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.

Cytomegalovirus pneumonitis after cardiac transplantation.

To evaluate the incidence and clinical features of cytomegalovirus (CMV) pneumonitis after cardiac transplantation, we identified 27 (16%) of 171 consecutive recipients in whom CMV pneumonitis was confirmed by strict diagnostic criteria. Cytomegalovirus pneumonitis occurred in 6 (30%) of 20 patients treated with azathioprine and prednisone, and 8 (25%) of 32 patients treated with azathioprine, cyclosporine, and prednisone, but only 13 (11%) of 119 patients treated with cyclosporine and prednisone. The incidence of CMV pneumonitis was not related to recipient preoperative CMV titers or to postoperative cardiac rejection, but there was a trend toward increased CMV pneumonitis in patients who received organs from CMV-positive donors. Mean onset of CMV pneumonitis was 2.9 +/- 1.6 (SD) months after transplantation. In the azathioprine-prednisone group, CMV was always associated with at least one other respiratory pathogen (Aspergillus, n = 5; Pneumocystis carinii, n = 2). In the two cyclosporine groups, CMV was either the sole respiratory pathogen (n = 9), or associated with P carinii (n = 11). Roentgenographically, diffuse bilateral hazy pulmonary opacities were present in 19 (70%) of 27 patients, but focal subsegmental opacity (26%), small pleural effusion (26%), and lobar consolidation (7%) were also observed. When bronchoscopy was performed, bronchoalveolar lavage was the most sensitive technique for detecting CMV (72%), whereas transbronchial biopsy (39%) and combined washings and brushings (33%) were relatively insensitive techniques. Respiratory failure and death occurred in 52% and 44%, respectively, of patients with CMV pneumonitis. In this population of immunocompromised hosts: (1) CMV pneumonitis, alone or with other respiratory pathogens, was a major cause of morbidity and mortality; (2) localized roentgenographic opacity did not exclude CMV pneumonitis; (3) bronchoalveolar lavage was the most sensitive bronchoscopic technique for detecting CMV pneumonitis.

Late fatal adenovirus pneumonitis in a lung transplant recipient.

Adenovirus (ADV) is increasingly recognized as a cause of morbidity and mortality in transplant recipients, but ADV pneumonitis has rarely been reported after lung transplantation. The few reported instances of ADV pneumonitis occurred mostly in children immediately after lung transplantation suggesting "primary" infection. We report a fatal case of ADV pneumonitis occurring in an adult, 4 years after unilateral lung transplantation, in whom the premortem diagnosis was not determined. Autopsy revealed severe necrotizing bronchitis, bronchiolitis, and interstitial pneumonitis. Characteristic smudgy intranuclear inclusions, immunohistochemistry for viral protein, in situ hybridization for viral genome, and postmortem lung cultures established ADV as the etiologic agent. ADV can cause fatal, occult respiratory infection in adult lung transplant recipients, remote from transplant surgery.

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.

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.

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.

Carcinoma of the lung after heart transplantation.

We have recently noted an unexpected high incidence of lung cancer in our population of cardiac allograft recipients. We conducted a retrospective review of cardiac transplantation at our institution to investigate the incidence, clinical course, and outcome of patients who developed lung cancer following heart transplantation. Nine patients--each with a history of smoking at 30 pack-years--developed lung cancer following heart transplantation, for an incidence of 1.56% of patients at risk. Eight of the patients were male > or = 50 years of age, representing 3.3% of the male transplant recipients in this age group. The interval from transplantation to diagnosis clustered around 3-5 years after transplantation, but in two instances (22%), a neoplasm was discovered within 6 months of transplantation. Almost half of the cancers were discovered incidentally, despite routine radiographic surveillance. Seven of 9 (78%) patients had stage IV disease at presentation. Median survival after diagnosis was 3 months, and five of the seven patients who died survived less than 4 months after diagnosis. We conclude that cardiac transplant recipients are at increased risk for development of lung cancer. Patients with a moderate to heavy smoking history might well be advised to undergo chest CT scanning in an aggressive search for occult lung cancer before cardiac transplantation is considered further. Finally, despite frequent radiologic examinations, these lung cancers are often diagnosed incidentally, are far advanced at the time of diagnosis, are not surgically resectable, and are poorly responsive to adjuvant therapy.

New strategies for early diagnosis of heart allograft rejection.

BACKGROUND: Allograft rejection is mediated by T cells that recognize allogeneic major histocompatibility complex (MHC) molecules via the direct and indirect pathway. The direct pathway involves T cells that react against MHC/peptide complexes expressed on the surface of donor antigen-presenting cells (APCs). In contrast, T cells involved in the indirect pathway recognize peptides derived from processing and presentation of allogeneic MHC molecules by self (recipient) APCs. To explore the relative contribution of these two pathways to rejection, we have evaluated the response of peripheral blood T cells from 50 heart transplant recipients against donor APCs (direct recognition) and against self APCs pulsed with synthetic peptides corresponding to the hypervariable region of the mismatched HLA-DR antigens of the donor (indirect recognition). METHODS: T cell reactivity against donor APCs was quantitated by measuring the expression of CD69 on allostimulated CD3+ LDA1+ cells. Reactivity to synthetic allopeptides was determined in limited dilution assays. RESULTS: Serial studies of the kinetics of direct and indirect recognition showed that both pathways contribute to early acute rejection episodes. Primary rejection was accompanied invariably by indirect recognition of a dominant allopeptide. Intermolecular spreading of T cell epitopes was observed during recurrent rejections. Enhanced recognition of donor alloantigens via the direct pathway was found predominantly during early rejection episodes. A single form of allorecognition was shown to occur in some rejection episodes. CONCLUSIONS: Monitoring of the direct and indirect pathway of allorecognition provides a reliable method for prediction and differential diagnosis of acute rejection of heart allografts.

Cytomegalovirus pneumonitis and lobar consolidation.

This report describes the occurrence of localized lobar consolidation caused solely by cytomegalovirus infection in two heart transplant recipients. This highly atypical and previously unreported radiographic manifestation of cytomegalovirus pneumonitis underscores the need for vigorous diagnostic evaluation of immunosuppressed patients since localized pneumonitis in the immunocompromised host does not exclude the possibility of opportunistic infection.

Platelet activation and fibrinopeptide formation in pulmonary hypertension.

Intravascular thrombosis is postulated to cause or to contribute to the development of uncharacterized ("primary") pulmonary hypertension (PPH). To assess whether there is ongoing platelet-fibrin thrombosis in patients with PPH, we measured specific markers of platelet activation: platelet factor 4 (PF4) and beta-thromboglobulin (BTG); of fibrin formation: fibrinopeptide A (FPA); and of fibrin dissolution: fibrinopeptide BB1-42 (FPBB1-42) in peripheral venous blood from 10 patients with PPH (group 2). Results were compared with those of normal volunteers (group 1, n = 9) and with results from patients with pulmonary hypertension secondary to congenital heart disease (group 3, n = 7). Both groups 2 and 3 exhibited severe pulmonary hypertension (mean pulmonary arterial pressure = 62 +/- 20 mm Hg and 70 +/- 13 mm Hg, respectively). Mean level of PF4, BTG, FPA, and FPBB1-42 in patients with pulmonary hypertension, either primary or secondary to congenital heart disease, did not differ from levels in normal subjects. Within group 2, levels of platelet proteins and fibrinopeptides did not differ between patients who were classified clinically as having plexogenic arteriopathy vs thromboembolic disease. These observations suggest that a sustained state of abnormal platelet activation and fibrin formation or dissolution is not present in patients with established pulmonary hypertension.

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.

Pulmonary vascular resistance in emphysema.

To assess the hemodynamic effects of pulmonary microvasculature disruption in emphysema, we examined resting pulmonary hemodynamics and lung function in 12 carefully identified patients with type A chronic obstructive pulmonary disease. Individuals with respiratory muscle weakness and intercurrent infection were excluded. Standard spirometry, helium dilution lung volumes, and single-breath carbon monoxide diffusing capacity (DCOSB) were obtained within 24 h of right heart catheterization. Resistance to pulmonary blood flow was assessed using the difference between pulmonary arterial (PA) diastolic and mean wedge pressures, and expressed as the pulmonary diastolic gradient (PDG). Mean FEV1/FVC was 51 +/- 8 percent, RV/TLC was 48 +/- 11 percent, DCOSB percent predicted was 62 +/- 29 percent, PaO2 was 72 +/- 11 mm Hg (FIO2, 0.21), and PaCO2 was 39 +/- 5 mm Hg. Mean PDG was 5 +/- 3 mm Hg (normal < or = 3 mm Hg) with normal PA pressures, indicating mildly elevated resistance to pulmonary blood flow. The PDG correlated most closely with DCOSB, rising in curvilinear fashion as DCOSB fell (r = -0.869, p < 0.001). These observations were compared with our previous report of analogous findings in patients with chronic, diffuse interstitial lung disease (ILD). In that group, PDG also increased curvilinearly as DCOSB fell (r = -0.839, p < 0.001). Subjects with FVC greater than 50 percent predicted had elevated PDG with normal pressures, while those with FVC less than 50 percent had pulmonary hypertension. The regression of PDG on DCOSB was strikingly similar to emphysema, although the slope in emphysema was less than that in ILD (p < 0.001). These observations suggest that elevated pulmonary vascular resistance in emphysema stems from disruption of the microcirculation in a fashion similar to that encountered in mild-moderate ILD. However, the magnitude of increase is not sufficient to generate resting pulmonary hypertension in the absence of disturbed gas exchange.

Pulmonary tuberculosis after lung transplantation.

During a 5-year study period, we diagnosed pulmonary tuberculosis in two (2%) of 94 lung and heart-lung transplant recipients. Each infection occurred 3 months after bilateral lung transplantation in the presence of evidence implicating donor-to-recipient transmission of the pathogen. The radiographic patterns of pulmonary tuberculosis were subtle: narrowing of the middle lobe bronchus of the right lung caused by an endobronchial granulomatous mass (n = 1) and a focal cluster of small nodules in the upper lobe of the left lung and small bilateral pleural effusions (n = 1). Each patient achieved complete clinical and radiographic response after antituberculous therapy. We conclude that Mycobacterium tuberculosis may be transmitted directly by a donor lung and may involve bronchial mucosa, pulmonary parenchyma, and pleura.

Superiority of end-to-end versus telescoped bronchial anastomosis in single lung transplantation for pulmonary emphysema.

OBJECTIVE: To assess the influence of surgical technique (telescoped versus end-to-end anastomosis) on the incidence of bronchial anastomotic complications in patients who underwent single lung transplantation for pulmonary emphysema. METHODS: Seventy-six adult recipients of single lung transplants for pulmonary emphysema were evaluated for the presence of 3 types of major bronchial anastomotic complications: ischemia, dehiscence, and severe stenosis. Surgical technique, clinical course, and mortality were reviewed retrospectively. RESULTS: The 3 major complications were observed in 11 (34%; ischemia), 8 (25%; dehiscence), and 11 (34%; severe stenosis) of 32 telescoped bronchial anastomoses. In contrast, ischemia, dehiscence, and severe stenosis occurred in only 4 (9%), 1 (2%), and 2 (5%) of 44 end-to-end anastomoses (P =.0087, P =.0034, and P =.0012, respectively). The relative risk of ischemia, dehiscence, and severe stenosis in telescoped anastomoses was 2.1, 2.5, and 2.5, respectively, compared with end-to-end anastomoses. Five (13%) telescoped anastomoses required stent placement as compared with only 2 (5%) end-to-end anastomoses (P =.1244). Early postoperative pneumonia was more common in the telescoped anastomosis group (56%) than in the end-to-end group (32%; P =.0380). There was a trend toward shorter survival in the telescoped anastomosis group (mean survival 1045 +/- 145 days) as compared with the end-to-end group (mean survival 1289 +/- 156 days), but these differences did not achieve statistical significance (P =.2410). CONCLUSIONS: In patients who underwent single lung transplantation for pulmonary emphysema, telescoped anastomoses were associated with a higher incidence of bronchial anastomotic complications than end-to-end anastomoses.

Utility of airway endoscopy in the diagnosis of respiratory complications of cardiac transplantation.

We evaluated 39 episodes (in 32 patients) of pulmonary parenchymal infiltrates following cardiac transplantation with fiberoptic bronchoscopy (FOB) in a prospective study of 94 consecutive recipients. Initial FOB established the diagnosis in 24/39 (62 percent) instances. Subsequent examinations included repeat FOB (five), open lung biopsy (five), needle aspiration (two), and autopsy (nine), establishing 49 diagnoses. Specific pathogens were identified in 45 instances, neoplasm in two, and idiopathic interstitial pneumonitis in two. Bronchoalveolar lavage alone yielded diagnoses in 63 percent and transbronchial biopsy and bronchial washings/brushings in 46 and 43 percent, respectively. Transbronchial biopsy suggested idiopathic interstitial pneumonitis in 17 instances, but four had spontaneous clearing, and open lung biopsy or autopsy showed alternative diagnoses (particularly CMV and Aspergillus) in 11. The main complication of FOB was moderate (25 to 100 ml) hemorrhage after transbronchial biopsy (10 percent); no severe episodes occurred despite elevated pulmonary vascular pressures. In this population of immunocompromised hosts: (1) bronchoalveolar lavage is the most sensitive bronchoscopic technique for detecting infection; (2) transbronchial biopsy is not useful in detecting CMV or Aspergillus infection; (3) pulmonary hypertension is associated with some risk of moderate but not severe hemorrhage after transbronchial biopsy.

Patent foramen ovale complicating heart transplantation. A window on posttransplantation hemodynamics.

A patient developed refractory hypoxemia and right-to-left shunt across a patent foramen ovale after orthotopic cardiac transplantation. The right-to-left shunt was produced by volume overload of the donor right ventricle during the period of early postoperative myocardial depression and resolved with preload reduction and diuresis. Increased preload of the right heart needs to be considered in the early postoperative management after cardiac transplantation. The foramen ovale of the donor and recipient should be evaluated at operation by visual and probe examination and securely closed if either is patent, since this pattern of hemodynamic changes is common following cardiac transplantation.

Adhesion molecules (E-selectin and ICAM-1) in pulmonary allograft rejection.

Vascular endothelial cells act as antigen-presenting cells in the lung allograft and stimulate alloreactive host lymphocytes. Activated lymphocytes and cytokines can induce expression of leukocyte-endothelial adhesion molecules that facilitate invasion of the allograft by circulating leukocytes. To define the role of endothelial HLA class II antigen and adhesion molecule expression in lung allograft rejection, we prospectively analyzed endothelial expression of HLA class II, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) antigens in 52 transbronchial biopsy specimens from 24 lung allograft recipients as compared to normal control subjects. Thirty-one of 52 specimens showed histologic rejection and 8 of 24 patients developed histologic obliterative bronchiolitis (OB) by the end of the study period. Increased expression of HLA class II antigen was seen in 32 of 52 (62%) lung allograft specimens, but increased expression did not correlate with acute rejection or OB. In contrast, E-selectin expression was seen in 30 of 52 (58%) biopsy specimens and was associated with acute rejection (p < 0.005) and with the development of OB (p < 0.05). Increased expression of ICAM-1 was seen in only 18 of 52 (35%) biopsy specimens and did not correlate with acute rejection or OB. These data suggest that E-selectin expression may be a tissue marker of acute and chronic lung rejection possibly by promoting leukocyte adhesion to the allograft endothelium. The high levels of endothelial HLA class II expression may reflect long-term antigenic stimulation of the allograft even in the absence of rejection.

Bronchocentric mycosis occurring in transplant recipients.

Although a variety of long-term, probably immunologically induced pulmonary changes have been described in recipients of both combined heart-lung and bone marrow transplantation, pulmonary infections continue to remain causes of significant morbidity and mortality as well. Herein we describe three patients (two heart-lung and one bone marrow transplant recipient) who had bronchocentric granulomatous mycosis, a tissue manifestation of fungal infection not previously described in the setting of a transplant host. Although one patient was being treated successfully with antifungal agents for his mucormycosis, two other patients eventually died of invasive aspergillosis. This emphasizes that although this process is histologically somewhat similar to bronchocentric granulomatosis, a high index of suspicion for infection needs to be maintained when this pathologic process is identified in a transplant host.

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.

Insufficiency fractures of the sacrum: a cause of low back pain after lung transplantation.

Insufficiency fractures of the sacrum were diagnosed during the first year after successful transplantation in four (5.6%) of 71 lung and heart-lung transplant recipients. Each patient had development of low back pain after minor or no trauma; all had osteoporosis. In each instance, plain radiographs failed to demonstrate the fracture, and the diagnosis was established by radionuclide bone scanning that demonstrated the characteristic "butterfly" (bilateral sacral fracture) or "half-butterfly" appearance (unilateral sacral fracture). Sacral insufficiency fractures, a significant cause of low back pain in lung transplant recipients, may be underdiagnosed in this population because routine radiographs do not usually reveal the fracture; bone scanning is the preferred diagnostic modality.