Liver failure, cirrhosis and HH Flashcards
Liver failure - definition
Can occur suddenly in a previously healthy liver – acute hepatic failure or more commonly as a result of decompensation of chronic disease – acute on chronic hepatic failure.
Fulminant hepatic failure is a clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function – encephalopathy in 7 days – hyperacute, 8-28 days – acute, 5-26 weeks – subacute.
Liver failure - causes
- Infections – viral hepatitis (especially B, C and cytomegalovirus), yellow fever or leptospirosis.
- Drugs / toxins – paracetamol, halothane, isoniazid, mushrooms or carbon tetrachloride.
- Vascular – Budd-Chiari syndrome or veno-occlusive disease (e.g. antiphospholipid syndrome).
- Others – alcohol, primary biliary cirrhosis, haemochromatosis, autoimmune hepatitis, α1-antitrypsin deficiency, Wilson’s disease, fatty liver of pregnancy, malignancy or HELLP.
Liver failure - signs
Jaundice, hepatic encephalopathy, fetor hepaticus (pear drops), asterixes, constructional apraxia (test with 5 pointed star) and signs of chronic liver disease (cirrhosis) when acute on chronic failure.
Hepatic encephalopathy
As the liver fails nitrogenous waste (ammonia) builds up in the circulation and passes to the brain. It is converted to glutamine by astrocytes causing an osmotic imbalance. Fluid moves into the cells leading cerebral oedema and symptoms – grade 1 – mood and sleep disturbance, grade 2 – drowsiness and slurred speech, grade 3 – stupor and confusion and grade 4 – coma.
Liver failure - investigations
- Bloods – FBC for infection or GI bleeding, Us and Es, LFTs, clotting, glucose, paracetamol level, hepatitis, CMV and EBV serology, ferritin, α1-antitrypsin, caeruloplasmin or autoantibodies.
- Microbiology – blood cultures, urine cultures and ascitic tap for microscopy, culture and sensitivity – if neutrophils >250/mm3 it indicates bacterial peritonitis.
- Radiology – CXR, abdominal ultrasound and Doppler flow studies of portal and hepatic veins.
Liver failure - general management
- Be sure to rule out sepsis, hypoglycaemia, GI bleeds (due to varices) and encephalopathy.
- Treat the cause where possible e.g. GI bleed, sepsis, paracetamol poisoning or malignancy.
- If the patient is malnourished get dietician input as good nutrition decreases mortality rates.
- If renal failure (hepatorenal syndrome) develops may require haemofiltration or haemodialysis.
- Avoid sedatives (and other drugs with hepatic metabolism) but treat seizures with lorazepam.
- Consider a PPI as prophylaxis against stress ulceration e.g. 40mg Omeprazole IV/PO OD.
- Liase early with the nearest transplant centre for appropriateness (King’s college criteria).
Liver failure - complication management
- Bleeding – give 10mg Vitamin K IV OD for 3 days, platelets, FFP and blood PRN and endoscopy.
- Infection – give 1-2g Cefuroxime IV OD until sensitivities are known (avoid gentamicin).
- Ascites – fluid restriction, low salt diet, daily weight and prescribe diuretics e.g. Furosemide.
- Hypoglycaemia – check regularly and give 50mL 50% Glucose if <2mmol or symptomatic.
- Encephalopathy – avoid sedatives and give 30-50mL Lactulose TDS OD and regular enemas (decreases number of nitrogen forming bowel organisms) – aim for 2-4 soft stools per day.
- Cerebral oedema – give 20% Mannitol IV and hyperventilate.
Liver failure - prognosis
Poor prognostic features are grade 3 or 4 encephalopathy, age >40 years, albumin <30 g/L, raised INR, drug induced or late onset hepatic failure.
There’s a 65% survival rate post-transplantation.
Hepatorenal syndrome
Renal failure in patients with chronic liver disease. It is not well understood but the initial event appears to be splanchnic arterial vasodilation followed by renal vasoconstriction.
Liver failure - prescribing
Avoid opiates, diuretics (increased risk of encephalopathy), oral hypoglycaemics or saline containing IV infusions. The effects of warfarin are enhanced.
- Hepatotoxic drugs – paracetamol, methotrexate, phenothiazines, isoniazid, azathioprine, oestrogen-6-mercaptopurine, salicylates, tetracycline and mitomycin (chemotherapy drug).
Kings college criteria for liver transplantation
- Paracetamol liver failure – arterial pH <7.3 24 hours after ingestion or all of the following – pro-thrombin time >100 seconds, creatinine >300 μmol/L and grade 3 or 4 encephalopathy.
- Non-paracetamol liver failure – PT >100 secs and 3 out of 5 of the following – drug induced, aged <10 or >40 years, >1 week to encephalopathy, PT >50 secs or bilirubin >300μmol/L.
Cirrhosis - definition
Kirrhos means yellow in Greek - cirrhosis implies irreversible liver damage. Histologically there is loss of the normal hepatic architecture with bridging fibrosis and nodular regeneration.
Cirrhosis - causes
Most common causes are chronic alcohol abuse and hepatitis B or C infection.
Rarer causes include non-alcoholic steatohepatitis, autoimmune diseases (PBC or PSC), genetic diseases (Wilson’s disease, haemochromotosis or α1-antitrypsin deficiency), cryptogenic (unknown), Budd-Chiari syndrome or drugs (e.g. amiodarone, methotrexate or methyldopa).
Cirrhosis - signs
Range from only deranged LFTs to decompensated end-stage liver disease.
- Hands – clubbing, palmar erythema, Dupuytren’s contracture, leuconychia (due to hypo-albuminaemia) or Terry’s nails (white proximally but distal third is red due to telangiectasia).
- Other signs - hyperdynamic circulation, spider naevi, xanthelasma, gynaecomastia, atrophic testes, loss of body hair, parotid enlargement, hepatomegaly or a small liver in later stages.
Cirrhosis - complications
- Hepatic failure – coagulopathy and raised INR (due to decreased factors II, VII, IX and X), encephalopathy causing confusion and asterixes, hypoalbuminaemia causing oedema and leuconychia, sepsis, spontaneous bacterial peritonitis or hypoglycaemia.
- Portal hypertension – ascites, splenomegaly and porto-systemic shunt which can lead to oesophageal varices (± upper GI bleeding) and caput medusae (enlarged peri-umbilical veins).
- Renal function – reduced hepatic clearance of immune complexes leads to them getting trapped in the kidneys causing IgA nephropathy. In addition hepatitis C virus and α1-antitrypsin deficiency are known to cause membranoproliferative glomerulonephritis.