Using Human-Centered Design to Improve a Surgery Resident Well-Being Program.

INTRODUCTION: Surgery resident mental health, burnout, and overall well-being are constantly scrutinized, and improving surgery resident well-being programs continuously requires refinement. We sought to evaluate the effectiveness of human-centered design (HCD) sprints to enhance our surgery resident well-being program. METHODS: An HCD sprint was conducted with 34 surgery residents in a single session using seven separate domains, including Mental Health/Reflection and Therapy; Mentoring or Faculty Engagement; Physical Well-being; Retreats; Scheduled Breaks or Free Time; Social Connection; and Well-being Lectures, Emails, or Curriculum. Responses were characterized as: "How might we", Suggestions, Useful, and Not Useful. RESULTS: Well-being Lectures, Emails, or Curriculum were overwhelmingly viewed, as Not Useful (77%), as was Mental Health/Reflection and Therapy (42%). Scheduled Breaks or Free Time was viewed as the most Useful (42%). This category also had the most suggestions and "How might we" ideas for improvement (41%). Lastly, Suggestions and "How might we" ideas were also common for improving Mentoring or Faculty Engagement (31% and 29%, respectively). These results were incorporated into multiple strategies to improve surgery resident well-being and also shared in a Department of Surgery Grand Rounds. CONCLUSIONS: Surgery resident well-being and a targeted approach by a well-being program are critical to a residency program, particularly with the arduous nature of surgical training during the pandemic resulting in periods of prolonged social isolation. HCD sprints are an effective means to refine a surgery resident well-being program and to involve the residents themselves in that process.

Trauma surgeon-performed peripheral arterial repairs are associated with equivalent outcomes when compared with vascular surgeons.

BACKGROUND: Civilian extremity trauma with vascular injury carries a significant risk of morbidity, limb loss, and mortality. We aim to describe the trends in extremity vascular injury repair and compare outcomes between trauma and vascular surgeons. METHODS: We performed a single-center retrospective review of patients 18 years or older with extremity vascular injury requiring surgical intervention between January 2009 and December 2019. Demographics, injury characteristics, operative course, and hospital course were analyzed. Descriptive statistics were used to examine management trends, and outcomes were compared for arterial repairs. Multivariate regression was used to evaluate surgeon specialty as a predictor of complications, readmission, vascular outcomes, and mortality. RESULTS: A total of 231 patients met our inclusion criteria; 80% were male with a median age of 29 years. The femoral vessels were most commonly injured (39.4%), followed by the popliteal vessels (26.8%). Trauma surgeons performed the majority of femoral artery repairs (82%), while vascular surgeons repaired the majority of popliteal artery injuries (84%). Both had a similar share of brachial artery repairs (36% vs. 39%, respectively). There were no differences in complications, readmission, vascular outcomes, and mortality. Median time from arrival to operating room was significantly shorter for trauma surgeons. There was a significant downward trend between 2009 and 2017 in the proportion of total and femoral vascular procedures performed by trauma surgeons. On multivariate regression, surgical specialty was not a significant predictor of need for vascular reintervention, prophylactic or delayed fasciotomies, postoperative complications, or readmissions. CONCLUSION: Traumas surgeons arrived quicker to the operating and had no difference in short-term clinical outcomes of brachial and femoral artery repairs compared with patients treated by vascular surgeons. Over the last decade, there has been a significant decline in the number of open vascular repairs done by trauma surgeons. LEVEL OF EVIDENCE: Therapeutic/Care Management, Level IV.

Outcomes of infants and children undergoing surgical repair of ventricular septal defect: a review of the literature and implications for research with an emphasis on pulmonary artery hypertension.

BACKGROUND: Pulmonary vascular disease resulting from CHDs may be the most preventable cause of pulmonary artery hypertension worldwide. Many children in developing countries still do not have access to early closure of clinically significant defects, and the long-term outcomes after corrective surgery remain unclear. Focused on long-term results after isolated ventricular septal defect repair, our review sought to determine the most effective medical therapy for the pre-operative management of elevated left-to-right shunts in patients with an isolated ventricular septal defect. METHODS: We identified articles specific to the surgical repair of isolated ventricular septal defects. Specific parameters included the pathophysiology and pre-operative medical management of pulmonary over-circulation and outcomes. RESULTS: Studies most commonly focused on histologic changes to the pulmonary vasculature and levels of thromboxanes, prostaglandins, nitric oxide, endothelin, and matrix metalloproteinases. Only 2/44 studies mentioned targeted pharmacologic management to any of these systems related to ventricular septal defect repair; no study offered evidence-based guidelines to manage pulmonary over-circulation with ventricular septal defects. Most studies with long-term data indicated a measurable frequency of pulmonary artery hypertension or diminished exercise capacity late after ventricular septal defect repair. CONCLUSION: Long-term pulmonary vascular and respiratory changes can occur in children after ventricular septal defect repair. Research should be directed at providing an evidenced-based approach to the medical management of infants and children with ventricular septal defects (and naturally all CHDs) to minimise consequences of pulmonary artery hypertension, particularly as defect repair may occur late in underprivileged societies.

Incoming residents' knot-tying and suturing skills: Are medical school boot camps sufficient?

INTRODUCTION: Many medical schools offer M4 boot camps to improve students' preparedness for surgical residencies. For three consecutive years, we investigated the impact of medical school boot camps on intern knot-tying and suturing skills when measured at the start of residency. METHODS: Forty-two interns completed questionnaires regarding their boot camp experiences. Their performance on knot-tying and suturing exercises was scored by three surgeons blinded to the questionnaire results. A comparison of these scores of interns with or without boot camp experiences was performed and statistical analysis applied. RESULTS: 26 of 42 (62%) interns reported boot camp training. There were no differences in scores between interns with or without a M4 boot camp experience for suturing [9.6(4.6) vs 9.8(4.1), p < 0.908], knot-tying [9.1(3.6) vs 8.4(4.1), p = 0.574], overall performance [2.0(0.6) vs 1.9(0.7), p = 0.424], and quality [2.0(0.6) vs 1.9(0.7), p = 0.665]) (mean(SD)). CONCLUSIONS: We could not demonstrate a statistically significant benefit in knot-tying and suturing skills of students who enrolled in M4 boot camp courses as measured at the start of surgical residency.

Observing pneumothoraces: The 35-millimeter rule is safe for both blunt and penetrating chest trauma.

BACKGROUND: As more pneumothoraxes (PTX) are being identified on chest computed tomography (CT), the empiric trigger for tube thoracostomy (TT) versus observation remains unclear. We hypothesized that PTX measuring 35 mm or less on chest CT can be safely observed in both penetrating and blunt trauma mechanisms. METHODS: A retrospective review was conducted of all patients diagnosed with PTX by chest CT between January 2011 and December 2016. Patients were excluded if they had an associated hemothorax, an immediate TT (TT placed before the initial chest CT), or if they were on mechanical ventilation. Size of PTX was quantified by measuring the radial distance between the parietal and visceral pleura/mediastinum in a line perpendicular to the chest wall on axial imaging of the largest air pocket. Based on previous work, a cutoff of 35 mm on the initial CT was used to dichotomize the groups. Failure of observation was defined as the need for a delayed TT during the first week. A univariate analysis was performed to identify predictors of failure in both groups, and multivariate analysis was constructed to assess the independent impact of PTX measurement on the failure of observation while controlling for demographics and chest injuries. RESULTS: Of the 1,767 chest trauma patients screened, 832 (47%) had PTX, and of those meeting inclusion criteria, 257 (89.0%) were successfully observed until discharge. Of those successfully observed, 247 (96%) patients had a measurement of 35 mm or less. The positive predictive value for 35 mm as a cutoff was 90.8% to predict successful observation. In the univariant analyses, rib fractures (p = 0.048), Glasgow Coma Scale (p = 0.012), and size of the PTX (≤35 mm or >35 mm) (P < 0.0001) were associated with failed observation. In multivariate analysis, PTX measuring 35 mm or less was an independent predictor of successful observation (odds ratio, 0.142; 95% confidence interval, 0.047-0.428)] for the combined blunt and penetrating trauma patients. CONCLUSION: A 35-mm cutoff is safe as a general guide with only 9% of stable patients failing initial observation regardless of mechanism. LEVEL OF EVIDENCE: Therapeutic, level III.

The diagnostic value of gastroesophageal reflux disease (GERD) symptoms and detection of pepsin and bile acids in bronchoalveolar lavage fluid and exhaled breath condensate for identifying lung transplantation patients with GERD-induced aspiration.

BACKGROUND: Gastroesophageal reflux disease (GERD) is thought to lead to aspiration and bronchiolitis obliterans syndrome after lung transplantation. Unfortunately, the identification of patients with GERD who aspirate still lacks clear diagnostic indicators. The authors hypothesized that symptoms of GERD and detection of pepsin and bile acids in the bronchoalveolar lavage fluid (BAL) and exhaled breath condensate (EBC) are effective for identifying lung transplantation patients with GERD-induced aspiration. METHODS: From November 2009 to November 2010, 85 lung transplantation patients undergoing surveillance bronchoscopy were prospectively enrolled. For these patients, self-reported symptoms of GERD were correlated with levels of pepsin and bile acids in BAL and EBC and with GERD status assessed by 24-h pH monitoring. The sensitivity and specificity of pepsin and bile acids in BAL and EBC also were compared with the presence of GERD in 24-h pH monitoring. RESULTS: The typical symptoms of GERD (heartburn and regurgitation) had modest sensitivity and specificity for detecting GERD and aspiration. The atypical symptoms of GERD (aspiration and bronchitis) showed better identification of aspiration as measured by detection of pepsin and bile acids in BAL. The sensitivity and specificity of pepsin in BAL compared with GERD by 24-h pH monitoring were respectively 60 and 45 %, whereas the sensitivity and specificity of bile acids in BAL were 67 and 80 %. CONCLUSIONS: These data indicate that the measurement of pepsin and bile acids in BAL can provide additional data for identifying lung transplantation patients at risk for GERD-induced aspiration compared with symptoms or 24-h pH monitoring alone. These results support a diagnostic role for detecting markers of aspiration in BAL, but this must be validated in larger studies.

Pepsin concentrations are elevated in the bronchoalveolar lavage fluid of patients with idiopathic pulmonary fibrosis after lung transplantation.

BACKGROUND: Aspiration of gastroesophageal refluxate has been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and the progression of bronchiolitis obliterans syndrome after lung transplantation. The goals of the present study were to identify lung transplant patients at the greatest risk of aspiration and to investigate the causative factors. MATERIALS AND METHODS: From September 2009 to November 2011, 252 bronchoalveolar lavage fluid (BALF) samples were collected from 100 lung transplant patients. The BALF pepsin concentrations and the results of transbronchial biopsy, esophageal function testing, barium swallow, and gastric emptying scan were compared among those with the most common end-stage lung diseases requiring lung transplantation: IPF, chronic obstructive pulmonary disease, cystic fibrosis, and α1-antitrypsin deficiency. RESULTS: Patients with IPF had higher BALF pepsin concentrations and a greater frequency of acute rejection than those with α1-antitrypsin deficiency, cystic fibrosis, or chronic obstructive pulmonary disease (P = 0.037). Moreover, the BALF pepsin concentrations correlated negatively with a lower esophageal sphincter pressure and distal esophageal amplitude; negatively with distal esophageal amplitude and positively with total esophageal acid time, longest reflux episode, and DeMeester score in those with chronic obstructive pulmonary disease; and negatively with the upright acid clearance time in those with IPF. CONCLUSIONS: Our results suggest that patients with IPF after lung transplantation are at increased risk of aspiration and a greater frequency of acute rejection episodes, and that the risk factors for aspiration might be different among those with the most common end-stage lung diseases who have undergone lung transplantation. These results support the role of evaluating the BALF for markers of aspiration in assessing lung transplant patients as candidates for antireflux surgery.

Aspiration, localized pulmonary inflammation, and predictors of early-onset bronchiolitis obliterans syndrome after lung transplantation.

BACKGROUND: We hypothesized that immune mediator concentrations in the bronchoalveolar fluid (BALF) are predictive of bronchiolitis obliterans syndrome (BOS) and demonstrate specific patterns of dysregulation, depending on the presence of acute cellular rejection, BOS, aspiration, and timing of lung transplantation. STUDY DESIGN: We prospectively collected 257 BALF samples from 105 lung transplant recipients. The BALF samples were assessed for absolute and differential white blood cell counts and 34 proteins implicated in pulmonary immunity, inflammation, fibrosis, and aspiration. RESULTS: There were elevated BALF concentrations of interleukin (IL)-15, IL-17, basic fibroblast growth factor, tumor necrosis factor-α, and myeloperoxidase, and reduced concentrations of α1-antitrypsin, which were predictive of early-onset BOS. Patients with BOS had an increased percentage of BALF lymphocytes and neutrophils, with a reduced percentage of macrophages (p < 0.05). The BALF concentrations of IL-1ß; IL-8; interferon-γ-induced protein 10; regulated upon activation, normal T-cell expressed and secreted; neutrophil elastase; and pepsin were higher in patients with BOS (p < 0.05). Among those with BOS, BALF concentrations of IL-1RA; IL-8; eotaxin; interferon-γ-induced protein 10; regulated upon activation, normal T-cell expressed and secreted; myeloperoxidase; and neutrophil elastase were positively correlated with time since transplantation (p < 0.01). Those with worse grades of acute cellular rejection had an increased percentage of lymphocytes in their BALF (p < 0.0001) and reduced BALF concentrations of IL-1ß, IL-7, IL-9, IL-12, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, interferon-γ, and vascular endothelial growth factor (p ≤ 0.001). Patients with aspiration based on detectable pepsin had increased percentage of neutrophils (p < 0.001) and reduced BALF concentrations of IL-12 (p < 0.001). CONCLUSIONS: The BALF levels of IL-15, IL-17, basic fibroblast growth factor, tumor necrosis factor-α, myeloperoxidase, and α1-antitrypsin at 6 to 12 months after lung transplantation are predictive of early-onset BOS, and those with BOS and aspiration have an augmented chemotactic and inflammatory balance of pulmonary leukocytes and immune mediators. These data justify the surgical prevention of aspiration and argue for the refinement of antirejection regimens.

Pulmonary cytokine composition differs in the setting of alcohol use disorders and cigarette smoking.

Alcohol use disorders (AUDs), including alcohol abuse and dependence, and cigarette smoking are widely acknowledged and common risk factors for pneumococcal pneumonia. Reasons for these associations are likely complex but may involve an imbalance in pro- and anti-inflammatory cytokines within the lung. Delineating the specific effects of alcohol, smoking, and their combination on pulmonary cytokines may help unravel mechanisms that predispose these individuals to pneumococcal pneumonia. We hypothesized that the combination of AUD and cigarette smoking would be associated with increased bronchoalveolar lavage (BAL) proinflammatory cytokines and diminished anti-inflammatory cytokines, compared with either AUDs or cigarette smoking alone. Acellular BAL fluid was obtained from 20 subjects with AUDs, who were identified using a validated questionnaire, and 19 control subjects, matched on the basis of age, sex, and smoking history. Half were current cigarette smokers; baseline pulmonary function tests and chest radiographs were normal. A positive relationship between regulated and normal T cell expressed and secreted (RANTES) with increasing severity of alcohol dependence was observed, independent of cigarette smoking (P = 0.0001). Cigarette smoking duration was associated with higher IL-1ß (P = 0.0009) but lower VEGF (P = 0.0007); cigarette smoking intensity was characterized by higher IL-1ß and lower VEGF and diminished IL-12 (P = 0.0004). No synergistic effects of AUDs and cigarette smoking were observed. Collectively, our work suggests that AUDs and cigarette smoking each contribute to a proinflammatory pulmonary milieu in human subjects through independent effects on BAL RANTES and IL-1ß. Furthermore, cigarette smoking additionally influences BAL IL-12 and VEGF that may be relevant to the pulmonary immune response.

Pulmonary inflammation after ethanol exposure and burn injury is attenuated in the absence of IL-6.

Alcohol consumption leads to an exaggerated inflammatory response after burn injury. Elevated levels of interleukin-6 (IL-6) in patients are associated with increased morbidity and mortality after injury, and high systemic and pulmonary levels of IL-6 have been observed after the combined insult of ethanol exposure and burn injury. To further investigate the role of IL-6 in the pulmonary inflammatory response, we examined leukocyte infiltration and cytokine and chemokine production in the lungs of wild-type and IL-6 knockout mice given vehicle or ethanol (1.11 g/kg) and subjected to a sham or 15% total body surface area burn injury. Levels of neutrophil infiltration and neutrophil chemoattractants were increased to a similar extent in wild-type and IL-6 knockout mice 24 h after burn injury. When ethanol exposure preceded the burn injury, however, a further increase of these inflammatory markers was seen only in the wild-type mice. Additionally, signal transducer and activator of transcription-3 (STAT3) phosphorylation did not increase in response to ethanol exposure in the IL-6 knockout mice, in contrast to their wild-type counterparts. Visual and imaging analysis of alveolar wall thickness supported these findings and similar results were obtained by blocking IL-6 with antibody. Taken together, our data suggest a causal relationship between IL-6 and the excessive pulmonary inflammation observed after the combined insult of ethanol and burn injury.

Inhalation injury severity and systemic immune perturbations in burned adults.

OBJECTIVE: We aimed to determine whether the severity of inhalation injury evokes an immune response measurable at the systemic level and to further characterize the balance of systemic pro- and anti-inflammation early after burn and inhalation injury. BACKGROUND: Previously, we reported that the pulmonary inflammatory response is enhanced with worse grades of inhalation injury and that those who die of injuries have a blunted pulmonary immune profile compared with survivors. METHODS: From August 2007 to June 2011, bronchoscopy was performed on 80 patients admitted to the burn intensive care unit when smoke inhalation was suspected. Of these, inhalation injury was graded into 1 of 5 categories (0, 1, 2, 3, and 4), with grade 0 being the absence of visible injury and grade 4 corresponding to massive injury. Plasma was collected at the time of bronchoscopy and analyzed for 28 immunomodulating proteins via multiplex bead array or enzyme-linked immunosorbent assay. RESULTS: The concentrations of several plasma immune mediators were increased with worse inhalation injury severity, even after adjusting for age and % total body surface area (TBSA) burn. These included interleukin (IL)-1RA (P = 0.002), IL-6 (P = 0.002), IL-8 (P = 0.026), granulocyte colony-stimulating factor (P = 0.002), and monocyte chemotactic protein 1 (P = 0.007). Differences in plasma immune mediator concentrations in surviving and deceased patients were also identified. Briefly, plasma concentrations of IL-1RA, IL-6, IL-8, IL-15, eotaxin, and monocyte chemotactic protein 1 were higher in deceased patients than in survivors (P < 0.05 for all), whereas IL-4 and IL-7 were lower (P < 0.05). After adjusting for the effects of age, % TBSA burn, and inhalation injury grade, plasma IL-1RA remained significantly associated with mortality (odds ratio, 3.12; 95% confidence interval, 1.03-9.44). Plasma IL-1RA also correlated with % TBSA burn, inhalation injury grade, fluid resuscitation, Baux score, revised Baux score, Denver score, and the Sequential Organ Failure Assessment score. CONCLUSIONS: The severity of smoke inhalation injury has systemically reaching effects, which argue in favor of treating inhalation injury in a graded manner. In addition, several plasma immune mediators measured early after injury were associated with mortality. Of these, IL-1RA seemed to have the strongest correlation with injury severity and outcomes measures, which may explain the blunted pulmonary immune response we previously found in nonsurvivors.

Implications of alcohol intoxication at the time of burn and smoke inhalation injury: an epidemiologic and clinical analysis.

Up to 50% of burn patient fatalities have a history of alcohol use, and for those surviving to hospitalization, alcohol intoxication may increase the risk of infection and mortality. Yet, the effect of binge drinking on burn patients, specifically those with inhalation injuries, is not well described. We aimed to investigate the epidemiology and outcomes of this select patient population. In a prospective study, 53 patients with an inhalation injury and a documented blood alcohol content (BAC) were grouped as BAC negative (n = 37), BAC = 1 to 79 mg/dl (n = 4), and BAC ≥ 80 mg/dl (n = 12). Those in the last group were designated as binge drinkers according to National Institute on Alcohol Abuse and Alcoholism criteria. Binge drinkers with an inhalation injury had considerably smaller %TBSA burns than did their nondrinking counterparts (mean %TBSA 10.6 vs 24.9; P = .065) and significantly lower revised Baux scores (mean 75.9 vs 94.9; P = .030). Despite binge drinkers having smaller injuries, the groups did not differ in terms of outcomes and resource utilization. Finally, those in the binge-drinking group had considerably higher carboxyhemoglobin levels (median 5.2 vs 23.0; P = .026) than did nondrinkers. Binge drinkers with inhalation injuries surviving to hospitalization had less severe injuries than did nondrinkers, although their outcomes and burden to the healthcare infrastructure were similar to the nondrinking patients. Our findings affirm the effect of alcohol intoxication at the time of burn and smoke inhalation injury, placing renewed emphasis on injury prevention and alcohol abuse education.

Gastroesophageal reflux disease in lung transplant patients with cystic fibrosis.

BACKGROUND: Gastroesophageal reflux disease (GERD) in lung transplant patients is being increasingly investigated because of its reported association with chronic rejection. However, information concerning the characteristics of GERD in cystic fibrosis (CF) patients is scarce. METHODS: We compared esophageal pH monitoring, manometry, gastric emptying studies, and barium swallow of 10 lung transplant patients with CF with those of 78 lung transplant patients with other end-stage pulmonary diseases. RESULTS: In lung transplant patients with CF, the prevalence of GERD was 90% (vs 54% controls, P = .04), of whom 70% had proximal reflux (vs 29% controls, P = .02). CONCLUSIONS: Lung transplant patients with CF have a significantly higher prevalence and proximal extent of GERD than do other lung transplant recipients. These data suggest that CF patients in particular should be routinely screened for GERD after transplantation to identify those who may benefit from antireflux surgery, especially given the risks of GERD-related aspiration and chronic allograft injury.

Medium and long-term outcomes after pneumatic dilation or laparoscopic Heller myotomy for achalasia: a meta-analysis.

Recent randomized studies comparing outcomes after pneumatic dilation (PD) and laparoscopic Heller myotomy (LHM) for the treatment of achalasia are conflicting and limited to short-term follow-up. Our meta-analysis compared the long-term durability of these approaches, with the hypothesis that LHM offers superior long-term remission compared with PD. We identified 36 studies published between 2001 and 2011 with at least 5 years of follow-up. Those studies describing PD included 3211 patients (mean age, 49.8 y). For PD, the mean 5-year remission rate was 61.9% and the mean 10-year remission rate was 47.9%. Overall, 1526 patients (mean age, 46.3 y) were treated with LHM; 83% received a fundoplication. In contrast, the mean 5- and 10-year remission rates after LHM were 76.1% and 79.6%, respectively. Finally, the perforation rate for LHM was twice that of PD (4.8% vs. 2.4%; P<0.05). We conclude that despite a higher frequency of perforation, LHM affords greater long-term durability.

Pulmonary immune changes early after laparoscopic antireflux surgery in lung transplant patients with gastroesophageal reflux disease.

BACKGROUND: The biologic mechanisms by which laparoscopic antireflux surgery (LARS) might influence the inflammatory process leading to bronchiolitis obliterans syndrome are unknown. We hypothesized that LARS alters the pulmonary immune profile in lung transplant patients with gastroesophageal reflux disease. METHODS: In 8 lung transplant patients with gastroesophageal reflux disease, we quantified and compared the pulmonary leukocyte differential and the concentration of inflammatory mediators in the bronchoalveolar lavage fluid (BALF) 4 weeks before LARS, 4 weeks after LARS, and 12 months after lung transplantation. Freedom from bronchiolitis obliterans syndrome (graded 1-3 according to the International Society of Heart and Lung Transplantation guidelines), forced expiratory volume in 1 second trends, and survival were also examined. RESULTS: At 4 weeks after LARS, the percentages of neutrophils and lymphocytes in the BALF were reduced (from 6.6% to 2.8%, P = 0.049, and from 10.4% to 2.4%, P = 0.163, respectively). The percentage of macrophages increased (from 74.8% to 94.6%, P = 0.077). Finally, the BALF concentration of myeloperoxide and interleukin-1ß tended to decrease (from 2109 to 1033 U/mg, P = 0.063, and from 4.1 to 0 pg/mg protein, P = 0.031, respectively), and the concentrations of interleukin-13 and interferon-γ tended to increase (from 7.6 to 30.4 pg/mg protein, P = 0.078 and from 0 to 159.5 pg/mg protein, P = 0.031, respectively). These trends were typically similar at 12 months after transplantation. At a mean follow-up of 19.7 months, the survival rate was 75% and the freedom from bronchiolitis obliterans syndrome was 75%. Overall, the forced expiratory volume in 1 second remained stable during the first year after transplantation. CONCLUSIONS: Our preliminary study has demonstrated that LARS can restore the physiologic balance of pulmonary leukocyte populations and that the BALF concentration of pro-inflammatory mediators is altered early after LARS. These results suggest that LARS could modulate the pulmonary inflammatory milieu in lung transplant patients with gastroesophageal reflux disease.

The prevalence and extent of gastroesophageal reflux disease correlates to the type of lung transplantation.

BACKGROUND: Evidence is increasingly convincing that lung transplantation is a risk factor of gastroesophageal reflux disease (GERD). However, it is still not known if the type of lung transplant (unilateral, bilateral, or retransplant) plays a role in the pathogenesis of GERD. STUDY DESIGN: The records of 61 lung transplant patients who underwent esophageal function tests between September 2008 and May 2010, were retrospectively reviewed. These patients were divided into 3 groups based on the type of lung transplant they received: unilateral (n=25); bilateral (n=30), and retransplant (n=6). Among these groups we compared: (1) the demographic characteristics (eg, sex, age, race, and body mass index); (2) the presence of Barrett esophagus, delayed gastric emptying, and hiatal hernia; and (3) the esophageal manometric and pH-metric profile. RESULTS: Distal and proximal reflux were more prevalent in patients with bilateral transplant or retransplant and less prevalent in patients after unilateral transplant, regardless of the cause of their lung disease. The prevalence of hiatal hernia, Barrett esophagus, and the manometric profile were similar in all groups of patients. CONCLUSIONS: Although our data show a discrepancy in prevalence of GERD in patients with different types of lung transplantation, we cannot determine the exact cause for these findings from this study. We speculate that the extent of dissection during the transplant places the patients at risk for GERD. On the basis of the results of this study, a higher level of suspicion of GERD should be held in patients after bilateral or retransplantation.

Early pulmonary immune hyporesponsiveness is associated with mortality after burn and smoke inhalation injury.

This prospective study aims to address mortality in the context of the early pulmonary immune response to burn and inhalation injury. The authors collected bronchoalveolar lavage fluid from 60 burn patients within 14 hours of their injury when smoke inhalation was suspected. Clinical and laboratory parameters and immune mediator profiles were compared with patient outcomes. Patients who succumbed to their injuries were older (P = .005), had a larger % TBSA burn (P < .001), and required greater 24-hour resuscitative fluids (P = .002). Nonsurvivors had lower bronchoalveolar lavage fluid concentrations of numerous immunomodulators, including C5a, interleukin (IL)-1ß, IL-1RA, IL-8, IL-10, and IL-13 (P < .05 for all). Comparing only those with the highest Baux scores to account for the effects of age and % TBSA burn on mortality, nonsurvivors also had reduced levels of IL-2, IL-4, granulocyte colony-stimulating factor, interferon-γ, macrophage inflammatory protein-1ß, and tumor necrosis factor-α (P < .05 for all). The apparent pulmonary immune hyporesponsiveness in those who died was confirmed by in vitro culture, which revealed that pulmonary leukocytes from nonsurvivors had a blunted production of numerous immune mediators. This study demonstrates that the early pulmonary immune response to burn and smoke inhalation may be attenuated in patients who succumb to their injuries.

A review of the role of GERD-induced aspiration after lung transplantation.

The increased prevalence of gastroesophageal reflux disease (GERD) in lung transplantation patients has been established; however, many questions persist regarding the relationship of GERD to aspiration and its potential to induce pulmonary allograft failure. Moreover, the biological implications of aspiration in lung transplantation have yet to be fully elucidated. The goal of this review was to assess the relationship between GERD and aspiration, focusing on the role of these events in the development of allograft injury after lung transplantation.

The protective role of laparoscopic antireflux surgery against aspiration of pepsin after lung transplantation.

BACKGROUND: The goal of this study was to determine, in lung transplant patients, if laparoscopic antireflux surgery (LARS) is an effective means to prevent aspiration as defined by the presence of pepsin in the bronchoalveolar lavage fluid (BALF). METHODS: Between September 2009 and November 2010, we collected BALF from 64 lung transplant patients at multiple routine surveillance assessments for acute cellular rejection, or when clinically indicated for diagnostic purposes. The BALF was tested for pepsin by enzyme-linked immunosorbent assay (ELISA). We then compared pepsin concentrations in the BALF of healthy controls (n = 11) and lung transplant patients with and without gastroesophageal reflux disease (GERD) on pH-monitoring (n = 8 and n = 12, respectively), and after treatment of GERD by LARS (n = 19). Time to the development of bronchiolitis obliterans syndrome was contrasted between groups based on GERD status or the presence of pepsin in the BALF. RESULTS: We found that lung transplant patients with GERD had more pepsin in their BALF than lung transplant patients who underwent LARS (P = .029), and that pepsin was undetectable in the BALF of controls. Moreover, those with more pepsin had quicker progression to BOS and more acute rejection episodes. CONCLUSION: This study compared pepsin in the BALF from lung transplant patients with and without LARS. Our data show that: (1) the detection of pepsin in the BALF proves aspiration because it is not present in healthy volunteers, and (2) LARS appears effective as a measure to prevent the aspiration of gastroesophageal refluxate in the lung transplant population. We believe that these findings provide a mechanism for those studies suggesting that LARS may prevent nonallogenic injury to the transplanted lungs from aspiration of gastroesophageal contents.

Laparoscopic antireflux surgery for gastroesophageal reflux disease after lung transplantation.

BACKGROUND: Although gastroesophageal reflux disease (GERD) is highly prevalent in lung transplantation, the pathophysiology of GERD in these patients is unknown. We hypothesize that the pathophysiology of GERD after lung transplantation differs from that of a control population, and that the 30-d morbidity and mortality of laparoscopic antireflux surgery (LARS) are equivalent in both populations. METHODS: We retrospectively compared the pathophysiology of GERD and the 30-d morbidity and mortality of 29 consecutive lung transplant patients with 23 consecutive patients without lung transplantation (control group), all of whom had LARS for GERD between November 2008 and May 2010. RESULTS: Both groups had a similar prevalence of endoscopic esophagitis and Barrett's esophagus , comparable manometric profiles, and similar prevalence of abnormal peristalsis. However, hiatal hernia was more common in controls than in lung transplant patients (57% versus 24%; P = 0.04). Lung transplant patients had a higher prevalence and severity of proximal GERD (65% versus 33%; P = 0.04). The 30-d morbidity and mortality following LARS were similar in both groups regardless of the higher surgical risk of lung transplants (median ASA class: 3 versus 2 for controls, P < 0.001). CONCLUSIONS: These results show that despite similar manometric profiles, lung transplant patients are more prone to proximal reflux than the general population with GERD; the prevalence of endoscopic esophagitis and Barrett's esophagus is the same in both groups of patients; a hiatal hernia is uncommon after lung transplantation; and the morbidity and mortality of LARS are the same for lung transplant patients as the general population with GERD.