Implementation of an Online External Ventricular Drain Training Module-An Educational Initiative to Improve Proficiency of Perioperative Health Care Providers: Results of a Retrospective Study.

BACKGROUND: An external ventricular drain (EVD) training module may improve the knowledge and proficiency of perioperative health care providers (HCPs). METHODS: We examined knowledge gaps, self-reported comfort in managing EVDs, and improvement in self-assessment scores among HCPs from 7 academic medical centers based on an online EVD training module. RESULTS: Of the 326 HCPs who completed the module, 207 (70.6%) reported being uncomfortable managing EVDs. The median pretest scores were 6 (interquartile range=2), and posttest scores were 8 (interquartile range=1), out of a maximum possible score of 9. The most frequent incorrectly answered questions were: (a) maximum allowed hourly cerebrospinal fluid volume drainage (51%), (b) the components of a normal intracranial pressure waveform (41%), and (c) identifying the correct position of the stopcock for accurate measurement of intracranial pressure (41%). The overall gain in scores was 2 (interquartile range=2) and highest among HCPs who had managed 1 to 25 EVDs (2.51, 95% confidence interval: 2.23-2.80), and without self-reported comfort in managing EVDs (2.26, 95% confidence interval: 1.96-2.33, P <0.0001). The majority of participants (312, 95.7%) reported that the training module helped them understand how to manage EVDs, and 276 (84.7%) rated the module 8 or more out of 10 in recommending it to their colleagues. CONCLUSIONS: This online EVD training module was well-received by participants. Overall, improved scores reflect enhanced knowledge among HCPs following completion of the module. The greatest benefit was observed in those reporting less experience and feeling uncomfortable in managing EVDs. The impact on the reduction in EVD-associated adverse events deserves further examination.

Carbon Dioxide, Blood Pressure, and Perioperative Stroke: A Retrospective Case-Control Study.

BACKGROUND: The relationship between intraoperative physiology and postoperative stroke is incompletely understood. Preliminary data suggest that either hypo- or hypercapnia coupled with reduced cerebrovascular inflow (e.g., due to hypotension) can lead to ischemia. This study tested the hypothesis that the combination of intraoperative hypotension and either hypo- or hypercarbia is associated with postoperative ischemic stroke. METHODS: We conducted a retrospective, case-control study via the Multicenter Perioperative Outcomes Group. Noncardiac, nonintracranial, and nonmajor vascular surgical cases (18 yr or older) were extracted from five major academic centers between January 2004 and December 2015. Ischemic stroke cases were identified via manual chart review and matched to controls (1:4). Time and reduction below key mean arterial blood pressure thresholds (less than 55 mmHg, less than 60 mmHg, less than 65 mmHg) and outside of specific end-tidal carbon dioxide thresholds (30 mmHg or less, 35 mmHg or less, 45 mmHg or greater) were calculated based on total area under the curve. The association between stroke and total area under the curve values was then tested while adjusting for relevant confounders. RESULTS: In total, 1,244,881 cases were analyzed. Among the cases that screened positive for stroke (n = 1,702), 126 were confirmed and successfully matched with 500 corresponding controls. Total area under the curve was significantly associated with stroke for all thresholds tested, with the strongest combination observed with mean arterial pressure less than 55 mmHg (adjusted odds ratio per 10 mmHg-min, 1.17 [95% CI, 1.10 to 1.23], P < 0.0001) and end-tidal carbon dioxide 45 mmHg or greater (adjusted odds ratio per 10 mmHg-min, 1.11 [95% CI, 1.10 to 1.11], P < 0.0001). There was no interaction effect observed between blood pressure and carbon dioxide. CONCLUSIONS: Intraoperative hypotension and carbon dioxide dysregulation may each independently increase postoperative stroke risk.

Anesthetic Management of Asleep and Awake Craniotomy for Supratentorial Tumor Resection.

Understanding how anesthetics impact cerebral physiology, cerebral blood flow, brain metabolism, brain relaxation, and neurologic recovery is crucial for optimizing anesthesia during supratentorial craniotomies. Intraoperative goals for supratentorial tumor resection include maintaining cerebral perfusion pressure and cerebral autoregulation, optimizing surgical access and neuromonitoring, and facilitating rapid, cooperative emergence. Evidence-based studies increasingly expand the impact of anesthetic care beyond immediate perioperative care into both preoperative optimization and minimizing postoperative consequences. New evidence is needed for neuroanesthesia's role in neurooncology, in preventing conversion from acute to chronic pain, and in decreasing risk of intraoperative ischemia and postoperative delirium.

Case Report: Yellow Fever Vaccine-Associated Neurotropic Disease and Associated MRI, EEG, and CSF Findings.

Yellow fever vaccine-associated neurotropic disease (YEL-AND) is a rare and serious complication following vaccination with the 17D live attenuated yellow fever vaccine. Cases of YEL-AND have presented as acute inflammatory demyelinating polyneuropathy, acute disseminated encephalomyelitis, and meningoencephalitis. To date, intracranial imaging of the progression and resolution of this disease has been minimally depicted in the literature. We present the case of a 67-year-old woman who developed YEL-AND following vaccination. Her diagnosis was complicated by imaging findings consistent with variant Creutzfeldt Jakob Disease. Her clinical history and the progression of her intracranial imaging is discussed in this case report.

Effects of androgens on early post-ischemic neurogenesis in mice.

Although androgens are reported to affect stroke outcomes by altering ischemic tissue damage, their effect on post-injury repair is unknown. Since neurogenesis has recently been recognized as contributing to stroke outcomes, we investigated the role of androgens on stroke-induced neurogenesis. Adult male mice were subjected to transient middle cerebral artery occlusion (MCAO) and neurogenesis was examined 1 week later by quantifying BrdU/doublecortin-positive and BrdU/NeuN-positive neurons in brain germinal regions as well as the injured striatum. To elucidate the role of endogenous androgens, post-MCAO neurogenesis was examined in gonadally intact males, intact males implanted with the androgen receptor antagonist flutamide, and surgically castrated males. Surgical castration or pharmacologic androgen receptor blockade had no effects on post-ischemic neurogenesis, except that continuous androgen receptor blockade unexpectedly suppressed maturation of newborn neurons (BrdU/NeuN-positive cells) in the dentate gyrus. Post-MCAO neurogenesis was also examined in surgically castrated mice treated with continuous release implants containing testosterone or dihydrotestosterone (DHT). Testosterone and DHT robustly inhibited post-ischemic neurogenesis in the dentate gyrus, and the more potent androgen DHT virtually abolished the presence of immature newborn neurons (BrdU/doublecortin-positive cells) in the injured striatum. Our data suggest that endogenous androgens do not alter post-stroke neurogenesis quantitatively, but the presence of supra-physiological androgen stimulation profoundly suppresses early neurogenesis in germinal brain areas and reduces cellular repair in injured tissue after cerebral ischemia. These results advance the understanding of the role that androgens play in stroke outcomes.

Gender and the injured brain.

Anesthesiologists are frequently confronted with patients who are at risk for neurological complications due to perioperative stroke or prior traumatic brain injury. In this review, we address the growing and fascinating body of data that suggests gender and sex steroids influence the pathophysiology of injury and outcome for these patients. Cerebral ischemia, traumatic brain injury, and epilepsy are reviewed in the context of potential sex differences in mechanisms and outcomes of brain injury and the role of estrogen, progesterone, and androgens in shaping these processes. Lastly, implications for current and future perioperative and intensive care are identified.

Sigma 1 receptor agonists act as neuroprotective drugs through inhibition of inducible nitric oxide synthase.

Postischemic administration of the sigma-1 agonists reduces ischemic brain injury; however, the mechanism is unclear. We hypothesized that the sigma-1 agonist (+)isoform of pentazocine (P(+)) reduces damage in part by ameliorating cell death mediated via inducible nitric oxide synthase (iNOS) and that the (-)isoform (P(-)) lacks this effect. We compared treatment with P(+) with or without the iNOS inhibitor aminoguanidine (AG) and also the effects of P(+) in iNOS deficient (iNOSKO) mice. A possible mechanism of neuroprotection is inhibition of iNOS expression. Male C57/Bl6 mice were subjected to transient middle cerebral artery occlusion (90 min) and drugs were administered with reperfusion: 1) P(+) with AG (P+/AG), 2) P(+), 3) P(-), 4) AG, or 5) placebo. iNOSKOs were treated with either P(+) or placebo. Infarction (triphenyltetrazolium chloride histology, 72 h) was reduced by P(+) treatment in striatum by 44% and in neocortex by 23% versus placebo (P < 0.05), a reduction comparable to AG effect. P(-) did not attenuate brain injury. There was no difference in P(+)/AG treatment compared with showed the same level of neuroprotection as P(+) alone. P(+) also did not provide further neuroprotection for iNOSKOs. We conclude that postischemic administration of P(+) reduces infarct volume in mice. Because AG provides no additional benefit to P(+) treatment and iNOSKOs do not benefit from P(+), we speculate that P(+) acts by suppressing cell death resulting from iNOS toxicity.