Asian Cardiovasc Thorac Ann 2007;15:149-153
© 2007 Asia Publishing EXchange Ltd
Surgical Embolectomy in Acute Massive Pulmonary Embolism
Ahmad A Amirghofran, MD,
Abbas Emami Nia, MD,
Ramin Javan, MD
Department of Cardiac Surgery, Shiraz University of Medical Sciences, Faghihi Hospital, Shiraz, Iran
For reprint information contact: Ahmad A Amirghofran, MD Tel: 98 917 111 0159 Fax: 98 711 235 5026 Email: amirghofranaa{at}yahoo.com, Department of Cardiac Surgery, Shiraz University of Medical Sciences, Faghihi Hospital, Shiraz, Iran.
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ABSTRACT
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Acute pulmonary embolism is a serious condition and despite diagnostic and therapeutic advances, mortality is still high. Anticoagulation, thrombolytic therapy, catheter embolectomy, and open pulmonary embolectomy are therapeutic options. Surgical embolectomy was considered the management of last resort, but recent studies show the effectiveness of this therapeutic modality. We reviewed our 7-year experience of pulmonary embolectomy in patients with acute massive pulmonary embolism from 1997 to 2004. Eleven patients underwent open embolectomy, 7 (64%) were male, and the mean age was 45.6 years. Pulmonary embolism occurred after major surgery in 5 patients (46%), 2 were diagnosed with malignancy and spinal cord injury, and no risk factors were detected in 4. The diagnosis was made by spiral computed tomography alone in 4 patients, and by angiography in 7. Cardiac arrest occurred in 3 patients preoperatively; 2 of them survived. Open pulmonary embolectomy is the most effective treatment for acute massive pulmonary embolism. Cardiac arrest is the worst prognostic factor. Less aggressive clot evacuation in patients who are diagnosed late appears to be effective in minimizing postoperative hemoptysis.
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INTRODUCTION
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Acute pulmonary embolism (PE) is considered a condition with high mortality. According to data published by the International Cooperation Pulmonary Embolism Registry in 1999, 2,454 patients with acute PE died within 90 days, most of these deaths were attributed to recurrent PE.1 Acute massive PE is an occlusion of the pulmonary artery (PA) by more than 50% of its cross-sectional area, resulting in hemodynamic compromise.2–5 Despite diagnostic and therapeutic advances, the rate of mortality due to acute PE remains as high as 30%.6–8 The mainstay of treatment of PE is anticoagulation with heparin. Other modalities include thrombolysis, catheter embolectomy, and surgical embolectomy. Thrombolytic therapy, although effective, is associated with a high rate of intracranial hemorrhage (3%).1 Catheter embolectomy that can be performed at the time of pulmonary angiography, is a good therapeutic modality but can fragment the embolus with further propagation into the peripheral pulmonary vasculature and increased risk of pulmonary hypertension.9 In the past, surgical embolectomy was known to be the last resort for management of PE. However, recent studies have questioned the validity of this belief and consider it an early modality.10 We describe our 7-year experience of 11 patients with acute massive PE who underwent emergency pulmonary embolectomy.
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PATIENTS AND METHODS
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All cases of acute massive PE who underwent emergency pulmonary embolectomy from 1997 to 2004 were reviewed retrospectively. The hospital records were reviewed for predisposing factors, time interval between the onset of symptoms and operation, preoperative evaluation, patients’ condition prior to surgery, operative technique, site of thrombi, morbidity, and mortality.
There were 11 patients with acute massive PE who underwent open pulmonary embolectomy (Table 1
). Seven (64%) patients were male, and the mean age was 45.6 years (range, 33 to 72 years). In 5 patients (45%), the event occurred following a surgical intervention: 2 (18%) had undergone recent coronary artery bypass grafting, one had brain surgery, one had aortic dissection surgery, and one had abdominoplasty. Two others were diagnosed with malignancy and spinal cord injury. No risk factors were found in 4 patients. The mean time between onset of symptoms and operation ranged from a few hours to 14 days (mean, 4.3 days; Table 2). The diagnosis was made by spiral computed tomography in 3 patients, one of whom underwent pulmonary angiography for confirmation. Seven patients were diagnosed by pulmonary angiography alone, and one was diagnosed intraoperatively. Transthoracic echocardiography was performed in 9 patients, which was indicative of embolism in all. Cardiac arrest occurred preoperatively in 3 patients and they entered the operating room on continuous cardiopulmonary resuscitation (CPR). Two patients were in a shock state, 5 were only dyspneic, and one had low cardiac output preoperatively.
All but one patient underwent sternotomy for the surgical approach. After pericardiotomy and full heparinization, the aorta and right atrium were cannulated and cardiopulmonary bypass (CPB) was instituted. In all patients, the embolectomy was carried out on a beating heart without aortic cross clamping. The main PA was opened longitudinally and retracted with Army-Navy retractors, especially to expose the right PA beneath the ascending aorta. In 2 patients, the right PA had to be opened between the aorta and the superior vena cava for better exposure. Russian forceps and ring forceps were used for removal of clots in the main pulmonary branches. Clots were removed from more distal branches by suction, a Fogarty catheter, or stone forceps (Figure 1). Irrigation and external lung compression were also used as additional maneuvers. These maneuvers were only occasionally found to be useful. Special care was taken to avoid damage to the already infarcted loose tissue in the distal pulmonary branches. In one patient who had an operation for aortic dissection 1 month prior to embolectomy, we chose the left thoracotomy approach to avoid obvious troublesome adhesions. Cardiopulmonary bypass was instituted between the femoral artery and vein in this patient, and the main PA was easily approached through the left thorax, with good exposure. In 6 patients, an inferior vena caval filter was inserted perioperatively; within 4 days after surgery in 5, and within 3 weeks in the other.
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Figure 1. The clot removed from the main pulmonary artery and its branches in one of the patients. Fragments are aligned to form the original shape.
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RESULTS
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Nine (82%) patients survived the operation and were discharged from the hospital. Two immediate deaths (18.18%) occurred in the operating room because of massive hemoptysis soon after weaning off CPB. One of these patients entered the operating room on CPR and the other had very low cardiac output. Both had symptoms of pulmonary embolism for several days, especially dyspnea for 4 and 7 days (Table 1
), and extensive embolectomy using forceps, a Fogarty catheter, and lung compression was carried out. A third death occurred one month postoperatively due to renal failure that was not a complication of surgery. The patient was discharged from the cardiac surgical service and later readmitted to the nephrology clinic. He was diagnosed with widespread malignancy and peritoneal seeding prior to death. Two other patients developed mild hemoptysis and recovered well during their hospital stay, with no sequelae. Another suffered hypoxic brain damage; she was still alive 5 years after the surgery but her most recent brain computed tomography scan showed diffuse brain atrophy.
Follow-up was completed in 6 of the 8 survivors. None of them had hemodynamic problems. One in whom an inferior vena caval filter was inserted, developed a repeat deep-vein thrombosis in the left lower extremity during the 3-year follow-up. This gradually improved to chronic organized thrombus, confirmed by both venography and color Doppler sonography. Postoperative complications were massive hemoptysis, (100 to 600 mL of blood per 24 hr) in 2 patients, mild hemoptysis (< 100 mL of blood per 24 hr) in 2, renal failure and hypoxic brain damage in one patient each. Two other patients who had symptoms for a relatively long time (2 and 3 days), underwent less aggressive clot evacuation and developed mild hemoptysis postoperatively.
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DISCUSSION
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Massive PE is defined as entrapment of a large embolus within the PA. If shock is induced, the mortality risk rises 3- to 7-fold; the majority of deaths occur within one hour of presentation.11 As the PA becomes obstructed, the increased afterload causes right ventricular strain and dilatation, hypokinesis, tricuspid regurgitation with annular dilatation of the tricuspid valve, and ultimately right ventricular failure.12,13 Pressure overload, however, causes a leftward shift of the interventricular septum, and together with pulmonary vasoconstriction results in decreased cardiac output and reduced blood oxygen content, and eventually, right ventricular ischemia, cardiac arrest, and death.14 Resumption of PA flow is the only way to interrupt this fatal cascade.
There is a wide consensus on using thrombolytics in massive PE, but controversy arises because reduced mortality has not yet been conclusively proved.8,13,15 However, these agents are contraindicated in up to 50% of patients because of recent surgery, trauma, stroke, hemorrhage, or CPR.16 According to the International Cooperative Pulmonary Embolism Registry, patients treated with a thrombolytic agent have an intracranial hemorrhage rate of 3%, which is a matter of great concern.1 Gulba and colleagues7 showed that patients treated with thrombolytics had higher rates of death, major hemorrhage, and recurrent embolism than their surgical counterparts. Generally, thrombolytic therapy should be given very cautiously to patients who are not potential candidates for open embolectomy.
Catheter embolectomy is a minimally invasive technique that can be performed during pulmonary contrast angiography. The clot is removed by suction of the PA through the jugular or femoral vein.9 Although a success rate of 80% was reported, available catheters tend to fragment the embolus, with distal showering of emboli to smaller inaccessible arterial branches, causing further pulmonary hypertension.9,17 Embolus recurrence is more common with this method than with open pulmonary embolectomy.18 The indications for surgical embolectomy are now extended beyond the traditional ones, such as failed medical therapy and contraindications to thrombolytics. In the past, open pulmonary embolectomy was the treatment of last resort for patients with PE, due to its high mortality rate. The average morbidity from different series between 1982 and 1999 was 30%.8 The approach has changed over time, and many centers are reporting open embolectomy as an integral part of their treatment algorithm for massive and submassive PE.10 A decrease of mortality after open pulmonary embolectomy from 57% in the 1960s to 6% in 2005 is proof of this.10,19 However, open pulmonary embolectomy is an immediate and definitive form of treatment for acute massive PE, with outstanding long-term results, and it should not be considered merely as a last resort.14 We performed transthoracic echocardiography as a fast, noninvasive, and available modality. It was performed early in the course of admission of all suspected cases. Any evidence of PE leads to further diagnostic evaluations. Few studies are available comparing medical versus surgical management of PE. In a nonrandomized comparison of surgical and medical treatment in hemodynamically compromised patients with massive PE, the medically treated group had a higher mortality rate, more hemorrhagic events, and a higher rate of recurrent PE.7
It has been shown in several studies that patients who enter the operating room on CPR have significantly higher mortality rates, compared to no CPR (73.7% vs 20%).20 There are two possible reasons for the poor prognosis in patients with CPR prior to surgery: there may be established organ dysfunction due to prolonged preoperative hypotension; and cardiac massage may displace a significant amount of embolic material into the distal pulmonary arterial tree, where it might be inaccessible.18
Massive hemoptysis was a major complication in this series and caused 2 deaths. Both of these patients had a delayed diagnosis (4 and 7 days from initial symptoms). Our explanation for this complication is that the clots in these patients had moved further peripherally and eventually caused infarction in lung parenchyma, due to the delayed diagnosis. This part of the lung becomes more susceptible to bleeding. Before beginning the operation, as the clots were fixed in place, no hemoptysis occurred. However, when we attempted to remove the clots aggressively from the distal branches using a Fogarty catheter and lung compression, the patient developed hemoptysis on weaning from CPB. This means that the connections between the capillaries and alveoli, which were produced due to parenchymal infarction, were filled with clots and we manually opened these connections. Consequently, bleeding into the respiratory system occurred. We applied this theory in the management of the last 2 patients who were diagnosed late (2 and 3 days). We exerted less aggressive clot evacuation, which resulted in only mild hemoptysis postoperatively. So, it appears reasonable to use less aggressive methods of clot removal from the peripheral vasculature in cases diagnosed late, to minimize the risk of massive hemoptysis.
We used stone forceps (Figure 2) for clot evacuation instead of ring forceps. This instrument, used by urologists to remove renal stones, has different sizes and tip angulations. This allows the surgeon to access more distant clots with a lower risk of fragmentation. We found this instrument to be very useful for gentle extraction of trapped particles of clot in medium-sized PA branches.
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Figure 2. Stone forceps used to evacuate renal stones. Different tip angles ease the evacuation of clots with minimal risk of fragmentation.
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Lack of transesophageal echocardiography in the operating room for evaluating residual clots after embolectomy was a limitation to our study. However, we assessed the amount of clot remaining by comparing PA pressure after embolectomy with normal PA pressure. As most cases have acute PE, adequate clot removal should result in near normal PA pressure; pressures above normal mean that some peripheral clots are still in place.
Sternotomy is considered the best approach for pulmonary embolectomy. Occasionally, due to prior surgery on the thorax and the resultant adhesion formation in the pericardium, as well as the urgency to reach the PA, this approach is not feasible. In one patient who had undergone surgery for aortic dissection, the PE had to be approached via a left thoracotomy. After femorofemoral cannulation, the left thorax was accessed. The main PA was easily characterized beneath the pericardium, and incised. This was much faster than dissecting adhesions through a sternotomy.
It was concluded from this experience that open pulmonary embolectomy is the most effective treatment for acute massive PE, and it should not be left as the last option. Cardiac arrest is the worst prognostic factor, especially if CPR is performed continuously prior to the operation. Less aggressive clot evacuation in patients who are diagnosed late seems to be good practice and an effective way of minimizing postoperative hemoptysis.
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ABSTRACT
INTRODUCTION
