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OBJECTIVE Airway obstruction after postoperative extubation is a dreaded but uncommon complication in patients undergoing circumferential cervical spine surgery (CCSS). The cuff leak test (CLT) has been utilized to assess air leak around the endotracheal tube which may reflect airway swelling. In this prospective observational study, we analyze the temporal evolution of CLT and perioperative factors that may influence it. METHODS Twenty patients undergoing single-stage CCSS were managed according to our extubation protocol. Patients were maintained intubated overnight following surgery. They were extubated if a CLT > 200 mL and both intensive care unit (ICU) and Neurosurgery teams agreed that it was safe. Patients extubated in the first postoperative day (8 of 20) comprised the early group, and the remaining patients (12 of 20) the delayed group. Patient and operative data were analyzed as a single group and comparing both groups. RESULTS The main indication for surgery was cervical deformity. Median number of levels fused was 5 anteriorly (range, 1-6) and 6 (range, 1-13) posteriorly. Patients were kept intubated for an average of 73.6 hours (range, 26-222 hours) and stayed in the ICU for 119.1 hours (range, 36-360 hours). There were 4 failed extubations and 3 patients (15%) required a tracheostomy. Patient profiles between both groups were very similar across most patient variables but differed significantly regarding infraglottic luminal area (p < 0.05). Patients with larger preoperative cuff leak values tended to have a shorter intubation period (p = 0.053). CONCLUSION This study objectively demonstrates the difficulties in airway management following CCSS and provides useful insight for preoperative planning and counseling. Local anatomic factors influence airway outcome more than operative factors. The study format does not allow for testing of interventions but we suggest that patients with favorable anatomy (larger infraglottic luminal area) may benefit from a less strict airway management protocol.

Inattentional blindness refers to when an individual fails to recognize an event or object due to their awareness being engaged in a different task and has been described in radiology. The purpose of this study is to determine whether the sensitivity of detecting diffusion-weighted imaging (DWI) lesions in spontaneous intracerebral hemorrhage (sICH) is reduced due to inattentional blindness.Using a prospective observational cohort, select sICH patients received an MRI scan within 72 h of admission. The scans were subject to an "official read" that occurred as part of the routine workflow. Separately, each scan underwent two "preliminary research reads" with task-specific instructions to detect DWI lesions. A "final research read" via three-party adjudication was used to calculate sensitivity and specificity for detecting these lesions. Board-certified neuroradiologists blinded to the clinical history of the patients reviewed all imaging.Amongst 121 sICH participants with research MRI scans, 49.6% (n = 60) scans were noted to have DWI lesion on their "final research read." The "official read" detected these DWI lesions with a sensitivity of 65% (95% CI, 52-77%). In contrast, the "preliminary research read" sensitivity for readers 1 and 2 was 98% (CI 95%, 91 to 100%) and 87% (CI 95%, 75 to 94%), respectively. Both were significantly different (p 0.05) from the sensitivity of the "official read."Given the increased sensitivity with task-specific instructions, our results suggest that inattentional blindness may be leading to the decreased detection of DWI lesions in patients with concomitant sICH.

Background Intracerebral hemorrhage has been associated with changes in various weather conditions. The primary aim of this study was to examine the collective influence of temperature, barometric pressure, and dew point temperature on the incidence of primary spontaneous intracerebral hemorrhage (sICH). Methods Between January 2013 and December 2016, patients with sICH due to hypertension or amyloid angiopathy with a known time of onset were identified prospectively. Meteorological variables 6 hours prior to time of onset were obtained from the National Oceanic Atmospheric Administration via two weather stations. Using a Monte-Carlo simulation, random populations of meteorological conditions in a 6-hour time window during the same years were generated. The actual meteorological conditions 6-hours prior to sICH were compared to those from the randomly generated populations. The false discovery rate method was used to identify significant meteorological variables. Results Time of onset was identified in 455 of 603 (75.5%) patients. Distribution curves for change in temperature, mean barometric pressure, and change in barometric pressure 6-hours prior to hemorrhage ictus were found to be significantly different from the random populations. (FDR approach P Conclusions We concluded that barometric pressure primarily influences the incidence of intracerebral hemorrhage. The association described in the literature between temperature and intracerebral hemorrhage is likely confounded by variations in barometric pressure.

Whether systolic blood pressure (SBP) is reliable in acute spontaneous intracerebral (sICH) by assessing agreement between simultaneous BP measurements obtained from cuff non-invasive blood pressure (NIBP) and radial arterial invasive blood pressure (AIBP) devices.Among 766 prospectively screened sICH subjects, 303 (39.5%) had NIBP and AIBP measurements. During the first 24 h, 2157 simultaneous paired measurement readings were abstracted. Paired NIBP/AIBP measurements were included in a Bland-Altman technique with 95% agreement limits and coefficients from regression analysis derived from a bootstrap procedure.Variance for SBP was 66.1 mmHg, which was larger than the 44.3 mg Hg for diastolic blood pressure (DBP) or the 46.1 mmHg for mean arterial pressure (MAP). Pairwise comparison of mean biases showed a significant difference between SBP when compared to DBP (p0.0001) or MAP (p0.0001). The mean bias between DBP and MAP was not different (p = 0.68). Regression-based Bland Altman analysis found significant bias (slope -0.16, 95% CI -0.23, -0.09, p0.05) over the range of mean SBP. Bias over the range of mean DBP or MAP was not significant.We concluded that SBP is an unreliable blood pressure measurement in patients with sICH.

Highlights There are limited data on pulse oximetry oxygen saturation (SpO2) targets in patients with COVID-19 respiratory failure Hyperoxia is common in critically ill patients and associated with worse outcomes Markers of systemic oxygen (O2) utilization suggest that hyperoxia occurs in this disease Adjusting SpO2 targets to systemic O2 utilization may limit hyperoxia Limiting hyperoxia in COVID-19 respiratory failure may improve outcomes, Background Management of hypoxemia in patients with severe COVID-19 respiratory failure is based on the guideline recommendations for specific SpO2 targets. However, limited data exist on systemic O2 utilization. The objective of this study was to examine systemic O2 utilization in a case series of patients with this disease. Patients and methods Between March 24, and April 9, 2020, 8 patients intubated for severe COVID-19 respiratory failure had near-simultaneous drawing of arterial blood gas (ABG), central venous blood gas (cVBG), and central venous oxygen saturation (ScvO2) at a mean of 6.1 days into hospitalization. Three patients were managed with indirect cardiac output (CO) monitoring by FloTrac sensor and Vigileo monitor (Edwards Lifesciences, Irvine, CA). The oxygen extraction index (OEI; SaO2-ScvO2/SaO2) and oxygen extraction fraction (OEF; CaO2-CvO2/CaO2 ≥ 100) were calculated. Values for hyperoxia (ScvO2 ≥ 90%), normoxia (ScvO2 71–89%), and hypoxia (ScvO2 ≤ 70%) were based on the literature. Mean values were calculated. Results The mean partial pressure of oxygen (PaO2) was 102 with a mean fraction of inspired O2 (FiO2) of 44%. One patient was hyperoxic with a reduced OEI (17%). Five patients were normoxic, but 2 had a reduced OEF (mean 15.9%). Two patients were hypoxic but had increased systemic O2 utilization based on OEF or OEI. Conclusion In select patients with severe COVID-19 respiratory failure, O2 delivery (DO2) was found to exceed O2 utilization. SpO2 targets based on systemic O2 utilization may help in reducing oxygen toxicity, especially in the absence of anaerobic metabolism. Further data are needed on the prevalence of systemic O2 utilization in COVID-19. How to cite this article Garg RK, Kimbrough T, Lodhi W, DaSilva I. Systemic Oxygen Utilization in Severe COVID-19 Respiratory Failure: A Case Series. Indian J Crit Care Med 2021;25(2):215–218.

Background: COVID-19 has been associated with increased risk of venous and arterial thromboembolism including ischemic stroke. We report on patients with acute ischemic stroke and concomitant COVID-19 in a diverse patient population. Methods: This is a retrospective analysis of patients hospitalized with acute ischemic stroke (AIS) and COVID-19 to our comprehensive stroke center in Chicago, IL, between March 1, 2020, and April 30, 2020. We reviewed stroke characteristics, etiologies, and composite outcomes. We then compared our cohort with historic patients with AIS without COVID-19 admitted in the same time frame in 2019 and 2020. Results: Out of 13 patients with AIS and COVID-19, Latinos and African-Americans compromised the majority of our cohort (76.8%), with age ranging from 31-80 years. Most strokes were cortical (84.6%) and more than 50% of patients had no identifiable source, and were categorized as embolic stroke of unknown source (ESUS). A trend toward less alteplase administration was noted in the COVID-19 stroke patients compared to the non-COVID group from 2020 and 2019 (7.1 vs. 20.7% p 0.435 and 7.1 vs. 27.2% p 0.178). Endovascular thrombectomy was performed in 3 (23%) patients. Systemic thrombotic complications occurred in 3 (23%) COVID-19 AIS patients. Median National Institutes of Health Stroke Scale and modified Rankin Scale at discharge were 11 (IQR 4-23) and 4 (IQR 3-4), respectively. In the logistic regression model corrected for age and sex, COVID-19 was associated with discharge to mRS > 2 (p 0.046, OR 3.82, CI 1.02-14.3). Eight patients (63.8%) were discharged home or to acute rehabilitation, and two deceased from COVID-19 complications. Conclusion: AIS in the setting of COVID-19 is associated with worse outcomes, especially among African-American and Latino populations. Large vessel disease with ESUS was common suggesting an increased risk of coagulopathy and endothelial dysfunction as a potential etiology.

Objective To report neurological manifestations seen in patients hospitalized with Coronavirus disease 2019 (COVID-19) from a large academic medical center in Chicago, Illinois. Methods We retrospectively reviewed data records of 50 patients with COVID-19 who were evaluated by the neurology services from March 1, 2020 - April 30, 2020. Patients were categorized into 2 groups based on timing of developing neurological manifestations: the “Neuro first” group had neurological manifestations upon initial assessment, and the “COVID first” group developed neurological symptoms greater than 24 h after hospitalization. The demographics, comorbidities, disease severity and neurological symptoms and diagnoses of both groups were analyzed. Statistical analysis was performed to compare the two groups. Results A total of 50 patients (48% African American and 24% Latino) were included in the analysis. Most common neurological manifestations observed were encephalopathy (n = 30), cerebrovascular disease (n = 20), cognitive impairment (n = 13), seizures (n = 13), hypoxic brain injury (n = 7), dysgeusia (n = 5), and extraocular movement abnormalities (n = 5). The “COVID-19 first” group had more evidence of physiologic disturbances on arrival with a more severe/critical disease course (83.3% vs 53.8%, p 0.025). Conclusion Neurologic manifestations of COVID-19 are highly variable and can occur prior to the diagnosis of or as a complication of the viral infection. Despite similar baseline comorbidities and demographics, the COVID-19 patients who developed neurologic symptoms later in hospitalization had more severe disease courses. Differently from previous studies, we noted a high percentage of African American and Latino individuals in both groups.

Rapidly progressive primary angiitis of the CNS (PACNS) is recognized as a clinical subtype of PACNS that is almost uniformly fatal. PACNS is usually characterized by subacute progression over several months. The most common symptoms are headaches and cognitive dysfunction, followed by focal neurologic deficits.1 Compared with this more indolent presentation, patients with rapidly progressive PACNS are more likely to present in coma with quadriparesis and MR imaging notable for bilateral infarcts.2 Various treatment combinations including high-dose corticosteroids, cyclophosphamide, azathioprine, methotrexate, rituximab, and plasma exchange have been described1,3; however, no good outcomes have been reported to date. The largest case series of 11 patients had only 1 survivor who at 14 months had a modified Rankin Scale (mRS) of 5 (bedridden, requiring constant nursing care).2 One other survivor of rapidly progressive PACNS had an mRS of 5 at the 3-month follow-up.4 We describe the treatment and outcome of a patient with rapidly progressive PACNS who returned to his premorbid baseline with an mRS of 0.

BACKGROUND/OBJECTIVE: Diffusion weighted imaging (DWI) lesions have been well described in patients with acute spontaneous intracerebral hemorrhage (sICH). However, there are limited data on the influence of these lesions on sICH functional outcomes. We conducted a prospective observational cohort study with blinded imaging and outcomes assessment to determine the influence of DWI lesions on long-term outcomes in patients with acute sICH. We hypothesized that DWI lesions are associated with worse modified Rankin Scale (mRS) at 3 months after hospital discharge. METHODS: Consecutive sICH patients meeting study criteria were consented for an magnetic resonance imaging (MRI) scan of the brain and evaluated for remote DWI lesions by neuroradiologists blinded to the patients’ hospital course. Blinded mRS outcomes were obtained at 3 months. Logistic regression was used to determine significant factors (p < 0.05) associated with worse functional outcomes defined as an mRS of 4–6. The generalized estimating equation (GEE) approach was used to investigate the effect of DWI lesions on dichotomized mRS (0–3 vs 4–6) longitudinally. RESULTS: DWI lesions were found in 60 of 121 patients (49.6%). The presence of a DWI lesion was associated with increased odds for an mRS of 4–6 at 3 months (OR 5.987, 95% CI 1.409–25.435, p = 0.015) in logistic regression. Using the GEE model, patients with a DWI lesion were less likely to recover over time between 14 days/discharge and 3 months (p = 0.005). CONCLUSIONS: DWI lesions are common in primary sICH, occurring in almost half of our cohort. Our data suggest that DWI lesions are associated with worse mRS at 3 months in good grade sICH and are predictive of impaired recovery after hospital discharge. Further research into the pathophysiologic mechanisms underlying DWI lesions may lead to novel treatment options that may improve outcomes associated with this devastating disease.

Nontraumatic convexity subarachnoid hemorrhage (cSAH) is a nonaneurysmal variant that is associated with diverse etiologies.With IRB approval, we retrospectively reviewed consecutive nontraumatic cSAH from July 1, 2006 to July 1, 2016. Data were abstracted on demographics, medical history, neuroimaging, etiology, and clinical presentation.We identified 94 cases of cSAH. The cases were classified according to the following etiologies: reversible cerebral vasoconstriction syndrome (RCVS) 17 (18%), cerebral amyloid angiopathy (CAA) 15 (16%), posterior reversible encephalopathy syndrome 16 (17%), cerebral venous thrombosis 10 (11%), large artery occlusion 7 (7%), endocarditis 6 (6%), and cryptogenic 25 (27%). Early rebleeding occurred in 9 (10%) patients. Time from initial imaging to CT rebleeding was 40 hours (range, 5-74). CAA was associated with the highest mean age at 75.8 and RCVS the lowest at 47.6 years (P.0001). Among patients with RCVS, initial vascular imaging was negative in 6 (35%), and repeat imaging documented vasoconstriction at a mean delay of 5 days (range, 3-16).There were significant differences among the subgroups in cSAH, with CAA presenting as older men with transient neurological deficits, and RCVS presenting as younger women with thunderclap headache. Rebleeding was seen in 10% of cSAH patients. One-third of RCVS patients with cSAH required repeat vascular imaging to diagnose vasoconstriction.

Objectives Higher glycemia on admission has been associated with diffusion weighted imaging (DWI) lesions in patients with spontaneous intracerebral hemorrhage (sICH). However, the influence of longitudinal glycemia after admission and during a patient's hospitalization on DWI lesions in sICH has not been studied. Our aim was to compare longitudinal glycemia in sICH patients with and without DWI lesions. Material and Methods Glycemia measurements were abstracted on participants enrolled in a prospective observational study examining predictors for DWI lesions in sICH. Univariate analysis was used to compare mean longitudinal glycemia in sICH patients with and without DWI lesions. Logistical regression was used to determine whether mean longitudinal glycemia was predictive of DWI lesions. Results DWI lesions were found in 60 of the 121 (49.6%) participants. Mean time-to-MRI was 99.6 h (SD ± 89). During this time interval, 2,101 glucose measurements were analyzed with a median number of 7 (IQR 12, 1-261) measurements per patient. Mean longitudinal glycemia was higher in the DWI positive group compared to the DWI negative group until time-to-MRI (132 mg/dL vs 122 mg/dL, p = 0.03). Mean longitudinal glycemia was found to be predictive of DWI lesions (OR 1.02, 95% CI 1.005 to 1.035, p = 0.011). Conclusions Mean longitudinal glycemia was higher in sICH patients with DWI lesions compared to those without DWI lesions. Future research into the association between higher glycemia and DWI lesions in sICH may provide insight into a pathophysiologic mechanism.

INTRODUCTION: Hypoxemia is a cardinal sign of patients with severe COVID-19 respiratory failure Current guidelines recommend an SpO2 of 92-96% to ensure adequate oxygenation and prevent anaerobic metabolism However, hyperoxia is associated with cellular toxicity and worse outcomes in critically ill patients The aim of this study was to examine the prevalence of hyperoxia and determine oxygenation utilization in a cohort of patients with severe COVID-19 respiratory failure METHODS: Between March 24 to April 9, 2020, 8 patients intubated for severe COVID-19 respiratory failure had nearsimultaneous drawings of arterial blood gas, central venous blood gas, central venous O2 (ScvO2) and arterial lactate levels at a mean of 6 1 days into their hospitalization Three patients were managed with the FloTrac sensor and Vigileo monitor (Edwards Lifesciences, Irvine, CA) to measure indirect cardiac output and determine the oxygen extraction fraction (OEF;CaO2-CvO2/CaO2 x 100) Also, the oxygen extraction index (OEI;SaO2-ScvO2/SaO2) and delta pCO2 (PcvO2-PaCO2) were calculated Hyperoxia was defined as a ScvO2 > 90% based on the literature Mean values were calculated for the results RESULTS: The mean age of the cohort was 55 3 years, 63% were men, and 50% were Hispanic The mean SaO2 was 96% and PaO2 was 102 mm Hg None of the patients had evidence of anaerobic metabolism as assessed by arterial lactate levels (mean=1 2 mmol/dL) or delta pCO2 (mean=1 1 mm Hg) Although the mean ScvO2 was 71 8%, 1 patient had evidence of hyperoxia Two patients had relative hyperoxia as evidenced by reduced OEI (mean 14 4%) and reduced OEF (15 9%) CONCLUSIONS: Our results suggest that a subset of patients with severe COVID-19 respiratory failure are at risk for hyperoxia based on ScvO2 Furthermore, a larger proportion of patients may have relative hyperoxia based on O2 utilization indexes Further prospective data are needed on the prevalence of hyperoxia in severe COVID-19 respiratory failure This may influence oxygenation targets and outcomes in patients with this deadly disease

Introduction Apnea testing remains essential for the clinical evaluation of brain death determination. In patients who test positive for SARS-CoV-2, disconnecting the patient from the ventilator and introducing high flow oxygen into the endotracheal tube increases the risk for aerosolization of airway secretions and exposure of the examiner. Methods Case report of a patient with an intracerebral hemorrhage that evolved to significant cerebral edema and herniation, who underwent apnea test using a method involving a t-piece and an HME filter. Results Patient successfully pronounced brain dead using a safe method to minimize exposure to SARS-CoV-2. Conclusion At a time where healthcare workers are at high risk of exposure to COVID-19, the above described method is a safe process for apnea testing in declaration of brain death.

There is a paucity of outcomes data in patients over 80 years presenting with intracerebral hemorrhage (ICH). The primary aim of our study is to describe outcomes in this patient population.Retrospective study of patients admitted with primary ICH from January 2012 to July 2018. Data were obtained from the Rush University Get With The Guidelines database; only patients 80 or above were included.A total of 1713 patients were screened and 220 patients met inclusion criteria. About 68.2% were female and mean age was 85.6 years old. Median ICH score on admission was 2 (IQR 1-3). Location of ICH included: deep (48.2%), lobar (40%), and cerebellum (9.5%). ICH etiologies included hypertensive (51.8%), cerebral amyloid angiopathy (26.8%), coagulopathy (5.9%), and the remaining were undetermined. CT angiograms were performed in 34.5% (n = 76) of patients; of these patients one arteriovenous malformation was identified. Patients underwent the following procedures: external ventricular drains (8.6%), decompression (3.6%), and ventriculoperitoneal shunts (1.8%). Tracheostomy and percutaneous gastrostomy placement were performed in 8.2%. About 4.5% had seizures and 1.5% were treated for status epilepticus. Disposition at hospital discharge included: subacute nursing facility ([SNF] 24.1%), acute rehabilitation (23.2%), hospice (18.2%), death (18.2%), home (11.8%), long-term acute care facility ([LTAC] 3.6%), and unknown (1%). Patients with an ICH score ≥2 on admission had a roughly 6 times higher chance of experiencing an unfavorable outcome (LTAC, SNF, or death), when compared to patients with lower ICH score.This study shows that a significant proportion (35%) of ICH patients ≥80 years old have a good outcome, with discharge to home or to rehabilitation. Our data suggest that older patients with ICH presenting with supratentorial hemorrhages (volume30 cc) without intraventricular extension can have good outcomes despite their age.

To investigate magnetic resonance imaging (MRI) detection of cerebral infarction (CI) in patients presenting with subarachnoid hemorrhage (SAH). CI is a well-known complication of SAH that is typically detected on computed tomography (CT). MRI has improved sensitivity for acute CI over CT, particularly with multiple, small, or asymptomatic lesions. With IRB approval, 400 consecutive SAH patients admitted to our institution from August 2006 to March 2011 were retrospectively reviewed. Traumatic SAH and secondary SAH were excluded. Data were collected on demographics, cause of SAH, Hunt Hess and World Federation of Neurosurgical Societies grades, and neuroimaging results. MRIs were categorized by CI pattern as single cortical (SC), single deep (SD), multiple cortical (MC), multiple deep (MD), and multiple cortical and deep (MCD). Among 123 (30.8 %) SAH patients who underwent MRIs during their hospitalization, 64 (52 %) demonstrated acute CI. The mean time from hospital admission to MRI was 5.7 days (range 0–29 days). Among the 64 patients with MRI infarcts, MRI CI pattern was as follows: MC in 20 (31 %), MCD in 18 (28 %), SC in 16 (25 %), SD in 3 (5 %), MD in 2 (3 %), and 5 (8 %) did not have images available for review. Most infarcts detected on MRI (39/64 or 61 %) were not visible on CT. The use of MRI increases the detection of CI in SAH. Unlike CT studies, MRI-detected CI in SAH tends to involve multiple vascular territories. Studies that rely on CT may underestimate the burden of CI after SAH.

Introduction: Re-bleeding can have significant adverse consequences, but has not been well described in isolated nontraumatic convexity subarachnoid hemorrhage (cSAH), and therefore we sought to report the clinical spectrum of re-bleed in this population. Methods: With IRB approval, we retrospectively reviewed consecutive nontraumatic cSAH admitted to our institution from August 1, 2006 to June 1, 2016. cSAH was defined as radiographic hemorrhage isolated to the convexities, without cisternal component. Trauma was excluded. Data was abstracted on demographics, medical history, neuroimaging, etiology, and clinical presentation. Good clinical outcome was defined as modified rankin score of 0-2 at 3 months. Results: Among 93 cSAH patients, re-bleed occurred in 9 (10%) patients. The mean age of patients with re-bleed was 55.6 years (range, 24-68) and 8 (89%) were women. The majority 6 (67%) were Hispanic. Most patients 8 (89%) presented with severe headache. The etiology of cSAH was reversible cerebral vasoconstriction syndrome (RCVS) in 6 (67%), amyloid angiopathy in 1 (11%), cerebral venous thrombosis (CVT) in 1 (11%), and post-procedural related in 1 (11%). Initial re-bleeding was new remote subarachnoid hemorrhage in 1 (11%) and new intracerebral hemorrhage in 8 (89%). Clinical symptoms of initial re-bleeding included isolated worsening headache in 2 (22%), focal neurological deficits in 4 (44%), and no clinical change in 3 (33%). Time from initial neuroimaging documenting cSAH to CT documenting re-bleed was 40 hours (range, 5 - 74), and re-bleed occurred within 60 hrs in most patients (89%). Two patients had subsequent re-bleeding (due to CVT and RCVS) documented at 1.9 and 11.8 hours after the initial re-bleed CT. Good clinical outcome was seen in 7 (78%) . Conclusion: Re-bleeding was seen in 10% of cSAH patients and in the majority of patients occurred early, within 2.5 days. Clinicians should be aware of this potential complication of cSAH.

Introduction: Although alterations in fibrinogen and fibrinogen degradation products are well-established after intravenous tissue plasminogen activator (IVtPA) in acute stroke, IVtPA is not recognized to cause markedly abnormal international normalized ratio (INR). Methods: With IRB approval, we prospectively screened 99 consecutive acute stroke patients who received IVtPA admitted from November 1, 2015 to July 1, 2016. Laboratory tests including INR, activated partial thromboplastin time (aPTT), fibrinogen, and d-Dimer were drawn at intervals of 6, 12, 24, and 48 hours. Data was collected on patient demographics, last known normal (LKN), IVtpA dose and timing, and National Institutes of Health Stroke Scale (NIHSS). Post-IVtPA coagulopathy was defined as INR ≥ 1.5. Reference range for fibrinogen was 190 - 395 mg/dL. Results: Among 44 patients prospectively enrolled, the mean age was 66.5 years (range, 32 to 91). Mean time from LKN to IVtPA administration was 2.6 hours (range 0.07 to 10.8). Initial pre-IVTPA mean NIHSS was 14 (range, 3 to 26) and 24 hour mean NIHSS was 7.4, (range 0 to 30). Mean pre-IVtPA INR was 1.05 (range, 0.9 to 1.4). Mean peak post-IVtPA INR was 1.28 (range 1.01 to 3.08). Mean deviation of actual to ideal IVtPA dose was 1.02 mg (range, 22.9 to 14.4). Post IVtPA coagulopathy occurred in 6 patients (14%), with peak INR noted at a mean of 13 hours after IVtPA administration (range, 5.6 to 18.6). Five patients of the six (83%) with post IVtPA coagulopathy had low fibrinogen, and mean fibrinogen nadir was 97 mg/dL (range, 37 to 242). Post-IVtPA coagulopathy was not significantly associated with initial NIHSS, 24 hour NIHSS, LKN to IVtPA time, or deviation of actual IVtPA dose from ideal dose. Conclusion: Post-IVtpA coagulopathy occurs in 14% of patients when studied prospectively and is associated with hypofibrinogenemia, but does not appear to correlate with severity of stroke or IVtPA dosing/timing.

Introduction: Intravenous tissue plasminogen activator (IVtPA) is a proven treatment in acute ischemic stroke but relies on weight-based dosing in a time sensitive manner. Errors in body weight estimation are common and may result in over or under-dosing of IVtPA. Methods: With IRB approval, we prospectively screened 99 consecutive patients who received IVtPA for suspected acute ischemic stroke from November 1, 2015 to July 1, 2016 as part of a prospective IVtPA study. Patients were included in this analysis who had complete data. Data was collected on patient demographics, National Institutes of Health Stroke Scale (NIHSS), body weight, and times of last known normal (LKN) and IVtPA administration. A significant error in IVtPA dosing was defined as a >10% difference in actual versus calculated IVtPA dose. Results: Among 42 patients prospectively enrolled, the mean age was 65.8 years (range, 32 to 89) and 30 (79%) of patients were transfers from outside Emergency Rooms. Mean time from LKN to IVtPA administration was 2.4 hours (range. 0.7 to 4.8). Initial pre-IVtPA mean NIHSS was 14 (range, 3 to 26). The mean % error in IVtPA dose was +1.9% (range, -29% to + 21%). Ten patients (24%) had a significant error in IVtPA dosing of > 10% of the dose, and 8 (80%) were over-doses. Patients with significant IVtPA dosing error did not differ in terms of age (65.8 vs 65.8, p 0.99), sex (female 55.6% vs 38.9%, p 0.45), race (white 70% vs 47%, p 0.28), height (164.8 vs 171.0 cm, p 0.1), or time from LKN to IVtPA (2.8 vs 2.3, p 0.15). Patients with significant IVtPA dosing errors had significantly lower baseline weight (70.3 vs 90.0 kilograms, p 0.029) and higher NIHSS (18.7 vs 12.6, p 0.018). Conclusion: Dosing errors of > 10% of the calculated IVtPA dose occur in nearly one-quarter of acute stroke patients treated in the community, and patients with lower weight and higher NIHSS were at higher risk of dosing errors.

Background and Purpose— Decreased diffusion (DD) consistent with acute ischemia may be detected on MRI after acute intracerebral hemorrhage (ICH), but its risk factors and impact on functional outcomes are not well-defined. We tested the hypotheses that DD after ICH is related to acute blood pressure (BP) reduction and lower hemoglobin and presages worse functional outcomes. Methods— Patients who underwent MRI were prospectively evaluated for DD by certified neuroradiologists blinded to outcomes. Hemoglobin and BP data were obtained via electronic queries. Outcomes were obtained at 14 days and 3 months with the modified Rankin Scale, a functional scale scored from 0 (no symptoms) to 6 (dead). We used logistic regression for dependence or death (modified Rankin Scale score 4–6). Results— DD distinct from the hematoma was found on MRI in 39 of 95 patients (41%). DD was associated with greater BP reductions from baseline and a higher risk of dependence or death at 3 months (odds ratio, 4.8; 95% confidence interval, 1.7–13.9; P =0.004) after correction for ICH score (1.8 per point; 95% confidence interval, 1.2–3.1; P =0.01). Lower hemoglobin was associated with worse ICH score, larger hematoma volume, and worse outcomes, but not DD. Conclusions— DD is common after ICH, associated with greater acute BP reductions, and associated with disability and death at 3 months in multivariate analysis. The potential benefits of acute BP reduction to reduce hematoma growth may be limited by DD. The prevention and treatment of cerebral ischemia manifested as DD are potential methods to improve outcomes.

The maintenance of sinus rhythm in patients with Atrial Fibrillation (AF) is difficult and is complicated by adverse drug reactions of antiarrhythmic drugs or the adverse events related with ablation procedures. Amiodarone can be used for preventing AF recurrence; but it has the risk of serious toxicities secondary to its iodinated nature. Dronedarone, an amiodarone analogue without iodine, has been shown to decrease the frequency of AF recurrence and to provide heart rate control during AF recurrence. Dronedarone is a benzofuran derivative; specifically N-[2-Butyl-3-[4-[3-(dibutylamino)propoxy]benzoyl]-5-benzofuranyl]methane-sulfonamide and its production process has been patented. In the ATHENA trial, dronedarone therapy was associated with a significant reduction in the combined primary endpoint of death from any cause or hospitalization due to cardiovascular causes. However, dronedarone has been noted to increase cardiovascular mortality among patients with advanced congestive heart failure (NYHA class III and IV). On March 18, 2009, the Cardiovascular and Renal Drugs Advisory Committee of the Food and Drug Administration (FDA) approved dronedarone for an indication of atrial fibrillation suppression, with a warning against its use in patients with NYHA class III and IV heart failure or recently decompensated heart failure.

Background and Purpose— There are few data on the effectiveness and side effects of antiepileptic drug therapy after intracerebral hemorrhage. We tested the hypothesis that antiepileptic drug use is associated with more complications and worse outcome after intracerebral hemorrhage. Methods— We prospectively enrolled 98 patients with intracerebral hemorrhage and recorded antiepileptic drug use as either prophylactic or therapeutic along with clinical characteristics. Antiepileptic drug administration and free phenytoin serum levels were retrieved from the electronic medical records. Patients with depressed mental status underwent continuous electroencephalographic monitoring. Outcomes were measured with the National Institutes of Health Stroke Scale and modified Rankin Scale at 14 days or discharge and the modified Rankin Scale at 28 days and 3 months. We constructed logistic regression models for poor outcome at 3 months with a forward conditional model. Results— Seven (7%) patients had a clinical seizure, 5 on the day of intracerebral hemorrhage. Phenytoin was associated with more fever ( P =0.03), worse National Institutes of Health Stroke Scale at 14 days (23 [9 to 42] versus 11 [4 to 23], P =0.003), and worse modified Rankin Scale at 14 days, 28 days, and 3 months. In a forward conditional logistic regression model, phenytoin prophylaxis was associated with an increased risk of poor outcome (OR, 9.8; 1.4 to 68.6; P =0.02), entering after admission National Institutes of Health Stroke Scale and age. Excluding patients with a seizure did not change the results. Levetiracetam was not associated with demographics, seizures, complications, or outcomes. Conclusions— Phenytoin was associated with more fever and worse outcomes after intracerebral hemorrhage.

The treatment of non-Newtonian fluids in tubular reactors is frequently encountered in industries, which may be studied by mathematical modeling. The modeling of endothermic reactions of non-Newtonian fluids in tubular reactors with radial dispersion has been done for Ostwald-de-Waele power law fluids. The coupled mass balance, heat balance and velocity equations have been dealt with. The model is solved using finite difference numerical methods. The effect of variation in the dimensionless parameters of the model has also been studied. In addition, the rheological parameter n also affects the reactor performance as well as the velocity profile. An increase in n leads to higher velocity distortion and a decrease in conversion and temperature.

Background and Purpose— The purpose of this study was to investigate time delays, adherence to guidelines, and their impact on outcomes in patients with warfarin-associated intracerebral hemorrhage transferred from community emergency departments to a comprehensive stroke center. Methods— We collected demographic, clinical, transfer time, treatment, and outcome data for patients transferred to our institution with warfarin-associated intracerebral hemorrhage from community emergency departments. Results— Among 928 patients with intracerebral hemorrhage, 56 (6%) with warfarin-associated intracerebral hemorrhage (median international normalized ratio, 2.55) were transferred to the comprehensive stroke center. Twenty patients received no acute reversal therapy before transfer, only 4 of whom had international normalized ratios ≤1.4 in the community emergency department. Median time of emergency department stay was 3.66 hours and median time to initiation of acute reversal therapy was 4.48 hours. Those who received ≥3 U of fresh–frozen plasma or recombinant activated Factor VIIa (11 patients) before transfer had lower repeat international normalized ratios and better discharge dispositions than those treated less aggressively. Conclusions— Treatment of warfarin-associated intracerebral hemorrhage in community emergency departments is often suboptimal and does not adhere to published guidelines. Treating coagulopathy aggressively before interhospital transfer may improve outcomes and warrants further investigation.

The intracerebral hemorrhage (ICH) score is a simple grading scale that can be used to stratify risk of 30 day mortality in ICH patients. A similar risk stratification scale for subarachnoid hemorrhage (SAH) is lacking. We sought to develop a risk stratification mortality score for SAH. With approval from the Institutional Review Board, we retrospectively reviewed 400 consecutive SAH patients admitted to our institution from August 1, 2006 to March 1, 2011. The SAH score was developed from a multivariable logistic regression model which was validated with bootstrap method. A separate cohort of 302 SAH patients was used for evaluation of the score. Among 400 patients with SAH, the mean age was 56.9 ± 13.9 years (range, 21.5–96.2). Among the 366 patients with known causes of SAH, 292 (79.8 %) of patients had aneurysmal SAH, 65 (17.8 %) were angiogram negative, and 9 (2 %) were other vascular causes. The overall in-hospital mortality rate was 20 %. In multivariable analysis, the variables independently associated with the in-hospital mortality were Hunt and Hess score (HH) (p

Conventional hemodialysis and hemoperfusion have been used for life-threatening phenobarbital poisoning. We report the successful use of continuous renal replacement therapy in a case of severe phenobarbital poisoning associated with severe coma and hypotension. Use of this modality led to clearance of phenobarbital with improvement in the clinical status of the patient.

Although cardiac abnormalities are well described among patients with acute brain injury, they have not been investigated systematically for acute subdural hemorrhage (SDH). We sought to investigate the prevalence and characteristics of cardiac abnormalities in patients with SDH.Consecutive adult patients admitted to Rush University Neurosciences Intensive Care Unit with a diagnosis of SDH were analyzed. Electrocardiograms (ECGs), obtained within 48 h of admission were reviewed. Myocardial injury, defined as troponin I elevation (0.09 ng/ml) on admission was identified.One hundred and fourteen patients admitted with SDH between 1 January 2010 and 31 December 2011 were included. Mean age was 67.9 years (SD 16.6 years), 60% were male. Comorbidities included hypertension (74%), diabetes mellitus (31%), cardiovascular disease (35%), and cerebrovascular disease (25%). The SDH was right-sided in 47%, and the most common location was frontoparietal (43%). SDH size was 14.4 ± 7.9 mm, with 4.6 ± 5.5 mm midline shift. One or more ECG abnormalities were found in 75% of patients. Troponin was elevated in nine patients. Cardiac abnormalities were not associated with SDH characteristics. Classic neurogenic ECG findings were not encountered.Although we found ECG abnormalities to be common in patients with SDH, they were not associated with SDH characteristics, and classic neurogenic findings were not observed. Myocardial injury was infrequent and not associated with SDH characteristics. While cardiac abnormalities in acute intracerebral injury often are attributed to neurocardiogenic causes, these are unlikely prominent mechanisms in SDH. Other medical causes need to be considered, as this will have important implications for management.

Background: The International Cooperative Study on the Timing of Aneurysm Surgery suggested that delayed cerebral vasospasm is a significant contributor to mortality (at 6 months) after subarachnoid hemorrhage (SAH). However, the Cincinnati population based study did not find cerebral vasospasm to be a significant contributor to short-term mortality. Methods: We reviewed 350 consecutive non-traumatic SAH patients who were hospitalized at our institution from August 1, 2006 to June 30, 2010. Data were collected on demographics, Hunt and Hess grade, presence of cerebral infarct, symptomatic vasospasm, and in-hospital mortality. Symptomatic vasospasm was defined as cerebral vasospasm that required intra-arterial therapy (pharmacologic vasodilators or angioplasty). Cerebral infarct was defined as any new radiographic infarct seen on CT or MRI (of any cause). Results: Among 350 patients with non-traumatic SAH, the mean age was 56.7 years (range, 21.5 to 89.1) and 68% were aneurysmal. The overall in-hospital mortality rate was 20.2% (71 patients). The causes of in-hospital mortality were withdrawal of support in 53 (75%), brain death in 14 (20%), and cardiopulmonary death in 4 (8%). The mean time to death was 8.1 (range 0 to 31) days, with 36% of deaths occurring within the first 2 days of hospitalization. Among patients with symptomatic cerebral vasospasm or cerebral infarct , 19% (26/139) died. In univariate and multivariate analyses, symptomatic cerebral vasospasm and cerebral infarct were not associated with in-hospital mortality. When the analysis was restricted to patients with aneurysmal SAH, cerebral vasospasm and cerebral infarct were still not predictive of in-hospital mortality. In multivariable analysis, the variables most associated with in-hospital mortality were Hunt and Hess score (HH) (p Conclusions: In-hospital mortality after SAH is associated with initial severity of hemorrhage, rebleeding, and age. Symptomatic cerebral vasospasm and cerebral infarct were not significant contributors of overall in-hospital mortality, and approximately one-third of in-hospital mortality after SAH occurs within the first 2 days of hospitalization. By design, studies that exclude patients with severe SAH tend to over-estimate the contribution of cerebral vasospasm on short-term mortality.

In patients with subarachnoid hemorrhage (SAH), higher hemoglobin (HGB) has been associated with better outcomes, but packed red blood cell (PRBC) transfusions with worse outcomes. We performed a prospective pilot trial of goal HGB after SAH.Forty-four patients with SAH and high risk for vasospasm were randomized to goal HGB concentration of at least 10 or 11.5 g/dl. We obtained blinded clinical outcomes at 14 days (NIH Stroke Scale and modified Rankin Scale, mRS), 28 days (mRS), and 3 months (mRS), and blinded interpretation of brain MRI for cerebral infarction at 14 days. This trial is registered at www.stroketrials.org.Forty-four patients were randomized. Patients with goal HGB 11.5 g/dl received more PRBC units per transfusion [1 (1-2) vs. 1 (1-1), P0.001] and more total PRBC units [3 (2-4) vs. 2 (1-3), P = 0.045]. Prospectively defined safety endpoints were not different between groups. HGB concentration was different between study groups from day 4 onwards. The number of cerebral infarctions on MRI (6 of 20 vs. 9 of 22), NIH Stroke Scale scores at 14 days [1 (0-9.75) vs. 2 (0-16)], and rates of independence on the mRS at 14 days (65% vs. 44%) and 28 days (80% vs. 67%) were similar, but favored higher goal HGB (P0.1 for all).Higher goal hemoglobin in patients with SAH seems to be safe and feasible. A phase III trial of goal HGB after SAH is warranted.

Many ICUs have implemented protocols for tight glucose control, but there are few data on hypoglycemia and neurologic outcomes in patients with subarachnoid hemorrhage (SAH).We prospectively ascertained 172 patients with SAH, who were treated according to a standard protocol for target glucose 80-110 mg/dl. Outcomes were assessed with the modified Rankin scale (mRS) at 14 days, 28 days, and 3 months.Worse neurologic injury at admission (P0.001) and a history of diabetes (P = 0.002) were associated with increased glucose variance. There was lower nadir glucose in patients with radiographic cerebral infarction (81 +/- 15 vs. 87 +/- 16 mg/dl, P = 0.02), symptomatic vasospasm (78 +/- 12 vs. 84 +/- 16 mg/dl, P = 0.04) and angiographic vasospasm (79 +/- 14 vs. 86 +/- 16 mg/dl, P = 0.01), but maximum and mean glucose values were not different. Glucose80 mg/dl was earlier and more frequent in patients with worse functional outcome at 3 months (P0.001). Progressive reductions in nadir glucose were associated with increasing functional disability at 3 months (P = 0.001) after accounting for neurologic grade and mean glucose. Severe hypoglycemia (40 mg/dl) occurred in one patient.In patients with SAH, nadir glucose80 mg/dl is associated with cerebral infarction, vasospasm, and worse functional outcomes in multivariate models. Protocols for target glucose 80-110 mg/dl effectively control hyperglycemia, but may place patients with SAH at risk for vasospasm, cerebral infarction, and poor outcome even when severe hypoglycemia does not occur.

OBJECTIVE: Intraventricular hemorrhage (IVH) is a serious complication of intracerebral hemorrhage (ICH). We hypothesized that antiplatelet medication use and platelet activity would be associated with more IVH. METHODS: We prospectively identified patients with spontaneous ICH and measured platelet activity on admission with the VerifyNow-Aspirin assay (Accumetrics, San Diego, CA). IVH volume was quantified with the Graeb scale, divided into categories of 0 (no IVH), 1 to 2 (minimal IVH), 3 to 5 (moderate IVH), and 6 and above (severe IVH). Antiplatelet medications were prospectively recorded. We used ordinal regression to measure the effect of platelet activity after correcting for ICH location and ICH volume. Outcomes were measured at 14 days or discharge with the National Institutes of Health Stroke Scale and modified Rankin Scale (mRS) and at 28 days and 3 months with the mRS. RESULTS: In our cohort of 73 patients, 36 had no IVH, 11 had minimal IVH, 10 had moderate IVH, and 16 had severe IVH. Aspirin and clopidogrel (P = 0.03 for both) were associated with less platelet activity. More IVH was related to reduced platelet activity (P = 0.01) after correction for ICH volume and location without contribution from aspirin or clopidogrel use. IVH was associated with worse National Institutes of Health Stroke Scale score (P = 0.002) and mRS score (P = 0.001) at 14 days and with mRS scores at 28 days (P = 0.02) and 3 months (P = 0.008). CONCLUSION: Reduced platelet activity was related to more IVH as a complication of ICH. The relationship of platelet activity to IVH deserves further study.

The maintenance of sinus rhythm in patients with Atrial Fibrillation (AF) is difficult and is complicated by adverse drug reactions of antiarrhythmic drugs or the adverse events related with ablation procedures. Amiodarone can be used for preventing AF recurrence; but it has the risk of serious toxicities secondary to its iodinated nature. Dronedarone, an amiodarone analogue without iodine, has been shown to decrease the frequency of AF recurrence and to provide heart rate control during AF recurrence. Dronedarone is a benzofuran derivative; specifically N-[2-Butyl-3-[4-[3-(dibutylamino)propoxy]benzoyl]-5-benzofuranyl]methane-sulfonamide and its production process has been patented. In the ATHENA trial, dronedarone therapy was associated with a significant reduction in the combined primary endpoint of death from any cause or hospitalization due to cardiovascular causes. However, dronedarone has been noted to increase cardiovascular mortality among patients with advanced congestive heart failure (NYHA class III and IV). On March 18, 2009, the Cardiovascular and Renal Drugs Advisory Committee of the Food and Drug Administration (FDA) approved dronedarone for an indication of atrial fibrillation suppression, with a warning against its use in patients with NYHA class III and IV heart failure or recently decompensated heart failure.

Background and Purpose— Antiplatelet medication use and reduced platelet activity may be associated with mortality after intracerebral hemorrhage (ICH). We tested the hypothesis that reduced platelet activity is associated with early ICH clot growth and worse outcomes. Methods— We prospectively identified patients with spontaneous ICH, measured platelet activity (VerifyNow-ASA, Accumetrics) on admission, and recorded antiplatelet medication use. ICH volume was calculated using computerized volumetric analysis. Data were analyzed with nonparametric statistics and repeated measures ANOVA as appropriate. Patients were prospectively followed for functional outcomes. Data are presented as mean±SD or median [Q1 to Q3]. Results— Reduced platelet activity (≤550 aspirin reaction units [ARU]) was associated with increased ICH volume growth ( P P =0.001), but without impact on outcomes. Reduced platelet activity was associated with worse modified Rankin Scores at 3 months ( P =0.02). Conclusions— Reduced platelet activity was associated with early ICH volume growth and worse functional outcome. Because platelet activity can be increased with platelet transfusion, increasing platelet activity is a potential method to reduce ICH volume growth and improve functional outcomes.

There are few predictors of acute lung injury (ALI) or the acute respiratory distress syndrome (ARDS) after subarachnoid hemorrhage (SAH). We hypothesized that cardiac troponin I, which is associated with cardiovascular morbidity, would also predict ALI. We prospectively enrolled 171 consecutive patients with SAH. Troponin was routinely measured on admission and the next day and subsequently if abnormal. We prospectively recorded the maximum troponin, in-hospital events, and clinical endpoints. ALI and ARDS were defined by standard criteria. Acute lung injury was found in 10 patients (6%), ARDS in an additional 14 (8%), and pulmonary edema without lung injury in 9 (5%). Maximum troponin was different in patients without lung injury or pulmonary edema (0.03 [0.02–0.12] mcg/l), ALI (0.17 [0.04–1.4]), or ARDS (0.31 [0.9–1.8], P

To the Editor, We were interested to read the article by Battey and colleagues [1] regarding the analysis of datasets of patients with intracerebral hemorrhage (ICH). It is asserted that patients who survive at least 5 days are more suitable for analysis for the effect of seizure medications (now the preferred term [2]). This technique, however, is itself likely to lead to a biased dataset, and such a selection criterion is particularly inappropriate to evaluate seizure medications. The analysis does not take the duration of treatment or dose of seizure medications given into account, but it is likely to be important. One day of phenytoin (while a comatose patient undergoes EEG monitoring) is not likely to be the same as 14 days of phenytoin, which is why we took care to show that longer duration of treatment is associated with more complications in patients with ICH [2], and subsequent worse functional outcomes. More intense therapy is also associated with more complications and worse outcome in patients with subarachnoid hemorrhage [3]. Similar to the metric of pack-years for smoking exposure instead of a dichotomous one, analysis utilizing total dose exposure is important and fundamental to investigations of adverse drug effects. Furthermore, in this manuscript, seizure medications are grouped together, but each medication is likely to have a different safety profile and each may have a different effect on complications and outcomes. Five days after ICH symptom onset seems to be an arbitrary time to assess the impact of seizure medications. We [2] and others [4] have found that seizures after ICH usually occur within 24 h of symptom onset. Restricting the analysis to those who have survived at least 5 days will introduce bias by excluding patients most likely to have a seizure as a marker of disease, or who die as a consequence of seizures [5]. Mortality after ICH usually has a nonneurologic cause after a few days [6], so it is unclear why seizure medications should affect mortality. If one were to wait until 5 days after ICH symptom onset to randomize patients in a clinical trial of seizure medications, there would be relatively few events to study. The authors emphasize that their initial results suggested that seizure medications are lifesaving after ICH, and that only by selecting the subset of patients who had survived 5 days could they see that this was false. The initial results are a feint, however, since there is no established mechanism by which seizure medications would reduce mortality. Early clinical seizures are not independently associated with outcomes [4]. Seizure medications probably reduce mortality vs. placebo in patients with status epilepticus, but it is not clear from these data why such treatment should reduce mortality in an unselected cohort. We agree that patients who are prescribed seizure medications are likely to have more severe neurologic disease, but the authors neither present data on how the excluded patients might have differed from the overall dataset (i.e., might bias it) nor cite statistical literature that calls for excluding patients in this manner. The usual technique is to adjust the whole eligible cohort for A. M. Naidech (&) M. B. Maas E. M. Liotta J. C. Guth S. U. Schuele Departments of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA e-mail: a-naidech@northwestern.edu