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Peritonitis, Acute

para>30% of patients are asymptomatic (1)[C]. ‚  
Geriatric Considerations

Signs and symptoms are frequently absent, particularly in pediatric and elderly patients (1)[B].

‚  

PHYSICAL EXAM


  • Tachycardia, fever, tachypnea, altered mental status
  • Abdominal distention, ascites, abdominal wall guarding and rigidity, rebound tenderness, hypoactive/absent bowel sounds

DIFFERENTIAL DIAGNOSIS


  • 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

DIAGNOSTIC TESTS & INTERPRETATION


Initial Tests (lab, imaging)
ALERT

Early diagnosis is essential to reduce mortality. Paracentesis should be performed in any patient with new ascites, including suspected SBP (5)[B].

‚  
  • 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.

ALERT

Lab interpretation: Ascitic fluid culture is negative in up to 50% of patients with SBP (1)[A].

‚  
  • 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].

ALERT

Imaging: Criteria or clinical suspicion for secondary peritonitis necessitates emergent CT scan. CT diagnostic for secondary peritonitis in 85% (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].

TREATMENT


GENERAL MEASURES


  • For SBP, control the effects of cirrhosis/ascites with salt restriction, spironolactone +/ ’ ˆ ’ 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].

MEDICATION


  • SBP empiric first-line treatment
    • Community-acquired SBP w/o recent Ž ²-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 Ž ²-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 cefoxatime 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].

SURGERY/OTHER PROCEDURES


  • 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 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).

ALERT

Mortality of SBP approaches 80% if the patient receives unnecessary exploratory laparotomy; conversely, mortality of secondary bacterial peritonitis approaches 100% if not treated surgically (1,3).

‚  

INPATIENT CONSIDERATIONS


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 Ž ²-blockers as part of their outpatient regimen, but during an episode of SBP Ž ²-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.

ONGOING CARE


FOLLOW-UP RECOMMENDATIONS


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.

DIET


  • NPO, total parental nutrition as necessary
  • Resume enteral feeding after return of bowel function
  • Sodium restriction can reduce future ascites (3)[A].

PROGNOSIS


  • 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.

COMPLICATIONS


  • Renal failure, liver failure, encephalopathy, coagulopathy
  • Secondary infection, iatrogenic infection, abscess, fistula formation, abdominal compartment syndrome
  • Sepsis/septic shock, cardiovascular collapse, adrenal insufficiency, respiratory failure, ARDS

REFERENCES


11 Alaniz ‚  C, Regal ‚  RE. Spontaneous bacterial peritonitis: a review of treatment options. P T.  2009;34(4):204 " “210.22 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 " “271.33 Wiest ‚  R, Krag ‚  A, Gerbes ‚  A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut.  2012;61(2):297 " “310.44 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 " “44.55 Runyon ‚  B; AASLD. 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 " “1653.66 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 Ž ² 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 ‚  

CODES


ICD10


  • K65.0 Generalized (acute) peritonitis
  • K65.2 Spontaneous bacterial peritonitis
  • K65.8 Other peritonitis
  • K65.9 Peritonitis, unspecified
  • K65.1 Peritoneal abscess

ICD9


  • 567.21 Peritonitis (acute) generalized
  • 567.23 Spontaneous bacterial peritonitis
  • 567.89 Other specified peritonitis
  • 567.9 Unspecified peritonitis
  • 567.22 Peritoneal abscess
  • 567.29 Other suppurative peritonitis

SNOMED


  • 67602004 Acute peritonitis
  • 11836002 Primary bacterial peritonitis (disorder)
  • 31860008 Acute bacterial peritonitis
  • 213293008 Aseptic peritonitis (disorder)

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.
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