A 58-year-old man with a 15-year history of alcohol use disorder presents to the emergency department with hematemesis and melena. On examination, he is tachycardic (HR 110/min), hypotensive (BP 88/54 mmHg), and has clinical signs of chronic liver disease including spider angiomata, ascites, and splenomegaly. Endoscopy reveals large esophageal varices with active bleeding. After initial resuscitation and blood transfusion, he receives variceal ligation. However, 48 hours later, he develops sudden-onset abdominal pain, fever (38.5°C), and worsening hemodynamic instability despite ongoing resuscitation. Repeat endoscopy shows no active variceal bleeding. What is the most likely diagnosis?

Explanation

## Clinical Diagnosis: Spontaneous Bacterial Peritonitis (SBP) ### Presentation Analysis This cirrhotic patient with ascites develops — 48 hours after a variceal bleed — the classic triad of SBP: - **Fever** (38.5°C) - **Abdominal pain** (new onset) - **Hemodynamic deterioration** despite resuscitation Repeat endoscopy confirms **no active variceal bleeding**, directing attention to an extraluminal cause of decompensation. ### Why SBP is the Most Likely Diagnosis **Key Point:** SBP is the most common serious infection in cirrhotic patients with ascites, occurring in 10–30% of hospitalised cirrhotics. GI bleeding is one of the strongest precipitants — bacterial translocation from the gut increases dramatically during acute variceal haemorrhage, and the risk of SBP within 48 hours of a bleed is well-established (Harrison's Principles of Internal Medicine, 21st ed.). | Feature | SBP | Esophageal Perforation | Acute Pancreatitis | |---------|-----|------------------------|-------------------| | **Setting** | Cirrhosis + ascites | Post-endoscopic procedure | Alcohol / gallstones | | **Pain** | Diffuse abdominal | Substernal / chest-dominant | Epigastric → back | | **Fever** | Yes | Yes (mediastinitis) | Low-grade | | **Hemodynamic instability** | Yes (sepsis) | Yes (mediastinitis/sepsis) | Variable | | **Ascitic fluid PMN** | >250 cells/μL (diagnostic) | Normal | Normal | | **Imaging** | CT: ascites, peritoneal enhancement | CXR: pneumomediastinum, free air | CT: pancreatic edema | | **Precipitant** | GI bleed, infection | EVL procedure (0.1–0.5%) | Alcohol, gallstones | ### Why Esophageal Perforation is Less Likely Here Esophageal perforation post-EVL is a **rare** complication (0.1–0.5%). Crucially, its dominant presentation is **chest pain, odynophagia, subcutaneous emphysema, and pneumomediastinum on imaging** — not primarily abdominal pain. The stem describes **abdominal pain** as the cardinal symptom, which is far more consistent with peritonitis from SBP. Furthermore, in a cirrhotic patient with ascites who has just had a GI bleed, SBP is orders of magnitude more probable than esophageal perforation. ### Diagnostic Approach - **Diagnostic paracentesis** is mandatory: ascitic fluid PMN ≥250 cells/μL confirms SBP even before culture results. - Blood cultures should be drawn simultaneously. ### Management (Harrison's / EASL Guidelines) 1. **Empirical antibiotics:** IV cefotaxime 2 g every 8 hours (or ceftriaxone) for 5 days 2. **IV albumin:** 1.5 g/kg on day 1 and 1 g/kg on day 3 — reduces hepatorenal syndrome and mortality 3. **Secondary prophylaxis:** Norfloxacin 400 mg/day (or ciprofloxacin) indefinitely after first episode 4. **Primary prophylaxis during GI bleed:** IV ceftriaxone 1 g/day for 7 days (reduces SBP risk) **Clinical Pearl:** All cirrhotic patients admitted with GI bleeding should receive antibiotic prophylaxis (ceftriaxone IV) to prevent SBP — this is a Grade A recommendation in EASL and AASLD guidelines. Failure to do so is a common exam and clinical pitfall. **High-Yield:** The diagnostic threshold for SBP is ascitic fluid PMN ≥250 cells/μL. Treatment should NOT be delayed pending culture results — empirical antibiotics plus albumin save lives.