Responding to Life-Threatening Pulmonary Embolic Disease
Top Papers of the Month
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Why is there so much institutional variation in the management of pulmonary embolic disease?
Despite being the “most preventable cause of death among hospitalized patients,” pulmonary embolic disease (PED) still manages to claim 100,000 to 180,000 lives a year in the United States.1 A recent “Top Paper” defined “massive” (5%) and “submassive” PED (20% to 25%).1 These 2 categories of PED, complicated by hypotension, syncope, cardiogenic shock, cardiac arrest (massive), and right ventricular (RV) dysfunction (submassive), are life-threatening. The information in the Top Paper, focusing on the submassive variety, is timely and should significantly change future practice.
The paper was organized according to the JAMA “Clinical Crossroads, Conferences with Patients and Doctors” format. It began with a case presentation, followed by pertinent questions, pathophysiology, diagnostic insights, therapy, specific recommendations for the patient presented, and final questions with discussion. The following are important points in the paper (definitely not all inclusive).
CASE PRESENTATION
A 60-year-old woman with shortness of breath was proven to have a saddle embolus on a CT scan (available for viewing in the article). Examination revealed neither hypotension nor right-sided heart findings (including jugular venous distension). But an echocardiogram demonstrated an elevated pulmonary artery pressure (45 mm Hg) and RV dilatation, hypokinesis, and systolic leftward deviated interventricular septum. In addition, troponin T levels were slightly elevated (0.15 ng/mL; normal 0 to 0.1 ng/mL).
DIAGNOSIS OF SUBMASSIVE PED
The minimal troponin “bump” is important. It reflects RV injury and increases the risk of death.2 The echocardiographic findings are critical as well. Since the definition of submassive PED requires RV dysfunction, the echocardiogram determined that the case under discussion was consistent with submassive PED. Patients in this echocardiographic category experience a higher incidence of hypotension, cardiogenic shock, cardiac arrest, and death.3
THERAPY
Immediate anticoagulation was accomplished (with fractionated heparin). More aggressive measures for submassive PED were considered, including fibrinolysis (with tissue plasminogen activator). References to 3 studies are provided in the Top Paper. Although no study yet has proven that fibrinolysis reduces mortality in submassive PED, other end points (e.g., mechanical ventilation) were improved (this therapy was recommended to the patient). Catheter-directed fibrinolysis, surgical embolectomy, and inferior vena cava filters were also discussed. Importantly, indications for filters were very restricted. Also, the filters should be retrievable.
FINAL QUESTIONS AND ANSWERS
The question that I would have asked led off discussion: Why does so much institutional variation in the management of PED exist? The discussant admitted that specific treatment of submassive PED requires more evidence for guideline implementation. In the meantime, I will be more cognizant of right-sided heart examination, echocardiography, troponin measurements, and the potential utility of fibrinolytics in a higher risk cohort. One suspects that these therapies will be the wave of the future.
REFERENCES:
1. Piazza G. Submassive pulmonary embolism. JAMA. 2013:309;171-180.
2. Stein PD, Matta F, Janjua M, et al. Outcome in stable patients with acute pulmonary embolism who had right ventricular enlargement and/or elevated levels of troponin. Am J Cardiol. 2010;106:558-563.
3. Kucher N, Rossi E, De Rosa M, et al. Prognostic role of echocardiography among patients with acute pulmonary embolism and a systolic arterial pressure of 90 mm Hg or higher. Arch Intern Med. 2005;165:1777-1781.