39 research outputs found

    Management of anticoagulant-related intracranial hemorrhage: An evidence-based review

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    The increased use of anticoagulants for the prevention and treatment of thromboembolic diseases has led to a rising incidence of anticoagulant-related intracranial hemorrhage (AICH) in the aging western population. High mortality accompanies this form of hemorrhagic stroke, and significant and debilitating long-term consequences plague survivors. Although management guidelines for such hemorrhages are available for the older generation anticoagulants, they are still lacking for newer agents, which are becoming popular among physicians. Supportive care, including blood pressure control, and reversal of anticoagulation remain the cornerstone of acute management of AICH. Prothrombin complex concentrates are gaining popularity over fresh frozen plasma, and reversal agents for newer anticoagulation agents are being developed. Surgical interventions are options fraught with complications, and are decided on a case-by-case basis. Our current state of understanding of this condition and its management is insufficient. This deficit calls for more population-based studies and therapeutic trials to better evaluate risk factors for, and to prevent and treat AICH

    Year in review 2011: Critical Care – neurocritical care

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    Contributions from the neurosciences to Critical Care in 2011 covered an array of topics. We learned about potential biomarkers for, and the effect of cerebral oxygen metabolism on, delirium, in addition to treatment of the latter. A group of investigators studied surface cooling in healthy awake volunteers, and incidence of infection associated with therapeutic hypothermia. The effects of statin and erythropoietin on stroke were revisited, and the role of adhesion molecule in the inflammatory reaction accompanying intracerebral hemorrhage was scrutinized. Biomarkers in subarachnoid hemorrhage and their relationship to vasospasm and outcome, and effect of daylight on outcome in this patient population, as well as a new meta-analysis of statin therapy were among the research in subarachnoid hemorrhage. Moreover, 2011 witnessed the publication of a multidisciplinary consensus conference's recommendations on the critical care management of subarachnoid hemorrhage. Results of studies regarding the diagnosis and vascular complications of meningitis were reported. Traumatic brain injury received its share of articles addressing therapy with hypertonic saline and surgical decompression, the development of coagulopathy, and biomarkers to help with prognostication. Finally, research on the treatment of Guillain-Barre syndrome in children, prediction of long-term need of ventilatory support, and pathophysiology of critical illness polyneuropathy and myopathy were reported

    Clinical review: Prevention and therapy of vasospasm in subarachnoid hemorrhage

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    Vasospasm is one of the leading causes of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Radiographic vasospasm usually develops between 5 and 15 days after the initial hemorrhage, and is associated with clinically apparent delayed ischemic neurological deficits (DID) in one-third of patients. The pathophysiology of this reversible vasculopathy is not fully understood but appears to involve structural changes and biochemical alterations at the levels of the vascular endothelium and smooth muscle cells. Blood in the subarachnoid space is believed to trigger these changes. In addition, cerebral perfusion may be concurrently impaired by hypovolemia and impaired cerebral autoregulatory function. The combined effects of these processes can lead to reduction in cerebral blood flow so severe as to cause ischemia leading to infarction. Diagnosis is made by some combination of clinical, cerebral angiographic, and transcranial doppler ultrasonographic factors. Nimodipine, a calcium channel antagonist, is so far the only available therapy with proven benefit for reducing the impact of DID. Aggressive therapy combining hemodynamic augmentation, transluminal balloon angioplasty, and intra-arterial infusion of vasodilator drugs is, to varying degrees, usually implemented. A panoply of drugs, with different mechanisms of action, has been studied in SAH related vasospasm. Currently, the most promising are magnesium sulfate, 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors, nitric oxide donors and endothelin-1 antagonists. This paper reviews established and emerging therapies for vasospasm

    Effect of alteplase use on outcomes in patients with atrial fibrillation: Analysis of the Initiation of Anticoagulation after Cardioembolic Stroke study

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    Background Intravenous alteplase improves outcome after acute ischemic stroke without a benefit in 90-day mortality. There are limited data on whether alteplase is associated with reduced mortality in patients with atrial fibrillation (AF)-related ischemic stroke whose mortality rate is relatively high. We sought to determine the association of alteplase with hemorrhagic transformation and mortality in patients with AF. Methods and Results We retrospectively analyzed consecutive patients with acute ischemic stroke between 2015 and 2018 diagnosed with AF included in the IAC (Initiation of Anticoagulation After Cardioembolic Stroke) study, which pooled data from stroke registries at 8 comprehensive stroke centers across the United States. For our primary analysis, we included patients who did not undergo mechanical thrombectomy (MT), and secondary analyses included patients who underwent MT. We used binary logistic regression to determine whether alteplase use was associated with risk of hemorrhagic transformation and 90-day mortality. There were 1889 patients (90.6%) who had 90-day follow-up data available for analyses and were included; 1367 patients (72.4%) did not receive MT, and 522 patients (27.6%) received MT. In our primary analyses we found that alteplase use was independently associated with an increased risk for hemorrhagic transformation (odds ratio [OR], 2.23; 95% CI, 1.57-3.17) but reduced risk of 90-day mortality (OR, 0.58; 95% CI, 0.39-0.87). Among patients undergoing MT, alteplase use was not associated with a significant reduction in 90-day mortality (OR, 0.68; 95% CI, 0.45-1.04). Conclusions Alteplase reduced 90-day mortality of patients with acute ischemic stroke with AF not undergoing MT. Further study is required to assess the efficacy of alteplase in patients with AF undergoing MT

    Comparing external ventricular drains-related ventriculitis surveillance definitions

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    OBJECTIVETo evaluate the agreement between the current National Healthcare Safety Network (NHSN) definition for ventriculitis and others found in the literature among patients with an external ventricular drain (EVD)DESIGNRetrospective cohort study from January 2009 to December 2014SETTINGNeurology and neurosurgery intensive care unit of a large tertiary-care centerPATIENTSPatients with an EVD were included. Patients with an infection prior to EVD placement or a permanent ventricular shunt were excluded.METHODSWe reviewed the charts of patients with positive cerebrospinal fluid (CSF) cultures and/or abnormal CSF results while they had an EVD in place and applied various ventriculitis definitions.RESULTSWe identified 48 patients with a total of 52 cases of ventriculitis (41 CSF culture-positive cases and 11 cases based on abnormal CSF test results) using the NHSN definition. The most common organisms causing ventriculitis were gram-positive commensals (79.2%); however, 45% showed growth of only 1 colony on 1 piece of media. Approximately 60% of the ventriculitis cases by the NHSN definition met the Honda criteria, approximately 56% met the Gozal criteria, and 23% met Citerio’s definition. Cases defined using Honda versus Gozal definitions had a moderate agreement (Îș=0.528; P&lt;.05) whereas comparisons of Honda versus Citerio definitions (Îș=0.338; P&lt;.05) and Citerio versus Gozal definitions (Îș=0.384; P&lt;.05) had only fair agreements.CONCLUSIONSThe agreement between published ventriculostomy-associated infection (VAI) definitions in this cohort was moderate to fair. A VAI surveillance definition that better defines contaminants is needed for more homogenous application of surveillance definitions between institutions and better comparison of rates.Infect Control Hosp Epidemiol 2017;38:574–579</jats:sec

    Rate of infarct-edema growth on CT predicts need for surgical intervention and clinical outcome in patients with cerebellar infarction

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    BACKGROUND: Up to 20% of patients with cerebellar infarcts will develop malignant edema and deteriorate clinically. Radiologic measures, such as initial infarct size, aid in identifying individuals at risk. Studies of anterior circulation stroke suggest that mapping early edema formation improves the ability to predict deterioration; however, the kinetics of edema in the posterior fossa have not been well characterized. We hypothesized that faster edema growth within the first hours after acute cerebellar stroke would be an indicator for individuals requiring surgical intervention and those with worse neurological outcomes. METHODS: Consecutive patients admitted to the neurological intensive care unit with acute cerebellar infarction were retrospectively identified. Hypodense regions of infarct and associated edema, infarct-edema , were delineated by using ABC/2 for all computed tomography (CT) scans up to 14 days from last known well. To examine how rate of infarct-edema growth varied across clinical variables and surgical intervention status, nonlinear and linear mixed-effect models were performed over 2 weeks and 2 days, respectively. In patients with at least two CT scans, multivariable logistic regression examined clinical and radiological predictors of surgical intervention (defined as extraventricular drainage and/or posterior fossa decompression) and poor clinical outcome (discharge to skilled nursing facility, long-term acute care facility, hospice, or morgue). RESULTS: Of 150 patients with acute cerebellar infarction, 38 (25%) received surgical intervention and 45 (30%) had poor clinical outcome. Age, admission National Institutes of Health Stroke Scale (NIHSS) score, and baseline infarct-edema volume did not differ, but bilateral/multiple vascular territory involvement was more frequent (87% vs. 50%, p \u3c 0.001) in the surgical group than that in the medical intervention group. On 410 serial CTs, infarct-edema volume progressed rapidly over the first 2 days, followed by a subsequent plateau. Of 112 patients who presented within two days, infarct-edema growth rate was greater in the surgical group (20.1 ml/day vs. 8.01 ml/day, p = 0.002). Of 67 patients with at least two scans, after adjusting for baseline infarct-edema volume, vascular territory, and NIHSS, infarct-edema growth rate over the first 2 days (odds ratio 2.55; 95% confidence interval 1.40-4.65) was an independent, and the strongest, predictor of surgical intervention. Further, early infarct-edema growth rate predicted poor clinical outcome (odds ratio 2.20; 95% confidence interval 1.30-3.71), independent of baseline infarct-edema volume, brainstem infarct, and NIHSS. CONCLUSIONS: Early infarct-edema growth rate, measured via ABC/2, is a promising biomarker for identifying the need for surgical intervention in patients with acute cerebellar infarction. Additionally, it may be used to facilitate discussions regarding patient prognosis

    Abstract Number ‐ 222: Spontaneous Simultaneous Bilateral Putaminal Hemorrhages in a Young Woman

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    Introduction Spontaneous simultaneous bilateral basalganglia hemorrhage is an exceedingly rare condition with significant morbidity and mortality. Hypertension is the most common underlying etiology followed by intoxication and metabolic causes1. Methods Here we describe a 39‐year‐old woman with a spontaneous simultaneous bilateral putaminal hemorrhages believed to be secondary to amphetamine (Adderall) use and undiagnosed hypertension. Results A 39‐year‐old right‐handed woman with history of attention‐deficit/hyperactivity disorder (ADHD) on dextroamphetamine‐amphetamine (Adderall), white coat hypertension and prior gestational hypertension was brought to the emergency department due to sudden‐onset left hemiparesis, left foot numbness, gait instability, and an abnormal sensation in her right ear. On arrival, blood pressure was 239/139 mmHg. Patient was noted to be somewhat drowsybut was consistently regarding,able to respond, and had anosognosia, hypophonia, a right gaze preference, mild dysarthria, left arm and leg hypotonia, left hemiparesis and hypoesthesia involving face, arm and leg and brisk reflexes on the left side.Head CT revelated bilateral putaminal hemorrhages measuring 10mL on the right and 3mL on the left,with no intraventricular hemorrhage and minimal right‐to‐left midline shift.Patient was admitted to the neuro ICU and treated with a nicardipine infusion. CTA/MRI/MRV/MRA and catheter angiography revealed no underlying structural pathology. Furthermore, patient had a normal platelet count and coagulation profile. Urine drug screen was positive for amphetamines, and serum metanephrines (0.59 nmol/L) and normetanephrines (1.2nmol/L) were elevated in the setting ofAdderall use. Nicardipine infusion was discontinued on day one and she was started on carvedilol 12 mg bid and amlodipine 5mg daily. Adderall was discontinued and patient was counseled on avoiding stimulant medications use. At time of discharge her dysarthria had resolved but her left hemiplegia remained unchanged. She was discharged on day 5 of hospital stay to an inpatient rehabilitation facility. She was started on fluoxetine 20 mg daily for motor recovery at the rehabilitation facility. At her two months follow‐up visit, she was noted to have significant improvement in her left‐sided strength, hypoesthesia and left facial droop but had developed left arm and leg spasticity. She was started on a trial of dry needling with physical therapy prior to consideration of anti‐spasmodic medications or Botox injections. At her office visit, her blood pressure had been well controlled on lisinopril 10 mg and amlodipine 10 mg daily. Conclusions Overall, this case report highlights that amphetamine (Adderall) use is a potential cause of spontaneoussimultaneousbilateralbasalgangliahemorrhage
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