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Vascular Medicine 2002; 7: 181–185 Massive pulmonary embolism: a remarkable case and review of treatment Joshua M Cooper and Joshua A Beckman Abstract: Although the clinical syndrome following pulmonary embolism (PE) may be subtle, in the case of massive PE the severity of the clinical presentation typically makes the picture more obvious. If more than two lobar pulmonary arteries become obstructed, the hemodynamic and respiratory consequences are severe, and may be life threatening. We present an unusual case where a patient experienced transient hemodynamic collapse during valsalva, and a massive saddle pulmonary embolus was discovered incidentally. Current treatment options for massive PE are then discussed. Key words: pulmonary embolism; thrombectomy/embolectomy; thrombolysis Case report A 68-year-old man presented to the emergency department because of a syncopal episode. At a health club with friends, just after using the leg press machine, he suddenly lost consciousness for 30 seconds. He reported no symptoms either before or after the syncopal episode. His friends took him out for dinner, and then brought him to the emergency department, where he began to experience mild chest pains which radiated to his upper back. His past medical history was signi cant for prostate cancer, treated with radical prostatectomy four years previously. He had no history of cardiovascular or pulmonary disease. He took no medications, did not smoke, and exercised daily without symptoms. In the emergency department, his pulse was 95 beats per minute, blood pressure was 112/64 mmHg, and respirations were 14 breaths per minute, with 98% oxygen saturation on room air. Signi cant physical ndings included a jugular venous pressure of 8 cm water, symmetric pulses and blood pressures, a normal lung exam, a normal cardiac exam, no edema or cyanosis, and intact radial and pedal pulses. His electrocardiogram revealed normal sinus rhythm, normal axis, normal intervals, and an occasional premature ventricular contraction with fusion. Laboratory values were remarkable as follows: creatinine 1.5 mg/dl, creatine kinase 695 U/l with ,1% MB fraction, and troponin I 1.1 ng/ml (normal 0–0.08). Because of the concern for aortic dissection as an explanation for intrascapular pain and syncope, a spiral CT scan with intravenous contrast was obtained. The CT scan revealed a massive saddle pulmonary embolus (Figure 1). In addition, the abdominal images demonstrated a 9.3 3 7.6 cm mass in the left kidney, with thrombus seen lling a left renal vein, extending to the midline and into the Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA Address for correspondence: Joshua A Beckman, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USA. Tel: +1 617 732 6186; Fax: +1 617 232 2749; E-mail: [email protected] Ó Arnold 2002 suprarenal inferior vena cava (Figure 2). Urgent echocardiography revealed normal left ventricular size and function with an ejection fraction of 50%. The interventricular septum was mildly attened and there was hypokinesis of the anterior free wall of the right ventricle, suggestive of right ventricular (RV) pressure overload. There was mild tricuspid regurgitation with a peak velocity of 3.5 m/s, indicative of a RV systolic pressure of 49 mmHg plus right atrial pressure. Because of the location and size of the embolus, surgical removal was felt to be the best treatment strategy. In the operating room, transesophageal echocardiography con rmed the presence of a massive saddle pulmonary embolus, extending into and nearly obstructing both the right and left main pulmonary arteries (Figure 3). Mild RV strain was noted. The patient underwent pulmonary embolectomy with complete removal of central venous thrombus, as well as left radical nephrectomy an inferior vena cava thromboectomy. Pathological evaluation of the renal mass revealed renal cell carcinoma, and the embolus contained a mixture of renal cell carcinoma and brin. Surgical resection margins revealed neither local invasion nor tumor-laden lymph nodes. The patient recovered and was discharged 6 days postoperatively on warfarin. He remained asymptomatic with no clinical evidence of tumor recurrence until 15 months later, when he was found to have hepatic and pulmonary metastases. Discussion PE remains a clinically challenging diagnosis, more often missed than found, with no decline in its incidental discovery at autopsy over the past 30 years.1 The 3-month mortality after PE is as high as 17%,2 and outcomes are closely linked to the degree of pulmonary vascular obstruction and resulting RV strain.3 As the extent of obstruction approaches 75%, the right ventricle must generate a systolic pressure in excess of 50 mmHg to preserve perfusion, a task that a normal right ventricle cannot accomplish acutely.4 When pulmonary artery obstruction overwhelms 10.1191/1358863x02vm441cr 182 JM Cooper and JA Beckman Figure 1 Computed tomography scan of the chest demonstrating a ‘saddle’ pulmonary embolus extending into the right and left main pulmonary arteries. Figure 2 Computed tomography scan of the abdomen demonstrating a left renal mass and thrombus in the left renal vein (arrows). (IVC, inferior vena cava.) the ability of the right ventricle to maintain cardiac output and adequate left ventricular lling, hemodynamic collapse rapidly occurs; 85% of deaths from massive PE occur within the rst 6 hours.4 The goal of therapy in massive PE is an improvement in forward ow and a reduction in RV afterload to avoid right Vascular Medicine 2002; 7: 181–185 ventricular failure. By reducing the degree of occlusion in the pulmonary vasculature and minimizing the humoral vasoconstrictors that emanate from intravascular thrombus, pulmonary vascular resistance and pulmonary artery pressure fall. Increasing the patent pulmonary artery cross-sectional area is the goal of every treatment strategy in massive Massive pulmonary embolism 183 Figure 3 Intraoperative echocardiogram. The ultrasound transducer is placed directly on the pulmonary artery at its main bifurcation. The thrombus almost completely occludes both the right and left main pulmonary arteries. PE. The three main modalities of reducing obstruction include thrombolysis, clot fragmentation, and clot removal. Treatment selection depends on several factors, including risk of bleeding, stability of the patient, resource availability, and the speci c characteristics of the thrombus burden. Thrombolysis Thrombolytic agents activate plasminogen to form plasmin on the surface of brin clots, resulting in brinolysis. This brin degradation occurs at the blood-thrombus interface and causes dissolution of the clot on its exposed surfaces. As the thrombus shrinks and fragments, it embolizes distally in the pulmonary arterial tree, while brinolysis continues. Thrombolytic therapy has been demonstrated to reduce clot burden in patients with PE more rapidly than heparin alone.5 There is no evidence that infusion of a thrombolytic agent into the pulmonary artery has any advantage over intravenous administration.6 The Food and Drug Administration has approved the use of urokinase (4400 IU/kg intravenously over 10 minutes, then 4400 IU/kg per hour for 12 hours), streptokinase (250 000 IU intravenously over 30 minutes, then 100 000 IU/hour for 24 hours), and tissue plasminogen activator (100 mg intravenously over 2 hours) for the treatment of PE. Systemic anticoagulation should be instituted after thrombolytic administration when the partial thromboplastin time is twice normal. The American Heart Association has issued a scienti c statement that recommends the consideration of thrombolysis for major PE in the setting of syncope, hypotension, severe hypoxemia, or heart failure.7 The data that demonstrate a mortality reduction from PE thrombolysis are quite sparse.8 There is only one randomized trial that studied patients with massive PE and hemodynamic collapse.9 It showed a strong life-saving effect of thrombolysis in this population, and was stopped after only eight patients were enrolled. In hemodynamically Vascular Medicine 2002; 7: 181–185 stable patients with major PE and RV dysfunction, thrombolysis has been retrospectively demonstrated to reduce 30day mortality.1 0 The bene t in this population is thought to be due to rapid improvement in lung perfusion demonstrated via improved RV function after thrombolysis, shown echocardiographically.1 1 This improvement in mortality, however, has not been universally reported,1 2 so thrombolysis for PE in hemodynamically stable patients with RV dysfunction remains controversial. Major hemorrhage remains the main risk of thrombolytic agents. The risk of intracranial hemorrhage has varied from 1.5% to 3% in various trials and registries.8 Major bleeding was seen in 22% of patients after thrombolysis in a large international PE registry.1 3 Because of the lack of randomized control trial data, the decision to use a thrombolytic agent for massive PE needs to be made on an individual case basis, with attention paid to risk factors for hemorrhage. Catheter fragmentation There are many different catheter designs that have been invented to attempt percutaneous fragmentation of a massive central pulmonary artery clot burden.1 4 The rationale of fragmentation involves clot embolization further into the pulmonary tree, where the total cross-sectional area of the vasculature is larger.1 4 It has also been pointed out, however, that the total obstructive cross-sectional area of the fragmented clot would potentially become much greater, which could more than offset the purported bene t of distal embolization.1 5 In fact, reports of pure clot fragmentation typically record either an unchanged or an increased pulmonary artery pressure immediately following the procedure.1 6 ,1 7 Most studies of mechanical disruption, however, have used adjunctive thrombolytic therapy. This combination treatment seems to be effective in restoring clinical and hemodynamic parameters in acutely ill patients with mas- 184 JM Cooper and JA Beckman sive PE.1 8 ,1 9 Theoretically, thrombolysis should proceed at a faster rate with the larger exposed surface area of fragmented thrombus. Technical problems with various fragmentation devices have included vascular wall damage, dif culty with device positioning, and the inability to adequately disrupt large or old thrombi. There are no randomized trials to clarify whether mechanical fragmentation is a useful component of acute therapy, whether or not thrombolytics are used. Catheter thrombectomy Thrombectomy is the ultimate goal of therapy for massive PE. The rst device to percutaneously extract intact thrombi used a metal suction cup, introduced either from the leg or the neck.2 0 Although a number of patients had successful clot extractions with this device and immediate hemodynamic improvement,2 1 this procedure has limitations. It requires a venous cutdown, can be complicated by reembolization of the clot being extracted or inability to access certain branches of the pulmonary artery, and there may be dif culty in removing old thrombus. Devices have also been designed that use Venturi jets to pulverize and aspirate thrombus material from the pulmonary arteries.2 2 ,2 3 While these catheters have been successfully used to remove a small percentage of thrombus material from fresh pulmonary artery emboli, the small catheter size (5 French) limits their ability to treat large central thrombi adequately. In addition, there can be a signi cant amount of blood aspiration with a prolonged procedure, and clots that have already formed stable brin crosslinks are not amenable to disruption by this method. Surgical embolectomy While surgical removal of a massive central pulmonary arterial embolus is the most de nitive treatment, it is also the most invasive. The decision to proceed to the operating room is dependent on the prompt availability of surgical resources, and it requires the surgeon to accept the signi cant possibility of a poor outcome. It is because of these issues that randomized trials have not been done and that the reported case series are necessarily affected by selection bias. Surgical embolectomy is typically reserved for the hemodynamically unstable patient, sometimes after failed thrombolysis. In one non-randomized case series of patients with massive PE complicated by shock, surgical therapy yielded a slightly lower mortality when compared with thrombolysis.2 4 The main predictor of mortality in patients undergoing surgical pulmonary embolectomy is pre-operative cardiac arrest requiring resuscitation. Patients with hemodynamic collapse prior to surgery have an operative mortality ranging from 43% to 84%.2 5 More recently, Aklog and colleagues reported the results of 29 consecutive patients with massive proximal PE, RV dysfunction, but preserved hemodynamics.2 6 In this setting, 89% of the patients were alive more than 1 month after surgery. Use of cardiopulmonary bypass may also improve survival.2 7 Conclusion Massive PE requires urgent therapy to restore pulmonary arterial ow. In the absence of treatment, mortality from Vascular Medicine 2002; 7: 181–185 PE remains high.2 8 Anticoagulation is the standard of care for PE, with the addition of thrombolysis or surgical embolectomy when the clot burden and clinical presentation warrant more aggressive treatment. Catheter-based treatments have not shown any additional therapeutic bene t. The optimal strategy for treating tumor-containing massive PE is unknown. In this case, we felt surgical removal of the saddle PE was most appropriate. The patient was hemodynamically stable, reducing the likelihood of intraoperative mortality. The PE was likely to be partially composed of carcinoma, making the prediction of the ef cacy of thrombolysis or the consequence of promoting distal embolization of tumor-containing material impossible. 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