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Liver failure


Some of the manifestations are of the causative diseases process, e.g. memory impairment in chronic alcoholism, extrapyramidal symptoms in Wilson’s disease and cardiac failure in haemochromatosis.


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Table 3. Summary of pathophysiology of acute and chronic liver failure.

Systemic hypotension

This may be due to bleeding, sepsis, dysrhythmia or reduced systemic vascular resistance in acute hepatic failure. Invasive monitoring should be used to optimise fluid status (see Shock module) and inotropes or vasoconstrictors used as appropriate. A significant percentage of patients respond to fluid alone.

Renal failure

This occurs in virtually all patients with significant liver damage after paracetamol due to toxicity, acute tubular necrosis and functional renal failure. Continuous veno-venous haemofiltration is the renal replacement method of choice – it causes less upset of ICP than haemodialysis.


Gram positive bacterial and fungal infections are common in AHF. Cultures should be taken in the event of unexplained deterioration. Ceftriaxone and amoxicillin are used in combination in ICU patients. Fluconazole is given to patients requiring ventilation. Empirical antifungal treatment may be given to patients who do not respond to antibiotic treatment. Fungal infection is the most common new infection after ICU day 5.


Coagulopathy is almost universal in AHF. Most patients do not bleed – due increased FVIII and failure to produce anticoagulant factors (such as antithrombin 3). Coagulopathy is due to underproduction of the vitamin K dependent clotting factors II, VII, IX and X.

PT should be measured twice daily. It is an important prognostic indicator and should not therefore be corrected unless surgery or ICP monitor insertion is intended. It should not be given for CVP line insertion. Fresh frozen plasma and possibly cryoprecipitate will be required in the circumstances above. Thrombocytopenia can occur (usually with paracetamol poisoning) and should be corrected if invasive procedures are undertaken.


Is caused by the inability to mobilise liver glycogen. Glucose should be measured every 2 hours in acute liver failure and a glucose infusion will often be required – but be wary of inducing hyponatraemia. Glucose should be given as low volume infusions of 20% dextrose, which must be via a CVP line.

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