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J Thorac Cardiovasc Surg 1995;110:861-0863
© 1995 Mosby, Inc.
BRIEF COMMUNICATIONS |
Darlinghurst, Australia
From the Cardiopulmonary Transplant Unit, St. Vincent's Hospital, Darlinghurst, New South Wales, Australia.
Acute reperfusion injury is a potentially life-threatening complication of lung transplantation. Typically, acute reperfusion injury becomes apparent within hours of completion of the transplant procedure and in its most severe form results in progressive hypoxemia, pulmonary hypertension, systemic hypotension, and diffuse opacification of the transplanted lung or lungs on chest x-ray films, a clinical syndrome known as the reimplantation response.
1 The pathophysiologic disturbance and clinical picture of acute reperfusion injury closely resembles adult respiratory distress syndrome (ARDS), a condition that has been successfully treated with inhaled nitric oxide (iNO). 2 In this report we describe two cases of severe acute reperfusion injury after lung transplantation that were treated with iNO. In both cases, iNO rapidly reversed the respiratory failure and associated hemodynamic abnormalities.
Case 1
A 50-year-old woman underwent left single lung transplantation because of smoking-induced emphysema on December 31, 1993. The donor was a 22-year-old woman who died after craniotomy. Arterial oxygen tension (PaO2) to inspired oxygen fraction (FiO2) ratio was 388 mm Hg before procurement. The ischemic time for the donor lung was 384 minutes. The initial postoperative PaO2/FiO2 ratio was 216 mm Hg. A chest x-ray film taken 1 hour after operation showed full expansion of the transplanted lung with no radiologic infiltrate. The patient was extubated at 12 hours after operation. During the next 45 minutes increasing dyspnea occurred. A repeat chest x-ray film showed diffuse opacification of the transplanted lung. Shortly after the film was obtained the patient had cardiorespiratory arrest. She required prolonged resuscitation before a stable cardiac rhythm could be reestablished and she remained critically ill during the next 6 hours with profound hypoxemia (PaO2/FiO2 ratio in the range of 70 to 80 mm Hg) and shock (mean systemic blood pressure between 45 and 55 mm Hg with severe oliguria) despite intravenous infusions of high-dose adrenaline and noradrenaline. Mean pulmonary artery wedge pressure remained in the range of 10 to 14 mm Hg but pulmonary vascular resistance (PVR) was markedly elevated (calculated mean PVR in the range of 350 to 400 dynes sec · cm-5). Administration of iNO was begun at an inspired concentration of 36 ppm. NO was added at the ventilator end of the inspiratory limb of a Servo 900C ventilator (Siemens, Solna, Sweden). Within the next 15 minutes PaO2 rose from 73 to 103 mm Hg and within 1 hour this value rose to 212 mm Hg. Hemodynamic changes in response to iNO are summarized in Table I. An attempt to wean the patient from iNO after 12 hours of administration was associated with an abrupt fall in PaO2 from 103 to 77 mm Hg and rise in PVR from 170 to 315 dynes sec · cm-5, which was reversed by reinstitution of iNO administration at 20 ppm. The patient was able to be weaned completely from iNO administration after 26 hours. By this time, the PaO2/FiO2 ratio was 192 mm Hg and the opacification in the transplanted lung noted on the previous chest x-ray film had largely cleared.
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A 29-year-old woman with cystic bronchiectasis underwent bilateral sequential single-lung transplantation on May 26, 1994. The donor was a 55-year-old man who died of spontaneous intracerebral hemorrhage. The PaO2/FiO2 ratio was 342 mm Hg when measured before lung procurement. The right lung was transplanted first without incident. The ischemic time for the right lung was 210 minutes. During implantation of the left lung, 10 minutes after reperfusion of the right lung, progressive hypoxemia and hypotension ensued. Cardiopulmonary bypass was established and implantation of the left lung completed. The ischemic time for the left lung was 330 minutes. After reperfusion of the left lung and weaning from cardiopulmonary bypass hypoxemia and hypotension again occurred. The patient was transferred to the intensive care unit but her condition continued to deteriorate. Intravenous noradrenaline administration was begun because of worsening systemic hypotension. A chest x-ray film showed diffuse opacification of the right lung with less marked changes in the left lung. A diagnosis of acute reperfusion injury was made and iNO administration was begun in a concentration of 10 ppm. As in the first case there was evidence of improvement within 15 minutes of the start of iNO administration with a rise in PaO2 from 57 mm Hg to 130 mm Hg. One hour after iNO administration began, the PaO2/FiO2 ratio had risen from 57 to 150 mm Hg and the pulmonary vascular resistance had fallen from 599 to 309 dynes sec · cm-5 (
Table I). The respiratory and hemodynamic parameters remained stable thereafter until an accidental increase in the concentration of iNO, which occurred after 18 hours of administration. The patient received an inhaled concentration of NO of 110 ppm for a period of approximately 30 minutes and became nauseated and restless. The methemoglobin level at this time was 19%. The administration of iNO was temporarily discontinued and the FiO2 increased to 0.85. Administration of iNO was recommenced at 10 ppm after 1 hour at which time the methemoglobin level had fallen to 13%. The methemoglobin level continued to fall exponentially during the next 5 hours. The iNO was withdrawn completely after 24 hours of administration. The patient was extubated 54 hours after operation.
Discussion
Acute reperfusion injury of the lung is characterized by increased pulmonary capillary permeability, pulmonary edema, and an acute rise in PVR. The latter abnormality has been found to be largely a result of a loss of endothelium-dependent NO-mediated relaxation. 3 In its most severe form, acute reperfusion injury results in ARDS. Both patients were critically ill at the time of introduction of iNO. Administration of iNO led to a rapid and dramatic improvement in lung function and stabilization of the circulation. The mechanism of the beneficial effect of iNO in acute reperfusion injury is likely to be similar to that seen in ARDS and related to two unique pharmacokinetic properties of iNO. First, iNO is only delivered to ventilated lung segments so that its vasodilator effect is confined to these segments, which thereby optimizes ventilation-perfusion matching. 2 Second, NO is rapidly inactivated after its diffusion into the bloodstream by binding to hemoglobin, 4 which prevents any systemic effect of the gas.
Recently, Adatia and associates 5 reported the use of iNO in the treatment of six patients with postoperative graft dysfunction after lung transplantation. They observed an average fall in PVR of 31% and a trend toward increased PaO2 in response to a 15-minute administration of 80 ppm iNO. Two of their patients had hypoxemia refractory to conventional treatment. Both showed a marked improvement in PaO2 in response to iNO, which was continued in low dosages for 40 and 69 hours, respectively. The dosage of iNO chosen in our first case was based on early studies in human beings in which a dose of 36 ppm was used. 2 In 10 patients awaiting cardiac transplantation, we observed no difference in the pulmonary vasodilator response between 10 and 40 ppm iNO (unpublished observations). For this reason we chose a dosage of 10 ppm iNO in the second case. The rapid development of methemoglobinemia in the second case highlights the potential toxicity of iNO therapy. 6 We did not observe any major sequelae after the accidental increase in iNO concentration, but the episode emphasizes the need for continuous monitoring of the iNO concentration and methemoglobin level during iNO therapy.
In conclusion, iNO rapidly reversed respiratory failure and shock in two patients who had severe acute reperfusion injury after lung transplantation, and we recommend that this therapy be considered for any patient who has this life-threatening complication after lung transplantation.
Footnotes
J THORAC CARDIOVASC SURG 1995;110:861-3 
References
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