Real-Time, Automated Detection of Ventilator-Associated Events: Avoiding Missed Detections, Misclassifications, and False Detections Due to Human Error.

OBJECTIVETo validate a system to detect ventilator associated events (VAEs) autonomously and in real time.DESIGNRetrospective review of ventilated patients using a secure informatics platform to identify VAEs (ie, automated surveillance) compared to surveillance by infection control (IC) staff (ie, manual surveillance), including development and validation cohorts.SETTINGThe Massachusetts General Hospital, a tertiary-care academic health center, during January-March 2015 (development cohort) and January-March 2016 (validation cohort).PATIENTSVentilated patients in 4 intensive care units.METHODSThe automated process included (1) analysis of physiologic data to detect increases in positive end-expiratory pressure (PEEP) and fraction of inspired oxygen (FiO2); (2) querying the electronic health record (EHR) for leukopenia or leukocytosis and antibiotic initiation data; and (3) retrieval and interpretation of microbiology reports. The cohorts were evaluated as follows: (1) manual surveillance by IC staff with independent chart review; (2) automated surveillance detection of ventilator-associated condition (VAC), infection-related ventilator-associated complication (IVAC), and possible VAP (PVAP); (3) senior IC staff adjudicated manual surveillance-automated surveillance discordance. Outcomes included sensitivity, specificity, positive predictive value (PPV), and manual surveillance detection errors. Errors detected during the development cohort resulted in algorithm updates applied to the validation cohort.RESULTSIn the development cohort, there were 1,325 admissions, 479 ventilated patients, 2,539 ventilator days, and 47 VAEs. In the validation cohort, there were 1,234 admissions, 431 ventilated patients, 2,604 ventilator days, and 56 VAEs. With manual surveillance, in the development cohort, sensitivity was 40%, specificity was 98%, and PPV was 70%. In the validation cohort, sensitivity was 71%, specificity was 98%, and PPV was 87%. With automated surveillance, in the development cohort, sensitivity was 100%, specificity was 100%, and PPV was 100%. In the validation cohort, sensitivity was 85%, specificity was 99%, and PPV was 100%. Manual surveillance detection errors included missed detections, misclassifications, and false detections.CONCLUSIONSManual surveillance is vulnerable to human error. Automated surveillance is more accurate and more efficient for VAE surveillance.Infect Control Hosp Epidemiol 2018;826-833.

Is GERD a Factor in Osteonecrosis of the Jaw? Evidence of Pathology Linked to G6PD Deficiency and Sulfomucins.

Osteonecrosis of the jaw (ONJ), a rare side effect of bisphosphonate therapy, is a debilitating disorder with a poorly understood etiology. FDA's Adverse Event Reporting System (FAERS) provides the opportunity to investigate this disease. Our goals were to analyze FAERS data to discover possible relationships between ONJ and specific conditions and drugs and then to consult the scientific literature to deduce biological explanations. Our methodology revealed a very strong association between gastroesophageal reflux and bisphosphonate-induced ONJ, suggesting acidosis as a key factor. Overgrowth of acidophilic species, particularly Streptococcus mutans, in the oral microbiome in the context of insufficient acid buffering due to impaired salivary glands maintains the low pH that sustains damage to the mucosa. Significant associations between ONJ and adrenal insufficiency, vitamin C deficiency, and Sjögren's syndrome were found. Glucose 6 phosphate dehydrogenase (G6PD) deficiency can explain much of the pathology. An inability to maintain vitamin C and other antioxidants in the reduced form leads to vascular oxidative damage and impaired adrenal function. Thus, pathogen-induced acidosis, hypoxia, and insufficient antioxidant defenses together induce ONJ. G6PD deficiency and adrenal insufficiency are underlying factors. Impaired supply of adrenal-derived sulfated sterols such as DHEA sulfate may drive the disease process.

Controlled trial for smoking cessation in a Navy shipboard population using nicotine patch, sustained-release buproprion, or both.

This study reports an experimental, randomized controlled clinical trial comparing three treatments for smoking cessation: sustained-release bupropion, nicotine patch, and combination nicotine and bupropion, to a counseling-only control group (N = 140), for smoking sailors aboard seven Navy ships. The purpose was to determine the effectiveness of different pharmcotherapies used in smoking cessation programs. Continuous abstinence was defined as the percentage of subjects who did not smoke since the quit date assessed at 6 and 12 months and having an expired carbon monoxide concentration of <10 ppm at educational sessions 2, 3, and 4. Nine subjects dropped out of the study, and 40 subjects were lost to follow-up. Eleven percent (15/140 subjects) had continuous abstinence at 12 months. The abstinence rates at 12 months were 47% in the control group, as compared with 27% in the nicotine patch/bupropion group, 20% in the nicotine patch group, and 7% in the bupropion group.