Lawson, Donna

Hospital medicine ward rounds are often conducted away from patients’ bedsides, but it is unknown if more time-at-bedside is associated with improved patient outcomes. Our objective is to measure the association between “time-at-bedside,” patient experience, and patient–clinician care agreement during ward rounds. Research assistants directly observed medicine services to quantify the amount of time spent discussing each patient’s care inside versus outside the patient’s room. “Time-at-bedside” was defined as the proportion of time spent discussing a patient’s care in his or her room. Patient experience and patient–clinician care agreement both were measured immediately after ward rounds. Results demonstrated that the majority of patient and physicians completely agreement on planned tests (66.3%), planned procedures (79.7%), medication changes (50.6%), and discharge location (66.9%), but had no agreement on the patient’s main concern (74.4%) and discharge date (50.6%). Time-at-bedside was not correlated with care agreement or patient experience ( P > .05 for all comparisons). This study demonstrates that spending more time at the bedside during ward rounds, alone, is insufficient to improve patient experience.

Chronic hyperglycemia inhibits the male gonadal axis. The present analyses test the hypothesis that acute glucose ingestion also suppresses LH and testosterone (T) secretion and blunts the LH-T dose-response function. The design comprised a prospectively randomized crossover comparison of LH and T secretion after glucose vs. water ingestion in a Clinical Translational Research Center. The participants were healthy men ( n = 57) aged 19–78 yr with body mass index (BMI) of 20–39 kg/m2. The main outcome measurements were deconvolution and LH-T dose-response analyses of 10-min data. LH-T responses were regressed on glucose, insulin, leptin, adiponectin, age, BMI, and CT-estimated abdominal visceral fat. During the first 120 min after glucose ingestion, for each unit decrease in LH concentrations, T concentrations decreased by 86 (27–144) ng/dl ( r = 0.853, P < 0.001). Based upon deconvolution analysis, glucose compared with water ingestion reduced 1) basal (nonpulsatile; P < 0.001) and total ( P < 0.001) T secretion without affecting pulsatile T output and 2) pulsatile ( P = 0.043) but not basal LH secretion. By multivariate analysis, pulsatile LH secretion positively predicted basal T secretion after glucose ingestion ( r = 0.374, P = 0.0042). In addition, the glucose-induced fall in pulsatile LH secretion was exacerbated by higher fasting insulin concentrations ( P = 0.054) and attenuated by higher adiponectin levels ( P = 0.0037). There were no detectable changes in the analytically estimated LH-T dose-response curves ( P > 0.30). In conclusion, glucose ingestion suppresses pulsatile LH and basal T secretion acutely in healthy men. Suppression is influenced by age, glucose, adiponectin, and insulin concentrations.