Octreotide for insulin overdose, combined with methamphetamine, linked to fatal mesenteric microvascular compromise

Severe hypoglycemia from insulin overdose is a critical medical emergency often complicated by comorbidities and concurrent substance use. Current management typically involves high-dose dextrose infusions. However, persistent hypoglycemia may necessitate agents like Octreotide to suppress endogenous insulin secretion. This case highlights a rare but fatal outcome where the interplay of insulin overdose, Octreotide administration, and recent methamphetamine use may have synergistically contributed to microvascular compromise and ischemia, a significant gap in understanding complex drug-substance interactions.

A 44-year-old male with chronic kidney disease stage 3b, insulin-dependent diabetes mellitus, and recent methamphetamine use presented with altered mental status following a self-reported insulin overdose of 240 units. Initial management included high-dose dextrose infusions for persistent severe hypoglycemia. When dextrose alone proved insufficient, Octreotide (dose not specified) was administered to suppress endogenous insulin secretion. The patient's clinical course was monitored for resolution of altered mental status and subsequent complications, including abdominal pain and respiratory distress, leading to computed tomography angiography and emergency laparotomy.

Following Octreotide administration, the patient initially stabilized, and altered mental status resolved. However, approximately five hours later, he developed acute abdominal pain, worsening encephalopathy, and respiratory distress, necessitating intubation. Computed tomography angiography revealed extensive portal and mesenteric venous gas, indicative of severe intestinal compromise. Emergency laparotomy confirmed widespread microvascular ischemia throughout the bowel. Importantly, there was no evidence of full-thickness intestinal infarction, strongly suggesting non-occlusive mesenteric ischemia (NOMI). Despite aggressive surgical intervention and resuscitation efforts, the patient's condition rapidly deteriorated, and he ultimately succumbed to his illness. This outcome underscores the severe, rapid progression of NOMI in this complex clinical scenario.

The patient developed acute abdominal pain and worsening encephalopathy approximately five hours after Octreotide administration, leading to fatal mesenteric microvascular compromise.