Associations of an eye-tracking task and pupillary metrics with age and ASA physical status score in a preoperative cohort.

Advanced age, American Society of Anesthesiologists physical status (ASA) classification and the presence of cognitive impairment are associated with an elevated risk of postoperative morbidity and mortality. The visual paired comparison (VPC) task, which relies on recognition of novel images, examines declarative memory. VPC scores have demonstrated the ability to detect mild cognitive impairment and track progression of neurodegenerative disease. Quantitative pupillometry may have similar value. We evaluate for associations between these variables of interest and the feasibility of performing these tests in the preoperative clinic. Prospective data from 199 patients seen in the preoperative clinic at a tertiary academic center were analyzed. A 5 min VPC task (Neurotrack Technologies, Inc, Redwood City, CA) was administered during their scheduled preoperative clinic visit. Pupillary light reflexes were measured at the same visit (PLR-3000™, Neuroptics Corp, Irvine, California).Thirty-four percent of patients were categorized as ASA 2 and 58% as ASA 3. Median age was 57 (IQR: 44-69). Associations were demonstrated between age and ASA physical status (Mann-Whitney U Test, p < 0.0001), maximum pupil size (Spearman Rank Correlation, r = - 0.40, p < 0.0001), and maximum constriction velocity (Spearman Rank Correlation, r = - 0.39, p < 0.0001). Our data also revealed an association between VPC score and age (Spearman Rank Correlation, p = 0.0016, r = - 0.21) but not ASA score (Kruskal-Wallis Test, p = 0.14). When compared to a nonsurgical cohort with no history of memory impairment, our population scored worse on the VPC task (Mann-Whitney U Test, p = 0.0002). A preoperative 5 min VPC task and pupillometry are feasible tests in the preoperative setting and may provide a valuable window into an individual's cognition prior to elective surgery.

Opioid-Free Anesthesia for Craniotomy.

BACKGROUND: Perioperative opioids are problematic following craniotomy as they can impede neurological examination because of excessive sedation and mask surgical complications. Multimodal anesthetic techniques including nerve blocks have been used successfully to deliver opioid-free anesthesia in other surgical populations; however, no clinical data evaluating opioid-free anesthesia for craniotomy exists within the current body of literature. MATERIALS AND METHODS: Six prospectively identified patients underwent supratentorial craniotomy at Emory University Hospital using a multimodal opioid-free anesthetic (OFA) technique consisting of preoperative scalp block, dexmedetomidine and intravenous acetaminophen. These opioid-free patients were matched by age, sex, incision length, and incision location to 18 retrospectively identified control patients who underwent craniotomy using conventional, opioid-based anesthetic techniques. Postoperative opioid consumption and pain scores were compared and analyzed for noninferiority. RESULTS: Noninferiority of the OFA technique was demonstrated for opioid consumption at all measured intervals from postanesthesia care unit arrival to 24 hours postoperatively. Noninferiority was also demonstrated with respect to average postoperative pain scores from 0 to 12 hours, 0 to 24 hours, as well as length of postanesthesia care unit stay. Noninferiority was not shown for time to first rescue opioid postoperatively, pain scores for the 12 to 24 hours postoperative period, or time to emergence from anesthesia. CONCLUSIONS: This pilot study demonstrates the feasibility of an OFA technique for patients undergoing supratentorial craniotomy and suggests that larger prospective randomized controlled trials are indicated to examine the role of multimodal anesthetic techniques for craniotomy.

Hemispheric Asymmetry on the Electroencephalogram during General Anesthesia Responsive to Blood Pressure Manipulations.

The electroencephalogram (EEG) has been extensively used to detect ischemia and the need for shunting during carotid endarterectomy. Limited literature exists using EEG data to detect ischemia in other surgeries. This case report depicts a 65-year-old man, with extensive vascular history including complete left carotid occlusion and severe right carotid stenosis, who presented for left first rib resection and left subclavian vein balloon angioplasty. Following induction of general anesthesia, frontal EEG (SedLine; Masimo Corporation, Irvine, CA, USA) demonstrated hemispheric asymmetry, which nearly resolved with vasoactive support. At three distinct periods, discordance reoccurred necessitating a higher mean arterial pressure threshold. This case demonstrates EEG patterns concerning for focal spectrographic ischemia and highlights the potential use of EEG signals to capture hypoperfusion and direct vasoactive therapy.

Correction to: Low-chloride- versus high-chloride-containing hypertonic solution for the treatment of subarachnoid hemorrhage-related complications: The ACETatE (A low ChloriE hyperTonic solution for brain Edema) randomized trial.

[This corrects the article DOI: 10.1186/s40560-020-00449-0.].

Low-chloride- versus high-chloride-containing hypertonic solution for the treatment of subarachnoid hemorrhage-related complications: The ACETatE (A low ChloriE hyperTonic solution for brain Edema) randomized trial.

BACKGROUND: Recent reports have demonstrated that among patients with subarachnoid hemorrhage (SAH) treated with hypertonic NaCl, resultant hyperchloremia has been associated with the development of acute kidney injury (AKI). We report a trial comparing the effect of two hypertonic solutions with different chloride contents on the resultant serum chloride concentrations in SAH patients, with a primary outcome aimed at limiting chloride elevation. METHODS: A low ChloridE hyperTonic solution for brain Edema (ACETatE) trial is a single-center, double-blinded, double-dummy, randomized pilot trial comparing bolus infusions of 23.4% NaCl and 16.4% NaCl/Na-acetate for the treatment of cerebral edema in patients with SAH. Randomization occurred when patients developed hyperchloremia (serum Cl- ≥ 109 mmol/L) and required hyperosmolar treatment. RESULTS: We enrolled 59 patients, of which 32 developed hyperchloremia and required hyperosmolar treatment. 15 patients were randomized to the 23.4% NaCl group, and 17 patients were randomized to the 16.4% NaCl/Na-acetate group. Although serum chloride levels increased similarly in both groups, the NaCl/Acetate group showed a significantly lower Cl- load at the end of the study period (978mEq vs. 2,464mEq, p < 0.01). Secondary outcome analysis revealed a reduced rate of AKI in the Na-acetate group (53.3% in the NaCl group vs. 11.8% in the Na-acetate group, p = 0.01). Both solutions had similar effects on ICP reduction, but NaCl/Acetate treatment had a more prominent effect on immediate post-infusion Na+ concentrations (increase of 2.2 ± 2.8 vs. 1.4 ± 2.6, (p < 0.01)). Proximal tubule renal biomarkers differed in concentration between the two groups. CONCLUSIONS: Our pilot trial showed the feasibility and safety of replacing 23.4% NaCl infusions with 16.4% NaCl/Na-acetate infusions to treat cerebral edema in patients with SAH. The degree of hyperchloremia was similar in the two groups. 16.4% NaCl/Na-acetate infusions led to lower Cl- load and AKI rates than 23.4% NaCl infusions. Further multi-center studies are needed to corroborate these results. TRIAL REGISTRATION: clinicaltrials.gov # NCT03204955, registered on 6/28/2017.

Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients.

BACKGROUND: Acute treatment of cerebral edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of cerebral edema for optimal efficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of cerebral edema. Clinicians must be able to select appropriate therapies for initial cerebral edema management based on available evidence while balancing efficacy and safety. METHODS: The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a panel in 2017. The group generated 16 clinical questions related to initial management of cerebral edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy. RESULTS: The panel generated recommendations regarding initial management of cerebral edema in neurocritical care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intracerebral hemorrhage, bacterial meningitis, and hepatic encephalopathy. CONCLUSION: The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or cerebral edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing cerebral edema in patients with bacterial meningitis, but not ICH. Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these critical clinical situations merits close monitoring for adverse effects. There is a dire need for high-quality research to better inform clinicians of the best options for individualized care of patients with cerebral edema.

Pain management in neurocritical care; an update.

PURPOSE OF REVIEW: Pain management in neurocritical care is a subject often avoided because of concerns over the side-effects of analgesics and the potential to cause additional neurological injury with treatment. The sedation and hypercapnia caused by opioids have been feared to mask the neurological examination and contribute to elevations in intracranial pressure. Nevertheless, increasing attention to patient satisfaction has sparked a resurgence in pain management. As opioids have remained at the core of analgesic therapy, the increasing attention to pain has contributed to a growing epidemic of opioid dependence. In this review, we summarize the most recent literature regarding opioids and their alternatives in the treatment of acute pain in patients receiving neurocritical care. RECENT FINDINGS: Studies on pain management in neurocritical care continue to explore nonopioid analgesics as part of a multimodal strategy aimed at decreasing overall opioid consumption. Agents including local anesthetics, acetaminophen, ketamine, gabapentinoids, and dexmedetomidine continue to demonstrate efficacy. In addition, the prolonged longitudinal course of many recent trials has also revealed more about the transition from acute to chronic pain following hospitalization. SUMMARY: In an era of increasing attention to patient satisfaction mitigated by growing concerns over the harms imposed by opioids, alternative analgesic therapies are being investigated with promising results.

Automated Pupillometry and Detection of Clinical Transtentorial Brain Herniation: A Case Series.

Introduction: Transtentorial herniation (TTH) is a life-threatening neurologic condition that typically results from expansion of supratentorial mass lesions. A change in bedside pupillary examination is central to the clinical diagnosis of TTH. Materials and. Methods: To quantify the changes in the pupillary examination that precede and accompany TTH and its treatment, we evaluated 12 episodes of herniation in three patients with supratentorial mass lesions using automated pupillometry (NeurOptics, Inc., Irvine, CA). Herniation was defined clinically by the onset of fixed and dilated pupils in association with decreased levels of consciousness. Automated pupillometry was measured simultaneously with the bedside clinical examination, but the clinical team was blinded to these results and could not act on the data. Data from the pupillometer were downloaded 1-2 times per week onto a secured laptop, and data processing was facilitated by the use of Mathematica 8.0. Results: Neurologic Pupil Index measurements, values generated by the pupillometer based on an algorithm that incorporates pupillary size and reactivity in a normal population, were found to be abnormal before 73% of TTHs. This abnormality occurred at a median of 7.4 h before TTH. All episodes of TTH were reversed after clinical intervention at a median of 43 min after the event. The value did not fall to 0 in 42% of clinical herniations, but it did decrease to very abnormal values of 0.5-0.8. Conclusions: The potential of automated pupillometry to guide the management of severely injured neurologic patients is intriguing and warrants further study in the critical care unit and beyond. The utility of a portable device in the combat setting may allow for triage of patients with severe neurologic injury.

Comparison of equivolume, equiosmolar solutions of mannitol and hypertonic saline with or without furosemide on brain water content in normal rats.

BACKGROUND: Mannitol and hypertonic saline (HS) are used by clinicians to reduce brain water and intracranial pressure and have been evaluated in a variety of experimental and clinical protocols. Administering equivolume, equiosmolar solutions in healthy animals could help produce fundamental data on water translocation in uninjured tissue. Furthermore, the role of furosemide as an adjunct to osmotherapy remains unclear. METHODS: Two hundred twenty isoflurane-anesthetized rats were assigned randomly to receive equivolume normal saline, 4.2% HS (1,368 mOsm/L 25% mannitol (1,375 mOsm/L), normal saline plus furosemide (8 mg/kg), or 4.2% HS plus furosemide (8 mg/kg) over 45 min. Rats were killed at 1, 2, 3, and 5 h after completion of the primary infusion. Outcome measurements included body weight; urinary output; serum and urinary osmolarity and electrolytes; and brain, lung, skeletal muscle, and small bowel water content. RESULTS: In the mannitol group, the mean water content of brain tissue during the experiment was 78.0% (99.3% CI, 77.9-78.2%), compared to results from the normal saline (79.3% [99.3% CI, 79.1-79.5%]) and HS (78.8% [99.3% CI, 78.6-78.9%]) groups (P < 0.001), whereas HS plus furosemide yielded 78.0% (99.3% CI, 77.8-78.2%) (P = 0.917). After reaching a nadir at 1 h, brain water content increased at similar rates for mannitol (0.27%/h [99.3% CI, 0.14-0.40%/h]) and HS (0.27%/h [99.3% CI, 0.17-0.37%/h]) groups (P = 0.968). CONCLUSIONS: When compared to equivolume, equiosmolar administration of HS, mannitol reduced brain water content to a greater extent over the entire course of the 5-h experiment. When furosemide was added to HS, the brain-dehydrating effect could not be distinguished from that of mannitol.

A review of scalp blockade for cranial surgery.

Neural blockade of the scalp may be used as an adjunct to general anesthesia or serve as the principal anesthetic for both intracranial and extracranial procedures. Effective scalp blockade typically requires anesthetizing multiple peripheral nerves; blockade of one or more of these is often used to diagnose and treat conditions such as chronic headache. Improved anatomic knowledge has refined the use of scalp blockade so that directed neural blockade is achieved. The vascularity of the scalp, proximity of arteries supplying the cerebral circulation, use of large volumes of local anesthetic, and presence of intracranial devices or bony defects require attention. The impact of perioperative scalp blockade on acute and chronic pain may offer insight into the benefits of perioperative neural blockade generally.

Infarct volume after hyperacute infusion of hypertonic saline in a rat model of acute embolic stroke.

INTRODUCTION: Hypertonic saline (HS) can treat cerebral edema arising from a number of pathologic conditions. However, physicians are reluctant to use it during the first 24 h after stroke because of experimental evidence that it increases infarct volume when administered early after reperfusion. Here, we determined the effect of HS on infarct size in an embolic clot model without planned reperfusion. METHODS: A clot was injected into the internal carotid artery of male Wistar rats to reduce perfusion in the middle cerebral artery territory to less than 40 % of baseline, as monitored by laser-Doppler flowmetry. After 25 min, rats were randomized to receive 10 mL/kg of 7.5 % HS (50:50 chloride:acetate) or normal saline (NS) followed by a 0.5 mL/h infusion of the same solution for 22 h. RESULTS: Infarct volume was similar between NS and HS groups (in mm(3): cortex 102 ± 65 mm(3) vs. 93 ± 49 mm(3), p = 0.72; caudoputamenal complex 15 ± 9 mm(3) vs. 21 ± 14, p = 0.22; total hemisphere 119 ± 76 mm(3) vs. 114 ± 62, p = 0.88, respectively). Percent water content was unchanged in the infarcted hemisphere (NS 81.6 ± 1.5 %; HS 80.7 ± 1.3 %, p = 0.16), whereas the HS-treated contralateral hemisphere was significantly dehydrated (NS 79.4 ± 0.8 %; HS 77.5 ± 0.8 %, p < 0.01). CONCLUSIONS: HS reduced contralateral hemispheric water content but did not affect ipsilateral brain water content when compared to NS. Infarct volume was unaffected by HS administration at all evaluated locations.

Emergency neurological life support: intracranial hypertension and herniation.

Sustained intracranial hypertension and acute brain herniation are "brain codes," signifying catastrophic neurological events that require immediate recognition and treatment to prevent irreversible injury and death. As in cardiac arrest, evidence supports the organized implementation of a stepwise management algorithm. Because there are multiple etiologies and many treatments that can potentially reverse cerebral herniation, intracranial hypertension and herniation was chosen as an Emergency Neurological Life Support (ENLS) protocol.

Preoperative preparation of the surgical patient with neurologic disease.

This article emphasizes some key points in the preoperative evaluation of patients with neurologic disease. The amount of neurologic disease in the general population is a difficult number to assess accurately. This is, in part, because of the wide-sweeping scope of neurologic disease. The International Classification of Diseases has the highest number of conditions attributable to neurologic disease. Patients with neurologic disease are commonly encountered, and their illness is often complicated by significant comorbid disease. It is important to think of the patient as a whole rather than the sum of his or her systems. While it is tempting to consider the traditional preoperative evaluation from a "cardiac clearance" point of view, we must resist this urge, and evaluate which risk factors we can modify and hopefully mitigate to optimize the perioperative period.

Preoperative preparation of the surgical patient with neurologic disease.

This article emphasizes some key points in the preoperative evaluation of patients with neurologic disease. The amount of neurologic disease in the general population is a difficult number to assess accurately. This is, in part, because of the wide-sweeping scope of neurologic disease. The International Classification of Diseases has the highest number of conditions attributable to neurologic disease. Patients with neurologic disease are commonly encountered, and their illness is often complicated by significant comorbid disease. It is important to think of the patient as a whole rather than the sum of his or her systems. While it is tempting to consider the traditional preoperative evaluation from a "cardiac clearance" point of view, we must resist this urge, and evaluate which risk factors we can modify and hopefully mitigate to optimize the perioperative period.

Pharmacologic management of brain edema.

Cerebral edema is an intrinsic response to a variety of structural and metabolic insults. It is a major contributing factor in the development of intracranial hypertension and brain herniation, underscoring the need for early identification through an integration of clinical and neuroimaging findings, followed by timely institution of measures to reduce brain edema and intracranial hypertension. The management of cerebral edema requires a comprehensive approach in which pharmacologic treatments play a central role. These include glucocorticoids, hyperosmolar agents, diuretics, and sedative-anesthetic agents. Basic, translational, and clinical studies are needed to further unravel mechanisms underlying brain edema, with the goal of identifying new treatment strategies. Promising targets include modulators of endothelial cell tight junction proteins and of aquaporin channel expression within the blood-brain barrier.

Mechanical thrombectomy of the internal carotid artery and middle cerebral arteries for acute stroke by using the retriever device.

We report a case of mechanical thrombectomy in which a new device, the Retriever, was used for acute cerebral ischemia in the setting of extensive occlusion of the left internal carotid and middle cerebral arteries. Excellent radiographic and clinical results were obtained. The Retriever is currently approved and available for foreign body extraction and for intracranial thrombectomy when used as part of the Mechanical Embolus Removal in Cerebral Ischemia, or MERCI, clinical trial. This device was able to retrieve and remove clots efficiently from the intracranial and extracranial circulation, offering a new therapeutic alternative in the treatment of acute cerebral ischemic disease.