Emergent operation for isolated severe traumatic brain injury: Does time matter?

BACKGROUND: It remains unclear whether the timing of neurosurgical intervention impacts the outcome of patients with isolated severe traumatic brain injury (TBI). We hypothesized that a shorter time between emergency department (ED) admission to neurosurgical intervention would be associated with a significantly higher rate of patient survival. METHODS: Our institutional trauma registry was queried for patients (2003-2013) who required an emergent neurosurgical intervention (craniotomy, craniectomy) for TBI within 300 minutes after the ED admission. We included patients with altered mental status upon presentation in the ED (Glasgow Coma Scale [GCS] score < 9). Patients with associated severe injuries (Abbreviated Injury Scale [AIS] score ≥ 2) in other body regions were excluded. In-hospital mortality of patients who underwent surgery in less than 200 minutes (early group) was compared with those who underwent surgery in 200 minutes or longer (late group) using univariate and multivariate analyses. RESULTS: A total of 161 patients were identified during the study time frame. Head computed tomographic scan demonstrated subdural hematoma in 85.8%, subarachnoid hemorrhage in 55.5%, and equal numbers of epidural hematoma and intraparenchymal hemorrhage in 22.6%. Median time between ED admission and neurosurgical intervention was 133 minutes. In univariate analysis, a significantly lower in-hospital mortality rate was identified in the early group (34.5% vs. 59.1%, p = 0.03). After adjusting for clinically important covariates in a logistic regression model, early neurosurgical intervention was significantly associated with a higher odds of patient survival (odds ratio, 7.41; 95% confidence interval, 1.66-32.98; p = 0.009). CONCLUSION: Our data suggest that the survival rate of isolated severe TBI patients who required an emergent neurosurgical intervention could be time dependent. These patients might benefit from expedited process (computed tomographic scan, neurosurgical consultation, etc.) to shorten the time to surgical intervention. LEVEL OF EVIDENCE: Prognostic study, level IV.

Clinical practices, complications, and mortality in neurological patients with acute severe hypertension: the Studying the Treatment of Acute hyperTension registry.

OBJECTIVE: To determine the demographic and clinical features, hospital complications, and predictors of 90-day mortality in neurologic patients with acute severe hypertension. DESIGN: Studying the Treatment of Acute hyperTension (STAT) was a multicenter (n=25) observational registry of adult critical care patients with severe hypertension treated with intravenous therapy. SETTING: Emergency department or intensive care unit. PATIENTS: A qualifying blood pressure measurement>180 mm Hg systolic or >110 mm Hg diastolic (>140/90 mm Hg for subarachnoid hemorrhage) was required for inclusion in the STAT registry. Patients with a primary neurologic admission diagnosis were included in the present analysis. INTERVENTIONS: All patients were treated with at least one parenteral (bolus or continuous infusion) antihypertensive agent. MEASUREMENTS AND MAIN RESULTS: Of 1,566 patients included in the STAT registry, 432 (28%) had a primary neurologic diagnosis. The most common diagnoses were subarachnoid hemorrhage (38%), intracerebral hemorrhage (31%), and acute ischemic stroke (18%). The most common initial drug was labetalol (48%), followed by nicardipine (15%), hydralazine (15%), and sodium nitroprusside (13%). Mortality at 90 days was substantially higher in neurologic than in non-neurologic patients (24% vs. 6%, p<.0001). Median initial blood pressure was 183/95 mm Hg and did not differ between survivors and nonsurvivors. In a multivariable analysis, neurologic patients who died experienced lower minimal blood pressure values (median 103/45 vs. 118/55 mm Hg, p<.0001) and were less likely to experience recurrent hypertension requiring intravenous treatment (29% vs. 51%, p=.0001) than those who survived. Mortality was also associated with an increased frequency of neurologic deterioration (32% vs. 10%, p<.0001). CONCLUSION: Neurologic emergencies account for approximately 30% of hospitalized patients with severe acute hypertension, and the majority of those who die. Mortality in hypertensive neurologic patients is associated with lower minimum blood pressure values, less rebound hypertension, and a higher frequency of neurologic deterioration. Excessive blood pressure reduction may contribute to poor outcome after severe brain injury.

Therapeutic hypothermia in acute ischemic stroke.

Induced hypothermia has been used for neuroprotection in cardiac and neurovascular procedures. Experimental and translational studies provide evidence for its utility in the treatment of ischemic cerebrovascular disease. Over the past decade, these principles have been applied to the clinical management of acute stroke. Varying induction methods, time windows, clinical indications, and adjuvant therapies have been studied. In this article the authors review the mechanisms and techniques for achieving therapeutic hypothermia in the setting of acute stroke, and they outline pertinent side effects and complications. The manuscript summarizes and examines the relevant clinical trials to date. Despite a reasonable amount of existing data, this review suggests that additional trials are warranted to define the optimal time window, temperature regimen, and precise clinical indications for induction of therapeutic hypothermia in the setting of acute stroke.

Impact of systems of care and blood pressure management on stroke outcomes.

Stroke is the third leading cause of death in the United States and the leading cause of disability. Stroke patients' outcomes are strongly determined by how long they remain untreated ("time is brain"). The Joint Commission's adoption of stroke performance improvement measures combined with the Centers for Medicare and Medicaid's more recent adoption in October 2009 make a systems approach to improving stroke outcomes a higher priority. As hospitals establish local and regional stroke care systems to meet these performance measures, treatment of emergent high blood pressure (BP) is a major consideration to improve rapid triage and management of acute stroke patients. Intravenous thrombolysis with tissue plasminogen activator (tPA) is a critical quality of care component for acute ischemic stroke (AIS) treatment, but its administration is contingent on BP management. For patients with AIS who are potentially eligible for tPA and patients with intracerebral hemorrhage, timely, controlled BP may improve patient outcomes. Appropriate BP management, however, is still controversial given the heterogeneity of stroke subtypes, the varying attributes of candidate antihypertensive agents, and both local and central hemodynamics. Additionally, organizational delivery system factors may be suboptimal at some hospitals. Under current hospital stroke performance measures, payment mechanisms, and emergency department throughput measures, the impact of BP management may become transparent to patients and payers, and have important consequences for hospital-derived stroke outcomes.

Metrics for measuring quality of care in comprehensive stroke centers: detailed follow-up to Brain Attack Coalition comprehensive stroke center recommendations: a statement for healthcare professionals from the American Heart Association/American Stroke Association.

BACKGROUND: Stroke is a major cause of disability and death. The Brain Attack Coalition has proposed establishment of primary and comprehensive stroke centers to provide appropriate care to stroke patients who require basic and more advanced interventions, respectively. Primary stroke centers have been designated by The Joint Commission since 2003, as well as by various states. The designation of comprehensive stroke centers (CSCs) is now being considered. To assist in this process, we propose a set of metrics and related data that CSCs should track to monitor the quality of care that they provide and to facilitate quality improvement. METHODS AND RESULTS: We analyzed available guideline statements, reviews, and other literature to identify the major features that distinguish CSCs from primary stroke centers, drafted a set of metrics and related data elements to measure the key components of these aspects of stroke care, and then revised these through an iterative process to reach a consensus. We propose a set of metrics and related data elements that cover the major aspects of specialized care for patients with ischemic cerebrovascular disease and nontraumatic subarachnoid and intracerebral hemorrhages at CSCs. CONCLUSIONS: The metrics that we propose are intended to provide a framework for standardized data collection at CSCs to facilitate local quality improvement efforts and to allow for analysis of pooled data from different CSCs that may lead to development of national performance standards for CSCs in the future.

Central retinal artery occlusion associated with intranasal methamphetamine use.

Stimulant abuse is associated with ischemic stroke. This report describes a 43-year-old woman with a central retinal artery occlusion following the use of intranasal methamphetamine. Toxicology testing should be considered in patients presenting with acute visual loss.

Acute Treatment of Cerebral Venous Thrombosis.

Correct and timely diagnosis of cerebral venous thrombosis (CVT) is imperative in determining the appropriate treatment plan. Clinical suspicion is crucial, followed by radiographic confirmation using CT, MRI, or conventional angiography. Emergency and critical care of the patient is important, including control of airway and circulation. Initially, the treatment of choice is anticoagulation with heparin. Consideration should be given to intrathrombus delivery of thrombolytic agents. Eventually, newer techniques such as laser, ultrasound, and suction may be considered.

Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Abnormal serum sodium levels (hyponatremia and hypernatremia) are frequently observed during the acute period after aneurysmal subarachnoid hemorrhage (SAH) and may worsen cerebral edema and mass effect. We performed this study to determine the prognostic significance of serum sodium concentration abnormalities. METHODS: We analyzed prospectively collected data for the placebo treatment group in a clinical trial conducted at 54 neurosurgical centers in North America. The presence of hypernatremia (serum sodium concentration of >145 mmol/L) and hyponatremia (serum sodium concentration of <135 mmol/L) was determined with serum sodium measurements obtained at admission and 3, 6, and 9 days after SAH. The effects of hypernatremia and hyponatremia on the risk of symptomatic vasospasm and on 3-month outcomes were analyzed after adjustment for the following potential confounding factors: age, sex, preexisting hypertension, admission Glasgow Coma Scale score, initial mean arterial pressure, subarachnoid clot thickness, intraventricular blood or intraparenchymal hematoma, ventricular dilation, and aneurysm size and location. RESULTS: Of 298 patients in the analysis, 58 (19%) developed hypernatremia and 88 (30%) developed hyponatremia. Hypernatremia was significantly associated with poor outcomes (odds ratio, 2.7; 95% confidence interval, 1.2-6.1). A positive correlation was observed between the highest sodium values recorded and Glasgow Outcome Scale scores at 3 months (P < 0.0001 by analysis of variance). Hyponatremia was not associated with 3-month outcomes (odds ratio, 1.9; 95% confidence interval, 0.9-4.3). Neither hypernatremia nor hyponatremia was associated with the risk of symptomatic vasospasm. CONCLUSION: Hyponatremia seems to be more common than hypernatremia after SAH. However, hypernatremia after SAH is independently associated with poor outcomes, and this association is independent of previously identified outcome predictors, including age and admission Glasgow Coma Scale scores. Further studies are needed to define the underlying mechanism of this association.

Early false-negative diffusion-weighted imaging in brainstem infarction.

It has been well established that acute ischemic lesions can be identified with diffusion-weighted imaging before they are detected on computed axial tomography or conventional magnetic resonance imaging sequences. Previous studies examining the sensitivity and specificity of diffusion-weighted imaging for acute stroke have dealt primarily with cortical stroke. Only limited information is available on the accuracy and temporal evolution of findings on diffusion-weighted imaging in patients with brainstem infarction. We present a case of lateral medullary infarction with false-negative diffusion-weighted imaging 16 hours after symptom onset and a brief review of the literature on the utility of diffusion-weighted imaging in early detection of brainstem stroke. Cases with false-negative initial imaging are increasingly more commonly reported in the literature, with initial images being obtained from 0.5 to over 24 hours after symptom onset. This delay in radiographic confirmation of brainstem stroke emphasizes the continuing need for accurate clinical diagnoses, especially in the early hours after symptom onset, when thrombolysis remains a treatment option. Delays in diagnosis and initiation of treatment of brainstem stroke may increase the associated morbidity and mortality.