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Objectives: Incorporation of a single daily assessment by a clinical pharmacist to improve adherence with a sedation protocol is associated with reduced duration of mechanical ventilation and intensive care unit (ICU) length of stay (LOS). We test the feasibility of incorporating a clinical pharmacist into more frequent sedation assessments and observed whether there are any potential differences in the sedatives administered., Methods: Prospective, quasi-experimental, pilot study of patients admitted to the medical ICU. Patients were included in the analysis if ≥18 years of age within the first 24 hours of initiation of mechanical ventilation. Our primary intent was to test the clinical feasibility surrounding more frequent sedation assessments by a clinical pharmacist by evaluating potential differences in time in target sedation range and sedative administration. Exploratory efficacy end points included time in target sedation range (0 to -2) using the Richmond Agitation Sedation Scale (RASS) and sedative exposure. Patients were assigned to receive either 3 assessments with a clinical pharmacist per day (intervention) or a single assessment by a clinical pharmacist per day (standard of care). During the assessments, clinical pharmacists participated in the RASS administration and made dosing adjustments according to an established sedation protocol., Main Results: Seventeen patients were enrolled (n = 6 intervention group, n = 11 standard of care). Duration of mechanical ventilation was similar in the 2 groups (intervention 100.0 hours [52.5-197.5] vs control 76.0 hours [46.0-201.0], P = .95), but patients in the intervention group exhibited a greater percentage time in the target RASS range (intervention 76.0% [53.7-81.5%] vs control 45.2% [35.3-67.0], P = .11) that was not statistically significant. Patients in the intervention group received less fentanyl per day (820.9 µg [227.3-1579.4] vs 1997 µg [1648.2-2477.2], P = .02) than in the control group., Conclusion: Incorporating a clinical pharmacist into more frequent daily sedation assessments was associated with a reduction in fentanyl administration. There were no observed differences in time in target sedation range or reduction in duration of mechanical ventilation.

The evidence linking delirium to poor outcomes after critical illness is compelling, including higher mortality, prolonged mechanical ventilation, longer length of intensive care unit stay, and long-term cognitive impairments. The attitude toward delirium in the neurologic community is shifting away from viewing it as an unmodifiable, inevitable consequence of severe illness to treating it is as a neurologic emergency, akin to seizures or encephalitis. Delirium, like other manifestations of critical illness encephalopathy, is an organ dysfunction syndrome. Given the brain's central role in maintaining homeostasis, brain failure may dysregulate many downstream functions of significant consequence in critically ill patients. The diagnosis of delirium may be confounded in patients with primary brain disorders, but nevertheless delirium symptoms in the neurologic population are also independently associated with worse outcomes. There is scant evidence for directed pharmacological treatment of delirium, but multicomponent care bundles that address the management of pain, agitation, sedation, and delirium are effective at reducing the burden of delirium in the general intensive care unit population. The management of delirium in the neurologic intensive care environment is mostly extrapolated from studies on general medical critical illness and noncritically ill neurologic patients. Further investigation into the unique risks and management needs of critically ill neurologic and neurosurgical patients is needed to reduce the burden of delirium in that population., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Purpose of Review: This article updates neurologists on recent insights and management strategies of intracerebral hemorrhage (ICH)., Recent Findings: Blood pressure reduction likely improves outcomes in patients with intracerebral hemorrhage, although not by the expected mechanism of reducing hematoma growth. One formulation of prothrombin complex concentrate for reversing severe bleeding associated with warfarin is now approved by the US Food and Drug Administration (FDA), and specific reversal therapies for the novel oral anticoagulants are in development. Neurologic monitoring frequently detects ICH worsening that requires an intervention. Platelet transfusion and pharmacologic platelet activation are promising and often used as part of patient management but have not yet been shown to improve patient outcomes., Summary: Measurable progress continues toward establishing effective therapies to improve outcomes in patients with ICH. Blood pressure reduction and reversal of medications that exacerbate bleeding are likely to improve outcomes. Recommendations for neuromonitoring will help clinicians at the bedside attend to the most important abnormalities and optimize later quality of life. This article reviews standards for diagnosis and severity of ICH, monitoring and treatment of complications in the hospital, available interventions, and the measurement of outcomes.

Anemia and bleeding are paramount concerns in neurocritical care and often relate to the severity of intracranial hemorrhage. Anemia is generally associated with worse outcomes, and efforts to minimize anemia through reduced volume of blood sampled are encouraged. Point-of-care-testing reliably detects the use of non-steroidal anti-inflammatory drugs that may worsen bleeding and reduce platelet activity, particularly in patients with intracerebral hemorrhage. How best to monitor the effect of platelet transfusion or platelet-activating therapy is not well studied. For patients known to take novel oral anticoagulants, drug-specific coagulation tests before neurosurgical intervention are prudent.

Objective: We tested the hypothesis that surveillance neuroimaging and neurologic examinations identified changes requiring emergent surgical interventions in patients with intracerebral hemorrhage (ICH)., Methods: Patients with primary ICH were enrolled into a prospective registry between December 2006 and July 2012. Patients were managed in a neuroscience intensive care unit with a protocol that included serial neuroimaging at 6, 24, and 48 hours, and hourly neurologic examinations using the Glasgow Coma Scale and NIH Stroke Scale. We evaluated all cases of craniotomy and ventriculostomy to determine whether the procedure was part of the initial management plan or occurred subsequently. For those that occurred subsequently, we determined whether worsening on neurologic examination or worsened neuroimaging findings initiated the process leading to intervention., Results: There were 88 surgical interventions in 84 (35%) of the 239 patients studied, including ventriculostomy in 52 (59%), craniotomy in 21 (24%), and both in 11 (13%). Of the 88 interventions, 24 (27%) occurred subsequently and distinctly from initial management, a median of 15.9 hours (8.9-27.0 hours) after symptom onset. Thirteen (54%) were instigated by findings on neurologic examination and 11 (46%) by neuroimaging. Demographics, severity of hemorrhage, and hemorrhage location were not associated with delayed intervention., Conclusions: More than 25% of surgical interventions performed after ICH were prompted by delayed imaging or clinical findings. Serial neurologic examinations and neuroimaging are important and effective surveillance techniques for monitoring patients with ICH.

Intracranial hemorrhage is a life-threatening condition, the outcome of which can be improved by intensive care. Intracranial hemorrhage may be spontaneous, precipitated by an underlying vascular malformation, induced by trauma, or related to therapeutic anticoagulation. The goals of critical care are to assess the proximate cause, minimize the risks of hemorrhage expansion through blood pressure control and correction of coagulopathy, and obliterate vascular lesions with a high risk of acute rebleeding. Simple bedside scales and interpretation of computed tomography scans assess the severity of neurological injury. Myocardial stunning and pulmonary edema related to neurological injury should be anticipated, and can usually be managed. Fever (often not from infection) is common and can be effectively treated, although therapeutic cooling has not been shown to improve outcomes after intracranial hemorrhage. Most functional and cognitive recovery takes place weeks to months after discharge; expected levels of functional independence (no disability, disability but independence with a device, dependence) may guide conversations with patient representatives. Goals of care impact mortality, with do-not-resuscitate status increasing the predicted mortality for any level of severity of intraparenchymal hemorrhage. Future directions include refining the use of bedside neuro-monitoring (electroencephalogram, invasive monitors), novel approaches to reduce intracranial hemorrhage expansion, minimizing vasospasm, and refining the assessment of quality of life to guide rehabilitation and therapy.

Introduction: Anemia is associated with poor outcomes in patients with aneurysmal subarachnoid hemorrhage (SAH). It remains unclear whether this association can be modified with more aggressive use of red blood cell (RBC) transfusions. The degree to which restrictive thresholds have been adopted in neurocritical care patients remains unknown., Methods: We performed a survey of North American academic neurointensivists, vascular neurosurgeons and multidisciplinary intensivists who regularly care for patients with SAH to determine hemoglobin (Hb) concentrations which commonly trigger a decision to initiate transfusion. We also assessed minimum and maximum acceptable Hb goals in the context of a clinical trial and how decision-making is influenced by advanced neurological monitoring, clinician characteristics and patient-specific factors., Results: The survey was sent to 531 clinicians, of whom 282 (53%) responded. In a hypothetical patient with high-grade SAH (WFNS 4), the mean Hb concentration at which clinicians administered RBCs was 8.19 g/dL (95% CI, 8.07 to 8.30 g/dL). Transfusion practices were comparatively more restrictive in patients with low-grade SAH (mean Hb 7.85 g/dL (95% CI, 7.73 to 7.97 g/dL)) (P < 0.0001) and more liberal in patients with delayed cerebral ischemia (DCI) (mean Hb 8.58 g/dL (95% CI, 8.45 to 8.72 g/dL)) (P < 0.0001). In each setting, there was a broad range of opinions. The majority of respondents expressed a willingness to study a restrictive threshold of ≤8 g/dL (92%) and a liberal goal of ≥10 g/dl (75%); in both cases, the preferred transfusion thresholds were significantly higher for patients with DCI (P < 0.0001). Neurosurgeons expressed higher minimum Hb goals than intensivists, especially for patients with high-grade SAH (β = 0.46, P = 0.003), and were more likely to administer two rather than one unit of RBCs (56% vs. 19%; P < 0.0001). Institutional use of transfusion protocols was associated with more restrictive practices. More senior clinicians preferred higher Hb goals in the context of a clinical trial. Respondents were more likely to transfuse patients with brain tissue oxygen tension values <15 mmHg and lactate-to-pyruvate ratios >40., Conclusions: There is widespread variation in the use of RBC transfusions in SAH patients. Practices are heavily influenced by the specific dynamic clinical characteristics of patients and may be further modified by clinician specialty and seniority, the use of protocols and advanced neurological monitoring.

Introduction: Severity of illness scores predict all-cause mortality after intracerebral hemorrhage (ICH), but do not differentiate between proximate mechanisms or predict the timing. We hypothesized that death by neurologic criteria [brain death (BD)], withdrawal of life support, and cardiovascular death would be distinct after ICH., Methods: We prospectively enrolled patients with spontaneous ICH without underlying vascular malformation or neoplasm. We recorded clinical data and the proximate mechanism of death (BD, withdrawal of life support, cardiovascular death, or other cause). Time to death was compared with Kaplan-Meier methods (log-rank test). Data are median (IQR)., Results: Among 89 patients, 15 had withdrawal of life support, 5 had BD, 2 died from cardiac arrest, and 3 died from other causes. Among patients who died, ICH score, age, Glasgow Coma Scale, NIH Stroke Scale, and proximate cause were not associated with the proximate mechanism of death. The time to death was different (P < 0.001) depending on the proximate mechanism. Patients with BD died 1 [0-1] 1 day after ICH, withdrawal of life support led to death 5 [1-13] days after ICH, cardiac death occurred 35 [35-85] days after ICH, and other causes led to death 33 [26-33] days after ICH. Among patients where life support was withdrawn, a higher ICH score on admission was related to earlier death (P = 0.002)., Conclusions: Proximate mechanisms of death after ICH occur at distinct times. Withdrawal of life support leads to earlier death in patients with a higher severity of injury. Medical causes of death can be effectively prevented after ICH.

Introduction: Longer length of stay (LOS) is associated with higher complications and costs in ICU patients, while hospital protocols may decrease complications and LOS. We hypothesized that medical complications would increase LOS after spontaneous subarachnoid (SAH) and intracerebral (ICH) hemorrhage after accounting for severity of neurologic injury in a cohort of consecutively admitted patients., Methods: We prospectively recorded admission characteristics, hospital complications, and LOS for 122 patients with SAH and 56 patients with ICH from February 2006 through March 2008. A multidisciplinary Neuro-ICU team included a dedicated pharmacist and intensivist on daily rounds. Hospital protocols set glucose control with intravenous insulin, ventilator bundles, pharmacist involvement, and hand hygiene. Associations were explored with univariate statistics (t-tests, ANOVA, or non-parametric statistics as appropriate) and linear regression (repeated after log transformation of ICU and hospital LOS)., Results: Factors associated with longer LOS after SAH and ICH were similar. In both SAH and ICH the strongest drivers of LOS were infection, fever, and acute lung injury. For SAH, vasospasm and Glasgow Coma Scale were also significant in some models, while in patients with ICH the volume of the initial bleed was significant in some models., Conclusion: LOS after spontaneous brain hemorrhage is driven by medical complications even after the adoption of dedicated intensive care medical staff, pharmacist involvement, and evidence-based protocols for ICU care. Further alterations in care will be necessary to eliminate "preventable" complications and minimize LOS after brain hemorrhage.