Acute Stroke, Deep Vein Thrombosis, and Pulmonary Embolism

Source: Wijdicks EFM, Scott JP. Pulmonary embolism associated with acute stroke. Mayo Clin Proc 1997;72:297-300.

Wijdicks and scott reviewed cases of pulmonary embolism (PE) complicating acute stroke at the Mayo Clinic over two decades, 1976-1995. PE occurred in 33 patients with hemorrhagic or ischemic strokes. The authors do not report the number of patients who had acute stroke during the period, leaving the incidence of post-stroke PE undetermined.

Three patients died from progressive cerebral edema and brain herniation after large hemisphere infarcts; small pulmonary emboli found at autopsy were incidental. Of the other 30 patients with clinically evident PE, 15 had ischemic stroke, and 15 had ganglionic or lobar hemorrhage. None had received prophylactic heparin administered intravenously or subcutaneously to prevent deep vein thrombosis (DVT). Four patients with PE had received intermittent pneumatic compression of the lower extremities but only while they were in the intensive care unit following surgical evacuation of a cerebral hematoma.

PE occurred from three days to four months (median, 20 days) after stroke onset. Fifteen patients died suddenly; all had massive PE at autopsy. Fifteen survivors had clinical symptoms and signs of PE, verified by ventilation perfusion scans and pulmonary angiography in eight patients.

Seven patients with middle cerebral artery territory ischemic strokes received anticoagulation with intravenous heparin. An inferior vena cava filter was placed in eight others with cerebral hemorrhage.

DVT was diagnosed in 11 of 30 patients and was always found in the flaccid paralyzed leg.


In an earlier study of 30 acute stroke patients who received no anti-thrombotic prophylaxis, Warlow et al (Lancet 1972;1:1305-1306) identified 18 with DVT diagnosed by fibrinogen uptake studies; four of the 18 developed PE. In a more recent analysis of pooled data, Clagett and associates (Chest 1995;108 [suppl]:312S-334S) reported an incidence of 42% of DVT diagnosed by fibrinogen uptake tests in 125 patients with acute ischemic stroke. The frequency of DVT was reduced to 26% (15/58) by the prophylactic use of low unfractioned heparin and reduced further to 17% (27/163) by the use of low-molecular-weight heparin. Intermittent pneumatic compression devices may be useful in stroke patients, but this has been insufficiently studied.

Based on these data, the American College of Chest Physicians’ Consensus Conference on Anti-thrombotic Therapy (Chest 1995;108 [suppl]:312S-334S) has recommended using low-dose unfractioned heparin or low-molecular-weight heparin to reduce the occurrence of DVT in patients with acute ischemic stroke.

Although Wijdicks and Scott have supplied no new information on the incidence of PE or its most effective means of prevention, the authors re-focus on an important clinical problem. The neurologist has a responsibility to make sure that prophylactic heparin therapy is begun at once in hospitalized patients with acute ischemic stroke and hemiparesis. In patients with cerebral hemorrhage and hemiplegia, the use of prophylactic anti-thrombotic therapy may be relatively or absolutely contraindicated. Such patients may be protected by applying intermittent pneumatic compression and graded elastic compression stockings along with vigorous passive range of motion. The significant occurrence of DVT in ischemic stroke patients, even when heparin prophylaxis is employed, demands that the mechanical measures mentioned above be used to supplement the effects of heparin. The effective prevention of post-stroke DVT and PE requires close coordination among physicians, nurses, and physical therapists. —jjc