Search

Background: Many ICUs have implemented protocols for tight glucose control, but there are few data on hypoglycemia and neurologic outcomes in patients with subarachnoid hemorrhage (SAH).Methods: We prospectively ascertained 172 patients with SAH, who were treated according to a standard protocol for target glucose 80-110 mg/dl. Outcomes were assessed with the modified Rankin scale (mRS) at 14 days, 28 days, and 3 months.Results: Worse neurologic injury at admission (P < 0.001) and a history of diabetes (P = 0.002) were associated with increased glucose variance. There was lower nadir glucose in patients with radiographic cerebral infarction (81 +/- 15 vs. 87 +/- 16 mg/dl, P = 0.02), symptomatic vasospasm (78 +/- 12 vs. 84 +/- 16 mg/dl, P = 0.04) and angiographic vasospasm (79 +/- 14 vs. 86 +/- 16 mg/dl, P = 0.01), but maximum and mean glucose values were not different. Glucose < 80 mg/dl was earlier and more frequent in patients with worse functional outcome at 3 months (P < 0.001). Progressive reductions in nadir glucose were associated with increasing functional disability at 3 months (P = 0.001) after accounting for neurologic grade and mean glucose. Severe hypoglycemia (<40 mg/dl) occurred in one patient.Conclusions: In patients with SAH, nadir glucose < 80 mg/dl is associated with cerebral infarction, vasospasm, and worse functional outcomes in multivariate models. Protocols for target glucose 80-110 mg/dl effectively control hyperglycemia, but may place patients with SAH at risk for vasospasm, cerebral infarction, and poor outcome even when severe hypoglycemia does not occur. [ABSTRACT FROM AUTHOR]

Introduction: There are few predictors of acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS) after subarachnoid hemorrhage (SAH). We hypothesized that cardiac troponin I, which is associated with cardiovascular morbidity, would also predict ALI.Methods: We prospectively enrolled 171 consecutive patients with SAH. Troponin was routinely measured on admission and the next day and subsequently if abnormal. We prospectively recorded the maximum troponin, in-hospital events, and clinical endpoints. ALI and ARDS were defined by standard criteria.Results: Acute lung injury was found in 10 patients (6%), ARDS in an additional 14 (8%), and pulmonary edema without lung injury in 9 (5%). Maximum troponin was different in patients without lung injury or pulmonary edema (0.03 [0.02-0.12] mcg/l), ALI (0.17 [0.04-1.4]), or ARDS (0.31 [0.9-1.8], P < 0.001). In ROC analysis, a cutoff of 0.04 mcg/l had 91% sensitivity and 42% specificity for ALI or ARDS (AUC = 0.75, P < 0.001). Troponin was associated with ALI or ARDS after accounting for neurologic grade in multivariate models without further contribution from pneumonia, packed red cell transfusion, gender, tobacco use, coronary artery disease, vasospasm, depressed ejection fraction on echocardiography, or CT grade. Lung injury was associated with worse functional outcome at 14 days, but not at 28 days or 3 months.Conclusion: Troponin I is associated with the development of ALI after SAH. [ABSTRACT FROM AUTHOR]

Introduction: Severity of illness scores predict all-cause mortality after intracerebral hemorrhage (ICH), but do not differentiate between proximate mechanisms or predict the timing. We hypothesized that death by neurologic criteria [brain death (BD)], withdrawal of life support, and cardiovascular death would be distinct after ICH.Methods: We prospectively enrolled patients with spontaneous ICH without underlying vascular malformation or neoplasm. We recorded clinical data and the proximate mechanism of death (BD, withdrawal of life support, cardiovascular death, or other cause). Time to death was compared with Kaplan-Meier methods (log-rank test). Data are median (IQR).Results: Among 89 patients, 15 had withdrawal of life support, 5 had BD, 2 died from cardiac arrest, and 3 died from other causes. Among patients who died, ICH score, age, Glasgow Coma Scale, NIH Stroke Scale, and proximate cause were not associated with the proximate mechanism of death. The time to death was different (P < 0.001) depending on the proximate mechanism. Patients with BD died 1 [0-1] 1 day after ICH, withdrawal of life support led to death 5 [1-13] days after ICH, cardiac death occurred 35 [35-85] days after ICH, and other causes led to death 33 [26-33] days after ICH. Among patients where life support was withdrawn, a higher ICH score on admission was related to earlier death (P = 0.002).Conclusions: Proximate mechanisms of death after ICH occur at distinct times. Withdrawal of life support leads to earlier death in patients with a higher severity of injury. Medical causes of death can be effectively prevented after ICH. [ABSTRACT FROM AUTHOR]