Embolia pulmonar

THROMBOLYTIC THERAPY FOR ACUTE PULMONARY EMBOLISM
A Critical Appraisal
Jamie L. Todd, MD and  Victor F. Tapson, MD*

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© 2009 American College of Chest Physicians

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Abstract
Pulmonary embolism (PE) is a prevalent condition that may account for > 300,000 deaths annually in the United Statesalone. Although thrombolytics have been studied as a treatment for acute PE since the 1960s, to date there have been only 11 randomized controlled trials comparing thrombolytic therapy to conventional anticoagulation, and the numbers of patients included in these trials has been small. Many studies confirm that thrombolytic therapy leads to rapid improvement in hemodynamic aberrations associatedwith PE, and this approach to massive PE with cardiogenic shock is a guideline-based practice. It is widely accepted that acute PE without associated right ventricular (RV) dysfunction or hemodynamic instability can be readily managed with standard anticoagulation. The appropriate therapy for submassive PE (PE associated with RV dysfunction but preserved systemic arterial BP) remains an area ofcontention, and definitive data proving mortality benefit in this setting are lacking. Further efforts at risk stratification may better determine who is in need of aggressive therapy. This article reviews historical aspects of and current evidence for thrombolytic therapy in acute PE with specific attention to bleeding risk, and data regarding hemodynamic parameters and mortality. We also discuss riskstratification techniques and propose a clinical algorithm for the incorporation of thrombolytic therapy.
A 77-year-old woman with a history of hypertension and left ventricular diastolic dysfunction presented to the emergency department with 1 week of unilateral calf swelling and dyspnea. She denied chest pain, palpitations, hemoptysis, syncope, or known risk factors for venous thromboembolism,except for her age. Examination revealed a slightly anxious elderly woman who was comfortable at rest but dyspneic with minimal movement. She was afebrile, the pulse was 66 beats/min while receiving β-blocker therapy, the respiratory rate was 22 breaths/min, and the BP, 140/86 mm Hg. The oxygen saturation was 88% on room air. There was no elevated jugular venous pressure, loud S2, or precordiallift. The right lower extremity was swollen from the ankle to the knee. Laboratory evaluation findings were notable for an elevated d-dimer level, a negative troponin T level, and a pro-brain natriuretic peptide (BNP) level that was elevated at 1,608 pg/mL (reference range, < 600 pg/mL). Arterial blood gas measurement revealed a pH of 7.45, PCO2 of 30 mm Hg, and PO2 of 59 mm Hg on room air, atrest. The ECG did not show right ventricular (RV) strain. She was placed on oxygen at 2 L/min, and subcutaneous enoxaparin was initiated. A CT angiography (CTA) scan of the chest revealed extensive pulmonary embolism (PE) in the left and right pulmonary arteries with extension into the right upper, right lower, and left lower lobe segmental and subsegmental pulmonary arteries. Ultrasound of the rightleg revealed nonocclusive thrombus in the proximal femoral vein. Transthoracic echocardiography demonstrated moderate RV enlargement with hypokinesis. The patient was admitted to the hospital ward where discussions of thrombolytic therapy ensued. As one might anticipate, highly divergent opinions emerged, and there was difficulty reaching a consensus.
This case illustrates the inadequate evidencebase and the varied opinions regarding the use of thrombolytic therapy for acute PE. Although PE may be responsible for as many as 300,000 deaths per year in the United States, the number of patients included in randomized controlled trials evaluating thrombolytics has been very small.1,2 To date, only 11 such studies3–13 have compared thrombolytic therapy to conventional anticoagulation in the...