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Management of Submassive Pulmonary Embolism

2010; Lippincott Williams & Wilkins; Volume: 122; Issue: 11 Linguagem: Inglês

10.1161/circulationaha.110.961136

1524-4539

Gregory Piazza, Samuel Z. Goldhaber,

Acute Ischemic Stroke Management

HomeCirculationVol. 122, No. 11Management of Submassive Pulmonary Embolism Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBManagement of Submassive Pulmonary Embolism Gregory Piazza and Samuel Z. Goldhaber Gregory PiazzaGregory Piazza From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass. and Samuel Z. GoldhaberSamuel Z. Goldhaber From the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass. Originally published14 Sep 2010https://doi.org/10.1161/CIRCULATIONAHA.110.961136Circulation. 2010;122:1124–1129Case presentation: A 58-year-old woman with a history of cigarette smoking, chronic obstructive pulmonary disease, and recent intensive care unit admission for pneumonia presented with sudden onset of right-sided chest discomfort and dyspnea. On physical examination, she was tachycardic (heart rate 110 beats per minute), normotensive (blood pressure of 128/72 mm Hg), tachypneic (24 breaths per minute), and hypoxemic (oxygen saturation 88% on room air). She had jugular venous distension to the angle of her mandible, a grade 2/6 holosystolic murmur that increased to grade 3/6 with inspiration at the left lower sternal border, lung fields clear to auscultation bilaterally, and mild symmetrical lower-extremity edema. The ECG was notable for sinus tachycardia and T-wave inversions across the anterior precordium. Laboratory evaluation was remarkable for a D-dimer level of 1104 ng/mL (normal <500 ng/mL) and a cardiac troponin I level of 1.4 ng/mL (normal 2.6 m/s, and loss of inspiratory collapse of the inferior vena cava (IVC).14 Regional RV dysfunction with severe free-wall hypokinesis and apical sparing (McConnell sign) is a specific finding in acute PE.15 An RV-to-LV end-diastolic diameter ratio of 0.9 or greater, assessed in the left parasternal long-axis view or the subcostal view, is an independent predictor of hospital mortality.16 Echocardiography is warranted to identify RV dysfunction in patients with acute PE and clinical evidence of RV failure or elevated levels of cardiac biomarkers.3 A simple score based on clinical parameters, echocardiographic findings, and cardiac biomarkers can be used to stratify patients with acute PE according to risk of adverse outcomes (Table 1).17Table 1. Illustrations of Risk Stratification for Acute PERiskClinical AppearanceVital SignsCardiac BiomarkersRV FunctionLowAppears wellNormalNormalNormal RV size and functionIntermediateAppears wellNormalElevatedModerate RV dysfunctionHighAppears illTransient or sustained hypotensionElevatedSevere RV dysfunctionSubmassive PE can also be diagnosed when RV enlargement on chest computed tomography, defined by an RV-to-LV diameter ratio >0.9, is observed.18 RV enlargement on chest computed tomography predicts increased 30-day mortality in patients with acute PE.18,19 Detection of RV enlargement by chest computed tomography is especially convenient for diagnosis of submassive PE, because it uses data acquired during the initial diagnostic scan.PathophysiologyDirect physical obstruction of the pulmonary arteries, hypoxemic vasoconstriction, and release of potent pulmonary arterial vasoconstrictors increase pulmonary vascular resistance and RV afterload. Acute RV pressure overload may result in RV hypokinesis and dilation, tricuspid regurgitation, and ultimately, RV failure. Patients with submassive PE may deteriorate over the course of several hours to days and develop systemic arterial hypotension, cardiogenic shock, and cardiac arrest. Elevated diastolic pressure causes deviation of the interventricular septum toward the LV and impairs LV filling. An abnormal transmitral flow pattern on Doppler echocardiography may be observed because left atrial contraction, represented by the A wave on transmitral Doppler, makes a greater contribution to LV diastole than passive filling, signified by the E wave. RV pressure overload may also result in increased wall stress and ischemia by increasing myocardial oxygen demand while simultaneously limiting its supply (Figure 1). Severe mismatch between myocardial oxygen demand and supply may lead to RV infarction. Download figureDownload PowerPointFigure 1. The pathophysiology of submassive PE. PVR indicates pulmonary vascular resistance.A combination of ventilation-to-perfusion mismatch, increases in total dead space, and right-to-left shunting explains the majority of gas-exchange abnormalities observed in patients with acute PE. Arterial hypoxemia and an increased alveolar-arterial oxygen gradient are the most commonly noted abnormalities of gas exchange. Hyperventilation, especially in patients with normal baseline pulmonary function, may result in hypocapnea and respiratory alkalosis.ManagementAnticoagulation remains the cornerstone of therapy. Current options for advanced therapy include fibrinolysis, catheter-assisted embolectomy, surgical embolectomy, and IVC filter insertion (Figure 2). The decision to select advanced therapy for submassive PE or to maintain anticoagulation alone must be individualized because of a paucity of trials to help guide management. Download figureDownload PowerPointFigure 2. An algorithm for management of patients with submassive PE. CT indicates computed tomography.FibrinolysisFibrinolysis functions as a "medical embolectomy" and, when successful, will rapidly reverse hemodynamic compromise and gas-exchange derangements. In patients with submassive PE, fibrinolysis relieves RV pressure overload and may avert impending hemodynamic collapse and death due to progressive RV failure. Fibrinolytic therapy may reduce the likelihood of developing chronic thromboembolic pulmonary hypertension.20 The 2008 American College of Chest Physicians' guidelines include fibrinolysis as an option for patients with submassive PE who are judged to have a low risk of bleeding (grade 2B).21 Patients with a low risk of bleeding have normal renal function, are not frail, and are not receiving dual-antiplatelet therapy.The Management Strategies and Prognosis of Pulmonary Embolism Trial-3 (MAPPET-3) randomized 256 patients with submassive PE to receive recombinant tissue plasminogen activator (tPA) 100 mg over a 2-hour period followed by unfractionated heparin infusion or placebo plus heparin anticoagulation.22 Compared with heparin anticoagulation alone, fibrinolysis resulted in a significant reduction in the primary study end point of in-hospital death or clinical deterioration that required escalation of therapy (defined as catecholamine infusion, rescue fibrinolysis, mechanical ventilation, cardiopulmonary resuscitation, or emergency surgical embolectomy).22 The difference was largely attributable to a higher frequency of open-label fibrinolysis due to "clinical deterioration" as determined by the treating clinician.22In a prospective study of 200 patients with submassive PE, echocardiography was performed at the time of diagnosis and after 6 months to determine the frequency of pulmonary hypertension.20 Estimated pulmonary artery systolic pressure at 6 months increased in 27% of patients receiving heparin alone, and nearly half of these patients were moderately symptomatic.20 The median decrease in pulmonary artery systolic pressure was only 2 mm Hg in patients treated with heparin alone compared with 22 mm Hg in those treated with tPA plus heparin.20 Estimated pulmonary artery systolic pressure at follow-up did not increase in any of the patients treated with tPA.20The Pulmonary Embolism International Thrombolysis Trial (PEITHO) is a large randomized controlled trial that began in 2007. The investigators plan to enroll 1000 patients in 12 countries to evaluate a primary clinical end point of all-cause mortality or hemodynamic collapse within 7 days in patients treated with the fibrinolytic agent tenecteplase plus heparin versus heparin alone. As of March 31, 2010, 453 patients had been randomized. Results are expected in 2013.The US Food and Drug Administration has approved tPA 100 mg administered as a continuous intravenous infusion over a 2-hour period for treatment of acute massive PE. Nevertheless, tPA is often used off-label to treat submassive PE. All patients being considered for fibrinolysis should be screened carefully for contraindications that make the bleeding risk prohibitive. The most dreaded complication of fibrinolysis is intracranial hemorrhage. An analysis from the International Cooperative Pulmonary Embolism Registry (ICOPER) observed that the risk of intracranial hemorrhage may be as high as 3%.2 A study from a center with experience in fibrinolysis for acute PE reported that the overall major bleeding rate may approach 20%.23 Major contraindications to fibrinolysis include intracranial mass; cerebrovascular event or neurosurgery within the prior 2 months; history of intracranial hemorrhage; recent major trauma; active or recent respiratory tract, gastrointestinal, or genitourinary bleeding; severe uncontrolled hypertension; recent prolonged cardiopulmonary resuscitation; thrombocytopenia (<50 000 platelets/μL); acute pericarditis or pericardial effusion; ongoing suspicion of aortic dissection; and recent surgery, invasive procedure, or internal organ biopsy.Fibrinolysis is most successful when administered within several days of acute PE. Although the efficacy of fibrinolysis is inversely proportional to the duration of symptoms, effective fibrinolysis can be observed up to 2 weeks after an acute event.24,25 Patients with more anatomically extensive PE achieve a greater response to fibrinolysis than those with smaller and peripherally located thrombi.25 On the basis of available data, local catheter-directed delivery of the fibrinolytic agent directly into the pulmonary artery does not appear to improve efficacy or safety. Therefore, peripherally administered fibrinolytic therapy is ordinarily preferred to catheter-directed fibrinolysis.26–28Intravenous unfractionated heparin is the preferred agent for immediate systemic anticoagulation in patients undergoing advanced therapy such as fibrinolysis (Table 2). Intravenous unfractionated heparin offers the advantage of immediate discontinuation and rapid reversal in the event of bleeding complications. In contrast to fibrinolysis in myocardial infarction, intravenous unfractionated heparin infusion is withheld during fibrinolysis in patients with acute PE.29 At the conclusion of the fibrinolytic infusion, the activated partial thromboplastin time should be checked. Unfractionated heparin infusion should be restarted without a bolus when the activated partial thromboplastin time is less than 80 seconds. If greater than 80 seconds, the activated partial thromboplastin time should be rechecked every 4 hours until it falls into the range at which heparin can be safely restarted. Table 2. How to Administer Fibrinolytic Therapy for Submassive PEaPTT indicates activated partial thromboplastin time.• Initiate anticoagulation with intravenous unfractionated heparin bolus and continuous infusion with a target aPTT of 60–80 seconds as soon as submassive PE is suspected• Stop heparin infusion when issuing the order to administer fibrinolysis• Infuse recombinant tPA 100 mg over a 2-hour period with careful monitoring for bleeding complications, including neurological checks every 15 minutes during the infusion• Obtain immediate post–fibrinolytic infusion aPTT• After the fibrinolytic infusion has concluded, do not restart heparin until the aPTT is <80 secondsAlternative Advanced TherapiesAlternatives to fibrinolysis may be considered when contraindications to fibrinolysis exist or when patients have failed to respond to an initial trial of fibrinolytic therapy. Approximately half of all patients with acute PE have contraindications to fibrinolysis. Alternative advanced therapies include catheter-assisted embolectomy, surgical embolectomy, and IVC filter insertion.Catheter-assisted embolectomy is an emerging technique for advanced therapy when full-dose fibrinolysis has failed or is contraindicated.30,31 Catheter-assisted techniques, such as low-dose "local" fibrinolysis and thrombus fragmentation or aspiration, have the greatest success when applied to large, centrally located thrombi within the first 5 days of symptoms. The combination of local fibrinolysis with mechanical thrombectomy is called "pharmacomechanical therapy."32Surgical embolectomy requires a median sternotomy and cardiopulmonary bypass. Surgical embolectomy is most effective in patients with large, centrally located thrombi. Perioperative mortality for patients undergoing surgical embolectomy has declined over the last 2 decades.33 Surgical embolectomy has been shown to be a safe and effective technique in the treatment of acute PE when performed by experienced surgeons.34,35IVC filter insertion should be considered in patients with submassive PE in whom fibrinolysis and embolectomy are contraindicated or unavailable. IVC filter insertion reduces the incidence of recurrent PE but has not been shown to lower long-term mortality.36 IVC filters do not halt ongoing thrombogenesis and appear to increase the risk of deep vein thrombosis.36 Retrievable IVC filters offer a safe and effective alternative to permanent filters and may be removed up to several months after insertion.37Case Presentation (continued): The patient immediately received unfractionated heparin by intravenous bolus and then continuous infusion. After screening for contraindications to fibrinolysis was performed and after discussion with the patient and her family about their preferences, the decision was made to proceed with fibrinolysis for submassive PE. Our recommendation to proceed with fibrinolysis was predicated on a low risk of bleeding and an increased risk of death due to recurrent PE and RV failure with anticoagulation alone. Unfractionated heparin infusion was discontinued, and 100 mg of tPA was administered over a 2-hour period. The patient began having gingival oozing during tPA administration; this was managed with gauze packing. At approximately 1 hour into fibrinolysis, her chest pain and dyspnea abated. After completion of the fibrinolytic infusion and when the activated partial thromboplastin time was less than twice the upper limit of normal, unfractionated heparin infusion was restarted without a bolus as a "bridge" to anticoagulation with warfarin. At her 2-week office visit, the patient felt well and had no chest pain or shortness of breath. A follow-up transthoracic echocardiogram 6 weeks later demonstrated normal pulmonary artery systolic pressures and normal RV size and systolic function.Sources of FundingDr Piazza is supported by a Research Career Development Award (K12 HL083786) from the National Heart, Lung, and Blood Institute.DisclosuresNone.FootnotesCorrespondence to Gregory Piazza, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E-mail [email protected] References 1 Glynn RJ, Danielson E, Fonseca FA, Genest J, Gotto AM Jr, Kastelein JJ, Koenig W, Libby P, Lorenzatti AJ, MacFadyen JG, Nordestgaard BG, Shepherd J, Willerson JT, Ridker PM. A randomized trial of rosuvastatin in the prevention of venous thromboembolism. N Engl J Med. 2009; 360: 1851–1861.CrossrefMedlineGoogle Scholar2 Goldhaber SZ, Visani L, De Rosa M. 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A prospective long-term study of 220 patients with a retrievable vena cava filter for secondary prevention of venous thromboembolism. Chest. 2007; 131: 223–229.CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. 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