Theory and Practice in Acute Venous Thrombosis

Abstract

The purpose of this review has been to outline the basis for proposing, and the details for implementing, a rational and consistent plan of therapy for the management of acute venous thrombosis. We have interpreted the entity of venous thrombosis as representing a common, frequently systemic disease, clinically manifest by focal intravascular coagulation. Concerning this disease, the specific etiology is unknown, the diagnostic criteria are crude and unsatisfactory, and although the clinical course is usually benign and self limited it may be unpredictably recurrent and fatal. We have also inferred that the difficulties in statistically validating any specific therapeutic measure are, for the present, extremely great, and that this problem will not be significantly lessened until an accurate test for thrombosis is devised. To construct a workable frame of reference for the clinical management of venous thrombosis within the limits of our present knowledge, we have formulated the concept of the temporary thrombotic state. Treatment is based upon the neutralization of hypercoagulability by anticoagulant drugs and upon a reduction of venous stasis by the removal of immobilization and a decrease in the size of the peripheral venous pool by elastic support. Various aspects of this therapeutic approach are described in detail and illustrated by selected case studies.

Coagulation And Fibrinolytic Studies During Pregnancy1

“…Owing to the increase in concentration of some coagulation factors and the decrease in fibrinolytic activity pregnancy has been considered as a hypercoagulable state, implying an increased capacity to form fibrin and an increased tendency to thrombosis. So far, no causal relationship has been demonstrated between intravascular thrombosis and alterations in any known coagulation factor (Owren, 1965;~o~n s o~, 1965;Eric~son, 1965;Wessler and Deykin, 1958). It must be recollected that the initial stage in thrombus formation is independent of plasma coagulation and depends on platelet function.…”

Diabetic Acidosis With Pancreatic Artery Thrombosis: Unusual Complication of Carcinoma of the Pancreas*

“…Kenny (11) suggested that the high incidence of thrombosis is due to secretion of an abnormal substance by the tumor cells, or to an undue secretion of an abnormal substance concerned in blood clotting. An interesting observation was added by Wessler and Deykin (14) who reported that the associated phlebitis was controlled by heparin, but not by dicoumarin medication.…”

“…The substance appears to inhibit naturally occurring factors which normally serve to maintain the fluid state of the circulating blood. The likely point of action of the tumor‐secreted substance, according to the findings of Wessler and Deykin (14), is in the final stages of blood coagulation, when endogenous heparin and its co‐factors antagonize thrombin. The thrombophilic state which is observed in such patients is an expected consequence of inhibition or neutralization of physiologic thrombin antagonism.…”

Fibrinolysin (Plasmin) Therapy in Acute Deep Thrombophlebitis

“…The third patient had a recurrence at 1 month and died 6 weeks later with pulmonary embolizatioii and congestive healrt failure. The fourth patient had reeurreniees at 1, 2, and 3 mnonths after discharge but for the subsequent 6 iimonths she had no further complaints other thani severe postphl]ebitic changes of the involved extremity.…”