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Gastrointestinal & Hepatic System

Liver Cirrhosis

An advanced stage of chronic liver disease characterized by irreversible scarring (fibrosis) and nodular regeneration, leading to disruption of liver architecture and function, and development of portal hypertension.

Also known as: Cirrhosis, End-Stage Liver Disease

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Referral and warning signs

When to refer

Refer ALL patients with suspected or confirmed cirrhosis to a specialist (Gastroenterologist/Hepatologist) for: Confirmation of diagnosis and etiology. Staging and prognostication (e.g., MELD score). Management of complications (ascites, HE, varices). HCC and variceal surveillance planning. Consideration for liver transplantation.

Red flags

  • New onset jaundice, ascites, or encephalopathy (decompensation)
  • Haematemesis or melaena (variceal bleeding)
  • Fever and abdominal pain in patient with ascites (SBP)
  • Deteriorating renal function (HRS)
  • Focal liver lesion on ultrasound or rising AFP (possible HCC)

Signs and symptoms

  • Compensated Cirrhosis (May be asymptomatic or have non-specific symptoms): Fatigue, malaise, anorexia, weight loss, mild RUQ discomfort.
  • Decompensated Cirrhosis (Development of complications):
  • - Jaundice (yellowing skin/eyes).
  • - Ascites (fluid accumulation in abdomen).
  • - Peripheral Oedema (leg swelling).
  • - Hepatic Encephalopathy (confusion, drowsiness, asterixis - flapping tremor).
  • - Oesophageal/Gastric Variceal Bleeding (haematemesis, melaena).
  • - Spontaneous Bacterial Peritonitis (SBP) (fever, abdominal pain in patient with ascites).
  • - Hepatorenal Syndrome (HRS) (progressive renal failure).
  • Stigmata of Chronic Liver Disease:
  • - Skin: Spider naevi (angiomata), palmar erythema, thin skin, easy bruising (ecchymoses), caput medusae (dilated abdominal veins).
  • - Endocrine: Gynaecomastia, testicular atrophy, loss of body hair (men); menstrual irregularities (women).
  • - Nails: Terry's nails (white proximal nail), clubbing.
  • - Other: Splenomegaly, hepatomegaly (early) or small/shrunken liver (late), parotid gland enlargement, Dupuytren's contracture (assoc. with alcohol).

Risk factors

  • Chronic Hepatitis B infection
  • Chronic Hepatitis C infection
  • Alcoholic Liver Disease (chronic excessive alcohol use)
  • Non-Alcoholic Fatty Liver Disease (NAFLD) / Non-Alcoholic Steatohepatitis (NASH) - associated with obesity, diabetes, metabolic syndrome.
  • Autoimmune Hepatitis
  • Primary Biliary Cholangitis (PBC)
  • Primary Sclerosing Cholangitis (PSC)
  • Hereditary Haemochromatosis (iron overload)
  • Wilson's Disease (copper overload)
  • Alpha-1-Antitrypsin Deficiency
  • Chronic right-sided heart failure ('cardiac cirrhosis')
  • Chronic Schistosomiasis (Hepatosplenic - causes portal hypertension often without true cirrhosis initially).

Diagnosis

Clinical assessment

Suspect based on stigmata of chronic liver disease, signs of portal hypertension, or presence of decompensating events (jaundice, ascites, encephalopathy, variceal bleed). Identify underlying cause.

Investigations

  • Liver Function Tests (LFTs): Often abnormal but non-specific. ALT/AST may be normal or elevated. Bilirubin, ALP, GGT may be elevated. Albumin typically low, INR/PT typically prolonged (reflect impaired synthetic function).
  • Complete Blood Count (CBC): Thrombocytopenia (low platelets) common due to hypersplenism. Anaemia may be present.
  • Renal Function (U&Es, Creatinine): Assess for hepatorenal syndrome.
  • Viral Hepatitis Serology (HBsAg, Anti-HCV): Identify underlying viral cause.
  • Autoimmune markers (ANA, ASMA, LKM-1, IgG levels), Iron studies (Ferritin, Transferrin Saturation), Copper studies (Ceruloplasmin): If specific causes suspected.
  • Abdominal Ultrasound with Doppler: Assess liver size/texture (nodularity), splenomegaly, ascites, portal vein diameter/flow, rule out HCC, rule out biliary obstruction.
  • Assessment of Fibrosis:
  • - Non-invasive markers (APRI, FIB-4).
  • - Transient Elastography (FibroScan): Measures liver stiffness, good correlation with fibrosis stage.
  • - Liver Biopsy: Gold standard for confirming cirrhosis and assessing etiology/activity, but invasive and less commonly needed if clinical/non-invasive tests confirm.
  • Upper GI Endoscopy (OGD): Screen for oesophageal/gastric varices in all newly diagnosed cirrhosis patients.
  • Alpha-fetoprotein (AFP): Tumour marker for HCC screening.

Diagnostic criteria

Histological confirmation via biopsy OR combination of clinical stigmata, imaging findings (nodular liver, splenomegaly, ascites, varices), laboratory abnormalities (thrombocytopenia, impaired synthetic function), and/or evidence of portal hypertension complications.

Management

Non-pharmacological management

  • Treat the Underlying Cause (if possible): Antivirals for HBV/HCV, Alcohol cessation, Weight loss/Metabolic control for NAFLD/NASH, Immunosuppression for autoimmune hepatitis, Chelation for iron/copper overload.
  • Lifestyle: Complete alcohol abstinence. Sodium restriction (<2g/day) for ascites/oedema. Maintain adequate nutrition (protein intake usually encouraged unless severe encephalopathy). Avoid NSAIDs, sedatives, potentially hepatotoxic drugs/herbs.
  • Vaccinations: Hepatitis A, Hepatitis B, Pneumococcus, Influenza.
  • Hepatocellular Carcinoma (HCC) Surveillance: Abdominal Ultrasound +/- AFP every 6 months.
  • Variceal Screening: Endoscopy at diagnosis, repeat periodically based on findings.
  • Liver Transplantation: Definitive treatment for end-stage liver disease (highly specialized centres).

Pharmacological treatment

  • Management of Complications:
  • - Ascites: Sodium restriction + Diuretics (Spironolactone +/- Furosemide). Start Spironolactone 50-100mg OD, titrate up (max 400mg). Add Furosemide 20-40mg OD, titrate up (max 160mg) if needed (maintain Spiro:Furo ratio ~100:40). Monitor weight, electrolytes, renal function. Large Volume Paracentesis (LVP) for tense ascites (give IV Albumin 6-8g per litre removed if >5L tapped).
  • - Spontaneous Bacterial Peritonitis (SBP): Diagnosis via ascitic tap (PMN >250/mm³). Treat with IV Ceftriaxone (or Cefotaxime). Secondary prophylaxis (e.g., oral Ciprofloxacin or Norfloxacin daily) after first episode.
  • - Hepatic Encephalopathy (HE): Identify/treat precipitants (infection, GI bleed, dehydration, electrolyte disturbance, sedatives). Lactulose oral/rectal (titrate to 2-3 soft stools/day). Rifaximin (non-absorbable antibiotic) may be added.
  • - Oesophageal Variceal Bleeding: Acute management (see UGIB - GI003): Resuscitation, Vasoactive drugs (Terlipressin/Octreotide), Antibiotic prophylaxis (Ceftriaxone), Urgent Endoscopy (Band ligation preferred). Secondary prophylaxis (after bleed): Non-selective Beta-blocker (Propranolol/Nadolol - titrate to HR 55-60 bpm) +/- Endoscopic band ligation.
  • - Primary Prophylaxis of Variceal Bleeding: For medium/large varices - Non-selective Beta-blocker OR Endoscopic band ligation.
  • - Hepatorenal Syndrome (HRS): Urgent specialist management. Vasoconstrictors (Terlipressin) + IV Albumin. Requires addressing underlying precipitants, often needs liver transplant.

Monitoring

  • Regular clinical follow-up (monitor for decompensation).
  • Monitor LFTs, renal function, electrolytes, CBC, INR.
  • Monitor nutritional status.
  • Regular HCC surveillance (Ultrasound +/- AFP Q6 months).
  • Regular Variceal screening/surveillance endoscopy.
  • Monitor adherence and side effects of medications.

Complications

  • Portal Hypertension -> Varices (oesophageal, gastric), Ascites, Splenomegaly/Hypersplenism
  • Hepatic Encephalopathy
  • Spontaneous Bacterial Peritonitis (SBP)
  • Hepatorenal Syndrome (HRS)
  • Hepatopulmonary Syndrome / Portopulmonary Hypertension
  • Coagulopathy / Bleeding risk
  • Hepatocellular Carcinoma (HCC)
  • Malnutrition / Sarcopenia
  • Increased susceptibility to infections

Prevention

  • Prevent/treat underlying causes (HBV/HCV treatment, alcohol cessation, manage NAFLD).
  • HBV vaccination.

Patient education

  • Explain cirrhosis as irreversible liver scarring.
  • Discuss underlying cause and importance of treating it (e.g., alcohol abstinence, antivirals).
  • Lifestyle modifications (diet - esp salt, alcohol avoidance).
  • Need for regular monitoring and screening (HCC, varices).
  • Recognizing signs of decompensation (jaundice, swelling, confusion, bleeding) and seeking urgent care.
  • Medication adherence (diuretics, beta-blockers, lactulose etc).
  • Importance of vaccinations.

Uganda-specific notes

HBV, alcohol, and potentially Schistosomiasis/Aflatoxin are major causes. Late presentation with decompensated disease is common. Access to diagnostics (FibroScan, AFP, endoscopy), treatments (DAAs, Rifaximin, Terlipressin, banding), and liver transplant is severely limited. Management focuses on clinical diagnosis, managing ascites/HE with available drugs, preventing variceal bleeding where possible, and palliative care.

References

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 6, Section 6.5.4 (including subsections on complications)

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