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.
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| 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.
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| 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.