A 31-year-old woman with a history of multiple sclerosis on treatment with interferon and bulimia nervosa, diagnosed two years ago, came to the emergency department for acute abdominal pain after a binge. She was undergoing individual and group psychotherapeutic treatment. She denies self-harm attempts or previous psychiatric admissions. She started binge eating when she was 15 years old in relation to the stress caused by exams and since then, her life has revolved around binge eating and purgative behaviours. She reports that binge eating interferes with a normal working and social life. Since the onset of the eating disorder, the number of binges exceeds monthly. The purgative measures she habitually uses are induced vomiting and laxatives.
The patient comes to the emergency department with severe abdominal pain of 7 hours' duration, accompanied by a feeling of fullness, nausea and vomiting. She reported having eaten a large amount of food in the last few hours, after which she had induced vomiting on several occasions without being effective.
Physical examination revealed the patient's thinness: height 159 cm, weight 42 kg (BMI: 17), the patient's abdomen was globular, tympanic, with scarce bowel sounds. Temperature 36.3 oC, blood pressure 125/65 mmHg and heart rate 75 bpm. Plain abdominal X-ray showed a large gastric dilatation.
Lymphocyte count: 19,800 with 93.5% neutrophils. Amylase 286 IU/l, glycaemia: 229 mg/dl, Na: 147 mmol/L, K: 3.2 mmol/L, LDH: 570 and creatinine kinase (CK) of 92.
He was prescribed IV fluids, enemas and nasogastric tube placement. Neither the enemas nor the nasogastric tube were effective.
Ten hours later, the patient went into preshock. Physical examination showed lividity in the lower limbs and weakness of the paedial pulses, as well as a heart rate of 120 bpm, blood pressure 80/60. Blood glucose: 430 mg/dl, amylase: 1,485 Ul/l, ALAT: 1,008 U/L, LDH: 8,102, CK: 8,310, C-reactive protein: 32 ng/ml and metabolic acidosis with pH: 7.07, PO2: 32 mmHg, PCO2: 78 mmHg, bicarbonate: 22.6 mEq/l and lactic acid of 33 mg/dl.
Computed tomography examination showed large gastric dilatation, occupying most of the abdominal cavity with a hydro-aerial level and aortic compression. The large gastric dilatation compresses the rest of the abdominal structures including the great vessels, aorta and cava and their branches, which is the cause of the low attenuation coefficient images identified in the pancreas and kidneys in relation to areas of ischaemia of these viscera.
Given the severity of the patient, and the absence of improvement with conservative measures, a laparotomy and gastrotomy was performed with extraction of food material (approximately 7 litres) from the gastric chamber, in which a large amount of undigested food debris was found. Two days later, a control CT scan was performed, which showed a significant decrease in the volume of the gastric chamber and the restoration of the aortic calibre, as well as the recovery of normal renal and pancreatic perfusion.
After 4 weeks of admission to the ICU, due to the existence of multi-organ failure related to hypoperfusion of abdominal viscera, acute hepatic failure due to toxic-ischaemic hepatitis and toxic-metabolic encephalopathy, pancreatic ischaemia, intestinal ischaemia, circulatory shock, abdominal ischaemic-perfusion syndrome, acute renal failure and acute respiratory failure, she was discharged from the ICU in good clinical condition.
