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Massive Pulmonary Embolism: Percutaneous Mechanical Thrombectomy during Cardiopulmonary Resuscitation
Massive Pulmonary Embolism: Percutaneous Mechanical Thrombectomy during Cardiopulmonary Resuscitation Mario Fava, MD, Soledad Loyola, MD, Hernán Bertoni, MD, and Alberto Dougnac, MD Seven patients with massive pulmonary embolism (PE) causing cardiac arrest underwent percutaneous mechanical thrombectomy (PMT) with Hydrolyser and Oasis catheters during cardiopulmonary resuscitation (CPR). Three received adjunctive recombinant tissue plasminogen activator. Thrombectomy was successful in restoring pulmonary perfusion in six patients (85.7%). One patient died of cardiac arrest. Systolic pulmonary pressure decreased after thrombectomy from a median of 73 mm Hg (range, 63–90 mm Hg) to 42 mm Hg (range, 32– 81 mm Hg; P < .05). There was one groin hematoma that required blood transfusion. In conclusion, massive PE causing cardiac arrest can be treated with PMT simultaneously with CPR maneuvers to rapidly revert circulatory collapse, with restoration of pulmonary circulation. Larger series are needed to validate this method. J Vasc Interv Radiol 2005; 16:119 –123 Abbreviations: CPR ⫽ cardiopulmonary resuscitation, PE ⫽ pulmonary embolism, PMT ⫽ percutaneous mechanical thrombectomy, rt-PA ⫽ recombinant tissue plasminogen activator
PULMONARY embolism (PE) causes or contributes to 50,000 –200,000 deaths per year in the United States (1,2). The mortality rate for massive PE producing shock is approximately 30% (3). It is one of the most frequent noncardiac causes of cardiac arrest (4), with mortality rates ranging from 65% to 95% in reported series (2,4). In fatal cases, the majority of deaths occur within 1 hour of presentation (2). This clinical situation is similar to the “golden hour” of myocardial infarction, stroke, and trauma, during which a timely approach to diagnosis and treatment of
massive PE with cardiac arrest can change the outcome (2). Percutaneous mechanical thrombectomy (PMT) and fragmentation are therapeutic options for patients with massive PE that have been used especially when there are contraindications to thrombolytic drugs. These mechanical therapies can help to immediately reverse cardiac arrest (5–9). The purpose of this article is to present our clinical experience in the treatment of massive PE causing cardiac arrest. We used PMT simultaneously with cardiopulmonary resuscitation (CPR).
MATERIALS AND METHODS From the Department of Interventional Radiology (M.F., S.L.) and Intensive Care Unit (A.D.), P. Universidad Catolica de Chile, Marcoleta #367, Santiago, Chile; and Department of Interventional Radiology (H.B.), Hospital Italiano, Buenos Aires, Argentina. Received March 18, 2004; revision requested June 3; final revision received and accepted September 3. From the SIR 2003 Annual Meeting. Address correspondence to M.F.; E-mail: fava@ med.puc.cl None of the authors have identified a conflict of interest. © SIR, 2005 DOI: 10.1097/01.RVI.0000146173.85401.BA
Patient Group Seven patients (four women, three men) with a mean age of 56 years (range, 30 –79 years) with sudden cardiac arrest secondary to massive PE were treated with PMT during CPR. All patients had pulseless electrical activity on initial assessment. Risk factors for thromboembolic disease in these patients were deep venous thrombosis in four patients, recent major surgery in two patients (cardiac
transplantation and hemicolectomy), prolonged immobilization in two, major trauma (femoral neck fracture) in one, and hypercoagulability in one. Four patients had contraindications to thrombolytic agents (two with recent major surgeries, one with major trauma, and one because of recent postpartum status). The other three patients received recombinant tissue plasminogen activator (rt-PA) after thrombectomy. The diagnosis of massive PE was established in three patients with computed tomographic (CT) angiography before the occurrence of cardiac arrest. Two cases studied with echocardiography before cardiac arrest demonstrated right ventricle failure. In the other four cases, clinical diagnosis was confirmed angiographically. All patients were transferred to the angiography suite during CPR to rapidly initiate therapy. CPR maneuvers were performed synchronously with PMT. The intensive care unit team and interventionalists worked coordinated on both sides of the table and there were instances in which PMT and cardiac compressions were performed simultaneously with fluoroscopy.
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Thrombectomy during CPR in Massive Pulmonary Embolism
Devices At random, the Hydrolyser thrombectomy catheter (6,8) (Cordis, Miami, FL) was used in four cases, and the Oasis thrombectomy catheter (8) (Boston Scientific, Galway, Ireland) was used in three cases. These devices are hydraulic recirculation PMT devices that use the Venturi effect. Heparinized saline solution is injected with an angiographic mechanical injector at 2.5–3.0 mL/sec at 750 psi through a narrow injection lumen that ends in a hairpin loop at the distal end of the catheters, which produce a Venturi effect that fragments adjacent thrombus and directs the debris to a evacuation lumen.
Semiquantitative estimation of removed thrombi was performed with use of a computer program developed for this purpose. The program calculates the thrombi-occluded area in the pulmonary arterial tree as a percentage with use of a standard diagram that was “shadowed” in thrombi-occluded areas (6). Institutional review board approval in our institution is not required for retrospective reports such as this. Study Endpoints The study endpoint was mortality equal or superior to that expected for cardiac arrest secondary to massive PE without endovascular recanalization.
Technique The access to pulmonary arteries was obtained by unilateral (n ⫽ 4) or bilateral (n ⫽ 3) common femoral vein puncture (Seldinger technique) with use of 6-F pigtail catheter(s). Nonionic contrast medium (Radiomiron 370; Schering, Berlin, Germany) was administered. Pulmonary arterial pressures were measured before and after PMT. The procedure was performed through an 80-cm, 8-F or 10-F sheath (Super Arrow-Flex Percutaneous Sheath Introducer Set; Arrow International, Reading, PA) selectively positioned to reach the thrombi. The thrombectomy catheters were positioned in the thrombus and moved in a forward/backward movement in the main and lobar arteries. Eight to 12 passes in a back-and-forth motion were performed with the Hydrolyser and Oasis catheters. Each pass takes 30 – 40 seconds. In the three cases with no contraindication to thrombolytic therapy, rt-PA (Actilyse; Boehringer Ingelheim, Ingelheim, Germany) was infused directly into the thrombus after PMT (10-mg bolus and infusion of 10 mg/h during 4 hours; total, 50 mg). The Urokinase Pulmonary Embolism Trial angiographic severity index was calculated (10). This index has a maximum value of 18, which corresponds to complete occlusion of both pulmonary arteries. An occlusion of two or more lobar arteries (index ⬎5) or equivalent smaller branches is angiographically considered a massive PE.
Statistical Analysis Data were analyzed with the use of the Wilcoxon test for paired values. A P value ⬍.05 was considered statistically significant. Results are presented as median values with ranges in parentheses.
RESULTS PMT was successful in restoring of pulmonary perfusion in six patients (85.7%). Duration of CPR was 10 –35 minutes, with a median of 25 minutes. The PMT devices’ activation time was 6 minutes (4 – 8 minutes). Injected saline solution volume during PMT was 300 – 400 mL. Recovered volume in the bag was 200 –300 mL. Systolic pulmonary artery pressure decreased from a median of 73.0 mm Hg (90 – 63 mm Hg) to 42 mm Hg (32– 81 mm Hg) immediately after thrombectomy (P ⬍ .05), and in three patients, pressure decreased to 34 mm Hg (33–36 mm Hg) after rt-PA infusion (P ⫽ NS). The Urokinase Pulmonary Embolism Trial Angiographic Severity Indexes (10) before and after PMT were 15 (14 –16) and 7 (5–10), respectively (P ⫽ .022). A median of 60% of thrombus (40%–70%) was removed, calculated by semiquantitative computer analysis. No difference was observed in quantity of thrombus removed between the Hydrolyser and Oasis thrombectomy devices.
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Complications There were no major complications directly related to PMT. Two patients treated with rt-PA developed a hematoma at the puncture site; one required transfusion of 2 U of blood. One patient did not recover from cardiac arrest caused by massive PE and died during the CPR and PMT procedure. Another patient had a brain infarction secondary to cardiac arrest but survived. Six patients were discharged within 30 days. A representative case is illustrated in Figure 1.
DISCUSSION Although its frequency is not well established, massive PE is one of the most frequent noncardiac causes of cardiac arrest (4,11). In a study by Wood (3) that included PE with pulmonary hypertension or right heart failure caused by massive PE, the incidence of cardiac arrest was 18%. In the series by Miller et al (12), cardiac arrest occurred in 29% of patients. Kurkciyan et al (4) established that massive PE causes 14.6% of cases of cardiac arrest of extracardiac origin. In the majority of cases of massive PE with cardiac arrest, there is pulseless electric activity/electromechanical dissociation and asystole (4,11). Comes et al (11) found that massive PE caused 36% of cases of unexplained sudden cardiac arrest among patients who had pulseless electric activity as the initial rhythm (11). In our series, all seven patients presented with pulseless electric activity and electromechanical dissociation. Mortality rates in massive PE when causing cardiac arrest are extremely high, as high as 70% in some series (3,11). Cardiac arrest will occur within 1–2 hours after the onset of clinical presentation in two thirds of fatal massive PE cases (1). A prompt clinical diagnosis of massive PE and treatment is necessary for optimal treatment in this “golden hour” (2). CPR maneuvers in these cases should be accompanied by causative treatment. When a patient’s condition is hemodynamically compromised, diagnostic methods as CT angiography, magnetic resonance angiography, and ventilation/perfusion lung scan are time-consuming. Echocardiography in patients in hemodynamically unstable
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Figure 1. (a) Initial pulmonary angiography shows bilateral thrombi with upper right lobe and lower left lobe occlusion and lower right lobe partial obstruction. Swan-Ganz catheter tip is seen in lower right pulmonary artery. (b) Bilateral PMT catheters were positioned during cardiac massage. (c) Left pulmonary thrombectomy with Hydrolyser Thrombectomy Catheter is shown, through a guiding catheter that enables contrast material injection to monitor response to thrombectomy. (d) Control image of PMT in left lower lobe artery shows partial recanalization. (e) The thrombectomy catheter is in a right upper lobe artery. (f) Final angiography shows patent right upper lobe artery.
condition is useful in assessing the severity of massive PE (2). Currently available data do not indicate that thrombolysis contributes to a significant increase in bleeding complications when administered during CPR. Other publications support the use of thrombolytic drugs during CPR (13) even though hemorrhagic complications occur; but considering the poor prognosis of patients with cardiac arrest, the possible benefits of thrombolysis outweigh the potential risks (14). We used rt-PA in three patients with no contraindication to thrombolytic drugs, with the rationale to remove the fragments of thrombus that migrated distally to the segmental and
more peripheral branches that were not reached by the PMT devices. PMT is a minimally invasive therapeutic option when thrombolytic drugs are contraindicated. PMT has maturated into a reliable and valuable therapeutic tool in acute vascular diseases. PMT devices are designed to achieve rapid clearance of acute occlusion in large vessels. PMT in massive PE provides efficacious and safe debulking of occlusive centrally located thrombus in pulmonary arteries, decreasing pulmonary artery pressure and improving hemodynamics (6,8). Its utility is limited in wall-adherent thrombi that are not occlusive because the catheters advance through the ad-
jacent patent lumen. The access to more peripheral pulmonary branch thrombi is difficult because of the rigidity of the thrombectomy catheters. Additionally, vessel wall disruption has been described experimentally with the AngioJet device (Possis, Minneapolis, MN) in vessels smaller than 6 mm (ie, segmental arteries) (15). More detailed descriptions of different devices are available in the literature (8,9). A small number of patients with massive PE treated with PMT are described in the literature (8). Major series used the Greenfield thrombectomy device, Amplatz thrombectomy device (7), Hydrolyser (6), and rotatable pigtail catheter. All had good clin-
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10-F sheath) and the use of thrombolytic drugs. The patient who died did not recover from cardiac arrest. There was no hemoptysis related to the PMT procedure. We have proposed an algorithm for the diagnosis and treatment of patients with cardiac arrest and suspected massive PE (Fig 2). In summary, PMT treatment of massive PE causing cardiac arrest can be performed simultaneously with CPR and is useful to reverse circulatory collapse. In this group of patients, there was a lower mortality rate than was expected. PMT can remove a significant volume of thrombi, sufficient to reverse cardiac arrest. PMT offers an alternative to surgical thrombectomy and pharmacologic thrombolysis, especially when there are contraindications to thrombolytic drugs. The reported technique will probably be improved in the future and warrants more evaluation.
Figure 2. Proposed algorithm for massive pulmonary embolism. Note.—PEA/EMD ⫽ pulseless electrical activity/ electromechanical dissociation; ECHO ⫽ echocardiography; RV ⫽ right ventricle.
ical results, with rapid restoration of pulmonary blood flow and decreased associated mortality. To our knowledge, there are no comparative studies of efficacy and safety among devices (ie, Amplatz TD, AngioJet, and rotatable pigtail catheter).
Complications There were no major complications directly related to PMT. The hematoma in the puncture site could result from the size of devices (most of the procedures were performed through a
References 1. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Prog Cardiovasc Dis 1975; 17:257–270. 2. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest 2002; 121:877–905. 3. Kasper W, Konstantinides S, Geibel A, et al. Management strategies and determinant of outcome in acute major pulmonary embolism: results of a multicenter registry. J Am Coll Cardiol 1997; 30:1165–1171. 4. Kurkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med 2000; 160:1529 –1535. 5. Elliot GC. Embolectomy, catheter extraction or disruption of pulmonary emboli. Curr Opin Pulm Med 1995; 1:298 –302. 6. Fava M, Loyola S, Huete I. Massive pulmonary embolism: treatment with the Hydrolyser thrombectomy device. J Vasc Interv Radiol 2000; 11:1159 – 1164. 7. Muller-Hulsbeck S, Brossmann J, Jahnke T. Mechanical thrombectomy of major and massive pulmonary embolism with use of Amplatz Thrombectomy device. Invest Radiol 2001; 36: 317–322. 8. Fava M, Loyola S. Applications of percutaneous mechanical thrombectomy (PMT) in pulmonary embolism. Tech Vasc Interv Radiol 2003; 6:53–58. 9. Sharafuddin MJA, Hicks ME. Current status of percutaneous mechanical
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thrombectomy. Part II: devices and mechanisms of action. J Vasc Interv Radiol 1998; 9:15–31. 10. Walsh PN, Greenspan RH, Simons M, et al. An angiographic severity index for pulmonary embolism. The Urokinase Pulmonary Embolism Trial: a national cooperative study. Circulation 1973; 47(suppl II):II101–II108. 11. Comes KA, De Rook FA, Rusell ML, et al. The incidence of pulmonary embolism in unexplained sudden cardiac
Fava et al
arrest with pulseless electrical activity. Am J Med 2000; 109:351–356. 12. Miller GA, Hall RJ, Paneth M. pulmonary embolectomy, heparin, and streptokinase: their place in the treatment of acute massive pulmonary embolism. Am Heart J 1977; 93:568 –574. 13. Spohr F, Bottiger B. Safety of thrombolysis during cardiopulmonary resuscitation. Drug Saf 2003; 26:367–379. 14. Janata K, Holzer M, Kurkciyan I, et al. Major bleeding complications in car-
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diopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism. Resuscitation 2003; 57:49 –55. 15. Biederer J, Schoene A, Reuter M, Heller M, Müller-Hülsbeck S. Suspected pulmonary artery disruption after transvenous pulmonary embolectomy using a hydrodynamic thrombectomy device: clinical case and experimental study on porcine lung explants. J Endovasc Ther 2003; 10:99 –110.
PULMONARY embolism (PE) causes or contributes to 50,000 –200,000 deaths per year in the United States (1,2). The mortality rate for massive PE producing shock is approximately 30% (3). It is one of the most frequent noncardiac causes of cardiac arrest (4), with mortality rates ranging from 65% to 95% in reported series (2,4). In fatal cases, the majority of deaths occur within 1 hour of presentation (2). This clinical situation is similar to the “golden hour” of myocardial infarction, stroke, and trauma, during which a timely approach to diagnosis and treatment of
massive PE with cardiac arrest can change the outcome (2). Percutaneous mechanical thrombectomy (PMT) and fragmentation are therapeutic options for patients with massive PE that have been used especially when there are contraindications to thrombolytic drugs. These mechanical therapies can help to immediately reverse cardiac arrest (5–9). The purpose of this article is to present our clinical experience in the treatment of massive PE causing cardiac arrest. We used PMT simultaneously with cardiopulmonary resuscitation (CPR).
MATERIALS AND METHODS From the Department of Interventional Radiology (M.F., S.L.) and Intensive Care Unit (A.D.), P. Universidad Catolica de Chile, Marcoleta #367, Santiago, Chile; and Department of Interventional Radiology (H.B.), Hospital Italiano, Buenos Aires, Argentina. Received March 18, 2004; revision requested June 3; final revision received and accepted September 3. From the SIR 2003 Annual Meeting. Address correspondence to M.F.; E-mail: fava@ med.puc.cl None of the authors have identified a conflict of interest. © SIR, 2005 DOI: 10.1097/01.RVI.0000146173.85401.BA
Patient Group Seven patients (four women, three men) with a mean age of 56 years (range, 30 –79 years) with sudden cardiac arrest secondary to massive PE were treated with PMT during CPR. All patients had pulseless electrical activity on initial assessment. Risk factors for thromboembolic disease in these patients were deep venous thrombosis in four patients, recent major surgery in two patients (cardiac
transplantation and hemicolectomy), prolonged immobilization in two, major trauma (femoral neck fracture) in one, and hypercoagulability in one. Four patients had contraindications to thrombolytic agents (two with recent major surgeries, one with major trauma, and one because of recent postpartum status). The other three patients received recombinant tissue plasminogen activator (rt-PA) after thrombectomy. The diagnosis of massive PE was established in three patients with computed tomographic (CT) angiography before the occurrence of cardiac arrest. Two cases studied with echocardiography before cardiac arrest demonstrated right ventricle failure. In the other four cases, clinical diagnosis was confirmed angiographically. All patients were transferred to the angiography suite during CPR to rapidly initiate therapy. CPR maneuvers were performed synchronously with PMT. The intensive care unit team and interventionalists worked coordinated on both sides of the table and there were instances in which PMT and cardiac compressions were performed simultaneously with fluoroscopy.
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Thrombectomy during CPR in Massive Pulmonary Embolism
Devices At random, the Hydrolyser thrombectomy catheter (6,8) (Cordis, Miami, FL) was used in four cases, and the Oasis thrombectomy catheter (8) (Boston Scientific, Galway, Ireland) was used in three cases. These devices are hydraulic recirculation PMT devices that use the Venturi effect. Heparinized saline solution is injected with an angiographic mechanical injector at 2.5–3.0 mL/sec at 750 psi through a narrow injection lumen that ends in a hairpin loop at the distal end of the catheters, which produce a Venturi effect that fragments adjacent thrombus and directs the debris to a evacuation lumen.
Semiquantitative estimation of removed thrombi was performed with use of a computer program developed for this purpose. The program calculates the thrombi-occluded area in the pulmonary arterial tree as a percentage with use of a standard diagram that was “shadowed” in thrombi-occluded areas (6). Institutional review board approval in our institution is not required for retrospective reports such as this. Study Endpoints The study endpoint was mortality equal or superior to that expected for cardiac arrest secondary to massive PE without endovascular recanalization.
Technique The access to pulmonary arteries was obtained by unilateral (n ⫽ 4) or bilateral (n ⫽ 3) common femoral vein puncture (Seldinger technique) with use of 6-F pigtail catheter(s). Nonionic contrast medium (Radiomiron 370; Schering, Berlin, Germany) was administered. Pulmonary arterial pressures were measured before and after PMT. The procedure was performed through an 80-cm, 8-F or 10-F sheath (Super Arrow-Flex Percutaneous Sheath Introducer Set; Arrow International, Reading, PA) selectively positioned to reach the thrombi. The thrombectomy catheters were positioned in the thrombus and moved in a forward/backward movement in the main and lobar arteries. Eight to 12 passes in a back-and-forth motion were performed with the Hydrolyser and Oasis catheters. Each pass takes 30 – 40 seconds. In the three cases with no contraindication to thrombolytic therapy, rt-PA (Actilyse; Boehringer Ingelheim, Ingelheim, Germany) was infused directly into the thrombus after PMT (10-mg bolus and infusion of 10 mg/h during 4 hours; total, 50 mg). The Urokinase Pulmonary Embolism Trial angiographic severity index was calculated (10). This index has a maximum value of 18, which corresponds to complete occlusion of both pulmonary arteries. An occlusion of two or more lobar arteries (index ⬎5) or equivalent smaller branches is angiographically considered a massive PE.
Statistical Analysis Data were analyzed with the use of the Wilcoxon test for paired values. A P value ⬍.05 was considered statistically significant. Results are presented as median values with ranges in parentheses.
RESULTS PMT was successful in restoring of pulmonary perfusion in six patients (85.7%). Duration of CPR was 10 –35 minutes, with a median of 25 minutes. The PMT devices’ activation time was 6 minutes (4 – 8 minutes). Injected saline solution volume during PMT was 300 – 400 mL. Recovered volume in the bag was 200 –300 mL. Systolic pulmonary artery pressure decreased from a median of 73.0 mm Hg (90 – 63 mm Hg) to 42 mm Hg (32– 81 mm Hg) immediately after thrombectomy (P ⬍ .05), and in three patients, pressure decreased to 34 mm Hg (33–36 mm Hg) after rt-PA infusion (P ⫽ NS). The Urokinase Pulmonary Embolism Trial Angiographic Severity Indexes (10) before and after PMT were 15 (14 –16) and 7 (5–10), respectively (P ⫽ .022). A median of 60% of thrombus (40%–70%) was removed, calculated by semiquantitative computer analysis. No difference was observed in quantity of thrombus removed between the Hydrolyser and Oasis thrombectomy devices.
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Complications There were no major complications directly related to PMT. Two patients treated with rt-PA developed a hematoma at the puncture site; one required transfusion of 2 U of blood. One patient did not recover from cardiac arrest caused by massive PE and died during the CPR and PMT procedure. Another patient had a brain infarction secondary to cardiac arrest but survived. Six patients were discharged within 30 days. A representative case is illustrated in Figure 1.
DISCUSSION Although its frequency is not well established, massive PE is one of the most frequent noncardiac causes of cardiac arrest (4,11). In a study by Wood (3) that included PE with pulmonary hypertension or right heart failure caused by massive PE, the incidence of cardiac arrest was 18%. In the series by Miller et al (12), cardiac arrest occurred in 29% of patients. Kurkciyan et al (4) established that massive PE causes 14.6% of cases of cardiac arrest of extracardiac origin. In the majority of cases of massive PE with cardiac arrest, there is pulseless electric activity/electromechanical dissociation and asystole (4,11). Comes et al (11) found that massive PE caused 36% of cases of unexplained sudden cardiac arrest among patients who had pulseless electric activity as the initial rhythm (11). In our series, all seven patients presented with pulseless electric activity and electromechanical dissociation. Mortality rates in massive PE when causing cardiac arrest are extremely high, as high as 70% in some series (3,11). Cardiac arrest will occur within 1–2 hours after the onset of clinical presentation in two thirds of fatal massive PE cases (1). A prompt clinical diagnosis of massive PE and treatment is necessary for optimal treatment in this “golden hour” (2). CPR maneuvers in these cases should be accompanied by causative treatment. When a patient’s condition is hemodynamically compromised, diagnostic methods as CT angiography, magnetic resonance angiography, and ventilation/perfusion lung scan are time-consuming. Echocardiography in patients in hemodynamically unstable
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Figure 1. (a) Initial pulmonary angiography shows bilateral thrombi with upper right lobe and lower left lobe occlusion and lower right lobe partial obstruction. Swan-Ganz catheter tip is seen in lower right pulmonary artery. (b) Bilateral PMT catheters were positioned during cardiac massage. (c) Left pulmonary thrombectomy with Hydrolyser Thrombectomy Catheter is shown, through a guiding catheter that enables contrast material injection to monitor response to thrombectomy. (d) Control image of PMT in left lower lobe artery shows partial recanalization. (e) The thrombectomy catheter is in a right upper lobe artery. (f) Final angiography shows patent right upper lobe artery.
condition is useful in assessing the severity of massive PE (2). Currently available data do not indicate that thrombolysis contributes to a significant increase in bleeding complications when administered during CPR. Other publications support the use of thrombolytic drugs during CPR (13) even though hemorrhagic complications occur; but considering the poor prognosis of patients with cardiac arrest, the possible benefits of thrombolysis outweigh the potential risks (14). We used rt-PA in three patients with no contraindication to thrombolytic drugs, with the rationale to remove the fragments of thrombus that migrated distally to the segmental and
more peripheral branches that were not reached by the PMT devices. PMT is a minimally invasive therapeutic option when thrombolytic drugs are contraindicated. PMT has maturated into a reliable and valuable therapeutic tool in acute vascular diseases. PMT devices are designed to achieve rapid clearance of acute occlusion in large vessels. PMT in massive PE provides efficacious and safe debulking of occlusive centrally located thrombus in pulmonary arteries, decreasing pulmonary artery pressure and improving hemodynamics (6,8). Its utility is limited in wall-adherent thrombi that are not occlusive because the catheters advance through the ad-
jacent patent lumen. The access to more peripheral pulmonary branch thrombi is difficult because of the rigidity of the thrombectomy catheters. Additionally, vessel wall disruption has been described experimentally with the AngioJet device (Possis, Minneapolis, MN) in vessels smaller than 6 mm (ie, segmental arteries) (15). More detailed descriptions of different devices are available in the literature (8,9). A small number of patients with massive PE treated with PMT are described in the literature (8). Major series used the Greenfield thrombectomy device, Amplatz thrombectomy device (7), Hydrolyser (6), and rotatable pigtail catheter. All had good clin-
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10-F sheath) and the use of thrombolytic drugs. The patient who died did not recover from cardiac arrest. There was no hemoptysis related to the PMT procedure. We have proposed an algorithm for the diagnosis and treatment of patients with cardiac arrest and suspected massive PE (Fig 2). In summary, PMT treatment of massive PE causing cardiac arrest can be performed simultaneously with CPR and is useful to reverse circulatory collapse. In this group of patients, there was a lower mortality rate than was expected. PMT can remove a significant volume of thrombi, sufficient to reverse cardiac arrest. PMT offers an alternative to surgical thrombectomy and pharmacologic thrombolysis, especially when there are contraindications to thrombolytic drugs. The reported technique will probably be improved in the future and warrants more evaluation.
Figure 2. Proposed algorithm for massive pulmonary embolism. Note.—PEA/EMD ⫽ pulseless electrical activity/ electromechanical dissociation; ECHO ⫽ echocardiography; RV ⫽ right ventricle.
ical results, with rapid restoration of pulmonary blood flow and decreased associated mortality. To our knowledge, there are no comparative studies of efficacy and safety among devices (ie, Amplatz TD, AngioJet, and rotatable pigtail catheter).
Complications There were no major complications directly related to PMT. The hematoma in the puncture site could result from the size of devices (most of the procedures were performed through a
References 1. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Prog Cardiovasc Dis 1975; 17:257–270. 2. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest 2002; 121:877–905. 3. Kasper W, Konstantinides S, Geibel A, et al. Management strategies and determinant of outcome in acute major pulmonary embolism: results of a multicenter registry. J Am Coll Cardiol 1997; 30:1165–1171. 4. Kurkciyan I, Meron G, Sterz F, et al. Pulmonary embolism as a cause of cardiac arrest: presentation and outcome. Arch Intern Med 2000; 160:1529 –1535. 5. Elliot GC. Embolectomy, catheter extraction or disruption of pulmonary emboli. Curr Opin Pulm Med 1995; 1:298 –302. 6. Fava M, Loyola S, Huete I. Massive pulmonary embolism: treatment with the Hydrolyser thrombectomy device. J Vasc Interv Radiol 2000; 11:1159 – 1164. 7. Muller-Hulsbeck S, Brossmann J, Jahnke T. Mechanical thrombectomy of major and massive pulmonary embolism with use of Amplatz Thrombectomy device. Invest Radiol 2001; 36: 317–322. 8. Fava M, Loyola S. Applications of percutaneous mechanical thrombectomy (PMT) in pulmonary embolism. Tech Vasc Interv Radiol 2003; 6:53–58. 9. Sharafuddin MJA, Hicks ME. Current status of percutaneous mechanical
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thrombectomy. Part II: devices and mechanisms of action. J Vasc Interv Radiol 1998; 9:15–31. 10. Walsh PN, Greenspan RH, Simons M, et al. An angiographic severity index for pulmonary embolism. The Urokinase Pulmonary Embolism Trial: a national cooperative study. Circulation 1973; 47(suppl II):II101–II108. 11. Comes KA, De Rook FA, Rusell ML, et al. The incidence of pulmonary embolism in unexplained sudden cardiac
Fava et al
arrest with pulseless electrical activity. Am J Med 2000; 109:351–356. 12. Miller GA, Hall RJ, Paneth M. pulmonary embolectomy, heparin, and streptokinase: their place in the treatment of acute massive pulmonary embolism. Am Heart J 1977; 93:568 –574. 13. Spohr F, Bottiger B. Safety of thrombolysis during cardiopulmonary resuscitation. Drug Saf 2003; 26:367–379. 14. Janata K, Holzer M, Kurkciyan I, et al. Major bleeding complications in car-
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diopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism. Resuscitation 2003; 57:49 –55. 15. Biederer J, Schoene A, Reuter M, Heller M, Müller-Hülsbeck S. Suspected pulmonary artery disruption after transvenous pulmonary embolectomy using a hydrodynamic thrombectomy device: clinical case and experimental study on porcine lung explants. J Endovasc Ther 2003; 10:99 –110.