Acute Peritonitis – Causes, Symptoms, Diagnosis, Treatment and Ongoing care
- Acute inflammation of the membrane that lines the visceral and parietal peritoneum
- 3 types are recognized:
- Primary: Spontaneous bacterial peritonitis (SBP)
- Secondary bacterial peritonitis (2BP): Associated with inflammation of a visceral organ
- Tertiary bacterial peritonitis (3BP): Persistent or recurrent infection after adequate initial therapy
- SBP implies an intra-abdominal bacterial infection without an apparent intra-abdominal source. It is a common complication of cirrhosis/chronic liver disease.
- 2BP is an intra-abdominal infection with a surgically treatable source.
- 3BP is often seen in patients with comorbidities or who are immunocompromised.
- Varies with underlying abdominal disease process
- Recurrence rates of SBP within 6 months as high as 43%; within 1 year 69%
- Predominant sex: Male > Female.
- SBP: 10–30% of patients with cirrhosis and ascites, with a mortality rate of 25%
- 2BP can be a consequence of visceral organ inflammation (e.g., appendicitis, diverticulitis); without perforation <10%, with perforation >50% chance of contracting 2BP
- Cirrhosis, ascitic fluid total protein level <1 g/dL, elevated bilirubin, upper GI bleeding, prior SBP
- Gut ischemia with reperfusion, indwelling IV and urinary catheters
- Massive transfusion, perioperative shock
- PEG tube insertion (increased risk of peritonitis if higher body mass index [BMI] and lower serum albumin) (1)
- Geriatric considerations: Mortality is greater in this age group. Symptoms may be muted.
- Prophylactic antibiotics indicated for cirrhotic patients with acute GI hemorrhage and following intra-abdominal surgery
- Prophylactic antibiotics for high-risk patients with recurrent peritonitis and low ascitic fluid total protein levels remain an area of controversy.
- Inflammation of the peritoneum owing to infectious, chemical (i.e., bile, blood, barium), mechanical, or neoplastic causes
- SBP: Seen in cirrhotics with portal hypertension; translocation of gut bacteria (gram negative > gram positive) across the gut wall or into mesenteric lymph nodes leads to infection and inflammation of ascites fluid.
- Bacterial seeding may occur in the presence of other infections, such as urinary tract infections (UTIs), pneumococcal sepsis, cellulitis, pharyngitis, and dental infections.
- 2BP: Ruptured peritoneal organ or tissue seeding the peritoneum with bacteria
- Most common pathogens:
- Primary: Escherichia coli (40%), Streptococcus sp. (15%), Klebsiella pneumoniae (7%), Pseudomonas sp. (5%), Proteus sp. (5%)
- Secondary: E. coli, Klebsiella, Proteus, Streptococcus, Enterococcus, Bacteroides, and Clostridium sp.
- Tertiary: Enterobacter, Pseudomonas, Enterococcus, Staphylococcus, and Candida sp.
- Primary: Associated with hepatic, cardiac, nephrotic, and malignancy-related ascites
- Perforation of bowel, most common site sigmoid; peritoneal abscess
- Abdominal trauma
- Continuous ambulatory peritoneal dialysis
- Appendicitis, diverticulitis, pancreatitis, acute cholecystitis
- Colitis: Infectious, inflammatory
- Peptic ulcer perforation
- Ischemic bowel
- Strangulation of the small bowel
- Postoperative (intraabdominal surgery)
- Pelvic inflammatory disease
- Iatrogenic: Endoscopic procedures, anastomotic dehiscence, and inadvertent bowel injury (mechanical, thermal, etc.)
- Abdominal pain
- Fever (>37.8°C [100°F]) ± increased white blood cells (WBCs). Note: Patients with advanced cirrhosis or severe sepsis may be mildly hypothermic.
- Nausea/vomiting, chills, anorexia, decrease in renal function, dyspnea, tachycardia, altered mental status (54% of cirrhosis patients owing either to infection or to hepatic dysfunction) (2)[B]
- Rebound tenderness, abdominal wall rigidity, abdominal distension with decreased or absent bowel sounds
- Abdominal pain may be diminished in patients with ascites because ascites fluid separates the visceral and parietal peritoneal surfaces.
Diagnostic Tests & Interpretation
Initial lab tests
- Basic metabolic panel, complete blood count (CBC) with differential, blood culture, urinalysis and culture, liver function tests (LFTs), lipase, prothrombin time (PT)/international normalization ratio (INR)/partial thromboplastin time (PTT)
- Ascitic fluid analysis (2)[B]:
- Cell count with differential, culture (false-negative in 80% patients), Gram stain, total protein, lactate dehydrogenase, glucose, amylase, albumin
- SBP: Absolute polymorphonuclear (PMN) count ≥250 cells/mm3 (if positive, culture typically grows 1 organism 90% of the time)
- 2BP: Absolute PMN count ≥250 cells/mm3 or WBC count ≥500 cells/mm3 (culture typically grows multiple organisms)
Follow-Up & Special Considerations
If no clinical improvement in 48–72 hours, repeat paracentesis to monitor treatment success (decrease in neutrophil count <50% original value and negative cultures).
- Supine/upright abdominal films and CXR: Free air in peritoneal cavity, large/small bowel dilatation, intestinal wall edema
- Sonograph or CT scan with enteral and IV contrast material: Intraabdominal mass, ascites, abscess, extravasation of water-soluble gut contrast material
- Ascites: Abdominal paracentesis
- Abscess: Ultrasound- or CT-guided percutaneous drainage
- Diagnostic laparotomy
- Colonoscopy to assess for colitis
Predominant PMN infiltration noted in ascitic fluid
- Abscess formation (subdiaphragmatic, subhepatic, peritoneal, pelvic)
- Ileus (volvulus, intussusception)
- Mesenteric adenitis, appendicitis, pancreatitis, cholecystitis, pelvic inflammatory disease (PID), pyelonephritis
- Ruptured ectopic pregnancy, tubo-ovarian cyst
- SBP: No antibiotic proven to be more efficacious than others (3,4,5,6)[A]:
- Cefotaxime 2 g IV q8h × 5–14 days; excellent penetration into ascites with no nephrotoxicity; common side effect is rash.
- Ceftriaxone 1 g q24h × 5–14 days
- Ampicillin-sulbactam 3 g IV q6h × 5–14 days (3,4)[A]
- Albumin 1.5 g/kg IV on day 1 and 1 g/kg on day 3 for hospitalized SBP patients to prevent hepatorenal syndrome (4,7)[A]
- Quinolones (e.g., norfloxacin, ofloxacin, ciprofloxacin) × 7 days
- Must cover anaerobic as well as gram-negative aerobic/facilitative organisms
- Agents active against anaerobic organisms include metronidazole, cefotetan, ticarcillin-clavulanate, piperacillin-tazobactam, ampicillin-sulbactam, imipenem
- 3BP: Long-term daily prophylactic regimens include norfloxacin 400 mg/d PO and trimethoprim-sulfamethoxazole 1 double-strength tablet PO daily (less expensive) (5)[A].
- Associated with chronic ambulatory peritoneal dialysis: Vancomycin plus gentamicin instilled in peritoneal cavity
- Prevention of SBP in patients with cirrhosis and GI bleeding: Antibiotic regimens as listed above for SBP
- Patients with ascitic fluid total protein levels <1 g/dL: Give prophylactic therapy during hospitalization only. Long-term antibiotics are controversial (2)[B].
- If on prophylactic therapy, 3BP should be treated with a different agent depending on culture results.
Treat paralytic ileus (nasogastric decompression); add respiratory support if needed.
Two phases (for 2BP): Emergent surgery, either laparoscopic or open abdomen, to remove etiologic agent; then once patient is stable, have a 2nd look within the abdomen.
- Volume resuscitation to prevent secondary organ system dysfunction; monitor urine output by Foley catheter.
- Antibiotics are started empirically to cover a broad spectrum of organisms once infection is suspected, with an ascitic fluid PMN count of ≥250 cells/mm3. The choice of antibiotic may be altered after culture and sensitivity results are obtained.
- Give adequate analgesics and antiemetics; if patient has severe nausea/vomiting, perform nasogastric decompression.
- Condition should improve within 24–72 hours of initial treatment. If no improvement, check for a persistent or recurrent infectious focus.
- Closely monitor for secondary infections after long-term antibiotics use or from a surgical wound site.
- NPO: IV fluids and electrolytes
- Total parenteral nutrition may be necessary.
- Enteral feedings after return of bowel sounds and passage of flatus and/or feces
- Mortality rate for SBP is 10–30%, with 1/2 of deaths caused by GI bleed, renal failure, or liver failure.
- 69% of patients with SBP have recurrence within 1 year and a mortality rate approaching 50%.
- Mortality of SBP is ∼80% if patient unnecessarily receives exploratory laparotomy.
- Uncomplicated 2BP <5% mortality rate; severe 30–50% mortality rate
- Presence of renal insufficiency is strongest prognostic indicator for mortality in SBP (2)[B].
- Other poor prognostic indicators: Peripheral leukocytosis, older age, ileus, high Child-Pugh score, malnutrition, or cancer
- Patients with hospital-acquired (vs. community-acquired) SBP have a greater risk of death (5)[A].
- Septicemia, septic shock
- Acute renal failure, liver failure
- Respiratory failure
- Abscess formation
- Abdominal compartment syndrome
1. Shah RD, Tariq N, Shanley C. Peritonitis from peg tube insertion in surgical intensive care unit patients: identification of risk factors and clinical outcomes.Surg Endosc. May 2009.
2. Sheer TA, Runyon BA. Spontaneous bacterial peritonitis. Dig Dis. 2005;23:39–46.
3. Runyon BA, Practice Guidelines Committee, American Association for the Study of Liver Diseases (AASLD). Management of adult patients with ascites due to cirrhosis. Hepatology. 2004;39:841–56.
4. Parsi MA, Atreja A, Zein NN. Spontaneous bacterial peritonitis: recent data on incidence and treatment. Cleve Clin J Med. 2004;71:569–76.
5. Frazee LA, Marinos AE, Rybarczyk AM et al. Long-term prophylaxis of spontaneous bacterial peritonitis in patients with cirrhosis. Ann Pharmacother.2005;39:908–12.
6. Lontos S, Gow PJ, Vaughan RB, et al. Norfloxacin and trimethoprim-sulfamethoxazole therapy have similar efficacy in prevention of spontaneous bacterial peritonitis. J Gastroenterol Hepatol. 2008;23:252–5.
7. Fernández J, Navasa M, Planas R, et al. Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis. Gastroenterology. 2007;133:818–24.
Cheong HS, Kang CI. Clinical significance and outcome of nosocomial acquisition of spontaneous bacterial peritonitis in patients with liver cirrhosis. Clinic Infec Dis. 2009;48(9):1230–6.
See Also (Topic, Algorithm, Electronic Media Element)
Appendicitis, Acute, Crohn Disease; Diverticular Disease; Ectopic Pregnancy; Pancreatitis
Algorithm: Abdominal Rigidity
- 567.9 Unspecified peritonitis
- 567.21 Peritonitis (acute) generalized
67602004 acute peritonitis (disorder)
- Patients with both SBP and 2BP will have ≥250 PMNs/mm3; however, SBP is typically unimicrobial, whereas 2BP is typically polymicrobial with an evident intraabdominal source of infection.
- 2BP typically also will have ≥2 of the following criteria:
- Total protein concentration >1 g/dL
- Glucose concentration <50 mg/dL (2.8 mmol/L)
- Elevated lactate dehydrogenase ≥225 units/L
- Peritoneal carcinomatosis, pancreatic ascites, hemorrhage into ascites, and tuberculous peritonitis are associated with ≥250 PMNs/mm3, but PMNs are often <50% of total WBCs. These forms of peritonitis are usually culture negative.
- SBP develops in preexisting ascites; it does not cause ascites.
- An ascitic fluid culture growing multiple organisms but with a PMN count of <250 cells/mm3 on analysis is most likely polymicrobial bacterascites secondary to bowel puncture with paracentesis needle. This is rare (<0.6% of all paracenteses, and morbidity is low) (2)[B].