Neeraj Badjatia

Defining Vasospasm After Subarachnoid Hemorrhage. What Is the Most Clinically Relevant Definition

Background and Purpose— Vasospasm is an important complication of subarachnoid hemorrhage, but is variably defined in the literature. Methods— We studied 580 patients with subarachnoid hemorrhage and identified those with: (1) symptomatic vasospasm, defined as clinical deterioration deemed secondary to vasospasm after other causes were eliminated; (2) delayed cerebral ischemia (DCI), defined as symptomatic vasospasm, or infarction on CT attributable to vasospasm; (3) angiographic spasm, as seen on digital subtraction angiography; and (4) transcranial Doppler (TCD) spasm, defined as any mean flow velocity >120 cm/sec. Logistic regression analysis was performed to test the association of each definition of vasospasm with various hospital complications, and 3-month quality of life (sickness impact profile), cognitive status (telephone interview of cognitive status), instrumental activities of daily living (Lawton score), and death or severe disability at 3 months (modified Rankin scale score 4–6), after adjustment for covariates. Results— Symptomatic vasospasm occurred in 16%, DCI in 21%, angiographic vasospasm in 31%, and TCD spasm in 45% of patients. DCI was statistically associated with more hospital complications (N=7; all P<0.05) than symptomatic spasm (N=4), angiographic spasm (N=1), or TCD vasospasm (N=1). Angiographic and TCD vasospasm were not related to any aspect of clinical outcome. Both symptomatic vasospasm and DCI were related to reduced instrumental activities of daily living, cognitive impairment, and poor quality of life (all P<0.05). However, only DCI was associated with death or severe disability at 3 months (adjusted OR, 2.2; 95% CI, 1.2–3.9; P=0.007). Conclusions— DCI is a more clinically meaningful definition than either symptomatic deterioration alone or the presence of arterial spasm by angiography or TCD.

Impact of tight glycemic control on cerebral glucose metabolism after severe brain injury: A microdialysis study*

Objectives:To analyze the effect of tight glycemic control with the use of intensive insulin therapy on cerebral glucose metabolism in patients with severe brain injury. Design:Retrospective analysis of a prospective observational cohort. Setting:University hospital neurologic intensive care unit. Patients:Twenty patients (median age 59 yrs) monitored with cerebral microdialysis as part of their clinical care. Interventions:Intensive insulin therapy (systemic glucose target: 4.4–6.7 mmol/L [80–120 mg/dL]). Measurements and Main Results:Brain tissue markers of glucose metabolism (cerebral microdialysis glucose and lactate/pyruvate ratio) and systemic glucose were collected hourly. Systemic glucose levels were categorized as within the target “tight” (4.4–6.7 mmol/L [80–120 mg/dL]) vs. “intermediate” (6.8–10.0 mmol/L [121–180 mg/dL]) range. Brain energy crisis was defined as a cerebral microdialysis glucose <0.7 mmol/L with a lactate/pyruvate ratio >40. We analyzed 2131 cerebral microdialysis samples: tight systemic glucose levels were associated with a greater prevalence of low cerebral microdialysis glucose (65% vs. 36%, p < 0.01) and brain energy crisis (25% vs.17%, p < 0.01) than intermediate levels. Using multivariable analysis, and adjusting for intracranial pressure and cerebral perfusion pressure, systemic glucose concentration (adjusted odds ratio 1.23, 95% confidence interval [CI] 1.10–1.37, for each 1 mmol/L decrease, p < 0.001) and insulin dose (adjusted odds ratio 1.10, 95% CI 1.04–1.17, for each 1 U/hr increase, p = 0.02) independently predicted brain energy crisis. Cerebral microdialysis glucose was lower in nonsurvivors than in survivors (0.46 ± 0.23 vs. 1.04 ± 0.56 mmol/L, p < 0.05). Brain energy crisis was associated with increased mortality at hospital discharge (adjusted odds ratio 7.36, 95% CI 1.37–39.51, p = 0.02). Conclusions:In patients with severe brain injury, tight systemic glucose control is associated with reduced cerebral extracellular glucose availability and increased prevalence of brain energy crisis, which in turn correlates with increased mortality. Intensive insulin therapy may impair cerebral glucose metabolism after severe brain injury.

Guidelines for prehospital management of traumatic brain injury 2nd edition

The information contained in these Guidelines, which reflects the current state of knowledge at the time of completion of the literature search (July 2006), is intended to provide accurate and authoritative information about the subject matter covered. Because there will be future developments in scientific information and technology, it is anticipated that there will be periodic review and updating of these Guidelines. These Guidelines are distributed with the understanding that the Brain Trauma Foundation, the National Highway Traffic Safety Administration, and the other organizations that have collaborated in the development of these Guidelines are not engaged in rendering professional medical services. If medical advice or assistance is required, the services of a competent physician should be sought. The recommendations contained in these Guidelines may not be appropriate for use in all circumstances. The decision to adopt a particular recommendation contained in these Guidelines must be based on the judgment of medical personnel, who take into consideration the facts and circumstances in each case, and on the available resources.

Metabolic Impact of Shivering During Therapeutic Temperature Modulation The Bedside Shivering Assessment Scale

Background and Purpose— Therapeutic temperature modulation is widely used in neurocritical care but commonly causes shivering, which can hamper the cooling process and result in increases in systemic metabolism. We sought to validate a grading scale to assist in the monitoring and control of shivering. Methods— A simple 4-point Bedside Shivering Assessment Scale was validated against continuous assessments of resting energy expenditure, oxygen consumption, and carbon dioxide production as measured by indirect calorimetry. Therapeutic temperature modulation for fever control or the induction of hypothermia was achieved with the use of a surface or endovascular device. Expected energy expenditure was calculated using the Harris–Benedict equation. A hypermetabolic index was calculated from the ratio of resting of energy expenditure to energy expenditure. Results— Fifty consecutive cerebrovascular patients underwent indirect calorimetry between January 2006 and June 2007. Fifty-six percent were women, and mean age 63±16 years. The majority underwent fever control (n=40 [80%]) with a surface cooling device (n=44 [87%]) and had signs of shivering (Bedside Shivering Assessment Scale >0, 64% [n=34 of 50]). Low serum magnesium was independently associated with the presence of shivering (Bedside Shivering Assessment Scale >0; OR, 6.8; 95% CI, 1.7 to 28.0; P=0.01). The Bedside Shivering Assessment Scale was independently associated with the hypermetabolic index (W=16.3, P<0.001), oxygen consumption (W=26.3, P<0.001), resting energy expenditure (W=27.2, P<0.001), and carbon dioxide production (W=18.2, P<0.001) with a high level of interobserver reliability (&kgr;w=0.84, 95% CI, 0.81 to 0.86). Conclusion— The Bedside Shivering Assessment Scale is a simple and reliable tool for evaluating the metabolic stress of shivering.

Consensus summary statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care: A statement for healthcare professionals from the Neurocritical Care Society and the European Society of Intensive Care Medicine

Neurocritical care depends, in part, on careful patient monitoring but as yet there are little data on what processes are the most important to monitor, how these should be monitored, and whether monitoring these processes is cost-effective and impacts outcome. At the same time, bioinformatics is a rapidly emerging field in critical care but as yet there is little agreement or standardization on what information is important and how it should be displayed and analyzed. The Neurocritical Care Society in collaboration with the European Society of Intensive Care Medicine, the Society for Critical Care Medicine, and the Latin America Brain Injury Consortium organized an international, multidisciplinary consensus conference to begin to address these needs. International experts from neurosurgery, neurocritical care, neurology, critical care, neuroanesthesiology, nursing, pharmacy, and informatics were recruited on the basis of their research, publication record, and expertise. They undertook a systematic literature review to develop recommendations about specific topics on physiologic processes important to the care of patients with disorders that require neurocritical care. This review does not make recommendations about treatment, imaging, and intraoperative monitoring. A multidisciplinary jury, selected for their expertise in clinical investigation and development of practice guidelines, guided this process. The GRADE system was used to develop recommendations based on literature review, discussion, integrating the literature with the participants’ collective experience, and critical review by an impartial jury. Emphasis was placed on the principle that recommendations should be based on both data quality and on trade-offs and translation into clinical practice. Strong consideration was given to providing pragmatic guidance and recommendations for bedside neuromonitoring, even in the absence of high quality data.

Relationship between hyperglycemia and symptomatic vasospasm after subarachnoid hemorrhage.

Objective:To determine the relationship between blood glucose levels (mg/dL) and occurrence of symptomatic vasospasm (VSP) and clinical outcomes after aneurysmal subarachnoid hemorrhage. Design:Retrospective observational study of 352 patients with subarachnoid hemorrhage admitted within 48 hrs of ictus between January 1995 and June 2002. Setting:Neurointensive care unit. Patients:Adult patients admitted after subarachnoid hemorrhage. Interventions:None. Measurements and Main Results:Variables included age; Hunt-Hess classification score; Fisher group; insulin use; infectious disease status; history of diabetes mellitus; and blood glucose values. Poor clinical outcome was defined by a modified Rankin score ≥3, and hyperglycemia was defined by a blood glucose level >140 mg/dL. Mean daily blood glucose values were assessed from admission to development of VSP or day 14. Mean admission blood glucose value, mean inpatient blood glucose value, insulin use, infectious disease status, Hunt-Hess classification score, Fisher group, and history of diabetes mellitus were entered in a Cox proportional hazards model. VSP occurred in 103 (29.2%) of 352 patients. Mean admission blood glucose values (176.6 ± 40.3 mg/dL vs. 162.3 ± 47.8 mg/dL; p = .01) and mean inpatient blood glucose values (166.2 ± 24.7 mg/dL vs. 155.8 ± 29.7 mg/dL; p = .001) were significantly higher in patients with VSP. Mean inpatient blood glucose value (relative risk, 1.01; 95% confidence interval, 1.0–1.03; p = .04), Hunt-Hess classification score ≥3 (relative risk, 2.23; 95% confidence interval, 1.21–3.99; p = .02), and Fisher group score of 3 (relative risk, 1.28; 95% confidence interval, 1.15–3.1; p = .05) increased the risk for VSP. Hyperglycemia was associated with longer length of stay in the neurointensive care unit (14.5 ± 7.1 days vs. 11.6 ± 5.4 days; p < .001) and poor outcome at discharge (modified Rankin score ≥3: 58.9% vs. 18.8%; p < .001). Conclusions:Mean inpatient blood glucose value is associated with the development of VSP and may represent a target for therapy to prevent VSP and improve clinical outcomes.

Hyperthermia and fever control in brain injury.

Fever in the neurocritical care setting is common and has a negative impact on outcome of all disease types. Meta-analyses have demonstrated that fever at onset and in the acute setting after ischemic brain injury, intracerebral hemorrhage, and cardiac arrest has a negative impact on morbidity and mortality. Data support that the impact of fever is sustained for longer durations after subarachnoid hemorrhage and traumatic brain injury. Recent advances have made eliminating fever and maintaining normothermia feasible. However, there are no prospective randomized trials demonstrating the benefit of fever control in these patient populations, and important questions regarding indications and timing remain. The purpose of this review is to analyze the data surrounding the impact of fever across a range of neurologic injuries to better understand the optimal timing and duration of fever control. Prospective randomized trials are needed to determine whether the beneficial impact of secondary injury prevention is outweighed by the potential risks of prolonged fever control.

Transcranial Doppler for predicting delayed cerebral ischemia after subarachnoid hemorrhage.

OBJECTIVETranscranial Doppler (TCD) is widely used to monitor the temporal course of vasospasm after subarachnoid hemorrhage (SAH), but its ability to predict clinical deterioration or infarction from delayed cerebral ischemia (DCI) remains controversial. We sought to determine the prognostic utility of serial TCD examination after SAH. METHODSWe analyzed 1877 TCD examinations in 441 aneurysmal SAH patients within 14 days of onset. The highest mean blood flow velocity (mBFV) value in any vessel before DCI onset was recorded. DCI was defined as clinical deterioration or computed tomographic evidence of infarction caused by vasospasm, with adjudication by consensus of the study team. Logistic regression was used to calculate adjusted odds ratios for DCI risk after controlling for other risk factors. RESULTSDCI occurred in 21% of patients (n = 92). Multivariate predictors of DCI included modified Fisher computed tomographic score (P = 0.001), poor clinical grade (P = 0.04), and female sex (P = 0.008). After controlling for these variables, all TCD mBFV thresholds between 120 and 180 cm/s added a modest degree of incremental predictive value for DCI at nearly all time points, with maximal sensitivity by SAH day 8. However, the sensitivity of any mBFV more than 120 cm/s for subsequent DCI was only 63%, with a positive predictive value of 22% among patients with Hunt and Hess grades I to III and 36% in patients with Hunt and Hess grades IV and V. Positive predictive value was only slightly higher if mBFV exceeded 180 cm/s. CONCLUSIONIncreased TCD flow velocities imply only a mild incremental risk of DCI after SAH, with maximal sensitivity by day 8. Nearly 40% of patients with DCI never attained an mBFV more than 120 cm/s during the course of monitoring. Given the poor overall sensitivity of TCD, improved methods for identifying patients at high risk for DCI after SAH are needed.

Frequency and clinical impact of asymptomatic cerebral infarction due to vasospasm after subarachnoid hemorrhage : Clinical article

OBJECT The authors sought to determine frequency, risk factors, and impact on outcome of asymptomatic cerebral infarction due to vasospasm after subarachnoid hemorrhage (SAH). METHODS The authors prospectively studied 580 patients with SAH admitted to their center between July 1996 and May 2002. Delayed cerebral ischemia (DCI) from vasospasm was defined as 1) a new focal neurological deficit or decrease in level of consciousness, 2) a new infarct revealed by follow-up CT imaging, or both, after excluding causes other than vasospasm. Outcome at 3 months was assessed using the modified Rankin Scale. RESULTS Delayed cerebral ischemia occurred in 121 (21%) of 580 patients. Of those with DCI, 36% (44 patients) experienced neurological deterioration without a corresponding infarct, 42% (51 patients) developed an infarct in conjunction with neurological deterioration, and 21% (26 patients) had a new infarct on CT without concurrent neurological deterioration. In a multivariate analysis, risk factors for asymptomatic DCI included coma on admission, placement of an external ventricular drain, and smaller volumes of SAH (all p < or = 0.03). Patients with asymptomatic DCI were less likely to be treated with vasopressor agents than those with symptomatic DCI (64 vs 86%, p = 0.01). After adjusting for clinical grade, age, and aneurysm size, the authors found that there was a higher frequency of death or moderate-to-severe disability at 3 months (modified Rankin Scale Score 4-6) in patients with asymptomatic DCI than in patients with symptomatic DCI (73 vs 40%, adjusted odds ratio 3.9, 95% confidence interval 1.3-12.0, p = 0.017). CONCLUSIONS Approximately 20% of episodes of DCI after SAH are characterized by cerebral infarction in the absence of clinical symptoms. Asymptomatic DCI is particularly common in comatose patients and is associated with poor outcome. Strategies directed at diagnosing and preventing asymptomatic infarction from vasospasm in patients with poor-grade SAH are needed.

Resuscitation and critical care of poor-grade subarachnoid hemorrhage.

As outcomes have improved for patients with aneurysmal subarachnoid hemorrhage, most mortality and morbidity that occur today are the result of severe diffuse brain injury in poor-grade patients. The premise of this review is that aggressive emergency cardiopulmonary and neurological resuscitation, coupled with early aneurysm repair and advanced multimodality monitoring in a specialized neurocritical care unit, offers the best approach for achieving further improvements in subarachnoid hemorrhage outcomes. Emergency care should focus on control of elevated intracranial pressure, optimization of cerebral perfusion and oxygenation, and medical and surgical therapy to prevent rebleeding. In the postoperative period, advanced monitoring techniques such as continuous electroencephalography, brain tissue oxygen monitoring, and microdialysis can detect harmful secondary insults, and may eventually be used as end points for goal-directed therapy, with the aim of creating an optimal physiological environment for the comatose injured brain. As part of this paradigm shift, it is essential that aggressive surgical and medical support be linked to compassionate end-of-life care. As neurosurgeons become confident that comfort care can be implemented in a straightforward fashion after a failed trial of early maximal intervention, the usual justification for withholding treatment (survival with neurological devastation) becomes less relevant, and lives may be saved as more patients recover beyond expectations.