To investigate risk factors of critical illness polyneuromyopathy (CIPM) in a general multidisciplinary intensive care unit (ICU). Prospective observational study in a 28-bed university multidisciplinary ICU. Four hundred and seventy-four (323 M/151 F, age 55 +/- 19) consecutive patients were prospectively evaluated. All patients were assigned admission Acute Physiology and Chronic Health Evaluation (APACHE II; 15 +/- 7) and Sequential Organ Failure Assessment (SOFA; 6 +/- 3) scores and were subsequently evaluated for newly developed neuromuscular weakness. Other potential causes of new-onset weakness after ICU admission were excluded before CIPM was diagnosed. Forty-four (23.8%) of 185 patients developed generalized weakness that met the criteria for CIPM. Patients with CIPM had higher APACHE II (18.9 +/- 6.6 vs 15.6 +/- 6.4, P = 0.004) and SOFA scores (8.4 +/- 2.9 vs 7.1 +/- 2.9, P = 0.013). According to multivariate logistic regression analysis, the following risk factors were independently associated with the development of CIPM: severity of illness at the time of ICU admission, administration of aminoglycoside antibiotics and high blood glucose levels. Analysis according to severity of illness stratification revealed the emergence of Gram (-) bacteremia as the most important independent predisposing factor for CIPM development in less severely ill patients. CIPM has a high incidence in the ICU setting. Our study revealed the association of aminoglycosides, hyperglycemia and illness severity with CIPM development, as well as the association between Gram (-) bacteremia and development of CIPM in less severely ill patient population.

Background. To determine whether automated office blood pressure (AOBP) readings are associated with left ventricular mass (LVM) index as closely as those of 2

Background: Automated office blood pressure (AOBP) measurement is superior to conventional office blood pressure (OBP) because it eliminates the “white coat effect” and shows a strong association with ambulatory blood pressure. Methods and Results: We conducted a cross‐sectional study in 146 participants with office hypertension, and we compared AOBP readings, taken with or without the presence of study personnel, before and after the conventional office readings to determine whether their variation in blood pressure showed a difference in blood pressure values. We also compared AOBP measurements with daytime ambulatory blood pressure monitoring and conventional office readings. The mean age of the studied population was 56±12 years, and 53.4% of participants were male. Bland–Altman analysis revealed a bias (ie, mean of the differences) of 0.6±6 mm Hg systolic for attended AOBP compared with unattended and 1.4±6 and 0.1±6 mm Hg bias for attended compared with unattended systolic AOBP when measurements were performed before and after conventional readings, respectively. A small bias was observed when unattended and attended systolic AOBP measurements were compared with daytime ambulatory blood pressure monitoring (1.3±13 and 0.6±13 mm Hg, respectively). Biases were higher for conventional OBP readings compared with unattended AOBP (−5.6±15 mm Hg for unattended AOBP and oscillometric OBP measured by a physician, −6.8±14 mm Hg for unattended AOBP and oscillometric OBP measured by a nurse, and −2.1±12 mm Hg for unattended AOBP and auscultatory OBP measured by a second physician). Conclusions: Our findings showed that independent of the presence or absence of medical staff, AOBP readings revealed similar values that were closer to daytime ambulatory blood pressure monitoring than conventional office readings, further supporting the use of AOBP in the clinical setting.

Intensive care unit-acquired weakness (ICUAW) is a common complication, associated with significant morbidity. Neuromuscular electrical stimulation (NMES) has shown promise for prevention. NMES acutely affects skeletal muscle microcirculation; such effects could mediate the favorable outcomes. However, optimal current characteristics have not been defined. This study aimed to compare the effects on muscle microcirculation of a single NMES session using medium and high frequency currents.

Postresuscitation hemodynamics are associated with hospital mortality/functional outcome. We sought to determine whether low-dose steroids started during and continued after cardiopulmonary resuscitation (CPR) affect postresuscitation hemodynamics and other physiological variables in vasopressor-requiring, in-hospital cardiac arrest. We conducted a two-center, randomized, double-blind trial of patients with adrenaline (epinephrine)-requiring cardiac arrest. Patients were randomized to receive either methylprednisolone 40 mg (steroids group) or normal saline-placebo (control group) during the first CPR cycle post-enrollment. Postresuscitation shock was treated with hydrocortisone 240 mg daily for 7 days maximum and gradual taper (steroids group), or saline-placebo (control group). Primary outcomes were arterial pressure and central-venous oxygen saturation (ScvO₂) within 72 hours post-ROSC. Eighty nine of 98 controls and 80 of 86 steroids group patients with ROSC were treated as randomized. Primary outcome data were collected from 100 patients with ROSC (control, n = 54; steroids, n = 46). In intention-to-treat mixed-model analyses, there was no significant effect of group on arterial pressure, marginal mean (95% confidence interval) for mean arterial pressure, steroids vs. control: 74 (68–80) vs. 72 (66–79) mmHg] and ScvO₂ [71 (68–75)% vs. 69 (65–73)%], cardiac index [2.8 (2.5–3.1) vs. 2.9 (2.5–3.2) L/min/m²], and serum cytokine concentrations [e.g. interleukin-6, 89.1 (42.8–133.9) vs. 75.7 (52.1–152.3) pg/mL] determined within 72 hours post-ROSC (P = 0.12–0.86). There was no between-group difference in body temperature, echocardiographic variables, prefrontal blood flow index/cerebral autoregulation, organ failure-free days, and hazard for poor in-hospital/functional outcome, and adverse events (P = 0.08–>0.99). Our results do not support the use of low-dose corticosteroids in in-hospital cardiac arrest. Trial Registration: ClinicalTrials.gov number: NCT02790788 ( https://www.clinicaltrials.gov ).