Spontaneous Bacterial Peritonitis: Diagnostic Criteria and Comprehensive Overview

Spontaneous bacterial peritonitis (SBP) is a critical condition characterized by the acute infection of ascitic fluid, the pathological accumulation of fluid within the abdominal cavity. This infection occurs without any evident primary intra-abdominal source, primarily affecting individuals with liver cirrhosis and ascites. While SBP can affect both adults and children, it is predominantly diagnosed in adults with advanced liver disease. The most frequently identified pathogens are gram-negative enteric bacteria, such as Escherichia coli and Klebsiella pneumoniae, indicating the gastrointestinal tract as the principal origin of infection. Prompt diagnosis and treatment are paramount due to the rapid progression of SBP to severe complications like septic shock and multi-organ failure. This article delves into the etiology, epidemiology, pathophysiology, clinical presentation, and crucially, the Spontaneous Bacterial Peritonitis Diagnosis Criteria, alongside contemporary management strategies and the pivotal role of an interprofessional healthcare team.

Etiology of Spontaneous Bacterial Peritonitis

The predominant causative agents in SBP are gram-negative aerobic bacteria, accounting for approximately 75% of cases. Within this group, Klebsiella pneumoniae is particularly prevalent, responsible for about half of these infections. Gram-positive aerobic bacteria contribute to the remaining cases, with Streptococcus pneumoniae and Viridans group streptococci being the most commonly isolated species.[3, 4]

Due to the typically high oxygen tension of ascitic fluid, anaerobic organisms are infrequently implicated in SBP. In the vast majority of SBP cases (around 92%), a single bacterial species is identified as the causative agent. However, polymicrobial infections have been reported in a smaller subset of patients.

A significant predisposing factor for SBP is chronic liver disease, particularly in patients with Child-Pugh Class C cirrhosis, indicative of severely decompensated liver function. This classification is associated with a markedly reduced survival rate. Decompensated cirrhotic patients are at the highest risk due to several factors. The primary route of infection is bacterial translocation from the intestinal lumen to mesenteric lymph nodes and subsequently to the ascitic fluid.

Several additional risk factors augment the susceptibility to SBP. A prior history of SBP significantly increases the likelihood of recurrence. Low complement levels, indicative of impaired immune function, and diminished hepatic protein synthesis, leading to prolonged prothrombin time (PT) and reduced ascitic fluid protein levels (below 1 g/dL), are also crucial risk factors. Long-term proton pump inhibitor (PPI) therapy is another recognized risk factor. PPIs elevate gastric pH, which can promote bacterial overgrowth in the gut and subsequent translocation.

It is noteworthy that while ascites is a hallmark of SBP in adults, a considerable proportion of children diagnosed with SBP do not present with ascites. The underlying reasons for this disparity remain unclear.[5]

Epidemiology of Spontaneous Bacterial Peritonitis

SBP affects both adults and children, with a bimodal age distribution in pediatric populations, peaking in neonates and children around five years old. The highest incidence is observed in patients with liver cirrhosis. However, SBP can complicate any condition leading to ascites, including Budd-Chiari syndrome, congestive heart failure, systemic lupus erythematosus, renal failure, and various malignancies. The prognosis associated with SBP in these contexts is generally poor. Approximately 10% to 25% of patients with ascites will develop SBP, and the condition carries a significant in-hospital mortality rate of around 20%.

Patients with a history of SBP are at increased risk of subsequent infections, often with drug-resistant organisms. Advanced age, the use of proton-pump inhibitors (PPIs), and undergoing SBP prophylaxis, such as selective intestinal decontamination, are also associated with an elevated risk of developing SBP.[6]

Pathophysiology of Spontaneous Bacterial Peritonitis

The pathophysiology of SBP is primarily attributed to bacterial translocation from the gastrointestinal (GI) tract. As mentioned, the majority of organisms isolated in SBP cases are gram-negative enteric bacteria, strongly suggesting the GI tract as the primary source. The frequent detection of enterotoxins in ascitic fluid further supports this theory of bacterial translocation.

An alternative, less common, route of infection is hematogenous spread from a distant infection site, such as a urinary tract infection. This is more likely to occur in immunocompromised individuals. Patients with liver cirrhosis often exhibit small intestinal bacterial overgrowth, largely due to slowed intestinal transit time. This bacterial overgrowth, combined with impaired liver function leading to reduced protein production (including low complement levels) and compromised phagocytic and reticuloendothelial system function, collectively diminishes the body’s ability to clear microorganisms. This cascade of events promotes bacterial migration and proliferation within the ascitic fluid.[7]

History and Physical Examination in SBP

A high index of suspicion for SBP is crucial in all patients presenting with ascites, particularly those exhibiting acute clinical deterioration. While the classic presentation of SBP includes fever, chills, and abdominal pain, a significant proportion of patients may be asymptomatic, and SBP can be an incidental finding. Fever is the most common symptom and a particularly valuable clinical indicator, as cirrhotic patients are often hypothermic. Other signs and symptoms may include diarrhea, paralytic ileus, new-onset or worsening hepatic encephalopathy (altered mental status) without other identifiable causes, new or worsening renal failure, or ascites refractory to diuretic therapy.

Physical examination findings in SBP can range from mild abdominal tenderness to guarding and rebound tenderness. However, the absence of fever or significant abdominal pain does not rule out SBP.

Spontaneous Bacterial Peritonitis Diagnosis Criteria and Evaluation

Rapid diagnosis and initiation of treatment are critical in SBP due to its potential for rapid progression to septic shock and multi-organ failure. The cornerstone of spontaneous bacterial peritonitis diagnosis criteria is the analysis of ascitic fluid obtained via paracentesis.

Ascitic Fluid Analysis:

Peritoneal fluid analysis is mandatory in all patients suspected of having SBP. This analysis includes:

• Cell count and differential: Specifically, the polymorphonuclear leukocyte (PMN) count.
• Gram stain and culture: To identify the causative organism and its antibiotic susceptibility.
• Lactate level and pH: Can provide additional supportive diagnostic information.

Polymorphonuclear Leukocyte (PMN) Count:

The primary diagnostic criterion for SBP is an elevated PMN count in ascitic fluid.

• A PMN count of ≥ 250 cells/μL (0.25 x 10^9/L) in ascitic fluid is the widely accepted diagnostic threshold for SBP. This criterion exhibits a high sensitivity (93%) for detecting SBP, although the specificity is slightly lower (94%).
• Historically, a threshold of >500 cells/μL was used, but the 250 cells/μL cut-off provides better sensitivity for earlier diagnosis and intervention.

Image: Microscopic view of ascitic fluid, highlighting cellular components relevant to SBP diagnosis.

Additional Diagnostic Procedures:

• Blood and Urine Cultures: Should be obtained prior to antibiotic administration. These cultures can help identify the source of infection and guide antibiotic therapy, although they are less specific for SBP diagnosis itself.
• Imaging Studies (CT Scan): If intra-abdominal perforation is suspected, computed tomography (CT) scanning is warranted as it is more sensitive than plain radiography for detecting small perforations.

Rapid Diagnostic Tests:

• Leukocyte Esterase Reagent Strip: A rapid reagent strip test for leukocyte esterase in ascitic fluid has shown promising results. It has demonstrated a high sensitivity (reported as 100% in some studies) compared to manual PMN counting for SBP diagnosis. This test offers a potentially more efficient method for rapid bedside diagnosis of SBP, but further large-scale evaluations are needed to confirm its widespread applicability and reliability.

High-Risk Patient Screening:

Patients at high risk for SBP should undergo diagnostic paracentesis even with minimal symptoms. High-risk categories include:

• Cirrhotic patients with gastrointestinal bleeding.
• Patients with a prior history of SBP.
• Cirrhotic patients with low ascitic fluid protein levels (<1.5 g/dL, some studies use <1 g/dL or <1.2 g/dL).
• Cirrhotic patients hospitalized for reasons other than SBP who have low ascitic protein concentration.

Treatment and Management of Spontaneous Bacterial Peritonitis

Prompt empiric antibiotic therapy is crucial in managing SBP.

Empiric Antibiotic Therapy:

• Intravenous third-generation cephalosporins (e.g., cefotaxime, ceftriaxone) are the recommended first-line empiric antibiotics. Therapy should be initiated in all patients with suspected SBP and a PMN count of ≥ 250 cells/μL in ascitic fluid.
• Adjustments to empiric therapy are necessary in specific situations:
  • Patients with recent beta-lactam antibiotic exposure.
  • Patients with suspected nosocomial SBP.
  • In these cases, initial antibiotic selection should consider local resistance patterns and susceptibility testing results when available. Broader-spectrum antibiotics like piperacillin-tazobactam or carbapenems might be considered.

Monitoring Treatment Response:

• Repeat ascitic fluid analysis: A follow-up paracentesis and ascitic fluid PMN count should be performed 48 hours after initiating antibiotic therapy to assess treatment efficacy.
• Treatment success is generally defined as a reduction in the ascitic fluid PMN count by at least 25% after 48 hours. Lack of improvement may indicate:
  • Antibiotic resistance.
  • Secondary bacterial peritonitis due to intra-abdominal perforation or abscess.
  • The need for surgical intervention in cases of secondary peritonitis.

Adjunctive Albumin Therapy:

• Intravenous albumin administration is recommended in addition to antibiotics for cirrhotic patients with SBP who meet specific high-risk criteria:
  • Serum creatinine > 1 mg/dL.
  • Blood urea nitrogen (BUN) > 30 mg/dL.
  • Total bilirubin > 4 mg/dL.
• Albumin has been shown to reduce in-hospital mortality and the incidence of renal impairment in these high-risk patients compared to antibiotic therapy alone.

Antibiotic Prophylaxis:

• Long-term antibiotic prophylaxis is indicated for high-risk patients to prevent recurrent SBP.
• Candidates for prophylaxis include:
  • Patients with a prior episode of SBP.
  • Cirrhotic patients with ascites and low ascitic fluid protein (<1.5 g/dL).
• Commonly used prophylactic antibiotics:
  • Norfloxacin.
  • Ciprofloxacin.
  • Trimethoprim-sulfamethoxazole.
• Antibiotic Resistance Considerations: Prolonged fluoroquinolone prophylaxis can promote antibiotic resistance, particularly in settings with high fluoroquinolone usage. In such cases, cefotaxime may be considered as an alternative treatment option for SBP. Piperacillin-tazobactam or carbapenems can also be used empirically if cefotaxime is not suitable.

Management of Renal Failure:

• Renal failure is a significant complication and a leading cause of mortality in SBP. Intravenous albumin can help mitigate the risk of renal failure.
• In patients who develop renal failure, treatment with octreotide or midodrine may be beneficial.

Differential Diagnosis of Spontaneous Bacterial Peritonitis

It is essential to differentiate SBP from other conditions presenting with abdominal pain and ascites:

• Perforated viscus
• Perinephric abscess
• Pyelonephritis
• Diverticulitis
• Appendicitis
• Mesenteric ischemia

These conditions typically require different diagnostic approaches and management strategies, often involving surgical intervention.

Prognosis of Spontaneous Bacterial Peritonitis

With timely diagnosis and appropriate treatment, the infection-related mortality of SBP is relatively low. However, the prognosis remains serious, especially for patients who develop sepsis. In-hospital mortality rates for SBP can be as high as 20-40%, and long-term mortality remains substantial, with 1- and 2-year mortality rates reported at 70% and 80%, respectively. The underlying severity of liver disease in patients who develop SBP significantly impacts long-term survival. Liver transplantation should be considered for eligible survivors of SBP.

Complications of Spontaneous Bacterial Peritonitis

SBP can lead to several serious complications:

• Renal failure
• Sepsis and septic shock
• Liver failure/insufficiency
• Tense ascites
• Bleeding or bowel perforation (rare complications of paracentesis)
• Spontaneous fungal peritonitis (less common but possible, particularly in patients with prior antibiotic exposure)

Deterrence and Patient Education for SBP

Preventive measures and patient education are crucial in managing SBP risk:

• Aggressive management of acute gastrointestinal bleeding in cirrhotic patients.
• Inpatient management for cirrhotic patients with ascites and low ascitic fluid protein (<1 g/dL).
• Long-term antibiotic prophylaxis for patients with a history of SBP.
• Patient education on the signs and symptoms of SBP, emphasizing the need for prompt medical attention.

Enhancing Healthcare Team Outcomes

Optimal management of SBP requires a collaborative interprofessional team approach. This team typically includes physicians, nurses, pharmacists, dietitians, and physical therapists. Effective communication and coordination are essential to address not only the acute infection but also the underlying conditions contributing to ascites. Pharmacists play a crucial role in medication management, ensuring avoidance of nephrotoxic or hepatotoxic drugs and counseling patients on alcohol abstinence. Nurses are vital for monitoring vital signs, abdominal girth, and weight, and for educating patients and families about SBP symptoms and the importance of timely hospital readmission if symptoms recur. Dietary and physical therapy consultations can address nutritional needs and mobility limitations. Early recognition of SBP by all team members and prompt intervention are critical to improving patient outcomes and reducing mortality.

Outcomes

Despite advances in diagnosis and treatment, SBP remains a serious condition with significant morbidity and mortality, particularly in patients with end-stage liver and kidney disease. Early diagnosis and aggressive treatment are crucial to improving survival rates and minimizing complications.

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