Fulminant hepatitis, or fulminant hepatic failure, is defined as a clinical syndrome of severe liver function impairment, which causes hepatic coma and the decrease in synthesizing capacity of liver, and develops within eight weeks of the onset of hepatitis. Several independent factors influence the survival of patients: age, the cause of liver disease, the degree and the duration of encephalopathy in relation to the onset of the disease, and the prevention of complications. Over the years many intensive treatments have been practiced. Liver transplantation is expensive, and patients who survive transplantation require life-long immunosuppression, clinical care and complications management. Without transplantation fulminant hepatitis and hepatic failure might be completely recovered spontaneously, and the patient could expect a normal life. Two cases of fulminant B hepatitis with intensive care treatment, and their survival despite unfavorable prognosis are presented in this paper. The management of patients with fulminant hepatitis required intensive monitoring and therapeutic measures, including corticosteroids. The prognosis for survival without transplantation in fulminant hepatitis is limited by the measures of medical treatment and new specific therapeutic modalities which must be developed through basic research.
Alloogenous blood and/or corresponding haemoproduct transfusion is an efficient and relatively safe supportive treatment. Despite the fact that pre transfusion investigation of both patients and donors ensure high degree of safety of this type of treatment, occurrence of adverse haemotherapy effects is possible and often unpredictable. Acute haemolytic transfusion reaction occur as a consequence of immune conflict between red blood cell membrane agents and specific antibodies present in plasma. Since it is impossible to completely avoid the occurrence of transfusion reactions, wherein acute transfusion haemolytic reaction present a serious, possibly life threatening complication, it is an imperative to continue to improve the knowledge on pathogenesis mechanisms leading to complications associated with these reaction and to define the most efficient therapeutical modalities.
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