抄録
The incidence of pulmonary thromboembolism in the total autopsied cases and the actual reported cases of pulmonary thromboembolism in Japan has gradually increased. Since there is no part of the history, physical examination or noninvasive laboratory findings that is specific, a tentative criteria for diagnosis of pulmonary thromboembolism is proposed based a scoring system. Pulmonary thromboembolism can be classified into 5 different types: (1) massive pulmonary thromboembolism, (2) recurrent or occult pulmonary thromboembolism, (3) diffuse pulmonary microthromboembolism, (4) submassive pulmonary thromboembolism, (5) pulmonary infarction. We have carried out a series of model experiments in order to clarify the mechanism of the development of pulmonary microthromboembolism and the production of pulmonary infarction. On the basis of this data, we suspect that hyperfibrinolysis, endothelial damages and activated permeability factors lead to the interstitial and alveolar edema in pulmonary microthromboembolism or severe hemorrhage in pulmonary infarction. The combination therapy of UK (480, 000 units) and DS (3, 000 mg) had two advantages: (1) inhibition of shortening of APTT, (2) economy of UK dosage. Laboratory monitoring for effective UK therapy showed a markedly reduced α2 PI to under 50% of normal levels and fibrinolysis associated with fibrinogenolysis. The therapeutic effects of heparin were assessed by prolonged APTT (45-250 sec) and elevated Anti-FXa activity (0.2-1.2 u/ml of plasma heparin concentration) as an indicator for the evaluation of anticoagulation activity and by normalized FPA, Fbg, FDP, Plg and AT III as an indicator for evaluation of antithrombolic activity.
