Hematogenic peritonitis
DEFINITION AND CLINICAL CONTEXT
Hematogenic (haematogenous) peritonitis refers to peritoneal infection resulting from organisms reaching the peritoneal cavity through the bloodstream rather than by direct perforation of an abdominal viscus. The syllabus uses this distinct term; in contemporary clinical practice, spontaneous bacterial peritonitis in patients with cirrhosis/ascites is the most familiar related syndrome, although bacterial translocation across the gut wall is also an important mechanism.
AETIOLOGY AND PATHOGENESIS
Potential settings include bacteraemia/sepsis, immunosuppression, cirrhosis with ascites and impaired host defence. Organisms may seed ascitic fluid from blood or translocate across intestinal mucosa and mesenteric lymphatics. Common organisms in spontaneous bacterial peritonitis include Escherichia coli, Klebsiella species and streptococci. Reduced complement and opsonic activity in cirrhotic ascites impair bacterial clearance.
CLINICAL FEATURES
Presentation ranges from fever, abdominal pain and tenderness to subtle deterioration in a patient with cirrhosis: worsening ascites, encephalopathy, renal dysfunction, hypotension or unexplained sepsis. Some patients are asymptomatic. Unlike secondary peritonitis, there may be no focal perforation or localised source.
DIAGNOSIS
Perform prompt diagnostic paracentesis in hospitalised patients with cirrhosis and ascites, especially with fever, abdominal symptoms, GI bleeding, encephalopathy, shock or renal deterioration. Ascitic fluid cell count and differential, culture (ideally inoculated into blood-culture bottles at bedside), albumin and total protein are required. Ascitic polymorphonuclear neutrophils ≥250 cells/mm³ establish SBP in the appropriate context, even if culture is negative. Obtain blood cultures and assess renal function, electrolytes, liver function and coagulation. If polymicrobial culture, very high neutrophils, low glucose, high LDH, localised signs or failure to respond, suspect secondary peritonitis and obtain urgent CT/surgical review.
TREATMENT
Start empirical IV antibiotics immediately after cultures/paracentesis without delaying treatment in an unstable patient. A third-generation cephalosporin is commonly used for community-acquired SBP; healthcare-associated infection, resistant organisms or severe sepsis require broader cover based on local resistance patterns. Give IV albumin in appropriate patients, particularly with renal dysfunction or high risk of renal failure, following guideline-based dosing. Stop or modify precipitating drugs where appropriate and treat sepsis/renal injury. Secondary prophylaxis with an oral antibiotic is considered after an SBP episode; primary prophylaxis is reserved for selected high-risk patients.
DIFFERENTIAL AND COMPLICATIONS
Differentiate SBP/haematogenous infection from secondary peritonitis due to perforation, tuberculous peritonitis, malignant ascites and pancreatitis. Complications include septic shock, hepatorenal syndrome, recurrent infection and death. Repeat paracentesis at about 48 hours is considered if response is inadequate or secondary peritonitis is suspected.