Carlton C. McGregor

Gastroparesis After Lung Transplantation: Potential Role in Postoperative Respiratory Complications

BACKGROUND We observed an unexpectedly high incidence of postoperative gastroparesis among lung and heart-lung transplant recipients. PURPOSE To identify the incidence of GI complications and to describe the clinical profiles of patients who developed symptomatic gastroparesis after lung transplantation. PATIENTS AND METHODS Retrospective study of GI symptoms and complications identified during 3 years of follow-up of 38 adult lung and heart-lung transplant recipients. RESULTS Sixteen of 38 patients (42%) reported one or more GI complaint and received a specific GI diagnosis. Nine of 38 patients (24%) complained of early satiety, epigastric fullness, anorexia, nausea, or vomiting. Gastroparesis was suspected when endoscopic evaluation revealed undigested food in the stomach after overnight fast and symptoms could not be attributed to peptide disease or cytomegalovirus gastritis. Delayed gastric emptying was confirmed by gastric scintigraphy. Mean gastric empty (t1/2) was 263 +/- 115 min (normal < 95 min). Gastroparesis occurred in 4 of 13 right lung, 2 of 12 left lung, 1 of 9 bilateral single lung, and 2 of 4 heart-lung recipients (p = NS). Patients responded partially to metoclopramide or cisapride, with the exception of two patients who required placement of jejunal feeding tubes secondary to severe symptoms. In long-term follow-up, symptoms resolved in all patients and treatment with medications or mechanical intervention was successfully discontinued. Four of nine patients (44%) suffering from gastroparesis developed obliterative bronchiolitis (OB). Food particles were discovered in the BAL fluid of two such symptomatic patients. In contrast, only 6 of 29 (21%) nonsymptomatic patients developed OB (p = 0.16). CONCLUSION Symptomatic gastroparesis is a frequent complication of lung or heart-lung transplantation that may promote microaspiration into the lung allograft.

Bone loss and fracture after lung transplantation.

BACKGROUND Osteoporosis is very common in patients with end-stage pulmonary disease. However, there are few prospective data on fracture incidence after lung transplantation. METHODS We prospectively evaluated changes in bone mass, fracture incidence, and biochemical indices of bone and mineral metabolism in 30 patients who completed 1 year of observation after lung transplantation. All received calcium, vitamin D, and therapy with one or more agents that inhibit bone resorption, initiated shortly after transplantation. RESULTS Before transplantation, only 20% of the patients had normal lumbar spine (LS) and femoral neck bone mineral density (BMD). After transplantation, 15 patients (50%) sustained significant bone loss at either the LS (-8.6+/-1.0%) or the femoral neck (-11.3+/-2.2%). Eleven (37%) patients (10 women) sustained a total of 54 atraumatic fractures. Pretransplantation LS BMD and T scores were significantly lower in those who sustained fractures (-2.809+/-0.32 versus -1.569+/-0.29; P<0.01). Fracture patients were more likely to have had pretransplantation glucocorticoid therapy (chi-square 5.687; P<0.02). The duration of pretransplantation glucocorticoid therapy was also longer in fracture patients (4.9+/-0.8 versus 1.3+/-0.4 years; P<0.001). Biochemical markers of bone resorption were significantly higher in patients who sustained bone loss and/or fractures. CONCLUSIONS We conclude that fractures are a significant problem in the first year after lung transplantation, even in patients who receive therapy to prevent bone loss. Women with low pretransplantation BMD and a history of pretransplantation glucocorticoid therapy are at greatest risk.

Clinical Investigations: Lung TransplantationGastroparesis After Lung Transplantation: Potential Role in Postoperative Respiratory Complications

BACKGROUND We observed an unexpectedly high incidence of postoperative gastroparesis among lung and heart-lung transplant recipients. PURPOSE To identify the incidence of GI complications and to describe the clinical profiles of patients who developed symptomatic gastroparesis after lung transplantation. PATIENTS AND METHODS Retrospective study of GI symptoms and complications identified during 3 years of follow-up of 38 adult lung and heart-lung transplant recipients. RESULTS Sixteen of 38 patients (42%) reported one or more GI complaint and received a specific GI diagnosis. Nine of 38 patients (24%) complained of early satiety, epigastric fullness, anorexia, nausea, or vomiting. Gastroparesis was suspected when endoscopic evaluation revealed undigested food in the stomach after overnight fast and symptoms could not be attributed to peptide disease or cytomegalovirus gastritis. Delayed gastric emptying was confirmed by gastric scintigraphy. Mean gastric empty (t1/2) was 263 +/- 115 min (normal < 95 min). Gastroparesis occurred in 4 of 13 right lung, 2 of 12 left lung, 1 of 9 bilateral single lung, and 2 of 4 heart-lung recipients (p = NS). Patients responded partially to metoclopramide or cisapride, with the exception of two patients who required placement of jejunal feeding tubes secondary to severe symptoms. In long-term follow-up, symptoms resolved in all patients and treatment with medications or mechanical intervention was successfully discontinued. Four of nine patients (44%) suffering from gastroparesis developed obliterative bronchiolitis (OB). Food particles were discovered in the BAL fluid of two such symptomatic patients. In contrast, only 6 of 29 (21%) nonsymptomatic patients developed OB (p = 0.16). CONCLUSION Symptomatic gastroparesis is a frequent complication of lung or heart-lung transplantation that may promote microaspiration into the lung allograft.

Incidence of pulmonary vein complications after lung transplantation: A prospective transesophageal echocardiographic study

OBJECTIVES This study attempted to document the incidence of pulmonary vein complications and their potential relation to clinical outcome in patients after lung transplantation. BACKGROUND Several case reports have documented the presence of pulmonary venous thrombosis causing graft failure in patients after lung transplantation. Because the presentation of these complications mimics that of other postoperative problems, the true incidence of pulmonary vein abnormalities remains unclear. Transesophageal echocardiography is ideally suited to examine the pulmonary veins in the postoperative setting. METHODS Twenty-one consecutive patients undergoing lung transplantation at our institution underwent transesophageal echocardiography within 32 days of transplantation (mean [+/- SD] 6.5 +/- 7.8 days). Special attention was placed on visualizing the pulmonary veins. RESULTS Six (29%) of the 21 patients were noted to have abnormalities of the pulmonary veins in the vicinity of the anastomotic site. After follow-up of 30 days, 4 of these patients (67%) had significant cardiovascular morbidity, and 2 died, compared with 1 (7%) of 15 patients with normal pulmonary veins (p = 0.03). The degree of obstruction of the pulmonary vein appeared to correlate with short-term outcome. CONCLUSIONS Abnormalities of the pulmonary veins are common after lung transplantation and are easily identified by transesophageal echocardiography. Occlusive thrombi appear to be detrimental to short-term outcome.

Immunologic monitoring in lung allograft recipients

To identify patients with increased risk of chronic lung allograft rejection, we assessed the utility of an in vitro biopsy-derived lymphocyte growth assay and serum anti-HLA antibody screening as a complement to currently available methods of monitoring lung allograft recipients. Lymphocyte growth assay was performed on bronchoscopic fragments of tissue cultured in medium with rIL-2. Seventy-nine biopsies from 31 lung transplant recipients were tested by lymphocyte growth assay, and results were correlated with histopathology findings. Positive lymphocyte growth was found in 12/26 (46%) episodes of acute rejection, 5/44 biopsies without rejection (11%), and 0/9 episodes of bronchitis. Positive lymphocyte growth was seen in 7/16 (44%) grade A1 rejections and in 5/10 (50%) grade A2 rejections, as opposed to only 5/44 (11%) grade A0 (no rejection) biopsies (P < 0.01 for both A1 and A2 with respect to A0). Actuarial probability of remaining free from obliterative bronchiolitis (OB)* tended to be higher in patients who did not exhibit lymphocyte growth in biopsies. Sequential samples of sera obtained at the time of the biopsy were screened for lymphocytotoxic anti-HLA antibodies. Twenty-two of 44 recipients (50%) developed anti-HLA antibodies during the first postoperative year, exhibiting greater than 10% reactivity to an HLA reference panel of lymphocytes in four or more consecutive serum samples. Actuarial survival of lung allograft recipients with anti-HLA antibodies (n = 22) was lower than in those without anti-HLA antibodies (n = 22; P = 0.03). Of the 22 antibody producers, 7/12 died as a consequence of OB. Of the 22 non-antibody-producers, 1/2 deaths occurred as a consequence of OB. Anti-HLA antibodies were present in 9/11 instances of OB (82% sensitivity) and in 13/33 patients without OB (61% specificity; P = 0.03). These data indicate that lung transplant recipients with positive lymphocyte growth and anti-HLA antibodies are at an increased risk of chronic allograft rejection.

Reduction in tuberculin skin-test conversions among medical house staff associated with improved tuberculosis infection control practices.

OBJECTIVE To assess the efficacy of an infection control program as measured by tuberculin skin-test (TST) conversion rates in medical house staff. DESIGN Observational study. SETTING University-based hospital in New York City serving a large indigent population. PARTICIPANTS Medical house staff. INTERVENTIONS TST conversions were measured every 6 months in medical house staff from June 1992 to June 1994. Compliance with the isolation policy was measured by identifying room locations 24 hours after admission of patients who had Mycobacterium tuberculosis recovered from respiratory specimens. RESULTS The TST conversion rate decreased from 5.8 to 0, 2.3, and 0 per 100 person years of exposure in successive 6-month periods. The estimated annual TST conversion rate among interns fell from 7 per 100 person years in June 1992 to 0 per 100 person years in June 1993 and 0 per 100 person years in June 1994 (P < .029). The proportion of patients with pulmonary tuberculosis who were isolated in negative-pressure rooms increased from 38% to 75% over the study period (P < .01). CONCLUSION Development of a multifaceted infection control program can decrease the risk of nosocomial tuberculosis infection in medical house staff.

Pulmonary nodules and masses after lung and heart-lung transplantation

The authors assess clinical and radiographic findings of pulmonary nodules and masses after lung and heart-lung transplantation. One hundred and fifty nine patients who survived at least 3 months after lung and heart-lung transplantation were followed by serial chest radiographs for a median of 27 months. Single or multiple lung nodules or masses were noted at chest radiography in 15 (9.4%) of 159 patients. Imaging findings and causes of these nodules and masses were reviewed retrospectively. Infection was found in 10 (6%) of 159 patients. Specific pathogens (11 pathogens in 10 patients) were Aspergillus (n = 4), Mycobacteria (n = 4), and other bacteria (n = 3). Noninfectious causes were found in 5 (3%) of patients and included B-cell lymphoma (n = 2), bronchogenic carcinoma (n = 2), and pulmonary infarcts (n = 1). Nodules and masses appeared a median of 11 months after transplantation (range: 0.2 to 36 months). Five patients (33%) had single lesions; the other 10 (67%) patients had multiple lesions (range 2 to 50). Aspergillus lesions were most commonly located in the upper lobes, were cavitary in three of four patients, and all were fatal. Nodules and masses arose in the transplanted lung in 12 (80%) of the patients, and in the native lung in 3 (20%) of the patients (2 bronchogenic carcinoma, 1 M. tuberculosis simulating bronchogenic carcinoma). Nodules and masses detected by chest radiography are not uncommon (9.4%) after lung and heart-lung transplantation. Infections are more common than noninfectious causes of posttransplant nodules and masses. Specific clinical and imaging characteristics may provide clues to etiology.

Variability of right ventricular functional recovery after lung transplantation

BACKGROUND The purpose of this study was to assess by echocardiography the effects of lung transplantation on recovery of right ventricular (RV) function in patients with preoperative RV dysfunction. METHODS Fourteen (20%) of 71 lung transplant recipients were identified by echocardiography as manifesting abnormal RV function before lung transplantation. These 14 patients were selected for follow-up echocardiographic study 8 months after transplantation. RESULTS RV function improved significantly in the study group. Mean RV end-diastolic area decreased from 26.8 +/- 7.9 cm2 to 20.1 +/- 4.7 cm2 (P < 0.01); mean RV end-systolic area decreased from 21.5 +/- 6.8 cm2 to 13.1 +/- 4.2 (P < 0.01); and mean RV fractional area change (FAC) increased from 20.4 +/- 3.3% to 35.8 +/- 8.9% (P < 0.001). A subgroup of four patients, however, exhibited no change in RV function. Patients who achieved improvement in RV function tended to be younger, had shorter duration of disease before transplantation, and had higher pulmonary arterial (PA) pressures before transplantation (PA systolic, 89 +/- 28 mmHg vs. 38 +/- 11 mmHg, P < 0.001; PA diastolic, 42 +/- 11 mmHg vs. 19 +/- 3 mmHg, P < 0.002). Each of the eight patients with primary pulmonary hypertension exhibited improvement in RV function (mean delta FAC +20.6 +/- 5.9%), while two of three patients with emphysema and both patients with idiopathic pulmonary fibrosis failed to achieve improvement in RV function (mean delta FAC +2.3 +/- 1.2%). CONCLUSIONS Improvement of RV function assessed by echocardiography occurs after lung transplantation, even in patients with severe preoperative RV dysfunction. However, the degree of improvement is variable and may depend on the degree of RV after-load reduction and the presence or absence of intrinsic myocardial disease. RV ejection parameters do not distinguish between these two possibilities.

Five cases of bacteraemia due to Gordonia species

Gordonia species are aerobic Gram-positive bacilli and a rare cause of human disease. To our knowledge, there are only two cases of human infection with Gordonia sputi reported in the literature. We report five cases of bacteraemia due to Gordonia species at our institution since 2005, including four caused by G. sputi. Three of these cases were likely related to chronic indwelling central venous catheters.

Salvage by volume reduction of chronic allograft rejection in emphysema

BACKGROUND We hypothesized that native lung volume reduction surgery (LVRS) would improve respiratory function in patients who had previously undergone single lung transplantation for emphysema and who were disabled by obliterative bronchiolitis. METHODS Seven single lung transplant recipients who had advanced bronchiolitis obliterans syndrome (BOS grade 3b), absence of active infection, and suitable anatomy underwent native LVRS. Mean time from lung transplantation to LVRS was 39 +/- 17 months. RESULTS Mean FEV1 rose from 684 +/- 164 ml before LVRS to 949 +/- 219 ml at 3 months after LVRS, an increment of 40% (p = .002). Mean 6-minute walk rose from 781 +/- 526 ft before LVRS to 887 +/- 539 ft at 3 months after LVRS (p = .031), and mean dyspnea index declined from 3.1 +/- 1.1 before LVRS to 1.6 +/- 0.5 at 3 months after LVRS (p = .010). Mean native lung volume declined from 2956 +/- 648 ml before LVRS to 2541 +/- 621 ml at 3 months after LVRS, but the change was not statistically significant (p = .12). Mean transplant lung volume was little changed before and after LVRS (2099 +/- 411 ml and 1931 +/- 607 ml, respectively, p = NS). There was also a trend toward increased ventilation and perfusion of the native lung and reduction in ventilation and perfusion of the transplant lung, but these changes did not achieve statistical significance. By six months after LVRS, three patients died (two as a consequence respiratory failure), and survivors began to show evidence of deteriorating spirometry. CONCLUSIONS LVRS is capable of salvaging respiratory function in chronic allograft rejection in emphysema by reducing native lung hyperinflation. These benefits, however, appear to be limited in magnitude and duration by the severity of the underlying allograft dysfunction.