Left Single Lung Transplantation Research Articles

Inhibition of regulated necrosis attenuates receptor-interacting protein kinase 1-mediated ischemia-reperfusion injury after lung transplantation.

Increasing evidence indicates that regulated necrosis plays a critical role during cell death caused by ischemia-reperfusion (IR) injury. Necroptosis is one form of regulated necrosis. Necrostatin-1 (Nec-1), an inhibitor of receptor-interacting protein kinase 1 (RIPK1), is known to reduce necroptosis. We investigated the effect of Nec-1 treatment on IR-induced lung injury in a rat lung transplant model. Lewis rats were divided into 4 groups (n = 6 each): (1) Control (no treatment), (2) Donor treatment (D), (3) Recipient treatment (R), and (4) Donor plus Recipient treatment (D+R) groups. Donor lungs were flushed and preserved for 18 hours at 4ºC before transplantation. Recipient animals underwent a left single lung transplant. After 2 hours of reperfusion, we assessed the physiologic function, cytokine expression, pathway activation, and the extent of necrosis. Pulmonary gas exchange in D+R group was significantly better than in the other 3 groups (p = 0.003). Lung edema was significantly lower in the D+R group compared with the Control group (p = 0.006). The expression of interleukin-6 in lung tissue and plasma was significantly reduced in the D+R group compared with the Control group (p = 0.036). The percentage of necrotic cells in D+R group was significantly lower than in the Control and D groups (p = 0.01), indicating Nec-1inhibited regulated necrosis. The administration of Nec-1 to both donor and recipient improved graft function after lung transplantation through the reduction of necroptosis. The inhibition of regulated necrosis appears to be a promising strategy to attenuate IR lung injury after lung transplantation.

Left Single Lung Transplantation Through Left Anterolateral Thoracotomy With Longitudinal Partial Sternotomy (Hemiclamshell): An Innovative Surgical Resource

IntroductionPulmonary fibrosis (PF) is one of the main indications for lung transplantation among end-stage respiratory diseases. PF represents a surgical challenge due to the pulmonary retraction, reduction of pleural space, and limitation for access of the lung hilum by elevation, specifically on the left lung. Unilateral sternothoracotomy, or hemiclamshell (HCS) approach, is the anterolateral thoracotomy with longitudinal partial sternotomy with possibility of cervical extension. This was initially described as a surgical approach for resection of lung apex tumors and of the cervicothoracic region, excision of mediastinal and thoracic wall tumors, and as an urgent incision for the repair of mediastinal and cervicothoracic vascular lesions. HCS is not usually described for liver transplantation. CaseA 62-year-old man who was a nonsmoker was diagnosed with idiopathic PF. After 3 years of medical management and follow-up, the patient was referred to us for a pretransplantation study. He presented with dyspnea grade III according to the Medical Research Council. In the radiograph of the chest and computed tomography of the thorax showed signs of pulmonary fibrosis predominantly left-lung associated with loss of volume and alteration of respiratory function tests. We performed left single lung transplantation through a left HCS approach. During implantation we converted the superior pulmonary vein into “neo-atrium” for the atrial anastomosis. The patient presented excellent evolution and was discharged from the hospital at 26 days. ConclusionWe present a case of left single lung transplantation by PF through an HCS approach as novel and effective resource for this type of procedure.

Single Lung Transplant Complicated by Anastomotic Pulmonary Artery Stenosis

SESSION TITLE: Transplantation SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Anastomotic pulmonary artery stenosis after lung transplantation is a rare complication. Endovascular stenting appears to be a safe and efficacious treatment modality1. CASE PRESENTATION: A 43-year-old female with COPD underwent a single left lung transplant. Four months post-transplant, she presented with progressive hypoxic respiratory failure. CT chest showed a new ill-defined 2.2 x 2.1 cm nodular opacity in the left lower lobe graft shown in Figure 1. Transbronchial biopsy was negative for rejection. Bronchoalveolar lavage showed Aspergillus antigen index of 7.56 and culture grew 1 colony of non-sporulating filamentous fungus. CT-guided biopsy of the lesion showed necrotic lung parenchyma. She was treated empirically with intravenous and inhaled Amphotericin B. Despite treatment, her respiratory failure worsened and she became heated high flow oxygen dependent. Quantitative nuclear lung perfusion scan showed an overall perfusion to the right native lung was calculated to be 77.04% with overall perfusion to the left graft lung calculated to be 22.96%. Right heart angiography confirmed significant stenosis of the left pulmonary artery shown in Figure 2. Placement of a 26 mm x 12 mm LD Mega stent resulted in minimal residual stenosis. Repeated nuclear lung perfusion showed overall perfusion of left graft lung increased to 57.34%. She was eventually discharged home on room air. DISCUSSION: Pulmonary artery stenosis is a rare complication after lung transplantation. It requires a high index of suspicion especially after ruling out rejection and infection etiologies. Open repair carries high mortality and morbidity risk. To date, there have been a few case reports and retrospective studies to support the safety and efficacy of percutaneous endovascular stent placement2. Our patient tolerated the procedure well and had significant clinical improvement. CONCLUSIONS: Percutaneous endovascular stent placement is gaining acceptance as the first choice treatment for pulmonary artery stenosis following lung transplant since it is better tolerated than open repair. It appears to be safe and efficacious. However, long-term outcomes are not clear at this point. Reference #1: Grubstein A et al. Angioplasty using covered stents in five patients with symptomatic pulmonary artery stenosis after single-lung transplantation. Cardiovasc Intervent Radiol, 2014; 37: 686-690. Reference #2: Anaya-Ayala JE et al. Endovascular management of early lung transplant-related anastomotic pulmonary artery stenosis. J Vasc Interv Radiol, 2015; 26: 878-882. DISCLOSURE: The following authors have nothing to disclose: Van Le, Amy Pope-Harman No Product/Research Disclosure Information

Case Report: Successful Lung Transplantation from a Donor Seropositive for Trypanosoma cruzi Infection (Chagas Disease) to a Seronegative Recipient.

The increasing shortage of organs for transplantation has prompted transplant programs to investigate the use of extended criteria donors, such as those with transmissible infectious diseases. Successful cases of organ transplantation (mostly kidney and liver) from Trypanosoma cruzi seropositive donors to seronegative recipients have been reported. We present a case of lung transplantation from a donor serologically positive for Chagas disease to a seronegative recipient, and provide a review of the literature. Left single lung transplantation was performed in a 44-year-old Spanish woman presenting with interstitial lung disease in February 2016. The deceased donor was a Colombian immigrant living in Spain who was serologically positive for Chagas disease. Oral administration of 5 mg/kg/day benznidazole divided in three doses for 60 days was given for specific Chagas disease prophylaxis after transplantation. Periodic follow-up with serological reverse transcription polymerase chain reaction to detect T. cruzi DNA were performed until 6 months after the end of treatment. All results were negative, indicating that transmission of T. cruzi had not occurred. In a review of the literature, two similar cases were identified in Argentina and the United States. In both cases T. cruzi infection was detected posttransplant in the recipients, after which they were treated with benznidazole. The course of the patient described herein confirms that lungs from donors with chronic T. cruzi infection can be used successfully as allografts, and that posttransplant prophylaxis with benznidazole may reduce the probability of transmission of T. cruzi to the recipient.

Rapid and strong de novo donor-specific antibody development in a lung transplant recipient: Short communication/case report

A 66-yo female patient (typed B*39:01, 44:02) underwent first left single lung transplant (typed B*81:01, 15:17) on 02/07/2016 with negative for DSA in current and historical samples. On 02/17/2016 strong de novo DSA (MFI=15,200, C1q+) to B81 were detected. The recipient has two children typed B*07:02, 44:02 B*27:03, 39:01, and had received multiple vaccinations. Twinrix, Zostavax and MMR vaccines contain viruses grown on live human lung fibroblasts (MRC-5, typed B*07:02, 44:02, and WI-38, typed B*08:01, 58:01). Each dose of vaccine used for injection is known to contain protein components of fibroblasts including HLA. Most likely rapid de novo DSA development is due to booster effect produced by five exposures to mismatched B locus alleles which share the following epitopes: 70IAQ, 65QIA, 65QIA+76esn, 69aa+80n, and 163ew+73te. The later three consist of paired non-self and self eplets. Although likelihood of bystander effect produced by multiple vaccinations is low its impact cannot be ruled out.

Lung transplantation for phase Ⅲ silicosis: a series of 32 cases

Objective: To evaluate the effect of lung transplantation for phase Ⅲ silicosis. Methods: From September 2002 to September 2015, 32 patients with end-stage silicosis underwent lung transplantation at Department of Thoracic Surgery, Affiliated Wuxi People's Hospital, Nanjing Medical University. There were 29 male and 3 female patients aged from 24 to 63 years. Thirty-two patients were diagnosed as phase Ⅲ silicosis by the local occupational disease prevention and control center. Fifteen patients were type Ⅰ respiratory failure and 17 patients were type Ⅱ. There were 14 cases accepted bilateral sequential lung transplantation and 18 cases accepted single lung transplantation, including 13 cases with right single lung transplantation and 5 cases with left single lung transplantation. Extracorporeal membrane oxygenation was used in 13 patients. Pulmonary function monitoring was performed at 3 months, 6 months, 1 year, and 2 years after lung transplantation. Clinical characteristics were compared using t-test, χ2 test and Fisher exact test between groups, Kaplan-Meier survival curve and Log-rank test were used to find out the factors affecting survival. Results: All the patients received lung transplantation successfully. One patient died of multiple organ failure, 1 died of sepsis, and 1 succumbed to sudden cardiac death. Twenty-nine patients were discharged from hospital. During follow-up, there were 5 deaths, two patients died of sepsis 7 months postoperatively, 1 died of renal failure 5 months post-transplant, 1 died of sudden cardiac death, and the remaining 1 patient died of bronchiolitis obliterans. Twenty-four patients lived a good quality of life, with survival rates of 90.6% at 3 months, 80.8% at 1 year, 76.7% at 3 years, and 76.7% at 5 years. Significant difference was not observed between single and bilateral lung transplantation about long-term survival rate. During follow-up pulmonary function post-transplant (3 months, 6 months, 1 year, and 2 years) were improved dramatically compared with preoperative level, and patients lived a good quality of life. Conclusion: Lung transplantation is beneficial for patients with phase Ⅲ silicosis, long-term survival is probable.

Giant cell interstitial pneumonia in patients without hard metal exposure: analysis of 3 cases and review of the literature

Giant cell interstitial pneumonia is a rare lung disease and is considered pathognomonic for hard metal lung disease, although some cases with no apparent hard metal (tungsten carbide cobalt) exposure have been reported. We aimed to explore the association between giant cell interstitial pneumonia and hard metal exposure. Surgical pathology files from 2001 to 2004 were searched for explanted lungs with the histopathologic diagnosis of giant cell interstitial pneumonia, and we reviewed the associated clinical histories. Mass spectrometry, energy-dispersive x-ray analysis, and human leukocyte antigen typing data were evaluated. Of the 455 lung transplants, 3 met the histologic criteria for giant cell interstitial pneumonia. Patient 1 was a 36-year-old firefighter, patient 2 was a 58-year-old welder, and patient 3 was a 45-year-old environmental inspector. None reported exposure to hard metal or cobalt dust. Patients 1 and 2 received double lung transplants; patient 3 received a left single-lung transplant. Histologically, giant cell interstitial pneumonia presented as chronic interstitial pneumonia with fibrosis, alveolar macrophage accumulation, and multinucleated giant cells of both alveolar macrophage and type 2 cell origin. Energy-dispersive x-ray analysis revealed no cobalt or tungsten particles in samples from the explanted lungs. None of the samples had detectable tungsten levels, and only patient 2 had elevated cobalt levels. The lack of appropriate inhalation history and negative analytical findings in the tissue from 2 of the 3 patients suggests that giant cell interstitial pneumonia is not limited to individuals with hard metal exposure, and other environmental factors may elicit the same histologic reaction.

Building a Lung Transplant Program

Building a Lung Transplant Program

Annexin V homodimer protects against ischemia reperfusion–induced acute lung injury in lung transplantation

ObjectiveWe hypothesized that administration of a homodimer of recombinant annexin V, diannexin, could shield phosphatidylserine on the endothelium, and inhibit leukocyte and platelet adhesion, thereby potentially reducing ischemia reperfusion injury (IRI) in lung transplantation. This hypothesis was tested using a rat syngeneic single left-lung transplant model. MethodsRats were randomly assigned to receive diannexin (DN group; n = 10) or normal saline (control group; n = 10). Diannexin (1000 μg/kg) was administered to the donor lung in the pulmonary flush solution, and to the recipient intravenously, 5 minutes after initiation of reperfusion. Grafts were reperfused for 2 hours. ResultsThe transplanted grafts in the DN group performed significantly better in gas exchange with higher partial pressure of oxygen (control group: 179 ± 121 vs DN group: 330 ± 54 mm Hg; P = .007) and lower partial pressure of carbon dioxide (control: 55.1 ± 26 vs DN: 34.2 ± 11 mm Hg; P = .04), as well as lower peak airway pressure (control: 20.5 ± 8.5 vs DN: 12.0 ± 7.9 cm H2O; P = .035) after 2 hours of reperfusion. Wet-to-dry lung weight ratio (P = .054), and alveolar fibrin deposition score (P = .04), were reduced in the DN group. Caspase-cleaved cytokeratin 18 in plasma (a marker of epithelial apoptosis) was significantly reduced in the DN group (P = .013). Furthermore, gene-expression levels of proinflammatory cytokines in the transplanted graft, including interleukin-6 (P = .04) and macrophage inflammatory protein 2 (P = .03) were significantly decreased in the DN group. ConclusionsA homodimer of recombinant annexin V reduced ischemia reperfusion injury in a lung transplant animal model, by reducing cell death and tissue inflammation.

Do we need to cool the lung graft after ex vivo lung perfusion? A preliminary study

BackgroundAfter normothermic ex vivo lung perfusion (EVLP), pulmonary grafts are usually flush-cooled and stored on ice until implantation although evidence for this practice lacks. We compared outcomes between 2 post-EVLP preservation strategies in a porcine left single-lung transplantation model. Material and methodsAfter cold flush and 2-h EVLP, donor lungs were prepared and split. In [C], (n = 5) lungs cooled on device to 15°C were preserved in ice-water; in [W] (n = 5), lungs were disconnected from EVLP at 37°C and kept at room temperature. The left lung was transplanted in a recipient animal. Posttransplant, 6 h-monitoring included hourly assessment of pulmonary vascular resistance, pulmonary artery pressure, plateau airway pressure, compliance, and oxygenation before and after exclusion of the right lung. Lung biopsies and bronchoscopy with bronchoalveolar lavage (BAL) were performed at retrieval, at the end of EVLP (R lung), and 1 and 6 h after reperfusion (L lung). ResultsLungs in [W] showed the highest compliance (P < 0.05) and the lowest plateau airway pressure (not statistically significant) throughout the whole reperfusion period. Oxygenation and pulmonary artery pressure were similar between groups. Pulmonary vascular resistance was stable in [C], but rose after reperfusion in [W]. Histologic signs of lung injury and BAL neutrophilia were more pronounced in [C] at 1 h (not statistically significant and P < 0.05, respectively). BAL cytokine levels and lung tissue expression of intercellular adhesion molecule 1 did not differ between groups. ConclusionsNormothermic preparation after EVLP results in similar graft performances compared with lung cooling after EVLP.

(113) - Optimal Oxygenation in Lung Graft Circulation during Ex Vivo Lung Perfusion

(113) - Optimal Oxygenation in Lung Graft Circulation during Ex Vivo Lung Perfusion

Right Native Lung Pneumonectomy Due to over Inflation Three Years after Left Single Lung Transplantation for Pulmonary Lymphangioleiomyomatosis

Native lung hyperinflation (NLH) is one of the known complications after single lung transplantation (SLT). Generally, satisfactory results are achieved in patients undergoing SLT when simultaneous (or second stage) volume reduction of the contralateral native lung is performed. Contralateral native lung pneumonectomy after SLT is rarely reported. In this article, we report a case of a successful, right pneumonectomy of the native lung, 3 years after a left single lung transplant for pulmonary lymphangioleiomyomatosis (PLAM). The patient's pulmonary function and quality of life improved significantly after a right pneumonectomy of the native lung.

Effect of inhaled tacrolimus on ischemia reperfusion injury in rat lung transplant model

Systemic tacrolimus therapy has been shown to protect against lung ischemia-reperfusion injury in animal models. We sought to investigate on a functional and cellular level if inhaled nanoparticle tacrolimus administered to the donor lung before procurement could similarly attenuate ischemia-reperfusion injury after lung transplant. An isogenic orthotopic rat model of single left lung transplant was used. Donor animals were pretreated with inhaled tacrolimus (treatment group) or inhaled lactose (controls) before lung procurement. Lung grafts were subjected to 3 hours of cold ischemia followed by 4 hours of reperfusion after graft implantation. Recipient animal arterial blood gas measurement and isograft wet to dry weight ratios were obtained. Macrophage, neutrophil, and T-cell accumulation and activation in lung isografts, including γδ T-cell, T-helper, and cytotoxic T-cell subtypes were analyzed by flow cytometry. Tacrolimus levels were measured in the lung isograft using liquid chromatography/mass spectrometry. Isograft cytokine levels were measured with commercial enzyme-linked immunosorbent assay and microbead array kits. Oxygenation in treatment group animals was significantly higher than in controls. The presence of macrophages, neutrophils, and all T-cell subtypes in the isografts as well as isograft levels of inflammatory cytokines were all less in the treatment group versus controls, although no single variable achieved statistical significance. Inhaled nanoparticle tacrolimus treatment of lung donors is associated with an attenuation of ischemia-reperfusion injury on a functional and cellular level in lung transplant.

Size matching in lung transplantation: An evidence-based review

The evidence base for size matching between donors and recipients in lung transplantation has not recently been reviewed in a comprehensive manner. Our aim in this study was to assimilate published studies that have addressed size matching of donors to recipients and to establish a pragmatic understanding of the range of lung sizes that may be used for lung transplantation. A comprehensive literature search was performed using Medline and PubMed up to and including September 2012, to identify scientific articles that relate to size matching between donors and lung transplant recipients. Seventy-two articles were identified, of which 21 had addressed the question of the impact of size mismatching on outcomes in lung transplantation. No study has specifically tested the consequences of intentionally mismatching above or below the hypothetical limits for double lung transplantation of a predicted total lung capacity for the donor of between 75% and 125% of the recipient predicted total lung capacity as set out in the ISHLT consensus report on lung donor acceptability criteria. Research is lacking that has robustly defined limits for size mismatch for single lung transplantation and for recipients with restrictive lung pathologies such as pulmonary fibrosis. Published research on the impact of size mismatching between lung transplant donors and recipients is limited by study design and size. It is centered on addressing the issue of mismatch in double lung transplantation in cohorts with a diagnostically heterogeneous make-up and in single lung transplant patients with chronic obstructive pulmonary disease.

A Rare Occurrence of Pulmonary Alveolar Proteinosis after Lung Transplantation

We present a case of pulmonary alveolar proteinosis (PAP) initially diagnosed 28 months after left single-lung transplantation for idiopathic pulmonary fibrosis. The diagnosis was based upon the presence of periodic acid-Schiff (PAS)-positive and surfactant immunostain-positive acellular lipoproteinaceous material within alveoli seen on transbronchial biopsy as well as in bronchoalveolar lavage fluid. The patient eventually also displayed a characteristic "crazy paving" pattern on radiographic imaging. Granulocyte macrophage-colony stimulating factor antibodies were negative, consistent with secondary PAP. PAP is a rare interstitial lung disease with only a few reported cases occurring after lung transplantation. The etiology is thought to be related to a defect in macrophage function caused by immunosuppression. Reduced immunosuppression has been associated with stabilization, but not reversal, of the condition in the case reported here. PAP is an exceptionally rare cause of dyspnea and radiographic infiltrates after lung transplantation and may be related to toxicity of immune-suppressive medications.

Inhibition of hydrogen sulfide generation contributes to lung injury after experimental orthotopic lung transplantation

BackgroundLung injury induced by ischemia or reperfusion significantly accounts for the risk of early mortality of lung transplantation (LT). Recent studies have demonstrated that hydrogen sulfide (H2S) and its endogenous synthase cystathionine-γ-lyase (CSE) confer protection against injury induced by ischemia or reperfusion in various organs. This prompted us to define the role of CSE/H2S pathway in transplantation-induced lung injury. MethodsWe performed single left LT in male Sprague–Dawley rats after 3 h of cold ischemia time. H2S donor NaHS (14 μmol/kg, intraperitoneally) or CSE inhibitor propargylglycine (37.5 mg/kg, intraperitoneally) was administered 15 min before the start of the LT. CSE protein expression, H2S generation, and the severity of pulmonary graft injuries were estimated at 24 h after reperfusion. ResultsBoth CSE protein expression and H2S generation were markedly decreased in transplanted rat lungs compared with those in sham-operated lungs. In the lung-transplanted rats, NaHS administration significantly improved pulmonary function and decreased lipid peroxidation and myeloperoxidase activity. In addition, NaHS inhibited the production of interleukin 1β but increased interleukin 10 levels in graft lung tissues. In contrast, propargylglycine further exacerbated pulmonary function and lung injuries after experimental orthotopic LT. ConclusionsTo our knowledge, this study for the first time has demonstrated that the suppression of CSE expression and H2S production is associated with transplantation-induced lung injury. Both exogenous and endogenous H2S seem to have protective effects against acute LT injury by their multiple functions including antioxidation and anti-inflammation, suggesting that modulation of H2S levels may be considered a potential therapeutic approach in LT.

The effect of β-2 adrenoreceptor agonist inhalation on lungs donated after cardiac death in a canine lung transplantation model

It is a matter of great importance in a donation after cardiac death to attenuate ischemia-reperfusion injury (IRI) related to the inevitable warm ischemic time. Donor dogs were rendered cardiac-dead and left at room temperature. The dogs were allocated into 2 groups: the β-2 group (n = 5) received an aerosolized β-2 adrenoreceptor agonist (procaterol, 350 μg) and ventilation with 100% oxygen for 60 minutes starting at 240 minutes after cardiac arrest, and the control group (n = 6) received an aerosolized control solvent with the ventilation. Lungs were recovered 300 minutes after cardiac arrest. Recipient dogs underwent left single-lung transplantation to evaluate the functions of the left transplanted lung for 240 minutes after the reperfusion. Oxygenation and dynamic compliance were significantly higher in the β-2 group than in the control group. The β-2 group revealed significantly higher levels of cyclic adenosine monophosphate and high-energy phosphates in the donor lung after the inhalation than before it. Histologic findings revealed that the β-2 group had less edema and fewer inflammatory cells. Our results suggest that β-2 adrenoreceptor agonist inhalation during the pre-procurement period may ameliorate IRI.

Activations of Mitogen-Activated Protein Kinases and Regulation of Their Downstream Molecules After Rat Lung Transplantation from Donors After Cardiac Death

Objectives Accepting organs donated after cardiac death (DCD) is an effective approach to the donor shortage. However, lung transplantations from DCD donors show severe rapid pulmonary graft dysfunction (PGD) followed by warm ischemia–reperfusion injury (IRI). This study sought to clarify the molecular mediators in warm IRI, including activation of mitogen-activated protein kinase (MAPK) and the downstream cascades. Methods We performed single left lung transplantation using organs from male Sprague-Dawley rats after 0 (CIT group), 30 (30WIT group), or 180 (180WIT group) minutes of warm ischemia time. Pulmonary graft functions were estimated by blood gas analysis. At 1 hour after reperfusion, the phosphorylation status of MAPKs (ERK, p38, and JNK) and the gene expression levels of transcription factors (Egr-1 and ATF-3) and immune mediators (MCP-1, MIP-2, PAI-1, ICAM-1, TNF-α, IL-1β, IL-6, and COX-2) in the grafts were examined using Western blotting and real-time polymerase chain reaction assays. Results Severe PGD was observed in the 180WIT group compared with transplanted lungs in the other groups, which exhibited good pulmonary graft function. ERK and JNK activations, as well as mRNA levels of transcription factors (Egr-1 and ATF3) significantly increased with greater warm ischemic times. The pattern of JNK activation correlated with the severity of PGD. MCP-1, ICAM-1, IL-1β, IL-6, and COX-2 were also up-regulated among the 180WIT group, although MIP-2 and PAI-1 showed no significant differences among the groups. Conclusions We suggest that the ERK and JNK pathways may play important roles to induce the injury caused by prolonged warm ischemia followed by reperfusion in the setting of lung transplantation from DCD donors.

Salvaging the dehisced lung transplant bronchial anastomosis with homograft aorta

This is a case of 50-year-old male who underwent left single lung transplantation for pulmonary fibrosis. He sustained a bronchial dehiscence with a pulmonary artery-bronchial fistula which was primarily repaired. One week later, there was complete bronchial dehiscence followed by a massive hemoptysis. At operation, following resection of necrotic donor bronchus there was a sizeable gap between donor and recipient bronchus, which was bridged with a cryopreserved aortic homograft. The homograft patch provided a satisfactory repair without malacia. The patient required retransplantation six months later for reasons unassociated with the repair. Homograft aorta proved useful material for salvaging the dehisced lung transplant bronchial anastomosis.

Extracorporeal Membrane Oxygenation as a Bridge to Lung Transplant: Midterm Outcomes

Extracorporeal membrane oxygenation (ECMO) is used occasionally as a bridge to lung transplantation. The impact on mid-term survival is unknown. We analyzed outcomes after lung transplant over a 19-year period in patients who received ECMO support. From March 1991 to October 2010, 1,305 lung transplants were performed at our institution. Seventeen patients (1.3%) were supported with ECMO before lung transplant. Diagnoses included retransplantation (n = 6), pulmonary fibrosis (n = 6), cystic fibrosis (n = 4), and chronic obstructive pulmonary disease (n = 1). Fifteen patients underwent double lung transplant, one patient had single left lung transplant and one patient had a heart-lung transplant. Venovenous and venoarterial ECMO were implanted in eight and nine cases, respectively. Median duration of support was 3.2 days (range, 1 to 49 days). Mean patient follow-up was 2.3 years. Thirty-day, 1-year, and 3-year survivals were 81%, 74%, and 65%, respectively, for the supported patients and 93%, 78%, and 62% in the control group (p = 0.56). Two-year survival was not affected by ECMO type, with survival of five out of nine patients supported by venoarterial ECMO vs seven out of eight patients supported by venovenous ECMO (p = 0.17). At 1- year follow-up, allograft function for the ECMO-supported patients did not differ from the control group (forced expiratory volume in one second, 2.35 L vs 2.09 L, p = 0.39) (forced vital capacity, 3.06 L vs 2.71 L, p = 0.34). Extracorporeal membrane oxygenation as a bridge to lung transplantation is associated with higher perioperative mortality but acceptable mid-term survival in carefully selected patients. Late allograft function did not differ in patients who received ECMO support before lung transplant from those who did not receive ECMO.