Chapter 39 (page 196)

The Pyloric Sphincteric Cylinder in Health and Disease

Go to chapter: 1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 | 16 | 17 | 18 | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | 27 | 28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 | 36 | 37 | 38 | 39
Chapter 39 (page 196)

Chapter 39

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).