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CASE REPORTS

Corrosive Gastric Outlet Obstruction : Is "Early" Surgical Repair Harmful
Prashant K Adivarekar, Gaurav Baheti, Dharmendra Singh, Sanjay B Raut
Gastric outlet obstruction due to accidental corrosive acid ingestion is as well known as it is discouraging. We present here three cases of corrosive prepyloric strictures and our management modalities. Having burnt our fingers in the first case we were wiser in planning a staged procedure for the next two patients with satisfying results and thus questioning the rationale of an early surgical intervention in these cases.

INTRODUCTION
Corrosive acid ingestion still remains a major health hazard in children and there is an urgent need for public awareness, proper and effective legislation, ensuring correct labelling and safe packaging. Because of the greater use of alkali in the household caustic injury caused by acids is relatively uncommon. Tendency of the acids to “lick the oesophagus and bite the pyloric antrum”1 is known, but recently gastric burns caused by alkali corrosives have been reported.2 We present here our experience in the management of patients with corrosive gastric outlet obstruction.

CASE REPORTS
Case 1
A three and half year old boy presented to us with history suggestive of gastric outlet obstruction since 5 days. Barium study revealed a abrupt cut off at the pylorus. Scopy done showed an inflamed pylorus with a non-passable stricture at the pre-pyloric region. Patient was explored and a Heinecke-Mickuliz pyloroplasty was done. Post-op was uneventful and the patient was discharged. A week after the discharge patient was brought with similar complaints. On careful probing, history of accidental ingestion of battery fluid was obtained. Repeat dye study showed abrupt cut off at the pyloric region. A feeding jejunostomy was done. Patient was discharged and was followed up after 8 weeks at which time a gastro-jejunostomy was done. Post-op was uneventful. Patient is asymptomatic and is thriving well.

Case 2
A seven year old girl had history of haematemesis following accidental ingestion of battery fluid for which she was treated at a private nursing home. Patient was referred to us for persistent vomiting with significant weight loss. Barium study showed dilatation of the stomach with abrupt cut off at the pylorus.
OGD scopy showed the pylorus to be inflamed and oedematous and the scope could not be negotiated across. (Fig. 2)
A feeding jejunostomy was done and the patient was discharged to allow for the complete healing process to take place. After two months a repeat barium study showed complete gastric outlet obstruction. The patient was explored. A tight prepyloric stricture was evident. A finneys type pyloroplasty was done. Post-op was uneventful. After 6 weeks the patient is asymptomatic, is gaining weight and barium study shows dye passing easily across into the duodenum. (Fig. 3)

Case 3
A seven year old girl was referred to us with history of corrosive ingestion 2 weeks back. OGD scopy done showed the presence of circumferential corrosive ulcer with pyloric obstruction. Patient had complaints of persistent vomiting with significant weight loss. A feeding jejunostomy was done and the patient was discharged, with the reparative surgery to be done after 6-8 weeks, to allow for the complete healing process to take place. Repeat Barium study showed abrupt cut off at the pyloric region, with the finding confirmed on gastroscopy. Patient underwent an explorative laparotomy 8 weeks after the initial insult which showed the presence of a prepyloric stricture. A finneys type pyloroplasty was done. At 6 weeks follow-up the patient is asymptomatic and is thriving well.

DISCUSSION
The first description of gastric burn without the involvement of the oesophagus was in 1828, which was a case of sulphuric acid ingestion.3,4 Viscosity and specific gravity of corrosive acids is lower than that of liquid alkalis, hence acids are associated with rapid transit through the oesophagus and the damage primarily occurs in the antrum of the stomach.5 Also the related antral spasm causes pooling of the corrosive at the antrum leading to burns at the antrum.6,7 Another reason for the greater susceptibility of the stomach is its columnar epithelium, whereas the oesophagus has a more resilient squamous epithelium.3 Some investigators have also reported cases of corrosive prepyloric strictures after alkali products instead of the solid or crystalline forms.2,4 The degree of mucosal injury depends on the nature of the agent, the amount and the concentration ingested, the amount of food in the stomach at the time of ingestion and the mode of ingestion.8-10

The management of gastric outlet obstruction is operative, but there is still some controversies especially in the timing of the surgery. In the first case we burnt our fingers, by an early intervention, for want of a proper history of corrosive ingestion. Once the history was confirmed we waited for the complete healing process to take place after which we went ahead with the reparative surgery. Hence reparative surgery is to be done after complete healing process is over. During this phase if any insult is added it will cause more extensive fibrosis.

The guidelines propagated by us are as follows:
Initial resuscitation with airway management and cardiovascular stability.

Fibreoptic endoscopy within 24-48 hours for grading the severity of injury.

In the early cases supportive medical therapy in the form of intravenous antibiotics, H2 receptor blockers and steroids which interfere with the inflammation, collagen synthesis, fibrosis and chronic scarring are advocated.

Drugs used : steroids (prednisolone or recently dexamethasone). Antacids, proton pump inhibitors.

A feeding jejunostomy is done for the maintenance of enteral nutrition and the patient is discharged.

Patient followed up after 6-7 weeks. Investigated with repeat barium study and endoscopy and accordingly the reparative surgery is planned.

Process of Healing
First 24 hours : Haemorrhage, thrombosis and marked inflammation.

After 48 hours : Thrombosis of the submucosal vessels, hence local necrosis and gangrene.

Till 3rd week : Necrotic tissue is sloughed, oedema decreases and neovascularisation begins.

3-6th week : Scar formation with fibroblast proliferation and commencement of stricture formation, mucosal re-epithelisation begins by the 4th week and is usually complete by the 6th week.

REFERENCES
1. Marks IN, Banks S, Werbeloff L, et al. The natural history of corrosive gastritis: report of five cases. Am J Dig Dis 1963; 8 : 509-24.
2. Ciftci AO, Senocak ME, Buyukpamukcu N, et al. Gastric outlet obstruction due to corrosive ingestion: incidence and outcome. Pediatr Surg Int 1999; 15 : 88-91.
3. Maggi ALC, Meeroff M. Stenosis of the stomach caused by corrosive gastritis. Gastroenterology 1953; 24 : 573-8.
4. McAuley CE, Steed DL, Webter MW. Late sequelae of gastric acid injury. Am J Surg 1985; 149 : 412-5.
5. Gray HK, Holmes CL. Pyloric stenosis caused by ingestion of corrosive substance: report of a case. Surg Clin North Am 1948; 28 : 1041.
6. Testa GF. Contributo radiologico experimentalle allo studio delle lesioni esofagee e gastriche nelle causticazioni de alkali. Radio Med 1938; 25 : 17.
7. Jalundhwala JM, Shah RC. Corrosive stricture of the stomach. Am J Surg 1967; 114 : 461-4.
8. Ritter FN, Newman MH, Newman DE. A clinical and experimental study of corrosive burns of the stomach. An Otol Rhinol Laryngol 1968; 77 : 830-42.
9. Chodak GW, Passaro E. Acid ingestion: Need for gastric resection. JAMA 1978; 239 : 225-6.
10. Lowe JE, Graham DY, Boisaubin EV, et al. Corrosive injury to the stomach, the natural history and the role of fibreoptic endoscopy. Am J Surg 1979; 137 : 803-6.

EARLY INTERVENTION
Double-blind trial in patients from 32 countries to assess whether budesonide is useful in the treatment of early onset mild persistent asthma. Their results showed that the drug was effective in reducing the likelihood of a severe asthma-related event, as well as increasing the number of symptom-free days.
Lancet Infect Dis 2003; 3 : 1066, 1071



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