Bacterial peritonitis is an acute inflammatory process due to bacterial infection in the peritoneal cavity. It has primary (spontaneous bacterial peritonitis — SBP, usually in patients with cirrhotic ascites) and secondary (related to gastrointestinal perforation, appendicitis, diverticulitis, postoperative contamination) forms. Secondary peritonitis is much more common and requires emergent surgical intervention. On CT, diffuse peritoneal thickening and enhancement, free intraperitoneal fluid/ascites, mesenteric fat stranding, fluid-level collections, and potentially free air (if perforation present) are seen. Peritoneal thickening is smooth and homogeneous — nodular thickening suggests peritoneal carcinomatosis or tuberculous peritonitis. On diffusion-weighted MRI, inflammatory fluid may show diffusion restriction. On US, free fluid, bowel wall thickening, and decreased peristalsis can be seen. Treatment consists of broad-spectrum antibiotics and surgical source control of the underlying cause.
Age Range
20-80
Peak Age
55
Gender
Equal
Prevalence
Common
In bacterial peritonitis, the infectious agent reaches the peritoneal cavity and triggers an inflammatory cascade on mesothelial surfaces. In secondary peritonitis, bacteria contaminate the peritoneal cavity from GI perforation (ulcer, diverticulitis, appendicitis, trauma) → peritoneal mesothelial cells encounter bacterial endotoxin and lipopolysaccharide (LPS) → pro-inflammatory cytokines (TNF-alpha, IL-1, IL-6) are released → vasodilation and increased capillary permeability → proteinaceous exudate fluid accumulates in the peritoneal cavity. This proteinaceous exudate appears denser than simple ascites on CT (15-30 HU vs 0-10 HU) and may show diffusion restriction on DWI due to protein and cellular debris. Inflammation creates vascular proliferation and edema on peritoneal surfaces → appears as enhancing peritoneal thickening on CT. Inflammatory infiltration in mesenteric fat tissue creates fat stranding — edema fluid leaks between fat lobules increasing fat density. If perforation is present, free air from the GI lumen accumulates in the peritoneal cavity — visible as free air anterior to the liver or subdiaphragmatically on CT. Inflammatory ileus reduces bowel peristalsis → bowel loop dilation and air-fluid levels develop.
Visualization of smooth, homogeneous peritoneal thickening and enhancement together with free intraperitoneal air on CT — finding combination indicating secondary bacterial peritonitis from GI perforation with emergent surgical indication.
In the portal venous phase, the parietal and visceral peritoneum shows diffuse, smooth thickening and prominent enhancement. While normal peritoneum is imperceptible on CT (1-2 mm), in peritonitis it thickens to 2-5 mm with intense enhancement. Thickening is smooth and homogeneous — no nodular component. This smooth pattern is critical in distinguishing bacterial peritonitis from peritoneal carcinomatosis (nodular thickening), tuberculous peritonitis (nodular + thickened omentum), and peritoneal mesothelioma (irregular nodular).
Report Sentence
Diffuse, smooth thickening and prominent enhancement of the parietal and visceral peritoneum are seen; consistent with acute peritonitis.
On non-contrast CT, free fluid is seen in the peritoneal cavity — peritonitis exudate is denser than simple ascites (15-30 HU vs 0-10 HU). Fluid collects gravity-dependently in the cul-de-sac, Morrison's pouch, paracolic gutters, and subphrenic spaces. Due to inflammatory debris or fibrin, fluid may be heterogeneous and show fluid-fluid levels. Dense, loculated collections suggest abscess formation. In SBP, ascites is usually pre-existing and homogeneous — infected ascites cannot be reliably distinguished from simple ascites on non-contrast CT.
Report Sentence
Free fluid is seen in the peritoneal cavity with density higher than simple ascites (__ HU); consistent with exudative/inflammatory fluid.
In secondary peritonitis from GI perforation, free intraperitoneal air is seen on CT. Air most commonly accumulates in the anterior peritoneal space between the anterior liver surface and abdominal wall (highest point in supine position). Subdiaphragmatic free air may accompany the Rigler sign — air seen on both sides of the bowel wall (intraluminal + extraluminal). Small amounts of free air can be detected with thin-section CT — using lung window (W:1500 L:-500) facilitates detection of small air bubbles. Identifying the perforation site is critical for treatment planning — focal wall defect, extraluminal oral contrast leak, and concentrated stranding around the perforation provide localization clues.
Report Sentence
Free air is seen in the anterior peritoneal space, consistent with gastrointestinal perforation; emergent surgical evaluation is recommended.
In peritonitis, diffuse fat stranding and haziness are seen in mesenteric fat tissue. Stranding is widespread throughout the mesentery — not focal (focal stranding suggests localized pathology like appendicitis or diverticulitis). Prominent stranding may also be seen in the greater omentum — 'dirty omentum' appearance. Mesenteric vessels become conspicuous within surrounding stranding — vascular engorgement indicates inflammatory hyperemia. In advanced cases, omental cake-like thickening may develop but this must be distinguished from peritoneal carcinomatosis.
Report Sentence
Diffuse mesenteric fat stranding and haziness are seen, consistent with acute peritoneal inflammation.
On B-mode US, free fluid is seen in the peritoneal cavity — inflammatory exudate may not be completely anechoic like simple ascites, and may contain low-level internal echoes and fibrin strands (thin hyperechoic lines). Bowel wall thickening (>3 mm) and decreased/absent peristalsis may accompany — paralytic ileus finding. Bowel loop dilation and air-fluid levels may be visible. Loculated collections (abscess) are thick-walled, heterogeneous with internal debris and sometimes gas echoes. US sensitivity for peritonitis diagnosis is lower than CT but valuable for rapid bedside assessment.
Report Sentence
Free fluid with internal echoes and bowel wall thickening are seen in the peritoneal cavity; consistent with acute peritonitis.
On DWI, inflammatory peritoneal fluid may show diffusion restriction — signal preservation at high b-values and low ADC values on the ADC map. Restriction is particularly prominent in loculated collections (abscess): ADC <1.0 x 10^-3 mm2/s. In diffuse peritoneal fluid, restriction may be less prominent but shows lower ADC values than simple ascites. DWI can also be used in treatment response follow-up when evaluated together with peritoneal thickening and enhancement.
Report Sentence
Diffusion restriction is seen in peritoneal fluid on DWI (ADC: __ x 10^-3 mm2/s), consistent with inflammatory/infectious content.
Criteria
Primary peritonitis developing in cirrhotic ascites without GI perforation. Ascitic fluid neutrophil count >250/mm3. Usually E. coli, Klebsiella, Streptococcus pneumoniae.
Distinct Features
No free air on CT. Ascites is pre-existing — peritoneal thickening and enhancement develop after infection. Treatment is antibiotics — no surgery needed.
Criteria
Peritoneal contamination from GI perforation (ulcer, diverticulitis, appendicitis, trauma, anastomotic leak). Polymicrobial infection.
Distinct Features
Free air frequently present. Focal wall defect and intense stranding at perforation site. Emergent surgical indication — source control mandatory. CT identification of perforation site guides surgical planning.
Criteria
Persistent or recurrent peritonitis despite treatment of secondary peritonitis. Usually nosocomial pathogens (Enterococcus, Candida, coagulase-negative staphylococci). More common in immunosuppressed patients.
Distinct Features
Persistent peritoneal thickening and collections on follow-up. Multiple loculated abscesses may develop. High mortality (30-60%). Repeated surgery or percutaneous drainage may be needed.
Distinguishing Feature
Peritoneal carcinomatosis shows NODULAR peritoneal thickening (omental cake) — bacterial peritonitis shows smooth, homogeneous thickening. Carcinomatosis is not clinically acute, has known primary malignancy history, no fever or leukocytosis.
Distinguishing Feature
TB peritonitis shows smooth or nodular peritoneal thickening, loculated ascites, omental thickening ('omental cake'), and rim-enhancing lymphadenopathy. Subacute/chronic course rather than acute. PPD/QuantiFERON and ascitic fluid ADA are elevated.
Distinguishing Feature
Peritoneal mesothelioma shows irregular, nodular peritoneal thickening and plaque-like lesions. Asbestos exposure history is important. Chronic course — no acute abdomen. Mass lesions in mesentery and omentum may accompany.
Distinguishing Feature
Sclerosing encapsulating peritonitis (cocoon syndrome) shows thick peritoneal membranes encapsulating bowel loops. Related to peritoneal dialysis history or beta-blocker use. No acute infection findings. Chronic intestinal obstruction presentation.
Urgency
emergentManagement
surgicalBiopsy
Not NeededFollow-up
specialist-referralBacterial peritonitis is a life-threatening condition requiring emergent medical/surgical intervention. In secondary peritonitis, emergent surgical source control (perforation repair, bowel resection, abscess drainage) and broad-spectrum IV antibiotic therapy are lifesaving. In SBP, antibiotic therapy is sufficient — no surgery needed. Treatment delay can lead to sepsis, septic shock, and multi-organ failure — mortality approaches 100% without treatment. CT is the gold standard for identifying perforation site, collection localization, and complication assessment. Percutaneous drainage may be an alternative for loculated abscesses. Treatment response is followed clinically + laboratory; control imaging is indicated for non-improvement or deterioration.
Bacterial peritonitis is a life-threatening condition requiring urgent treatment. SBP needs paracentesis and antibiotic therapy, secondary peritonitis requires surgical intervention. Early diagnosis reduces mortality.