Intensive care unit-acquired hypernatremia is an independent predictor of increased mortality and length of stay.

PURPOSE: The purpose of this study is to examine the impact of hypernatremia acquired after intensive care unit (ICU) admission on mortality and length of stay (LOS). MATERIALS AND METHODS: Data for this observational study were collected from patients admitted between January 1, 2008, and September 30, 2010 to 344 ICUs in the eICU Research Institute. RESULTS: Of the 207702 eligible patients, 8896 (4.3%) developed hypernatremia (serum Na >149 mEq/L). Hospital mortality was 32% for patients with hypernatremia and 11% for patients without hypernatremia (P < .0001). Intensive care unit LOS was 13.7 ± 9.7 days for patients with hypernatremia and 5.1 ± 4.6 for patients without hypernatremia (P < .0001). Multivariate analysis showed that hypernatremia was an independent risk factor for hospital mortality with a relative risk (RR) of 1.40 (95% confidence interval, 1.34-1.45) and ICU LOS with a rate ratio (RtR) of 1.28 (1.26-1.30). The RR for mortality and RtR for ICU LOS increased with increasing severity strata of hypernatremia, but the duration of hypernatremia was not associated with mortality. CONCLUSIONS: Hypernatremia developed following ICU admission in 4.3% of patients. Hypernatremia was independently associated with a 40% increase in risk for hospital mortality and a 28% increase in ICU LOS. Severity, but not duration of ICU-acquired hypernatremia was associated with hospital mortality.

Association between intensive care unit-acquired dysglycemia and in-hospital mortality.

OBJECTIVE: Our objective was to quantify the association between intensive care unit-acquired dysglycemia (hyperglycemia, hypoglycemia, and high variability) and in-hospital mortality. DESIGN: Retrospective, observational study. SETTING: eICU Research Institute participating hospitals with an active tele-ICU program between January 1, 2008, and September 30, 2010, representing 784,392 adult intensive care unit patients. PATIENTS: A total of 194,772 patients met inclusion criteria with an intensive care unit length of stay >48 hrs. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Acute Physiology and Chronic Health Evaluation IV standardized mortality ratios were calculated for dysglycemia present at admission and acquired in the intensive care unit. Intensive care unit-acquired dysglycemia was modeled using multivariable modified Poisson regression to account for confounding not incorporated in Acute Physiology and Chronic Health Evaluation. Dysglycemia severity was assessed by the relative risk of in-hospital mortality associated with the maximum, time-weighted average daily glucose; lowest glucose value throughout the intensive care unit stay; and quintiles of variability (coefficient of variation). The association of duration beyond thresholds of dysglycemia on mortality was also modeled. The adjusted relative risk (95% confidence interval) of mortality for the maximum intensive care unit average daily glucose was 1.13 (1.04-1.58), 1.43 (1.30-1.58), 1.63 (1.47-1.81), 1.76 (1.55-1.99), and 1.89 (1.62-2.19) for 110-150 mg/dL, 151-180 mg/dL, 180-240 mg/dL, 240-300 mg/dL, and >300 mg/dL, respectively, compared to patients whose highest average daily glucose was 80-110 mg/dL. The relative risk of mortality for the lowest glucose value was 1.67 (1.37-2.03), 1.53 (1.37-1.70), 1.12 (1.04-1.21), and 1.06 (1.01-1.11) for <20 mg/dL, 20-40 mg/dL, 40-60 mg/dL, and 60-80 mg/dL, respectively, compared to patients whose lowest value was 80-110 mg/dL. The relative risk of mortality increased with greater duration of hyperglycemia and with increased variability. The relative risk for the highest compared to lowest quintile of variability was 1.61 (1.47-1.78). The association of duration of hyperglycemia on mortality was more pronounced with more severe hyperglycemia. CONCLUSIONS: The risk of mortality progressively increased with severity and duration of deviation from euglycemia and with increased variability. These data suggest that severe intensive care unit-acquired hyperglycemia, hypoglycemia, and variability are associated with similar risks of mortality.

Postischemic inotropic support of the dysfunctional heart.

OBJECTIVE: To determine relative adenine nucleotide regeneration and improvement in left ventricular (LV) function using three commonly used adrenergic agents--epinephrine, dobutamine, and phenylephrine---during reperfusion after a period of global ischemia. After initial resuscitation from cardiac arrest, adrenergic agents are frequently required to support postischemic LV dysfunction. However, the relative effectiveness and associated bioenergetic changes associated with these agents in the postischemic heart are unclear. DESIGN: Prospective, controlled laboratory study. SETTING: University research laboratory. SUBJECTS: Isolated, perfused Sprague-Dawley rat hearts. INTERVENTIONS: After 20 mins of global ischemia, isolated rat hearts were reperfused for 30 mins with Krebs-Henseleit solution alone (control, n = 8), or with the addition of equipotent doses of epinephrine 1 microM (n = 8), dobutamine 0.3 microM (n = 8), or phenylephrine 50 microM (n = 8). In a second experiment, an alpha-1 antagonist, prazosin was given with phenylephrine to block the presumed alpha-1 agonist effect of phenylephrine. MEASUREMENTS AND MAIN RESULTS: A constant volume balloon was placed in the left ventricle to measure LV pressure and derived parameters of LV function. Adenine nucleotide concentrations were derived at various time points using high-performance liquid chromatography. During reperfusion, the phenylephrine group had significant improvement in LV function and cardiac efficiency in contrast to epinephrine and dobutamine. Total adenine nucleotides tended to be highest in the phenylephrine group with significant increases in adenosine diphosphate and adenosine monophosphate and no significant loss of adenosine triphosphate. The phenylephrine-induced increase in heart rate and developed pressure could be blocked with an alpha-1 antagonist, prazosin. CONCLUSIONS: In the isolated reperfused heart, phenylephrine, mediated by alpha-1 agonism, significantly improves postischemic LV dysfunction without worsening the overall myocardial metabolic state.