Acute Pancreatitis as an Unusual Complication of Corrosive Ingestion

We read with great interest the case report “Unusual presentation and complication of caustic ingestion. Case report” by Lionte et al. in the March 2007 issue of Journal of Gastrointestinal and Liver Diseases (1). We report a young patient who presented with acute corrosive ingestion and developed pancreatitis 10 days after ingestion. A 25 year old young female presented as an emergency case following accidental ingestion of 100ml of hydrochloric acid (HCl). She vomited immediately after HCl ingestion. At admission, she was hemodynamically stable with saliva drooling. On examination, she had a red, swollen tongue and her oropharynx was edematous and inflamed. Nothing could be given by mouth, only intravenous fluids and intravenous proton pump inhibitor (PPI). Her liver function tests, hemogram, renal function tests, chest X-ray, urine routine examination, ECG, abdominal X-ray and ultrasonography were normal. The esogastroduodenoscopy performed two days after ingestion revealed erythema and edema of oropharynx, Grade II A injury in esophagus, grade II B injury in stomach and duodenum (2). On day 10 she had severe epigastric pain radiating to her back associated with vomiting. On examination she had epigastric tenderness. Her serum amylase and lipase levels were more than 3 times elevated. Her serum calcium, serum lipids were normal, abdominal ultrasound did not show sludge or stones in gallbladder, common bile duct was normal and abdominal Xray was normal with no evidence of perforation. Contrastenhanced CT of the abdomen showed a bulky pancreas. Continuous tube aspiration, intravenous fluids, prophylactic antibiotics, analgetics and PPI but nothing oral were given. Symptoms improved over the next 5 days. On day 16, a liquid diet was initiated, following which she had recurrent vomiting. She underwent repeated endoscopy which showed similar lesions in the esophagus, stomach, and also in the first part of the duodenum. There was stricture at D1 and D2 junction which could not be passed by the endoscope. The patient underwent a feeding jejunostomy. After 3 weeks, a barium swallow and meal showed esophageal stricture with reduced capacity of the stomach. She underwent dilatation of the esophageal stricture with a 7mm Savary-Gillard dilator. Further three sessions of dilatation with a 9 mm dilator followed. The intention was to dilate the esophageal stricture and then to perform balloon dilatation of the duodenal stricture. Acid injury is usually limited to the stomach: 6-20% of patients have associated esophageal and small intestinal injuries (2). The subsequent sparing of the duodenum is thought to be due to a pyloric spasm induced by the irritant acid in the antrum and the alkaline duodenal pH (3). Our patient had circumferential ulceration at D1 and D2, which led to duodenal stricture. She developed pancreatitis, with high amylase and lipase levels in the setting of severe pain in the abdomen, due to papillary edema consecutive to corrosive ingestion. Necrotizing pancreatitis has been reported in patients with transmural necrosis and perforation of the stomach (3). Our report supports the description of two out of nine patients in the surgical series who had pancreatic head necrosis and distal necrotizing pancreatitis with involvement of duodenal mucosa (4). However, even in initially stable patients, significant injuries of the duodenum and pancreas should be suspected and actively searched for. Sandeep Nijhawan Pankaj Jain Dept. Gastroenterology SMS Medical College Jaipur, Rajasthan, India