Ann Thorac Surg 2001;71:364-366
© 2001 The Society of Thoracic Surgeons
Case report
Nitric oxide usage after posttraumatic pneumonectomy
Feza Nurozler, MDa,
Michael Argenziano, MDa,
Mark E. Ginsburg, MDa
a Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, New York, USA
Accepted for publication May 17, 2000.
Address reprint requests to Dr Argenziano, c/o Dr Ginsburg, Division of Cardiothoracic Surgery, 161 Fort Washington Ave, Atchley Pavilion, Rm 310, New York, NY 10032
e-mail: ma66{at}columbia.edu
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Abstract
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Pneumonectomy is rarely required in the surgical management of thoracic traumatic injuries with high mortality rates. Right heart failure due to elevated pulmonary artery pressure and the adult respiratory distress syndrome have been leading causes of mortality reported after posttraumatic pneumonectomy. The beneficial effect of inhaled nitric oxide has been shown in pulmonary hypertension and in adult respiratory distress syndrome. We report the use of inhaled nitric oxide in the perioperative management of a patient undergoing emergent pneumonectomy.
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Introduction
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Pneumonectomy is rarely required in the surgical management of thoracic traumatic injuries. However, in cases of major hilar vascular or proximal bronchial trauma, pneumonectomy may be unavoidable. Traditionally, patients requiring pneumonectomy for control of hemorrhage or airway management have had high mortality rates, in some series approaching 50% to 67% [1, 2]. Right heart failure due to elevated pulmonary artery pressure and the adult respiratory distress syndrome (ARDS) have been leading causes of mortality reported after posttraumatic pneumonectomy. Adult respiratory distress syndrome in these patients is characterized by intrapulmonary shunting, which results in arterial hypoxemia, and by acute pulmonary hypertension due to microvascular vasoconstriction [3]. Contributing factors to these elevations in pulmonary vascular resistance (PVR) and ARDS include cytokine release associated with hemorrhagic shock, massive blood product transfusion, and anatomic reduction of pulmonary vascular capacitance. After pneumonectomy, sudden elevation of PVR in the remaining lung results in right ventricular strain, dilatation, and in many cases leads to overt right heart failure. Nitric oxide (NO), initially described as an endothelium-derived relaxation factor, has been implicated in a wide variety of physiologic and pathophysiologic processes. Nitric oxide is synthesized by the vascular endothelium and acts as a natural local vasodilator. Inhaled NO has been shown to cause pulmonary vasodilation in primary pulmonary hypertension [4], in pulmonary hypertension secondary to congenital heart disease [5], and in ARDS [6]. The beneficial effects of inhaled NO on arterial oxygenation and mechanical ventilatory requirements have been reported in the management of pulmonary edema after elective pulmonary resections [7]. In contrast to intravenously administered vasodilators, inhaled NO does not cause systemic hypotension and selectively improves the perfusion of ventilated regions, thus improving arterial oxygenation [6]. We report the use of inhaled NO in the perioperative management of a patient undergoing emergent pneumonectomy for control of hemorrhage after penetrating chest trauma.
A 24-year-old man presented to the emergency department after sustaining a gunshot wound to the anterior chest. Upon initial assessment, arterial blood pressure was 90/50 mm Hg and pulse rate was 120 beats/min. The patient was intubated endotracheally and examination revealed a single right infraclavicular gunshot wound in the anterior axillary line, with no identifiable exit wound. A right chest tube was placed, which immediately drained 1.5 L of blood. Within minutes, the systolic blood pressure decreased to 60 mm Hg and the patient became unresponsive. As 6 units of packed red blood cells were transfused, increasing the blood pressure to 100/60 mm Hg, the patient was transferred to the operating room. In the operating room the patient was explored through a right anterolateral thoracotomy, which revealed a complex proximal right pulmonary arterial injury not amenable to repair. Because of ongoing blood loss, the decision was made to perform a right extrapericardial pneumonectomy. No other intrathoracic injuries were identified, and the patient was closed and transferred to the intensive care unit in stable hemodynamic condition. During the procedure, the patient received an additional 10 units of packed red blood cells as well as 6 units of platelets. At the close of the procedure, intraoperative transesophageal echocardiography revealed mild right ventricular dilatation with moderate tricuspid regurgitation, but no evidence of ventricular dysfunction. Upon arrival to the intensive care unit the patient was hemodynamically stable, with cardiac output of 5 L/min, pulmonary artery pressure 40/20 mm Hg, and a PaO2 of 120 mm Hg on an FiO2 of 0.40. Despite this, inhaled nitric oxide was instituted prophylactically, at a dose of 5 ppm. The patient remained stable for the first 36 hours, until the morning of postoperative day 2, when arterial oxygenation worsened (PaO2 69 on FiO2 1.0, positive end-expiratory pressure +12), pulmonary artery pressures increased (70/25 mm Hg), and cardiac output decreased (3.5 L/min). Chest radiography revealed diffuse hazy opacification of the left lung and echocardiography demonstrated right ventricular dilatation and mild diffuse hypokinesis. At this point, inhaled NO was increased to 20 ppm, and furosemide diuresis was begun. On postoperative day 3, the patient began to improve, with reductions in pulmonary artery pressure (40/20 mm Hg) and improvements in arterial oxygenation (PaO2 of 110 on FiO2 of 0.50), and ventilator support was weaned. Over the next 24 hours, chest radiography revealed clearing of the left lung field and cardiac output improved to 6 L/min. Inhaled NO was weaned off slowly on postoperative day 5, and on day 6, the patient was extubated and transferred to the step-down unit. The patient made an uneventful subsequent recovery and was discharged on postoperative day 11. The time course of inhaled NO and corresponding data are summarized in Table 1.
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Comment
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Pneumonectomy is rarely required in the management of the thoracic trauma patient. However, in the setting of hilar vascular injury or proximal airway disruption in an unstable patient, urgent pneumonectomy may be needed, with high attendant mortality. In published series, mortality rates as high as 63% have been reported, with most intraoperative deaths resulting from uncontrollable hemorrhage and most postoperative deaths attributable to right heart failure. In patients who survive the intraoperative period, survival depends upon aggressive management of pulmonary hypertension, right ventricular dysfunction, and noncardiogenic pulmonary edema [1, 2]. These pulmonary vascular and parenchymal effects are mediated by a number of concurrent pathophysiologic processes, including cytokine release associated with hemorrhagic shock, massive blood product transfusion, fluid overload, and anatomic reduction of pulmonary vascular capacitance. The interplay between hemorrhagic shock and pneumonectomy is complex, and has been studied by Cryer and associates [2], who compared cardiopulmonary responses to shock resuscitation in pigs undergoing hemorrhagic shock alone, pneumonectomy alone, or hemorrhagic shock plus pneumonectomy. In this animal model, higher PVR and lower stroke volume indices were found in survivors of shock plus pneumonectomy than in those undergoing either insult alone, suggesting a synergistic effect of pneumonectomy and shock resuscitation in the development of right heart failure and acute lung injury. It is reasonable to hypothesize, thus, that the high mortality associated with posttraumatic pneumonectomy results from the combined pathophysiologic effects of shock resuscitation and pneumonectomy, either of which might be tolerable in the absence of the other.
The management of pulmonary hypertension and acute lung injury after emergent pneumonectomy is a challenging problem. Mainstays of management include expeditious control of blood loss, avoidance of excessive volume and blood product administration, pharmacologic inotropic support, optimization of arterial oxygenation, and control of pulmonary hypertension. Because intravenously administered vasodilators produce dilation of both systemic and pulmonary circulations, their effectiveness in lowering PVR may be limited by significant systemic hypotension as well as hypoxemia due to increased intrapulmonary shunting [8]. Inhaled NO is an extremely effective, specific pulmonary vasodilator with no appreciable systemic hemodynamic effects [4–7]. In contrast to intravenously administered vasodilators, inhaled NO is preferentially delivered to arterioles immediately subjacent to ventilated alveoli, selectively improves perfusion of ventilated regions, and therefore improves ventilation-perfusion matching and arterial oxygenation [6]. The time course and dose response of inhaled NO for systemic oxygenation and pulmonary hypertension have been studied in patients with ARDS [9]. According to this study, longer time and larger doses of inhaled NO are required for pulmonary vasodilation than for improvement in oxygenation. This study also revealed that the improvement in oxygenation reaches a maximum at 10 ppm and, at higher doses, drifts back toward the baseline, whereas pulmonary artery pressure presents a continuous dose-dependent reduction. These combined beneficial effects on arterial oxygenation and PVR in the absence of adverse systemic effects make inhaled NO a particularly useful adjunct in the management of the posttraumatic pneumonectomy patient. However, it should be remembered that higher doses than 10 ppm of inhaled NO can cause deterioration of oxygenation. This case represents a report of inhaled NO use in this setting. Further randomized prospective studies need to be done to determine the beneficial effects of inhaled NO on the management of pulmonary hypertension and acute lung injury after emergent pneumonectomy.
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References
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Abstract
Introduction
