Management Of Fulminant Hepatic Failure Research Articles

Management of fulminant hepatic failure in children--an analysis of 56 cases.

Management of fulminant hepatic failure in children--an analysis of 56 cases.

LIVER TRANSPLANTATION FOR FULMINANT HEPATIC FAILURE

In conclusion, the availability of liver transplantation has dramatically advanced the management of fulminant hepatic failure. A major responsibility of the gastroenterologist/hepatologist involved in the care of patients with liver failure is early decision making regarding likelihood of spontaneous recovery and consideration toward referral to a transplantation center. In particular, patients with exposure to drugs or toxins (other than acetaminophen); patients with presumed non-A, non-B hepatitis; children or older patients; patients with prolonged jaundice; profoundly jaundiced patients; or patients with severe coagulopathy should be given the highest consideration for urgent transplantation. Supportive care should take into account the potential complications of bleeding, sepsis, cerebral edema, renal failure, and respiratory failure. Such complications are the major limiting factors that prevent patients with fulminant hepatic failure from undergoing liver transplantation and contribute to the majority of postoperative deaths among patients who undergo transplantation. If these issues are heeded, and in light of emerging therapeutic modalities and surgical innovations, it is anticipated that ongoing improvement of the overall outcome of patients with fulminant hepatic failure will continue to be seen.

Fulminant Hepatic Failure

Fulminant hepatic failure is a complex clinical syndrome that has a diverse etiology, an unpredictable course, and a high mortality rate. The acutely ill patient admitted to the ICU with this condition often presents a challenge to the intensive care staff because of the life-threatening, multi-system complications. This article presents a review of the etiology, complications, and management of fulminant hepatic failure.

Management of fulminant hepatic failure

Management of fulminant hepatic failure

Advances in transplantation

Transplantation is a rapidly evolving field. Advances in solid organ transplantation are occurring in the fields of surgery, anaesthesiology, critical care medicine, immunology and pathology. Candidate selection has become more precise to enable optimal timing of transplantation. This is most evident among patients with fulminant hepatic failure. Advances in surgical approach and perioperative care have resulted in improved survival and the development of new procedures. These steps have been complemented, indeed enabled, by the introduction of immunosuppressive agents with great potency combined with remarkable selectivity. This chapter presents some aspects of organ transplantation that highlight these advances. The discussion of the management of fulminant hepatic failure addresses changes in the preoperative care of patients and the issues surrounding candidate selection. The section below focuses on FK 506 which has facilitated developments in transplantation of pancreatic islet cells, small bowel and xenografts.

Liver transplantation after paracetamol overdose.

To evaluate the role of liver transplantation after paracetamol overdose. Prospective study of consecutive candidates for transplantation and performance of transplantation over 18 months. Liver unit, King's College Hospital, London. Fulfilment of indicators of poor prognosis, selection for transplantation, transplantation, survival. 30 of 37 patients considered to have a reasonable prognosis with intensive medical care survived. Of 14 of 29 patients considered to have a very poor prognosis and registered for urgent liver transplantation, six received liver transplants, four of whom survived, while seven died and one survived without a transplant. Three of 15 patients with poor prognostic indicators but not selected for transplantation survived. Liver transplantation will have a definite but limited role in the management of fulminant hepatic failure induced by paracetamol.

Etiology and Clinical Pattern of Fulminant Hepatitis in Iraq

Of 253 prospectively studied cases of acute viral hepatitis (AVH), 47 were fulminant (18.6%). There were 15 males and 32 females. Their age ranged from 7 to 60 years (mean, 29 years). Serological evidence of AVH-A was found in one case (2%), AVH-B in 13 cases (28%), AVH-D in one case (2%), and AVH-NANB in 32 cases (68%). Fulminant hepatitis was found in 2.6% of AVH-A cases, in 16.25% of AVH-B cases, in one of two AVH-D superinfections, and in 24.8% of the AVH-non-A, non-B (NANB) cases. The clinical picture in the two main etiological categories, namely the AVH-B and the AVH-NANB, showed that the latter possessed a more prolonged and severe clinical course with higher mortality (P<0.001). It also showed a higher mortality in females of the child bearing age, compared with males of the same age group (P<0.001).

Effect of ranitidine on acetaminophen-induced hepatotoxicity in dogs

The effect of ranitidine administration upon the hepatotoxic effect produced by a multidose acetaminophen administration regimen was examined. Seventy-two dogs received three subcutaneous injections of acetaminophen (750, 200, 200 mg/kg body wt) in DMSO (600 mg/ml) at time zero, 9 hr later, and 24 hr after the first dose. Ten control animals (group I) were not given ranitidine, the remaining 62 dogs received an intramuscular injection of ranitidine 30 min before each acetaminophen dose. Three different doses of ranitidine were used (mg/kg body wt): 50 mg, group II (33 dogs); 75 mg, group III (14 dogs); 120 mg, group IV (15 dogs). Ranitidine reduced the expected acetaminophen-induced hepatoxicity in a dose-response manner. Moreover, a significant correlation was found between the ranitidine dose and the survival rate, as evidenced by transaminase levels in the serum and histology of the liver. This model of fulminant hepatic failure induced by acetaminophen and its modulation with ranitidine provides clinical investigators with a research tool that will be useful in the future investigation of putative medical and surgical therapies being investigated for use in the clinical management of fulminant hepatic failure. Because of the size of the animal used in this model, frequent and serial analyses of blood and liver were available for study to determine the effect of therapy within a given animal as opposed to within groups of animals.

Hemodialysis-Hemoperfusion in Fulminant Viral Hepatitis

It is theorized that charcoal hemoperfusion and hemodialysis with a highly permeable membrane should be synergistic in the management of fulminant hepatic failure. Previous studies have shown marked differences between these two treatments in their effects in the various biochemical abnormalities of this serious clinical problem. Survival rates in patients treated with charcoal hemoperfusion approximate the rates in those treated with hemodialysis with a highly permeable membrane but are only slightly better than in untreated cases. The excellent recovery of two patients with fulminant viral hepatitis in stage III and IV coma treated with this combined regimen indicates that further studies should be done to confirm this thesis.

Liver transplantation in the management of fulminant hepatic failure

Liver transplantation is now performed for the treatment of fulminant hepatic failure, but the selection of patients for this procedure has been incompletely described. We used worsening hepatic encephalopathy, clinical evidence of brain edema, and prolongation of the prothrombin time after 24–48 h of intensive medical treatment as key factors influencing the decision to recommend liver transplantation. Thirty-seven patients (29 adult, 8 pediatric) were admitted with fulminant hepatic failure. Ten improved with medical treatment, so liver transplantation was not recommended. Twentyseven deteriorated despite medical treatment. Eight of these, 7 with grade 4 hepatic encephalopathy and persistent coagulopathy, did not receive transplantation because of contraindications (n = 5), failure to find a donor (n = 1), or refusal of therapy (n = 2). None of these survived. Sixteen of the other 19 patients developed grade 4 hepatic encephalopathy, 5 had brain edema, and all had persistent coagulopathy, so liver transplantation was performed. One year actuarial survival was 58%. This retrospective analysis confirms that survival exceeding 50% can be obtained with liver transplantation in patients with fulminant hepatic failure. Additional studies of prognostic markers are needed to define the role of liver transplantation in the management of this disease.

Peritoneal Dialysis in Fulminant Hepatic Failure

None of the modes of temporary liver support seems to improve survival in fulminant hepatic failure complicated by “grade four” coma. The authors assessed the efficacy of rapid exchange peritoneal dialysis in five consecutive patients with fulminant hepatic failure and grade four coma. Four had concurrent acute renal failure and the prognosis for combined hepatic and renal failure is extremely poor irrespective of mode of therapy. Despite this poor prognosis, three of the five recovered completely, four regained consciousness during the initial peritoneal dialysis and the level of consciousness improved during six of 10 periods of peritoneal dialysis. Two of these patients died two weeks after beginning peritoneal dialysis; and in both autopsy showed massive hepatic necrosis and no evidence of hepatic regeneration. These preliminary results compare favorably with those of hemoperfusion in grade four coma. We conclude that rapid exchange peritoneal dialysis offers a number of theoretical advantages over hemo perfusion and merits further evaluation in the management of fulminant hepatic failure.

The influence of ammonia and octanoic acid on liver regeneration in the rat.

1. We have investigated the effect of intermittent doses of ammonia and octanoic acid on liver regeneration in the rat after partial hepatectomy. Regeneration was assessed by uptake of tritiated thymidine into liver deoxyribonucleic acid. 2. We have found a reduction in hepatic regenerative response in animals treated with ammonium acetate as a source of ammonia. 3. No inhibiting effect of octanoic acid on liver regeneration was found, at the dose used. 4. The implications of the results for management of fulminant hepatic failure are discussed.

Management of Fulminant Hepatitis by Vigorous Supportive Treatment-Reply

<h3>In Reply.—</h3> I was gratifying to learn that Drs Vij and Tandon and their associates have been able to confirm results published by our group in which we advocated aggressive but conservative medical management of fulminant hepatic failure. Although our results are comparable, there are some differences in our approaches to management. For example, we employed neomycin as a standard form of management in each of our patients, whereas Drs Vij and Tandon empirically used ampicillin. I quite agree with them that the use of conservative but aggressive medical management is appropriate in the treatment of fulminant hepatic failure. Careful observation of fluid and electrolyte management, the employment of fresh frozen plasma to maintain satisfactory prothrombin levels, and close monitoring of blood gases represent a superior means of treatment when compared with more unique but potentially harmful approaches.

Approaches to the Management of Fulminant Hepatic Failure

This discussion has concerned the management of fulminant hepatic failure with stage III or IV encephalopathy occurring in a patient with previously normal liver function. Basic medical management must include special attention to the metabolic, neurologic, hemorrhagic, and infectious complications common to this syndrome as well as aggressive supportive care. Because the mortality rate remains high in spite of these measures, a variety of other approaches to therapy continue to be evaluated. These include corticosteroid administration, exchange transfusion, plasmapheresis, and the development of extracorporeal hepatic support systems.