Vitamin D Supplementation in Mechanically Ventilated Patients in the Medical Intensive Care Unit.

BACKGROUND: The utility of vitamin D (VITD) supplementation during critical illness and whether it may alter outcomes, including mortality and ventilator-free days, is unclear. We performed a retrospective cohort study in a generalizable population to investigate this question. METHODS: We included all mechanically ventilated adults admitted to the medical intensive care unit (ICU) service at a tertiary center from 2009 to 2012 who were in the ICU for at least 72 hours. Patients were grouped as having received or not received VITD at any time during the first 7 days of their ICU stay, and we adjusted for the following covariates with multivariable analyses: simplified acute physiology score, age, gender, admission diagnosis, race/ethnicity, admission season, admission day of the week, and VITD supplementation prior to admission. RESULTS: Among the 610 included patients, 281 received VITD, and 329 did not. There were no differences in outcomes between these groups. However, we did find significantly more ventilator-free days (21.0±2.6 [adjusted mean days±standard error] vs 17.6±2.4, P=0.04) and ICU-free days (18.5±2.5 vs 16.3±2.3, P=0.03) in patients who were taking VITD prior to admission (n=91) vs those who were not (n=519). No patients who were taking VITD before admission died vs 34.5% of those who were not (estimated odds ratio=4.9×10-7 , 95% CI=3.1×10-7 to 7.5×10-7 , P<0.0001). CONCLUSION: These results suggest that VITD supplementation during critical illness may not provide benefit and that further research investigating potential supplementation in ambulatory patients at high risk of ICU admission (eg, severe underlying chronic disease) is warranted.

Acid aspiration-induced airways hyperresponsiveness in mice.

The role of gastroesophageal reflux and micro-aspiration as a trigger of airways hyperresponsiveness (AHR) in patients with asthma is controversial. The role of acid reflux and aspiration as a direct cause of AHR in normal subjects is also unclear. We speculated that aspiration of a weak acid with a pH (1.8) equivalent to the upper range of typical gastric contents would lead to AHR in naive mice. We further speculated that modest reductions in aspirate acidity to a level expected during gastric acid suppression therapy (pH 4.0) would impede aspiration-induced AHR. BALB/c female mice were briefly anesthetized with isoflurane and allowed to aspirate 75 microl of saline with HCl (pH 1.8, 4.0, or 7.4) or underwent sham aspiration. Mice were re-anesthetized 2 or 24 h later, underwent tracheostomy, and were coupled to a mechanical ventilator. Forced oscillations were used to periodically measure respiratory impedance (Zrs) following aerosol delivery of saline and increasing doses of methacholine to measure for AHR. Values for elastance (H), airways resistance (R(N)), and tissue damping (G) were derived from Zrs. Aspirate pH of 1.8 led to a significant overall increase in peak R(N), G, and H compared with pH 4.0 and 7.4 at 2 and 24 h. Differences between pH 7.4 and 4.0 were not significant. In mice aspirating pH 1.8 compared with controls, airway lavage fluid contained more neutrophils, higher protein, and demonstrated higher permeability. We conclude that acid aspiration triggers an acute AHR, driven principally by breakdown of epithelial barrier integrity within the airways.