Although it is well known that fulminant hepatic failure (FHF)might be often complicated with disseminated intravascular coagulation (DIC), its bedside diagnosis and control are rather confused. Hemostatic change after replacement therapy might be helpful to distinguish wheather the abnormal clotting tests are owing to the defects of protein synthesis or to excessive consumption. A 38-year-old woman with relapse of acute myeloblastic leukemia and FHF(post-transfusion hepatitis, type of non-A,non-B) received 2 courses of plasma exchange therapy (4 and 3L) using Hemonetics M-30 with 6,000 U/day of heparin sodium continuous i.v. and died on 4th hospital day. Postmortem necropsy revealed massive hepatic necrosis and fibrin thrombi in kidneys. Before the beginning of plasma exchange, results of bedside tests were as follow;platelets 44×109/l(decreased from 240 within a week ), PT over 90", aPTT 26", fibrinogen 120 mg/dl and serum FDP 10 mcg/ml. Serial observations of hemostatic parameters 1, 4, 8 and 12 hours after the end of exchange therapy disclosed that apparent half life time of each factors were remarkably shortened. For example, T 1/2 of factor I, E, VE, XI, antithrombin EE (AT IE) and alpha-2 plasmin inhibitor(AP) were 4, 14.5, 1-5, 4.7, 15 and 2.6 hours, respectively. In crossed immunoelectrophoresis of AT III and AP, patient plasma showed abnormal peaks of each protein which were considered to be enzyme-inhibitor complexes. Plasminogen was not detected before therapy(0 % by S-2251 and less than 5 % by Rocket IEP) in spite of AP remaining (16 % by S-2251, 25 % by Rocket IEP) and FDP was elevated to 80 mcg/ml at 4 hours after exchange. These findings indicated that, in some case of FHF, FDP did not increase because of absence of plasminogen even if accompanied with DIC.
Alternating therapeutic plasma exchange (TPE) with double plasma molecular adsorption system (DPMAS) for the treatment of fulminant hepatic failure (FHF)
