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Interact CardioVasc Thorac Surg 2008;7:591-594. doi:10.1510/icvts.2008.176735 © 2008 European Association of Cardio-Thoracic Surgery
Expedient pulmonary embolectomy for acute pulmonary embolism: improved outcomesDivision of Cardiothoracic Surgery, Department of Surgery, Maimonides Medical Center, 4802 10th Avenue, 4th Floor, Brooklyn, NY 11219, USA Received 30 January 2008; received in revised form 8 April 2008; accepted 10 April 2008
*Corresponding author. Tel.: +1 (718) 283-7686; fax: +1 (718) 283-7392.
Indications regarding surgical pulmonary embolectomy for treatment of submassive/massive acute pulmonary embolism remain controversial. An institutional experience with pulmonary embolectomy for acute pulmonary embolism (APE) was reviewed. A retrospective analysis of all patients undergoing pulmonary embolectomy for APE from September 2004 to January 2007 was conducted. Demographic data, clinical presentation and outcomes were analyzed. Fifteen patients underwent surgery for APE over a period of 27 months [average age 59.6 (range 35–89) years, (seven male, eight female)]. Six (40%) patients were admitted with known APE and nine patients exhibited post admission APE (seven – after surgical procedures, two – after cerebrovascular accident). Clinical presentation included dyspnea (86.67%), hemodynamic instability requiring continuous vasopressor support (40%), echocardiographic evidence of right ventricular dilatation (80%). Ten patients undergoing early/expedient embolectomy all survived while delayed surgery in the other five patients (>24 h) was associated with 60% mortality. Expanding indications for early surgical pulmonary embolectomy has stemmed from reliable echocardiographic identification of right ventricular compromise and recognition of these findings as harbingers of subsequent hemodynamic embarrassment. Our series underscores the benefit of early consideration and performance of pulmonary embolectomy in these critically ill patients.
Key Words: Pulmonary embolism; Echocardiogram; Emergency
Despite improving diagnostic modalities and widespread efforts at prophylaxis, acute pulmonary embolism (APE) continues to be a common healthcare problem, with mortality rates reported as high as 15% [1–3]. Massive APE, associated with hemodynamic collapse, carries a mortality rate as high as 70% if not treated within the initial hours following diagnosis [4–7]. Additionally, patients surviving their initial APE have demonstrated significant late mortality (7% – 1 week, 13% – 1 month, and 18% – 3 months) [1]. Some authors accept this as an indication for early surgery with or without cardiopulmonary bypass (CPB). Mortality rate for patients undergoing embolectomy for massive APE ranges from 11–64% [8–10]. Submassive APE is typically associated with significant pulmonary arterial lumen obstruction (>50%), and echocardiographic evidence of right ventricular dilatation and/or hypokinesis [10, 11]. Increasingly, surgical embolectomy has been applied to these patients who exhibit borderline hemodynamic instability responsive to initial supportive measures [9–11]. We sought to examine our own experience with surgical pulmonary embolectomy for APE, in an attempt to identify patient characteristics and treatment modalities that affected clinical outcomes.
2.1. Study population A retrospective review identified 15 patients with APE who underwent pulmonary embolectomy between September 2004 and January 2007. Five patients underwent surgery >24 h (Group 1) after the diagnosis of APE had been made and 10 patients underwent surgery within 24 h of diagnosis (Group 2). Demographic data, co-morbidities, preoperative hemodynamic status, diagnostic studies, time to operating room from the time of diagnosis and postoperative outcomes were reviewed. Transesophageal echocardiogram was performed intraoperatively in all patients. Pulmonary embolectomy was performed using median sternotomy and standard cannulation/CPB techniques. Longitudinal arteriotomies of the main pulmonary artery and right pulmonary artery (between ascending aorta and superior vena cava) were performed in seven patients. The remaining eight patients underwent main pulmonary artery arteriotomy, extending into the left and right branches. Thromboembolectomy was accomplished by forcep extraction and irrigation of the pulmonary arterial tree. Fourteen cases were performed on normothermic CPB without aortic cross-clamping. The single patient with atrial septal defect repair required aortic cross clamping/arrest. Inferior vena cava filters were placed in all patients (preoperatively – 5, intraoperatively – 9, postoperatively – 1). Continuous values are expressed as mean±S.D., and the differences between the two groups were evaluated using unpaired t-test. Categorical differences in the two groups were evaluated using 2-test. For all tests a P-value <0.05 was considered significant.
Seven males and eight females were evaluated. Six (40%) patients were referred from nearby hospitals. In seven (46.6%) patients, APE was subsequent to either surgery or trauma within 6–15 days. Two (13.3%) patients suffered cerebrovascular accident (CVA) in the preceding 14 days. Nine (60%) patients experienced a recent change in clinical status, with significant predisposition to deep venous thrombosis (DVT). Acute DVT was documented by Duplex in 10 (66.7%) patients. One patient had a history of prior DVT. Eight (53.3%) patients required preoperative intubation. Computed tomography (CT) scan proved APE in all patients, 12 (80%) of which demonstrated a saddle embolism. Right ventricular dilatation/hypokinesis was demonstrated on echocardiography in 12 (80%) patients, of which six were borderline hemodynamically stable and, therefore, met criteria for the diagnosis of submassive APE. The remaining six patients with echocardiographic evidence of right ventricular strain proved hemodynamically unstable despite numerous supportive maneuvers and, therefore, met criteria for the diagnosis of massive APE. Overall, seven (47%) patients met criteria for massive APE and underwent embolectomy as their initial therapeutic option. Four (27%) patients initially received thrombolytic therapy with no improvement, and showed evidence of right ventricular strain on serial echocardiogram. Three (20%) patients bore contraindications to thrombolytic therapy (recent brain surgery – 1, subarachnoid hemorrhage – 1, upper GI bleed – 1). There was no difference between the groups in age, gender, preoperative use of trombolytics, vasopressors and ventilatory support and preoperative presence of right heart dysfunction (Table 1).
Patients in Group 2 required significantly less ventilator and intensive care unit days. Five (33.3%) patients suffered postoperative morbidities, including respiratory failure, pneumonia, sepsis, GI bleeding and pericardial effusion. Overall mortality was 20%. All three mortalities had delayed surgery (Group 1). Deaths were associated with prolonged ventilator support, pneumonia and multi-organ system failure. Of the twelve discharged patients, survival rate at a mean follow-up time of eight months was 100%.
Standard initial therapy for PE of any type remains anticoagulation with heparin. Thrombolytic therapy has traditionally been reserved for massive APE, but has not convincingly reduced the mortality. Additionally, thrombolytic therapy is fraught with twice the risk of significant hemorrhage when compared to heparin anticoagulation [1, 7, 13, 14]. Surgical embolectomy has been considered only for massive APE. Some authors have, though, questioned the overall role of this treatment and have alternatively suggested the use of right heart catheter techniques [1, 5, 12]. These techniques, however, could be associated with thrombus fragmentation, distal embolization, and excessive mortality rates as high as 30% [12]. The role of acute surgical embolectomy for submassive APE has been addressed by a number of authors [10–12]. They emphasize the importance of the central position of the clot in patients considered for surgery [11]. Improved interpretation of echocardiography has provided new insights for timing of surgical intervention. Identification of right ventricular compromise with chamber dilatation/hypokinesis is now recognized as a harbinger of subsequent circulatory collapse. With early recognition of impending circulatory failure, an opportunity for emergent surgery appears to be of benefit for both in-hospital patients and those from neighboring institutions where CPB is not available. In our series, one-third of patients had delayed (>24 h) pulmonary embolectomy (Group 1) and sustained a 60% mortality rate. This resulted from delayed diagnosis or untimely surgical intervention. Clearly, willingness to consider and perform surgical embolectomy early is paramount to patient survival. None of the ten (Group 2) patients undergoing surgical embolectomy within 24 h of APE endured any major morbidity or mortality. Since the benefits of surgical intervention diminish sharply 24 h following APE diagnosis, our clinical approach involves strong consideration of emergent surgery in patients with early hemodynamic changes and echocardiographic proof of right ventricular dysfunction/hypokinesis (Fig. 1).
Complete extraction of all pulmonary thrombus including fragments in the distal pulmonary tree was effective in reestablishing forward pulmonary flow and decompression of the obstructed right ventricle. Persistence in removal of distal thrombi is important and requires repetitive distal irrigation and thrombus removal by a variety of techniques including forceps extraction, repetitive irrigation and Fogarty embolectomy. We recognize that the patient sample size and retrospective nature of this report is a limitation. However, given the acuteness, severity and relative infrequency of massive and submassive APE, it is unlikely that any significant randomized study comparing medical vs. surgical options will be forthcoming. Our experience with this severely ill group of patients suggests that traditional heparin anticoagulation with or without thrombolytic therapy is not the optimal treatment. The results of the study support an early surgery for patients with massive or submassive APE following echocardiographic proof of right heart dilation/dysfunction or signs of impending circulatory decompensation.
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