eMedicine Specialties > Emergency Medicine > Infectious Diseases

Spontaneous Bacterial Peritonitis

Author: Steven M Bandy, MD, FACEP, Adjunct Clinical Professor of Emergency Medicine, Pikeville College School of Osteopathic Medicine and Virginia College of Osteopathic Medicine; Consulting Staff, Department of Emergency Medicine, Johnston Memorial Hospital; Medical Director, Rejuvenage Medspa; Operational Medical Director, Virginia Operations, Wings Air Rescue Ambulance Service
Contributor Information and Disclosures

Updated: Dec 2, 2009

Introduction

Background

Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Generally, no source of the infecting agent is easily identifiable, but contamination of dialysate can cause the condition among those receiving peritoneal dialysis (PD). Spontaneous bacterial peritonitis occurs in both children and adults and is a well-known and ominous complication in patients with cirrhosis.¹ Of patients with cirrhosis who have spontaneous bacterial peritonitis, 70% are Child-Pugh class C. In these patients, the development of spontaneous bacterial peritonitis is associated with a poor long-term prognosis. Once thought to occur only in those individuals with alcoholic cirrhosis, spontaneous bacterial peritonitis is now known to affect patients with cirrhosis from any cause.

Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing spontaneous bacterial peritonitis.

Spontaneous bacterial peritonitis can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as congestive heart failure and Budd-Chiari syndrome.

Pathophysiology

The mechanism for bacterial inoculation of ascites has been the subject of much debate since Harold Conn first recognized it in the 1960s.

Enteric organisms have traditionally been isolated from more than 90% of infected ascites fluid in spontaneous bacterial peritonitis, suggesting that the GI tract is the source of bacterial contamination. The preponderance of enteric organisms, in combination with the presence of endotoxin in ascitic fluid and blood, once favored the argument that spontaneous bacterial peritonitis was due to direct transmural migration of bacteria from an intestinal or hollow organ lumen, a phenomenon called bacterial translocation. However, experimental evidence suggests that direct transmural migration of microorganisms might not be the cause of spontaneous bacterial peritonitis.

Evidence suggests that the long-term prophylaxis of patients with cirrhosis with fluoroquinolones, often norfloxacin, has led to selective intestinal decontamination and high-level fluoroquinolone resistance. This has been supported by published data that show a higher predominance of gram-positive pathogens in ascitic fluid cultures than previously reported.

An alternative proposed mechanism for bacterial inoculation of ascites suggests a hematogenous source of the infecting organism in combination with an impaired immune defense system. Nonetheless, the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains the source of much debate.

A host of factors contributes to the formation of peritoneal inflammation and bacterial growth in the ascitic fluid. A key predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to decreased intestinal transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, contributes to an increased number of microorganisms and decreased capacity to clear them from the bloodstream, resulting in their migration into and eventual proliferation within ascites fluid.

Interestingly, adults with spontaneous bacterial peritonitis typically have ascites, but most children with spontaneous bacterial peritonitis do not have ascites. The reason for and mechanism behind this is the source of ongoing investigation.

Frequency

United States

In patients with ascites, the prevalence may be as high as 18%. This number has grown from 8% over the past 2 decades, most likely secondary to an increased awareness of spontaneous bacterial peritonitis and heightened threshold to perform diagnostic paracentesis.

Mortality/Morbidity

The spontaneous bacterial peritonitis mortality rate ranges from 40-70% in adult patients with cirrhosis and is lower in children with nephrosis. Patients with concurrent renal insufficiency have been shown to be at a higher risk of mortality from spontaneous bacterial peritonitis than those without concurrent renal insufficiency. Mortality from spontaneous bacterial peritonitis may be decreasing among all subgroups of patients because of advances in its diagnosis and treatment.

Race

No race predilection is known.

Sex

In patients with ascites, both sexes are affected equally.

Age

Although the etiology and incidence of hepatic failure differ between children and adults, in those individuals with ascites, the incidence of spontaneous bacterial peritonitis is roughly equal. Two peak ages for spontaneous bacterial peritonitis are characteristic in children: one in the neonatal period and the other at age 5 years.

Clinical

History

A broad range of signs and symptoms are seen in spontaneous bacterial peritonitis (SBP). A high index of suspicion must be maintained when caring for patients with ascites, particularly those with acute clinical deterioration.

• Completely asymptomatic cases have been reported in as many as 30% of patients.
• Fever and chills occur in as many as 80% of patients.
• Abdominal pain or discomfort is found in as many as 70% of patients.
• Worsening or unexplained encephalopathy
• Diarrhea
• Ascites that does not improve following administration of diuretic medication
• Worsening or new-onset renal failure
• Ileus

Physical

• Abdominal tenderness: This is found in more than 50% of patients with spontaneous bacterial peritonitis. Findings on the abdominal examination can range from mild tenderness to overt rebound and guarding. In some cases, the abdominal examination mimics an acute intra-abdominal catastrophe requiring emergency surgical evaluation.
• Hypotension (5-14%)
• Signs of hepatic failure such as jaundice and angiomata

Causes

• Etiologic agents
  • Traditionally, three fourths of spontaneous bacterial peritonitis infections have been caused by aerobic gram-negative organisms (50% of these being Escherichia coli), with one fourth of these infections are due to aerobic gram-positive organisms (19% streptococcal species). E coli is demonstrated in the image below.
  • 
    

    

    Gram-negative Escherichia coli.

    [ CLOSE WINDOW ]

    

    Gram-negative Escherichia coli.

  • However, some data suggest that the percentage of gram-positive infections may be increasing.^2,3 One study cites a 34.2% incidence of streptococci, ranking in second position after Enterobacteriaceae.³ Viridans group streptococci (VBS) accounted for 73.8% of these streptococcal isolates.
  • Anaerobic organisms are rare because of the high oxygen tension of ascitic fluid.
  • A single organism is noted in 92% of cases, and 8% of cases are polymicrobial.
• Risk factors
  • Patients with cirrhosis who are in a decompensated state are at the highest risk of developing spontaneous bacterial peritonitis.⁴
  • Low complement levels are associated with the development of spontaneous bacterial peritonitis. Patients at greatest risk for spontaneous bacterial peritonitis have decreased hepatic synthetic function with associated low total protein level or prolonged prothrombin time (PT).
  • Patients with low protein levels in ascitic fluid (<1 g/dL) have a 10-fold higher risk of developing spontaneous bacterial peritonitis than those with a protein level greater than 1 g/dL.

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