Gastrointestinal

Spontaneous bacterial peritonitis: diagnosis and prophylaxis

Clinical Overview and When to Suspect SBP

— Bacterial translocation from gut lumen → mesenteric lymph nodes → systemic circulation → ascitic fluid

— Impaired opsonic activity in low-protein ascites (ascitic protein <1.5 g/dL is the key vulnerability marker)

— Reticuloendothelial dysfunction in cirrhosis allows bacteremia to seed sterile ascites

— Cirrhotic ascites is by far the dominant substrate (~10–30% annual incidence in hospitalized cirrhotics)

— Less commonly: nephrotic syndrome, severe heart failure with ascites, fulminant hepatic failure

— Not typical in malignant ascites (rare to develop SBP)

— E. coli (most common), Klebsiella, Streptococcus pneumoniae, other streptococci, enterococci

— Rising MDR organisms (ESBL, VRE) in nosocomial SBP and recent healthcare exposure

— Polymicrobial or anaerobic growth → think secondary peritonitis, not SBP

— Any cirrhotic with ascites admitted to hospital for any reason — get diagnostic paracentesis

— Fever, abdominal pain, ileus, worsening encephalopathy, unexplained AKI, hypotension, new acidosis

— GI bleed in cirrhosis (high SBP risk — prophylaxis indicated)

— Up to 13% of SBP is asymptomatic at presentation

Board pearl: On Step 3, every cirrhotic admitted with ascites gets a diagnostic paracentesis within 12–24 hours of admission, regardless of how "well" they look. Failure to tap is the most common wrong answer. Empiric antibiotics without tap is also wrong unless tap is impossible.

Definition: Spontaneous bacterial peritonitis (SBP) is infection of pre-existing ascitic fluid in the absence of a surgically treatable intra-abdominal source (no perforation, abscess, or contiguous infection).

Pathophysiology:

Who gets SBP:

Microbiology — single organism, gram-negative dominance historically:

When to suspect (must be a low threshold):

Mortality: Untreated ~90%; even with prompt treatment, in-hospital mortality 20–40% and 1-year mortality ~70%.

Presentation Patterns and Key History

— Fever or hypothermia (~70%)

— Diffuse abdominal pain or tenderness (~60%)

— New or worsening hepatic encephalopathy — often the only clue

— Unexplained AKI or hepatorenal physiology

— Hypotension, tachycardia, or new metabolic acidosis

— Ileus, nausea, vomiting, diarrhea

— Leukocytosis without obvious source

— Etiology and severity of cirrhosis (Child-Pugh, MELD)

— Prior SBP episodes — recurrence rate ~70% at 1 year without prophylaxis

— Recent variceal bleed (up to 20% develop infection within a week)

— Current PPI use (associated with increased SBP risk)

— Beta-blocker use (nonselective beta-blockers — controversy if SBP with hypotension)

— Recent healthcare exposure, antibiotic use, hospitalization → predicts MDR organisms

— Adherence to lactulose, rifaximin, diuretics, sodium restriction

— GI bleeding

— New confusion in stable cirrhotic

— Rising creatinine without clear cause

— Increasing diuretic requirement or refractory ascites

— Any sepsis physiology in a cirrhotic

Key distinction: Secondary bacterial peritonitis (perforated viscus, abscess) presents with localized pain, peritoneal signs, free air, polymicrobial fluid, and very high ascitic protein/LDH/glucose abnormalities. Missing this distinction is fatal because secondary peritonitis needs surgery, not just antibiotics.

Step 3 management: When asked "next best step" in a cirrhotic with any new symptom — encephalopathy, AKI, fever, pain, hypotension — the answer is almost always diagnostic paracentesis before antibiotics, even before imaging in most stems. Document the indication clearly to support the procedure note and billing.

Classic triad is unreliable — fever + abdominal pain + worsening ascites is present in a minority. SBP is frequently subtle or silent.

Common presenting features (any one should trigger paracentesis):

Key historical elements to extract:

Triggers that should make you tap even harder:

Physical Exam Findings and Hemodynamic Assessment

— May look deceptively well — examine carefully

— Asterixis, somnolence, disorientation suggest encephalopathy (often the only SBP clue)

— Jaundice, scleral icterus, temporal wasting reflect underlying cirrhosis severity

— Baseline cirrhotic vasodilation means "normal" BP may actually be relative hypotension

— MAP <82 mmHg in cirrhosis is associated with worse renal outcomes

— Tachycardia may be absent if patient is on nonselective beta-blocker

— Fever absent in up to 30% — hypothermia is an ominous sign

— Distension, shifting dullness, fluid wave consistent with ascites

— Tenderness often diffuse and mild; rebound and guarding are uncommon in SBP

— Localized peritoneal signs → think secondary peritonitis and obtain imaging

— Reduced bowel sounds from ileus

— Caput medusae, umbilical hernia, flank fullness — chronic portal hypertension stigmata

— Spider angiomata, palmar erythema, gynecomastia, testicular atrophy, Dupuytren contracture

— Splenomegaly (often hard to palpate through ascites)

— Lower extremity edema

— Grade encephalopathy (West Haven 0–IV)

— Asterixis on wrist extension

— Any change from baseline mental status warrants paracentesis

Board pearl: Hemodynamic assessment in cirrhosis — these patients have low SVR, high cardiac output baseline. When SBP-induced sepsis hits, they decompensate rapidly into hepatorenal syndrome–AKI. Early albumin (1.5 g/kg day 1, 1 g/kg day 3) is part of SBP management specifically to prevent this circulatory collapse — not just fluid resuscitation.

CCS pearl: On the CCS case, when you see ascites + any clinical change, order paracentesis immediately along with CBC, CMP, coagulation, lactate, blood cultures × 2, urinalysis, and CXR. Don't wait for imaging to drain.

General appearance:

Vital signs — sepsis physiology can be blunted in cirrhosis:

Abdominal exam:

Stigmata of chronic liver disease:

Neurologic exam — critical:

Diagnostic Workup — Paracentesis and Ascitic Fluid Analysis

— Site: left lower quadrant, lateral to rectus, 2 fingerbreadths cephalad and medial to ASIS

— Use ultrasound guidance to reduce bleeding and dry-tap complications

— Coagulopathy is not a contraindication; routine FFP/platelets before tap are not recommended (bleeding rate <1%)

— Avoid if DIC or clinically apparent hyperfibrinolysis

— Cell count with differential (most important — drives diagnosis)

— Bacterial culture — inoculate 10 mL into each blood culture bottle at bedside (increases yield from ~50% to ~80%)

— Total protein, albumin (for SAAG), LDH, glucose

— Gram stain (low sensitivity ~10% but useful if positive)

— Cytology if malignancy suspected (separate large-volume sample)

— AFB/fungal cultures if TB or atypical exposure

— SBP = ascitic PMN ≥250 cells/mm³ regardless of culture result

— Culture-negative neutrocytic ascites (CNNA): PMN ≥250, culture negative → treat as SBP

— Monomicrobial non-neutrocytic bacterascites: PMN <250 but positive culture → repeat tap; treat if symptomatic

— CBC, CMP, lactate, coagulation, blood cultures × 2 before antibiotics

— UA, CXR to rule out alternative sources

— Lactic acidosis suggests severe sepsis

Key distinction: SAAG ≥1.1 g/dL = portal hypertension (cirrhosis, HF, Budd-Chiari). SAAG <1.1 suggests peritoneal disease (malignancy, TB, pancreatitis) — these patients essentially do not develop classic SBP and a positive culture/high PMN means look harder for another source.

Step 3 management: Order the tap, then start empiric antibiotics immediately after fluid is obtained if PMN ≥250 or high clinical suspicion — do not wait for culture results.

Diagnostic paracentesis is the cornerstone — perform within 12–24 hours of admission in every cirrhotic with ascites.

Send the following from ascitic fluid:

Diagnostic criteria:

Adjusting PMN for traumatic tap: subtract 1 PMN per 250 RBCs.

Concurrent workup:

Diagnostic Workup — Distinguishing Secondary Peritonitis and Advanced Studies

— Total protein >1 g/dL

— Glucose <50 mg/dL

— LDH > upper limit of normal serum LDH

— Polymicrobial Gram stain or culture (especially anaerobes, fungi, multiple organisms)

— Ascitic CEA >5 ng/mL or alkaline phosphatase >240 U/L (specific for gut perforation)

— Failure of PMN to decrease by ≥25% on repeat tap at 48 hours despite appropriate antibiotics

— Localized peritoneal signs, pneumoperitoneum, surgical history

— Suspected secondary peritonitis → CT abdomen/pelvis with IV contrast (and oral/rectal if perforation considered)

— Look for free air, abscess, bowel wall thickening, perforation, diverticulitis, appendicitis

— Renal function permitting; use caution with contrast in HRS-AKI but do not delay critical imaging

— Atypical organism on culture

— Suspected secondary peritonitis

— Nosocomial SBP or recent antibiotic exposure (higher resistance risk)

— Failure to clinically improve

— Expect ≥25% decline in PMN; if not, broaden antibiotics and image

— Procalcitonin can support bacterial infection but does not replace fluid analysis

— Leukocyte esterase reagent strips on ascitic fluid — point-of-care screen, not definitive

— MELD-Na score on admission to risk-stratify mortality and transplant urgency

Board pearl: Polymicrobial growth + high protein + low glucose + high LDH in ascitic fluid = secondary peritonitis. Call surgery and image. This is a classic Step 3 distractor where the test rewards recognizing the need for surgical consultation and CT, not just escalating antibiotics.

Why this matters: Treating secondary bacterial peritonitis as SBP delays surgery and is fatal. ~5% of "SBP" is actually secondary.

Runyon's criteria for secondary peritonitis (≥2 of 3 in ascitic fluid):

Additional clues to secondary peritonitis:

When to image:

Repeat paracentesis at 48 hours — when?

Advanced labs:

Risk Stratification and First-Line Management Logic

— Diagnostic paracentesis with full fluid panel

— Blood cultures × 2, lactate, CBC, CMP, coags, UA, CXR

— Empiric IV antibiotics within 1 hour of suspicion if PMN ≥250 or sepsis physiology

— IV albumin to prevent HRS-AKI

— Hold nonselective beta-blockers if SBP with hypotension, AKI, or refractory ascites

— Hold nephrotoxins (NSAIDs, aminoglycosides, IV contrast if possible)

— Lactulose for encephalopathy; rifaximin add-on if recurrent

— Community-acquired, no recent antibiotic exposure → 3rd-generation cephalosporin (cefotaxime or ceftriaxone)

— Nosocomial SBP, recent antibiotics, healthcare exposure, severe sepsis → broad-spectrum: piperacillin-tazobactam or carbapenem ± vancomycin if MRSA/VRE risk

— Local antibiogram should guide regional choices

— Indicated when: Cr >1 mg/dL, BUN >30 mg/dL, or total bilirubin >4 mg/dL

— Dose: 1.5 g/kg on day 1, then 1 g/kg on day 3

— Reduces HRS incidence from ~30% to ~10% and mortality from ~30% to ~10%

— Higher MELD score

— AKI at presentation

— Hepatic encephalopathy

— Bacteremia, nosocomial origin, MDR organism

— Failure of PMN to decrease by ≥25% at 48 hours

Step 3 management: When the stem gives you a cirrhotic with ascitic PMN ≥250, the correct order set is paracentesis (done) → cefotaxime IV + albumin → admit. Do not pick "outpatient ciprofloxacin" — that's prophylaxis, not treatment.

Initial management sequence (think CCS order set):

Risk stratification for empiric antibiotic choice:

Albumin indication and dosing (high yield):

Markers of poor prognosis:

Disposition: Most SBP patients require inpatient admission; ICU for sepsis, encephalopathy grade III–IV, severe AKI, or hemodynamic instability.

Pharmacotherapy — First-Line Antibiotic Regimens

— Cefotaxime 2 g IV q8h for 5–7 days (gold standard, most studied)

— Ceftriaxone 1–2 g IV q24h — equally acceptable, easier dosing

— Coverage: gram-negatives (E. coli, Klebsiella), streptococci

— 5 days is sufficient if clinical and PMN response — no benefit to longer courses in uncomplicated SBP

— Fluoroquinolone (ciprofloxacin or levofloxacin) IV → PO if not on quinolone prophylaxis and low local resistance

— Avoid if patient was on norfloxacin/cipro prophylaxis (resistance likely)

— Piperacillin-tazobactam 4.5 g IV q6–8h OR

— Carbapenem (meropenem 1 g IV q8h) if ESBL risk or critically ill

— Add vancomycin or daptomycin if MRSA or VRE risk (catheters, recent MRSA, severe sepsis)

— De-escalate based on culture and susceptibility

— 1.5 g/kg on day 1 (within 6 hours of diagnosis)

— 1 g/kg on day 3

— Use 25% albumin product

— Hold nonselective beta-blockers if hypotension, AKI, or refractory ascites

— Avoid NSAIDs, aminoglycosides, ACEi/ARBs during acute episode

— PPIs — reassess indication; routine prophylactic PPI is associated with increased SBP risk

— Lactulose titrated to 2–3 soft stools/day for concurrent HE

— Expect clinical improvement and ≥25% PMN drop by 48 hours

— Repeat tap only if not improving or atypical features

— Transition to oral antibiotic acceptable if culture identifies susceptible organism and patient improving

Board pearl: Cefotaxime + albumin is the canonical SBP answer for community-acquired disease. Pip-tazo or meropenem is the answer for nosocomial or sick-looking patients with recent healthcare exposure.

Community-acquired SBP — first-line:

Penicillin/cephalosporin allergy:

Nosocomial SBP or healthcare-associated (recent hospitalization, recent antibiotics, MDR risk):

Albumin (do not forget — it's part of pharmacotherapy):

Adjuncts and what to avoid:

Duration and response assessment:

Expanded Pharmacology — Resistance, Refractory Disease, and Source Control

— ESBL-producing Enterobacterales — require carbapenem

— VRE — daptomycin or linezolid

— MRSA — vancomycin (target trough 15–20 if severe) or daptomycin

— Candida peritonitis (rare in true SBP) — echinocandin; consider secondary source

— Nosocomial onset (>48h after admission)

— Healthcare exposure within 90 days

— Recent broad-spectrum antibiotic

— Prior MDR colonization or infection

— Septic shock at presentation

— Repeat diagnostic paracentesis

— Broaden antibiotics empirically pending data

— Obtain CT abdomen/pelvis to rule out secondary peritonitis — abscess, perforation, ischemia

— Surgical consultation if any concern for surgical source

— By definition there is no surgical source — if one is found, it is no longer SBP

— Indwelling peritoneal catheters (rare in cirrhotics, common in PD patients): if SBP-like syndrome → that's PD peritonitis, different organisms and management

— Tunneled peritoneal drains for malignant ascites can become infected — typically polymicrobial

— Routine antifungals not indicated

— Add if persistent fever despite appropriate antibiotics, recent broad-spectrum antibiotic, TPN, or Candida on culture

— De-escalate based on susceptibility within 48–72 hours

— Document indication, duration, and stop date in the medical record

— Consider transition from IV to PO once afebrile and improving

CCS pearl: If your CCS patient is not improving at 48 hours, your next orders are repeat paracentesis, blood cultures, CT abdomen/pelvis with contrast, surgical consult, and broaden antibiotics to piperacillin-tazobactam or meropenem. Don't just "continue cefotaxime and observe."

MDR organism considerations (rising globally):

Risk factors prompting broad empiric coverage:

Failure to respond at 48 hours (PMN not declining ≥25%):

Source control concept in "spontaneous" peritonitis:

Antifungal considerations:

Antibiotic stewardship Step 3 angle:

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher baseline mortality and frailty; delirium often the only SBP sign

— Lower threshold to tap and admit

— Goals-of-care discussion earlier — many are not transplant candidates

— Adjust antibiotic doses for age-related GFR decline

— Polypharmacy review — discontinue NSAIDs, reassess PPIs, review beta-blockers

— SBP is the leading precipitant of HRS-AKI in cirrhosis

— Use AKI-HRS criteria: rise in Cr ≥0.3 mg/dL within 48h or ≥50% from baseline within 7 days, no improvement after 2 days off diuretics + albumin challenge (1 g/kg/day × 2 days), no shock, no nephrotoxins, no structural disease

— Treat HRS-AKI with terlipressin (preferred where available) or norepinephrine + albumin; midodrine + octreotide + albumin if outpatient/floor

— Avoid aminoglycosides absolutely — high nephrotoxicity in cirrhosis

— Adjust cefotaxime/ceftriaxone minimally; piperacillin-tazobactam needs renal dose adjustment

— Hold ACEi/ARBs, NSAIDs, diuretics during acute AKI

— Higher Child-Pugh/MELD → higher SBP mortality

— All cirrhotics with SBP should be evaluated for liver transplantation — SBP is a defining event for transplant referral

— MELD exception points may apply in select cases

— PD peritonitis is not SBP — different definition (cloudy effluent, WBC >100 with >50% PMN, organism on culture)

— Treated with intraperitoneal antibiotics; cefazolin + ceftazidime empirically

Board pearl: Every patient who survives an episode of SBP should be referred for liver transplantation evaluation — 1-year mortality is ~70% without transplant. This referral is a frequent "next best step" answer on Step 3.

Step 3 management: Document MELD-Na at diagnosis, place transplant referral order, hold nephrotoxins, and add albumin — all in the same admission order set.

Elderly cirrhotics:

Renal impairment / AKI / HRS:

Hepatic impairment severity:

Dialysis patients with peritoneal dialysis:

Special Populations — Pregnancy, Pediatrics, and Other Subgroups

— Cirrhotic pregnancy is rare but increasingly seen with autoimmune hepatitis, NAFLD, post-transplant

— Ascites uncommon but possible with portal hypertension or Budd-Chiari (think pregnancy-associated hypercoagulability)

— Cefotaxime and ceftriaxone are pregnancy-compatible (category B historically) — preferred

— Avoid fluoroquinolones (cartilage concerns) and tetracyclines

— Albumin is safe in pregnancy

— MFM and hepatology co-management; delivery planning for variceal risk

— Rare; seen in nephrotic syndrome (low protein ascites, impaired opsonization) and biliary atresia or other pediatric cirrhosis

— Pneumococcus and gram-negatives common

— Cefotaxime is first-line

— Nephrotic children — pneumococcal vaccination is key prevention

— Often Streptococcus pneumoniae or E. coli

— Diagnostic tap criteria same (PMN ≥250)

— Treat with ceftriaxone; ensure pneumococcal and meningococcal vaccination

— Peritonitis in this population is usually surgical (anastomotic leak, biliary leak) — image and consult surgery

— On immunosuppression — atypical organisms, fungi possible

— Consider TB peritonitis (high protein, lymphocyte-predominant, low SAAG, ADA elevated)

— Fungal peritonitis in profoundly immunosuppressed

— Higher baseline SBP risk

— TIPS may reduce ascites volume and SBP recurrence but worsens encephalopathy

Key distinction: TB peritonitis classically shows lymphocyte-predominant ascitic fluid with high protein, low SAAG (<1.1), elevated adenosine deaminase, and chronic indolent presentation — not classic SBP. Diagnosis often requires peritoneal biopsy via laparoscopy.

Pregnancy:

Pediatric SBP:

Nephrotic syndrome–associated peritonitis:

Post–liver transplant patients:

HIV / immunocompromised cirrhotics:

Refractory ascites / TIPS patients:

Complications and Adverse Outcomes

— Most feared SBP complication; develops in ~30% without albumin, ~10% with appropriate albumin

— Functional renal failure from splanchnic vasodilation and renal vasoconstriction

— Treatment: terlipressin + albumin (FDA-approved 2022) or norepinephrine + albumin in ICU

— Definitive treatment: liver transplantation

— Cirrhotic sepsis has higher mortality than non-cirrhotic

— Vasopressor of choice: norepinephrine

— Stress-dose steroids for refractory shock (relative adrenal insufficiency common)

— SBP is a top precipitant

— Manage with lactulose, rifaximin, treat infection, correct electrolytes (hypokalemia, alkalosis worsen HE)

— Avoid benzodiazepines

— SBP and bleeding feed each other; bleeding raises SBP risk (gut translocation)

— All cirrhotics with UGIB get ceftriaxone 1 g IV daily × 7 days prophylactically

— ~70% at 1 year without prophylaxis

— Indication for indefinite oral antibiotic prophylaxis (see chunk 15)

— In-hospital 20–40%

— 1-year mortality 50–70% even after recovery

— 2-year mortality ~80%

— Bacteremia (~50% of SBP)

— Acute-on-chronic liver failure (ACLF) — multi-organ failure on cirrhotic substrate; high short-term mortality

— Spontaneous bacterial empyema (hepatic hydrothorax infection) — analogous condition, treat similarly

Board pearl: A cirrhotic with SBP who develops rising creatinine despite holding diuretics and getting albumin challenge has HRS-AKI. Next step: terlipressin + albumin and transplant evaluation, not more fluids or diuretics.

Hepatorenal syndrome–AKI (HRS-AKI):

Sepsis and septic shock:

Hepatic encephalopathy:

Variceal bleeding:

Recurrence:

Mortality:

Other:

When to Escalate Care — ICU, Consult, and Inpatient Triage

— Septic shock or vasopressor requirement

— Hepatic encephalopathy grade III–IV (airway protection)

— Active GI bleeding with hemodynamic instability

— Respiratory failure or hepatic hydrothorax requiring ventilation

— Severe AKI requiring CRRT

— Lactate >4 mmol/L, MAP <65 despite fluids

— Hepatology — all SBP cases, for transplant evaluation and ongoing management

— Transplant surgery / center referral — first SBP episode is a transplant-defining event

— General surgery — any suspicion of secondary peritonitis (high ascitic protein/LDH, low glucose, polymicrobial, peritoneal signs, free air)

— Interventional radiology — therapeutic paracentesis, TIPS evaluation

— Infectious disease — MDR organisms, treatment failure, atypical pathogens

— Nephrology — HRS-AKI, RRT decisions

— Palliative care — end-stage cirrhosis not eligible for transplant

— Hemodynamically stable, grade I–II HE, no AKI → general medical floor with q4h vitals

— Borderline hemodynamics, escalating O2 needs, grade II–III HE → step-down/telemetry

— Identify primary outpatient hepatologist

— Schedule post-discharge paracentesis if needed

— Initiate prophylactic antibiotic before discharge

— Vaccinations updated during admission if possible

— Goals-of-care conversation in patients not eligible for transplant

CCS pearl: On the CCS interface, your "consult" orders should include hepatology and transplant evaluation for any first SBP episode — this is a guideline-mandated action that the case is testing for, not optional.

All SBP requires inpatient admission — no outpatient management.

ICU admission criteria:

Consultation triggers:

Floor vs step-down considerations:

Transition planning starts on day 1:

Key Differentials — Same-Category (Peritonitis and Ascitic Fluid Infections)

— Surgical source: perforation, abscess, appendicitis, diverticulitis, ischemic bowel

— Polymicrobial, anaerobic, high protein (>1 g/dL), low glucose (<50), high LDH

— Localized peritoneal signs, free air on imaging

— Requires surgery + broad antibiotics, not antibiotics alone

— PMN ≥250 with negative culture

— Treat exactly like SBP

— Same mortality as culture-positive SBP

— Positive culture, PMN <250

— Often transient colonization; repeat tap

— Treat if symptomatic or if repeat shows PMN ≥250

— Multiple organisms with PMN <250 — often iatrogenic from bowel puncture during paracentesis

— Observe; consider antibiotics if symptomatic

— Cloudy effluent, fever, abdominal pain in PD patient

— Effluent WBC >100/mm³ with >50% PMN

— Intraperitoneal antibiotics (vancomycin or cefazolin + ceftazidime)

— Distinct entity, do not confuse with SBP

— Subacute course, fever, weight loss, ascites

— Lymphocyte-predominant, high protein, low SAAG, elevated ADA

— Diagnosis often by laparoscopy with biopsy

— RIPE therapy

— Immunocompromised, recent broad-spectrum antibiotics

— Candida most common

— Echinocandin; remove catheters; rule out surgical source

Key distinction: PMN ≥250 = treat as SBP regardless of culture. Two positive organisms on Gram stain or culture = think secondary peritonitis until proven otherwise.

Secondary bacterial peritonitis:

Culture-negative neutrocytic ascites (CNNA):

Monomicrobial non-neutrocytic bacterascites (MNB):

Polymicrobial bacterascites:

Peritoneal dialysis peritonitis:

Tuberculous peritonitis:

Fungal peritonitis:

Key Differentials — Other-Category Causes of Abdominal Pain or Decompensation in Cirrhotics

— Triggered by GI bleed, infection (UTI, pneumonia), electrolyte derangement, constipation, sedatives, dehydration

— Always tap to rule out SBP — but also do UA, CXR, blood cultures

— Diagnosed after excluding other causes of AKI

— SBP is the most common precipitant, but not always

— Hematemesis, melena, hypotension

— Endoscopy, octreotide, ceftriaxone (which also acts as SBP prophylaxis)

— Worsening ascites, abdominal pain, GI bleeding

— Doppler US to diagnose

— Anticoagulation case-by-case

— Sudden severe abdominal pain, hemoperitoneum, shock

— Imaging: CT abdomen

— Embolization or surgery

— Jaundice, fever, leukocytosis, tender hepatomegaly

— Maddrey discriminant function, MELD; steroids if eligible

— Can mimic infection

— Older patients, vascular disease, lactic acidosis

— CT angiography

— Especially in alcohol-related cirrhosis

— Lipase, CT

— Common alternative infections precipitating cirrhotic decompensation

— Always work up alongside SBP

Board pearl: In a cirrhotic with new encephalopathy, the mandatory minimum infection workup is: paracentesis, blood cultures, urinalysis with culture, and chest X-ray. Missing any of these is a common Step 3 wrong answer.

Hepatic encephalopathy without SBP:

Hepatorenal syndrome without infection:

Variceal hemorrhage:

Portal vein thrombosis:

Hepatocellular carcinoma rupture:

Acute alcoholic hepatitis:

Ischemic colitis or mesenteric ischemia:

Pancreatitis:

UTI/pyelonephritis, pneumonia, cellulitis (e.g., from edematous legs):

Secondary Prevention, Discharge Medications, and Long-Term Plan

— Acute GI bleeding in cirrhotic: ceftriaxone 1 g IV daily × 7 days, then transition to oral if appropriate

— Low-protein ascites (<1.5 g/dL) PLUS one of: Cr ≥1.2, BUN ≥25, Na ≤130, Child-Pugh ≥9 with bili ≥3 → norfloxacin 400 mg PO daily (or ciprofloxacin 500 mg PO daily where norfloxacin unavailable)

— Indefinite norfloxacin 400 mg PO daily OR

— Ciprofloxacin 500 mg PO daily OR

— TMP-SMX DS one tablet daily (alternative, watch hyperkalemia and renal function)

— Continue until transplant, resolution of ascites, or death

— Diuretics: spironolactone + furosemide in 100:40 ratio, titrated to ascites and electrolytes — restart cautiously after AKI resolves

— Lactulose titrated to 2–3 soft stools/day

— Rifaximin 550 mg BID if recurrent HE

— Nonselective beta-blocker for varices — restart cautiously; avoid if refractory ascites with hypotension or AKI

— Discontinue/avoid: NSAIDs, ACEi/ARBs in advanced disease, unnecessary PPIs

— Pneumococcal (PCV20 or PCV15 + PPSV23)

— Annual influenza

— Hepatitis A and B if non-immune

— COVID-19 per current guidelines

— Tdap, zoster (recombinant), RSV per age

— Sodium <2 g/day

— Fluid restriction only if Na <125 mmol/L

Step 3 management: Every SBP discharge order set must include: oral prophylactic antibiotic, hepatology follow-up, transplant referral, lactulose, vaccinations updated, NSAIDs discontinued, diuretics carefully resumed, and outpatient labs in 1–2 weeks.

Primary prophylaxis indications (no prior SBP):

Secondary prophylaxis (prior SBP episode):

Other discharge medications:

Vaccinations (high yield):

Sodium and fluid restriction:

Follow-Up, Monitoring Parameters, and Counseling

— Hepatology visit within 1–2 weeks of discharge

— Repeat CMP and CBC at 1 week to monitor renal function, electrolytes, response to diuretics

— MELD-Na recalculated at each visit

— Therapeutic paracentesis as needed for symptomatic ascites (with albumin replacement 6–8 g per liter removed if >5 L)

— Quinolone prophylaxis: watch for tendinopathy, QT prolongation, C. difficile, MDR colonization

— TMP-SMX: monitor potassium and creatinine

— Reassess prophylaxis indication periodically; do not stop without hepatology input

— Any new symptom, encephalopathy, or AKI → repeat paracentesis

— Routine surveillance paracentesis is not standard, but low threshold for diagnostic tap is essential

— Ultrasound ± AFP every 6 months in all cirrhotics — continue during and after SBP recovery

— EGD per current Baveno guidelines; nonselective beta-blocker or band ligation based on findings

— Strict alcohol abstinence in alcohol-related cirrhosis; refer to addiction medicine, AA, naltrexone or acamprosate consideration

— Weight management in MASH/NAFLD-related cirrhosis

— Medication review at every visit — patients often resume NSAIDs for pain

— Sodium-restricted diet education with dietitian referral

— Sick-day rules: fever, confusion, abdominal pain → ED immediately

— Pneumococcal and influenza vaccine reminders

— Transplant pathway education and listing requirements (e.g., 6-month sobriety in many programs — though increasingly individualized)

Board pearl: HCC screening with abdominal ultrasound every 6 months continues lifelong in cirrhotics regardless of SBP history. This is a commonly tested ambulatory management point.

Post-discharge follow-up cadence:

Monitoring on prophylactic antibiotics:

Recurrence surveillance:

Hepatocellular carcinoma screening:

Variceal surveillance:

Counseling priorities:

Ethical, Legal, and Patient Safety Considerations

— Discuss risks: bleeding (<1%), bowel perforation (rare), infection at site, post-paracentesis circulatory dysfunction

— In an encephalopathic patient lacking capacity, obtain consent from legal surrogate; if emergent and surrogate unavailable, proceed under implied/emergency consent and document carefully

— Document indication, ultrasound use, technique, fluid sent, and complications

— Hepatic encephalopathy fluctuates — reassess capacity at each major decision

— Use the four-prong test: understanding, appreciation, reasoning, communicating a choice

— A patient refusing paracentesis with grade II HE likely lacks capacity; engage surrogate

— Patients ineligible for transplant (active substance use without engagement, severe comorbidity, social barriers) need early palliative care involvement

— Discuss code status, DNR/DNI, and ceiling-of-care decisions on admission, not at the point of crisis

— Acknowledge the inequities in transplant access (insurance, geography, race) — Step 3 may probe ethical handling

— Medication reconciliation at discharge — confirm prophylactic antibiotic prescribed, diuretics adjusted, NSAIDs discontinued, beta-blocker decision documented

— Send discharge summary to PCP and hepatologist within 48 hours

— Schedule follow-up appointment before discharge, not "call to schedule"

— Teach-back method for sodium restriction, lactulose titration, and red-flag symptoms

— Address health literacy and language barriers with interpreter services

— Failure to perform admission paracentesis (sentinel quality measure)

— Missed secondary peritonitis (delayed surgery is catastrophic)

— Nephrotoxic exposures during admission (NSAIDs, contrast, aminoglycosides)

— Benzodiazepine administration in encephalopathic patients

Step 3 management: "Failure to perform admission diagnostic paracentesis in a cirrhotic with ascites" is a national quality measure — institutions track and report it.

Informed consent for paracentesis:

Capacity assessment:

Goals of care and transplant candidacy:

Transition-of-care safety (high-yield Step 3):

Patient safety events to prevent:

Mandatory reporting: Not typical for SBP per se; however, suspected elder abuse or neglect in a decompensated cirrhotic with poor adherence and unsafe home environment must be reported per state law.

High-Yield Associations and Rapid-Fire Clinical Facts

Board pearl: If the stem mentions ascitic PMN 250 (or anything ≥250) — pick cefotaxime + IV albumin and refer to transplant. This single fact pattern is highly tested.

Diagnostic threshold: Ascitic PMN ≥250 cells/mm³ = SBP.

Most common organism: E. coli, then Klebsiella, then Streptococcus pneumoniae.

First-line community-acquired antibiotic: Cefotaxime 2 g IV q8h × 5 days.

Albumin dosing: 1.5 g/kg day 1 + 1 g/kg day 3 — when Cr >1, BUN >30, or bilirubin >4.

Albumin reduces: HRS and mortality by ~two-thirds when added to antibiotics.

SAAG ≥1.1 = portal hypertension; SAAG <1.1 = peritoneal disease (rarely true SBP).

Secondary peritonitis criteria (Runyon): protein >1, glucose <50, LDH > serum upper limit; 2 of 3.

Repeat tap at 48h if not improving; expect ≥25% PMN drop.

Variceal bleed prophylaxis: Ceftriaxone 1 g IV daily × 7 days.

Long-term prophylaxis: Norfloxacin 400 mg PO daily (or cipro/TMP-SMX).

Indication for primary prophylaxis in no-prior-SBP cirrhotic: ascitic protein <1.5 + (Cr ≥1.2, BUN ≥25, Na ≤130, or Child-Pugh ≥9 with bili ≥3).

1-year recurrence without prophylaxis: ~70%.

1-year mortality even after recovery: 50–70% — refer all to transplant.

HRS-AKI treatment: Terlipressin + albumin (preferred) or norepinephrine + albumin.

Avoid in acute SBP: NSAIDs, aminoglycosides, ACEi/ARBs, IV contrast (if avoidable), nonselective beta-blockers (if hypotensive/AKI).

PPI use in cirrhotics: associated with increased SBP risk — reassess indication.

Inoculate culture bottles at bedside with 10 mL each — increases yield from 50% to 80%.

Coagulopathy does not require correction before paracentesis.

GI bleed in cirrhotic = give ceftriaxone empirically (lowers infection AND mortality).

TB peritonitis: lymphocyte-predominant, high protein, low SAAG, elevated ADA.

HCC surveillance: US ± AFP q6 months lifelong.

Vaccinate cirrhotics: pneumococcal, HAV, HBV, influenza annually, COVID, zoster.

Board Question Stem Patterns

Key distinction: Step 3 stems often hinge on whether the next step is diagnostic (paracentesis) vs therapeutic (antibiotics) vs surgical (CT + surgery) vs preventive (prophylaxis) — read carefully to identify which decision node is being tested.

Pattern 1 — Classic SBP: 55-year-old man with alcohol-related cirrhosis presents with fever and confusion. Ascites present. Paracentesis: PMN 480/mm³, total protein 0.8 g/dL, culture pending. Answer: Start cefotaxime IV + IV albumin; admit.

Pattern 2 — Subtle SBP: Cirrhotic patient admitted for "worsening encephalopathy"; no fever or pain. Question asks next best step. Answer: Diagnostic paracentesis before treating encephalopathy.

Pattern 3 — Secondary peritonitis trap: PMN 600 but ascitic protein 3.0, glucose 30, LDH 400. Gram stain shows multiple organisms. Answer: CT abdomen/pelvis + surgical consult + broaden antibiotics — not just cefotaxime.

Pattern 4 — Albumin question: SBP confirmed; patient has Cr 1.6 and bili 5.2. Next step in addition to antibiotics? Answer: IV albumin 1.5 g/kg now and 1 g/kg on day 3.

Pattern 5 — Prophylaxis after bleed: Cirrhotic with upper GI bleed, hemodynamically stabilized. Answer: Ceftriaxone 1 g IV daily × 7 days.

Pattern 6 — Long-term prophylaxis: Cirrhotic just recovered from first SBP. Discharge plan? Answer: Norfloxacin 400 mg PO daily indefinitely + transplant referral + vaccinations.

Pattern 7 — Primary prophylaxis: Cirrhotic, no prior SBP, ascitic protein 0.9 g/dL, Cr 1.4, Na 128. Answer: Start norfloxacin prophylaxis.

Pattern 8 — HRS trigger: SBP patient with rising creatinine despite albumin challenge and no diuretics. Answer: HRS-AKI → terlipressin + albumin, transplant evaluation.

Pattern 9 — Wrong-answer trap: Cirrhotic with PMN 200 and positive E. coli culture (MNB). Answer: Repeat paracentesis; treat if symptomatic or PMN now ≥250.

Pattern 10 — Failure to improve: 48 hours into cefotaxime, PMN dropped from 600 to 550 (no improvement). Answer: Repeat tap, CT abdomen, surgical consult, broaden antibiotics.

Pattern 11 — Outpatient cirrhotic follow-up: When to image for HCC? Answer: Ultrasound every 6 months.

One-Line Recap

SBP is infection of pre-existing ascitic fluid in cirrhosis, diagnosed by ascitic PMN ≥250 cells/mm³, treated empirically with cefotaxime (or ceftriaxone) plus IV albumin (1.5 g/kg day 1, 1 g/kg day 3), with mandatory liver transplant referral and indefinite oral antibiotic prophylaxis after recovery.

Board pearl: When in doubt on Step 3 — tap the belly, give cefotaxime and albumin, refer to transplant, and discharge on norfloxacin.

Diagnosis: Every hospitalized cirrhotic with ascites gets a diagnostic paracentesis within 24 hours — coagulopathy is not a contraindication; inoculate culture bottles at the bedside to boost yield; PMN ≥250 establishes the diagnosis regardless of culture; Runyon's criteria (protein >1, glucose <50, LDH > serum ULN) flag secondary peritonitis requiring CT and surgery.

Treatment: Community-acquired SBP → cefotaxime 2 g IV q8h × 5 days; nosocomial or septic → piperacillin-tazobactam or carbapenem ± vancomycin; add IV albumin when Cr >1, BUN >30, or bilirubin >4 — this single intervention cuts HRS and mortality dramatically; hold NSAIDs, ACEi/ARBs, aminoglycosides, and nonselective beta-blockers if AKI or hypotension.

Prevention: Ceftriaxone × 7 days for any cirrhotic with GI bleeding; norfloxacin 400 mg daily indefinitely after first SBP episode or as primary prophylaxis when ascitic protein <1.5 plus renal/sodium/Child-Pugh risk markers; update pneumococcal, hepatitis A/B, influenza, and COVID vaccines.

Long-term: First SBP is a transplant-defining event — 1-year mortality without transplant approaches 70%; continue HCC surveillance every 6 months; reassess medications, especially PPIs and beta-blockers, and reinforce alcohol abstinence, sodium restriction, and lactulose adherence at every visit.