The Pyloric Sphincteric Cylinder in Health and Disease

1 - Introduction

Mon, 01 Jan 0001 00:00:00 +0000

Introduction #

There has long been disagreement about various aspects of the structure and function of the "gatekeeper" (Greek pyloros, from pyle = gate and ouros = guard). In recent years the problem has often been mentioned in anatomy, physiology, gastroenterology, radiology and even in nuclear medicine. For instance, while referring to manometric and gastric emptying studies, Schuurkes and van Nuenten (1984) pointed out that there was considerable controversy as to whether a true pyloric sphincter existed in most species, and especially in man.

According to Reeve (1981) many functional aspects of sphincters are poorly understood; the exact mechanism of control of the transfer of chyme from stomach to duodenum through the pylorus is still not clear. Malagelada (1983) states that controversy surrounds the motor activity and function of the antroduodenal junction; there is disagreement as to whether the pylorus functions as a separate unit or as an integral part of the distal antrum. Ehrlein et al. (l984) reiterate that pyloric motility is poorly understood, and according to Funch-Jensen (l987) there are many unsolved questions. Malagelada (1990) states that the stomach performs multiple functions with a deceivingly simple anatomy; this is regarded as the key to the investigator's frustration when trying to uncover its secrets. One source of the many controversies surrounding the pylorus may be species differences, according to Schulze-Delrieu et al. (1984).

In view of the divergent and sometimes conflicting views expressed, the aim of the present investigation is to examine, firstly, certain aspects of the anatomy and physiology of the gastroduodenal junction and secondly, to try and elucidate some aspects of the more common pathological conditions affecting the region.

In their investigations Camilleri et al. (l985) stated that radionuclide and manometric emptying studies provided closely interrelated physiological studies and might be regarded as complementary diagnostic tools in the investigation of some of these problems. It is our submission that radiographic studies, provided they are integrated with other modes of investigation, may similarly be regarded as an important and complementary diagnostic tool. It is recognized that radiology has certain demerits. For instance, it is hardly possible to quantify gastric emptying radiologically; barium sulphate in suspension, although non-soluble, non-absorbable and non-toxic, may separate from solids and liquids, rendering radiographic emptying studies of little value.

On the other hand upper gastrointestinal radiography has certain advantages. For instance, it displays anatomic detail exquisitely (Velchik et al l989). One may add that the same holds true for movements of the stomach and duodenum; these are clearly observable and recordable under physiological conditions in the intact stomach as well as after pharmacological modification. The absence of intraluminal tubes eliminates the possibility that they may modify physiological contractions or prevent sphincters from closing properly. Also, in experimental motility studies it has not been determined, as far as we are aware, what effects gastrostomy or duodenostomy has on motility. In radiology this is not a complicating factor.

There is a tendency, especially in physiology, to dismiss radiological investigations as "purely visual observations." This sounds rather illogical, as observation, by the nature of things, is a visual impression. On the other hand it would not be unreasonable to question the interpretation of these visual observations.

According to Texter (l963) radiology has been so successful in the demonstration of pathological processes, that there has been a tendency to overlook its application as an investigative aid in the exploration of normal physiological forms of movement. Edwards and Rowlands (l968) pointed out that various methods had been applied to the study of antral and pyloric movements and the transport of contents, but that each had its own limitations and interfered in some way with the mechanism. No single method had given a clear, acceptable picture, although radiology kept the best perspective.

The present investigation originated in, and was conducted from, the Radiological Department. The image or action observed, was regarded as a fact; its interpretation might be open to question. At all times radiological findings were critically evaluated and, where possible, considered in conjunction with other findings.

The designation "barium meal" appears to be something of a misnomer, as it implies the swallowing of solids, while a liquid is in fact imbibed. In view of the important differences between gastric emptying of solids and liquids, the term was considered to be ambiguous and was avoided where possible.

In descriptions of cases the clinical features were either not discussed or kept to a minimum, as the aim of the investigation is the discussion of anatomical, physiological and radiological features and of the pathogenesis.

In background descriptions and reviews of the literature the method followed was to present quotations in chronological order so as to obtain an historical perspective. Quotations were not identified by superscript number but by authors' names and dates for ready identification and a brief historical overview.

A number of intriguing entities will be encountered, such as the fickle pylorus and the sphincteric paradox of Winans (l976) (Chap. 15), the errant or wandering antrum (Chap. 2), and the Janus-like sphincteric mechanism, looking backwards (into the stomach) as well as forwards (into the duodenum) (Chap. 3). An event horizon is described (Chap. 14), which is perhaps another way of saying "we don't know." In addition the vagaries of the vagus nerves described by Skandalakis et al. (l986) (Chap. 8) will have to be faced.

But first of all it is necessary to consider some uncertain and almost undefinable concepts, viz. the "pyloric antrum," "sphincters," and "peristalsis."

References #

Camilleri M, Malagelada JR, Brown ML, et al. Relation between antral motility and gastric emptying of solids and liquids in humans. Am J Physiol l985, 249 (Gastrointest Liver Physiol 12): G580-G585.
Edwards DAW, Rowlands EN. Physiology of the gastroduodenal junction. In: Handbook of Physiology, edit Code C.F. Sect 6, Vol 4. American Physiological Society, Washington l968, pp 1985-2000.
Ehrlein HJ, Keinke O, Schemann M. Studies on the process of gastric emptying. In: Gastrointestinal Motility, edit RomanÿC. MTP Press, Lancaster l984, pp 111-118.
Funch-Jensen P. Basal upper gastrointestinal motility in healthy people. Scand J Gastroenterol l987, 22 Suppl 128, 52-61.
Malagelada JR. Gastric, pancreatic and biliary responses to a meal. In: Physiology of the Gastrointestinal Tract, Vol 2, edit Johnson LR. Raven Press, New York l983, pp 893-924.
Malagelada JR. Where do we stand on gastric motility? Scand J Gastroenterol l990, 25 Suppl l75, 42-51.
Reeve DRE. Anatomy of the sphincters of the alimentary canal. In: Alimentary Sphincters and their Disorders, edit Thomas PA, Mann CV. MacMillan Publ, London l98l, pp 1-26.
Schulze-Delrieu K, Ehrlein HJ, Blum AL. Mechanics of the pylorus. In: Gastric and Gastroduodenal Motility, edit Akkermans LMA, Johnson AG, Read NW. Praeger Publ, New York l984, pp 87-102.
Schuurkes JAJ, van Nueten JM. Gastroduodenal co-ordination. In:Gastric and Gastroduodenal Motility, edit Akkermans LMA, Johnson AG, Read NW. Praeger Publ, New York l984, p 119.
Skandalakis LJ, Gray SW, Skandalakis JE. The history and surgical anatomy of the vagus nerve. Surg Gynaec Obstet l986, 162, 75-85.
Texter EC. Motility in the gastrointestinal tract. J Amer Med Assoc l963, 184, 640-647.
Velchik MG, Reynolds JC, Alavi A. The effect of meal energy content on gastric emptying. J Nucl Med l989, 30, 1106-1110.
Winans CS. The fickle pylorus (Editorial). Gastroenterology l976, 70, 622-623.

2 - Some Uncertain Concepts

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Some Uncertain Concepts #

1. The Pyloric Antrum #

Willis (l682) introduced the term "antrum pylori" (Greek antron = cave) to indicate the part of the stomach adjoining the pylorus; no further demarcation was given. Cunningham (1906) pointed out that the term was ambiguous and that it was rarely possible to obtain a clear anatomical conception of what it meant; it was largely responsible for much of the obscurity associated with the pyloric part of the stomach. Lewis (1912) also drew attention to the confusion caused by the term.

Forssell (1913) was totally opposed to the designation "antrum," as, in his view, it was vague and had no foundation in anatomical fact. Müller (l921) pointed out that the word was used in different senses; some authors used it to denote a small area close to the pylorus while others considered it to be the entire "transverse" stomach.

Cole et al. (l932) defined "antrum" as the portion of the stomach between the sulcus angularis and the pyloric valve; the fan-shaped muscle constituted a small portion of its distal end (Fig. 3.4). Golden (l937), on the other hand, used the term as a synonym for Forssell's canalis egestorius (i.e., the fan-shaped muscle) (Fig. 3.3).

While discussing a series of cases of gastric carcinoma, Coller et al. (l941) stated that in the majority the lesion was located either in the prepyloric region or in the pyloric antrum, from which it is concluded that these are different entities. In view of the ambiguities and lack of anatomical definition, Torgersen (l942) advocated abolition of the term "antrum."

Clarity is not forthcoming from the descriptions of Jenkinson (l955), who stated that the pyloric canal, approximately 3.0 cm in length, was located on the oral side of the "pyloric sphincter"; the antrum was said to be the region extending from the pyloric canal to the incisura angularis on the lesser curvature (Fig. 2.1). In another sentence the antrum was defined as the part of the stomach between the sulcus intermedius and the duodenum.

Fig. 2.1. Pyloric antrum according to Jenkinson. P.S., pyloric sphincter; P.C., pyloric canal; S.I., sulcus intermedius; I.A., incisura angularis. (In another sentence the antrum was said to be the region between the sulcus intermedius and the duodenum.)

Not only do anatomists disagree among themselves about the concept "antrum", but Foulk et al (l957) pointed out that gastric landmarks and boundaries differed in their details for the pathologist, the surgeon, the endoscopist and the radiologist. Grossman (l958) stated that many writers had commented on the lack of uniformity of terms and the ambiguity of some of them; according to him the pyloric portion was usually divided into the pyloric canal adjacent to the sphincter, and the pyloric vestibule or antrum adjacent to the corpus. He preferred to name functional divisions of the stomach in terms of their secretory characteristics; "pyloric gland area" was suggested for the mucus secreting, gastrin producing zone and "oxyntic gland area" for the acid producing region.

According to Edwards (l96l) it was widely accepted that the antrum represented the portion of the stomach distal to the incisura, which approximately defined the boundaries of the pyloric mucosal zone. Although some anatomists and clinicians adhered to this definition, du Plessis (l963), as a surgeon, was concerned with the fact that the pyloric mucosal zone was often larger than the anatomical antrum. Tanner (l964) pointed out that there was extreme variability in the extent of antral mucosa; if it were equated with the antrum, the boundaries of the latter would also be variable.

Moe et al. (l965) looked upon "antrum" as the pyloric mucosal zone. According to Capper et al (l966) the antrum was more of a physiologic concept than an anatomical one, and was best defined as the distal part of the stomach which contained and released gastrin; for antrectomy to be adequate, this zone had to be defined accurately and all of the gastrin-secreting mucosa had to be removed.

Carlson et al. (l966) and Code and Carlson (l968) defined the antrum as the region caudad to the incisura angularis. In terms of motor function it was divided into two segments of varying length (Fig. 2.2). The more caudad portion, called the terminal segment, participated in a simultaneous, segmental contraction called terminal antral contraction (TAC); the length of the segment was not fixed and its dimensions might change. The cephalad segment of the antrum was not involved in TAC but the two segments constituted a functional motor unit and contracted in a coordinated way.

Edwards and Rowlands (l968) again drew attention to the confusion in nomenclature; in their view the term "antrum" denoted the proximal part of the thickened muscle mass adjacent to the pylorus, and not the part of the stomach distal to the incisura angularis.

Fig. 2.2. Pyloric antrum according to Carlson et al. I.A., incisura angularis; T.A., terminal antrum

Fig. 2.3. Pyloric antrum according to Gray's Anatomy (American Edition). P.A., pyloric aperture; S.I., sulcus intermedius; P.V., pyloric vestibule; I.A., incisura angularis

Different definitions of the pyloric antrum were encountered in the American and British editions of an anatomical textbook, both published in the same year. In the 29th American edition of Gray's Anatomy of the Human Body (l973) the antrum was said to be located on the caudal side of the sulcus intermedius, the latter being 2.5cm from the aperture (Fig 2.3); the pyloric vestibule was said to be on the oral side of the sulcus, extending to the incisura angularis. It was also stated categorically that the antrum was much smaller than the pyloric mucosal zone. In the 35th British edition of Gray's Anatomy (l973) the antrum was said to be on the oral side of the sulcus intermedius (Fig 2.4).

Fig. 2.4. Pyloric antrum according to Gray's Anatomy (British Edition). P.A., pyloric aperture; S.I., sulcus intermedius

Strickland and Mackay (l973) again equated "antrum" with the pyloric mucosal zone. According to Spiro (l977) the antrum was too loosely defined, but was usually considered to be the portion of the stomach beyond the angulus. It differed from the remainder of the stomach in that its motor activity was greater, its mucosa was different (being the source of gastrin production) and it had an absence of mucosal folds (Comment: The angulus, seen endoscopically, corresponds to the incisura angularis. Radiology shows that mucosal folds are by no means absent in the normal living, distal stomach.)

Stave and Brandtzaeg (l978) considered the "distal" antrum to be the region extending proximally from the pylorus for a distance of 3.0 cm. Polak et al. (l977), Royston et al (l978) and Dockray (l978) equated "antrum" with the pyloric mucosal zone. According to Ito (l98l) the antrum is proximal to the pyloric canal. (Comment: Ito's pyloric canal would have been considered to be the terminal antrum by Stave and Brandtzaeg.) Szurszewski (l98l) defined the antrum by drawing an imaginary line from the incisura angularis to a point opposite it on the greater curvature; the region between the line and the gastroduodenal junction was looked upon as the antrum (Fig. 2.5). The muscular zone between the intermediate sphincter (sulcus intermedius) and the gastroduodenal junction formed the terminal antrum. Bolondi et al (l984) considered the antrum to be the region extending from the angulus to the pyloric aperture. The terminal antrum was described as the immediate prepyloric region by King et al (l984). Ganong (l985) again equated "antrum" with the gastrin secreting mucosal zone.

Fig. 2.5. Pyloric antrum according to Szurszewski. P.A., pyloric aperture; S.I., sulcus intermedius; I.A., incisura angularis; T.A., terminal antrum

According to K.L. Moore (l985) the pyloric part of the stomach consists of a narrow portion 1.0 to 2.0 cm long, which is continuous with the pylorus and called the pyloric canal, and a wider pyloric antrum on the oral side of the canal.

J.G. Moore et al (l986) described a midgastric transverse band in humans, which, in their view, represented an anatomic separation between the gastric reservoir (the fornix and corpus) and the antrum; the entire region between the transverse band and pylorus was considered to be the antrum. Collins et al. (1991) ascribed an important role to the transverse band in differential emptying of solids and liquids; it appeared to be responsible for the initial retention of solids. (It appears if the transverse band may correspond to the musculus sphincter antri, i.e. a loop at the termination of the oblique fibres of the muscularis externa, described by Torgersen in l942. It was also called the lower segmental loop and formed the oral boundary of the sinus.)

Discussion #

One has to agree with Cunningham (1906), Forssell (1913) and Torgersen (1942) that the term "antrum" has been used in many different senses, that it is ambiguous and responsible for much of the obscurity associated with the pyloric part of the stomach. For instance, a number of authors equated "antrum" with the pyloric mucosal zone (Moe et al 1965; Strickland and Mackay 1973; Polak et al. 1977; Ryston et al. 1978; Dockray 1978; Ganong 1985), yet it has been shown that this zone is not constant and may migrate up and down the stomach in cases of gastric and duodenal ulceration (Chap. 5). Tanner (1964) mentioned the "extreme variability" in the extent of pyloric mucosa. In anatomy again, it has been stated categorically that the antrum is much smaller than the pyloric mucosal zone (Gray 1973).

Numerous other examples of conflicting views have been quoted above. It seems that the antrum may be errant or wandering in more ways than one, and that for this reason it is a designation which is best avoided.

References #

Bolondi L, Bortolotti M, Santi V, et al. Measurement of gastric emptying time by real-time ultrasonography. Gastroenterology l985, 90, 752-759.
Capper WM, Butler TJ, Buckler KG, et al. Variation in size of the gastric antrum: measurement of alkaline area associated with ulceration and pyloric stenosis. Ann Surg l966, 163, 281-290.
Carlson HC, Code CF, Nelson RA. Motor action of the canine gastroduodenal junction: a cineradiographic, pressure and electrical study. Amer J Dig Dis l966, ll, 155- 172.
Code CF, Carlson HC. Motor activity of the stomach. In: Handbook of Physiology Sect 6: Alimentary Canal, Vol 4: Motility. Amer Physiol Soc, Washington DC l968, pp 1903-1916.
Cole LG and Collaborators. Important anatomical data of the digestive tract. Radiology l932, l8, 471-520.
Coller FA, Kay EB, McIntyre RS. Regional lymphatic metastases of carcinoma of the stomach. Arch Surg l941, 43, 748-761.
Collins PJ, Houghton LA, Read NW, et al. Role of the proximal and distal stomach in mixed solid and liquid meal emptying. Gut 1991, 32, 615-619.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
Dockray GJ. Gastrin overview. In: Gut Hormones, edit Bloom SR, Grossman MI, Churchill Livingstone, London l978, pp 129-139.
Du Plessis DJ. The importance of the pyloric antrum in peptic ulceration. South Afr J Surg l963, 1, 3-11.
Edwards D. Some radiological aspects of pyloric disease. Proc Roy Soc Med l96l, 54, 933-937.
Edwards DAW, Rowlands EN. Physiology of the gastroduodenal junction. In: Handbook of Physiology Sect 6: Alimentary Canal Vol 4: Motility. Amer Physiol Soc, Washington DC l968, l985-2000.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr l9l3, Suppl 30, 1-265.
Foulk WT, Comfort MW, Butt HR, et al. Peptic ulcer near the pylorus. Gastroenterology l957, 32, 395-403.
Ganong WF. Review of Medical Physiology. Lange Medical Publications, Los Altos l985, 12th Edit, p 401.
Golden R. Antral gastritis and spasm. J Amer Med Assoc l937, 109, 1497-1500.
Gray H. Anatomy of the Human Body. 29th American Edition, ed Goss CM. Lea and Febiger, Philadelphia l973, p 1220.
Gray H. Gray's Anatomy. 35th British Edition, ed Warwick R, Williams PH. Longman Co, Edinburgh l973, p 1273.
Grossman MI. The names of the parts of the stomach. Gastroenterology l958, 34, 1159-1162.
Ham AW. Histology. JB Lippincott Co, Philadelphia l969, 7th edit, p 655.
Ito S. Functional gastric morphology. In: Physiology of the Gastrointestinal Tract. Ed Johnson LR, Raven Press, New York l98l, Vol 1, pp 517-550.
Jenkinson EL. The pyloric antrum of the stomach. Amer J Roentgen Rad Ther l955, 73, 905-937.
King PM, Adam RD, Pryde A, et al. Relationships of human antroduodenal motility and transpyloric fluid movement: non-invasive observations with real-time ultrasound. Gut l984, 25, 1384-1391.
Lewis FT. The form of the stomach in human embryos with notes upon the nomenclature of the stomach. Amer J Anat l9l2, 13, 477-503.
Moe RE, Klopper PJ, Nyhus LM. Demonstration of the functional anatomy of the canine gastric antrum. Amer J Surg l965, 110, 277-285.
Moore KL. Clinically Oriented Anatomy. Williams and Wilkins Publ, Baltimore 2nd ed, 1985.
Moore JG, Dubois A, Christian PE, et al. Evidence for a midgastric transverse band in humans. Gastroenterology 1986, 91, 540-545.
M�ller E. Anatomischen und r�ntgenologischen Untersuchungen über Form, Bau und Lage des Magens. Erg Anat l921, 23, 310. Quoted by Torgersen (l942).
Polak JM, Sullivan SN, Bloom SR, et al. Enkephalin-like immunoreactivity in the human gastrointestinal tract. Lancet l977, l, 972-974.
Royston CMS, Polak J, Bloom SR, et al. G cell population of the gastric antrum, plasma gastrin, and gastric acid secretion in patients with and without duodenal ulcer. Gut l978, l9, 689-698.
Spiro HM. Clinical Gastroenterology. Macmillan Publ, New York l977, 2nd ed, p 148.
Stave R, Brandtzaeg P. Immunohistochemical investigation of gastrin producing cells (G cells). Scand J Gastroent l978, 13, 199-203.
Strickland RG, Mackay IR. A reappraisal of the nature and significance of chronic atrophic gastritis. Amer J Dig Dis l973, 18, 426-440.
Szurszewski JH. Electrical basis for gastrointestinal motility. In: Physiology of the Gastrointestinal Tract. Ed Johnson LR, Raven Press, New York l98l, Vol 2, pp 1435- 1466.
Tanner NC. The surgical treatment of peptic ulcer. Brit J Surg l964, 51, 5-23.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, l-191.
Willis T. Opera omnia. Amstelaedami l682. Quoted by Cunningham (1906).

2 What is a Sphincter? #

The definition of sphincter (Greek sphinkter = that which binds tight, binder) remains elusive. Williams (l962) pointed out that early anatomists and surgeons saw and felt a narrow powerful band of muscle enclosing the distal end of the stomach and concluded that it was a sphincter controlling the width of the lumen; later observers thought the sphincter could be part of the circular musculature of the pyloric canal, constituting an inherent part of the gastroduodenal pump. He called the pyloric sphincter a muscularis propria ring, consisting mainly of circular but also containing some longitudinal fibres, which surrounds the pyloric aperture; it narrows the distal end of the stomach to the point at which the lumen can be occluded by a mucosal plug. The sphincter also takes part in pump-like contractions of the fan-shaped muscle to close the pyloric canal.

3 - The Walls of the Stomach and Duodenum

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The Walls of the Stomach and Duodenum #

At upper abdominal operations, with the organs in situ, a slight groove may be seen in the glistening serosal surface at the gastroduodenal junction. In the groove a small, superficial subserosal vein, lying vertically across the front of the gut, may be evident; this is the prepyloric vein, draining into the right gastric vein (Chap. 7). The groove and the prepyloric vein indicate the position of the pyloric ring. At palpation a sudden transition is felt at the ring between the thick walls of the pyloric region and the thin walls of the duodenum.

The wall of the pyloric part of the stomach and of the proximal 2.0 to 3.0 cm of the duodenum is composed of four coats. From without inwards these are the serous, muscular, submucous and mucous coats. The mucous coat is separated from the luminal contents by a layer of gastric mucus.

4 - The Submucous Coat

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The Submucous Coat #

The submucous coat is a layer of strong but loose areolar tissue with some elastic fibres, lying between the muscularis mucosae and the muscularis externa; it is rich in mast cells, macrophages, lymphocytes, eosinophilic leucocytes and plasma cells. It forms a bed in which the vessels and nerves break up before entering the mucous membrane; consequently it contains arteries, veins, lymphatics and Meissner's nerve plexuses. The plexuses form part of the autonomic nervous system and contain postganglionic sympathetic fibres as well as pre- and postglanglionic parasympathetic fibres. The nerve cells are all parasympathetic.

Stomach

In the stomach the submucous layer does not contain any glands. It is wider than that of the duodenum and extends into the rugae of the stomach, forming the core of each "mucosal" fold. A gastric mucosal fold, in other words, consists of a central core of submucous tissue (constituting the major part of the fold), with a layer of mucosa on each surface.

During injection of the submucous lymphatic plexus of the pyloric region, Jamieson and Dobson (1907) found that fluid ran most readily in an orad direction; however, it also filled a plexus on the orad side of the pyloric ring, and spread into the duodenal plexus. This was ascribed to well-marked continuity of the gastric and duodenal submucous lymphatic plexuses. The findings differ from those of Horton (l928, l931) who investigated the spread of India ink injected into the submucous layer of the pyloric part of the stomach. While it spread out in all directions from the needle point, it was halted at the pyloric ring, none passing into the submucosa of the duodenum. To Horton (l928, l931) this indicated a complete block between the submucous coat of the stomach and that of the duodenum.

Williams (l962) examined aspects of the mucosa and submucosa of the pyloro-duodenal junction in 48 fresh post-operative partial gastrectomy specimens. The gastric submucosa contained loosely knit connective tissue and was found to be considerably wider than that of the duodenum. The muscularis mucosae on the gastric side was clearly visible as a thin, continuous band closely applied to the mucosa, thickening as it approached the pylorus. At the pyloric ring it split up, sending fibres into the mucosa, and finally petering out in a washer-like band of fibrous tissue applied to the muscular ring; in this way the mucosa was firmly bound to the muscle. Injection of India ink into the submucosal layer of the stomach showed that its flow was halted abruptly at the pylorus, none passing into the submucosa of the duodenum; the band of fibrous tissue was the point at which the flow stopped. This point was situated either at the apex of the pyloric muscular ring, or on the duodenal or gastric aspect of the ring. According to Williams (l962) these findings as well as those of Horton (l928, l931) confirmed the fact that the gastric mucosa was firmly bound to the muscle at the "sphincter", and that there was no direct communication between the submucosal compartments of the stomach and the duodenum. (Comment: the sphincter was equated with the pyloric ring).

Duodenum #

The submucous coat of the duodenum is appreciably narrower than that of the stomach; it also differs from the gastric submucosa in that it contains glands, viz. the duodenal glands of Brunner. (Comment: As a possible link between Brunner's glands and transpyloric extension of gastric carcinoma cannot be excluded, as described in Chapter 33, they will be discussed in some detail). Vasoactive intestinal peptide (VIP), substance P and met-enkephalin immunoreactive neuronal elements are present in the duodenal submucosa (vide infra).

Brunner's glands are small acino-tubular glands in the submucosa of the duodenum. Their deep, secretory portions consist of branched and coiled tubules which extend to the circular muscularis externa. Their ducts pierce the muscularis mucosae to open on the luminal surface of the mucosa, in the depths of the crypts between the intestinal glands. Brunner's glands are composed of tall cuboidal cells with dark basal nuclei and a clear cytoplasm, their glandular portions extending into the ducts.

In the majority of subjects they commence at the pyloro-duodenal junction and are most numerous in the first part of the duodenum, gradually decreasing in number toward the third and fourth parts. Occasionally they extend into the upper part of the jejunum; in exceptional cases some Brunner's glands may be present in the pyloric sphincteric cylinder. Horton (l928) examined 84 anatomical specimens and found that they commenced abruptly at the distal portion of the pyloric "sphincter" in all subjects except one; in this single instance they extended for a distance of 8.0 mm across the "sphincter" into the stomach.

Landboe-Christensen (l944) examined the proximal delimitation of the Brunner gland area in 53 anatomical specimens of various age groups. It was found that the border might lie: (1) on the duodenal steep, i.e. the almost perpendicular duodenal side of the pyloric ring, (2) at the top of the ring itself and (3) on the sloping gastric side of the ring. The border between Brunner's glands and pyloric mucosa might run in a regular circle, might be wavy or dentate, or might present one or more tongues or linear extensions. The border might be sharp but in some cases there was a narrow transitional zone, usually on the duodenal side of the ring. Occasionally scattered or solitary islets of Brunner's glands were seen in the pyloric mucosa. In the age group of 25 years and under, the border was on the duodenal side of the ring in half the cases; as age advanced, the border tended to spread on to the pyloric ring and in subjects over 50 years of age the pyloric ring was crossed by Brunner islets in up to four-fifths of the cases. The border also tended to become less sharp with advancing age.

Brunner's glands produce a mucous secretion which forms a protective lining on the duodenal mucosa, preventing epithelial damage by chemical or mechanical trauma (Florey and Harding l934; Griffith and Harkins l956). The mucin secreted has a high bicarbonate content, rendering it alkaline and affording further protection against acid gastric chyme (Griffith and Harkins l956). However, it is possible that the alkaline secretion in the duodenum originates from the surface epithelium and not from Brunner's glands (Flemstr�m and Garner l984). In man Brunner's glands have been shown to contain and secrete epidermal growth factor (EGF) (Elder et al. l978; Heitz et al. l978), a peptide comprising 53 amino acids (Gregory l975). EGF is also produced in the submandibular salivary glands (Hollenberg l979). Mouse EGF is chemically similar to human urogastrone, a polypeptide prepared from urine (Elder et al. l978). Mouse EGF and human urogastrone are closely related structures and seem to be identical in biologic activity; physical data on human EGF suggest that the material is urogastrone (Elder et al. l978).

Both polypeptides have a number of biologic effects in common, including inhibition of gastric acid secretion and a cytoprotective effect on the gastroduodenal mucosa. Intraduodenal as well as intragastric instillation of EGF prevents the development of experimental duodenal and gastric ulcers in the rat (Kirkegaard et al l983). Both substances are powerful mitogens, causing epithelial proliferation and keratinization of squamous epithelial cells in tissue cultures (Elder et al. l978). Experimental intragastric installation of EGF increases the synthesis and contents of DNA and RNA in the gastroduodenal mucosa (Dembinski et al. l982). It was suggested that EGF and urogastrone might have a role in the control of gastric secretion as well as in mucosal growth and the known rapid turnover of cells lining the gut (Elder et al. l978).

By means of immunohistochemical studies in the rat Kirkegaard et al (l98l) demonstrated a dense network of vasoactive intestinal polypeptide (VIP) immunoreactive nerve fibres around the acini of Brunner's glands as well as small ganglia with VIP immunoreactive nerve-cell bodies close to the glands. Intravenous infusions of VIP increased bicarbonate, protein and mucin output from the Brunner's glands, and it was suggested that physiological secretion from these glands might be stimulated by the VIP nerves. Ferri et al. (l984) studied the innervation of Brunner's glands in humans in specimens obtained during gastrectomy for gastric or extragastric carcinoma. In the duodenal submucosa numerous VIP and substance P nerve fibres were noted in the ganglia of Meissner's plexus and in the internodal strands. VIP immunostaining also revealed a rich supply of fibres at the periphery of Brunner's glands, but only a few of these were seen to enter the glands and reach the acinar cells. Nerve bundles immunostained for met- enkephalin ran in the internodal strands of the duodenal submucosa and formed dense networks in occasional ganglia. The study showed that in cases of gastric carcinoma in man, the Brunner's glands did not have the rich supply of VIP containing nerves as was the case in rats.

Immunohistochemical studies in the rat showed that as in man, EGF was almost exclusively present in the secretory cells of Brunner's glands (Kirkegaard et al. l984). It was shown that VIP stimulated secretion of EGF and bicarbonate from Brunner's glands, an effect which was inhibited by somatostatin. According to Kirkegaard et al. (l984) the mechanism controlling Brunner's gland secretion was complex and not fully elucidated. The autonomic nervous system, local factors and a hormonal mechanism were probably all involved.

According to Skov Olsen et al. (l985) evidence has accumulated to show that cholinergic, adrenergic and VIP-containing nerves innervate and thereby influence the secretion from Brunner's glands. They confirmed the presence of VIP containing nerves in these glands in the rat. The influence of the sympathetic nervous system and adrenergic agonists on basal and VIP stimulated flow rate and secretion of EGF from Brunner's glands was studied. It was confirmed that the sympathetic nervous system had an inhibitory effect on Brunner's gland secretion. Chemical sympathectomy increased the flow rate and output of EGF (but depleted the glands of EGF) whereas the alpha-adrenergic agonist noradrenaline inhibited the secretion. VIP was found to increase Brunner's gland secretion and total output of EGF; VIP probably also increased the synthesis of EGF.

Fuse et al. (l990) determined the thickness of Brunner's glands in surgically resected duodenal ulcer specimens and normal controls. The maximum mean thickness in controls was l.54 � 0.38 mm; in duodenal ulceration it varied widely from 0.5 to 5.0 mm. In most duodenal ulcer cases the glands were thickest within 1.0 cm of the centre of the ulcer; in a small minority of cases of duodenal ulceration the layer of Brunner's glands remained diffusely thin. It was concluded that Brunner's glands became hyperplastic in duodenal ulceration, especially near the ulcer; this was probably a defense mechanism against acid and peptic digestion. In cases of healed duodenal ulceration Brunner's glands were thin at the centre of the scar; this histological finding corresponded to the depressed, scarred area observed endoscopically, and suggested decreased mucosal resistance.

Discussion #

The fact that the submucosa of the first part of the duodenum is much narrower than that of the stomach, and that it contains multiple Brunner's glands which pierce the muscularis mucosae (thus virtually attaching the mucosa to the muscular layer), means that its inherent ability to move is much less than that of the submucosa of the pyloric sphincteric cylinder. This may be of some importance in transpyloric prolapse of gastric mucosa (Chap. 38). It probably also accounts for the fact that normally duodenal mucosal folds are smaller, and less mobile, than mucosal folds of the pyloric sphincteric cylinder.

Brunner's glands have been shown to become hyperplastic in duodenal ulceration; this was considered to be a defense mechanism against digestion by acid gastric juice.

In a few cases of pyloric adenocarcinoma, where extension into the duodenum had occurred, we have noted that Brunner's glands were not infiltrated (Chap. 33). The question arises whether this signifies that Brunner's glands, by virtue of their secretions or some other mechanism, act as a biological or anatomical barrier preventing further spread of gastric carcinoma down the duodenum; this aspect will be discussed in more detail in Chapter 33.

References #

Dembinski A, Gregory H, Konturek SJ, et al. Trophic action of epidermal growth factor on the pancreas and gastroduodenal mucosa in rats. J Physiol l982, 325, 35-42.
Elder JB, Williams G, Lacey E, et al. Cellular localization of human urogastrone - epidermal growth factor. Nature l978, 271, 466-467.
Ferri GL, Botti P, Biliotti G, et al. VIP, substance P and metenkaphalin immunoreactive innervation of the human gastrodudodenal mucosa and Brunner's glands. Gut l984, 25, 948-952.
Flemström G, Garner A. Some characteristics of duodenal epithelium. In: Mucus and Mucosa. Pitman, London l984. Ciba Foundation Symposium 109, 94-108.
Florey HW, Harding HE. Further observations on the secretion of Brunner's glands. J Path Bact l934, 39, 255-276.
Fuse Y, Tsuchihashi Y, Takamasu M, et al. Thickness of Brunner's glands and its clinical significance in duodenal ulcer disease. Scand J Gastroenterol l990, 25, 165-172.
Gregory H. Isolation and structure of urogastrone and its relationship to epidermal growth factor. Nature l975, 257, 325-327.
Griffith CA, Harkins HN. The role of Brunner's glands in the intrinsic resistance of the duodenum to acid-pepsin digestion. Ann Surg l956, 243, 160-172.
Heitz PU, Kasper M, Van Noorden S, et al. Immunohistochemical localization of urogastrone to human duodenal and submandibular glands. Gut 1978, 19, 408-413.
Hollenberg MD. Epidermal growth factor - urogastrone, a polypeptide acquiring hormonal status. Vitam Horm l979, 37, 69-110.
Horton BT. Pyloric musculature, with special reference to pyloric block. Amer J Anat l928, 41, 197-225.
Horton BT. Pyloric block with special reference to the musculature, myenteric plexus and lymphatic vessels. Arch Surg l931, 22, 438-462.
Jamieson JK, Dobson JF. The lymphatic system of the stomach. Lancet l907, 1, 1061-1066.
Kirkegaard P, Lundberg JM, Poulsen SS, et al. Vasoactive intestinal peptidergic nerves and Brunner's gland secretion in the rat. Gastroenterology l98l, 8l, 872-878.
Kirkegaard P, Skov Olsen P, Poulsen SS, et al. Epidermal growth factor inhibits cystamine induced duodenal ulcers. Gastroenterology l983, 85, 1277-1283.
Kirkegaard P, Skov Olsen P, Poulsen SS, et al. Exocrine secretion of epidermal growth factor from Brunner's glands: stimulation by VIP and acetylcholine. Regulatory Peptides l983, 7, 367-372.
Kirkegaard P, Olsen PS, Nexo E, et al. Effect of vasoactive intestinal polypeptide and somatostatin on secretion of epidermal growth factor and bicarbonate from Brunner's glands. Gut l984, 25, 1225-1229.
Landboe-Christensen E. The duodenal glands of Brunner in man: their distribution and quantity. Acta Path Microbiol Scand l944, Suppl 52, ll-267.
Skov Olsen P, Poulsen SS, Kirkegaard P. Adrenergic effects on secretion of epidermal growth factor from Brunner's glands. Gut l985, 26, 920-927.
Williams I. Closure of the pylorus. Brit J Rad l962, 35, 653-670.

5 - The Mucous Membrane or Mucosa

Mon, 01 Jan 0001 00:00:00 +0000

The Mucous Membrane or Mucosa #

The mucous membrane of the stomach and first part of the duodenum consists of 3 layers; an outermost muscularis mucosae, a middle lamina propria and an innermost glandular epithelial lining, bordering the lumen.

Stomach #

Muscularis Mucosae #

The muscularis mucosae, a thin layer of smooth muscle, forms the border between the mucosa and submucosa. It consists of outer longitudinal and inner circular fibres; from the inner layer strands of smooth muscle cells extend through the lamina propria toward the luminal surface between the gastric glands. It is surmized that contraction of these strands may compress the glands, thereby facilitating their emptying (Bloom and Fawcett l975).

Lamina Propria #

The lamina propria occupies the narrow region between the muscularis mucosae and the surface epithelial cells with their glands. It extends into the area between the necks of the glands and forms a basement membrane on which the epithelial cells rest. There is little lamina propria in the fornix and body, where the gastric glands are numerous and closely packed; it is more prominent in the cardiac and pyloric zones (Ito l967).

The lamina propria consists of a delicate network of collagenous and reticular fibres and a few fibroblasts or reticular cells. The meshes of the network contain plasma cells, mast cells, eosinophilic leucocytes and lymphocytes. Local accumulations of lymphocytes may occur in the cardiac and pyloric regions. Strands of smooth muscle traverse this layer, which also contains fine capillaries, lymphatic vessels and nerve fibres.

Epithelial Lining #

The entire luminal surface of the mucosa is covered by a layer of simple columnar cells, called the surface mucus cells. Numerous tubular invaginations of the surface, the gastric pits or foveolae, are lined by the same type of cell (Ito l967). In the pyloric region the pits are deeper than in the remainder of the stomach, extending at least halfway to the muscularis mucosae. They are V-shaped, tapering off into the glands that open into them (Bevelander and Ramaley l979).

The mucus-secreting columnar cells lining the luminal surface and the pits are joined near their free surfaces to each other by tight junctions (Ham l974). It is surmized that this arrangement forms one of the mechanisms by which the underlying layers are protected against luminal acid. The supranuclear portions of the cells just below their free surfaces contain dense, homogeneous, spherical or ovoid granules consisting of a type of mucigen (Bloom and Fawcett l975). Upon release into the lumen, the granules give rise to the layer of mucus that covers the luminal surface of the mucosa. In the cells of the gastric pits, the granules become progressively less abundant at deeper levels, and in the bottom of the pits they from only a thin layer immediately beneath the cell surface. Cells of this kind continue into the necks of the gastric glands. Under physiological conditions, the surface mucus cells are continuously desquamated into the lumen and are completely replaced every 3 days (Ham l974; Bloom and Fawcett l975). Newly formed cells appear in the deeper parts of the foveolae and in the necks of the glands; these are slowly displaced upward and continually replace those lost on the surface.

Three Mucosal Zones #

The entire thickness of the mucous membrane in all parts of the stomach is occupied by a multitude of glands which open into the bottom of the gastric pits. The blind ends of the glands extending into the mucosa are slightly expanded and coiled, sometimes dividing into 2 or 3 branches. On the basis of the cell population in the glands, the gastric mucosal coat is differentiated into 3 zones:

Cardiac Zone #

This zone consists of a narrow, ring-shaped area around the gastro-oesophageal junction, containing the cardiac glands. These glands have wide lumina and shallow pits and are composed overwhelmingly of mucus-secreting cells. They may contain a few neuroendocrine cells, also called APUD cells on account of their capacity to synthesize monoamines through a process of Amine Precursor Uptake and Decarboxylation (vide infra). In the transitional area, where this zone is continuous with the second or oxyntic zone, a few parietal cells may be present. The glands of the cardiac zone secrete mucus and very little, if any, enzymes.

Oxyntic Zone #

This zone comprises the greater part of the fornix and corpus, i.e. the proximal two-thirds or more of the stomach. The glands are variously known as fundic glands, proper gastric glands or principal gastric glands. As one of their most important properties is the secretion of gastric acid, Grossman (l958) suggested the term "oxyntic" (Greek: acid- forming) as an appropriate indicator of this glandular zone. The mucosa here is much deeper than in the cardiac zone and contains a greater number of glands. The pits are shallow and the glands extending from the bottoms of the pits are 2 to 3 times as long as the pits are deep.

Each principal gastric gland is composed of 4 kinds of cells (Bevelander and Ramaley l979):

Chief, zymogenic or peptic cells. These are situated mostly in the deeper parts of the glands. They exhibit secretory granules containing the precursors of pepsin.
Parietal or oxyntic cells. These are most numerous in the necks of the glands. They do not border directly on the lumen, but are crowded away from it by peptic cells. Each cell is roughly triangular in shape, with the apex projecting towards the lumen between the sides of two peptic cells that border it. These cells are intensely acidophilic, contain the gastric proton pump mechanism, and produce the antecedent of hydrochloric acid; they are also believed to elaborate intrinsic factor. The secretion of oxyntic cells must pass between adjacent peptic cells that almost cover them, to reach the lumen.
Neck mucous cells. These cells resemble the mucous cells of the cardiac and pyloric zones. They are relatively few in number and are lodged between the parietal cells in the necks of the glands; they are smaller than the surface mucous cells and their mucigen granules are larger and less dense than those of the surface cells (Bevelander and Ramaley l979). The secreted mucus is somewhat different from that secreted by the surface mucous cells (Leeson l976).
Neuroendocrine or APUD cells. These small, granulated cells occur singly in the epithelium of the gastric mucosa (Bloom and Fawcett l975). They are scattered between the peptic cells and are few in number. It is accepted that some of these cells are the site of synthesis and storage of serotonin (5-hydroxytryptamine). Cells of the APUD line are much more numerous in the pyloric mucosal zone and will be described separately (Chap. 9).

The glands of the oxyntic zone produce nearly all the enzymes and hydrochloric acid secreted in the stomach; they also produce some of the mucus.

Pyloric Zone #

This zone comprises roughly the distal third of the stomach. Normally it extends further along the lesser curvature than the greater, but its boundaries may vary (vide infra). The pits are deeper in this zone than elsewhere in the stomach, extending into the mucous membrane for half its thickness. The glands are also of a simple, branched tubular type, but they branch more extensively and the tubules are coiled.

The glands contain the following types of cells:

Mucous cells resembling the neck mucous cells of the oxyntic glands. These large, mucus-secreting cells constitute the overwhelming number of cells in the pyloric glands. They have a pale cytoplasm containing indistinct granules, the nucleus is often flattened against the base of a cell, and short microvilli covered by a layer of mucus, are present on the luminal surface.
Parietal cells. A few isolated parietal cells may be present among the mucous cells (Ito l967). Parietal cells also occur in the transitional region between the pyloric and oxyntic zones (Bevelander and Ramaley l979).
Neuroendocrine or APUD cells. These cells are much more numerous in the pyloric than in the cardiac and oxyntic zones; when compared with the mucous cells they are still relatively few in number. With light microscopy they have been called enterochromaffin cells. With electron microscopy their cytoplasmic granules are clearly visible after staining with chromium or silver salts. On the basis of their staining reactions, the cells have been divided into two types, viz. argentaffin cells, in which the granules reduce silver without pretreatment, and argyrophilic cells, in which a reducing substance is required before the granules will react with silver (Bloom and Fawcett l975) (Chap. 9).

The glands of the pyloric mucosal zone do not produce enzymes, but secrete mucus; this zone is also an important producer of endocrine, paracrine or neurocrine regulatory peptides by virtue of the APUD cells contained in its glands (Chap 9).

Anatomical Extent and Boundaries of the Pyloric Mucosal Zone #

The various mucosal zones of the stomach are not sharply delimited, and along the borderlines the glands of one region mingle with those of the adjoining region; intermediate glands may be present between the pyloric and body (i.e. oxyntic) mucosal zones (Bloom and Fawcett l975).

The extent of the pyloric mucosal zone, and its boundaries on the oral and aboral sides, may be determined by microscopic, macroscopic, surgical and other methods. The microscopic identification of the pyloric mucosa in morbid anatomical specimens is probably the most accurate method of determining the boundaries of this zone. For instance, it has been stated in histology that the pyloric mucosal zone usually comprises the distal 4-5cm of the stomach, and that it extends farther along the lesser curvature than the greater (Bloom and Fawcett 1975).

Border on Aboral Side

Using macroscopic techniques in 53 fresh, non-diseased post-mortem specimens, Landboe-Christensen (l944) found that the border between pyloric and duodenal mucosa might lie either on the perpendicular, duodenal side of the pyloric ring, at the top of the ring, or on the sloping gastric side of the ring. With ageing there was a tendency for the border to shift from the duodenal to the gastric side of the ring.

Using microscopic methods in 110 cases of partial gastrectomy for duodenal ulcer, Oi and Sakurai (l959) came to essentially similar conclusions. In all specimens the border was within 5.0 mm of the summit of the pyloric "sphincter muscle" (presumably the pyloric ring), either on the duodenal or on the gastric side. The pyloric mucosa was in direct contact with the duodenal mucosa, i.e. the border could be identified as a line, in contrast to the border between pyloric and oxyntic mucosa, which consisted of a transitional zone of varying width.

Border on Oral Side

Landboe-Christensen (l944) studied the extent of the pyloric mucosal zone on the oral side by macroscopic tehcniques in 47 non-diseased, fresh post-mortem specimens. In all instances this zone was longer on the lesser than on the greater curvature, covering on average 7.2 cm of the lesser, and 5.2 cm of the greater curvature. The average percentage of the lesser curvature covered was 44 percent, and the average percentage of the greater curvature covered was 12 percent. The border between pyloric and oxyntic mucosa was irregular, often dentate or tortuous, and as a rule a number of islets of oxyntic mucosa were encountered in the pyloric zone. There was a transitional area of varying width between the two zones. In practice, a line drawn from the junction of the upper three- fifths and lower two-fifths of the lesser curvature, running downwards and to the right, indicates the approximate boundary of pyloric mucosa (Fig. 5.1).

Dean and Mason (l964) studied 117 fresh gastric resection specimens microscopically (resected for either duodenal or gastric ulcer). In l8 cases of duodenal ulcer the average length of pyloric mucosa along the lesser curvature was 9.0cm, and along the greater curvature 7.4 cm. On an average the pyloric mucosa extended for l.5cm further up the lesser than the greater curvature. In the majority of all duodenal ulcer specimens the transitional zone between pyloric and oxyntic mucosa varied from 0.5 to 5.0 cm in width, the average width being 1.0cm. The upper limit of the pyloric mucosa showed wide individual variations. Patients with gastric ulcers tended to have a greater extent of pyloric mucosa than those with duodenal ulcers, and women with gastric ulcers had more pyloric mucosa than men with gastric ulcers.

Fig. 5.1. Relationship between pyloric sphincteric cylinder and pyloric mucosal zone in normal stomach. Arrows, contracted sphincteric cylinder; broken line, approximate border between pyloric and oxyntic mucosal zones.

Schrager et al. (l967) studied the "antrum" microscopically in 45 normal stomachs obtained at necropsy, in 75 resection specimens of duodenal ulcer and in 40 specimens of gastric ulcer. Normal stomachs showing clear histology were not easily obtained due to the speed with which autolysis occurs after death; in only 13 could measurements be made. Normally the average length of pyloric mucosa between the "sphincter" (i.e. the pyloric ring) and the boundary zone on the lesser curvature was 8.9 cm, with an average "sphincter" to cardia distance of 22.5 cm. Thus the pyloric zone encompassed 40 percent of the lesser curvature. On the greater curvature the average figures were 4.8 cm, 39 cm and 12 percent respectively. Comparative studies showed that in the majority of duodenal ulcer patients the pyloric zone was larger than in normal controls, and in the majority of gastric ulcer cases it was almost twice the normal size.

In surgical pH monitoring tests, Capper et al. (l962, l966) found a wide variation in size between the small pyloric zone of duodenal ulcer and the larger zone of gastric ulcer cases. With duodenal ulceration the zone was usually of normal size or smaller, extending to a line 3.0 to 4.0 cm from the pylorus. (In their only normal subject, the pyloric zone was 4.0 to 5.0 cm in length.) In gastric ulcer cases the pyloric zone was very much larger, at times encompassing the whole of the lesser curvature. Capper et al. concluded that the junction between the distal alkaline, pyloric zone and the proximal oxyntic zone was not static, but that it might migrate up and down the stomach. The alkaline zone could have been a normal "antrum", but it could also have represented oxyntic mucosa which had been altered by gastritis. Royston et al. (l978) found in patients with duodenal ulcer, that the mean area of the "antrum", as defined histologically, was double the mean antral area defined as the alkaline zone in the pH studies of Capper et al. (l962, l966).

The test of Moe et al (l965, l966) was based on the differential excretion of dyestuffs from the gastric corpus and the "antrum" in dogs. The mean area of the "antrum" was found to occupy 20 percent of the total gastric area, with a range of 10 to 30 percent. A modification of the test was used by Hedenstedt et al (l967) in humans, the results being controlled histologically. On the whole, the pyloric zone was found to be larger than that determined by Moe's test. In all cases the extent of pyloric mucosa was greater on the lesser than on the greater curvature. Amdrup et al (l972) used the congo red test for a precise determination of the "antrum" prior to antrectomy for gastric ulcers. In their experience the "antrum" in gastric ulcer cases was often larger than in duodenal ulcer cases, sometimes extending high up on the lesser curvature and occasionally as far as the cardia.

Duodenum #

The duodenal mucous membrane also consists of 3 layers, but these differ from those of the stomach in several respects.

6 - Electrical Potential Difference at the Gastroduodenal Mucosal Junction

Mon, 01 Jan 0001 00:00:00 +0000

Electrical Potential Difference at the Gastroduodenal Mucosal Junction #

It has long been known that the mucosal surface of the upper gastrointestinal tract is electrically negative with respect to serosa, skin and blood. The size of the electrical potential difference (PD), measured in millivolts (mv), is greatest in the oxyntic mucosal zone in the corpus of the stomach. Andersson and Grossman (1965) found that the mucosal surface of the corpus was at a potential of -44mV with respect to blood, while the figures for the "antrum" and duodenal bulb were -35mV and -7mV respectively. When an intraluminal electrode was manipulated from the duodenum into the stomach, there was a change to a more negative potential in the stomach. The greatest change in PD occurred as the electrode passed from the duodenum into the stomach. It occurred abruptly, was uniform, sharp, well-defined and coincided with what they called the anatomical sphincter (the pyloric ring) and the mucosal border. It was shown by these authors as well as by Durbin (1967) that the change in PD was a reliable means of identifying the gastroduodenal junction.

During endoscopic studies of the pylorus, Blackwood (1969) correlated visual identification of the pyloric ring with PD measurements. In all 7 normal subjects a significant PD change occurred within 1.0 cm of the true pyloric ring. In 2 studies in which a PD change occurred 3.0 to 4.0 cm beyond a visualized ring, the latter was shown to be a false ring, mimicking the pylorus and caused by antral deformity.

Geall et al (1970) confirmed that PD measurements between the mucosal surface and venous blood gave identical values to the PD between mucosa and serosa, but that mucosa-skin PD measurements varied and were less reliable. They thought that the technique might have various applications, e.g. in the investigation of transport mechanisms.

During experimental studies PD measurements were used as an accurate method of identifying the gastroduodenal mucosal junction in canines by Isenberg and Csendes (1972). Fisher and Cohen (1973) confirmed that the junction of the stomach and duodenum as seen radiologically in normal human subjects (Chap. 11, 13), was marked by a PD change of -33mV.

Kaye et al (1976) and White et al (1981) used PD measurements to determine the gastroduodenal mucosal junction in humans.

Discussion #

A significant change in electrical potential difference (PD) occurs at the gastroduodenal mucosal junction, located on, or close to, the top of the pyloric ring (the right pyloric loop) (Chaps. 3, 5). PD measurements are a reliable means of determining the gastroduodenal mucosal junctions in the intact, living canine and human stomachs.

References #

Andersson S, Grossman MI. Profile of pH, pressure and potential difference at gastroduodenal junction in man. Gastroenterology l965, 49, 364-371.
Blackwood WD. Pylorus identification. Gastroenterology l969, 57, 163-167.
Durbin RP. Electrical potential difference of the gastric mucosa. In: Handbook of Physiology Sect 6: Alimentary Canal, Vol 2 : Secretion, edit Code CF, Heidel W. Amer Physiol Soc, Washington DC l968, pp 879-888.
Fisher R, Cohen S. Physiological characteristics of the human pyloric sphincter. Gastroenterology l973, 64, 67-75.
Geall MG, Code CF, McIlraith DC, et al. Measurement of gastrointestinal transmural electric potential difference in man. Gut l970, 11, 34-37.
Isenberg JI, Csendes A. Effect of octapeptide of cholecystokinin on canine pyloric pressure. Amer J Physiol l972, 222, 428-431.
Kaye MD, Mehta SJ, Showalter JP. Manometric studies of the human pylorus. Gastroenterology l976, 70, 477-480.
White CM, Poxon V, Alexander-Williams J. A study of motility of normal human gastroduodenal region. Dig Dis Sci l98l, 26, 609-617.

7 - Arteries, Veins, Lymphatics

Mon, 01 Jan 0001 00:00:00 +0000

Arteries, Veins, Lymphatics #

Arterial Supply #

The arterial supply of the stomach is derived from all three branches of the coeliac artery, which arises from the front of the aorta between the crura of the diaphragm (Last l984). It is a short wide trunk, surrounded by the coeliac lymph nodes and flanked by the coeliac ganglia of the sympathetic system.

The first branch, the left gastric artery, runs to the left, giving off an ascending oesophageal branch, and supplying the upper part of the stomach; it may also give rise to the left hepatic artery (Moore l980). It then turns downwards between the two layers of the lesser omentum, running to the right along the lesser curvature. It divides into two parallel branches, which give off branches to the anterior and posterior gastric walls and which anastomose freely with arteries from the greater curvature. The two branches of the left gastic artery then anastomose with the two branches of the right gastric artery in the region of the incisura angularis.

The second branch of the coeliac trunk, the hepatic artery, passes downwards as far as the first part of the duodenum. It then turns forwards at the opening into the lesser sac (epiploic foramen) and curves upwards into the space between the two layers of the lesser omentum towards the porta hepatis, to supply the liver. As it turns into the lesser omentum the hepatic artery gives off the gastro-duodenal and right gastric arteries. The latter passes to the left between the two layers of the lesser omentum, along the lesser curvature of the stomach, dividing into two branches which anastomose with the branches of the left gastric artery. The right gastric artery also gives off branches to the anterior and posterior gastric walls, anastomosing with branches from the right gastro- epiploic artery.

The gastro-duodenal artery passes downwards behind the first part of the duodenum, which it supplies by multiple small branches; it then divides into the superior pancreatico-duodenal artery, supplying the second part of the duodenum and head of the pancreas, and the right gastro-epiploic artery. The latter turns to the left, passes along the greater curvature of the stomach between the layers of the greater omentum, giving off branches to the anterior and posterior gastric walls. It anastomoses with the left gastro- epiploic artery at about the midportion of the greater curvature (Menguy l976).

The third branch of the coeliac trunk, the splenic artery, passes to the left along the upper border of the pancreas, behind the peritoneum and the stomach, to supply the spleen. During its course it gives off branches to the pancreas; just before entering the splenic hilum it gives off the short gastric arteries supplying the gastric fornix, and the left gastro-epiploic artery. The latter passes downwards and to the right along the greater curvature of the stomach, between the two layers of the greater omentum, to anastomose with the right gastro-epiploic artery at the midportion of the greater curvature. It gives off branches to the anterior and posterior gastric walls, which anastomose with branches of the gastric arteries along the lesser curvature. Other branches, the epiploic arteries, pass downwards between the layers of the greater omentum.

Branches from the arterial arcades on the lesser and greater curvatures ramify through the submucosa, forming a rich arterial network from which branches arise to supply the mucus membrane. Because of this arrangement the mucosa is not supplied by end arteries, with the possible exception of the mucosa along the lesser curvature, which appears to receive its arterial supply directly from branches of the right and left gastric arteries (Menguy l976).

The first 2 cm of the duodenum is supplied by multiple small branches from the hepatic and gastroduodenal arteries (Last l984). According to Cunningham (l947) the first part of the duodenum occupies the frontier zone between the coeliac and superior mesenteric vascular supplies, and the vessels which supply it vary considerably in their size and mode of origin; the peculiarity of its blood supply may partly account for the frequency with which it is the seat of ulceration.

Venous Drainage #

The position of the gastric veins is similar to that of the arteries along the lesser and greater curvatures. All the gastric veins drain either directly or indirectly into the portal system, which carries venous blood to the liver.

The left gastric vein runs to the left along the lesser curvature, receiving the oesophageal veins below the oesophageal hiatus in the diaphragm. Usually it drains directly into the portal vein at the superior border of the pancreas.

The right gastric vein runs along the lesser curvature to the right, towards the pylorus, joining the portal vein behind the first part of the duodenum. It receives the prepyloric vein, a small vein running vertically across the anterior surface of the gastro-duodenal junction on the pyloric ring; it is an important visual guide to the situation of the ring (Chap. 3).

The left gastro-epiploic vein, running to the left along the greater curvature, and the short gastric veins, drain into the splenic vein or its tributaries. Having received tributaries from the pancreas as well as the inferior mesenteric vein, the splenic ultimately joins the superior mesenteric vein to form the portal vein.

The right gastro-epiploic vein runs to the right as far as the head of the pancreas. Usually it turns downwards to join the superior mesenteric vein, draining into the portal vein. Considerable variations may occur and the right gastro-epiploic may enter the portal vein directly, or it may join the splenic vein. There is no gastroduodenal vein.

The veins from the first 2 cm of the duodenum drain into the prepyloric vein (Last l984).

Lymphatic Drainage #

In a meticulous study of 30 post-mortem specimens, Jamieson and Dobson (l907) found that the lymph vessels in the walls of the stomach arise in the subepithelial interglandular tissue of the mucosa, from where they pass outwards between the glands to communicate with each other in the peri-glandular plexus. Vessels proceed from here into the subglandular plexus between the glands and muscularis mucosae. Short vessels then pierce the muscularis mucosae to break up on its outer surface to form the submucous plexus. Large vessels draining this plexus pass outwards through the muscular coats, communicating with the networks among the muscle fibres, and open into the subserous plexus. From the latter valved collecting vessels radiate to the curvatures of the stomach to enter the omenta. By means of injection techniques it was shown that fluid passed from the submucous to the subserous plexus, but not in the reverse direction.

Doubt had been expressed by previous authors as to the continuity of the gastric and duodenal plexuses. Jamieson and Dobson (l907) found that injection of the gastric submucous plexus showed free communication with the submucous plexus of the duodenum. Injection of the gastric subserous plexus showed a sharp demarcation at the pyloric ring, with the fluid flowing in the direction of the gastric curvatures. In only one specimen could direct communication between the gastric and duodenal subserous plexuses be demonstrated. However, many of the collecting vessels from the pyloric subserous network ran downwards over the duodenum to reach the subpyloric glands, and as they received vessels from the duodenum it was surmized that an indirect communication was formed in this way.

Horton (l928) on the other hand, demonstrated by means of injections of India ink that an almost complete block existed between the submucous lymphatics of the stomach and those of the duodenum at the pylorus. In contrast, the subserous lymphatics of the pyloric region were continuous with those of the duodenum.

Coller et al. (l94l) divided the lymphatics of the stomach into intramural, intermediary and extramural systems. The intramural system consists of 3 networks, viz. submucosal, intermuscular and subserosal. The submucosal lymphatic channels communicate freely throughout the submucosa of the stomach and to a lesser degree with the submucosal lymphatics of the duodenum; they also communicate freely with the intermuscular and subserosal networks. The intermediary system consists of numerous small channels between the subserosal network and the extramural collecting systems. The extramural system consists of four major zones of lymphatic drainage, corresponding to the arterial supply of the stomach. Ultimately all zones drain into the coeliac nodes around the coeliac arterial trunk on the anterior aspect of the aorta.

According to Eker (l951) the stomach should be considered to have the following 4 zones of lymphatic drainage:

The first zone comprises the upper two-thirds of the lesser curvature and a large part of the body of the stomach. The lymphatic drainage is into the left gastric nodes lying along the left gastric artery. These nodes are joined by lymphatics coming down from the lower part of the oesophagus, and their efferents proceed to the coeliac nodes.
The second zone of lymphatic drainage is from the distal part of the lesser curvature, including the lesser curvature of the pyloric region, to the suprapyloric nodes along the right gastric artery. Eker (l951) stressed the fact that this zone consists of "only a small area in the lower part of the pyloric region". Efferent channels from the suprapyloric nodes drain to the hepatic and ultimately to the coeliac and aortic nodes.
Most of the pyloric part of the stomach as well as the right (i.e. lower) half of the greater curvature constitute the third zone. The extramural lymphatics from these areas drain into the right gastro-epiploic nodes in the gastrocolic ligament, lying along the right gastro-epiploic vessels, and into the pyloric nodes on the anterior surface of the head of the pancreas. The direction of lymph flow is from above downwards, towards the pylorus and the nodes between the head of the pancreas and second part of the duodenum. From these groups, collectively called the subpyloric glands (which also drain the first part of the duodenum), efferent vessels pass along the gastro-duodenal artery to the hepatic nodes along the hepatic artery, and thence to the coeliac nodes.
The fourth zone is from the left (i.e. upper) half of the greater curvature and the gastric fornix. From here lymph vessels pass to the left gastro-epiploic nodes, lying along the left gastro-epiploic artery, proceed to the pancreatico-lienal nodes along the splenic artery, and ultimately to the coeliac nodes.

Lehnert et al. (l985) studied the distribution of lymph and blood capillaries by light and transmission electron microscopy in 16 endoscopic biopsy and surgical resection specimens of human gastric mucosa and submucosa. Four were normal and 12 showed evidence of gastritis. A clear distinction between small mucosal blood and lymph capillaries was not always possible with light microscopy; a distinction could be made by electron microscopy. This showed blood capillaries at all levels of the lamina propria, and especially at its upper levels, as well as in the submucosa. Lymph capillaries on the other hand, could not be demonstrated in the upper and middle regions of the lamina propria; lymphatics were only present in the deep lamina propria adjacent to the muscularis mucosae. Larger lymph vessels were observed in the submucosa. It was concluded that the entire human gastric mucosa had a rich supply of blood capillaries, many of which were adjacent to the gastric glands and surface epithelium, but that lymphatic capillaries were present only in the deep lamina propria. It seemed if earlier descriptions, derived from light microscopy, needed revision.

Discussion #

Investigators differ on the question of continuity of gastric and duodenal lymphatics. According to Jamieson and Dobson (l907), who injected lymph plexuses in the gastric submucosa, free communication existed between gastric and duodenal submucosal lymphatics; this was also the view of Coller et al. (l941). Horton (l928, l931) and Williams (l962) on the other hand, during injections of India ink into the gastric submucosal space, found a complete block at the pylorus, with no communication between gastric and duodenal submucosal lymphatics. The differing results could be due to differences in methodology; whereas Jamieson and Dobson (l907) injected lymphatic plexuses, it seems that the injections of Horton (l928, l931) and Williams (l962) were done into the submucosal space.

According to Jamieson and Dobson (l907) the gastric and duodenal subserous lymphatics did not communicate, while Horton (l928, l931) found that they were continuous. All authors agree that the gastric submucous and gastric subserous lymphatic systems communicate freely. There is general agreement about extramural lymphatic drainage away from the stomach. These factors are of importance in the spread of gastric carcinoma, and especially when spread of pyloric carcinoma into the duodenum has to be considered (Chap. 33).

The findings of Eker (l951) show that extramural lymphatic drainage from the region of the pyloric sphincteric cylinder is downwards, to the suprapyloric and subpyloric glands.

Lehnert et al. (l985) thought that the low incidence of lymph node metastasis in early gastric carcinoma, where the lesion is confined to the mucosa, could be due to the rarity of lymph capillaries (as opposed to blood capillaries) in the mucosa.

References #

Coller FA, Kay EB, McIntyre RS. Regional lymphatic metastases of carcinoma of the stomach. Arch Surg l941, 43, 748-761.
Cunningham DJ. Text-book of Anatomy. Edit Brash JC, Jamieson EB. Oxford Univ Press, 8th ed, London l947, p 1457.
Eker R. Carcinomas of the stomach: investigation of the lymphatic spread from gastric carcinomas after total and partial gastrectomy. Acta Chir Scand l951, 101, 112-126.
Horton BT. Pyloric musculature, with special reference to pyloric block. Amer J Anat l928, 41, 197-225.
Horton BT. Pyloric block with special reference to the musculature, myenteric plexus and lymphatic vessels. Arch Surg l931, 22, 438-462.
Jamieson JK, Dobson JF. The lymphatic system of the stomach. Lancet l907, l, l061-l066.
Last RJ. Anatomy: Regional and Applied. Churchill Livingstone, 7th ed, London l984, p 280.
Lehnert T, Erlandson RA, Decosse JJ. Lymph and blood capillaries of the human gastric mucosa: a morphologic basis for metastasis in early gastric carcinoma. Gastroenterology l985, 89, 939-950.
Menguy R. Surgery of Peptic Ulcer. WB Saunders Co, Philadelphia l976, p 4.
Moore KL. Clinically Oriented Anatomy. Williams Wilkins Co, Baltimore l980, p 176.
Williams I. Closure of the pylorus. Brit J Rad l962, 35, 653-670.

8 - Nerves

Mon, 01 Jan 0001 00:00:00 +0000

Nerves #

Classically the autonomic nervous system consists of two components, cholinergic and adrenergic nerves; the former are contained mostly in the parasympathetic, and the latter mostly in the sympathetic division. For the past 4 decades a third component of the autonomic system, which is neither cholinergic nor adrenergic, has been recogized; the principal active substance released from these nerves in the gastrointestinal tract is a purine nucleotide; they have been called purigenic nerves by Burnstock (l972). An increasing number of peptides with a dual localization in endocrine cells and peripheral nerves in the walls of the gastrointestinal tract has now been recognized. This has led to the concept of a three-part autonomic control system consisting of cholinergic, adrenergic and peptidergic nerves (Bishop et al. l977).

Parasympathetic Nerve Supply #

The parasympathetic nerve supply to the stomach is derived from the anterior and posterior vagal trunks and their branches. Afferent fibres are also present in the vagi, which are mixed nerves.

Anterior Vagus #

The anterior vagal trunk, which is derived mainly from the left vagus nerve but which includes fibres from the right vagus and also some sympathetic fibres from the splanchnic nerves, enters the abdominal cavity through the oesophageal hiatus in the diaphragm. It is usually single but may be divided into two or even three trunks. The manner of distribution of its branches is in the main constant (Latarjet et al. l921; McCrea l924).

Having supplied several fine twigs to the lower end of the oesophagus and cardiac part of the stomach, the anterior trunk breaks up into its main branches.

According to Latarjet three main sets of branches are present:

The first set, consisting of 4 to 5 direct branches, emanating "one below the other", supplies the upper part of the lesser curvature. These nerves do not form a plexus and can be dissected separately. A few filaments from the sympathetic supply join these direct branches via the coeliac plexus. One of the branches in this group is always bigger than the others and very distinct; Latarjet (l921) called it the principal anterior nerve of the lesser curvature. It innervates the area from the cardia to the pyloric vestibule, and does not proceed beyond the latter (Fig 8.1).
Branches emanating from the vagal supply to the liver. These branches, usually 3 to 5 in number, descending in the lesser omentum, "fall like rain" on the superior margin of the pylorus and first part of the duodenum. Latarjet called them the superior pyloric nerves (Fig 8.1).
The third set consists of vagal filaments from the hepatic branches, accompanying the sympathetic nerves along the right gastroepiploic artery next to the greater curvature. They provide a few vagal twigs to the inferior margin of the pylorus. Latarjet called these the inferior pyloric nerves (Fig 8.1).

According to Latarjet (l921) the anterior vagus can be divided into two distinct functional divisions. The first division, consisting of the direct branches, supplies the fornix and body, i.e. the "reservoir" part of the stomach. The second division, through the hepatic branches, supplies the pylorus and first part of the duodenum, i.e. the "sphincteric" part of the stomach. (Comment: According to Latarjet, the principal anterior nerve of the lesser curvature does not supply the pylorus; the pylorus and first part of the duodenum are innervated by the superior and inferior pyloric nerves, emanating from the hepatic branches). Latarjet found the innervation in dogs to be similar to that in man.

The papers of McCrea (l924), Mitchell (l940) and Jackson (l948) describe personal investigations and provide an analysis of the literature. The following findings are pertinent to the present discussion.

According to McCrea (l924) the anterior vagal trunk breaks up into 3 to 6 main branches. To the left a group of gastric branches arise, supplying the anterior surface of the cardia, the fornix and proximal portion of the body of the stomach. These may or may not form an anterior gastric plexus.

Fig. 8.1. Diagram of gastric branches of anterior vagus. 1., Direct branches; 2., branches emanating from vagal supply to liver (superior pyloric nerves); 3., branches emanating from vagal supply to liver (inferior pyloric nerves); H., hepatic branch or branches; A.L., anterior nerve of Latarjet (principal anterior nerve of lesser curvature)

On the right there are the following three main groups of branches:

The first or hepatic branch proceeds laterally in the lesser omentum towards the porta hepatis; it is frequently duplicated. Its terminal twigs are divided into 2 series, viz. a proximal which supplies the porta hepatis, and a distal, which turns downwards towards the pylorus. From the latter twigs pass (a) to the pylorus and first part of the duodenum; (b) along the right gastric artery to the region of the pyloric canal; (c) to run deep to the pylorus with the gastroduodenal artery towards the head of the pancreas and second part of the duodenum; (d) to run proximally on the wall of the hepatic artery, and (e) to communicate with sympathetic twigs passing to the gall bladder. Communications with sympathetic twigs are common.
The second branch on the right, a large nerve, passes downwards between the layers of the lesser omentum, a short distance from, and parallel to, the lesser curvature of the stomach. It is distributed to the anterior surface of the pyloric "antrum" and body of the stomach, but does not reach the pyloric "canal".
The third branch lies on and follows the lesser curvature along the attachment of the lesser omentum; it descends as far as the incisura angularis. All these branches may communicate with the coeliac sympathetic plexus, and in the region of the fornix communications are received from the posterior vagal trunk.

McCrea (l924) concludes that the pyloric canal, pyloric "sphincter" and first part of the duodenum are supplied by the hepatic branches of the anterior vagus. The remainder of the stomach is supplied by the gastric, and second and third right branches. It is stated specifically that the second branch supplies the anterior surface of the "antrum" and body, but that it does not reach the pyloric "canal". McCrea found the distribution of the vagi in the abdomen of the cat, dog and rabbit to be essentially similar to that of man.

Mitchell's (l940) findings differ in certain minor respects from those of McCrea (l924). According to Mitchell some of the lowermost gastric branches (which primarily supply the cardia, fornix and upper lesser curvature) reach almost, but not quite, to the pylorus.

The hepatic branches (of which there are two to four), running towards the right to the porta hepatis, divide at the hepatic artery, one branch passing upwards to the liver and the other downwards to the pylorus and coeliac plexus. In one out of 15 specimens the uppermost hepatic branch divided into three: one to the porta hepatis, one to the cystic duct and gall bladder, and the third to the pylorus.

The greater anterior gastric nerve (i.e. McCrea's second branch) supplies two pyloric twigs according to Mitchell (l940). The first arises near the upper end of the lesser curvature, passes almost horizontally between the layers of the lesser omentum as far as the hepatic artery, then turns downwards on the left side of the hepatic artery to reach the pylorus and proximal part of the duodenum. It often bifurcates, sending one branch upwards to the liver and the other downwards to the pylorus, and it is connected to the hepatic plexus. The other pyloric twig usually arises from the greater anterior gastric nerve about halfway along the lesser curvature, and passes obliquely between the layers of the lesser omentum to the pyloric "antrum", some fibres reaching the pyloric "sphincter". This twig arises at a lower level, but supplies the pylorus proximal to the branch first described.

Thus according to McCrea (l924) and Mitchell (1940), the main innervation of the pyloric region from the anterior vagus occurs via its hepatic branches. According to Mitchell (l940) the pylorus is also innervated by twigs arising in the greater anterior gastric vagal branch, running between the layers of the lesser omentum.

Jackson (l948) studied the distribution of the vagus in 50 cadavers. The hepatic branches of the anterior trunk, running to the porta hepatis, were identified in 43 cases. In the first case the hepatic branch was followed to its termination and was found to supply the first few centimeters proximal to the pylorus, the pylorus itself and the first part of the duodenum. In the remainder of the dissections attention was concentrated on the more proximal parts of the branches, and the hepatic branches were followed only to the fissure of the ductus venosus. The principal anterior nerve of the lesser curvature described by Latarjet (l921) was found in 28 instances. From its origin it passed along the lesser curvature, returning to the stomach generally from 2.5-9 cm proximal to the pylorus; the closest any branch of this nerve came to the pyloric "sphincter" was 2.5 cm.

Skandalakis et al. (l986) reiterate that separation of the anterior vagal trunk into anterior gastric and hepatic divisions is usually found on the surface of the distal oesophagus at the gastro-oesophageal junction. Usually a major branch of the anterior gastric division forms the principal anterior nerve of the lesser curvature (nerve of Latarjet). In most instances it can be traced to the level of the incisura; occasionally it may proceed as far as the first part of the duodenum (in these cases the pylorus is still innervated via the hepatic branch). It may also be absent, the "antrum" being supplied by branches arising from the anterior vagal trunk proximal to the origin of the hepatic division. Many variations exist, and Skandalakis et al. (l986) referred to "the vagaries of the vagus nerve". However, these authors point out that the usual supply to the pylorus is a descending branch (or branches) from the hepatic division before it reaches the liver; occasionally the pyloric branch may arise from the anterior gastric division.

Posterior Vagus #

The posterior vagal trunk, which is derived mainly from the right vagus nerve but includes fibres from the left vagus and some sympathetic fibres, enters the abdomen through the oesophageal hiatus in the diaphragm on the posterior surface of the oesophagus. The number and direction of its branches is more constant than that of the anterior vagus (Latarjet l921; Skandalakis et al. l986). Shortly after entering the abdomen it divides into 2 main divisions. The larger or coeliac division proceeds to the coeliac and other abdominal sympathetic plexuses. The smaller or posterior gastric division first gives off fine twigs to the lower oesophagus and fornix. It then continues along the lesser curvature, giving off 4 to 6 posterior gastric branches. Latarjet (l921) called the most inferior and also the largest of these branches the principal posterior nerve of the lesser curvature; this has subsequently become known as the posterior nerve of Latarjet. Together with the other posterior branches it innervates the posterior wall of the stomach, with the exception of the pylorus and immediate prepyloric region. It also anastomoses with sympathetic twigs from the coeliac plexus, as well as with the principal anterior nerve of the lesser curvature.

McCrea's (l924) findings are similar to those of Latarjet, but he terms the branch from which the posterior gastric twigs arise, the "stem". Thus the stem gives off branches to the posterior aspect of the proximal portion of the body of the stomach. It then continues downwards, giving off branches to the posterior surface of the body and pyloric "antrum", the most distal being distributed in the region of the incisura angularis. According to McCrea the posterior vagus does not reach the pyloric canal.

Mitchell's (l940) findings are almost identical. What he calles the posterior gastric nerve (McCrea's "stem") gives off branches at intervals which pass to the stomach, but the terminal branches extend only to the pyloric "antrum", failing to reach the pyloric "sphincter". Slender hepatic twigs may also be given off towards the porta hepatis.

In 50 dissections of the posterior vagal trunk, Jackson (l948) charted the gastric branches and determined the point of origin of the coeliac branch. The principal posterior nerve of the lesser curvature (nerve of Latarjet) was identified in 19 instances. It proceeded along the lesser curvature in the direction of the pylorus, but, before reaching it, turned across the posterior surface of the stomach towards the greater curvature. Jackson concluded that the vagal supply to the pylorus was via the hepatic branches of the anterior vagus.

According to Skandalakis et al. (l986) the posterior gastric division forms the posterior nerve of Latarjet. The posterior gastric division usually terminates higher on the lesser curvature than the anterior gastric division; in a small minority of cases it reaches the pylorus. The most frequent pattern of the posterior gastric division is that described by McCrea (l924), which is a typical, but not universal, pattern.

Parasympathetic Ganglia #

The left vagus supplies efferent preganglionic fibres mainly to the anterior surface, and the right vagus mainly to the posterior surface of the stomach. In addition both vagi send branches to the coeliac plexus. The parasympathetic preganglionic vagal fibres penetrate the layers of the gastric wall, to form synapses in the ganglion cells of the plexus of Auerbach between the longitudinal and circular muscle coats, and in the plexus of Meissner in the submucosa. From the ganglia postganglionic fibres emerge to supply the musculature and mucosa. According to Horton (l928), Auerbach's plexus is continuous from the pyloric region to the duodenum.

In addition to the myenteric (Auerbach's) and submucous (Meissner's) plexuses, Rash and Thomas (l962) described a third group, namely the subserous plexuses; they also mentioned the differentiation of enteric neurones into argyrophilic Dogiel Type I cells with short dendrites, and argyrophobic Dogiel Type II with fewer but longer dendrites. According to Smith (l970) the axons of argyrophilic neurones do not leave the plexuses and do not reach muscle fibres; their function is to coordinate peristalsis. The axons of argyrophobic cells, which are strongly cholinergic, form secondary and tertiary plexuses and supply muscle fibres; they act by initiating contractions. The general effect of myenteric plexus damage is loss of coordinated muscular contractions which serve to propel luminal contents caudally; this may lead to local muscular hypertrophy, e.g. hypertrophic pyloric stenosis (Chap 23).

Discussion #

The investigators quoted, namely Latarjet (l921), McCrea (l924), Mitchell (l940), Jackson (l948) and Skandalakis et al. (l986), found that the main, and in most cases the only, nerve supply from the anterior vagus to the pylorus is via its hepatic branch or branches. The region supplied in this way encompasses the distal "few centimetres" of the stomach, the pylorus and first part of the duodenum. While none of the authors referred to the findings of Cunningham (l906), Forssell (l913) or Torgersen (l942), it is clear that the region of the pylorus innervated in this way, corresponds to the pyloric sphincteric cylinder.

In the vast majority of cases the principal anterior nerve of the lesser curvature (nerve of Latarjet) does not innervate the sphincteric cylinder. A few exceptions were mentioned. Mitchell (l940) stated that in some cases a few fibres from the anterior vagus might reach the pylorus directly from gastric branches higher up. Skandalakis et al. (l986) found that Latarjet's nerve might occasionally proceed as far as the duodenum; in these cases there was still a separate branch from the hepatic division to the pylorus.

The investigators quoted found that the posterior vagus (including the posterior nerve of Latarjet) does not usually innervate the pylorus and prepyloric region, the most distal twigs extending only as far as the incisura angularis or the "commencement of the antrum". It is clear that the region which is not innervated by the posterior vagus, corresponds to the pyloric sphincteric cylinder. One of the few exceptions was mentioned by Skandalakis et al. (l986); in a small minority of cases they found that fibres of the posterior gastric division could reach the pylorus.

It is concluded that the vagal supply to the pyloric sphincteric cylinder (which includes the pyloric ring musculature) and to the first part of the duodenum, occurs via the hepatic branch of the anterior vagus in the vast majority of cases; the hepatic branch (or branches) breaks up into the superior and inferior pyloric nerves, supplying the cylinder. It is of interest to note that, when first describing the pyloric sphincteric cylinder in l906, Cunningham surmized that its powerful musculature was probably under control of a special innervation.

Sympathetic Nerve Supply #

The sympathetic nerve supply to the stomach is almost entirely derived from the coeliac plexus. The gastric branches of the coeliac plexus accompany the vessels supplying the stomach, and the maximum number are found alongside the left gastric, hepatic and phrenic arteries, while others accompany the splenic, right gastric and gastro-epiploic vessels.

According to McCrea (l924) these nerves can be grouped as follows:

Fibres from the coeliac plexus accompany the left inferior phrenic artery, wind across the anterior aspect of the lower oesophagus, communicate with branches of the anterior vagus, and are distributed to the cardia and fornix.
Fibres from the coeliac plexus pass with the left gastric artery and divide into three groups: (a) Fibres passing with the oesophageal and superior branches of this artery to the cardia and proximal part of the body of the stomach; these twigs communicate with branches of the anterior and posterior vagal trunks. (b) Fibres passing with the main stem of the artery along the lesser curvature to supply the anterior and posterior surfaces of the body of the stomach and pyloric "antrum". (c) Fibres passing between the layers of the lesser omentum towards the porta hepatis, communicating with hepatic branches of the anterior vagal trunk in most instances.
Fibres passing from the coeliac plexus along the hepatic artery and distributed with its branches. They reach the pyloric region of the stomach with the right gastric and right gastroepiploic arteries.

In all major respects Mitchell's (l940) description agrees with that of McCrea, although he adds some exceptions. According to Mitchell the terminal twigs accompanying the main branch of the left gastric artery, i.e. group 2b of McCrea, did not reach the pylorus in any of the 15 specimens examined by him, but united with the nerve filaments lying alongside the right gastric artery. The right gastric branches, (group 3 of McCrea) supply the upper parts of the pyloric region.

Sympathetic Ganglia #

Preganglionic sympathetic fibres end in the coeliac ganglia; efferent fibres emerging from the coeliac ganglia to accompany the arteries are postganglionic. Even though they traverse the enteric ganglia they probably have no functional relationship to the enteric plexuses; they are distributed with the postganglionic vagal fibres emerging from the plexuses.

Afferent visceral fibres from the stomach travel the same course in reverse, to ganglion cells in the posterior spinal nerve roots. They do not synapse in, or arise from, sympathetic ganglia. Although the sympathetic nerves are motor, they also carry fibres from sense organs in the viscera.

Discussion #

It seems that the main sympathetic supply to the pyloric region occurs via fibres accompanying the hepatic artery and its branches.

Peptidergic System #

The peptidergic system refers to a widespread group of cells, derived from neuroectoderm embryologically and having certain biochemical features in common. They are also referred to as neuroendocrine cells and belong to the APUD cell line, based on their capacity to synthesize monoamines through a process of amine precursor uptake and decarboxylation. During recent years a large number of biologically active peptides, produced by APUD cells, have been demonstrated in central and peripheral neurogenic tissues as well as in the walls of the gastrointestinal tract (Chap. 9). Some of the peptides, notably gastrin and vasoactive intestinal peptide (VIP), were first detected in the gut and subsequently in the brain; others, such as somatostatin, enkephalin and neurotensin were first identified in brain tissue and subsequently in the walls of the alimentary tract. Substance P has long been known to be present in both locations.

Most of the monoamines have several molecular forms or sizes. Some types are released into the circulation, producing their biological effects in distant target organs; these can be looked upon as true hormones acting in an endocrine way. Others act locally in the vicinity of their site of origin in a paracrine way. A third group functions as neurotransmitters, acting in a neurocrine way. A clearcut separation of endocrine, paracrine and neurocrine functions is not always feasible. Burnstock (l986) pointed out that thinking mainly in terms of antagonistic parasympathetic cholinergic and sympathetic adrenergic control of functions, is no longer tenable. The involvement of a multiplicity of neurotransmitters and of sophisticated peripheral control mechanisms such as neuromodulation and co-transmission, has to be recognized. This is accomplished through non-cholinergic, non-adrenergic nerves of the purigenic system.

APUD cells and regulatory peptides in the pyloric region of the stomach will be discussed in somewhat greater detail in the next chapter.

References #

Bishop AC, Polak JM, Buchan AMJ, et al. Third division of the autonomic nervous system: an important element in gut control. Gut l977, 18, A962.
Burnstock G. Purigenic nerves. Pharm Rev l972, 24, 509-581.
Burnstock G. Autonomic neuromuscular junctions: current developments and future directions. J Anat l986, 146, 1-30.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr l913, Suppl 30, 1-265.
Horton BT. Pyloric musculature with special reference to pyloric block. Amer J Anat l928, 41, 213.
Jackson RG. Anatomic study of the vagus nerves. Arch Surg l948, 57, 333-352.
Latarjet A, Wertheimer P. L'énervation gastrique. Données expérimentales. Déductions cliniques. J Méd Lyon l921, 36, 1289-1302.
Latarjet A. Note préliminaire sur l'innervation et l'énervation de l'estomac. Lyon Méd l921, 130, 166-167.
Latarjet A, Cluzet M, Wertheimer P. Effects de la section et de l'excitation des nerfs propres de l'estomac sur la motricité de cet organe. C R Soc Biol l921, 84, 985-987.
Latarjet A. Section des rameaux gastriques du vague. La Presse Med l921, 41, 409.
McCrea ED. The abdominal distribution of the vagus. J Anat (London) l924, 59, l8-40.
Mitchell GAC. A macroscopic study of the nerve supply of the stomach. J Anat (London) l940, 75, 50-63.
Rash RM, Thomas MD. The intrinsic innervation of the gastro-oesophageal and pyloro-duodenal junctions. J Anat l962, 96, 389-396.
Skandalakis LJ, Gray SW, Skandalakis JE. The history and surgical anatomy of the vagus nerve. Surg Gynaec Obstet l986, 162, 75-85.
Smith B. Disorders of the myenteric plexus. Gut l970, ll, 271-274.
Torgerson J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.

9 - Regulatory Peptides

Mon, 01 Jan 0001 00:00:00 +0000

Regulatory Peptides #

For a brief historical review of the regulatory peptides, one is indebted to Royston et al (l978) and others. It was pointed out that Solcia and his colleagues (l967) described endocrine-like cells in the gastric "antrum" which were argyrophilic, but non-argentaffin in quality. The next year McGuigan (l968), by means of an immunofluorescent technique, identified gastrin in cells of the antral mucosa, which he named G cells. Bussolati and Pearse (l970), using immunofluorescent and silver techniques, showed that these two types of cell were the same.

G cells belong to the APUD cell line; the technique of immunocytochemistry shows the precise localization of the cells in the walls of the gastrointestinal tract. Individual cells contain secretory granules in the basal part of the cytoplasm, whereas the Golgi complex is supranuclear. In the pyloric mucosal zone most of the cells extend to the lumen in a pyramidal way, with tufts of microvilli at the apex; these probably act as receptor sites. Secreted peptides are demonstrated by radioimmunoassay of tissue extracts.

The following regulatory peptides appear to be among the more important in the present context.

Gastrin #

Edkins (1906) showed that an extract of pyloric mucosa administered intravenously stimulated secretion of gastric acid and pepsinogen; he suggested that the active principle was of hormonal origin and named it gastrin. It was soon apparent that this action was similar to that of histamine, and many authorities considered gastrin and histamine to be the same substance. As pointed out by Dockray (l978), nearly 60 years of uncertainty about the existence, nature and specificity of the antral hormone gastrin, and its relationship to histamine, followed. This was resolved when Gregory and Tracy (l96l, l964) isolated two related heptadecapeptides from hog antral mucosa, which proved to be gastrin. It was shown to occur in highest concentration in the pyloric mucosal zone, where its concentration was 500 times higher than in the corpus of the stomach (McGuigan l968).

Gastrin producing G cells originate from neuroectoderm together with other cells of the APUD series. They have a clear appearance, are piriform in shape and located in the mid and deep zones of the pyloric mucosal glands; electronmicroscopy shows that they possess microvilli extending into the lumen and that secretory granules are present in the basal parts of the cells. This organisation allows for secretion of hormone into the bloodsteam in response to luminal stimuli (Dockray l978). Normally there are approximately half a million G cells per cmª in the stomach in man, amounting to a total of approximately 10 million G cells (Mortensen l980).

Synthesis of gastrin I and II occurs predominantly in the G cells of the pyloric mucosal zone; less important sources are G cells in the duodenum, D cells in the islands of Langerhans in the pancreas, and isolated G cells in the proximal acid producing region of the fornix and body of the stomach. Some authorities hold that normally G cells do not occur in the oxyntic zone of the stomach; they may however, be present in pathological conditions (Stave and Brandtzaeg l976).

While G cells are interspersed among the more frequent mucus producing cells, the question arises whether their spatial distribution is equal to that of the pyloric mucosal zone; are G cells found throughout the pyloric mucosa, or are they confined to certain areas of this zone? Stave and Brandtzaeg (l976) pointed out that there were few quantitative data on the actual G cell mass of the stomach at that time; however, variations in the numbers of antral G cells had been reported in relation to pathological states. By means of immunohistochemical methods these authors attempted a systematic mapping of the numerical distribution of G cells in the human stomach and duodenum in specimens resected for peptic ulcer. In a small series (8 gastric ulcer cases and 8 cases of duodenal ulcer with uraemia), no G cells were found in the oxyntic zone of the stomach. A low number occurred in the transitional zone at the proximal border of the antrum (Comment: The term "antrum" was not defined, but appeared to be equated with the pyloric mucosal zone). In the gastric ulcer group no significant difference was found between the numbers of G cells at various levels of the "antrum"; in the cases of duodenal ulcer with uraemia there was a statistically significant increase in the number of G cells from the proximal to the distal part of the "antrum". The first part of the duodenum contained considerably fewer G cells than the "antrum", and the numbers in the duodenum were virtually equal in the two groups.

In a second and larger series of cases, Stave and Brandtzaeg (l978) determined the antral density, mucosal distribution and total mass of G cells in gastric resection specimens. The series of 42 cases consisted of 12 cases of gastric ulcer, 14 cases of duodenal ulcer with uremia, 11 cases of duodenal ulcer without uremia, and 5 cases of gastric carcinoma. Immuno-reactive G cells were not seen in the oxyntic zone of the stomach in any of the cases, and low numbers occurred in the transitional zone along the proximal border of the pyloric antrum. The first part of the duodenum contained only a fifth to an eighth of the number in the "distal antrum". (The distal antrum was now said to be the area extending proximally from the pylorus for a distance of 3.0cm). In the duodenal ulcer group, as well as in the group of duodenal ulcer with uraemia, and the gastric carcinoma group, the density of G cells increased from the proximal to the distal part of the antrum; in the group of gastric ulceration the overall density in various parts of the antrum remained the same. G cell density was found to be significantly lower along the lesser curvature and on the anterior and posterior walls than along the greater curvature. This held true in all patient groups excepting that of duodenal ulcer with uraemia. It was concluded that the densest concentration of G cells occurred in the terminal antrum, i.e. the distal 3.0cm of the stomach; that the G cell density was significantly higher along the greater than along the lesser curvature; that individual variations existed in the antral G cell density, the total G cell mass and the spatial distribution of G cells in the antrum; that a transitional zone, of varying width, occurred in all patients; and that the G cell density in the distal antrum was lower in patients with gastric ulceration than in the other patient categories.

A study by Royston et al. (l978) showed results similar to those of Stave and Brandtzaeg (l976, l978). The highest density of G cells was found in "antral" mucosal glands near the pylorus, the number gradually decreasing in an orad direction until the junctional zone between antrum and corpus was reached, where a marked decrease in numbers occurred. These authors found significant direct correlations between antral area and G cell density, between peak acid output and G cell population, and between basal plasma gastrin and G cell density.

G cells act in an endocrine rather than a paracrine or neurocrine way; being secreted into the bloodstream, circulating gastrin (consisting of different molecular types) produces its effects on distant target cells. It should therefore be looked upon as a hormone. There is evidence that some gastrin is also secreted into the lumen, but the physiological significance of this is not clear (Uvnäs-Wallensten l978). Gastrin or its synthetic analogues has a number of effects on the upper gastrointestinal tract, some of the most important being stimulation of hydrochloric acid, pepsinogen and intrinsic factor secretion by the stomach; stimulation of bicarbonate and enzyme secretion by the pancreas; increase in tone of the lower esophageal sphincter; increase in amplitude of smooth muscle contractions in the stomach and jejunum (Theron and Meyer l976); and trophic action on the fundic mucosa, pentagastrin inducing hypertrophy of the mucosa and increases in DNA, RNA and protein synthesis (Johnson and Guthrie l976; Dockray l978). Removal of the "antrum" leads to atrophy of the oxyntic glandular zone (Dockray l978).

Gastrin release is induced by vagal activity, mechanical distension of the stomach, certain food constituents, and is controlled by intra-antral pH (Uvnäs-Wallensten l978). Acidification of antral mucosa inhibits release of gastrin and is probably an important physiological mechanism for the control of gastrin secretion (Walsh and Grossman l975). The kidneys and small intestine catabolise gastrin (Dockray l978).

Hypergastrinaemia is produced by the following conditions: (1) gastrinomas, which generally arise in the pancreas, occasionally in the duodenum and only rarely in the "antrum" (Yalow and Berson l970; Gregory and Tracy l975; Dockray l978); (2) removal or disease of organs participating in the catabolism of gastrin, e.g. after loss of kidney function or after extensive small bowel resection (Dockray l978); (3) pernicious anaemia, in which the atrophic gastritis may spare the antrum and in which there is a tendency toward hyperplasia of G cells, resulting in serum gastrin concentrations which may be in the gastrinoma range (Yalow and Berson l970; Dockray l978). Achlorhydric and hypochlorhydric patients also tend to have high circulating gastrin concentrations due to diminished acid inhibition (Dockray l978); (4) increased secretion from antral G cells (Walsh and Grossman l975).

Somatostatin #

Krulich et al. (l968, l969) and Brazeau et al (l973) isolated a tetradecapeptide from ovine, and Schally et al (l976) from porcine hypothalamic tissue, which was shown to inhibit release of growth hormone (GH) from the pituitary gland. Later named somatostatin, it has subsequently been found to be widely distributed in the central nervous system (Brownstein et al. l975; Arimura et al. l978; Forssmann et al. l979), the gastrointestinal tract (Arimura et al. l975, l978) and other organs in experimental animals and man. Using radioimmunoassay the distribution in rat organs other than the central nervous system was determined (Arimura et al. l975, l978); it was shown that the pancreas had the highest concentration, namely 34ng/mg protein, followed by the stomach with a concentration of 12ng/mg. In the stomach the hormone was found in the pyloric and oxyntic mucosal zones but not in the cardiac zone. The total amount in either the pancreas or stomach was greater than in the hypothalamus; the duodenum, jejunum and ileum contained lesser amounts, ranging from 1.2 to 1.8ng/mg protein. Other organs such as the liver, spleen, kidneys and adrenals did not contain significant amounts.

Combined immunocytochemical and histological methods for demonstrating endocrine granules showed that somatostatin was present in D cells in the islet system of the pancreas (Polak et al. l975) and in morphologically similar D cells in the gastrointestinal tract (Polak et al. l976), localized predominantly in the midzone of the mucosal glands. According to Bloom and Polak (l978) the highest concentration of D cells occurs in the pancreas and pyloric mucosal zone, where the incidence is more than 31 cells per mm². In the remainder of the stomach and duodenum there are 11 to 30 cells per mm², and in the jejunum 1 to 10 cells per mm²; in the ileum and colon the number is zero.

Somatostatin not only suppresses the secretion of growth hormone, but possesses a wide variety of inhibitory actions on other pituitary and extra-pituitary secretions. It suppresses the release of thyroid-stimulating hormone by the pituitary, the release of glucagon, insulin and exocrine secretions by the pancreas, the secretion of cholecystokinin, motilin and secretin by the intestine, and the secretion of gastrin, gastric acid and pepsin by the stomach (Pearse et al. l977; Konturek et al. l978).

Experimental lowering of "antral" pH induces a release of somatostatin by D cells in the pyloric mucosal zone. It appears that somatostatin suppresses gastric acid secretion by direct action on the parietal cells of the cardiac and oxyntic mucosal zones (Arimura et al. l978). Lowering the pH also inhibits the secretion of gastrin; consequently low pH suppresses both gastric acid and gastrin secretion (Arimura et al. l978). Somatostatin is considered to be a potent vasoconstrictor of the intestinal circulation, and some of the inhibitory effects in the gastrointestinal tract may be the result of diminished mesenteric blood flow (Konturek et al. l978). It also suppresses motility of the intestine and contractions of the gall bladder and it possesses neurotrophic effects. The findings suggest that somatostatin not only serves as a hypophysiotrophic hormone, but also as a neurotransmitter (Vale et al. l977).

Somatostatinomas of the pancreas have been documented; patients had hypoglucagonaemia, hypoinsulinaemia and mild diabetes, with remission of hyperglycaemia after removal of the tumor (Ganda et al. l977; Larsson et al. l977).

Holle et al. (l985) determined the number of somatostatin-secreting D cells in the "antrum", pre- and post-operatively, in 20 patients with duodenal and 8 with gastric ulceration. In patients with a normal population of gastrin-immunoreactive G cells, the D cells were within the normal range. High G cell values were accompanied by high D cell values and low G cell values by low D cell values. The G cell to D cell ratio was 8:1 in duodenal, and 6.6:1 in gastric ulceration. Morphologic coupling of the gastrin- somatostatin system in the "antrum" was assumed; this was constant in ulcer disease both before and after vagotomy.

According to Holle et al. (l985) the almost exclusively inhibitory function of somatostatin, combined with the proximity to glucagon A and insulin B cells in the pancreas, as well as to parietal and gastrin G cells in the stomach, raises the question of a paracrine-like mechanism. However, in addition to the direct interaction of somatostatin D cells with neighbouring cells, adrenergic and cholinergic pathways also appear to exist.

Vasoactive Intestinal Peptide (VIP) #

Said and Mutt (l970) isolated a polypeptide with strong vascular effects from porcine small intestine. Termed vasoactive intestinal peptide (VIP), it was subsequently purified by Said and Mutt (l972). For some time VIP was considered to be a solely gastrointestinal hormone; later studies, however, demonstrated VIP in central and peripheral neurons, suggesting a neurotransmitter function (Larsson et al. l976). It is now known that VIP nerves have an ubiquitous occurrence in the body, being particularly numerous in the gastrointestinal, genito-urinary and respiratory tracts (Alumets et al. l978). In the peripheral autonomic system these nerves were shown to occur in various regions, including the superior and inferior mesenteric ganglia, and the submucous (Meissner's) and myenteric (Auerbach's) plexuses of the intestinal wall (Said l978).

Structures believed to exert a sphincteric function receive a particularly rich supply of VIP nerves, more so than the smooth muscle of adjacent regions. Among these are the oesophago-gastric junction, the pyloric "sphincter", sphincter of Oddi, internal anal sphincter, and the openings of the ureters and urethra into the trigonum of the bladder. The very rich supply of VIP nerves is a consistent finding in the smooth muscle of all recognized sphincters; it is thought that an evaluation of the density of VIP innervation may assist in anatomically defining a sphincter (Alumets et al. l978) (Chap. 2).

Using immuno-fluorescent techniques, Polak et al (l974) determined the cellular distribution of VIP in the mammalian (dog, pig and baboon) gastrointestinal tract, mucosal samples being taken from the gastric fornix, pyloric "antrum", duodenum, jejunum, ileum and colon. The distribution of cells was found to be wide; they were present in all regions examined, the highest number occurring in the colon in all three species. According to Bloom and Polak (l978) the highest concentration of VIP cells, more than 31 per mm², occurred in the colon. There were 11 to 30 cells per mm² in the duodenum, and in the stomach, including the pyloric mucosal zone, the concentration was 1 to 10 cells per mm². The relative numerical frequency of these cells in the different gastric mucosal zones was not determined in detail. Small numbers of cells occurred in the pancreas.

Walsh (l983) pointed out that while VIP was originally thought to be located in gastrointestinal endocrine-type cells, later data were consistent with a purely neural localization in the gut; VIP was also distributed throughout the brain and in peripheral nerves outside the gastrointestinal tract. In the stomach Ferri et al. (l984) found a dense VIP-containing nerve supply around oxyntic and pyloric mucosal glands. In the duodenum VIP (and substance P) were present in striking nerve networks in the villi and muscularis mucosae and around blood vessels. VIP was also immunostained in nerve bundles and neuronal perikarya between the lobules of Brunner's glands, while very few fibres reached the proximity of the acinar cells of these glands (Chap. 4).

The biological actions of VIP are numerous and include vasodilatation, lowered blood pressure, increased cardiac output, glycogenolysis and relaxation of smooth muscle (Piper et al. l970). VIP release from the gut was demonstrated upon electric stimulation of the vagus in pigs; significant inhibition of gastric secretion was associated with enhanced VIP release (Said l978). The physiological role of VIP, however, was uncertain (Said l978), but it appeared to be implicated in the following actions: it might serve as a neurotransmitter in the central nervous as well as the peripheral autonomic systems; its wide distribution in many tissues and the relatively constant plasma values suggested that it probably acted as a neurotransmitter in a paracrine, rather than in an endocrine, way (Modlin et al. l978). The VIP neurons have been shown to be under dual (both vagal and splanchnic) control of the autonomic system; release of VIP into venous effluent has been correlated with specific physiological mechanisms known to be mediated via non-cholinergic and non-adrenergic nerve fibres, and elicited by electrical stimulation of the vagus nerves (Fahrenkrug et al. l977). Vagal stimulation caused a frequency-dependent increase in the release of VIP; splanchnic stimulation caused a decrease in the release of VIP, an action which was annulled by alpha-adrenergic blockade. The inhibitory effect of splanchnic stimulation significantly diminished vagally induced VIP release. It was suggested that VIP functioned as the mediator of actions in the gastrointestinal tract known to be elicited via non-cholinergic, non- adrenergic vagal fibres (Fahrenkrug et al. l977).

VIP may participate in the regulation of gastrointestinal tone, motility and secretion (Said l978). It has been proposed as a possible neurotransmitter of inhibitory nerves of the gut (Fahrenkrug et al. l977, l978) and it appears likely that it is involved in sphincter relaxation (Alumets et al. l978). It is a strong candidate as a neurotransmitter responsible for relaxation of the lower oesophageal sphincter (Goyal et al. l980) and the internal anal sphincter in some vertebrates (Biancani et al. l985). It inhibits the amplitude of smooth muscle contractions of the gastric "antrum" in canines (Morgan et al. l978); its usual effect on gastrointestinal smooth muscle is relaxation (Walsh l983).

VIP appears to be an important mediator of paraneoplastic syndromes associated with islet-cell tumors of the pancreas, especially the watery diarrhoea hypokalaemia achlorhydria (WDHA or Verner-Morrison) syndrome. Although disputed by some authors, the findings of Welbourn et al (l978) left little doubt that a WDHA syndrome could occur in association with a pancreatic or certain neural tumors. Other tumors which may secrete large amounts of VIP or VIP-like peptides are neuroblastoma, ganglioneuroma, pheochromocytoma, medullary thyroid carcinoma and bronchogenic carcinoma (Said l978).

Substance P #

While studying the biological effects of extracts of intestinal wall on isolated jejunum preparations, Von Euler and Gaddum (l930) described contractions occurring as a result of a "novel" or unknown substance. Its effects were two fold: it lowered arterial pressure (presumably as a result of vasodilatation), and it caused contraction of smooth muscle in various organs. Fourty years later Chang and Leeman (l970) isolated and identified the unknown factor as an 11-amino-acid peptide called substance P. It was shown to be present in various tissues, including the central nervous system; particularly high concentrations occurred in the posterior horns of the spinal cord.

In the gastrointestinal tract, substance P containing nerve fibres and cell bodies are encountered along its entire length; they are least prominent in the oesophagus and upper part of the stomach (Polak and Bloom l98l). According to Walsh (l983) the highest concentrations occur in the duodenum. Substance P neuronal cell bodies are mainly located in the myenteric plexuses; their nerve fibres richly innervate the circular musculature, whereas the longitudinal muscle contains only a sparse network of fibres. Substance P nerve fibres are also in close contact with the blood vessels (Polak and Bloom l98l).

In the human gastric mucosa Ferri et al. (l984) demonstrated substance P immunoreactivity in the oxyntic zone in a few, thin fibres only. Fibres containing this peptide were more numerous and interconnecting in the "antrum" 3.0cm above the pyloric aperture. In the duodenum substance P (and VIP) were present in striking nerve networks in the villi as well as in the muscularis mucosae and around blood vessels. The peptide was also immunostained in nerve fibres in the submucosa, in neuronal perikarya between the lobules of Brunner's glands and in Meissner's plexus.

Substance P has been found to cause contraction of the muscularis mucosae; it is also a well-known vasodilator (Ferri et al. l984).

Enkephalin #

Hughes et al (l975) isolated two endogenous opiate-like compounds from pig brain. The two pentapeptides, endorphin and enkephalin, were subsequently demonstrated in other mammalian species (Polak et al. l977).

The distribution of endorphins and enkephalins in man was studied by a combination of immunocytochemistry and radioimmunoassay (Polak et al l977, l978). Endorphin immuno-reactivity was found to be confined to the intermediate and anterior lobes of the pituitary. Enkephalins on the other hand, were found to have a much wider distribution, being present in many areas of the central nervous sytem, spinal cord and peripheral nerves and being widely distributed in the gastrointestinal tract (Polak et al. l977; Skov Olsen et al. l98l). It was of interest that enkephalins were absent from the pituitary.

In the gastrointestinal tract enkephalin was found in most areas, the highest concentration being in the "antrum" (i.e. the pyloric mucosal zone) with lesser amounts in the duodenum and jejunum and even less in the colon; it was not present in the gastric fornix. The "antrum" contained 31 to 103 ng/gm wet weight, the duodenum l7 to 93 ng/gm, and the colon 6 to 15 ng/gm; the gall bladder and pancreas contained smaller amounts (Polak et al. l977, l978). Distribution of enkephalin cells closely paralleled the localization as determined by radioimmunoassay. According to Polak et al (l977) enkephalin was found in endocrine cells of the "antrum" and duodenum similar to G cells; it was presumed that the peptide could be stored either within gastrin containing granules or in different granules, as several granule types might occur in the same cell. However, the exact intracellular localization of these peptides was not clear; according to Skov Olsen (l98l) enkephalins were localized to specific endocrine-paracrine cells (other than G cells) of the APUD series, as well as to nerve fibres of the myenteric plexuses.

In the human gastric mucosa Ferri et al (l984) found metenkephalin immunoreactivity in a few scattered nerve bundles in the basal parts of the mucosa and in the muscularis mucosae. Enkephalins were rapidly degraded by blood and were unlikely to have a hormonal function; a paracrine function was more probable (Skov Olsen l98l).

The localization of enkephalins in neural tissue parallels that of opiate receptor sites (Polak et al. l978). Both are found in high concentrations in areas associated with sensory input of pain signals; the small molecular size and short half-life of this peptide suggest a neurotransmittive function. The pharmacology of morphia probably provides the best clue as to the role of enkephalins. Morphia acts by increasing muscle tone, delaying gastric emptying and slowing intestinal transit. In the gastrointestinal tract enkephalins may act in a similar manner; gastrointestinal enkephalins may aid in the control of intestinal motility, whereas brain enkephalins are thought to be involved in pain tolerance.

Konturek et al. (l978, l980) determined the effects of enkephalin on the gastrointestinal tract in canines. The results showed that enkephalin mimicked most of the motor effects of opiates; following administration there was a decrease in the rate, but increase in the amplitude of gastric contractions, with a delay in gastric emptying. In the small bowel enkephalin caused a marked reduction in postprandial spike potential activity, and conversion of the fed pattern of activity to a fasting pattern. Intra-arterial enkephalin and morphia increased intraluminal pressure values dose dependently, and decreased mesenteric vascular resistance.

Galanin #

Bishop et al (l986) showed that galanin immunoreactivity was localized exclusively to neuronal elements in the walls of the gastrointestinal tract in the rat, pig and man, and that it occurred at all levels of the tract. Galanin immunoreactive neuronal cells were noted in the submucous plexuses and immunoreactive nerves were present in all layers of the wall, with the possible exception of the mucosa; most fibres were located in the muscle layers. In the human stomach galanin immunoreactive nerves were equally numerous in the "antrum" and fornix. Preliminary pharmacological experiments showed that galanin caused smooth muscle contractions in the rat intestine and induced mild hyperglycaemia (Bishop et al. l986); it appeared to act as a regulatory factor in the control of gastrointestinal motility.

A close relationship existed between galanin and VIP immunoreactivity, both peptides occurring in the same ganglion cells of the submucous plexuses. The distribution of galanin and VIP immunoreactive nerves in the walls of the gastrointestinal tract was also similar, with the following exceptions: galanin fibres were infrequent in the mucosal layer as compared with VIP fibres, which formed dense mucosal plexuses; and galanin nerves did not appear to be associated with the vascular system of the gastrointestinal tract. (Bishop et al. 1986).

Neurotensin #

According to Buchan et al. (l977) the neurotensin secreting N cell is a typical endocrine cell with a connection to the lumen via microvilli and electron dense secretory granules grouped at the basement membrane. Radioimmunoassay and immunocytochemistry of fresh surgical and endoscopic samples showed that the highest concentration of neurotensin occurs in ileal mucosa, with significant amounts in the jejunum and only traces in the pyloric mucosal zone and duodenum. The concentration of neurotensin in plasma rises after a meal, but its function is still unclear. In the belief that it is a modulator of secretory and motor functions of the stomach, Blackburn et al (l980) infused it intravenously into healthy volunteers at a dose of 2.4 pmol/kg/min, designed to mimic postprandial levels. It was found that neurotensin caused significant inhibition of pentagastrin stimulated gastric acid and pepsin secretion. It also caused significant delay in gastric emptying, making it one more candidate for the hormone postulated to be released from the small intestine and to cause a feedback delay in gastric emptying.

Discussion #

Although individual variations in the distribution of APUD cells in the gastrointestinal tract exist, it is generally agreed that the highest density of gastrin producing G cells occurs in the distal 3.0cm of the stomach, i.e. in that part of the pyloric mucosal zone which lines the sphincteric cylinder. The number gradually decreases in an orad direction until the junctional zone between pyloric and oxyntic mucosa is reached, where a marked decrease in numbers occurs. The first part of the duodenum contains a fifth to an eighth of the number of G cells in the distal stomach. The physiological effects of gastrins, and the sequelae of overproduction in gastrinomas, are well known and need no recapitulation. In a small series of cases of gastric carcinoma Stave and Brandtzaeg (l978) found that the density of G cells increased from the proximal to the distal part of the "antrum", as in normal subjects. In acid corrosive injury to the gastric mucosa damage of G cells may produce histamine-fast achlorhydria, occurring as part of a delayed gastric syndrome (Chap. 39).

In the stomach somatostatin occurs mainly in the pyloric and oxyntic, and not in the cardiac mucosal zones.

Vasoactive intestinal peptide has a predominantly neural localization in the gastrointestinal tract. A dense VIP containing nerve supply occurs around glands in the pyloric and oxyntic mucosal zones; in the duodenum VIP is encountered in neuronal elements between the lobules of Brunner's glands. A particularly rich supply of VIP nerves occurs in structures believed to exert a sphincteric function, a factor which may assist in anatomically defining a sphincter. To the best of our knowledge this finding has not yet been utilized to determine the exact roles of the pyloric ring and pyloric sphincteric cylinder in the mechanism at the pylorus.

Substance P-containing nerve fibres in the gastrointestinal tract occur in highest density in the duodenal villi, muscularis mucosae, blood vessels, Meissner's plexuses and between the lobules of Brunner's glands. In the stomach these fibres have been found to be numerous and interconnecting in the "antrum" 3.0 cm proximal to the pyloric aperture. This is the region of the left pyloric loop in man; whether the occurrence is of any significance in relation to the sphincteric cylinder is not known. Substance P fibres are much less prominent in the upper part of the stomach.

In the gastrointestinal tract enkephalin occurs in highest concentration in the pyloric mucosal zone. Like morphia it causes a decrease in rate, but increase in amplitude of gastric contractions, with delay in emptying. Its effect on cyclical contractions of the sphincteric cylinder has not been determined; it is surmized that it will be of a similar nature.

Galanin immunoreactive fibres are equally numerous in the "antrum" and fornix; the peptide causes smooth muscle contractions and appears to act as a regulatory factor in motility.

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Gregory RA, Tracy HJ. The preparation and properties of gastrin. J Physiol l96l, 156, 523-543.
Gregory RA, Tracy HJ. The constitution and properties of two gastrins extracted from hog antral mucosa. Gut l964, 5, 103-117.
Gregory RA, Tracy HJ. The chemistry of gastrins. In: Gastrointestinal Hormones. edit Thompson JC. Univ Texas Press, Austin l975, pp 13-24.
Holle GE, Buck E, Pradayrol L, et al. Behavior of somatostatin-immunoreactive cells in the gastric mucosa before and after selective proximal vagotomy and pyloroplasty in the treatment of gastric and duodenal ulcers. Gastroenterology l985, 89, 736-745.
Hughes J, Smith TW, Kosterlitz HW, et al. Identification of two related pentapeptides from the brain with potent opiate agonist activity. Nature l975, 258, 577-579.
Johnson LR, Guthrie PD. Stimulation of DNA synthesis by big and little gastrin. Gastroenterology l976, 71, 599-602.
Konturek SJ, Krol R, Pawlik W, et al. Pharmacology of somatostatin. In: Gut Hormones, edit Bloom SR, Churchill Livingstone, New York l978, pp 457-462.
Konturek SJ. Pawlik E, Tasler J, et al. Effects of enkephalin on the gastrointestinal tract. In: Gut Hormones, edit Bloom SR, Churchill Livingstone, London l978, pp 507-512.
Konturek SJ. Opiates and gastrointestinal tract. Amer J Gastroenterol l980, 74, 285-291.
Krulich L, Dhariwal APS, McCann S. Stimulatory and inhibitory effects of purified hypothalamic extracts on growth hormone release from rat pituitary in vitro. Endocrinology l968, 83, 783-790.
Krulich L, McCann S. Effect of GH-releasing factor and GH-inhibiting factor on the release and concentration of GH in pituitaries incubated in vitro. Endocrinology l969, 85, 319-324.
Larsson LI, Fahrenkrug J, Schaffalitzky de Muckadell O, et al. Localization of vasoactive intestinal polypeptide (VIP) to central and peripheral neurons. Proc Nat Acad Science l976, 73, 3197-3200.
Larsson LI, Hirsch MA, Holst JJ, et al. Pancreatic somatostatinoma: clinical features and physiological implications. Lancet l977, l, 666-668.
McGuigan JE. Gastric mucosal intracellular localization of gastrin by immunofluorescence. Gastroenterology l968, 55, 315-327.
Modlin IM, Mitchell SJ, Bloom SR. The systemic release and pharmacokinetics of VIP. In: Gut Hormones, edit Bloom SR, Churchill Livingstone, New York l978, pp 470-474.
Morgan KF, Schmalz PF, Szurszewski JH. The inhibitory effects of vasoactive intestinal polypeptide on the mechanical and electrical activity of canine antral smooth muscle. J Physiol l978, 282, 437-450.
Mortensen NJM. The anatomy of the gastrin cell. Ann Roy Coll Surg l980, 62, 462-469.
Pearse AGE, Polak JM, Bloom SR. The newer gut hormones: cellular sources, physiology and clinical aspects. Gastroenterology l977, 72, 746-761.
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10 - Ultrasonography of Normal Anatomy

Mon, 01 Jan 0001 00:00:00 +0000

Ultrasonography of Normal Anatomy #

Conventional surface Ultrasonography of the Normal Infantile Pylorus #

The sonographic appearance of infantile hypertrophic pyloric stenosis (IHPS) was first described by Teele and Smith (l977) (Chap. 23). Subsequently a number of authors investigated the sonographic features of the normal infantile pylorus.

In transverse section the normal pylorus presents as a hypoechoic ring with a central echogenic core, resembling a "doughnut" or "target" (Fig. 10.1). By comparing sonographic images with histological sections Blumhagen and Coombs (l98l) were able to show that the hypoechoic ring coresponded to the muscular layer in the wall, while the more echogenic central core was formed by the mucosal and submucosal layers, including the muscularis mucosae. On these views the overall diameter of the ring, as well as the thickness of the sonolucent muscular layer, could be measured. The width of the hypoechoic muscular layer in normal infants between the ages of 2 and 10 weeks, was found to be approximately 3.0 mm.

Fig. 10.1. Transverse ultrasonic section of normal pyloric ring showing "doughnut" (arrow). The hypoechoic ring is the muscular, and the inner echogenic core the mucosal/submucosal component of the ring

Strauss et al. (l98l), using a static gray-scale B-scan unit and subsequently a real-time unit with a 5MHz focused transducer, considered the infantile pylorus to be within normal limits if its overall diameter measured 1.5cm or less.

Longitudinal sections of the normal pylorus, on which the canal length can be measured, may also be obtained. In tracing the thin, hypoechoic muscular layer distally to the gastric outlet, Blumhagen and Noble (l983) found the "antral" muscular layer to vary from 1.5 to 3.0 mm in thickness in normal infants. Khamapirad and Athey (l983), using digital gray-scale static equipment and a 5MHz focused transducer, studied transverse and longitudinal sonographic images of the pylorus in 12 normal infants between the ages of one and 6 weeks. The normal pyloric ring was similar in appearance to the mass of IHPS but was less than 1.0cm in diameter.

In a control group of 24 normal infants ranging in age from 2 days to 32 weeks, Graif et al. (l984) found the mean and standard deviation for the transverse diameter to be 7.45 � 2.2 mm. The mean single wall thickness was 2.3 mm with a standard deviation of � 0.7 mm, while the mean length of the pylorus was 12.0 mm with a standard deviation of � 3.7 mm.

Wilson and Vanhoutte (l984) measured what they called the true pyloric muscle length in l7 normal babies, and found the range to vary from 12.0 to 15.0 mm.

Stunden et al. (l986), in 88 normal infants under the age of 5 months, found the mean overall diameter of the pylorus to be 9.1 � 1.1mm, the mean muscle thickness 1.6 � 0.4 mm, and the mean canal length 8.3 � 2.5 mm. These measurements were all obtained with the pylorus in its most contracted state. Additional information could be obtained when the pylorus was viewed in real-time. Normally the pyloric "canal" was seen to relax, allowing fluid to pass from stomach to duodenum. Some variation in overall diameter and muscle thickness did occur, probably representing alterations in muscle tone.

According to Stringer et al. (l986) the thickness of the inner echogenic layer, consisting of the mucosa, muscularis mucosae and submucosa, normally varies between 2.5 and 3.5 mm in infants.

Swischuk (l989) found the hypoechoic outer muscular layer to measure only 1.0 mm in normal infants. At times it was too thin to be measureable.

Discussion #

The anatomy of the pyloric ring may be determined accurately by means of non-ionizing, non-invasive sonography in normal human subjects. This has been done in a number of volunteers, in whom it was confirmed that the ring consists mainly of mucosal and submucosal tissues, surrounded by a relatively thin, peripheral muscular ring (Chap. 11). The relative paucity of muscular fibres in the pyloric ring suggests that it is unlikely to be a sphincter in the usually accepted sense of the word.

References #

Blumhagen JD, Coombs JB. Ultrasound in the diagnosis of hypertrophic pyloric stenosis. J Clin Ultrasound l98l, 9, 289-292.
Blumhagen JD, Noble HGS. Muscle thickness in hypertrophic pyloric stenosis: sonographic determination. Amer J Roentg l983, 140, 221-223.
Graif M, Itzchak Y, Avigad I. et al. The pylorus in infancy: overall sonographic asssessment. Pediatr Radiol l984, 14, 14-17.
Khamapirad T, Athey PA. Ultrasound diagnosis of hypertrophic pyloric stenosis. J Pediatr l983, 102, 23-26.
Strauss S, Itzchak Y, Manor A, et al. Sonography of hypertrophic pyloric stenosis. Amer J Roentg l98l, 135, 1057-1058.
Stringer DA, Daneman A, Brunelle F, et al. Sonography of the normal and abnormal stomach (excluding hypertrophic pyloric stenosis) in children. J Ultrasound Med l986, 5, 183-188.
Stunden RJ, Le Quensne GW, Little KET. The improved ultrasound diagnosis of hypertrophic pyloric stenosis. Pediatr Radiol l986, 16, 200-205.
Swischuk LE. Imaging of the Newborn, Infant and Young Child. Williams and Wilkins, Baltimore, 3rd ed l989, pp 394-413.
Teele RL, Smith EH. Ultrasound in the diagnosis of idiopathic hypertrophic pyloric stenosis. New Engl J Med l977, 296, 1149-1150.
Wilson DA, Vanhoutte JJ. The reliable sonographic diagnosis of hypertrophic pyloric stenosis. J Clin Ultrasound l984, 12, 201-204

Endoscopic Ultrasonography of the Layer Structure of the Gastric Walls #

B-mode and real-time ultrasonography is a well-established and valuable diagnostic procedure in the examination of various intra-abdominal conditions. However, factors such as obesity, alimentary gas and ribs may limit the resolution and field of view in conventional surface echography. Hisanaga et al (l980) developed a sonographic scanner which could be introduced into the lumen of the stomach; as the gastric walls are quite thin, adjacent organs such as the pancreas could be observed from within the gastric lumen.

11 - Anatomy of the Pyloric Ring

Mon, 01 Jan 0001 00:00:00 +0000

Anatomy of the Pyloric Ring #

In fresh specimens a narrow (3.0mm to 4.0 mm) annular thickening, the pyloric ring, is felt in the wall of the gut at the gastro-duodenal junction. At laparotomy it may be difficult to palpate (Edwards and Rowlands l968), due to the effects of muscle relaxants administered during anaesthesia. On radiographs taken during the motor quiescent phase of the interdigestive myoelectric complex, the ring presents as a deep, clearcut, annular indentation separating the barium in the lumen of the stomach from that in the duodenum (Fig 11.1).

Fig. 11.1. Radiograph of normal pyloric ring (arrow) in motor quiescent phase of interdigestive myoelectric complex

Radiographic Anatomy #

Edwards (l96l) found the length of the ring, as measured on radiographs, to vary between 1.0mm and 12.0mm; the mean length was 1.7mm. It was not stated whether these measurements were taken during motor quiescent or during contraction phases. (Comment: the term "width" is preferred to "length" as used by Edwards. Normally, the width of the pyloric ring may vary, depending on the stage of contraction of the pyloric sphincteric cylinder, as described in Chapter 13).

Present Investigations #

The width and height of the pyloric ring, and the diameters of the pyloric aperture, sphincteric cylinder and duodenal bulb, were measured on radiographs of 10 adult subjects, taken at a time when no visible motor activity was evident, i.e. during the motor quiescent phase of the interdigestive myoelectric complex (Fig 11.2, Table 11.1). All subjects had been referred for radiographic examination because of vague upper abdominal symptoms. In none could an organic lesion be demonstrated; clinically and radiologically the stomach and duodenum were considered to be normal in all. The mean width of the ring was 4.7mm and the mean height 11.1mm; the depth was approximately the same on the greater and lesser curvature sides.

Fig. 11.2. Diagram of pyloric ring in motor quiescent phase. W, width; H, height; DB, duodenal bulb; PA, pyloric aperture; PSC, pyloric sphicteric cylinder

The inner margin of the ring surrounds the pyloric aperture, i.e. the opening by which the lumen of the stomach communicates with that of the duodenum. In the motor quiescent phase the diameter of the aperture varied from 5.0 to 13.0mm, with a mean of 8.7mm. The mean diameter of the sphincteric cylinder was 57.1mm, and the mean diameter of the duodenal bulb 35.8mm. (Comment: Owing to magnification factors the real measurements will be approximately four-fifths of the figures given).

Table 11.1 Radiographic measurements during the motor quiescent phase of the interdigestive complex


Case	Width of ring (mm)	Height of ring (mm)	Diameter Aperture	Diameter sphincteric cylinder (mm)	Diameter duodenal bulb (mm)

1	4.0	15.0	11.0	60.0	45.0
2	5.0	13.0	10.0	61.0	38.0
3	6.0	11.0	6.0	54.0	26.0
4	4.0	11.0	6.0	64.0	30.0
5	7.0	14.0	11.0	50.0	40.0
6	8.0	13.0	13.0	74.0	40.0
7	3.0	5.0	6.0	60.0	50.0
8	3.0	11.0	10.0	40.0	35.0
9	4.0	6.0	9.0	45.0	26.0
10	3.0	12.0	5.0	63.0	28.0
Average	4.70	11.1	8.7	57.1	35.8

Conclusion

It is concluded that the pyloric ring causes an appreciable constriction of the lumen at the gastroduodenal junction. Furthermore it is seen that the pyloric aperture is patent during the motor quiescent phase.

Microscopic Anatomy #

Illustrations of microscopic sections of the normal pyloric ring are occasionally encountered in published papers. In most instances the purpose is to illustrate some feature of the stomach in the vicinity of the pylorus and the ring is seen incidentally. On examining such illustrations the anatomical build of the ring may be studied.

Horton (l928) illustrated 3 normal stomachs sectioned 6 hours post-mortem. In all it is seen that the pyloric ring is not a structure consisting solely of muscular tissue. While its "base" is formed by muscularis externa, the top or inner part of the ring( i.e. the part surrounding the aperture) consists of a mucosal fold (made up of a core of submucosa with a layer of mucosa on each surface, as described in Chapter 5). In Horton's illustration of a 6 months old foetus the height of the outer muscular component of the pyloric ring is 14.0mm and the height of the inner mucosal fold, or mucosal component, also 14.0mm. In a 4 month old infant the muscular division of the ring measures 3.4cm in height and the mucosal division 2.0cm. In a one year old child the measurements are 3.5cm and 1.5cm respectively. It is clear in these subjects that the inner part of the pyloric ring consists of mucosal and submucosal, and not of muscular tissue.

Cole (l928) held that the abrupt interruption separating the lumen of the stomach from that of the duodenum (i.e. the pyloric ring) is a muco-membranous fold consisting solely of mucosa and submucosa with its acompanying muscularis mucosae. The circular fibres of the muscularis externa end at the base of the "pyloric fold", which should be looked upon as a valve and not as a sphincter, according to Cole (l928). Scott's (l946) observations led him to conclude that normally a thick mucosal fold caps the pyloric "sphincter" (from which it may be concluded that the ring consists of both the "sphincter" and an overlying mucosal fold).

In illustrations of Manning and Gunter (l950) the following measurements may be made: in a 66 year old subject the external muscular component of the ring is 3.0cm in height, and the inner mucosal/submucosal component 2.5 cm. In a 78 year old subject the figures are 2.5cm and 2.0cm respectively, and in a 58 year old subject 3.5cm and 2.0cm respectively. Williams (l962) illustrated two fresh, adult, partial gastrectomy specimens. In one the muscular component of the ring measures l8.0mm in height and the mucosal/submucosal component 9.0mm. In the other the figures are 21.0mm and 11.0mm respectively.

Present investigations #

Although the nature and function of the pyloric ring is often debated, few deliberate attempts have been made to determine its microscopic anatomy. Consequently sections of the ring were done more than 6 hours post-mortem in 7 subjects varying in age from 9 months to 83 years, who had succumbed to non-gastrointestinal causes; a total of 20 sections were examined (Table 11.2). In all cases the pyloric ring is seen to consist of muscular and mucosal/submucosal components (Fig 11.3). For instance, in a 9 month old subject the muscular component is seen to be 2.0mm in height, and the overlying mucosal component 1.0mm. In a 5 year old subject the approximate figures are 5.5mm and 1.5mm respectively, and in a 44 year old subject 5.5mm and 1.5mm respectively.

Fig. 11.3. Microscopic section of normal pyloric ring. The muscular component measures 4.5 mm, the mucosal/submucosal component 1.5 mm in height

Table 11.2 Results of postmortem examination in seven subjects

Fig. 11.3. Microscopic section of normal pyloric ring. The muscular component measures 4.5 mm, the mucosal/submucosal component 1.5 mm in height

Table 11.2 Results of postmortem examination in seven subjects


Subject	Age	Sex	Specimen number	Total wall thickness (mm)	Thickness of muscle layers	Thickness of mucosal/submucosal component

A.R.	9m	M	1	3.0	2.0	1.0
			2	3.0	2.0	1.0
			3	3.5	2.5	1.0
C.J.	5y	M	4	7.0	5.5	1.5
			5	6.0	5.0	1.0
			6	6.5	5.5	1.0
			7	7.0	5.5	1.5
A.W.	34y	M	8	6.5	5.0	1.5
			9	6.0	5.0	1.0
D.J.	44y	M	10	7.0	5.5	1.5
			11	7.0	5.5	1.5
			12	7.0	5.5	1.5
			13	6.0	5.0	1.0
			14	6.5	5.0	1.5
K.P.	55y	F	15	5.0	3.5	1.5
			16	5.5	4.0	1.5
			17	5.0	4.0	1.0
L.S.	76y	M	18	11.0	9.0	2.0
A.W.	83y	F	19	6.5	5.5	1.0
			20	6.5	5.5	1.0

y = years
m = months

12 - The Pylorus at Rest: Open or Closed?

Mon, 01 Jan 0001 00:00:00 +0000

The Pylorus at Rest: Open or Closed? #

In considering the mechanism of the pylorus it is of importance to determine, first of all, if the aperture is open or closed at rest. By “at rest” is meant conditions pertaining after an overnight fast, in which the stomach is empty except for normally occurring intraluminal gas, swallowed saliva and gastric secretions; it denotes the motor quiescent phase of the interdigestive myo-electric complex, with absence of radiologically discernible motor activity.

As indicated in Chap. 15, a number of authors held the view that the canine and human pylorus was surrounded by a narrow zone of raised pressure which was tonically contracted "at rest", closing the aperture; with the advent of an “antral” peristaltic wave the aperture relaxed (Brink et al. l965; Isenberg and Csendes l972; Fisher and Cohen l973). Other authors found or inferred that the pylorus was patent under fasting conditions, that it was not surrounded by a zone of elevated basal pressure, and that it did not act antagonistically to oncoming peristaltic waves (Atkinson et al. l957; Andersson and Grossman l965; Kaye et al. l976; McShane et al. l980; White et al. l98l; Gaffney et al. l987).

It can be assumed that an open pyloric aperture will allow the passage of liquids, while a closed pylorus will not. For this reason a fluid barium suspension has been used to determine the patency, or otherwise, of the aperture.

Present Investigations #

Patients and Methods #

A total of 100 adult, ambulatory outpatients were examined radiologically after an overnight fast. All had been referred for routine radiographic studies because of vague abdominal symptoms; patients with definite clinical symptoms and signs such as recurrent epigastric pain, weight loss, vomiting, haematemesis, melaena or a palpable mass, were excluded from the study.

Patients were examined in the erect and supine positions, each being asked to swallow three mouthfuls (45 ml) of a barium suspension in quick succession. The viscosity of the suspension was approximately four times that of water, the specific gravity was 2.004 and the consistency that of thick soup. These features ensured a fluidity which was less than that of water, but probably slightly more than that of chyme.

The state of the pylorus was determined by TV fluoroscopy and radiography, not more than one or two “spot” films being exposed (size of radiation field 14.5 x ll.5 cm). As soon as this had been done, more barium was swallowed (usually with the addition of effervescent salts)), and the conventional barium examination, for which the patient had been referred, was completed. If this revealed an organic lesion, the case was also excluded. In this group of 100 patients, in other words, the upper gastrointestinal tract was considered to be normal clinically as well as radiologically.

Ethical Considerations. In 52 patients the screening time due to the procedure varied from 5 to 15 seconds; in 48 patients it was longer, varying from 25 to 60 seconds. (In all the technique of intermittent screening was used). The anterior and posterior skin doses of x- radiation were measured and found to be negligible. As a small field (14.5 x ll.5 cm) limited to the upper abdomen was involved, it was felt that the extra radiation, received as a result of the procedure, could be discounted.

Results #

In 52 of the 100 patients the swallowed, liquid barium suspension passed rapidly down the oesophagus, traversed the stomach and flowed through the pyloric aperture in one smooth movement, without any delay or hold-up at the pylorus. This occurred in the absence of visible motor movements in the stomach. In many cases the head of barium was in the duodenum while the “tail end” was still in the oesophagus (Fig. 12.1). In all cases the normal, deep annular indentation of the pyloric ring between the stomach and duodenum became clearly visible as soon as the barium had traversed the aperture (Fig. 11.1). The part of the stomach on the immediate oral side of the ring (the pyloric sphincteric cylinder) was expanded without being unduly distended.

The width of the barium column in the pyloric aperture, between the lips of the ring, indicated the diameter of the aperture. It was measured on the films and varied from a minimum of 4.0mm to a maximum of 10.0 mm between subjects, the diameter in the majority being in the 5.0 to 10.0 mm range. (Owing to technical factors minor geometrical magnification occurs during radiographic filming, and the true measurements will be approximately four-fifths of those measured on the films).

In 48 patients there was some delay or hold-up at the ring; in the majority the delay varied from approximately 40 to 90 seconds; in a few it lasted for 2 or 3 minutes. The following are representative cases:

Fig. 12.1. Rapid swallowing in fasting stomach. Barium suspension traverses pyloric aperture, which is patent (arrow). “Tail end” of barium still in oesophagus. Absence of gastric motor movements

Case Reports

Case 12.1 J.S., male aged 28 years. Having swallowed 3 mouthfuls of barium suspension, a hold-up lasting 41 seconds occurred at the pyloric ring (counting had started as soon as the barium entered the gastric fornix). For the first 20 seconds of this period no gastric motor movements were seen; the distal 3.0 to 4.0 cm of the stomach was expanded without being unduly distended. At 20 seconds two successive, incomplete, “segmental” or “cylindrical” contractions of this region occurred (see Chap. 13), followed by commencing emptying into the duodenum at 41 seconds (Fig 12.2). (By “incomplete” is meant a minor to moderate degree of narrowing of the lumen, i.e. not bisecting the barium column).
Case 12.2 S.A., female aged 28 years. There was a hold-up at the pyloric ring lasting 85 seconds. For the first 30 seconds of this period no gastric contractions were seen. Subsequently two incomplete cylindrical contractions of the distal 3.0 to 4.0 cm occurred, followed by commencing emptying into the duodenum at 85 seconds.
Case 12.3 H.A., male aged 61 years. The hold-up at the pyloric ring lasted 128 seconds. At l8 seconds 2 or 3 incomplete contractions occurred, followed by a long period of inactivity. Eventually a few contractions reappeared, associated with emptying at 128 seconds.





`Fig. 12.2 A-D. Patient J.S. Initial hold-up at pyloric ring (A, B). Successive, incomplete contractions of pyloric sphincteric cylinder (arrow). Emptying into duodenum (C, D)`

Generally speaking a similar sequence of events was seen in the majority of patients in this group, namely a short hold-up at the pyloric ring, followed by 2 or 3 incomplete (or occasionally maximal) contractions of the pyloric sphincteric cylinder and commencing emptying into the duodenum (Fig. 12.3). The degree of dynamic narrowing of the lumen, as seen radiologically, probably corresponds to the amplitude as measured manometrically. This varied greatly among subjects.

Fig. 12.3. The first of two or three maximal contractions of pyloric sphincteric cylinder (arrows) preceding emptying into duodenum

In a minority of subjects in this group the period of hold-up at the pyloric ring was longer, lasting at least 90 seconds and sometimes as long as 2 to 3 minutes. In these patients the stomach invariably had a long, hanging, fish-hook shape, with a sagging greater curvature, which is evidence of hypotonia (Chap. 19). Tilting the table to an angle of 45 degrees, and turning the patient into the left anterior oblique position (i.e. with the right side down), invariably caused immediate emptying into the duodenum even in the absence of visible motor activity.

The following case is an example:

Case 12.4 S.M., female aged 50 years. In the erect position there was sagging of the greater curvature, which was located low down in the abdomen opposite the 5th lumbar vertebra; the shape of the stomach was compatible with hypotonicity. The first incomplete contraction of the pyloric sphincteric cylinder was seen at 60 seconds, with another occurring at 100 seconds. Up to 230 seconds no emptying had occurred. The table was then tilted to 45 degrees and the patient turned into the left anterior oblique position. Immediate emptying occurred in this position in the absence of visible contractions of the pyloric region, indicating patency of the pyloric aperture.

Discussion #

It is concluded that the pyloric aperture was open at rest in 52 of 100 normal subjects. Its diameter, as measured on the films, varied from a minimum of 4.0 mm to a maximum of 10.0mm in different subjects.

In the remaining 48 subjects some delay or hold-up occurred at the pyloric ring. In the majority of these the hold-up lasted from 40 to 90 seconds; in a few the hold-up was longer, lasting from 90 seconds to 3 minutes. In this latter subgroup the delay at the pylorus was associated with hypotonicity or sagging of the greater curvature of the stomach. Tilting the table by 45 degrees and turning the patient into the left anterior oblique position, caused immediate gastric emptying in the absence of radiologically visible contractions. It is concluded that visible contractions are not necessary for emptying of liquid barium in this position.

It appears that the delay in emptying in these 48 subjects was either due to hypotonicity of the gastric musculature (Chap. l9), or to closure of the pyloric aperture. Different types of closure of the aperture may occur (Chap. 13); in the present cases the pyloric sphincteric cylinder was expanded, and the radiological features suggest that closure of the aperture was due to converging or spiral (“iris-like”) gastric mucosal folds (Chap. 13).

References #

Andersson S, Grossman MI. Profile of pH, pressure and potential difference at gastroduodenal junction in man. Gastroenterology l965, 49, 364-371.
Atkinson M, Edwards DAW, Honour AJ, et al. Comparison of cardiac and pyloric sphincters. Lancet l957, 273, 918-922.
Brink BM, Schlegel JF, Code CF. The pressure profile of the gastroduodenal junctional zone in dogs. Gut l965, 6, 163-171.
Fisher RS, Cohen S. Physiological characteristics of the human pyloric sphincter. Gastroenterology l973, 64, 67-75.
Gaffney PR, Gleeson DJ, Hall JW, et al. The manometric findings at the human pylorus: the evidence against the presence of a tonic sphincter. Scand J Gastroenterol l987, 22, 525-532.
Isenberg JI, Csendes A. Effect of octapeptide of cholecystokinin on canine pyloric pressure. Amer J Physiol l972, 222, 428-431.
Kaye MD, Mehta SJ, Showalter JP. Manometric studies of the human pylorus. Gastroenterology l976, 70, 477-480.
McShane AJ, O'Morain C, Lennon JR, et al. Atraumatic non-distorting pyloric sphincter pressure studies. Gut l980, 21, 826-828.
White CM, Poxon V, Alexander-Williams J. A study of motility of normal human gastroduodenal region. Dig Dis Sci l98l, 26, 609-617.

13 - Radiographic Examination of Normal Motility

Mon, 01 Jan 0001 00:00:00 +0000

Radiographic Examination of Normal Motility #

Introduction #

In radiographic studies of the upper gastrointestinal tract, only the contrast material in the lumen is visible, the actual walls of the tract being invisible.

The contrast material usually consists of one or more of the following:

Insoluble, non-absorbable barium sulphate in fluid suspension. Where such a suspension is used, it represents the luminal contents, and being radio-opaque, is visualized as an image of positive contrast. In the "conventional" radiographic study a low density barium suspension is used with a specific gravity of 2.004 and a viscosity approximately four times that of water. The consistency approximates that of thick soup but may, if required, be increased to that of a paste. Commercial preparations contain additives regulating consistency and taste.
Water soluble, absorbable iodine-containing solutions, also providing images of positive contrast, but with lower radio-opacity than barium.
Air, which may be swallowed or introduced via tubes, providing negative contrast.
Carbondioxide gas, affording an intraluminal, negative contrast agent. The gas is liberated in the lumen by swallowed, commercially available gas-producing granules or powders.

In the "conventional" radiographic study, barium sulphate with or without the addition of air or gas is used, affording clear and sharply defined images of the contrast column in the lumen. As pharmacologically active substances are not usually administered, normally occurring, physiological movements of the contrast column may be studied. While the rate of flow of a fluid contrast agent depends to a large extent on its viscosity, we noted no naked eye differences in the type or range of movements, whether "conventional" fluid barium suspension, barium paste or a watery iodine solution was used as contrast agent. (Comment: The "range" of movement seen radiologically roughly corresponds to the amplitude as determined at manometry).

The comparatively large volume of barium used in the conventional radiographic study (much less being used in the double-contrast method) may obscure some of the intraluminal features, confirming the dictum that "barium reveals but also conceals". Consequently use is made of compression techniques, by which some of the suspension is pressed away, to reveal the macroscopic mucosal folds and other intraluminal features.

In the double-contrast radiographic study, a coating of the luminal surface of the mucosa is obtained by swallowing a small volume of a micropulverized, dense, more viscous barium preparation; positioning the patient ensures equal allround coating. The parenteral administration of an antimuscarinic pharmacological agent causes temporary paralysis of the muscular walls with expansion of the lumen; this is enchanced by introducing a large volume of carbondioxide gas into the lumen. Under these circumstances naked-eye movements are no longer discernible; moreover, distension of the lumen with stretching of the walls effaces the macroscopic mucosal folds. The micropulverized barium enters minute furrows between the areae gastricae on the inner surface of the mucosa, thus rendering the areae gastricae, or surface mucosal pattern, visible (Fig. 13.1). In the present investigation, whenever motility patterns were studied, the conventional barium examination was used.

Fig. 13.1. Double contrast study with gas distended lumen. Fine, reticular pattern indicates areae gastricae or surface mucosal pattern

Validation Studies #

It is regarded as axiomatic in radiology that a temporary, circumferential, physiological narrowing of the barium column in the lumen of a hollow muscular tube is due to contraction of the walls of the tube. This supposition has not always been accepted universally. It has been argued, especially in physiology, that a barium column may appear to be narrowed in cases of incomplete filling of the lumen. Alternatively, even with complete filling, a passive "falling together" of the walls (as opposed to active contraction) may narrow the column. Whether these objections are valid or not may be determined by combining alternative modes of investigation, e.g. manometry, with radiological imaging procedures.

In the present context intraluminal pressure profiles and specially devised living anatomical studies have been done in an effort to validate the radiological observations.

Intraluminal Pressure Profiles #

While investigating mucosal fold movements in the distal 3.0 to 4.0 cm of the stomach, i.e. within the confines of the anatomical pyloric sphincteric cylinder, as well as in the duodenum, intraluminal pressure studies were combined with radiological imaging procedures in 11 normal subjects (Keet et al l978) (Chap. 15). These investigations may, at the same time, be utilized to determine the relationship between intraluminal pressures and radiologically demonstrable, physiological movements of the circumference of the barium column in these regions. (In this context "movements" do not imply propulsion or retropulsion of contents).

Ethical Considerations. All subjects taking part were informed, volunteer, adult, male ambulatory outpatients who had been referred for an upper gastro-intestinal radiographic study because of vague abdominal symptoms. None had had any significant clinical signs at the preliminary clinical examination. Only patients in whom no organic lesion could be demonstrated in the oesophagus, stomach and duodenum at the radiological examination were admitted to the study; it was cleared by the Ethical Committee.

Patients, Materials and Methods #

Pressure recordings were obtained by means of an air-filled system and a miniature balloon, placed on the immediate oral side of the pyloric aperture (i.e. in the lumen of the pyloric sphincteric cylinder) in 5 subjects, and in the second or third parts of the duodenum in 6 other subjects.

A pressure sensitive system usually used for cardiovascular physiology, with some modifications, was employed. It consisted of a monitor (Statham SP1400) (Statham Instruments Inc., Los Angeles), a miniature transducer (Statham P37B), a recorder (Statham SP2006) and a catheter, 125 cm in length, with an outside diameter of 2.0mm. A miniature balloon 38 mm in length and 8.0 mm in diameter, covered the 6 endholes of the catheter. The volume of air introduced into the balloon to achieve zero pressure was 0.8 ml. After an overnight fast the balloon was manipulated into position under TV screening, with the subject in the erect position. Four mouthfulls of a fluid barium suspension were swallowed to delineate the lumen and for purposes of localization. In the absence of visible motor activity the diameter of the pyloric sphincteric cylinder was approximately eight times the diameter of the balloon (visible because of its air content), and the diameter of the duodenum three times that of the balloon. Artifacts such as subject movement, coughing and pressure increases produced during compression procedures were identified and excluded. Pressure increases were correlated with motility of the barium column as viewed radiographically, and vice versa.

Results in Stomach #

In the pyloric sphincteric cylinder the base line of the curve represented intraluminal pressure while the cylinder was distended, in the absence of radiologically visible motor activity (Fig. 15.1). The following two distinct waves of pressure increase were noted manometrically:

Irregularly occurring, nonrhythmic contractions, causing intraluminal pressure increases varying from 9.0 to 34 mm Hg (the majority being in the range of 12 to 25 mm Hg). These waves lasted for 5 to 21 seconds (the majority being in the 6 to 10 second range) (Fig. 15.1), occurred repeatedly in all subjects and conform to Type II contractions (Code and Carlson l968; Shepard l97l).
In two of the subjects compound waves, consisting of a rise in base line pressure of 3.0 to 5.0mm Hg and lasting for 10 to 40 seconds, on which were superimposed waves of shorter duration (3 to 5 seconds) and higher amplitude (up to 12 mm Hg), were recorded; these conform to Type III waves (Shepard l97l).

Simultaneous radiological TV monitoring showed that both waves of pressure increase were associated with a concentric narrowing of the barium column characteristically occurring in this situation (see below). The higher the amplitude of the pressure wave, the greater the luminal narrowing appeared to be radiologically.

Conclusion #

It was concluded that the narrowing of the barium column was due to active contraction of the walls.

Results in Duodenum #

In the second and third parts of the duodenum the base line again represented intraluminal pressure in the absence of radiologically visible motor activity. Two waves of pressure increase were noted manometrically:

Nonrhythmic, simple, brief monophasic waves, causing intraluminal pressure increases of 4.0 to 35 mm Hg (the majority being in the 7.0 to 34 mm Hg range), and lasting 2 to 8 seconds (Fig. 13.2). These waves occurred repeatedly in all subjects and conform to Type I duodenal waves (Foulk et al. l954; Vantrappen et al. l965; Friedman et al l965); it was suggested that they should be designated phasic waves (Texter l968).
In two of the subjects nonrhythmic, complex waves consisting of a rise in base line pressure of 3.0 to 4.0 mm Hg and lasting from 40 seconds to 2½ minutes, with superadded peaks of l9 to 23 mm Hg lasting for 5 to 6 seconds, were seen occasionally. These conform to Type III duodenal waves (Foulk et al. l954; Vantrappen et al. l965; Friedman et al. l965); it was suggested that they should be designated tonic waves (Texter l968).

During both types of waves radiologically visible, circumferential narrowing of the luminal barium column occurred simultaneously with the increases in pressure (see also Chap. 15).

Fig. 13.2. Four monophasic duodenal pressure waves. Each was associated with a radiologically visible contraction. During each wave mucosal folds changed in direction to become longitudinal. Base line indicates intraluminal pressure in absence of motor activity. Ten-second marker on zero line

Conclusion #

It was concluded that the narrowing of the intraluminal barium column was due to active contraction of the walls.

Living Anatomical Studies #

The living anatomy was investigated in a number of patients who had to undergo cholecystectomy during the ordinary course of events (Keet and Heydenrych l982). The investigation was designed to determine the spatial relationship between the barium column in the lumen and the walls.

Ethical Considerations. The study was undertaken in informed, adult, white, volunteer patients who had been admitted to hospital with definite indications for cholecystectomy. All aspects of the procedure had been considered carefully beforehand by ourselves, our peers and the Head of the Department of Surgery; no objections were raised. The Ethical Committee indicated that it could find no objection to the procedure.

Patients, materials and methods #

Six patients were examined. On completion of the cholecystectomy, and before closure of the abdomen, the stomach and duodenum were shown to be normal by means of direct inspection and palpation. Two fine, flexible stainless metal wires, similar to the wires used in the leads of myocardial pacemakers, were attached to the serosal surface of the pyloric region of the stomach and first part of the duodenum by means of superficial, interrupted, absorbable sutures (Fig. 13.3). One wire was attached to the lesser and the other to the greater curvature, the free "duodenal" ends of both wires being brought to the surface (as in the case of a postoperative T-tube) through the cholecystectomy incision, which was subsequently closed in the usual way.

Approximately 8 days later, on the day before discharge, each patient had a limited radiographic study as follows: after an overnight fast 4 to 5 mouthfulls of the usual liquid barium suspension was swallowed in the erect position, so as to outline the horizontal part of the gastric lumen and to extend well up into the vertical part. The space between the metal wires on the serosal surfaces and the luminal barium indicated the thickness of the wall; during the motor quiescent stage it was approximately 4.0 to 5.0 mm. After emptying into the duodenum had commenced, gastric contractions were studied by means of radiographic TV monitoring and appropriate radiographs.

Fig. 13.3. Radiograph showing living anatomy. Two fine, flexible metal wires (retouched) are attached to serosal surfaces of lesser and greater curvatures. The space between the wires and intraluminal barium indicates the cylindrical muscular contraction

Results #

Narrow, circumferential indentations of the barium column appeared in the body of the stomach and proceeded to move in a caudal direction. Opposite the indentations the fine, flexible wires remained in their original position, showing that these indentations were due to contraction waves in the walls and not "falling together" of the walls. At a point 3.0 to 4.0 cm orally to the pyloric ring each wave became stationary, at the same time initiating a concentric, cylindrical narrowing of the barium column in the remaining part of the stomach, as far as and including the area of the ring. Again the wires were seen to remain in their original position. During a contraction the space between the wires and the luminal barium widened to approximately 8.0 to 10.0 mm all round, indicating an active, tube-like or cylindrical contraction of the muscular walls, 3.0 to 4.0 cm in length (Fig. 13.3). After a second or two of maximal contraction, the walls relaxed and the cycle was repeated.

On completion of the radiological examination the wires were removed by gentle traction on their external ends. None of the patients suffered any discomfort or untoward sequelae; recovery was normal.

Conclusion #

It is concluded that the narrowing of the intraluminal barium column was not due to a passive falling together of the walls, as the fine, flexible wires on the serosal surface remained in their original positions. The narrowing of the column was due to active contraction of the walls between the serosa and the barium containing lumen. (Endoscopic ultrasonography confirms that "peristaltic" contraction of the wall produces wall thickening, as mentioned in Chapter 10).

Motor Divisions of Stomach #

According to Code and Carlson (l968) the stomach has 3 functional regions corresponding to its anatomic divisions, namely the fundus, corpus and pyloric antrum, which, in their view, is the region stretching from the incisura angularis to the pylorus. (Comment: While the concept of these "anatomical" divisions appears to be widely accepted, it is shown in Chapters 2 and 3 that the division is of an arbitrary nature and not based on anatomical facts). In terms of motor activity Code and Carlson (l968) divided the antrum into two segments of varying length. The caudal portion participates in a simultaneous segmental contraction called the terminal antral contraction (TAC), previously described by Carlson, Code and Nelson (l966). The cephalad portion of the antrum, according to these authors, is not usually involved in TAC; however, at times TAC involves only the distal one to two centimeters of the antrum, and at other times almost the entire antrum. During TAC a simultaneous contraction of the terminal segment of the antrum occurs, a phenomenon which corresponds to antral systole previously described by Golden (l937). The cephalad and terminal (or caudal) segments of the antrum, together with the pylorus (also called the pyloric canal or pyloric sphincter) constitute a functional motor unit according to Code and Carlson (1968); the separate parts vary in their dimensions but contract in a co-ordinated way. The pyloric canal closes vigorously with contraction of the terminal antrum. (Comment: According to these authors the pyloric ring constitutes the pyloric sphincter. The pyloric canal is equated with the aperture).

Ruch and Patton (l973) state that morphologically, histologically and functionally the stomach is divided into 3 parts, viz. the fundus, corpus and pyloric antrum or pars pylorus, a narrower, more muscular, non-acid secreting region. The fundus and corpus together form a somewhat bulbous, thin-walled storage and secretory chamber, while food is fragmented and mixed with digestive juices in the "antrum". There is no structural discontinuity between these regions, which are only modifications of a basic pattern.

From the point of view of motility, other authors divided the stomach into two parts, namely a proximal one third and a distal two thirds (Kelly l98l; Funch-Jensen l987). The division was said to be based not on the usually accepted anatomical considerations, but on the type of smooth muscle activity. During swallowing the proximal part of the stomach relaxes, which allows filling without a significant increase in pressure. It acts as a receptacle and determines to a large extent the emptying of liquids. The distal two thirds shows active peristalsis which propagate luminal contents towards the pylorus, thereby effecting the emptying of solids.

In terms of motor function, based on the muscular anatomy, radiologically visible contraction patterns, manometrically recordable pressure waves and myoelectric activity, it is our view that the stomach should be divided into three parts namely (1) the fornix, (2) the corpus and sinus and (3) the distal 3.0 to 4.0 cm (Keet l957) (Fig. 13.4).

Fig. 13.4. In terms of motor activity the stomach should be divided into three parts. 1., fornix; 2., corpus and sinus; 3., distal 3-4 cm

Fornix #

This region roughly encompasses the proximal one sixth of the stomach. The muscular coat is at its thinnest in this region and consists of outer longitudinal, middle circular and inner oblique fibres. The entire cardiac mucosal zone as well as the upper part of the oxyntic zone are located in this region. During radiographic examinations this part of the stomach is seen to be capable of slow expansion and contraction (depending on the degree of filling), but no other intrinsic motility, such as peristaltic activity, is discernible. This correlates well with manometric findings, in which it has been shown that motor activity in the fornix consists almost entirely of slow, low amplitude phasic changes in pressure or tone (Lind et al. l961; Code and Carlson l968; Granger et al. l985). It has also been found that myoelectric activity is absent in the fornix (Kelly and Code l97l; Koch et al. l987).

Corpus and Sinus #

This region extends from the base of the fornix as far as an imaginary line 3.0 to 4.0 cm orally to the pyloric aperture. The muscular coat in its proximal part again consists of outer longitudinal, middle circular and inner oblique fibres, while the oblique layer terminates in its distal part. The major part of the oxyntic mucosal zone as well as the proximal part of the pyloric mucosal zone are located in this region. (The extent of the pyloric mucosal zone is discussed in Chap. 5).

During radiological examinations narrow, annular constricting waves, moving in a caudal direction (i.e. peristaltic waves) are seen in this part. They commence as shallow circumferential indentations of the barium column in the corpus, some distance above the incisura angularis, and may or may not become deeper as they proceed. This agrees with manometric and other physiological findings, where it has been shown that peristaltic contractions originate in the orad part of the corpus and migrate towards the pylorus (Smith et al. l957; Rhodes et al. l966; Carlson et al. l966; Granger et al. l985; Koch et al. l987). On the basis of intraluminal pressure changes, these peristaltic waves are divided into Type I waves (producing pressure increases of less than 5.0 cm of water) and Type II waves (producing pressure increases of more than 5.0 cm of water) (Code et al. l952; Smith et al. l957; Carlson et al. l966). The two types are essentially similar, being simple, monophasic waves, differing only in amplitude (Code and Carlson l968). It was surmised that the main function of Type I waves was mixing (with a secondary function of propulsion) and the main function of Type II waves propulsion (and secondarily mixing).

While both Type I and Type II waves are of a peristaltic nature, a third type namely Type III waves, may occur. These are complex waves, characterized by a rise in base-line pressure on which either Type I or Type II waves are superimposed. They are seldom present and of little consequence in the stomach (Code et al. l952). Radiologically Type III waves are usually not recognizable in the stomach.

The frequency of barium-induced peristaltic (i.e. Type I and Type II) waves in this part of the stomach, as seen radiologically, is approximately 3 per minute in man and 5 per minute in dogs (Smith et al l957; Rhodes et al. l966; Carlson et al. l966). Underlying myoelectric activity occurring here consists of slow waves (also known as basic electrical rhythm, pacesetter potential or electrical control activity) and spike activity (spike bursts, action potential or electrical response activity) (Chap. 16). Slow waves originate on the greater curvature in the upper part of the corpus, where spontaneous depolarizations occur at a frequency of 3 cycles per minute in man (Kwong et al. l970; Couturier et al. l972; Funch-Jensen l987), and 5 cycles per minute in canines (Weber and Kohatsu l970; Kelly et al. l97l). Contraction occurs when spike activity is superimposed on slow waves.

Distal 3-4 cm #

The muscular coat is at its thickest in this part of the stomach and consists of outer longitudinal and inner circular fibres. The thickening of the circular musculature commences almost imperceptibly 3.0 to 4.0 cm from the pylorus, increases gradually in an aboral direction and ends abruptly in the muscular ring (i.e. the muscular component of the pyloric ring) which surrounds the aperture. There is no structural discontinuity between the musculature of this region and that of the more proximal part of the stomach on its oral side (the sinus). Aborally the circular musculature of the ring is sharply demarcated from that of the duodenum by a fibrous septum (Chap. 3).

The musculature of the distal 3.0 to 4.0 cm of the stomach forms the pyloric sphincteric cylinder, as described by Cunningham (l906), the circular musculature of which consists of a system of rings or loops according to Forssell (l913), Cole (l928) and Torgersen (l942) (Chap. 3). It was shown that the loops deviate from the lesser curvature, where they meet in a muscle torus or knot, to encircle the greater curvature in a fan-like shape. The right muscular loop forms the peripheral part of the pyloric ring (Chap. 11). The greater curvature part of the left loop (which is less well-developed than the right) is situated 3.0 to 4.0 cm orally to the right loop and corresponds to the sulcus intermedius; the circular loops are connected by intervening circular as well as by the overlying longitudinal fibres.

The interior of this part of the stomach is lined by pyloric mucosa. However, the pyloric mucosal zone is not limited to this region, but extends orally into the more proximal part of the stomach (i.e. the sinus) for a variable distance (Chap. 5).

Myoelectric activity in the distal 3.0 cm of the stomach differs from that in the corpus and sinus in that a marked velocity increase in basic electrical rhythm occurs here (Chap. 16). This is associated with a "rapid spread of peristalsis" or a "nearly simultaneous contraction" of this part of the stomach, responsible for its behaviour as a motor unit (Chap. 16).

Do Gastric Peristaltic Waves Progress as far as the Pyloric Aperture? #

In a consideration of motility patterns of the distal 3.0 to 4.0 cm of the stomach, it is necessary to determine if gastric peristaltic waves normally proceed as far as the pyloric aperture.

Golden (l937) stated that each narrow peristaltic wave proceeding down the stomach terminated in "antral systole", i.e. a segmental or concentric contraction of the entire canalis egestorius described by Forssell (l913), which corresponds to the pyloric sphincteric cylinder.

Other authors differed. During simultaneous cineradiographic and kymographic studies in man, Smith et al. (l957) found that both Type I and Type II waves invariably progressed over the antrum toward the pylorus in a peristaltic manner. In some cases the pylorus failed to relax as barium was driven towards it (which implied that the waves proceeded as far as the pylorus); in other cases the wave faded just proximal to the pylorus.

14 - The Pylorus at Gastroscopy

Mon, 01 Jan 0001 00:00:00 +0000

The Pylorus at Gastroscopy #

Schindler (l936) described the interior of the stomach as seen at gastroscopy in patients lying on their left side. In this position the pyloric part falls to the left and forward towards the anterior abdominal wall. While radiologists perceive the incisura angularis as an indentation of the lesser curvature side of the barium column, gastroscopists see it as a prominence or "kind of fold" in the inside of the stomach, called the angulus or angle. According to Schindler the stomach could be divided into two parts: the part above the angulus or pars digestoria, and the part between the angulus and pylorus or pars egestoria. If little air is used for inflation at gastroscopy, another prominent fold, the musculus sphincter antri, becomes visible on the anterior and posterior walls and greater curvature at the level of the angulus. It is a separate entity from the angulus, is probably formed by contraction of the muscularis externa and is usually not demonstrable radiologically.

According to Schindler (l936) peristaltic waves always commence distally to the musculus sphincter antri. Gastroscopically these waves are seen as circular elevations moving towards the pylorus and accompanied by a shortening of the "antrum" until closure of the pylorus is complete. This is often accompanied by the formation of radial mucosal folds, giving the closed pylorus a stellate appearance.

Torgersen (l942) showed that the musculus sphincter antri consisted of a loop at the termination of the oblique fibres of the muscularis externa of the corpus. It was also called the lower segmental loop and formed the oral boundary of the sinus (Chap. 3). Consequently it did not take part in the contractions of the pyloric sphincteric cylinder.

Gastroscopically the pylorus is seen to be open most of the time, according to Johnson (l961). As a wave of peristalsis passes down the "antrum" and reaches the pylorus, the latter is seen to close. It remains closed for only a few seconds, then relaxes, remaining open until it is reached by the next peristaltic wave.

Rider et al. (l967) described the dynamic anatomy of the "antrum" and pylorus. Numerous combined fluroscopic and gastroscopic studies showed that peristaltic waves proceeded through the corpus and proximal part of the "antrum" towards the pylorus. Each wave caused a "pinch-off" in the antrum, creating the appearance of a rosette-like sphincter, called the proximal sphincter. The area beyond this sphincteric action was still part of the stomach and represented the "distal antrum" or "pyloric channel". With relaxation of the proximal sphincter a small, circular distal opening became evident beyond it, which was the pyloric aperture surrounded by the true pyloric ring. It was pointed out that the proximal sphincter could easily be mistaken for the pyloric ring, and in such cases it could erroneously be concluded that a gastroscope which had passed this area was in the duodenal bulb.

Comment: From the above description it is clear that contraction of the "proximal sphincter" is the same occurrence as contraction of the left pyloric loop as seen radiologically (Chap.13). The dynamic anatomy seen at gastroscopy and radiology tallies with the morbid anatomy described by Cunningham (l906), Forssell (l913) and Torgersen (l942). The part of the stomach on the caudal side of the "proximal sphincter", called the "distal antrum" or "pyloric channel", is the pyloric sphincteric cylinder.

According to Code and Carlson (l968) each terminal antral contraction (TAC) seen at gastroscopy, produces a diaphragm across the stomach with a central orifice. The size of the orifice depends on the strength of the contraction. Retropelled contents are forced with varying degrees of vigor through this orifice in an oral direction.

Comment: The diaphragm across the stomach with a central orifice again corresponds, in our view, to contraction of the left pyloric loop (Chap. 13). Not only gastric contents, but at times also gastric mucosal folds, are retropelled through the contraction ring of the left loop, by powerful contractions of the pyloric sphincteric cylinder (Chaps. 13, 36).

At gastroscopy Edwards and Rowlands (l968) found that ripples of contraction sometimes moved down the gastric wall to a well-defined ring where the large bag of the stomach joined the commencement of the "antral funnel". The ring often contracted to a narrow bore, at times obliterating the lumen, and could be mistaken for the pylorus. The true pylorus was situated at the end of the funnel. At times annular contraction waves with a frequency of 3 per minute moved long the "antrum" to the gastro-duodenal junction, propelling mucus. Sometimes the mucus would be retropelled from the funnel in an oral direction. The findings were ascribed to intermittent and possibly haphazard activity of the stomach due to the conditions pertaining at gastroscopy, such as the distension of the stomach, the stress of the subject, and the administration of sedative drugs.

Comment: In our view the well-defined ring at the commencement of the "pyloric funnel", which could be mistaken for the pylorus, again corresponds to the left pyloric loop, while the "pyloric funnel" corresponds to the sphincteric cylinder. The retropulsion of mucus through the ring is the result of normal contractile activity of the cylinder; normal retropulsion of barium occurs in the same way (Chap. 13). Blackwood (l969) pointed out that the correct interpretation of a ring structure in the pyloric region could present problems at gastroscopy, especially when it had an unusually large diameter, when a second ring was seen beyond it, or when radiology revealed a gastric lesion obviously distal to the ring structure visualized. In such cases it could be difficult to determine if one was dealing with the pyloric ring or with a different ring. In an attempt to improve the endoscopic evaluation of the pyloric region, he localized the pylorus by electrical potential difference (PD) measurements under direct gastroscopic vision. Of 9 studies, 7 revealed a significant PD change within 1.0 cm of the visualized ring, confirming the visual diagnosis of a normal pyloric ring. In all 7 cases the radiological appearance was normal. Two studies showed the PD change 3.0 to 4.0 cm beyond the visualized ring. In both, radiological abnormalities were evident in the stomach (one had an "antral" ulcer with narrowing, the other a "narrowed antrum"). These were regarded as cases of antral deformity mimicking the pylorus, i.e. false pyloric rings.

Comment: From the published radiographs of the 2 abnormal cases, it seems that the pyloric sphincteric cylinder was contracted in both. The "antral" ulcer in the first case was located within the cylinder. The rings visualized in these 2 cases must have been at the oral end of the contracted cylinder, i.e. in the situation of the left pyloric loop. The PD change 3.0 to 4.0 cm distal to the visualized rings confirms the above interpretation.

Of a total of l8 ring-like structures seen in the "distal antrum" at gastroscopy, Blackwood (l969) found 14 to be normal pyloric rings. Four of the l8 were "antral" deformities mimicking the true pyloric ring. It was concluded that about 4 out of 5 ring structures seen in the "distal antrum" would be pylorus, while about 1 out of 5 would be a different ring. The following criteria were suggested as aids in identifying rings in the distal antrum: the normal pylorus should be visualized distal to the occlusive portion of the "antral peristaltic wave" and remain patent and immobile between antral contractions. It should have the appearance of a sharply defined circumferential mucosal diaphragm projecting at nearly right angles to the antral wall. In cases of antral narrowing however, the wall would be observed to taper gradually to a narrowed area. An antral contraction wave might be seen to move smoothly in a caudal direction, distal to a ring-like structure. If mucosa distal to a ring was extruded proximally, it was likely that "antrum" was present distal to this particular ring. Blackwood (l969) finally defined the normal pylorus as a localized circumferential narrowing formed by a thin septum of mucosa with a small central aperture seen only, and remaining patent, between antral contractions, without mucosa or other landmarks being visualized distally.

According to Dagradi (l969), once the tipe of the gastroscope has been insinuated beyond the angulus, deep, rhythmic, sequential propagative waves of the "antrum" are commonly observed. These originate at the angulus, traverse the "antrum" and recede into the distance. On advancing the fiberoptic instrument, the waves are seen to terminate at a certain point of closure, where longitudinal mucosal folds are drawn together as if by a purse string. From this point a retrograde prolapse of bunched-up mucosa develops, somewhat resembling the opening of the petals of a flower bud; the point of closure has been likened to a rosette or "fleurette". Relaxation of the contraction ring follows, revealing the cavity of the "prepyloric antrum" and at its distal end the pyloric orifice. Normally the orifice is ring-like in configuration when seen head-on or oval if seen tangentially; at times it may be observed to contract or expand, changing slowly in diameter. Occasionally a false pyloric orifice may be seen which can be confusing. This usually occurs in association with a distal "antral" ulcer; the true nature of such a localized, unrelenting contraction ring becomes evident if the pyloric orifice can be observed distal to it.

Comment: The rosette-like point of closure again corresponds to contraction of the left pyloric loop, situated at the commencement of the pyloric sphincteric cylinder (Chap. 13). Retrograde prolapse or movement of mucosal folds during contraction of the cylinder is clearly visible radiographically (Chap. 13).

At endoscopy Kaye et al. (l976) found that the pylorus was frequently very narrow, but that it was usually not completely closed except during the terminal phase of an "antral" contraction.

Maratka (l984) mentioned that a congenital septum or an acquired fibrous septum (secondary to ulcer scarring) in the antral area might simulate the pylorus and could be called a "pseudopylorus".

Comment: The permanent "pseudopylorus" formed by a septum is obviously quite distinct from the normal intermittent, ring-like contractions of the left pyloric loop with its central aperture.

According to Varis (l989) endoscopy may fail to demonstrate motor disorders of the stomach, for instance in conditions such as diabetic gastroparesis.

Comment: One of the few shortcomings of endoscopy in the examination of the upper gastrointestinal tract is its inability to demonstrate the full range of gastric motor movements under physiological conditions. The very presence of an endoscope in the stomach with mechanical distension of the gastro-oesophageal junction, renders the examination unphysiological; so does air distension of the gastric lumen. Only movements ahead of the light source are seen and these cannot be correlated with those occurring more proximally.

Discussion #

In the light of the anatomy as described by Cunningham (l906), Forssell (l913) and Torgersen (l942), and the radiological forms of movement as described by Torgersen (l942) and Keet (1957), the sequence of events as seen at gastroscopy, can probably be stated to be as follows: once the tip of the gastroscope is beyond the angulus but some distance proximally to the pylorus (with the gastric lumen distended by air), the pyloric aperture is visualized and seen to be open most of the time. At times ripples of contraction are seen, and at times annular contraction waves with a frequency of 3 per minute (peristaltic waves) move along the distal corpus and sinus to a well-defined ring, formed by the left pyloric loop. On the caudal side of the ring longitudinal mucosal folds may be seen to recede into the distance and end at the pyloric aperture (Fig. 14.1).

Fig. 14.1. Contraction ring formed by left pyloric loop. On caudal side of ring longitudinal mucosal folds recede into the distance, ending at pyloric aperture

The region of the stomach between the ring (the left pyloric loop) and the pyloric aperture is the pyloric sphincteric cylinder. The ring may narrow (Fig.14.2) and contract to a narrow bore, through which mucus or at times mucosal folds may be retropelled. This indicates the stage of maximal contraction of the sphincteric cylinder as seen radiologically (Chap. 13).

Fig. 14.2. Further narrowing of ring (left pyloric loop). The region beyond the ring and between it and the pyloric aperture (not visible) is the sphincteric cylinder

As the contraction causes the lumen to "disappear", the event itself (except for the contraction of the left loop) is not visible gastroscopically. In this sense maximal contraction of the pyloric sphincteric cylinder causes, gastroscopically speaking, an event horizon in the distal stomach. After a few seconds the sphincteric cylinder (including its left loop) relaxes, revealing the pyloric aperture, which is seen to be open (Fig. 14.3).

Fig. 14.3. Pyloric aperture distal to the ring

Should the tip of the gastroscope be closer to the pylorus, the pyloric aperture itself may be seen to close or open to a certain extent, in the absence of contraction of the sphincteric cylinder (marked air distension of the lumen may prevent contraction of the cylinder). In this case the variation in size of the aperture is thought to be due to iris-like action of the mucosal folds (Chap.13).

References #

Blackwood WD. Pylorus identification. Gastroenterology l969, 57, 163-167.
Code CF, Carlson HC. Motor activity of the stomach. In: Handbook of Physiology, Sect 6: Alimentary Canal Vol 4: Motility, edit Code CF. Amer Physiol Soc, Washington DC l968, pp 1903-1916.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edinb l906, 45, 9-47.
Dagradi AE. The gastric antrum and the pyloric orifice. Gastroint Endosc l969, 16, 43-44.
Edwards DAW, Rowlands EN. Physiology of the gastroduodenal junction. In: Handbook of Physiology, Sect 6: Alimentary Canal Vol 4: Motility, edit Code CF. Amer Physiol Soc, Washington DC l968, pp 1985-2000.
Forssell G. Über die Beziehung der Röntgenbilder des menslichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr 1913, Suppl 30, 1-265.
Johnson HD. The pylorus: its function and some surgical considerations. Proc Roy Soc Med l961, 54, 938-940.
Kaye MD, Mehta SJ, Showalter JP. Manometric studies of the human pylorus. Gastroenterology l976, 70, 477-480.
Keet AD. The prepyloric contractions in the normal stomach. Acta Rad l957, 48, 413-424.
Maratka Z. Terminology, definitions and diagnostic criteria in digestive endoscopy. Scand J Gastroenterol l984, l9, Suppl 103, 31-38.
Rider JA, Moeller HC, Puletti EJ. Gastroscopic observations of the dynamic anatomy of the antrum and pylorus. Gastroint Endosc l967, 14, 100- 101.
Schindler R. Gastroscopic observation concerned with the gross anatomy of the stomach: the musculus sphincter antri, observation of the position of the stomach, the mucosal folds. Amer J Dig Dis l936, 3, 149-153.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.
Varis K. Diabetic gastroparesis (a review). Scand J Gastroenterol l989, 24, 897-903.

15 - Manometry at the Gastroduodenal Junction

Mon, 01 Jan 0001 00:00:00 +0000

Manometry at the Gastroduodenal Junction #

Atkinson et al. (l957) stated that although the pyloric sphincter was a well-defined anatomical structure, there was doubt whether it functioned physiologically as a sphincter in the sense that it closed the stomach off from the duodenum. Using a system of small air-filled balloons and air-filled, open-tipped tubes, these authors investigated intraluminal pressure profiles in the pyloro-duodenal region in normal subjects as well as in patients with active duodenal ulceration and with non-ulcer dyspepsia. Measurements were taken in the fasting stomach and in stomachs containing a mixture of food and barium sulphate. In no instance could a band of increased pressure be obtained anywhere in the region of the duodenal cap, pyloric canal or pyloric "antrum". While phasic pressure waves were recorded in the pyloric region on many occasions, and while it was possible to correlate radiologically visible peristaltic waves inthe corpus and "antrum" with the pressure records, no convincing evidence of independent contractions at the gastroduodenal junction (i.e. the pyloric ring) was found. It was concluded that the diameter of the pyloric ring was more than 7.0 mm most of the time, whether the stomach was empty or not. These authors could not demonstrate a physiological sphincter in the sense of a tonically contracted muscular ring which kept the lumen tightly closed and which relaxed intermittently to allow gastric contents to pass into the duodenum.

The phasic pressure waves recorded on the gastric side of the ring were deemed capable of causing partial or complete obliteration of the lumen. Each contraction was found to be intermittent and brief, and involved a segment 3.0 to 4.0 cm in length. It probably reduced the bore of the pyloric canal and closed it momentarily. (Comment: "Pyloric canal" was equated with the pyloric aperture). Atkinson et al. (l957) concluded that the pylorus was normally relaxed; there was no evidence that it acted antagonistically to peristaltic or other phasic pressure waves.

Andersson and Grossman (l965), using a system of small (5.0 to 10 mm diameter) water- filled balloons, recorded intraluminal pressures of the pyloro-duodenal region in normal, fasting, supine human subjects. As a balloon was withdrawn from the duodenum through the pylorus, a change in pressure occurred only rarely. During 7 of 130 withdrawals, i.e. in approximately 5 percent of instances, a transient pressure peak of variable magnitude occurred when the balloon passed the "sphincter". It was concluded that the pyloric sphincter was usually not detectable by pressure measurements and that these measurements could not be used as a means of identifying the pylorus. The luminal diameter of the resting pylorus in supine subjects appeared to be greater than 10.0 mm.

Brink et al. (l965) measured intraluminal pressures of the gastroduodenal region in canines. Having performed a gastrostomy and duodenostomy in each animal, cannulae were inserted into the stomach and duodenum through which water-filled, open-tipped tubes and small balloons were introduced into the lumen. As the pressure-detecting units were withdrawn, an increase in resting pressure occurred when the gastroduodenal junctional zone was reached. The magnitude of the change in pressure varied with the cross-sectional diameter of the detecting instrument. With the open-tip tube, elevation of pressure occurred in the junctional zone in 15 of 25 tests on 5 dogs. The mean length of the zone of increased pressure varied from 1.1cm to 1.6 cm. With balloons an increase in pressure was detected more often. The frequency with which they were able to demonstrate a high pressure zone rose as the size of the balloon sensor was increased. With a 7.0 mm diameter balloon, a rise in pressure was seen in 97 percent of 58 observations. Instillation of acid into the duodenum caused an increase in the pressure peaks of the junctional zone, with a simultaneous increase in amplitude of duodenal contractions (type I pressure waves) and a cessation of motor activity in the "antrum". It was concluded that there was a narrow zone of raised pressure at the gastroduodenal junction in fasting dogs, in which the diameter of the lumen was less than 7 mm most of the time.

Carlson et al. (l966) investigated motor action of the canine gastroduodenal junction by means of combined cineradiographic, manometric and electrical studies. Small intraluminal water-filled balloons were positioned in the first part of the duodenum and within 3.0 to 4.0 cm of the pyloric ring on the gastric side, i.e. in the "terminal antrum". The balloons were connected to external strain gauge transducers by means of cannulae. When a Type II contraction (Chap. 13) reached a point 3.0 to 4.0 cm from the pyloric ring, the terminal antrum and pyloric canal distal to it contracted simultaneously, or almost simultaneously, in a segmental way; such vigorous terminal antral contractions (TAC) caused sharp elevations in intraluminal pressures. The pyloric canal almost always contracted with the terminal antrum. (Comment: "Pyloric canal" was equated with the pyloric aperture). The mean duration of TAC was 3.1 seconds, the mean time interval between completion of cycles 12.7 seconds, and the mean rate 4.8 per minute.

Isenberg and Csendes (l972), using open-tipped perfused tubes as pressure sensors, measured intraluminal pressures in canines prepared with gastric and duodenal cannulas. The sensors were moved in 1.0 cm increments back and forth across the pylorus. Mean resting pyloric pressure when the sensors were moved from the stomach to duodenum was 14.8 cm H²0; when they were moved from duodenum to stomach, it was 8.9 cm H²0. Intravenous infusion of cholecystokinin octapeptide produced an increase in pyloric pressure. Mean sphincter length was 1.8 cm. It was concluded that the dog pylorus was tonically contracted and that the resting tone was increased by octapeptide of cholecystokinin. Fisher and Cohen (l973) used infused open-tipped catheters for their manometric studies of the gastroduodenal junction in 28 normal, fasting human subjects. All measurements were made with the subject lying on the right side. At the duodenogastric junction a high pressure zone approximately 1.5 cm in length was recorded. The pressure here varied from 2.5 to 11.7 mm Hg above the intra-abdominal pressure, with a mean magnitude of 5.0 mm Hg. During duodenal acidification with 0.1N HCl the pyloric pressure increased from its basal level of 5.0mm Hg to 25.0 mm Hg, an increase occurring in all l7 subjects tested. Intraduodenal olive oil also significantly increased pyloric pressure. An "antral" peristaltic contraction was associated with a brief drop in pyloric pressure, followed by a sequential contraction of the pylorus and the duodenum. This motor behaviour did not occur consistently and could be recorded in several subjects only.

Fisher and Cohen (l973) concluded that the human pylorus had the physiological characteristics of a true gastrointestinal sphincter, since (1) it was distinguised by a zone of elevated pressure which relaxed with "antral" peristalsis; (2) the high pressure zone contracted in response to physiological duodenal stimuli, and (3) an increase in pyloric pressure was associated with a diminution in reflux of duodenal contents into the stomach. Compared with other gastrointestinal sphincters, the high pressure zone was narrow and had a low resting magnitude, which might explain the failure of previous studies to recognize it. They considered their perfused catheters to be more sensitive than balloon sensors which had been used in some previous investigations. Although the presence of a high pressure zone at the gastroduodenal junction implied sphincteric properties, these authors pointed out that an alternative explanation might be that the high pressure zone was simply a manifestation of the anatomical configuration of the "pyloric channel". In that case the findings would not be of any functional significance.

Kaye et al. (l976) did not agree with Fisher and Cohen (l973) that perfused catheters were more sensitive than balloon sensors. As each sensor in a perfused catheter assembly had of necessity a restricted radial disposition, an important limitation was imposed on sphincteric assessment. In their opinion balloon sensors were less accurate, but not less sensitive than perfused catheters. For these reasons they used a circumferentially sensitive pressure sensor, consisting of a silastic diaphragm around a fluid-filled chamber containing a miniature transducer. The overall circumference was 6.0mm, the device being both accurate and sensitive to pressure around the whole circumference. Pressures were recorded in 8 healthy, fasting human subjects lying in the supine position. Transient phasic pressure rises were occasionally observed at the gastroduodenal junction (as indicated by a change in electrical potential difference as described in Chap. 6), but in no instance was a zone of tonically elevated pressure demonstrated convincingly. The most striking evidence for a pyloric high pressure zone in any of the 8 subjects was a sustained rise of only 1.0 or 2.0 mm Hg, corresponding to a 26mV change in potential difference.

Because the miniature transducer assembly was not suitable for the introduction of solutions into the duodenum, additional studies were done with a six-lumen, open-tipped, continuously perfused catheter system similar to that of Fisher and Cohen (l973), its overall diameter being 5.4 mm. Ten healthy, fasting, supine human subjects were studied, firstly in the basal state, subsequently during infusion of 0.1N HCl into the duodenum and lastly after instillation of olive oil into the duodenum. During the basal withdrawal studies a pressure elevation was seen in 1 of 3 pressure-transmitting catheters in 2 of the 10 subjects. Such tonic elevations of pressure were seen more frequently during intraduodenal infusion of HCl and installation of olive oil, but in only one subject was a rise of pressure noted in all 3 leads; this was quite small and occurred over a distance of only 0.5 cm. These elevations were felt to be due to mucosal apposition of the catheter orifice as it traversed the narrowest part of the gastroduodenal region. It was also shown that the right lateral position, as used by Fisher and Cohen (l973), could cause 90 degree angulation at the gastroduodenal junction with increased resistance to flow and therefore an increase in intraluminal pressure.

With both types of assembly, Kaye et al. (l976) recorded phasic elevations in most subjects from both duodenum and "antrum". The "antral" motor activity was usually most prominent at, and immediately proximal to the gastroduodenal junction. These authors concluded that they were unable to demonstrate a zone of tonically elevated pressure at the gastroduodenal junction in healthy subjects, despite the use of accurate and sensitive manometric systems. They inferred that the pylorus was open for most of the time in fasting, healthy young individuals. This conclusion was considered to be consistent with endoscopic observations, which showed that the pylorus was usually not completely closed except during the terminal phase of "antral" contractions (Chap. 14).

Valenzuela et al. (l976) assessed pyloric sphincter pressures in normal, fasting human subjects as well as in patients with gastric ulcer and duodenal ulcer. All individuals were examined in the right recumbent position by means of an open-tipped, water-perfused catheter assembly. Intra-duodenal pressure was used as a zero reference and pyloric pressure was measured as a zone of sustained elevated pressure without considering peak phasic contractions. Basal pyloric sphincter pressure was found to be 10.2 ± 1.2 mm Hg. During perfusion of acid into the duodenum the pressure was almost doubled, to 20.2 ± 1.8mm Hg. This was prevented by the prior administration of atropine. Metoclopramide increased pyloric sphincter pressure in normal subjects as well as in patients with gastric ulcer and duodenal ulcer.

While comparing the findings of Fisher and Cohen (l973) with those of Kaye et al. (l976), Winans (l976) was moved to conclude that the pylorus was "fickle". Whereas Fisher and Cohen (l973) presented evidence to show that it was a true sphincter in the anatomical and physiological sense, the findings of Kaye et al. (l976) cast doubt upon the legitimacy of that claim. Could the divergent experimental results be reconciled? Winans (l976) thought that an explanation might be found in differences in methodology. The right decubitus study position of Fisher and Cohen (l973), for instance, might have narrowed the pyloric lumen mechanically, producing an artifactual high pressure zone. Other seemingly minor but potentially important methodological differences were possible. During combined radiographic and manometric studies Keet et al. (l978) recorded fasting intraluminal pressures in the pyloric sphincteric cylinder by means of an air-filled system and a miniature balloon in 5 normal adult subjects in the erect position (Chap. 13). The following two distinct waves of pressure increase in the pyloric sphincteric cylinder were noted:

Irregularly occurring, nonrhythmic contractions, causing pressure increases varying from 9 to 34 mm Hg (the majority being in the range of 12 to 25 mm Hg). These waves lasted from 5 to 21 seconds (the majority being in the 6 to 10 second range), and occurred repeatedly in all subjects (Fig. 15.1). Simultaneous radiographic TV monitoring showed that each of these waves was associated with a typical maximal contraction of the pyloric sphincteric cylinder (Chap. 13). The waves also conformed to contractions of the "terminal antrum" (TAC) described by Carlson, Code and Nelson (l966), Code and Carlson (l968) and Shepard (l97l), called Type II waves.

Fig. 15.1. Two Type II pressure waves of pyloric sphincteric cylinder. Simultaneous radiography showed typical contraction of cylinder during both waves. Base line indicates intraluminal pressure in absence of radiologically visible motor activity. 10- second marker on zero line

In two of the subjects compound waves, consisting of a rise in base line pressure of 3 to 5 mm Hg and lasting for 10 to 40 seconds, on which were superimposed waves of shorter duration (3 to 5 seconds) and higher amplitude (up to 12 mm Hg) were seen. These conformed to Type III waves (Shepard l97l). (Comment: Radiologically both types of waves were associated with typical contractions of the pyloric sphincteric cylinder. Compound waves are usually ascribed to additional increases in tone. Contractions of the cylinder in the full stomach are usually quite regular, tending to occur at a rate of 3 per minute. The fact that pressure waves occurred irregularly in this investigation, might have been due to the fact that a small volume of liquid barium was used. Houghton et al pointed out that emptying of solids was associated with an increase in frequency of "antral" peristaltic waves; vide infra).

No attempt was made by Keet et al. (l978) to record contractions of the pyloric ring (right pyloric loop) and the sphincteric cylinder separately.

McShane et al. (l980) studied pyloric sphincter pressures in 32 patients under basal conditions, after stimulation with HCl and after posture changes. A single fine perfused catheter, 2.0mm in diameter, with 2 diametrically opposite side openings, was placed in the duodenum at endoscopy; resting pyloric pressures were measured during catheter withdrawal 3 to 5 hours later. In 28 of the 32 patients no rise in pressure occurred in the pyloric region. One patient of the remaining 4 showed a temporary rise in pressure which did not recur at repeat examinations, and in the other 3 there were pressure rises of 3.0, 3.0 and 6.0 mm Hg respectively. It was concluded that it was not possible to demonstrate any significant zone of pressure change at the pylorus in the basal state. Posture changes and instillation of 0.1N HCl into the duodenum did not affect the results. It was thought that the conflicting results previously obtained by Fisher and Cohen (l973) and by Valenzuela et al. (l976) might have been due to the fact that in their investigations the catheter was withdrawn too soon after intubation, at a time when the intubation itself might have affected the sphincter tone. Moreover, the catheters of Fisher and Cohen (l973) had 3 times the diameter of those used by McShane et al. (l980), which could also have affected their results; Brink et al. (l965) had shown previously that the larger the diameter of a pressure detecting unit, the greater were the pressures recorded. They implication was that the zones of elevated pressure recorded by Fisher and Cohen (l973) and by Valenzuela et al (l976), might have been due to muscle excitation and resistance to stretch, and might not have been a true indication of basal pyloric sphincter tone. McShane et al. (l980) concluded that the pyloric sphincter remained patent under fasting conditions, with a luminal diameter greater than 2.0 mm. They supported the concept of the pylorus as a "filter pump", having the ability to filter particles greater than 2.0 mm in diameter, while allowing fluid and chyme to enter the duodenum continuously.

In discussing the uncertainties pertaining to the action of the human pylorus, White et al. (l98l) thought that there had been a failure to obtain adequate pressure recordings from within the lumen. Pull-through techniques would not be applicable if the pylorus were open most of the time. It was necessary to determine the timing of closure of the pylorus with respect to contractions of the "antrum" and duodenal bulb. Consequently continuous records of intraluminal pressures had to be obtained simultaneously from the "antrum", pylorus and duodenal bulb. In order to achieve this end an open-tipped, water- perfused, six-channel catheter assembly with an external diameter of 6.0.mm was used. The middle opening was placed within the pylorus while other pressure channels recorded from the "mid-antrum" and the distal duodenal bulb. Measurements were taken in 15 fasting, normal human subjects in the right recumbent position. It was found that basal pressures in the "antrum", pylorus and duodenal bulb were the same relative to atmospheric pressures; there was no gradient of basal pressure across the pylorus. During withdrawal of the catheters through the pylorus a change in basal pressure did not occur.

White et al. (l98l) recorded a total of 264 "antral", 213 pyloric and 834 duodenal pressure waves. The majority of pyloric contractions were related to an "antral" contraction, and most of these were also associated with a duodenal contraction. In this way a concerted contraction of the whole gastroduodenal region occurred. However, independent contractions of all three areas were also encountered; 70 per cent of duodenal and 36 per cent of pyloric contractions were independent. Powerful contractions of the "antrum" were usually associated with related contractions of the pylorus and duodenum. Less powerful contractions of the "antrum" were usually independent. It was concluded that the human pylorus did not cause a zone of elevated basal pressure; apart from a brief closure during contraction, the pylorus was always open. Dooley et al. (l985), commenting on the contradictory results of previous investigators, pointed out that the motility of the upper gastrointestinal tract during fasting was not a static one and marked variations were seen during the various phases of the interdigestive motility complex (IDMC). It was conceivable that the pylorus could show cyclic variation with the different phases of the complex. Consequently pyloric pressure was monitored continuously for 300 minutes at a time, in 6 healthy fasting adult subjects. A perfused catheter system was used with 2 "antral" and 2 duodenal side openings. A Dent (l976) sleeve, 4.5 cm in length and with an outer diameter of 6.0mm, was incorporated in the multilumen tube assembly between the duodenal and antral ports, and placed in the pylorus under fluroscopic control, with measurements obtained in the supine position. The pylorus was assessed for the possible presence of an elevated basal pressure zone, using baseline duodenal pressure as a reference. Pyloric pressure was also analyzed for each separate phase of the IDMC, and the frequency and amplitude of its phasic contractions were determined.

Dooley et al. (l985) found that basal pyloric pressure in the fasting state showed no elevation above baseline duodenal pressure during phase III of the IDMC. In phases I and II, basal pyloric pressures varied in different subjects, being elevated in some but not in others. Subjects studied on separate days often showed different patterns of activity, and it appeared that duodenal acidification gradually increased basal pyloric pressure. The pylorus also showed phasic activity, which was maximal in phase III. The exact significance of this activity was not clear. The sleeve device did not allow any firm conclusions to be drawn on the phasic activity of the pylorus in relation to that of the "antrum" on the one hand, and that of the duodenum on the other.

Using a system of perfused catheters and a pull-through technique, Gaffney et al. (l987) found that the presence of a high pressure zone at the pylorus was very variable. Of 170 records made, a high pressure zone was present in 53 percent while no change in pressure was found in 47 percent. The subject's position had no effect on the presence of a high pressure zone, which refuted the premise of Kaye et al. (l976) that the zone of elevated pressure found by Fisher and Cohen (l973) might be artifactual. In addition the pylorus showed no response to duodenal acidification. It was concluded that the evidence weighed heavily against the presence of a tonic sphincter at the pylorus.

Houghton et al. (l988) investigated the normal patterns of pressure activity in the "antrum", pylorus and duodenum and their relationship to changes in "antral" and duodenal pH, under fasting conditions and after ingestion of chocolate milk. By this procedure the relationship between motor events and transpyloric flow of acid gastric secretions could be determined. An eleven-channel intraluminal probe was used, incorporating a sleeve sensor 4.5 cm in length positioned across the pylorus. The maximum diameter of the manometric assembly was 6.5 mm. The "short pyloric sphincter" was identified by continuous measurements of transmucosal electrical potential difference (Chap. 6). The sleeve sensor in the pylorus consistently registered a higher basal pressure from the pylorus than from the adjacent "antral" and duodenal ports. However, it was conceded that the recording of pyloric tone might depend on the width of the manometric probe in relation to the pyloric aperture; the higher basal pressure might be an artifact. The most common fasting motor pattern consisted of regular co-ordinated contractions, most of which involved the "antrum" and duodenum, and showed evidence of propagation with transient reductions in duodenal pH. Ingestion of milk changed the motor pattern to one which was composed of pressure waves confined to the pylorus with few waves in the "terminal antrum" or proximal duodenum. These isolated pyloric pressure waves were gradually replaced by propagated "antroduodenal" contractions occurring at a regular frequency. The liquid component of a mixed meal emptied rapidly in an exponential manner, whereas the solid remained in the gastric fornix until 80 per cent of the liquid had emptied, and then emptied in a linear manner; the onset of solid emptying was associated with an increase in the frequency of antral pressure waves.

Discussion #

Gaffney (l987) pointed out that the results of pyloric manometric studies conflict, some showing evidence of a sphincter at the pylorus, and others not. As examples of the former, the following may be mentioned:

Brink et al. (l965) demonstrated a narrow (1.1cm to 1.6cm) zone of raised intraluminal pressure at the gastroduodenal junction in canines. Isenberg and Csendes (l972) found the dog pylorus to be tonically contracted, the sphincter length being 1.8 cm. Fisher and Cohen (l973) recorded a pyloric high pressure zone, 1.5 cm in length, in humans; to them it had the characteristics of a true sphincter, but it was acknowledged that it could simply be a manifestation of the normal configuration of the pyloric channel. Valenzuela et al. (l976) found that the basal pyloric sphincter pressure was elevated in normal human subjects lying on the right side; they looked upon the pyloric ring as a sphincter in the usually accepted sense. Using a sleeve sensor, Houghton et al. (l988) consistently registered a higher basal pressure from the pylorus than from the adjacent antral and duodenal ports. This was ascribed to the pyloric sphincter, but it was acknowledged that it might be artefactual.

These findings were not accepted universally. Kaye et al. (l976) pointed out that the results of Fisher and Cohen (l973) could have been influenced by the fact that subjects were examined in the right lateral decubitus position; in this position there could be angulation of catheters with increased resistance to flow and consequent increase in intraluminal pressure. Valenzuela et al. (l976) similarly examined patients lying on their right side. However, Gaffney et al. (l987) found that the subject's position had no effect on the presence of a high pressure zone, refuting the premise of Kaye et al. (l976).

It is doubtful if the findings of Brink et al. (l965) and of Isenberg and Csendes (l972) can be regarded as physiological, as each experimental animal had both a gastrostomy and a duodenostomy, which might have influenced the results. Many authors failed to find evidence of a tonically contracted ring structure at the pylorus. Atkinson et al. (l957) were unable to demonstrate independent contraction of the pyloric ring; they found that the pylorus was normally relaxed and did not act antagonistically to phasic pressure waves. Andersson and Grossman (l965), Kaye et al. (l976), McShane et al. (l980), White et al. (l98l), Dooley et al. (l985) and Gaffney et al. (l987) found no convincing manometric evidence of a zone of tonically elevated basal pressure at the pylorus. McShane et al. (l980) stated that the pyloric sphincter remained patent under fasting conditions. Apart from a brief closure during contraction, the pylorus was always open, according to White et al. (l98l). Kelly (l983) and Gaffney et al. (l987) concluded that the evidence weighed heavily against the presence of a tonic sphincter at the pylorus.

Winans (l976) attributed the divergent results of manometric studies to differences in methodology and differences in position of the subjects examined. Whereas the human pylorus was easily identifiable as a gross anatomic structure, it eluded identification as a functioning sphincter. Winans (l976) called this a "sphincteric paradox", and referred to the pylorus as being "fickle". Adding to the confusion is the lack of agreement on the definition of a sphincter (Chap. 2) and its relation to a high pressure zone.

In determining the manometric features of the pylorus, none of the authors quoted, with the exception of Keet et al. (l978), referred to or took note of the muscular anatomy of the region as determined by Cunningham (l906), Forssell (l913) and Torgersen (l942) (Chap. 3). According to this concept the pyloric ring consists of an aboral thickening of the cylinder, and constitutes an inherent part of the cylinder both anatomically and functionally. The closest any of the authors came to the concept of a sphincteric cylinder at the pylorus, was the recognition of the "terminal antrum" as a functional unit by Carlson, Code and Nelson (l966), Code and Carlson (l968) and Shepard (l97l). However, the terminal antrum had not been defined in terms of muscular anatomy, whereas the sphincteric cylinder had.

The sphincteric mechanism at the pylorus will probably prove to be less paradoxical once the muscular component of the pyloric ring (the right pyloric loop) is no longer regarded as a separate structure, but is acknowledged to be an inherent part (i.e. the aboral end) of the pyloric sphincteric cylinder.

References #

Andersson S, Grossman MI. Profile of pH, pressure, and potential difference at gastroduodenal junction in man. Gastroenterology l965, 49, 364-371.
Atkinson M, Edwards DAW, Honour AJ, et al. Comparison of cardiac and pyloric sphincters. Lancet l957, 273, 918-922.
Brink BM, Schlegel JF, Code CF. The pressure profile of the gastroduodenal junctional zone in dogs. Gut l965, 6, 163-171.
Carlson HC, Code CF, Nelson RA. Motor action of the canine gastroduodenal junction: a cineradiographic, pressure and electric study. Amer J Dig Dis l966, 11, 155-172.
Code CF, Carlson HC. Motor activity of the stomach. In: Handbook of Physiology, Sect 6: Alimentary Canal, Vol 4: Motility. American Physiological Soc, Washington DC l968, pp 1903-1906.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
Dent JA. A new technique for continuous sphincter pressure measurement. Gastroenterology l976, 7l, 263-267.
Dooley CP, Reznick JB, Valenzuela JE. A continuous manometric study of the human pylorus. Gastroenterology l985, 89, 821-826.
Fisher RS, Cohen S. Physiological characteristics of the human pyloric sphincter. Gastroenterology l973, 64, 67-75.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr 1913, Suppl 30, 1-265.
Gaffney PR, Gleeson DJ, Hall JW, et al. The manometric findings at the human pylorus: the evidence against the presence of a tonic sphincter. Scand J Gastroenterol l987, 22, 525-532.
Houghton LA, Read NW, Heddle R, et al. Motor activity of the gastric antrum, pylorus and duodenum under fasted conditions and after a liquid meal. Gastroenterology l988, 94, 1276-1284.
Houghton LA, Read NW, Heddle R, et al. Relationship of the motor activity of the antrum, pylorus and duodenum to gastric emptying of a solid-liquid mixed meal. Gastroenterology l988, 94, 1285-1291.
Isenberg JI, Csendes A. Effect of octapeptide of cholecystokinin on canine pyloric pressure. Amer J Physiol l972, 222, 428-431.
Kaye MD, Mehta SJ, Showalter JP. Manometric studies of the human pylorus. Gastroenterology l976, 70, 477-480.
Keet AD, Vermaak JC, Mouton J. Intraluminal pressure profiles and mucosal movements in the stomach and duodenum. Amer J Gastroenterol l978, 69, 144-148.
Kelly KA. Motility of the stomach and gastroduodenal junction. In: Physiology of the Gastrointestinal Tract. Vol 1, Edit Johnson LR. Raven Press, New York l98l, pp 393-410.
McShane AJ, O'Morain C, Lennon JR, et al. Atraumatic non-distorting pyloric sphincter pressure studies. Gut l980, 21, 826-828.
Shepard RS. Human Physiology. JB Lippincott Co, Philadelphia l97l, p 417.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.
Valenzuela JE, Defilippi C, Csendes A. Manometric studies on the human pyloric sphincter: effect of cigarette smoking, metoclopramide and atropine. Gastroenterology l976, 70, 481-483.
White CM, Poxon V, Alexander-Williams J. A study of motility of normal human gastroduodenal region. Dig Dis Sci l98l, 26, 609-617.
Winans CS. The fickle pylorus (editorial). Gastroenterology l976, 70, 622-623.

16 - Myoelectric Activity at the Gastroduodenal Junction

Mon, 01 Jan 0001 00:00:00 +0000

Myoelectric Activity at the Gastroduodenal Junction #

The presence of rhythmic electrical activity in the musculature of the gastric "antrum" of anaesthetized dogs was first reported by Alvarez and Mahoney (1922) and has since been confirmed repeatedly. Bozler (l945) recorded the electrical potentials of the dog, cat and guinea pig stomachs by means of non-polarizable differential electrodes. In the dog, the differential potential associated with each peristaltic contraction showed three main deflections, designated the R, S and T waves. The shape of the recorded potential was identical with that of cardiac muscle but differed from it in that it lasted from 5 to 8 seconds, i.e. it had a slow phase. Species differences were noted; in the guinea pig stomach a slow potential could be observed only in the region of the pylorus. In the cat the same action potentials as in the dog were obtained as long as the contractions in the stomach were weak. If movements were strong enough to be easily visible, brief spike potentials were superimposed on the slow phases; the number and frequency of the spikes increased with the strength of the contraction. At that time the significance of the spikes was not known.

Bass et al. (l96l) found that a rhythmic electric complex could be recorded regularly from the "antrum" in dogs. Called the basic electric rhythm (BER), its frequency was about 4.4 per minute. Bursts of relatively rapid changes in potential, fast or spike activity, occurred in association with approximately 40 percent of BER complexes. (In the duodenal bulb a similar basic electric rhythm and fast or spike activity was recorded.) Both types of activity became attenuated at the pylorus and usually disappeared in it. Although some of the fast activity of the antrum occasionally extended into the pylorus, it was felt that in the dog the pylorus acted as an "electric insulator" between the stomach and duodenum.

Daniel and Chapman (l963) pointed out that all investigators had recorded a more or less constant electrical wave in vitro from the body and "antrum" of both the resting and the contracting stomach. Its frequency varied from 3 to 6 per minute, depending on the species and the type of preparation. In the contracting stomach an electrical wave, which they called the primary wave, preceded each peristaltic contraction. In the dog's stomach these propagated electrical waves did not vary in shape with the presence or absence of motor activity. It was concluded that the electrical activity of the dog stomach preceded and appeared to control the spread of peristaltic contractions, but went on relatively unchanged in the absence of peristalsis.

Daniel and Chapman (l963) also investigated the electrical activity of the dog stomach by means of a monopolar technique. When the electrodes were oriented transversely to the longitudinal muscle fibres, the primary waves with a frequency of 3 to 6 per minute were the most prominent and consistent feature. In the upper third of the stomach the typical electrical wave was small and disappeared near the fundus. Activity progressed distally along an array of electrodes parallel to the greater curvature, at a velocity increasing from 0.3 cm per second in the body of the stomach to 3.0 to 4.0 cm per second as the wave neared the antrum, thus correlating electrical events with descriptions of a rapid spread of peristalsis in the antral region. Activity at the antral electrodes was often nearly simultaneous. In the antrum, but not in the body of the stomach, the primary wave was often followed by secondary smaller deflections which were sometimes fused; these were present only when visible, active peristalsis was evident. Visible antral peristaltic contractions followed the primary waves by 6 to 9 seconds and the secondary waves by 1 to 2 seconds. Daniel and Chapman (l963) described the events as follows: an electrical wave, probably originating in the cardia, travelled slowly down the stomach at a velocity of slightly more than 0.5 cm/sec until it reached the pyloric "antrum", where its velocity increased to 4 cm/sec. The wave recurred periodically at the same frequency of 3 to 6 per minute as the contractions of the stomach, and appeared to precede and initiate gastric motility. However, there was a variable relationship between electrical and mechanical events, as the primary electrical wave might continue unchanged after inhibition of motility. In the "antrum" of the dog secondary spikes accompanied motility and disappeared with it. Secondary spikes could only be recorded in the antral part of the dog's stomach, while in the cat and guinea pig stomach they occurred in the cardia.

Daniel (l965) studied the drug responses of the "antrum" and duodenal bulb in the dog, using intra-arterial infusions of drugs and combined recordings of electrical and mechanical activity. In the inactive antrum an electrical rhythm of 4 to 5 waves per minute occurred, resembling the QRS complex in the heart, and called the initial potential. It was propagated distally over most of the antrum at a velocity of 0.3 to 1.0 cm per second, but at a distance of 2.0 to 4.0cm from the pylorus the velocity increased, reaching 2.0 to 4.0 cm per second in the terminal two centimeters of the antrum; the amplitude also increased near the pylorus. In the active or contracting antrum, the above repetitive initial potential was followed by a second potential, consisting of repetitive negative going spikes in the terminal two centimeters; they did not appear to be propagated.

Daniel (l965) showed that infusion of adrenaline or noradrenaline caused inhibition of antral second potentials and contractions. Intra-arterial infusion of acetylcholine and nicotine led to the production or enhancement of second potentials and contractions; in addition, premature initial potentials might be produced and these were often propagated in an antiperistaltic direction. In the duodenum, slow waves occurred at a rhythm of l7 to l9 per minute, irrespective of mechanical activity; when contractions occurred they were preceded by a series of fast spike potentials. Acetylcholine and other cholinergic stimulants produced or increased fast spikes and contractions in the duodenum. Atropine prevented all the excitatory effects of acetylcholine and other cholinergic stimulants in both the antrum and duodenum. Bortoff and Weg (l965) studied the relationship between antral and duodenal slow waves at the gastroduodenal junction. Using feline anatomical preparations, they confirmed that spontaneous electrical activity of the pyloric "antrum" consisted of periodic depolarizations; these antral slow waves could be associated with spike potentials which were thought to initiate contractions. There was an extension of antral slow waves across the pylorus into the proximal duodenum; consequently muscular contractions initiated in the antrum could extend into the duodenum, thereby co-ordinating the activities of the antrum, pylorus and duodenal bulb. Although the results were not as definite in the dog as in the cat, they differed from those of Bass et al. (l961), who had concluded that the pylorus acted as an electric insulator, separating the electrical activity of the stomach from that of the duodenum. Bortoff and Weg (l965) found that extension of antral slow waves into the proximal duodenum could be eliminated by a transverse incision through the musculature at the gastroduodenal junction, the mucosa and submucosa being left intact; this indicated that continuity of the gastroduodenal musculature was a necessary condition for transmission of antral slow waves into the proximal duodenum. It was surmized that electrical slow waves were generated by longitudinal muscle cells; they could be recorded in the stomach in the absence of any apparent mechanical activity.

Carlson et al. (l966) simultaneously recorded intraluminal pressures, intramural electrical activity and contractions as seen cineradiographically, in fasted dogs. In the gastroduodenal junctional zone the electrical activity consisted of cyclic changes in potential, recognized as BER of the antrum, and occurring at a rate of 5.1 per minute. Between rhythmic antral BER complexes, elevations with superimposed rapid spike activity, also described as "fast activity", occurred. The presence or absence of motor activity did not affect the frequency of antral BER cycles, but did affect the contours. Motor action was associated with spike configurations; in every instance of cineradiographically identified contraction, the electric record showed associated spike activity. According to Carlson et al. (l966), a recognizable interval usually elapsed between the appearances of BER complexes at separate electrodes in the upper part of the stomach. The mean velocity of the conduction of a BER complex increased as it approached the pyloric "canal". In the body of the stomach there was a slow propagation of 0.5 cm per second, increasing to about 2.0 cm per second in the antrum. In the terminal three centimeters of the antrum simultaneous or nearly simultaneous BER complexes were recorded from different electrodes; this was consistent with the development of a simultaneous or nearly simultaneous contraction of the entire terminal antrum as seen at cineradiography.

Motor activity in the pyloric "canal", as in the antrum, was associated with fast activity in the electrical record, and occurred with the same frequency and rhythm as the fast activity in the adjacent antrum. Contraction of the pyloric canal occurred simultaneously with, or shortly after, the onset of a terminal antral contraction (TAC). (Comment: The pyloric canal was equated with the pyloric aperture). The electrical activity in the proximal duodenum was characterized by cyclic changes in potential, with a mean rate of l7.2 per minute, designated BER of the duodenum. Duodenal contractions occurred synchronously with the BER, but their precise timing with reference to contractions in the adjacent pyloric canal was irregular; BER of the stomach and duodenum did not appear to be in phase.

Although the technique of obtaining electrical records from cutaneous electrodes, called electrogastrography, had been known for a number of years, it was further developed by Nelson and Kohatsu (l968). These authors defined the slow wave in the stomach as a controlled, rhythmic, regularly propagated, moving annulus of electrical depolarization travelling from the cardia to the pylorus, and accelerating during its passage; it could be viewed as a conducted action potential. When mechanical or contractile waves were present, the electrical and mechanical waves were synchronous. The relationship of peristaltic to electric waves could be considered as locked in time but graded in amplitude from no coupling (i.e. a mechanically quiescent stomach) to complete coupling (i.e. a peristaltic wave of maximum amplitude synchronous with each electrical wave). There was a 1:1 time relationship of the peristaltic and electrical waves. In human subjects studied by means of surgical implantation of stainless steel electrodes directly into the muscle, it was found that the rate in the fasting stomach was 3 ± 0.4 cycles per minute.

Daniel and Irwin (l968) pointed out that muscular contractile activity in the stomach was rhythmic and propagated in a well co-ordinated way. Rhythmic contractions in unanaesthetized man recurred at a mean frequency of 3 per minute and in the dog at 5 per minute. Regular, propagated electrical activity was associated with this regular contractile activity. The rhythm of the elctrical activity was the same whether the stomach was contracting or inactive; during contractile activity, a second electrical component appeared. In the inactive stomach the rhythmically occurring electrical complex, previously called the basic electric rhythm (BER) or pacesetter potential, was termed the "initial potential" or "initial polarization" by Daniel and Irwin (l968). It seemed to commence some 15 to 20 cm above the pylorus in human subjects and was normally propagated toward the pylorus; both the size and the rate of propagation of the initial potential increased as it progressed. In the anaesthetized dog it had a propagation velocity of 0.1 to 0.2 cm per second near its origin, increasing to 1.5 to 4.0 cm per second in the antrum. The same general scheme had been noted previously by Carlson et al. (l966). According to Daniel and Irwin (l968) the more rapid spread of electrical activity over the antrum presumably provided the mechanism responsible for its behaviour as a motor unit.

In the active or contracting stomach, a second electrical deflection occurred, corresponding in time to the mechanically recorded contractile activity. This had previously been called "spiking potentials", "fast activity" or "action potential"; Daniel and Irwin (l968) suggested the term "second potential". It was phased by the initial potential and was typically recorded as a prolonged negative deflection, or as a series of negative spikes. Spikes were usually seen only in the terminal 2.0 or 3.0 cm of the dog antrum.

Abolishing contractile activity with moderate doses of catecholamines or atropine was associated with disappearance of the second potential according to Daniel and Irwin (l968). Activation of contraction in a previously inactive stomach resulted in the reappearance of second potentials. Thus it appeared that second potentials were associated with, or initiated, the contractile process. The second potential, unlike the initial potential, was not propagated; it could be produced locally by the local intra- arterial infusion of acetylcholine, without appearing at electrodes a few millimeters distant in either direction. It was surmized that the second potential as well as its associated contractile activity might be produced or affected by local release of chemical mediators or neurohormones, i.e. it appeared to be under local control. Daniel and Irwin (l968) found that rhythmic duodenal electrical activity in dogs, recurring at a rate of l7 per minute, existed within one millimeter of rhythmic gastric electrical activity recurring at a rate of 4.3 to 5.1 per minute. There was a possibility of coupling between the gastric and duodenal electrical rhythms since the frequency of the two rhythms could indicate a 3:1 or 4:1 coupling. These authors did not agree with Bass et al (l961) that the stomach and duodenum were electrically insulated by an interposed electrically silent zone; such insulation could only be achieved by a continuous lipid membrane, and no such structure existed at the gastroduodenal junction.

Bortoff and Davis (l968) instituted in vivo animal studies to determine whether or not transmission of slow waves across the gastroduodenal junction occurred, to study the effect of myenteric denervation on slow wave transmission and to observe the effects of vagal and splanchnic nerve stimulation. Using suction electrodes applied to the serosal surface in cats, dogs, rhesus monkeys and baboons, it was shown that "antral" slow waves spread across the junction into the proximal duodenum, where they periodically augmented depolarizations of duodenal slow waves, thereby increasing the probability of duodenal spiking. After functional myenteric denervation the duodenal spread of antral slow waves continued, indicating that it was a myogenic process; this probably occurred via bundles of antral longitudinal muscle extending across the pylorus and interdigitating with duodenal longitudinal musculature. (Comment: Some longitudinal muscle fibres normally extend across the pylorus from the stomach to the duodenum as described in Chapter 3). However, the spread could be modulated neurologically; vagal stimulation increased both amplitude and duration of antral slow waves, augmenting depolarization on both sides of the junction and increasing spike activity. Thus duodenal spiking was temporally related to antral slow waves. Splanchnic stimulation had mixed effects, causing either excitation similar to that of vagal stimulation, or inhibition of antral slow waves. It appeared if the spread of antral slow waves into the proximal duodenum constituted the primary mechanism for co-ordination of the mechanical activity at the gastroduodenal junction.

Kwong et al (l970) studied the electrical activity of the gastric "antrum" up to 6.0 cm from the pylorus in 56 patients with upper gastrointestinal pathology, and in 12 patients with gall-stones acting as controls; at operation electrodes were implanted through the serosa and others attached to the mucosa by means of suction. The same frequency was recorded from the mucosal and serosal electrodes and the main components of the wave forms were the same. In the control patients the wave frequency was approximately 3 per minute, which was significantly less than the frequency in patients with gastric ulceration, duodenal ulceration and gastric carcinoma. The general pattern of the wave forms was the same in all groups, although areas replaced by tumor were electrically silent. It was concluded that while there were differences in frequency, no differences in the pattern of electrical activity appeared which might be of diagnostic significance in these conditions.

Duthie et al. (l97l) studied the pacesetter potential in the stomach and duodenum in patients undergoing cholecystectomy. Electrodes were implanted under the serosa in the gastric "antrum" and in the duodenum as far as the duodenal papilla, the indifferent electrode being placed on the skin of the abdomen. The frequency and amplitude of the electrical waves were measured, and where possible also the conduction times. In the antrum the frequency of the pacesetter potential was stable during recordings made at rest. The waveform was similar to that obtained from electrodes sucked on to the mucosa as found by Kwong et al. (l970), and the mean frequency of about 3.12 cycles per minute was also similar. Action potentials were seen only occasionally in the unstimulated stomach. In the duodenum, from 10 to 12cm distal to the pylorus, the frequency of the pacesetter potential was about 12 cycles per minute. In the proximal 4.0 to 5.0 cm of the duodenum, the predominant pattern consisted of 3 cycles/min as in the antrum, occasionally superimposed on 12 cycles/min. However, no direct relationship could be established between the frequency of the gastric (3 cycles/min) and duodenal (12 cycles/min) intrinsic activities. The conduction velocity of the electrical waves in the antrum between 4.0 and 1.5 cm from the pylorus was about 0.5 cm per second. Across the pyloric region it was approximately 2.0cm per second, i.e. about four times as fast.

Ingestion of water, citrate or oleate significantly slowed the frequency of the pacesetter potential in the "antrum"; the injection of morphine was followed by an increase in action potentials both in the antrum and the duodenum. Duthie et al (l97l) concluded that the 3 cycles/min rhythm of the antrum passed into the proximal duodenum, but they were not able to detect any relationship between this frequency and the intrinsic 12 cycles/min frequency of the remainder of the duodenum. The route of conduction from the stomach to the duodenum was probably via the longitudinal muscle fibres continuing from the antrum across the pylorus.

Sarna (l975) suggested that the inherent rhythmic myoelectrical activity of the stomach should be termed electrical control activity. When motor activity was present, the electrical control activity was accompanied by a second component with or without superimposed fast oscillating potential changes, for which he suggested the appellation electrical response activity.

El-Sharkawy et al. (l978) simultaneously recorded mechanical and intracellular electric activity from canine and human gastric musculature, and found regional differences in the electrical signal that caused contractions. Phasic contractions in the "terminal antrum" were initiated by spike potentials whereas phasic contractions in the corpus and orad antrum were regulated by the plateau potential.

Smout et al. (l980) called the first kind of electrical activity, i.e. the omnipresent periodic activity that is not indicative of contractile activity, the electrical control activity (ECA). Electrical response activity (ERA) only occurs in connection with phasic contractile activity, but is time-locked to ECA; it does not always consist of spikes. ERA may be absent, as in the motor quiescent phase of the interdigestive myoelectric complex. According to Szurszewski (l98l) a phasic gastric contraction is usually a mechanical manifestation of an electrical event occurring in smooth muscle cells. A spontaneous electrical signal originates in the musculature of the midcorpus, which can be identified as a pacemaker region. The signal complex is propagated circumferentially around the stomach and longitudinally to the gastroduodenal junction. In canines intracellularly recorded action potentials from antral circular musculature, in the region extending from the intermediate sphincter to the gastroduodenal junction, distinguishes it from more orad regions of the stomach; similar features were likely to exist in human musculature. (Comment: The intermediate sphincter is synonymous with the left pyloric loop as described in Chap. 3). The "antrum" can be divided into orad and terminal parts, according to Szurszewski (l98l). In the corpus and proximal antrum the electrical wave forms are the same, and coincide closely with contraction of the circular muscle fibres; in the terminal 2.0 to 3.0 cm of the antrum, characteristic electrical activity is seen during contraction. The action potential in this region has an initial, rapid depolarization and a plateau potential with oscillations in potential superimposed on the plateau potential.

Stoddard et al. (l98l) reiterated that gastric myoelectric activity is characterized by the presence of regular slow waves in the distal two-thirds of the stomach, the orad third being an electrically silent area. The mean slow wave frequency is species dependent, being approximately 3 cyles per minute in man and 5 cycles per minute in dogs, with little day to day variation. The rhythm is normally remarkably stable, with only occasional irregularities of a few cycles' duration.

You and Chey (l984) pointed out that it had not been clarified whether or not a slow wave (pacesetter potential or PSP) per se was associated with a mechanical contraction. A prevailing view was that gastric contractions resulted from the occurrence of spike activity (action potential), and not from the slow wave alone; the function of the slow wave was considered to consist of setting the pace and direction of gastric contractions. However, some authors had reported an intimate relationship between contractile activity and PSP in the canine stomach, whether spike activity was present or not; a similar relationship had been found in human antral muscle segments (You et al. l980). These observations suggested that PSP in the stomach might also promote phasic contractions. In a study of the relationship between electrical and mechanical activities of the "distal antrum" in humans and canines, it was found that phasic contractions were recorded by sensitive ministrain gauges implanted on the serosal surface, although electrical activity showed only PSP's without action potentials or second potentials. (The distal antrum was defined as the region 2.0 cm proximal to the pylorus). Intraluminal manometry could not always recognize these phasic contractions; the number of contractions recorded by manometry was less than 50 percent of the PSP's accompanied by action potentials or second potentials. No gastric contractions were recorded when pacesetter potentials occurred without action potentials.

You and Chey (l984) found that gastric dysrhythmia, including tachygastria, could be induced by epinephrine. During dysrhythmia phasic contractions disappeared and no contractions occurred in association with action potentials. Tachygastria was considered to be present when PSP occurred regularly in a frequency of more than 7 cycles per minute; bradygastria indicated a frequency of less than 3 cycles per minute. Because of the insensitivity mentioned above, intraluminal manometry might not be able to detect gastric dysrhythmia.

Geldof et al. (l986) reiterated that gastric myoelectric activity could be recorded by peroral (suction) electrodes, by serosal electrodes placed at laparotomy, and by electrodes attached to the abdominal skin (electrogastrography). In a series of patients with unexplained nausea and vomiting, these authors recorded abnormal myoelectric activity by means of electrogastrography in almost 50 percent; the abnormal recordings were characterized by instability of the gastric pacemaker frequency, tachygastrias and absence of the normal increase in amplitude in the postprandial recording.

Discussion #

Periodic, rhythmic electrical activity, propagated in an aboral direction, occurs in the musculature of the stomach in man and other higher vertebrates. These waves, consisting of cyclical changes in potential, are variously known as primary waves, basic electrical rhythm (BER), slow waves, initial potential, pacesetter potential (PP) and electrical control activity (ECA). The waves occur at a rate of approximately 3 per minute in man and 6 per minute in dogs. They are omnipresent, precede and control the spread of peristalsis (Daniel and Chapman l963), but continue unchanged in the absence of peristalsis and do not indicate contractile activity.

Bursts of relatively rapid changes in potential, variously known as secondary waves, fast or spike potentials, second potential, fast activity, action potentials and electrical response activity (ERA), occur in association with some BER complexes. They are not propagated, appear to initiate contractions, and are associated with motor action.

A number of authors demonstrated a velocity increase in BER from approximately 0.3 cm per second in the corpus of the stomach to 3.0 or 4.0 cm per second in the terminal two to three centimeters of the "antrum", both in dogs (Daniel and Chapman l961, l963; Carlson et al. l966) and in man (Daniel and Irwin l968; Duthie et al. l97l). This corresponded to a "rapid spread of peristalsis" in, or "a nearly simultaneous contraction" of the terminal antrum. According to Daniel and Irwin (l968) the more rapid spread of electrical activity over the "terminal antrum" presumably provided the mechanism responsible for its behaviour as a motor unit.

The rapid progression of BER in the "terminal antrum" probably also points to some distinguishing feature or specialization of the musculature in this region. It is surmized that it is linked to the specialized musculature of the pyloric sphincteric cylinder described by Cunningham (1906), Forssell (1913) and Torgersen (l942), with its typical motor activity as discussed in Chapters 3, 13 and 15. ## References

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Geldof H, van der Schee EJ, van Blankenstein M, et al. Electrogastrographic study of gastric myoelectrical activity in patients with unexplained nausea and vomiting. Gut l986, 27, 799-808.
Hamilton JW, Bellahsene BE, Reichelderfer M, et al. Human electrogastrograms: comparison of surface and mucosal recordings. Dig Dis Sci l986, 31, 33-39.
Kwong NK, Brown BH, Whittaker GE, et al. Electrical activity of the gastric antrum in man. Brit J Surg l970, 57, 913-916.
Nelson TS, Kohatsu S. Clinical electrogastrography and its relationship to gastric surgery. Amer J Surg l968, 116, 215-222.
Sarna SK. Gastrointestinal electrical activity: terminology. Gastroenterology l975, 68, 1631-1635.
Smout AJPM, van der Schee ET, Grashuis JL. The electrogastrogram and what it shows. Dig Dis Sci l980, 25, l79-l87.
Stoddard CJ, Smallwood RH, Duthie HL. Electrical arrhythmias in the human stomach. Gut l98l, 22, 705-712.
Szurszewski JH. Electrical basis for gastrointestinal motility. In: Physiology of the Gastrointestinal Tract. Vol 2, edit Johnson LR. Raven Press, New York l98l, pp 1435-1466.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, l-191.
You CH, Lee KY, Chey WY, et al. In vitro myoelectric study of antral muscle from patients with tachygastria. Dig Dis Sci l980, 25, A17.
You CH, Chey WY. Study of electromechanical activity of the stomach in humans and dogs with particular attention to tachygastria. Gastroenterology l984, 86, 1460-1468.

17 - Ultrasonography of Pyloric Motility and Gastric Emptying

Mon, 01 Jan 0001 00:00:00 +0000

Ultrasonography of Pyloric Motility and Gastric Emptying #

Bateman et al (l977) measured the rate of gastric contractions by means of ultrasound pulse-echo scanning. As the procedure was non-invasive, non-ionizing and non- traumatic, it had certain advantages over other modes of examination. After an overnight fast normal subjects seated in the upright position imbibed 500 ml orange cordial warmed to 37ºC. Using a standard, commercially available B-scanner with a 1.5 MHz probe, the fluid in the stomach presented as an echo-free, transonic region. A quantitative display of the movement of the anterior and posterior walls of the "antrum" could be obtained in T-M (time motion) mode, and a permanent photographic record could be made. A continuous A-mode record of the wall movements was obtained simultaneously on video-tape.

In the normal stomach a biphasic response to the liquid meal was seen. Initially the "antral" contraction waves were slow and irregular, but after 7 to 15 min they appeared more frequently at regular 20 second intervals. The temperature of the fluid appeared to be of importance as gastric contraction waves were found to be inhibited at temperatures lower than 37ºC. Intravenous administration of 15 mg or 30 mg propantheline caused cessation of the contractions for periods of up to 3 hours. The method was found to be particularly suited to the measurement of contraction rates.

Holt et al. (l980) used real-time ultrasonic imaging to study contractions in the pyloric "antrum" and body of the stomach in 10 healthy subjects after a liquid test meal of 500 ml warmed orange juice. In 5 subjects scanning was also performed at intervals after a variety of solid and liquid meals. In all cases a real-time ultrasonic scanner containing 4 rotating transducers of 2.5 MHz was used; scans were done with the subject standing or seated upright. Real-time ultrasonic images were recorded on video-casettes and permanent photographic records were obtained.

In the resting state the distended, liquid-filled "antrum" was visualized as a rounded, echo-free or transonic zone. After the liquid meal contraction of the "antrum" was absent or weak for up to 5 minutes, but this was followed by regular contractions occurring with a frequency of 3 per minute, i.e. a contraction every 20 seconds; these were taken to be peristaltic waves. Propantheline 30 mg intravenously abolished the "antral" movements, while metoclopramide 10 mg intravenously enhanced the magnitude and frequency of the contractions. It was said that the images produced by real-time ultrasonic techniques closely resembled those seen during barium screening studies.

King et al. (l984) examined l7 normal subjects using a rotating transducer real-time ultrasound scanner with a 5 MHz probe. Subjects were examined seated in the upright position after an overnight fast and after imbibing 500 ml warmed orange cordial to which 0.5 g of chopped and sieved bran was added. The bran particles suspended in the fluid luminal contents acted as a sonic marker, thus allowing identification of movement through the pylorus. Forward flow indicated movement of particles from the stomach to the duodenum and retrograde flow movement from the duodenum into the stomach.

Images of the bran particles, the "distal or terminal antrum", pylorus and duodenum were obtained. (Comment: The "terminal antrum" was defined as the immediate prepyloric area. More detailed definitions of the terms "antrum" and "terminal antrum" were not given.) The timing and duration of the terminal antral contractions (TACs), proximal duodenal contractions, and periods of forward and retrograde flow through the pylorus in each individual were then compared in order to establish the relationships between them. The duration of a terminal antral contraction was about 4 seconds (mean 3.93 seconds ± 0.8). Pyloric closure invariably occurred as the gastric peristaltic wave reached the pylorus at the midpoint of the terminal antral contraction. Contractions of the first part of the duodenum were seen to occur just after the midpoint of the majority (86 percent) of terminal antral contractions. The vast majority (92 percent) of duodenal contractions occurred immediately after the terminal antral contraction, 5.5 percent occurred simultaneously with it and 2.5 percent were ectopic. Contraction of the first part of the duodenum lasted about 5 seconds (mean 4.93 seconds SD ± 1.75).

Transpyloric fluid movement was reflected by the movement of the bran particles. It occurred as brief episodes when the pylorus was open. Forward flow occurred in 81 percent of the cycles of contraction and lasted about 2 to 4 seconds. The majority of these episodes occurred after relaxation of the terminal antrum, pylorus and duodenum, while 25 percent occurred just before the terminal antral contraction. The discrete episodes of forward flow thus occurred as the terminal antrum, pylorus and duodenum were relaxed at the end or the start or each peristaltic cycle. Occasionally there was no forward flow in spite of terminal antral and duodenal contractions.

Retrograde flow, in episodes lasting up to 5 seconds, occurred in the vast majority of observed cycles of contraction. Most of these episodes were seen just before the terminal antral contraction, with 39 percent following it. A brief period of forward flow often ended abruptly and was sometimes immediately followed by a period of retrograde flow.

Bolondi et al. (l985) measured gastric emptying times in l8 normal subjects and 36 patients with functional dyspepsia, using a high-resolution real-time scanner with a 3.5 MHz linear array transducer. Having measured the transverse diameter and length of the "antrum" before and after a mixed solid-liquid meal, the volume of the "antropyloric" region was calculated and the time taken for its emptying determined. The antrum was taken to be the area extending from the "angle region" to the pylorus. Significantly longer emptying times were observed in patients with functional dyspepsia as compared with normal subjects. It was stated that various phases of antral peristalsis, such as propulsion waves, grinding movements and retropulsion could be studied by means of ultrasonic techniques, but no further particulars of these movements were given. King et al. (l985) used real-time ultrasonic imaging to study the temporal relationships between contractions of the terminal antrum, pylorus and proximal duodenum in 22 normal subjects. The methodology was similar to that of their previous study (King et al. l984). A total of 259 cyclical periods of motor activity were observed during 32 recordings, a general pattern being seen in all.

Terminal antral contractions occurred in 98 percent of the cyclical periods of motor activity. The duration of the terminal antral contraction was relatively constant at about 4 seconds (mean 3.6 ± 0.6 sec) and pyloric closure occurred at the midpoint of these contractions. The pylorus then opened as the terminal antrum relaxed and remained open until the next TAC started. Pyloric closure occurred with each terminal antral contraction and was not seen at any other time. During the few (2 percent) cyclical periods of motor activity in which terminal antral contractions did not occur, the pyloric "channel" (presumably the pyloric aperture) remained widely patent. The observations provided no evidence of independent pyloric function, i.e. independent function of the pyloric ring, in the post-prandial state in humans. Sixty-seven percent of the TACs were associated with contraction of the duodenal bulb. Ninety-four percent of duodenal bulb contractions occurred about 1 second after pyloric closure. The remaining 6 percent were ectopic, i.e. apparently unco-ordinated with TACs. Duodenal bulb contractions lasted approximately 5 seconds.

Discussion #

Real-time ultrasonic scanning plays an important role in the investigation of pyloric motility, pyloro-duodenal co-ordination and transpyloric fluid movement. Contractions of the pyloric region (designated pyloric "antrum" or "terminal antrum") closely resemble motility seen during radiological studies.

None of the authors quoted above related their findings to the specialized muscular anatomy of the pyloric sphincteric cylinder as described by Cunningham, Forssell and Torgersen (Chap. 3). However, it appears if the "terminal antrum" corresponds to the sphincteric cylinder. The finding that closure of the pyloric aperture occurs with each terminal antral contraction tallies with radiological observations that muscular closure of the aperture occurs during contraction of the sphincteric cylinder. According to ultrasonography the aperture closes as a gastric peristaltic wave reaches the midpoint of the terminal antrum, i.e. during terminal antral contraction (TAC). Radiologically it is seen that the aperture closes progressively during ongoing contraction of the cylinder. However, there is also an interplay between the right and left loops of the cylinder. If the left loop closes first, propulsion of contents into the duodenum occurs; if the right loop (surrounding the aperture) closes first, retropulsion from the cylinder (and not from the duodenum) into the more proximal part of the stomach occurs (Chap. 13). During maximal contraction of the cylinder both loops are tightly contracted and the aperture is closed.

In ultrasonography "forward flow" from stomach to duodenum, and "retrograde flow" from duodenum to stomach was described in association with TAC. The question arises whether true duodenogastric reflux was observed or whether retrograde movement of contents from the contracting sphincteric cylinder occurred.

With ultrasonography pyloro-duodenal co-ordination may be studied. This is hardly possible with conventional radiology; although it has been attemped by others, it has not been pursued in the present investigation. Ultrasonography has an advantage over radiology in that transpyloric flow of liquid contents may be quantified, using bran particles as sonic markers. Other advantages are that it is non-ionizing, non-invasive and non-traumatic.

Ultrasonography failed to identify independent action of the pyloric ring in the post- prandial state; this seems to confirm the view that the ring as such does not function as a sphincter.

References #

Bateman DN, Leeman S, Metreweli C, et al. A non-invasive technique for gastric motility measurement. Brit J Rad l977, 50, 526-527.
Bolondi L, Bortolotti M, Santi V, et al. Measurement of gastric emptying time by real-time ultrasonography. Gastroenterology l985, 89, 752-759.
Holt S, McDicken WN, Anderson T, et al. Dynamic imaging of the stomach by real-time ultrasound: a method for the study of gastric motility. Gut l980, 21, 597-601.
King PM, Adam RD, Pryde A, et al. Relationships of human antroduodenal motility and transpyloric fluid movement: non-invasive observations with real- time ultrasound. Gut l984, 25, 1384-1391.
King PM, Heading RC, Pryde A. Co-ordinated motor activity of the human gastroduodenal region. Dig Dis Sci l985, 30, 219-224, 24.

18 - Radionuclides in the Investigation of Gastric Emptying

Mon, 01 Jan 0001 00:00:00 +0000

Radionuclides in the Investigation of Gastric Emptying #

Griffith et al. (l966, l968) enumerated some of the techniques which had been used up to that time in the investigation of gastric emptying. For example, a previously administered meal could be aspirated at intervals, giving an indication of the rate of emptying. This showed that fluids left the stomach in an exponential manner; however, the technique was non-physiological and inaccurate, and required repeated naso-gastric intubations.

The time taken for a radio-opaque meal to leave the stomach could also be determined. This method could give rise to inaccuracies as it was possible that radio-opaque barium could separate from the meal, or alternatively, could become adherent to the mucosa; in both instances it would leave the stomach at a rate different to that of the meal. Moreover, the rate of emptying could not be quantified, and little information was obtained about the pattern of emptying.

Griffith et al,. (l966, l968) first used radionuclides in the study of gastric emptying. A technique was described in which a standard meal of porridge and eggs was labelled with radio-active chromium (⁵¹Cr), the rate at which it left the stomach being determined by means of external gamma counting. Subjects with and without gastro- duodenal disease were examined in the supine position, care being taken to differentiate the radio-activity emanating from the stomach from that of the small bowel. It was found that most of the meal left the stomach in an exponential manner. It also appeared that the rate of emptying of the stomach was constant for any one person whether there was gastro-duodenal disease or not.

Emptying of Liquids and Solids #

Heading et al. (l974) used different radio-isotopes to label the liquid and solid components of a standard meal; by this method emptying of liquids and solids could be assessed separately but simultaneously. The liquid component, consisting of cornflakes and milk, was labelled with ^113mIn DTPA chelate. The solid component consisted of small pieces of filter paper impregnated with ^99mTc sulphur colloid and coated with a thin film of perspex. In 15 normal subjects emptying of the aqueous phase approximated to a simple exponential process, but the solid phase marker appeared to empty at a constant rate. In almost all subjects this was substantially slower than emptying of the liquid phase, and there was poor correlation between the two rates.

In a review of gastric emptying tests up to that time, Sheiner (l975) pointed out that the choice of isotope used for labelling meals varied widely between workers. For the liquid component ¹¹³In-DTPA chelate was often used, while ⁵¹Cr, ¹²⁹Cs and ^99mTc-human albumin microspheres (HAM) had all been used to determine emptying of the more solid components. The gamma emission was measured by scintiscanning or by fixed detectors in a gamma camera. The results of gastric emptying studies could be expressed in diverse ways. The rate and patterns of emptying were influenced by a variety of factors such as the fluidity of the meal, the pH, osmolarity and volume of the food eaten and the specific gravity and viscosity of the more solid components.

Meyer et al. (l976) stated that previous measurements of gastric emptying of solid foods had depended on external counting of surface adsorbed isotopes, without verification that isotopic labels remained attached to the food in the stomach. It was shown that up to 90 percent of ⁵¹Cr adsorbed to scrambled eggs could become detached in the stomach. Moreover, much of the egg was dissolved by HCl and pepsin, increasing the amount of ⁵¹Cr which entered the liquid phase. A method was developed in which ^99mTc sulphur colloid was injected intravenously into chickens in vivo. The colloid was phagocytised by Kupfer cells, incorporated intracellularly and absorbed uniformly throughout the liver substance. Less than 10 percent of the tag administered in this way separated from the fed liver in the stomach. Chicken liver tagged with ^99mTc in vivo was found to be an appropriate marker of the rate of emptying of solid food. Tests showed that ^99mTc-tagged liver left the stomach in a linear, zero-order pattern. The same amount of solid appeared to be transferred into the duodenum per hour regardless of the size of the meal. By contrast, the liquid component of a meal left the stomach more rapidly, in an exponential or first-order pattern (i.e. linear on a semilogarithmic plot). Referring to the previous investigations of Griffith et al. (l966, l968), who had found that solid food left the stomach in an exponential fashion, it was stated that the discrepancy might have been due to liquefaction of the ⁵¹Cr marker used. The observations of Meyer et al. (l976) that liquids emptied faster than solids and that liquids emptied in a first-order fashion while solids emptied in a zero- order pattern, supported the concept that the human stomach handled liquids and solids by different processes.

Heading et al. (l976), using methods similar to those in their previous study (Heading et al l974), found that the posture of a patient and the composition of a meal might modify emptying patterns. In normal control subjects and duodenal ulcer patients, liquid emptying was faster than solid emptying and could be represented as a monoexponential process. Solid emptying followed a different pattern, better represented as a linear emptying with time. In patients who had undergone Billroth II partial gastrectomy there was no evidence of differential emptying of liquids and solids. Malagelada (l977) described the striking changes undergone by a solid liquid meal in the stomach during the postprandial period. Gastric and duodenal aspiration of a meal of meat labelled with ⁵¹Cr and containing water with polyethylene glycol, showed that the volume of solids was decreased by solubilization and partial digestion in the stomach. At the same time, endogenous secretions expanded the liquid phase of the gastric contents. Because of these processes, the gap between the percentage of solids in the stomach and that entering the duodenum gradually disappeared during the postprandial period, and gastric secretions rapidly replaced the water imbibed as the main intragastric liquid. It was thought that the process of retaining solids in the stomach and allowing liquids to empty into the duodenum, would expose the solid nutrients to continuously renewed, fresh gastric juice.

Canine gastric emptying of a digestible solid, an indigestible solid and a liquid was studied by Hinder and Kelly (l977), by quantitating the rate of appearance of gastric markers in the duodenum. Bovine liver tagged with ⁵⁷Co-cyanocobalamine, 7.0 mm diameter radio-opaque plastic spheres and one percent or 10 percent dextrose tagged with ³H polyethylene glycol (³HPEG) were used for the digestible solid, the indigestible solid and liquid respectively. The rate of gastric emptying of cubed liver was found to be similar, whether the liver was given alone or with solutions of the rapidly emptying one percent dextrose; the rate of emptying was slowed by 10 percent dextrose. Homogenization of the liver speeded emptying. The homogenized liver emptied even faster when dispensed in one percent dextrose, and emptied more slowly when dispersed in 10 percent dextrose, but in both instances the liver emptied at the same rate as the solution with which it was mixed. Indigestible spheres were nearly all retained, whereas the liver and dextrose were emptied. It was concluded that the stomach emptied liquids while solids were retained for reduction to a smaller size, after which they were discharged at the same rate as the liquid then present in the stomach.

Meyer (l979) pointed out that while external gamma counting of food markers to measure gastric emptying should theoretically obviate the need for sampling gastric contents, the method was not entirely free from difficulties. The distribution of radiolabels was not necessarily precise, as labels of the aqueous phase might adhere to the solids, and overlap could contribute to inaccuracies in gamma counting. Even when a radiolabel accurately identified a portion of the solid phase, that portion might empty at rates dependent on the size of its particles. Meyer (l980) nevertheless pointed out that short half-life, low- energy, gamma-emitting nuclide labels were safe for the investigation of gastric emptying processes. The phagocytosis of circulating colloidal nuclides such as ^99mTc and ^113mIn by the Kupfer cells of the liver of living donor animals had reduced labelling time. Hepatocytes could be labelled with ⁵⁷Co or ⁵⁹Fe in donor animals to provide tagged liver. The high chemical affinity of elemental ¹²³I for starch in foods and the chemical conjugation of radioiodine to hemicellulose have also provided methods for labelling food constituents. Having identified some of the artifacts in counting, methods have been instituted to correct them.

Horowitz et al. (l982) in an extensive review, pointed out that major advantages of radionuclide studies of gastric emptying were that they were simple and noninvasive, did not interfere with normal physiological mechanisms in the stomach, and allowed the simultaneous labelling of solid and liquid components of a meal. Methodological problems limiting the specificity and sensitivity of radionuclide tests included factors such as angulation of gamma rays originating within the stomach, causing them to be counted outside the gastric region of interest. Most of these minor problems were capable of correction.

According to Horowitz et al. (l982), emptying of labelled solids was usually linear after an initial lag phase. The lag phase reflected the movement of food from the fundus to the "antrum". Emptying of liquids was generally nonlinear, with a minimal lag period, and could be represented as a monoexponential, volume dependent process. Consequently it appeared that solid and liquid components of a meal were emptied in different ways. The pressure gradient across the gastroduodenal junction, largely controlled by the tone of the fundus, was the major factor controlling the emptying of liquids. The "antropyloric musculature" was of major importance in controlling the emptying of solid food, the end point being the passage of particles less than 1.0mm in size. Both these processes were also controlled from the duodenum by receptors responding to carbohydrate, fat and protein, with resultant slowing of gastric emptying.

Collins et al. (l983) assessed gastric emptying of a mixed solid and liquid meal in normal subjects, using ^99mTc sulphur colloid as the solid, and ^113mIn-DTPA as the liquid marker. It was shown that large errors in the measurements were possible, due to the variation in tissue attenuation caused by the changing depth of the radionuclide within the stomach. A technique for the correction of attenuation was described, using factors derived from a lateral image of the stomach. Normal solid emptying was found to be slower than liquid emptying and was characterised by a delay or lag period, which was followed by linear emptying; liquid emptying followed a single exponential pattern. Increasing the calorie content of the meal prolonged the lag period of solid and slowed liquid emptying. Whereas previous studies using other radionuclides in normal subjects had shown day-to-day variation in gastric emptying rates within normal subjects, as well as variations in rates between subjects (Heading et al. l976), this study showed that the day-to-day variation in gastric emptying within individual subjects was not significant. On the other hand, statistically significant differences were present in solid and liquid emptying between different subjects and groups.

Camilleri et al. (l985) studied the possible relation between "antral" phasic pressure activity and the emptying of solids and liquids from the normal human stomach after a mixed meal. Simultaneous antral manometry and radioscintigraphy were performed in 14 normal individuals after ingestion of a meal labelled with ^99mTc sulphur colloid in cooked egg (solid component) and ¹¹¹In DTPA (liquid component). Phasic pressure activity was recorded in the "distal antrum", i.e. 1.0 cm proximal to the gastroduodenal junction. During early precipitous emptying of liquids, occurring during the lag phase for solids, there was no relation between liquid emptying and "antral" motility. During the solid-emptying period however, there was a positive correlation between emptying of solids and "antral" motility. In addition, during the solid-emptying phase, a possible association was noted between antral phasic pressure activity and the emptying of liquids. The data are consistent with a role for antral pressure activity in trituration of solid food and a role for the "antrum" in the subsequent propulsion of solids and liquids from the stomach. Read et al. (l986) determined gastric emptying time by labelling a solid test meal with ^99mTechnetium sulphur colloid; the meal included labelled mashed potato mixed in water but was of homogeneous consistency. In normal subjects the stomach emptied exponentially with a half time of 1.2 ± 0.3 hours. A residue of up to 12 percent of the food (mean 6 percent) was present in the stomach 4 hours ater eating the meal. Although the radionuclide was mixed with liquid which reconstituted the mashed potato, they found no difference in the rate of emptying of the meal whether the marker was in the water used for reconstitution or whether it was incorporated in chicken liver. This supported the results of Hinder and Kelley (l977), who had shown that the solid and liquid components emptied at the same rate from meals of homogeneous consistency, but at different rates from meals composed of well separated solid and liquid components (such as the steak and water meal used by Meyer et al. in l976).

Camilleri et al. (l986) studied "antral" motility and gastric emptying in patients with clinically suspected upper gastrointestinal dysmotility. For the motility studies manometry was performed with a multiple-lumen perfusion assembly, and for gastric emptying a mixed solid and liquid meal was employed, ¹³¹I-Fibre being incorporated into the meal as a solid, nondigestible marker, and ^99mTc-DTPA as the aqueous marker. Solid emptying was found to be significantly prolonged in patients with "antral" hypomotility (but not in those with intestinal dysmotility). The prolongation was characterised both by an increase in the duration of the lag phase and a slower emptying rate in the postlag emptying phase (the lag phase being defined as the interval between the ingestion of the meal and the first appearance of ¹³¹I in the proximal small intestine). The half-times for liquid emptying were significantly prolonged in antral hypomotility as well as in intestinal dysmotility, but it was more marked in the former. These authors came to the conclusion that radionuclide gastric emptying and manometric studies provided closely interrelated physiologic information and could be regarded as complementary diagnostic tools.

Velchik et al. (l989) pointed out that while gastric empyting was influenced by meal weight and composition (the relative percentages of carbohydrate, protein and fat), the effect of meal energy content had not been thoroughly investigated. By means of radioinuclide techniques these authors showed that gastric emptying was progressively delayed by increasing the energy or caloric content of a standard meal.

Discussion #

The rate and pattern of gastric emptying is influenced by multiple factors, e.g. the composition, volume, osmolarity, pH and fluidity of a meal, the specific gravity, viscosity, digestibility and size of the more solid components, the posture of the subject (Heading et al. l974; Sheiner l975), and emotional states (Velchik et al. l989).

The advantages of radionuclide studies of gastric emptying are that they are simple, noninvasive, do not interfere with normal physiological processes and allow simultaneous labelling of solid and liquid components of a meal (Horowitz et al. l982; Velchik et al. l989).

The observations of Heading et al. (l974), Meyer et al. (l976) and Horowitz et al (l982) indicate that the stomach handles liquids and solids by different processes. The liquid component of a meal leaves the stomach more rapidly than solids, and is emptied in an exponential or first order pattern (Heading et al. l974; Meyer et al. l976). The pressure gradient across the gastro-duodenal junction is a major factor influencing emptying of liquids, and is largely controlled by the tone of the fundus (Horowitz et al. l982). During early emptying of liquids (occurring in the lag phase for solids), there is no relationship between "distal antral" motility and liquid emptying, as shown by simultaneous manometric and radioscintigraphic studies (the "distal antrum" was defined as the region 1.0 cm proximal to the gastro-duodenal junction) (Camilleri et al. l985).

Although it is true that upper gastrointestinal radiography is not quantitative and not suitable for analyzing the complex process of gastric emptying in its entirety, one agrees with Velchik et al. (l989) that it exquisitely displays anatomic detail. As contractions of the walls are clearly visible (Chap. 13), much information can be gained about the early stages of emptying of a liquid barium suspension (Chap 13). The influence of gastric tone (Chap. 19) and the posture of the subject (Chap. 20) is of major importance in the emptying of liquid barium. During the early stages emptying of the suspension usually occurs in the absence of both gastric peristaltic waves and contractions of the pyloric sphincteric cylinder, although shallow ripples of contraction of the gastric walls may be evident (Chap. 13). During later stages regular, cyclical contractions of the sphincteric cylinder occur at a rate of 3 per minute (Chaps. 13, 15). In the barium studies it is not possible to determine unequivocally whether individual contractions of the cylinder are associated with propulsion of liquid contents into the duodenum, or with retropulsion into the stomach, or with both (Chap. 13). However, progressive filling of the duodenum occurs in association with regular contractions of the cylinder, which suggests that one of the functions is propulsion.

Solids are emptied at a slower rate than liquids and in a linear or zero-order pattern (Heading et al l974; Meyer et al. l976). Hinder and Kelly (l977) showed that a distinction had to be made between the emptying of digestible and indigestible solids, and that larger solid particles were retained for reduction to a smaller size before emptying. The volume of solids may be decreased by solubilization and partial digestion in the stomach (Malagelada l977). Solids only empty after an initial delay or lag phase (Horowitz et al. l982; Collins et al. l983).

The "antropyloric muscle" is of major importance in controlling emptying of solid food (Horowitz et al. l982); a positive correlation exists between "antral" motility and emptying of solids (Camilleri et al. l986). This was confirmed by Velchik et al. (l989), who stated that the emptying of solids was largely determined by the "antrum and duodenopyloric mechanism". None of the authors quoted above correlated their findings with the muscular anatomy of the distal stomach as described by Cunningham (l906), Forssell (l913) and Torgersen (l942).

Radiographically the emptying of a mixed meal consisting of liquids, solids and barium sulphate suspension, is seen to be associated with vigorous cyclical contractions of the pyloric sphincteric cylinder (Chap. 13). Solids present as defects in the barium; softish solids may be observed to change in shape during contraction of the cylinder. It is our submission that cyclical contractions of the pyloric sphincteric cylinder will explain the "antropyloric muscular function" mentioned by Horowitz et al (l982), the "antral phasic pressure activity" of Camilleri et al (l986) and the "antral and duodenopyloric mechanism" of Velchik et al (l989).

Camilleri et al. (l986) found that antral phasic pressure activity played a role not only in propulsion of liquids and solids from the stomach, but also in trituration of solid food. Contraction of the pyloric sphincteric cylinder may at times be associated with retropulsion of barium suspension into the stomach (Chap. 13), retropulsion of its mucosal folds (Chap. 13), and retropulsion of sessile mucosal polyps (Chap. 36). Whether propulsion or retropulsion occurs, depends on the interplay between the right and left pyloric muscular loops (Chap. 13). It is probable that contraction of the cylinder, especially in the absence of propulsion or retropulsion, may be associated with trituration of solid particles. In diabetic gastroparesis failure of contraction of the cylinder was seen to be associated with failure of trituration (and propulsion) of solid tablets (Chap. 37).

According to Camilleri et al. (l986) radionuclide and manometric emptying studies provide closely interrelated physiological studies and may be regarded as complementary diagnostic tools. It seems that upper gastrointestinal radiographic studies may likewise assist in the clarification of problems of gastric emptying.

References #

Camilleri M, Malagelada JR, Brown ML, et al. Relation between antral motility and gastric emptying of solids and liquids in humans. Amer J Physiol l985, 249 (Gastrointest Liver Physiol 12) : G580-G585.
Camilleri M, Brown ML, Malagelada JR. Relationship between impaired gastric emptying and abnormal gastrointestinal motility. Gastroenterology l986, 9l, 94-99.
Collins PJ, Horowitz M, Cook DJ, et al. Gastric emptying in normal subjects: a reproducible technique using a single scintillation camera and computer system. Gut l983, 24, 1117-1125.
Cunningham DJ. The varying form of the stomach in man and the anthropoid age. Trans Roy Soc Edin l906, 45, 9-47.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Forschr Geb Röntgenstr l913, Suppl 30, 1-265.
Griffith GH, Owen GM, Kirkman S, et al. Measurement of rate of gastric emptying using Chromium - 51. Lancet l966, 1, 1244-1245.
Griffith GH, Owen GM, Campbell H, et al. Gastric emptying in health and in gastroduodenal disease. Gastroenterology l968, 54, 1-7.
Heading RC, Tothill P, McLoughlin GP, et al. Gastric emptying rate measurement in man: a method for simultaneous study of solid and liquid phases. Gut l974, 15, 841.
Heading RC, Tothill P, McLoughlin GP, et al. Gastric emptying rate measurement in man: a double isotope scanning technique for simultaneous study of solid and liquid phases. Gastroenterology l976, 71, 45-50.
Hinder RA, Kelly KA. Canine gastric emptying of solids and liquids. Amer J Physiol l977, 233 (Endocrinol Metab Gastro-intest Physiol 2): E335-E340.
Horowitz M, Cook DJ, Collins PJ, et al. The application of techniques using radionuclides to the study of gastric emptying. Surg Gynaec Obstet l982, 155, 737-744.
Malagelada JR. Quantification of gastric solid-liquid descrimination during digestion of ordinary meals. Gastroenterology l977, 72, 1264-1267.
Meyer JH, MacGregor IL, Gueller R, et al. ^99mTc-tagged chicken liver as a marker of solid food in the human stomach. Amer J Dig Dis l976, 21, 296-304.
Meyer JH. New dimensions in gastric physiology. Dig Dis Sci l979, 24, 97-100.
Meyer JH. Gastric emptying of ordinary food: effect of antrum on particle size. Amer J Physiol l980, 239 (Gastroint Liver Physiol 2); G133-G135.
Read NW, Al-Janabi MN, Holgate AM, et al. Simultaneous measurement of gastric emptying, small bowel residence and colonic filling of a solid meal by the use of the gamma camera. Gut l986, 27, 300-308.
Sheiner HJ. Gastric emptying tests in man. Gut l975, 16, 235-247.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, l-l91.
Velchik MG, Reynolds JC, Alavi A. The effect of meal energy content on gastric emptying. J Nucl Med l989, 30, 1106-1110.

19 - Gastric Tone and the Pyloric Sphincteric Cylinder

Mon, 01 Jan 0001 00:00:00 +0000

Gastric Tone and the Pyloric Sphincteric Cylinder #

Schulze-Delrieu (l986) pointed out that there was much uncertainty about the concept "gastric tone". It was a term that had been widely used at the beginning of this century and it was thought that tone determined the mechanical responsiveness of the stomach. Radiologists elaborated on this concept by assuming that a long, angulated "fish-hook" stomach reflected a low gastric tone; such a hypotonic stomach was associated with delayed gastric emptying and gastric stasis. On the other hand a short, globular, "steerhorn" stomach indicated a high gastric tone, i.e. it was hypertonic, and was associated with rapid gastric emptying.

Determination of Tone #

In order to determine gastric tone, Stadaas and Aune (l970) recorded intragastric pressure-volume relationships in 27 patients with dyspepsia, the tension generated by the gastric walls being measured over a range of balloon volumes. A thin-walled intragastric plastic balloon was filled stepwise with known volumes of water; after each step the intragastric pressure was recorded. If balloon pressures for all volumes were low, muscular tension of the gastric wall was low, i.e. the stomach was considered to be hypotonic. If balloon pressures were high, muscular tension of the wall was high and the stomach was hypertonic.

In a study of gastric tone Schulze-Delrieu (l983) examined the changes in gastric dimensions that accompanied the accommodation of volume by the stomach. He pointed out that while distension of the stomach was seen during routine radiographic studies, it had not been determined whether all the walls distended to the same degree, whether distension occurred mostly in the transverse axis or in the longitudinal axis, and which muscular structures were primarily concerned with volume accommodation. Excised stomachs of herbivores (rabbits) and carnivores (cats) were immersed in carboxygenated physiological solution and the shape and dimensions of the stomach, the response to filling, the intragastric pressures and the effects of drugs were determined. It was found that in both herbivores and carnivores the length and angulation of the lesser curvature were little affected by filling of the stomach. During volume accommodation gastric distension occurred mostly in the proximal stomach and along the greater curvature. Filling the stomach increased the length of the gastric circumference. These features could be explained on the muscular build of the stomach as a whole as determined by Pernkopf (l929) and Torgersen (l945). Another reason for the sizeable expansion of the greater curvature was that this curvature was concave while the lesser curvature was convex with respect to the lumen.

Normally, according to Schulze-Delrieu (l983), intraluminal pressures rose sharply on filling the stomach and declined thereafter. Carbachol, a known stimulant of gastric smooth muscle, caused contraction with a shortening of the longitudinal axis, as well as tubular contraction of the "antrum" and an increase in intragastric pressure. Isoproterenol, a known inhibitor of gastric smooth muscle, caused a more elongated shape, a flaccid appearance and a decrease in intragastric pressure. The findings provided experimental proof that the degree of gastric muscle tension was reflected in the overall configuration of the stomach. The existence of correlations between the configuration and the state of activity or tone of the musculature was demonstrated, thereby confirming the assumptions of early radiologists, according to Schulze-Delrieu (l983). Consequently measurements of gastric size and configuration provide one method of assessing gastric tone.

Another method is to measure tone by its effects on gastric volume rather than on gastric pressure. This was done by Azpiroz and Malagelada (l985, G229) who had developed an electronic barostat allowing the measurement of tone by recording changes in the intragastric volume of air. The barostat consisted of an intragastric air-filled bag, the pressure in the bag being kept constant electronically. When the stomach relaxed, air was injected into the bag; when it contracted, air was withdrawn. Gastric tone could be monitored from the barostat as variations in intrabag volume. Simultaneously intraluminal pressure activity was recorded by implanted manometric catheters. Tonic changes undetected by manometry were clearly registered by the barostat. In dogs it was found that marked changes in gastric tone were induced by meals. Receptive relaxation during feeding was followed by a low-tone accommodation period; this in turn was followed by a period of sustained high tonicity.

Azpiroz and Malagelada (l985, G501) demonstrated that nutrients in the small bowel could affect gastric tone. Fat infused into the proximal small bowel induced gastric relaxation in canines, whereas protein had only a modest effect and carbohydrate had no effect. In contrast, protein and carbohydrate infused into the distal small bowel markedly reduced gastric tone, whereas fat had no effect. These authors defined gastric tone as sustained muscular contraction of the gastric wall; variations in gastric tone probably mediated important physiological functions such as accommodation to a meal and emptying of liquids.

Schulze-Delrieu (l986) stated that physiologists working with isolated strips of gastric musculature abhorred the term gastric tone, as it was imprecise and reflected a judgment on gastric muscle tension as gained from purely visual or radiographic inspection. However, more precise measurements of gastric tone had been made with the use of gastric balloons. In his view gastric tone referred to the tension generated by the gastric walls. It affected the ability of the stomach to accommodate volume and to generate the driving force for gastric emptying. Experimental studies (Schulze-Delrieu l983) provided proof that the degree of gastric muscle tension development was reflected in the overall configuration of the stomach. If it was stimulated, the stomach was short and globular; if it was inhibited, the stomach was long and flaccid. The longitudinal musculature of the proximal greater curvature had a pivotal role in the overall control of gastric tone. According to Azpiroz and Malagelada (l990) tonic muscular contraction of the stomach (i.e. gastric tone), determines the balance between gastric accommodation and emptying. Tone is finely regulated by multiple interacting mechanisms; reflexes arising from different regions of the upper gastrointestinal tract may modulate the gastric emptying process (and hence presumably gastric tone).

An unusual but well-documented case of gastric atony was described by Telander et al (l978). This concerned a 5 months old child who presented with massive gastric distension and intractable gastric stasis. No evidence of organic narrowing or occlusion was found at the pylorus during 3 separate exploratory operations. Biopsy of the gastric wall revealed no abnormality of the ganglion cells in the myenteric plexuses and the smooth muscle cells of the tunica muscularis were normal. A gastric pressure-volume response obtained through a gastrostomy revealed no concomitant increase of intragastric pressure during stepwise increments of volume, indicating a complete lack of gastric tone, i.e. gastric atony. The cause was considered to be absence of electrical potential normally coupling electrical and mechanical activity, diminished sensitivity of the gastric smooth muscle to excitatory stimuli and probably an ectopic antral pacemaker. (Chap.16).

Discussion #

Hypotonicity #

Mainly as a result of the investigations of Stadaas and Aune (l97O), Schulze-Delrieu (l983, l986) and Azpiroz and Malagelada (l985) it may now be accepted that the radiographic image of a long, angulated, "fish-hook" stomach with a sagging greater curvature is due to hypotonicity of the gastric musculature. The hypotonic stomach is associated with decreased or absent peristalsis, absent cyclical contractions of the pyloric sphincteric cylinder and delayed emptying of liquid barium in the erect position (Chap. 13, 20). Changing the position of the subject to the left anterior oblique recumbent position, causes immediate, gravitational emptying of liquid barium, showing that pylorospasm is not a factor in these cases (Chap. 20).

In most instances gastric hypotonicity is of idiopathic origin and presumably of little clinical significance. More severe degrees, sometimes progressing to acute gastric dilatation, may occur in a variety of conditions e.g. post-operatively, after severe trauma and in electrolyte disturbances.

Hypertonicity #

A short, transversely situated, "steerhorn" stomach on the other hand, is now known to be the result of gastric hypertonicity. In these cases immediate emptying of liquid barium usually commences in the erect position, before the onset of peristalsis or cyclical contractions of the pyloric sphincteric cylinder (Chap. 13).

References #

Azpiroz F, Malagelada JR. Physiologic variations in canine gastric tone measured by an electronic barostat. Amer J Physiol l985, 248, G229 - G237.
Azpiroz F, Malagelada JR. Intestinal control of gastric tone. Amer J Physiol l985, 249, G501 - G509.
Azpiroz F, Malagelada JR. Perception and reflex relaxation of the stomach in response to gut distension. Gastroenterology l990, 98, ll93 - ll98.
Pernkopf E. Beiträge zur vergleichenden Anatomie des Vertebratenmagens. Zeitschr gesamte Anat l929, 91, 329 - 362.
Schulze-Delrieu K. Volume accommodation by distension of gastric fundus (rabbit) and gastric corpus (cat). Dig Dis Sci l983, 28, 625 - 632.
Schulze-Delrieu K. Selected Summaries: Gastric Tone. Gastroenterology l986, 90, 1298 - 1299.
Stadaas J, Aune S. Intragastric pressure-volume relationship before and after vagotomy. Acta Chir Scand l970, 136, 611 - 615.
Telander RL, Morgan KG, Kreulen DL, et al. Human gastric atony with tachygastria and gastric retention. Gastroenterology l978, 75, 497 - 501.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l945, Suppl 45, 1 - 191.

20 - Pylorospasm

Mon, 01 Jan 0001 00:00:00 +0000

Pylorospasm #

There has been much uncertainty about the concept "pylorospasm". For many years radiologists considered pylorospasm to be due to spasm of the pyloric ring, where the ring was equated with the pyloric sphincter. It was thought that spasm of the ring (or "sphincter") closed the pyloric aperture, thereby delaying gastric emptying and causing retention. In other words, whenever the barium-filled stomach showed delayed emptying, or failed to empty within a certain prescribed time (in the absence of an organic lesion), older radiologists were inclined to label the condition "pylorospasm". This diagnosis was made commonly, was usually accepted by clinicians, and probably had an erroneous bearing on the perception of many intra-abdominal conditions.

Radiological Features #

Hughson (1925) for example, stated that spasm of the pylorus (as manifested by delayed gastric emptying) formed the basis of the radiological diagnosis in many pathologic conditions of the gastrointestinal tract. The great majority of cases of radiologically diagnosed pylorospasm were directly attributable to pathological conditions either of the stomach itself or of other abdominal viscera. He quoted previous studies in which radiological examinations had revealed delayed gastric emptying, considered to be due to pylorospasm, in 27 percent of duodenal ulcer and 89 percent of gastric ulcer cases. This led him to believe that radiologists had thrown much light on the relation of pylorospasm to intra-abdominal disease.

Bastianelli (1925) had reservations about the above radiological interpretation of pylorospasm. He agreed that in certain patients, especially neurotic individuals, a type of pylorospasm of nervous origin could occur; this was defined as a more or less permanent closure of the pylorus, not relieved by contractions of the "antrum" as seen at radiological examinations. It is clear that in this instance spasm of the pyloric ring was inferred. A similar type of pylorospasm was reflex spasm, occurring as a result of lesions of other abdominal organs, e.g. pathology of the gall bladder or appendix. In these cases there was increased tonicity of the pyloric canal and pyloric ring (the term "canal" indicated the pyloric aperture). Reflex spasm, causing a delay in gastric emptying, could also occur as a result of gastric hyperacidity. However, referring to the work of Cole (1913), Bastianelli (1925) stated that in many instances the radiological observations could not be accepted without question. Pylorospasm was much more likely to consist of a tonic contraction of the entire "antrum" rather than an isolated contraction of the "sphincter", as physiological observations favoured a simultaneous contraction of the whole region. It appeared to him that the question of pylorospasm needed revision.

Deaver and Burden (1929) were also impressed by the frequent radiological diagnosis of pylorospasm in intra-abdominal conditions (where pylorospasm was equated with spasm of the pyloric ring, which was considered to be the sphincter). It led these surgeons to believe that disease of the gall bladder or appendix caused symptoms which were attributable to reflex pylorospasm. It was assumed, moreover, that reflex pylorospasm prevented regurgitation of alkaline duodenal contents into the stomach, causing gastric hyperacidity and ulceration. In order to alleviate the symptoms in gastric ulceration, duodenal ulceration and chronic cholecystitis, the now obsolete operation of hemi- sphincterectomy was devised. During this procedure the anterior half of the pyloric "sphincter" (i.e. the pyloric ring) was excised; in their view this prevented further pylorospasm and relieved the symptoms in most cases.

Problems of Definition #

What exactly is meant by pylorospasm? During conventional radiological examinations, with the patient in the erect position, and in the absence of an organic lesion in the upper gastrointestinal tract, it is not unusual to observe a delay in gastric emptying of liquid barium suspension. This, in many instances, is still considered to be caused by pylorospasm, by which is implied spasm of the pyloric ring, which is equated with the sphincter. The question may well be asked whether the ring is spastic in these cases. If it were, it could be expected to remain spastic irrespective of the position of the patient. In order to determine whether this is the case, the following investigations were done.

Patients and Methods #

Fifty adult, ambulatory out-patients, each showing a long, "hanging", atonic stomach with a marked delay in gastric emptying of liquid barium in the erect position (an appearance usually ascribed to pylorospasm), were selected for examination. These patients were encountered during the ordinary course of events, having been referred for routine radiographic study because of vague upper abdominal symptoms. None had any objective signs of upper gastrointestinal disease at a prior clinical examination. The following is a representative case:

Case Report

Case 20.1.J.B., 47 year old male. After swallowing the first 3 mouthfuls of Micropaque in the erect position, the stomach was seen to be of the long, hanging, atonic type, the sagging greater curvature forming the most dependent part (Fig. 20.1A). The distal part of the stomach curved upwards and was filled up to the presumed position of the pyloric ring. Peristalsis and cyclical contractions of the pyloric sphincteric cylinder were absent, with total absence of gastric emptying for the first 5 minutes. This would have been interpreted as "pylorospasm" by many investigators. The head of the examining table was then lowered to an angle of 45 degrees, while the patient was rotated 45 degrees onto the right side (i.e. the tilted left anterior oblique radiological position). Immediate emptying of liquid barium occurred in the continued absence of both peristalsis and contractions of the pyloric sphincteric cylinder, revealing a normal pyloric ring surrounding a patent aperture (Fig 21.1B). On re-assuming the erect position, gastric emptying ceased once again.

A B

Fig. 20.1. A Case J.B. Erect position. Long, atonic stomach, the sagging greater curvature forming most dependent part. Absence of peristalsis, cyclical activity of sphincteric cylinder and emptying of fluid barium. B Case J.B. Oblique tilted position. Normal pyloric ring and patent aperture. Immediate emptying of fluid barium in continued absence of peristalsis and cyclical activity of sphincteric cylinder

In 49 of the patients the features were identical to the case quoted. The findings show that the delay in gastric emptying was not due to pylorospasm, in the sense that the pyloric ring was spastic, as neither spasm nor delayed emptying was present in the tilted oblique position; it would be highly improbable for spasm to manifest itself in the erect position only. It was much more likely that the delay in gastric emptying was due to one or both of the following factors: (1) primarily aperistaltic, hypotonic stomach; (2) the erect position of the subject. In these cases, in the erect position, the pyloric aperture is at a higher level than the lowermost part of the greater curvature, which bulges downward. While the aperture is patent, the lack of tone (Chap. 19) and/or cyclical contractions of the pyloric sphincteric cylinder (Chap. 18) causes failure of emptying. In the tilted oblique position the aperture is manipulated so as to become the lowermost part of the stomach. While contractions of the cylinder remain absent, passive, gravitational emptying of liquid content occurs, showing the aperture to be patent, without evidence of spasm of the ring. (In one of the 50 cases a delay in gastric emptying occurred in both the erect and the tilted oblique positions; the cause of this remained unclear.)

Discussion #

It appears possible that Hughson (l925), Deaver and Burden (l929) and others were led to believe that absent or delayed emptying of fluid barium in hypotonic stomachs in the erect position, was due to pylorospasm, which was equated with spasm of the pyloric ring. It was claimed, moreover, that such "pylorospasm" was a frequent accompaniment of intra-abdominal pathology. In the historical context it is of interest to note that Bastianelli (l925) questioned their radiological interpretation of "pylorospasm". Even today an inactive, hypotonic, barium containing stomach showing delayed or absent emptying in the erect position is often, and we believe mistakenly, ascribed to pylorospasm. According to Torgersen's views (l942) it would be highly unlikely for the pyloric ring (the right pyloric loop) as such, to become spastic; as no dividing line exists between the musculature of the ring and that of the remainder of the sphincteric cylinder, any possible spasm would involve the entire cylinder.

Pathogenesis #

Torgersen (1942) showed an illustration in which the canine canalis egestorius (i.e. pyloric sphincteric cylinder), in its entirety, was spastic. He postulated that the appearance of pylorospasm was identical to that seen in a maximal or near maximal normal contraction of the sphincteric cylinder (Chap. 13) during certain stages of vomiting (Chap. 26) and in cases of infantile hypertrophic pyloric stenosis (IHPS) (Chap. 23). All these conditions had the same anatomical "substratum", namely contraction of the musculature of the entire sphincteric cylinder.

Astley (1952) described 10 well-documented cases of infantile pylorospasm in which the spasm involved the canalis egestorius as defined anatomically by Forssell (1913) (Chap. 3). In all these infants, who presented with vomiting, a prepyloric narrowing simulating infantile hypertrophic pyloric stenosis was seen at the radiological examination. The narrowing persisted for periods ranging from 10 minutes to over an hour; it differed from IHPS in degree but not in the extent or shape of the area affected. Continued observation showed that it was neither constantly narrowed nor completely devoid of peristalsis as in IHPS; after a variable interval the narrowed segment relaxed to a certain extent and in some cases it eventually attained a normal calibre. In a few instances the relaxation occurred suddenly while in others intermittent contraction and relaxation was seen. There can be little doubt that these cases of infantile pylorospasm were due to spasm of the pyloric sphincteric cylinder. Astley (1952) mentioned the fact that the radiological appearance simulated a stage in the normal cycle of contraction of what he called the "prepylorus".

Wood and Astley (1952), during an investigation of the causes of vomiting in young infants, described the clinical findings in a group of 12 cases in which the symptoms closely resembled those of IHPS. Some of the cases previously mentioned by Astley (1952) appear to be included in this group. A palpable pyloric tumor was found in 8 of the cases (the term "tumor" indicated a clinically detectable swelling). It resembled the tumor of IHPS, although it differed in consistency, being softer, and it was less well defined. It was usually palpable immediately before or just after a vomit, relaxed quickly and could not be felt repeatedly; as the clinical findings resembled IHPS the condition was called "pseudo-pyloric stenosis". Radiological examination in 4 of the 12 babies showed infantile pylorospasm, i.e. a cylindrical prepyloric narrowing simulating IHPS. However, it lacked the constancy and aperistalsis of IHPS, and continued observation showed that it widened eventually. In 5 of the 12 babies who were operated upon, neither pyloric hypertrophy nor tumor was found, showing that the features were due to spasm of the sphincteric cylinder. In their investigations into the causes of vomiting in more than 100 infants, Astley (1952) and Wood and Astley (1952) did not describe any cases of pylorospasm in which spasm was limited to the pyloric ring.

Craig (l955) pointed out that a palpable, contractile tumor was present in 98 percent of infants with IHPS over the age of 2 weeks. The same significance could not always be attached to the palpation of a contractile pyloric tumor in babies under 2 weeks of age. Initially 2 cases were encountered, both babies under 2 weeks, in whom recurrent regurgitation was associated with a contractile pyloric tumor. Over a period of weeks the symptoms as well as the pyloric tumor disappeared, the only treatment having been daily gastric lavages. Because of the clinical features IHPS was excluded as a cause of the condition. Craig (l955) instituted a prospective study in which 21 infants less than 2 weeks of age, presenting with repeated vomiting but otherwise normal, were examined. Contractile pyloric tumors were palpated in l7. With repeated gastric lavages symptoms subsided within 7 to 14 days, while the tumors disappeared after a period of time varying from 4 weeks to 3 months. In a control group of 115 healthy newborn infants with uninterrupted progress and no feeding difficulties, a palpable pyloric tumor was felt in 25. Of the 21 who were followed up, the tumor disappeared within 6 weeks to 3 months. The pyloric tumors had a fusiform or spheroidal shape and a firm or distinctly hard consistency. They were felt to contract and relax repeatedly, became firmer as feeding continued, and were palpated at successive examinations. A feature of all cases was the large amount of mucus in the gastric lavages. Some of the cases were examined radiologically but this appeared to be incomplete and yielded little relevant information. One of the symptomatic babies, who had a large pyloric tumor resembling IHPS in all respects, was referred for operation, at which no tumor was found.

According to Craig (1955) these cases indicated that a hard, contractile pyloric tumor could be felt in the absence of organic change of the musculature. It was considered to be due to spasm of the fan-shaped pyloric musculature described by Cole (l928). It was evidence not of muscular hypertrophy but of muscular spasm, and resembled the cases of pseudo-pyloric stenosis previously described by Astley (l952).

Atkinson et al. (l957) stated that the concept of spasm of the pylorus presumably derived from the belief that a physiological sphincter existed at the pylorus. It was widely believed that the pyloric ring acted as a sphincter. However, during manometric studies they were unable to find any evidence of a physiological sphincter at the pylorus, and in no instance could a band of increased pressure be demonstrated anywhere at the pyloroduodenal junction (Chap. 15). Although phasic pressure waves were recorded repeatedly in a 4.0 to 5.0 cm long segment of the prepyloric region, no evidence of independent contraction was found at the gastroduodenal junction, i.e. at the pyloric ring. For most of the time the lumen surrounded by the pyloric ring or "sphincter" was more than 7.0 mm in diameter. The closure of the ring was intermittent and brief, occurring as part of the phasic contraction which periodically involved the whole pyloric region. Atkinson et al. (l957) concluded that the concept of spasm of the pyloric ring had been grossly overworked as an explanation for a variety of symptoms.

According to Levin (l971) pylorospasm could at times mimick the "elongated", narrowed pylorus of adult hypertrophic pyloric stenosis.

Swischuk (l978, l980) considered pylorospasm to be a spasm of the "antropyloric" region, by which was meant a tubelike, segmental area extending orally from the ring. It could be difficult to distinguish pylorospasm from some cases of IHPS; in pylorospasm, however, the narrowing was not as intense and there were slight changes in the configuration. A similar deformity of the antropyloric region could also occur in association with gastric ulceration in neonates.

Franken (l982) found infantile pylorospasm a difficult entity to define; the appearances could be very similar to those of IHPS on radiographic study. However, the narrowing seen in infantile pylorospasm was not as constant as in IHPS, and in infantile pylorospasm some peristaltic movement did occur in the affected area. It could be difficult to convince the surgeon that the patient had infantile pylorospasm and not IHPS.

Ultrasonic Features #

Direct viewing of the pyloric musculature is achieved by means of ultrasonic examination (Chap. 10). Blumhagen and Coombs (l98l) showed that a persistent contraction of the circular musculature of the "distal antrum and pylorus", creating a cylindrical muscle mass resembling IHPS, might be seen during ultrasonic examinations in infants. According to these authors, contraction of the "distal antrum" and pylorus (and not of the pyloric ring) constituted pylorospasm.

Blumhagen and Noble (l983) found that spasm of the "distal antrum and pylorus" could be differentiated ultrasonically from IHPS by measuring the single wall muscle thickness. Normally the muscle thickness in infants varies between 1.5 and 3.0 mm; in IHPS it varies between 3.0 and 6.0 mm. Whenever the single wall muscle thickness is 4.0 mm or more, it can be regarded as IHPS.

Wilson and Vanhoutte (l984) determined the true length of the pyloric muscle by means of ultrasonography in l7 normal infants; the range varied from 12.0 to 15.0 mm. Similar results were obtained by Graif et al. (l984), who found the mean length of the pylorus (pyloric musculature) to be 12.0 mm with a standard deviation of 3.7 mm. It is clear that this is the anatomical region which may contract during pylorospasm, i.e. a relatively long area which includes the pyloric ring, as opposed to an isolated contraction of the ring only. This was confirmed by Stunden et al. (l986), who measured the length of the pyloric canal in normal infants "with the pylorus in its most contracted state". The mean length of the canal was 8.3 ± 2.5mm, and on occasion it was up to 14.0 mm in length.

With longitudinal ultrasonic views of the pylorus Haller and Cohen (l986) found the length of the pyloric musculature in normal infants to be up to l8.0 mm. Ultrasonically the contraction of this muscular cylinder in pylorospasm could simulate IHPS. However, with spasm the contracted region was not quite as rigid as in IHPS, and the appearance changed on subsequent examinations.

Operative and Experimental Features #

Larson et al (l967) described 10 adult cases in whom radiographs showed clear evidence of adult hypertrophic pyloric stenosis (AHPS), i.e. a cylindrical pyloric narrowing (Chap. 24). At operation the stomach was found to be normal in 5, showing that the narrowing was of a temporary, spastic nature, in other words due to pylorospasm.

During operations on 5 suspected cases of AHPS, Bateson et al. (l969) noted that on touching the pylorus with a gloved finger, the pyloric and adjacent "antral" muscle contracted, becoming hard and pale; the affected region was approximately 2.5 cm in length and resembled AHPS, but the contraction was temporary and of a spastic nature.

Keet and Heydenrych (l97l) found that electrical and mechanical stimulation of the vagus trunks in the oesophageal hiatus of the diaphragm in canines, caused a 3.0 cm long cylindrical area of contraction in the pyloric region. It corresponded exactly to the anatomical pyloric sphincteric cylinder as described by Cunningham (l906), Forssell (l913) and Torgersen (l942), lasted as long as the stimulus was applied, and was clearly of a spastic nature.

Case Reports

The following are some of the cases of pylorospasm which we have encountered:

21 - Congenital Anomalies

Mon, 01 Jan 0001 00:00:00 +0000

Congenital Anomalies #

Congenital anomalies of the pyloric region of the stomach are rare (Thompson et al. l968; Lamesch and Schneider l973; Korber and Glasson l977). The cause is usually thought to be localized vascular impairment occurring during foetal life (Bremer l944; Louw l959).

Pyloric Atresia #

Almost all cases of gastric atresia occur in the pyloric region (Franken l982). The condition may present as a membrane occluding the lumen, as a gap in continuity, or a fibrous cord intervening between patent portions at the gastroduodenal junction. Some cases have been associated with epidermolysis bullosa (Korber and Glasson l977; Franken l982). Clinically the condition presents as upper abdominal distension in a newborn infant, with bile-free vomiting from birth (Davis and Douglas l961; Thompson et al. l968; Bronsther et al. l97l). Maternal hydramnios occurs in approximately 50 percent of cases (Thompson et al. l968; Bronsther et al. l97l).

Radiographic examination shows the stomach to be distended, with complete absence of gas in the remainder of the gastrointestinal tract. In the erect abdominal film this gives rise to a single air-fluid level in the stomach, topped by a gas bubble (the "single bubble" sign) (Davis & Douglas l961; Becker et al. l963; Bronsther et al. l97l). According to Franken (l982) neonatal gastric hypotonia, which is a much more frequent condition, may give a similar appearance. (In hypotonia gastric inactivity with lack of peristalsis and cyclical contraction of the pyloric sphincteric cylinder may delay gastric emptying as described in Chapter l9).

Discussion #

Gastric atresia usually affects the region of the pyloric sphincteric cylinder; whether it is limited to the cylinder is not known.

References #

Becker JM, Schneider KM, Fischer AE. Pyloric atresia. Arch Surg l963, 87, 413-416.
Bremer JL. Diverticula and duplications of the intestinal tract. Arch Path l944, 38, 132-140.
Bronsther B, Nadeau MR, Abrams MW. Congenital pyloric atresia: a report of three cases and a review of the literature. Surgery l97l, 69, 130-136.
Davis DA, Douglas KR. Congenital pyloric atresia, a rare anomaly. Ann Surg l96l, 153, 418-422.
Franken EA. Gastrointestinal Imaging in Pediatrics. Harper and Row, Philadelphia l982, 2nd ed, p 138.
Korber JS, Glasson MJ. Pyloric atresia associated with epidermolysis bullosa. J Pediatr l977, 90, 600-601.
Lamesch A, Schneider H. Atr�sie et st�nose congenitales du pylore. Acta Paed Belgica l973, 27, 169-183.
Louw JH. Congenital intestinal atresia and stenosis in the newborn; observations on its pathogenesis and treatment. Ann Roy Coll Surg l959, 25, 209- 234.
Thompson NW, Parker W, Schwartz S, et al. Congenital pyloric atresia. Arch Surg l968, 97, 792-796.

Duplications #

True or complete duplication of the stomach or any other entire region of the gastrointestinal tract is exceedingly rare. More common (but also rare) incomplete duplications may be defined as spherical or tubular enteric formations which lie in contiguity with the normal alimentary tract and which share with it a common blood supply, and usually a common muscle coat (Abrami and Dennison l961). These cyst-like structures, or duplication cysts, usually do not communicate with the normal lumen. They may have a mucosal lining and may be pedunculated (Kammerer l969). They may occur along the entire alimentary tract, the most common site being the ileum and the least common the stomach (Abrami and Dennison l961; Kremer et al. l970). Over a 21 year period Sieber (l956) encountered 25 cases of gastrointestinal tract duplications, only 4 of which involved the stomach. Duplications of the pyloric region are particularly rare (Grosfeld et al. l970).

Duplication cyst of the stomach is a communicating or non-communicating cyst lined by gastric, intestinal or pancreatic epithelium, and usually located along the greater curvature (Kremer et al. l970). Occasionally it may be situated in the wall of the pyloric region; in such cases encroachment on the lumen may produce gastric outlet obstruction (Grosfeld et al. l970), or an appearance resembling infantile hypertrophic pyloric stenosis (Abrami and Dennison l96l; Kammerer l969). In non-communicating duplication cysts accumulation of acid and pepsin may produce a local inflammatory reaction, perforation, abscess formation and peritonitis; this was seen in 6 of 9 patients described by Kremer et al. (l970).

Discussion #

Gastric duplication does not appear to be related anatomically to the pyloric sphincteric cylinder.

References #

Abrami G, Dennison WM. Duplication of the stomach. Surgery l96l, 49, 794-801.
Grosfeld JL, Boles ET, Reiner C. Duplication of pylorus in the newborn: a rare cause of gastric outlet obstruction. J Ped Surg l970, 5, 365-369.
Grosfeld JL, O'Neill JA, Clatworthy HW. Enteric duplications in infancy and childhood: an l8 year review. Ann Surg l970, 172, 83-90.
Kammerer GT. Duplication of stomach resembling hypertrophic pyloric stenosis. J Amer Med Assoc l969, 207, 2101-2102.
Kremer RM, Lepoff RB, Izant RJ. Duplication of the stomach. J Pediat Surg l970, 5, 360-364.
Sieber WK. Alimentary tract duplications. Arch Surg l956, 73, 383- 392.

Congenital Double Pylorus #

Congenital double pylorus is an extremely rare condition. In reviewing their cases of gastro-intestinal duplications encountered over an l8 year period, Grosfeld et al. (l970) did not mention a single example of this anomaly. A case was reported by Christien et al (l97l), but subsequently doubt was expressed as to the congenital nature of the lesion (Hansen et al. l972). Acquired double pylorus, due to pyloroduodenal fistula, is not nearly as rare and is a well documented condition (Chap. 31).

Sufian et al. (l977) described a case which appears to be of true congenital origin. It concerned a 30 year old female with a long history of epigastric pain and aspirin and ethanol abuse. The radiological examination revealed two pyloric apertures; gastroscopy failed to show any abnormality. Although no evidence of active or previous ulceration was found at operation, a partial gastrectomy was performed. The resection specimen revealed a second pyloric opening 2.0 cm in length and 1.0cm in diameter, adjacent to the normal pylorus. The mucosa and muscularis mucosae of both apertures were normal, but a nodule of ectopic pancreatic tissue was situated in the wall of the second opening.

Gupta and Hollander (l977) described a case of achalasia of the oesophagus occurring in a 56 year old female. During endoscopic examination a double pyloric aperture was an unexpected finding. There was no evidence of peptic ulcer disease and it was considered to be a case of double pylorus of congenital origin.

Williams et al. (l98l) mentioned the case of a 35 year old male who had had duodenal ulcer symptoms for 5 years. Endoscopy showed a duodenal ulcer and a double pylorus proximal to the ulcer. At operation a septum between the 2 apertures was excised. It was composed of normal mucosa with a complete ring of muscularis mucosae, and the case was considered to be a double pylorus of congenital origin.

Discussion #

Congenital double pylorus is extremely rare and cases have not been encountered by us. Acquired double pylorus due to pyloroduodenal fistula is much less rare and is well documented.

References #

Christien G, Branthomme J, Volny L, et al. Pylore double: malformation congénitale. Sem Hôp Paris l97l, 47, 1485-1488.
Grosfeld JL, O'Neill JA, Clatworthy HW. Enteric duplications in infancy and childhood: an l8 year review. Ann Surg l970, l72, 83-90.
Gupta A, Hollander D. Duplication of the pylorus found concomitantly with achalasia: congenital or peptic etiology? Amer J Dig Dis l977, 22, 829-830.
Hansen HO, Kronborg O, Pedersen T. The double pylorus. Scand J Gastroenterol l972, 7, 695-696.
Sufian S, Ominsky S, Matsumoto T. Congenital double pylorus: a case report and review of the literature. Gastroenterology l977, 73, 154-157.
Williams RS, Gilmore IT, Johnson AG. Congenital double pylorus: a case report. Brit J Surg l98l, 68, 65.

Pyloric Membrane, Web or Diaphragm #

Pyloric membrane, web or diaphragm has been defined as a thin, circumferential mucosal septum in the pyloric region, projecting intraluminally perpendicular to the long axis of the "antrum". It is composed of two layers of gastric mucosa, with a central core of submucosa and muscularis mucosae; the external muscular and serous coats do not take part in its formation. In the majority of cases a central or eccentric aperture is present, varying from a pinhole to several millimeters in diameter; in a few cases the membrane was unperforated or complete (Rowling l959; Melamed et al. l960; Gerber l965; Parrish et al. l968; Felson et al. l969; Bell et al. l977; Mitchell et al. l979; Jinkins et al. l980).

Pyloric membrane is generally regarded as a congenital anomaly. It is usually associated with symptoms and signs of gastric outlet obstruction. In incomplete membranes symptoms may only occur in adult life, the aperture preventing obstruction for many years (Cremin l969; Jinkins et al. l980). The condition has been described in premature and newborn infants, in older infants and children (Touroff and Sussman l940; Gerber l965; Farman et al. l968; Cremin l969; Bell et al. l977; Fujioka et al. l980; Jinkins et al. l980), and in adults (Farman et al l968; Felson et al l969; Melamed et al l960; Ghent and Denton l974; Ghahremani l974), the ages in adults ranging from 32 to 85 years.

A typical radiographic sign is a radiolucent line 2.0 to 3.0 mm in width, perpendicular to the long axis of the "antrum", representing the membrane (Felson et al. l969). The region between the membrane and the pyloric aperture may be filled with barium, resembling the duodenal bulb; the "double-bulb" appearance is another chracteristic sign (Parrish et al. l968; Felson et al. l969; Bell et al. l977).

In the great majority of cases described in the literature, the membrane was located 1.0 to 4.0 cm proximal to the pyloric aperture; it could perhaps best be designated a "prepyloric" membrane in these cases (vide infra). In a few instances it was very close to, or at the pylorus ("true pyloric membrane"); one case of Rowling (l959), one of Dineen and Redo (l963), one of Gerber (l965), two of Felson et al. (l969) and one of Mitchell (l979) fall into this category. In isolated instances (one case of Felson et al., and one of Ghahremani), a membrane was seen 7.0cm proximal to the pylorus.

In the prepyloric category, the distance of the membrane from the pyloric aperture varied from 1.0 to 2.0 cm in children (Bell et al. l978), and from 1.5 to 4.5 cm in adults (Ghahremani l974). The majority of membranes in adults were located at a distance of 1.5 to 4.0 cm from the pylorus (Rowling l959; Melamed et al. l960; Parrish l968; Cremin l969; Felson et al. l969; Ghahremani l974; Bell et al. l977; Mitchell et al. l979; Jinkins et al. l980).

Discussion #

We have not encountered reports in which the prepyloric membrane was described in relation to the pyloric sphincteric cylinder. However, in many descriptions and their accompanying illustrations, it was noted that the prepyloric membrane occurred in the location of the left pyloric loop. This is especially well demonstrated in illustrations accompanying the case report of Rowling (l959), that of Melamed et al (l960), the 3 cases of Parrish et al. (l968), the 2 of Cremin (l969), the one of Ghent and Denton (l974), most of the 10 cases of Bell et al. (l977), the 2 cases of Fujioka et al (l980) and the 4 of Jinkins et al. (l980). It appears to us (but it has not been proved) that, in the majority of cases, the prepyloric mucosal membrane occurs on the luminal aspect of the left pyloric loop of the muscularis externa, in the same way as the mucosal and submucosal parts of the pyloric ring are located on the luminal aspect of the right pyloric loop (to form the pyloric ring). It is interesting to note that Parrish et al. (l968) found a definite thickening in the muscularis externa underlying the membrane in one of their cases; this could conceivably be due to the left loop.

Fujioka et al. (l980) also reported 2 cases of pseudowebs, in whom radiographic examination had shown typical signs of prepyloric membranes; at operation and endoscopy no abnormality was found. In these cases the "webs" were probably caused by prominent, circular mucosal folds. It should be possible to differentiate permanent webs from circular mucosal folds by the characteristic movements and change in position of the folds during contraction of the sphincteric cylinder, as discussed in Chapters 2 and 13. However, a circular mucosal fold may occasionally be permanent, simulating a web (Chap. 28).

References #

Bell MJ, Ternberg JL, McAlister W, et al. Antral diaphragm: cause of gastric outlet obstruction in infants and children. J Pediatr l977, 90, 196- 202.
Bell MJ, Ternberg JL, Keating JP, et al. Prepyloric gastric antral web: a puzzling epidemic. J Pediat Surg l978, 13, 307-313.
Cremin BJ. Congenital pyloric antral membranes in infancy. Radiology l969, 92, 509-512.
Dineen JP, Redo SF. Pyloric obstruction due to mucosal diaphragm. Surgery l963, 53, 674-676.
Farman J, Cywes S, Werbeloff L. Pyloric mucosal diaphragms. Clin Rad l968, l9, 95-99.
Felson B, Berkmen YM, Hoyumpa M. Gastric mucosal diaphragm. Radiology l969, 92, 513-517.
Fujioka M, Fisher S, Young LW. Pseudoweb of the gastric antrum in infants. Ped Radiol l980, 9, 73-75.
Gerber BC. Prepyloric diaphragm, an unusual abnormality: a case report. Arch Surg l965, 90, 472-480.
Ghent CN, Denton D. Mucosal diaphragm of the gastric antrum: case report and review of the literature. Canad J Surg l974, 17, 274-278.
Ghahremani GG. Nonobstructive mucosal diaphragms or rings of the gastric antrum in adults. Amer J Roentg Rad Ther Nucl Med l974, 121, 236- 247.
Jinkins JR, Ball TI, Clements JL, et al. Antral mucosal diaphragms in infants and children. Ped Radiol l980, 9, 69-72.
Melamed A, Haukohl RS, Callan E. Pyloric antral mucosal diaphragm with transpyloric mucosal prolapse. Radiology l960, 74, 452-457.
Mitchell KG, McGowan A, Smith DC, et al. Pyloric diaphragm, antral web, congenital antral membrane: a surgical rarity? Brit J Surg l979, 66, 572-574.
Parrish RA, Kanavage CB, Wells JA, et al. Surg Gynaec Obstet l968, 127, 999-1004.
Rowling JT. The prepyloric septum: a rare anomaly. Brit J Surg l959, 47, 162-166.
Touroff ASW, Sussman RM. Congenital prepyloric membranous obstruction in premature infant. Surgery l940, 8, 739-755.

Ectopic Pancreatic Tissue #

Samuel (l955) pointed out that barium-filled ducts in ectopic pancreatic tissue, embedded in the wall of the stomach, may simulate an intramural diverticulum. Moore and Kaplan (l956) found that a small mass of aberrant pancreatic tissue may be loosely attached to the serosal surface of the upper intestine, or it may occur in the subserosal, submuscular or submucosal regions of the gastric walls. Radiographically it usually presents as an elevated mound with a central dimpling and an opening formed by ducts. When the dimpling is filled with barium, it may resemble a polyp with an ulcer at its tip; when the ducts are filled, it resembles a diverticulum.

Besemann et al. (l97l) confirmed that most aberrant pancreatic nodules occurred in the upper gastrointestinal tract, usually in the duodenum, but occasionally in the stomach near the pylorus.

Case Report #

Case 21.1. D.J., 22 year old male, had a long history of dyspepsia not responding to anti-ulcer treatment. Two days before admission there had been an episode of haematemesis. Gastroscopy showed a small orifice on the posterior gastric wall close to the pyloric aperture. It was thought to be either an intramural diverticulum or a double pylorus; radiographic examination was requested for further elucidation. This showed a small, branching, diverticular structure approximately 1.0 cm in length, on the greater curvature side of the pyloric sphincteric cylinder within 1.0 cm of the pylorus (Fig. 21.1). It remained constant in appearance irrespective of the degree of contraction of the cylinder, the contractions being normal. At laparotomy no evidence of ulceration was seen. A nodule of abnormal tissue measuring approximately 2.0 cm in diameter was palpated in the gastric wall at the site indicated by endoscopy and radiology. Gastrostomy revealed a small orifice extending into the nodule, which was removed by local excision. Histology showed it to consist of endo- and exocrine pancreatic tissue located in the muscular coat of the stomach.

Fig. 21.1. Case D.J. Small, branching, diverticulum-like structure (arrow) on greater curvature side of pyloric sphincteric cylinder

Discussion #

In this case a small nodule of ectopic pancreatic tissue in the wall of the greater curvature of the pyloric sphincteric cylinder did not affect the movements of the cylinder to any appreciable extent. Radiographically the lesion mimicked an intramural diverticulum (Chap. 22).

References #

Besemann EF, Auerbach SH, Wolfe WW. Importance of roentgenologic diagnosis of aberrant pancreatic tissue in the gastrointestinal tract. Amer J Roentg Rad Ther Nucl Med l969, 107, 71-76.
Moore MB, Kaplan IW. Heterotopic pancreatic tissue in the stomach. Amer J Gastroenterol l956, 26, 699-705.
Samuel E. Gastric diverticula. Brit J Radiol l955, 28, 574-578.

22 - Partial or Intramural Gastric Diverticulum

Mon, 01 Jan 0001 00:00:00 +0000

Partial or Intramural Gastric Diverticulum #

The term partial gastric diverticulum was first used by Samuel (l955) to indicate a projection of the mucosa into, but not through the muscular coats of the stomach. As it does not extend as far as the serosa, external inspection of the stomach at operation will not reveal any abnormality. He described a case, diagnosed by radiography and subsequently confirmed at operation, in whom a partial diverticulum was located on the greater curvature of the pyloric "antrum" approximately 1.0mm orally to the pyloric ring. It was surrounded by a shallow, smooth-walled defect which was considered to be due to oedema. Radiographically it had to be differentiated from a gastric ulcer, a small ulcerated tumor and ectopic pancreatic tissue (in which barium-filled ducts might resemble small diverticula) (Chap. 21). However, these conditions could be excluded because of the smooth outline and narrow neck of the diverticulum, the normal mucosal pattern in its vicinity and the absence of associated spasm.

Flachs et al. (l965) described 2 similar cases. In both the partial diverticulum was situated on the greater curvature close to the pyloric ring. In one of the cases it was mistaken for a gastric ulcer, resulting in partial gastrectomy. The resection specimen showed a mucosal pouch protruding into the submucosa, with the muscular layer intact and the serosa smooth and glistening. It was pointed out that a mucosal pouch could show variable filling with barium during the radiographic examination; the surrounding musculature might contract to such an extent that it could disappear almost completely. In contrast, a gastric ulcer showed little change in appearance.

Rabushka et al. (l968) described the radiographic appearances of a case (confirmed at operation) in which a partial diverticulum, entirely contained within the wall of the stomach, was situated on the greater curvature 4.0 to 5.0 cm proximal to the pylorus. (In another case a diverticulum on the greater curvature of the pars media was also considered to be of the intramural variety, but this was not proved and it could possibly have been a "conventional" diverticulum).

The condition is rare. Treichel et al. (l976) encountered 4 patients (one of whom had 2 intramural diverticula) during the course of 10,000 routine upper gastrointestinal barium investigations. All cases were confirmed by endoscopy and 2 also by operation. The diverticula typically occurred on the greater curvature of the "antrum" within 1.0 to 4.0 cm of the pylorus, measured 4.0 to 10.0 mm in diameter, presented as round or oval pouches with narrow necks, and changed to some extent in size and shape during contraction of the walls. Complete filling of a diverticulum could be achieved by administering a spasmolytic during a double contrast examination. In the case where radiography showed 2 diverticula, endoscopy initially failed to reveal the lesions; however, they were visualized at a second attempt. It was stated that the lesions were easier to detect by radiography than by endoscopy.

Treugut and Olsson (l980) described another case in which the lesion typically presented at radiography as a smooth-walled, lenticular, intramural outpouching on the greater curvature of the "antrum" approximately 3.0 cm proximal to the pylorus. It varied somewhat in size but never exceeded 10.0 mm in diameter. The ostium was surrounded by a circular fold; in other respects the mucosal folds were normal, which differentiated it from a gastric ulcer and an ulcerated tumor. Confirmation was obtained by endoscopy and operation.

Cockrell et al. (l984) encountered reports of 13 cases in the literature and added 3 of their own. To them the striking feature was the unique location of the lesion on the greater curvature of the "distal antrum". There was no explanation for its occurrence in this particular situation and the etiology remained unknown.

Dickinson and Freeman (l986) reviewed the radiographic and endoscopic features of the condition and described 6 cases of their own. All were diagnosed at radiography, 4 being confirmed by endoscopy. It was pointed out that while a partial gastric diverticulum was a rare and clinically insignificant lesion, it was liable to cause diagnostic confusion and might lead to inappropriate treatment (e.g. partial gastrectomy) if not recognized.

We have encountered the following 3 cases of intramural gastric diverticula during the last 13,600 upper gastrointestinal barium investigations.

Case Reports

Case 22.1. M.W., 55 year old female, complained of cramp-like epigastric pains diurnally and occasionally nocturnally after a late evening meal. At times she felt nauseous. Physical examination revealed signs of chronic bronchitis and iron deficiency anaemia. Gastroscopy showed a sliding hiatus hernia without oesophagitis. No evidence of ulceration or other lesion was seen in the stomach and duodenum. A second gastroscopy six years later showed no abnormality in the oesophagus, stomach and duodenum. Repeat gastroscopy the following month was difficult due to lack of patient co-operation. The oesophagus was normal. The pyloric region appeared somewhat hyperaemic and oedematous, the remainder of the stomach being normal. The duodenum could not be visualized. Barium radiographic examination at that time showed a small diverticulum on the greater curvature of the pyloric sphincteric cylinder approximately 2.5 cm proximal to the pyloric ring (Fig. 22.1A). Its neck, which was surrounded by a shallow, smooth-walled indentation of the barium in the lumen, was 0.7 mm in diameter. During contraction of the cylinder it was seen to be situated midway between the right and left pyloric loops (Fig. 22.1B) in the situation where the pyloric pseudo-diverticulum occurs normally (Chap. 13). At times, during near maximal contraction of the cylinder, it disappeared, only to reappear during the next cycle of filling.

A	B
`Fig. 22.1. A Case M.W. Small intramural diverticulum (arrow) on greater curvature of pyloric sphincteric cylinder 2.5 cm proximal to pyloric ring. B Case M.W. Partial contraction of sphincteric cylinder. Intramural diverticulum (arrow) situated on rim of physiological pseudodiverticulum (PD), midway between right and left pyloric loops`

Because of the features enumerated in the discussion it was diagnosed as an intramural or partial gastric diverticulum. It was certainly not an ulcer as witnessed by repeated gastroscopies. The fact that it was not seen at gastroscopy does not come as a surprise as Treichel et al. (l976) had found that the lesion was easier to detect by radiography than by endoscopy. Cockrell et al. (l984) stated that an intramural diverticulum may be difficult to detect endoscopically if its ostium is hidden by a fold or if it occurs in an area which is contracting.

Case 22.2. G.V., 32 year old female, complained of a vague feeling of fullness and occasional pain in the epigastrium. Physical examination revealed some epigastric tenderness. After a month's treatment with antacids the symptoms disappeared. Radiographic examination at that time showed a small diverticular-like structure on the greater curvature of the pyloric sphincteric cylinder approximately 3.0 cm proximal to the pyloric ring, i.e. midway between the right and left pyloric loops, in the position where the pyloric pseudo-diverticulum usually occurs (Fig. 22.2A). It was surrounded by a shallow, smooth-walled, lenticular indentation of the barium in the lumen. During contraction of the cylinder it changed in shape and became smaller (Fig. 22.2B); it was diagnosed as an intramural or partial diverticulum. Absence of associated spasm, normal mucosal folds in the vicinity and change in size during contraction ruled out an ulcer. The patient was lost to follow-up and did not return for gastroscopy.

A	B
`Fig. 22.2. A Case G.V. Intramural diverticulum (arrow) on greater curvature of sphincteric cylinder 3.0 cm proximal to pyloric ring. B Case G.V. Contraction of sphincteric cylinder. Intramural diverticulum (arrow) between right and left pyloric loops now smaller`

Case 22.3. J.V., l9 year old female, complained of "acidity", of several months' duration. Gastroscopy showed mucosal erosions in the lower oesophagus, probably due to reflux oesophagitis. The gastric fornix and corpus were normal; on the greater curvature of the "antrum" a "pseudodiverticulum" was seen. Radiographic examination 14 months later, for the same complaint, showed an intramural diverticulum on the greater curvature within 2.0 cm of the pylorus. Cyclical contractions of the pyloric sphincteric cylinder were normal; during contraction of the right and left pyloric loops, a normal, physiological pseudodiverticulum was seen with an intramural diverticulum on its greater curvature aspect (Fig. 22.3).

Fig. 22.3. Case J.V. Normal contraction of pyloric muscle torus (MT) and right (RPL) and left (LPL) pyloric loops. Intramural diverticulum (arrow) on rim of physiological pseudodiverticulum (PD)

Discussion #

According to Cockrell et al. (l984) the striking feature of the lesion was its unique location on the greater curvature of the "distal antrum". No ready explanation could be found for its occurrence in this particular situation and the etiology remained unknown.

We believe the explanation probably lies in the anatomical build of the pyloric sphincteric cylinder as described previously (Chap. 3). In all 3 our cases the intramural diverticulum occurred on the greater curvature between the right and left pyloric loops, a fact which became clear during contraction of the loops. In this region the musculature of the cylinder is at its thinnest; it is surmized that the intramural diverticulum consists of a projection of mucosa and submucosa into the relatively sparse muscle fibres. It is best visible when the region is distended, becoming compressed or smaller during contraction of the muscular rings and intervening musculature. According to the descriptions of Samuel (l955), Flachs et al. (l965), Treugut and Olsson (l980) and Cockrell et al. (l984) their cases will also fall into this category, and so will some of the cases described by Rabushka et al. (l968), Treichel et al. (l976) and Dickinson and Freeman (l986).

An intramural gastric diverticulum should not be confused with the pseudo-diverticulum of the pylorus, which is a fleeting, physiological outpouching of all layers of the wall occurring normally during contraction of the sphincteric cylinder (Chap.13). An intramural gastric diverticulum may be seen on the greater curvature aspect of the physiological pseudodiverticulum during a stage of contraction of the sphincteric cylinder.

Whether it is a congenital or acquired lesion, is not known.

References #

Cockrell CH, Cho SR, Messmer JM, et al. Intramural gastric diverticula: a report of three cases. Brit J Radiol l984, 57, 285-288.
Dickinson RJ, Freeman AH. Partial gastric diverticula: radiological and endoscopic features in six patients. Gut l986, 27, 954-957.
Flachs K, Stelman HH, Matsumoto PJH. Partial gastric diverticula. Amer J Roentg Rad Ther Nucl Med l965, 94, 339-342.
Rabushka SE, Melamed M, Melamed JL. Unusual gastric diverticula: report of two cases. Radiology l968, 90, 1006-1008.
Samuel E. Gastric diverticula. Brit J Radiol l955, 28, 574-578.
Treichel J, Gerstenberg E, Palme G, et al. Diagnosis of partial gastric diverticula. Radiology l976, ll9, 13-18.
Treugut H, Olsson SA. Intramurales Magendivertikel. Fortschr Geb Röntgenstr Nuklearmed l980, 133, 327-328.

23 - Infantile Hypertrophic Pyloric Stenosis

Mon, 01 Jan 0001 00:00:00 +0000

Infantile Hypertrophic Pyloric Stenosis #

Although a few isolated cases of infantile hypertrophic pyloric stenosis (IHPS) had been reported previously, Hirschsprung (l888) is generally regarded as the first author to have recognized it as a separate clinical entity. At that time the tendency was to designate the condition congenital hypertrophic pyloric stenosis. At present, the clinical features and management are well understood, and will not be recapitulated. It may be useful to discuss the images seen during radiographic and ultrasonic examinations, especially in relation to anatomical factors, and to consider some of the theories regarding the etiology and pathogenesis.

Anatomical Localization and Radiographic Features #

Cunningham (1906) studied the morbid anatomical appearances in "a considerable number" of cases of IHPS, and found the muscular hypertrophy to be limited to the anatomical pyloric sphincteric cylinder, which includes the pyloric ring (Chap. 3). The affected area was almost 2.54 cm in length and had the look and feel of a hard, solid cylinder. It was sharply demarcated from the duodenum on its aboral, and from the pyloric vestibule on its oral side. In more severe cases the narrowing was greatest at the two ends, the cylinder in those cases assuming an oval or fusiform shape, somewhat like an olive. In all cases the musculature of the remainder of the stomach was normal. The relative extent to which each of the two muscular layers was involved in the hypertrophy was not the same in every case. While some observers believed that the circular musculature had undergone the greater degree of hypertrophy, Cunningham (1906) found that both layers were involved. Nevertheless the circular layer of the cylinder remained 3 to 4 times as thick as the longitudinal in his cases.

Forssell (l913) emphasized that muscular hypertrophy in cases of IHPS was localized to the canalis egestorius, i.e. the pyloric sphincteric cylinder of Cunningham (1906) (Chap. 3). The radiographic appearances of the contracted canalis in IHPS corresponded exactly to those of a maximal normal contraction of the pyloric sphincteric cylinder (Chap. 13); while the contraction was cyclical and of a fleeting nature in normal subjects, it was constant in IHPS. The muscular hypertrophy was associated with functional abnormalities of the closing mechanism of the canalis egestorius. The autoplastic movements of the mucous membrane were also involved (Chaps. 2, 13).

Meuwissen and Sloof (l932, l934) were the first to state that the purpose of the radiological examination was not to demonstrate the indirect features of the condition, such as gastric hyperperistalsis and retention, but to visualize the lesion itself, i.e. the contracted pyloric canal, in its longest dimension. The average length of the canal in normal infants was only 1.0 to 2.0 mm, while in the majority of cases of IHPS it was very long and narrow, ranging from 12.0 to 24.0 mm in length. In a minority of cases the range was from 3.0 to 11.0 mm. (Owing to magnification factors the actual length was about nine-tenths of that measured on the films). Radiologically the thin, permanently contracted canal, containing a single, central streak of barium in the lumen, resembled a string. These authors were the first to describe the "string sign" of IHPS, and also mentioned concave indentations of the distal stomach on either side of the string, caused by the bulging pyloric musculature, which became known as the "shoulder sign" (Fig. 23.1). There was complete absence of peristalsis in the contracted region. According to Meuwissen and Sloof (l932, l934) the contraction was largely due to spasm, with or without associated muscular hypertrophy.

Fig. 23.1 A-F. More common radiographic signs of infantile hypertrophic pyloric stenosis (after Astley, 1952). A Central "beak". B Beak with adjacent concave indentations (shoulder sign). C Beak, gap and cap. D String sign. E Longitudinal mucosal folds. F Concave indentation base of cap. Pyloric "tit" (arrow)

Frimann-Dahl (l935) reported 3 cases and showed that muscular hypertrophy was not limited to the pyloric ring, as was commonly thought, but that it was up to 20.0 mm in length and involved the entire canalis egestorius. In his cases the musculature of the canalis was hypertrophied and strongly contracted, whereas the ring itself showed little thickening.

Runström (l939), in a study of 107 cases of IHPS, described the main patho- anatomical finding as a tumor as hard as cartilage, 2.0 to 3.0 cm in length and 1.5 cm thick, involving the muscular part of the stomach which had been designated the canalis egestorius by Forssell (l913); the muscular hypertrophy was not localized to the pyloric sphincter (i.e. the pyloric ring), but involved the entire canalis. Radiologically the contracted canalis presented as a tube with a narrow lumen 2.0 to 3.0 cm in length, completely lacking in "peristaltic motility". In contrast, the remainder of the stomach showed increased peristalsis, which invariably stopped at the oral end of the constriction. In addition a change occurred in the autoplastic movements of the mucosa, with mucosal folds filling the narrow passage in the contracted canalis; these factors resulted in a delay in gastric emptying.

Torgersen's (l942) microscopic sections showed that muscular hypertrophy in IHPS involved the two sphincteric loops together with the intervening fibres, i.e. the entire canalis egestorius. As the musculature of the remainder of the stomach was normal, he concluded that it was a pathological process limited to the canalis. Hypertrophy of the muscular wall with resultant narrowing of the lumen gave rise to the radiological picture of a permanently contracted pyloric canal. Torgersen (l942) agreed with Forssell (l913) that the radiological appearance of IHPS conformed to that seen in a maximal or near maximal contraction of the normal canalis. Contraction of the circular fibres of the muscularis externa produced narrowing of the lumen, and contraction of the longitudinal fibres produced shortening; the exact picture seen would depend on which of the two forms of contraction had gained supremacy.

Astley (l952) reiterated that in IHPS the prepyloric portion of the stomach was constantly narrowed and devoid of peristalsis. Radiologically this might present in a number of ways (Fig. 23.1). In some infants in whom no gastric emptying occurred for a considerable time, the distended stomach was seen to end in a small triangular projection or "antral beak". On either side of the beak a concave indentation occurred in the distal stomach due to the bulging pyloric musculature. Whem emptying did take place, the narrowed channel might present as a hair-line of barium, or as 2 or 3 parallel lines (crowded mucosal folds), or as a canal with a width of up to 3.0 mm. The canal was often slightly curved (concave upwards) and its length could vary between 8.0 and 30.0 mm. A concave indentation of the base of the duodenal bulb, again caused by the bulging pyloric muscle mass, might be present, resulting in a mushroom or umbrella-like appearance of the bulb. Incomplete filling of the stenotic area appeared as a gap between the "beak" and the cap.

According to Astley (l952) the following conditions could mimic the radiographic appearances of IHPS, and should be considered in the differential diagnosis:

A stage in the normal, cyclical contraction of the region. Referring to Forssell (l913), he mentioned that a maximal normal contraction of the canalis egestorius (Chap. 13) might simulate the contraction of IHPS. While the former is of a fleeting nature, the latter is permanent.
Infantile pylorospasm. In a series of 10 vomiting babies Astley (l952) noted that the normal process of widening of the prepyloric channel to its full calibre was considerably delayed in these cases. The narrowing persisted for 10 minutes to over an hour and simulated IHPS. However, continued observation showed that the segment was neither constantly narrowed nor devoid of peristalsis as it was in IHPS. After an interval gradual, or at times a more sudden relaxation occurred. The features were due to pylorospasm (Chap. 20) and were sometimes erroneously diagnosed as IHPS.
Gastric inactivity, i.e. failure of barium to leave the stomach due to absence of peristalsis. The retention could simulate that occurring in IHPS.

In a minority of cases of IHPS, the radiological findings were less easy to interpret; according to Astley (l952) these were cases in which filling of the stenotic area and duodenal bulb was of a fleeting nature, or in which free gastric emptying occurred.

Shopfner (l964) described an additional radiological sign of IHPS, namely the pyloric tit. This consisted of a sharp projection from the lesser curvature of the filled part of the stomach at the oral end of the constriction (Fig. 23.1). The tit was also seen in 2 cases of pylorospasm, and had exactly the same appearance as in IHPS, but disappeared when the spasm relaxed. The narrowing of pylorospasm resembled IHPS but disappeared within 5 to 10 minutes, enabling a differentiation to be made between the two conditions.

Not all the radiological signs occur in every case. In 14 proved cases of IHPS Haran et al (l966) noted the string sign in 11, the beak sign in 11, the tit sign in 6 and the shoulder sign in 5. These authors also described the doubletrack sign, consisting of 2 parallel linear streaks of barium with an interposed radiolucent band in the constricted channel. (Comment: The sign seems to be similar to one previously described by Astley in l952). While infantile pylorospasm might resemble IHPS radiologically, the "double-track" was not evident in their cases of spasm.

The radiographic features have been reviewed by Shuman et al. (l967), Haller and Cohen (l986) and others.

Swischuk et al. (l980, l989) pointed out that pylorospasm produced an "antral" deformity which was virtually indistinguishable from some forms of true IHPS. However, in spasm the configuration was less permanent, showing slight variations from time to time. The same authors described a number of cases of unusual, atypical or incomplete hypertrophy of the pyloric musculature, in which barium studies led to puzzling "antral" configurations, including funnel antrum, spiculated antrum, pyloric niche, and the lesser curve mass. The spiculated antrum was thought to be due to hypertrophied rings of circular muscularis externa, and the lesser curve mass to selective hypertrophy of the muscle torus (Chap. 25). With ultrasound and its ability to visualize the pyloric musculature directly, the diagnosis of IHPS in these cases left no room for doubt. The following cases illustrate some of the radiological features of IHPS:

Case Reports

Case 23.1. B.G., 21 day old male, was admitted for projectile vomiting. Radiographic examination showed almost total obstruction in the pyloric region with gastric distension. The obstruction presented as a sharp cut-off transverse to the long axis of the stomach, with a tiny central "beak" (Fig 23.2). These appearances are generally accepted to be indicative of IHPS, and in our view can be explained as follows: hypertrophy of the musculature of the pyloric sphincteric cylinder causes a mass which occludes the lumen, preventing its filling with barium (this has sometimes been referred to as "amputation of the antrum"). The tiny "beak" indicates filling of the commencement of the occluded pyloric canal. At operation the diagnosis of IHPS was confirmed.

Fig. 23.2. Case B.G. Sharp cut-off pyloric region causing obstruction. Presumed extent of pyloric muscular hypertrophy (straight arrows). Central "beak" (curved arrow)

Case 23.2. B.B., 28 day old male, had a history of post-feeds vomiting for the previous 2 weeks. Radiographic examination showed a severe, constant narrowing 2.0cm in length in the pyloric region of the stomach, causing obstruction. The narrowing was string-like in appearance and at its proximal end associated with concave indentations into the stomach (Fig. 23.3). The appearance is compatible with IHPS and can be explained as follows: hypertrophy of the musculature of the entire length of the pyloric sphincteric cylinder causes a pronounced narrowing of the lumen, which is permanent. Muscular hypertrophy surrounding the narrowed lumen indents the stomach, causing concave defects. The diagnosis of IHPS was confirmed at operation.

Fig. 23.3. Case B.B. String-like narrowing 2.0cm in length (arrows) due to pyloric muscular hypertrophy

Case 23.3. M.M., male aged 10 days, was admitted with a history of vomiting since birth. Radiographic examination initially showed total obstruction of the pyloric region ("amputation of the antrum") (Fig. 23.4A). After 15 minutes, barium filled the pyloric canal, which was permanently contracted and approximately 2.0 cm in length (Fig. 23.4B); two longitudinal mucosal folds were seen in the contracted canal. There was a concave indentation of the base of the duodenal bulb. The appearance is that of IHPS and can be explained as follows: muscular hypertrophy of the entire length of the pyloric sphincteric cylinder initially obstructs the lumen; somewhat later filling of the permanently formed pyloric canal occurs. Muscular hypertrophy surrounding the latter indents the base of the duodenal bulb. Ramstedt operation two days later confirmed IHPS.

A	B
`Fig. 23.4. A Case M.M. Initial total obstruction pyloric region ("amputation of antrum"). Presumed extent of pyloric muscular hypertrophy (arrows). B Case M.M. Permanently formed pyloric canal, containing longitudinal mucosal folds, due to IHPS (arrows). Concave indentation base of duodenal bulb`

Case 23.4. C.V., male aged 15 days, was admitted for projectile vomiting and dehydration. Radiographic examination showed a constant narrowing, 1.5 cm in length, in the pyloric region, with a concave indentation of the base of the duodenal bulb (Fig. 23.5). At times a small dilatation was seen in the centre of the narrowed canal. The appearance is indicative of IHPS and can be explained as follows: the entire length of the musculature of the pyloric sphincteric cylinder is hypertrophied, causing narrowing of the lumen and a permanently contracted pyloric canal, as well as a concave indentation of the base of the duodenal bulb. The dilatation in the centre of the narrowed canal is probably an outward bulge between the right and left pyloric loops. The diagnosis was confirmed at a Ramstedt operation a few days later.

Fig. 23.5. Case C.V. Permanently formed pyloric canal due to IHPS. Concave indentation base of bulb. Small central dilatation in canal

Anatomical Localization and Ultrasonic Features #

Using a grey-scale unit with a 5MHz nonfocused transducer, Teele and Smith (l977) first described the sonographic appearances in 5 babies with IHPS. By passing the transducer transversely over the right lateral abdominal wall at the level of the costal margin, the region of the pylorus was scanned through the liver; the hypertrophied pyloric musculature presented as a round or oval echolucent mass with a central stellate collection of echoes. The average antero-posterior diameter of each mass was 2.3 cm, with a range of 1.8 to 2.8 cm. They were unable to identify a similar soft tissue mass in normal babies. An echolucent mass could also be produced by the gastric "antrum" or duodenal bulb filled with fluid, and by the hepatic flexure of the colon filled with stool, but in those instances the appearance was evanescent and did not have the typical central collection of echoes seen in IHPS.

Subsequently, various authors determined the measurements of the pyloric mass in IHPS by direct viewing during ultrasonic examinations. Strauss et al. (l98l) examined 20 infants aged from 14 to 49 days with IHPS, initially using a static gray-scale B-scan and later a real-time unit with a 5 MHz focused transducer. The pylorus was considered to be abnormally thickened if it measured 1.5 cm or more in its ventral-dorsal diameter. (In surgically controlled cases the pyloric mass of IHPS measured approximately 1.5 cm in diameter). In 16 of the cases the mass measured from 1.5 cm to 3.0 cm. It presented as a round anechoic mass with a central collection of echoes. In addition the pyloric "canal" was seen to be elongated to 20 mm. Real-time scanning showed an absence of movement of gastric contents across the pyloric canal.

Blumhagen and Coombs (l98l) examined 23 proven cases of IHPS between the ages of 2 and 10 weeks, using a B-scanner with a 6.0 mm focused 7.5 MHz transducer. In all cases the hypoechoic single muscle layer was 4.0 mm thick or thicker. The thick hypoechoic ring in the pyloric region was the sole criterion by which IHPS was diagnosed. The fundamental advantage of ultrasonography over other methods of diagnosis was that it visualized the hypertrophied muscle directly. Occasionally a hypoechoic ring might be formed by the muscle layers of the normal "distal antrum" as seen on parasagittal sections near the midline, but in those cases the layer was less than 4.0 mm in thickness. A false positive sonograph might be obtained in pylorospasm, in which there was persistent contraction of the circular musculature of the "distal antrum" and pylorus, creating a cylindrical muscle mass. In those cases the muscle was also less than 4.0 mm in thickness. The length of the hypertrophied muscle in IHPS was found to be variable, with some patients having only a short segment of hypertrophy and others a more elliptical mass. In a larger series of cases Blumhagen and Noble (l983) followed the normal hypoechoic muscle layer of the proximal stomach distally to the gastric outlet. Where the thickness of the muscle layer of the distal antrum and pylorus was 4.0 mm or more, a confident diagnosis of IHPS could be made. (The thickness varied from 3.0 mm to 6.0 mm in IHPS, being approximately 4.5 mm in the majority of cases). It was stated that at sonography the hypertrophied antral and pyloric circular musculature formed a thick, rounded cylinder having the appearance of a hypoechoic ring in cross section, and an ellipse with an echogenic core in sections parallel to the long axis. The best safeguard against making a false positive sonographic diagnosis is to identify the continuity of the thickened pyloric muscular layer with that of the remainder of the stomach, and to measure its thickness, rather than to measure the diameter of the mass, as advocated by previous authors.

Khamapirad and Athey (l983) obtained transverse and longitudinal sonographic images in l8 babies between the ages of one and 6 weeks with IHPS. A constant finding was a hypoechoic mass greater than 1.0 cm in diameter and containing a round or stellate central echogenic area. (The diameter of the mass ranged from 1.2 cm to 2.2 cm, with an average of l.7 cm). This was considered to be one of the main criteria for the diagnosis, the other being the ability to demonstrate a continuation of the hypoechoic mass with the gastric "antrum".

Graif et al. (l984) considered previous sonographic measurements in IHPS to have been inconclusive, especially in borderline cases. In order to increase the diagnostic accuracy of the modality other parameters and features of the hypertrophied muscle were evaluated, using a high resolution real-time unit with a 10 MHz transducer. In 22 infants with IHPS between the ages of 2 and 10 weeks the following measurements were obtained (mean and standard deviations were given respectively): the transverse diameter of the pylorus was 13.4 ± 1.6mm, the single wall thickness 4.5 ± 0.9 mm, and the mean pyloric length was 84 percent longer than that of normals. It was noted that high resolution, high frequency real-time scanning also showed the pressure effects of the hypertrophied muscle on the adjacent "antrum" by direct vision, confirming the fact that the concave indentations were caused by the muscle mass. (Comment: In radiology hypertrophy of the muscular wall is inferred from the configuration of intraluminal barium).

Wilson and Vanhoutte (l984) held that the true pyloric muscle length was the most important criterion for the diagnosis of IHPS. This was obtained by rotating the transducer from a short axis image of the pylorus until a maximum long axis was produced. In 16 proven cases of IHPS the true pyloric muscle length ranged from 2.0 to 2.6 cm. In 17 normal controls the range varied from 12.0 mm to 15.0 mm. It was felt that measurements of the true pyloric muscle length approached more closely the established radiological criterion of an elongated pyloric muscle and that it defined the anatomic abnormality seen at surgery more clearly. It was concluded that a true pyloric muscle length of 2.0 cm or more was a reliable sonographic sign of IHPS.

Stunden et al. (l986) achieved 100 percent accuracy in the ultrasound diagnosis of IHPS in 112 cases. Criteria used included measurements of the pyloric diameter, muscle thickness, canal length, real-time observation of the function of the pylorus and gastric peristalsis. Statistics showed that canal length was the only factor which could discriminate precisely between a normal and an hypertrophied pylorus. The overall diameter of the ring in IHPS was usually more than 11.0 mm (normal 11.0 mm or less) and the thickness of the muscle layer in the wall more than 2.5 mm (normal less than 2.5 mm). The canal length in IHPS was more than 16mm (normal less than 15 mm). When viewing the hypertrophied pylorus in real-time, relaxation of the canal did not occur, little fluid passed through it and gastric peristalsis was increased.

Carver et al. (l988) pointed out that in most of the previous publications where normal and abnormal ranges for length, breadth and muscle thickness were determined, there was often an overlap between the normal and abnormal ranges for all three measurements. By using a 7.5 MHz real-time sector scanner they estimated pyloric muscle volume and correlated this with body weight. In 21 babies with surgically confirmed IHPS, the pyloric muscle index was obtained by dividing the pyloric muscle volume in cubic centimeters by the body weight in kilograms. If this index was less than 0.4 the pylorus was normal, and if more than 0.4 the diagnosis of IHPS could be made with confidence.

In many instances Bowen (l988) was unable to identify the normal pyloric muscles with 5 MHz mechanical sector transducers; the normal pyloric muscle was much easier to demonstrate with computed sonography using a 5 MHz linear transducer. Normally pyloric dimensions might vary during real-time ultrasonic scanning, probably related to peristaltic contractions involving the pyloric muscle itself; the contracted gastric antrum might simulate an elongated pyloric channel of IHPS.

Pathogenesis and Etiology #

Meuwissen and Sloof (l932, l934) were of the opinion that the condition was entirely due to spasm of the pyloric muscle, causing a permanent contraction. This might or might not be associated with muscular hypertrophy.

Torgersen (l942) thought the simplest explanation would be that the circular musculature of the canalis egestorius had developed disproportionately strongly in comparison with the longitudinal musculature. During foetal life the circular musculature was laid down earlier and reached considerable thickness before the longitudinal layer was differentiated (Chap. 3). It seemed possible that regressive changes in the powerful circular musculature, which normally occurred at or near birth, had not taken place. Torgersen (l949) later also pointed out that the pyloric sulcus had an asymmetrical position in relation to the axis of the transverse part of the stomach, being closer to the angulus on the lesser curvature side. In IHPS genetic causes might lead to excessive asymmetry with consequent hypertrophy of the musculature of the canalis (i.e. the sphincteric cylinder).

Meeker and De Nicola (l948) described IHPS in a newborn infant; it had caused gastric outlet obstruction on the 2nd day of life and required operation on the 4th day. The etiology was unclear, and the question was whether muscular hypertrophy had preceded or followed pylorospasm. As the condition appeared to be congenital in their case, it was thought that it had occurred too early in life for spasm to have caused hypertrophy. By means of light microscopy Belding and Kernohan (l953) studied the myenteric plexuses and thickness of the muscle layers in normal controls, in 9 cases of IHPS and in 5 cases of adult hypertrophic pyloric stenosis (AHPS). In both IHPS and AHPS the number of myenteric ganglion cells and myenteric nerve fibre tracts per unit area of muscle tissue showed a real decrease in the pyloric region, while it remained quantitatively normal in the remainder of the stomach and in the duodenum. A constant finding was that the majority of myenteric ganglion cells in the pyloric region also showed degenerative changes, consisting of indistinct nuclear membranes, fragmentation or disintegration of the nucleolus, and disintegration of the cytoplasm with loss of cell membranes. Such changes were not present in the myenteric ganglion cells in the remainder of the stomach and in the duodenum, nor were they evident in normal controls. These pathological changes could be due to exhaustion caused by excessive vagal stimulation. According to these authors thickening of the muscularis externa in the normal stomach commences at a point just below the gastric incisura, extends to the pyloro-duodenal junction, and consists mainly of an increase in thickness of the circular musculature. In IHPS and AHPS the circular muscle of the pylorus was 2 to 4 times as thick as in normal controls, while it remained normal, or showed only a slight increase in thickness, in the remainder of the stomach and the duodenum. Microscopically the hypertrophied circular muscle of IHPS and AHPS had an irregular pattern with muscle fibres running in all directions, resembling a leiomyoma. The disorganization of muscle fibres was not evident in the stomach above the stenosed area and in the duodenum, neither was it seen in the normal stomach. It was unlikely that the ganglionic changes were secondary to the muscle hypertrophy and there appeared to be primary changes in both the myenteric ganglia and the musculature.

Carter and Powell (l954) recorded 12 examples of pyloric stenosis in parent and child, and drew attention to the increased risk of the disease in offspring of parents who were themselves affected. It was thought that genetic predisposition was a strong probability in the pathogenesis. However, environmental factors also had to be considered.

McKeown and MacMahon (l955) traced 112 adults who had been operated upon for IHPS in infancy. They had 29 children, none of whom exhibited pyloric stenosis. This and several other series examined by these authors, led them to conclude that a simple genetic hypothesis was unlikely. The condition could more plausibly be attributed to early postnatal environmental factors.

Friesen et al (l956) also using light microscopy, studied the myenteric nerve plexuses in normal controls and in l9 infants with IHPS. In the normal foetus at 12 weeks' gestation, the myenteric nerve layer of the pylorus appeared as an almost continuous layer of immature, completely undifferentiated nerve cells with little, if any segmentation into nests or plexuses. At 14 to 16 weeks there was a tendency towards elongated plexuses of cells which were still undifferentiated. At 26 weeks the myenteric layer showed organization into definite plexuses which contained, in addition to the undifferentiated cells, some cells with vesicular nuclei. Shortly after birth more mature cells appeared in the plexuses. Mature ganglion cells with abundant cytoplasm, prominent cell and nuclear membranes with nucleoli first appeared between the second and the fourth week after full-term gestation. The shift was toward differentiation so that recognizable mature ganglion cells were present in the normal pylorus from one to 5 months, with only a few undifferentiated cells being visible. In IHPS, at 4 to 8 weeks after birth, the plexuses contained no mature ganglion cells, having a cellular development similar to that of a normal pylorus several weeks earlier in age. It was concluded that failure of development or maturation of the ganglion cells was present, rather than degeneration of the cells as had been postulated by previous authors. The "degenerated" or "disintegrated" appearances previously described were probably cells which had never developed completely.

Roberts (l959) studied normal controls and biopsy specimens obtained at pyloromyotomy in 25 cases of IHPS. True hypertrophy of both longitudinal and circular muscle layers was evident, which he ascribed to overwork. The myenteric plexuses were examined for the quality and quantity of neural elements, i.e. nerve cells, supporting cells of Schwann and nerve fibrils. In IHPS the constituent cells had less cytoplasm and were more tightly packed than in normal controls, with fewer well-differentiated nerve cells in evidence. The size of ganglia tended to be smaller and the intervals between them greater than in normal specimens. The large continuous sheets of ganglia seen in the normal pylorus were absent, and it was concluded that there were quantitative as well as qualitative changes in the myenteric ganglia in IHPS.

Rintoul and Kirkman (l961) studied the morphological appearance of the myenteric ganglion cells and the structure of the nerve fibre tracts in biopsy specimens in 38 infants with IHPS. With silver staining two distinct ganglion cell types were recognized: (1) Type I Dogiel cells, showing a marked affinity for silver. While they were present in the control specimens, they were absent or virtually absent from the pyloric ganglia in cases of IHPS; this suggested that these cells were either congenitally absent, or that they had degenerated. (2) Type II Dogiel cells, which were less argentophylic. These were present and uniformly distributed throughout the myenteric ganglia in both the control and biopsy material. No clear evidence of degeneration of ganglion cells, such as had been described earlier, was found. However, it was admitted that early degenerative changes might not have been revealed by the silver staining process.

Friesen and Pearse (l963) studied the histological and histochemical features of the pyloric ganglion cells in biopsy material in 15 cases of IHPS; post-mortem studies were done in 2 additional cases. In IHPS the ganglion cells in the pylorus were not arranged in an evenly dispersed layer between the longitudinal and circular musculature. Cells were present in clumps within the thin longitudinal musculature, with infrequent extensions into the underlying circular layer. While numerous cells were present, few were large, mature cells, the majority being small and immature; these cells were enzymatically active and the histological appearances were not those of degenerated or dead cells. However, there was lack of mitochondrial and other oxidative enzymes characteristic of the mature cell. The features suggested arrest of the normal development of ganglion cells in the pyloric area. Mature ganglion cells containing numerous mitochondria were present in large numbers in the gastric wall above the pylorus in cases of IHPS, as well as in the pylorus in normal stomachs. The results supported the theory that motor acitivity such as pylorospasm preceded the development of hypertrophy of the pyloric circular musculature. According to Heinisch (l967) the etiology and pathogenesis of IHPS and AHPS remained obscure. Macroscopically and microscopically these conditions could not be differentiated from each other. As the pathological process was not limited to the pyloric ring, but also encompassed the immediate prepyloric area, Heinisch suggested that it should be termed "antrumhypertrophy" instead of pyloric hypertrophy. In his experimental work on rabbits, Heinisch attached glass spheres to the interior of the gastric fundus through a gastrostomy. This caused an "impairment of the functional unity" of the stomach; after 4 weeks a definite pyloric muscular thickening, which could not be distinguished from pyloric hypertrophy, occurred. Heinisch (l967) thought that the muscular hypertrophy was a compensatory mechanism due to the functional impairment of the proximal part of the stomach.

Smith (1970) noted that hypertrophic pyloric stenosis could occur in Chagas disease, in which myenteric plexus damage occurs. The general effect of this is loss of co-ordinated muscle contractions which propel the bolus analwards, leading to local hypertrophy and hyperplasia of smooth muscle.

Dodge (l970) found that pentagastrin injections of 3 pregnant bitches produced pyloric muscle hypertrophy and duodenal ulceration in some of the offspring.

Keet and Heydenrych (l97l) showed that electrical and mechanical stimulation of the vagal nerve trunks in the oesophageal hiatus of the diaphragm in canines, produced a temporary, tubular contraction of the pyloric sphincteric cylinder, approximately 3.0cm in length and exactly resembling hypertrophic pyloric stenosis. Increasing the stimulus caused the contraction to become firmer, until it became a rubbery hard cylinder simulating the "olive" of IHPS. It lasted as long as the stimulus was applied, while the remainder of the stomach remained flaccid. A similar result was obtained with mechanical stimulation (Chap. 32).

Dodge (l973), in a wide ranging review of the genetics of the condition, concluded that IHPS had a familial distribution but that this did not obey simple Mendelian laws. A single X-linked gene whose effects were greatly modified by other genetic and/or environmental factors would explain the increased risk to male relatives of female probands, but the excess of males with IHPS could not be accounted for by X-linkage, as male to male transmission occurred with greater frequency than expected. The most likely explanation for the distribution pattern was that multiple genetic and environmental factors, including a modifying effect of sex, operated together to produce IHPS. Female patients carried a heavier genetic load and were more likely to have affected male relatives. Suggested environmental factors were the maternal blood group, primogeniture, and the occurrence of stress shortly before birth.

Karim, Morrison and Parks (l974) administered daily pentagastrin injections to 12 bitches during the second half of pregnancy. Among 59 offspring 14 developed pyloric muscle hypertrophy, and 8 others pyloroduodenal ulcers. No muscle hypertrophy was seen in the controls.

Rogers et al. (l975) found no difference in circulating plasma gastrin levels in babies with and without IHPS, and concluded that gastrin stimulation was an unlikely cause of the muscle hypertrophy. An alternative hypothesis could be an abnormal response to intermittent milk feeding. This would release cholecystokinin and secretin from the duodenal mucosa, causing contraction, and ultimately hypertrophy, of the pylorus.

Dodge and Karim (l976) again found that pentagastrin administered to pregnant bitches produced typical pyloric muscular hypertrophy in some of their offspring. This occurred in 16 out of 56 puppies; some had duodenal ulceration. The findings indicated a variation in the response, with some pups showing no pathological changes while others were markedly affected. It suggested that individual inherent susceptibilities, such as genetic and environmental factors, were important determinants of the response.

In electron microscopic studies of the pyloric parasympathetic ganglia in IHPS, Jona (l978) found no abnormalities in the neurons and interstitial cells of the nerve plexuses; the maturation process of the ganglia proceeded normally. A small number of large axons, the significance of which was unclear, was present. While there was a marked increase in the overall thickness of the circular musculature, the individual muscle cells appeared normal. In view of the essentially normal morphology, Jona suggested that a "functional" etiology should be considered.

According to Swischuk (l980) evidence was accumulating to suggest that prolonged spasm or overactivity of the "antropyloric muscle" was the primary problem in infants with IHPS. It was probable that multiple causes of the muscular spasm could be operating.

While numerous factors had been proposed as the cause of IHPS, Haller and Cohen (l986) reiterated that the precise etiology remained uncertain.

Discussion #

In the radiological examination, here as elsewhere, only the barium suspension in the lumen is visible, and from the luminal appearances the alterations in the walls are inferred (Chap. 13). With ultrasonography the actual muscle mass causing narrowing of the lumen can usually be demonstrated. Consequently ultrasound has become the investigation of choice for suspected IHPS in many centers. Pilling (l983) discussed the relative sensitivity of radiology and ultrasound in the diagnosis. Of 26 cases with palpable pyloric tumors the mass was not detected by ultrasound in 2; in these cases, as well as in cases without palpable masses, an upper gastrointestinal radiological series was deemed necessary.

Pathogenesis #

In considering the pathogenesis, it should be noted that many authors held the view that the pyloric canal was elongated in IHPS (Shopfner l964; Shuman et al. l967; Teele and Smith l977; Strauss et al. l98l; Graif et al. l984; Stunden et al. l986; Bowen l988). The same was implied by Meuwissen and Sloof (l932, l934) and by Jenkinson (l955). While terminological uncertainties have to be taken into account, it is clear that in all these instances the "pyloric canal" was equated with the pyloric ring, which was considered to be the sphincter. Meuwissen and Sloof, for instance, stated that the average length of the pyloric canal was 1.0 to 2.0 mm in normal infants, which tallies with the width of the ring. According to these authors the essential factor in the pathogenesis was hypertrophy and elongation of the pyloric ring or "sphincter".

However, in dissections of morbid anatomical specimens of IHPS, Cunningham (l906) had shown previously that muscular hypertrophy involved the entire length of the sphincteric cylinder; it included, but was not limited to, the ring. Forssell (1913) and Torgersen (l942) showed convincingly that the musculature of the entire canalis egestorius (the sphincteric cylinder) was involved in the hypertrophy; the findings were subsequently confirmed by Frimann-Dahl (l935), Runstr"m (l939) and Astley (l952). Although he did not refer to the anatomical findings of Cunningham (l906), Forssell (l913) and Torgersen (l942), Heinisch (l967) noted that muscular hypertrophy was not confined to the pyloric ring but also involved the prepyloric region, which led him to suggest the term "antrumhypertrophy" for the condition. Analysis of our own cases also shows that the pyloric sphincteric cylinder in its entirety, is involved.

The premise that the pyloric canal is hypertrophied and elongated in IHPS (where "canal" is equated with the pyloric ring or sphincter), is difficult to accept. In view of the evidence quoted it appears much more likely that the entire pyloric sphincteric cylinder is involved in the hypertrophy, causing a permanently formed pyloric canal with concomitant motility disturbances. Normally the canal is a fleeting, physiological structure, being fully formed at the end of a maximal, cyclical contraction of the sphincteric cylinder (Chap. 13); in IHPS it is permanent, due to muscular hypertrophy of the entire cylinder.

In their investigations of IHPS many authors (Teele and Smith l977; Strauss et al. l98l; Blumhagen and Coombs l98l; Blumhagen and Noble l983; Khamapirad and Athey l983; Graif et al. l984) failed to consider the fundamental anatomical findings of Cunningham (l906), Forssell (l913) and Torgersen (l942); this may account for much of the uncertainty surrounding the pathogenesis.

Etiology #

In considering the etiology, it has to be pointed out that numerous theories have been formulated (some of which will be mentioned or recapitulated briefly). Most authors agree that the cause remains obscure. Freeman (l929) pointed out that the gizzard in graminivorous birds was situated in exactly the same location as the pyloric mass in IHPS. Normally in birds, food is mixed with gastric juice in the proventriculus or glandular stomach, and ground in the gizzard or muscular stomach. Similarly, in some higher mammals such as the coloured anteater, the gastric outlet is occupied by a heavy muscular mass in the same situation as the "tumor" in IHPS. It was thought that the condition could be of an atavistic nature, a reversion to a more primitive form.

According to Torgersen (l942, 1949) the most likely explanation was a genetic disturbance associated with excessive asymmetry; this could delay or impede regressive changes in the circular musculature of the sphincteric cylinder, normally occurring at or near birth.

Prolonged pylorospasm was suggested as a possible cause by Meeker and De Nicola (l948). A genetic defect was also postulated by Carter and Powell (l954) and by Rintoul and Kirkman (l96l). McKeown and MacMahon (l955) mentioned the possibility of environmental factors. Belding and Kernohan (l953) demonstrated degeneration of neurons in the myenteric ganglia of the affected region; Rintoul and Kirkman (l96l) were unable to substantiate these findings, but postulated an absence of argyrophilic Type I Dogiel cells from pyloric myenteric ganglia in IHPS.

Friesen et al. (l956) suggested delay in maturation of myenteric ganglion cells; this statement was questioned by Roberts (l959), as premature infants did not have an increased incidence of IHPS. Skoryna et al (l959) thought a congenital neuro-muscular dysfunction of the pyloric sphincteric cylinder could be responsible for both the infantile and adult forms. Friesen and Pearse (l963) found the ganglion cells in the affected region to be present in clumps and not arranged in evenly dispersed layers; many cells were small and immature, suggesting failure or arrest of normal development.

Heinisch (l967) produced hypertrophic pyloric stenosis in rabbits by suturing glass spheres to the interior of the fornix. Keet and Heydenrych (l97l) found that electrical and mechanical stimulation of the vagal trunks in the oesophageal hiatus of the diaphragm (in canines), produced temporary muscular contraction of the pyloric sphincteric cylinder, indistinguishable from IHPS.

Dodge (l970, l973, l976) as well as Karim et al. (l974) produced IHPS in some newborn pups by administration of pentagastrin to the mothers (other probands developed pyloroduodenal ulcers).

Rogers et al. (l975) and Moazam et al (l978) found no difference in plasma gastrin levels in infants with and without IHPS, concluding that gastrin stimulation was an unlikely cause of the muscular hypertrophy.

In view of the fact that the pyloric parasympathetic ganglia and individual muscle cells appeared normal at electron microscopy, Jona (l978) suggested a "functional" etiology. Swischuk (l980) thought that prolonged spasm of the "antropyloric muscle" (which could be due to a variety of causes) was the primary event.

Conclusion #

It has been shown that the pyloric sphincteric cylinder is a specialized muscular region of the stomach (Chap. 3), normally lined by pyloric mucosa (Chap. 5). In the vast majority of subjects its vagal supply occurs exclusively via the hepatic branch or branches (Chap. 8). Its motility is unique (as far as the stomach is concerned) in that it contracts cyclically in a "segmental" or "systolic", rather than a peristaltic way (Chap. 13). The contractions depend on and are triggered by underlying myoelectric activity (Chap. 16). In our view any one, or a combination of these factors, may have a bearing on the pathogenesis.

The contraction of the hypertrophied musculature in IHPS closely resembles a normal maximal or near-maximal contraction of the pyloric sphincteric cylinder (Chap. 13). In the former the contraction is permanent, in the latter of a fleeting nature, occurring in cycles with a frequency of approximately 3 per minute during active gastric emptying of solids. Normally when the cylinder is fully contracted, its lumen is obliterated by closely packed longitudinal mucosal folds; barium-filling of furrows between the folds may resemble lines or strings (Chap.13). A similar appearance of the mucosa is seen in IHPS, where barium-filling of longitudinal mucosal furrows in the hypertrophied and contracted cylinder gives rise to the "string sign" (Fig. 23.0). In a sense IHPS can be looked upon as the pathological counterpart of a maximal normal, physiological contraction of the sphincteric cylinder.

Radiologically and ultrasonically the narrowing of pylorospasm resembles that of IHPS in many respects (Meuwissen and Sloof l932; Torgersen l942; Astley l952; Shopfner l964; Haran et al. l966; Swischuk l980; Blumhagen and Coombs l98l; Bowen l988), showing that pylorospasm is not limited to the pyloric ring, but involves the entire pyloric sphincteric cylinder.

References #

Astley R. The radiology of infantile pyloric stenosis. Brit J Rad l952, 25, 342-350.
Belding HH, Kernohan JW. A morphologic study of the myenteric plexus and musculature of the pylorus with special reference to the changes in hypertrophic pyloric stenosis. Surg Gynaec Obstet l953, 97, 322-334.
Blumhagen JD, Coombs JB. Ultrasound in the diagnosis of hypertrophic pyloric stenosis. J Clin Ultrasound l98l, 9, 289-292.
Blumhagen JD, Noble HGS. Muscle thickness in hypertrophic pyloric stenosis: sonographic determination. Amer J Roentg l983, 140, 221-223.
Bowen A. The vomiting infant: recent advances and unsettled issues in imaging. Radiol Clin North Amer l988, 26, 377-392.
Carter CO, Powell BW. Two-generation pyloric stenosis. Lancet l954, 1, 746-748.
Carver RA, Okorie M, Steiner GM, et al. Infantile hypertrophic pyloric stenosis: diagnosis from the pyloric muscle index. Clin Rad l988, 38, 625- 627.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
Dodge JA. Production of duodenal ulcers and hypertrophic pyloric stenosis by administration of pentagastrin to pregnant and newborn dogs. Nature l970, 225, 284-285.
Dodge JA. Genetics of hypertrophic pyloric stenosis. Clin Gastroent l973, 2, 523-538.
Dodge JA, Karim AA. Induction of pyloric hypertrophy by pentagastrin. An animal model for infantile hypertrophic pyloric stenosis. Gut l976, 17, 280-284.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr. 1913, Suppl 30, 1-265.
Freeman L. Discussion: The management of recurrent ulcer following partial gastrectomy, by Balfour DC. Ann Surg l929, 90, 535-545.
Friesen SR, Boley JO, Miller DR. The myenteric plexus of the pylorus: its early normal development and its changes in hypertrophic pyloric stenosis. Surgery l956, 39, 21-29.
Friesen SR, Pearse AGE. Pathogenesis of congenital pyloric stenosis: histochemical analysis of pyloric ganglion cells. Surgery l963, 53, 604-608.
Frimann-Dahl J. Über den Nachweis der sogenannten kongenitalen Pylorus-hypertrophie durch Röntgenuntersuchung. Acta Rad l935, 16, 331-334.
Graif M. Itzchak Y, Avigad I, et al. The pylorus in infancy: overall sonographic assessment. Pediatr Radiol l984, 14, 14-17.
Haller JO, Cohen HL. Hypertrophic pyloric stenosis: diagnosis using ultrasound. Radiology l986, 161, 335-339.
Haran PJ, Darling DB, Sciammas F. The value of the double-track sign as a differentiating factor between pylorospasm and hypertrophic pyloric stenosis in infants. Radiology l966, 86, 723-725.
Heinisch HM. Die sogenannte Pylorushypertrophie im Tierversuch. Klin Wochenschr l967, 45, 1251-1252.
Hirschsprung H. F"lle von angeborener Pylorusstenose, beobachtet bei Säuglingen. Jahrb Kinderheil, l888, 28, 61-68.
Jenkinson EL. The pyloric antrum of the stomach. Amer J Roentg Rad Ther Nucl Med l955, 73, 905-937.
Jona JZ. Electron microscopic observations in infantile hypertrophic pyloric stenosis. J Pediatr Surg l978, 13, 17-20.
Karim AA, Morrison JE, Parks TG. The role of pentagastrin in the production of canine hypertrophic pyloric stenosis and pyloroduodenal ulceration. Brit Journ Surg l974, 61, 327.
Keet AD, Heydenrych JJ. Hiatus hernia, pyloric muscle hypertrophy and contracted pyloric segment in adults. Amer J Roentg Rad Ther Nucl Med l97l, 113, 217-228.
Khamapirad T, Athey PA. Ultrasound diagnosis of hypertrophic pyloric stenosis. J Pediatr l983, 102, 23-26.
McKeown T, MacMahon B. Infantile hypertrophic pyloric stenosis in parent and child. Arch Dis Child l955, 30, 497-500.
Meeker CS, De Nicola RR. Hypertrophic pyloric stenosis in a newborn infant. J Pediatr l948, 33, 94-97.
Meuwissen T, Sloof JP. Die roentgenologische Diagnose der kongenitalen, hypertrophischen Pylorusstenose. Acta Paediatr Scand l932, 14, l9- 48.
Meuwissen T, Slooff J. Roentgen examination of pyloric canal of infants with congenital hypertrophic pyloric stenosis. Amer J Dis Child l934, 48, 1304-1315.
Moazam F, Rodgers BM, Talbert JL, et al. Fasting and postprandial serum gastrin levels in infants with congenital hypertrophic pyloric stenosis. Ann Surg l978, 188, 623-625.
Pilling DW. Infantile hypertrophic pyloric stenosis: a fresh approach to the diagnosis. Clin Rad l983, 34, 51-53.
Rintoul JR, Kirkman NF. The myenteric plexus in infantile hypertrophic pyloric stenosis. Arch Dis Child l96l, 36, 474-480.
Roberts PAL. Pathology of infantile hypertrophic pyloric stenosis. Proc Roy Soc Med l959, 52, 1022-1023.
Rogers IM, Drainer IK, Moore MR, et al. Plasma gastrin in hypertrophic pyloric stenosis: a hypothesis disproved? Arch Dis Childh l975, 50, 467- 471.
Runström G. On the roentgen-anatomical appearance of congenital pyloric stenosis during and after the manifest stage of the disease. Acta Paediatr Scand l939, 26, 383-433.
Shopfner CE. The "pyloric tit" in hypertrophic pyloric stenosis. Amer J Roentg Rad Ther Nucl Med l964, 91, 674-679.
Shuman FI, Darling DB, Fisher JH. The radiographic diagnosis of congenital hypertrophic pyloric stenosis. J Pediatr l967, 71, 70-74.
Skoryna SC, Dolan HS, Gley A. Development of primary pyloric hypertrophy in adults in relation to the structure and function of the pyloric canal. Surg Gynec Obstet l959, 108, 83-92.
Smith B. Disorders of the myenteric plexus (progress report). Gut 1970, 11, 271-274.
Strauss S, Itzchak Y, Manor A, et al. Sonography of hypertrophic pyloric stenosis. Amer J Roentg l98l, 136, 1057-1058.
Stunden RJ, Le Quesne GW, Little KET. The improved ultrasound diagnosis of hypertrophic pyloric stenosis. Pediatr Radiol l986, 16, 200-205.
Swischuk LE, Heyden CK, Tyson KR. Atypical muscle hypertrophy in pyloric stenosis. Amer J Roentg l980, 134, 481-484.
Swischuk LE. Radiology of the Newborn and Young Infant. Williams and Wilkins, Baltimore, 2nd ed l980, pp 364-381.
Swischuk LE. . Williams and Wilkins, Baltimore, 3rd ed l989, pp 394-413.
Teele RL, Smith EH. Ultrasound in the diagnosis of idiopathic hypertrophic pyloric stenosis. New Eng J Med l977, 296, 1149-1150.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.
Torgersen J. The developmental anatomy of the pyloric canal and the etiology of infantile pyloric stenosis. Acta Rad l949, 32, 435-438.
Wilson DA, Vanhoutte JJ. The reliable sonographic diagnosis of hypertrophic pyloric stenosis. J Clin Ultrasound l984, 12, 201-204.

24 - Adult Hypertrophic Pyloric Stenosis

Mon, 01 Jan 0001 00:00:00 +0000

Adult Hypertrophic Pyloric Stenosis #

Although cases of hypertrophy of the pyloric musculature in adults (AHPS) had been reported previously, Morton (l930) first concluded that the condition seemed to constitute a definite clinical entity. He described 3 cases, aged 63, 42 and 39 years, in each of in each of whom radiographic examination had shown a constant, tubelike narrowing of the pyloric ring and immediate prepyloric area, 2.5 to 3.0 cm in length in one of the cases. (Measurements were not given in the other two). At operation the lesion was found to be due to hypertrophy of the pyloric muscularis externa in all instances; there were no associated lesions such as gastric or duodenal ulceration.

Kirklin and Harris (l933) described the radiographic signs of AHPS as elongation and narrowing of the pyloric canal together with evidence of gastric outlet obstruction. While these signs were not pathognomonic, a distinctive sign was a concave indentation of the base of the duodenal bulb, produced by partial invagination of the hypertrophied pyloric muscle into the duodenum. (Comment: It has subsequently been shown that various other conditions, ranging from normal contraction of the pyloric sphincteric cylinder to pyloric carcinoma, may produce similar duodenal indentation, as described in Chapters 13 and 33). In 50 cases of pyloric muscular hypertrophy in adults associated lesions of the upper gastrointestinal tract, such as gastric and duodenal ulceration, were present in 35.

North and Johnson (l950) stated that many cases of secondary pyloric hypertrophy, i.e. cases in whom the hypertrophy was associated with either benign or malignant gastric ulceration, had been reported prior to that time. The associated lesion was often situated away from the pyloric region in the more proximal part of the stomach. In primary AHPS, on the other hand, there were no associated gastric lesions. They were able to collect 59 case reports of verified primary AHPS, and described 5 cases of their own. It was stated that the lesion was not always easily recognizable at operation, a firm mass, or at least a thickening, being usually but not invariably palpable. When the condition was suspected, and when the exterior of the stomach appeared normal, a gastrostomy with examination of the lumen and palpation of the wall was necessary. Although the normal variations in the thickness of the pyloric musculature had not been clearly defined at that time, Truesdale (1915) had previously determined that the normal thickness of the "sphincter" (presumably referring to the pyloric ring) was 5.0 mm on an average, while Horwitz et al. (l929) found the range in thickness to vary from 3.8 to 8.5 mm with an average of 5.8 mm; both made their measurements upon fixed specimens in which the "sphincter" had been sectioned. North and Johnson (l950) found that in most of the recorded cases of primary AHPS in which data were available, the pyloric muscle measurements were considerably above this normal range and the same applied in their cases. The outstanding pathological feature of the lesion was hypertrophy and hyperplasia of the circular muscle layer, which was thickest at the pyloric ring, diminishing gradually over the "antrum" for a distance of 3.0 to 4.0 cm. The longitudinal muscle coat might also show a moderate grade of hypertrophy and the submucosa and mucosa might contain foci of cellular infiltration, consisting of plasma cells, lymphocytes and some neutrophils. Macroscopically the condition caused an unyielding tumor occupying the distal 3.0 to 4.0 cm of the stomach. The macroscopic appearances of infantile hypertrophic pyloric stenosis (IHPS) and primary adult hypertrophic pyloric stenosis (AHPS) were almost identical.

McNaught (l957) described 5 cases of AHPS, in 3 of whom there was no associated lesion, while in 2 an associated gastric ulcer was found at operation. It appears from the description that the ulcer was away from (i.e. proximal to) the area of muscular hypertrophy in both cases. This author found the lesion in AHPS to be comparable to simple hypertrophic pyloric stenosis in infants, and to him it was clear that the lesion was limited to the canalis egestorius or pyloric sphincteric cyclinder, as postulated by Torgersen (1942).

Craver (l957) reported 11 cases of AHPS encountered during a 24 year period. In 5 of these there was no concomitant upper gastrointestinal lesion, in 3 there was associated gastric ulceration, in 2 associated duodenal ulceration and in one associated haemorrhagic gastritis. (Comment: It is not stated clearly what the location of the gastric ulcers was, but it appears if they were proximal to the area of muscular hypertrophy). The gross appearance at operation resembled that found in IHPS, with a firm, unyielding, fusiform or circular tumor mass occupying the distal 3.0 to 4.0 cm of the stomach. The consistency varied from that of soft rubber to cartilage and it was thickest at the pyloro- duodenal junction, thinning out gradually over the "antrum"; distally it stopped abruptly at the pyloric ring. In 8 of the cases measurements showed that the muscular thickness ranged from 12 to 20 mm, with an average of 15.4 mm. This was 2 to 3 times the average thickness (7.1 mm) found in a series of normal controls. Microscopically there was both hypertrophy and hyperplasia of the circular layer, the muscular fibres being increased in size as well as in number. There were no inflammatory changes or oedema.

In a series of 25 cases coming to laparotomy, Desmond and Swynnerton (l957) found associated gastric ulceration in 12, duodenal ulceration in 6, pyloric ulceration in one and mucosal prolapse in 2, while 6 cases had no associated lesion (some cases had more than one associated condition). At operation the lesion presented as a white, regular, glistening muscular mass with a normal serosa and a loose, lax submucosa. (Comment: The finding is similar to the appearance seen during experimental truncal vagal stimulation in canines as described in Chap. 32). It could readily be differentiated from a grey, irregular, infiltrative type of carcinoma. Lumsden and Truelove (l958) described cases which showed that AHPS might be a sequel to IHPS, or it might arise de novo in adults. In the first category 5 patients who had received medical treatment for hypertrophic pyloric stenosis in infancy, showed radiological abnormalities campatible with AHPS in later life. Similar cases were described by other authors (Chap. 23); most of these adult cases were symptom-free.

Skoryna et al. (l959) described 6 cases with the morphology based on Torgersen's anatominal concepts. In 2 cases there was hypertrophy of the circular musculature of the pyloric canal (i.e. presumably the pyloric sphincteric cylinder) without other macroscopic lesions in the stomach and duodenum (one of the cases showed microscopic evidence of chronic gastritis); these were labelled cases of diffuse primary pyloric hypertrophy without associated proximal gastric lesions. In one case hypertrophy of the circular musculature of the "pyloric canal" was associated with a gastric ulcer on the lesser curvature 6.0 cm orally to the pylorus (i.e. approximately 3.0 cm orally to the commencement of the sphincteric cylinder) together with associated chronic gastritis; this was called a case of diffuse primary pyloric hypertrophy associated with a proximal gastric lesion. In another case there was moderate hypertrophy of the musculature of the entire pyloric canal, with a relatively greater degree of hypertrophy of the circular muscle on the lesser curvature at the muscle knot; there was no associated gastric or duodenal lesion, and Skoryna et al. (1959) considered it to be an example of primary pyloric hypertrophy of the focal type. (This case is also quoted in Chap. 25). One case exhibited benign ulceration within the confines of the "pyloric canal" (with muscular hypertrophy of its walls), and another had pyloric muscle hypertrophy with extensive surrounding adhesions and fibrosis, suggesting a previous inflammatory process (probably a duodenal ulcer). These 2 cases were considered to be pyloric muscular hypertrophy secondary to a distal obstructive lesion, e.g. obstructive complications of pyloric or duodenal ulceration.

Knight (l961) described 7 cases of AHPS; four of these were of a focal nature and are considered elsewhere (Chap. 25). Two of the remaining cases had diffuse enlargement of the pyloric musculature similar to IHPS, without evidence of gastric or duodenal ulceration. Gallstones were present in one of these, for which a cholecystectomy was performed. Both cases needed pyloroplasty. In the last case there was diffuse pyloric muscular hypertrophy involving a segment 2.5 cm in length, with a benign gastric ulcer 6.0 cm proximal to the pylorus. According to Knight (1961), hypertrophy in IHPS involves the entire circumference, while in the adult it may involve only a localized segment of the pyloric musculature. In IHPS hypertrophy always seems to occur as a primary condition, without associated upper gastro-intestinal pathology, while in the adult associated peptic ulceration or gastritis is common. This author found the thickness of the "pylorus" in 10 fresh post-mortem adult stomachs to range from 4.0 to 7.0 mm, with an average of 5.1 mm, while the thickness ranged from 10 to 15 mm in AHPS. The gross appearance of the pylorus in AHPS was similar to that of IHPS.

Edwards (1961) recognized two types of AHPS, viz. an idiopathic form, in which no other gastric lesion was present, and a secondary form in which there was some associated lesion such as gastric or duodenal ulceration or gastric carcinoma. It was stated that the etiology remained doubtful and among the possibilities to be considered were persistence of the infantile form, degeneration of the myenteric plexus and long continued pylorospasm. Pathologically the circular musculature was increased in thickness from the usual 3.0 to 8.0 mm to a maximum of 30 mm with an average of 15 mm. Radiologically elongation and narrowing of the pyloric canal was present.

Christiansen and Grantham (l962) collected 56 case reports published subsequent to the review by North and Johnson (l950), and added 2 of their own. In both their cases the gross and histological appearances were indistinguishable from those of IHPS. Of the 58 cases reviewed, 34 had no associated lesion in the upper gastrointestinal tract, but the remaining 24 had associated pathology, the most common lesions being gastritis (9), cholecysititis (7) and hiatus hernia (4).

Seaman (l963) reported 27 cases of AHPS, of which l8 had an associated gastric ulcer and 2 more had evidence of previous gastric ulceration. It is not clear from the description what the position of the gastric ulcer was in each case. Most of the other cases had microscopic evidence of gastritis, while 2 had duodenal ulceration (one of these also had a gastric ulcer.) There was no evidence of obstruction in the duodenal ulcer cases. While accepting the normal measurements of Horwitz (l929), Craver (l957) and Knight (l961), Seaman (l963) found that the thickness of the pyloric musculature in his cases varied from 9.0 to 15 mm, with an average of 11.2 mm. He found the gross appearance of AHPS to be similar to that of IHPS, the thickest portion of the musculature being at the pyloroduodenal junction, ending abruptly at the duodenum, but decreasing gradually as it faded into the "antrum" on the gastric side. Seaman based the morphology of the lesion in AHPS on the muscular anatomy as determined by Forssell (l913), Cole (l928) and Torgersen (l942).

Wieser et al. (l963) reviewed 44 operatively confirmed cases of AHPS. The condition was defined as any non-carcinomatous wall-thickening in the canalis egestorius, irrespective of its etiology. Two types were recognized, viz. a purely muscular form and a mixed form in which additional evidence of gastritis was present in the mucosa and submucosa. Twenty percent of the cases were associated with hiatus hernia, and gastric ulceration was present in 50 percent; this was probably not coincidental, the ulceration being deemed to be secondary to the pyloric stenosis. Radiologically there was elongation and narrowing of the pyloric canal with a prepyloric outpouching, altered peristalsis and a concave indentation of the base of the duodenal bulb. The condition had to be differentiated from early pyloric carcinoma. Keynes (l965) found that 132 cases of simple, primary or idiopathic hypertrophic pyloric stenosis in adults, i.e. muscular hypertrophy without associated lesions, had been described in the English literature up to that time. These included 64 case reports collected from, or added to the literature by North and Johnson (l950), as well as 56 cases reviewed by Christiansen and Grantham (l962) and 2 new cases added by them. Keynes (l965) described the clinical, radiological and pathological findings in 12 new cases of AHPS, 6 of whom had associated peptic ulceration (3 duodenal, 2 gastric and one pyloric), and were designated "complicated" AHPS. The remaining 6 had no associated upper gastro-intestinal lesion and were of the "simple" variety. The gross appearance of the pylorus in diffuse AHPS, both in the simple and the complicated types, was similar to that in IHPS: a smooth, firm or rubbery hard tumor occupied the region of the pylorus, ending abruptly at the duodenum, where it was at its thickest. From here the muscular thickening gradually decreased towards the proximal end of the pyloric canal. Histologically there was hypertrophy of the circular fibres with occasional moderate longitudinal muscular hypertrophy. Keynes (l965) noted no abnormality in the ganglion cells of the myenteric plexuses. The affected region was limited to the pyloric "canal" (pyloric sphincteric cylinder) as described by Cunningham (1906), Horton (1928) and Torgersen (l942). In infants the hypertrophy was always of the simple variety, since it occurred in the absence of other gastro-intestinal pathology, but in adults it could be complicated. Although simple AHPS was uncommon, Keynes (l965) did not believe it was as rare as the literature seemed to suggest.

Du Plessis (l966) described 6 cases of what he termed primary hypertrophic pyloric stenosis commencing in adult life without apparent cause. Gastric resection was performed in 2, both of which showed atrophic gastritis and gastric ulceration. These cases would have been classified secondary AHPS by North and Johnson (1950), and primary AHPS associated with a proximal gastric lesion by Skoryna (l959), Knight (l961) and Christiansen and Grantham (l962). Keynes (l965) would have designated them "complicated" AHPS. Du Plessis (l966) looked upon them as "primary" as he considered the gastric ulceration to be the effect of stasis secondary to the pyloric stenosis. In both resection specimens the circular muscle along the greater curvature showed a marked increase in thickness at the pylorus and for a distance of 2.5 cm proximally. Along the lesser curvature the circular muscle was increased in thickness at the pylorus and up to 1.5 cm proximally. In contrast the longitudinal musculature showed a decrease in thickness over the pylorus and for some distance proximally. The ganglion cells in the myenteric plexuses of the 2 cases appeared normal. In 4 cases there was no associated pathology in the stomach and duodenum. Biopsies taken at the time of operation in all 6 cases showed atrophic gastritis and confirmed the deficiency in the longitudinal musculature.

Interpreting his findings on the anatomical concepts of Torgersen (l942), Du Plessis (l966) suggested that the cause of AHPS was a deficiency of the longitudinal musculature of the pyloric canal (i.e. pyloric sphincteric cylinder), which would result in a failure of the canal to shorten during contraction. This would cause an imbalance of longitudinal and circular muscle contractions resulting in functional obstruction. The circular fibres of the fan-shaped muscle would gradually become hypertrophied as a result of repeated ineffective contractions, adding a mechanical element to the obstruction.

Larson et al. (l967) enumerated the generally accepted radiographic signs as lengthening and narrowing of the pyloric canal with an intact mucosal relief, a contrast filled cleft in the centre of the canal and a crescentic indentation of the duodenal bulb. In 10 cases in whom radiographs showed clear evidence of AHPS, surgical exploration revealed a normal stomach in 5, pyloric carcinoma in 2, AHPS in 1, AHPS and a gastric ulcer in 1, while one case showed evidence of prior surgical treatment for IHPS. It was concluded that there was little direct correlation between the radiographic appearance of pyloric elongation and narrowing on the one hand, and pyloric muscle thickness on the other.

Bodon and Haake (l968) called attention to the frequent association of AHPS with hiatus hernia and reported 11 cases of their own. In these cases the surgical solution was to correct the pyloric hypertrophy by means of pyloroplasty or antrectomy, necessitating an abdominal (as opposed to a transthoracic) approach. At operation the diagnosis of pyloric hypertrophy was not difficult, the hypertrophied muscle presenting as a mass 4.0 to 10 mm thick and 1.0 to 5.0 cm long.

At gastroscopy the hypertrophied muscle resembles the uterine cervix, according to Schuster and Smith (l969). The pyloric opening presents as a hole of fixed diameter in the centre of the mound, thus contrasting with the actively mobile pyloric region of normal subjects. The affected region, unlike the normal "antrum", does not respond to anticholinergics.

Bateson et al. (l969) described l7 cases of AHPS, in 4 of whom there was an associated lesser curvature gastric ulcer, and in one a prepyloric ulcer. None of these cases had associated duodenal ulceration. Macroscopically every case showed hypertrophy of the "pyloric and prepyloric muscle", stopping abruptly at the "pyloric canal" (i.e. pyloric aperture) and thinning out gradually over the adjacent part of the "antrum". Although the hypertrophy was most marked at the pyloroduodenal junction, it also involved the wall of the pyloric "antrum", and a more accurate title according to Bateson et al. (l969) would have been hypertrophic pyloric channel disease, the pyloric channel being defined as the area between the duodenum and a point 2.5 cm proximal to the duodenum. In 5 of the cases it was noted that on touching the pylorus with a gloved finger during operation, the pyloric and adjacent antral muscle contracted, becoming hard and pale. (Comment: a similar appearance was seen during experimental truncal vagal stimulation as described in Chapter 32). This spasm probably accounted as much for the radiological appearances as did the degree and extent of muscle hypertrophy and, in their opinion, made careful measurement of the muscle thickness an academic exercise of doubtful value. Microscopically hypertrophy and hyperplasia of the circular muscle fibres was seen with fibrous tissue between the hypertrophied bundles in every case.

In his review Levin (l97l) came to the conclusion that the radiographic diagnosis of AHPS could not be made with a high degree of confidence. While the signs of hypertrophic pyloric stenosis were diagnostic in infants, this was not always the case in adults. Nevertheless several reports had indicated that AHPS represented persistence of a mild form of IHPS. In his view the poor correlation between the radiographic and pathologic findings led to the conclusion that the elongated, narrowed pylorus was at times due to spasm. In those patients proved to have AHPS, gastric or duodenal ulceration or gastritis had been present in the majority. Indirect evidence suggested that these conditions were the sequelae and not the cause of pyloric muscle hypertrophy. It was important to exclude pyloric carcinoma as a cause of the narrowing in every case.

Discussion #

Most authors agree that adult hypertrophic pyloric stenosis (AHPS) is a rare condition. In approximately 17,000 upper gastrointestinal barium examinations over a 5 year period we diagnosed the condition not more than 3 or 4 times; these patients were lost to follow-up and the diagnosis could not be verified.

Types of AHPS #

Primary, Idiopathic or Simple #

AHPS may occur in the absence of other pathology in the upper gastrointestinal tract. An analysis of 129 verified cases encountered in the literature, showed that 51 had no associated lesions (Table 24.1). In addition to the above Morton (1930) described 3, North and Johnson (1950) 5, Lumsden and Truelove (1958) 5, Christiansen and Grantham (l962) 2, and Larsen et al. (l967) one case of verified AHPS without concomitant lesions. (These were individual cases, not forming part of larger groups). These cases have been termed primary (North and Johnson l950), idiopathic (Edwards l96l) or simple (Keynes l965) AHPS. In order to differentiate the condition from focal hypertrophic pyloric stenosis Skoryna et al. (l959) designated them cases of diffuse primary pyloric hypertrophy without associated proximal gastric lesions.

Table 24.1. Analysis of 129 verified cases of AHPS encountered in the literature


Authors	No. of verified AHPS cases	No. of AHPS cases without associated lesions

Kirklin & Harris (1933)	50	15
Desmond & Swynnerton (1957)	25	6
Craver (1957)	11	5
McNaught (1957)	5	3
Skoryna et al. (1959)	6	2
Knight (1961)	3	2
Keynes (1965)	12	6
Bateson et al. (1969)	17	12

TOTAL	129	51

AHPS: adult hypertrophic pyloric stenosis

25 - Focal Hypertrophy and Focal Spasm of the Pyloric Musculature in Adults

Mon, 01 Jan 0001 00:00:00 +0000

Focal Hypertrophy and Focal Spasm of the Pyloric Musculature in Adults #

In l952 Bachmann reported 12 cases with localized areas of hypertrophy of the pyloric musculature in adults. In each instance the hypertrophied area was situated on the lesser curvature; it was found as incidental pathology in a series of 600 autopsies and none of the cases had any other abnormalities of the stomach and duodenum. The cases were divided into three groups according to their relationship to the pyloric "sphincter". (Comment: the "sphincter" was equated with the pyloric ring). In the first group (5 cases) the thickening was situated directly in the "sphincter"; it resembled an enlarged version of the normal sphincter, consisting mainly of circular but also containing some irregular and longitudinal muscle fibres. In the second group (4 cases) the thickening was located a very short distance orally to the "sphincter", being separated from it by a narrow zone of normal tissues. In the third group (3 cases) it was situated in the "sphincter" as well as in the immediate prepyloric part. In the first two groups it appeared to be of a rounded or nodular character (while differing distinctly from a myoma), and in the third group it was rather longer than wide. In considering the pathogenesis, Bachmann asked himself whether these cases indicated that a certain part of the pyloric musculature was liable to undergo hypertrophy by virtue of its having a specialized function or structure.

Keet (l956) reported 2 adult operative cases in which the gastric resection specimens showed, as incidental pathology, a localized area of thickening of the pyloric musculature on the lesser curvature of the stomach. In the first case a true muscular hypertrophy was present; in the second the thickening appeared to be in the nature of a spasm, as it disappeared during the course of a few hours. We believe that the localized or focal pyloric muscular thickening in these two cases lends itself to a rational explanation on anatomical grounds, as indicated below.

Case Reports #

Case 25.1. G.V.L., 50 year old male, was admitted for partial gastrectomy because of a non-healing gastric ulcer, having had ulcer symptoms for the previous 12 years. Radiographic examination 6 years prior to admission had shown a tiny excrescence on the lesser curvature of the stomach 1.5 cm proximal to the pylorus, which was interpreted as a gastric ulcer. Three years prior to admission a second radiographic examination reported an ulcer niche on the lesser curvature, but failed to state its exact situation. Four months before admission a third radiographic examination showed a large gastric ulcer niche halfway up the lesser curvature in the region of the incisura angularis; there was no sign of the ulcer previously mentioned proximal to the pylorus. At operation the gall bladder was distended and contained calculi; there were no adhesions to the duodenum or pylorus. Palpation of the stomach in situ revealed a thickening of softish consistency in the pylorus on the lesser curvature side, diagnosed provisionally as a gastric polyp. A large gastric ulcer of the middle of the lesser curvature was seen and felt. Partial gastrectomy was done, the duodenum being divided 3.0 cm distal to the pyloric ring, well beyond the palpable thickening. A retrocolic gastrojejunal anastomosis was made and a cholecystectomy performed.

The macroscopic pathological examination of the resection specimen showed a large gastric ulcer on the lesser curvature 7.0 cm proximal to the pylorus. A mucosal fold, approximately l.0 cm high, separated the lumen of the stomach from that of the duodenum. In the pylorus, on the lesser curvature side and jutting into this mucosal fold, a rounded, pea-sized, rubbery hard mass was situated in the gastric wall. The mucosa, which was freely mobile on the underlying layers, was less mobile over the mass. There was no naked-eye evidence of ulceration locally. Microscopic examination showed the mass to consist of hyperplasia of the circular muscle (Fig. 25.1); it was not a myoma as it was not well defined and merged gradually into the surrounding circular muscle. The submucosa overlying the thickening was rather thin and contained numerous blood vessels. The pyloric mucosa and submucosa showed infiltration with inflammatory cells and changes of chronic gastritis. The ulcer on the middle of the lesser curvature proved to be a chronic, benign ulcer penetrating into the muscle layers.

Fig. 25.1. Case G.V.L. Microscopic section of pyloric nodule on lesser curvature side of pyloroduodenal junction, showing great hypertrophy of circular muscle fibres. Thin overlying submucosa

Case 25.2 M.B., 58 year old female, was admitted because of achylia gastrica. Radiographic examination showed an irregularity on the lesser curvature at the incusura angularis, which was regarded as a probable early gastric carcinoma. Partial gastrectomy was performed. The macroscopic examination of the fresh resection specimen showed a few hemorragic spots in its proximal part. At the pylorus, on the lesser curvature side, a hard pea-sized nodule was felt in the gastric wall. It was not particualrly well defined and was presumed to be a local thickening of the pyloric musculature. Microscopic examination showed well marked chronic gastritis with a few erosive defects in the mucosa and fibrotic tissue in the submucosa. When the specimen was handled again a few hours after it had been received, it was noted that the nodule previously felt at the pylorus on the lesser curvature side had disappeared. Except for the chronic gastritis no microscopical abnormalities were seen in the pylorus. Comments: Care should be taken with the interpretation of localized thickenings in gastric resection specimens, as these may be artifacts due to the application of clamps. This can be ruled out in the first case, since the thickening was felt with the stomach in situ and before clamps were applied. In the second case there was no obvious damage to the gastric wall at the site, such as one would expect after a clamp. The question may also arise whether the muscular thickening in the first case was not caused by healing of the old ulcer. Several points mitigate against this. The tiny excrescence originally interpreted as an ulcer niche was situated some distance orally to the pyloric aperture and not at the orifice, where the muscular thickening was subsequently felt. Second, the microscopic appearances were quite different from those of a healed gastric ulcer. Third, reference to the original radiographs raised serious doubt as to whether the excrescence was in fact an ulcer and not due to barium filling a furrow between mucosal folds.

The cases show, therefore, that there was focal thickening of the pyloric musculature, located in both cases on the lesser curvature at the pyloric aperture. In the first case the thickening was due to muscle hypertrophy, in the second to a temporary spasm. In both cases it was an incidental finding, and in both there was evidence of chronic gastritis, with an active gastric ulcer halfway up the lesser curvature in the first case.

From the above it will be clear that the focal muscular thickening in our 2 cases occurred in the exact situation of the pyloric muscle torus or muscle knot as described by Torgersen (l942). To the best of our knowledge these were the first cases to be reported in which it was shown that the anatomic basis for this entity derived from Torgersen's interpretation of the anatomy. Subsequently a number of authors based their findings in focal pyloric hypertrophy as well as in adult hypertrophic pyloric stenosis on the anatomy as determined by Cunningham (l906), Forssell (l913) and Torgersen (l942) (Chap. 3).

While Bachmann (1952) did not refer to Torgersen's findings, it is interesting to note that the hypertrophy in his first first group of cases occurred in exactly the same situation, and he in fact stated that the appearance resembled an enlarged version of a normal section of that region. Morphologically the cases described in Bachmann's second and third groups appear to be related to the first. Referring to the normal prepyloric contractions as described earlier (Chap. 13), it seems that the muscular hypertrophy in his second group occurred in the area where the peristaltic wave stops, i.e. a short distance orally to the pyloric aperture. The site and extent of muscular hypertrophy in his third group corresponds to the area of contraction on the lesser curvature normally occurring during a near maximal contraction of the pyloric sphincteric cylinder.

Skoryna et al. (l959), in their description of 6 cases of adult hypertrophic pyloric stenosis, included one case with moderate thickening of the entire pyloric "canal", with an additional small nodular mass on the lesser curvature side of the "canal" (i.e. at the muscle knot). Pathologically this proved to be a muscular nodule composed of circular fibres, diagnosed as focal hyperplasia of the muscle knot. There was no associated ulceration.

Mack (l959) described another case of focal hypertrophy of the muscle torus.

In 4 of the 7 cases of adult hypertrophic pyloric stenosis described by Knight (l96l), the hypertrophy was of a focal nature. In two of these it was localized to the muscle knot on the superior aspect (i.e. lesser curvature side) of the pyloric ring. In both the nodule was l.0 cm in diameter and consisted of circular muscle fibres. In the third case the hypertrophy was more extensive, involving the greater curvature and posterior wall, but not encircling the lumen, and extending proximally from the pyloric ring for a distance of 3.0 to 4.0 cm (i.e. the length of the sphincteric cylinder). In the fourth case a l.0 cm nodule of circular muscle fibres was found in the pylorus on the greater curvature side. None of these cases had associated gastric or duodenal ulceration, but chronic gastritis was present in two. Knight concluded that focal hypertrophy was not necessarily limited to the muscle knot, but that it could occur anywhere in the pyloric musculature. Whether it represented an early stage of diffuse hypertrophy was not known.

Heidenblut (l96l) described a case in whom a benign gastric ulcer was situated in the anterior gastric wall l.5 cm proximal to the pyloric ring. Directly opposite the ulcer in the posterior gastric wall a localized area of muscular thickening was found. It was thickest at the pylorus and extended for a short distance proximally into the "antrum", gradually thinning out. Microscopically it consisted of hypertrophied circular fibres. Changes of chronic gastritis were present in the mucosa and submucosa.

Wellman et al. (l964) described the autopsy findings in an elderly patient in whom an area of focal muscular hypertrophy occurred on the lesser curvature of the pyloric and immediate prepyloric region. The hypertrophy was confined to the circular musculature and was diagnosed as torus hyperplasia. A superficial erosion was seen in the overlying mucosa but no ulceration or ulcer scar was evident.

Seaman (l963, l966) described 4 adult cases of focal hypertrophy of the pyloric muscle in which the hypertrophy was limited to the muscle torus or knot. In all cases a firm, rounded, intramural mass was palpated at the lesser curvature aspect of the pyloric ring in the situation of the muscle knot. It varied in diameter in the different cases from 1.0 to 2.0 cm. In one case there was associated cholelithiasis and an hiatus hernia, in another a duodenal ulcer, and in a third associated atrophic gastritis; none was associated with a gastric ulcer. In all cases microscopic examination showed focal hypertrophy of the pyloric musculature. Of the 4 cases, one showed no definite radiographic abnormality. Two cases exhibited a widening of the space between the base of the duodenal bulb and the distal "antrum" on the lesser curvature side, i.e. a widening of the lesser curvature side of the pyloric ring. The fourth case showed a flattening of the distal lesser curvature of the "antrum" with a small protrusion which was not constant and not caused by an ulcer. Aron et al. (l973) described the case of an elderly female in whom radiographic examination showed an hiatus hernia and a large filling defect on the lesser curvature side of the "distal antrum" with narrowing of the antral outlet. Endoscopy revealed oesophagitis while an irregular submucosal lesion measuring 2.5 cm x 0.5 cm was seen approximately l.0 to 2.0 cm proximal to the pylorus on the lesser curvature side; biopsy showed a normal mucosa. At operation a localized, firm, nodular mass measuring 3.0 cm in length and extending from the pylorus to the "distal antrum" on the lesser curvature, was found. Histology revealed marked hypertrophy of the circular musculature, diagnosed as torus hyperplasia which had presented as a gastric pseudotumor.

Liebermann-Meffert and Allgöwer (l977) investigated the morphology of the pylorus and "antrum" in gastric ulcer disease. In a series of 77 cases the ulcer was adjacent to the pylorus in 10, and in other parts of the stomach in 67. Focal areas of muscle hypertrophy which distorted either the "antrum", the pyloric ring or both were commonly found. The hypertrophy was not uniform but irregular, involving different parts of the pylorus and "antrum" to a variable degree. The findings were not described in detail nor interpreted in the light of the anatomy as determined by Cunningham (1906), Forssell (1913) and Torgersen (1942).

Discussion #

At least 27 cases of focal hypertrophy (including one of focal spasm) of the pyloric musculature in adults have been described in detail in the literature. Seventeen were not associated with other lesions in the upper gastrointestinal tract and apparently occurred de novo. Four cases were associated with chronic or atrophic gastritis (one also had achylia gastrica), one with an acute erosion, 2 with hiatus hernia, 2 with gastric and one with duodenal ulceration.

In 17 cases the hypertrophy (or spasm in one case) was limited to the pyloric muscle torus or knot. (The l7 cases in this group do not tally with the l7 mentioned above). Normally contraction of the pyloric muscle knot is a fleeting occurrence, being part of cyclical contraction of the sphincteric cylinder; it causes an evanescent widening of the lesser curvature part of the pyloric ring (Chap. 13). In focal hypertrophy of the muscle knot the mass occurs in the same situation and is permanent. The condition may be considered to be the pathological counterpart of a physiological stage of contraction.

Radiographically Seaman (l966) noted a permanent widening of the lesser curvature side of the pyloric ring in 2 of his 4 cases of torus hyperplasia. In retrospect this was also present in our Case 25.1. A similar but very advanced case was described by Aron et al. (l973). Torus hyperplasia should be considered in the radiological differential diagnosis of permanent widening of the lesser curvature side of the pyloric ring.

In 7 of the remaining l0 cases (described by Bachmann) the focal hypertrophy, while not strictly limited to the muscle torus, occurred in the same region and can probably be explained on the same basis. In 3 the hypertrophy occurred elsewhere in the pyloric musculature; this also applied to the cases of Liebermann-Meffert and Allgöwer (l977), which were not described individually.

It is concluded that focal hypertrophy is limited to the pyloric muscle torus in many instances, but this is not invariably the case and it may also occur elsewhere in the pyloric musculature. It may occur de novo or be associated with gastric ulceration (located more proximally in the stomach), chronic or erosive gastritis, hiatus hernia and duodenal ulceration. Whether it represents an early stage of diffuse adult hypertrophic pyloric stenosis is not known.

References #

Aron JM, Newman A, Heaton JW. Torus hyperplasia of the pyloric antrum presenting as a gastric pseudotumor. Gastroenterology l973, 64, 634 - 636.
Bachmann KD. Über umschriebene, plattenförmige Muskelhyperplasien im Antrum und Pylorus ("Muskelplatten"), Beitr path Anat l952, 112, 97 - 103.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9 - 47.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr 1913, Suppl 30, 1 - 265.
Heidenblut A. Herdförmige gutartige Pylorushypertrophie des Erwachsenen. Fortschr Geb Röntgenstr Nuklearmed 1961, 94, l75 - 181.
Keet AD. Focal hypertrophy of the pyloric musculature in adults. Arch Path l956, 61, 20 - 23.
Knight CD. Hypertrophic pyloric stenosis in the adult. Ann Surg l96l, 153, 899 - 910.
Liebermann-Meffert D, Allgöwer M. The morphology of the antrum and pylorus in gastric ulcer disease. Prog Surg 1977, 15, 109 - 139.
Mack HC. Adult hypertrophic pyloric stenosis. Arch Int Med 1959, 104, 574 - 579.
Seaman WB. Hypertrophy of the pyloric muscle in adults. Radiology l963, 80, 753 - 764.
Seaman WB. Focal hypertrophy of the pyloric muscle: torus hyperplasia. Amer J Roentg Rad Ther Nucl Med l966, 96, 388 - 392.
Skoryna SC, Dolan HS, Gley A. Development of primary pyloric hypertrophy in adults in relation to the structure and function of the pyloric canal. Surg Gynaec Obstet l959, 108, 83 - 92.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1 - 191.
Wellman KF, Kagan A, Fang H. Hypertrophic pyloric stenosis in adults: survey of the literature and report of a case of the localized form (torus hyperplasia). Gastroenterology l964, 46, 601 - 608.

26 - Nausea, Retching and Vomiting

Mon, 01 Jan 0001 00:00:00 +0000

Nausea, Retching and Vomiting #

The mechanism of vomiting in mammals is complex and in spite of experimental studies some aspects are still not fully understood. It is usually accepted that the vomiting sequence consists of 3 successive phases: nausea initially, followed by retching, often leading to forcible expulsion of gastric contents through the mouth, i.e. ejection or vomiting. During these stages a co-ordinated sequence of movements occurs, involving, amongst others, the upper small bowel, stomach, oesophagus, diaphragm, voluntary abdominal muscles and glottis.

The complex movements of the ejection phase occur with extreme rapidity. Some features visible during radiographic investigation of this phase have been described by Lumsden and Holden (l969); as these involve the proximal stomach, the gastro- oesophageal junction, oesophagus and laryngo-pharynx, the details fall outside the scope of the present investigation.

Nausea #

During radiological examinations Barclay (l936) noted absence of gastric peristalsis in cases of nausea, as well as sagging of the lowermost part of the greater curvature which he attributed to loss of gastric tone. Lumsden and Holden (l969) described a similar, sudden descent of the greater curvature in a number of patients with nausea; they had no radiographic record of the occurrence.

During routine barium studies in the erect position, one of our patients would occasionally complain of nausea after having swallowed the first few mouthfuls of the suspension. Under these circumstances the following was seen: the lower part of the greater curvature sagged, causing an increase in the diameter of the distal part of the stomach, indicating loss of tone (Chap. 19). Simultaneously peristaltic contractions in the body of the stomach, cyclical contractions of the pyloric sphincteric cylinder and gastric emptying ceased. The appearance of the stomach was similar to that seen after administration of anticholinergic agents. The following is an example of what is usually observed in cases of nausea:

Case Report #

Case 26.1. G.C., male aged 24 years, was referred for barium study because of vague upper gastrointestinal symptoms. Having swallowed the first 3 mouthfuls of barium, the patient complained of feeling nauseous; there was no retching but he was unable to continue drinking. Initially the stomach appeared to have a normal tone, but the greater curvature sagged, moderate gastric dilatation occurred and peristaltic activity and cyclical contractions of the pyloric sphincteric cylinder ceased. A trickle of barium had entered the duodenal bulb but no further gastric emptying occurred (Fig. 26.1). He was advised to sit down. After 15 minutes the nausea disappeared and the examination could be resumed. Gastric tone, peristalsis, sphincteric cylinder activity and emptying became normal; no organic lesion was detected.

Fig. 26.1. Case G.C. Moderate dilatation of stomach, sagging of greater curvature, and absence of peristalsis and cyclical activity of pyloric sphincteric cylinder

According to Monges et al. (l974) the first electromyographic phenomena of nausea are the disappearance of spiking activity in the stomach and small intestine, and the slowing, decrease in amplitude and disturbance in propagation of the basal electrical rhythm (BER). These events may occur before the patient experiences nausea.

You et al. (l980) recorded gastric myoelectric activity in control subjects and in a group of patients with unexplained nausea, epigastric bloating and vomiting; the technique entailed the use of a peroral suction electrode. As no mention was made of actual retching or vomiting during the investigations, it would appear that recordings were obtained during the phase of nausea. One of the electrodes was attached to the gastric mucosa 1.0 cm orally to the pyloric ring, and another 3.0 cm orally to the ring, i.e. within the confines of the pyloric sphincteric cylinder (others were attached further orally, and 2 were located in the duodenum). In contrast to the normal, regular pacesetter potential (PP) with a frequency of 3 to 4 cycles per minute, all 9 patients showed abnormal "antral" myoelectric activity, characterized by tachygastria or tachyarrhythmia and propagation of the PP in either the orad or aborad direction. Although all 9 patients with nausea, bloating and vomiting studied by You et al. (l980) had antral arrhythmias, Stoddard et al. (l98l) described 5 patients with antral arrhythmia without any gastrointestinal symptoms at all. In their view the association between antral arrhythmia and disturbed gastric motility remained unclear, although it was possible that such arrhythmia might be associated with delay in gastric emptying.

Hamilton et al. (l986) studied the BER in 20 normal control subjects and in 5 patients with nausea and vomiting of longer than 6 months' duration. All patients had delayed gastric emptying as diagnosed by radionuclide scanning techniques, and 4 had previously been diagnosed as diabetic gastroparesis. The BER was recorded from the abdominal surface by means of a cutaneous electrode, and was shown to be similar in form and frequency to recordings obtained by mucosal suction electrodes. In one normal subject and in 4 of the 5 patients, periods occurred in which BER rates exceeded 5 per minute. In a normal subject the period of tachygastria lasted only 2.5 minutes and the subject remained asymptomatic. In patients, tachygastria lasted for periods of 4 minutes and was associated with nausea; the nausea resolved when the fast rate abated. The fifth patient was asymptomatic during the recording and had no tachygastria. Again it appeared if the recordings were done during periods of nausea and not while retching or vomiting occurred.

Using cutaneous electrodes, Geldof et al. (l986) recorded gastric myoelectrical behaviour by electrogastrography in 48 patients with prolonged, unexplained nausea and vomiting, and in 52 normal control subjects, in the fasting and post-prandial states. In 30 of the 48 patients gastric emptying studies were done, using a radiolabelled solid meal. No mention was made of actual retching or vomiting during the investigations, and it seems if the recordings were done during the phase of nausea. The patient group could be divided into 2 subgroups: in 25 patients all electrogastrographic parameters were identical to the control group, while in 23 abnormal myoelectrical activity was found, characterised by instability of the gastric pacemaker frequency, tachygastrias in both the fasting and postprandial states, and absence of the normal increase in amplitude in the postprandial tracing. This last characteristic was correlated with delayed gastric emptying of solids. Not all patients displayed all three abnormal features; tachygastria lasting between 3 and 14 minutes for instance, was seen in 8 of the patients. It is generally assumed that no motor activity is present during a tachygastria (Telander et al l978; You et al. l980; You and Chey l984; Geldof et al. l986), which is generated in an "antral" ectopic focus and which overrides the normal gastric pacemaker (Telander et al. l978). It was concluded that in a heterogeneous group of patients with unexplained nausea and vomiting, a subgroup could be discerned with abnormal myoelectrical activity which was related to the symptoms.

Kerlin (l989) studied the contractile activity of the stomach and small intestine in 20 patients with longstanding, idiopathic nausea and vomiting, in the fasting and postprandial states. Records were obtained by a low compliance infusion system from the gastric "antrum" (four sites), the duodenum and the jejunum; it appears if the studies were done during the stage of nausea. Only two patients had contractile abnormalities during fasting. After a solid-liquid test meal, the contractility of the gastric "antrum" was significantly impaired in patients as compared with normal controls. It was concluded that postprandial "antral" hypomotility was a major abnormality in patients with unexplained nausea and vomiting.

Retching #

The retching phase is characterized by a series of violent spasmodic abdomino-thoracic contractions with the glottis closed. During this time the inspiratory movements of the chest wall and diaphragm are opposed by the expiratory contractions of the abdominal musculature. At the same time movements of the stomach and its contents take place. Whereas a patient will complain of disagreeable sensations during nausea, speech is not possible during retching. The characteristic movements furnish a ready diagnostic sign of the retching phase.

During gastroscopic observations retching usually interferes to such an extent with the examination that it is difficult to observe the motor behaviour of the stomach. Schindler (l937) studied retching on two occasions during gastroscopy and noted that longitudinal folds appeared in the previously smooth "antrum", thickened quickly, came together and completely closed the "antrum". (Comment: The description tallies with contraction of the pyloric sphincteric cylinder during which the folds become longitudinal, so that only longitudinal folds are seen in the fully contracted cylinder) (Chap. 13).

Torgersen (l942) stated that the canalis egestorius (pyloric sphincteric cylinder) contracted during vomiting, and referred to previous work by Groedel who had illustrated the contraction of the two loops and the intervening musculature during vomiting.

Lumsden and Holden (l969) gave a detailed description of the movements of the stomach and duodenum in vomiting as seen in 3 cases during diagnostic radiological investigations. They did not refer to, and did not base their findings on, the concept of the pyloric sphincteric cylinder. In their first case, during retching, a constriction was described and illustrated in the proximal part of the "antrum". The greater curvature in this region showed a deep notch and was closely approximated to the lesser curvature. (Comment: From the description and illustration it is clear that the constriction and deep notch correspond to contraction of the left pyloric loop, with a collection of barium in the pyloric sphincteric cylinder on its aboral side). On an exposure taken immediately afterwards, the prepyloric region had hardly changed. (Comment: In the illustration a collection of barium is seen in the sphincteric cylinder between the right and left pyloric loops). At this stage the body of the stomach had also contracted and barium was being expelled through the cardia. In their second case, during retching, there was some barium in the "antrum", separated from the main mass of barium in the stomach by an annular constriction involving both curvatures of the stomach and superficially resembling the pylorus. (Comment: The appearance in the illustration is identical to contraction of the left pyloric loop) (Chap. 13).

In their third case vomiting occurred suddenly, a radiograph being taken at that exact moment. Some barium was trapped between the contracted "proximal part of the antrum" and the closed pylorus. (Comment: The trapped barium as illustrated appears to be in the pyloric sphincteric cylinder between the right and left pyloric loops).

The following are examples of cases we observed during retching:

Case Reports #

Case 26.2. M.J., female aged 29 years. Having swallowed 2 mouthfuls of barium, the patient suddenly started to retch. A film exposed at that moment showed a tightly contracted pyloric sphincteric cylinder containing longitudinal mucosal folds, with folds on its oral side bulging into the gas-distended gastric lumen (Fig. 26.2). The appearance is identical to that seen during a stage of the normal contraction of the pyloric sphincteric cylinder (Chap. 13). Afterwards retching stopped, more barium was swallowed and cyclical contractions of the cylinder became normal. No lesion was detected in the upper gastrointestinal tract.

Fig. 26.2. Case M.J. Tightly contracted pyloric sphincteric cylinder, containing longitudinal mucosal folds (straight arrow). Retropelled folds bulging into gastric lumen (curved arrows)

Case 26.3. E.W., female aged 34 years. Having swallowed 4 mouthfuls of barium in the erect position, the patient suddenly started to retch; barium had reached the pyloric aperture but had not traversed it, while some was still in the oesophagus. As soon as retching started a film was exposed. This showed contraction of the left pyloric loop with a "round" collection of barium on its aboral side, i.e. in the sphincteric cylinder (Fig. 26.3A). A segmental or systolic contraction of this collection followed, terminating in a tightly contracted cylinder containing a longitudinal mucosal fold (Fig. 26.3B); this corresponded to maximal contraction of the sphincteric cylinder. During contraction barium contained in the cylinder was propagated not into the duodenum, but in a retrograde way into the more proximal part of the stomach. When retching ceased, normal cyclical contractions of the pyloric sphincteric cylinder and gastric emptying commenced. No organic lesion was found.

A	B
`Fig. 26.3. A Case E.W. Contraction of left pyloric loop (curved arrow). Round collection of barium in partially contracted sphincteric cylinder (straight arrow). B Case E.W. Maximally contracted sphincteric cylinder containing a longitudinal mucosal fold (arrow).`

Vomiting #

Lang et al. (l986) examined the gastrointestinal motor correlates of vomiting in canines by means of implanted extramural strain gauge transducers. One of the motor responses was a retrograde peristaltic contraction commencing in the middle of the small intestine and moving in an orad direction through the small intestine to the gastric "antrum". Ejection did not occur after a consistent delay following the "antral retrograde peristaltic contraction", i.e. there was no evidence that the antral contraction correlated with vomitus ejection. This was consistent with previous findings that the stomach did not provide the propulsive force for vomitus ejection; it was more likely that the propulsive force was provided by contractions of the abdominal or respiratory muscles. The small intestinal retrograde peristaltic contraction, leading to gastric "antral" contractions, was probably mediated peripherally by muscarinic cholinergic receptors as it was selectively blocked by atropine (which does not readily cross the blood-brain barrier).

During routine barium studies we observed the act of ejection in 5 or 6 patients. Because of violent movements it was usually not possible to obtain satisfactory radiographs. The following is a representative case:

Case Report #

Case 26.4. S.S., female aged 42 years. After swallowing two mouthfuls of barium, it accummulated in the pyloric region. Incomplete contractions of the pyloric sphincteric cylinder, not propagating the barium into the duodenum, soon started. Almost immediately the patient felt nauseous and retching commenced. At this stage the pyloric sphincteric cylinder contracted maximally, giving rise to an appearance sometimes called "amputation of the antrum". Immediately afterwards a long spastic contraction occurred in the body of the stomach, associated with ejection. Two contracted areas were then present in the stomach, namely the contracted sphincteric cylinder, and a larger region of contraction of the body of the stomach. At that stage most of the remaining barium was in the upper part of the stomach, above the contracted regions. Subsequent clinical examination revealed no obvious cause for the vomiting.

Discussion #

With the exception of Torgersen (l942), none of the authors quoted above based their descriptions of nausea, retching and vomiting on the muscular anatomy of the stomach as previously determined by Cunningham (l906), Forssell (l913) and Torgersen himself.

Our radiographic observations show that nausea is characterized by loss of gastric tone, absence of peristalsis and cyclical contractions of the pyloric sphincteric cylinder, and lack of emptying of fluid barium in the erect position. A number of authors described the electromyographic phenomena recorded during nausea (Monges et al. l974; You et al. l980, l984; Hamilton et al. l986; Geldof et al. l986). It is probable that some of the electrical arrhythmias may be associated with the appearances seen at radiography. Pressure studies of Kerlin (l989) confirmed that postprandial "antral" hypomotility was a major factor in unexplained nausea.

The representative cases described here show that retching is associated with contraction of the pyloric sphincteric cylinder; this is well seen during radiographic studies. Although Lumsden and Holden (l969) did not base the morphology in their cases on the anatomy as described by Torgersen (l942), accompanying illustrations leave little doubt that the pyloric sphincteric cylinder was contracted in all. Wood and Astley (l952) and others (Chap. 20) described a temporary narrowing in the pyloric region closely resembling infantile hypertrophic pyloric stenosis, in vomiting infants. Judging by the descriptions it involved the pyloric sphincteric cylinder. The endoscopic appearances described by Schindler (l937) also tally with contraction of the sphincteric cylinder.

Radiography shows that the cylinder is contracted during ejection. By means of strain gauge transducers in canines Lang et al. (l986) demonstrated an "antral retrograde peristaltic contraction", which appears to tally with contraction of the cylinder; this contraction, however, did not provide the propulsive force for ejection. Radiographically a second, longer area of contraction was seen in the upper part of the stomach during ejection, in addition to the contraction of the cylinder in one of our cases (Case 26.4).

References #

Barclay AE. The Digestive Tract. Cambridge University Press, London l936, p 268.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
Forssell G, Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr l913, Suppl 30, l-265.
Geldof H, Van der Schee EJ, Van Blankenstein M, et al. Electrogastrographic study of gastric myoelectrical activity in patients with unexplained nausea and vomiting. Gut 1986, 27, 799-808.
Hamilton JW, Ballahsene BE, Reichelderfer M, et al. Human electrogastrograms: comparison of surface and mucosal recordings. Dig Dis Sci l986, 31, 33-39.
Kerlin P. Postprandial antral hypomotility in patients with idopathic nausea and vomiting. Gut l989, 30, 54-58.
Lang IM, Sarna SK, Condon RE. Gastrointestinal motor correlates of vomiting in the dog: quantification and characterization as an independent phenomenon. Gastroenterology l986, 90, 40-47.
Lumsden K, Holden WS. The act of vomiting in man. Gut l969, l0, 173-179.
Monges H, Salducci J, Naudy B. Electrical activity of the gastrointestinal tract in dog during vomiting. In: Gastrointestinal Motility, edit Daniel EE. Mitchell Press, Vancouver l974, pp 479-488.
Schindler R. Gastroscopy. University of Chicago Press, Chicago l937, p 145.
Stoddard CJ, Smallwood RH, Duthie HL. Electrical arrhythmias in the human stomach. Gut 1981, 22, 705-712.
Telander RL, Morgan KG, Kreulen DL, et al. Human gastric atony with tachygastria and gastric retention. Gastroenterology l978, 75, 497- 501.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, pp 38, 39.
Wood BSB, Astley R. Vomiting of uncertain origin in young infants. Arch Dis Child l952, 27, 562-568.
You CH, Lee KY, Chey WY, et al. Electrogastrographic study of patients with unexplained nausea, bloating and vomiting. Gastroenterology l980, 79, 311-314.
You CH, Chey WY. Study of electromechanical activity of the stomach in humans and dogs with particular attention to tachygastria. Gastroenterology l984, 86, 1460-1468.

27 - Duodenogastric Reflux

Mon, 01 Jan 0001 00:00:00 +0000

Duodenogastric Reflux #

Regurgitation of alkaline duodenal juice into the stomach has long been of interest. Previously it was assumed to be a normal, protective reaction in cases of gastric hyperacidity (Olch l928). The studies by Du Plessis (1960, 1962, 1965) and Lawson (l964) tended to show the converse, namely that it might be damaging to the gastric mucosa. It was found that transpyloric duodenogastric reflux constituted one of the causes of chronic and atrophic gastritis, with an attendant decrease in gastric mucosal resistance to ulceration (Du Plessis l960, l965). Transstomal reflux after gastro- enterostomies caused a severe atrophic gastritis (Du Plessis l962).

Under experimental conditions in canines, duodenogastric reflux caused superficial gastritis, atrophic gastritis and epithelial proliferation with an increase in mitotic acitivity (Lawson l964). Excessive reflux of duodenal contents into the stomach appeared to be a factor in the pathogenesis of gastric ulceration (Capper l967; Delaney et al. l970). The canine gastric mucosal barrier was destroyed by lysolecithin and phospholipase A, and if the human gastric mucosa behaved similarly, regurgitation of duodenal contents could be damaging (Davenport l970). In guinea-pigs, lysolecithin produced gastric mucosal damage with macroscopic erosions, showing that reflux from the duodenum was an important factor in causing gastritis and gastric erosions (Orchard et al. l977). Bile salts caused a degradation of gastric mucus in pigs, thus damaging the protective layer on the luminal surface of the epithelium (Marriott et al. l977; Schrager and Oates l978).

Previous Tests #

Various tests have been devised to determine the ability of the pylorus to prevent duodenogastric reflux.

The concentration of bile acid conjugates in fasting gastric aspirates has long been used as a quantitative measure of duodenogastric reflux (Du Plessis l965; Kaye and Showalter l974; Valenzuela and Defilippi l976; Hoare et al. l978). Although it is a useful guide it has obvious limitations and may not always be reliable since duodenogastric regurgitation may result simply from the presence of an indwelling gastric tube itself (Capper et al. l966).

A radiographic test was devised by Capper et al. (l966). By threading a thin-bore soft rubber tube through the pylorus, gastrografin was injected directly into the lumen of the duodenum. (Rigid plastic tubes were found to be unsuitable as their stiffness interfered with the normal sphincteric action and rendered the pylorus incompetent). With the tube in situ, and with no contrast medium in the stomach, reflux could be observed on the radiological TV monitor, being categorized as minimal, moderate or gross. Special attention was paid to the relationship of reflux to duodenal contraction waves.

In his investigations Grech (l970) used Capper's test with minor modifications. Keighley et al. (l975) employed a further modification; after injection of 20 ml dilute barium suspension into the duodenum through the transpyloric tube, the tube was withdrawn, followed by 3 minutes of radiographic screening to observe whether reflux was present.

Using a radioactive test, Rhodes et al (l969) injected a dose of ¹⁴C-tagged bile salts intravenously. The concentration of secreted radio-active bile salts in aspirated gastric juice was measured, the value serving as an index of duodenal regurgitation. In Wormsley's (l972) test an indicator substance (polyethylene glycol) was injected into the duodenum, followed by aspiration of gastric juice; this entailed the use of both an intragastric and an intraduodenal tube.

Kim et al. (l972) and Keighley et al. (l975) pointed out that the diagnosis of reflux alkaline gastritis could be made by a combination of gastric analysis, gastroscopy and biopsy. Reflux was present endoscopically, according to Hoare et al. (l978), if there was a pool of bile in the stomach or if reflux occurred throughout the examination. It was acknowledged that the presence of a duodenal tube or gastroscope might lead to reflux. Previously Flint and Grech (l970) had stated that gastroscopy was not a satisfactory method of assessing pyloric reflux when vagal blocking drugs were used. Connell (l978) stated that endoscopy in itself had marked effects on gastro-intestinal motility, and implied that it was not satisfactory for assessing pyloric reflux.

Sophisticated electrical pacing techniques have been used experimentally. Kelly and Code (l977) examined duodenogastric reflux in canines, in which pacing from a site in the distal duodenum reversed the direction of the pacesetter potential from aborad to orad, reversing the direction of propagation of duodenal contents, and resulting in duodenogastric reflux.

Valenzuela and Defilippi (l976) used manometric techniques for direct measurement of pyloric sphincter pressures; this entailed the presence of polyvinyl catheters through the pylorus. By the combined use of duodenal marker perfusion and miniature intraluminal strain gauge transducers, Rees et al (l979) determined the relationship between antroduodenal motor activity, duodenogastric reflux and gastric emptying. Although these refined techniques have yielded valuable data, there remains the lingering suspicion that the presence of gastric or transpyloric tubes might have influenced the results. Cole (l969) had stated previously that even the nausea felt by most intubated patients might account for bile entering the stomach. Rovelstad (l976) reiterated that tube studies could impair the normal closing mechanism of the pylorus.

A radioactive test, based on the differential excretion of iminodiacetic acid (IDA) by the liver, was described by Muhammad et al. (l980). Following the intravenous administration of ^99mTc-labelled p-butyl-IDA, which is completely secreted into the bile, radioactivity was measured in the stomach (in post-gastrectomy patients) by means of a gamma camera. Reflux was expressed as a percentage of the total excreted radioactivity. Nicolai et al. (l980) injected ^99mTc-labelled diethyl-IDA intravenously, followed by aspiration of the tracer from the stomach through a double- lumen nasogastric tube, allowing quantification of reflux. The test also involved the intravenous injection of cholecystokinin to produce gallbladder contraction, with constriction of the pylorus as a side effect. Ehrlein (l98l) pointed out that the function of the pyloric sphincter in preventing duodenogastric reflux had not been clarified. (It was explained that the term "pyloric sphincter" in this context referred to the pyloric ring). It was difficult to record contractions over a long period of time in humans. In animals it was possible to measure the external diameter of the pylorus with induction coils, and to determine pressure changes simultaneously by means of implanted strain gauge transducers (Ehrlein l980). The method was used in canines to investigate possible co-ordination of gastric and duodenal motility, gastroduodenal reflux at the same time being observed fluoroscopically. In the digestive state the pylorus opened when a peristaltic wave involved the commencement of the "antrum", closing when the wave reached the pyloric sphincter. Contraction maxima of the duodenal bulb most often occurred a fraction of a second before, or after, contraction maxima of the pyloric sphincter. Consequently there was incomplete closure of the pylorus during duodenal contraction, allowing duodenogastric reflux to occur; it was produced by atypical segmental contractions of the bulb. In the interdigestive state different phases were encountered. In the first phase, in the absence of contractile activity in the stomach and duodenum, no reflux occurred. In the second and third phases imperfect timing of pyloric and duodenal contractions, as in the digestive state, sometimes resulted in duodenogastric reflux.

Various derivatives of ^99mTc-IDA have now been used extensively in the study of duodenogastric reflux, notably ^99mTc-BIDA (butyl iminodiacetic acid) and ^99mTc-HIDA. These tests have certain minor limitations in common (Thomas et al, l984). For instance, anatomical definition of the stomach was often complicated by overlap of the left lobe of the liver and the duodeno-jejunal flexure; delineation of the gastric "antrum" was poor, and as it was close to the duodenal bulb, minor degrees of reflux might not be detectable; and computer analysis of small volumes of reflux might be difficult to interpret.

Two further limitations of the cholescintigraphic tests, in our view, are the following:

As only bile constituents are labelled, the tests apply to reflux of bile into the stomach; they are not a measure of reflux of the other constituents of duodenal juice, of which pancreatic exocrine secretion is the most important. It may be useful to have a test able to demonstrate reflux of duodenal contents (as opposed to bile only), into the stomach.
At present the tests do not visualize the pylorus clearly, i.e. it is not possible to determine the extent of contraction or relaxation of the pyloric region in relation to reflux.

A Double-Contrast Radiographic Test for Duodenogastric Reflux #

As a modification of the double-contrast upper gastrointestinal radiographic examination, we have described the following radiographic test for duodenogastric reflux (Keet l982). In this test the pylorus is clearly visualized and its diameter can be determined during reflux; in addition, the relationship of reflux to pyloric and duodenal contractions may be studied. The test is non-invasive and does not entail the use of catheters, intubation or the administration of pharmacological agents (which may alter motility).

The patient, standing behind the radiological TV monitor after a 12-hour overnight fast, is instructed to swallow 4 to 5 mouthfuls of a micropulverized barium suspension, e.g. Micropaque (Adcock-Ingram, Johannesburg) ordinarily used for upper gastrointestinal radiographic examinations. Immediately afterwards a gas-producing agent is swallowed, e.g. 2 x 50 Gastrast tablets (Toho Kagaku Kenyusho, Tokyo), followed by 2 mouthfuls of water containing a few drops of Telament liquid (Adcock Ingram, Johannesburg). The barium accumulates in the lower part of the stomach while the gas distends the fornix. While the patient is instructed not to eructate, the table is immediately tilted into the horizontal position. With the arms abducted throughout the examination, the supine subject is now rotated into the left anterior oblique position (right side down) till barium enters the duodenal bulb. As soon as duodenal filling is achieved, the subject is rotated rapidly through 90 degrees into the right anterior oblique position. This causes the remaining barium in the stomach to descend into the fornix, while the gas is displaced and ascends into the pyloric region, which now constitutes the uppermost part of the stomach. Consequently the first part of the duodenum is filled with barium, while the pyloric region up to the ring is filled with gas (Fig. 27.1). The competence of the pylorus can now be studied, radiographs being taken at appropriate times. Duodenogastric reflux through the pylorus into the gas-containing part of the gastric lumen is clearly visible (Fig. 27.2). (This should not be confused with the normal orad movement of barium often seen during contraction of the pyloric sphincteric cylinder as described in Chap. 13). Should no reflux be observed, or should the duodenum empty its contents prematurely, positioning of the patient is repeated. Generally speaking, the manoeuvre is repeated 4 to 5 times during each test. The effects of compression of the second or third parts of the duodenum may also be studied.

Fig. 27.1. Duodenal bulb filled with barium. Pyloric sphincteric cylinder filled with gas and distended

Fig. 27.2. Reflux of barium (arrow) from the duodenum into the pyloric sphincteric cylinder, which is relaxed

Advantages #

The main advantages of this method appear to be the following:

Because of the clear images produced by radiography, the diameter and competence of the pylorus may be studied in relation to both duodenal contraction waves and the motility of the pyloric part of the stomach, i.e. the pyloric sphincteric cylinder. Little attention has been paid to duodenogastric reflux in relation to pyloric motility in previous investigations.
If it is assumed that the barium suspension in the duodenal lumen represents duodenal contents, the procedure will determine the presence or absence of reflux of duodenal contents, i.e. of duodenal juice (in contrast to bile only).
No medication (e.g. anticholinergics or cholecystokinin) is administered, thus allowing the study of pyloric competence in the absence of pharmacological modification.
There is no gastric intubation (thus eliminating nausea) and the pylorus is not traversed by a tube (or has been traversed immediately before observation, as in the test of Keighley et al. l975).
The test is quick and simple to perform, and may be followed by a "conventional" upper gastrointestinal radiographic examination.

Disadvantages #

Radiation to the patient should be considered, but measurements showed that this was minimal and could be discounted since a small (11.0 x 8.0 cm), localized aperture was used, not more than two 11.0 x 8.0 cm film exposures were needed for record purposes, and screening time generally did not exceed 90 to 120 seconds.
In a minority of patients, depending on the direction of the pyloroduodenal axis, it may not be possible to obtain a side view of the duodenum and pylorus, the barium-filled bulb being projected over the pyloric aperture.
The examination is performed in the interdigestive phase and in the supine position only.
While there is no doubt about the ability of the procedure to illustrate the presence or absence of reflux, quantification cannot be accurate as only a rough impression of the quantity of reflux is gained.

Results in Normal Subjects #

Having received approval of the Ethical Committee, the test was performed in 14 informed, volunteer, asymptomatic male medical students between the ages of 23 and 27 years. In 9 of the subjects no duodenogastric reflux occurred. In 2 subjects there was minimal reflux on one occasion only (three further "rotating manoeuvres" failed to produce reflux). In 3 subjects moderate reflux occurred. In each it was seen two or three times during four "rotating manoeuvres". One of these subjects was re-tested a week later, with similar results.

Duodenal Motility

In all 14 normal subjects duodenal peristalsis appeared normal on the TV monitor and the duodenum emptied normally. In all there also occurred retrograde movement of barium in the duodenal lumen, which appeared to result from "segmental" contraction waves in the third part of the duodenum. While these contractions did not proceed along the duodenal walls, but remained localized to the third part, they forced barium in an orad direction, at times as far as the bulb; barium in the lumen distal to these contractions was forced in an aborad direction.

In all normal subjects the second part of the duodenum was also compressed as far as possible by means of the gloved hand on the anterior abdominal surface. This did not occlude the lumen completely, did not prevent aborad movement, and did not initiate retrograde movement. The results were the same with and without partial compression of the second part of the duodenum.

Pyloric Motility

As indicated previously (Chap. 3), the muscular part of the pyloric ring is considered to be the terminal annular thickening of the pyloric sphincteric cylinder, as described by Cunningham (1906), Forssell (l913) and Torgersen (l942). The cylinder, which is 3.0 to 4.0 cm in length, normally contracts in a segmental (as opposed to "peristaltic") way (Chap. 13). As the ring forms an inherent part of the cylinder, it closes and opens with contraction and relaxation of the cylinder respectively. In all subjects these contractions were normal. Reflux in the 5 subjects occurred either during maximal relaxation of the sphincteric cylinder, (Fig. 27.2), or when it was in a state of partial contraction (Fig. 27.3). It never occurred during maximal contraction of the cylinder.

Fig. 27.3. Barium filling to show partial contraction of sphincteric cylinder. At this stage the pyloric aperture (arrow) is widely patent

Results in Patients #

Having received approval of the Ethical Committee, the test was performed in 100 patients between the ages of l8 and 79 years who, during the ordinary course of events, had been referred for radiographic examinations because of upper gastro-intestinal symptoms, e.g. dyspepsia and epigastric pain.

No Lesion Detected

In 48 patients no macroscopic organic lesion could be demonstrated in the upper gastro- intestinal tract; these were considered to be patients with non-ulcer dyspepsia. Eighteen (± 37 percent) had minimal to moderate duodenogastric reflux. In all cases reflux occurred during those stages of the pyloric cycle in which the pyloric sphincteric cylinder was relaxed (Fig. 27.2), or partially contracted (Fig. 27.3). Reflux never occurred during maximal contraction of the cylinder.

Duodenal Ulceration

In our series there were 25 cases of active duodenal ulceration or duodenal deformity typical of ulceration, l8 (approximately 72 percent) showing moderate duodenogastric reflux.

Gastric Ulceration

We encountered 9 cases of chronic benign ulcer on the lesser curvature of the stomach at varying distances proximal to the pyloric sphincteric cylinder, i.e. not within the cylinder itself. Seven of these showed moderate reflux. In the present series no cases of benign gastric ulceration within the pyloric sphincteric cylinder were seen.

Malignant Gastric Ulceration

In our series 2 cases of malignant gastric ulceration (proved by biopsy) were diagnosed. In one case, with the ulcer on the lesser curvature close to the pylorus (i.e. within the sphincteric cylinder), there was moderate to marked reflux. In the second case, with the ulcer at the incisura angularis, no reflux was seen.

Sliding Hiatus Hernia with Free Gastro-Oesophageal Reflux

There were 9 cases in the present series, 4 showing reflux of duodenal contents into the stomach.

Combined Lesions

In the present series 7 cases had combined lesions, e.g. duodenal ulceration and hiatus hernia. Most of these showed reflux. One of these cases had constant spasticity of the pyloric sphincteric cylinder with irregular and transverse mucosal folds (Fig. 27.4). It was diagnosed radiologically and endoscopically as spasm and chronic gastritis affecting the cylinder. In addition the duodenal bulb was deformed due to ulceration. In this case moderate to marked duodenogastric reflux occurred. Owing to the tube-like spasm of the cylinder, the pyloric aperture was neither fully open nor fully closed, but fixed in a state of partial patency.

Fig. 27.4. Barium filling of spastic pyloric sphincteric cylinder in a case of chronic gastritis. Duodenal bulb deformed

Duodenal Motility

In the last 40 patients of the series, special attention was paid to duodenal motility. In 32 of these the aborad and orad movements of intraluminal barium were identical to those in normal controls. In 8 no orad movement of contrast was seen in the second and third parts of the duodenum, yet in half of these cases duodenogastric reflux occurred. One's impression was that physiological duodenal movements were probably of little consequence in the mechanism of reflux. (By experimentally reversing the pacesetter potential in the duodenum in canines by electrical stimulation, Kelly and Code l977 did produce reflux.)

Pyloric Motility

As in normal control subjects, reflux in patients only occurred while the pyloric sphincteric cylinder was relaxed or in a state of partial contraction; it never occurred during maximal contraction of the cylinder.

Subsequent Tests #

Shortly after the above radiographic test for duodenogastric reflux was described (Keet l982), a similar procedure was mentioned by Hughes et al. (l982). Minimal reflux was considered to be a slight trickle through the pylorus, moderate reflux that which extended to the "antral" region of the stomach, and gross reflux that which extended to the body of the stomach. Duodenogastric reflux was found to be present in 6 (27 percent) of 22 normal subjects and in 128 (32 percent) of 396 patients with non-ulcer dyspepsia. Statistically there was no significant difference in incidence between the normal controls and dyspeptic patients.

Using a ^99mTc-EHIDA test, Niemela et al (l984) found reflux in 14 of 33 normal controls. With a similar test Wolverson et al (l984) noted duodenogastric reflux in 6 of 13 normal controls. With a nasogastric aspiration technique Wolverson et al (l984) found that 8 of 15 normal controls had reflux. By measuring the intragastric bile acid concentration by means of a nasogastric suction technique, Gotthard et al. (l985) showed that large fluctuations in reflux might occur during a 24 hour measuring period. Of 12 normal control subjects 10 showed reflux, with low daytime values and frequent high peaks in bile acid concentration during the night.

Discussion #

Normal subjects

Du Plessis (l965) stated that slight duodenogastric reflux was a normal occurrence. Capper et al. (l966) found no reflux in 15 normal controls, while it occurred in one out of 12 normal subjects in Flint and Grech's (l970) series. Nevertheless Flint and Grech were of the opinion that the pylorus was normally competent, i.e. it did not allow reflux. Rovelstad (l976) stated that it was debatable whether duodenogastric reflux was a normal phenomenon, while Donovan et al (l977) found no reflux in normal controls. Nicolai et al. (l980) on the other hand, demonstrated a median reflux of 4.3 percent of an intravenously injected dose of radioactive technetium-labelled IDA.

In 5 of 14 normal subjects, and in l8 of 48 non-ulcer dyspeptic patients, Keet (l982) found minimal to moderate duodenogastric reflux. Hughes et al. (l982) found reflux in 6 of 22 normal subjects and in 128 of 396 patients with non-ulcer dyspepsia, the incidence in the two groups being more or less the same. Similar results were obtained by Niemela et al. (l984), who noted reflux in 14 of 33 normal control subjects, and by Wolverson et al. (l984) who found reflux in 6 of 13 controls. The findings of Gotthard et al. (l985) pointed to large fluctuations in reflux, with higher peaks occurring nocturnally.

It is concluded that mild to moderate duodenogastric reflux occurs in approximately one third of normal subjects, and in one third of patients with non-ulcer dyspepsia, as shown (inter alia) by the radiological tests of Keet (l982) and Hughes et al. (l982). In other words, the pylorus is normally not competent in a significant percentage of normal subjects and approximately the same percentage of patients with non-ulcer dyspepsia.

Duodenal Ulceration

Du Plessis (l965) stated that in some cases of duodenal ulceration, reflux was excessive. Capper et al. (l966) found moderate or gross reflux in 33 percent or duodenal ulcer cases, Donovan et al (l977) in 24 percent, while Valenzuela and Defilippi (l976) stated that the incidence of reflux in patients with duodenal ulceration was not significantly different from that in controls. Of 7 cases Nicolai et al. (l980) found increased reflux in 2 only; in both, pyloric deformity was also present.

In our series there were 25 cases of active duodenal ulceration or duodenal deformity typical of ulceration, l8 (approximately 72 percent) showing moderate duodenogastric reflux. Hughes et al. (l982) found reflux in 53 percent of one group of patients with duodenal ulcer, and in 32 percent of patients in another group. Of 60 patients with duodenal ulceration Wolverson et al. (l984) found 32 (53 percent) to be reflux positive.

It is concluded that duodenogastric reflux occurs in a significant percentage of cases with duodenal ulceration; the incidence, as reported by different authors, varies from approximately 24 percent to approximately 72 percent. As cyclical activity of the pyloric sphincteric cylinder is normal in the vast majority of cases of duodenal ulceration (Chap. 30), the reflux is difficult to explain on the basis of pyloric dysfunction.

Gastric Ulceration

Du Plessis (l965) found the concentration of bile acid conjugates in fasting gastric aspirates to be abnormally high in cases of gastric ulceration. Capper et al. (l966) found moderate or gross reflux in 66 percent of gastric ulceration patients, while Rhodes et al (l969) and Delaney et al. (l970) mentioned an increased incidence of bile reflux in patients with gastric ulceration. Flint and Grech (l970) stated that the pylorus was incompetent in gastric ulceration and chronic alcoholic gastritis, while the results of Valenzuela and Defilippi (l976) suggested pyloric "sphincter" incompetence in gastric ulceration. Nicolai et al. (l980) found increased reflux in l8 gastric ulcer cases.

In our series (Keet l982) there were 9 cases of benign ulcer on the lesser curvature of the stomach at varying distances proximal to the sphincteric cylinder, i.e. not within the cylinder. Seven of these showed moderate reflux. In the series of Hughes et al. (l982) reflux was present in 21 of 46 patients with gastric ulcer. Although there appeared to be a higher proportion of gastric ulcer patients with reflux, the results did not reach statistical significance when compared with the other dyspeptic patients examined. The impression was that there was no direct association between the degree of reflux and the presence of peptic ulceration, according to Hughes et al. (l982). Niemela et al. (l984) found that of l9 patients with gastric ulcer in the body of the stomach, l7 had reflux. Two patients had both gastric and duodenal ulceration, both showing reflux. Twelve patients had prepyloric and antral gastric ulcers, 8 showing reflux. Of 30 patients with gastric ulceration Wolverson et al. (l984) found l7 (53 percent) to be reflux positive. Gotthard et al. (l985) examined 11 patients with prepyloric ulcer disease (i.e. with the ulcer situated within 2.0 cm of the pyloric ring); in all the intragastric concentrations of bile acid were measured over a 12 hour period. The mean bile acid concentrations in prepyloric ulcer patients were found to be significantly higher than in both controls and duodenal ulcer patients, diurnally as well as nocturnally.

Gastric ulceration is often associated with spasm of the pyloric sphincteric cylinder (Chap. 29). Spasm of the cylinder resembles a normal, partial contraction; at this stage the pyloric aperture is normally open (Chap. 13). In spasm the aperture is "fixed" in the open position. It is surmized that for this reason a high incidence of duodenogastric reflux is to be expected in gastric ulceration.

Malignant Gastric Ulceration

In our series (Keet l982) 2 malignant gastric ulcers were found. In one case, with the ulcer on the gastric lesser curvature close to the pylorus (i.e. within the sphincteric cylinder), there was moderate to marked reflux. In the second case, with the ulcer at the incisura angularis, no reflux was seen.

Sliding Hiatus Hernia with Gastro-Oesophageal Reflux

Donovan et al. (l977) noted duodenogastric reflux in 3 of 8 patients with hiatus hernia. In 10 cases of hiatus hernia Nicolai et al. (l980) found no evidence of increased reflux. In our series (Keet l982) there were 9 cases of hiatus hernia, 4 showing reflux of duodenal contents. There seems to be an association between hiatus hernia and spasm of the pyloric sphincteric cylinder; this may allow increased duodenogastric reflux and may ultimately lead to biliary oesophagitis (Chap. 32).

Combined Lesions

In the present series 7 cases had combined lesions, e.g. duodenal ulceration and hiatus hernia; most of these showed reflux. One of these cases showed a constant spasm of the pyloric sphincteric cylinder with irregular and transverse mucosal folds (Fig. 27.4). It was diagnosed radiologically and endoscopically as spasm and gastritis affecting the cylinder; in addition the duodenal bulb was deformed due to ulceration. In this case moderate to marked duodenogastric reflux occurred. Owing to the tube-like spasm of the cylinder, the pyloric aperture was neither fully open nor fully closed, but fixed in the patent position.

Pyloric Motility

Both in normal controls and in patients, duodenogastric reflux only occurred while the pyloric sphincteric cylinder was relaxed or in a state of partial contraction; it never occurred during maximal contraction of the cylinder. During relaxation of the cylinder there is absence of muscular closure of the aperture; mucosal closure may be present (Chap. 13). During partial contraction of the cylinder, occurring as a phase of cyclical contractile activity, the pyloric aperture is open (Chap. 13). Spasm of the cylinder resembles partial, physiological contraction, and is associated with patency of the aperture; it differs from a physiological contraction in that its contraction is permanent. Consequently increased duodenogastric reflux is to be expected in spasticity of the pyloric sphincteric cylinder.

The above does not imply that the phase of contraction of the sphincteric cylinder is the only factor in the pathogenesis of duodenogastric reflux.

Duodenal Motility

Both in normal subjects and in patients, duodenal peristaltic waves and "segmental" contraction waves in the third part of the duodenum appeared to be of little consequence in duodenogastric reflux (vide supra). However, in experimental studies in canines Ehrlein (l981) found that the timing between contractions of the duodenal bulb and the pyloric "sphincter" (right pyloric loop) was not perfect. Contraction maxima of the duodenal bulb often occurred slightly before or after contraction maxima of the "sphincter". Consequently the pyloric aperture was often inadequately closed during contraction of the duodenal bulb, resulting in reflux.

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Keet AD. A new, tubeless radiological test for duodenogastric reflux. South Afr Med J l982, 61, 78-81.
Keighley MRB, Asquith P, Alexander-Williams J. Duodenogastric reflux: a cause of gastric mucosal hyperaemia and symptoms after operations for peptic ulceration. Gut l975, 16, 28-32.
Kelly KA, Code CF. Duodenal-gastric reflux and slowed gastric emptying by electrical pacing of the canine duodenal pacesetter potential. Gastroenterology l977, 72, 429-433.
Kim SK, Rogers LS, Heitzman RE. Reflux alkaline gastritis. Amer J Roentg Rad Ther Nucl Med l972, 115, 271-274.
Lawson HH. Effect of duodenal contents on the gastric mucosa under experimental conditions. Lancet l964, 1, 469-472.
Marriott C, Kellaway IW, Martin GP. The effect of bile salts on the physical properties of mucus (abstract). In: Mucus in Health and Disease. Edit Elstein M, Parke DV. Plenum Press, London l977, p 509.
Muhammed I, McLoughlin GP, Holt S, et al. Non-invasive estimation of duodenogastric reflux using technetium-^99mbutyliminodiacetic acid. Lancet l980, 2, 1162-1165.
Nicolai JJ, Silberbusch J, Van Roon F, et al. A simple method for the quantification of biliary reflux. Scand J Gastroenterol l980, 15, 775- 780.
Niemela S, Heikkila J, Lehtola J. Duodenogastric reflux in patients with gastric ulcer. Scand J Gastroenterol l984, 19, 896-898.
Olch IY. Duodenal regurgitation as a factor in neutralisation of gastric acidity. Arch Surg l928, 16, 125-138.
Orchard R, Reynolds K, Fox B, et al. Effect of lysolecithin on gastric mucosal structure and potential difference. Gut l977, l8, 457-461.
Rees WDW, Go VLW, Malagelada JR. Simultaneous measurement of antroduodenal motility, gastric emptying and duodenogastric reflux in man. Gut l979, 20, 963-970.
Rhodes J, Bernardo DE, Phillips SF, et al. Increased reflux of bile into the stomach in patients with gastric ulcer. Gastroenterology l969, 57, 241-252.
Rovelstad RA. The incompetent pyloric sphincter; bile and mucosal ulceration. Amer J Dig Dis l976, 21, 165-173.
Schrager J, Oates MDG. Relation of human gastro-intestinal mucus to disease states. Brit Med Bull l978, 34, 79-82.
Thomas WEG, Jackson PC, Cooper MJ, et al. The problems associated with scintigraphic assessment of duodenogastric reflux. Scand J Gastroenterol l984, l9 (Suppl 92), 36-40.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.
Valenzuela JE, Defilippi C. Pyloric sphincter studies in peptic ulcer patients. Amer J Dig Dis l976, 21, 229-232.
Wolverson RL, Sorgi M, Mosimann F, et al. The incidence of duodenogastric reflux in peptic ulcer disease. Scand J Gastroenterol l984, l9 (Suppl 92), 149-150.
Wormsley KG. Aspects of duodenogastric reflux in man. Gut l972, 13, 243-250.

28 - Gastritis and Erosions in the Pyloric Sphincteric Cylinder

Mon, 01 Jan 0001 00:00:00 +0000

Gastritis and Erosions in the Pyloric Sphincteric Cylinder #

Holsti (l931) stated that inflammatory alterations of gastritis usually affected the mucosa, but that changes also occurred in the deeper layers of the wall in 66 percent of cases, and even the serous layer might be involved. He performed detailed histological studies of the intramural ganglia in gastric resection specimens affected by chronic gastritis (in the absence of peptic ulceration). Compared with normal controls, the ganglia of gastritis showed marked changes affecting the periganglionar, capsular and intraganglionar structures. The outstanding feature was an increase in connective tissue both in the periganglionar and intraganglionar regions, coupled with intraganglionar infiltration of inflammatory cells and degeneration of ganglion cells; in some ganglia hardly a single normal cell was seen. The changes were more marked in Auerbach's than in Meissner's plexus and more advanced in the pyloric than in the fundic zone. The intensity of the condition varied from case to case, from ganglion to ganglion, and even from one part of a ganglion to another. The spatial spread of the process was uneven, but two components of the wall, namely the mucosa and Auerbach's plexuses, were always involved.

Schindler et al. (l937) pointed out that at that time the normal histological picture of the gastric mucosa was still being debated. Specimens for examination were rarely obtained from healthy stomachs as postmortem changes altered the picture and healthy stomachs were not resected. Minor histological changes did not indicate active disease but were the normal reaction to external irritants, such as hot or cold food; those changes were not due to chronic gastritis. Gastroscopy could be carried out in normal persons, and on the basis of systematic gastroscopic investigations it was suggested that chronic gastritis could be divided into 3 types: superficial, atrophic and hypertrophic. Demonstrating the mucosal folds by means of radiological relief techniques was of little value in the diagnosis of chronic gastritis.

Golden (l937) defined gastritis as inflammation of the gastric wall of unknown etiology, which began in and might be limited to the mucosa, but which frequently extended to the deeper layers and even to the serosa. It could be generalized, but was often patchy and not infrequently it was limited to, or had its maximum effect in, the antrum. The term "antrum" was used synonymously with the canalis egestorius as described by Forssell (l913), while antral systole and diastole indicated contraction and relaxation of the canalis respectively. As the canalis egestorius was the most important part of the stomach as far as motility was concerned, inflammatory change here could be expected to produce serious disturbances in gastric motive function.

Golden (l937) agreed with Schindler et al. (l937) and other previous authors that in many cases of gastritis the change in the mucous membrane could not be demonstrated by radiology, and the condition could only be diagnosed by gastroscopy. In other cases, however, the canalis exhibited motility disorders which were readily apparent during the radiological examination; in some there was absence of contraction (absence of "antral systole"), while in others a greater or lesser degree of "antral" spasm was seen. The spasm could vary from marked contraction to failure of full relaxation of the canalis. Involvement of the deeper layers of the wall by inflammatory infiltration and fibrosis could hamper or prevent normal movements of the muscularis mucosae and consequently of the mucosal folds (Chaps. 2, 13); as a result the folds failed to change in direction as they normally did during antral systole, causing them to appear exaggerated. These features enabled Golden (l937) to make a radiological diagnosis of "antral gastritis and spasm" in appropriate cases. The prepyloric narrowing was sometimes associated with mucosal erosions which at that time were only demonstrable by gastroscopy or histological examination.

In histological studies of 100 partial gastrectomy specimens, Magnus (l946) found that inflammatory gastritis affecting the pyloric region consisted of two types. The first type, acute erosive pyloric gastritis, was characterized by polymorphonuclear infiltration of the mucosa, with lesser numbers of lymphocytes, plasma cells and eosinophils. The glandular epithelium showed degenerative changes, there was capillary hyperaemia with mucosal oedema, and erosions were visible on the surface. The typical erosion had the size of a pin's head and involved only the superficial part of the mucosa, i.e. it did not extend through the mucosa and muscularis mucosae into the submucosa; erosions varied in number from a few to over a hundred in individual cases. The second type, chronic atrophic gastritis, was characterized by atrophy of the glandular parenchyma, fibrosis in the mucosa and submucosa, intense infiltration of the interstitial tissue by plasma cells and lymphocytes, and intestinal metaplasia of the gastric epithelium. There was a transition from acute erosive to chronic atrophic pyloric gastritis, and the two types were sometimes found together.

MacDonald and Rubin (l967) found that gastric suction biopsy studies of gastritis had been disappointing; blind suction biopsy often missed the pyloric mucosal zone and specimens of pyloric mucosa were seldom obtained. Examination of the entire length of gastrectomy specimens by means of the Swiss roll technique afforded better results. For a variety of reasons the definition and classification of chronic gastritis remained unsatisfactory. Correlation between the radiological mucosal fold pattern and histological findings was poor.

Studies by Gear et al. (l97l), (Chap. 29), showed that ulcers of the body of the stomach were associated with more extensive and more severe gastritis than ulcers of the prepyloric region. In the latter gastritis was usually localized to the distal stomach, it was often superficial and showed little evidence of atrophic change or metaplasia. The fact that gastritis persisted in spite of healing of the gastric ulceration, indicated that it was the basic disease process and not simply a zonal change secondary to the ulcer. By means of fibreoptic gastroscopy Whitehead et al. (l972) obtained fresh, multiple full- thickness biopsy specimens from all parts of the gastric mucosa in a large number of patients. They proposed a classification of chronic gastritis applicable to all zones of the mucosa, based on the following features: First, the mucosal type had to be established, e.g. pyloric mucosa had to be differentiated from pseudopyloric metaplasia of body mucosa. Second, the grade had to be determined; chronic atrophic gastritis (in which there was atrophy of tubules) could be subdivided into mild, moderate and severe grades. Third, the stage of activity had to be established; both superficial and atrophic gastritis could be either active or quiescent. Fourth, the presence and type of metaplasia had to be determined; it was acknowledged that difficulties could arise in recognizing mucosal type when severe gastritis was associated with metaplasia or atrophy. In their classification the degree of atrophy, rather than the degree of chronic cellular infiltration, was graded. It was also established that intestinal metaplasia nearly always occurred in mucosa which was the site of atrophic gastritis.

Strickland and Mackay (l973) reviewed the nature of chronic atrophic gastritis in relation to the structure and function of the pyloric antrum, where "antrum" was equated with the pyloric mucosal zone. Two distinct types of atrophic gastritis were recognized. In Type A, tests for parietal cell autoantibody and intrinsic factor antibody were positive; there was sparing of antral mucosa, with diffuse changes in the corpus, and severe impairment of gastric secretion. In Type B, parietal cell autoantibody and intrinsic factor antibody reactions were negative; there was definite antral involvement with focal changes in the corpus, and moderate impairment of gastric secretion. Benign gastric ulceration of the corpus was found to be associated with Type B atrophic gastritis; the more proximally the ulcer was located in the stomach, the more extensive the gastritis and the more severe the impairment of acid secretion proved to be. Chronic atrophic gastritis persisted after ulcer healing, supporting the view that gastric ulcer originated from chronic gastritis.

Rao et al. (l975) stated that the term chronic gastritis carried different connotations for the clinician, the pathologist and the radiologist. Previously little attention had been given to determining the degree of chronic cellular infiltration involving the full thickness of the gastric mucosa. They supported the use of terms which described the morphological abnormalities found in mucosal biopsies, namely the degree of cellular infiltration of the whole mucosa and the presence or absence of atrophy. A simple descriptive classification of chronic gastritis into mild, moderately severe and severe grades, with or without atrophy or metaplasia, was recommended. Mucosal biopsies in 241 patients with a variety of upper abdominal conditions showed chronic gastritis in 184. Only 3 of the patients were diagnosed as true superficial gastritis, where the cellular infiltration was limited to the lamina propria between the pits.

Op den Orth and Dekker (l976) described erosions as superfical mucosal defects which did not penetrate the muscularis mucosae. A flat erosion was a mucosal defect without reaction in the adjacent parts, while a varioliform or complete erosion indicated a mucosal defect surrounded by an elevated zone; the elevated zone had been variously interpreted as a circular contraction of the muscularis mucosae, oedema, leucocytic infiltration, or fibrosis. It was pointed out that erosions could occur as solitary lesions or in combination with other upper gastro-intestinal pathology, e.g. gastric or duodenal ulceration; whether a gastric erosion itself ever developed into a gastric ulcer was controversial. Because of the raised zone surrounding it, an erosion could be visualized fairly easily with double-contrast radiography as a tiny, constant fleck of barium surrounded by a radiolucent halo; some erosions tended to be linear rather than circular. In some cases erosions in the prepyloric area were associated with prominent or irregular mucosal folds; the radiographic diagnosis of erosions was found to be reliable, and correlated well with their endoscopic demonstration.

Roesch (l978) pointed out that gastric erosions occurred very commonly and were often multiple. In the acute type the epithelial defect was not surrounded by inflammatory reaction, while the chronic type had an elevated, bulging border. Only the chronic type was detectable radiologically, presenting as a small fleck with a surrounding halo. Endoscopy showed that almost 60 percent of chronic erosions occurred in the antral region, and that they were often associated with prominent mucosal folds. Radiological demonstration of these bead-like prepyloric folds was highly suspicious of chronic erosions, even in the absence of a central punctate barium-filled depression. Where erosions were followed-up for 5 years or longer, the transformation of multiple antral erosions into hyperplastic folds could often be seen.

Morson and Dawson (l979) reiterated that the most accurate diagnosis of gastritis was made on biopsies taken under direct vision through a fibrescope. Their classification, which was made on histological grounds, entailed 3 types, namely chronic superfical gastritis, atrophic gastritis (both of which might be either active or quiescent), and gastric atrophy. Active superficial gastritis might be accompanied by small erosions. In atrophic gastritis the essential feature was not the increase in inflammatory cells in the lamina propria, but the reduction or atrophy of the deep glands, accompanied by intestinal metaplasia in the "antrum". Attention was drawn to the fact that in both superficial and atrophic gastritis, submucous fibrosis and thickening of the muscularis externa had been reported, giving rise to "antral" deformity which was recognizable radiologically.

Freise et al. (l979) did four year follow-up studies in 64 patients with gastric erosions. The most common site of multiple erosions was the "antral" region. Erosions were frequently seen in combination with other upper gastrointestinal conditions such as gastric or duodenal ulceration or hiatus hernia. In 10 percent of cases chain-like multiple erosions developed into a persistent, prominent gastric mucosal fold, usually in the "antrum". When such a fold was seen, it could be taken to be the result of a chain of erosions. There was no evidence that erosions led to chronic gastric ulceration, polyps or malignancy.

Karvonen et al. (l983) classified erosions according to their endoscopic morphology. In the complete type there was a surrounding elevated border; incomplete or flat erosions were surrounded by a red halo, and haemorrhagic erosions were punctate bleeding spots. In 86 percent of 117 patients with gastric erosions (but without other upper gastrointestinal pathology), the lesions occurred only in the antral or prepyloric part of the stomach, and in the majority of patients presented as multiple erosions. Some showed features of both the complete and incomplete types, and were characterized by their location on prominent prepyloric mucosal folds. Nesland and Berstad (l985) noted a specific endoscopic appearance, consisting of standing prepyloric mucosal folds, redness and erosions, in a considerable number of patients presenting with dyspepsia; they called the condition erosive prepyloric changes (EPC) and divided it into three grades on the basis of the endoscopic features. In grade 1 there were standing mucosal folds, independent of peristalsis, running either transversely or longitudinally in the "antral" lumen. In grade 2 the same appearance was seen with red spots or streaks situated on top of the folds. In grade 3 the previous 2 appearances were associated with macroscopic erosions, described as white, fibrin-covered spots with red halos. EPC grades 2 and 3 were found in 26 percent of 1001 consecutive patients examined endoscopically. After excluding all patients with ulcer, carcinoma, post- operative conditions and upper gastro-intestinal bleeding, a group of 651 patients with non-ulcer dyspepsia remained; EPC grades 2 or 3 were seen in 210. In a group of 34 asymptomatic volunteers, grade 2 was found in 5 cases and grade 3 in one case. The frequency of grades 2 and 3 of erosive prepyloric changes appeared to be higher in non- ulcer dyspepsia than in patients with peptic ulceration and also varied with age. The highest frequency encountered was 52 percent, in patients with non-ulcer dyspepsia in the 40 to 49 year age group. The entity prepyloric erosive changes probably represented a form of antral gastritis. It might have a bearing on the radiological diagnosis of antral gastritis. Although the redness and often also the erosions were not visible radiologically, the permanent and coarse mucosal folds should be evident.

Berstad and Nesland (l985) stated that the three grades of EPC were merely different expressions of the same process. While the superficial mucosal state might regress or progress to another grade, the prominent, standing prepyloric mucosal folds were of a permanent nature. Histological verification was obtained in 88 percent of cases of endoscopically visible grade 3 erosions; they were always accompanied by an element of acute inflammation with infiltration of neutrophil polymorphs. In the vast majority there was an additional chronic inflammatory infiltration of lymphocytes and plasma cells. Intramucosal fibrosis was present in all biopsy specimens. Clinically, EPC appeared to be related to non-ulcer dyspepsia. The symptoms could be suggestive of gastric ulcer, while endoscopy proved the absence of ulceration. The findings supported the theory that EPC was a disease entity of its own, to be differentiated from ulcer disease. The permanent feature of the condition, namely standing mucosal folds, was independent of the ongoing inflammatory activity in the surface layer; whether contractions in the deeper muscular layers contributed to the fold formation was not known.

Berstad and Nesland (l987) reiterated that EPC was an endoscopic diagnosis based on the presence of standing prepyloric folds, with or without different types of erosions. Standing folds were defined as transverse or parallel folds in the prepyloric region, which might run into the pylorus itself and which were independent of peristaltic movements. They did not believe that EPC and peptic ulceration were aspects of the same disease process; EPC could not be considered to be merely a form of antral gastritis.

Hojgaard et al. (l987) pointed out that clinicians, endoscopists and pathologists defined gastritis in different ways. Pathoanatomical gastritis occurred very commonly and the prevalence increased with age. These authors found no correlation between dyspepsia (in patients without peptic ulceration) and endoscopic signs suggesting gastritis, or histological gastritis. It was concluded that gastritis did not seem to constitute a clinical entity in non-ulcer dyspepsia.

Karvonen et al. (l987) studied 130 patients with gastric mucosal erosions, occurring in the absence of peptic ulceration, by endoscopic biopsy; most were located in the "antrum". In their view erosions were inconsistent phenomena, probably with different pathogeneses and etiologies. Some incomplete erosions were associated with abuse of analgesics, but those located on prepyloric mucosal folds appeared to be associated with duodenal ulceration or duodenitis. The study suggested that prepyloric erosions constituted an entity of their own; in most instances the mucosa of the corpus was well preserved despite ageing, the appearance being similar to that of duodenal ulcer disease.

Present Investigations #

Patients and Methods #

During routine upper gastrointestinal barium examinations, a presumptive radiological diagnosis of "antral gastritis" was made from time to time. Most of these patients subsequently had endoscopic investigations (unfortunately biopsies were not taken in all). After a suitable interval the patients' clinical notes were perused and a final diagnosis obtained.

A total of 50 cases who were diagnosed radiologically, and confirmed endoscopically, as chronic "antral" gastritis were studied. The following are examples of the more pronounced cases:

Case Reports #

Case 28.1. G.G., 52 year old male. Radiographic examination showed a moderate degree of constant contraction of the pyloric sphincteric cylinder, with absence of normal, cyclical contraction and relaxation; the contraction fixed the pyloric aperture in the open position (Fig. 28.1). The stomach appeared to be hypertonic; rapid emptying of fluid barium occurred. Endoscopic biopsy of the "antral" region revealed acute on chronic gastritis; no evidence of malignancy was seen. Repeat endoscopic biopsy two months later showed acute on chronic inflammatory reaction in the lamina propria, with eosinophylic infiltration and without evidence of intestinal metaplasia. Stainings for Helicobacter pylori were positive. A third endoscopic biopsy two months after the second, showed chronic gastritis with intestinal metaplasia. Stainings for Helicobacter pylori were negative.

Fig. 28.1. Case G.G. Moderate degree of constant contraction of pyloric sphincteric cylinder (arrows). Cyclical activity absent. Pyloric aperture patent

Case 28.2 J.C., 63 year old male, was a know case of ethanol abuse and liver cirrhosis. Radiographic examination showed a marked degree of constant contraction of the pyloric sphincteric cylinder, which contained prominent, irregular, immobile mucosal folds (Fig. 28.2 A-D).





`Fig. 28.2 A-D. Case J.C. Constant contraction of sphincteric cylinder with absent cyclical activity. Irregular, immobile folds in cylinder`

Peristaltic waves were normal in the remainder of the stomach, but stopped abruptly at the commencement of the cylinder, which showed total absence of cyclical contraction and relaxation. Endoscopy revealed chronic "antral" gastritis; a few small erosions were noted in the first part of the duodenum.

Case 28.3 L.M., 50 year old female. Radiographic examination showed pronounced, constant contraction of the pyloric sphincteric cylinder; occasionally a minor degree of relaxation occurred, but cyclical contraction and relaxation was absent and most of the time the appearance remained as illustrated (Fig. 28.3). Prominent circular and irregular mucosal folds which appreared to be immobile, were present in the contracted cylinder. A concave indentation was seen in the base of the duodenal bulb. Endoscopy revealed a number of mucosal erosions as well as an appearance of severe "antral" gastritis. This was still present at a second endoscopy 8 months later, indicating chronicity.

Fig. 28.3. Case L.M. Constant contraction of sphincteric cylinder (arrows), with prominent irregular, static mucosal folds

Case 28.4 C.C., 36 year old female. Radiographic examination showed the pyloric sphincteric cylinder to be markedly contracted most of the time; at such times it contained longitudinal mucosal folds (Fig. 28.4A). Occasionally it relaxed to a certain extent, when a fold changed in direction to become circular (Fig. 28.4B); relaxation was never complete and cyclical activity was absent. Endoscopy revealed an erosion on the lesser curvature side of the pyloric region; touching the mucosa caused haemorrhage. The endoscopic diagnosis was erosive antral gastritis.


A
`Fig. 28.4. A Case C.C. Marked contraction of sphincteric cylinder, with longitudinal mucosal folds B Case C.C. Some relaxation of cylinder. A mucosal fold has changed in direction to become circular. Cyclical activity absent`	B

Case 28.5 J.M., 45 year old male. The pyloric sphincteric cylinder remained partially contracted throughout the radiographic examination, with complete absence of normal, cyclical contraction and relaxation. At least one prominent, circumferential mucosal fold, which did not change in position, was present in the partially contracted cylinder (Fig. 28.5). Initially it was difficult to distinguish between a permanent, circumferential mucosal fold and a prepyloric septum. Endoscopy revealed prominent, thickened prepyloric mucosal folds with an abnormal, whitish, granular surface. Endoscopic biopsy showed lymphocytic and plasma cell infiltration of the lamina propria; in some areas atypical epithelium, presumably due to inflmmatory change, was seen. The endoscopic diagnosis was chronic "antral" gastritis.

Fig. 28.5. Case J.M. Partial contraction of sphincteric cylinder, with absent cyclical activity. Prominent static, circular mucosal fold in cylinder (arrow)

Discussion #

A brief review of the literature shows that many aspects of gastritis are still controversial; even its definition is contentious. It has been stated that clinicians, pathologists and endoscopists defined "gastritis" in different ways (Hojgaard et al. l987). Others held that the term "chronic gastritis" had different connotations for the clinician, the pathologist and radiologist (Rao et al. l975). Authors differ on the subdivision of gastritis into various types and grades. It is agreed, however, that the diagnosis in the intact stomach can only be made by means of endoscopy, biopsy and microscopy. As the deeper layers of the wall are also involved in many instances, a full investigation would entail histologic examination of resection specimens.

The cases quoted here show that certain radiologically recognizable alterations may be associated with chronic "antral" gastritis, perhaps more correctly termed chronic gastritis affecting the pyloric sphincteric cylinder. (One of the cases was diagnosed as erosive haemorrhagic gastritis). The radiologically recognizable alterations are:

Partial but constant contraction of the sphincteric cylinder; the degree of contraction was usually described as "moderate" or "marked". In these cases radiologically visible peristaltic waves in the corpus and sinus of the stomach appeared normal, but each wave stopped at the commencement of the partially contracted cylinder. In some cases the cylinder showed minor degrees of contraction and relaxation, but maximal cyclical contraction and relaxation at a rate of 3 cycles per minute was absent in all. The appearance closely resembles that of pylorospasm (Chap. 20).
In some cases the pyloric aperture was seen to be fixed in the open position as a consequence of partial contraction of the cylinder; this appearance may be associated with duodenogastric reflux (Chap. 27). It is presumed that the lack of cyclical activity of the cylinder may have a bearing on trituration and the emptying of solids (Chap. 18).
Prominent irregular and/or circular mucosal folds showing restricted movements or no movement at all. In view of the restricted movements of the walls of the cylinder it is not surprising that "independent but co-ordinated" movements of the inner mucosal layer should also be curtailed or absent (Chaps. 2, 13). It is surmized that cellular infiltration in the mucosa, submucosa, muscular layers and neuronal elements occurring in chronic gastritis, partially accounts for the restricted movements.
Theoretically the static, irregular mucosal folds projecting into the lumen should hamper duodenogastric reflux occurring as a result of patency of the pyloric aperture in some cases.
A presumptive radiological diagnosis of chronic gastritis affecting the sphincteric cylinder, was only made if the above features occurred in the absence of other pathology in the upper gastrointestinal tract (e.g. gastric ulceration or hiatus hernia).
According to Nesland and Berstad (l985) and Karvonen et al. (l987), erosive prepyloric change (EPC) was a condition characterized by standing mucosal folds and erosions; it was diagnosed endoscopically and appeared to be an entity of its own. Radiographically a standing mucosal fold may also be recognized, as seen in Fig. 28.5. In this case it concerned a circular fold which failed to change in position. It was associated with lymphocytic and plasma cell infiltration, no mention being made of erosions.

References #

Berstad A, Nesland AA. Prepyloric erosions and related changes: review. Scand J Gastroenterol l985, 20, 779-782.
Berstad A, Nesland AA. Erosive prepyloric changes: a new entity. Scand J Gastroenterol l987, 22, Suppl 128, 94-100.
Forssell G. Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr l913, Suppl 30, 1-265.
Freise J, Hofmann R, Gebel M, et al. Follow-up study of chronic gastric erosions. Endoscopy l979, 11, 13-17.
Gear MWL, Truelove SC, Whitehead R. Gastric ulcer and gastritis. Gut l97l, 12, 639-645.
Golden R. Antral gastritis and spasm. J Amer Med Assoc l937, 109, 1497-1500.
Holsti O. On the condition of the intramural ganglia in the stomach in cases of gastritis. Acta Med Scand l93l, 76, 316-342.
Holsti O. On the nature of the pylorus affections which simulate ulcus. Acta Med Scand l93l, 76, 343-393.
Hojgaard L, Matzen P, Christoffersen P. Gastritis: a clinical entity? Scand J Gastroenterol l987, 22, Suppl 128, 90-93.
Karvonen AL, Sipponen P, Lehtola J, et al. Gastric mucosal erosions: an endoscopic, histological and functional study. Scand J Gastroenterol l983, l8, 1051-1056.
Karvonen AL, Kekki M, Lehtola J, et al. Prepyloric erosions: an entity of its own among erosive gastric lesions. A morphologic and dynamic study of gastric mucosa in patients with gastric erosions. Scand J Gastroenterol l987, 22, 1095-1101.
MacDonald WC, Rubin CE. Gastric biopsy: a critical evaluation. Gastroenterology l967, 53, 143-170.
Magnus HA. The pathology of simple gastritis. J Path Bact l946, 58, 431-439.
Morson BC, Dawson IMP. Gastrointestinal Pathology. Blackwell Scientific Publications, London 2nd ed, l979, p 91.
Nesland AA, Berstad A. Erosive prepyloric changes in persons with and without dyspepsia. Scand J Gastroenterol l985, 20, 222-228.
Op den Orth JO, Dekker W. Gastric erosions: radiological and endoscopic aspects. Radiol Clin l976, 45, 88-99.
Rao SS, Krasner N, Thomson TJ. Chronic gastritis: a simple classification. J Path l975, 117, 93-96.
Roesch W. Erosions of the upper gastrointestinal tract. Clin Gastroenterol l978, 7, 623-634.
Schindler R, Ortmayer M, Renshaw JF. Chronic gastritis. J Amer Med Assoc l937, l08, 465-468.
Strickland RG, Mackay IR. A reappraisal of the nature and significance of chronic atrophic gastritis. Amer J Dig Dis l973, 18, 426-440.
Whitehead R, Truelove SC, Gear WML. The histological diagnosis of chronic gastritis in fibreoptic gastroscope biopsy specimens. J Clin Path l972, 25, 1-11.

29 - Gastric Ulceration and the Pyloric Sphincteric Cylinder

Mon, 01 Jan 0001 00:00:00 +0000

Gastric Ulceration and the Pyloric Sphincteric Cylinder #

Johnson (l957, 1965) and Johnson et al. (l964) held that gastric ulcers should not only be classified anatomically according to their distance from the pylorus, but also in accordance with their associated acid-secretory or patho-physiological characteristics. While most gastric ulcer patients were acid hyposecretors, some were moderate and others hypersecretors of acid. On this basis the following 3 types of gastric ulcers were recognized: Type I consisted of those cases in whom the ulcer was situated to the left of and above the gastric angulus (the angulus being defined as the lowest point of the lesser curvature), without macroscopic abnormalities of the prepyloric region, the pylorus or duodenum; these cases were associated with a low level of acid secretion and possibly hyposecretion of mucus. Type II consisted of those cases in which a gastric ulcer to the left of the angulus was associated with, and probably secondary to, an ulcer or its scar in the pylorus or duodenum; these patients were moderate and sometimes hypersecretors of acid. Type III included all gastric ulcers on or near the pylorus, and might be combined with a duodenal ulcer or a Type II gastric ulcer proximally; these patients usually had hypersecretion of acid. Type III was subdivided as follows: (1) ulcers within one inch (2.54 cm) of the pylorus, called true prepyloric ulcers; (2) ulcers to the right of the angulus but further than 2.54 cm from the pylorus, called "other antral" ulcers. It was concluded that gastric ulcers near the pylorus and those occurring with a duodenal ulcer should be looked upon as a disease of acid hypersecretion; in these cases there was a marked blood group O predominance, the ulcers nearest the pylorus carrying the highest proportion of blood group O. Gastric ulcers in the body of the stomach, occurring in patients in whom the duodenum was normal, were usually characterized by acid hyposecretion; in these patients there was no evidence of group O preponderance, but in fact an excess of blood group A. The findings showed that the pathogenesis differed in different types of gastric ulcers.

In their endoscopic studies of the mucosal morphology in 200 patients with chronic gastric ulceration, Stadelmann et al. (l97l) classified the ulcers according to their anatomical location, i.e. whether they were situated in the "prepyloric antrum", at the angulus, in the middle of the body or in the subcardial region. A close relationship existed between the location of the ulcer and the maximal acid secretion. Ulcers of the "prepyloric antrum" were similar to duodenal ulcers, having hyperchlorhydria, while those at the angulus had normochlorhydria and subcardial ulcers had hypochlorhydria. It was concluded that the maximal acid output decreased the farther the ulcer was away from the pylorus.

In an extensive review Brooks (l985) divided chronic, benign, recurrent gastric ulcers into the following subgroups: (1) corpus or fundus ulcers; (2) antral or prepyloric ulcers; (3) pyloric channel ulcers; (4) a combination of any of the above with duodenal ulceration; (5) ulcers resistant to healing under treatment.

In view of the fact that the present investigation is primarily concerned with the muscular anatomy of the stomach and motility, we divided gastric ulcers into 2 types, viz. those situated proximally to the pyloric sphincteric cylinder and those occurring within the cylinder, i.e. within 3.0 cm to 4.0 cm of the pyloric aperture.

Gastric Ulceration Proximal to the Pyloric Sphincteric Cylinder #

In a radiological investigation of 200 patients with large, chronic benign gastric ulcers on the lesser curvature of the pars media, Steigman (l943) found associated "antral spasm" (which he equated with pylorospasm) in a small percentage of cases. At times the spasm was persistent and quite marked, the whole "antrum" distal to the ulcer being contracted throughout the examination. (Comment: On accompanying illustrations it appears if the "antral spasm" is limited to the pyloric sphincteric cylinder).

Lilja (l953, l954) pointed out that in cases of ulceration at the incisura angularis, associated changes in the pyloric part of the stomach were not unknown but had not been subjected to a systematic analysis. In his radiological investigations Lilja found that gross ulceration at the incisura was usually associated with an impairment of gastric motility in the distal stomach, consisting of altered peristalsis with dilatation of the sinus. Of 21 cases with a large ulcer at the incisura, radiological examination showed dilatation of the sinus in 18; in 4 cases in which the ulcer was smaller, the sinus was not dilated. In some of these cases the appearance of the canalis egestorius (i.e. the pyloric sphincteric cylinder) also deviated from the normal, showing a cylindrical contraction in several. In others it contained irregular and oblique mucosal folds, while its contractions were atypical and occurred at infrequent intervals. At times there was a non-characteristic functional impairment of the canalis with the pylorus remaining widely patent.

Histological examination in one of these cases showed chronic inflammatory changes in the mucosa of the canalis with infiltration of plasma cells and hyperplasia of lymph follicles. Another case showed follicular and antral gastritis. In all cases destruction of the muscularis externa, with fibrous replacement, was seen at the site of the ulcer (at the incisura). Lilja (l953, l954) concluded that in cases of ulceration at the incisura angularis, associated changes were frequently seen in the canalis egestorius. The most common appearance was a more or less permanent contraction of the canalis of varying severity, resembling adult hypertrophic pyloric stenosis (AHPS) in the most pronounced cases. Lilja (l959) subsequently stated that the changes in the canalis were so common that they had to be regarded as an inherent part of the radiological appearance in cases of deep ulceration at the incisura. In some cases it was found that the contraction of the canalis persisted for periods of 2 to 4 years after healing of the ulcer. In their description of 6 cases of AHPS, Skoryna et al. (l959) included one case in which pyloric muscular hypertrophy was associated with a lesser curvature gastric ulcer situated 6.0 cm orally to the pylorus (Chap. 24). The muscular hypertrophy involved the canalis egestorius as described by Torgersen (l942). It was surmized that the pyloric hypertrophy was probably the primary lesion.

Knight (l961) described a case of a 37 year old male in which a benign gastric ulcer, 6.0 cm proximal to the pylorus, was associated with AHPS (Chap. 24). The area of muscular hypertrophy was 2.5 cm in length and the walls measured 1.5 cm in thickness, i.e. it appeared to be a typical case of AHPS limited to the pyloric sphincteric cylinder. Whether there was a causal relationship between the gastric ulcer and the pyloric hypertrophy was not clear. (Two other cases of AHPS described by Knight were not associated with gastric ulceration). According to him it was likely that the gastric ulcer was the result rather than the cause of the AHPS. This was consistent with the experimental findings of Dragstedt et al. (l954), who had previously produced gastric ulceration in dogs by occluding the pylorus.

Burge et al. (l963) described 2 adult cases in each of which a benign gastric ulcer situated high on the lesser curvature was associated with what they called the "pyloric channel syndrome". In one case radiography showed a narrowed pyloric �antrum� suggesting malignancy, while operation revealed severe benign organic stenosis of the pyloric area with a tiny eccentric aperture. In the second case, in which radiography showed tapering of the prepyloric stomach and deformity of the duodenal cap (in addition to the high gastric ulcer), microscopic examination of the resection specimen revealed unilateral pyloric muscle hypertrophy with small round-cell infiltration and fibrosis. It was thought that the pyloric channel syndrome, with associated gastric stasis, was the probable cause of the gastric ulceration in these cases.

During histological examination of resection specimens in 37 cases of chronic gastric ulceration, Du Plessis (l963) found associated atrophic gastritis of the whole of the pyloric gland area in 62 percent of cases, and of half the pyloric gland area in 92 percent. (Comment: In cases of gastric ulceration the pyloric glandular zone may be more extensive than in normal controls as described in Chapter 5).

Garret et al. (l966) studied antral contraction waves by means of small water-filled balloons placed in the "distal antrum" in normal controls and 13 patients with benign gastric ulceration. In 10 of the patients the ulcer was situated at or below the incisura angularis but orally to the pyloric region. The amplitude and duration of Type II waves were similar in health and gastric ulcer patients, but there was a significant reduction in the number of these waves in the ulcer group. Normal motility patterns were obtained after the ulcer had healed. It was concluded that the gastric ulcer had a secondary effect on motility; there could be an interruption between action potentials and the contractile mechanism of antral smooth muscle.

Schrager et al. (l967) performed histological studies of the "antrum" in 40 resection specimens obtained from cases of gastric ulceration. In 31 cases the ulcer was situated at a distance of 5.0 cm to 10.0 cm proximal to the pylorus; in 5 cases it was at a distance of 2.5 cm to 5.0 cm, and in 4 cases at a distance of 0 cm to 2.5 cm from the pylorus. While a zone of gastritis surrounded the ulcer in all instances, the main inflammatory changes were found in the "antrum". These consisted of widespread destruction of pyloric glands, intestinalization, and in a few cases complete mucosal atrophy, usually associated with marked fibrosis in the submucosa. In 7 stomachs (it is not clear what the exact situation of the ulcer was in these cases) the changes had been severe enough to produce stenosis of the "antrum". Schrager et al. (l967) quoted a number of previous authors who had found that the inflammatory changes of gastritis in cases of gastric ulceration were confined to the "antrum". These changes were much more intense in cases of gastric ulceration than in duodenal ulceration; while intestinal metaplasia was uncommon in duodenal ulceration, it was frequently encountered in cases of gastric ulcer. Most previous authors held the view that the inflammatory changes preceded the ulceration, and that the inflammation of the antrum was the more fundamental change.

Kwong et al. (l970) studied the electrical activity in the distal 6.0 cm of the "antrum" in patients with gastric ulceration by means of serosal electrodes implanted at operation and mucosal electrodes introduced via nasogastric tubes. Recordings in 12 control subjects showed a wave frequency of 3 cycles per minute; there was a significantly higher frequency in 8 patients with gastric ulceration. The amplitude of the waves, the shape of the wave forms and the conduction time of the electrical impulses were the same in the two groups.

Gear et al. (l97l) pointed out that gastric ulcer was frequently associated with chronic gastritis, but that the relationship between the two was controversial. Some previous studies had suggested that gastritis was the primary change, with the gastric ulcer supervening; other studies had indicated that the ulcer was the primary lesion with gastritis an accompanying zonal change. Features of the gastritis associated with chronic benign gastric ulcer in 35 untreated cases were studied by means of fibreoptic gastroscopy and biopsy; there were 14 prepyloric ulcers and 21 in the body of the stomach. Biopsies were taken in the prepyloric area, from the middle of the lesser curvature, from the high lesser curvature and the middle of the greater curvature. A marked difference in the distribution and severity of the gastritis in the two subgroups was found, the changes being more severe and more extensive in ulcers of the body of the stomach. In general, there was a tendency for the more severe atrophic changes to be found distally in the "antrum" and on the lesser curvature, while the greater curvature was least affected. Another group of 28 patients with gastric ulceration had a gastroscopy before and after medical treatment. In most cases biopsy specimens from the second examination showed a similar, or worse, grade of gastritis than those from the first. In a third group of patients, in whom the gastric ulceration had been treated by vagotomy and pyloroplasty, the atrophic gastritis and intestinal metaplasia commonly became worse after surgery.

Gear et al. (l97l) concluded that the gastritis associated with chronic gastric ulcer was regional, with the distal part of the stomach and midpart of the lesser curvature the most severely affected. Ulcers of the body of the stomach were associated with more extensive and more severe gastritis than ulcers of the prepyloric region. It was felt that gastritis was the basic disease process with gastric ulceration a secondary phenomenon. Lawson (l972) studied the antral mucosa by means of gastroscopy and biopsy in 25 patients with gastric ulceration "in the usual position" along the lesser curvature. (Comment: It appears if the ulcers were situated a considerable distance proximally to the pyloric aperture). The biopsies were taken at a point half-way between the ulcer and the pyloric aperture, in an area in which the antral mucosa appeared normal macroscopically. In 10 cases the surface epithelium, pyloric glands and mitotic activity were normal. In the remaining 15 cases marked histological changes were seen, with chronic atrophic gastritis in 7 and increased mitotic activity in 8. The findings supported the view that a diffuse mucosal lesion of the "antrum" was associated with gastric ulceration situated proximally to the antrum. It was not clear whether the gastritis or the gastric ulcer was the primary event.

Fisher and Cohen (l973) studied pyloric sphincter pressures in 10 patients with gastric ulceration, both before and after healing, and in 10 normal control subjects. (Comment: The pyloric ring was equated with the sphincter). The ulcer was situated high on the lesser curvature in 1 case, on the middle of the lesser curvature in 4, in the prepyloric region in 3 and in the "pyloric channel" in 2. Intraluminal pressures were determined by means of an open-tipped, 5-lumen catheter assembly, with all patients in the right lateral decubitus position. It was found that the gastroduodenal junction of patients with an active gastric ulcer was characterized by a zone of high pressure similar to that in normal subjects. The pyloric pressure in patients with gastric ulcer was 4.2 ± 0.9 mm Hg as compared to 6.2 ±: 1.3 mm Hg in normal subjects. Duodenal acidification in normal subjects increased the pyloric pressure to 25 mm Hg, but had no effect in patients with active gastric ulceration. Intravenous administration of secretin and cholecystokinin gave similar results. The studies suggested pyloric sphincter dysfunction in patients with gastric ulceration, probably leading to increased duodenogastric reflux. As similar findings were obtained after healing, it appeared unlikely that gastric ulceration was the cause of the pyloric incompetence. (Comment: The results of manometric studies in normal subjects by Fisher and Cohen are discussed in Chap. 15). Fisher and Boden (l975) subsequently reported that pyloric sphincter dysfunction could be reversed by gastric acidification, but that the mechanism of the dysfunction remained unclear.

Liebermann-Meffert and Allgöwer (l977) pointed out that while the factors leading to gastric ulceration were not fully understood, some abnormality of the pylorus, e.g. antral stasis or duodenogastric reflux, had been implicated. In an attempt to elucidate the problem, detailed studies of anatomical changes in the pyloric region were performed in 77 surgical resection specimens of patients with gastric ulceration. In 10 the ulcer was immediately adjacent to the pylorus ("pyloric ulcers") while in 67 it was situated in other parts of the stomach ("non-pyloric ulcers"); the findings were compared with those of 50 control subjects. While all controls had a soft antropyloric wall, considerable patchy induration of the wall was felt in 41 of 54 gastric ulcer specimens. The pyloric diameter in controls had a range of 15 mm to 22 mm; in the ulcer specimens the range was 10mm to 22 mm. In 22 of 45 ulcer specimens the pyloric ring was smaller than the lower limit of normal, and bouginage was found to be difficult as the ring was more rigid than in controls, although it had not caused obstruction.

According to Liebermann-Meffert and Allgöwer (l977) the pyloric and prepyloric musculature was of uniform thickness in control subjects, while nodular or fusiform muscular thickening, often involving only part of the circumference, was frequently found in ulcer specimens (Chap. 25). In 9 of these cases the muscular hypertrophy was circular, involving the whole pyloric ring uniformly. In all cases considerable fibrosis was seen in the thickened musculature. Diffuse submucosal thickening, probably due to a combination of oedema and connective tissue hypertrophy, was found in the ulcer cases, and the mucosa often appeared coarse and roughened. The number of Auerbach's plexuses and the corresponding number of nerve cells was significantly reduced in cases of gastric ulcer, being only half that seen in controls. All the changes occurred in the antropyloric wall irrespective of the site of the ulcer. It was concluded that the thickness of the gastric wall at the pylorus and in the distal 5.0 cm of the "antrum", was increased in patients with gastric ulcer. Although the mucosa, submucosa and muscular layers were affected, the changes were most marked in the latter. Muscle hypertrophy was not necessarily uniform, was usually associated with fibrosis, and histological abnormalities of the muscle cells were common. The intramural ganglia were markedly reduced in number and those which were present commonly showed abnormal nuclei. Since the muscle and ganglia were involved in normal motility, it was reasoned that the above features were consistent with a disturbance of normal physiological mechanisms at this site. Whether this was a cause or the consequence of duodenogastric reflux, or whether it formed a link in the chain of events leading to gastric ulceration, remained uncertain.

In 8 cases in whom a gastric ulcer was situated on the lesser curvature or anterior gastric wall, Meister et al. (l979) found histologically verified chronic atrophic gastritis and intestinal metaplasia with mild or moderate dysplasia in all. These mucosal changes were especially prominent in the proximal regions of the resection specimens.

Liebermann-Meffert et al. (l98l) found that intraoperative electrical stimulation of the vagal trunks caused a distinct intragastric pressure rise in patients with gastric ulcer, duodenal ulcer, combined gastric and duodenal ulcer, and in non-ulcer controls. However, the amplitude, duration and integrated motor response in the stomach was significantly greater in the patients with gastric ulcer than in the other groups. It was concluded that gastric ulceration did not cuase hypomotility of the gastric reservoir (i.e. the corpus and fundus), but that it was probably associated with a disturbance of the antral pump mechanism. The intrinsic morphological alterations of the antropyloric wall could render antral contractions less effective, leading to impaired gastric drainage and stasis. In a further study of the pathomorphology of the antropyloric wall in peptic ulcer disease, Liebermann-Meffert and Allgöwer (l98l) found that abnormalities of the muscle fibres and Auerbach's plexuses, and the replacement of contractile muscular tissue by fibrous tissue, might impair antropyloric motor function, having a bearing on gastric emptying and duodenogastric reflux. The changes were always more severe in gastric than in duodenal ulceration, and did not occur in controls. While the pyloric aperture was somewhat rigid to distension in all peptic ulcer patients, its mean diameter was not significantly smaller than in controls and there was no stenosis of the pyloric ring which could account for gastric stasis.

Miller et al. (l980) pointed out that while patients with Type I gastric ulcers had less acid in their stomachs than normal controls, it was debatable whether this indicated actual hyposecretion, or whether it was due to increased back-diffusion of hydrogen ions across the mucosal barrier, or to neutralization by refluxed duodenal contents. In a study of 7 patients with chronic benign gastric ulceration above the incisura, it was found that gastric acid output in response to an ordinary solid-liquid meal was significantly less than in normal controls. In the patient group the emptying rate of solids was consistently lower than in controls while emptying of liquids remained normal. The gastric ulcer patients also had increased intragastric bile acid concentrations.

In his review Brooks (l985) found that a gastric ulcer in the corpus was usually associated with hyposecretion of acid and pepsin, decrease in the "antral" gastrin content, reduced amplitude of "antral" contractions, an incompetent pylorus, increased bile reflux, and delayed emptying of solids.

We have noted that gastric ulcers in the more proximal parts of the stomach were sometimes associated with contraction or motility disturbances of the pyloric sphincteric cylinder. The following are representative cases:

Case Reports #

Case 29.1 C.W., 60 year old male, presented with intermittent epigastric pain and malaena. Radiographic examination showed a gastric ulcer, 2.5 cm in diameter, in the posterior wall of the upper corpus, approximately 10 cm proximal to the pylorus; the features were those of a benign ulcer. There was constant contraction (or spasticity) of the pyloric sphincteric cylinder, the contracted region being 3.0 to 4.0 cm in length (Fig. 29.1). Cyclical contraction and relaxation of the cylinder, normally occurring at a rate of 3 cylces per minute, was absent; the contraction of the cylinder "fixed" the pyloric aperture in the open or patent position. Mucosal folds in the contracted cylinder appeared normal, but their movements were restricted. A shallow, concave identation of the base of the duodenal bulb, caused by the pyloric ring, was evident. Peristaltic waves in the remainder of the stomach were normal; emptying of liquid barium appeared normal. Two weeks later a Billroth I partial gastrectomy confirmed the large, chronic gastric ulcer. No macroscopic abnormality was seen or felt in the pyloric region. Histology of the ulcer proved it to be benign; microscopic examination of the pyloric region was not carried out.



`Fig. 29.1 A-D. Case C.W. Constant contraction or spasticity of pyloric sphincteric cylinder. Cyclical activity absent. Pyloric aperture "fixed" in patent position (B-D)`

Case 29.2 I.H., 59 year old male, presented with longstanding epigastric pain and malaena. Radiographic examination showed a large ulcer in the posterior wall of the midcorpus. Endoscopic biopsy confirmed the ulcer; the gastric mucosa showed intestinal metaplasia with prominent acute and chronic inflammatory cells, diagnosed as subacute gastritis. No evidence of malignancy was found. After anti-ulcer therapy the patient was temporarily lost to follow-up, but reappeared three years later. Radiographic examination showed the following: after the first two mouthfuls of barium a large ulcer on the posterior wall of the corpus was evident as before (Fig. 29.2A). Before barium entered the duodenum a constant, deep spastic incisura was seen in the pyloric region of the distal greater curvature; swallowing more barium showed it to be due to contraction of the left pyloric loop (Fig. 29.2B). The pyloric sphincteric cylinder between the left loop and the pyloric aperture remained partially contracted, normal cyclical contraction and relaxation being absent. The pyloric aperture remained patent and emptying of fluid barium appeared normal; the appearances were unchanged throughout the examination.

Further treatment followed. Radiographic examination 18 months later showed the ulcer, the prominent contraction of the left pyloric loop and contraction of the remainder of the cylinder to be unchanged (Fig. 29.2C). Endoscopic biopsy confirmed the previous findings. Radiographic examination and endoscopic biopsy after another 5 years showed no change. Billroth II partial gastrectomy confirmed the presence of a large, chronic, benign gastric ulcer on the posterior wall of the corpus; it had penetrated into the pancreas. No organic lesion was seen or felt in the pyloric region.


`Fig. 29.2 A,B. A Case I.H. Large gastric ulcer posterior wall of corpus (open arrow). Deep spastic incisura distal greater curvature (curved arrow). B Case I.H. The spastic incisura is caused by constant contraction of the left pyloric loop (curved arrow).`



`Fig. 29.2 C-F Case I.H. Eighteen months later the gastric ulcer (open arrow), contraction of the left pyloric loop (curved arrow) and contraction of the sphincteric cylinder are unchanged`

Case 29.3 V.D., 30 year old male, complained of epigastric pain not responding to antacids. Radiographic examination showed a gastric ulcer 1.5cm in diameter, on the lesser curvature at the angulus (Fig. 29.3A); no signs of malignancy were seen. Intially there was marked contraction of the pyloric sphincteric cylinder, which contained a few prominent mucosal folds; this was associated with delay in emptying of liquid barium. After barium had filled the cylinder, it was seen to remain contracted throughout the examination; although a minor degree of relaxation occurred occasionally, the apperances remained as illustrated most of the time, with absence of cyclical activity (Fig. 29.3B). Longitudinal mucosal folds were evident in the contracted cylinder. Endoscopic biopsy showed a benign looking gastric ulcer in the corpus. Microscopically there was mixed inflammatory cell infiltration, diagnosed as acute on chronic gastritis. No evidence of malignancy was seen. Repeat endoscopy 2 months later showed that the ulcer had healed.


A
`Fig. 29.3. A Case V.D. Gastric ulcer on lesser curvature at angulus (open arrow). Marked contraction of sphincteric cylinder (filled arrow). B Case V.D. Gastric ulcer at angulus (open arrow). Constant contraction of sphincteric cylinder (filled arrows) with absent cyclical activity.`	B

Discussion #

Chronic Benign Gastric Ulceration #

Many authors found evidence of chronic or atrophic gastritis in the pyloric region in cases where gastric ulceration was located more proximally in the stomach (Lilja l959; Burge et al. l963; du Plessis l963; Schrager et al. l967; Gear et al. l97l; Lawson l972; Meister et al. l979). Some investigators looked upon "antral" gastritis as the primary event (Schrager et al. l967; Gear et al. l97l), while others pointed out that the relationship between gastritis and gastric ulceration remained controversial (Lawson l972; Liebermann-Meffert and Allgöwer 1977).

Narrowing of the pyloric region in cases of chronic, benign gastric ulceration in the region of the angulus has been described by several authors. Steigman (l943) for instance, noted "antral spasm" in a small percentage of cases where the ulcer was located at the incisura angularis. Lilja (l953, l954) found the canalis egestorius (i.e. the pyloric sphincteric cylinder) to be contracted in some of these cases of gastric ulceration. The cylindrical contraction might resemble AHPS, or it might be less severe and be more in the nature of an impairment of motility; irregular and oblique mucosal folds might be present in the contracted region, and the pylorus might be patent. Burge et al. (l963) called the condition the "pyloric channel syndrome", while Schrager et al (l967) termed it "stenosis of the antrum".

Motility disturbances of the pyloric region in cases of gastric ulceration of the corpus were described by Garret et al. (l966) during manometric studies, by Kwong et al. (l970) during myoelectrical investigations and by Miller et al. (l980) in gastric emptying studies.

One case in which AHPS was associated with a gastric ulcer located 6.0cm proximal to the pylorus was described by Skoryna et al. (l959), and another by Knight (l96l) (Chap. 24); the latter author considered AHPS to be the cause of the ulcer. According to Liebermann-Meffert and Allgöwer (l977) nodular or fusiform thickening in the pyloric and prepyloric musculature, with mucosal and submucosal changes, reduction in the number of Auerbach's plexuses and fibrosis, occurred not uncommonly in association with gastric ulceration more proximally in the stomach; these alterations caused a disturbance of normal motility and of the "antral pump mechanism".

The cases described here show that a chronic, benign gastric ulcer, situated away from (i.e. orally to) the pyloric region, may be associated with contraction of the pyloric sphincteric cylinder. In a recent series of 65 consecutive cases of chronic gastric ulceration, where the ulcer was located more proximally in the stomach (usually in the region of the angulus on or near the lesser curvature), we noted a constant contraction of the pyloric sphincteric cylinder in 10. (Comment: Although histology of the ulcer was obtained in all instances, microscopic examination of the pyloric region was not considered to be a routine examination and was not done). This confirms the findings of Lilja (l953, l954), and will probably also explain some of the appearances described by Steigmann (l943), Schrager et al. (l967), and others.

Contraction of the pyloric sphincteric cylinder may be associated with increased duodenogastric reflux (Chap. 27), fixation of the pyloric aperture in the "open" position (Chap. 20), decreased cyclical activity (Chap. 20), delayed emptying of solids (Chap. 18) and diminished trituration (Chap. 18). Among the abnormalities encountered in patients with gastric ulceration in the corpus of the stomach, Brooks (l985) mentioned increased bile reflux, incompetent pylorus, reduced amplitude of gastric "antral" contractions and delayed gastric emptying of solids. It appears possible that contraction of the pyloric sphincteric cylinder may be a factor in the pathophysiology of these cases.

Why some cases of ulceration in the gastric corpus should be associated with contraction of the pyloric sphincteric cylinder and others not, is not known. It is not clear whether gastric ulceration or contraction of the cylinder is the primary event. We have not been able to establish a clear relationship between the size, chronicity or exact situation of the ulcer on the one hand, and contraction of the cylinder on the other.

Malignant Gastric Ulcer #

Contraction of the pyloric sphincteric cylinder in the presence of an ulcer in the corpus does not necessarily indicate a benign ulcer. During the present investigation the following case, proving the opposite, was encountered.

Case Report #

Case 29.4 F.F., 29 year old female, presented with epigastric pain and loss of weight. Radiographic examination showed an ulcer 1.5 cm in diameter on the lesser curvature of the stomach at the incisura angularis (Fig. 29.4 (A-D). A cylindrical contraction, 3.0 cm in length and containing a longitudinal mucosal fold, was seen in the pyloric region; a prominent pseudo-diverticulum was evident on the greater curvature side of the contraction, the appearances tallying with contraction of the pyloric sphincteric cylinder. Occasionally a minor degree of relaxation occurred, but most of the time the contraction remained as illustrated, with absence of normal cyclical activity. (Fig. 29.4 A-D). Response to anti-ulcer therapy was poor. Endoscopic biopsy 6 months later showed an ulcer at the angulus with surrounding induration. Microscopically the base of the ulcer consisted of fibrinopurulent material, fibrotic tissue and well-differentiated adenocarcinoma cells. Billroth II partial gastrectomy confirmed the large ulcer with indurated edges on the lesser curvature. Microscopically a well- differentiated adenocarcinoma, infiltrating locally through the muscularis externa into the subserosal tissue, was seen. The adjacent gastric mucosa showed areas of intestinal metaplasia. Microscopic examination of l7 lymph nodes revealed no carcinoma cells. It was concluded that the appearance of a chronic ulcer with dense fibro-collagenous tissue and carcinoma cells in the base, was compatible with so-called "ulcer cancer", i.e. carcinoma originating in a chronic gastric ulcer.



`Fig. 29.4 A-D Case F.F. Malignant ulcer at incisura angularis (open arrow). Constant contraction of pyloric sphincteric cylinder with absent cyclical activity (filled arrows)`

Gastric Ulceration Within the Pyloric Sphincteric Cylinder

Golden (l937) pointed out that the narrowing of antral gastritis and spasm, as seen on radiographs, was confined to that part of the stomach which normally exhibited antral systole and diastole, i.e. the pyloric sphincteric cylinder (Chap. 28). A similar contraction could occur in cases of prepyloric ulceration, where the ulcer was surrounded by contraction of the "fan-shaped muscle". According to Golden (l937) it had been customary to attribute "antral spasm" in these cases to the ulcer, but as the same spasm could occur in gastritis without ulceration, it was more likely that the spasm was due to the inflammatory change in the gastric wall. As pointed out above, an identical contraction might occur in cases where the ulcer was located more proximally in the stomach.

Magnus (l954) examined various features of 421 surgical resection specimens in cases of gastric ulceration. A total of 131 ulcers were located within 2.5 cm of the pylorus, 50 were situated between 2.5 to 5.0 cm from the pylorus and the remainder were located further proximally. No morphological difference was found between the ulcers in the various situations.

Raffensperger (l955) described an adult case in whom a prepyloric gastric ulcer, situated on the greater curvature 1.0 cm proximally to the pylorus, was diagnosed radiologically. Initially no associated narrowing was seen, but as the ulcer healed a prepyloric narrowing containing prominent irregular mucosal folds, became evident. Five weeks after the original diagnosis the radiographic appearance of adult hypertrophic pyloric stenosis (AHPS) was seen, and at operation the gross appearance was that of typical AHPS. Microscopically the thickening consisted solely of muscular tissue without evidence of associated oedema or inflammation. A healed gastric ulcer was also present. The condition was considered to be AHPS which had developed within five weeks around a healing, prepyloric gastric ulcer.

It has been mentioned that Johnson (l957, l965) and Johnson et al. (l964) divided gastric ulcers into three types, depending on the associated acid secretory characteristics. Prepyloric ulcers (occurring within 2.54 cm of the pylorus) and other antral ulcers (occurring to the right of the angulus but further than 2.54 cm from the pylorus) were associated with acid hypersecretion, resembled duodenal ulcers clinically, and constituted Type III gastric ulcers.

Foulk et al. (l957) stated that the "pyloric channel" was not a well-delineated anatomical entity, and that gastric landmarks and boundaries differed in their details for the radiologist, the endoscopist, the surgeon and the pathologist (Chap. 2). For that reason the literature on "pyloric and pyloric-channel" ulcers was confusing. The proximal boundary of the so-called pyloric channel was difficult to define, and the term merely described a region of the stomach near the pylorus rather than a definite anatomical entity. The length of the anatomical pyloric channel was variable, but was approximately 2.0 cm. Pyloric channel ulcers were defined as ulcers occurring between the gastroduodenal junction and an imaginary line 2.0 cm above the junction; the term pyloroduodenal ulcers was used to indicate ulcers which straddled the junction. These authors studied three groups of patients with surgically treated peptic ulcer near the pylorus. There were 35 cases with pyloric channel ulcers, 29 with pyloroduodenal and l9 with duodenal ulcers. Clinically there were no features which permitted a differentiation of pyloric channel ulcers from the other two groups.

In their description of 6 cases of AHPS, Skoryna et al. (l959) included one case in which an ulcer of the pyloric canal was associated with hypertrophy of the musculature of the canalis egestorius as described by Torgersen (l942) (Chap. 24).

Texter et al. (l959) also drew attention to the confusion which existed concerning the terminology of the distal portion of the stomach. These authors looked upon the pyloric sphincter as the muscular ring surrounding the lumen of the gastroduodenal junction, and the pyloric channel or pyloric canal as the narrow space encompassed by the ring. Ulceration of the pyloric channel consequently indicated an ulcer involving the ring. This concept of pyloric channel ulcers differed from that of Foulk et al. (l957), who would have termed these pyloroduodenal ulcers. In a clinical study of 67 cases of pyloric channel ulcers Texter et al. (l959) found that although the symptoms were not pathognomonic, they differed significantly from those of gastric ulcers occurring elsewhere in the stomach, and from those of uncomplicated duodenal ulcers.

Burge et al. (l963) described a pyloric channel syndrome occurring in association with gastric ulceration. The ulcer in these cases could be located either high on the lesser curvature or in the pyloric channel. Pathologically the pylorus and prepyloric region showed small round cell infiltration and muscle hypertrophy with fibrous replacement of muscle cells. These features were apt to cause a narrowing of the pylorus and prepyloric region.

Murray et al. (l967) described features in 47 patients who underwent operation for pyloric channel ulcers. (Comment: From the description it is clear that the pyloric channel was equated with the pyloric aperture). Preoperative radiologic examination was obtained in 42 of the patients and the diagnosis of pyloric channel disease was confirmed in 41. There was associated duodenal ulcer disease in 25 cases, while 8 patients had an associated lesser curvature gastric ulcer and 10 associated hiatus hernia. Clinically pyloric channel ulcer was frequently associated with a symptom complex called the pyloric syndrome. Dysfunction of the "antral" evacuation mechanism was noted in one half of the patients. The ulcer was usually associated with low gastric acidity, and histologically it appeared to occur in gastric mucous membrane.

Gear et al. (l97l) found gastritis associated with prepyloric ulcers to be much less severe, and also less extensive, than that associated with ulcers in the body of the stomach. In both groups of ulcers the gastritis occurred predominantly in the distal part of the stomach and along the middle of the lesser curvature. Superficial or atrophic gastritis was found to persist or even worsen after healing of the ulcer, whether the treatment was medical or surgical.

Liebermann-Meffert and Allgöwer (l977, l98l), in their study of surgical resection specimens, found that the changes in the antropyloric wall occurring in association with pyloric ulceration, were similar to those seen in gastric ulceration elsewhere in the stomach (see above); these included abnormalities of Auerbach's plexuses and the muscularis externa with replacement of contractile muscular tissue by fibrous tissue. It was thought that this might impair antropyloric motor function. Lawson (l98l) stated that a prepyloric ulcer differed from a duodenal or mid lesser curvature gastric ulcer in a number of ways. For instance, it had a high recurrence rate when treated by parietal cell vagotomy and it was associated with a variable level of gastric acid secretion. The degree and distribution of chronic severe gastritis in 15 antrectomy specimens removed for prepyloric ulceration was examined. In 6 of the cases the prepyloric ulcer was on the lesser curvature; in these cases there were localized areas of severe chronic gastritis along the middle of the anterior and posterior walls of the "antrum", with a tongue of gastritis extending upwards along the lesser curvature as far as the fundus. In 3 cases, where the prepyloric ulcer was situated on the greater curvature, localized areas of gastritis also occurred, the least affected area being along the lesser curvature. The widest area of gastritis was seen on the anterior and posterior walls of the greater curvature of the "antrum", with a tongue-like extension to the fundus. In 6 cases the ulcer had healed at the time of histological examination. The general pattern of the distribution of severe gastritis was similar to that in the 9 other cases, the main area affected being the lesser curvature in both the fundus and antrum. It was concluded that localized areas of severe chronic gastritis occurred in the "antrum" in all cases of prepyloric ulceration. A tongue-like process of gastritis extended from the "antrum" to the fundus along the particular curvature on which the ulcer was situated. In prepyloric ulceration not the whole of the "antrum" was involved, as appeared to be the case in many specimens resected for mid lesser curvature gastric ulcer. The fact that the mucosa failed to return to normal after healing of the ulcer in 6 cases, confirmed the previous findings of Gear et al. (l97l), and suggested that chronic gastritis was not a secondary effect of the ulcer but could be an important factor in its pathogenesis.

Brooks (l985) found that patients with pyloric and duodenal ulcers showed a similar tendency to hypersecretion, but that peak acid outputs were significantly lower in the prepyloric ulcer group.

Lauritsen (l988, l989) stated that although it was generally believed that prepyloric ulcers resembled duodenal ulcers with respect to their acid secretory patterns, clinical trials had shown that patients with prepyloric ulcer disease were more resistant to treatment with H2-receptor antagonists than patients with duodenal ulcer disease. Their treatment remained a therapeutic challenge; for that reason the effects of a proton pump inhibitor (omeprazole) were studied in 176 patients with active prepyloric ulcers (all gastric ulcers below the angulus were considered to be "prepyloric"). The results were said to be encouraging.

The following are representative cases of ulceration within the pyloric sphincteric cylinder:

Case Reports #

Case 29.5 S.S., 32 year old female, complained of heartburn and intermittent epigastric pain of two years' duration. Radiographic examination showed a constant fleck of barium, indicating an active ulcer, within the pyloric sphincteric cylinder approximately 1.5 cm proximal to the pyloric aperture (Fig. 29.5). The cylinder was partially contracted, and remained contracted throughout the examination, with absence of normal, cyclical contraction and relaxation. Emptying of fluid barium was not delayed. Anti-ulcer therapy was commenced and proved beneficial. Endoscopy 5 months later showed a superficial, healing gastric ulcer in the anterior wall of the pyloric region, without evidence of malignancy. Follow-up endoscopy showed healing of the ulcer. The duodenum was normal. Considerable duodenogastric reflux was present.

Fig. 29.5. Case S.S. Ulcer (open arrow) within confines of pyloric sphincteric cylinder, which is partially contracted (filled arrows)

Case 29.6 M.T., 20 year old male, complained of dyspepsia, loss of appetite and epigastric pain of several months' duration. Radiographic examination showed a constant fleck of barium, 1.5 cm in diameter, indicating an active ulcer, on the lesser curvature side of the pyloric sphincteric cylinder (Fig. 29.6). The cylinder was somewhat deformed, partially contracted and unchanging in appearance throughout the examination, with absent cyclical activity; it contained prominent oblique and circular mucosal folds which were drawn in towards the ulcer and did not change in direction (Fig. 29.6). The duodenal bulb filled poorly. Response to anti-ulcer therapy was poor. Endoscopy 3 months later confirmed the presence of a benign gastric ulcer in the pyloric region. Billroth I partial gastrectomy with truncal vagotomy in May l984 showed a chronic, benign gastric ulcer 1.0 cm proximal to the pylorus. Microscopic examination revealed absence of malignancy. The gastric mucosa showed evidence of chronic gastritis.

Fig. 29.6. Case M.T. Ulcer (open arrow) in sphincteric cylinder, which is deformed and permanently contracted (filled arrows). Circular, unchanging mucosal folds drawn in towards ulcer

Case 29.7 A.J., 35 year old female, complained of intermittent epigastric pain and postprandial nausea of 5 years' duration. Radiographic examination showed an active ulcer niche on the lower lesser curvature at the commencement of the pyloric sphincteric cylinder (Fig. 29.7). Prominent oblique mucosal folds were drawn in toward the ulcer; (they may also be described as radiating fan-like from the ulcer). The sphincteric cylinder between the ulcer and the pyloric aperture was deformed, filled poorly, contained prominent oblique mucosal folds, and remained unchanging in appearance with absent cyclical activity. The mucosal folds remained fixed in the same position, showing no macroscopic movements. The duodenal bulb filled poorly. Endoscopic biopsy the same month showed a chronic, active ulcer in the prepyloric region without evidence of malignancy. The duodenum was normal. The gastric mucosa in the vicinity of the ulcer showed acute inflammatory cells in the lamina propria with areas of fibrosis and intestinal metaplasia, diagnosed as acute on chronic gastritis. Anti-ulcer therapy was commenced; the patient failed to return for follow-up.

Fig. 29.7. Case A.J. Ulcer (arrow) in sphincteric cylinder, which is deformed. Absent cyclical activity. Prominent, unchanging, oblique mucosal folds drawn in towards ulcer

Case 29.8 L.J., 56 year old female, had a long history of dyspepsia and nocturnal epigastric pain. Radiographic examination showed a constant contraction of the pyloric sphincteric cylinder, the contracted region being approximately 2.0cm in length, with absence of normal cyclical contractile activity (Fig. 29.8). A constant niche on the greater curvature side of the contracted cylinder indicated an active ulcer. The pyloric aperture was "fixed" in the open position and rapid emptying of fluid barium occurred. Anti-ulcer therapy resulted in symptomatic improvement. Endoscopic biopsy a month later showed two active ulcers in the pyloric region, without macroscopic evidence of malignancy. Biopsy was difficult on account of narrowing, only fibrino-purulent material being obtained. Repeat endoscopy after 4 months showed healing of both ulcers; further endoscopy showed no residual ulceration, narrowing or other abnormality.

Fig. 29.8. Case L.J. Constant contraction of pyloric sphincteric cylinder (filled arrows). Ulcer in contracted cylinder (open arrow)

Discussion #

The great majority, if not all, cases of chronic, benign ulcers in the pyloric sphincteric cylinder are associated with contraction of the cylinder. In a recent series of 20 consecutive cases of gastric ulceration within 3.0 to 4.0 cm of the pyloric aperture, we noted contraction of the cylinder in all. The degree of contraction may vary from moderate (Fig. 29.5) to severe (Fig. 29.8), and will have a bearing on the radiographic appearance. Contraction of the cylinder implies diminished or absent cyclical activity of its musculature (Chap. 13) which, in turn, may delay emptying of solids and hamper trituration (Chap.18). In some cases contraction is associated with deformity of the cylinder (Fig. 29.6, 29.7). Cyclical activity is absent in these cases as well.

Normally mucosal folds lie in a circular or spiral direction in the distended pyloric sphincteric cylinder, changing to longitudinal when the cylinder contracts (Chap. 13). (This is one of the best examples of co-ordinated movements of the muscularis externa and mucosa originally described by Forssell) (Chap. 13). As movements of the cylinder are diminished or absent in cases of local gastric ulceration, it is to be expected that mucosal fold movements will also be curtailed or absent. In addition some ulcers within the cylinder are associated with an "indrawing" and fixation of mucosal folds (Fig. 29.6, 29.7), further hampering their movements. It is surmized that the impeded or curtailed mucosal fold movements seen in cases of gastric ulceration within the cylinder, may further hamper the processes of expulsion and trituration.

It has been said that the acid-secretory characteristics of pyloric and duodenal ulcers are similar (Johnson l957, l966; Stadelmann et al. l97l; Brooks l985). The present findings show that there are important differences between ulcers within the pyloric sphincteric cylinder on the one hand, and duodenal ulcers (Chap. 30) on the other hand, as far as motility patterns of the cylinder are concerned.

References #

Brooks FP. The pathophysiology of peptic ulcer disease. Dig Dis Sci l985, 30, Suppl ll, 15S-29S.
Burge H, Gill AM, Lewis RH. The pyloric channel syndrome and gastric ulceration. Lancet l963, 1, 73-75.
Dragstedt LR, Oberhelman HA, Evans SO, et al. Antrum hyperfunction and gastric ulcer. Ann Surg l954, 140, 396-404.
Du Plessis DJ. The importance of the pyloric antrum in peptic ulceration. South Afr J Surg l963, 1, 3-11.
Fisher RS, Cohen S. Pyloric sphincter dysfunction in patients with gastric ulcer. New Engl J Med l973, 288, 273-276.
Fisher RS, Boden G. Reversibility of pyloric sphincter dysfunction in gastric ulcer. Gastroenterology l975, 69, 591-597.
Foulk WT, Comfort MW, Butt HR, et al. Peptic ulcer near the pylorus. Gastroenterology l957, 32, 395-403.
Garret JM, Summerskill WHJ, Code CF. Antral motility in patients with gastric ulcer. Amer J Dig Dis l966, ll, 780-789.
Gear MWL, Truelove SC, Whitehead R. Gastric ulcer and gastritis. Gut l97l, 12, 639-645.
Golden R. Antral gastritis and spasm. J Amer Med Assoc l937, 109, 1497-1500.
Johnson HD. The clasification and principles of treatment of gastric ulcers. Lancet l957, 2, 518-520.
Johnson HD. Love AHG, Rogers NC, et al. Gastric ulcers, blood groups, and acid secretion. Gut l964, 5, 402-411.
Johnson HD. Gastric ulcer: classification, blood group characteristics, secretion patterns and pathogenesis. Ann Surg l965, 162, 996-1004.
Knight CD. Hypertrophic pyloric stenosis in the adult. Ann Surg l961, 153, 899-910.
Kwong NK, Brown BH, Whittaker GE, et al. Electrical activity of the gastric antrum in man. Brit J Surg l970, 57, 913-916.
Lauritsen K. Effect of omeprazole and cimetidine on prepyloric gastric ulcer: double blind comparative trial. Gut l988, 29, 249-253.
Lauritsen K. Omeprazole in the treatment of prepyloric ulcer: review of the results of the Danish Omeprazole Study Group. Scand J Gastroenterol l989, 24, Suppl l66, 54-57.
Lawson HH. The pyloric antrum in patients with gastric ulcer. South Afr Med J l972, 46, 894-895.
Lawson HH. A histological assessment of prepyloric ulceration and a hypothesis relating to acid secretion. Scand J Gastroenterol l98l, 16, Suppl 67, 141-147.
Liebermann-Meffert D, Allgöwer M. The morphology of the antrum and pylorus in gastric ulcer disease. Prog Surg l977, 15, 109-139.
Liebermann-Meffert D, Müller C, Allgöwer M. Gastric hypermotility and antropyloric dysfunction in gastric ulcer patients. Scand J Gastroent l98l, 16, Suppl 67, 5-7.
Liebermann-Meffert D, Allgöwer M. Neuromuscular tissue defects and antropyloric dysfunction in peptic ulcer. Scand J Gastroent l98l, 16, Suppl 67, 111-113.
Lilja B. Gastric block: a disturbance of gastric motive function. Acta Rad l953, 39, 353-367.
Lilja B. Gastric motive function with particular reference to the activity of the conducting system in the stomach. Acta Rad l954, 41, 225-246.
Lilja B. Motor activity of the stomach. Acta Rad l959, Suppl l80, 1- 94.
Magnus HA. The pathology of peptic ulceration. Postgrad Med J l954, 30, 131-136.
Meister H, Holubarsch CH, Haferkamp O, et al. Gastritis, intestinal metaplasia and dysplasia versus benign ulcer in stomach and duodenum and gastric carcinoma: a histotopographical study. Path Res Pract l979, 164, 259-269.
Miller LJ, Malagelada JR, Longstreth GF, et al. Dysfunctions of the stomach with gastric ulceration. Dig Dis Sci l980, 25, 857-864.
Murray GF, Ballinger WF, Stafford ES. Ulcers of the pyloric channel. Amer J Surg l967, 113, 199-203.
Raffensperger EC. Time required for the development of pyloric muscle hypertrophy in an adult. Gastroenterology l955, 28, 458-462.
Schrager J, Spink R, Mitra S. The antrum in patients with duodenal and gastric ulcers. Gut l967, 8, 497-508.
Skoryna SC, Dolan HS, Gley A. Development of primary pyloric hypertrophy in relation to the structure and function of the pyloric canal. Surg Gynaec Obstet l959, 108, 83-92.
Stadelmann O, Elster K, Stolte M, et al. The peptic gastric ulcer: histotopographic and functional investigations. Scand J Gastroenterol l97l, 6, 613-623.
Steigmann F. Considerations on the diagnosis of large gastric ulcers and implications as to treatment. Amer J Dig Dis l943, 10, 88-93.
Texter EC, Smith HW, Bundesen WE, et al. The syndrome pylorique: clinical and physiologic observations. Gastroenterology l959, 36, 573-579.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.

30 - Duodenal Ulceration and the Pyloric Sphincteric Cylinder

Mon, 01 Jan 0001 00:00:00 +0000

Duodenal Ulceration and the Pyloric Sphincteric Cylinder #

As far as we are aware the contractile behaviour of the pyloric sphincteric cylinder in cases of duodenal ulceration has not been described. However, other features of the pyloric part of the stomach in duodenal ulceration have been studied extensively, and a consideration of some of these may give an indication of the type of motility which can be expected.

Griffith et al. (l966) examined the rate of gastric emptying in a small number of cases of uncomplicated duodenal ulceration by means of radio-isotope labelled solid meals, and found it to be faster than normal. Buckler (l967), in a study of 193 patients with uncomplicated duodenal ulcer, found no significant difference in the total emptying time of a solid meal as compared with normal subjects, and concluded that the pattern of gastric emptying in duodenal ulcer patients was similar to that of normal individuals.

Schrager et al. (l967) performed histological examinations of the "antrum" in 75 surgical resection specimens of duodenal ulceration. In a third of the cases the duodenal ulcer was adjacent to the pyloric mucosa, and in the remainder it was 2.0 cm distal to the "sphincter". The duodenal mucosa surrounding the ulcer was normal. In all cases mild, diffuse inflammatory alterations, involving the whole of the antral mucosa, were noted; these consisted of lymphocytic and plasma cell infiltration, with variable degrees of pyloric gland destruction and intestinalization. In the great majority of cases less than 25 percent of pyloric glands were damaged; in a small minority there was a 25 to 50 percent reduction in glands, and in some of these an increase in fibrous tissue in the submucosa was observed. The changes were more severe along the lesser curvature near the boundary zone between the "antral" and body mucosa, i.e. the part furthest removed from the ulcer; the body mucosa appeared completely normal. It was concluded that duodenal ulceration was associated with mild inflammatory change of the gastric antral mucosa, in contrast to gastric ulceration, which was accompanied by much more severe inflammatory alterations.

Griffith et al. (l968), in a second series of cases, again found the gastric emptying rate of solids to be more rapid in duodenal ulceration than in normal controls, while George (l968) found that the mean emptying time of a fluid test-meal in 34 patients with uncomplicated duodenal ulcer did not differ from that of controls.

Kwong et al. (l970) studied the electrical activity of the distal 6.0 cm of the "antrum" by means of serosal electrodes implanted at operation for duodenal ulceration. The general patterns of the wave forms, the amplitude of the waves and the conduction time of the electrical impulses were the same as in normal controls. However, the frequency of the waves was increased, being approximately 6 cycles per minute in duodenal ulcer as opposed to 3 cycles per minute in controls. Cobb et al. (l97l), in a study of 12 duodenal ulcer patients and normal controls, found no difference in the pattern of gastric emptying of liquids in the two groups.

Fordtran and Walsh (l973) studied gastric emptying of solid meals in 7 patients with duodenal ulcer and 6 normal subjects. Using an infusion of sodiumbicarbonate to control intragastric pH and to act as a buffer, it was found that the duodenal ulcer patients emptied the meal buffer at a much more rapid rate than normal controls. It was acknowledged that the emptying rate of the buffer might not necessarily be the same as the emptying rate of the total mass in the stomach.

Using a solid meal labelled with Indium ^113m DPTA, Howlett et al. (l976) compared gastric emptying in 27 duodenal ulcer patients with 26 normal subjects. The half emptying time did not differ significantly in the two groups; when applying a method of principal component analysis to the results, a number of duodenal ulcer patients showed a relative slowing of the rate during the later phase of gastric emptying. It was suggested that the faster emptying previously found by Griffith et al. (l966, l968) and by Fordtran and Walsh (l973) might have been due to the fact that their meals had twice the volume of that of Howlett et al. (l976).

Liebermann-Meffert et al. (l98l) studied the response of gastric musculature to electrical vagal stimulation during intraoperative vagomotor tests in different groups of patients. Although a pressure rise occurred in all groups, it was found that the amplitude and duration of the contractions, and the integrated motor response was significantly greater in patients with gastric ulcer than in patients with duodenal ulcer. It was concluded that the motility disorder of the gastric musculature in duodenal ulceration was less evident than in gastric ulceration and seemed to be of minor importance. During histological studies of the antropyloric wall in peptic ulcer disease, Liebermann-Meffert and Allgöwer (l98l) found that less thickening occurred in duodenal ulcer than in gastric ulcer; the abnormal features of muscle and ganglion cells were also less severe in duodenal ulceration.

Lam et al. (l982), using a marker-dilution method, found that duodenal ulcer patients emptied liquid meals more rapidly than normal subjects.

Earlam et al. (l985) found histological evidence of chronic "antral" gastritis in 33 of 36 patients with duodenal ulceration who required surgery after prolonged but unsuccessful medical therapy. Of these, 24 had chronic superficial, and 9 chronic atrophic gastritis. The high incidence of antral gastritis was considered to be a striking finding; it was thought that it could be related to the severe symptoms in this particular group of cases.

According to Brooks (l985) duodenal ulceration should be looked upon as a heterogeneous syndrome which includes the following: (1) acute erosions; (2) uncomplicated ulcers; (3) bleeding; (4) perforation; (5) gastric outlet obstruction; (6) ulcers resistant to healing under treatment, and (7) recurrent ulceration after surgery. Not all patients will exhibit the same abnormalities in function; in some, gastric motor function may show an increase in frequency and amplitude of "antral" contractions with accelerated emptying of solids. On the whole associated gastritis of antral mucosa is a common finding. Holt et al. (l986) pointed out that gastric emptying rate measurements in patients with duodenal ulcer had produced conflicting results. Many previous studies had failed to identify any gastric emptying abnormality, while in others the rate was found to be faster than in normal controls. The conflicting results might have been due to factors such as differences in experimental methods and differences in meal composition; the exact stage at which emptying was measured in relation to the treatment or healing of a duodenal ulcer was also important. Using ^113m In as a marker of the liquid, and ^99m Tc as a marker of the solid phase, measurements of gastric emptying rates were undertaken in duodenal ulcer patients before, during and after therapy with cimetidine, as well as in control subjects. Before therapy there were no significant differences in the rate or pattern of gastric emptying in duodenal ulcer patients as compared with normal controls. This implied that gastric motor function in the two groups was similar, and the results did not agree with the findings of previous investigators who had found abnormally fast emptying in duodenal ulcer patients. During treatment, however, the emptying rate of particles became faster. The findings suggested that cimetidine had no marked effect on the emptying of the liquid component of a meal, but that there was a specific effect of the emptying of the solid phase. Gastric emptying patterns from control subjects and from healed duodenal ulcer patients were remarkably similar.

Williams et al. (l986) measured gastric emptying of citric acid, glucose and fat meals by means of a double-sampling, dye-dilution technique, while maintaining intragastric pH at a constant level. Acid, glucose and fat inhibited gastric emptying in a dose-dependent fashion in duodenal ulcer patients as well as in normal controls. Duodenal ulcer patients emptied all three types of meals faster than normals, but differences only occurred at the lower doses of glucose or with the less potent doses of acid and fat. It was concluded that differences in gastric emptying of liquid meals in duodenal ulcer patients, as compared with normals, were small; the variable responses obtained with different concentrations might explain some of the inconsistencies found by previous workers.

Hui et al. (l986) performed endoscopic biopsies in 213 patients with active duodenal ulceration and diagnosed active chronic antral gastritis in 99 percent. The degree of chronic inflammation was assessed histologically by the infiltration of polymorphs and chronic inflammatory cells and by the severity of mucosal degeneration. In the majority of patients antral gastritis was considered to be of a moderate degree. In non-ulcer controls active chronic antral gastritis occurred in 50 percent and in a milder form. It was concluded that the exact relationship of chronic antral gastritis to duodenal ulceration was uncertain. Healing of the duodenal ulcer was accompanied by histological improvement of the antral gastritis.

Present Investigations #

Patients and Methods #

We examined the contractile behaviour of the pyloric sphincteric cylinder in duodenal ulceration by means of upper gastrointestinal radiography in the following groups of patients:

Group 1. Sixty consecutive patients with active duodenal ulceration receiving and responding to medical treatment. All had been referred from the outpatient department with the clinical diagnosis of duodenal ulcer. In most cases the symptoms had been present for several months to a year; some had had symptoms and signs of chronic, recurrent duodenal ulceration and had received anti-ulcer therapy intermittently for the previous one to four years. Many had previous radiographic and/or endoscopic examinations, in which the diagnosis had been confirmed. Only patients in whom a definite ulcer niche could be seen radiologically or endoscopically in the duodenal bulb, were admitted to the study; patients with additional upper gastrointestinal pathology, e.g. gastric ulceration or hiatus hernia, were excluded.

Group 2. Seventeen cases of chronic recurring duodenal ulceration not responding satisfactorily to medical therapy. All had endoscopically proven active duodenal ulceration and all were candidates for the operation of sero-myotomy and parietal cell vagotomy.

In 58 of 60 cases of the first group, and in 15 of l7 cases of the second group, contractions of the pyloric sphincteric cylinder were normal. The following are examples from the 58 cases of the first group:

Case Reports #

Case 30.1. P.K., 44 year old male, a known case of duodenal ulceration, had received anti-ulcer therapy for some months; at the time of examination he was still symptomatic. Radiographic examination revealed no lesion in the oesophagus and stomach; the duodenal bulb was deformed and showed a niche on its lesser curvature side, indicating an active duodenal ulcer. Contractions of the pyloric sphincteric cylinder were normal. The distended cylinder contained several transverse (i.e. circular) mucosal folds (Fig. 30.1A). During contraction of the cylinder the folds changed in direction to longitudinal, only longitudinal folds being evident in the maximally contracted cylinder, with formation of the pyloric canal (Fig. 30.1B). The rate of cyclical contractions of the cylinder was normal at about 3 or 4 per minute. It is not possible to determine the amplitude of individual contractions radiographically; descriptions such as "maximal" or "near maximal" may give some indication of the degree of contraction. Radiographically the range and degree of contraction appeared to be normal.

A	B
`Fig. 30.1 A,B. Case P.K. A Transverse (i.e. circular) mucosal folds in distended pyloric sphincteric cylinder. Ulcer niche in duodenal bulb. B Normal contraction of sphincteric cylinder. Longitudinal mucosal folds in fully contracted pyloric canal. Ulcer niche in duodenal bulb`

Case 30.2. W.C., 33 year old male, a known case of duodenal ulceration, presented with epigastric pain and malaena. Radiographic examination showed no abnormality in the oesophagus and stomach. The duodenal bulb was deformed and contained an ulcer niche (not clearly visible in illustration) (Fig.30.2A). Cyclical contractions of the pyloric sphincteric cylinder occurred at a rate of 3 to 4 per minute; the range of individual contractions appeared to be normal, varying from full expansion (Fig. 30.2A) to maximal or near maximal contraction (Fig. 30.2B). A month after the examination the duodenal ulcer perforated, necessitating laparotomy and omental plugging of the perforation; the stomach was normal at operation.

A	B
`Fig. 30.2 A,B. Case W.C. A Pyloric sphincteric cylinder distended. Deformed duodenal bulb due to active ulceration. B Normal contraction of sphincteric cylinder. Duodenal bulb deformed`

Discussion #

In 73 of 77 cases of duodenal ulceration, cyclical contractions of the pyloric sphincteric cylinder were found to be normal in character, range and frequency. (It has to be reiterated that these features were determined while using a fluid barium suspension). Normal contractions were seen irrespective of the size of the ulcer, its exact position (whether located in the apex, centre of base of the duodenal bulb) and irrespective of the degree of deformity and/or narrowing of the bulb (in 9 of the cases there was appreciable narrowing).

In 2 of 60 cases in the first group in whom normal contractions of the cylinder were absent, the stomach was aperistaltic, hypotonic and moderately dilated, with delayed emptying in the erect position; this was not due to duodenal narrowing or obstruction, the cause of the aperistalsis being undetermined. In 2 of 17 cases in the second group with absent cyclical activity, atypical contraction of the cylinder was noted.

It has been stated that the acid-secretory characteristics of duodenal and pyloric ulcers are similar (Chap. 29). The present findings show that there are important differences in the motility patterns of the pyloric sphincteric cylinder in the two conditions. Normal contractions usually occur in duodenal ulceration while severe motility disturbances are present in pyloric ulceration (Chap. 29). The findings confirm those of Liebermann- Meffert and Allgöwer (l98l), who stated that motor disorders of the gastric musculature were less evident in duodenal than gastric ulceration and were, in fact, of minor importance in duodenal ulceration.

"Antral" gastritis may occur in cases of duodenal ulcer, but is usually of a mild, diffuse type; gastric ulceration is associated with much more severe inflammatory alterations, according to Schrager et al. (l967). Liebermann-Meffert and Allgöwer (l98l) found that abnormal features of the muscular layers and ganglion cells were less severe in duodenal than in gastric ulcer. Earlam et al. (l985) described a high incidence of chronic superficial and chronic atrophic antral gastritis in a selected group of duodenal ulcer patients, all requiring operation after prolonged but unsuccessful medical therapy. Brooks (l985) looked upon gastritis of the antral mucosa as a common finding in duodenal ulceration. Hui et al. (l986) found active, chronic gastritis in almost all patients with duodenal ulcer; in the majority it was of moderate severity.

The less severe grades of pyloric gastritis occurring in association with duodenal ulcer (as opposed to the more severe gastritis in pyloric and other gastric ulcers) probably accounts for the normal motility of the pyloric sphincteric cylinder in the former.

References #

Brooks FP. The pathophysiology of peptic ulcer disease. Dig Dis Sci l985, 30, Suppl 11, 15S-29S.
Buckler KG. Effects of gastric surgery upon gastric emptying in cases of peptic ulceration. Gut l967, 8, 137-147.
Cobb JS, Bank S, Marks IN, et al. Gastric emptying after vagotomy and pyloroplasty. Amer J Dig Dis l97l, 16, 207-215.
Earlam RJ, Amerigo J, Kakavoulis T, et al. Histological appearances of oesophagus, antrum and duodenum and their correlation with symptoms in patients with duodenal ulcer. Gut l985, 26, 95-100.
Fordtram JS, Walsh JH. Gastric acid secretion rate and buffer content of the stomach after eating; results in normal subjects and in patients with duodenal ulcer. J Clin Invest l973, 52, 645-657.
George JD. Gastric acidity and motility. Amer J Dig Dis l968, 13, 376-383.
Griffith GH, Owen GM, Kirkman S, et al. Measurement of rate of gastric emptying using Chromium-51. Lancet l966, 1, 1244-1245.
Griffith GH, Owen GM, Cambell H, et al. Gastric emptying in health and in gastroduodenal disease. Gastroenterology l968, 54, 1-7.
Holt S, Heading RC, Taylor TV, et al. Is gastric emptying abnormal in duodenal ulcer? Dig Dis Sci l986, 31, 685-692.
Howlett PJ, Sheiner HJ, Barber DC, et al. Gastric emptying in control subjects and patients with duodenal ulcer before and after vagotomy. Gut l976, l7, 542-550.
Hui WM, Lam SK, Ho J, et al. Chronic antral gastritis in duodenal ulcer: natural history and treatment with prostaglandin E1. Gastroenterology l986, 91, 1095-1101.
Kwong NK, Brown BH, Whittaker GE, et al. Electrical activity of the gastric antrum in man. Brit J Surg l970, 57, 913-916.
Lam SK, Isenberg JI, Grossman MI, et al. Rapid gastric emptying in duodenal ulcer patients. Dig Dis Sci l982, 27, 598-604.
Liebermann-Meffert D, Müller C, Allgöwer M. Gastric hypermotility and antropyloric dysfunction in gastric ulcer patients. Scand J Gastroenterol l98l, 16, Suppl 67, 5-7.
Liebermann-Meffert D, Allgöwer M. Neuromuscular tissue defects and antropyloric dysfunction in peptic ulcer. Scand J Gastroenterol l98l, 16, Suppl 67, 111-113.
Schrager K, Spink R, Mitra S. The antrum in patients with duodenal and gastric ulcers. Gut l967, 8, 497-508.
Williams NS, Elashoff J, Meyer JH. Gastric emptying of liquids in normal subjects and patients with healed duodenal ulcer disease. Dig Dis Sci l986, 31, 943-952.

31 - Pyloroduodenal Fistula or Acquired Double Pylorus

Mon, 01 Jan 0001 00:00:00 +0000

Pyloroduodenal Fistula or Acquired Double Pylorus #

Whereas a double pylorus had previously been presumed to be of congenital origin, Hansen et al. (1972) described 2 cases in which the clinical and endoscopic findings indicated that it was usually an acquired lesion. The first case was a 55 year old male with a known prepyloric gastric ulcer. Follow-up gastroscopy showed that the ulcer had perforated into the duodenum, forming a short fistulous communication between the stomach and duodenum, which had the appearance of a second pyloric aperture. In the second case a known duodenal ulcer had perforated through the pyloric ring into the stomach, with a similar result. In both cases a mucosal septum was situated between the 2 apertures.

Drapkin et al. (1974) described a case in which a deep ulcer on the lesser curvature of the "antrum" eventually perforated into the duodenal bulb, forming an acquired pyloro- duodenal fistula. At endoscopy two pyloro-duodenal openings, separated by a mucosal septum, were seen. A catheter inserted into one opening re-entered the "antrum" through the other.

Engle (1975) collected 7 cases from the literature and described another case in which a prepyloric gastric ulcer had penetrated into the duodenum. The radiological appearance was that of a short gastroduodenal fistula, extending from the distal stomach to the duodenal bulb on the lesser curvature side. The accessory canal was separated from the normal pylorus by a septum or bridge of mucosa, which conceivably could simulate a filling defect or mass lesion at a radiographic study. It was stated that cases had probably been misdiagnosed previously and that the condition was more common than the number of reported cases would suggest. A similar case was reported by Bender and Soffa (1975).

Hegedus et al. (1978) studied the developmental history as well as the clinical, endoscopic and radiological features of 11 cases of acquired double pylorus encountered among 7,932 consecutive radiographic studies over a 3 year period. They were able to show how a known prepyloric gastric ulcer penetrated the wall and eventually perforated into the duodenal bulb to form a second "pyloric canal". This left no doubt about the acquired nature of the lesion. In 7 of the patients peptic ulcer symptoms disappeared at the time of formation of the fistula, rendering surgical interference unnecessary. It was said that the gastric side of the fistula might not be visible endoscopically, as it could be covered by fibrin or necrotic material; it was easier to recognize the condition radiologically.

Tallman et al. (1979) reported another 4 cases. In the first case 2 constantly patent pyloric openings with intact mucosal margins were seen gastroscopically. The duodenum could be visualized through both channels. The patient had had a prepyloric gastric ulcer for the previous 8 years. In another case a radiographic study showed a short fistulous tract leading from the superior portion of the "antrum" to the superior fornix of the duodenal bulb. In a third case gastroscopy showed a rosary of oedematous mucosal folds; although a fistula was not visible initially, a pediatric endoscope inserted through the occluded opening entered the duodenum. Two subsequent radiographic studies failed to reveal the fistula. In the fourth case a lesser curvature prepyloric ulcer had led to 2 fistulous communications between the stomach and duodenum, resulting in a tri- channelled pylorus.

Thompson et al. (1982) estimated that approximately 60 cases had been described up to that time. The fistulous communication usually extended from the lesser curvature of the "distal antrum" to the superior fornix of the duodenal bulb; less commonly it was located on the greater curvature side. The radiological appearance was usually characteristic; endoscopy sometimes failed to diagnose the condition.

During 6810 consecutive radiographic studies over a 2 year period we encountered 5 cases of acquired double pylorus (Keet and Bezuidenhout 1984). Four will be described briefly:

Case Reports #

Case 31.1. S.K., 67 year old male, was admitted with a history of burning epigastric pain of 4 months' duration. It commenced a few hours after meals, woke him at night and was relieved by food and antacids. Occasionally it radiated to the back. There was no history of haematemesis or malaena. Twenty years prior to admission he had had a bout of similar symptoms.

Physical examination revealed epigastric tenderness. A radiographic study, done elsewhere, showed an irregular narrowing 3.5 cm in length at the pylorus (Fig. 31.1A); it had been interpreted as a carcinoma. Repeat radiological examination showed that the narrowing was in reality a fistulous connection between the distal end of the pyloric sphincteric cylinder and the base of the duodenal bulb on the lesser curvature side. It was adjacent to, and located on the posterior aspect of the pylorus. The sphincteric cylinder remained partially contracted as illustrated, neither maximal contraction nor maximal expansion occurring. The duodenal bulb was deformed. The condition was diagnosed as an acquired double pylorus, i.e. a pyloroduodenal fistula as a result of a perforating ulcer. Endoscopy showed a benign pyloric ulcer filled with necrotic material. It had perforated into the duodenum and the instrument could be manipulated into the duodenum through the pylorus as well as through the channel formed by the perforation.

A	B
`Fig. 31.1 A,B. Case S.K. A Narrow, irregular channel between pyloric sphincteric cylinder and duodenal bulb, diagnosed as carcinoma. Normal pyloric aperture not filled with barium. Cylinder partially contracted. B Resection specimen. Arrow through pyloroduodenal fistula. Pyloric aperture visible behind arrow`

At operation considerable fibrotic reaction was encountered and the duodenum had to be dissected from the pancreas. A truncal vagotomy, antrectomy and Billroth I anastomosis was performed. The resection specimen showed a second aperture between the stomach and duodenum next to the normal pylorus, with a bridge of mucosal tissue between the 2 apertures (Fig. 31.1B) confirming the diagnosis of pyloroduodenal fistula or so-called double pylorus. Case 31.2. J.N., 55 year old male, complained of burning epigastric pain of 4 months' duration. It commenced an hour after meals and was relieved by food and antacids. There was intermittent nausea with some loss of appetite and weight. Previously he had been treated for ischaemic heart disease, gout, ethanol and aspirin abuse.

Physical examination revealed gouty tophi at various joints, moderate hypertension and epigastric tenderness. A radiographic study showed an extra channel extending from the distal end of the pyloric sphincteric cylinder to the superior fornix of the duodenal bulb on the lesser curvature side (Fig. 31.2). The sphincteric cylinder remained partially contracted throughout the examination, with a deep incisura on the greater curvature due to contraction of the left pyloric loop, as illustrated. There was some deformity of the duodenal bulb. The condition was diagnosed as an acquired double pylorus, presumably the result of penetration of a pyloric ulcer into the duodenum.

Fig. 31.2. Case J.N. Fistula between pyloric sphincteric cylinder and base of duodenal bulb on lesser curvature side (arrow). Constant contraction of sphincteric cylinder. Pyloric aperture patent

Anti-ulcer treatment was commenced. Initially the patient was lost to follow-up, but endoscopy 3 months later showed a posteriorly situated, deep prepyloric ulcer. No definite penetration into the duodenum could be demonstrated, but the examination was difficult and incomplete on account of fixation of tissues. After an episode of haematemesis a month later, a second endoscopy showed the same ulcer to be filled with blood clot. Because of increasing fixation it was not possible to manipulate the instrument through the pylorus into the duodenum.

The patient returned a year later after a massive haematemesis. Following ressuscitation, a laparotomy was performed at which an inflammatory mass was palpated on the posterior aspect of the pylorus. After a truncal vagotomy had been performed it was found that a pyloric ulcer had penetrated deeply into the pancreas, necessitating considerable dissection. The pancreas formed the base of the ulcer; from here it had burrowed into the duodenum. The pyloric ring was intact. The findings confirmed the presence of a gastro-duodenal fistula as a result of a penetrating pyloric ulcer. An antrectomy with Billroth I anastomosis was done. Histologically the ulcer was benign, with chronic gastritis and intestinal metaplasia in the surrounding gastric mucosa.

Case 31.3 S.D., 44 year old female, was a known case of pyloric ulceration. Three years before admission an active ulcer on the lesser curvature of the pyloric sphincteric cylinder had been diagnosed at radiological examination. Follow-up endoscopy after anti-ulcer therapy had shown healing of the ulcer with some residual deformity of the pyloric region.

She then presented with a recurrence of symptoms. Endoscopy showed pyloric deformity. Radiographic examination three weeks later revealed an ulcer on the lesser curvature of the pyloric sphincteric cylinder, on the immediate oral side of the ring, with a fistulous communication between the ulcer and the superior fornix of the duodenal bulb (Fig. 31.3). Prominent, permanent circular mucosal folds were present in the cylinder, which remained partially expanded throughout the examination with complete absence of cyclical contraction and relaxation. Repeat endoscopy the following week confirmed the presence of a prepyloric ulcer with a pyloro-duodenal fistula.

Fig. 31.3. Case S.D. Ulcer lesser curvature side of sphincteric cylinder with fistula (arrow) to base of duodenal bulb. Partial expansion of cylinder. Permanent, circular mucosal folds in cylinder

Case 31.4 W.S., 54 year old male, presented with a history of intermittent epigastric pain, aggravated by meals, relieved by alkalies and at times associated with vomiting, of 4 years' duration. Physical examination revealed epigastric tenderness. The first endoscopic examination showed a small, superficial, benign ulcer on the lesser curvature of the stomach approximately l.0cm proximal to the pylorus. After initial improvement the symptoms recurred. Radiographic examination three years later showed a narrow fistula extending from the lesser curvature of the pyloric sphincteric cylinder, 1.0cm proximal to the pylorus, to the superior fornix of the duodenal bulb. The cylinder remained in a state of partial contraction throughout the examination, while the pyloric aperture appeared normal. Control endoscopic examination confirmed the presence of a benign prepyloric ulcer, described as "deep"; the first part of the duodenum was deformed but a pyloro-duodenal fistula could not be identified. A second radiographic study confirmed the findings of the first. At the third radiological study (six months after the first) a fistulous communication was again noted between the prepyloric lesser curvature ulcer and the superior fornix of the duodenal bulb (Fig. 31.4A). The pyloric sphincteric cylinder remained partially contracted throughout the examination, occasionally reaching the pseudo-diverticulum stage, but never relaxed fully (Fig. 31.4B). Subsequently truncal vagotomy and antrectomy was done elsewhere for "chronic prepyloric ulcer". Unfortunately the resection specimen was discarded and was not available for examination.

A	B
`Fig. 31.4 A,B. Case W.S. A Fistula (arrow) between sphincteric cylinder and duodenal bulb on lesser curvature side. Cylinder partially contracted. Pyloric aperture patent. B Sphincteric cylinder contracted to pseudo-diverticulum stage. It never relaxed fully`

Einhorn et al. (1984) reviewed the literature of acquired double pylorus and reported 4 new cases with long term follow-up. In 36 cases the fistula extended from the lesser curvature of the "antrum" to the superior portion of the duodenal bulb. In 28 of these it had originated from "antral" ulcers, in 2 from "pyloric channel" ulcers and in 6 from duodenal ulcers. In 9 cases the fistula was situated between the greater curvature and the inferior portion of the duodenal bulb, 7 originating from antral ulcers, one from a pyloric channel ulcer and one from a duodenal ulcer. The radiological appearance of a double pylorus was said to be characteristic, consisting of two channels of barium separated by a smooth band of soft tissue which represented the intervening mucosal septum. The endoscopic appearance was also typical, the aperture of the fistula being clearly visible in the majority of cases. With the endoscope in the "distal antrum", it was frequently possible to insert a biopsy instrument into the fistula and visualize its tip within the duodenum by viewing through the pylorus.

None of the cases of acquired double pylorus reported up to 1984 had been associated with malignancy (Einhorn et al. 1984). Friehling and Rosenthal (1985) subsequently described an unusual case of gastric carcinoma in which the radiological appearance of a double-channel pylorus was the result of partition of the pyloric aperture by the tumor, no fistula being present.

The radiological features of two more (unconfirmed) cases of benign, acquired pyloro- duodenal fistula were subsequently described by Hurwitz and Friedman (1987).

Discussion #

Acquired double pylorus or pyloro-duodenal fistula occurring as a result of perforation of a peptic ulcer has also been known by the terms pseudo-pylorus, tunnel ulcer, pyloric diaphragm, antral mucosal band and pyloric septum (Drapkin et al. 1974; Hegedus et al 1978). None of the authors quoted, with the exception of Keet and Bezuidenhout (1984), described the condition in relation to the concept of the pyloric sphincteric cylinder.

Our cases had the following features in common: In all the pyloro-duodenal fistula extended from the superior aspect of the distal part of the pyloric sphincteric cylinder to the superior fornix of the duodenal bulb, i.e. it was situated on the lesser curvature side. (As reported in the literature the fistula may occasionally occur on the greater curvature side).

In all 4 cases the sphincteric cylinder remained partially contracted (or, in other words, incompletely expanded) throughout the radiological examination; although minor degrees of contraction and relaxation did occur, these movements were never maximal. This is best illustrated in Fig. 31.2, in which a permanent contraction of the left pyloric loop on the greater curvature, opposite the commencement of the fistula, is seen. In Case 31.4 the contraction at times reached the pseudo-diverticulum stage (Fig. 31.4B), before reverting to incomplete expansion (Fig. 31.4A).

It is concluded that our cases of acquired pyloro-duodenal fistula were associated with motility disturbance of the pyloric sphincteric cylinder, consisting of a restriction in the range of contraction and relaxation. Theoretically this could have an effect on emptying and trituration of solids (Chap. 18). Emptying of liquid barium occurred without undue delay through both orifices.

References #

Bender MD, Soffa DJ. Acquired double pylorus: a case report. Radiology l975, 116, 325-326.
Drapkin RL, Otsuka AL, Castellanos HL et al. Acquisition of a pyloric septum or pyloric duodenal fistula. Gastroenterology l974, 66, 1234-1236.
Einhorn RI, Grace ND, Banks PA. The clinical significance and natural history of the double pylorus. Dig Dis Sci l984, 29, 213-218.
Engle R. Tunnel ulcer with double pyloric canal. Radiology l975, 116, 323-324.
Friehling JS, Rosenthal LE. Gastric carcinoma presenting as double-channel pylorus on upper gastrointestinal series. Dig Dis Sci l985, 30, 269- 273.
Hansen HO, Kronborg O, Pedersen T. The double pylorus. Scand J Gastroenterol l972, 7, 695-696.
Hegedus V, Poulsen PE, Reichardt J. The natural history of the double pylorus. Radiology l978, 126, 29-34.
Hurwitz J, Friedman L. Pyloroduodenal fistula: a benign complication of peptic ulcer disease. South Afr Med J 1987, 72, 56-58.
Keet AD, Bezuidenhout DJJ. Dubbele pilorus en piloroduodenale fistels. South Afr Med J l984, 66, 740-742.
Tallman JM, Clements JL, Gilliam JH, et al. The multi-channelled pylorus. Clin Rad l979, 30, 337-341.
Thompson WM, Kelvin FM, Gedgaudas RK, et al. Radiologic investigation of peptic ulcer disease. Rad Clin North Amer l982, 20, 701-720.

32 - Gastro-oesophageal Reflux Disease (GERD) and the Pyloric Sphincteric Cylinder

Mon, 01 Jan 0001 00:00:00 +0000

Gastro-oesophageal Reflux Disease (GERD) and the Pyloric Sphincteric Cylinder #

Hiatus Hernia in Infants #

Roviralta (l951) described 3 cases of partial thoracic stomach in infants associated with hypertrophic pyloric stenosis (IHPS), and called the combination the phreno-pyloric syndrome. It was believed that raised intragastric pressure secondary to the obstruction at the pylorus forced the stomach into the chest. Among 115 children with a partial thoracic stomach, Astley and Carré (l954) encountered 5 who also had hypertrophic pyloric stenosis, while another 3 had "infantile pylorospasm". The pylorospasm in all 3 cases was described as an inconstant narrowing of the pyloric "antrum", (Chap. 20), the radiographic appearance simulating IHPS to such a degree that Astley (l956) later called them cases of pseudo-hypertrophic pyloric stenosis. The symptomatology suggested that initially there was gastroesophageal reflux due to a partial thoracic stomach, followed by the superimposition of hypertrophic stenosis a few weeks later. Thus vomiting commenced soon after birth, and at the age of 2 to 3 weeks the symptoms and signs of hypertrophic stenosis, such as projectile vomiting, visible peristalsis and a palpable mass were superadded.

Forshall (l955) described the findings in 93 infants with gastroesophageal reflux and hiatus hernia. In 58 cases the cardia was incompetent but situated below the diaphragm. Eight of these required Ramstedt's operation for IHPS, while others had visible gastric peristalsis with temporary palpable masses in the pyloric region.

Astley (l956) stated that the association of hiatus hernia and hypertrophic pyloric stenosis was not a very common combination, but that the frequency was enough to suggest something more than a chance occurrence. He found no ready explanation for the association of these two conditions.

Stewart (l960), in discussing a paper by Herrington (l960), was impressed by the frequency of pyloric hypertrophy in cases of hiatus hernia; in many instances it resembled infantile hypertrophic pyloric stenosis.

Johnston (l960), in a series of 76 cases of hiatus hernia in childhood, found that 8 (10.5 percent) also had hypertrophic pyloric stenosis. Some of those without hypertrophic stenosis showed visible gastric peristalsis with forcible or even projectile vomiting, which to him was an indication of a gastric emptying disorder, giving rise to functional pyloric obstruction. It was reasoned that this raised the intragastric pressure, thus forcing the cardia into the chest.

Bowen (l988) pointed out that criteria for diagnosing hiatus hernia in infants remained unsettled, but that it was generally agreed that the retrograde passage of material from the stomach into the oesophagus was the crux of the matter, regardless of whether or not a hiatal hernia could be demonstrated convincingly.

In a number of infants we have noted a combination of hiatus hernia and IHPS; however, no systematic study was done in infants to determine in which percentage of hiatus hernia cases IHPS also occurred. The following is an example of one of our cases:

Case Reports

Case 32.1. E.B., 5 weeks old female infant, was admitted with a history of vomiting after feeds and recurrent bilateral pneumonia. Radiographic examination showed a severe, constant narrowing of the pyloric sphincteric cylinder, with a "string sign" typical of IHPS (Fig. 32.1A). The gastro-oesophageal junction was patulous with free and persistent gastro-oesophageal reflux, diagnosed radiographically as a sliding hiatus hernia (Fig. 32.1B). Some aspiration of refluxed barium occurred. At operation the next day a pyloric "olive" measuring approximately 2.3 cm x 0.8 cm, typical of IHPS, was found. Ramstedt pyloromyotomy was done; post-operatively vomiting stopped and the patient made an uneventful recovery.

Fig. 32.1 A,B. Case E.B. A Constant narrowing of pyloric sphincteric cylinder with string sign (arrows), typical of idiopathic hypertrophic pyloric stenosis. B Patulous gastro-oesophageal junction with free reflux (arrow)

Hiatus Hernia in Adults #

Wieser et al. (l963), describing the radiographic appearances of adult hypertrophic pyloric stenosis (AHPS), noted that a fifth of their 44 patients with pyloric hypertrophy also had hiatus hernia (Chap. 24).

Burge (l964) found a high incidence of "pyloric channel disease" in cases of hiatus hernia. The pyloric pathology in these cases consisted of pyloric and prepyloric muscle hypertrophy, mucosal stenosis and external scarring, in varying combinations. Some had previous ulcers in the immediate vicinity of the pyloric ring. Of 5 cases operated on for hiatus hernia, 2 had pyloric mucosal stenosis and 3 stenosis of the pyloric ring with external scarring (presumably due to previous ulceration.) One of these cases also had considerable prepyloric muscular hypertrophy.

Burge et al. (l966) found that pyloric channel disease was more frequently associated with symptomatic hiatus hernia than duodenal ulceration. It was stated that this benign disease at the pylorus had previously frequently been overlooked, both during the radiological examination and at operation. The pylorus and duodenum were studied in 44 consecutive cases of hiatus hernia subjected to operation. Concomitant duodenal ulceration was present in 22 and pyloric channel disease in 34. (The apparent discrepancy was due to the frequent association of duodenal ulceration and pyloric channel disease in the same patient.) It was reiterated that pyloric channel disease included mucosal stenosis, gastritis, pyloric and prepyloric muscle hypertrophy, and scarring. It is clear that Burge (l964) and Burge et al. (l966) described pathological changes in the pylorus not limited to muscular hypertrophy, and presumably due to previous ulceration in many of the cases. However, pyloric channel disease also occurred without evidence of ulceration, and in those cases there was not only pyloric ring change but also a definite prepyloric component, as shown by a contracted and deformed prepyloric region on radiography, and by muscle hypertrophy at operation. In all these cases a long history of duodenal or pyloric disease almost invariably preceded the symptoms of hiatus hernia. Burge (l964) and Burge et al. (l966) did not refer to the findings of Cunningham (1906) and Torgersen (l942), and it appears that few of their cases of pyloric channel disease would fit into the category of muscular hypertrophy of the pyloric sphincteric cylinder.

Radiographic Studies #

Patients and Methods #

In a previous study of 134 consecutive adult cases of hiatus hernia, we noted a contracted pyloric region, conforming to contraction of the pyloric sphincteric cylinder, in l9 (Table 32.1) (Keet and Heydenrych l97l). Strict criteria were adhered to in the radiographic diagnosis of hiatus hernia. A sliding hernia was only diagnosed if it could be demonstrated from below the diaphragm, and if it is was associated with free and persistent gastro-oesophageal reflux in the Trendelenburg position. In order to achieve this, the patient was instructed to swallow 6 to 7 mouthfuls of a commercial barium suspension, followed by a swallow of water in the erect position. This served to fill the stomach with contrast medium, while the water cleared the oesophagus. The patient was then placed in the Trendelenburg position, and various manoeuvres were done in an effort to demonstrate a sliding hernia. An irreducible hiatus hernia was diagnosed if it was obvious that a part of the stomach was situated permanently above the diaphragm in both the erect and Trendelenburg positions.

Table 32.1. Contracted Pyloric Segment in Hiatus Hernia


	Series 1 n	Series 2 n

Sliding hiatus hernia without contracted pyloric segment	112	65
Sliding hiatus hernia with contracted pyloric segment	16	27
Irreducible hiatus hernia without contracted pyloric segment	3	24
Irreducible hiatus hernia with contracted pyloric segment	2	9
Sliding and rolling hiatus hernia with contracted pyloric segment	1	0
Total	134	125
Total hiatus hernia cases without contracted pyloric segment	115	89
Total hiatus hernia cases with contracted pyloric segment	19	36
Per cent hiatus hernia cases with contracted pyloric segment	14.2	28.8

In all cases gastric peristaltic waves and contractions of the pyloric sphincteric cylinder were carefully observed radiographically. Normal cyclical contractions of the cylinder (Chap. 13) were evident in 112 cases of sliding, and in 3 cases of irreducible hiatus hernia. Contraction of the pyloric sphincteric cylinder was diagnosed if this region failed to relax fully during the examination, which implied markedly diminished or absent cyclical activity. This was seen in 16 cases of sliding hiatus hernia, in 2 of irreducible hiatus hernia and in one where the hernia was of a combined sliding and rolling type. In these cases contraction of the cylinder ranged from what can be described as moderate (Fig. 32.5B), to severe (Fig. 32.2B) grades; perhaps more important is the fact that in all, the range and/or frequency of cyclical contraction and relaxation of the cylinder was severely curtailed.

More recently we examined a second series of 125 cases of hiatus hernia. Permanent contraction of the pyloric sphincteric cylinder, to greater or lesser degree, was present in 36 (28 percent). There were 92 cases of sliding hernia, 27 showing a contracted cylinder, and 33 cases of irreducible hiatus hernia, 9 with a contracted cylinder (Table I). Comparison of the two series of cases shows that the total percentage of cases of hiatus hernia with a contracted pyloric sphincteric cylinder, has almost doubled in the second series. The reason for this is not clear, but it is presumed that only the more severe grades of contraction were included in the first series. Few cases of contracted pyloric sphincteric cylinder could be controlled surgically, as almost all our cases of hiatus hernia which came to operation had a transthoracic approach for the repair of the hernia. The following cases were done via an abdominal route:

Case Reports

Case 32.2. A.G.C., female aged 64 years. Ten years previously a hiatus hernia had been diagnosed radiographically. At the present examination a large, sliding hiatus hernia with free gastro-oesophageal reflux was demonstrated in the Trendelenburg position (Fig. 32.2A). A constant contraction of the sphincteric cylinder, 5.0 cm in length, was seen (Fig. 32.2B). Its walls were smooth and regular, without evidence of local mucosal destruction, a niche, filling defect or other organic lesion. Emptying of fluid barium suspension was not delayed. At operation there was a hard, tumour-like contraction in the pyloric part of the stomach, extending proximally from the pyloric ring for a distance of 5.0 cm. The contraction was of such severity that the mass appeared avascular and greyish and at first simulated a carcinoma. However, gentle massaging caused it to relax, followed immediately by recurring contraction. A pylorosplasty was done at which the muscularis externa was seen to be three times the normal thickness. The mucosa bulged through the incision and the surgeon had no doubt that it was a case of adult hypertrophic pyloric stenosis (AHPS). There was no other local lesion. The hernia was repaired and a truncal vagotomy performed. Repeat radiological examination 7 months later showed a post-pyloroplasty appearance.

A
B
`Fig. 32.2 A,B. Case A.G.C. Large, sliding hiatus hernia (black arrows). Contracted pyloric sphincteric cylinder (white arrows)`

It seems that, while the radiological abnormality may be unequivocal, the operative findings, as far as the pyloric part is concerned, may be of an uncertain nature, as in the following case:

Case 32.3. F.V., male aged 75 years, was admitted for mild obstructive jaundice of 10 days' duration. There had been colicky epigastric pain for the previous 5 months, as well as acidity and heartburn for years. Oral and intravenous cholecystography revealed poor concentration of the opaque medium with calculi in the gallbladder and a dilated common bile duct containing stones. (At the time sonography of the gall bladder had not been perfected). The radiological examination showed a large, irreducible hiatus hernia (Fig. 32.3). A contraction of the pyloric sphincteric cylinder, 4.5 cm in length, with a tendency toward formation of a pseudodiverticulum on its greater curvature side, was constantly present; there was no evidence of any other lesion locally or in the remainder of the stomach. The diagnosis of contracted pyloric sphincteric cylinder, resembling AHPS, in association with hiatus hernia was made. At operation a cholecystectomy was done and calculi were removed from the common bile duct. The surgeon stated that the pyloric area of the exposed stomach felt a little thicker than usual. Had his attention not been drawn to it beforehand, it is doubtful if he would have commented on it in his operative notes. No other gastric lesion was detected. Because of the patient's age, it was decided not to repair the hernia at that time. Repeat radiographic examination 5 months later showed the irreducible hiatus hernia and the contracted pyloric sphincteric cylinder to be unchanged.

Fig. 32.3. Case F.V. Large irreducible hiatus hernia (black arrow). Contracted pyloric sphincteric cylinder

In this case two points are worth noting:

33 - Pyloric Carcinoma

Mon, 01 Jan 0001 00:00:00 +0000

Pyloric Carcinoma #

As pointed out by Castleman (l936), there was a time when it was widely believed that gastric carcinoma did not invade the duodenum. In most of the earlier text-books of surgery and surgical pathology it was stated that, while carcinoma of the stomach spread extensively in many directions by means of lymphatic and haematogenous metastases and through direct extension, it stopped abruptly at the pyloric ring. However, on reviewing the literature, Castleman (l936) collected 38 case reports of gastric carcinoma in which duodenal spread of the tumor had occurred. In the majority the extent of duodenal invasion was not more than 1.0 to 2.0 cm, but in isolated cases it could be as much as 5.0 cm. In view of these findings it was necessary to remove most of the first part of the duodenum in resections for gastric carcinoma.

In his own investigation Castleman (l936) examined microscopic preparations of 134 surgical and 65 autopsy specimens of pyloric carcinoma which had accumulated in his department during the previous 34 years. There was microscopic invasion of the duodenum in 6 (9 percent) of the autopsy, and in 15 (11 percent) of the surgical specimens. The extent of duodenal spread in the 21 cases varied from 4.0 mm to 2.3 cm. (In most of the surgical specimens carcinoma cells were found at the distal cut edge, i.e. the tumor had been transected). Spread usually occurred along the submucosa, often in the lymphatics, and rarely involved the mucosa. It was stated that spread had taken place deep to Brunner's glands (i.e. between Brunner's glands and the muscularis externa) and in the accompanying illustrations it appeared as if these glands were not involved. Usually duodenal infiltration was so slight that the surgeon had difficulty in palpating the thickened duodenal wall and it could only be detected microscopically. It was recommended that at least 3.0 cm of the duodenum be removed during gastric resection for carcinoma at the pylorus.

Dixon and Stevens (l936) drew attention to 6 cases of linitis plastica of the stomach in which histologically similar but separate, discrete lesions were found elsewhere in the gastrointestinal tract, namely in the oesophagus, jejunum, colon and rectum. No mention was made of direct extension into the duodenum in these cases. The authors had encountered 37 similar case reports in the literature.

Coller et al. (l941) studied the routes and extent of spread in 53 cases of gastric carcinoma. Duodenal involvement was seen in 14 cases (26.4 percent). In some it had occurred through direct extension of the tumor, and in others via submucosal and intermuscular lymphatic channels. The exact extent of duodenal spread was not mentioned.

Zinninger and Collins (l949) studied microscopic sections of gastric resection specimens in 36 cases of carcinoma of the stomach without any gross evidence of invasion of the duodenum. Microscopically 9 (25 percent) showed duodenal invasion by carcinoma. If only those cases were considered in which the lesion was situated within 5.0 cm of the pylorus, there were 9 cases out of 30 (30 percent) in which duodenal invasion had occurred. The extent of duodenal spread was as follows: in 2 cases it was 3.0 mm, in 4 cases 7.0 to 15.0 mm, in 2 cases 20.0 mm and in one case 60.0 mm. (The latter was an unusual case. It appeared to be a benign gastric ulcer, but was diagnosed microscopically as a mucoid scirrhous carcinoma with widespread extension. The cell types in the other 8 cases were not mentioned). The invasion of the duodenum seemed to be mostly by direct infiltration of the muscle or extension through the subserosal lymphatics. In 3 of the 9 cases spread had taken place in the submucosa. In some cases an isolated lymph node adjacent to the duodenum beyond the pylorus contained metastases without any carcinoma being found in the duodenal wall. No mention was made of carcinomatous infiltration in relation to Brunner's glands.

Eker (l951) studied the lymphatic spread of gastric carcinoma in 70 total and 100 partial gastrectomy specimens. Generally speaking extension into the oesophagus was much more frequent than spread into the duodenum. In the 70 specimens of total resection, 32.8 percent showed involvement of the oesophagus, while in the entire material of 170 cases only 2 tumors were found to have extended into the duodenum. It appeared as if the pyloric "sphincter" formed a barrier which prevented distal spread of carcinoma; similar circumstances did not pertain at the gastro-oesophageal junction.

Subsequently Eker and Efskind (l952) analyzed the frequency and extent of spread of gastric carcinoma within the different layers of the wall. For this purpose 42 total and 38 partial gastrectomy specimens were examined. Duodenal extension of the tumor was apparent in 14 of the 80 specimens. In all 14 cases the distance of duodenal infiltration beyond Brunner's glands was said to be short. Microscopically the cases were divided into adenocarcinomas, mucinous scirrhus carcinomas and colloid carcinomas.

It was found that gastric adenocarcinoma spread mainly in the mucosa and submucosa of the stomach, with spread decreasing gradually in the muscle layers toward the subserous layer. Spread in the subserous layer was slight, a fact which was especially obvious in the highly differentiated adenocarcinomas. In the 6 cases of gastric adenocarcinoma with duodenal extension, the spread in the mucous membrane stopped at the point where Brunner's glands commenced, i.e. at the line of demarcation between the stomach and duodenum. In other words, the duodenal mucosa was not involved by spread of gastric adenocarcinoma across the pylorus, while the other duodenal layers were.

In gastric mucinous scirrhus carcinomas conditions were found to be different. In most of these cases there was little spread in the gastric mucosa, most of the spread occurring in the submucosa and deeper layers of the gastric wall. In 6 of these cases duodenal extension of the tumor had occurred; in 4 of the 6 cases mucosal involvement stopped at the gastroduodenal junction, the duodenal mucosa being spared. In the other 2 cases the duodenal mucosa was involved for a distance of 2.0 mm in the first and 7.0 mm in the second case. All the other duodenal layers were involved in the spread. In gastric colloid carcinoma, the characteristics of spread in the gastric wall resembled those of adenocarcinoma in some cases, and mucinous scirrhus carcinoma in others. On the whole the greatest spread occurred in the submucous layer. In 2 cases infiltration of the duodenum had occurred, but further particulars of these were not given. The results seemed to justify the conclusion that the less differentiated carcinomas spread more readily to the duodenum than the highly differentiated tumors. In addition, the tendency to spread in the various layers of the wall was stronger in the stomach than in the duodenum.

In a wide-ranging study of gastrectomy specimens obtained from cases of gastric carcinoma, Eker and Efskind (1960) found the following: In 865 partially resected stomachs infiltration of the lower border was seen in 2.4 percent. In 256 totally resected stomachs infiltration of the lower border was present in 0.8 percent. Tumors involving the sphincteric cylinder (both adenocarcinoma and scirrhus carcinoma) infiltrated the lower border in 3.6 percent. The rarity with which distal extension of tumor occurred was ascribed to a barrier effect of the pyloric "sphincter", or to different peristaltic effects in the duodenum.

Majima et al. (l964) examined 833 subtotal resection specimens of cases of gastric carcinoma. Duodenal invasion was encountered in 151 cases (18.1 percent); the frequency of duodenal invasion depended on the location of the tumor in the stomach. If only those tumors within 1.0cm of the pyloric ring were considered, the incidence of duodenal invasion was 37.0 percent. In cases where the gastric tumor was located 3.0 to 4.0 cm proximal to the ring, the incidence was 4.1 percent. (Almost all these cases were associated with spread of carcinoma to other structures, e.g. the peritoneum and lymph nodes).

Of the cases with duodenal invasion, the serosa of the duodenum was involved in 115 (76.2 percent); in none of these cases could a continuous extension into the mucosal coat of the duodenum be demonstrated. However, in a few cases carcinoma of the prepyloric region extended directly into the duodenal submucosa at an early stage, in the absence of extragastric spread. In 92 percent of cases the extent of spread into the duodenum was 1.0 cm or less. In 6.6 percent it was between 1.0 and 2.0 cm, and in 0.7 percent it varied from 2.0 to 2.4 cm. In some of these cases the line of division of the duodenum was involved by carcinomatous infiltration, indicating that the duodenal invasion extended further than the distance given. The pattern of duodenal invasion was continuous in 54 percent of cases, discrete in 34 percent, and both continuous and discrete in 10 percent. In the 5 cases of duodenal mucosal invasion, spread had occurred via the lymphatic channels and not through continuous direct extension.

Fernet et al. (l965) described 7 cases of scirrhous carcinoma of the stomach (linitis plastica) which had spread within the wall of long segments of the alimentary tract, producing an appearance of leathered induration similar to that seen in the stomach. Occasionally the process extended downward as far as the sigmoid colon. This tubal spread was due to a neoplastic infiltrate in the intramural tissue spaces, producing a diffuse induration and separation of the mucosa, submucosa and muscularis. Spread occurred in the longitudinal lymph channels, mainly in the submucosa and subserosa, leaving the muscular layer relatively intact; the lymph spaces were clogged with small round or oval undifferentiated cells with a positive mucin reaction. Metastatic spread also occurred to the mesenteric lymph nodes and the intestinal serosa. It appeared as if the longitudinal spread in linitis plastica was quite different from that of glandular carcinoma, as the appearance of leathered induration was not observed in well- differentiated adenocarcinoma. Tubal spread seemed to occur only in linitus plastica or similar undifferentiated forms of carcinoma. No detailed description of conditions at the pyloro-duodenal junction in these cases was given.

Paramanandhan (l967) reviewed the literature on duodenal spread of gastric carcinoma for the period 1865 to 1965, and found great variations in the reported incidences. He studied the frequency and extent of duodenal invasion in 29 necropsy specimens of gastric adenocarcinoma. Invasion of the serosa and lymph nodes was apparent in all cases. The subpyloric group of lymph nodes was involved in 24 cases, 20 of these showing invasion of the duodenum. Thus duodenal spread had occurred in 20 of the 29 cases, giving an incidence of 68.9 percent. There was a discrepancy between the macroscopic and microscopic appearances, as only 3 of the 20 cases showed macroscopic evidence of duodenal invasion. Microscopically the spread often involved the duodenal mucosa and submucosa. The submucosal layer was the most frequently affected, being followed by the serosa and the other layers of the wall. In 17 cases duodenal invasion occurred chiefly via the lymphatics, but it was difficult to determine whether this was primarily via the submucous or via the subserosal lymph vessels. In 3 cases extension appeared to be by direct infiltration of sheets of anaplastic cells. The duodenal surface epithelium appeared to remain intact. Although they were often compressed by dilated lymphatics containing tumor cells, Brunner's glands appeared to be particularly resistant. In all cases there was some degree of lymphocytic infiltration of the duodenum, due to lymphatic stasis. As all cases with duodenal invasion showed involvement of the subpyloric group of glands, spread could be due to a downward or retrograde lymph flow resulting from a block of the nodes. The extent of duodenal spread varied from 0.5 cm to 22.6 cm. In more than half the cases no tumor tissue occurred beyond the first 3.0 cm of the duodenum, while in one case extension was seen for a distance of 22.6 cm.

In discussing the pathology and prognosis of carcinoma of the stomach, Hawley et al. (l970) analyzed the findings in 205 patients who underwent total or partial gastrectomy. Cases were divided into the following types: (1) well-differentiated adenocarcinoma; (2) poorly differentiated or anaplastic carcinoma; (3) linitis plastica type. One of the difficulties in the grading was the great variability in the degree of cellular differentiation in different parts of the same tumor. The amount of lymphocytic and plasma cell infiltration had a significant effect on the prognosis; five out of 7 patients with a heavy infiltration of such cells survived over 5 years. The feature with the worst influence on prognosis was lymph gland involvement. Linitis plastica was a type of carcinoma which had to be considered separately; here submucosal and muscular infiltration involved part or all of the stomach, sometimes without mucosal ulceration. Three cases of mucosal carcinoma, in which areas of malignant change were confined to the mucous membrane, were encountered; these were discovered incidentally during histological examinations of gastrectomy specimens removed for peptic ulceration. According to Öhman et al. (l972) gastric carcinomas could be graded histologically into the following types: (1) highly differentiated adenocarcinoma; (2) moderately differentiated adenocarcinoma; (3) poorly differentiated adenocarcinoma; (4) undifferentiated or expansive carcinoma; (5) linitis plastica; (6) gelatinous type. The highly differentiated adenocarcinomas had the best prognosis while there was no prognostic difference between the moderately and poorly differentiated and undifferentiated types. The prognostic significance of the degree of differentiation was probably linked to dissimilarities in longitudinal growth along the wall and the occurrence of lymph node metastases. Linitis plastica, which was also undifferentiated, spread in a different, infiltrative manner and had the worst prognosis of all. While all gastric carcinomas contained some amount of mucus, abundant mucinous masses were present in gelatinous carcinoma.

Ming (l973) reiterated that gastric carcinomas are highly infiltrative tumors, extending rapidly to the serosa. From here tumor cells may implant on other parts of the peritoneum; lymphatic and vascular spread is common. On gross examination of his cases the lesion often appeared to end sharply at the gastroduodenal junction, but it had been documented repeatedly that tumor extension into the duodenum was not uncommon. In many of those cases the duodenal invasion was mostly subserosal and the mucosa was not involved. The reason for the latter phenomenon was not known. Intramural spread of a highly infiltrative tumor to other parts of the small bowel and colon as reported by Fernet et al. (l965) appeared to be very rare.

Koehler et al. (l977) reviewed 111 consecutive cases with gastric adenocarcinoma. Spread of tumor to the duodenum was evident on gross inspection of the resected specimens in 7 cases (6 percent). In 6 patients (5 percent) radiographic abnormalities of the duodenum due to the transpyloric extension of gastric carcinoma were evident. (In the other case gastric outlet obstruction prevented radiological evaluation of the duodenum). In 2 patients without duodenal invasion, radiographic deformities of the duodenal bulb were due to inflammatory changes adjacent to the gastric tumor, and in one case the duodenal bulb was deformed due to metastatically enlarged adjacent lymph nodes. Microscopically the duodenum was involved in 20 cases (18 percent). Tumor cells were noted predominantly in the muscular and submucous layers of the duodenum, but mucosal invasion was noted occasionally. From the literature they concluded that in as many as half the cases with duodenal involvement, the tumor extended no more than 1.0 cm beyond the pylorus.

Joffe et al. (l977) described 4 cases with intraluminal filling defects of the duodenal bulb secondary to transpyloric prolapse of polypoid gastric carcinomas. It was pointed out that primary adenocarcinoma of the duodenum practically never arose in the bulb, and that intraluminal filling defects of the duodenum due to malignant lymphoma or metastatic malignancy were rare. Radiologically the cases had to be differentiated from prolapse of gastric mucosa (Chap. 38).

Present Investigations #

Patients and Methods #

In an effort to further elucidate duodenal spread and some other features of pyloric carcinoma, we did a retrospective study of 50 consecutive cases encountered in the radiological department over a period of 3 years. These patients had been referred for examination from the out-patient department during the ordinary course of events. At the time a barium radiographic study was the primary investigation for suspected gastric carcinoma. Because of the heavy work load and other reasons endoscopy was generally reserved for conditions such as haematemesis and radiologically negative dyspepsia, and for obtaining biopsies in cases of gastric ulceration. Moreover endoscopy was considered to have certain shortcomings in the diagnosis of gastric malignancy, especially in the pyloric region. Whereas the oral border of the lesion is usually clearly visualized endoscopically, narrowing and deformity may preclude passage of the instrument and the full extent of the lesion, as well as possible duodenal involvement, may not be evident. The barium suspension, on the other hand, usually traverses most narrowings to enter the duodenum, and the aboral border of the lesion may be seen.

Pyloric carcinoma was defined, somewhat arbitrarily, as a gastric carcinoma which, at the radiographic investigation, was seen to extend to the pyloric ring or to within 2.0 cm of the ring. Cases in which the aboral border of the lesion was more than 2.0 cm away from the ring were excluded. On average the duration of symptoms in these patients was from 4 to 12 months, i.e. they presented at a rather late stage of the disease; radiologically the lesions left little room for doubt. Cases of early gastric carcinoma, in which the lesion is limited to the mucosa, were not encountered, presumably because of the late presentations.

All cases were subsequently confirmed by endoscopic biopsy and/or operation, and the histology was obtained in 40 (Table 33.1). In 10 of the unresectable cases the surgeons deemed histological confirmation unnecessary. The 44 operations consisted of 24 Billroth II and 2 Billroth I partial gastrectomies, 16 palliative gastro-enterostomies and 2 exploratory laparotomies (in which widespread metastases precluded surgical palliation).

Table 33.1 Fifty cases of Pyloric Carcinoma

Radiographic examination	Endoscopic biopsy	Operation	Histology

50	38	44	40

The following are representative cases:

34 - Malignant Lymphoma

Mon, 01 Jan 0001 00:00:00 +0000

Malignant Lymphoma #

In a historical review of malignant lymphoid tumors of the gastrointestinal tract, Dawson et al (l96l) found that these tumors had been reported more frequently in the stomach than in the remainder of the digestive tract. Up to that time at least 293 reports of lymphoid tumors of the stomach had appeared in the literature, but no clear distinction had been made between lymphomas originating primarily in the stomach and those affecting the stomach as a manifestation of generalized, disseminated lymphomatous disease. According to these authors the tumors could be classified as primary if the following conditions were met: there should be no palpable superficial lymphadenopathy and no enlargement of the mediastinal lymph nodes; the total and differential white blood count should be within normal limits; at laparotomy the bowel (or gastric) lesion should predominate, the only lymph nodes obviously affected being those in its immediate neighbourhood; and finally the liver and spleen should be free of tumor.

Rappaport (l966) proposed a histological classification of the lymphomas which also included Hodgkin's disease. For the past two or three decades his classification, as well as five or six others, have been widely used.

Naqvi et al. (l969) found that approximately 1,200 cases of gastric lymphomas had been recorded, and reviewed 100 cases of their own. In their experience the stomach was the part of the gastrointestinal tract most frequently involved, and the prepyloric region the site most commonly affected.

In discussing the pathology Ming (l973) stated that, in the stomach, malignant lymphoma develops in the mucosa, from where the tumor cells infiltrate the submucosa and muscularis. Seeing that this mode of growth is similar to that of carcinoma, it often assumes the gross characteristics of carcinoma and macroscopic differentiation of the two conditions may be difficult. Grossly the tumors may be ulcerated with rolled borders, while others are polypoid. There may be extensive infiltration and thickening of the gastric wall and/or mucosal folds. Histologically there is dense infiltration, with varying degrees of admixture of mature and immature lymphoid cells and histiocytic (reticulum) cells; there is a lack of fibrous tissue proliferation. While mucosal glands may be absent, the remaining gastric glands usually retain their normal architecture. The presence of reticulum fibres and absence of stainable mucin are features in favour of lymphoma (as opposed to carcinoma).

Katz et al. (l973) described 15 cases of disseminated lymphoma with gastric involvement. The following abnormal findings were noted at gastroscopy: enlarged, nondistensible rugae in 13 cases, multiple superficial ulcerations in 11, nodular ulcerations in 8 and large polypoid masses in 4. Biopsy furnished a positive diagnosis in not more than 2 of the 15 cases. The poor yield was ascribed to the infiltrative submucosal nature of secondary lymphoma and the superficial capacity of endoscopic biopsies. The gastroscopic appearance was found to be of greater help in the diagnosis of gastric lymphoma than biopsies, directed brush cytology or cytology washings.

Meyers et al. (l975) pointed out that the radiographic features of primary gastric lymphoma were not specific and included polypoid masses, ulcerations, thickening of the walls and generalized enlargement of the rugae. These appearances could simulate ulcerated carcinoma, gastric ulceration, granulomatous disease or hypertrophic rugae due to other causes, e.g. Menetrier's disease. While lymphoma may occur anywhere in the stomach, they reiterated that it commonly involved the pyloric and prepyloric area. In 7 proved cases they noted a definite tendency for the condition to spread submucosally from the distal stomach into the duodenum, resulting in radiographically discernible contour deformities, filling defects or ulcerations in the duodenal bulb. These features seldom occur in gastric adenocarcinoma (Chap. 33), and were regarded as characteristic of lymphoma, permitting a specific diagnosis to be made. In one of their cases, which was described in detail, duodenal spread occurred both superficial and deep to the lamina propria. This surrounded, but apparently did not invade, the glands of Brunner.

Koehler et al. (l977) analyzed the records of l9 patients who underwent gastric resection for lymphoma. Three of these had microscopic evidence of invasion of the duodenum, and in one of these the duodenal involvement was evident radiographically and grossly.

Lim et al. (l977) defined primary gastric lymphoma as a tumor apparently originating in the stomach, with no clinical, laboratory or radiographic evidence of systemic involvement at the time of initial evaluation. They analyzed 50 consecutive cases and found the most common localities to be the "antrum", the pyloric area and lesser curvature. According to Rappaport's (1966) classification, the diffuse histiocytic type occurred in 23 of their 50 patients, the well differentiated lymphocytic type in 12, the mixed lymphocytic histiocytic in 5, the poorly differentiated lymphocytic in 5, Hodgkin's disease in 3, and unclassified lymphoma in 2 cases. The prognosis for survival was much better than in gastric carcinoma since the latter condition presented with a far higher incidence of serosal penetration and nodal and distant metastases. The treatment of choice was gastric resection (44 of their cases being resectable), while radiotherapy and chemotherapy constituted additional therapeutic options.

Seeing that the therapy and prognosis of gastric lymphoma differ significantly from those of adenocarcinoma, Hricak et al. (l980) reiterated that correct diagnosis was essential. By reviewing the radiographic and pathological features in 81 cases, they investigated the incidence of spread from the stomach into the oesophagus, and from the stomach into the duodenum. In 60 of the cases the tumor appeared to have originated primarily in the stomach, and only 5 of these showed involvement of adjacent nodes, the mesentery or small bowel. In 21 patients the involvement was mainly extrinsic, the stomach being secondarily involved. Radiographically transpyloric extension was seen in 27 of the 81 cases. In 7 the "antrum" was the only site of tumor involvement, 6 of these showing transpyloric extension. Histologically the tumor was found to have a submucosal origin (according to Ming it originated in the mucosa). Submucosal extension across the pylorus was seen in l9 of the 27 cases. Zornoza and Dodd (l980) pointed out that the gross appearance and microscopic characteristics of the lesion were identical in the primary gastric and disseminated forms. The only differences between them were the distribution of the disease and the potential for future spread. Disseminated lymphoma was a lethal process that ran a rapid course. Although moderate stiffening of the gastric walls might occur in the intraluminal fungating form, peristaltic waves were not completely absent. The diffusely enlarged and distorted gastric rugae appeared to be more or less fixed.

Craig and Gregson (l98l) reiterated that one of the findings strongly suggesting the diagnosis of lymphoma was mucosal involvement extending across the pylorus into the duodenum. The US National Cancer Institute (l982), in a retrospective study of over 1,000 cases, published a revised and modified classification of non-Hodgkin's lymphoma based on six previous classifications, including that of Rappaport (l966). This has become known as the "Working Formulation for non-Hodgkin's Lymphomas". It is based primarily on clinical correlations, especially survival curves, age, sex, presenting sites and stage of the disease. Other recent classifications have been based, in part, upon modern concepts of the immune system and lymphoid physiology.

According to Sandler (l984), whose views differ from those of Ming (l973), primary gastric lymphomas arise from lymphoid tissue in the lamina propria and extend laterally along the submucosal layer. As the mucosa is not involved in the first place, endoscopy and endoscopic biopsy are unreliable diagnostic modalities. The muscular layer is generally spared till a late stage of the disease. The diffuse infiltration by mature and immature lymphoid cells and histiocytic cells may result in large, rigid folds or the appearance of linitis plastica. The lesions may also be of a polypoid or fungating nature. They do not constrict the lumen or interfere with peristalsis, and pyloric obstruction is unusual.

Because the tumor is predominantly submucosal, the diagnosis of gastric lymphoma by endoscopic biopsy can be difficult, according to Fork et al. (l985); in one report a success rate of only 44 percent was achieved.

Only a few cases of malignant gastric lymphomatous disease have been encountered in our department in many thousands of upper gastrointestinal barium investigations during the past 3 to 4 years. The following are two of the cases:

Case Reports #

Case 34.1 G.C., l7 year old male, had a two year history of epigastric pain, vomiting, weight loss and retardation of growth. Physical examination revealed severe iron deficiency anaemia. Radiographic study showed multiple lobulated filling defects in the corpus and sinus of the stomach, constant irregularity of the greater and lesser curvatures and a narrowing at the commencement of the pyloric sphincteric cylinder, in the region of the left pyloric loop (Fig. 34.1). The cylinder was partially contracted throughout the examination, never contracting or relaxing maximally; this was associated with a patent pyloric aperture measuring 4.0 mm in diameter. Gastric emptying of fluid barium was delayed. Endoscopy showed diffuse, nodular infiltration of the entire corpus and "antrum", with contact bleeding. The infiltration surrounded the pyloric orifice, which was patent. The duodenum could not be visualized. Histology, according to the "Working Formulation", revealed a high grade, malignant, non-Hodgkin lymphoma. Bone marrow biopsy was normal.

Fig. 34.1. Case G.C. Irregularities of lesser and greater curvatures extending to commencement of pyloric sphincteric cylinder. Cylinder partially contracted (arrows). Pyloric aperture patent

At operation the entire stomach from the gastro-oesophageal junction to the pylorus was found to be involved by lymphomatous infiltration, and a total gastrectomy with an oesophago-jejunal anastomosis was performed. Macroscopically the resection specimen showed diffuse thickening of the walls with effacement of the normal mucosal pattern. Microscopically tumor cells extended from the mucosa into the muscular layer and in several areas as far as the serosa. Electron microscopically the cells were determined to belong to the lymphoma group, the condition being diagnosed by a combination of light microscopy, electron microscopy and immunocytology as a large cell (B-cell), immunoblastic lymphoma. The distal border of the resection specimen was free of tumor cells and liver biopsy was normal. A few enlarged mesenteric lymph nodes proved to be of reactive type.

Case 34.2 J.J., 43 year old male, presented with intermittent epigastric pain, vomiting, loss of appetite and loss of weight, of one year's duration. Physical examination revealed epigastric tenderness. Radiographic study showed a constant irregularity of the lower part of the lesser curvature, with a permanent, ulcer-like projection; a large, lobulated filling defect was present in the duodenal bulb (Fig. 34.2). The pyloric sphincteric cylinder remained expanded throughout the examination, failing to contract, and the pyloric orifice remained patent. The appearances were ascribed to a mass lesion, probably with ulceration, infiltrating the distal lesser curvature of the stomach and the first part of the duodenum. At endoscopy a deformity of the gastric "antrum", presumably due to external compression was seen, while the pyloric ring appeared normal. A large polypoid, lobulated mass measuring approximately 4.0 cm in diameter, was present in the duodenal bulb; the surrounding duodenal mucosa appeared normal. The biopsy specimen was inadequate but the possibility of malignant lymphoma was mentioned. Abdominal sonography showed no abnormality in the pancreas, liver, gall bladder and kidneys. Chest radiographs and bone marrow trephine biopsies were normal.

Fig. 34.2 Case J.J. Irregularity lower lesser curvature with ulcer-like projection. Pyloric sphincteric cylinder expanded. Pyloric aperture patent (arrow). Large, lobulated filling defect in duodenal bulb

At laparotomy two apparently separate mass lesions were found, one in the first part of the duodenum and the other in the distal stomach. Several enlarged perigastric lymph nodes were present. The liver and spleen appeared normal. Frozen sections suggested malignant lymphomatous disease, and a Billroth II partial gastrectomy was performed. Macroscopically the resection specimen showed several tumor nodules, varying in diameter from 1.5 cm to 4.0 cm, in the mucosa; some were ulcerated. The surrounding mucosa felt indurated. Microscopically the nodules consisted of mixed cellular infiltration; the majority of cells were of a lymphoid type while histiocytes, plasma cells and eosinophils were also present. Similar cells, as well as Reed Sternberg cells were seen in the lymph nodes. The condition was diagnosed as mixed cellularity Hodgkin's lymphoma.

Discussion #

Although primary malignant lymphoma may occur anywhere in the stomach, several authors commented on the fact that the pyloric region is the site most commonly affected (Naqvi et al l969; Meyers et al. l975; Lim et al. l977). It usually develops from lymphoid tissue in the mucosa (Ming l973), submucosa (Hricak et al. l980) or lamina propria (Sandler l984). In the early stages peristalsis may be impaired (Ngan and James l973), but it is usually not completely absent (Zornoza and Dodd l980), as the muscular layer is not infiltrated till a late stage (Sandler l984). In Case 34.1 radiographic examination showed widespread infiltration of the proximal part of the stomach, extending as far as the commencement of the pyloric sphincteric cylinder, which was in a state of partial contraction with absent cyclical activity; this is an uncommon presentation of malignant gastric lymphoma. In Case 34.2 there was radiographic and operative evidence of widespread involvement of the distal stomach, including the pyloric sphincteric cylinder and the first part of the duodenum, with destruction of normal anatomical features. The failure of cyclical activity of the sphincteric cylinder may be expected to hamper propulsion and trituration of solids.

Malignant gastric lymphoma has a definite tendency to extend across the pylorus into the duodenum (Meyers et al. l975; Hricak et al. l980; Craig and Gregson l98l); the spread usually occurs submucosally (Meyers et al. l975; Hricak et al. l980; Sandler l984), although mucosal spread has also been mentioned (Craig and Gregson l98l). Spread of gastric adenocarcinoma into the duodenum, although not as rare as postulated some decades ago, is less likely to occur (Chap. 33).

In one of 7 cases of duodenal spread of malignant gastric lymphoma, Meyers et al. (l975) noted that Brunner's glands were surrounded, but not invaded, by lymphomatous cells. (A possible relationship between pyloric adenocarcinoma and Brunner's glands of the duodenum is discussed in Chap. 33).

Whether malignant gastric lymphoma affects cells of the APUD system in the stomach is not known.

References

Craig O, Gregson R. Primary lymphoma of the gastrointestinal tract. Clin Rad l98l, 32, 63-71.
Dawson IMP, Cornes JS, Morson BC. Primary malignant lymphoid tumors of the intestinal tract. Brit J Surg l96l, 49, 80-89.
Fork FT, Haglund U, Hogstrom H, et al. Primary gastric lymphoma versus gastric cancer: an endoscopic and radiographic study of differential diagnostic possibilities. Endoscopy l985, l7, 5-7.
Hricak H, Thoeni RF, Margulis AR, et al. Extension of gastric lymphoma into the esophagus and duodenum. Radiology l980, 135, 309-312.
Katz S, Klein MG, Winawer SJ, et al. Disseminated lymphoma involving the stomach: correlation of endoscopy with directed cytology and biopsy. Amer J Dig Dis l973, l8, 370-374.
Koehler RE, Hanelin LG, Laing FC, et al. Invasion of the duodenum by carcinoma of the stomach. Amer J Roentg Rad Ther Nucl Med l977, 128, 201-205.
Lim FE, Hartman AS, Tan EGC, et al. Factors in the prognosis of gastric lymphoma. Cancer l977, 39, 1715-1720.
Meyers MA, Katzen B, Alonso DR. Transpyloric extension to duodenal bulb in gastric lymphoma. Radiology l975, 115, 575-580.
Ming SC. Tumors of the esophagus and stomach. In: Atlas of Tumor Pathology. 2nd Series, Fasc 7, Armed Forces Institute of Pathology, Wash. D.C. l973, pp 231-238.
Naqvi MS, Burrows L, Kark AE. Lymphoma of the gastrointestinal tract: prognostic guides based on 162 cases. Ann Surg l969, 170, 221-231.
Ngan H, James KW. Clinical Radiology of the Lymphomas. Butterworth Co, London l973, pp 105-131.
Rappaport H. Tumors of the hematopoietic system. In: Atlas of Tumor Pathology, Sect 3, Fasc 8, Armed Forces Institute of Pathology, Wash. D.C. l966, pp 97-160.
Sandler RS. Primary gastric lymphoma: a review. Amer J Gastroenterol l984, 79, 21-25.
United States National Cancer Institute: Sponsored Study of Classifications of Non-Hodgkin's Lymphomas. Cancer l982, 49, 2112-2135.
Zornoza J, Dodd GD. Lymphoma of the gastrointestinal tract. Sem Roentg l980, 15, 272-287.

35 - Malignancy at the Gastro-Oesophageal Junction

Mon, 01 Jan 0001 00:00:00 +0000

Malignancy at the Gastro-Oesophageal Junction #

It has been shown that some cases of hiatus hernia are associated with motility disturbances of the pyloric sphincteric cylinder (Chap. 32). In most cases of malignancy at, or in the immediate vicinity of the gastro-oesophageal junction, we have also noted contraction of the pyloric sphincteric cylinder to greater or lesser degree. The malignancy involved either the gastric fornix or the lower oesophagus; in some cases it was difficult to determine (for a variety of reasons) whether the lesion was primarily gastric or primarily oesophageal.

The incidence of contracted pyloric sphincteric cylinder in cases of malignancy at the cardia has not been determined, but it appears if it occurs in the majority of cases. We have become aware of the association only recently; to the best of our knowledge it has not been described previously.

The following are examples of 11 cases which have been encountered:

Case Reports #

Case 35.1S.S., 67 year old male, presented with increasing dysphagia. Radiographic examination showed a constant, irregular filling defect of the lower 5.0 to 6.0 cm of the oesophagus, typical of carcinoma; it extended as far as the gastro-oesophageal junction, i.e. through the oesophageal hiatus in the diaphragm (Fig. 35.1D). The pyloric sphincteric cylinder showed a constant contraction, appearing to be "fixed" midway between maximum contraction and maximum dilatation, with absent cyclical activity (Fig. 35.1A-C). Most of the time the pyloric aperture contained barium, i.e. it was patent; at times it contained a single mucosal fold. At oesophagoscopy only the upper border of the carcinoma could be visualized; biopsy was unsuccessful. Repeat radiography a month later showed extension of the oesophageal lesion with only a trickle of barium entering the stomach.





`Fig. 35.1. A-DCase S.S. A-C Constant contraction pyloric sphincteric cylinder with absent cyclical activity. D Irregular filling defect lower oesophagus extending through diaphragmatic hiatus, indicating carcinoma.`

Case 35.2M.B., 59 year old female presented with dysphagia. Oesophagoscopy and biopsy revealed a poorly differentiated squamous cell carcinoma of the oesophagus at 26.0cm. Radiography confirmed the lesion, which appeared to extend to just above the cardia. There was constant contraction of the pyloric sphincteric cylinder, which appeared to be "fixed" midway between maximum contraction and relaxation, with absent cyclical activity; this caused the pyloric aperture to remain widely patent (Fig. 35.2). Laparotomy for staging the oesophageal carcinoma revealed metastatic lymphadenopathy at the coeliac axis; the stomach appeared normal, showing that the contraction of the sphincteric cylinder was of a functional nature.

Fig. 35.2. Case M.B. Double contrast examination. Constant contraction of pyloric sphincteric cylinder with absent cyclical activity. Pyloric aperture patent.

Case 35.3 M.A., female aged 50 years, presented with dysphagia of one year's duration. Radiographic examination showed a carcinoma 5.0 cm in length in the lower oesophagus. There was marked contraction or spasm of the entire pyloric sphincteric cylinder, with a prominent pseudo-diverticulum on its greater curvature side (Fig. 35.3). Occasionally a minor degree of movement was seen; most of the time the appearance remained as indicated. Subsequent oesophagoscopies confirmed carcinomatous involvement of the lower third of the oesophagus.

Fig. 35.3. Case M.A. Constant, near maximal contraction of pyloric sphincteric cylinder with pseudo-diverticulum on greater curvature side.

Case 35.4V.M., male aged 38 years. Radiographic examination showed constant irregularity and narrowing of the lower 4.0 cm of the oesophagus, extending through the hiatus to the gastro-oesophageal junction (Fig. 35.4). The diagnosis of carcinoma was confirmed by oesophagoscopy. Constant contraction of the pyloric sphincteric cylinder, similar to that of the previous cases, was present.

Fig. 35.4. Case V.M. Carcinoma lower oesophagus, extending through hiatus in diaphragm (arrow).

Discussion #

The area with the highest prevalence of oesophageal carcinoma in the world is the Transkei region of South Africa (Sagar l989). The majority of patients first consult traditional healers, by whom they are treated, presenting at a hospital only when the disease has reached an advanced stage. At Tygerberg Hospital it is not unusual to see 3 or 4 new cases of advanced oesophageal carcinoma per week.

Common factors in the 11 cases mentioned here, are: (1) In all the malignant lesion involves the gastro-oesophageal junction and/or the region immediately above the junction, i.e. the intrahiatal part of the oesophagus. This is well seen in Case 35.4. (2) In all cases partial contraction (i.e. spasm) of the pyloric sphincteric cylinder was evident. Why the cylinder should show motility disturbances in these cases is not known. One possibility is that the malignant process may involve the vagus nerves in the oesophageal hiatus of the diaphragm. Keet and Heydenrych (l97l) showed that experimental stimulation of the vagi at this site caused contraction of the pyloric sphincteric cylinder (Chap. 32).

Permanent contraction or spasm of the pyloric sphincteric cylinder will impair trituration and gastric emptying of solids (Chap. 18). As the swallowing of solids becomes impossible in advanced oesophageal carcinoma, this should have theoretical implications only. Gastric emptying of fluids is not delayed by moderate contraction of the sphincteric cylinder (Chap. 13, 18), and fluids reaching the stomach through the oesophageal lesion should empty without undue delay. Moderate contraction of the cylinder "fixes" the pyloric aperture in the patent position (Chap. 20), so that increased duodenogastric reflux may be expected (Chap. 27).

References #

Keet AD, Heydenrych JJ. Hiatus hernia, pyloric muscle hypertrophy and contracted pyloric segment in adults. Amer J Roentg Rad Ther Nucl Med l97l, 113, 217-228.
Sagar PM. Aetiology of cancer of the oesophagus : geographical studies in the footsteps of Marco Polo and beyond. Gut l989, 30, 561-564.

36 - Sessile Polyps in the Sphincteric Cylinder

Mon, 01 Jan 0001 00:00:00 +0000

Sessile Polyps in the Sphincteric Cylinder #

A number of gastric lesions may present as polyps; however, the term polyp is usually used to indicate a benign epithelial tumor (Marshak and Lindner l97l).

In 2420 double-contrast radiographic studies of the stomach Gordon et al (l980) encountered polyps in 38 (1.6 %). Most were of an inflammatory or hyperplastic nature; none was associated with gastric malignancy. Solitary polyps tended to occur in the "antrum", while multiple polyps (usually 2 or 3) were more often located in the gastric fornix and body. Two-thirds were less than 1.0cm in diameter, only one being larger than 2.0cm; most were sessile and could not be removed by a snare. The surrounding mucosa was either normal or showed evidence of acute or chronic gastritis. However, Laxen et al (l983), in a study of 183 patients with gastric polyps, found epithelial dysplasia and increased prevalence of intestinal metaplasia in most.

The following case shows interesting features:

Case Report #

Case 36.1. W.V.W., 46 year old male, presented with vague upper abdominal symptoms. Cholecystectomy had been done 3 years previously. Radiographic examination showed a round, polyp-like lesion 1.5cm in diameter and surrounded by a circular mucosal fold, in the centre of the pyloric sphincteric cylinder (Fig 36.1A). Cyclical contractions of the cylinder were normal; during contraction the polyp moved in an orad direction, and with maximal contraction it was located approximately 2.0cm more orally (Fig 36.1B). Gastroscopy confirmed the presence of a benign, sessile polyp; histologically the mucosa was normal. At gastrostomy the polyp could not be located. Follow-up radiography and gastroscopy 3 years later showed it to be unchanged.

Fig. 36.1 A,B. Case W.V.W. A Round, sessile, benign polyp (arrowed) in centre of pyloric sphincteric cylinder. B Near maximal contraction of sphincteric cylinder. The polyp (arrowed) has moved in an orad direction

In a case of Peutz-Jeghers syndrome, a pair of sessile mucosal polyps in the pyloric sphincteric cylinder also moved in an orad direction during contraction of the cylinder.

Peutz-Jeghers Syndrome #

The three salient features of this syndrome are polyp formation in the gastrointestinal tract, mucocutaneous melanin pigmentation and inheritance through an autosomal dominant gene (Morson and Dawson l979). The polyps, which are hamartomas, are most common in the small bowel, but not infrequently occur in the stomach and colon. The condition usually presents in childhood with attacks of recurrent colic due to intussusception caused by the small bowel polyps, or it may present as iron deficiency anaemia due to haemorrhage. Macroscopically the polyps may be sessile but not infrequently they are pedunculated with short, broad pedicles (Morson and Dawson l979). Microscopically there is proliferation of the muscularis mucosae to form a branching pattern, clothed with essentially normal gastric mucosa.

The following case is an example:

Case Report #

Case 36.2. A.P., girl aged 16 years, was admitted with a history of recurrent malaena (for which blood transfusions had been necessary) and symptoms of iron deficiency anaemia. On examination hyperpigmented "freckles" were seen around the mouth, on the buccal mucosa and on the fingers and feet. (Her father had similar areas of pigmentation). Other findings were a hypochromic microcytic anaemia and sedimentation rate of 20.0 mm/hr. Rectal examination revealed no abnormality but tests for stool occult blood were positive. Radiological examination showed two round, polypoid defects, each l.5cm in diameter, within the confines of the pyloric sphincteric cylinder (Fig 36.2A). The distal margins of the defects were 1.0 and 3.0cm respectively from the pyloric aperture; no stalks were seen. During contraction of the cylinder the defects moved in an orad direction, the distance from their distal margins to the pylorus increasing to 4.0cm and 5.2cm respectively (Fig 36.2B). These movements occurred regularly during the examination.

Fig. 36.2 Case A.P. Peutz-Jeghers syndrome. A Sessile polyps close to pyloric aperture in relaxed pyloric sphincteric cylinder.

Fig. 36.2 B.Sphincteric cylinder contracted. The polyps have moved in an orad direction

A number of polyps were also seen in the second and third parts of the duodenum, at the duodeno-jejunal junction and in the upper jejunum. A double-contrast barium enema examination revealed no abnormality in the colon.

At endoscopy the presence of 2 sessile prepyloric mucosal polyps was confirmed. In addition 2 smaller but similar polyps were seen in the body of the stomach; none of the polyps had a stalk. Because of technical complications biopsies were not done. A clinical and radiological diagnosis of Peutz-Jeghers syndrome was made. While under investigation symptoms of upper small bowel obstruction supervened, necessitating a laparotomy. A jejuno-jejunal intussusception was found and reduced. Gastrostomy, duodenostomy and jejunostomy were done at which polyps were removed from the stomach, duodenum and jejunum.

The histology of the gastric polyps showed prominent, branching processes of muscularis mucosae with overlying columnar cell epithelium, without evidence of dysplasia. The diagnosis of hamartomatous polyps of the Peutz-Jeghers type was made. The patient made an uneventful recovery.

Discussion #

It is not unusual for pedunculated polyps in the pyloric sphincteric cylinder to be extruded into the duodenum. Consequently they may be visualized either in the pyloric region of the stomach or in the duodenum at a single radiographic examination.

The 2 cases described here had sessile polyps on the mucosa of the sphincteric cylinder. During contraction of the latter the polyps moved in an orad direction, and with maximal contraction were clearly situated farther from the pyloric aperture than in the partially contracted or non-contracted phases. This seems to confirm the fact that the pyloric mucosa may move in an orad direction during contraction of the sphincteric cylinder, a phenomenon first described by Golden (l937) (Chap 13).

References #

Golden R. Antral gastritis and spasm. J Amer Med Assoc l937, 109, 1497-1500.
Gordon R, Laufer I, Kressel HY. Gastric polyps found on routine double-contrast examination of the stomach. Radiology l980, 134, 27-30.
Laxen F, Kekki M, Sipponen P, et al. The gastric mucosa in stomachs with polyps: morphologic and dynamic evaluation. Scand J Gastroenterol l983, l8, 503-511.
Marshak RH, Lindner AE. Polypoid lesions of the stomach. Sem Roentg l97l, 6, 151-167.
Morson BC, Dawson IMP. Gastrointestinal Pathology, 2nd ed, Blackwell Scientific Publications, London l979, p 82.

37 - Diabetes Mellitus

Mon, 01 Jan 0001 00:00:00 +0000

Diabetes Mellitus #

Disturbances in gastrointestinal motility with associated symptoms such as vomiting, diarrhoea and constipation have long been recognized as complications of diabetes mellitus. Rundles (1945) described 4 diabetic patients with diarrhoea or alternating diarrhoea and constipation who also had pronounced anorexia and nausea. Radiological examination in all revealed abnormal gastric retention.

Kassander (1958) described 6 cases of poorly controlled diabetes mellitus with upper gastrointestinal manifestations, a condition he called "gastroparesis diabeticorum". In all cases the stomach showed sluggish peristalsis with retention of barium. There was no evidence of an organic lesion causing obstruction and all cases had a patulous pylorus through which the gastric contents could be expressed by hand. It was concluded that these cases represented a disturbance of propulsion, and more specifically of expulsion, of gastric contents. The gastric retention was considered to be similar to that occurring after truncal vagotomy and to be due to diabetic neuropathy involving the vagus nerves. The gastric manifestations could also occur in asymptomatic diabetic patients.

Marshak and Maklansky (l964) mentioned 4 similar cases and reiterated that diabetic gastropathy consisted of gastric retention in the absence of an obstructing lesion at the pylorus. In some cases there was a marked decrease in peristalsis while in others peristalsis was normal.

Zitomer et al. (l968) found that gastric neuropathy typically occurred in patients with a long history of inadequately controlled, moderately severe diabetes mellitus. The symptoms were generally mild and nonspecific, vomiting of undigested food from the previous day being one of the main manifestations. Radiologically the most constant and striking finding, occurring in 34 of their 35 cases, was sluggish, ineffectual and irregularly occurring peristalsis; on occasion peristalsis was absent altogether. There appeared to be decreased or absent propulsive motor activity, associated with abnormal gastric retention of food residues and barium, resembling a bezoar. The malfunction of gastric emptying and consequent unpredictable food absorption probably contributed to poor diabetic control. Despite the considerable delay in gastric emptying, barium could invariably be expressed by palpation through the pylorus, which remained patulous. If the patient was placed on his right side, passive gravitational emptying of liquid contents occurred, while solids tended to be retained. Overall the incidence of clinically significant gastric neuropathy was extremely low in diabetes mellitus, a figure of less than one per cent being mentioned.

Goyal and Spiro (l971) agreed that clinical manifestations of diabetic gastropathy occurred in a very small proportion of cases. While the gastric retention resulting from the reduction of peristaltic contractions resembled the hypomotility of truncal vagotomy, suggesting an autonomic neuropathy, other factors might play a role. It was known, for instance, that hyperglycaemia as well as glucagon inhibited gastric motility.

Scarpello et al. (l976) measured the rate of emptying of isotopically labelled solid meals, using ^99mTc-labelled sulphur colloid as a marker and a gamma camera. The gastric emptying rate in 29 insulin-dependent well-controlled diabetics was compared with that in l8 normal controls. No statistically significant difference in gastric emptying rate between controls and diabetics with or without autonomic neuropathy was found. Only 3 diabetics had greatly delayed gastric emptying, but in one of these the test had previously given a normal result.

Campbell et al. (l977) used a double isotope scintiscanning technique in order to differentiate between solid and liquid emptying in 12 patients with diabetes mellitus (6 with and 6 without objective evidence of autonomic neuropathy), and in 20 non-diabetic controls. Gastric stasis was demonstrated in 3 patients with autonomic neuropathy. In patients without stasis the normal differentiation between solid and liquid emptying was impaired, suggesting an abnormality of "antral" peristalsis.

Gramm et al. (l978) reviewed the radiological findings in 43 patients with diabetic gastric neuropathy. (It was said that the condition was seen more often on account of the increased longevity of diabetic patients). In the majority the stomach had an elongated, sausage-shaped configuration; there was sluggish, irregular gastric peristalsis with retention of solid food and barium in the absence of an organic obstruction at the pylorus.

Feldman et al. (l979) found that many patients with longstanding, insulin-dependent diabetes mellitus had reduced acid secretory responses to sham feeding (suggesting vagal neuropathy) and normal responses to infused food. Both in diabetics with nausea and vomiting and in patients without upper gastrointestinal symptoms, abnormal gastric retention of a nonabsorbable meal marker occurred. The findings supported earlier observations that gastric secretory and motor functions could be impaired in asymptomatic diabetics.

Malagelada et al. (l980) studied gastric motility by means of pressure transducers in the fornix, "antrum" and duodenum in fasting diabetic patients with symptomatic gastroparesis, as well as in asymptomatic diabetics and normal controls. Healthy subjects and asymptomatic diabetes mellitus patients averaged 2 phase III migrating motor complexes per 180 minutes, while most diabetics with gastroparesis had no such complexes. Whether analogous "antral" muscle dysfunction occurred postprandially in diabetic patients with gastroparesis was uncertain. However, as the emptying of solids might be delayed, it seemed likely that "antral" motor activity could be abnormal as it was the main mechanism responsible for the emptying of solids (Chap. 18). According to Feldman and Schiller (l983) the pathogenesis of diabetic gastroparesis remained uncertain, but the evidence supported the view that a vagal autonomic neuropathy was responsible. Feldman et al. (l984), using a radioloic method for assessing gastric emptying of radio-opaque, indigestible solid particles with simultaneous radionuclide scintigraphy of an ¹¹¹In-labelled standard meal, showed that patients with insulin-dependent diabetes mellitus had an abnormally slow gastric emptying rate for indigestible solids; emptying of digestible solids and liquids was close to normal.

Camilleri and Malagelada (l984) studied the fasting and fed manometric profiles of the stomach and proximal small intestine in 14 patients with the clinical diagnosis of diabetic gastroparesis. In 11 of the patients reduction in "antral" pressure activity with absent interdigestive migrating motor complexes was seen. Three patients exhibited a "peculiar continuous 3 minute antral contractile activity". In the small intestine abnormal manometric patterns were observed in 12 patients, in 9 of whom non-propagated, long bursts of powerful contractions occurred. The findings indicated that both in the stomach and small bowel the motility disorder was not invariably of a paretic type. In the stomach a reduction in frequency of amplitude of "antral" motor activity was the rule, but in a minority of patients prolonged periods of contraction of low amplitude (less than 20 mm Hg), occurred. This motor pattern indicated an abolition of the physiological cyclic activity and was distinctly abnormal; the consistently low amplitude might be insufficient to triturate solid food and empty the stomach. Clinically these patients had the same symptoms as those with "antral" hypomotility, for whom the term gastroparesis was perhaps more appropriate.

In symptomatic diabetic gastroparesis patients Achem-Karam et al. (l985) demonstrated abnormal "antral" and duodenal activity, characterized by absence of phase III of the interdigestive migrating motor complex; in 3 out of 6 patients the complex was also absent in the remainder of the proximal small bowel. The findings confirmed some of those previously described by Malagelada et al. (l980) and Camilleri and Malagelada (l984).

Using a dual radionuclide technique, Wright et al. (l985) investigated gastric emptying of solids and liquids in diabetic gastroparesis patients and normal controls. In both groups the emptying rate of liquids was normal; emptying of solids was markedly delayed in the diabetic group.

With a similar technique Horowitz et al. (l987) determined the effects of the prokinetic drug cisapride in 20 insulin-dependent diabetic patients who had delayed gastric emptying of the solid or liquid component of a meal, or both. It was found that cisapride increased the emptying rate of both solids and liquids.

Yoshida et al. (l988) found no morphologic abnormalities of the abdominal vagus nerves, the gastric musculature and myenteric plexuses in patients with diabetic gastroparesis.

In a review Varis (l989) defined diabetic gastroparesis as a delay of gastric emptying without gastric outlet obstruction in patients with long-standing insulin requiring diabetes mellitus. Characteristically the emptying of solids was delayed; in most cases the emptying rate of liquids was within the normal range, although it might be decreased in some patients. All normal motility patterns, e.g. adaptive relaxation and the maintenance of tone in the proximal stomach, "antropyloric" peristaltic movements and phase III of the interdigestive migrating motor complex might be lacking or abnormal. The "antral" motility disorder, leading to retention of solid foods, was considered to be the most characteristic feature of the condition.

As endoscopy may fail to demonstrate motor disorders of the stomach (Varis l989), it does not play an important role in the diagnosis. However, endoscopy does show gastric mucosal pathology such as acute erosions and gastritis, occurring in the majority of patients with diabetic ketoacidosis (Carandang et al. l969), and it may help to exclude mechanical pyloric obstruction (Camilleri and Malagelada l984).

From the above it is clear that gastric motility disturbances may occur both in symptomatic and asymptomatic diabetes mellitus patients. In a small percentage of cases these disorders may progress to diabetic gastroparesis, a condition usually occurring in patients with a long history of inadequately controlled, insulin-dependent diabetes mellitus.

We have had occasion to do upper gastrointestinal radiological examinations in numerous diabetic patients for a variety of reasons, over a period of years. Motility disturbances were found in a small number of patients, both in insulin-dependent and non-insulin dependent cases. The following are some of the cases with radiologically recognisable abnormalities.

Case Reports #

Case 37.1. D.R., 40 year old male had a long history of ethanol abuse and insulin- dependent diabetes mellitus which had been treated inadequately. For several weeks there had been dyspepsia, loss of appetite and nausea. Radiologically primary and secondary oesophageal peristaltic waves were normal. After an overnight fast the stomach contained food residues; the pyloric aperture was patent, measuring 9.0. mm in diameter (Fig. 37.1A). Gastric peristaltic waves were decreased both in frequency (i.e. less than 3 per minute) and intensity (i.e. failing to "bi-sect" the organ). The pyloric sphincteric cylinder was in a state of partial contraction most of the time (Fig. 37.1B). Cyclical contraction and relaxation of the cylinder, normally occurring at a frequency of 3 per minute (Chaps. 13, 15), was lacking. No obstructing lesion was seen at the pylorus and the duodenum appeared normal. Sonographically the gall bladder, liver, spleen and kidneys were normal; there was no ascites. The patient refused endoscopic examination.

Fig. 37.1. A,B. Case D.R. A Food residues in stomach. Pyloric aperture patent. Gastric peristaltic activity diminished. B Pyloric sphincteric cylinder (arrows) contracted most of the time.





`Fig. 37.1. C-F. Case D.R. After treatment and clinical improvement. Lessened contraction of sphincteric cylinder. Some movement evident but normal cyclical activity absent. Note pancreatic calcification`

Six months later, after proper diabetic control, he had improved clinically. On this occasion the stomach contained less residual food. Shallow gastric peristaltic waves were present, while the pyloric sphincteric cylinder remained partially contracted throughout the examination (Fig. 37.1C). Although this was less marked than on the previous occasion, normal cyclical activity remained absent and no maximal or complete contractions were seen. Peristaltic activity in the duodenum appeared to be decreased. Active peristaltic contractions with a fast passage of barium was noted in the jejunum. The films also showed scattered areas of calcification in the pancreas and the case was diagnosed as diabetic gastroparesis and chronic alcoholic pancreatitis. Case 37.2. T.M., 64 year old female with longstanding insulin-dependent diabetes mellitus and psychotic symptoms, was admitted with epigastric pain and episodes of vomiting. Radiological examination showed a decrease in frequency and intensity of gastric peristaltic waves; there was a lack of cyclical contraction and relaxation of the pyloric sphincteric cylinder, which remained in a state of partial contraction throughout the examination; this was associated with a patulous pyloric orifice measuring 1.2 cm in diameter. Sonographically the gall bladder, liver, spleen, kidneys and aorta were normal. The pancreas could not be visualized owing to obesity.

Attempts at controlling the diabetes in a peripheral hospital were only partially successful. She was readmitted 14 months later in a disorientated state with uncontrolled diabetes mellitus, diffuse abdominal pain and diarrhoea. Abdominal sonography was normal. Upper gastrointestinal radiological examination after an overnight fast showed numerous food residues in the stomach. Gastric peristalsis was decreased as before. The pyloric sphincteric cylinder remained partially contracted with absent cyclical activity, and contained food residues and unidentified tablets which she had found in the ward and swallowed the previous day (Fig. 37.2). (Each tablet measured 1.1 cm in diameter on the films; owing to magnification the true diameter would be in the region of 8.0 to 9.0 mm). The pyloric aperture remained patulous and no obstructing lesion was seen. The condition was diagnosed as diabetic gastroparesis.

Fig. 37.2. Case T.M. Absent cyclical activity of pyloric sphincteric cylinder. Pyloric aperture patulous. Retention of food residues and 8.0mm diameter tablets

Case 37.3. F.J., 64 year old female with longstanding, non-insulin dependent diabetes mellitus had received oral anti-diabetic therapy for 8 years. She was admitted for dyspepsia, epigastric pain and diabetic retinopathy. Upper gastrointestinal radiological examination showed a small benign-looking gastric polyp immediately below the gastro- oesophageal junction. Gastric peristaltic waves were shallow and appeared sluggish. The pyloric sphincteric cylinder was partially contracted throughout the examination; while minor degress of movement of the walls were discernable, there was a total lack of cyclical contraction and relaxation, the appearance remaining more or less unchanged (Fig. 37.3). The pyloric aperture remained patent, having a diameter of approximately 1.0 cm; continuous emptying of fluid barium occurred through the patulous pylorus. At gastroscopy a small, benign polyp was removed. The remainder of the stomach, the pylorus and duodenum showed no lesion. The motility disturbance of the pyloric sphincteric cylinder with the patulous pyloric aperture was thought to be compatible with diabetic gastroparesis.





`Fig. 37.3. A-D Case F.J. Pyloric sphincteric cylinder permanently contracted. Cyclical activity absent. Pyloric aperture patulous with diameter of 1.0 cm`

Case 37.4. M.J., 63 year old female was admitted for ischaemic heart disease, loss of weight and anorexia. She was a known case of non-insulin dependent diabetes mellitus and had received oral therapy for the previous 10 years. There was severe target organ involvement with diabetic retinopathy. Upper gastro-intestinal radiological examination showed a constant contraction of the pyloric sphincteric cylinder which remained unchanged throughout the examination (Fig. 37.4); this was thought to be compatible with early diabetic gastroparesis.

Fig. 37.4. Case M.J. Permanent contraction of pyloric sphincteric cylinder (arrows)

Discussion #

The above patients all had symptoms and signs warranting the clinical diagnosis of diabetic gastroparesis. Radiological studies in all showed absent cyclical activity of the pyloric sphincteric cylinder. It has been shown that normal motility of the sphincteric cylinder consists of alternating cycles of contraction and relaxation, occurring at a rte of approximately 3 per minute (Chap. 13); in diabetic gastroparesis these cycles are absent, the cylinder remaining in a state of permanent, partial contraction. As a maximal or complete contraction of the cylinder does not occur, there is a failure of muscular closure of the pyloric aperture (Chap. 13), which remains patent.

The patulous pylorus allows continuous emptying of fluid barium (Case 37.3). Emptying of solid food residues is retarded (Cases 37.1 and 37.2) due to failure of normal cyclical contraction of the sphincteric cylinder, i.e. failure of the normal mechanism of propulsion of solids. The retention of solid tablets with a diameter of 8.0 mm (Case 37.2) indicates failure of trituration of these tablets.

These conclusions tally with some of those of previous authors, and especially with those of Malagelada et al. (l980) and Camilleri and Malagelada (l984). However, we believe that the "antral" motor dysfunction mentioned by them as well as by Achem-Karam etal (l985) and others, can be placed on a firm anatomical footing if reference is made to the findings of Cunningham (l906), Forssell (l913) and Torgersen (l942) (Chap. 3).

The sustained contraction of the pyloric sphincteric cylinder seen radiologically in diabetic gastroparesis will also explain the "peculiar continuous 3 minute antral contractile activity" found by Camilleri and Malagelada (l984) during manometric studies in some of their patients. One agrees with these authors that the disorder is not invariably of a paretic type; in fact, there appears to be hypomotility due to a spastic or hypertonic condition of the gastric smooth musculature, and in particular of the pyloric sphincteric cylinder.

References #

Achem-Karam SR, Funakoshi A, Vinik AI, et al. Plasma motilin concentration and interdigestive motor complex in diabetic gastroparesis: effect of metoclopramide. Gastroenterology l985, 88, 492-499.
Camilleri M, Malagelada JR. Gastric motility in disease. In: Gastric and Gastroduodenal Motility, ed Akkermans LMA, Johnson AG, Read NW. Praeger Publ, New York l984, pp 213-214.
Camilleri M, Malagelada JR. Abnormal intestinal motility in diabetics with the gastroparesis syndrome. Eur J Clin Invest l984, 14, 420-427.
Campbell IW, Heading RC, Tothill P, et al. Gastric emptyin in diabetic autonomic neuropathy. Gut l977, l8, 462-467.
Carandang NV, Schuman BM, Whitehouse FW. The gastric mucosa of patients in diabetic ketoacidosis: a gastro-camera study. Gastroint Endosc l969, 16, 156-158.
Cunningham DJ. The varying form of the stomach in man and the anthropoid ape. Trans Roy Soc Edin l906, 45, 9-47.
Feldman M, Corbett DB, Ramsey EJ, et al. Abnormal gastric function in long- standing, insulin-dependent diabetic patients. Gastroenterology l979, 77, 12-17.
Feldman M, Schiller LR. Disorders of gastrointestinal motility associated with diabetes mellitus. Ann Int Med l983, 98, 378-384.
Feldman M, Smith HJ, Simon TR. Gastric emptying of solid radio-opaque markers: studies in healthy subjects and diabetic patients. Gastroenterology l984, 87, 895-902.
Forssell G, Über die Beziehung der Röntgenbilder des menschlichen Magens zu seinem anatomischen Bau. Fortschr Geb Röntgenstr 1913, Suppl 30, 1-265.
Goyal RK, Spiro HM. Gastrointestinal manifestations of diabetes mellitus. Med Clin North Amer 1971, 55, 1031-1044.
Gramm HF, Reuter K, Costello P. Radiologic manifestations of diabetic gastric neuropathy and its differential diagnosis. Gastrointes Radiol l978, 3, 151-155.
Horowitz M, Maddox A, Harding PE, et al. Effect of cisapride on gastric and oesophageal emptying in insulin-dependent diabetes mellitus. Gastroenterology l987, 92, 1899-1907.
Kassander P. Asymptomatic gastric retention in diabetics (gastroparesis diabeticorum). Ann Int Med l958, 48, 797-812.
Malagelada JR, Rees WDW, Mazzotta LJ, et al. Gastric motor abnormalities in diabetic and postvagotomy gastroparesis: effect of metoclopramide and bethanecol. Gastroenterology l980, 78, 286-293.
Marshak RH, Maklansky D. Diabetic gastropathy. Amer J Dig Dis l964, 9, 366-370.
Rundles RW. Diabetic neuropathy: general review with report of 125 cases. Medicine l945, 24, 111-160.
Scarpello JHB, Barber DC, Hague RV, et al. Gastric emptying of solid meals in diabetics. Brit Med J l976, 2, 671-673.
Torgersen J. The muscular build and movements of the stomach and duodenal bulb. Acta Rad l942, Suppl 45, 1-191.
Varis K. Diabetic gastroparesis (a review). Scand J Gastroenterol l989, 24, 897-903.
Wright RA, Clemente R, Wathen R. Diabetic gastroparesis: an abnormality of gastri emptying of solids. Amer J Med Sci l985, 289, 240-242.
Yoshida MM, Schuffler MD, Sumi SM. There are no morphologic abnormalities of the gastric wall or abdominal vagus in patients with diabetic gastroparesis. Gastroenterology l988, 94, 907-910.
Zitomer BR, Gramm HF, Kozak GP. Gastric neuropathy in diabetes mellitus: clinical and radiologic observations. Metabolism l968, l7, 199-211.

38 - Prolapse of Gastric Mucosa into the Duodenum

Mon, 01 Jan 0001 00:00:00 +0000

Prolapse of Gastric Mucosa into the Duodenum #

In 1911 Schmiedin described a case of gastric outlet obstruction in which, at operation, a fold of gastric mucous membrane was found to have acted like a ball-valve at the pylorus. The fold could be pushed into the pyloric aperture. While the pre-operative radiographs demonstrated the fold, they did not show definite evidence of prolapse into the duodenum. At operation the fold was excised, resulting in complete recovery of the patient. This appears to be the first description of a case in which redundant gastric mucosa caused significant symptoms.

Eliason and Wright (l925) described a case of a 56 year old male who was operated on for a suspected benign tumor of the stomach. Before opening the stomach a doughy mass was felt projecting through the dilated pylorus into the duodenum. During palpation the mass slipped into the stomach and could not be pushed back into the duodenum. Gastrostomy showed that the entire mucous membrane of the pyloric region was freely mobile on the underlying muscle coat and that it could be pushed through the pylorus, causing invagination of a complete mucous membrane cuff into the duodenum.

Eliason et al. (l926) described a case of a 61 year old male in which the pre-operative radiographs showed a defect extending through the pylorus into the base of the duodenal bulb. It was thought to be a pedunculated tumor of the stomach but operation revealed redundant gastric mucosal folds extending through the pylorus into the duodenum. In another case, that of a 29 year old male, radiographs showed a similar defect in the base of the duodenal bulb. At operation it was found that the pyloric mucous membrane was freely mobile upon the muscle coat and that it had prolapsed through the pylorus into the duodenum. A healed duodenal ulcer was also present.

These appear to be the first recorded cases of prolapse of gastric mucosa into the duodenum. Since that time additional cases have been reported, and by l952 at least 80 verified and 177 unverified cases had been described in the literature. (Comment: "Unverified" indicates cases diagnosed radiologically but not verified by other means. It is possible that the radiological appearances in some of these cases might have been due to normal anatomical variations). These case reports were collected and analyzed in a thesis in which various aspects of the condition were considered (Keet 1952). Subsequently more cases have been reported (vide infra).

At present there appears to be uncertainty, if not scepticism, about the diagnosis, and a need exists for continued investigation of different aspects of the condition. In particular, it seems necessary to determine to what extent the pyloric mucosa is normally mobile in relation to the underlying layers of the wall, and if it is capable of prolapsing into the duodenum.

Normal Mobility of the Mucosa #

Cunningham (1906) pointed out that the mucosa of the stomach is closely bound to the submucosa which, in turn, is loosely attached to the muscularis externa. Forssell (l923, l939) showed that two types of mucosal movements exist: (1) co-ordinated movements of the muscularis externa and the muscularis mucosae, which determine to a large extent the size, shape and position of the macroscopic folds; (2) "mucosal autoplastik", i.e. the inherent ability of the mucosa to move, which accounts for the fine, surface mucosal patterns (Chaps. 2, 13).

Cole (l928) showed that the pyloric valve is normally displaced into the duodenum after death. This normal appearance may be mistaken for prolapse of gastric mucosa, and has to be kept in mind whenever the diagnosis of prolapse has to be considered at autopsy.

Golden (l937) stated that the gastric mucosa was normally freely mobile on the muscular layers. This could readily be demonstrated by the separation of mucosa from muscle wall in the fresh specimen at autopsy, as well as by the projection of the mucous membrane over the edge of the muscle when the living stomach was cut at operation. Scott (l946) confirmed this view, but stated that normally the extent of movement was not sufficient to allow prolapse of gastric mucosa into the duodenum. he found it impossible to pull the gastric mucosa through the pylorus into the duodenum by means of surgical forceps in a series of 126 autopsies in which the stomach was normal. There was one exception, a case of severe cardiovascular disease and myocardial infarction. In this case the gastric mucosal folds could be manipulated into the duodenum comparable to the appearance seen in prolapse of the mucosa at operation.

Bralow and Melamed (l947) examined a number of normal stomachs within three hours post mortem and found that a small amount of gastric mucosa could be pulled through the pylorus, simulating a minor degree of prolapse. Ferguson (l948) concluded from observations at autopsy that the mucosa of the normal stomach was movable relative to the muscularis externa, but in no case sufficiently mobile to allow it to be drawn into the duodenum. Manning and Highsmith (l948) confirmed Golden's observation that the gastric mucosa was freely movable over the muscular coat. Manning and Gunter (l950) concluded that there was a certain looseness of the antral mucosa in the normal. In prolapse it was exaggerated and redundant folds could lie in the pyloric aperture or could easily be drawn through the aperture into the duodenum for variable distances. Keet l952 examined 10 normal stomachs approximately 24 hours post-mortem and found that a fold of pyloric mucous membrane (the mucosal/submucosal component of the pyloric ring) projected into the lumen of the duodenum in every case, confirming the observation of Cole (l928). Surgical forceps were used to determine to what extent the mucosa could be elevated from, or shifted on, the underlying layers in a 2.0 cm wide band on the oral side of the pyloric aperture, i.e. in the pyloric sphincteric cylinder. In a child 8 years of age it was not possible to elevate or shift the mucosa. In all adults the mucous membrane could be lifted from 5.0 mm to 1.0 cm from the muscular coat. Such a fold could be pulled beyond the pyloric ring (right pyloric loop) for a distance of 5.0 to 10.0 mm into the duodenum. At distances greater than 2.0 cm from the aperture it was still possible to elevate the mucosa into folds, which could be moved in all directions but could not be drawn into the duodenum. It was concluded that a certain degree of prolapse of the gastric mucosa could be produced artificially in adults at autopsy by traction on the mucosa close to the pyloric aperture. The greatest extent to which the mucosa could be drawn into the duodenum was one centimeter. Anything greater than this should probably be regarded as abnormal, and in young persons the distance was probably much less.

Williams (l962) examined aspects of the mucosa in 48 fresh post-operative partial gastrectomy specimens, removed because of gastric or duodenal ulceration. The gastric mucosa was found to be soft and pliable and to move easily over the muscularis externa. This was due to the fact that the gastric submucosal coat is normally much wider than that of the duodenum (Chapter 4). Finger pressure could push the mucosa into the pyloric ring, but owing to its attachment at the ring it rose in thebase of the duodenal bulb in a circumferential, two-layered fashion, like a clerical collar. In all cases a mucosal protrusion of 1.0 to 3.0 cm into the duodenum could be produced in this way. According to Williams (l962) a similar minor degree of physiological herniation of gastric mucosa into the base of the duodenal bulb frequently occurs during forceful contraction of the "pyloric press".

Pathoanatomical Diagnosis #

In the 2 cases of Hawley et al. (l949) which came to autopsy it was found that the gastric mucosa slid easily over the muscularis and could be lifted through the pylorus for distances of as much as 2.5 cm. This was considered to be definitely abnormal. In 2 of the 6 cases studied by Manning and Gunter (l950) the submucosa was very loose, slipping freely over the muscularis, and the redundant antral folds could be drawn into the duodenum for a distance of 2.0 cm. In both cases the entire circumference of the mucosa was involved. Histological examination showed chronic inflammatory change in the prolapsed mucosa, submucosa and muscularis mucosae. There appeared to be some hypertrophy of the musculature of the pyloric "sphincter". In 2 of the cases the prolapse consisted of tongue-like projections of gastric mucosa extending into the duodenum. In the 2 other cases in whom a radiological diagnosis of prolapsed gastric mucosa had been made, the patho-anatomical findings were not quite convincing and in our opinion could have been due to post mortem projection of the mucosal part of the pyloric ring into the duodenum.

Zimmer (l950) as well as Manning and Gunter (l950) stated that many pathologists failed to search for the condition at autopsy. The following features were considered to be typical of gastric mucosal prolapse: (1) gross protrusion of gastric mucosa into the duodenal bulb which is quite evident as soon as the stomach and duodenum are opened; (2) the mucosa may not protrude through the aperture but can easily or readily be drawn through it. The latter statement should probably be qualified by the provision that normally the gastric mucosa can be drawn into the bulb for a distance of one centimeter.

Surgical Diagnosis #

If the stomach and duodenum are exposed and inspected at operation, no abnormality will be seen in uncomplicated cases. At palpation no abnormality may be felt in either the stomach or duodenum, as the prolapsing mucosa is so soft that it cannot be felt through the walls (Rendich l923; Eliason et al. l926). A softish mass may be felt in the duodenum (Ferguson l948) or in the pyloric region while the duodenum feels normal (Schmiedin 1911; Norgore and Shuler 1945; MacKenzie et al. 1946; Zacho 1948; Nygaard and Lewitan 1948; Teng 1962). In some cases a doughy, tumor-like mass could be felt in the duodenum, which disappeared under palpation (Eliason et al. 1926; Bohrer and Copleman 1938). In others it could be slipped back and forth between the stomach and duodenum (MacKenzie et al. 1946; Nygaard and Lewitan 1948).

Because of these features all stomachs should be opened at operation whenever the condition is suspected (Scott 1946). In the cases quoted above, folds of redundant gastric mucosa were seen after the stomach had been opened. In several cases big prepyloric folds occluded the aperture, acting like a valve (Schmieden 1911; Eliason et al. 1926; Zacho 1948; Keet 1952, 1953). In other ocases the incision was carried through into the duodenum. When both the stomach and duodenum were opened, redundant folds of gastric mucosa protruding into the duodenum were usually quite evident (Meyer and Singer 1931; Bohrer and Copleman 1938; MacKenzie et al. 1946). In most cases the prepyloric folds were movable on the muscular coat and could easily be pulled into the duodenum for variable distances (Rees 1937; Ferguson 1948; Hawley et al. 1949). In the case of Hawley et al. (1949) for instance, the pyloric mucosa could be drawn through the aperture for a distance of 2.0 cm. In one of the cases described by Rees (1937) the largest gastric mucosal fold was 3.0 cm in height and 4.0 cm in length. It could be pushed through the pylorus into the duodenum with ease. Rees (1937) described another case in which the duodenum was opened first. A soft mass of tissue consisting of a ring of gastric mucosa was seen to project through the pyloric aperture. A similar appearance was seen in a case of Archer and Cooper (1939), where a protrusion of gastric mucosa through the pylorus, viewed from the duodenal side, resembled external haemorrhoids about the anus. In a case of Köhler (1950) the duodenum was also opened first. Initially no sign of prolapse was seen but compressing the prepyloric area caused mucosal folds to escape from the pylorus. In the case of White et al. (1966), a scope inserted through a duodenal incision showed gastric mucosa protruding through the pylorus.

In cases where partial gastrectomy is performed because of prolapse per se, or because of an associated lesion (e.g. gastric or duodenal ulceration), the resection specimen may show large circumferential folds of gastric mucosa which can be manipulated into the duodenum. When such a specimen is placed in formalin, the range of movement of the mucosa becomes progressively less with the passage of time (Keet 1952).

Although the entire circumference of the prepyloric mucosa is usually involved in prolapse of the gastric mucosa, a case of active duodenal ulceration was encountered at surgery in which tongue-like, linear processes of gastric mucosa had prolapsed into the duodenal bulb (Keet 1952).

Gastroscopic Diagnosis #

Moersch and Weir (1942) and later Tesler (1947) visualized large tumor-like masses of redundant gastric mucosa projecting into the lumen of the stomach at gastroscopy. However, in their cases the folds did not prolapse into the duodenum. Scott (1946) did not obtain postive recognition of folds of redundant gastric mucosa slipping though the pylorus in his cases. Manning and Highsmith (1948) reported gastroscopic confirmation in one case. Ten of the cases of Hawley et al (1949) were examined gastroscopically, the condition being visualized in 2. At gastroscopy White et al. (1966) visualized large, hyperaemic oedematous prepyloric folds which pushed back into the stomach as the "sphincter" closed, in their case. The mucosa had a granular and inflammatory appearance and oozed fresh blood.

The diagnosis of prolapse of gastric mucosa into the duodenum has been confirmed gastroscopically in a few cases only. The value of gastroscopy was to rule out gastritis and erosions in cases which had been diagnosed radiologically (Scott 1946). Van Noate et al. (1948) believed that failure to recognize the condition at gastroscopy might be due to inflation of the stomach, the distension causing the previously prolapsed mucosa to return to a more normal position.

Radiological Diagnosis #

The radiological diagnosis of circumferential prolapse of gastric mucosa into the duodenum depends primarily on the demonstration of a rounded or irregularly lobulated filing defect situated centrally in the base of the duodenal bulb. The defect has been described as circular (Eliason et al. 1926; Rees 1937; Bohrer and Copleman 1938; Zimmer 1950), semicircular (Pendergrass and Andrews 1935), irregularly circular (Eliason et al. 1926; Bohrer and Copleman 1938) or arch-shaped (Köhler 1950). The shape of the defect caused by the extruded or prolapsed gastric mucosal folds has been likened to an umbrella (Rees 1937; Van Noate et al. 1948; Fermin 1950; Köhler 1950; Manning and Gunter 1950), a mushroom (Scott 1946; Bralow and Melamed 1947; Hawley et al. 1949; Fermin 1950) and a cauliflower (Scott 1946; Bralow and Melamed 1947; Nygaard and Lewitan 1948). It should be possible to show that the defect is continuous with gastric rugae stretching from the prepyloric area through the pyloric aperture (Scott 1946; Nygaard and Lewitan 1948; Hawley et al. 1949; Todd and Brennan 1957).

The defect in the base of the bulb is not constant, but varies in size and shape (Scott 1946; Nygaard and Lewitan 1948; Hawley et al 1949; Köhler 1950; Keet 1952). This variation is evident not only at different examinations, but also during different stages of the same examination. Most authors seem to associate this characteristic with the position of the patient. It has been frequently stated that the defect is more readily seen with the patient in the horizontal position (Eliason et al. 1926; Rubin 1942; MacKenzie et al. 1946; Manning and Gunter 1950; Zimmer 1950), while others state that it is best seen in the upright position (Köhler 1950). According to some it is equally well seen in the prone and upright positions (Bohrer and Copleman 1938; Scott 1946; Nygaard and Lewitan 1948; Fermin 1950). At times the prolapse may be reduced (Scott 1946) and no defect will be evident (Rees 1937). In our experience the upright position has proved preferable. The duodenal bulb can usually be seen to advantage in this position, and as pointed out by Köhler (1950), the erect posture is the best for a study of peristalsis and for finding a suitable degree of compression. It seems as if the changing nature of the defect may be the result of contractile activity in the distal stomach, rather than changes in the position of the patient.

Bralow and Melamed (1947) thought that mucosal prolapse ensued whenever there was a failure of the normal orad movement of the mucosa during antral systole as described by Golden (1937) (Chap 13). Nygaard and Lewitan (1948) stated that the duodenal defect changed its volume coincident with antral systole and diastole, being more extensive during systole and less obvious in diastole. In the illustrations of one of the cases of Manning and Highsmith (1948) prolapse was only evident during "antral systole". Manning and Gunter (1950) reasoned that inflammatory change in the muscularis mucosae in these cases interfered with its contractility, thus preventing the normal orad movement of the mucosa. Zimmer (1950) noted that changes in the duodenal defect took place during peristaltic activity, and Fermin (1950) stated that prolapse seemed to disappear when gastric peristalsis became less and when the tone of the stomach decreased. In three of our verified cases the size of the defect in the duodenal bulb was seen to be related to the degree of contraction of the pyloric sphincteric cylinder (Keet 1952). In these cases a shallow defect might be visible during relaxation or inactivity of the cylinder. During contraction the duodenal defect became more extensive, reaching its greatest volume with maximal contraction of the cylinder. The same feature was seen in most of our unverified cases as well. It was not unusual for the duodenal bulb to appear normal prior to contraction of the cylinder, with the defect only appearing during contraction.

In contrast, Stiennon (1960) noted that tortuous prepyloric rugae sometimes "prolapsed backward", i.e. in an orad direction, through an advancing peristaltic wave. In most cases a somewhat stronger or tighter wave finally forced the mucosa through the pylorus. A similar phenomenon was described by White et al. (1966), who reported that the hyperaemic and oedematous prepyloric folds pushed back into the stomach as the "sphincter" closed. It was shown in Chapter 13 that orad movement of the mucosa in the pyloric sphincteric cylinder may occur normally during contraction of the cylinder. Furthermore sessile mucosal polyps in the cylinder may move in an orad direction during contraction of the cylinder (Chap. 36).

Levin (l97l) again stated that the duodenal defect of prolapsed gastric mucosa became more prominent during "gastric systole", and that the shape of the bulb reverted to normal during "gastric diastole".

The following are examples of further cases encountered by us:

Case Reports

Case 38.1 J.S., 35 year old male had intermittent, burning epigastric pain apparently related to meals, for the previous 5 years. Large meals occasionally caused vomiting. Clinical examination was negative. Radiology revealed no abnormality in the oesophagus and stomach. During phases of distension or partial contraction of the pyloric sphincteric cylinder, the duodenal bulb appeared normal (Fig. 38.1A). With maximal contraction of the sphincteric cylinder an umbrella- like or mushroom-like defect appeared in the base of the duodenal bulb; it was continuous with longitudinal mucosal folds extending through the fully formed pyloric canal (Fig. 38.1B), and the diagnosis of prolapse of gastric mucosa into the duodenum was made. Gastroscopy showed a few prominent mucosal folds which appeared to be redundant and capable of prolapsing into the duodenum. No evidence of ulceration or other pathology was seen.

Fig. 38.1 A. Case J.S. Partial contraction of pyloric sphincteric cylinder. Base of duodenal bulb normal

Fig. 38.1 B. Case J.S. Maximal contraction of sphincteric cylinder. Umbrella-like defect base of bulb, continuous with longitudinal mucosal folds in pyloric canal

Case 38.2 A.A., 20 year old male, a known case of duodenal ulceration, had received anti-ulcer therapy for the preceding year. Because of a recurrence of symptoms radiographic examination was requested.

Several prominent, tortuous mucosal folds were seen in the pyloric sphincteric cylinder while it was relaxed; the base of the duodenal bulb appeared normal, but there was a possible ulcer near its apex (Fig. 38.2A). During maximal contraction of the pyloric sphincteric cylinder an umbrella-like defect appeared in the base of the duodenal bulb, continuous with longitudinal gastric mucosal folds stretching through the fully formed pyloric canal (Fig. 38.2B). The case was diagnosed as prolapse of gastric mucosa and probable active duodenal ulceration. Control double contrast radiographic examination a month later failed to show the prolapse. At this examination administration of an anticholinergic substance relaxed the gastric walls and insufflation of air caused luminal distension, factors which prevented the sphincteric cylinder from contracting.

Fig. 38.2 A. Case A.A. Prominent, tortuous mucosal folds in relaxed pyloric sphincteric cylinder. Base of duodenal bulb normal. Possible duodenal ulcer

Fig. 38.2 B. Case A.A. Maximal contraction of sphincteric cylinder. Umbrella-like defect base of bulb, continuous with longitudinal mucosal folds in pyloric canal

Case 38.3 M.W., 51 year old male, complained of vague upper abdominal symptoms of 4 months' duration. Clinical examination revealed no abnormality and he was referred for radiological examination. During partial contraction of the pyloric sphincteric cylinder the base of the duodenal bulb showed a shallow, concave indentation (Fig. 38.3A). During maximal contraction of the cylinder an umbrella-like defect was seen in the base of the bulb, with longitudinal mucosal folds in the fully formed pyloric canal (Fig. 38.3B). The case was diagnosed as prolapsed gastric mucosa.

Fig. 38.3 A,B. Case M.W. A Partial contraction of sphincteric cylinder. Shallow, concave indentation base of duodenal bulb. B Case M.W. Maximal contraction of cylinder. Umbrella-like defect base of bulb continuous with longitudinal mucosal folds in pyloric canal

Discussion #

Most of the authors quoted agree that normally there is a certain looseness of the mucosa in the pyloric region of the stomach (i.e. presumably in the pyloric sphincteric cylinder). Scott (l946) found that this was not sufficient to allow prolapse of gastric mucosal folds into the duodenum. Manning and Gunter (l950) stated that in patients with marked prolapse of the gastric mucosa the mucosal looseness was exaggerated and the redundant folds could lie either in the pyloric canal (presumably the pyloric aperture), or could easily be drawn through it into the duodenum for variable distances. Keet (l952) confirmed a certain looseness of the mucosa of the sphincteric cylinder in normal, adult, fresh post-mortem specimens. Williams (l962) showed that a minor degree of extrusion of the gastric mucosa through the pyloric aperture, of not more than 3.0 mm, might occur normally during forceful contraction of the "pyloric press" (presumably the pyloric sphincteric cylinder).

Cases verified at surgery and post-mortem leave little doubt that prolapse of gastric mucosa into the duodenum does occur and that the condition should be recognized as a separate entity.

Types and Grades of Prolapse #

Circumferential. In the majority of cases transpyloric prolapse of gastric mucosa is of a circumferential nature, in which a whole cuff of gastric mucosa prolapses into the duodenal bulb. This has sometimes been divided into mild (synonyms: minimal, slight, early), moderate and severe grades (Scott 1946; Nygaard and Lewitan 1948; Manning and Gunter 1950).

Linear or Tongue-like. Occasionally 2 or 3 tongue-like processes of gastric mucosa, involving only part of the circumference, extend into the duodenum (Hawley et al. 1949; Manning and Gunter 1950). This appearance may be associated with duodenal ulceration as found in verified cases (Zimmer 1950; Keet 1952). In these cases the typical mushroom-like defect of circumferential prolapse is not evident, but 2 or more longitudinal folds extend through the pyloric aperture, each ending independently in the bulb.

Not infrequently a single gastric mucosal fold is seen to extend through the pyloric aperture into the base of the bulb. This is considered to be a normal appearance (Scott 1946; Bralow and Melamed 1947; Hawley et al. 1949) and may have a phylogenetic basis. Torgersen (1942) found a similar appearance in certain lower vertebrates and considered it to be a functional mucosal "torus" in man.

Relationship to Cyclical Activity of Sphincteric Cylinder #

In the present cases as well as in some of those described previously (Keet l952) it is clear that prolapse of gastric mucosa may only occur during maximal contraction of the pyloric sphincteric cylinder. A number of other authors came to essentially similar conclusions, although they used terms such as "antral systole", "gastric systole" and "peristaltic activity" to indicate the concept of contraction of the sphincteric cylinder (Nygaard and Lewitan l948; Fermin l950; Zimmer l950; Levin l97l). According to Bralow and Melamed (l947) prolapse ensued when there was failure of the normal orad movement of the mucosa during "antral systole" as originally described by Golden (l937) (Chap. 13). In our view prolapse almost amounts to expulsion of gastric mucosal folds into the duodenum, together with luminal contents. It is surmized that it may indicate failure of the normal mechanism of "independent but co-ordinated" contractions involving the muscularis externa and mucosa, as described by Forssell (l923, l939) (Chap. 2, 13). It seems as if the occurrence of prolapse depends on the degree of contraction of the pyloric sphincteric cylinder, rather than the position of the patient, in many cases.

On the other hand prolapse of gastric mucosa into the duodenum may also be fickle and unpredictable; its occurrence and extent may vary between examinations and even during a single examination.

The Radiological Differential Diagnosis #

Normal. A number of authors have commented on the fact that the base of the duodenal bulb may normally have a semicircular or concave outline, which may easily be mistaken for a semicircular or mushroom-shaped defect due to prolapsed mucosa (Scott 1946; Bralow and Melamed 1947; Manning and Highsmith 1948; Hawley et al. 1949; Keet 1952; Todd and Brennan 1957). The concave defect often becomes more prominent during maximal contraction of the pyloric sphincteric cylinder (Chap. 13).

Depending on the direction of the pyloro-duodenal axis, the circular indentation of the base of the bulb caused by the normal pyloric ring, may sometimes appear to be exaggerated. This is especially evident when the bulb is seen obliquely from the base. If, in addition the sphincteric cylinder is contracted, producing longitudinal mucosal folds running toward the aperture, the appearance may mimic prolapse closely. In one of the illustrations of Rappaport et al. (1952), a round defect of the base of the bulb with radial striae of barium was said to indicate prolapse of gastric mucosa; however, this could just as well have been a normal stage of contraction of the cylinder. There seems to be little doubt that in many instances, and perhaps even in the majority of non-verified cases, the radiological diagnosis rested upon faulty interpretation of these normal appearances, leading to false positive diagnoses.

Adult Hypertrophic Pylorid Stenosis. A number of authors mentioned adult hypertrophic pyloric stenosis in the differential diagnosis (Pendergrass and Andrews 1935; Scott 1946; Hawley et al. 1949; Keet 1952). In this condition the hypertrophied musculature of the pyloric sphincteric cylinder indents the base of the duodenal bulb, producing a concave defect which may be mistaken for prolapse. The narrowed pyloric canal contains longitudinal mucosal folds converging on the aperture, again mimicking prolapse (Chap. 24). In adult hypertrophic pyloric stenosis the bulbar defect is due to pressure from without, and tends to be constant. In prolapse there is an intraluminal bulbar defect which tends to change in size and shape. Differences are also seen in the motility of the cylinder in the two conditions. Whereas the cylinder may contract and expand normally in prolapse, it remains more or less permanently contracted in hypertrophic stenosis. A complicating factor is that prolapse of gastric mucosa may co-exist with adult hypertrophic pyloric stenosis or narrowing and constriction of the cylinder (Pendergrass and Andrews 1935; Archer and Cooper 1939; MacKenzie et al. 1946; Zacho 1948; Manning and Gunter 1950; Keet 1952).

Prolapsed Benign Pedunculated Gastric Polyps. Prolapsed polyps have long been known to produce rounded defects in the duodenal bulb (Eliason et al 1926; Pendergrass and Andrews 1935). Short and Young (1968) collected 30 cases from the literature and found the majority to be benign adenomas. However, prolapsing lipomas, myomas, fibromyomas and other types of benign gastric polyps may occur. A feature of these defects is that they may vary in position, at times being seen in the confines of the sphincteric cylinder and at other times in the duodenal bulb.

Prolapsed Primary Gastric Carcinoma. Occasionally a prolapsed primary gastric carcinoma may produce a rounded intraluminal filling defect in the first part of the duodenum. Joffe et al. (1977) described 4 cases of this nature, all gastric adenocarcinomas, 2 being pedunculated and 2 sessile (Chap. 33).

Associated Gastroduodenal Lesions #

Most cases of prolapse of gastric mucosa into the duodenum occurred de novo, in the absence of other lesions of the upper gastrointestinal tract. However, in a considerable number of cases other lesions were also encountered during the radiological, surgical or post mortem examinations. The most frequent associated conditions were the following:

Duodenal Ulceration. Not infrequently active duodenal ulceration was encountered (Pendergrass 1930; Scott 1946; Manning and Gunter 1950; Zimmer 1950; Keet 1952). Cases associated with healed duodenal ulceration were also described (Eliason et al. 1926; Archer and Cooper 1939; Fermin 1950).

Gastric Ulceration. Melamed and Hiller (1943) described a case in which a large gastric ulcer was situated on the prolapsed mucosa. In other cases active gastric ulceration was located elsewhere in the stomach, i.e. away from the prolapsing mucosa (Hawley et al. 1949; Keet 1952).

Changes in the Pyloric Musculature. Changes of a hypertrophic or fibrotic nature in the pyloric musculature with consequent narrowing of the pyloric aperture were reported by various authors. Meyer and Singer (1931), Archer and Cooper (1939) and Zacho (1948) noted a perceptible thickening in the pyloric musculature in some of their cases. In a verified case of Ferguson (1948) the pyloric muscle was greatly hypertrophied. In his 3 cases Rees (1937) found the pyloric muscle to be constricted, having the appearance of a white fibrous ring in one case. Manning and Gunter (1950) noted thickening of the pyloric muscular ring in 4 of their 6 cases. Zimmer (1950) described a case with a duodenal ulcer and acute inflammatory changes in the pyloric mucosa and musculature. From these descriptions no clear picture emerged as to the nature and extent of the pyloric hypertrophy.

Cases with an abnormally wide pyloric aperture have also been described. Eliason et al. (1926) noted this feature in one case which came to operation. In the cases described by Nygaard and Lewitan (1968) and by Köhler (1950), the radiographs showed the pyloric aperture to be widely dilated.

Gastritis. Differences of opinion regarding the histology, pathogenesis and classification of gastritis have been referred to previously (Chap. 28). In the present context it is to be expected that different authors may have used different criteria in diagnosing gastritis. A number of cases of transpyloric prolapse of gastric mucosa have been described in which "gastritis" was mentioned as an associated lesion.

Bohrer and Copleman (1938) described one case in which there was associated acute and subacute gastritis. In two verified cases of Norgore and Shuler (1945) the pyloric region showed evidence of chronic gastritis. Histological examination of the resected mucosa in 5 operated patients described by Scott (1946), showed a slight increase in lymphocytes, plasma cells and eosinophils throughout the mucosa and submucosa; however, this was not considered sufficient to warrant a diagnosis of gastritis. Judd and Moe (1947) described a case in which erosive gastritis and infiltration by plasma cells were present. A verified case described by Nygaard and Lewitan (1948) had chronic gastritis and healed erosions. One of the 3 verified cases of Hawley et al (1949) showed a moderate infiltration of the gastric mucosa with plasma cells and lymphocytes. The second case showed no gross evidence of gastritis, and the third, in which 2 gastric ulcers were also present, had acute on chronic inflammatory reaction in the pyloric area. Two cases of verified circular prolapse studied by Manning and Gunter (1950) both showed chronic gastritis with heavy infiltration of lymphocytes and plasma cells in the prolapsed mucosa, submucosa and muscularis mucosae. In his verified case Teng (1962) found the submucosa to be thickened and oedematous; there was mild inflammatory reaction without ulceration. White et al. (1966) found the prepyloric mucosal folds to be hyperaemic and oedematous with a granular, inflammatory appearance.

Possible True Complications #

Ulceration and Haemorrhage. Cases with superficial ulceration of the prolapsed mucosa and consequent slow oozing of blood from the ulcerated surfaces were described by a number of authors (Pendergrass and Andrews 1935; Bohrer and Copleman 1938; Archer and Cooper 1939; MacKenzie et al 1946; Scott 1946; White et al. 1966). In some cases massive gastro-intestinal haemorrhage occurred (Ferguson 1948; Moon and Speed 1949; Fredel 1960). The above authors usually regarded ulceration and haemorrhage as a true complication of the condition.

Obstruction of the Pyloric Aperture by Redundant Gastric Mucosal Folds. Gastric mucosa prolapsing into the duodenum may, at times, pile up in the form of large, redundant prepyloric folds causing obstruction at the gastric outlet (Schmiedin 1911; Eliason et al 1926; Scott 1946; Judd and Moe 1947; Zacho 1948; Fredell 1960). (In the 2 cases of Zacho there was associated pyloric muscular hypertrophy). It seems that redundant prepyloric mucosal folds, causing obstruction, may also be regarded as a true complication.

Malignancy and Prolapse of Gastric Mucosa #

Malignancy does not appear to be a complication of gastric mucosal prolapse. The presence of benign papillomata on prolapsed mucosa was reported by Pendergrass and Andrews (1935). In one of the polyps a small plaque of malignant tissue was encountered; it was considered to be an incidental finding not directly related to the prolapse. One other case associated with malignancy was described, namely that of Rubin (1942), in which the malignant polypoid process involved the entire gastric mucosa. This appeared to be a case of general gastric polyposis with malignant degeneration, not confined to the prolapsed mucosa. According to Nygaard and Lewitan (1948) no instance of malignant change in a true case of transpyloric mucosal prolapse had been reported up to that time. This statement still appears to be valid at the present time. However, a primary gastric carcinoma may prolapse into the duodenum, causing a rounded, intraluminal filling defect in the bulb, as described by Joffe et al. (1977).

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39 - Acid Corrosive Injuries and the Pyloric Sphincteric Cylinder -

Mon, 01 Jan 0001 00:00:00 +0000

Acid Corrosive Injuries and the Pyloric Sphincteric Cylinder #

Acid and alkali corrosives affect the body tissues in different ways (Donner et al l98l). It is generally agreed that ingestion of corrosive acids primarily damages the stomach, and particularly its distal half, with little involvement of the oesophagus. Alkali ingestion on the other hand, primarily damages the pharynx and oesophagus, and only rarely involves the stomach (Steigmann and Dolehid l956; Marks et al l963; Poteshman l967; Ritter et al l968; Allen et al l970; Franken l973; Nicosia et al l974; Donner et al l98l; Gimmon and Durst l98l; Jena and Lazarus l985).

Acid corrosives cause rapid coagulation necrosis of one or more layers of the gastric wall (Steigmann and Dolehid l956; Donner et al l98l; Gimmon and Durst l98l). Occasionally this may be limited to the mucosa, in which case healing may occur, but the process is much more likely to involve the deeper layers as well (Gimmon and Durst l98l). The squamous epithelium of the oesophagus apparently offers resistance to acid compounds. In 16%-20% of cases of acid corrosive gastritis however, associated oesophageal injury is seen (Karon l962; Poteshman l967; Gimmon and Durst l98l).

Alkaline corrosives tend to dissolve tissues in the mouth, pharynx and oesophagus, and is neutralized by gastric acid in the stomach. However, in 20% of cases of alkaline corrosive injury the stomach is also affected (Nicosia et al l974).

By l98l over 200 cases of acid corrosive gastric injury had been documented (Gimmon and Durst l98l), while only a few cases of alkaline corrosive injury had been reported in the literature (Ritter et al l968; Allen et al l970; Nicosia et al l974). The degree and extent of gastric involvement in corrosive injuries depends on a number of factors, including the nature of the caustic substance, its concentration and viscosity, the quantity swallowed, the duration of contact with the gastric wall, and whether it was taken on an empty or a full stomach (Ritter et al l968; Allen et al l970; Franken l973; Nicosia et al l974; Jena and Lazarus l985).

As described by Marks et al (l963), Ritter et al (l967), Franken (l973) and others, the course of corrosive damage can be divided into different phases. In the immediate, acute phase an inflammatory exudate occurs on the mucosal aspect of the gastric wall; there is mucosal ulceration and necrosis, accompanied by oedema and an intense inflammatory reaction in the surrounding tissues. Full thickness burns of the wall are seen with diffuse gangrenous areas in the submucosa and muscularis externa, and fibrinous peritonitis. This is soon followed by marked inflammatory reaction and vascular congestion, with resultant haemorrhage. After 2 to 5 days sloughing and ulceration may occur with a distinct possibility of perforation.

In patients who do not succumb during the acute phase, fibroblastic activity commences. There is progressive cicatrization during the following 2 to 4 weeks, leading to stricture formation. In cases of severe burns the mucosa and submucosa do not regenerate. The fibrosis produces a narrow, non-distensible lumen of varying length, but often extending proximally from the pylorus as far as the incisura angularis. Symptoms of gastric outlet obstruction usually commence 4 to 6 weeks after the acute phase.

The damage to the gastric walls also entails loss of gastrin producing and other endocrine cells as well as loss of intrinsic nerves in the affected parts (Steigmann and Dolehid l956). Karon (l962) described a delayed gastric syndrome, occurring 2 to 6 weeks after ingestion of acid. This consists of tight stenosis in the distal two-thirds or distal half of the stomach, producing obstruction and vomiting, while the damage to the gastrin producing cells causes a histamine-fast achlorhydria. Similar cases, some having additional gastric ulcers, were described by Marks et al (l963) and Gimmon and Durst (l981). The gross anatomical and radiological resemblance to carcinoma of the stomach was stressed by Karon (l962), Marks et al (l963), Franken (l973), Gimmon and Durst (l98l) and Jena and Lazarus (l985). The following cases are examples of acid corrosive injuries:

Case Reports #

Case 39.1 L.M., female aged 29 years, accidentally swallowed a cupful of hydrochloric acid. This was followed by burning restrosternal and epigastric pain and continuous vomiting. Radiographic examination a week later revealed no abnormality in the oesophagus. A severe stricture, causing almost total occlusion of the lumen and commencing as a funnel-shaped narrowing in the region of the incisura angularis, was seen in the distal third of the stomach (Fig 39.1). At times a trickle of barium traversed the stricture, which was constant; the sphincteric cylinder and pyloric aperture were unidentifiable, with total absence of cyclical contraction and relaxation. Repeat examination after another week showed similar features, although the stricture appeared to be somewhat less severe. Antrectomy and Billroth I anastomosis 3 weeks after the incident showed the distal 5.0 to 6.0cm of the stomach to be oedematous and stenotic; the duodenum appeared normal. Microscopically severe fibrotic change was seen in the submucosa, with areas of necrosis and partial regeneration in the mucosa.

Fig. 39.1. Case L.M. Funnel-shaped, severe stricture in distal stomach

Case 39.2 D.P., 23 year old male, swallowed half a tumblerful of hydrochloric acid in an attempted suicide. After some hours he was admitted to a peripheral hospital where gastric lavage with dilute alkali was performed. Dysphagia and continuous vomiting necessitated oesophagoscopy after 10 days. This showed mucosal erosions and moderate oesophageal stenosis at 33cm. Upper gastrointestinal barium examination revealed a constant narrowing of the distal third of the stomach with absent cyclical contraction and relaxation of the pyloric sphincteric cylinder (Fig 39.2). This was associated with a patent pylorus and rapid emptying of fluid barium. The entire duodenum showed loss of mucosal pattern with rigid walls; immediately beyond the duodeno-jejunal flexure a 3.0cm long stenotic area was evident.

Fig. 39.2. Case D.P. Constant narrowing distal third of stomach. Pyloric aperture patent. Absent cyclical activity of pyloric sphincteric cylinder. Duodenal walls rigid. Stenosis proximal jejunum

Discussion #

As can be expected, the above cases show that acid corrosive injury of the stomach is not contained by anatomical boundaries, and therefore not necessarily limited to the pyloric sphincteric cylinder or to the pyloric mucosal zone. Usually the walls of the cylinder are damaged as part of a more extensive injury; the result is that the pyloric sphincteric cylinder is no longer recognizable as a functional unit. In Case 39.1 the cylinder was almost totally occluded as part of a more extensive stricture, causing obstruction to the flow of fluid barium. In Case 39.2 partial contraction of the cylinder "fixed" the pyloric aperture in the open position, leading to rapid emptying of fluid barium; theoretically the lack of cyclical contraction of the cylinder in this case should hamper trituration (Chap 18) and delay the emptying of solids (Chap 18).

A consequence of corrosive injury of the pyloric mucosal zone is that gastrin producing G-cells in this location may be affected, leading to a histamine-fast achlorhydria. It is probable that cells producing other regulatory peptides, e.g. somatostatin, vasoactive intestinal peptide and enkephalin (Chap 9) will also be damaged.

References #

Allen RE, Thoshinsky MJ, Stallone RJ, et al. Corrosive injuries of the stomach. Arch Surg l970, 100, 409-413.

Donner MW, Saba GP, Martinez CR. Diffuse diseases of the oesophagus: a practical approach. Sem Roentg l98l, 16, 198-213.

Franken EA. Caustic damage of the gastrointestinal tract: roentgen features. Amer J Roentg Rad Ther Nucl Med l973, 118, 77-85.

Gimmon Z, Durst AL. Acid corrosive gastritis: a plea for delayed surgical approach. Amer J Surg l98l, 141, 381-383.

Jena GP, Lazarus C. Acid corrosive gastritis. South Afr Med J l985, 67, 473- 474.

Karon AB. The delayed gastric syndrome with pyloric stenosis and achlorhydria following the ingestion of acid: a definite clinical entity. Amer J Dig Dis l962, 7, 1041- 1046.

Marks IN, Bank S, Werbeloff L, et al. Natural history of corrosive gastritis: report of five cases. Amer J Dig Dis l963, 8, 509-524.

Nicosia JF, Thornton JP, Folk FA, et al. Surgical management of corrosive gastric injuries. Ann Surg l974, 180, 139-143.

Potesham NL. Corrosive gastritis due to hydrochloric acid ingestion. Amer J Roentg Rad Ther Nucl Med l967, 99, 182-185.

Ritter FN, Newman MH, Newman DE. A clinical and experimental study of corrosive burns of the stomach. Ann Otol Rhin Laryng l968, 77, 830-841.

Steigmann F, Dolehid RA. Corrosive (acid) gastritis: management of early and late cases. New Engl J Med l956, 254, 981-986.