Acute renal failure and common metabolic disturbances represent potentially modifiable factors contributing to sepsis-associated encephalopathy. However, a true causal relationship has yet to be demonstrated. Our study confirms the prognostic significance of mild alteration of mental status in patients with sepsis.
Background and objectives Increasing experimental evidence suggests that acute respiratory distress syndrome (ARDS) may promote AKI. The primary objective of this study was to assess ARDS as a risk factor for AKI in critically ill patients.Design, setting, participants, & measurements This was an observational study on a prospective database fed by 18 intensive care units (ICUs). Patients with ICU stays .24 hours were enrolled over a 14-year period. ARDS was defined using the Berlin criteria and AKI was defined using the Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease criteria. Patients with AKI before ARDS onset were excluded.Results This study enrolled 8029 patients, including 1879 patients with ARDS. AKI occurred in 31.3% of patients and was more common in patients with ARDS (44.3% versus 27.4% in patients without ARDS; P,0.001). After adjustment for confounders, both mechanical ventilation without ARDS (odds ratio [OR], 4.34; 95% confidence interval [95% CI], 3.71 to 5.10) and ARDS (OR, 11.01; 95% CI, 6.83 to 17.73) were independently associated with AKI. Hospital mortality was 14.2% (n=1140) and was higher in patients with ARDS (27.9% versus 10.0% in patients without ARDS; P,0.001) and in patients with AKI (27.6% versus 8.1% in those without AKI; P,0.001). AKI was associated with higher mortality in patients with ARDS (42.3% versus 20.2%; P,0.001).Conclusions ARDS was independently associated with AKI. This study suggests that ARDS should be considered as a risk factor for AKI in critically ill patients.
When adjusted for risk-exposure time and severity at admission and during the ICU stay, BSI was associated with a 3-fold increase in mortality, but considerable variation occurred across BSI subgroups. Focusing on BSI subgroups may be valuable for assessing quality of care in ICUs.
Intrahospital transport increases the risk of complications in ventilated critically ill patients. Continuous quality improvement programs should include specific procedures to minimize intrahospital transport-related risks.
Extradural clonidine produces analgesia in adults. To assess its efficacy in children, we randomized 45 pediatric patients aged 1-7 yr presenting for a subumbilical surgery into three groups of 15 each. After halothane and N2O/O2 induction, and with a double-blind protocol, caudal anesthesia was performed with 1 mL/kg of 0.25% bupivacaine. Epinephrine 1/200,000 was added in one group (EG), 1 microgram/kg of clonidine in another group (CG), and no additional medication in the last group (BG). Postoperative analgesia was evaluated using the Broadman "objective pain/discomfort scale" (OPS) at 1-h intervals until the first analgesic administration. There were no differences among the groups in age, weight, duration of surgery, baseline systolic arterial pressure, and heart rate. The mean (+/- SD) duration of analgesia was longer in the CG (987 +/- 573 min) than in the EG (377 +/- 341 min) and BG (460 +/- 439 min); P < 0.01. The maximal OPS scores were lower in the CG than in the EG and BG (2.3 +/- 1.6 vs 3.4 +/- 1.4 and 3.4 +/- 1.8, respectively; P < 0.05). More patients in the CG (n = 7) than in the EG (n = 1) and BG (n = 2) required no postoperative analgesia; P < 0.05. No differences were found among the groups for the minimal respiratory rate and minimal Spo2 values in the postoperative phase, and there were no differences among the groups for heart rate and systolic arterial pressure during the 3 h after caudal anesthesia. We conclude that the duration of postoperative analgesia with caudal bupivacaine was significantly increased by the addition of 1 microgram/kg of clonidine.
A multistate model that appropriately handled VAP as a time-dependent event produced lower VAP-AM values than conditional logistic regression. VAP-AM varied widely with case-mix. Disease severity at VAP onset markedly influenced VAP-AM; this may contribute to the variability of previous estimates.
IntroductionTo assess the prevalence of dysnatremia, including borderline changes in serum sodium concentration, and to estimate the impact of these dysnatremia on mortality after adjustment for confounders.MethodsObservational study on a prospective database fed by 13 intensive care units (ICUs). Unselected patients with ICU stay longer than 48 h were enrolled over a 14-year period were included in this study. Mild to severe hyponatremia were defined as serum sodium concentration < 135, < 130, and < 125 mmol/L respectively. Mild to severe hypernatremia were defined as serum sodium concentration > 145, > 150, and > 155 mmol/L respectively. Borderline hyponatremia and hypernatremia were defined as serum sodium concentration between 135 and 137 mmol/L or 143 and 145 respectively.ResultsA total of 11,125 patients were included in this study. Among these patients, 3,047 (27.4%) had mild to severe hyponatremia at ICU admission, 2,258 (20.3%) had borderline hyponatremia at ICU admission, 1,078 (9.7%) had borderline hypernatremia and 877 (7.9%) had mild to severe hypernatremia. After adjustment for confounder, both moderate and severe hyponatremia (subdistribution hazard ratio (sHR) 1.82, 95% CI 1.002 to 1.395 and 1.27, 95% CI 1.01 to 1.60 respectively) were associated with day-30 mortality. Similarly, mild, moderate and severe hypernatremia (sHR 1.34, 95% CI 1.14 to 1.57; 1.51, 95% CI 1.15 to 1.99; and 2.64, 95% CI 2.00 to 3.81 respectively) were independently associated with day-30 mortality.ConclusionsOne-third of critically ill patients had a mild to moderate dysnatremia at ICU admission. Dysnatremia, including mild changes in serum sodium concentration, is an independent risk factor for hospital mortality and should not be neglected.
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