A 66-year-old man with a recent prosthetic knee infection, status postprosthesis removal, was admitted with recurrent septic arthritis. On his seventh hospital day, as he was signing his discharge paperwork, he developed acute respiratory distress. On physical examination, he was tachycardic to 118 beats/min, relatively hypotensive from 144/78 mm Hg earlier in the day to 94/54 mm Hg, and hypoxemic, with an oxygen saturation of 94% on a 100% nonrebreather facemask. The ECG showed sinus tachycardia. An urgent contrast-enhanced chest computed tomogram (CT) demonstrated large saddle pulmonary embolism (PE) and severe right ventricular (RV) enlargement, with an RV diameterto-left ventricular (LV) diameter ratio of 1.8 (Figure 1). The patient was administered a bolus of intravenous unfractionated heparin followed by a continuous infusion. An urgent bedside transthoracic echocardiogram showed severe RV dilation, moderateto-severe pulmonary hypertension, and RV pressure overload as suggested by systolic deviation of the interventricular septum toward the LV (Figure 2). The Vascular Medicine and Cardiac Surgery services were consulted for consideration of advanced therapies. Because of concern for major bleeding associated with fibrinolytic therapy in the setting of recent major surgery, surgical pulmonary embolectomy was recommended.
IntroductionDespite advances in diagnostics and therapeutics, acute PE remains a life-threatening condition with an in-hospital mortality rate of ≈7% for all-comers and 31% for patients with hemodynamically unstable (massive) PE.1 Current management algorithms emphasize risk stratification to identify patients who may benefit from early advanced therapies in addition to anticoagulation.2-4 Risk categories of massive, submassive, and low-risk PE are based on clinical, radiological, and laboratory criteria. Massive PE is characterized by systemic arterial hypotension, syncope, cardiogenic shock, cardiac arrest, or respiratory failure. Submassive PE is defined by evidence of RV dysfunction on imaging (RV/LV diameter >0.9 on contrastenhanced chest CT or RV dilation and hypokinesis on echocardiography), elevated cardiac biomarkers (such as cardiac troponin), or both, in a patient with preserved systemic arterial pressure. Submassive PE comprises a patient population at increased risk of adverse outcomes and early mortality. Low-risk PE patients have none of these features and typically have an uneventful clinical course when treated with therapeutic anticoagulation alone.Advanced therapies are often considered for patients with submassive or massive PE to rapidly relieve RV pressure overload and avert hemodynamic deterioration. Advanced therapies for reperfusion include systemic fibrinolysis, catheter-based pharmacomechanical intervention, and surgical pulmonary embolectomy. A recent meta-analysis showed a 1.7% absolute mortality