Venous Thrombosis
A. Deep venous thrombosis
1. Definition. Deep venous thrombosis occurs when a blood clot forms in the lower extremities or in the pelvic veins. The gravity of deep venous thrombosis stems from the tendency of the thrombi to become pulmonary emboli. This tendency is especially pronounced for clots located above the popliteal fossa.
2. Predisposing factors
a. Immobilization. The muscles in the legs act as pumps to maintain venous return from the lower extremities. Inactivity of these muscles leads to venous stasis, with subsequent development of thrombophlebitis. Stasis is likely to occur during surgery, prolonged bed rest, and prolonged periods in one position.
b. Venous incompetence. Venous valvular incompetence and the presence of varicose veins increase the incidence of thrombophlebitis.
c. CHF. In CHF, cardiac output is reduced, as is venous return from the legs.
d. Injury. Direct mechanical injury to the lower extremities may lead to blood clot formation and the development of thrombophlebitis.
e. Hypercoagulable states. Malignancy, estrogen use, and hyperviscosity syndrome may produce a hypercoagulable state, increasing the risk of thrombophlebitis.
3. Clinical features
a. Symptoms. The patient usually presents with unilateral leg pain and swelling.
b. Physical signs. In general, the physical examination is unreliable. Tenderness on compression of the calf muscles, increased resistance during dorsiflexion of the foot (Homans' sign), and an increase in the circumference of the affected leg by at least 1 cm suggest the presence of deep venous thrombosis.
4. Diagnosis
a. Noninvasive studies. Impedance plethysmography and Doppler ultrasonography are useful tests for the detection of deep venous thrombosis.
b. Invasive studies. Contrast venography currently is the most effective way to demonstrate the area of blood clot. This technique is associated with complications, including adverse reactions to the contrast agent and postvenography thrombophlebitis.
5. Therapy. Anticoagulants prevent additional clot formation and allow the body's autolytic system to lyse effectively and heal deep venous thrombosis. Anticoagulation therapy is usually maintained for 3–6 months.
a. Anticoagulation with intravenous heparin is indicated in the acute treatment of deep venous thrombosis. LMWH appears to be as effective as unfractionated heparin. Although the low–molecular-weight form is more expensive, it does not require laboratory monitoring. In cases of heparin-induced thrombocytopenia, a direct thrombin inhibitor should be substituted for heparin.
b. After adequate treatment with heparin, oral anticoagulation with warfarin is begun.
6. Prophylaxis. There is substantial medical evidence that the incidence of deep venous thrombosis for hospitalized patients can be reduced by the following methods.
a. Rapid mobilization. Prolonged bed rest should be avoided when possible. The increasingly rapid mobilization of patients following MI has significantly reduced the incidence of thromboembolic complications following this disease.
b. Increasing deep venous flow
(1) Antithromboembolic stockings and pneumatic compression devices compress the superficial veins, thereby increasing deep venous flow and reducing stasis and the incidence of thromboembolism.
(2) Foot exercises and avoidance of leg crossing are further methods of preventing deep venous thrombosis.
c. “Minidose†heparin. Intermittent doses of subcutaneous heparin given at 8- hour intervals inhibit factors X and XI in the clotting cascade without producing overt anticoagulation. This treatment significantly reduces the incidence of deep venous thrombosis in both medical and surgical patients on bed rest.
P.39
B. Superficial thrombophlebitis
Unlike deep venous thrombosis, in which a thrombus may break off and become a pulmonary embolism, superficial thrombophlebitis has little potential for embolic complications. Patients with superficial thrombophlebitis may present with a painful tender cord that can be easily palpated in the lower extremities. In the absence of concomitant deep venous thrombosis, anticoagulation is not indicated. Superficial thrombophlebitis is treated with elevation of the legs, heat, and administration of salicylates or other NSAIDs.
A. Deep venous thrombosis
1. Definition. Deep venous thrombosis occurs when a blood clot forms in the lower extremities or in the pelvic veins. The gravity of deep venous thrombosis stems from the tendency of the thrombi to become pulmonary emboli. This tendency is especially pronounced for clots located above the popliteal fossa.
2. Predisposing factors
a. Immobilization. The muscles in the legs act as pumps to maintain venous return from the lower extremities. Inactivity of these muscles leads to venous stasis, with subsequent development of thrombophlebitis. Stasis is likely to occur during surgery, prolonged bed rest, and prolonged periods in one position.
b. Venous incompetence. Venous valvular incompetence and the presence of varicose veins increase the incidence of thrombophlebitis.
c. CHF. In CHF, cardiac output is reduced, as is venous return from the legs.
d. Injury. Direct mechanical injury to the lower extremities may lead to blood clot formation and the development of thrombophlebitis.
e. Hypercoagulable states. Malignancy, estrogen use, and hyperviscosity syndrome may produce a hypercoagulable state, increasing the risk of thrombophlebitis.
3. Clinical features
a. Symptoms. The patient usually presents with unilateral leg pain and swelling.
b. Physical signs. In general, the physical examination is unreliable. Tenderness on compression of the calf muscles, increased resistance during dorsiflexion of the foot (Homans' sign), and an increase in the circumference of the affected leg by at least 1 cm suggest the presence of deep venous thrombosis.
4. Diagnosis
a. Noninvasive studies. Impedance plethysmography and Doppler ultrasonography are useful tests for the detection of deep venous thrombosis.
b. Invasive studies. Contrast venography currently is the most effective way to demonstrate the area of blood clot. This technique is associated with complications, including adverse reactions to the contrast agent and postvenography thrombophlebitis.
5. Therapy. Anticoagulants prevent additional clot formation and allow the body's autolytic system to lyse effectively and heal deep venous thrombosis. Anticoagulation therapy is usually maintained for 3–6 months.
a. Anticoagulation with intravenous heparin is indicated in the acute treatment of deep venous thrombosis. LMWH appears to be as effective as unfractionated heparin. Although the low–molecular-weight form is more expensive, it does not require laboratory monitoring. In cases of heparin-induced thrombocytopenia, a direct thrombin inhibitor should be substituted for heparin.
b. After adequate treatment with heparin, oral anticoagulation with warfarin is begun.
6. Prophylaxis. There is substantial medical evidence that the incidence of deep venous thrombosis for hospitalized patients can be reduced by the following methods.
a. Rapid mobilization. Prolonged bed rest should be avoided when possible. The increasingly rapid mobilization of patients following MI has significantly reduced the incidence of thromboembolic complications following this disease.
b. Increasing deep venous flow
(1) Antithromboembolic stockings and pneumatic compression devices compress the superficial veins, thereby increasing deep venous flow and reducing stasis and the incidence of thromboembolism.
(2) Foot exercises and avoidance of leg crossing are further methods of preventing deep venous thrombosis.
c. “Minidose†heparin. Intermittent doses of subcutaneous heparin given at 8- hour intervals inhibit factors X and XI in the clotting cascade without producing overt anticoagulation. This treatment significantly reduces the incidence of deep venous thrombosis in both medical and surgical patients on bed rest.
P.39
B. Superficial thrombophlebitis
Unlike deep venous thrombosis, in which a thrombus may break off and become a pulmonary embolism, superficial thrombophlebitis has little potential for embolic complications. Patients with superficial thrombophlebitis may present with a painful tender cord that can be easily palpated in the lower extremities. In the absence of concomitant deep venous thrombosis, anticoagulation is not indicated. Superficial thrombophlebitis is treated with elevation of the legs, heat, and administration of salicylates or other NSAIDs.
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