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Ann Thorac Surg 2000;69:1681-1685
© 2000 The Society of Thoracic Surgeons
a Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Virginia Health Sciences Center, Charlottesville, Virginia, USA
Address reprint requests to Dr Kron, Department of Surgery, University of Virginia Health Sciences Center, Box 310, Charlottesville, VA 22908
e-mail: ikron{at}virginia.edu
Presented at the Forty-sixth Annual Meeting of the Southern Thoracic Surgical Association, San Juan, Puerto Rico, Nov 4–6, 1999.
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Abstract |
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Methods. We performed a retrospective study of all lung transplant recipients at our institution from June 1990 until June 1998. One hundred patients received 120 organs during this time period. We compared two groups of patients in this study: those experiencing a significant reperfusion injury (22%) and those who did not (78%).
Results. In-hospital mortality was significantly greater in patients experiencing reperfusion injury (40.9% versus 11.7%, p < 0.02). Posttransplantation reperfusion injury also resulted in prolonged ventilation (393.5 versus 56.8 hours, p < 0.001) and an increased length of stay in both the intensive care unit (22.2 versus 10.5 days, p < 0.01) and in the hospital (48.8 versus 25.6 days, p < 0.03). The incidence of reperfusion injury could not be attributed to length of donor organ ischemia (221.5 versus 252.9 minutes, p < 0.20). The clinical impact of reperfusion injury was significantly greater in patients undergoing transplantation for preexisting pulmonary hypertension (6/14) than those with chronic obstructive pulmonary disease or emphysema alone (6/54) (42.9% versus 11.1%, p < 0.012).
Conclusions. Clinically significant pulmonary reperfusion injury increased in-hospital mortality and morbidity resulting in prolonged ventilation, length of stay in the intensive care unit, and cost of hospitalization. The incidence of reperfusion injury was not dependent upon the duration of donor organ ischemia but increased with the presence of preoperative pulmonary hypertension. These findings suggest that recipient pathophysiology and donor allograft quality may play important roles in determining the incidence of reperfusion injury.
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Introduction |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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Immediate graft dysfunction after pulmonary transplantation is believed to be a manifestation of ischemia-reperfusion (IR) injury. Up to 97% of transplanted lungs will have some degree of perihilar edema during the immediate postoperative period [4]. Although not well defined, it has become apparent that IR injury may contribute significantly to recipient morbidity. This increase in morbidity translates into an increased utilization of critical care resources as well as both intensive care unit (ICU) and hospital length of stay [5]. Originally, reperfusion injury was thought to be due to either inadequate preservation techniques or prolonged graft ischemia before implantation. Recent reports have been unable to link poor graft function to the interval of graft ischemia [4, 6].
Other reports have confirmed an increased incidence of clinically significant IR injury in recipients with preoperative pulmonary artery hypertension. Investigators believe that an increased postoperative transpulmonary gradient due to increased pulmonary arterial pressures may drive fluid across a damaged respiratory endothelium and epithelium exacerbating an evolving reperfusion injury. Reports to date have not been able to confirm a quantitative link between the degree of postimplantation pulmonary artery hypertension and the degree of clinically significant IR injury [7].
Efforts to reduce IR injury have focused mainly on improvements in preservation techniques. Despite the abundance of experimental evidence suggesting that improved efforts to preserve the lung’s vascular endothelium may result in a reduction in IR injury, very little clinical translation has been achieved [8, 9]. Extracellular preservation solutions and techniques directed toward preserving or augmenting the NO/cGMP pathway are slowly making their way into the clinical arena. Controlled randomized trials may help to better understand the process of IR and provide novel approaches to pulmonary preservation.
The purpose of this retrospective review was to define the incidence of IR injury after lung transplantation at our institution. Additionally, we hoped to better quantitate the morbidity and mortality associated with IR injury. Finally, we hoped to define a population of patients and associated factors that could be linked to an increased incidence of IR injury after pulmonary transplantation.
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Patients and methods |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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2 analysis. All values are expressed as means ± the standard errors. Significant differences are reported for p values less than 0.05. |
Results |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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PaO2/FiO2 ratios
Recipients experiencing a clinically significant IR injury also had worse overall pulmonary function, which was quantified by measuring their PaO2/FiO2 ratios during the first 48 hours after transplantation. The RI group had a significantly worse blood oxygen content for a given inspired FiO2 than did the NRI group at both 24 hours (158.2 ± 24.2 versus 264.2 ± 12.1, p < 0.001) and 48 hours (146.6 ± 20.2 versus 282.6 ± 14.7, p < 0.001) postimplantation. Again, there were no significant differences in the PaO2/FiO2 ratios at 24 and 48 hours in either group (Table 3). These data were combined with the CXR score to determine which patients were to be included in the RI group.
Mean pulmonary arterial pressures
Of note, there were no statistically significant differences between the mean pulmonary arterial pressures of the two groups at any time point (Table 3). Additionally, there were no significant improvements in the mean pulmonary artery pressure after lung transplantation in either group during the first 48 hours posttransplantation.
Outcomes
There was a higher mortality rate for patients experiencing a significant IR injury after lung transplantation. Of the 22 patients experiencing a clinically significant IR injury, 9 died in the hospital. This mortality rate was significantly higher than those patients not experiencing a clinically significant reperfusion injury (40.9% versus 11.5%, p < 0.002) (Table 4).
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Duration of graft ischemia
No correlation between the duration of graft ischemia after donor harvest and the incidence of IR injury could be demonstrated. The RI group received lungs that were ischemic on the average of 253 ± 22.0 minutes. There was no significant difference between the RI group and the NRI group, whose graft ischemia time averaged 221 ± 11.8 minutes.
Cause of recipient pulmonary failure
Despite the investigator’s inability to correlate the incidence or severity of IR injury to the measured mean pulmonary arterial pressures, those patients who were transplanted for elevated pulmonary arterial pressure (n = 14) experienced an increased incidence of RI compared with a group of patients transplanted for emphysematous (n = 54) changes alone (42.9% versus 11.1%, p < 0.012) (Table 5). No other significant differences could be demonstrated when the specific cause of recipient pulmonary failure was analyzed with regard to incidence of IR injury (Table 2).
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Comment |
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TopAbstractIntroductionPatients and methodsResultsCommentReferences |
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Defining the patient group experiencing a clinically significant IR injury after pulmonary transplantation is not a completely objective process. The grading of CXR is often open to subjective interpretation. However, when combined with clinical suspicion on the basis of poor PaO2/FiO2 ratios and negative bronchoscopy, the team can be rather certain that the graft is suffering a clinically significant IR injury within the first 48 hours after transplantation. Other reports have confirmed that these criteria can predict which patients may be at risk for an increased ICU LOS due to a prolonged need for ventilatory assistance [4, 5].
The exact mechanisms at work in the initiation and propagation of a clinically significant IR injury after lung transplantation are not completely understood. Investigators have propagated the belief that the vascular endothelium becomes damaged during the process of lung harvest and preservation [8, 9]. IR injury is then believed to represent the graft’s inability to prevent edema formation due to a dysfunctional pulmonary vascular endothelium. Recent reports have confirmed these suspicions. One study confirmed an increase in transcapillary radiolabeled transferrin flux immediately after graft implantation and during periods of acute rejection [10]. More recently, investigators have demonstrated a correlation between the degree of permeability of the alveolar-capillary barrier and the duration of graft ischemia before implantation by calculating the edema fluid to plasma protein ratio in a small group of patients undergoing pulmonary transplantation [11]. These data would appear to confound reports claiming the lack of correlation between the duration of graft ischemia and the incidence of clinically significant IR injury. However, the authors of this report demonstrated that it was the ability of the respiratory epithelium to clear alveolar edema which determined the overall outcome after the initiation of IR injury in the transplanted lung. A better understanding of this mechanism may provide insight into the process of IR injury in the lung and allow for the development of improved preservation techniques.
Initial reports have demonstrated an increase in mortality and morbidity associated with the occurrence of posttransplantation IR injury [5, 7]. Our data also confirm these reports. The mortality rate for recipients at our institution who experienced a clinically significant reperfusion injury was 40.9%. We did not analyze data regarding the increased incidence of acute rejection, infectious complications, or the incidence of chronic rejection in this patient population. A full investigation into these specific morbidities may provide additional insight into the true clinical implications of posttransplantation IR injury. We did, however, measure the increased utilization of resources generated during the support of those patients who experienced a clinically significant IR injury. Our report confirms that this patient group experiences a worse postoperative outcome and in the process requires prolonged ventilatory support resulting in a subsequent increase in ICU LOS, hospital LOS, and hospital costs.
Multiple reports have been generated on the occurrence of IR injury in those patients undergoing pulmonary transplantation for pulmonary hypertension [7, 12, 13]. Intuitively, one would suspect that those recipients undergoing single lung transplantation for pulmonary hypertension would experience an increased incidence of IR injury after transplantation due to the increased pulmonary blood flow and pressure experienced by the implanted lung. This in turn would lead to an increase in pulmonary edema formation and worsening graft function requiring prolonged ventilatory support. Investigators initially reported that this was not the case. The short-term outcome for single lung transplantation in a small series of patients demonstrated excellent outcome for patients suffering from pulmonary hypertension [14]. More recently, investigators are linking preoperative pulmonary hypertension to an increased incidence of in-hospital mortality as well as an increased incidence of IR injury after single lung transplantation [7, 12, 13]. This phenomenon is most likely due to the inability of the remaining native recipient lung to support the patient during periods of severe graft dysfunction which can be seen with significant IR injury or episodes of acute rejection. Recipients who are transplanted for emphysema are capable of improving the severe V/Q mismatch seen with primary graft dysfunction by shunting flow to the native lung. Patients with severe preoperative pulmonary artery hypertension cannot overcome the high vascular resistance of the native lung and are unable to divert flow from the graft during periods of severe dysfunction [7, 15]. Therefore, the relationship for an increased incidence of IR injury in the setting of pulmonary hypertension may not necessarily be a causal one, but may actually represent the inability of the native lung to support the patient during periods of severe graft dysfunction. This statement is further supported by the inability of investigators to link measured pulmonary arterial hypertension in the postoperative period to the incidence or severity of IR injury [7]. The inability of the native lung to support the recipient during periods of graft dysfunction results in a prolonged need for critical care support and exposes the patient to the increased mortality and morbidities associated with the delivery of that care. Perhaps these patients would be better served by double lung transplantation.
IR injury occurs in 20% to 30% of lung transplant recipients and results in increased patient mortality and morbidity requiring an increased consumption of hospital resources. Although IR injury may not necessarily be linked to a specific recipient pathophysiology, preexisting pulmonary hypertension may serve to unmask the incidence and severity of IR injury in the transplanted lung. The condition of the graft at the time of implantation may play an important role in the incidence of IR injury. Improved techniques of graft preservation may ensure that those mechanisms necessary to either prevent or ameliorate IR injury are well preserved at the time of implantation despite pulmonary insults before lung donation.
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C. E. Reed General thoracic surgery and the Southern Thoracic Surgical Association: the second 25 years Ann. Thorac. Surg., November 1, 2003; 76(90050): S14 - 16. [Full Text] [PDF]
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J. D. Christie, R. M. Kotloff, A. Pochettino, S. M. Arcasoy, B. R. Rosengard, J. R. Landis, and S. E. Kimmel Clinical Risk Factors for Primary Graft Failure Following Lung Transplantation Chest, October 1, 2003; 124(4): 1232 - 1241. [Abstract] [Full Text] [PDF]
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I. Kutschka, S. P. Sommer, J. M. Hohlfeld, G. Warnecke, M. Morancho, S. Fischer, A. Haverich, M. Struber, and the Hannover Thoracic Transplant Program In-situ topical cooling of lung grafts: early graft function and surfactant analysis in a porcine single lung transplant model Eur. J. Cardiothorac. Surg., September 1, 2003; 24(3): 411 - 419. [Abstract] [Full Text] [PDF]
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A. R. Glanville Inhaled Nitric Oxide after Lung Transplantation: No More Cosmesis? Am. J. Respir. Crit. Care Med., June 1, 2003; 167(11): 1463 - 1464. [Full Text] [PDF]
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M. O. Meade, J. T. Granton, A. Matte-Martyn, K. McRae, B. Weaver, P. Cripps, and S. H. Keshavjee A Randomized Trial of Inhaled Nitric Oxide to Prevent Ischemia-Reperfusion Injury after Lung Transplantation Am. J. Respir. Crit. Care Med., June 1, 2003; 167(11): 1483 - 1489. [Abstract] [Full Text] [PDF]
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M. Sugita, P. Ferraro, A. Dagenais, M.-E. Clermont, P. Barbry, R. P. Michel, and Y. Berthiaume Alveolar Liquid Clearance and Sodium Channel Expression Are Decreased in Transplanted Canine Lungs Am. J. Respir. Crit. Care Med., May 15, 2003; 167(10): 1440 - 1450. [Abstract] [Full Text] [PDF]
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 S. H. Merchant, D. M. Gurule, and R. S. Larson Amelioration of ischemia-reperfusion injury with cyclic peptide blockade of ICAM-1 Am J Physiol Heart Circ Physiol, April 1, 2003; 284(4): H1260 - H1268. [Abstract] [Full Text] [PDF]
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T. M. Aziz, T. M. Pillay, P. A. Corris, J. Forty, C. J. Hilton, A. Hasan, and J. H. Dark Perfadex for clinical lung procurement: is it an advance? Ann. Thorac. Surg., March 1, 2003; 75(3): 990 - 995. [Abstract] [Full Text] [PDF]
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M. de Perrot, M. Liu, T. K. Waddell, and S. Keshavjee Ischemia-Reperfusion-induced Lung Injury Am. J. Respir. Crit. Care Med., February 15, 2003; 167(4): 490 - 511. [Abstract] [Full Text] [PDF]
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W. M. Chatila, S. Furukawa, J. P. Gaughan, and G. J. Criner Respiratory Failure After Lung Transplantation Chest, January 1, 2003; 123(1): 165 - 173. [Abstract] [Full Text] [PDF]
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I. Friedrich, J. Spillner, E.-X. Lu, M. Barnscheidt, O. Kuss, A. Sablotzki, F. U. Schade, and J. Borgermann Induction of endotoxin tolerance improves lung function after warm ischemia in dogs Am J Physiol Lung Cell Mol Physiol, January 1, 2003; 284(1): L224 - L231. [Abstract] [Full Text] [PDF]
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M. de Perrot, Y. Imai, G. A. Volgyesi, T. K. Waddell, M. Liu, J. B. Mullen, K. McRae, H. Zhang, A. S. Slutsky, V. M. Ranieri, et al. Effect of ventilator-induced lung injury on the development of reperfusion injury in a rat lung transplant model J. Thorac. Cardiovasc. Surg., December 1, 2002; 124(6): 1137 - 1144. [Abstract] [Full Text]
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S. M. Fiser, C. G. Tribble, A. K. Kaza, S. M. Long, J. A. Kern, D. C. Cassada, J. Linden, J. Rieger, V. E. Laubach, A. Matisoff, et al. Adenosine A2A receptor activation decreases reperfusion injury associated with high-flow reperfusion J. Thorac. Cardiovasc. Surg., November 1, 2002; 124(5): 973 - 978. [Abstract] [Full Text] [PDF]
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G. Warnecke, M. Struber, J. M. Hohlfeld, J. Niedermeyer, S. P. Sommer, and A. Haverich Pulmonary preservation with Bretscheider's HTK and Celsior solution in minipigs Eur. J. Cardiothorac. Surg., June 1, 2002; 21(6): 1073 - 1079. [Abstract] [Full Text] [PDF]
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A. G. Duarte and S. Lick Predicting Outcome in Primary Graft Failure Chest, June 1, 2002; 121(6): 1736 - 1738. [Full Text] [PDF]
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S. M. Fiser, C. G. Tribble, S. M. Long, A. K. Kaza, J. A. Kern, D. R. Jones, M. K. Robbins, and I. L. Kron Ischemia-reperfusion injury after lung transplantation increases risk of late bronchiolitis obliterans syndrome Ann. Thorac. Surg., April 1, 2002; 73(4): 1041 - 1048. [Abstract] [Full Text] [PDF]
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 M. Kurusz, J. D Roach Jr, R. A Vertrees, M. K Girouard, and S. D Lick Leukocyte filtration in lung transplantation Perfusion, March 1, 2002; 17(2_suppl): 63 - 67. [Abstract] [PDF]
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 M. M. Chakinala, M. H. Kollef, and E. P. Trulock Critical Care Aspects of Lung Transplant Patients J Intensive Care Med, January 1, 2002; 17(1): 8 - 33. [Abstract] [PDF]
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M. R. Karamsetty and J. R. Klinger NO: More Than Just a Vasodilator in Lung Transplantation Am. J. Respir. Cell Mol. Biol., January 1, 2002; 26(1): 1 - 5. [Full Text] [PDF]
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