Prevalence of delayed gastric emptying and gastroesophageal reflux in patients with end-stage lung disease.
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Gastric Emptying↗
Biomedical subjects
Charles Hoopes
Publications and source records attributed to Charles Hoopes.
The prevalence of distal and proximal gastroesophageal reflux in patients awaiting lung transplantation.
OBJECTIVE: To determine the prevalence and proximal extent of gastroesophageal reflux (GERD) in patients awaiting lung transplantation. BACKGROUND: GERD has been postulated to contribute to accelerated graft failure in patients who have had lung transplantations. However, the prevalence of reflux symptoms, esophageal motility abnormalities, and proximal esophageal reflux among patients with end-stage lung disease awaiting lung transplantation are unknown. METHODS: A total of 109 patients with end-stage lung disease awaiting lung transplantation underwent symptomatic assessment, esophageal manometry, and esophageal pH monitoring (using a probe with 2 sensors located 5 and 20 cm above the lower esophageal sphincter). RESULTS: Reflux symptoms were not predictive of the presence of reflux (sensitivity, 67%; specificity, 26%). Esophageal manometry showed a high prevalence of a hypotensive lower esophageal sphincter (55%) and impaired esophageal peristalsis (47%) among patients with reflux. Distal reflux was present in 68% of patients and proximal reflux was present in 37% of patients. CONCLUSIONS: These data show that in patients with end-stage lung disease: 1) symptoms were insensitive and nonspecific for diagnosing reflux; 2) esophageal motility was frequently abnormal; 3) 68% of patients had GERD; 4) in 50% of the patients with GERD, acid refluxed into the proximal esophagus. We conclude that patients with end-stage lung disease should be screened with pH monitoring for GERD.
Adult↗
c-Kit immunophenotyping and metalloproteinase expression profiles of mast cells in interstitial lung diseases.
Diverse interstitial lung diseases (ILD) demonstrate mesenchymal infiltration by an abundance of activated mast cells whose role in parenchymal fibrogenesis remains unclear. Since mast cells differentiate in a dynamic, tissue-specific manner via signals transduced by c-Kit receptor, we examined the effect of ILD microenvironments on c-Kit expression and metalloproteinase phenotypes of mesenchymal mast cell populations. Immunohistochemical and flow cytometric analyses characterized surface expression of c-Kit on mast cells in tissues obtained from patients with idiopathic pulmonary fibrosis, systemic sclerosis, sarcoidosis, and lymphangioleiomyomatosis, thus identifying a unique immunophenotype not shared by normal lung mast cells. Isolation of c-Kit+/FcepsilonRI+/CD34- mast cells via immunocytometric sorting of heterogeneous cell populations from mechanically disaggregated lung tissues permitted analysis of gene expression patterns by two-step real-time polymerase chain reaction. Transcriptional profiling identified expression of c-Kit and the neutral serine proteases, tryptase and chymase, establishing the identity of sorted populations as mature mast cells. Mast cells harvested from ILD tissues demonstrated characteristic metalloproteinase phenotypes which included expression of matrix metalloproteinase (MMP)-1 and a disintegrin and metalloproteinase (ADAM)-9, -10, and -17. Immunohistochemical co-localization guided by gene profiling data confirmed expression of chymase, MMP-1, and ADAM-17 protein in subpopulations of mast cells in remodelling interstitium. Gene profiling of harvested mast cells also showed increased transcript copy numbers for TNFalpha and CC chemokine receptor 2, which play critical roles in lung injury. We conclude that ILD microenvironments induce unique c-Kit receptor and metalloproteinase mast cell phenotypes.
Cell Differentiation↗
Idiopathic pulmonary fibrosis: how often is it really idiopathic?
The cause of idiopathic pulmonary fibrosis (IPF) is unknown. The pathology suggests that IPF results from serial lung injury. It has been suggested that gastroesophageal reflux disease (GERD) may relate to the cause or the progression of the disease. The aims of this study were to determine the prevalence of GERD, the clinical presentation of GERD, and the manometric and reflux profiles in patients with end-stage IPF. Between July 2003 and October 2004, 18 patients with IPF on the lung transplant waiting list were referred for evaluation to the Swallowing Center of the University of California San Francisco. On the basis of the results of the pH monitoring test (5 and 20 cm above the lower esophageal sphincter), the patients were divided into two groups: group A, 12 patients (66%), GERD+; group B, 6 patients (34%), GERD-. The incidence of heartburn and regurgitation was similar between GERD+ and GERD- patients; reflux was clinically silent in one third of GERD+ patients. Reflux was associated with a hypotensive lower esophageal sphincter and abnormal esophageal peristalsis, and it was present in the upright and supine position. The reflux often extended into the proximal esophagus. These results show the following: (1) Two thirds of patients with IPF had GERD; (2) symptoms could not distinguish between those with and without GERD; (3) reflux occurred in the presence of a hypotensive lower esophageal sphincter and abnormal esophageal peristalsis; and (4) reflux occurred in the upright and supine positions, and often extended into the proximal esophagus. We conclude that patients with IPF should be screened for GERD, and if GERD is present, a fundoplication should be performed before or shortly after lung transplantation.
Chi-Square Distribution↗
Use of bivalirudin, a direct thrombin inhibitor, and its reversal with modified ultrafiltration during heart transplantation in a patient with heparin-induced thrombocytopenia.
Heparin-induced thrombocytopenia (HIT) is an increasingly common clinical finding in patients presenting for cardiac transplantation. Bivalrudin, a reversible direct thrombin inhibitor, is a molecular anti-coagulant with short half-life and the potential for removal by intraoperative hemofiltration. Herein we describe the dosing and intraoperative management of bivalrudin anti-coagulation in a patient undergoing urgent cardiac transplantation in the context of recently diagnosed HIT.
Adult↗
Profound hypoxemia resulting from shunting across an inadvertent atrial septal tear after left ventricular assist device placement.
UNLABELLED: Defects within the interatrial septum (IAS) can be a source of significant right-to-left shunting and hypoxemia, particularly after placement of a left ventricular assist device (LVAD). We report a case of LVAD placement in which an unrecognized IAS tear occurred intraoperatively, leading to profound arterial desaturation. Transesophageal echocardiography (TEE) was instrumental in making the diagnosis. Certain intraoperative events increased the pressure gradient between the right and left atria, aggravating hypoxemia. We recommend that patients undergoing LVAD placement be screened intraoperatively with TEE for unrecognized IAS defects. Re-examination of the IAS should occur on weaning from cardiopulmonary bypass. IMPLICATIONS: A traumatic atrial septal defect after atrial cannulation caused a right-to-left intracardiac shunt on initiation of left ventricular assist device support that was further aggravated by chest closure and pleural suction, culminating in severe hypoxemia.
Adult↗