Der Anaesthesist
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Clinical Trial
[The effect of substitution with AT III- and PPSB-concentrates in patients with terminal liver insufficiency].
Patients with end-stage liver disease frequently develop combined coagulopathies due to increased procoagulant and fibrinolytic turnover as well as thrombocytopenia. The onset of clinical symptoms of a haemorrhagic diathesis requires balanced substitution of coagulation factors, since fresh frozen plasma alone does not always maintain a sufficient haemostatic potential in these patients. This substitution commonly follows standard rules based on the assumption that 0.5-1 IU of a coagulation factor or inhibitor concentrate given per kg body weight will increase its endogenous activity by 1%. We set out to investigate the validity of this standard regime in patients with end-stage liver disease scheduled for orthotopic liver transplantation. ⋯ In patients with end-stage liver disease standard rules for substitution with AT III-concentrate are adequate only for patients with CLF. In patients with ALF higher AT III doses are required to achieve the expected effect on endogenous AT III activity. Procoagulant activity, as reflected by PT, can be increased by 1% when 1.6 IU/kg PPSB concentrate is given. However, this study shows the effects of coagulation concentrates only 30 min after administration. An increased volume of distribution and increased turnover may explain the poor recovery of AT III activity in the ALF group, indicating that the dose of coagulation concentrate should be estimated against the background of the patient's clinical symptoms and diagnosis.
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A 45-year-old, healthy, well-trained man climbed within 12 hours from 300 m above sea level to a shelter at 2500 m in the Tyrolean Alps. During the following 3 days he undertook ski tours to the surrounding mountains up to 3356 m. On the 4th day he suddenly suffered from headache, coughing and very severe dyspnoea even at rest, accompanied by loss of appetite and the feeling of suffocation. ⋯ HAPE is a non-cardiogenic pulmonary edema which develops in healthy individuals usually above 3000 m. Among the predisposing factors are rapid ascent, severe physical effort, diminished hypoxic ventilatory response and abnormal fluid balance. The treatment of choice is descent to a lower altitude, administration of oxygen and of nifedipine and expiratory positive airway pressure.