Thromboembolism

Abstract

Dr. Frederick K. Heath: The common denominator, prerequisite to an understanding of the mechanisms upon which present day therapy of thromboembolism is based, is the increased tendency of the blood to clot. This may be demonstrated by the Lee-White method of determining the clotting time by which, if lucite or paraffin coated tubes are used, an actual decrease in coagulation time below the normal may be noted. Why the blood tends to clot faster is not known but poor muscle tone, venous stasis and tissue damage seem to be predisposing factors. At any rate, clotting occurs and a thrombus is formed. In about 90 per cent of instances, this develops below the inguinal ligaments, most frequently in the deep veins of the calf. Early in its evolution no signs or symptoms are found. As the clot grows, inflammation of the vein wall, representing the reparative phase, may result in tenderness; obstruction of the vein may produce mild edema of the tissue drained. With growth of the ‘tail’ to involve larger veins, more venous obstruction and more edema may result until, with adherence of the ‘tail,’ definite venous obstruction is present and swelling of the calf ensues. At this juncture a considerable inflammatory reaction is present producing the common findings of pain, tenderness, fever, leukocytosis and elevation of the sedimentation rate. When these are marked, vasospasm may also occur. The typical picture is now one of acute thrombophlebitis as described by Ochsner. When the inflammatory process is less severe, or perhaps earlier in the course, the pattern resembles phlebothrombosis. Whether more profound differences exist between these clinical entities is not yet clear. The rate of healing is variable but takes place first by adherence of the clot and its ‘tail,’ which occurs about the fifth day, and then by endothelialization, completed by the tenth to twelfth day if growth can be prevented. These time factors are important not only because upon them is based the duration of anticoagulant therapy but also because they suggest when ligation is most needed. The breaking-off of the thrombus or its ‘tail’ before these are adherent, with consequent pulmonary embolization, is a major event, in the pathologic sequence and may produce a dramatic clinical picture. Again this aspect is variable, ranging from small emboli producing mild pleuritic pain with no signs to massive embolization causing sudden death. Between these extremes, deep constant pain, cyanosis, reflex dyspnea, cough and hemoptysis (rather infrequently), râles and, occasionally, pleural effusion may be encountered. Serious impairment of the pulmonary arterial flow and an accentuated pulmonic second sound may herald right heart failure and electrocardiographic evidence of acute cor pulmonale; nor should the presence of abdominal findings of pain and muscular spasm fail to suggest the possibility of a basal infarct with diaphragmatic irritation. The appearance of signs or symptoms referable to the lungs or pleura should always call to mind the possibility of thromboembolism. The aim of anticoagulant therapy is to prolong blood coagulation so as to prevent further growth of the thrombus in the vein of origin. If this can be done, the thrombus will become adherent and repair may take place before the ‘tail’ breaks off to become an embolus. When embolization has already occurred, the aim is not only to attain the same end at the original site so as to prevent further potential embolus formation but also to prevent proximal propagation of the thrombus which forms behind the embolus lodged in the lungs. This is carried out by the use of heparin and dicumarol with daily careful clotting and prothrombin time determinations. Statistics indicate that the results of anticoagulant therapy are excellent both in achieving a favorable local result as well as in preventing pulmonary embolization or its recurrence. Fatal pulmonary embolization, subsequent pulmonary embolization and venous thrombosis have each been reduced to about 1 per cent. Hemorrhage has been the only serious toxic manifestation of anticoagulant therapy. It is infrequent with adequate control and can be successfully combatted by the use of plasma and blood, and by vitamin K when dicumarol is the anticoagulant. Contraindications to anticoagulants exist: subacute bacterial endocarditis, hemorrhagic blood dyscrasias, recent threatened abortion, obstetrical cases near term and after a recent central nervous system operation. Anticoagulants obviously cannot be used prophylactically in the immediate preoperative period. They should be used with caution in liver disease or renal insufficiency and in patients with ulceration or malnutrition and in very old patients. At the present time, bilateral ligation of the femoral vein distal to the point of entry of the deep femoral vein is the surgical approach of choice. No obvious advantages can be expected from this mode of therapy which make it superior to anticoagulants. It is therefore usually reserved for situations in which anticoagulant therapy cannot be used.