Classification and treatment

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The ability to classify pulmonary embolism in terms of severity is useful when determining treatment strategies and patient prognosis. The classification scheme in T.a.b.le.4 utilizes symptomatology, blood gas derangements, and hemodynamic factors to place patients in one of five categories which correlate with a percentage of vascular occlusion. Class I patients are usually discovered on screening studies performed for other reasons. These patients have less than 20 per cent occlusion of the pulmonary arterial circulation and are asymptomatic. Patients with class II pulmonary embolism (20-30 per cent vascular occlusion) have the complex of findings associated with classic minor embolism: chest pain, hyperventilation, and anxiety, together with mild hemodynamic changes. Class III and IV (> 30 per cent vascular occlusion) patients present with more significant hypoxia as well as hemodynamic instability and shock. In class V pulmonary embolism (> 50 per cent vascular occlusion), shock and syncope are common features. Supportive measures are instituted based on clinical condition. Oxygen should be effectively delivered to provide a PaO2 above 60 mmHg (8 kPa). Pulmonary artery pressure should be monitored to help guide fluid resuscitation, particularly in patients in classes II to V where fluid is administered to help support hypotension and increase right ventricular stroke volume. Endpoints of therapy are an increase in overall cardiac output and urine production, an improvement in stroke volume, and stabilization of blood pressure. With continued cardiovascular compromise, the short-term use of norepinephrine (noradrenaline) has beneficial inotropic and pressor effects. However, the use of epinephrine (adrenaline), isoproterenol, dopamine, and dobutamine should all be considered and utilized as each individual clinical situation warrants. Hydralazine may also reduce pulmonary vascular resistance, decreasing right ventricular afterload.

Table 4 Classification of pulmonary embolism

Heparin therapy is instituted by administering a loading dose of 100 to 150 units/kg intravenously, followed by continuous infusion of 10 units/kg/h, and monitoring the partial thromboplastin time with a goal of 1.5 to 2 times control values. This management, together with supplemental oxygen therapy, may be all that is necessary for patients with class I and II pulmonary embolism. The heparin should be continued for 7 to 10 days to prevent propagation of clot, while the thrombus becomes adherent to the wall of the vessel during that time. The patient should be given oral warfarin (coumarin) while on heparin to allow several days of overlap while the prothrombin time becomes therapeutic (1.5 to 2 times control). This regimen prevents further embolization in over 90 per cent of these patients. Duration of therapy is controversial; however, at least 6 months of anticoagulation is recommended.

In patients with class III and IV pulmonary embolism, thrombolytic therapy should be initiated in an attempt to overcome hemodynamic compromise and improve clinical findings more rapidly than with heparinization. However, thrombolytic therapy has not been shown to improve overall mortality ( N§tloD§L.H..eart, Lung,, and

Blood Institute. .1974). The three agents most commonly used are streptokinase, urokinase, and tissue plasminogen activator. Streptokinase is effective systemically at a loading dose of 250 000 units, followed by infusion of 100 000 units/h intravenously for 12 to 24 h. Systemic administration of urokinase begins with a loading dose of 300 000 units and is followed by continuous infusion for 12 to 24 h at 300 000 units/h. Tissue plasminogen activator should be used at a dose of 0.5 mg/kg administered over 4 h. Regional (directed) infusion of these agents, particularly urokinase, can achieve faster clearance of thrombi ( Goldhaber.ef a/ 1987).

Contraindications to the use of thrombolytics include surgery within the previous 7 days, gastrointestinal bleeding in the previous 3 months, history of bleeding diathesis, hypertensive related cerebrovascular accident, or active intracranial process. If initiation of thrombolytic treatment is followed by a bleeding episode, the agent should be discontinued and 5 mg of aminocaproic acid administered to reverse the lytic state.

The short half-life of these drugs (streptokinase, 80 min; urokinase, 15 min; tissue plasminogen activator, 4 min) may be a consideration in their use. Heparin should be instituted following thrombolytic therapy as outlined previously.

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