Background and Purpose-To assess the prevalence of premorbid undernutrition and its impact on outcomes 1 month after stroke. Methods-The study recruited from consecutive stroke admissions during a 10-month period. Premorbid nutritional status (using the subjective global assessment [SGA]), premorbid functioning (modified Rankin scale [MRS]), and stroke severity (National Institutes of Health Stroke Scale [NIHSS] score) were assessed at admission. The associations between premorbid nutritional status, poor outcome (defined as MRS Ն3), and mortality were examined before and after adjustment for confounding variables, including age, gender, stroke risk factors, stroke severity, and admission serum albumin. Results-Thirty of 185 patients were assessed as having undernutrition at admission. Significant unadjusted associations were observed between undernutrition and poor outcome (odds ratio [OR], 3.4; 95% CI, 1.3 to 8.7; Pϭ0.01), and mortality (OR, 3.1, 95% CI, 1.3 to 7.7; Pϭ0.02) at 1 month. NIHSS, age, and premorbid MRS were also significantly associated with poor outcomes. After adjustment for these factors, the effect size of associations remained important but not significant (poor outcome: OR, 2.4; 95% CI, 0.7 to 9.0, Pϭ0.18; mortality: OR, 3.2; 95% CI, 1.0 to 10.4, Pϭ0.05). Conclusions-Premorbid undernutrition, as assessed using the SGA, appears to be an independent predictor of poor stroke outcome. Stroke prevention strategies should target undernutrition in the population at risk for stroke to improve outcomes.

K E Y W O R D S emotion, objectivity, science inquiry, scientific practices, subjectivity J Res Sci Teach. 2018;1-29. wileyonlinelibrary.com/journal/tea V C 2018 Wiley Periodicals, Inc. | 1

Information from the study has assisted planners and educators to identify clusters of nurses to target for interventions in this area. Results will also be used to assess the success of any interventions.

Background and Purpose: Previous research has attempted to analyze the relationship between post-stroke hyperthermia and prognosis. These analyses have been hindered by a lack of information about the time course and determinants of temperature change after stroke. Methods: Serial temperatures were measured until 48 h after ischaemic stroke in a prospectively recruited cohort. Potential determinants of temperature, including stroke severity [measured using the National Institutes of Health Stroke Scale (NIHSS)], infection and paracetamol use were recorded. Mixed-effects models were used to model serial temperature measurements over time, adjusted for significant determinants. Results: In 155 patients the mean temperature rose from 36.5°C at the time of stroke to 36.7°C approximately 36 h later. The factors with significant multivariable associations with serial temperatures were: first- and second-order time components, infection, paracetamol administration and the interaction between stroke severity (NIHSS ≧6) and time (all p < 0.1). Patients with admission NIHSS ≧6 had a mean temperature rise of 0.35°C during the first 36 h after stroke, compared with a rise of 0.17°C in those with NIHSS ≤5. Conclusions: Temperature spontaneously rises during the first 36 h after stroke, particularly after severer stroke and in the presence of infection.