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Division of Cardiothoracic Surgery, University of Tennessee Health Science Center, Memphis, Tennessee
Accepted for publication February 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 (Email: dweiman{at}utmem.edu).
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| Introduction |
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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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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.
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D. S. Weiman Reply Ann. Thorac. Surg., May 1, 2010; 89(5): 1703 - 1703. [Full Text] [PDF] |
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