Reduced Hospital Duration of Stay Associated with Revised Emergency Department-Intensive Care Unit Admission Policy: A before and after Study.

BACKGROUND: Emergency department (ED) and hospital crowding adversely impacts patient care. Although reduction methods for duration of stay in the ED have been explored, few focus on medical intensive care unit (MICU) patients. OBJECTIVE: To quantify duration of stay or mortality changes associated with a policy intervention that changed the role of an MICU resident to "screen" and write MICU admission orders in the ED to instead meet the patient and write orders in the MICU if there was an available bed. The intervention moved "screening" bed management-appropriateness discussions to the MICU attending or fellow level. METHODS: We performed a retrospective before and after study at an urban, level 1 trauma center of adults admitted to the MICU from the ED during the first 6 months in 2009 before, and the corresponding 6 months in 2010, after the intervention. We collected demographics, ED, MICU, and hospital duration of stay, duration of mechanical ventilation, Acute Physiology and Chronic Health Evaluation (APACHE) scores, and mortality from electronic medical records. Linear models compared duration of stay differences; logistic regression compared in-hospital mortality. T-tests assessed APACHE score changes before and after the policy change. Analyses were adjusted for age and sex. RESULTS: We included 498 patients, average age 66 years (±18), 52% male. Hospital duration of stay decreased 18% from 6.8 to 5.6 days (unadjusted p = 0.029). MICU duration of stay decreased from 3.5 to 3.3 days (unadjusted p = 0.34) and ED duration of stay from arrival to physical transfer decreased 40 min (375 to 324 min; unadjusted p = 0.006). Mortality and APACHE scores were unchanged. CONCLUSIONS: A streamlined admission intervention from the ED to the MICU was associated with decreased ED and hospital duration of stay without altering mortality.

Diarrhea: Initial Evaluation and Treatment in the Emergency Department.

Diarrhea generates a wide range of diagnostic considerations and has profound individual and public health significance. The setting and circumstances under which a patient presents with diarrhea drastically influences the concern brought to the encounter. Nausea, vomiting, and diarrhea are often provisionally labeled "gastroenteritis" with appropriate expectant management. In resource-poor countries, the significance of diarrhea is even greater. This review focuses on diarrhea and its initial evaluation and management in the emergency department.

Environmental, pharmacological, and genetic modulation of the HD phenotype in transgenic mice.

The HD-N171-82Q (line 81) mouse model of Huntington's disease (HD), expresses an N-terminal fragment of mutant huntingtin (htt), loses motor function, displays HD-related pathological features, and dies prematurely. In the present study, we compare the efficacy with which environmental, pharmacological, and genetic interventions ameliorate these abnormalities. As previously reported for the R6/2 mouse model of HD, housing mice in enriched environments improved the motor skills of N171-82Q mice. However, life expectancy was not prolonged. Significant improvements in motor function, without prolonging survival, were also observed in N171-82Q mice treated with Coenzyme Q10 (CoQ10, an energy metabolism enhancer). Several compounds were not effective in either improving motor skills or prolonging life, including Remacemide (a glutamate antagonist), Celecoxib (a COX-2 inhibitor), and Chlorpromazine (a prion inhibitor); Celecoxib dramatically shortened life expectancy. We also tested whether raising cellular antioxidant capacity by co-expressing high levels of wild-type human Cu/Zn superoxide dismutase 1 (SOD1) was beneficial. However, no improvement in motor performance or life expectancy was observed. Although we would argue that positive outcomes in mice carry far greater weight than negative outcomes, we suggest that caution may be warranted in testing Celecoxib in HD patients. The positive outcomes achieved by CoQ10 therapy and environmental stimuli point toward two potentially therapeutic approaches that should be readily accessible to HD patients and at-risk family members.

Nuclear-targeting of mutant huntingtin fragments produces Huntington's disease-like phenotypes in transgenic mice.

Huntington's disease (HD) results from the expansion of a glutamine repeat near the N-terminus of huntingtin (htt). At post-mortem, neurons in the central nervous system of patients have been found to accumulate N-terminal fragments of mutant htt in nuclear and cytoplasmic inclusions. This pathology has been reproduced in transgenic mice expressing the first 171 amino acids of htt with 82 glutamines along with losses of motoric function, hypoactivity and abbreviated life-span. The relative contributions of nuclear versus cytoplasmic mutant htt to the pathogenesis of disease have not been clarified. To examine whether pathogenic processes in the nucleus disproportionately contribute to disease features in vivo, we fused a nuclear localization signal (NLS) derived from atrophin-1 to the N-terminus of an N171-82Q construct. Two lines of mice (lines 8A and 61) that were identified expressed NLS-N171-82Q at comparable levels and developed phenotypes identical to our previously described HD-N171-82Q mice. Western blot and immunohistochemical analyses revealed that NLS-N171-82Q fragments accumulate in nuclear, but not cytoplasmic, compartments. These data suggest that disruption of nuclear processes may account for many of the disease phenotypes displayed in the mouse models generated by expressing mutant N-terminal fragments of htt.