Fig 1. Transfusion requirements of platelet concentrate.
After 44 days the patient was discharged in very good condition under anticoagulation therapy with acetylsalicylic acid 100 mg/day and warfarin (international normalized ratio, 2.5 to 3.5). Thirteen months later the same patient was hospitalized in our hospital due to a mechanical failure of the HeartMate XVE left ventricular assist device. This time circulating antibodies were not detected. Now the same anticoagulation management was carried out to exchange the HeartMate XVE with the HeartMate II. After termination of the extracorporeal circulation, 100% of the heparin was antagonized by protamine. No anticoagulation was given. Five hours later a re-thoracotomy was necessary due to bleeding. On the second postoperative day, argatroban (2 g/kg/ min) was started with an acid activated partial thromboplastin time from 45 to 55 seconds when blood loss of the drains was lower than 50 mL/hr. Postoperative acute renal failure developed in the patient, which required dialysis for 12 days. Sixteen days after the operation we combined argatroban with acetylsalicylic acid 100 mg three times a week. Before discharge, a new electrode of the pacemaker was implanted and argatroban was switched to warfarin. The patient was discharged on postoperative day 49 in very good condition with anticoagulation therapy, with warfarin and acetylsalicylic acid that was reduced to 100 mg on 3 days per week because of a platelets function test-100 closure time of more than 300 seconds.
Comment Several options to avoid heparin in heart surgery with extracorporeal circulation are described, such as danaparoid-sodium (Orgaran [Organon GmbH, Oberschleiheim, Germany]) and hirudin with moderate success concerning postoperative bleeding complications [1]. Argatroban was only used postoperatively after HIT developed [1]. In 2001, Aouifi published a series of 10 patients with HIT and showed that danaparoid was often associated with excessive bleeding and greater blood transfusion [2]. During cardiopulmonary bypass, inhibition of platelet aggregation by prostacyclin (in this study epoprostenol sodium) was © 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
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considered a safer anticoagulation in patients with HIT II than danaparoid-sodium. Iloprost was used safely during cardiopulmonary bypass in patients with HIT by several other authors [3–5]. Therefore, we used iloprost and heparin to undergo cardiopulmonary bypass in a patient with a heparin-induced thrombocytopenia with circulation antibodies for implantation of a left ventricular assist device. Intraoperatively, no thrombosis occurred. Its short elimination half-life of 45 minutes and hepatic metabolism are important aspects for use of argatroban in patients with renal failure [6]. In a clinical study with end-stage renal disease, argatroban 2 g/kg/min provided safe, adequate anticoagulation to enable successful hemodialysis. The implantation of left ventricular assist device is possible in patients with heparin-induced thrombocytopenia. This case demonstrates that the application of heparin for initiation of a cardiopulmonary bypass in combination with iloprost is a safe procedure. The complete antagonism with protamine at the end of the cardiopulmonary bypass minimizes the postoperative bleeding complications.
References 1. Christiansen S, Jahn UR, Meyer J, et al. Anticoagulative management of patients requiring left ventricular assist device implantation and suffering from heparin-induced thrombocytopenia type II. Ann Thorac Surg 2000;69:774 –7. 2. Aouifi A, Blanc P, Piriou V, et al. Cardiac surgery with cardiopulmonary bypass in patients with type II heparininduced thrombocytopenia. Ann Thorac Surg 2001;71:678 – 83. 3. Addonizio VP, Jr, Fisher CA, Kappa JR, Ellison N. Prevention of heparin-induced thrombocytopenia during open heart surgery with iloprost (ZK36374). Surgery 1987;102:796 – 807. 4. Kappa JR, Fisher CA, Todd B, et al. Intraoperative management of patients with heparin-induced thrombocytopenia. Ann Thorac Surg 1990;49:714 –23. 5. Shorten G, Comunale ME, Johnson RG. Management of cardiopulmonary bypass in a patient with heparin-induced thrombocytopenia using prostaglandin E1 and aspirin. J Cardiothorac Vasc Anesth 1994;8:556 – 8. 6. Di Nisio M, Middeldorp S, Buller HR. Direct thrombin inhibitors. N Engl J Med 2005;353:1028 – 40.
Acute Pulmonary Edema After Pericardial Drainage for Cardiac Tamponade John M. Karamichalis, MD, Andrei Gursky, MD, Ganpat Valaulikar, MD, James W. Pate, MD, and Darryl S. Weiman, MD, JD Division of Cardiothoracic Surgery, University of Tennessee Health Science Center, Memphis, Tennessee
Pericardial effusions with tamponade may present a clinical challenge in management for the cardiothoracic Accepted for publication Feb 2, 2009. Address correspondence to Dr Weiman, Division of Cardiothoracic Surgery, University of Tennessee Health Science Center, 910 Madison Avenue, 2nd Floor, Memphis, TN 38163; e-mail:
[email protected].
0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2009.02.001
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surgeon. We report a case of acute pulmonary edema secondary to the rapid release of a chronic traumatic pericardial effusion that resulted in the death of the patient. (Ann Thorac Surg 2009;88:675–7) © 2009 by The Society of Thoracic Surgeons
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ericardiocentesis for the treatment of pericardial tamponade may lead to a variety of complications. More commonly, these include lacerations of the right ventricle or coronary arteries, arrhythmias, hypotension, and pneumothorax. Acute pulmonary edema has rarely been reported [1– 4]. We describe a patient with a chronic traumatic pericardial effusion in whom severe pulmonary edema developed after pericardial drainage that resulted in hemodynamic collapse and death. Various mechanisms for this physiologic derangement are discussed.
FEATURE ARTICLES
A 19-year-old woman was involved in a motor vehicle accident. Her injuries included cerebral contusion, bilateral rib fractures with pulmonary contusions, and a grade II to III liver laceration. She required bilateral tube thoracostomies and prolonged endotracheal intubation necessitating a tracheostomy. She eventually improved, recovered from her injuries, and was discharged home. The patient presented to the emergency department 8 weeks after her initial injury with increasing fatigue and shortness of breath. On admission, her initial vital signs showed a heart rate of 110 beats/minute, blood pressure 120/80 mm Hg, with no pulsus paradoxus noted. She had mild jugular venous distention, normal heart sounds, and clear breath sounds bilaterally. Computed tomography imaging revealed a large pericardial effusion and an enlarged inferior vena cava. Her systolic blood pressure dropped rather suddenly to 90 mm Hg, and she became increasingly tachycardic. She was taken to the operating room for an emergency pericardial decompression. Attempts to intubate her failed due to a subglottic stenosis at the previous tracheostomy site. A subxiphoid pericardial window was performed while she was being ventilated by mask. A total of 1600 mL of pericardial fluid was drained, resulting in immediate improvement of her hemodynamics. Arterial blood gases and oxygen saturations remained normal throughout the procedure. While the patient was being transferred from the operating room to the intensive care unit, her peripheral oxygen saturations suddenly dropped to 70% and her respirations became increasingly labored. Attempted endotracheal intubation again failed, and an emergent redo-tracheostomy was performed. The patient continued to have difficulties with oxygenation and ventilation because of copious secretions of frothy pulmonary edema fluid that had to be continuously cleared from the tracheostomy tube and ventilatory circuit. The patient subsequently became progressively bradycardic and sustained a circulatory collapse. Bilateral tube thoracostomies were performed with minimal improvement. Further resuscitative attempts failed and she died.
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Comment Acute pulmonary edema after pericardiocentesis for cardiac tamponade is an unusual complication [1–5]. It was first described in 1983 by Vandyke and colleagues [6], who hypothesized that left ventricular dysfunction after pericardiocentesis for chronic tamponade may be related to acute hemodynamic changes from interventricular volume mismatch in the setting of elevated systemic vascular resistance and tachycardia. The initial left ventricular response is characterized by optimization of the Frank-Starling mechanism. Release of the tamponade may allow a sudden increase in pulmonary venous return thereby overloading the left ventricle while systemic vascular resistance remains high. Further increments in preload into the left ventricle can cause increasing wall stress, a reduction in stroke volume, and pulmonary edema. This response may be related to the magnitude and the velocity at which the load develops and to the extent of peripheral vascular resistance. Other proposed mechanisms include stunning of myocardium from primary alterations in intramyocardial blood distribution, myocardial ischemia, and subendothelial hemorrhage during tamponade persisting after relief of the tamponade. Whether pericardiocentesis provides a milieu for the development of myocardial stunning or a variant of reperfusion injury remains unknown. The tracheal stenosis in this patient might have created large fluctuations in her intrathoracic pressures that might have increased her transpulmonary pressures. The transpulmonary pressures are thought to have a role in reexpansion pulmonary edema after drainage of large pleural effusions, and it is possible that these pressures increased the risk that pulmonary edema would develop after this pericardial effusion was drained [7]. Although the exact pathophysiologic mechanism for left ventricular dysfunction after pericardiocentesis remains speculative, the abrupt disproportionate increase in left ventricular wall stress, coupled with the chronicity of tamponade and compensation by increased peripheral vascular resistance, may be critical determining factors. Myocardial stunning may have a contributory affect, considering the almost complete and uniform recovery of function seen in previously reported surviving patients. In patients with chronic effusion and tamponade, it appears prudent to initially decompress the pericardium gradually until the pathophysiology of tamponade is resolved. As proposed by Vandyke and colleagues [1], subsequent fluid should be drained gradually through an indwelling catheter while the patient’s hemodynamic variables are monitored. Although it is sometimes necessary to remove large amounts of fluid rapidly to restore normal blood pressure, it might be better to remove enough fluid to bring the central venous pressure and systemic blood pressure to normal, and then to use a catheter for slowly removing the remaining effusion. This may permit adaptive changes in coronary flow, myocardial mechanics, and wall stress by minimizing abrupt fluctuations in loading conditions otherwise associated
with a more rapid decompression of the pericardial space.
References 1. Shenoy M, Dhar S, Gittin R, Sinha A, Sabado M. Pulmonary edema following pericardiotomy for cardiac tamponade. Chest 1984;86:647– 8. 2. Glasser F, Fein A, Feinsilver S, Cotton E, Niederman M. Non-cardiogenic pulmonary edema after pericardial drainage for cardiac tamponade. Chest 1988;94:869 –70. 3. Naunheim K, Wood L, Little A. Pulmonary edema as a complication of pericardial drainage. Surg Gynecol Obst 1987;65:165– 6. 4. Bernal J, Pradhan J, Tchokonte R, Afonso L. Acute pulmonary edema following pericardiocentesis for cardiac tamponade. Can J Cardiol 2007;23:1155– 6. 5. Ditchey R, Engler R, LeWinter M. The role of the right heart in acute cardiac tamponade in dogs. Circ Res 1981;48:701–10. 6. Vandyke WH Jr, Cure J, Chakko CS, Gheorghiade M. Pulmonary edema after pericardiocentesis for cardiac tamponade. N Engl J Med 1983;309:595– 6. 7. Barbetakis N, Samanidis G, Paliouras D, Tsilikas C. Reexpansion pulmonary edema following video-assisted thoracic surgery for recurrent malignant pleural effusion. Interact Cardio Vasc Thorac Surg 2008;7:532–34.
Development of Bilateral Diffuse Pulmonary Arteriovenous Fistula After Fontan Procedure: Is There Nonhepatic Factor? Bo Sang Kwon, MD, Eun Jung Bae, MD, Gi Beom Kim, MD, Chung Il Noh, MD, Jung Yun Choi, MD, and Yong Soo Yun, MD Department of Pediatrics, College of Medicine, Seoul National University, Seoul, Korea
The cause of pulmonary arteriovenous fistulas after a cavopulmonary anastomosis is not clearly known, but the previous studies regarding their causes have been focused mainly on the hepatic factors. We report two unusual Fontan cases with multiple bilateral pulmonary arteriovenous fistulas. One of them died of progressive hypoxia, and the other underwent multiple coiling. Our cases suggest that potentially lethal diffuse pulmonary arteriovenous fistulas may develop bilaterally in spite of balanced hepatic effluent flow to pulmonary circulation through factors other than a hepatic factor. (Ann Thorac Surg 2009;88:677– 80) © 2009 by The Society of Thoracic Surgeons
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ome patients with complex congenital heart defects who have been palliated by connecting the systemic veins directly to the pulmonary circulation are known to develop pulmonary arteriovenous fistulas (PAVFs) [1]. Now it is well known that even in patients who do not have macroscopic PAVFs, significant intrapulmonary
Accepted for publication Dec 18, 2008. Address correspondence to Dr Bae, 28 Yongon-dong, Chongno-gu, Seoul, 110-744, Korea; e-mail:
[email protected].
© 2009 by The Society of Thoracic Surgeons Published by Elsevier Inc
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shunting occurs, which subsequently causes desaturation [2]. Their exact pathogenesis remains unknown. However, it is presumed that development of PAVFs is related to the diversion of hepatic venous flow away from the pulmonary circulation [3]. Although the absence of pulsatile flow may be a pathogenetic factor, there is a paucity of data unrelated to the hepatic factor. We report herein two unusual Fontan cases of multiple bilateral PAVFs which developed in spite of even hepatic effluent flow to the pulmonary circulation.
Case Reports Patient 1 A 13-year-old boy was born with corrected transposition of the great arteries, pulmonary atresia with confluent pulmonary arteries, patent ductus arteriosus, ventricular septal defect, mitral atresia, a morphologically small left ventricle with segmental anatomy (S,L,L), and an aorta arising from the right ventricle. At 18 months of age, he underwent a lateral-tunnel Fontan procedure with an intra-atrial Gore-Tex patch baffle (W. L. Gore & Assoc, Flagstaff, AZ). A 4-mm baffle fenestration was created. At postoperative follow-ups, he developed normally without apparent cyanosis. At 11 years of age, he began complaining of dyspnea on exertion and showed cyanosis with transcutaneous oxygen saturation of 82% ⬃ 83%, measured by pulse oximetry with a hemoglobin level of 18.3 g/dL at that time. Cardiac catheterization revealed the mean pulmonary artery pressure (11 mm Hg) the mean left atrial pressure (8 mm Hg), and the pulmonary-to-systemic flow ratio (0.9). Mixed venous saturation was 74%, systemic arterial saturation was 88%, left upper pulmonary venous saturation was 91%, left lower pulmonary venous saturation was 98%, right upper pulmonary venous saturation was 93%, and right lower pulmonary venous saturation was 97%. Test balloon occlusion of the fenestration in room air resulted in an insufficient increase in arterial oxygen saturation from 88% to 91% and a decrease in systemic flow from 5.1 to 4.2 L/min/m2. In addition, the position of the fenestration was contiguous to the cardiac vein. For these reasons, device closure of the fenestration was not performed. However, pulmonary angiography demonstrated multiple reticular patterns of the peripheral pulmonary vasculature with simultaneous visualization of contrast in the pulmonary arteries and veins, a characteristic of PAVFs in both lungs, as well as a patent fenestration (Fig 1). Bubble contrast echocardiography also showed abnormal findings. Initially there was coil embolization of the left upper PAVFs, which were relatively, largely based on angiographic findings and venous desaturation. Nevertheless, systemic arterial desaturation did not improve. Inferior and superior caval venography showed an even flow distribution to both lungs. Chest and abdominal computed tomography (CT) demonstrated no abnormal findings in the liver except mild hepatosplenomegaly. Biochemical liver function tests were within the normal range. Under general anes0003-4975/09/$36.00 doi:10.1016/j.athoracsur.2008.12.065
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