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The Liver - Part 5: acute liver failure

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VOL: 102, ISSUE: 02, PAGE NO: 26

Helen L. Day, MSc, BSc, RGN, RSCN, DipN, is paediatric critical care clinical educator and outreach facilitator

Rachel M. Taylor, MSc, RGN, RSCN, DipRes, is nurse researcher; both at Paediatric Liver Centre, King's College Hospital, London

Acute liver failure (ALF) is of sudden onset, with catastrophic clinical consequences. It is preferable to refer patients presenting with ALF to a specialist centre as transplantation may be required.

Acute liver failure (ALF) is of sudden onset, with catastrophic clinical consequences. It is preferable to refer patients presenting with ALF to a specialist centre as transplantation may be required.

Definition of acute liver failure
Acute liver failure is an umbrella term with subgroups of hyperacute, acute and subacute liver failure. Bhaduri and Mieli-Vergani (1996) suggest ALF is 'a rare multisystem disorder in which severe impairment of liver function, with or without encephalopathy, occurs in association with hepatocellular necrosis in a patient with no recognised underlying chronic liver disease'.

Aetiology
The causes of ALF are:

- Infective: hepatitis, adenovirus, Epstein-Barr virus, cytomegalovirus, echovirus, varicella, salmonella, tuberculosis, septicaemia, malaria, leptospirosis;

- Drugs: acetaminophen (paracetamol), allopurinol, amiodarone, antibiotics, carbamazepine, halothane, Ecstasy, isoniazid, non-steroidal anti-inflammatory drugs, phenytoin, sodium valproate;

- Toxins: mushroom poisons, herbal medicines, carbon tetrachloride, yellow phosphorus, industrial solvents;

- Metabolic: galactosaemia, tyrosinaemia, hereditary fructose intolerance, neonatal haemochromatosis, Niemann-Pick disease type C, Wilson's disease, mitochondrial cytopathies, congenital disorders of glycosylation;

- Autoimmunity;

- Vascular/ischaemic: Budd-Chiari syndrome, acute circulatory failure, heat stroke, acute cardiac failure, cardiomyopathies;

- Infiltrative: leukaemia, lymphoma; haemophagocytic lymphohistiocytosis (HLH).

Clinical features and management
Encephalopathy

The pathogenesis of encephalopathy is not fully understood and is probably multifactorial. Ammonia, fatty acids and intracerebral amino acid and neurotransmitter imbalances have been suggested as causative agents (O'Grady, 2000). Most patients with ALF have some degree of encephalopathy, ranging from grade 1 to grade 4 (Table 1). Management is that of intracranial hypertension, which may include:

- Monitoring: raised intracranial pressure (ICP) and prolonged cerebral perfusion pressure (CPP) of <50mmhg, or="" icp="" consistently="" 40mmhg="" are="" associated="" with="" poor="" neurological="" recovery="" in="" adults.="" measuring="" icp="" and="" cpp="" is="" advisable="" so="" that="" therapeutic="" interventions="" can="" be="" initiated="" to="" manipulate="" them="" (sizer="" et="" al,="" 2003)="" and="" thus="" prolong="" survival="" for="" patients="" awaiting="" transplantation.="" subdural="" bolt="" systems="" are="" used="" for="" adults="" and="" children.="" inr="" and="" platelet="" count="" are="" normalised="" before="" icp="" bolt="" insertion;="">

- Positioning: patients should be nursed with the neck in midline position and associated head elevation of approximately 30 degs to optimise jugular venous return in the management of raised ICP;

- Inotropes: using inotropes to induce hypertension to improve CPP may be useful;

- Muscle relaxants and sedation;

- Mannitol and hypertonic saline: persistent intracranial hypertension (20mmHg for 5 mins) may be treated using osmotic diuretic therapy, such as mannitol 20 per cent or hypertonic saline, in line with local guidelines (Bayir et al, 2003; Sizer et al, 2003);

- Anticonvulsants: if there is evidence of seizure activity, phenytoin may/should be considered and maintained until liver function is normalised;

- Hypothermia and cooling: mild hypothermia has been proposed to delay the onset of encephalopathy and prevent cerebral oedema, potentially serving as a bridge to transplantation (Jalan et al, 1999). Hypothermia is used in patients with head injury to reduce brain metabolic rate, thus reducing cerebral blood volume and ICP (Klein, 1999).

Coagulopathy

Profound compromise of hepatocyte function results in life-threatening coagulopathy, often compounded by disseminated intravascular coagulation. Management involves keeping platelets 50x109/L, especially for invasive procedures or line removal. Intravenous vitamin K should be administered daily (Bansal and Dhawan, 2004; O'Grady, 2000). Stress ulceration in ALF is common and a common site of haemorrhage, so prophylaxis with H2-receptor antagonists or proton pump inhibitors is advised (O'Grady, 2000). Fresh-frozen plasma may protect patients from haemorrhage for invasive procedures but will mask a deteriorating INR/PT, which should be considered when assessing clinical status.

Renal failure

Renal failure may be secondary to hypotension and sepsis. It is common in the early stages of acetaminophen overdose as a consequence of direct renal toxicity. Early intervention with continuous veno-venous haemodiafiltration (CVVHD) is recommended (Bansal and Dhawan, 2004; Ellis and Wendon, 1996).

Metabolic derangements

Profound hypoglycaemia is common, as is metabolic acidosis as lactic acid levels increase. Hypokalaemia, hyponatraemia, hypocalcaemia, hypomagnesaemia and hypophosphataemia may be observed (Bansal and Dhawan, 2004). Management includes high concentrations of intravenous dextrose, CVVHD for lactic acidosis and electrolyte corrections.

Haemodynamic abnormalities

Sepsis is the main cause of mortality in ALF. The high cardiac output, low systemic vascular-resistant state associated with sepsis results in profound hypotension and multiorgan dysfunction syndrome. Management includes CVVHD and fluid management, inotropic and vasopressor support, intravenous antibiotics, antifungals and antivirals (O'Grady, 2000).

Outcome
Survival depends on the underlying aetiology, which makes predicting outcome difficult. A low chance of survival (<20 per="" cent)="" is="" useful="" in="" deciding="" whether="" to="" list="" a="" patient="" for="" transplantation,="" which="" has="" a="" one-year="" survival="" of="" 60-70="" per="" cent,="" compared="" with="" 95="" per="" cent="" in="" those="" transplanted="" for="" chronic="" disease="" (o'grady="" 2000).="">

Summary
Clinical complexity presents health professionals with a significant challenge if a patient with ALF is to survive. While efforts to develop pharmacological therapies and biomechanical techniques serve as a bridge to spontaneous recovery, liver transplantation is the most successful treatment for most cases.

- This article has been double-blind peer-reviewed.

For related articles on this subject and links to relevant websites see www.nursingtimes.net

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