Primary Graft Dysfunction and Long-term Pulmonary Function After Lung Transplantation

Whitson, Bryan A.; Prekker, Matthew E.; Herrington, Cynthia; Whelan, Timothy; Radosevich, David M.; Hertz, Marshall I.; Dahlberg, Peter S.

doi:10.1016/j.healun.2007.07.018

Cited by 228 publications

(178 citation statements)

References 16 publications

(20 reference statements)

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“…As per the International Society of Heart and Lung Transplantation definition, PGD cases had diffuse alveolar infiltrates involving the lung allograft(s) that spared the native lung in the case of single lung transplantation; Pa O 2 /FI O 2 less than 200 mm Hg; and no other secondary cause of graft dysfunction, as defined in detail in prior publications (2,3,5,13,18). This definition of ''any grade 3 PGD'' has been adopted in a number of recent investigations (19)(20)(21)(22)(23). In addition, we conducted sensitivity analyses using patients with grade 3 PGD present at 72 hours, as in prior studies (3,5,8,13).…”

Section: Definition Of Primary Graft Dysfunctionmentioning

confidence: 99%

Plasma Levels of Receptor for Advanced Glycation End Products, Blood Transfusion, and Risk of Primary Graft Dysfunction

Christie¹,

Shah²,

Kawut³

et al. 2009

Am J Respir Crit Care Med

122

106

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Rationale:The receptor for advanced glycation end products (RAGE) is an important marker of lung epithelial injury and may be associated with impaired alveolar fluid clearance. We hypothesized that patients with primary graft dysfunction (PGD) after lung transplantation would have higher RAGE levels in plasma than patients without PGD. Objectives: To test the association of soluble RAGE (sRAGE) levels with PGD in a prospective, multicenter cohort study. Methods: We measured plasma levels of sRAGE at 6 and 24 hours after allograft reperfusion in 317 lung transplant recipients at seven centers. The primary outcome was grade 3 PGD (Pa O 2 /FI O 2 , 200 with alveolar infiltrates) within the first 72 hours after transplantation. Measurements and Main Results: Patients who developed PGD had higher levels of sRAGE than patients without PGD at both 6 hours (median 9.3 ng/ml vs. 7.5 ng/ml, respectively; P 5 0.028) and at 24 hours post-transplantation (median 4.3 ng/ml vs. 1.9 ng/ml, respectively; P , 0.001). Multivariable logistic regression analyses indicated that the relationship between levels of sRAGE and PGD was attenuated by elevated right heart pressures and by the use of cardiopulmonary bypass. Median sRAGE levels were higher in subjects with cardiopulmonary bypass at both 6 hours (P 5 0.003) and 24 hours (P , 0.001). sRAGE levels at 6 hours were significantly associated with intraoperative red cell transfusion (Spearman's r 5 0.39, P 5 0.002 in those with PGD), and in multivariable linear regression analyses this association was independent of confounding variables (P 5 0.02). Conclusions: Elevated plasma levels of sRAGE are associated with PGD after lung transplantation. Furthermore, plasma sRAGE levels are associated with blood product transfusion and use of cardiopulmonary bypass.

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Section: Definition Of Primary Graft Dysfunctionmentioning

confidence: 99%

Plasma Levels of Receptor for Advanced Glycation End Products, Blood Transfusion, and Risk of Primary Graft Dysfunction

Christie¹,

Shah²,

Kawut³

et al. 2009

Am J Respir Crit Care Med

122

106

View full text Add to dashboard Cite

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“…Primary graft dysfunction (PGD), defined as the occurrence of acute lung injury (ALI) in the allograft within 72 hours of transplantation (1), is a leading cause of death early after lung transplantation (2) and is a risk factor for chronic allograft rejection (3,4). Although PGD is typically attributed to ischemia-reperfusion injury of the allograft, systemic inflammation plays a critical role (5)(6)(7).…”

mentioning

confidence: 99%

Obesity and Primary Graft Dysfunction after Lung Transplantation

Lederer¹,

Kawut

Wickersham

et al. 2011

Am J Respir Crit Care Med

137

102

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Rationale: Obesity has been linked to acute lung injury and is a risk factor for early mortality after lung transplantation. Objectives: To examine the associations of obesity and plasma adipokines with the risk of primary graft dysfunction after lung transplantation. Methods: We performed a prospective cohort study of 512 adult lung transplant recipients with chronic obstructive pulmonary disease or interstitial lung disease enrolled in the Lung Transplant Outcomes Group Study. In a nested case-control study, we measured plasma leptin, adiponectin, and resistin before lung transplantation and 6 and 24 hours after lung transplantation in 40 cases of primary graft dysfunction and 80 control subjects. Generalized linear mixed models and logistic regression were used to estimate risk ratios and odds ratios. Measurements and Main Results: Grade 3 primary graft dysfunction developed within 72 hours of transplantation in 29% participants. Obesity was associated with a twofold increased risk of primary graft dysfunction (adjusted risk ratio 2.1; 95% confidence interval, 1.7-2.6). The risk of primary graft dysfunction increased by 40% (confidence interval, 30-50%) for each 5 kg/m 2 increase in body mass index after accounting for center, diagnosis, cardiopulmonary bypass, and transplant procedure. Higher plasma leptin levels were associated with a greater risk of primary graft dysfunction (sexadjusted P ¼ 0.02). The associations of both obesity and leptin with primary graft dysfunction tended to be stronger among those who did not undergo cardiopulmonary bypass. Conclusions: Obesity is an independent risk factor for primary graft dysfunction after lung transplantation.

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“…However, primary graft dysfunction (PGD), infection, and rejection remain as important contributors to mortality after lung transplantation. PGD is the most common postoperative complication, occurring in 25% of recipients [10,11]. The treatment of PGD varies with the severity of lung injury, with general supportive care in low grade forms.…”

Section: Harefield Hospitalmentioning

confidence: 99%

Mechanical ventilation after lung transplantation

Thakuria

Romano

Carby

et al. 2016

Journal of Critical Care

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IntroductionTo explore the hypothesis that early ventilation strategies influence clinical outcomes in lung transplantation, we have examined our routine ventilation practices in terms of tidal volumes (Vt) and inflation pressures.Methods 124 bilateral lung transplants between 2010 and 2013 were retrospectively assigned to low (<6ml/kg), medium (6-8ml/kg) and high (>8ml/kg) Vt groups based on ventilation characteristics during the first 6 hours after surgery. Those same 124 patients were also stratified to low-pressure (<25cm H2O) and high-pressure (≥25cm H2O) groups. ResultsEighty per cent of patients were ventilated using pressure control mode. Low, medium and high tidal volumes were applied to 10%, 43%, and 47% of patients respectively. After correcting for patients requiring extracorporeal support, there was no difference in short to mid-term outcomes among the different Vt groups. Low inflation pressures were applied to 61% of patients, who had a shorter length of ICU stay (5 vs. 12 days; p=0.012), higher FEV1 at 3 months (77.8% vs. 60.3%; p<0.001), and increased 6-month survival rate (95% vs. 77%; p=0.008). ConclusionLow Vt ventilation has not been fully adopted in our practice. Ventilation with higher inflation pressures, but not tidal volumes, were significantly associated with poorer outcomes after lung transplantation.Response to Reviewers: Dear Prof. Lumb, Article ID: JCRC-D-15-00340 -Mechanical ventilation following lung transplantationWe are most grateful to the reviewers for taking the time and care to appraise this manuscript, and for your constructive critique. We have addressed all of the points that were raised and have amended the manuscript accordingly. We feel that your suggestions has significantly improved the original manuscript.Responses to Reviewer #1 Reviewer #1: "The manuscript does not add anything new to the literature. It has been known for a very long time that excessive tidal volume and/or inflation pressures adversely affect patient outcome."Author response: We are grateful that you have taken the time to review our manuscript, although we are disappointed by your conclusions. We have made detailed arguments in both the introduction and discussion that highlight the need for this work within lung transplantation, combined with our unique approach to this clinical problem. Your statement is in direct opposition with the views of the other reviewers, who have helpfully pointed out the potential importance of our study within this field. Your critique also fails to acknowledge the major ongoing debate regarding the special importance of driving pressures, and the relative roles of tidal volumes and pressures in acute lung injury. As a rebuttal, we would respectfully suggest that our manuscript does add to the existing body of knowledge on this topic. As stated in the manuscript, we believe that our manuscript fills an important gap within the literature on VALI by providing new observations on lung ventilation practices in lung transplant recipients, a population that was...

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Primary Graft Dysfunction and Long-term Pulmonary Function After Lung Transplantation

Cited by 228 publications

References 16 publications

Plasma Levels of Receptor for Advanced Glycation End Products, Blood Transfusion, and Risk of Primary Graft Dysfunction

Plasma Levels of Receptor for Advanced Glycation End Products, Blood Transfusion, and Risk of Primary Graft Dysfunction

Obesity and Primary Graft Dysfunction after Lung Transplantation

Mechanical ventilation after lung transplantation

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