ICU · gi-nutrition

Acute Severe Intra-Abdominal Infection and Peritonitis — Comprehensive (Primary/SBP, Secondary, Tertiary, Source Control, Open Abdomen)

Also known as Spontaneous bacterial peritonitis · SBP · Secondary peritonitis · Tertiary peritonitis · Intra-abdominal infection · Complicated intra-abdominal infection · Source control · Damage control laparotomy · Open abdomen · Candida peritonitis · Anastomotic leak

Acute severe intra-abdominal infection with peritonitis is one of the most common and most lethal surgical emergencies managed in the ICU, with mortality ranging from <5% for uncomplicated community-acquired infection up to 30-50% for tertiary (persistent/recurrent) peritonitis in the critically ill. Peritonitis is classified into THREE pathophysiologically and therapeutically distinct categories. PRIMARY (SPONTANEOUS BACTERIAL) PERITONITIS (SBP): infection of cirrhotic ascites WITHOUT an identifiable intra-abdominal surgical source; monomicrobial (E. coli ~70%, Klebsiella, then gram-positives); diagnosed by ascitic polymorphonuclear (PMN) count >250 cells/mm3 (do NOT wait for culture — ~50% culture-negative); treated with a THIRD-GENERATION CEPHALOSPORIN (cefotaxime 2 g IV q8h for 5 days) PLUS ALBUMIN 1.5 g/kg day 1 then 1 g/kg day 3 (the landmark Sort 1999 NEJM trial proved albumin REDUCES hepatorenal syndrome from 33% to 10% and in-hospital mortality from 29% to 10%); NO surgery/source control required. SECONDARY PERITONITIS: infection from an intra-abdominal SOURCE requiring operative or interventional control — perforated viscus (appendicitis, diverticulitis, peptic ulcer, ischaemic bowel), anastomotic leak, bowel infarction, post-surgical leak; POLYMICROBIAL (gram-negative enteric bacilli + anaerobes (Bacteroides) + Enterococcus); management is SOURCE CONTROL + broad-spectrum antibiotics — source control is MANDATORY and antibiotics alone cannot cure secondary peritonitis. SOURCE CONTROL = all physical measures to eliminate a source and restore anatomy: DRAIN (pus/fluid), DEBRIDE (necrotic/infected tissue), DIVERT (defunction the bowel), and in the critically ill/physiologically exhausted patient a DAMAGE-CONTROL laparotomy (control contamination, temporary abdominal closure, resuscitate in ICU, planned re-operation). EMPIRIC ANTIBIOTICS: piperacillin-tazobactam OR a carbapenem (meropenem) + metronidazole for broad gram-negative + anaerobic cover; add Enterococcus cover (esp. healthcare-associated); add an antifungal (an echinocandin or amphotericin/fluconazole) for fungal (Candida) peritonitis. DURATION is SHORT: 4-7 days after adequate source control (STOP-IT trial, NEJM 2015 — ~4 days as good as ~8 days). TERTIARY PERITONITIS: persistent or recurrent peritonitis after >48h of apparently appropriate treatment of secondary peritonitis, or persistent intra-abdominal infection in the critically ill without a clear drainable source; reflects immune dysregulation/immune paresis as much as infection; organisms are MDR — Enterococcus (incl. VRE), Pseudomonas, Acinetobacter, MRSA, and Candida; management is CULTURE-DIRECTED, broad-spectrum, anti-fungal-inclusive therapy, repeat source-control assessment, and aggressive ICU support; mortality 30-50%. OPEN ABDOMEN management (negative pressure wound therapy/VAC, planned re-laparotomy 'on-demand' vs 'planned', and delayed primary fascial closure) is the strategy for the physiologically deranged patient in whom closure would cause abdominal compartment syndrome or where a second-look is required. DIAGNOSIS rests on CT abdomen with contrast (free intraperitoneal gas = perforation; fluid collections/abscess; fat stranding; ischaemia), diagnostic paracentesis (for SBP), and — selectively — diagnostic laparoscopy or diagnostic peritoneal lavage (now largely supplanted by CT and FAST ultrasound).