After reading this note you will be able to describe the clinical approach to a patient with ascites, recognise spontaneous bacterial peritonitis (SBP), order and interpret the key investigations, and outline immediate and definitive management – remembering to verify drug choices and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
- Ascites: pathological accumulation of fluid in the peritoneal cavity, detectable clinically or by imaging.
- Spontaneous bacterial peritonitis (SBP): infection of ascitic fluid without an intra‑abdominal source, diagnosed when the ascitic fluid polymorphonuclear leukocyte (PMN) count ≥ 250 cells/µL and/or a positive culture.
Anatomy and physiology you need
| Structure | Relevance to ascites |
|---|---|
| Peritoneal cavity | Space where fluid collects |
| Portal venous system | ↑ portal pressure drives transudation |
| Hepatic sinusoids | Fibrosis reduces oncotic pressure |
| Lymphatics | Impaired drainage worsens fluid build‑up |
| Diaphragm | Negative intrathoracic pressure influences fluid shift |
| Splanchnic vasculature | Vasodilation → arterial under‑filling → RAAS activation |
Causes and risk factors
| Category | Common Kenyan context |
|---|---|
| Cirrhosis (alcoholic, viral hepatitis B/C) | Leading cause |
| Congestive heart failure | Right‑sided failure |
| Nephrotic syndrome | Low plasma oncotic pressure |
| Peritoneal carcinomatosis | Ovarian, gastric, colorectal |
| Tuberculous peritonitis | HIV co‑infection raises risk |
| HIV‑related liver disease | Opportunistic infections, ART hepatotoxicity |
| Malaria (severe) | Capillary leak, hepatic congestion |
| Sickle cell disease | Hepatic sequestration, portal hypertension |
| Autoimmune (systemic lupus, rheumatic fever) | Vasculitis affecting liver/spleen |
| Post‑surgical or traumatic leaks | Rare in rotations |
Pathophysiology
Portal hypertension → ↑ hydrostatic pressure → fluid transudates into peritoneum
↓ hepatic synthetic function → ↓ albumin → ↓ plasma oncotic pressure → fluid shift
Splanchnic arterial vasodilation → effective hypovolemia → RAAS & sympathetic activation → sodium & water retention → further fluid accumulation
In cirrhosis, bacterial translocation from gut → ascitic fluid colonisation → SBP (PMN ≥ 250/µL)
Clinical features
History – what to ask
| Domain | Key questions | Rationale |
|---|---|---|
| Onset & progression | “When did you first notice abdominal swelling? Has it increased rapidly or slowly?” | Rapid accumulation suggests infection, hemorrhage or cardiac decompensation; gradual points to chronic portal hypertension. |
| Volume & distribution | “Is the swelling confined to the abdomen or does it extend to the legs, scrotum, or chest?” | Peripheral edema or pleural effusion indicates generalized fluid overload or hypo‑albuminaemia. |
| Pain & tenderness | “Do you have abdominal pain, especially sharp or worsening after meals?” | Pain may signal peritoneal irritation (SBP), bowel obstruction, or hepatic capsular stretch. |
| Fever / systemic signs | “Any recent fever, chills, night sweats?” | Fever is the hallmark of spontaneous bacterial peritonitis (SBP) or tuberculous peritonitis. |
| Gastro‑intestinal symptoms | “Nausea, vomiting, loss of appetite, early satiety, change in bowel habit?” | Reduced intake worsens hypo‑albuminaemia; vomiting may be due to portal gastropathy or bowel edema. |
| Hepatic history | “History of hepatitis B/C, alcohol use, prior liver disease, transfusions?” | Underlying cirrhosis is the commonest substrate for ascites. |
| HIV / TB / malaria | “HIV status, recent TB treatment, malaria episodes, travel to endemic areas?” | HIV, TB peritonitis, malaria‑related hepatic congestion are important tropical contributors. |
| Sickle‑cell / rheumatic disease | “Do you have sickle‑cell disease or rheumatic fever?” | Sickle‑cell can cause hepatic sequestration; rheumatic heart disease can cause right‑sided failure and ascites. |
| Medications & toxins | “Use of diuretics, NSAIDs, herbal remedies, antiretrovirals?” | NSAIDs can precipitate renal dysfunction; diuretics may mask early SBP. |
| Recent procedures | “Paracentesis, endoscopy, abdominal surgery in the past 2 weeks?” | Iatrogenic bacterial translocation is a risk for SBP. |
| Lifestyle & nutrition | “Alcohol intake, diet quality, weight loss?” | Malnutrition worsens oncotic pressure deficit. |
Examination – what to look for and why
| Finding | Interpretation |
|---|---|
| Abdominal girth (measure at umbilicus) | Quantifies ascites; rapid increase suggests infection or hemorrhage. |
| Fluid wave / shifting dullness | Confirms free fluid; shifting dullness indicates large volume. |
| Tenderness or guarding | Peritoneal irritation → possible SBP or perforation. |
| Fever, tachycardia | Systemic response to infection (SBP, TB) or sepsis. |
| Jaundice | Indicates cholestasis or advanced liver disease. |
| Spider naevi, palmar erythema, caput medusae | Stigmata of chronic portal hypertension. |
| Peripheral edema, sacral edema | Low albumin or right‑heart failure contributing to fluid shift. |
| Auscultation – breath sounds | Dullness at bases = pleural effusion (hepatic hydrothorax). |
| Cardiac exam (JVP, murmurs) | Right‑sided heart disease can mimic or aggravate ascites. |
| Signs of chronic liver disease (splenomegaly, testicular atrophy) | Support cirrhotic aetiology. |
| Skin lesions (cutaneous TB, Kaposi) | May point to TB or HIV‑related causes. |
| Neurological status | Encephalopathy suggests advanced hepatic dysfunction, influences management urgency. |
Differential diagnosis
| Condition | Points toward it | How to separate from cirrhotic ascites/SBP |
|---|---|---|
| Congestive heart failure | Bilateral leg edema, JVD, hepato‑jugular reflux | Cardiac exam, echocardiography, BNP, pleural effusion predominates |
| Nephrotic syndrome | Heavy proteinuria, hypo‑albuminaemia, edema | Urine dipstick, renal function, lack of portal hypertension signs |
| Tuberculous peritonitis | Low‑grade fever, night sweats, TB exposure | Ascitic fluid lymphocyte predominance, high ADA, PCR for TB |
| Peritoneal carcinomatosis | Rapidly enlarging abdomen, weight loss, known malignancy | Cytology positive for malignant cells, CT shows peritoneal nodules |
| Pancreatic ascites | History of pancreatitis, epigastric pain | Ascitic fluid high amylase, low SAAG |
| Budd‑Chiari syndrome | Hepatomegaly, painful ascites, abdominal wall veins | Doppler US shows hepatic vein obstruction |
| Parasitic (schistosomiasis) | Exposure to freshwater, eosinophilia | Stool ova, serology, peri‑portal fibrosis on imaging |
Investigations
| Test | What it answers | Meaning of result |
|---|---|---|
| Diagnostic paracentesis (cell count, differential, culture) | Presence of infection, SAAG | PMN > 250 cells/µL = SBP; SAAG ≥ 1.1 g/dL = portal hypertension |
| Ascitic fluid albumin & serum albumin (SAAG) | Etiology (portal vs non‑portal) | SAAG ≥ 1.1 g/dL → cirrhosis, heart failure; < 1.1 g/dL → TB, malignancy, pancreatitis |
| Ascitic fluid total protein | Prognostic for SBP risk | Low protein (< 1 g/dL) = higher SBP risk |
| Gram stain & culture (aerobic & anaerobic) | Identify causative bacteria | Positive culture confirms SBP; organism guides antibiotics |
| Serum electrolytes, renal function, bilirubin, INR | Baseline organ status, Child‑Pugh | Guides diuretic choice, albumin need, transplant urgency |
| CBC with differential | Leukocytosis, anemia | Elevated WBC supports infection; anemia may suggest chronic disease |
| HIV test | Underlying immunosuppression | Positive → higher TB/SBP risk, influences prophylaxis |
| Hepatitis B/C serology | Etiology of liver disease | Chronic infection → long‑term antiviral planning |
| Abdominal ultrasound (with Doppler) | Liver morphology, portal vein flow, presence of masses, splenomegaly | Confirms cirrhosis, rules out obstruction, detects HCC |
| CT abdomen (if indicated) | Detailed anatomy, peritoneal nodules, bowel pathology | Differentiates malignancy, TB, perforation |
| TB PCR or culture on ascitic fluid | Specific TB diagnosis | Positive → tuberculous peritonitis |
| Serum-ascites albumin gradient (SAAG) repeat if initial inconclusive | Re‑assessment | Same interpretation as above |
Diagnosis and severity
- Ascites is confirmed when abdominal fluid is demonstrable clinically or by imaging and a diagnostic tap yields fluid.
- Portal‑hypertensive ascites: SAAG ≥ 1.1 g/dL, usually low protein, accompanied by cirrhotic stigmata.
- Non‑portal ascites: SAAG < 1.1 g/dL, higher protein, consider TB, malignancy, pancreatitis.
- Spontaneous Bacterial Peritonitis (SBP) is diagnosed when:
- Ascitic PMN count > 250 cells/µL and no intra‑abdominal source on imaging, or
- Positive culture from ascitic fluid with compatible clinical picture, even if PMN count is lower.
- Severity grading (used to guide urgency and level of care):
| Category | Criteria | Clinical implication |
|---|---|---|
| Mild SBP | PMN > 250 cells/µL, stable vitals, no renal dysfunction (creatinine ≤ 1.5 mg/dL), no encephalopathy | Outpatient or short inpatient course, oral/IV antibiotics, albumin optional |
| Severe SBP | Hypotension, shock, renal impairment (creatinine rise ≥ 0.3 mg/dL), hepatic encephalopathy, or lactate > 2 mmol/L | Requires ICU‑level monitoring, IV antibiotics, albumin infusion, aggressive fluid/renal support |
| Complicated ascites | Refractory to diuretics, recurrent SBP, large‑volume paracentesis > 5 L repeatedly | Consider TIPS, transplant evaluation, long‑term prophylaxis |
- Overall severity of liver disease is staged with Child‑Pugh and MELD scores (derived from bilirubin, INR, creatinine, encephalopathy, ascites). Higher scores correlate with poorer prognosis and influence decisions about TIPS, transplant, or palliative care.
Management
Immediate stabilisation
- Airway‑breathing‑circulation – give supplemental O₂ if SpO₂ < 94 %; place large‑bore IV cannula, give crystalloid bolus if hypotensive (systolic < 90 mmHg) after checking for signs of fluid overload.
- Diagnostic paracentesis within 12 h of admission (or sooner if fever, abdominal pain, encephalopathy) – send fluid for cell count, culture (aerobic/anaerobic), albumin, protein, glucose and cytology.
- Empirical antibiotics – start a third‑generation cephalosporin (e.g., cefotaxime) plus oral quinolone if local resistance patterns dictate; give IV albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 to reduce renal failure risk.
- Hold diuretics if SBP is confirmed until infection is controlled; correct electrolyte disturbances (especially hyponatraemia, hypokalaemia).
Definitive treatment
| Goal | Intervention | Rationale |
|---|---|---|
| Eradicate infection | Continue chosen antibiotic for 5‑7 days (adjust per culture) | Prevent recurrence and resistance |
| Maintain circulatory volume | Albumin as above + cautious saline if needed | Reduces hepatorenal syndrome |
| Control ascites | Sodium restriction ≤ 2 g/day; start spironolactone (aldosterone antagonist) ± furosemide (loop) in 100:40 ratio | Improves natriuresis, avoids hyperkalaemia |
| Prevent recurrence | Long‑term norfloxacin or trimethoprim‑sulfamethoxazole prophylaxis in survivors of SBP | Lowers repeat SBP risk |
| Treat underlying liver disease | Counsel on abstinence, vaccinate (HAV, HBV), start antiviral therapy for hepatitis B/C if indicated, refer for transplant evaluation when MELD high | Addresses root cause |
| Manage complications | Renal dysfunction → consider terlipressin + albumin; hepatic encephalopathy → lactulose, rifaximin; variceal bleed risk → beta‑blocker or endoscopic banding after infection settled | Tailors care to organ failures |
Monitoring & safety
- Vitals q4 h (temperature, BP, HR, respiratory rate).
- Fluid balance strict input‑output chart; daily weight.
- Renal function (creatinine, urea) daily for first 3 days, then every 48 h.
- Electrolytes (Na⁺, K⁺, Mg²⁺) daily while on diuretics/albumin.
- Ascitic fluid repeat paracentesis if no clinical improvement after 48 h.
- Drug safety – avoid nephrotoxic agents (NSAIDs, aminoglycosides); monitor for antibiotic‑associated C. difficile.
Contra‑indications / safety notes
- Albumin infusion contraindicated in severe heart failure with pulmonary oedema.
- Spironolactone avoided in hyperkalaemia > 5.5 mmol/L.
- Beta‑blockers withheld in acute SBP with systolic BP < 90 mmHg or refractory ascites.
Complications and prognosis
- Renal failure / hepatorenal syndrome – most common cause of death; early albumin and vasoconstrictor therapy improves survival.
- Refractory ascites – may need large‑volume paracentesis with albumin or transjugular intra‑hepatic portosystemic shunt (TIPS).
- Spontaneous bacterial peritonitis recurrence – up to 30 % within a year without prophylaxis.
- Hepatic encephalopathy – precipitated by infection; worsens prognosis.
- Variceal bleeding – infection increases portal pressure; risk peaks during SBP episode.
- Mortality – 30‑day mortality after SBP ranges 20‑30 %; overall 1‑year survival depends on liver disease severity (MELD, Child‑Pugh).
High‑yield exam points
- Look‑alike conditions: tuberculous peritonitis, peritoneal carcinomatosis, pancreatic ascites, heart failure‑related transudate.
- Commonest wrong first step: delaying paracentesis > 12 h; examiners expect bedside tap as the first diagnostic move.
- Examiner bedside questions:
- “What fluid analysis results confirm SBP?” (PMN ≥ 250 cells/µL).
- “Why give albumin with antibiotics?” (prevents renal dysfunction).
- “How would you differentiate TB peritonitis from SBP on ascitic fluid?” (lymphocytic predominance, high ADA).
- “What is the next step if the patient develops worsening renal function on day 2?” (add vasoconstrictor therapy, reassess albumin, stop nephrotoxic drugs).
Clinical case
Case: A 48‑year‑old man with known alcoholic cirrhosis (Child‑Pugh B) presents with fever 38.5 °C, diffuse abdominal pain and increasing abdominal girth over 2 days. On exam: tense ascites, shifting dullness, mild asterixis, BP 100/62 mmHg, HR 112 bpm. bedside paracentesis yields cloudy fluid; PMN count 420 cells/µL, culture pending.
Questions
- What is the immediate management?
Start IV cefotaxime, give albumin 1.5 g/kg, obtain full labs, and hold diuretics.
- **If the culture later grows E. coli resistant to cefotaxime, what is the next step?**
Switch to a carbapenem (e.g., meropenem) and continue albumin; adjust based on susceptibility.
- What secondary prophylaxis should be offered on discharge?
Oral norfloxacin (or trimethoprim‑sulfamethoxazole) for 6 months to prevent SBP recurrence.
Practice questions
Question 1
A 55‑year‑old woman with hepatitis B cirrhosis presents with fever, abdominal tenderness and a new tense ascites. Paracentesis shows PMN 300 cells/µL. What is the most appropriate next step?
A. Start oral ciprofloxacin only
B. Begin IV third‑generation cephalosporin and give albumin
C. Order CT abdomen before any treatment
D. Increase spironolactone dose
Answer: B. Begin IV third‑generation cephalosporin and give albumin
Explanation: SBP requires prompt IV antibiotics and albumin to reduce renal failure risk.
Question 2
A patient with known cirrhosis and SBP is improving on antibiotics, but his serum creatinine rises from 1.1 to 2.0 mg/dL on day 3. Which intervention is indicated?
A. Stop albumin infusion
B. Add terlipressin and continue albumin
C. Switch to nephrotoxic analgesic for pain control
D. Increase diuretic dose
Answer: B. Add terlipressin and continue albumin
Explanation: Worsening renal function suggests hepatorenal syndrome; vasoconstrictor therapy with albumin is recommended.
Question 3
Which ascitic fluid finding most strongly suggests tuberculous peritonitis rather than SBP?
A. PMN ≥ 250 cells/µL
B. Lymphocyte predominance with high ADA
C. Low protein (< 1 g/dL)
D. Positive Gram stain
Answer: B. Lymphocyte predominance with high ADA
Explanation: TB peritonitis typically shows lymphocytic exudate and elevated adenosine deaminase.
Question 4
A 60‑year‑old man with decompensated cirrhosis has refractory ascites despite maximal diuretics. Which of the following is the best next therapeutic option?
A. Increase sodium restriction to 1 g/day
B. Perform large‑volume paracentesis without albumin
C. Refer for TIPS placement
D. Start high‑dose oral steroids
Answer: C. Refer for TIPS placement
Explanation: TIPS reduces portal pressure and is indicated for refractory ascites when other measures fail.
Question 5
During a bedside exam, a student notes a fluid wave and shifting dullness. The examiner asks why these signs are present in ascites. What is the correct explanation?
A. Increased intra‑abdominal pressure pushes the diaphragm upward
B. Fluid creates a palpable wave that transmits across the abdomen; shifting dullness occurs when fluid displaces air‑filled bowel on percussion
C. Enlarged liver compresses the stomach causing a wave‑like sensation
D. Hyperdynamic circulation causes pulsatile abdominal wall
Answer: B. Fluid creates a palpable wave that transmits across the abdomen; shifting dullness occurs when fluid displaces air‑filled bowel on percussion
Explanation: Both signs are physical manifestations of free fluid in the peritoneal cavity.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.