| Fulminant hepatic failure (FHF) occurs when the rate andextent of liver cell death are not adequately balanced by regenerative activity. Two forms of liver cell death are recognized: apoptosis and necrosis. A number of causes of FHF have been shown, predominantly in experimental animal models, to induce one or the other form of liver cell death .FHF is a devastating illness of varied causes, carrying considerable mortality and affecting patients with previously healthy livers. The clinical presentation varies widely but encephalopathy is the defining criterion. Management requires a multidisciplinary approach, including rapid triage, moni- toring, and referral to a transplantation center for further evaluation. The only treatment option that is curative is liver transplantation. However, because of shortage of cadaveric organ donors and/or delay in their availability, only 10% of FHF patients ultimately receive a transplant. This has led to development of artificial liver support systems with an idea to bridge the time to transplantation and/or recovery from FHF. Thus the major thrust is now to develop bioreactors, e.g., Extracorporeal Liver Assist Device (ELAD), Bioartificial Liver (BAL), etc.But in our country, there are more difficulty in treating FHF patients with Bioartificial Liver, liver transplantation and so on. The mortality of FHF in our country is higher than that in western countries. So, we analysis the epidemiology, the clinal presentation, the prognosis of FHF and so on, and write this article. We desire that something discussed in this article will be useful in understanding this disease, judging the prognosis and treating patients.Methods The retrospective analysis is performed in this study to 53 FHF cases hospitalized in the digestive and infectious disease departments of our hospital, which are divided into acute hepatic failure(AHF) group and subacute hepatic failure(SHF) group according to the diagnosis suggestion of international hepatopathy committee. These cases are also divided into the survivors and the nonsurvivors according to their prognosis. These cases all have hepatic encephalopathy. The observing contents include: 1.Epide- miology: sex, the relation of age and incidence rate, the relation of age and prognosis; 2.Etiology:the etiologic feature, the relation of etiological factor and prognosis; 3.Clinical presentation: the occurring time of hepatic encephalopathy in the AHF group and in the SHF group, the symptom in early stage, comparison between the complication in AHF group and the complication in SHF group, the relation of complication and prognosis; 4.Laboratory examination: the relation of prognosis and biochemical index in serum such as the transaminase, the bilirubin, the bile acid and so on; 5.Therapy: plasma exchange and internal medicine therapy.Results 1. In our study the incidence rate of male to female was 1.52:1. The on-set peak happened in the 20-60- year-old men. The survival rate of the men who were younger than 30 old was 50%. The survival rate of the 30-39-year-old men was 10%. The other men all died. 2.The percent of the patients infected hepatitis virus reached to 50.94%. 3.The symptoms in early stage were inertia, anorexia, nausea, emesis etc. Bleeding, ascites, infec- tion and hepatorenal syndrome were the main complications. There was no statistical difference on the incidence rate of the complications between the AHF and the SHF except that the incidence rate of ascites was higher in SHF group than that in AHF group. 4. A phenomena that in serum the transaminase becomes less and less and the bilirubin becomes more and more was more obvious in the death group than that in the survivors. The serum levels of AST/ALT, TBIL/DBIL, TBA were significantly higher in the blood samples from the death group than in those from the survivor group: 1.40±0.43 vs. 0.86±0.31 for AST/ALT, 2.32±0.16 vs. 1.91±0.39 for TBIL/ DBIL, and 178.9±25.1 vs. 92.4±35.2 μmol/L for TBA. The levels of serum TCHO was significantly lowerer in the blood samp... |
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