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BACKGROUND: Since 2005, the Lung Allocation Score (LAS) has prioritized patient benefit and post-transplant survival, reducing waitlist to transplant time to less than 200 days and decreasing mortality on the waitlist. A current challenge is the wait for the waitlist—the time between patient’s transplant-eligible diagnosis and waitlist registration. METHODS: We investigated whether sociodemographic (age, sex, race, insurance, marital status, median household income) and clinical (FEV(1) % of predicted, body mass index, depression/anxiety, alcohol/substance misuse, absolute/relative contraindications) factors influenced referral and waitlist registration. We conducted a retrospective cohort study through chart review of hospitalized patients on the University of Chicago general medicine service from 2006–2014 meeting transplant-eligible criteria and ICD-9 billing codes for cystic fibrosis (CF) and pulmonary fibrosis (PF). We analyzed the times from transplant-eligibility to referral, work-up, and waitlist using Kaplan-Meier curves and log-rank tests. RESULTS: Overall, referral rates for transplant-eligible patients were 64%. Of those referred, approximately 36% reach the lung transplant waitlist. Referred CF patients were significantly more likely to reach the transplant waitlist than PF patients (CF 60% vs. PF 22%, p

Lung transplantation is a well established treatment option for selected patients with endstage pulmonary diseases (Weill et al., J Heart Lung Transplant. 2015;34(1):1–15). Bronchial and pulmonary secretions after lung transplantation are a common cause of post-operative morbidity for recipients (Duarte and Lick, Chest Surg Clin N Am. 2002;12(2):397–416). Their clinical impact may frequently be underestimated and this can lead to significant complications. Consequently, patients may experience potential delays in their overall recovery after lung transplantation. As outcomes after lung transplantation have significantly improved over the last decade, this complex therapeutic strategy has become more prevalent (Chambers et al., J Heart Lung Transplant. 2017;36:1047–1059). With increasing clinical encounters with these challenging patients, it is essential for critical care physicians and allied providers to have applied knowledge and adequate skill sets to support lung recipients during the recovery. This is particularly important in the immediate post-operative phase and crucial after extubation. This review defines such pulmonary secretions and the pathophysiology involved. We provide a review of the applicable evidence available in this context.

Background Although postoperative predicted forced expiratory volume in the first second and diffusing capacity of lung (ppoFEV 1 % and ppoDLCO%, respectively) have been identified as independent predictors of postoperative pulmonary complications after open lobectomy, it has been suggested that their predictive abilities may not extend to patients undergoing minimally invasive lobectomy. Methods We evaluated outcomes in 805 patients undergoing isolated lobectomy through open (n = 585) or minimally invasive approaches (n = 220) using a prospective database. Demographic and physiologic data were extracted and compared with complications classified as pulmonary, cardiac, other, mortality, and any. Results Patients included 428 women and 377 men; mean age was 65.0 years. Minimally invasive patients were older (66.6 versus 64.3 years, p = 0.006), had better ppoFEV 1 % (71.5% versus 65.6%, p p = 0.017), and less often underwent induction therapy (0.5% versus 4.8%, p = 0.003). Pulmonary and other complications were less common after minimally invasive lobectomy (3.6% versus 10.4%, p = 0.0034; 8.6% versus 15.8%, p = 0.008). Operative mortality occurred in 1.4% of minimally invasive patients and 3.9% of open patients ( p = 0.075). Pulmonary complication incidence was related to predicted postoperative lung function for both minimally invasive and open approaches. On multivariate analysis with stratification for stage, ppoFEV 1 % and ppoDLCO% were predictive of pulmonary complications for both minimally invasive and open approaches. Conclusions Our results suggest that the predictive abilities of ppoFEV 1 % and ppoDLCO% are retained for minimally invasive lobectomy and can be used to estimate the risk of pulmonary complications.

Airway complications remain a major cause of morbidity and mortality after cardiothoracic transplantation. The reported incidence of airway ischemic complications varies widely, contributed to by the lack of a universally accepted grading system and standardized definitions. Furthermore, the majority of the existing classification systems fail to integrate the wide range of possible bronchial complications that may develop after lung transplant. Hence, a Working Group was created by the International Society for Heart and Lung Transplantation with the aim of elaborating a universal definition of adult and pediatric airway complications and grading system. One such area of focus is to understand the problem in the context of a more standardized consensus of classifying airway ischemia. This consensus definition will have major clinical, therapeutics, and research implications.

The purpose of this contribution is to review the development and scope of postgraduate training and educational affairs of the International Society of Heart and Lung Transplantation.

Purpose of review This review presents a concise update on clinical donation after cardiac death (DCD or DDCD) lung transplantation. Lung allografts have predominantly been procured from donors after determination of neurologic death but will not meet the existing demand. A steadily increasing need for lungs is evident worldwide, especially in an era of improved outcomes for recipients. Other solid organ utilization from donors after determination of cardiac death has markedly increased internationally, but the utilization rate of lungs from such donors is still considerably less. The multifaceted reasons for this discrepancy are considered, and the recent evidence available supporting DCD for lung transplantation in clinical practice is presented in context. The recent experimental research studies are not within the remit of this appraisal. Recent findings The more recent and markedly increased lung recipient cohorts showed very satisfactory survival outcomes for DCD transplantation in several programs. The overall utilization rate, however, remains low. The background and the rationale of lung donor allograft expansion to proactively include DCD allografts from controlled (Maastricht category III donors) is re-emphasized in this review. The feasibility of other DCD categories for lung transplantation is considered. This is particularly prudent with the advent of the ex-vivo lung perfusion modality in pulmonary procurement. Summary Despite evidence for adequate survival outcomes and reported favorable primary graft dysfunction rates, DCD lung transplantation remains underutilized in most countries. Waiting times could be notably reduced and mortality of lung candidates arguably decreased by a more decided and appropriate implementation of proven DCD lung transplant strategies.

OBJECTIVES: Obesity has been thought to predispose patients to excess morbidity after lung resection because of decreased diaphragm excursion, reduced lung volumes and relative immobility. We assessed the relationship of body mass index (BMI) to acute outcomes after major lung resection. METHODS: Information from our database of lung resections was evaluated for the period 1980–2011. Univariate analysis for adverse events (pulmonary, cardiovascular, other and overall) was used to select variables for inclusion in multivariate logistic regression analyses. Missing values were imputed. BMI was categorized as underweight (

Sarcoma originating from the pulmonary veins represents one of the rarest subtypes of sarcoma. We report the case of a 52-year-old woman presenting with cough and scant hemoptysis and ultimately diagnosed with a primary intimal sarcoma of the left inferior pulmonary vein extending into the left lower lobe of the lung. To our knowledge, this is the first reported case of such pathology in the literature. We present the case and critically appraise the literature for sarcomas of the great vessels.

Lung transplantation is now a well established treatment option for several end-stage respiratory diseases. Survival after lung transplantation has significantly improved over the last decade. The primary limitation to increased utilization of lung transplantation remains donor scarcity. Suitable allografts have been procured from donors after determination of neurologic death and from donors after determination of cardiac death (DDCD or DCD). Historically, the first human lung transplantation performed, utilized an allograft procured after cardiovascular death, also referred to as nonheart-beating donor.The experience at University of Wisconsin in 1993 reintroduced DCD lung transplantation with the first successful clinical case.A potential additional lung allograft source, DCD lung transplantation has been established with very acceptable outcomes observed by several centers. We provide the relevant background for the rationale of donor allograft expansion to include DCD lungs from controlled (Maastricht category III donors).This review considers the available evidence for DCD lung transplantation and compares reported primary graft dysfunction rates and current survival data available.

Background It has been previously shown that donor treatment with aprotinin or inhaled nitric oxide reduces reperfusion injury after lung transplantation in animals. These studies used living donors with normal lungs. However, the main source of lungs for transplantation is brain-dead donors. Brain death causes systemic inflammatory response and lung injury, rendering the organ susceptible to reperfusion injury after transplantation. We hypothesized that treatment with aprotinin or inhaled nitric oxide after brain death would improve the donor inflammatory response and reduce lung reperfusion injury after transplantation. Methods Brain death was induced in 24 rats by intracranial balloon inflation. Subsequently, the animals received intravenous aprotinin ( n = 8), inhaled nitric oxide ( n = 7), or no treatment ( n = 9) for 5 hours. The lungs were retrieved and reperfused for 2 hours using recipient rats. Results After brain death, oxygenation deteriorated earlier and significantly more in rats that received treatment, especially with nitric oxide. Treatment did not reduce the donor systemic inflammatory response as assessed by serum levels of proinflammatory cytokines. Oxygenation, airway pressure, pulmonary vascular resistance, lung water index and bronchoalveolar lavage cytokine levels were similar after reperfusion of grafts from all three groups of donors. Conclusions Donor treatment with aprotinin or inhaled nitric oxide does not improve lungs that have been injured by brain death.

Rat lung allograft rejection is mediated by collagen type V (col(V)) specific T-helper-cell 17 (Th17) cells. Adoptive transfer of these cells is sufficient to induce rejection pathology in isografts, whereas tolerance to col(V) suppresses allograft rejection. Therefore, we tested whether regulatory T cells from tolerant rats could suppress the Th17-mediated rejection in the syngeneic model of lung transplantation.Rats were subjected to syngeneic left lung transplantation, and acute rejection was induced by adoptive transfer of lymph node cells from col(V)-immunized rats. Tolerance was induced by intravenous injection of col(V), and spleen lymphocytes were used for adoptive transfer. CD4+ T cells were depleted using magnetic beads. Lung isografts were analyzed using micro-positron emission tomography imaging and histochemistry. The transvivo delayed type hypersensitivity assay was used to analyze the Th17 response.Adoptive cotransfer of col(V)-specific effector cells with cells from col(V)-tolerized rats suppressed severe vasculitis and bronchiolitis with parenchymal inflammation, and the expression of interleukin (IL)-17 transcripts in mediastinal lymph nodes induced by effector cells alone. Analysis by transvivo delayed type hypersensitivity showed that the reactivity to col(V) was dependent on the presence of tumor necrosis factor-alpha and IL-17 but not interferon-gamma. Depletion of CD4+ T cells from the suppressor cell population abrogated the col(V)-specific protection.Th17-mediated acute rejection after lung transplantation is ameliorated by CD4+ col(V)-specific regulatory T cells. The mechanism for this Th17 suppression is consistent with tolerance induction to col(V). The goal of transplantation treatment, therefore, should target Th17 development and not suppression of T-cell activation by suppressing IL-2.

Sympathetic discharge and hypertensive crisis often accompany brain death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor brain death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain death was induced by intracranial balloon inflation in rats, with or without alpha-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after brain death or sham procedure and reperfused using recipient rats. In a fourth group, brain death was induced and the lungs were retrieved 5 h after brain death and reperfused. Postreperfusion, lungs retrieved early from untreated brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockade-treated donors. Lungs retrieved late from brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor brain death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury.

Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by alpha-adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.

Patients with irreversible lung injury listed for lung transplantation increasingly face the dilemma of requiring a “bridge” to transplantation, which has prompted the development of alternative lung support devices. The utility of extra-corporal lung support to improve outcomes for various indications is still in evolution. We review the indications for lung support and the types of extracorporeal support systems and assess the evidence available for device support therapy for respiratory failure. We conclude that device therapy for reversible lung failure should be decided on an individual patient basis. No generic recommendations can currently be made.

Lung transplantation is the only established therapeutic option for several end-stage respiratory diseases. Limited mostly by lack of suitable allografts, the results have measurably improved over the last decade. Numerous surgical and pharmaceutical improvements have had positive impact on outcomes. The potential for critical care issues and the need for interdisciplinary management remains paramount. Cardiac, renal, and metabolic complications are frequently encountered in the acute postoperative phase. Allograft rejection and infectious diseases as well as problems related to immunosuppressive regimen are seen later after lung transplantation. Neurologic manifestations with a range of etiologies are discussed here in this context.

Lung transplantation is the only established therapeutic option for several end-stage respiratory diseases. Limited mostly by lack of suitable allografts, the results have measurably improved over the last decade. Numerous surgical and pharmaceutical improvements have had positive impact on outcomes. The potential for critical care issues and the need for interdisciplinary management remains paramount. Cardiac, renal, and metabolic complications are frequently encountered in the acute postoperative phase. Allograft rejection and infectious diseases as well as problems related to immunosuppressive regimen are seen later after lung transplantation. Neurologic manifestations with a range of etiologies are discussed here in this context.

Purpose of review Primary graft dysfunction (PGD), a form of acute lung injury after lung transplantation, has a significant impact on clinical outcomes after lung transplantation. This potentially reversible graft impairment occurs after ischemia-reperfusion injury. This review describes the expanding body of literature evaluating the central role of innate immune activation, nonadaptive responses and dysregulation in the development of PGD after lung transplant. Recent findings The innate immune system, highlighted by Toll-like receptor pathways and neutrophil migration and influx, plays an important role in the initiation and propagation of ischemia-reperfusion injury. Recent plasma biomarker and gene association studies have identified several genes and proteins composing innate immune pathways to be associated with PGDs. Long pentraxin-3 and Toll-like receptors, as well as inflammasomes and Toll-interacting protein, are associated with the development of PGD after lung transplantation. Summary Innate immune pathways are involved in the development of PGD and may provide attractive targets for therapies. It may be possible to prevent or treat PGD, as well as to allow pre-transplant PGD risk stratification. To improve understanding of the mechanisms behind clinical risk factors for PGD will require further in-depth correlation of donor-specific and recipient-related triggers of nonadaptive immune responses.

Background Tolerance to collagen structures has been shown to inhibit the progression of autoimmune scleroderma and rheumatoid arthritis. More recently, tolerance induction to collagen type V (colV) in experimental models of lung transplantation was shown to ameliorate the complex pathology known as "chronic rejection." The link between colV autoimmunity and progressive graft dysfunction and subsequent development of bronchiolitis obliterans syndrome (BOS) has been established in human lung transplant recipients. We hypothesized that intravenous injection of colV inhibits development of lung fibrosis in a bleomycin-induced lung injury mouse model. Methods Experimental animals were injected intravenously with saline or colV 10 days before intratracheal instillation of bleomycin. Pulmonary inflammation was monitored and quantified for the presence of cells in the bronchoalveolar lavage (BAL) fluid by flow cytometry and histology of lung tissue. Results ColV–pre-treated animals showed a significant reduction in lung inflammation compared with non-treated animals, according to histology and morphometry. The number of inflammatory cells in the BAL fluid was significantly reduced and associated with a lower proportion of γδ T cells and CD4 + T cells in the colV–pre-treated group. Matrix metalloproteinase-2 and -9 (MMP-2 and -9; also known as gelatinase A and gelatinase B, respectively) levels in the BAL fluid were significantly reduced in colV–pre-treated mice compared with the non-treated mice. In addition, intravenous injection of colV was associated with a significant reduction in the relative expression of interleukin (IL)-6, IL-17 and IL-22 in cells present in BAL fluid at 7 and 14 days after bleomycin instillation. Conclusions Pre-treatment by intravenous injection of colV inhibits bleomycin-induced pulmonary fibrosis by inhibiting IL-6 and IL-17 production. Fibrosis treatment in this context therefore should target induction of colV tolerance and Th17 development.

Background Combined heart–kidney transplantation (HKTx) is increasing in frequency, but long-term outcomes are unknown and appropriately comparative analysis is lacking. Methods This study was a retrospective review of prospectively collected data for 19 HKTx patients. Patient and graft survival, graft rejection and coronary allograft vasculopathy (CAV) were compared for HKTx vs recipients of a heart ( n = 515) or kidney alone ( n = 3,188) or both organs at separate time-points ( n = 8). Results Patient and graft survival did not differ for HKTx vs any group. HKTx time to first rejection episode was significantly prolonged for both organs vs single-organ recipients. The incidence of CAV was significantly lower for HKTx. Conclusions HKTx provides outcomes similar to those for solitary heart or kidney transplantation. There may be an immunologic advantage to receiving organs in a combined fashion. Such allocation of organs seems medically appropriate; however, more refined strategies are needed to identify optimal recipient populations.

Background It remains unclear which donor and recipient factors influence long-term allograft function in lung transplantation (LTx). Methods From October 1988 to February 2005, a total of 280 recipients underwent LTx at our center. Donor data and cause of death (CoD) were analyzed. The CoD was categorized according to rate of increase in intracranial pressure at the time of death. Each donor and recipient factor was correlated with long-term graft function. Recipient details, type of transplant, indication for transplant, and time on waiting list were analyzed. Recipients were stratified based on allograft ischemia time (AIT): 0 to 6, 6 to 8, 8 to 10, and >10 hours. Results Mean donor age was 30.9 years (36.7% male); 49.8% were cytomegalovirus (CMV) positive. Donor CoD was characterized by a slow rise in intracranial pressure (ICP) in 34.4%, rapid ICP in 18.7%, an intermediate ICP in 44.3%, and with no rise in 2.6%. A graft survival benefit was seen with female donors (P = .048); 34.4% of recipients ultimately developed graft failure at long term follow-up. Mean recipient age was 48 years; 63% were male and mean body-mass index (BMI) was 23.6; 60.2% had single lung transplantation, and mean wait list time was 323 days. Mean AIT totaled 421 minutes. Graft survival was longer with AIT of 8 to 10 hours compared to 6 to 8 hours (P = .03). Conclusions Donor factor analysis implied only female donor status conferred a long-term graft survival advantage. Intracranial pressure rise differences appear clinically unimportant. Prolonged cold ischemic time (>10 hours) or low recipient BMI did not adversely affect allograft function in our review.

Background Primary graft dysfunction (PGD) after lung transplantation (LTx) carries a significant mortality and clinical management is controversial. Extracorporeal membrane oxygenation (ECMO) has been used infrequently for recovery from acute lung injury (ALI) in this setting. We reviewed our experience with ECMO after primary LTx. Methods The present study is a retrospective analysis of all LTx patients between 1991 and 2004. Twenty-two patients sustained severe PGD with subsequent placement on ECMO. We analyzed indications and 30-day, 1-year and 3-year mortality. Complications and incidence of multiple-organ failure (MOF) were determined. Critical appraisal of the evidence available to date was performed. Results A total of 297 LTxs were performed during the study period, with 97.5%, 88.6% and 73.8% survival at 30 days, 1 year and 3 years, respectively. Twenty-two patients (7.9%) had severe allograft dysfunction leading to ECMO support. Twelve patients received single-lung (SLTx), 8 double-lung (BLTx), 1 single-lung/kidney (SLKTx) and 1 heart/lung (HLTx) transplantation. Thirty-day, 1-year and 3-year survival of LTx recipients with ECMO support post-operatively were 74.6%, 54% and 36%, respectively. MOF was the predominant cause of death (58.3%) in patients on ECMO support for PGD. Conclusions Our data suggest that, in addition to prolonged ventilation and pharmacologic support, ECMO should be considered as a bridge to recovery from PGD in lung transplantation. Early institution of ECMO may lead to diminished mortality in the setting of ALI despite the high incidence of MOF. Late institution of ECMO was associated with 100% mortality in this investigation.

Background: The increasing prevalence of obesity is a public health concern and perceived as a potential risk factor in open heart surgery. We critically appraised the literature available regarding postoperative complications in obese patients. Methods: A single-center retrospective evaluation of complication rates (1999—2004) in cardiac surgical patients categorized by body mass index (BMI) was conducted. The overall incidenceofcomplications(CX),renalfailure(RF),hemodialysis(HD), atrialfibrillation(AF),cardiacarrest(CA),infections(INF),stroke(CVA and TIA), prolonged ventilation (VENT), and pulmonary embolism (PE) were observed. Patients with normal BMI (20—30) served for comparison, obesity and extreme obesity (ExtOb) were defined as BMI 30—40 and � 40, respectively. Results: In our institutional review of 1920 patients, 1780 met the inclusion criteria with BMI < 20 (n = 53), 20—30 (n = 1056), 30—40 (n = 592), and � 40 (n = 79) based on National Health and Nutrition Examination Survey (NHANES) criteria. Significant increase in complications (STS database guideline definitions) were observed with a BMI � 40, 58% versus 47% (p = 0.04). Extremely obese patients (ExtOb) had increased length of stay (LOS) (11.4 days vs 9.6 days; p � 0.01), rate of renal failure (14.3% vs 5%; p � 0.01) and prolonged ventilation (39%; p = 0.01) compared to non-obese patients. Extremely obese had no significant increase in hemodialysis (7.3% vs 3.2%; p = 0.11) or stroke (5.2% vs 2.9%; p = 0.29). Obese patients (Ob) had increased LOS (10 days vs 9.6 days; p = 0.04) and prolonged ventilation (28.3% vs 23.5%; p = 0.03). Conclusions: Cardiac surgery can be performed without significant increase in perioperative and 30-day mortality in obese and extremely obese patients. Overall complication rates and LOS in patients with BMI � 40 is increased and demands attention. We provide evidence that rates of few specific complications increase with extreme obesity. For risk stratification in the setting of an obesity epidemic, we advocate an interdisciplinary approach in obese patients undergoing elective cardiac surgery.

Pulmonary embolism (PE) continues to be a significant cause of morbidity and mortality. It is estimated that nearly 200,000 to 300,000 PEs are diagnosed annually in the United States: approximately 1 per 1000 persons per year. Additionally, PE is associated with 50,000 to 100,00 0death sannually. 1 Operativ eintervention ,although rarely performed, is indicated in patients with massive embolism resulting in hemodynamic instability. Massive embolism is defined as a PE associated with systolic pressures less than 90 mm Hg or a 40 mm Hg or greater decrease from baseline for longer tha n1 5minutes. 2 Patient swit hsuc hemboli cburde nofte nrapidly progress to refractory hypotension and subsequent cardiopulmonary arrest. This patient population may benefit from surgical embolectomy.

Mitral valve dysfunction after orthotopic heart transplantation may cause symptoms refractory to medical therapy. In this report, we present a patient who underwent mitral annuloplasty for severe symptomatic mitral valve insufficiency 9 years after heart transplantation, and we critically appraise the literature available for mitral valve dysfunction in this setting. Mitral valve repair, when feasible, should be considered for mitral insufficiency after transplantation to improve functional status and reduce the risk of retransplantation--this is particularly prudent in view of chronic donor shortage.

Purpose: SLTx is advocated to optimize organ availability for endstage obstructive or fibrotic respiratory disease.Contra-lateral native lung hyperinflation in recipients with obstructive lung disease may limit functional improvements after SLTx. We hypothesized that recipients with fibrotic lung disease will achieve higher best FEV1 after SLTx than obstructive recipients. Methods and Materials: Single centre, retrospective review of recipients surviving more than 12 months after SLTx for fibrotic or obstructive disease was performed. Pre-transplant spirometry, total lung capacity (TLC) and residual volume (RV) were correlated with the best achieved FEV1 after SLTx. The best post-transplant FEV1 was compared between the fibrotic and obstructive recipients. Results: 57 SLTx recipients were included, 35 obstructive, median age 55yrs (range 37-64), 22 fibrotic, 57yrs (30-64). Post-SLTx survival was not different between the two groups 7.4 v 6.5 yrs respectively. Pre-transplant lung function showed significantly higher TLC (7.99 v 3.50 l, p 0.001Mann-WhitneyU test), RV (5.91 v 1.36 l, p 0.001) and lower FEV1 (0.66 v 1.59 l/s, p 0.001) in obstructive recipients compared with fibrotics. Post-SLTx, the maximal achieved FEV1 was significantly higher in fibrotics (2.38 v 1.83 l/s, p 0.0004). The best post-SLTx FEV1 was corrected for sex, height & age as % predicted FEV1 and showed higher values in the fibrotic group (72.8% v 57.3%, p 0.002). There was no correlation between pre-transplant % predicted TLC or RV and post-SLTx % predicted FEV1in obstructive recipients (r 0.11 p 0.6 Spearman). Conclusions: SLTx recipients for fibrotic lung disease achieve better maximal FEV1 than those with obstructive disease. Our data suggest that native lung hyperinflation in patients with obstructive disease may not be the only factor to account for this difference. Single lung transplantation should be the operation of choice in patients with fibrotic lung disease. The lower achieved lung function in obstructive disease is more complex than hyperinflation and requires further investigation.

Purpose: Brain death is accompanied by hypertensive crisis followed by hypotension. We examined the role of the haemodynamic changes in the systemic neutrophil activation and lung injury. Procedures: Rats (n 49) were anaesthetised and ventilated. Brain death was induced by intracranial balloon inflation in 37: a) “BD” group (n 13); b) “Phentolamine” group (n 12) received phentolamine before balloon inflation to prevent hypertension; c) “Noradrenaline” group (n 12) received intravenous infusion of noradrenaline after brain death to correct hypotension. In 12 rats (Sham) a balloon was inserted, but not inflated. Arterial blood gases and blood neutrophil CD11b/CD18 were measured for 4 h. Lungs were examined with transmission electron microscopy (TEM). Results: In BD, balloon inflation increased mean arterial pressure (MAP) to 150 14.5 mmHg (p 0.001). MAP then fell to a hypotensive plateau (p 0.001). In Phentolamine, the drug decreased MAP by 31 6.9%. Subsequent balloon inflation increased MAP, but not higher than Sham levels (p 0.8). MAP then fell to a plateau, similar to BD (p 0.4). In Noradrenaline, plateau MAP was increased to Sham levels (p 0.3). The BD group had significant metabolic acidosis (MA)(p 0.001), increased alveolo-arterial difference in partial oxygen pressure (P[A-a]O2)(p 0.036) and higher neutrophil CD11b/CD18 levels (p 0.01), compared with Sham. In Phentolamine, P[A-a]O2 and CD18 were similar to Sham, but MA was worse (p 0.001) and CD11b was higher (p 0.049). In Noradrenaline, all variables were similar to Sham (p 0.05). TEM revealed areas of full-thickness capillary-alveolar membrane rupture in BD and Noradrenaline. Lungs from Sham and Phentolamine were normal. Conclusions: The hypertensive crisis associated with brain death can cause stress failure of the pulmonary capillaries, neutrophil activation and lung dysfunction in the transplant donor, which are blocked by phentolamine. Further neutrophil activation and lung injury can be induced by neurogenic hypotension and organ ischaemia, and are reversed by noradrenaline. Optimal donor management requires control of both phases.

AMELIORATED REPERFUSION INJURY IN LUNG TRANSPLANTATION AFTER REDUCTION OF BRAIN DEATH INDUCED INFLAMMATORY GRAFT DAMAGE IN THE DONOR C.H. Wigfield, H.D. Golledge, B.K. Shenton, J.A. Kirby, J.H. Dark, Department of Cardiothoracic Surgery and Transplantation, Freeman Hospital, Newcastle upon Tyne, United Kingdom; Comparative Biology Centre, University of Newcastle, Newcastle upon Tyne, United Kingdom; Department of Surgery, University of Newcastle, Newcastle upon Tyne, United Kingdom