Abstract
The present study examined the clinical features of 41 stroke patients (mean age, 68.0 ± 9.1 years) with pulmonary embolism (PE). Lung scintigraphy or autopsy was performed in order to diagnose PE. The primary diagnosis was cerebral infarction in 28 patients, cerebral hemorrhage in 10, and subarachnoid hemorrhage in 3. The most frequent symptoms in the 41 patients were dyspnea, hypotension, tachypnea, tachycardia, and chest pain. Clinical examinations revealed that hypoxemia was accompanied by a low partial pressure of carbon dioside in the arterial blood (PaCO2) and that the serum lactic dehydrogenase activity (LDH) tended to increase gradually before PE, reaching a peak within 2 weeks after PE. The strongest risk factors associated with PE were a bedridden state due to disturbance of consciousness and motor paresis, and heart disease. Atrial fibrillation was observed in 17 of 29 patients with heart disease. The mortality rate was 39% among the PE patients. Twenty-one patients received thrombolytic therapy with urokinase and/or anticoagulant therapy with heparin and/or warfarin.
Fourteen of the 21 patients survived, and the efficacy of the above therapies was thus 67%. Early detection of PE requires close scrutiny of the clinical symptoms and an analysis of the arterial blood gases in addition to the use of lung scintigraphy or other methods. In order to prevent PE, stasis in the leg veins must be decreased by early rehabilitation after the stroke as well as leg elevation and the use of elastic stockings during the acute stage because a bedridden state may easily cause stasis in the leg veins, and thrombi may be formed soon after the stroke, Management of heart function is also important for stroke patients with heart disease in order to prevent PE. The LDH changes seen in most PE patients suggest that LDH activity could provide an indicator for the risk of PE.
