Liver Cirrhosis

Established cirrhosis - advanced fibrosis with architectural distortion - was long considered irreversible. Current evidence shows that fibrosis regression is possible when the causative injury is removed or treated: HBV-related cirrhosis regresses in a proportion of patients after years of effective antiviral therapy suppressing HBV DNA; HCV-related cirrhosis shows fibrosis improvement after successful cure with DAA therapy in most patients; alcohol-related cirrhosis improves significantly with sustained abstinence; NASH-related cirrhosis shows regression with significant weight loss. Fibroscan kPa values measurably decrease with effective treatment in fibrosis stages F2–F3 and early F4. True established F4 cirrhosis with severe architectural distortion and portal hypertension is less reversible - the goal becomes preventing progression and complications rather than reversal.

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome caused by the accumulation of ammonia and other gut-derived toxins in the blood when a failing liver cannot clear them. The gut produces ammonia from protein digestion and bacterial metabolism; in cirrhosis with porto-systemic shunting, this ammonia bypasses the liver and reaches the brain. Symptoms range from subtle changes in personality, concentration, and sleep pattern (covert HE) to confusion, disorientation, asterixis (liver flap tremor), and coma in overt HE. Treatment has two components: treating precipitating triggers (GI bleeding, infection, dehydration, constipation, sedative medications, electrolyte disturbance) and reducing ammonia production and absorption. Lactulose is the primary agent - it acidifies the colon, trapping ammonia as ammonium and accelerating its excretion; titrated to produce 2–3 soft stools daily. Rifaximin 550mg twice daily is added for secondary prevention of recurrent episodes.

Spontaneous bacterial peritonitis (SBP) is infection of ascitic fluid without any obvious abdominal source of infection - it occurs because the ascitic fluid of cirrhotic patients has reduced antibacterial activity and bacteria translocate from the gut through the damaged intestinal barrier. It presents with fever, worsening abdominal pain in the context of ascites, and deteriorating liver and kidney function. Diagnosis requires ascitic fluid sampling by paracentesis: a neutrophil count above 250/mm³ in the ascitic fluid confirms SBP. SBP is immediately life-threatening - it carries 20–30% in-hospital mortality and is a major precipitant of hepatorenal syndrome, which sharply worsens prognosis. Treatment is immediate cefotaxime IV for 5 days combined with IV albumin (1.5g/kg on day 1 and 1g/kg on day 3) - the albumin dramatically reduces the development of hepatorenal syndrome and mortality. Secondary prophylaxis with oral norfloxacin or ciprofloxacin daily prevents recurrent SBP after the first episode.

Nutrition in liver cirrhosis requires careful balancing. Protein intake should not be restricted in stable cirrhosis - inadequate protein causes muscle wasting (sarcopenia), which independently worsens cirrhosis prognosis and functional status. We recommend 1.2–1.5g protein/kg body weight daily for cirrhotics. In ascites, sodium restriction to less than 2g (88mmol) per day is essential - table salt, pickles, papads, salted snacks, and processed foods are the primary sodium sources in Indian diets and must be reduced or eliminated. Small, frequent meals are better tolerated than large meals - the compressed stomach capacity caused by ascites and splenomegaly produces early satiety. A late-evening carbohydrate snack reduces overnight gluconeogenesis from muscle breakdown in cirrhotics, who are effectively in a prolonged fasting state overnight due to impaired hepatic glycogen storage.

Liver transplant assessment is appropriate for patients whose liver disease has reached a stage where medical management cannot prevent progressive deterioration and near-term mortality. MELD score above 15 - which correlates to a 90-day mortality risk high enough to justify the operative risk of transplant - is the threshold for listing assessment in most transplant centres. Child-Pugh C cirrhosis with recurrent decompensation (repeated ascites requiring hospitalisation, recurrent variceal haemorrhage, recurrent hepatic encephalopathy) despite optimal medical management is also a transplant indication. HCC within Milan criteria in a cirrhotic liver (single lesion ≤5 cm or ≤3 lesions each ≤3 cm) is a transplant indication that treats both the cancer and the underlying cirrhosis simultaneously and offers the best long-term HCC-free survival of any treatment.

All patients with cirrhosis - regardless of aetiology, current clinical status, or Child-Pugh class - require 6-monthly liver ultrasound with serum AFP measurement. This surveillance schedule is universal for cirrhotics because all types of cirrhosis carry elevated HCC risk. Additional HCC risk factors - chronic HBV infection (even without cirrhosis in certain contexts), male sex, age above 55, active alcohol use, co-existing metabolic syndrome, and elevated baseline AFP - may warrant more frequent or enhanced imaging surveillance. Screen-detected HCC - found on routine 6-monthly scan before symptoms develop - is substantially more likely to be within Milan criteria and eligible for curative treatment than symptom-detected HCC found after the tumour has grown to cause pain or weight loss.