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* From the Departments of Pulmonary and Critical Care Medicine (Drs. Khan, Mehta, and Arroliga), Internal Medicine (Dr. Salloum), Radiology (Dr. O'Donovan), and Biostatistics (Mr. Mascha), The Cleveland Clinic Foundation, Cleveland, OH; and The Cardiovascular Research Institute (Dr. Matthay), University of California, San Francisco, CA.
Correspondence to: Alejandro C. Arroliga, MD, FCCP, Department of Pulmonary and Critical Care Medicine, Cleveland Clinic Foundation—G62–156, 9500 Euclid Ave, Cleveland, OH 44195; e-mail: Arrolia{at}ccf.org
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Abstract |
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Study objectives: (1) To describe the incidence of PRR in lung transplant recipients, (2) to identify the predictors of PRR, (3) to examine the correlation of suspected predictors with the severity of PRR, and (4) to evaluate the impact of PRR on morbidity and mortality of lung transplant recipients.
Design: Retrospective review of clinical records and radiographic studies.
Setting: Tertiary care referral center.
Patients: Ninety-nine consecutive patients with end-stage lung disease undergoing lung transplantation between February 1990 and October 1995.
Methods: Review of clinical records and postoperative chest radiographs of all lung transplant recipients to identify patients who experienced PRR. Chest radiographs of patients with PRR were graded for severity on a scale of 0 (none) to 5 (very severe). Demographic, pre- and perioperative factors were also evaluated along with short- and long-term survival of patients with PRR.
Results: Fifty-six of 99 lung transplant recipients (57%) experienced PRR. The median ischemia time of patients with and without PRR was 168 and 180 min, respectively (p = 0.62). The incidence of PRR was 51% in patients without preoperative pulmonary hypertension, 78% in mild to moderate pulmonary hypertension, and 58% in patients with severe pulmonary hypertension (p = 0.10). Incidence and severity of PRR was similar in patients receiving right, left, or double-lung transplantation. Similarly, age and sex of the recipients and underlying lung disease did not affect the incidence or severity of PRR. The incidence and severity of PRR was higher in patients undergoing cardiopulmonary bypass during lung transplantation. Patients with PRR had prolonged duration of mechanical ventilation and ICU stay. Overall, PRR did not affect the survival of the patients. However, survival of female lung transplant recipients was significantly better than male recipients (median survival, 60 vs 21 months; p = 0.02).
Conclusions: Acute pulmonary edema or PRR occurs frequently (57%) after lung transplantation. In this series, PRR was not associated with a prolonged ischemia time, preoperative pulmonary hypertension, the type of lung transplant, underlying lung disease, or age or sex of recipients. However, use of cardiopulmonary bypass during surgery was associated with increased incidence and severity of PRR. Also, the development of PRR resulted in prolonged mechanical ventilation and a longer ICU stay, but did not affect survival. Female lung transplant recipients survived significantly longer than male recipients. The reason for this difference in survival is unclear.
Key Words: acute pulmonary edema • lung transplantation • pulmonary reimplantation response
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Introduction |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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The occurrence of noncardiogenic pulmonary edema in the immediate postoperative period after lung transplantation is termed pulmonary reimplantation response (PRR). It is thought to be an ischemic vascular injury of the allograft that results in increased protein permeability of the lung microcirculation after reperfusion, which can result in interstitial and alveolar edema.1
Although PRR has been studied extensively in animals,2 3 4 5 6 limited information is available after lung transplantation in humans. For example, the incidence of PRR has not been established. Similarly, potential clinical predictors such as duration of ischemia time, preoperative pulmonary hypertension, underlying lung disease, and single-lung vs double-lung transplantation have not been well evaluated.
Therefore, there were four objectives of this study: to determine the incidence of PRR in a large number of consecutive lung transplant recipients, to determine whether any clinical factors predict the development of PRR, to examine the correlation of potential clinical predictors with the severity of PRR, and to evaluate the impact of PRR on morbidity and mortality of lung transplant recipients.
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Materials and Methods |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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65 years old with
chronic progressive end-stage pulmonary disease with projected life
expectancy of < 12 to 18 months. Preoperative right heart
catheterization was performed in all candidates age 
50 years old
and in those with suspected pulmonary hypertension on echocardiogram.
Bilateral lung transplantation was used in patients with cystic
fibrosis (CF), bilateral bronchiectasis, and in some patients with
primary pulmonary hypertension (PPH). In case of single-lung
transplantation, the side to be transplanted was determined primarily
by quantitative ventilation-perfusion scintigraphy: the lung with a
poorer ventilation-perfusion ratio was usually transplanted. The
decision to use cardiopulmonary bypass during surgery was based on the
presence of preoperative pulmonary hypertension and the response of
arterial oxygen tension, arterial carbon dioxide tension, elevation of
pulmonary artery pressure (PAP), and reduction in cardiac index during
one-lung ventilation.
Donor Selection and Lung Preservation
Standard donor selection criteria were applied.9
Organ harvesting was started with infusion of prostaglandin
E1 via a central vein beginning 15 min before
aortic cross-clamping, using 10 ng/kg/min prostaglandin
E1 and gradually increasing the rate of infusion
according to BP tolerance to a maximum of 80 ng/kg/min. Lung perfusion
cooling was performed using modified Euro-Collins solution at 4°C
into the main pulmonary artery. At least 4 L Euro-Collins solution was
used for the flush. Ventilation of the donor was continued with room
air during lung perfusion. The trachea was stapled with the lungs
two-thirds inflated. The lung was removed and placed in a sterile
plastic bag filled with Euro-Collins solution at 4°C.
Transplantation of the lung in the recipient was performed using the standard technique for single and bilateral sequential lung transplant.10 11 Systolic arterial and venous pressures, cardiac output, PAP, and arterial blood gases were closely monitored during the surgical procedure. In single-lung transplantation, allograft ischemia time was measured from aortic cross-clamping at organ procurement to the time of reperfusion after completion of the lung transplant. In bilateral sequential transplantation, ischemia time of the second lung was used.
Immunosuppression
Intravenous methylprednisolone (500 mg) was given
perioperatively immediately before graft perfusion. Standard induction
triple-drug immunosuppression consisting of cyclosporin (3 to 6 mg/kg),
azathioprine (2.5 mg/kg), and methylprednisolone (125 mg every 8 h
for 48 h followed by 20 mg bid until resumption of oral
medication) was initiated. The dose of azathioprine was adjusted to
maintain the WBC count > 4,000/µL.
Postoperative Management
Routine postoperative intensive care management was
performed.12
All patients had pulmonary artery catheters
for measuring central venous pressure, PAP, mean pulmonary artery
occlusion pressure, and cardiac output. Careful attention was given to
fluid balance to avoid fluid overload. Prophylactic antibiotics were
started perioperatively and ganciclovir was used in recipients with
cytomegalovirus mismatch (donor positive/recipient negative and donor
negative/recipient positive). Weaning from the ventilator was initiated
as early as possible after the surgery. Chest radiographs were obtained
on the day of surgery and at least once daily thereafter during the ICU
stay. All patients had bronchoscopy at least on alternate days to
remove secretions and to examine the bronchial anastomotic site.
Tracheal aspirate was obtained daily and examined for infection.
Bronchoscopy was also performed to do a BAL and to obtain protected
brush specimen for the diagnosis of infection whenever a new lung
infiltrate was identified on chest radiographs. Blood cultures were
also done daily during the ICU stay. Infection was suspected clinically
when lung infiltrates were associated with fever and hypoxemia.
Transbronchial biopsies of the allograft, in the first postoperative
week to diagnose rejection, were done at the discretion of the lung
transplant physician taking care of the patient. Patients with an acute
rejection diagnosis were treated with bolus methylprednisolone of 15
mg/kg (maximum, 1.0 g) IV once daily for 3 days after excluding
infection.
Identification of PRR
All chest radiographs in the first 5 postoperative days were
reviewed by a chest radiologist (P.B.O.) to identify pulmonary
infiltrates. The mean ratio of PaO2
to the fraction of inspired oxygen
(FIO2) was recorded in the first
24 h after the lung transplantation. PRR was diagnosed when the
following criteria were present within the first 24 h of
transplant: (1) allograft infiltrates on chest radiographs, (2)
hypoxemia with FIO2 0.30 to
maintain arterial oxygen tension 65 mm Hg, (3) pulmonary artery
occlusion pressure 12 mm Hg, and (4) absence of infection and
rejection. Chest radiographs showing lung infiltrates after 24 h
of lung transplantation were not categorized as PRR.
Severity of lung infiltrates on chest radiographs was graded using a categorical scale from 0 (none) to 5 (severe) as shown in Table 1 . Lungs on the chest radiograph were divided into three zones. Area of the lung above the aortic arch was labeled as upper zone, area of the lung below the pulmonary veins as lower zone, and the area of the lung between upper and lower zones was labeled as middle zone. The severity of PRR on chest radiographs increased with the number of zones involved.
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Statistical Analysis
Univariate analysis was performed to test for association
between PRR and potential baseline risk factors (age, sex, underlying
diagnosis, type and side of transplant, and cardiopulmonary bypass),
hospital outcome variables (ICU stay, duration of mechanical
ventilation and length of hospital stay, ischemia time, and mean PAP),
and long-term survival. A two-sided t test was used for
comparing the PRR and no PRR groups on continuous variables, Wilcoxon
rank-sum test for ordinal variables, and a likelihood ratio
2 test for categorical variables. Correlation
between PRR grade 0 to 5 and either continuous or ordinal variables was
assessed with Spearman correlation coefficient. The association of
baseline categorical factors with severity of PRR was assessed with
Wilcoxon rank-sum test or Kruskal-Wallis test. Baseline predictors of
long-term survival in these patients were assessed with Kaplan-Meier
curves or Cox proportional hazards regression models and log-rank
tests.
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Results |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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The mean allograft ischemia time was 236 min (range, 164 to 458 min) for double-lung transplant and 168 min (range, 80 to 358 min) for single-lung transplant. Thirty-seven (37%) patients required cardiopulmonary bypass during the surgery. The median time on cardiopulmonary bypass was 105 min (range, 46 to 198 min).
Prevalence of PRR by Risk Factors
Overall, 56 of 99 recipients (57%) experienced PRR after lung
transplantation. The mean
PaO2/FIO2
ratio in these patients was significantly lower in the first 24 h
after transplant than in patients who did not have PRR
(254 ± 110 vs 404 ± 137; p < 0.001).
The mean age of patients with PRR was similar to those who did not have PRR (44 ± 13 years vs 41 ± 14 years; p = 0.43; Table 2 ). Twenty-eight of 50 men (56%) and 28 of 49 women (57%) experienced PRR. Thus, no association was found between sex and development of PRR (p = 0.91).
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Allograft ischemia time did not predict PRR. The median ischemia time of patients with PRR was 168 min compared with 180 min for those patients who did not have PRR (p = 0.62). The maximal allograft ischemia time was 458 min.
Sixty of the 99 patients underwent preoperative right heart catheterization. Thirty of these 60 patients had normal PAP (mean, < 25 mm Hg). Eighteen patients had mild to moderate pulmonary hypertension (mean PAP, 25 to 50 mm Hg), and 12 had severe pulmonary hypertension (mean PAP, > 50 mm Hg). The incidence of PRR was 51% in patients without pulmonary hypertension, 78% in the mild to moderate group, and 58% in patients with severe pulmonary hypertension. The differences among the three groups were not significant (p = 0.10).
Thirty-seven patients required cardiopulmonary bypass during surgery. The mean time on cardiopulmonary bypass (pump time) was 109 min (quartiles, 71, 141 min). Patients who required cardiopulmonary bypass during surgery (26 of 37 patients; 70%) had significantly higher rate of PRR compared with those who did not (30 of 62 patients; 48%; p = 0.03; Table 2 ).
Severity Grade of PRR by Risk Factors
Chest radiographs of patients who experienced PRR after lung
transplantation were graded on a severity scale of 0 (none) to 5 (very
severe; Table 1
). As shown in Table 3
, patients with higher PRR grade had lower
PaO2/FIO2
ratio (p < 0.001). In this study, ischemia time of the allograft did
not predict the degree of PRR (Table 3) . Similarly, underlying lung
disease, age, or sex of the recipient as well as type or side of
transplant did not correlate with the severity of the PRR. However,
patients who required cardiopulmonary bypass during surgery had
significantly higher grade of PRR on chest radiograph or arterial blood
gas abnormalities compared with those who did not (median severity
grade, 2.0 vs 0.5; Wilcoxon-rank sum test, p = 0.01; Fig 2
). The duration of pump time did not correlate with the severity of PRR.
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Of the patients who were discharged from the hospital (n = 79) after the surgery, the mean follow-up time was 52 months (range, 30 to 90 months). The overall median Kaplan-Meier survival of patients (including postoperative deaths) was 34 months (range, 0 to 90 months).
Survival of female lung transplant recipients was significantly better than that of male recipients (median survival, 60 months vs 21 months; p = 0.02; Fig 3 ). The median survival of patients who had PRR was 28 months compared with 36 months for patients who did not have PRR (p = 0.99; Fig 4 ). Thirty-day survival of patients who experienced PRR was 86% (95% confidence interval [CI], 77 to 95%) compared with 84% (95% CI, 73 to 95%) in patients without PRR. Thus, PRR also did not affect the long-term survival of the patients. One-year survival was 68% (95% CI, 56 to 80%) in patients with PRR compared with 65% (95% CI, 51 to 79%) in patients without PRR. Similarly, 3-year survival was also similar in the two groups (49% vs 48%).
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Discussion |
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TOPAbstractIntroductionMaterials and MethodsResultsDiscussionConclusionReferences |
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12 mm Hg, (3) hypoxemia
(FIO2 0.30 to maintain arterial
oxygen tension of 65 mm Hg), and (4) no evidence of infection or
rejection. In addition to arterial hypoxemia, PRR may be associated
with systemic hypotension and a reduction of cardiac
output.15
The pathogenesis of PRR is not fully understood;
however, various cytokines and the generation of free oxygen
radicals4
during reperfusion of the allograft have been
implicated in its causation. Both ischemia and reperfusion seem to be
essential to the development of PRR. Although PRR has been extensively
investigated in animal models,2
16
17
18
only limited data
is available in human lung transplant recipients. Parenchymal infiltrates in the allograft consistent with PRR are a radiologic finding in the first 24 h of the postoperative period. Herman19 reported this process in 13 of 14 single-lung transplant recipients. In another study, 24 of 40 single-lung transplant recipients (60%) had PRR.14 PRR begins in the first 24 h after lung transplantation and generally worsens over time, reaching its peak in 4 to 7 days. In this study, 56 of 99 patients (57%) demonstrated infiltrates on chest radiographs within 24 h after transplantation, along with arterial hypoxemia. When lung infiltrates and hypoxemia developed after 24 h, fluid overload, infection, or allograft rejection were the usual causes. In our patients, we excluded infection by regular cultures of tracheal aspirate, blood cultures, BAL, and protected brush specimens. Because allograft rejection is uncommon in the first 24 h of lung transplantation, transbronchial biopsies were performed in patients who had lung infiltrates after the first 24 h at the discretion of the transplant physician.
Which lung transplant recipients are susceptible to PRR is not clearly known. Earlier reports suggest that prolonged allograft ischemia time predisposes to PRR.20 Sleiman et al14 studied 40 patients who received single-lung transplants and found that the mean ischemia time of patients with PRR was higher (241 ± 103 min) than patients who did not have PRR (155 ± 71 min). Other studies21 22 have suggested that an ischemia time of up to 6 h does not result in clinical dysfunction of the allograft. The ischemia time in our patients was much shorter than in other studies, but similar to the ischemia time reported recently by Christie et al.22 The median ischemia time was 168 min (quartiles, 142, 211 min) in patients with PRR and 180 min (quartiles, 150, 221 min) without PRR, with the longest ischemia time being 458 min. Thus, we believe that the relatively short ischemia time in our study resulted in failure to identify ischemia time as a risk factor for PRR.
PRR probably results from increased capillary permeability of the lung microcirculation. In single-lung transplant recipients with pulmonary hypertension, the majority of the pulmonary artery blood flow is directed toward the allograft because of the lower vascular resistance. Hence, patients with pulmonary hypertension are expected to have more severe degree of PRR. Bando et al23 reported 63% incidence of PRR in patients with pulmonary hypertension (12 of 19 patients), which is similar to the incidence in this study (56%). Kawaguchi et al3 have shown that, in a rat model, severity of PRR depends on severity of pulmonary hypertension. In this study, PRR developed in 51% of patients without pulmonary hypertension, 78% of patients with mild to moderate pulmonary hypertension, and 58% of patients with severe pulmonary hypertension (p = 0.10). Among those who underwent right heart catheterization (n = 60), the mean PAP was 32 ± 17 mm Hg in patients with PRR and 33 ± 16 mm Hg in patients who did not have PRR (p = 0.28). Moreover, the incidence of PRR in double-lung transplant recipients was similar to that of single-lung transplant recipients, suggesting that double-lung transplantation was not better than single-lung transplantation in preventing PRR.
Some patients require cardiopulmonary bypass during lung
transplantation. The general recommendation is that cardiopulmonary
bypass should be avoided during lung transplant because it adds
technical complexity to the procedure and increases ischemia time by
prolonging operative time. Cardiopulmonary bypass also induces cytokine
production (interleukin [IL]-1, IL-6, IL-8, tumor necrosis factor,
and interferon-
), probably in part because of contact of the blood
with the pump membrane. Some of these cytokines may increase lung
capillary permeability and have been implicated in ischemia-reperfusion
injury after lung transplantation.24
Some clinical studies
have suggested that patients requiring cardiopulmonary bypass during
lung transplantation may have a greater degree of allograft
dysfunction25
and an increased alveolar-arterial oxygen
difference.26
In this study, the incidence of PRR was
higher in patients who underwent cardiopulmonary bypass compared with
those did not (70% vs 48%; p = 0.03). Moreover, patients who
underwent cardiopulmonary bypass had a higher grade of PRR compared
with those who did not undergo cardiopulmonary bypass (Fig 2)
.
Finally, we analyzed the data to determine whether the underlying lung disease was associated with the severity of PRR. Patients with IPF had a slightly higher incidence and severity of PRR compared with patients with other diseases, but the difference was not statistically significant). Interestingly, patients with PPH did not have a more severe degree of PRR.
Patients who experienced PRR required longer duration of mechanical ventilation and required additional days of ICU stay compared with patients who did not have PRR. Overall, the hospital stay of patients with and without PRR was not different. However, in patients who survived the surgery and were discharged from the hospital, the number of hospital days correlated with the severity of PRR (p = 0.006; Spearman correlation; Table 3 ). Moreover, patients with a higher grade of PRR had an increased duration of mechanical ventilation (p < 0.001) and required more days in the ICU (p = 0.001). Despite prolonging the ICU stay, PRR had no impact on 30-day survival.
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Footnotes |
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Received for publication June 12, 1998. Accepted for publication February 3, 1999.
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