Assessment of Basilar Artery Reactivity in Stroke and Subarachnoid Hemorrhage Using Wire Myograph.

Blood flow regulation of normal cerebral arteries is a critical and important factor to supply the brain tissue with nutrients and oxygen. Stroke insult results in a disruption or reduction in cerebral arteries' blood flow with subsequent brain tissue damage. Hemorrhagic stroke is one type of stroke and accounts for about 13 % of all of stroke insults. In this type of stroke, the cerebral artery breaks open and causes bleeding in or surrounding the brain. Subsequently, this bleeding causes blood vessels to constrict in a process called vasospasm, in which the vessels narrow and impede the blood flow to brain tissue. Hemorrhagic stroke is the major cause of prolonged constriction of cerebral arteries. This leads to partial brain damage and sometimes death in patients with aneurysmal subarachnoid hemorrhage. Among the key delicate techniques to assess small blood vessel functionality is the wire myograph, which can be utilized in several cerebral injury models including stroke. The wire myograph is a device that provides information about the reactivity, stiffness, and elasticity of small blood vessels under isometric conditions. In this book chapter, we describe the techniques involved in wire myography assessment and the different measures and parameters recorded; we describe the utility of this technique in evaluating the effects of subarachnoid hemorrhage on basilar artery sensitivity to different agonists.

Response of brain oxygen to therapy correlates with long-term outcome after subarachnoid hemorrhage.

BACKGROUND: Brain oxygen (PbtO2) monitoring can help guide care of poor-grade aneurysmal subarachnoid hemorrhage (aSAH) patients. The relationship between PbtO2-directed therapy and long-term outcome is unclear. We hypothesized that responsiveness to PbtO2-directed interventions is associated with outcome. METHODS: Seventy-six aSAH patients who underwent PbtO2 monitoring were included. Long-term outcome [Glasgow Outcome Score-Extended (GOS-E) and modified Rankin Scale (mRS)] was ascertained using the social security death database and structured telephone interviews. Univariate and multivariate regression were used to identify variables that correlated with outcome. RESULTS: Data from 64 patients were analyzed (12 were lost to follow-up). There were 530 episodes of compromised PbtO2 (<20 mmHg) during a total of 7,174 h of monitor time treated with 1,052 interventions. Forty-two patients (66 %) survived to discharge. Median follow-up was 8.5 months (range 0.1-87). At most recent follow-up 35 (55 %) patients were alive, and 28 (44 %) had a favorable outcome (mRS ≤3). In multivariate ordinal regression analysis, only age and response to PbtO2-directed intervention correlated significantly with outcome. Increased age was associated with worse outcome (coeff. 0.8, 95 % CI 0.3-1.3, p = 0.003), and response to PbtO2-directed intervention was associated with improved outcome (coeff. -2.12, 95 % CI -4.0 to -0.26, p = 0.03). Patients with favorable outcomes had a 70 % mean rate of response to PbtO2-directed interventions whereas patients with poor outcomes had a 45 % response rate (p = 0.005). CONCLUSIONS: Response to PbtO2-directed intervention is associated with improved long-term functional outcome in aSAH patients.

Perfusion-CT assessment of blood-brain barrier permeability in patients with aneurysmal subarachnoid hemorrhage.

BACKGROUND: The goal of this study was to determine which clinical and radiographic variables in patients with subarachnoid hemorrhage (SAH) are associated with in vivo blood-brain barrier permeability (BBBP) assessments obtained using perfusion-CT (PCT) technology. METHODS: SAH patients with confirmed aneurysm etiology and with PCT and angiogram within 24 hours of each other were included, and relationships between clinical and imaging variables were analyzed using random-effects generalized linear models. RESULTS: One thousand one hundred and sixty two vascular territories from 83 patients were evaluated in this study. The mean BBBP increased by severity of vasospasm on DSA, however, in multivariate analysis, only mean transit time (MTT), cerebral blood volume (CBV), and severity of hydrocephalus were significantly associated with BBBP. Increased BBBP was not associated with angiographic vasospasm severity in multivariate analysis. CONCLUSION: Perfusion-CT assessment of BBBP may serve as a unique and useful biomarker in conjunction with angiography, additional perfusion-CT parameters, and clinical assessments, especially in characterizing microvascular dysfunction, or even in targeting treatments. However, future prospective studies will be required to definitively establish its clinical utility in the care of SAH patients.

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 (kappa(w)=0.84, 95% CI, 0.81 to 0.86). CONCLUSIONS: The Bedside Shivering Assessment Scale is a simple and reliable tool for evaluating the metabolic stress of shivering.

Energy expenditure in patients with nontraumatic intracranial hemorrhage.

BACKGROUND: Patients with intracerebral (ICH), intraventricular (IVH) and subarachnoid hemorrhage (SAH) have increased morbidity and mortality compared with other forms of stroke. We postulate that the systemic inflammatory state triggered by these forms of nontraumatic intracranial hemorrhage (IH) translates into higher nutrition requirements than traditionally assumed. In order to test this hypothesis, we performed a retrospective study comparing the resting energy expenditure (REE) of 14 mechanically ventilated IH patients with the REE of 6 severe traumatic brain injury (sTBI) patients (a disease known to induce an increased metabolic state). METHODS: Using nonparametric analysis, we compared 2 contemporary cohorts of patients-IH and sTBI-who required mechanical ventilation and who underwent indirect calorimetry (IC) within 7 days after the ictus. RESULTS: Fourteen patients with nontraumatic IH (IVH, 2; SAH, 9; SAH/ICH, 1; ICH/SAH/IVH, 2) who underwent IC within 7 days from injury were identified; median age: 59 (28-84) years, median admission Glasgow Coma Scale (GCS): 6 (4-9), and median APACHE II: 19.5 (15-28). A control cohort of 6 patients with sTBI was identified; median age: 57.5 (18-80) years, admission GCS: 6.5 (4-8), and APACHE II: 16 (11-31). Sedation was used in 11/14 patients with IH and in 5/6 severe TBI patients. No patient was pharmacologically paralyzed. Median REE was 1810 (1124-2806) and 2238 (1860-2780) kcal/d for the IH and for the sTBI patient cohorts, respectively. Using Wilcoxon signed ranks test, the 2 patient groups were found comparable in regard to baseline clinical variables and disease severity (APACHE II). We did not identify a statistically significant difference in the REE between these 2 cohorts of patients (p = .25). CONCLUSIONS: Patients with severe TBI and patients with IH have similar increments in metabolic rate during the initial phase (1 week from onset) of their disease. This information needs to be confirmed in a larger cohort of patients. If reproduced, our results suggest that nontraumatic IH patients are at high risk of inadequate nutrition if their metabolic rate is estimated after conventional nutrition practice.

Online assessment of brain tissue oxygen autoregulation in traumatic brain injury and subarachnoid hemorrhage.

Monitoring of brain tissue oxygenation (ptiO2) enables early diagnosis of secondary cerebral ischemia and may guide a cerebral perfusion pressure (CPP) orientated therapy. The purpose of our study was to explain the concept of ptiO2-autoregulation, defined as the ability of the brain to maintain ptiO2 despite changes in CPP, and to show the different states of ptiO2-autoregulation we found. Microcatheters to assess ptiO2 and intracranial pressure were implanted into cerebral 'tissue at risk' of patients suffering from traumatic brain injury or subarachnoid hemorrhage. By using a multimodal neuromonitoring setup and in-house built software we assessed and displayed online the relationship between ptiO2 and CPP based on a data buffer consisting of 12 h. Depending on the linear regression slope (bptiO2 = delta ptiO2/delta CPP), we defined the state of ptiO2-autoregulation as present (0 < or = bptiO2 < or = 1/6), moderate (1/6 < bptiO2 < or = 1/3), impaired (bptiO2 > 1/3) or inverse (bptiO2 < 0). When ptiO2-autoregulation is present, an elevation in CPP is ineffective to raise ptiO2. In contrast, an increase in CPP elevates ptiO2 more pronounced in impaired than in moderate ptiO2- autoregulation, but decreases ptiO2 in inverse ptiO2-autoregulation. We conclude that online assessment of ptiO2-autoregulation gives valuable information on which patient will benefit from an increase in CPP and which CPP should be achieved to do so.

Patterns of energy expenditure in intensive-care patients.

We studied the changes in energy expenditure (EE) in response to multiple injury (n = 6), subarachnoidal hemorrhage (n = 8), low-cardiac-output syndrome after open-heart surgery (n = 6), and uncomplicated coronary artery surgery (n = 10). Measurements were made during 5 consecutive days. In the multiple injury group, EE was 30% higher than predicted basal EE (range 10-52%) within 27 h after trauma, and this hypermetabolism remained unchanged throughout the study. After subarachnoidal hemorrhage, EE was 18% higher than predicted (range 0-45%) and the operation caused only a minor further increment in EE. Also, these patients remained hypermetabolic throughout the study. In the low-cardiac-output syndrome group, the increase in EE was less prominent (mean 15%, range 0-34%), but the pattern of hypermetabolism was similar to that observed in the multiple injury and subarachnoidal hemorrhage groups. The metabolic response to uncomplicated coronary artery surgery resembled the response to general surgery. We conclude that 1) there is an early consistent increase in EE in various groups of surgical intensive-care patients; 2) with appropriate treatment of the circulation, a prompt hypermetabolic response to surgical trauma is maintained even during low-cardiac-output syndrome; and 3) the marked hypermetabolism after subarachnoidal hemorrhage at the central nervous system is an integral part of the hypermetabolic response to injury.