> Table of Contents > Peritonitis, Acute
Peritonitis, Acute
Justin Thomas Ertle, BS, MD
Marie L. Borum, MD, EdD, MPH
image BASICS
  • Definition: inflammation of the peritoneum
  • Classification:
    • Aseptic: due to chemical irritation or systemic inflammation of peritoneum
    • Bacterial: due to infection of peritoneal fluid
  • Bacterial peritonitis types:
    • Primary/spontaneous bacterial peritonitis (SBP): infection of ascitic fluid without known source; typically monomicrobial
    • Secondary bacterial peritonitis: infection of peritoneal fluid from a detectable intra-abdominal source (i.e., perforation); typically polymicrobial
    • Tertiary bacterial peritonitis: persistent infection despite adequate therapy
  • In patients with ascites, the incidence of SBP in a 1-year period is 10-25% (1).
  • Secondary bacterial peritonitis correlates with incidence of the underlying pathology (e.g. colitis, appendicitis, diverticulitis, PUD).
  • 57% of patients with secondary bacterial peritonitis progressed to tertiary peritonitis (2).
  • SBP: In asymptomatic patients with cirrhosis and ascites, the prevalence is <3.5% in outpatients and 8-36% in the nosocomial setting (3).
  • In patients with cirrhosis and ascites, 5% of peritonitis is secondary rather than SBP (4).
  • Mechanism
    • SBP:
      • Primary mechanism is bacterial translocation via lymphatic spread through mesenteric lymph nodes into ascitic fluid.
      • Cirrhotic patients have multiple secondary mechanisms:
        • Small intestinal bacterial overgrowth (SIBO) and increased intestinal mucosal permeability to bacteria both increase bacterial translocation.
        • Decreased cellular and humoral immunity increases susceptibility to bacterial translocation
    • Secondary bacterial peritonitis
      • Spillage/translocation of bacteria from inflamed or perforated intraperitoneal organs or introduction of bacterial through instrumentation—for example, peritoneal dialysis, intraperitoneal chemotherapy
    • Tertiary bacterial peritonitis
      • Occurs in secondary peritonitis with inadequacy of source control or altered host immunity
  • Microbiology
    • SBP
      • Escherichia coli (46%), Streptococcus spp. (30%), Klebsiella (9%), and Staphylococcus (6%). Increasing rate of gram-positive and resistant organisms (e.g., extended-spectrum &bgr;-lactamase-producing [ESBL] E. coli, MRSA, enterococcus) in the nosocomial setting
    • Secondary bacterial peritonitis:
      • E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, Clostridium
  • SBP: advanced cirrhosis with ascites, bacterascites, malnutrition, upper GI bleed, PPI usage, prior SBP
    • Acid suppression with PPIs been shown to promote SIBO increasing SBP, and hospitalized cirrhotics receiving PPIs are at increased risk of developing SBP (3).
    • 70% of cases of SBP are seen in patients with Child-Pugh class C cirrhosis (1).
  • Secondary bacterial peritonitis: Factors associated with perforation or fluid translocation, for example, peritoneal dialysis, H. pylori and NSAIDs causing ulcers, vascular disease causing bowel ischemia, ETOH abuse causing pancreatitis
  • SBP prophylaxis is beneficial when risk factors are present, including ascitic fluid protein concentration <1.0 g/dL, esophageal varices, or history of previous SBP
    • Prior SBP: prophylactic norfloxacin or TMP/SMX PO daily (5)[A].
    • Cirrhosis and GI bleed: 7-day course of ceftriaxone 2 g IV daily or norfloxacin BID, IV while bleeding, PO as tolerated (5)[A]
    • Cirrhotic ascites with low ascitic fluid protein (<1.5 g/dL) and either renal impairment (creatinine ≥1.2, BUN ≥25, or serum Na ≤130) or liver failure (Child score ≥9, bilirubin ≥3): prophylactic norfloxacin PO daily (3,5)[A]
  • Limit use of PPIs to only proven indications, as PPIs increase incidence of SIBO (5)[B].
  • Tachycardia, fever, tachypnea, altered mental status
  • Abdominal distention, ascites, abdominal wall guarding and rigidity, rebound tenderness, hypoactive/absent bowel sounds
  • Liver disease: acute hepatitis, decompensated cirrhosis
  • Luminal disease: abscess formation, ileus, volvulus, intussusception, mesenteric adenitis, pancreatitis, cholecystitis, malignancy, peritoneal carcinomatosis
  • Extraluminal disease: ruptured ectopic pregnancy, tubo-ovarian abscess, PID, severe UTI, and/or pyelonephritis
  • Systemic disease: tuberculosis, pneumonia, MI, porphyria, SLE
Initial Tests (lab, imaging)
  • Immediate evaluation
    • Perform paracentesis, blood, and urine cultures before administration of antibiotics (1,5)[B].
    • Ascitic fluid studies should minimally include culture (use aerobic and anaerobic blood culture bottles), Gram stain, cell count with differential, and albumin (1)[B]; if assessing for secondary peritonitis also include LDH, total protein and glucose.
  • SBP: bacterascites and ascitic fluid PMN >250 cells/mm3
  • Culture-negative neutrocytic ascites: negative ascites culture, ascitic fluid PMN >250 cells/mm3
  • Nonneutrocytic bacterascites: positive ascites culture, ascitic fluid PMN <250 cells/mm3
  • Secondary peritonitis: PMN >250 cells/mm3 on ascitic fluid analysis, with any of the following criteria:
    • Polymicrobial culture or two of the following: ascitic fluid total protein >1 g/dL, glucose <50 mg/dL, or LDH >225 mU/mL. Sensitivity for perforation 96%, sensitivity for nonperforation secondary peritonitis 50% (5)[B]
    • Secondary peritonitis with perforation is likely with alkaline phosphatase >240 U/l or CEA >5 ng/mL, sensitivity 92% (5)[B].
  • Ultrasound or CT scan with enteral and IV contrast shows intra-abdominal mass, ascites, abscess, or extravasation of contrast in secondary peritonitis
  • Abdominal or chest x-ray may show free air in peritoneal cavity, large/small bowel dilatation, intestinal wall edema in secondary peritonitis.
Follow-Up Tests & Special Considerations
  • If asymptomatic bacterascites, recent antibiotic exposure, nosocomial atypical organism, or no clinical improvement, repeat paracentesis in 48 hours to resolution, defined as decrease in PMNs of 25% or negative cultures (1)[C].
  • In hemorrhagic ascites, PMN count can be corrected by subtracting 1 PMN per 250 RBCs (3)[A].
  • For SBP, control the effects of cirrhosis/ascites with salt restriction, spironolactone +/− furosemide, albumin infusion after large volume paracentesis, and/or lactulose for encephalopathy (5)[A].
  • Avoid nephrotoxic medications (e.g., NSAIDs) or other renal insults (5)[C].

  • SBP empiric first-line treatment
    • Community-acquired SBP w/o recent &bgr;-lactam antibiotic use: 3rd-generation cephalosporins, preferably cefotaxime, 2 g IV q8h for 5 days (5)[A]
    • SBP in absence of previous quinolone use/prophylaxis, vomiting, shock, hepatic encephalopathy, or serum creatinine >3 mg/dL: Ofloxacin 400 mg PO can be substituted for cefotaxime (5)[B].
    • Nosocomial SBP or recent &bgr;-lactam antibiotic: Empiric therapy based on local susceptibility of patients with cirrhosis for resistant bacteria (e.g., ESBL Enterobacteriaceae, MRSA) (6)[B]
    • Symptomatic bacterascites with PMN count <250 cells/mm3: cefotaxime 2 g IV q8h while awaiting sensitivities (5)[B]
    • Second-line antibiotic regimens include fluoroquinolones (levofloxacin), piperacillin/tazobactam, or vancomycin (5)[C].
    • SBP with renal or hepatic impairment (serum creatinine >1 mg/dL, BUN >30 mg/dL, or total bilirubin >4 mg/dL): Add albumin 1.5 g/kg within 6 hours and 1 g/kg on day 3 (1)[A],(5)[B].
  • Secondary bacterial peritonitis
    • Empiric broad spectrum antibiotic coverage for polymicrobial infection; IV cefotaxime or other 3rd- to 4th-generation cephalosporin plus metronidazole is one option for an initial regimen.
    • In peritoneal dialysis associated infection, intraperitoneal route superior to IV (6)[A]
  • Tertiary bacterial peritonitis
    • If no unrepaired perforations or leaks, conservative medical management. This includes antibiotics (guided by prior susceptibilities if available) and early enteral nutrition to prevent atrophy and maintain immunocompetence (2)[B].
    • In recurrent or persistent peritoneal dialysis associated infection, removal of the PD catheter is warranted (6)[A].
  • SBP
    • Medical management
  • Secondary bacterial peritonitis
    • Emergent surgical management, including source control with open laparotomy to repair any perforated viscus and eradicate infected material, is the first-line treatment (2)[A],(5)[B].
  • Tertiary bacterial peritonitis
    • If no unrepaired perforations or leaks, additional surgery for severe abdominal infection is correlated with deterioration and significant mortality (2).
Admission Criteria/Initial Stabilization
  • Acute peritonitis typically warrants inpatient admission.
  • In patients with cardiogenic or septic shock, invasive monitoring with early goal-directed fluid therapy
  • Patients who present with peritonitis can be severely hypovolemic. In these cases, volume resuscitation is critical. In patients with significant renal or hepatic dysfunction, albumin decreases mortality (1)[A],(5)[B].
  • Cirrhotic patients often take &bgr;-blockers as part of their outpatient regimen, but during an episode of SBP, &bgr;-blockers increase mortality, hepatorenal syndrome, and hospital stay in SBP patients (5)[B].
  • Nasogastric tube placement can prevent aspiration in patients with vomiting or GI bleeding.
Patient Monitoring
Normalization of vital signs with resolution of leukocytosis indicates improvement.
  • SBP: If follow-up paracentesis is performed after 48 hours to evaluate resolution, PMN decrease >25% is expected.
  • Development of leukopenia indicates immune exhaustion and poor prognosis.
  • NPO, total parental nutrition as necessary
  • Resume enteral feeding after return of bowel function
  • Sodium restriction can reduce future ascites (3)[A].
  • SBP
    • For inpatients with first episode of SBP, mortality ranges from 10% to 50% (3).
    • Prognosis is improved if antibiotics are started early, prior to onset of shock or renal failure.
    • Strongest negative prognostic indicator is renal insufficiency.
    • Other poor prognostic factors include nosocomial acquisition, old age, high Child-Pugh-Turcotte or MELD score, malnutrition, malignancy, peripheral leukopenia, and antibiotic resistance (3).
    • Patients with prior SBP have 1-year recurrence rate of 40-70% and 1-year mortality of 31-93% (1,3).
  • Secondary bacterial peritonitis:
    • In-hospital mortality of treated patients is 67% (4).
    • Mortality approaches 100% if not treated surgically, especially if secondary to perforation (2,4).
    • Prognosis is worse in perforated etiologies.
1. Alaniz C, Regal RE. Spontaneous bacterial peritonitis: a review of treatment options. P T. 2009;34(4):204-210.
2. Panhofer P, Izay B, Riedl M, et al. Age, microbiology and prognostic scores help to differentiate between secondary and tertiary peritonitis. Langenbecks Arch Surg. 2009;394(2):265-271.
3. Wiest R, Krag A, Gerbes A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut. 2012;61(2):297-310.
4. Soriano G, Castellote J, Alvarez C, et al. Secondary bacterial peritonitis in cirrhosis: a retrospective study of clinical and analytical characteristics, diagnosis and management. J Hepatol. 2010;52(1):39-44.
5. Runyon, B. Introduction to the revised American Association for the Study of Liver Diseases practice guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013;57(4):1651-1653.
6. Ballinger A, Palmer SC, Wiggins KJ, et al. Treatment for peritoneal dialysis-associated peritonitis. Cochrane Database Syst Rev. 2014;(4):CD005284.
Additional Reading
  • Bajaj JS, O'Leary JG, Wong F, et al. Bacterial infections in end-stage liver disease: current challenges and future directions. Gut. 2012;61(8):1219-1225.
  • Cheong HS, Kang CI, Lee JA, et al. Clinical significance and outcome of nosocomial acquisition of spontaneous bacterial peritonitis in patients with liver cirrhosis. Clin Infect Dis. 2009;48(9):1230-1236.
  • Deshpande A, Pasupuleti V, Thota P, et al. Acid-suppressive therapy is associated with spontaneous bacterial peritonitis in cirrhotic patients: a meta-analysis. J Gastroenterol Hepatol. 2013;28(2):235-242.
  • Ghassemi S, Garcia-Tsao G. Prevention and treatment of infections in patients with cirrhosis. Best Pract Res Clin Gastroenterol. 2007;21(1):77-93.
  • Jain P. Spontaneous bacterial peritonitis: few additional points. World J Gastroenterol. 2009;15(45):5754-5755.
  • Koulaouzidis A, Bhat S, Karagiannidis A, et al. Spontaneous bacterial peritonitis. Postgrad Med J. 2007;83(980):379-383.
  • Koulaouzidis A, Bhat S, Saeed AA. Spontaneous bacterial peritonitis. World J Gastroenterol. 2009;15(9):1042-1049.
  • Mandorfer M, Bota S, Schwabl P, et al. Nonselective &bgr; blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology. 2014;146(7):1680.e1-1690.e1.
See Also
Appendicitis, Acute; Cirrhosis of the Liver; Diverticular Disease; Peptic Ulcer Disease
  • K65.0 Generalized (acute) peritonitis
  • K65.2 Spontaneous bacterial peritonitis
  • K65.8 Other peritonitis
Clinical Pearls
  • Maintain a high index of suspicion for SBP in cirrhotic patients with ascites. SBP occurs in preexisting ascites and carries a high mortality, especially if presenting with GI bleed.
  • Early diagnosis and treatment reduces mortality.
  • Paracentesis is necessary to diagnose SBP.
  • Emergent CT scan should be performed if there is suspicion of secondary bacterial peritonitis.
  • Distinguishing SBP from secondary bacterial peritonitis is essential, as SBP treatment consists of antibiotic therapy whereas secondary bacterial peritonitis necessitates emergent surgical intervention.
  • Renal function is an important prognostic indicator for SBP. Albumin administration decreases the incidence of renal failure and mortality in patients with renal or hepatic impairment or large-volume paracentesis.