Abstract
Acute gastric dilation after binge eating may lead to ischaemic necrosis and perforation of the gastric wall. Though rarely seen owing to the rich blood supply of the stomach, its sequelae may be avoided by prompt decompression of the dilated stomach. We present such a case heretofore rarely reported from India.
Case report
A 20-year-old male with no known comorbidity had just completed a regular month-long religious fast with a heavy dinner of more than usual quantity. After 1–2 h, he started complaining of sharp, severe, non-radiating upper abdominal pain, which progressed to involve the entire abdomen. He had no vomiting.
Admitted 8 h after the onset of symptoms, he had tachycardia (pulse: 135/min), hypotension (BP: 100/80 mm Hg), tachypnoea (rate: 34/min), normal saturation (SpO2: 95%), and normal temperature (36.5°C). He was conscious and oriented, but in severe pain, with a rigid grossly distended silent abdomen not moving with respiration. He had not passed urine since the onset of symptoms.
A nasogastric tube was inserted, but it produced no aspirate and did not reduce the abdominal distension. An erect chest radiograph revealed a pneumoperitoneum. His blood investigations were all within normal limits, as shown in the table:
After vigorous fluid resuscitation, an exploratory laparotomy was carried out, revealing much undigested food debris lying free in the peritoneal cavity. There was no perforation in the duodenum, nor lower oesophagus. A large rent in the gastric fundus along its greater curve (Figure 1) was found. The gastric wall adjacent the tear was thinned out.
Gastric perforation at fundus.
Devitalized tissue was excised, and primary closure in two layers was performed. A feeding jejunostomy was fashioned 15 cm distal to the duodeno-jejunal flexure. A thorough peritoneal wash was carried out, and two drains were placed in the pelvis and right subhepatic space. Mechanical ventilation and inotropic support with noradrenaline and vasopressin were provided, but 19 h later, he succumbed to septicaemia.
Discussion
The rich blood supply of the stomach makes ischaemic necrosis and perforation rare. Dilation may occur from adhesive ileus, chronic outlet obstruction from neglected duodenal ulceration or pancreatic tumour, infection, parturition, central nervous system lesions, and trauma. 1 Bulimia may precipitate acute gastric dilatation, particularly after episodes of anorexia, which is more common in females. 2 In the upper gastrointestinal tract, oesophageal perforation (the Boerhaave syndrome) is related to binge eating, 3 while gastric and duodenal perforations are not commonly associated with it. When the intragastric pressure exceeds 30 cm H2O, 4 the intramural blood supply reduces. During fasting or starvation, the stomach undergoes atony and muscular atrophy. Sudden ingestion of large quantities of food may thus overtax an already weakened gastric wall.5, 6 Another risk factor contributing to mortality and morbidity in these cases is the infamous ‘refeeding syndrome’, occurring due to fluid and electrolyte shifts after breaking a prolonged starvation state. The metabolic switch to using fat and protein as the main source of energy in starvation when followed by sudden refeeding can result in decreased serum levels of phosphate, potassium, and magnesium. 7 Another condition that can lead to perforation of the adult gastrointestinal tract is Pigbel disease, caused by Clostridium perfringens and occurring commonly in immunocompromised or malnourished individuals. It has also been reported to occur among those who break their starved state by eating either large quantities of meat (pork) or trypsin inhibitor-containing foods like sweet potatoes, soybeans or peanuts. 8
The distended fundus may press against the right diaphragmatic crus and so create a one-way valve, 9 which occludes the oesophago-gastric junction, thus prohibiting vomiting.
A gastric splash should be looked for; a radiograph may reveal an air-fluid level in a markedly distended stomach, 6 which may be confirmed by ultrasound or a CT scan showing the distended stomach extending into the pelvis. 10
If identified early, gastric dilation can be decompressed by nasogastric decompression, though if this is no longer possible, a surgical decompression is urgently indicated.
Once perforation has occurred, a massive chemical peritonitis ensues, resulting in a mortality rate of 80%. 11
Footnotes
Declaration of conflicting interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
Patient's consent
Informed written consent was obtained from the patient's relative regarding publishing of his medical data.