Acute Pulmonary Embolism

Posted by Graham McMahon • July 16th, 2010

Pulmonary embolism should be suspected in all patients who present with new or worsening dyspnea, chest pain, or sustained hypotension without an obvious alternative cause. The diagnostic workup should be tailored to the severity of the clinical presentation on the basis of whether the patient is hemodynamically stable or unstable.  A review by Agnelli et al. explores the optimal diagnostic strategy and management, according to the clinical presentation.

Clinical Pearls

When is the D-dimer assay useful in the diagnosis of acute pulmonary embolism?

In patients with hemodynamic stability, the diagnosis of pulmonary embolism should follow a sequential diagnostic workup that integrates clinical probability assessment, D-dimer testing, and (if necessary) multidetector computed tomography or ventilation-perfusion scanning. The use of the D-dimer assay is of limited value in patients with a high clinical probability of pulmonary embolism. The specificity of an increased D-dimer level is reduced in patients with cancer, pregnant women, and hospitalized and elderly patients. Most hospitalized patients should not undergo D-dimer testing when pulmonary embolism is suspected.

What duration of anticoagulation is recommended after acute pulmonary embolism?

The duration of long-term anticoagulation should be based on the risk of recurrence after stopping vitamin K antagonists, the risk of bleeding while receiving treatment, and the patient’s preference. In patients with pulmonary embolism secondary to a temporary (reversible) risk factor, therapy with vitamin K antagonists should be given for 3 months. Patients with unprovoked pulmonary embolism, those with cancer, and those with recurrent unprovoked pulmonary embolism are candidates for indefinite anticoagulation with periodic reassessment of the risk-benefit ratio.

Morning Report Questions

Q: How should hemodynamically unstable patients with acute pulmonary embolism be managed?

A: Hemodynamically unstable patients are candidates for more aggressive treatment, such as pharmacologic or mechanical thrombolysis. Percutaneous mechanical thrombectomy (thrombus fragmentation and aspiration) and surgical embolectomy should be restricted to high-risk patients with an absolute contraindication to thrombolytic treatment or those in whom thrombolytic treatment has not improved hemodynamic status or as an alternative to surgical embolectomy if immediate access to cardiopulmonary bypass is unavailable.

Q: What risk factors should be considered when evaluating a patient with acute pulmonary embolism?

A: Shock and sustained hypotension identify patients at high risk for an adverse outcome. Right ventricular hypokinesis and dilatation have been shown to be independent predictors of 30-day mortality in hemodynamically stable patients. Patients with elevated levels of B-type natriuretic peptide (BNP) and pro-BNP were shown to be at increased risk for an adverse in-hospital outcome, as compared with patients with normal levels. Among hemodynamically stable patients, the association between an increased troponin level and right ventricular dysfunction on echocardiography identifies a group of patients at particularly high risk for an adverse outcome.

Figure 1. Diagnostic Workup for Pulmonary Embolism.

One Response to “Acute Pulmonary Embolism”

  1. I find it interesting that this is written by internal medicine/cardiology, and that there’s little-to-no reference to the Emergency Medicine community. Perhaps evaluations are done differently in Italy, but in the US a large percentage–if not the vast majority–of acute PE evaluations are performed by emergency physicians.

    The only EM-related reference is the “Geneva Score,” with a “low probability” score still giving you an 8% probability of PE.

    I would disagree with the diagnostic algorithm that the article presents as well; if you get a d-dimer on everyone with “low probability” for PE, you’re going to be irradiating a ton of people without pulmonary embolism because of the d-dimer’s terrible specificity. There’s certainly a role for the PERC rule, which this article does not present.

    Two final thoughts on anticoagulation: 1) I think it’s at least worth a mention that no good RDBCT has ever been done to show that anticoagulation works for PE, and 2) Dr. Agnelli has (at least in the past) received money from GSK, maker of Fondaparinux.

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