Medicine chapters
Cirrhosis and ascites (including spontaneous bacterial peritonitis)
What cirrhosis is, its causes (hepatitis C first in Pakistan), signs of chronic liver disease, how to grade it with Child-Pugh and MELD, and how to investigate and treat ascites, spontaneous bacterial peritonitis and hepatorenal syndrome.
- Cirrhosis is diffuse fibrosis with regenerating nodules; in Pakistan hepatitis C is the leading cause. Grade it with Child-Pugh (bilirubin, albumin, PT, ascites, encephalopathy) or MELD.
- Tap every new or worsening ascites: SAAG 11 g/L or more = portal hypertension; neutrophils over 250/mm³ = SBP.
- Treat ascites with salt restriction and spironolactone (add furosemide), and large-volume paracentesis with albumin; treat SBP with an IV cephalosporin plus albumin, then prophylaxis.
On this page
Overview
Cirrhosis is the end stage of many chronic liver diseases. Long-standing injury causes fibrosis, the liver architecture is destroyed, and regenerating nodules form. Two consequences explain almost every complication: liver cell failure (low albumin, clotting failure, jaundice, encephalopathy) and portal hypertension (varices, ascites, splenomegaly).
Cirrhosis may be compensated (no complications, often silent) or decompensated (ascites, variceal bleeding, encephalopathy or jaundice). Decompensation sharply worsens the outlook.
Causes
| Common | Less common |
|---|---|
| Hepatitis C (commonest in Pakistan) | Autoimmune hepatitis |
| Hepatitis B (with or without D) | Primary biliary cholangitis, primary sclerosing cholangitis |
| Alcohol | Haemochromatosis, Wilson disease (young patients) |
| Non-alcoholic fatty liver disease (NAFLD/MASLD) | α1-antitrypsin deficiency, cystic fibrosis |
| Budd-Chiari syndrome, chronic heart failure (cardiac cirrhosis) | |
| Drugs (methotrexate), cryptogenic |
Pathology
- Hepatic stellate cells are activated, turn into myofibroblasts and lay down collagen.
- Micronodular cirrhosis (nodules under 3 mm, uniform): typical of alcohol and biliary disease.
- Macronodular cirrhosis (variable, larger nodules): typical of viral hepatitis.
- Repeated injury destroys the reticulin framework, so regeneration forms disorganised nodules rather than normal lobules.
Clinical features
Signs of chronic liver disease
| Area | Signs |
|---|---|
| Hands | Palmar erythema, leuconychia (low albumin), clubbing, Dupuytren contracture (alcohol), asterixis (encephalopathy) |
| Face and chest | Jaundice, spider naevi (upper body, more than 5 is significant), gynaecomastia, parotid swelling (alcohol), fetor hepaticus |
| Abdomen | Splenomegaly, ascites, caput medusae, liver small or enlarged and firm, loss of body hair, testicular atrophy |
| General | Muscle wasting, bruising, ankle oedema |
Many signs come from raised oestrogen (poor breakdown) and portal hypertension.
In a young patient with cirrhosis, always check caeruloplasmin and urinary copper (Wilson disease) and iron studies, because both are treatable.
Complications of cirrhosis
- Portal hypertension and variceal bleeding (see the GI bleeding chapter)
- Ascites and spontaneous bacterial peritonitis
- Hepatic encephalopathy
- Hepatorenal syndrome
- Hepatopulmonary syndrome and portopulmonary hypertension
- Hepatocellular carcinoma
- Infections, malnutrition, osteoporosis
Investigations
Severity
- Albumin and prothrombin time/INR are the best measures of how well the liver works. Albumin below 28 g/L carries a poor outlook.
- Bilirubin rises late. Transaminases may be normal.
- Low sodium shows advanced disease (or over-diuresis). Raised creatinine is a bad sign.
- Low platelets reflect hypersplenism (pooling in a big spleen) and low thrombopoietin.
Cause
Viral markers (HBsAg, anti-HCV), autoantibodies and immunoglobulins, iron studies and ferritin, copper and caeruloplasmin (always in young patients), α1-antitrypsin, alcohol history.
Imaging and other tests
- Ultrasound: coarse, nodular liver, splenomegaly, ascites, portal vein flow; screens for HCC.
- Transient elastography (FibroScan): measures liver stiffness; reduces the need for biopsy.
- Upper GI endoscopy: screens for varices.
- Alpha-fetoprotein: for HCC; a value over about 200 ng/mL strongly suggests HCC.
- Liver biopsy: the gold standard when the cause or stage is unclear.
Grading severity
Child-Pugh score
| Points | 1 | 2 | 3 |
|---|---|---|---|
| Bilirubin (µmol/L) | Under 34 | 34–50 | Over 50 |
| Albumin (g/L) | Over 35 | 28–35 | Under 28 |
| Prothrombin time (seconds prolonged) | 1–4 | 4–6 | Over 6 |
| Ascites | None | Mild | Moderate to severe |
| Encephalopathy | None | Mild | Marked |
Class A: 5–6. Class B: 7–9. Class C: 10–15. Kumar quotes 1-year survival of about 82% for A, 62% for B and 42% for C.
Bilirubin 45 µmol/L (2), albumin 30 g/L (2), PT prolonged by 5 s (2), mild ascites (2), no encephalopathy (1)
Total = 2 + 2 + 2 + 2 + 1 = 9 → Child-Pugh class B
MELD score
Uses bilirubin, creatinine and INR (newer versions add sodium). It predicts short-term mortality and is used to prioritise patients for liver transplant; a MELD of 20 or more (or Child C) should prompt referral. See the transplant chapter for a worked example.
Child-Pugh is "ABCDE": Albumin, Bilirubin, Clotting (PT), Distension (ascites), Encephalopathy.
General management of cirrhosis
- Treat the cause: antivirals for HBV and HCV, stop alcohol, venesection, copper chelation, steroids for AIH. Fibrosis can regress.
- Nutrition: adequate calories and protein; salt restriction (about 2 g sodium a day); late-evening snack.
- Vaccinate against hepatitis A and B (and pneumococcus, influenza).
- Avoid alcohol, NSAIDs and aspirin (bleeding, kidney injury), sedatives, and nephrotoxic drugs.
- Surveillance: 6-monthly ultrasound (with or without AFP) for HCC; endoscopy for varices; non-selective beta-blocker or banding for large varices.
- Refer for transplant when decompensated (Child C, MELD 20 or more, refractory ascites, SBP, hepatorenal syndrome).
Ascites
Why it forms
- Splanchnic arterial vasodilatation (nitric oxide and other vasodilators) lowers the effective arterial blood volume.
- The kidney senses underfilling and activates the renin-angiotensin-aldosterone system, sympathetic nerves and ADH, so it retains sodium and water (secondary hyperaldosteronism). Urine sodium becomes very low.
- Portal hypertension increases hydrostatic pressure in the sinusoids and gut, so fluid and lymph leak into the peritoneum.
- Low albumin lowers oncotic pressure and adds to it.
Clinical features
Abdominal swelling, shifting dullness or fluid thrill, ankle oedema, umbilical hernia, breathlessness when tense. A right-sided pleural effusion (hepatic hydrothorax) may occur through small diaphragm defects. New or worsening ascites should prompt a search for a trigger: SBP, HCC, portal vein thrombosis, alcohol, or stopping diuretics.
Diagnostic tap (always do it)
Take a sample from every patient with new ascites and every admitted patient with ascites. Send for:
- Cell count: neutrophils over 250 cells/mm³ = SBP.
- Gram stain and culture (inoculate blood culture bottles at the bedside).
- Albumin (to calculate SAAG) and total protein.
- Cytology, amylase, and ADA if TB is suspected.
Serum-ascites albumin gradient (SAAG)
SAAG = serum albumin − ascitic albumin (same day).
| SAAG 11 g/L or more (portal hypertension) | SAAG under 11 g/L (peritoneum or low protein) |
|---|---|
| Cirrhosis | Peritoneal carcinomatosis |
| Budd-Chiari syndrome, veno-occlusive disease | Tuberculous peritonitis |
| Heart failure, constrictive pericarditis, tricuspid regurgitation | Pancreatic ascites |
| Massive liver metastases | Nephrotic syndrome |
Serum albumin 28 g/L, ascitic albumin 8 g/L
SAAG = 28 − 8 = 20 g/L → 11 or more → portal hypertension (e.g. cirrhosis)
Compare: serum albumin 30 g/L, ascitic albumin 22 g/L → SAAG 8 g/L → think TB or malignancy
In heart failure and constrictive pericarditis, the SAAG is high and ascitic protein is high (over 25 g/L), because the normal sinusoids leak protein. In cirrhosis, SAAG is high but protein is low. Tuberculous peritonitis (common in Pakistan): low SAAG, high protein, lymphocytes, raised ADA.
Management of ascites
- Dietary salt restriction: reduce sodium (about 2 g, or 80–90 mmol, a day). Avoid sodium-rich drugs and IV saline where possible.
- Spironolactone first: start 100 mg daily, increase stepwise up to 400 mg daily. It blocks the effect of the high aldosterone. Side effects: hyperkalaemia, painful gynaecomastia (eplerenone or amiloride are alternatives).
- Add furosemide (20–40 mg, increased if needed) if the response is poor or potassium rises.
- Aim: weight loss of about 0.5–0.7 kg a day (up to 1 kg if there is ankle oedema). Check weight daily and electrolytes every 1–2 days.
- Stop diuretics if sodium falls below about 128 mmol/L, creatinine rises, potassium is high, or encephalopathy develops.
- Fluid restriction only if sodium is below about 128 mmol/L.
Spironolactone is the first diuretic because cirrhotic ascites is driven by secondary hyperaldosteronism; furosemide alone works poorly.
Large-volume paracentesis
- For tense or refractory ascites; large volumes can be drained in one go.
- Removing more than about 5 litres risks post-paracentesis circulatory dysfunction (worsening vasodilatation, kidney injury, hyponatraemia).
- Prevent this by giving human albumin about 8 g per litre removed.
6 litres of ascites drained
Albumin = 8 g × 6 = 48 g → about 50 g IV albumin (e.g. 250 mL of 20% albumin)
Refractory ascites
Ascites that does not respond to maximum diuretics, or recurs quickly, or diuretics cannot be used because of side effects. Options: repeated paracentesis with albumin, TIPS (if no significant encephalopathy and adequate liver and heart function), and liver transplant.
Spontaneous bacterial peritonitis (SBP)
- Infection of ascites without a surgical source. Bacteria (usually gut organisms) translocate into blood and seed the fluid.
- Organisms: E. coli, Klebsiella, enterococci and streptococci.
- Features may be minimal: mild abdominal pain, fever, new confusion, worsening kidney function or unexplained deterioration. Many have no peritonism.
- Diagnosis: ascitic neutrophils over 250 cells/mm³. Do not wait for culture; it is often negative.
- Treatment: IV third-generation cephalosporin (cefotaxime or ceftriaxone) plus IV albumin (reduces hepatorenal syndrome and death). Adjust to culture and local resistance.
- Prophylaxis: after one episode, long-term norfloxacin 400 mg daily (or ciprofloxacin/co-trimoxazole); primary prophylaxis is considered when ascitic protein is below 10 g/L with advanced disease, and during variceal bleeding.
- Kumar: mortality 10–15%; recurrence about 70% within a year. SBP is an indication for transplant assessment.
Multiple organisms on culture, very high protein, very low glucose or gas under the diaphragm suggest secondary peritonitis (perforation), which needs imaging and surgery, not SBP treatment alone.
Any cirrhotic patient with ascites who becomes confused, febrile or develops kidney injury needs a diagnostic tap for SBP.
Hepatorenal syndrome (HRS)
- Functional kidney failure in advanced cirrhosis with ascites. The kidneys are structurally normal (they work again after transplant).
- Mechanism: extreme splanchnic vasodilatation → low effective blood volume → intense renal vasoconstriction.
- Features: rising creatinine, low urine output, urine sodium very low (under 10 mmol/L), bland urine, normal kidneys on ultrasound, no improvement after stopping diuretics and giving albumin for 2 days.
- Triggers: SBP, over-diuresis, large paracentesis without albumin, GI bleeding, NSAIDs, nephrotoxic drugs.
- Treatment: stop diuretics and nephrotoxins, albumin plus a vasoconstrictor (terlipressin, or noradrenaline); improves kidney function in about half. Liver transplant is the definitive treatment.
Hepatopulmonary syndrome and portopulmonary hypertension
- Hepatopulmonary syndrome: intrapulmonary vascular dilatation causes hypoxaemia. Clues: clubbing, cyanosis, platypnoea (breathless on sitting up) and orthodeoxia (oxygen saturation falls when upright). Diagnose with contrast (bubble) echocardiography. Improves after transplant.
- Portopulmonary hypertension: pulmonary arterial hypertension in portal hypertension.
Prognosis
- Compensated cirrhosis can be stable for years; about half survive 5 years overall.
- Poor signs: albumin under 28 g/L, sodium under 125 mmol/L, raised creatinine, persistent jaundice, refractory ascites, variceal bleeding, encephalopathy, a small liver.
Expect: commonest cause of cirrhosis in Pakistan (HCV); signs of chronic liver disease and their cause; micronodular vs macronodular; Child-Pugh items and classes; MELD for transplant listing; pathogenesis of ascites (splanchnic vasodilatation, secondary hyperaldosteronism); SAAG cut-off of 11 g/L and its causes; TB peritonitis pattern; neutrophil count over 250/mm³ for SBP, organisms and treatment with cephalosporin plus albumin; norfloxacin prophylaxis; spironolactone first and why; albumin with paracentesis; hepatorenal syndrome features and terlipressin; hepatopulmonary syndrome with orthodeoxia.
Quick revision
- Cirrhosis = fibrosis + regenerating nodules; complications from liver failure and portal hypertension.
- HCV is the leading cause in Pakistan; screen young patients for Wilson disease.
- Albumin and PT best show liver function; low platelets from hypersplenism.
- Child-Pugh: bilirubin, albumin, PT, ascites, encephalopathy; A 5–6, B 7–9, C 10–15.
- SAAG 11 g/L or more = portal hypertension; low SAAG = TB, cancer, pancreatitis, nephrotic.
- SBP: neutrophils over 250/mm³; IV cephalosporin + albumin; norfloxacin prophylaxis.
- Ascites: salt restriction, spironolactone 100–400 mg, add furosemide; stop if Na below 128.
- Paracentesis over 5 L: albumin 8 g per litre removed.
- HRS: functional, urine Na very low; terlipressin + albumin; transplant.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What does a high serum-ascites albumin gradient mean?
A SAAG of 11 g/L or more means the ascites is caused by raised pressure in the portal system, most often cirrhosis.
Why give albumin after draining a large volume of ascites?
Removing many litres worsens the low effective blood volume and can cause kidney injury; albumin at about 8 g per litre removed prevents this.
How is spontaneous bacterial peritonitis diagnosed?
By an ascitic neutrophil count above 250 cells/mm³ in a patient with ascites and no surgical source of infection, even before culture results are back.
Why do the kidneys fail in hepatorenal syndrome when they look normal?
Severe vasodilatation in the gut circulation lowers effective blood volume, and the kidneys respond by clamping down their own blood vessels. The failure is functional and reverses after liver transplant.