High incidence of venous thromboembolic events in lung transplant recipients.

BACKGROUND: Previous studies have reported a 12% incidence of venous thromboembolic events (VTEs) in lung transplant recipients (LTRs). Characterization of risk factors for VTEs in LTRs is lacking. We identified the incidence and risk factors associated with post-transplant VTEs. METHODS: A retrospective review of 153 LTRs from 1994 to 2006 was performed. Patients were categorized by age, race, gender, weight, underlying diagnosis, procedure, ischemic time, length of stay (LOS), cardiopulmonary bypass (CPB), location and number of VTEs, mobility, immunosuppression, renal, hepatic, hematologic and coagulation profiles and nutritional status. RESULTS: A single VTE occurred in 29% of LTRs within the study period. Fifty-eight percent had multiple VTEs and 7% had a radiologically confirmed pulmonary embolism. Median time from transplant to first VTE was 69 days. Sixty percent of VTEs occurred within 1 year, 20% of which occurred within the first month, 19% between 2 and 5 years, and 13% at beyond 5 years post-transplant. Seventy-six percent of VTEs occurred during hospitalization, 19% during outpatient status. Forty-eight percent were of the upper extremity and 47% were of the lower extremity. Sixty-one percent of LTRs were taking cyclosporine and 39% tacrolimus. VTE and non-VTE groups were similar in age, weight, body mass index (BMI), ischemic time, procedure or underlying diagnosis precipitating the need for transplant. Univariate analysis revealed LOS and CPB as significant predictors of a single VTE (p = 0.036, hazard ratio [HR] 1.006 and p = 0.045, HR 1.91, respectively). Multivariate analysis revealed only CPB as a significant predictor (p = 0.047, HR 1.929). CONCLUSIONS: Analysis of a cohort of LTRs for a median period of 1.5 years revealed a VTE incidence much higher than previously reported, especially within the first month after transplantation.

Chronic cough and dyspnea in ice hockey players after an acute exposure to combustion products of a faulty ice resurfacer.

The aim of this study was to characterize pulmonary function and radiologic testing in ice hockey players after exposure to combustion products of a faulty ice resurfacer. Our patients were 16 previously healthy hockey players who developed chronic cough and dyspnea after exposure. Symptom questionnaires, pulmonary function tests (PFTs), bronchoprovocation testing, cardiopulmonary exercise testing, high-resolution computed tomography (CT) imaging, and impulse oscillometry (IOS) were all used. A normal group was used for PFTs and IOS controls. Patients had onset of cough within 72 h of exposure. Ninety-two percent complained of dyspnea, 75% chest pain, and 33% hemoptysis. Eight percent were initially hospitalized for their symptoms. Eighty-five percent were treated with systemic steroids and 39% with inhaled bronchodilators. Six months postexposure, 54% complained of cough and 46% complained of dyspnea on exertion. All patients had normal PFTs; 8.3% had a significant bronchodilator response. All had normal exercise tests (mean VO2max = 90 +/- 3% predicted) and chest CTs. With IOS, 80% had a significant bronchodilator response (decreased resistance > 12% and SD score > 1; mean change = 21.1 +/- 9.9%, mean SD score = 3.1 +/- 2.5). No correlation existed between changes in resistance or reactance and spirometric values. Patient symptoms correlated significantly with bronchodilator response on IOS resistance (R=0.61, p=0.03). More than 50% of patients exposed to the combustion products of a faulty ice resurfacer remained symptomatic six months after exposure. Despite persistence of symptoms, conventional pulmonary function tests and radiologic evaluation did not reveal airway abnormalities. IOS showed evidence of increased airway resistance and small-airway disease, which correlated with patient symptoms.