Reprinted from Eating Disorders Review
November/December Volume 26, Number 6
©2015 iaedp
Q. One of my patients with bulimia nervosa (BN) has terrible problems with gastric motility. Are there any concerns about this condition in patients with eating disorders? (DL, Pittsburg, PA)
A. Two recent cases illustrate the seriousness of gastric dilatation and gastric necrosis, which can occur in patients with BN–and anorexia nervosa (AN) as well–who eat a huge amount of food in a short time.
A team of Spanish gastroenterologists recently reported a case of gastric necrosis following acute gastric dilatation. Dr. Jorge Navarrete-Panach and colleagues treated a 36-year-old woman who presented at their hospital’s emergency room with sudden onset of epigastric pain throughout her abdomen (Rev Esp Enferm Dig. 2015; 107: 577). Twenty-four hours before she was admitted, the woman had eaten a large amount of food at one sitting. When she was examined, her abdomen was painful and distended, with signs of peritoneal irritation. A complete blood count showed neutrophilic leukocytosis without electrolyte disorders, and abdominal x-ray films and abdominal computed tomographic scan showed a massive and dilated stomach, from the diaphragm to the iliac bone.
Because of the progressive deterioration of the patient, emergency surgery was performed, with total gastrectomy and esophagoplasty. Extensive necrosis of the posterior wall and gastric fundus and patchy necrosis were seen throughout the greater curvature. The specimen from the total gastrectomy was massively dilated and necrotic, measuring 40 cm along the greater curvature and 11 cm along the lesser curvature. After surgery the patient was assessed by a team of psychiatrists, and admitted for treatment of her eating disorder. She had no further complications.
In a second case, reported by Dr. Seung-Mok Youm and fellow anesthesiologists in South Korea, a 21-year-old woman with a history of BN arrived at the emergency room complaining of severe abdominal pain after eating a huge meal 5 hours before (Korean J Anesthesiol 2015 Apr;68(2):188-92. doi: 10.4097/kjae.2015.68.2.188. Epub 2015 Mar 30). On arrival at the emergency room, extreme abdominal distension was detected and the patient’s legs changed color; the patient had a history of BN and AN, and she had a relatively low body mass index (18.44 kg/m2). CT scans suggested severe gastric dilatation, so abdominal compartment syndrome was suspected, and emergency laparotomy was scheduled. An abrupt hemodynamic collapse developed just after the operation started. In spite of active resuscitation for 29 minutes, the patient did not recover.
Dr. Youm and colleagues attributed the cause of death to the sustained release of an unexpectedly large amount of potassium into the bloodstream from ischemic tissue. Acute kidney injury might have already developed since her urine output was nearly zero for a couple of hours. The emergency team failed to predict lethal hyperkalemia because the patient’s electrolyte analysis findings in the emergency room were almost normal, and there had not been any reported cases of acute gastric dilatation with fatal hyperkalemia.
Acute gastric dilatation is seldom reported, and gastric necrosis is very uncommon because the stomach has a very rich blood supply. This rare complication of an eating disorder can occur after a large intake of food over a very short period. About 60% of patients with AN or BN have altered gastric motility, which places them at risk of developing severe gastric dilatation, just as in these two cases. Even in cases of acute gastric dilatation without necrosis or perforation, the mortality may reach more than 15%, so it is important to monitor such patients closely after decompression surgery.
— SC
