In acute liver failure (alf) there is a defect in synthesis of coagulation factors in addition there is a disseminated intravascular coagulation which is followed by an impairment of the microcirculation. With an early substitution of Antithrombin III (AT III) we tried to stop this situation. In 22 patients (10 female, 12 male, age 10-68) with alf presenting with hepatic coma (grade I-IV) we studied the time course of AT III plasma activity (the study started in December 1978 and is continued until now). AT III was measured with the chromogenic substrate method. When AT III activity fell below the level of 80% of normal, we started to substitute AT III and to give low dose heparin (125-500 U/hrs). In addition in case of bleeding or a decrease of coagulation factors or fibrinogen under the hemostatic active concentration, complexes of prothrombin and fibrinogen were administered. Besides the usual conservative treatment for alf, patients in coma (grade IV) were undergoing baboon liver perfusion. The rapid fall of the hepatic coagulation factors stopped. In patients, who still were able to synthesize coagulation factors a reincrease of these factors after administration of AT III was seen and there was a further fall in fibrinogen. The dosage of AT III in alf required to bring AT III to normal values depended on the degree of intravascular coagulation. The average dose in our study was 250 U/3 hrs. The clinical course of alf was prolonged in all patients and 7 patients with the prognostic deleterious colombindex (sum of factors II + V + VIII) < 75% eventually survived the alf. The coagulation disorders in alf can be treated with an early substitution of AT III; thus, there is more time for liver regeneration. Our results suggest an improved prognosis of the acute liver failure.

tíber die rationelle Behandlung von Vergiftungen mit Alkyiphosphaten (E 605 und verwandten Pflanzenschutzmitteln der Phosphorsäureester-Gruppe) ist auch in dieser Wochenschrift mehrfach berichtet worden (3, 5). Die moderne Therapie besitzt in dem Pyridin-2-aldoxim-methyljodid (PAM) ein spezifisches Antidot, das die durch Alkylphosphate phos-

In connection with the "endogenous acetylcholine-poisoning" due to organophosphorous compounds beside the clinical important muscarinic and nicotinic symptoms an activation of the sympathetic nervous system (adrenal medulla, sympathetic ganglia) is expected. Therefore a kinetic profile of norepinephrine and epinephrine in the plasma of two patients with severe parathion-poisonings was taken up through the whole period of the intensive-medical treatment. The method used was HPLC with electrochemical detection. The parathion-concentration of the same plasma samples were measured, too. The result were individual different courses with periodically appearing, markedly increased plasma catecholamine values. A direct correlation of catecholamines with the parathion-concentration was not recognizable. A possible influence of the atropine-treatment as well as of stress-factors is discussed but estimated as not responsible for the observed peaks.

In two 19-year-old girls with Wilson's disease the condition took a fulminant course, including a poor general state, marked haemolysis and ascites. In the first patient the diagnosis was histologically confirmed only after three weeks, and onset of treatment with penicillamine was therefore delayed. With this medication the concentrations of alkaline phosphatase, cholinesterase and total bilirubin returned to normal, but again became abnormal after about seven weeks. Despite substitution of clotting factors thromboplastin time remained reduced. She died 82 days after the onset of symptoms. In the second patient, treatment with penicillamine was started at once, without waiting for histological confirmation. All laboratory values became normal and remained so. It is concluded from these observations that liver transplantation is indicated if the abnormal values for cholinesterase, thromboplastin time and bilirubin do not remain normal after six weeks and if the initial suppression of alkaline phosphatase continues or occurs again.

During the intensive medical treatment of a finally fatal parathion poisoning (survival time 7 days) with shock symptoms (lung and kidney) the kinetic profiles of both plasma and urinary catecholamines were taken up. In addition the parathion concentrations of the same plasma samples were measured. There could have been found plasma catecholamine profiles exhibiting peak concentrations in the initial phase, followed by a period of 4 days without any detectable plasma epinephrine and finally an extreme elevation of both catecholamines in the last period before death. The excretion patterns confirmed the plasma results. Imaginable pathophysiological mechanisms in consideration of the shock induced renal insufficiency are discussed. The question is raised whether the kinetics of plasma catecholamines may be a possible marker for the prognosis of organophosphate poisoning.