A Proposed Intervention to Decrease Resident-Performed Cataract Surgery Cancellation in a Tertiary Eye Care Center.

BACKGROUND: Cataracts are the leading cause of preventable blindness globally. As a result, competence in cataract surgery is an important component of ophthalmology residency training. Residency programs must optimize the number of cataract surgery cases to train proficient physicians. However, the rate of cataract surgery cancellations is high, and some are canceled because of preventable causes. OBJECTIVE: To evaluate the effect of mandatory on-site preadmission testing, including having a physical examination, on resident-performed cataract surgery cancellation rates. METHODS: For this study, patients scheduled for cataract surgery at the Wills Eye Hospital resident cataract clinic between January 2015 and November 2015 were enrolled and randomized into 2 groups: usual care or intervention. The patients randomized to the usual care group were instructed to complete preadmission testing and to have a physical examination with their primary care physician. The patients randomized to the intervention group were escorted to a Wills Eye Hospital-affiliated cardiologist to complete preadmission testing and to have a physical examination. Patients in both groups received a reminder call before the cataract surgery. RESULTS: A total of 441 patients were included in the study-240 patients in the usual care group and 201 patients in the intervention group. The overall cataract surgery cancellation rate was 14.5%; the rate was 12.4% in the intervention group and 16.3% in the usual care group (P = .28). The patients receiving the intervention were more likely to have preadmission testing and a physical examination than the patients in the usual care arm (P <.001). CONCLUSIONS: Facilitating the completion of preadmission testing for patients decreased the rates of resident-performed cataract surgery cancellation at a Wills Eye Hospital resident clinic and has the potential to improve patient outcomes and prevent blindness.

ß2-Adrenoceptor signaling in airway epithelial cells promotes eosinophilic inflammation, mucous metaplasia, and airway contractility.

The mostly widely used bronchodilators in asthma therapy are ß2-adrenoreceptor (ß2AR) agonists, but their chronic use causes paradoxical adverse effects. We have previously determined that ß2AR activation is required for expression of the asthma phenotype in mice, but the cell types involved are unknown. We now demonstrate that ß2AR signaling in the airway epithelium is sufficient to mediate key features of the asthmatic responses to IL-13 in murine models. Our data show that inhibition of ß2AR signaling with an aerosolized antagonist attenuates airway hyperresponsiveness (AHR), eosinophilic inflammation, and mucus-production responses to IL-13, whereas treatment with an aerosolized agonist worsens these phenotypes, suggesting that ß2AR signaling on resident lung cells modulates the asthma phenotype. Labeling with a fluorescent ß2AR ligand shows the receptors are highly expressed in airway epithelium. In ß2AR-/- mice, transgenic expression of ß2ARs only in airway epithelium is sufficient to rescue IL-13-induced AHR, inflammation, and mucus production, and transgenic overexpression in WT mice exacerbates these phenotypes. Knockout of ß-arrestin-2 (ßarr-2-/-) attenuates the asthma phenotype as in ß2AR-/- mice. In contrast to eosinophilic inflammation, neutrophilic inflammation was not promoted by ß2AR signaling. Together, these results suggest ß2ARs on airway epithelial cells promote the asthma phenotype and that the proinflammatory pathway downstream of the ß2AR involves ßarr-2. These results identify ß2AR signaling in the airway epithelium as capable of controlling integrated responses to IL-13 and affecting the function of other cell types such as airway smooth muscle cells.

Complementary anti-inflammatory effects of a ß-blocker and a corticosteroid in an asthma model.

Glucocorticosteroids are the mainstay treatment for chronic asthma; however, adverse effects can limit their usefulness. We previously determined in experimental asthma that chronic administration of ß2-adrenoceptor inverse agonists reduced airway hyperresponsiveness and indexes of inflammation. However, the effect of co-administration of glucocorticosteroids with ß2-adrenoceptor inverse agonists is unknown. Therefore, we evaluated the anti-inflammatory effect of co-administration of dexamethasone, a glucocorticosteroid, and nadolol, a ß2-inverse agonist, in a murine asthma model. We measured eosinophils and cytokines in bronchoalveolar lavage fluid and mucin content in epithelial cells after exposure to different concentrations of dexamethasone and nadolol. Dexamethasone was administered for 3 days and nadolol for 24 days prior to ovalbumin challenge. Both drugs were continued during five daily intranasal challenges with ovalbumin. Independent administration of dexamethasone (0.4 mg/kg/day) or nadolol (25 ppm) reduced bronchoalveolar lavage eosinophils by 58% and 36%, respectively (P < 0.05). Co-administration of both drugs yielded an additive reduction in eosinophils (81%, P < 0.05). Co-administration of both drugs (dexamethasone 0.4 mg/kg/day and nadolol 25 ppm) also yielded a greater reduction in mucin volume density (83%) than either drug alone (18% for dexamethasone and 62% for nadolol) and greater than high-dose dexamethasone (71%) alone (P < 0.05). Similarly, co-administration of both drugs (dexamethasone 0.4 mg/kg/day and nadolol 25 ppm) yielded an additive effect on the reduction of type 2 cytokines in bronchoalveolar lavage fluid equivalent to the administration of a 10-fold higher dose of dexamethasone. In Summary, the simultaneous administration of a glucocorticosteroid and a ß2-adrenoceptor inverse agonist was more effective at reducing indexes of airway inflammation than either drug given alone; suggesting nadolol may possess "glucocorticoid-sparing" properties.