Medical Case: Acute diarrhoea and abdominal pain in a cirrhotic patient

Diarrhoea, abdominal pain and fever are common reasons for emergency admission, but the differential diagnosis can be broad and sometimes unexpected.

Case presentation

It is a hot August afternoon when a 58-year-old man is brought by his wife to the emergency room of the University Hospital in Hamburg. He has been unwell for about 12 hours, with watery diarrhoea, nausea, and diffuse abdominal cramps. Earlier that day he began to feel feverish and unusually fatigued.

On arrival, the patient is alert but looks tired and sweaty. His vital signs are: temperature 38,6 °C, blood pressure 110/70 mmHg, heart rate 105/min, respiratory rate 20/min, oxygen saturation 96% on room air. Physical examination reveals a mildly distended abdomen with diffuse tenderness, no guarding or rebound. No jaundice is immediately apparent, and his skin and extremities show no rash or lesions. Heart and lung auscultation are unremarkable.

Past medical history

He has alcohol-related cirrhosis (Child-Pugh B, no prior encephalopathy), type 2 diabetes mellitus with poor glycemic control, and arterial hypertension. Medications: propranolol, metformin. No known allergies. The couple has not yet gone on holiday for the summer (only a few weekend trips to the nearby seaside). They reported a trip to the Canary Islands the previous December.

First investigations

• Blood tests: WBC 12.500/µL, Hb 13,6 g/dL, platelets 92.000/µL, CRP 168 mg/L, creatinine 1,4 mg/dL, bilirubin 2,2 mg/dL, INR 1,6, glucose 278 mg/dL.
• Arterial blood gas: pH 7,36, lactate 2,9 mmol/L.
• Electrolytes: mild hyponatremia (Na 131 mmol/L).
• ECG: sinus tachycardia at 105/min, QTc 460 ms, no ischemic changes.
• Chest X-ray: normal.
• Abdominal ultrasound: cirrhotic liver with moderate splenomegaly, no ascites.

Initial impression in ED

The team considers acute infectious gastroenteritis, most likely foodborne, possibly complicated by dehydration in the context of cirrhosis. The patient is hydrated with intravenous saline and given paracetamol for fever. He is admitted to the observation ward for monitoring.

Clinical course

For the first few hours in the observation ward, the patient is treated with intravenous fluids (2 L of crystalloid over 4 hours) and paracetamol for fever. The working diagnosis remains infectious gastroenteritis, given the acute diarrhoea, abdominal cramps, moderate leukocytosis, and absence of alarming abdominal or systemic signs. No cultures are ordered at this stage.

Six hours later, the nurse finds the patient increasingly drowsy, sweaty, and clammy. His new vital signs are: blood pressure 88/55 mmHg, heart rate 122/min, temperature 39,4 °C, SpO₂ 93% in room air. Urine output has dropped significantly.

Repeat laboratory results show marked worsening: WBC 18.700/µL, platelets 62.000/µL, bilirubin 3,8 mg/dL, creatinine 2,1 mg/dL, CRP 320 mg/L, and lactate 5,5 mmol/L. Arterial blood gas confirms metabolic acidosis (pH 7,30 - HCO₃⁻ 18 mmol/L).

A repeat ECG demonstrates persistent sinus tachycardia with nonspecific ST-T abnormalities; no arrhythmias are observed. High-sensitivity troponin is modestly elevated at 45 ng/L, interpreted as demand ischemia. Chest X-ray remains unchanged.

At this point, the diagnosis shifts from presumed gastroenteritis to sepsis of unclear origin. Blood cultures are immediately drawn, and a stool sample is sent for bacterial culture, though the patient has no further bowel movements. At this stage, the team is primarily considering a severe enteric infection in a cirrhotic host, and expects the cultures to reveal common foodborne pathogens such as Salmonella enteritidis or Campylobacter jejuni. Empiric broad-spectrum intravenous antibiotics are started with piperacillin–tazobactam (4,5 g every 8 hours), and the patient is transferred urgently to the Intensive Care Unit. Norepinephrine infusion is initiated to maintain a MAP above 65 mmHg.

During the night, approximately 4 hours after admission to the ICU, while under close monitoring, new skin findings appear: a rapidly enlarging, exquisitely painful violaceous patch on the left calf, which evolves within hours into large hemorrhagic bullae. The skin around the lesion is tense, warm, and erythematous.

Surgeons are called for urgent evaluation, with suspected necrotizing fasciitis. At bedside, they confirm severe pain disproportionate to the physical findings and a rapidly expanding area of necrosis.

The patient is taken immediately to the operating room for surgical exploration. Intraoperatively, extensive edema of the subcutaneous tissue and fascia is observed, with areas of necrosis but preserved muscle. Wide debridement of non-viable tissue is performed. Multiple specimens are collected for microbiological analysis, including swabs of the bullae, deep tissue samples, and fascia biopsies, with the expectation of isolating typical necrotizing soft tissue pathogens such as Streptococcus pyogenes, Staphylococcus aureus, or anaerobes including Clostridium species. A vacuum-assisted closure (VAC) system is applied for temporary wound management.