Clinical experience with transcranial Doppler ultrasonography as a confirmatory test for brain death: a retrospective analysis.

BACKGROUND: Transcranial Doppler (TCD) ultrasonography to demonstrate cerebral circulatory arrest (CCA) is a confirmatory test for brain death (BD). The primary aim of this retrospective study was to evaluate the practical utility of TCD to confirm BD when clinical diagnosis was not feasible due to confounding factors. Secondary aims were to evaluate the reasons for inability of TCD to confirm BD and to assess the outcome of patients not brain dead according to the TCD criteria. METHODS: TCD waveforms and medical records of all the patients examined to confirm suspected BD between 2001 and 2007, where clinical diagnosis was not possible, were analyzed. BD was diagnosed based on CCA criteria recommended by the Task Force Group on cerebral death of the Neurosonology Research Group of the World Federation of Neurology. Final outcome of patients and the use of other ancillary tests were noted. RESULTS: Ninety patients (61 males), aged 40 ± 21 (range 3-84) years underwent TCD examination for confirmation of suspected BD. TCD confirmed BD in 51 (57%) patients and was inconclusive in 38 (43%), with no flow signals on the first examination in 7 (8%) patients and the waveform patterns in 31 (35%) being inconsistent with BD. Fourteen of the 19 patients who had CCA pattern in at least one artery but did not meet all the criteria for BD were subsequently found brain dead according to SPECT/clinical criteria or suffered cardiovascular death. CONCLUSION: Using the conventional criteria, TCD confirmed BD in a large proportion, of patients where clinical diagnosis could not be made. The presence of CCA pattern in one or more major cerebral artery may be prognostic of unfavorable outcome, even when BD criteria are not satisfied.

Cerebral blood flow and the injured brain: how should we monitor and manipulate it?

PURPOSE OF REVIEW: Cerebral ischemia plays a major role in the pathophysiology of the injured brain, including traumatic brain injury and subarachnoid hemorrhage, thus improvement in outcome may necessitate monitoring and optimization of cerebral blood flow (CBF). To interpret CBF results in a meaningful way, it may be necessary to quantify cerebral autoregulation as well as cerebral metabolism. This review addresses the recent evidence related to the changes in CBF and its monitoring/management in traumatic brain injury. RECENT FINDINGS: Recent evidence on the management of patients with traumatic brain injury have focused on the importance of cerebral autoregulation in maintaining perfusion, which necessitates the measurement of CBF. However, adequate CBF measurements alone would not indicate the amount of oxygen delivered to neuronal tissues. Technologic advancements in measurement devices have enabled the assessment of the metabolic state of the cerebral tissue for the purpose of guiding therapy, progress as well as prognostification. SUMMARY: Current neurocritical care management strategies are focused on the prevention and limitation of secondary brain injury where neuronal insult continues to evolve during the hours and days after the primary injury. Appropriately chosen multimodal monitoring including CBF and management measures can result in reduction in mortality and morbidity.

Accuracy of transcranial Doppler ultrasonography and single-photon emission computed tomography in the diagnosis of angiographically demonstrated cerebral vasospasm.

OBJECT: The goal of this study was to assess the accuracy of the routine clinical use of transcranial Doppler (TCD) ultrasonography and SPECT in predicting angiographically demonstrated vasospasm. METHODS: Following receipt of institutional review board approval, the authors reviewed the records of patients with subarachnoid hemorrhage who had been admitted between 2004 and 2005 and underwent TCD ultrasonography and SPECT evaluations within 24 hours of cerebral angiography. Patients were categorized based on the presence or absence of vasospasm and/or hypoperfusion in the anterior cerebral arteries (ACAs), middle cerebral arteries (MCAs), and basilar arteries (BAs) or posterior cerebral arteries (PCAs) according to each imaging modality. Logistic regression was used to estimate the odds ratio (OR) of an angiographically demonstrated vasospasm also detected on TCD ultrasonography and SPECT. RESULTS: One hundred fifty-two patients (101 women) with a mean age (+/- standard deviation) of 53 +/- 13 years were included in the study. In the ACA, the OR of a vasospasm on TCD ultrasonography was 27 (95% confidence interval [CI] 3-243) and on SPECT 0.97 (95% CI 0.36-2.6); in the MCA, 17 (95% CI 5.4-55) and 2.0 (95% CI 0.71-5.5), respectively; in the BA, 4.4 (95% CI 0.72-27) and 5.6 (95% CI 0.89-36), respectively. There was no substantial change in the relative odds of a vasospasm when the findings on TCD ultrasonography and SPECT were considered jointly. CONCLUSIONS: Transcranial Doppler ultrasonography appears to be highly predictive of an angiographically demonstrated vasospasm in the MCA and ACA; however, its diagnostic accuracy was lower with regard to vasospasm in the BA. Single-photon emission computed tomography was not predictive of a vasospasm in any of the vascular territories assessed.

Prolonged propofol anesthesia is not associated with an increase in blood lactate.

BACKGROUND: Lactic acidosis is considered an early sign of propofol infusion syndrome. In this study, we investigated the changes in lactate and pH with propofol versus volatile anesthesia (VA) of long duration. METHODS: Demographic and intraoperative data were recorded retrospectively from the anesthesia records of patients who underwent elective spine surgery longer than 8 h. Propofol patients were matched 1:2 to VA patients, based on anesthesia time (AT) (+/-30 min) and blood loss (BL) (+/-500 mL). RESULTS: Of 246 patients identified, 50 received propofol (AT = 10 +/- 2 h, BL = 1955 +/- 1409 mL) and were matched to 100 VA cases (AT = 10 +/- 1 h, BL = 1801 +/- 1543 mL), and of those, 40 and 72 patients, respectively, had complete lactate data at baseline and at 8 h after anesthesia and were included in the main analysis. The propofol group received 8.8 +/- 2 mg x kg(-1) x h(-1) of propofol. The VA group age was older than the propofol group (58 +/- 12 vs 51 +/- 15 yr, respectively, P = 0.002), but there was no difference between the groups in gender, ASA grade, intraoperative hemodynamic variables, and use of vasopressors. After 8 h, the VA group had a larger increase in arterial lactate from baseline compared with the propofol group (change from baseline: propofol, 0.48 +/- 0.72 mmol/L; VA, 1.2 +/- 1.2 mmol/L, P = 0.001). CONCLUSIONS: During prolonged spine surgery >8 h, VA was associated with higher serum lactate, when compared with propofol infusion. Prospective studies are needed to elucidate the exact mechanisms and clinical implications of this finding.

Cerebral autoregulation and anesthesia.

PURPOSE OF REVIEW: This review will examine the recent literature on anesthesia and monitoring techniques in relation to cerebral autoregulation. We will discuss the effect of physiologic and pharmacological factors on cerebral autoregulation alongside its clinical relevance with the help of new evidence. RECENT FINDINGS: Intravenous anesthesia, such as combination of propofol and remifentanil, provides best preservation of autoregulation. Among inhaled agents sevoflurane appears to preserve autoregulation at all doses, whereas with other agents autoregulation is impaired in a dose-related manner. SUMMARY: Intraoperative cerebral autoregulation monitoring is an important consideration for the patients with neurologic disease. Transcranial Doppler based static autoregulation measurements appears to be the most robust bedside method for this purpose.

A Case Report of Thalamic Infarction after Lumbar Drain: A Unique Cause of Perioperative Stroke?

In the case presented, a patient has an unexplained episode of hypertension during aneurysm clipping. Following the procedure, the patient was discovered to have bilateral thalamic infarctions unrelated to the vascular location of the aneurysm. After a review of the case, it becomes apparent that intracranial hypotension caused by lumbar over drainage of cerebrospinal fluid (CSF) is the likely cause of both the episode of intraoperative hypertension and the thalamic infarcts. It is often presumed that having an open dura protects against intracranial hypotension and subsequent herniation. We present this case to suggest that opening the dura might not be protective in all cases and anesthesiologists must pay particular attention to the rate of CSF drainage. Lumbar CSF drainage is a technique frequently employed during neurological surgery and it is important for anesthesiologists to understand the signs, symptoms, and potential consequences of intracranial hypotension from rapid drainage.

Esmolol blunts postoperative hemodynamic changes after propofol-remifentanil total intravenous fast-track neuroanesthesia for intracranial surgery.

STUDY OBJECTIVE: To investigate whether esmolol is effective in attenuating postoperative hemodynamic changes related to sympathetic overdrive. DESIGN: Clinical study. SETTING: Operating room of a university hospital. PATIENTS: 60 ASA physical status I, II, and III patients, age 18 to 65 years, scheduled for elective craniotomy for supratentorial neurosurgery. INTERVENTIONS: Patients were given total intravenous anesthesia (TIVA) during emergence from anesthesia and up to 60 minutes after extubation. Those patients who had hypertension (defined as an increase in systolic blood pressure >20% from baseline values) and tachycardia (defined as an increase >20% in heart rate from baseline) received a loading dose of 500 microg/kg esmolol in one minute, followed by an infusion titrated stepwise (50, 100, 200, and 300 microg/kg per min) every two minutes. MEASUREMENTS: The mean dose and duration of esmolol therapy were measured. MAIN RESULTS: Of 60 patients, 49 (82%) who received propofol-remifentanil TIVA developed significant tachycardia and hypertension soon after extubation. Treatment with esmolol (500 microg/kg in bolus maintained at a mean rate of 200 +/- 50 microg/kg per min) effectively controlled hypertension and tachycardia in 45 of 49 patients (92%; P < 0.05) within a mean 4.30 +/- 2.20 minutes. After extubation, mean esmolol infusion time was 29 +/- 8 minutes. CONCLUSION: In patients undergoing elective neurosurgery with propofol-remifentanil TIVA, a relatively small esmolol dose and short infusion time effectively blunts early postoperative arterial hypertension and tachycardia.

Neurointensive care; impaired cerebral autoregulation in infants and young children early after inflicted traumatic brain injury: a preliminary report.

The objective of this report is to describe cerebral autoregulation after severe inflicted pediatric traumatic brain injury (iTBI). We examined cerebral autoregulation of both cerebral hemispheres (mean autoregulatory index; ARI) in children <5 years with Glasgow Coma Scale (GCS) score of <9 and no evidence of brain death within the first 48 h of pediatric intensive care unit (PICU) admission. Discharge and 6-month Glasgow Outcome Scale (GOS) scores were collected. GOS of <4 reflected poor outcome. All three iTBI and all seven noninflicted TBI (nTBI) patients had admission GCS score of <9. Eight of 10 patients had Autoregulatory Index (ARI) of <0.4 (impaired cerebral autoregulation) of at least one hemisphere. All children with iTBI had poor outcome, and none had intact cerebral autoregulation in both hemispheres. Children with nTBI had better overall outcome than those with iTBI. Two of the children with nTBI had intact autoregulation in both hemispheres and good outcome. Two of the three children with iTBI had differential effects on autoregulation between hemispheres despite bilateral injury. These are, to our knowledge, the first data on cerebral blood flow autoregulation in the unique setting of iTBI and provide a rationale for further study of their relationship to outcome and effects of therapy.

Dexmedetomidine sedation during awake craniotomy for seizure resection: effects on electrocorticography.

Patients with refractory seizures may undergo awake craniotomy and cortical resection of the seizure area, using intraoperative functional mapping and electrocorticography (ECoG). We used dexmedetomidine in 6 patients, transitioning successively from the asleep-awake-asleep method, through a combined propofol/dexmedetomidine sedative infusion, to dexmedetomidine as the only sedation. Initial experience with the asleep-awake-asleep method in 2 patients was successful with the replacement of propofol/laryngeal mask anesthesia, 20 to 30 minutes before ECoG testing, by dexmedetomidine infusion, maintained at 0.2 mcg kg-1 h-1 throughout neurocognitive testing. Propofol anesthesia was reintroduced for resection. One patient received combined dexmedetomidine (0.2 mcg kg-1 h-1) and propofol (200 mcg kg-1 min-1) infusions for sedation. Both infusions were stopped 15 minutes before ECoG. Subsequently, they were restarted and the epileptic foci resected. Three patients received dexmedetomidine as the sole sedative agent, together with scalp block local anesthesia, and incremental boluses totaling 150 to 175 mcg of fentanyl per case. Dexmedetomidine was started with 0.3 mcg kg-1 boluses and maintained with 0.2 to 0.7 mcg kg-1 h-1for craniotomy, testing, and resection. The infusion was paused for 20 minutes in 1 patient to allow improvement in neurocognitive testing. This occurred within 10 minutes. All patients enjoyed good hemodynamic control, with blood pressure maintained within 20% of initial values, and made uneventful recoveries. The surgical conditions were all reported as favorable. Dexmedetomidine can be used singly for sedation in awake craniotomy requiring ECoG. Individual dose ranges vary, but a bolus of 0.3 mcg kg-1 with an infusion of 0.2 mcg kg-1 min-1 is a good starting point, allowing accurate mapping of epileptic foci and subsequent resection.

Impact of basilar artery vasospasm on outcome in patients with severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: The purpose of the present study was to evaluate the impact of basilar artery (BA) vasospasm on outcome in patients with severe vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Sixty-five patients with clinically suspect severe cerebral vasospasm after aSAH underwent cerebral angiography before endovascular treatment. Vasospasm severity was assessed for each patient by transcranial Doppler measurements, angiography, and (99m)Tc-ethylcysteinate dimer single-photon emission computed tomography (ECD-SPECT) imaging. Percentage of BA narrowing was calculated in reference to the baseline angiogram. RESULTS: BA narrowing >or=25% was found in 23 of 65 patients, and delayed brain stem (BS) hypoperfusion, as estimated by ECD-SPECT, was found in 16. Fourteen of 23 patients with BA narrowing >or=25% experienced BS hypoperfusion, whereas only 2 of 42 patients with >or=25% BA narrowing experienced BS ischemia (P<0.001). Stepwise logistic regression after adjusting for age with Hunt and Hess grade, Fisher grade, hydrocephalus, and aneurysmal location as covariables revealed BA narrowing >or=25% and delayed BS hypoperfusion to be significantly and independently associated with unfavorable 3-month outcome (P=0.0001; odds ratio, 10.1; 95% CI, 2.5 to 40.8; and P=0.007; odds ratio, 13.8, 95% CI, 2.18 to 91.9, respectively). CONCLUSIONS: These findings suggest for the first time that BA vasospasm after aSAH is an independent and significant prognostic factor associated with poor outcome in patients with severe cerebral vasospasm requiring endovascular therapy. Further study should be done to evaluate the role of interventional therapy on outcome in patients with posterior circulation vasospasm.

Cerebral autoregulation and CO2 reactivity in anterior and posterior cerebral circulation during sevoflurane anesthesia.

The purpose of the study was to compare cerebral autoregulation (CA) and CO2 reactivity (CO2R) between the anterior and posterior circulation under sevoflurane anesthesia. We studied 9 adult ASA physical status I patients (22-47 yr) scheduled for elective orthopedic surgery. Blood flow velocity in the middle cerebral artery (Vmca) and in the basilar artery (Vba) were measured using transcranial Doppler ultrasonography. For CA testing, arterial blood pressure was increased using phenylephrine infusion. CA was quantified with the autoregulatory index (ARI). CO2R was investigated at PaCO2 of 30 +/- 2.8 mm Hg, 39.4 +/- 2.6 mm Hg, and 48.7 +/- 2.8 mm Hg. Linear regression analysis was used for CO2R. We found ARI was preserved in both arteries: ARImca (middle cerebral artery) = 0.72 +/- 0.2; ARIba (basilar artery) = 0.66 +/- 0.2; P = 0.5. With regard to CO2R, Vmca increased with slope of 1.7 cm/s/mm Hg PaCO2, Vba increased with slope of 1.5 cm/s/mm Hg PaCO2; P = 0.83. Absolute Vmca was higher compared with Vba; P < 0.05. We conclude that in healthy individuals under 0.5 MAC of sevoflurane and small-dose remifentanil: 1) mean flow velocities of BA are less than those of MCA; 2) autoregulation and CO2R are preserved in the basilar artery and are similar to those of MCA.

Clinical experience with dexmedetomidine for implantation of deep brain stimulators in Parkinson's disease.

The pharmacologic profile of the alpha-2 agonist dexmedetomidine (Dex) suggests that it may be an ideal sedative drug for deep brain stimulator (DBS) implantation. We performed a retrospective chart review of anesthesia records of patients who underwent DBS implantation from 2001 to 2004. In 2003, a clinical protocol with Dex sedation for DBS implantation was initiated. Demographic data, use of antihypertensive medication, and duration of mapping were compared between patients who received Dex (11 patients/13 procedures) and patients who did not receive any sedation (controls: 8 patients/9 procedures). There were no differences in severity of illness between the two groups. Dex provided patient comfort and surgical satisfaction with mapping in all cases, and significantly reduced the use of antihypertensive medication (54% in the Dex group, versus 100% in controls, P = 0.048). In DBS implantation, sedation with Dex did not interfere with electrophysiologic mapping, and provided hemodynamic stability and patient comfort. Routine use of Dex in these procedures may be indicated.

The incidence and risk factors for hypotension during emergent decompressive craniotomy in children with traumatic brain injury.

We conducted a retrospective cohort study in children <13 yr with traumatic brain injury (TBI) at a Level 1 pediatric trauma center to describe risk factors for intraoperative hypotension (IH) during emergent decompressive craniotomy. Between 1994 and 2004, 108 children underwent emergent decompressive craniotomy for TBI. Overall, 56 (52%) patients had IH. Independent risk factors for IH were each 10 mL estimated blood loss/kg (ARR 1.15 95% CI 1.08-1.22), each mm of computed tomography (CT) midline shift (ARR 1.04 95%CI 1.01-1.07), each 10 mL of CT lesion volume (ARR 1.03 95%CI 1.01-1.05), and emergency department (ED) hypotension (5/5 patients with ED hypotension had IH). CT midline shift > or =4 mm predicted IH (ARR 1.67 95% CI 1.06-2.63), independent of blood loss. IH occurred frequently during emergent decompressive craniotomy in children with TBI. ED hypotension, blood loss, CT lesion volume, and CT midline shift predicted IH. Anesthesiologists can expect children with preoperative CT midline shift > or =4 mm to have IH during this procedure.

Clinical features of fever associated with poor outcome in severe pediatric traumatic brain injury.

We describe the incidence and etiology of fever and the relationship between fever characteristics and outcome in children with severe traumatic brain injury (TBI). We conducted a retrospective study of children <14 years and with Glasgow Coma Scale (GCS) score of <9 admitted to a level I pediatric trauma center intensive care unit (PICU) between 1998 and 2003. We examined whether fever characteristics were associated with poor outcome (hospital discharge GCS score <13 and discharge disposition of either death or discharge to a skilled nursing facility). PICU length of stay (LOS) and hospital LOS were also examined. Data are presented as means and medians (SD), and P < 0.05 reflects significance. Ninety-three records were reviewed. Patients were 5.7 (SD 4.1) years old, 70% were male, and the average admission GCS score was 5. Mortality rate was 14%. Forty-eight (52%) patients had fever, and 23 (48%) of those patients had infectious fever. Each additional febrile episode was associated with a twofold higher risk of patients having a hospital discharge GCS score of <13 (odds ratio 2.4, 95% confidence interval 1.2-5.0) and having a 0.4-day longer PICU LOS (P < 0.001). Patients with infectious fever had a 0.9-day longer PICU LOS (P < 0.001). Patients with any fever in the PICU had an increased HLOS (0.9 days; P < 0.001). Our data suggest that in severe pediatric TBI, both fever and infection were common, and both were associated with longer LOS. Patients with higher fever burden had poor hospital discharge GCS score.