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Ann Thorac Surg 2004;77:697-699
© 2004 The Society of Thoracic Surgeons


Case report

Successful resuscitation of a patient with acute massive pulmonary embolism using emergent embolectomy

Georgios P. Georghiou, MDa, Ron Brauner, MDa, Marius Berman, MDa, Alon Stamler, MDa, Lucio Glanz, MDb, Bernardo A. Vidne, MDa*, Eldad Erez, MDa

a Departments of Cardiothoracic Surgery and Anesthesiology, Rabin Medical Center, Beilinson Campus, Petah Tiqva, Israel
b Department of Anesthesiology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

Accepted for publication April 29, 2003.

* Address reprint requests to Dr Vidne, Department of Cardiothoracic Surgery, Rabin Medical Center, Beilinson Campus, Petah Tiqva 49100, Israel
e-mail: bvidne{at}clalit.org.il


    Abstract
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
Acute massive pulmonary embolism is associated with a high mortality rate. Prompt diagnosis and treatment are mandatory for a successful outcome. Although thrombolysis is effective, it is associated with a high rate of bleeding complications. This report describes the use of emergent pulmonary embolectomy as an effective and aggressive therapeutic approach to a massive saddle pulmonary embolism in a 66-year-old woman. With the application of specific surgical techniques and good interdisciplinary cooperation, pulmonary embolectomy may serve as more than a last resort for the management of this clinically unstable and dangerous condition.


    Introduction
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
The diagnosis and treatment of pulmonary embolism (PE) demands an interdisciplinary approach with medical, surgical, and radiologic techniques. However, despite substantial advances mortality and recurrence rates remain high. Massive PE with cardiovascular collapse, indicating significant obliteration of the pulmonary vasculature, has a very grim prognosis. Such patients pose a challenge for both the anesthesiology and surgical teams, as well as for emergency room personnel. We describe a timely and aggressive diagnostic and therapeutic approach that can yield success.

A 66-year-old woman sought medical help because of an event of sudden-onset respiratory distress, chest pain, and loss of consciousness, with continual respiratory distress after consciousness was regained. Her medical history included stable angina pectoris, status post transient ischemic attack, and fracture of the left ankle 1-week before admission. The left ankle was treated by plaster cast, limiting the patient's freedom of movement.

On admission, vital signs were borderline (respiratory rate 30/minute, heart rate 110/minute, and blood pressure 95/50 mm Hg) with cyanosis. Electrocardiography revealed sinus tachycardia (heart rate 102/minute), S1Q3 pattern in standard leads, incomplete right bundle branch block, and negative T waves in leads III, aVF, and V1–V3. A presumptive diagnosis of PE was made, and a bolus of 10,000 U heparin was given intravenously. Oxygen therapy and a continuous infusion of heparin was initiated at 1000 U/hour. Transthoracic echocardiography revealed right ventricular dilatation and moderate tricuspid regurgitation. Spiral contrast computed tomography scan of the chest revealed a large saddle embolus at the bifurcation of the main pulmonary artery, protruding into the left and right pulmonary arteries and almost occluding them (Fig 1). Because of these findings and right ventricle deterioration, including tricuspid insufficiency, we decided to perform emergent pulmonary embolectomy, and the patient was taken to the operating room 4 hours after admission.



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Fig 1. Spiral contrast computed tomography scan of the chest illustrating a large saddle thrombus protruding into the left and right pulmonary arteries.

 
Preoperative findings included cyanosis, orthopnea, tachypnea (respiratory rate 40/minute), tachycardia (heart rate 120/minute), systemic hypotension (blood pressure 80/60 mm Hg), jugular venous distension, and metabolic acidosis. Shortly after induction of anesthesia, when the patient was already prepared and draped and full median sternotomy was completed, systemic blood pressure fell, end-tidal CO2 decreased, and the patient's state rapidly deteriorated to cardiac arrest. Pericardiotomy was performed with immediate resuscitation by cardiac massage and an intravenous bolus of 2 mg of adrenaline. The heart started beating again, but the patient was hypotensive (systolic blood pressure < 50 mm Hg) and she required continuous cardiac massage while we did purse-strings for the cannulation incision sites. The patient was heparinized and placed on cardiopulmonary bypass (CPB) using aortic and single right atrial cannulation. The total time of cardiac massage before the initiation of CPB was 8 minutes. The procedure was performed with aortic cross-clamping, cold crystalloid cardioplegia, and mild hypothermia (32°C). A transverse arteriotomy was made in the main pulmonary artery, and with the use of simple, gallbladder forceps, the huge saddle clot was gently extracted en bloc under direct vision from the main pulmonary artery and the right and left pulmonary arteries. The lungs were compressed manually to mobilize the peripheral clots. Total CPB time was 66 minutes, and aortic occlusion time was 24 minutes. Weaning from the heart-lung machine was successful on the first attempt with only moderate inotropic support. The postbypass course was uneventful. There were no postoperative complications. Mass size of the embolus was 7x4.5x2 cm. Follow-up transesophageal echocardiography revealed normal right ventricle contractility and no emboli. Venous sonography indicated a thrombus in the left popliteal vein. The patient was discharged on warfarin, keeping the international normalized ratio at around 2.0. At the 13-month follow-up visit there was no recurrence of the pulmonary embolism.


    Comment
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
Massive PE is caused by the interaction of a large embolism with underlying cardiopulmonary disease to produce hemodynamic instability. If shock is induced, the mortality risk rises three- to sevenfold; the majority of deaths occur within 1 hour of presentation. To take advantage of this small window of opportunity, the immediate integration of historical information, physical findings, and readily available laboratory data are necessary, combined with a structured physiologic approach to diagnosis and resuscitation [1].

Treatment with thrombolysis is often effective, but it is associated with a high frequency of major bleeding complications, especially intracranial hemorrhage. The International Cooperative Pulmonary Embolism Registry reported a 3% rate of intracranial bleeding in patients with PE treated with thrombolytic therapy [2]. Similar findings were also noted in two smaller contemporary PE registries [3, 4].

These observations, together with the 89% survival rate reported by the largest contemporary single-center study of emergent pulmonary embolectomy [5], prompted us to consider pulmonary embolectomy as an alternative to thrombolysis for our patient. We were concerned about both the massive size of the embolus as well as the near-total occlusion of the main pulmonary artery. Pulmonary embolectomy could ensure that the patient was treated before she became very ill, while providing a definitive means of removing the large pulmonary embolus. The method was associated with very few complications, and the patient was fit for early discharge.

Being aware that right ventricular hypokinesis and dilatation are associated with an increased rate of mortality and recurrent PE [5], we decided on emergent operation at the point of impending hemodynamic instability with moderate right ventricular dysfunction, despite preserved systemic arterial pressure [6]. This was the cornerstone of our management strategy. Our success hinged on the fact that the patient suffered cardiac arrest, the strongest predictor of operative mortality [5], in the operating room after full median sternotomy was done.

Specific aspects of the surgical technique minimized perioperative morbidity and mortality. The procedure was performed with aortic cross-clamping, cold crystalloid cardioplegia, and mild hypothermia. Avoiding ischemic injury to the stunned right ventricle decreases postoperative right heart dysfunction. Keeping the heart unloaded and well-perfused during embolectomy aids the resuscitation of the stunned right ventricle, most likely by regenerating depleted energy stores. Another key component of our surgical approach was the complete avoidance of blind instrumentation of the fragile pulmonary arteries. Such maneuvers can be traumatic and may lead to fatal pulmonary hemorrhage.

Acute massive saddle PE is an unstable and dangerous clinical situation warranting consideration during evaluation. Surgical embolectomy is one of several available treatment modalities and should not be considered merely as a last resort for desperate situations. A critical mass of severely ill patients with PE and devoted personnel with adequate resources are fundamental requirements for a successful effort in surgical embolectomy. Our patient had a very severe and rapidly deteriorating case of massive PE. Her good outcome after emergent surgical pulmonary embolectomy emphasizes the importance of rapid diagnosis, aggressive therapeutic approach, and effective cooperation between the emergency physician, cardiologist, radiologist, cardiac surgeon, and anesthesiologist.


    Acknowledgments
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 
The authors thank Gloria Ginzach and Charlotte Sachs of the Editorial Board, Rabin Medical Center, Beilinson Campus, for their assistance.


    References
 Top
 Abstract
 Introduction
 Comment
 Acknowledgments
 References
 

  1. Kenneth E.W. Major pulmonary embolism. Review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest 2002;121:877-905.[Abstract/Free Full Text]
  2. Goldhaber S.Z., Visuni L., De Rosa M. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER). Lancet 1999;353:1386-1389.[Medline]
  3. Meyer G., Gisselbrecht M., Diehl J.L., et al. Incidence and predictors of major hemorrhagic complications from thrombolytic therapy in patients with massive pulmonary embolism. Am J Med 1998;105:472-477.[Medline]
  4. Hamel E., Pacouret G., Vincentelli D., et al. Thrombolysis or heparin therapy in massive pulmonary embolism with right ventricular dilatation: results from a 128-patient monocenter registry. Chest 2001;120:120-125.[Abstract/Free Full Text]
  5. Akloq L., Williams C.S., Byrne J.G., et al. Acute pulmonary embolectomy. A contemporary approach. Circulation 2002;105:1416-1419.[Abstract/Free Full Text]
  6. Cannon C.P., Goldhaber S.Z. Cardiovascular risk stratification of pulmonary embolism. Am J Cardiol 1996;78:1149-1151.[Medline]



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This Article
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Right arrow Author home page(s):
Georgios P. Georghiou
Marius Berman
Alon Stamler
Bernardo A. Vidne
Eldad Erez
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