Transcranial volumetric imaging using a conformal ultrasound patch.

Accurate and continuous monitoring of cerebral blood flow is valuable for clinical neurocritical care and fundamental neurovascular research. Transcranial Doppler (TCD) ultrasonography is a widely used non-invasive method for evaluating cerebral blood flow1, but the conventional rigid design severely limits the measurement accuracy of the complex three-dimensional (3D) vascular networks and the practicality for prolonged recording2. Here we report a conformal ultrasound patch for hands-free volumetric imaging and continuous monitoring of cerebral blood flow. The 2 MHz ultrasound waves reduce the attenuation and phase aberration caused by the skull, and the copper mesh shielding layer provides conformal contact to the skin while improving the signal-to-noise ratio by 5 dB. Ultrafast ultrasound imaging based on diverging waves can accurately render the circle of Willis in 3D and minimize human errors during examinations. Focused ultrasound waves allow the recording of blood flow spectra at selected locations continuously. The high accuracy of the conformal ultrasound patch was confirmed in comparison with a conventional TCD probe on 36 participants, showing a mean difference and standard deviation of difference as -1.51 ± 4.34 cm s-1, -0.84 ± 3.06 cm s-1 and -0.50 ± 2.55 cm s-1 for peak systolic velocity, mean flow velocity, and end diastolic velocity, respectively. The measurement success rate was 70.6%, compared with 75.3% for a conventional TCD probe. Furthermore, we demonstrate continuous blood flow spectra during different interventions and identify cascades of intracranial B waves during drowsiness within 4 h of recording.

Emergency Neurological Life Support: Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is a subset of stroke due to spontaneous bleeding within the parenchyma of the brain. It is potentially lethal, and survival depends on ensuring an adequate airway, proper diagnosis, and early management of several specific issues such as blood pressure, coagulopathy reversal, and surgical hematoma evacuation for appropriate patients. ICH was chosen as an Emergency Neurological Life Support (ENLS) protocol because intervention within the first hours may improve outcome, and it is critical to have site-specific protocols to drive care quickly and efficiently.

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.

Current practices of triple-H prophylaxis and therapy in patients with subarachnoid hemorrhage.

BACKGROUND: Medical management of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) includes hypertensive, hypervolemic, and hemodilution ("triple-H") therapy. However, there is little information regarding the indications and guidance used to initiate and adjust triple-H therapy. METHODS: A 43-item questionnaire was e-mailed to 375 members of the Neurocritical Care Society. Questions were designed to investigate the diagnostic approach to cerebral vasospasm and prophylactic and therapeutic administration of triple-H therapy. RESULTS: Completed surveys were received from 167 respondents (45% response proportion). Eighty-six percent of respondents worked in hospitals with neurointensive care units (NICUs). SAH patients in hospitals with a NICU had longer ICU stay (P = 0.037) and had indwelling central venous catheters for longer (P < 0.01). Centers without dedicated NICUs were more likely to induce prophylactic hypervolemia (P < 0.01). Twenty seven percent of respondents (n = 45) reported using prophylactic hypervolemia in patients with SAH, while 100% reported inducing hypervolemia for severe or symptomatic vasospasm. Twelve percent (n = 20) of respondents reported inducing prophylactic hypertension, while all reported inducing hypertension with severe or symptomatic vasospasm. Half of respondents relied on the mean arterial pressure and half on systolic blood pressure as the clinical parameter for blood pressure titration. The most widely used agents to induce hypertension were phenylephrine (48%) and norepinephrine (39%). There was little variation in the use of hemodilution therapy comparing patients with or without evidence of vasospasm. CONCLUSIONS: There are substantial differences in the administration of prophylactic triple-H, but there was high agreement on indication for therapeutic use. There was wide variability in the extent of ICU monitoring, diagnostic approach, physiologic parameters and values used as target of therapy. NICU availability was associated with more intensive monitoring. Lack of evidence and guidelines for triple-H therapy might largely explain these findings.

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.

Effects of anemia and hypotension on porcine optic nerve blood flow and oxygen delivery.

BACKGROUND: Perioperative ischemic optic neuropathy occurs after major surgical procedures, which are often associated with hypotension, anemia, or venous congestion. However, the effects of these conditions on optic nerve (ON) blood flow are unknown and cannot be studied adequately in humans. METHODS: Farm-raised pigs were anesthetized with isoflurane, kept normocapnic and normothermic, and subjected to conditions of euvolemic or hypovolemic hypotension (mean arterial pressure 50-55 mm Hg), anemia (hematocrit 17%), venous congestion, and combinations thereof. Control animals were kept euvolemic and normotensive for the entire experiment. Fluorescent microspheres were used to measure cerebral blood flow (CBF) and ON blood flow at baseline and after experimental conditions, and to calculate oxygen delivery (DO2). RESULTS: No significant changes in CBF or ON blood flow or DO2 occurred with euvolemic hypotension (n = 5), compared with controls (n = 12). Hypovolemic hypotension (n = 4) resulted in stable CBF and cerebral DO2, but significant reductions in ON DO2 (P = 0.032). The significant increase in CBF associated with anemia (n = 6) resulted in stable cerebral DO2. In contrast, ON blood flow did not significantly change with anemia, with (n = 5) or without (n = 6) euvolemic hypotension, resulting in significant reductions in ON DO2 (P < 0.01). CONCLUSION: Compensatory mechanisms for porcine CBF maintain stable DO2 under specified conditions of hypotension or anemia, whereas ON compensatory mechanisms were unable to maintain blood flow and to preserve DO2. The authors conclude that the porcine ON is more susceptible to physiologic perturbations than the brain.

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.

Perioperative Vision Loss in Cervical Spinal Surgery.

STUDY DESIGN: Retrospective multicenter case series. OBJECTIVE: To assess the rate of perioperative vision loss following cervical spinal surgery. METHODS: Medical records for 17 625 patients from 21 high-volume surgical centers from the AOSpine North America Clinical Research Network who received cervical spine surgery (levels from C2 to C7) between January 1, 2005, and December 31, 2011, inclusive, were reviewed to identify occurrences of vision loss following surgery. RESULTS: Of the 17 625 patients in the registry, there were 13 946 patients assessed for the complication of blindness. There were 9591 cases that involved only anterior surgical approaches; the remaining 4355 cases were posterior and/or circumferential fusions. There were no cases of blindness or vision loss in the postoperative period reported during the sampling period. CONCLUSIONS: Perioperative vision loss following cervical spinal surgery is exceedingly rare.