What a failing liver stops doing
Every liver question becomes easier if you reason from lost function rather than memorising complications. A healthy liver detoxifies ammonia, synthesises albumin and clotting factors, metabolises drugs and bilirubin, and stores glycogen and vitamins. When it fails, each of those functions produces a predictable clinical picture that the exam then asks you to prioritise.
Loss of ammonia detoxification produces hepatic encephalopathy: confusion, asterixis or flapping tremor, personality change, sleep reversal and eventually coma. Loss of albumin synthesis lowers oncotic pressure and produces ascites and peripheral oedema. Loss of clotting factor synthesis prolongs the prothrombin time and INR, causing bruising, petechiae and gastrointestinal bleeding. Impaired bilirubin handling produces jaundice, pruritus, dark urine and clay-coloured stools.
Portal hypertension is the mechanical consequence of a scarred liver. Blood backs up and finds collateral routes, producing oesophageal and gastric varices, caput medusae, splenomegaly and haemorrhoids. Varices are thin-walled and rupture catastrophically, which is why any report of haematemesis or melaena in a cirrhotic client is the highest-priority finding in the item.
Laboratory patterns to recognise include elevated AST and ALT in hepatitis, elevated ammonia in encephalopathy, low albumin, prolonged PT and INR, elevated bilirubin, and low platelets from splenic sequestration.
- •No detox of ammonia → encephalopathy and asterixis
- •No albumin → ascites and oedema
- •No clotting factors → prolonged INR and bleeding
- •Portal hypertension → varices, splenomegaly, caput medusae
Managing the four complications
For bleeding varices the priority is airway protection and circulatory support: position the client to prevent aspiration, apply oxygen, establish large-bore intravenous access, and prepare for octreotide infusion, endoscopic band ligation or balloon tamponade. Beta blockers such as propranolol are used long-term to lower portal pressure. Avoid anything that raises intra-abdominal pressure, including straining, coughing and vigorous suctioning.
For ascites the nursing focus is measurement and comfort. Weigh the client daily at the same time on the same scale, measure abdominal girth at a marked location, restrict sodium, administer diuretics such as spironolactone with furosemide, and position semi-Fowler's to ease breathing. Before a paracentesis, have the client void to prevent bladder puncture; afterwards monitor for hypotension and hypovolaemia from rapid fluid shift.
For hepatic encephalopathy, lactulose is the answer the exam wants. It acidifies the bowel, traps ammonia as ammonium and excretes it in stool. Titrate to two or three soft stools a day; more than that risks dehydration and hypokalaemia, and none means the dose is insufficient. Rifaximin reduces ammonia-producing gut flora. Protein is no longer aggressively restricted, but excessive protein loads are avoided and neurological status is monitored closely.
For infection, spontaneous bacterial peritonitis presents with fever, abdominal pain and worsening ascites, and it is confirmed by diagnostic paracentesis. Cirrhotic clients are functionally immunocompromised, so a low-grade fever deserves attention rather than reassurance.
| Complication | Key findings | Priority nursing action |
|---|---|---|
| Oesophageal varices | Haematemesis, melaena, hypotension | Protect airway, large-bore IV access, prepare octreotide and endoscopy |
| Ascites | Distension, dyspnoea, weight gain | Daily weight and girth, sodium restriction, semi-Fowler's |
| Hepatic encephalopathy | Confusion, asterixis, high ammonia | Lactulose titrated to 2–3 soft stools daily; safety measures |
| Coagulopathy | Bruising, prolonged INR | Soft toothbrush, electric razor, avoid IM injections |
| Spontaneous bacterial peritonitis | Fever, abdominal pain | Notify provider, prepare for diagnostic paracentesis |
Hepatitis: transmission, precautions and prevention
Hepatitis A and E are transmitted by the faecal-oral route, usually through contaminated food or water. Prevention rests on hand hygiene, safe food handling and, for hepatitis A, vaccination. Contact precautions apply for incontinent or diapered clients. These infections are acute and self-limiting and do not become chronic.
Hepatitis B, C and D are bloodborne and transmitted through needle sharing, unprotected sex, perinatal exposure and occupational needlestick injury. Standard precautions are sufficient in most care settings. Hepatitis B is vaccine-preventable and the vaccine is a three-dose series recommended for all health care workers. Hepatitis C has no vaccine but is now curable with direct-acting antiviral therapy. Hepatitis D only occurs alongside hepatitis B.
Teaching for any client with viral hepatitis includes avoiding alcohol and hepatotoxic drugs, especially acetaminophen above recommended limits, resting during the acute phase, eating small frequent meals with adequate carbohydrate, not donating blood, and using barrier protection for bloodborne types. Household contacts of hepatitis A cases may receive immune globulin.
Practise these patterns with the gastrointestinal question guide, the infection control article and the adult health question sets, which include unfolding case studies on decompensated cirrhosis.
- •Hepatitis A and E: faecal-oral, acute, hand hygiene and food safety
- •Hepatitis B: bloodborne, vaccine-preventable, can become chronic
- •Hepatitis C: bloodborne, no vaccine, curable with antivirals
- •All types: no alcohol, caution with acetaminophen, no blood donation