Neurocritical care
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The aim of this narrative review is to describe the toxicologic confounders of brain death currently reported in the literature to offer guidance for physicians assessing brain death after a toxic exposure. We established an a priori definition of a "brain death mimic" as an unresponsive, intubated patient missing some, but not all brainstem reflexes. We completed a review of the literature utilizing MEDLINE and EMBASE to find case reports of patients of all ages in English, French, and Spanish meeting the criteria and hand searched the references of the results. ⋯ The most common means by which the cases failed brain death examination prerequisites was via normal neuroimaging. The xenobiotics in this review should be considered in cases of poisoning resulting in loss of brainstem reflexes and addressed before brain death determination. Brain death diagnosis should not be pursued in the setting of normal cerebral imaging or incomplete evaluation of brain death prerequisites.
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With increasing prevalence of chronic diseases, multimorbid patients have become commonplace in the neurosurgical intensive care unit (neuro-ICU), offering unique management challenges. By reducing physiological reserve and interacting with one another, chronic comorbidities pose a greatly enhanced risk of major postoperative medical complications, especially cardiopulmonary complications, which ultimately exert a negative impact on neurosurgical outcomes. ⋯ This knowledge enables neurosurgeons, neuroanesthesiologists and neurointensivists to function with a heightened level of vigilance in the care of these high-risk patients and can inform the perioperative neuro-ICU management with individualized strategies able to minimize the risk of untoward outcomes. This review highlights potential pitfalls in the intra- and postoperative neuro-ICU period, describes common preoperative risk stratification tools and discusses tailored perioperative ICU management strategies in multimorbid neurosurgical patients, with a special focus on approaches geared toward the minimization of postoperative cardiopulmonary complications and unplanned reintubation.
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Review
Effect of Desmopressin on Platelet Dysfunction During Antiplatelet Therapy: A Systematic Review.
An increasing number of patients receive antiplatelet therapy. Patients exposed to surgery while receiving platelet inhibitors hold an increased bleeding risk. Especially in neurosurgery and neurocritical care patients, bleeding and hematoma expansion are feared complications as even minor bleedings may be hazardous. The objective of this systematic review was to investigate the effect of desmopressin (1-deamino-8-D-arginine vasopressin, DDAVP) on platelet function during antiplatelet therapy in patients undergoing non-cardiac surgery, patients who experience spontaneous or traumatic hemorrhage, healthy individuals and in animals. ⋯ The present data hold biochemical evidence that DDAVP improves platelet function during antiplatelet therapy in humans and animals. The need for randomized trials is evident in order to evaluate the potential clinical effect of DDAVP in management of patients with spontaneous or traumatic hemorrhage, or undergoing neurosurgery, while receiving antiplatelet therapy.
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Endoplasmic reticulum stress (ERS) plays a vital role in mediating apoptosis in the brain following cardiac arrest (CA). Studies have shown that therapeutic hypothermia (TH) provides neuroprotection through anti-apoptosis; however, the effects of temperature variability in TH on the brain remain unclear. In this study, we investigated the different effects of temperature variability through extracorporeal membrane oxygenation on apoptosis and ERS in the brain following CA. ⋯ TH can reduce neuronal apoptosis by ERS, while temperature variability does not attenuate this beneficial effect.
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To compare the assessment of cerebral autoregulation by cerebrovascular reactivity indices based on intracranial pressure (Pressure Reactivity Index, PRx) and on transcranial Doppler (Mean Velocity Index, Mx) during controlled variations of arterial blood pressure in severe brain injury. Primary outcome was the agreement between both cerebrovascular reactivity indices measured by the Bland-and-Altman method. Secondary outcomes were the association of cerebrovascular reactivity indices with arterial blood pressure variation, and the comparison of optimal cerebral perfusion pressures determined by both indices. ⋯ Cerebral vasoreactivity indices calculated with intracranial pressure or transcranial Doppler show only moderate agreement. Both indices nonetheless suggest substantially higher optimal cerebral perfusion pressure than those currently provided by international guidelines.