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2025 PACUPrep BCCCP Preparatory Course Ascites & Spontaneous Bacterial Peritonitis Diagnostic & Classification Strategies for Ascites & SBP

Lesson 35, Topic 2

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Diagnostic & Classification Strategies for Ascites & SBP

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Diagnostic & Classification Strategies for Ascites & Spontaneous Bacterial Peritonitis

Learning Objective

Apply diagnostic and classification criteria to assess a patient with ascites and spontaneous bacterial peritonitis (SBP) and guide initial management.

1. Clinical Assessment

Early recognition of ascites and spontaneous bacterial peritonitis (SBP) relies on a focused history, physical examination findings, and vital sign trends in patients with cirrhosis.

History

Progressive abdominal distension, discomfort, early satiety, or dyspnea.
New onset of fever, abdominal pain or tenderness, or altered mental status.
Potential precipitating events: recent gastrointestinal bleeding, hospitalization, non-adherence to diuretics, proton pump inhibitor (PPI) use, or a history of prior SBP.

Physical Exam

Classic signs of ascites: shifting dullness on percussion, a palpable fluid wave, and bulging flanks.
Signs of peritonitis: rebound tenderness, guarding, or rigidity. Note that these classic peritoneal signs are often subtle or absent in SBP compared to secondary peritonitis.

Vital Signs & Labs

Fever (temperature >38°C or 100.4°F) or hypothermia, especially in elderly or immunocompromised individuals.
Tachycardia and hypotension, which may indicate systemic inflammatory response syndrome (SIRS) or sepsis.
Evidence of end-organ dysfunction, such as new or worsening renal dysfunction or hyponatremia.

Key Pearl: The Urgency of Paracentesis

Any hospitalized patient with cirrhosis and ascites warrants a diagnostic paracentesis, even if asymptomatic. Delays in performing this procedure beyond 12 hours from admission are associated with a significant increase in in-hospital mortality.

2. Diagnostic Paracentesis

A timely diagnostic paracentesis is the gold standard procedure to diagnose SBP and characterize the etiology of ascites.

Indications & Timing

All patients with new-onset or worsening ascites.
Any patient with ascites and clinical suspicion of infection (e.g., fever, pain) or hemodynamic instability.
Target Timeframe: The procedure should be performed within 12 hours of hospital admission.

Technique & Sample Handling

Site Selection: The preferred sites are the left or right lower quadrant, lateral to the rectus sheath, or a midline infra-umbilical approach in an area with a palpable fluid pocket.
Ultrasound Guidance: Strongly recommended for obese patients, those with prior abdominal surgery, or when fluid is difficult to localize. It significantly reduces the risk of complications like bleeding or bowel perforation.
Sample Inoculation: Inoculate at least 10 mL of ascitic fluid directly into both aerobic and anaerobic blood culture bottles at the bedside.
Lab Aliquots: Send additional fluid in sterile tubes for a cell count with differential, total protein, albumin, LDH, and glucose. Cytology should be ordered if malignancy is suspected.

Clinical Pearl: Maximizing Culture Yield

Bedside inoculation of blood culture bottles is a critical step. This practice can double the diagnostic yield of ascitic fluid cultures compared to sending the fluid in a sterile container for inoculation in the laboratory.

3. Ascitic Fluid Analysis

Key ascitic fluid parameters are essential to differentiate SBP from other conditions like portal hypertensive ascites and secondary bacterial peritonitis.

Diagnostic Criteria & Interpretation

PMN Count: An absolute polymorphonuclear (PMN) leukocyte count ≥250 cells/mm³ is diagnostic for SBP. This applies to both culture-positive SBP and culture-negative neutrocytic ascites (CNNA).
Serum-Ascites Albumin Gradient (SAAG): A SAAG ≥1.1 g/dL strongly suggests that ascites is due to portal hypertension (sensitivity >97%). It is calculated by subtracting the ascitic fluid albumin from the serum albumin.
Total Protein & Other Markers: A low total protein (<2.5 g/dL) is typical for uncomplicated cirrhotic ascites. An elevated protein, low glucose, or high LDH should raise suspicion for secondary bacterial peritonitis (e.g., from a perforated viscus) or other causes like malignancy or tuberculosis.

Interpretation of Key Ascitic Fluid Parameters
Parameter	Typical in Cirrhosis	Diagnostic Threshold	Clinical Implication
PMN Count	<250 cells/mm³	≥250 cells/mm³	Spontaneous Bacterial Peritonitis (SBP)
SAAG	≥1.1 g/dL	<1.1 g/dL	Suggests non-portal hypertensive cause
Total Protein	<2.5 g/dL	>2.5 g/dL	Consider cardiac ascites or secondary peritonitis
LDH	Low (fluid/serum ratio <0.6)	Elevated	Suggests secondary peritonitis, malignancy
Glucose	Approximately serum level	Low (<50 mg/dL)	Suggests secondary peritonitis, malignancy
Culture Yield	35–65%	—	Increased with bedside bottle inoculation

Clinical Pearl: Culture-Negative Neutrocytic Ascites (CNNA)

Patients with a PMN count ≥250 cells/mm³ but a negative ascitic fluid culture have CNNA. This condition carries a similar prognosis to culture-positive SBP and must be treated with empiric antibiotics in the same manner.

4. Laboratory & Imaging Modalities

Paracentesis should be complemented with serum studies and imaging to exclude alternate etiologies and assess for vascular complications of cirrhosis.

Serum Studies

Standard Labs: A complete blood count (CBC), comprehensive metabolic panel (to assess renal and hepatic function), coagulation profile, and serum albumin are essential.
Kidney Function: Monitor serum creatinine closely. A rise of ≥0.3 mg/dL or ≥50% from baseline indicates acute kidney injury (AKI), a common and serious complication of SBP.

Emerging Biomarkers

Serum Procalcitonin: May aid in the diagnosis of SBP, with reported sensitivity and specificity around 82-86%.
Ascitic Calprotectin: A promising marker with high reported sensitivity (~91%) and specificity (~87%) for SBP.
Other investigational markers include ascitic fluid lactoferrin and macrophage inflammatory protein-1β.

Imaging

Ultrasound with Doppler: Confirms the presence and distribution of ascites and is crucial for evaluating portal vein patency and flow, which can rule out portal vein thrombosis or Budd-Chiari syndrome.
Cross-sectional Imaging (CT/MRI): Not routinely required for SBP diagnosis but indicated to identify malignancy, abscess, or bowel perforation when secondary peritonitis is suspected based on ascitic fluid analysis (e.g., high protein, multiple organisms on Gram stain).

5. Classification Systems

Standardized systems for grading ascites and categorizing SBP are vital for guiding the intensity of therapy, including dietary measures, diuretic management, and antibiotic selection.

Ascites Grading (International Ascites Club)

This system classifies ascites by severity, which directly influences management.

Figure 1: International Ascites Club Grading System. The grade of ascites dictates therapy, from sodium restriction and diuretics for Grades 1-2 to large-volume paracentesis (LVP) for Grade 3.

SBP Acquisition Category

Community-acquired: Infection diagnosed at admission or within 48 hours.
Nosocomial: Infection develops more than 48 hours after hospitalization.
Health care–related: Patient had a recent hospitalization or invasive procedure within the last 30 days.

Prognostic Scoring Systems

Child-Pugh Score: Assesses the severity of chronic liver disease (Classes A, B, C).
MELD Score: Predicts 3-month mortality and is used to prioritize patients for liver transplantation. Higher scores correlate with increased risk and mortality from SBP.

Key Pearl: Management by Classification

Classification directly drives management. Grade 3 (tense) ascites requires therapeutic large-volume paracentesis (LVP) followed by albumin infusion (6–8 grams per liter of fluid removed) to prevent post-paracentesis circulatory dysfunction. The SBP acquisition category (e.g., nosocomial) guides empiric antibiotic choice to cover for multi-drug resistant (MDR) organisms.

References

Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the AASLD. Hepatology. 2021;74(2):1014–1048.
Dever JB, Sheikh MY. Spontaneous bacterial peritonitis: bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther. 2015;41(12):1298–1307.
Popoiag RE, Fierbințeanu-Braticevici C. Spontaneous bacterial peritonitis: update on diagnosis and treatment. Rom J Intern Med. 2021;59(4):345–350.
Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology. 2004;39(3):841–856.
Moore KP, Wong F, Gines P, et al. The management of ascites in cirrhosis: report on the consensus conference of the International Ascites Club. Hepatology. 2003;38(1):258–266.
Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and SBP. N Engl J Med. 1999;341(6):403–409.
European Association for the Study of the Liver. EASL clinical practice guidelines for management of decompensated cirrhosis. J Hepatol. 2018;69(2):406–460.
Gaetano JN, Micic D, Aronsohn A, et al. The benefit of paracentesis on hospitalized adults with cirrhosis and ascites. J Gastroenterol Hepatol. 2016;31(6):1025–1030.
Mercaldi CJ, Lanes SF. Ultrasound guidance decreases complications and cost in thoracentesis and paracentesis. Chest. 2013;143(2):532–538.
Yang Y, Li L, Qu C, et al. Diagnostic accuracy of serum procalcitonin for SBP in end-stage liver disease: a meta-analysis. Medicine (Baltimore). 2015;94(49):e2077.
Fernandes SR, Santos P, Fatela N, et al. Ascitic calprotectin is a novel and accurate marker for SBP. J Clin Lab Anal. 2016;30(6):1139–1145.
Soriano G, Castellote J, Alvarez C, et al. Secondary bacterial peritonitis in cirrhosis: retrospective study of characteristics, diagnosis and management. J Hepatol. 2010;52(1):39–44.

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