Acute hepatic failure - Hindawi

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nancy, lymphoma, ischemic hepatitis from shock and other low output car- diac states, and acute Bud
FULMINANT HEPATIC FAILURE

Acute hepatic failure ROGER W ILLIAMS, MD, FRCP, FRCS, FRCPE, FRACP, FACP(HON), JULIA WENDON, MRCP

R WILLIAMS, J WENDON. Acute hepatic faulure. Can J Gastroenterol 1993; 7(7):535-541. The etiology of acute liver failure in patients without pre-existing liver disease varies depending on geographical location. In the United Kingdom, acetaminophen toxicity remains the most common cause while worldwide, viral hepatitis B is the most prevalent cause. The management of patients with acute liver failure requires the application of good basic intensive care - recently, the advent of liver transplantation has widened the therapeutic options available. Careful attention to cardiovascular monitoring and manipulation of hemodynamic variables is required and mechanical ventilation is needed in patients who progress to grade III/IV encepaholopathy. Renal replacement therapy is best achieved using a continuous hemodiafiltration system rather than hemodialysis in patients who present with acute liver failure. The development of cerebral edema is a common and frequently fatal complication, and requires meticulous care involving intracranial pressure monitoring. Patients are functionally immunosupressed and require frequent bacteriological surveillance, the incidence of both bacterial and fungal sepsis being very high. In some patients, such as those with lymphoma presenting as acute liver failure, specific chemotherapeutic regimens may be available. The advent ofliver transplantation has offered a great advance in the management of acute liver failure but requires stringent patient selection such that those patients with a good chance of spontaneous recovery Jo not undergo transplantation, while those with a poor prognosis can be considered.

Key Words: Fulminant hepatic failure, Intensive care, Transplantation

lnsuffisance hepatique aigue

RESUME:

L'etiologie de l'insuffisance hepatique aigue chez les patients qui n'avaient eu aucune maladie hepatique auparavant, varie selon les lieux geographiques. Au Royaume-Uni, la toxicite liee a l'acetaminophene en dcmeure la plus frequente cause, alors qu'ailleurs clans le monde, on l'attribue surtout au virus de l'hepatite B. Le traitement des patients en insuffisance hepatique aigue exige de tres bons soins intensifs, et recemment, la mise au point des transplantations hepatiques a diversifie les options therapeutiques offertes. Une attention particuliere doit etre accordee a la surveillance cardiovasculaire et ala manipulation des Institute of Liver Studies, King's College Hospital and King's College School of Medicine and Dentistry, London, United Kingdom Correspondence: Dr Roger Williams, Institute of Liver Studies, King's College Hospital and King's College School of Medicine and Dentistry, Bessemer Road, London, United Kingdom SES 9PJ CAN J GASTROENTEROL VOL 7 No 7 SEPTEMBER/OC TOBER 1993

F

ULMINANT HEPATIC FAILURE (FHF)

is the term used to describe patients with a very rapid progression of symptoms and signs of liver failure, with development of encephalopathy within eight weeks of symptom onset (1) in patients without preceding liver disease. A similar group of patients are those with late onset hepatic failure (LOHF), defined as the onset of encephalopathy within eight weeks to six months of the development of symptoms - again , in patients without preceding liver disease (2). The stratification of patients with respect to the speed of onset of encephalopathy is of great importance since this, in association with etiology, carries prognostic implications and is of special importance when transplantation is being considered as a therapeutic option. A number of alterative classifications based largely on time interval between onset of symptoms/jaundice and development of encephalopathy, and including such terms as 'subfulminant hepatic failure' have been described (3). Analysis of our data showed those with the most rapidly progressive disease who developed encephalopathy within seven days of the onset of jaundice had the best prognosis. On the basis of this analysis, we have proposed a new division and classification of hyperacute, acute and subacute hepatic failure to encompass the whole range of liver failure (Table 1).

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WILLIAMS ANO W ENJ.X)N

variables hemoclynamiques, et une ventilation mecanique est souvent necessaire chez les patients qui evoluenr vers une encephalopathie de classe III/IV. Le traitement substitutif renal s'cffectuc mieux au moyen d'un systeme d'hemofiltration continue qu'au moyen de l'hemodialyse chez les patients en insuffisance hepatique aiguc. L'installation d'oedeme cerebral est une complication frequente et souvent fatale pour laquelle ii faut surveiller de pres la pression intracr:iniennc. Les patients se trouvent fonctionnellement immunosuppnmes et neccssitent aussi une surveillance hacteriologiquc frequence puisque !cs infections, tant fongiques quc bacteriennes sont frequentes. Chez certairu sujets atreints de lymphomes avec insuffisance heparique aigue, des schemas chimiotherapeutiques sont offerts. La mise au point de la transplantation hepatique a pcrmis au traitement de l'insuffisance hepatique 40 years; serum bilirubin >300 µmol/L; time from onset of jaundice to encephalopathy more seven days; or a prothrombin time of >50 s. Regardless of the decision co transplant, aggressive intensive care management is pivotal in the care of patients with liver failure, acute and chronic, and its sequelae. Patients who may be suitable for transplantation or the specialist care that liver units can provide should be considered for trans-

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fer early, rather than late, in the course of their disease, before the development of hemodynamic instability and cerebral edema. In patients in whom transplantation is appropriate, support is needed to maintain other organ function and, thus, suitability for transplantation while awaiting a suitable donor. In patients in whom transplantation is not appropriate, optimal support of failing organs is required co promote as beneficial an environment as possible to optimize the potential for liver regeneration and to overcome sepsis.

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induced fulminam hepatic failure by late administration of acecylcysteine. Lancer 1990;i:1572-3. Keays R, Harrison PM, WendonJA, Gimson AES, Alexander GJM, Williams R. Intravenous acetylcysteine in acetaminophen induced fulminant hepatic failure: A prospective controlled trial. Br Med J 1991;303:1026-9. Harrison PM, Wendon JA, Oimson AES, Alexander GJM, Williams R. Improvement by acetylcysteine of haemodynamics and oxygen crampon in fulminant hepatic failure. N Engl J Med !991;324:1852-8. Burgundcr JM, Varriale A, Lauterburg BH. Effect of N-acetylcysteine on plasma cysteine and glutathione following paracetamol administration. Eur J Clin Pharmacol 1989;36:127-31. Horowitz JD, Henry CA, Syrjanen ML, et al. Nitroglycerine/ N-acecylcysteine in the management of unstable angina pectoris. Eur Heart J 1988;9(Suppl A):95-100. Basile A, Hughes R, Harrison P, et al. Elevated brain concentrations of 1,4-benzodiazcpines in fulminant hepatic failure. N Engl J Med 1991;325:473-8. O'Grady JG, G imson AE, O'Brien CJ, Pucknell A, Hughes RD, Williams R. Controlled trials of charcoal hcmoperfusion and prognostic factors in fulminant hepatic failure. Oastroentcrology 1988;94: 1186-92. Davenport A, Will EJ, Davison AM. Effect of posture on intracranial pressure and cerebral perfusion pressure in patients with fulminanr hepatic and renal failure after acetaminophen self-poisoning. Crit Care Me