What prophylactic measures are available?

Approaches to prophylaxis of deep venous thrombosis include antithrombotic drugs and pneumatic-compressive devices. Both heparin and warfarin are effective in preventing deep

venous thrombosis. Subcutaneous heparin offers a low risk of bleeding and rapid onset of prophylaxis but is ineffective in patients undergoing prostate or hip surgery. Low-dose warfarin (with prolongation of the prothrombin time to 1.2-1.3 times normal) also has a low risk of bleeding and is effective in patients with trauma, bums, and hip surgery. It takes several days, however, to develop a full antithrombotic effect. Antiplatelet drugs such as aspirin and dipyridamole are not effective in prophylaxis.

Intermittent pneumatic-compressive devices effect prophylaxis by maintaining venous flow in the lower extremities and are especially efficacious in patients who cannot receive anticoagulant medications. Modalities available include compressive devices applied to the feet alone, covering the calves, or extending to the thighs. No version has been shown to provide superior prophylaxis.

Should all deep venous thromboses be treated with anticoagulation?

No. Deep venous thromboses are treated primarily to prevent fatal pulmonary embolism. Because the risk of fatal embolism is low for deep venous thromboses limited to calf veins, many authorities do not recommend anticoagulation in this setting. Lack of extension into the popliteal system must be confirmed and followed (for 14 days) by impedance plethysmography. If this or other reliable tests for popliteal extension are not available, deep venous thromboses in the calf should be treated.

Where do most pulmonary emboli originate?

Thromboses in the deep veins of the lower extremities account for 90-95% of pulmonary emboli. Less common sites of origin include thromboses in the right ventricle; in upper-extremity, prostatic, uterine, and renal veins; and, rarely, in superficial veins.

Are pulmonary embolism and pulmonary infarction synonymous terms?

No. The pulmonary parenchyma is supplied by both the pulmonary and bronchial (systemic) circulations. Pulmonary infarction results when embolized lung parenchyma is inadequately perfused by the bronchial circulation. Infarction complicates only 10% of pulmonary emboli. The two conditions are treated in the same fashion.

What are the most common findings on chest roentgenogram and electrocardiogram (ECG) in patients with pulmonary emboli?

Most patients with pulmonary embolism have a normal chest roentgenogram. When the chest roentgenogram is abnormal, the findings are nonspecific and include an elevated hemidiaphragm, focal or multifocal infiltrates, pleural effusion, platelike atelectasis, enlarged pulmonary arteries, focal oligemia (Westermark’s sign), and right ventricular enlargement. Most patients with pulmonary embolism present with sinus tachycardia. Other EKG findings include arrythmias (premature atrial and ventricular beats, first-degree atrioventricular (AV) block, supraventricular arrhythmia); right ventricular strain (right axis deviation, right ventricular hypertrophy); p-pulmonale; right bundle-branch block; S,S2S3 and SjQjTj pattern; and depression, elevation, or inversion of S-T and T waves.

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