Introduction: Septic shock complicated by multiple organ dysfunction is a leading cause of death in critically ill patients. Infections caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli are particularly challenging because antimicrobial resistance may delay effective therapy. The gastrointestinal tract is increasingly recognized as an amplifier of systemic inflammation through barrier disruption and bacterial translocation, particularly in patients with chronic enteropathy and severe malnutrition. Case presentation: A 29-year-old man with a history of intestinal tuberculosis, inflammatory bowel disease, and recent nephrotic syndrome presented with chronic watery diarrhea, vomiting, oliguria, and scleral icterus. Admission findings included leukocytosis, lymphopenia, a neutrophil-to-lymphocyte ratio of 25.9, acute kidney injury, hyponatremia, profound hypoalbuminemia (12.1 g/L), and procalcitonin above 32 ug/L. His course progressed to encephalopathy, recurrent seizures, upper gastrointestinal bleeding, coagulopathy, and vasopressor-dependent shock with anuric renal failure requiring continuous renal replacement therapy. Blood cultures grew ESBL-producing E. coli, and contrast-enhanced abdominal computed tomography showed diffuse bowel wall thickening. Serial biomarkers revealed progressive lymphopenia, persistent hypoalbuminemia, and rising lactate (10.5 mmol/L), consistent with immune-metabolic failure and a persistent inflammation, immunosuppression, and catabolism syndrome (PICS)-like trajectory. He died on the intensive care unit on day 10 due to refractory multiorgan failure. Conclusion: In vulnerable hosts with chronic enteropathy and malnutrition, marked gastrointestinal involvement combined with serial immune-metabolic biomarkers may help identify early high-risk deterioration and support repeated source reassessment and timely antimicrobial optimization.