“…Bile acids were investigated as markers of retrograde aspiration, although, a temporal link along with a dose-response effect was observed with the earlier development of BOS. Furthermore, bile acids carry a plausible biologic activity toward lung injury (38,39,42,43), thus this study also supports their active role, whether primary or contributive to other agents, toward the development of chronic lung allograft dysfunction.…”
Gastro-esophageal reflux and related pulmonary bile acid aspiration were prospectively investigated as possible contributors to postlung transplant bronchiolitis obliterans syndrome (BOS). We also studied the impact of aspiration on pulmonary surfactant collectin proteins SP-A and SP-D and on surfactant phospholipids-all important components of innate immunity in the lung. Proximal and distal esophageal 24-h pH testing and broncho-alveolar lavage fluid (BALF) bile acid assays were performed prospectively at 3-month posttransplant in 50 patients. BALF was also assayed for SP-A, SP-D and phospholipids expressed as ratio to total lipids: phosphatidylcholine; dipalmitoylphosphatidylcholine; phosphatidylglycerol (PG); phosphatidylinositol; sphingomyelin (SM) and lysophosphatidylcholine. Actuarial freedom from BOS was assessed.Freedom from BOS was reduced in patients with abnormal (proximal and/or distal) esophageal pH findings or BALF bile acids (Log-rank Mantel-Cox p < 0.05). Abnormal pH findings were observed in 72% (8 of 11) of patients with bile acids detected within the BALF. BALF with high levels of bile acids also had significantly lower SP-A, SP-D, dipalmitoylphosphatidylcholine; PG and higher SM levels (Mann-Whitney, p < 0.05). Duodeno-gastro-esophageal reflux and consequent aspiration is a risk factor for the development of BOS postlung transplant. Bile acid aspiration is associated with impaired lung allograft innate immunity manifest by reduced surfactant collectins and altered phospholipids.
“…Bile acids were investigated as markers of retrograde aspiration, although, a temporal link along with a dose-response effect was observed with the earlier development of BOS. Furthermore, bile acids carry a plausible biologic activity toward lung injury (38,39,42,43), thus this study also supports their active role, whether primary or contributive to other agents, toward the development of chronic lung allograft dysfunction.…”
Gastro-esophageal reflux and related pulmonary bile acid aspiration were prospectively investigated as possible contributors to postlung transplant bronchiolitis obliterans syndrome (BOS). We also studied the impact of aspiration on pulmonary surfactant collectin proteins SP-A and SP-D and on surfactant phospholipids-all important components of innate immunity in the lung. Proximal and distal esophageal 24-h pH testing and broncho-alveolar lavage fluid (BALF) bile acid assays were performed prospectively at 3-month posttransplant in 50 patients. BALF was also assayed for SP-A, SP-D and phospholipids expressed as ratio to total lipids: phosphatidylcholine; dipalmitoylphosphatidylcholine; phosphatidylglycerol (PG); phosphatidylinositol; sphingomyelin (SM) and lysophosphatidylcholine. Actuarial freedom from BOS was assessed.Freedom from BOS was reduced in patients with abnormal (proximal and/or distal) esophageal pH findings or BALF bile acids (Log-rank Mantel-Cox p < 0.05). Abnormal pH findings were observed in 72% (8 of 11) of patients with bile acids detected within the BALF. BALF with high levels of bile acids also had significantly lower SP-A, SP-D, dipalmitoylphosphatidylcholine; PG and higher SM levels (Mann-Whitney, p < 0.05). Duodeno-gastro-esophageal reflux and consequent aspiration is a risk factor for the development of BOS postlung transplant. Bile acid aspiration is associated with impaired lung allograft innate immunity manifest by reduced surfactant collectins and altered phospholipids.
“…Bile aspiration secondary to duodeno-GER has been associated with severe pulmonary injury. Cytotoxicity may result in disruption of cellular membranes or alteration of cellular cationic permeability depending on the bile acid concentration [27,33,40]. These findings suggest that refluxates, including bile acids, play an important role in BO pathogenesis in lung transplant patients.…”
Microaspiration due to gastroesophageal reflux (GER) has been suggested as a factor contributing to the development and exacerbation of several respiratory disorders. To explore the relationship between GER and respiratory disorders, we histologically examined the bilateral lungs of a rat gastroduodenal contents reflux model, which was previously used to investigate the histogenesis of Barrett's esophagus and esophageal carcinoma. GER was surgically induced in male Wistar rats. The bilateral lungs of the reflux rats were examined with hematoxylin and eosin (HE), PAS-Alcian blue, and Azan staining at 10 and 20 weeks after surgery. Immunohistochemical staining of CD68 and α-SMA was also performed. Aspiration pneumonia with severe peribronchiolar neutrophilic and lymphocytic infiltrates, goblet cell hyperplasia, prominence of blood vessels, and increased thickness of the smooth muscle layer were detected. Bronchiolitis obliterans (BO)-like lesions comprising granulation tissue with macrophages, spindle cells, and multinucleated giant cells in the lumen of respiratory bronchioles were observed in the bilateral lungs of the reflux animals. These findings suggest that the severe inflammation and the BO-like lesions may play a role in exacerbation of the forced expiratory volume in 1 second (FEV 1) in human cases. In conclusion, we speculate that repetitive microaspiration due to GER may contribute to the exacerbation of various respiratory diseases, particularly asthma and chronic obstructive pulmonary disease (COPD), and the development of BO syndrome following lung transplantation. The reflux model is a good tool for examining the causal relationships between GER and respiratory disorders.
“…They have been found to be associated with neonatal respiratory distress syndrome [5], bile pneumonia [5], alveolitis, bronchioloitis obliterans [6,7], and exaggerated injury in ventilator associated pneumonias [8,9]. There is understandably a paucity of studies done on humans but experimental studies conducted on rats [10], rabbits [11] and pigs [12], have demonstrated that bile acids cause inflammation and cytotoxic effects on histologic examinations. Similarly, broncho-alveolar lavage studies have found a positive correlation between increased bile acid levels and inflammatory markers in blood, increased neutrophilia [13], inflammation in alveoli and ventilator associated pneumonias [9].…”
Anesthetic related fatality is rare in this time and age in young patients who are ASA II (American Society of Anesthesiologists). Our patient had a very unfortunate anesthetic mortality due to aspiration of bilious vomit. A posthumous diagnosis of post Endoscopic Retrograde Cholangio-pancreatography (ERCP) pancreatitis leading to ileus was missed before surgery. There is a brief literature search about perils of bile aspiration, post ERCP pancreatitis and why pancreatitis is a lethal combination with acute respiratory distress syndrome (ARDS).
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