Carotid artery dissection and non-aneurysmal subarachnoid hemorrhage following carotid endarterectomy.

Stroke continues to be a major public health issue resulting in high mortality and severe long-term disability. Carotid endarterectomy (CEA) plays an important role in the prevention of ischemic stroke. Complications associated with CEA can be life threatening and prompt recognition is crucial. In this report, we present a patient who presented to the hospital with progressive headache, 2 weeks following CEA. He was neurologically intact and hypertensive. Non-contrast head computed tomography (CT) scan showed convexity subarachnoid hemorrhage (SAH). He was found to have a left internal carotid artery dissection. Patients who present to the hospital following CEA with headache and hypertension benefit from a non-contrast head CT scan. The presence of SAH can be a warning sign of cerebral hyperperfusion syndrome. Carotid artery dissection is also a disease entity that can occur in the post-operative period. Prompt recognition and treatment is crucial for the management of these disease entities.

Standardized Criteria to Initiate External Ventricular Drain (EVD) Weaning in a Neurological Intensive Care Unit to Increase the Safety of EVD Discontinuation and Reduce the Need for a Shunt.

Introduction Patients with subarachnoid hemorrhages (SAH) with external ventricular drains (EVD) can develop chronic hydrocephalus (HCP), requiring permanent cerebrospinal fluid (CSF) diversion via an external shunt. Two different strategies have been used to assess for dependence on EVD: 1) prompt closure, and 2) gradual weaning. Gradual weaning of EVDs is performed by increasing drainage resistance to outflow over days. However, when to start one strategy or the other is up to the physician. No uniform guidelines exist raising a question: Are standardized criteria necessary to initiate the EVD weaning process for SAH patients to increase the safety of EVD discontinuation and reduce the need for a shunt? This study shares criteria used to initiate EVD weaning that displayed increased safety of EVD discontinuation for patients with subarachnoid hemorrhage requiring EVD, particularly with regards to length of hospital stay (LOS), hospital-acquired infection rates, and ventriculoperitoneal shunt/endoscopic third ventriculostomy (VPS/ETV) placement. Methods One hundred and fifty-one SAH patients from January 2016 to January 2019 were analyzed. 60 aneurysmal SAH (aSAH) and 18 non-aneurysmal nontraumatic SAH (naSAH) patients required EVD placement. A gradual EVD weaning protocol was initiated if patients met the following criteria: 1. The reason for EVD placement has resolved or is resolving, 2. The quantity of CSF output is <250mL over 24 hours, 3. Quality of CSF is nonbloody, 4. Intracranial Pressure (ICP) must be within normal limits, and 5. The patient must be neurologically stable. It was acceptable to initiate the weaning process when the patient had mild cerebral vasospasm, but not moderate to severe cerebral vasospasm. EVD weaning was performed by increasing the drain (chamber) height by 5 millimeters of mercury every 24 hours if the criteria were met. Charts were reviewed for LOS, infection rates, and rate of VPS/ETV. Gender, age, race, wean failure incidence, Hunt-Hess scores, modified Fisher scores, and syndrome of inappropriate antidiuretic hormone/cerebral salt wasting (SIADH/CSW) rates were obtained. Results The average LOS for aSAH patients with EVD was 20.35 days. The incidence of VPS/ETV was 11%. A chi-square analysis revealed that aSAH patients had higher rates of VPS/ETV placement (p<0.001) and EVD wean failures (p<0.001) than naSAH patients. aSAH patients had a lower incidence of VPS/ETV placement of 11% compared to 21% nationally. Conclusions Standardized criteria to initiate EVD weaning provided a reduction in VPS/ETV placement among aSAH patients compared to national averages and provided a uniform approach to EVD management. Comparable infection rates and LOS for SAH patients requiring EVDs compared to national averages were found.

Ketamine and Its Emergence in the Field of Neurology.

The quest for a safe and effective anesthetic medication in the mid-20th century led to the discovery of CI-581, which was later named ketamine. Ketamine was labeled a "dissociative anesthetic" due to the state of sensory deprivation that it induces in the subjects receiving it. Although it enjoyed widespread use at the beginning of the Vietnam war, its use rapidly waned due to its psychedelic effect and it became more popular as a recreational drug, and in the field of veterinary medicine. However, as we gained more knowledge about its multiple sites of action, it has reemerged as a useful anesthetic/analgesic agent. In the last decade, the field of neurology has witnessed the growing use of ketamine for the treatment of several neurological conditions including migraine, status epilepticus, stroke, and traumatic brain injury (TBI). Ketamine acts primarily as a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist. The binding of ketamine to NMDA receptors leads to decreased frequency and duration of Ca+2 channel opening and thus inhibits glutaminergic transmission. This mechanism has proven to be neuroprotective in several neurological conditions. Ketamine does not increase intracranial pressure (ICP), and it maintains cerebral perfusion pressure (CPP) by increasing cerebral blood flow. Ketamine has also been shown to inhibit massive slow waves of neurological depolarizations called cortical spreading depolarizations (CSD), usually seen during acute neurological injury and are responsible for further neurological deterioration. Unlike other anesthetic agents, ketamine does not cause cardiac or respiratory suppression. All these favorable mechanisms and cerebral/hemodynamic actions have led to increased interest among clinicians and researchers regarding the novel uses of ketamine. This review will focus on the use of ketamine for various neurological indications.

Concomitant central venous sinus thrombosis and subdural hematoma in acute promyelocytic leukemia: middle meningeal artery embolization enables safe anticoagulation. Illustrative case.

BACKGROUND: Acute promyelocytic leukemia (APL) has long been associated with coagulation disorders. The proposed mechanism is a combination of fibrinolysis, proteolysis, platelet dysfunction, thrombocytopenia, and possibly disseminated intravascular coagulation. Hemorrhagic complications are prominent. OBSERVATIONS: In this case, a 25-year-old female with newly diagnosed APL developed extensive cerebral venous thrombosis (CVT) and was initiated on a protocol with idarubicin and all-trans retinoic acid. The general recommendation for treating CVT is anticoagulation to stabilize the existing thrombus and prevent propagation. The patient was initiated on a heparin drip, but her clinical course was complicated by subdural hemorrhage (SDH) and epidural hemorrhage in the setting of thrombocytopenia. Anticoagulation was held, and her CVT propagated on follow-up imaging. To restart anticoagulation for CVT with a limited risk of SDH, the authors pursued middle meningeal artery (MMA) embolization. The patient was transitioned to apixaban and discharged to home. LESSONS: MMA embolization enables safe anticoagulation in patients with concomitant CVT and SDH. The authors report the complex clinical course and effective management of this rare clinical scenario.