The Future of Neurocritical Care Research: Proceedings and Recommendations from the Fifth Neurocritical Care Research Network Conference.

The Fifth Neurocritical Care Research Network (NCRN) Conference held in Boca Raton, Florida, in September of 2018 was devoted to challenging the current status quo and examining the role of the Neurocritical Care Society (NCS) in driving the science and research of neurocritical care. The aim of this in-person meeting was to set the agenda for the NCS's Neurocritical Care Research Central, which is the overall research arm of the society. Prior to the meeting, all 103 participants received educational content (book and seminar) on the 'Blue Ocean Strategy®,' a concept from the business world which aims to identify undiscovered and uncontested market space, and to brainstorm innovative ideas and methods with which to address current challenges in neurocritical care research. Three five-member working groups met at least four times by teleconference prior to the in-person meeting to prepare answers to a set of questions using the Blue Ocean Strategy concept as a platform. At the Fifth NCRN Conference, these groups presented to a five-member jury and all attendees for open discussion. The jury then developed a set of recommendations for NCS to consider in order to move neurocritical care research forward. We have summarized the topics discussed at the conference and put forward recommendations for the future direction of the NCRN and neurocritical care research in general.

The Role of Osmotic Therapy in Hemispheric Stroke.

BACKGROUND: Decompressive hemicraniectomy (DHC) can be lifesaving in hemispheric stroke complicated by cerebral edema. Conversely, osmotic agents have not been shown to improve survival, despite their widespread use. It is unknown whether medical measures can similarly confer survival in certain patient subgroups. We hypothesized that osmotic therapy (OT) without DHC may be associated with a greater likelihood of survival in particular populations depending on demographic, radiologic, or treatment characteristics. METHODS: We performed a retrospective cohort analysis of patients with large anterior circulation strokes with an NIH stroke scale (NIHSS) ≥10 who received OT. We compared clinical, radiologic, and treatment characteristics between two groups: (1) those who survived until discharge with only OT (medical management success) and (2) those who required either DHC or died (medical management failure). RESULTS: Thirty patients met eligibility criteria. Median NIHSS was 19 [interquartile range (IQR) 13-24], and median GCS was 10 [IQR 8-14]. Forty-seven percent of the medical management cohort survived to discharge. Demographic characteristics associated with medical management success included NIHSS (p = 0.009) and non-black race (p = 0.003). Of the various interventions, the administration of OT after 24 hours and a smaller hypertonic saline dose was also associated with survival to discharge (p = 0.038 and 0.031 respectively). CONCLUSION: Our results suggest that patients with moderate size hemispheric infarcts on presentation and those who do not require OT within the first 24 h of stroke may survive until discharge with medical management alone. Black race was also associated with conservative management failure, a finding that may reflect a cultural preference toward aggressive management. Further prospective studies are needed to better establish the utility of medical management of hemispheric edema in the setting of moderate size hemispheric infarcts.

Clinical trial design in the neurocritical care unit.

Clinical trials provide a robust mechanism to advance science and change clinical practice across the widest possible spectrum. Fundamental in the Neurocritical Care Society's mission is to promote Quality Patient Care by identifying and implementing best medical practices for acute neurological disorders that are consistent with the current scientific knowledge. The next logical step will be to foster rapid growth of our scientific body of evidence, to establish and disseminate these best practices. In this manuscript, five invited experts were impaneled to address questions, identified by the conference organizing committee as fundamental issues for the design of clinical trials in the neurological intensive care unit setting.

Factors predicting prognosis after decompressive hemicraniectomy for hemispheric infarction.

The authors reviewed 42 consecutive cases of decompressive hemicraniectomy after hemispheric ischemic stroke to assess predictors of outcome. On univariate analysis, advanced age and history of hypertension were significantly associated with unfavorable outcome, whereas thrombolysis was protective. Side of infarction, pupillary nonreactivity, degree of preoperative midline shift, and timing of surgery did not predict outcome. On multivariate analysis, older age independently predicted poor recovery (odds ratio 2.9 per 10-year increase in age).

Hematoma growth is a determinant of mortality and poor outcome after intracerebral hemorrhage.

BACKGROUND: Although volume of intracerebral hemorrhage (ICH) is a predictor of mortality, it is unknown whether subsequent hematoma growth further increases the risk of death or poor functional outcome. METHODS: To determine if hematoma growth independently predicts poor outcome, the authors performed an individual meta-analysis of patients with spontaneous ICH who had CT within 3 hours of onset and 24-hour follow-up. Placebo patients were pooled from three trials investigating dosing, safety, and efficacy of rFVIIa (n = 115), and 103 patients from the Cincinnati study (total 218). Other baseline factors included age, gender, blood glucose, blood pressure, Glasgow Coma Score (GCS), intraventricular hemorrhage (IVH), and location. RESULTS: Overall, 72.9% of patients exhibited some degree of hematoma growth. Percentage hematoma growth (hazard ratio [HR] 1.05 per 10% increase [95% CI: 1.03, 1.08; p < 0.0001]), initial ICH volume (HR 1.01 per mL [95% CI: 1.00, 1.02; p = 0.003]), GCS (HR 0.88 [95% CI: 0.81, 0.96; p = 0.003]), and IVH (HR 2.23 [95% CI: 1.25, 3.98; p = 0.007]) were all associated with increased mortality. Percentage growth (cumulative OR 0.84 [95% CI: 0.75, 0.92; p < 0.0001]), initial ICH volume (cumulative OR 0.94 [95% CI: 0.91, 0.97; p < 0.0001]), GCS (cumulative OR 1.46 [95% CI: 1.21, 1.82; p < 0.0001]), and age (cumulative OR 0.95 [95% CI: 0.92, 0.98; p = 0.0009]) predicted outcome modified Rankin Scale. Gender, location, blood glucose, and blood pressure did not predict outcomes. CONCLUSIONS: Hematoma growth is an independent determinant of both mortality and functional outcome after intracerebral hemorrhage. Attenuation of growth is an important therapeutic strategy.

Early mortality following spontaneous intracerebral hemorrhage.

The authors reviewed the charts of 1,421 patients with cerebral hemorrhage to determine the cause of death. Limitation or withdrawal of life-sustaining interventions was the most common cause of death (68%) followed by brain death (28%). Neurologic reasons were the most common cause of delayed decisions to withdraw or limit therapy. Brain death was more common in African Americans, whereas life-sustaining interventions were withdrawn or limited early more often in whites.

Mannitol bolus preferentially shrinks non-infarcted brain in patients with ischemic stroke.

Changes in brain tissue volume in six patients who had acute complete middle cerebral artery (MCA) infarctions and CT evidence of midline shift were measured using the brain boundary shift integral (BBSI) on sequential T1-weighted MR images acquired before and after a 1.5-g/kg bolus infusion of mannitol. At 50 to 55 minutes after the baseline scan, total brain volume decreased by 8.1 +/- 2.8 mL (0.6%, p < 0.005). Brain in the noninfarcted hemisphere shrank more (0.8 +/- 0.4%) than in the infarcted hemisphere (0.0 +/- 0.5%, p < 0.05).

Safety of hemodynamic augmentation in patients treated with Guglielmi detachable coils after acute aneurysmal subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Guglielmi detachable coils (GDC) used in the treatment of intracranial aneurysms do not always completely occlude the aneurysm. Thus, after an acute subarachnoid hemorrhage (SAH), there is a theoretical risk of rebleeding from coiled aneurysms, especially when blood pressure is elevated. The aim of this study is to determine whether use of hemodynamic augmentation (HA) to treat delayed ischemic deficits (DID) will increase the risk of rebleeding in these patients. METHODS: Delayed ischemic deficits developed in 12 (7 women and 5 men, aged 31 to 64 years) of 51 patients treated with GDC for acute SAH over a 4-year period. Aneurysms in all 12 patients were >/=80% obliterated with GDC, and there was >/=90% obliteration of 78% of the aneurysms. Hemodynamic augmentation with fluids, phenylephrine, dopamine, and/or dobutamine was used to treat DID for a mean duration of 3 days (range 1 to 11 days). RESULTS: With HA, mean arterial blood pressure (MAP) rose 15% (range 0 to 30%) and systolic blood pressure (SBP) rose 13% (range 0 to 29%) above baseline. MAP was maintained at >10% above baseline for 65% of the treatment period. The maximum MAP was 104 to 170 mm Hg (mean 140 mm Hg), and maximum SBP was 154 to 261 mm Hg (mean 210 mm Hg). No patient had rebleeding or any significant complication during the course of therapy. CONCLUSIONS: Based on this limited series of patients, we believe that it may be safe to use HA in patients treated with GDC for SAH.

Factors associated with withdrawal of mechanical ventilation in a neurology/neurosurgery intensive care unit.

OBJECTIVE: The objective of this study was to identify factors associated with the decision to withdraw mechanical ventilation from patients in a neurology/neurosurgery intensive care unit. Specifically, the following factors were considered: the severity of the neurologic illness, the healthcare delivery system, and social factors. DESIGN: Retrospective analysis of prospectively collected clinical database. SETTING: Neurology/neurosurgery intensive care unit of a large academic tertiary care hospital. PATIENTS: Patients were 2,109 nonelective admissions to the neurology/neurosurgery intensive care unit who received mechanical ventilation over a period of 82 months. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The average age was 56 +/- 19.7 yrs, 53% were male, and 81% were functionally normal before admission. The median Glasgow Coma Scale score was 14, the average Acute Physiology and Chronic Health Evaluation II severity of illness score was 13.5 +/- 8.3, and probability of death was 18.2 +/- 22.0%. Mechanical ventilation was withdrawn from 284 (13.5%). Factors that were independently associated with withdrawal of mechanical ventilation were as follows: more severe neurologic injury [admission Glasgow Coma Scale score (odds ratio 0.86/point, confidence interval 0.82-0.90), diagnosis of subarachnoid hemorrhage (odds ratio 2.44, confidence interval 1.50-3.99), or ischemic stroke (odds ratio 1.72, confidence interval 1.13-2.60)], older age (odds ratio 1.04/yr, confidence interval 1.03-1.05), and higher Acute Physiology and Chronic Health Evaluation II probability of death (odds ratio 1.03/%, confidence interval 1.02-1.04). Mechanical ventilation was less likely to be withdrawn if patients were African-American (odds ratio 0.50, confidence interval 0.36-0.68) or had undergone surgery (odds ratio 0.44, confidence interval 0.2- 0.67). Marital status, premorbid functional status, clinical service (neurology vs. neurosurgery), attending status (private vs. academic), and type of health insurance were not associated with decisions to withdraw mechanical ventilation. CONCLUSIONS: We conclude that decisions to withdraw mechanical ventilation in the neurology/neurosurgery intensive care unit are based primarily on the severity of the acute neurologic condition and age but not on characteristics of the healthcare delivery system. Care is less likely to be withdrawn from African-American patients or those who had surgery.

Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage.

A zone of hypoperfusion surrounding acute intracerebral hemorrhage (ICH) has been interpreted as regional ischemia. To determine if ischemia is present in the periclot area, the authors measured cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) with positron emission tomography (PET) in 19 patients 5 to 22 hours after hemorrhage onset. Periclot CBF, CMRO2, and OEF were determined in a 1-cm-wide area around the clot. In the 16 patients without midline shift, periclot data were compared with mirror contralateral regions. All PET images were masked to exclude noncerebral structures, and all PET measurements were corrected for partial volume effect due to clot and ventricles. Both periclot CBF and CMRO2 were significantly reduced compared with contralateral values (CBF: 20.9 +/- 7.6 vs. 37.0 +/- 13.9 mL 100 g(-1) min(-1), P = 0.0004; CMRO2: 1.4 +/- 0.5 vs. 2.9 +/- 0.9 mL 100 g(-1) min(-1), P = 0.00001). Periclot OEF was less than both hemispheric OEF (0.42 +/- 0.15 vs. 0.47 +/- 0.13, P = 0.05; n = 19) and contralateral regional OEF (0.44 +/- 0.16 vs. 0.51 +/- 0.13, P = 0.05; n = 16). In conclusion, CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia. Thus, the authors found no evidence for ischemia in the periclot zone of hypoperfusion in acute ICH patients studied 5 to 22 hours after hemorrhage onset.

Autoregulation of cerebral blood flow surrounding acute (6 to 22 hours) intracerebral hemorrhage.

BACKGROUND: Arterial hypertension is common in the first 24 hours after acute intracerebral hemorrhage (ICH). Although increased blood pressure usually declines to baseline values within several days, the appropriate treatment during the acute period has remained controversial. Arguments against treatment of hypertension in patients with acute ICH are based primarily on the concern that reducing arterial blood pressure will reduce cerebral blood flow (CBF). The authors undertook this study to provide further information on the changes in whole-brain and periclot regional CBF that occur with pharmacologic reductions in mean arterial pressure (MAP) in patients with acute ICH. METHODS: Fourteen patients with acute supratentorial ICH 1 to 45 mL in size were studied 6 to 22 hours after onset. CBF was measured with PET and (15)O-water. After completion of the first CBF measurement, patients were randomized to receive either nicardipine or labetalol to reduce MAP by 15%, and the CBF study was repeated. RESULTS: MAP was lowered by -16.7 +/- 5.4% from 143 +/- 10 to 119 +/- 11 mm Hg. There was no significant change in either global CBF or periclot CBF. Calculation of the 95% CI demonstrated that there is less than a 5% chance that global or periclot CBF fell by more than -2.7 mL x 100 g(-1) x min(-1). CONCLUSION: In patients with small- to medium-sized acute ICH, autoregulation of CBF was preserved with arterial blood pressure reductions in the range studied.

Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage.

OBJECTIVE: To determine whether mortality rate after intracerebral hemorrhage (ICH) is lower in patients admitted to a neurologic or neurosurgical (neuro) intensive care unit (ICU) compared to those admitted to general ICUs. BACKGROUND: The utility of specialty ICUs is debated. From a cost perspective, having fewer larger ICUs is preferred. Alternatively, the impact of specialty ICUs on patient outcome is unknown. Patients with ICH are admitted routinely to both general and neuro ICUs and provide an opportunity to address this question. SETTING: Forty-two neuro, medical, surgical, and medical-surgical ICUs. MEASUREMENTS AND MAIN RESULTS: The study was an analysis of data prospectively collected by Project Impact over 3 yrs from 42 participating ICUs (including one neuro ICU) across the country. The records of 36,986 patients were merged with records of 3,298 patients from a second neuro ICU that collected the same data over the same period. The impact of clinical (age, race, gender, Glasgow Coma Scale score, reason for admission, insurance), ICU (size, number of ICH patients, full-time intensivist, clinical service, American College for Graduate Medical Education or Critical Care Medicine fellowship), and institutional (size, location, medical school affiliation) characteristics on hospital mortality rate of ICH patients was assessed by using a forward-enter multivariate analysis. Data from 1,038 patients were included. The 13 ICUs that admitted >20 patients accounted for 83% of the admissions with a mortality rate that ranged from 25% to 64%. Multivariate analysis adjusted for patient demographics, severity of ICH, and ICU and institutional characteristics indicated that not being in a neuro ICU was associated with an increase in hospital mortality rate (odds ratio [OR], 3.4; 95% confidence interval [CI], 1.65-7.6). Other factors associated with higher mortality rate were greater age (OR, 1.03/year; 95% CI, 1.01-1.04), lower Glasgow Coma Scale score (OR, 0.6/point; 95% CI, 0.58-0.65), fewer ICH patients (OR, 1.01/patient; 95% CI, 1.00-1.01), and smaller ICU (OR, 1.1/bed; 95% CI, 1.02-1.13). Having a full time intensivist was associated with lower mortality rate (OR, 0.388; 95% CI, 0.22-0.67). CONCLUSIONS: For patients with acute ICH, admission to a neuro vs. general ICU is associated with reduced mortality rate.

Hemodynamic monitoring in the neurological intensive care unit.

The neurointensivist needs to have a thorough understanding of hemodynamic issues and the interaction of the brain and the cardiovascular system. Before one decides to intervene and try to correct an apparent "abnormal hemodynamic parameter" one needs to think whether such an intervention is indeed warranted and what effect the intervention would have on the cerebral circulation. The neurointensivist thus needs to approach these issues differently from the approach an internist or general intensivist would take.

Sodium disturbances frequently encountered in a neurologic intensive care unit.

Most sodium disturbances in patients with CNS lesions result from disturbed water regulation. Possible systemic and iatrogenic causes must be evaluated prior to treatment. Insufficient secretion of ADH leads to hypernatremia if fluid intake is inadequate and can be treated with either fluid or hormone replacement. Care must be exercised in patients with acute diabetes insipidus because of the potentially variable and transient nature of the disturbance. Hyponatremia usually results from inappropriate secretion of ADH and should be managed aggressively in symptomatic patients with loop diuretics and hypertonic saline. However, very rapid correction or overcorrection should be avoided. Patients with SAH and hyponatremia should not be fluid restricted because of the risk of exacerbating vasospasm but treated with large volumes of isotonic or mildly hypertonic saline.

Reversible left ventricular dysfunction associated with raised troponin I after subarachnoid haemorrhage does not preclude successful heart transplantation.

Transient abnormalities in ECGs, echocardiograms, and cardiac enzymes have been described in the acute setting of subarachnoid haemorrhage. In addition, left ventricular dysfunction has been reported at the time of brain death. A patient with an acute subarachnoid haemorrhage who presented with raised troponin I (TnI) concentrations and diffuse left ventricular dysfunction is described. After declaration of brain death 32 hours later, the heart was felt initially not suitable for transplantation. A normal cardiac catheterisation, however, lead to successful transplantation of the donor heart. Raised catecholamine concentrations and metabolic perturbations have been proposed as the mechanisms leading to the cardiac dysfunction seen with brain death. This may be a biphasic process, allowing time for myocardial recovery and reversal of the left ventricular dysfunction. Awareness of this phenomenon in the acutely ill neurologic population needs to be raised in order to prevent the unnecessary rejection of donor hearts.

Effects of fluid management on edema volume and midline shift in a rat model of ischemic stroke.

BACKGROUND AND PURPOSE: The purpose of this study was to investigate the effects of fluid management on brain water content (BW) and midline shift (MLS) after a focal cerebral ischemic insult. METHODS: A suture model was used to induce focal cerebral ischemia for 90 minutes (n=44). The rats were randomly assigned to 3 groups 2. 5 hours after reperfusion: dehydration (n=24), control (n=8), or hydration (n=12). BW was obtained with the wet-dry weight method 24 hours after middle cerebral artery (MCA) occlusion. In addition, MRI were obtained (n=31) 24 hours after the onset of ischemia so that the ratio of hemispheric volumes ipsilateral (IH) and contralateral (CH) to the infarct and the extent of MLS could be obtained. RESULTS: Across the range from moderate dehydration to intravascular volume expansion with isotonic saline, BW of the IH increased linearly as a function of change in body weight (r(2)=0.89), whereas few changes in relation to body weight were observed in CH, indicating a preferential effect of fluid management on the infarcted hemisphere. Furthermore, the hemispheric volume ratio (IH/CH) and MLS also increased in relation to changes in body weight. However, paradoxical increases in BW, IH/CH, and extent of MLS were observed in comparison with controls when severe dehydration was produced with high-dose mannitol. CONCLUSIONS: Changes in ischemic BW by fluid management correlated closely with changes in body weight except when high-dose mannitol was used. Mannitol, as a dehydrating agent, may be associated with bimodal effects, with a high dose aggravating ischemic BW.

No reduction in cerebral metabolism as a result of early moderate hyperventilation following severe traumatic brain injury.

OBJECT: Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs). METHODS: Nine patients were studied a mean of 11.2+/-1.6 hours (range 8-14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6+/-1.8 and their mean age 27+/-9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30+/-2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls. Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59+/-0.44 ml/100 g/minute [p < 0.01] and 0.31+/-0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5+/-8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8+/-0.56 ml/100 g (p < 0.001), OEF rose to 0.45+/-0.13 (p < 0.02), and CvO2 fell to 8.3+/-3 vol% (p < 0.02); CMRO2 remained unchanged. CONCLUSIONS: The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.

Artificial neural networks improve the prediction of mortality in intracerebral hemorrhage.

BACKGROUND: Artificial neural network (ANN) analysis methods have led to more sensitive diagnosis of myocardial infarction and improved prediction of mortality in breast cancer, prostate cancer, and trauma patients. Prognostic studies have identified early clinical and radiographic predictors of mortality after intracerebral hemorrhage (ICH). To date, published models have not achieved the accuracy necessary for use in making decisions to limit medical interventions. We recently reported a logistic regression model that correctly classified 79% of patients who died and 90% of patients who survived. In an attempt to improve prediction of mortality we computed an ANN model with the same data. OBJECTIVE: To determine whether an ANN analysis would provide a more accurate prediction of mortality after ICH when compared with multiple logistic regression models computed using the same data. METHODS: Analyses were conducted on data collected prospectively on 81 patients with supratentorial ICH. Multiple logistic regression was used to predict hospital mortality, then an ANN analysis was applied to the same data set. Input variables were age, gender, race, hydrocephalus, mean arterial pressure, pulse pressure, Glasgow Coma Scale score, intraventricular hemorrhage, hydrocephalus, hematoma size, hematoma location (ganglionic, thalamic, or lobar), cisternal effacement, pineal shift, history of hypertension, history of diabetes, and age. RESULTS: The ANN model correctly classified all patients (100%) as alive or dead compared with 85% correct classification for the logistic regression model. A second ANN verification model was equally accurate. The ANN was superior to the logistic regression model on all objective measures of fit. CONCLUSIONS: ANN analysis more effectively uses information for prediction of mortality in this sample of patients with ICH. A well-validated ANN may have a role in the clinical management of ICH.

Progression of mass effect after intracerebral hemorrhage.

BACKGROUND AND PURPOSE: While the evolution of mass effect after cerebral infarction is well characterized, similar data regarding intracerebral hemorrhage (ICH) are scant. Our goal was to determine the time course and cause for progression of mass effect after ICH. METHODS: Patients with spontaneous supratentorial ICH who underwent >/=2 CT scans were identified in our prospectively collected database. CT lesion size and midline shift of the pineal and septum pellucidum were retrospectively measured and correlated with clinical and CT characteristics. Causes for increased midline shift were determined by 2 independent observers. RESULTS: Seventy-six patients underwent 235 scans (3.1+/-1.3 per patient). Initial CT was obtained within 24 hours of ICH in 66. Twenty-five scans were repeated on day 1, 80 on days 2 through 7, 31 on days 8 through 14, and 24 >14 days after ICH. Midline shift was present on 88% of the initial scans. There were 17 instances of midline shift progression: 10 occurred early (0.2 to 1.7 days) and were associated with hematoma enlargement, and 7 occurred late (9 to 21 days) and were associated with edema progression. Progression of mass effect due to edema occurred with larger hemorrhages (P<0.05). Of 65 scans repeated for clinical deterioration, only 10 were associated with increased mass effect. CONCLUSIONS: Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks, associated with increase in edema. The clinical significance of later-developing edema is unclear.

Predictors of acute hospital costs for treatment of ischemic stroke in an academic center.

BACKGROUND AND PURPOSE: We sought to determine predictors of acute hospital costs in patients presenting with acute ischemic stroke to an academic center using a stroke management team to coordinate care. METHODS: Demographic and clinical data were prospectively collected on 191 patients consecutively admitted with acute ischemic stroke. Patients were classified by insurance status, premorbid modified Rankin scale, stroke location, stroke severity (National Institutes of Health Stroke Scale score), and presence of comorbidities. Detailed hospital charge data were converted to cost by application of department-specific cost-to-charge ratios. Physician's fees were not included. A stepwise multiple regression analysis was computed to determine the predictors of total hospital cost. RESULTS: Median length of stay was 6 days (range, 1 to 63 days), and mortality was 3%. Median hospital cost per discharge was $4408 (range, $1199 to $59 799). Fifty percent of costs were for room charges, 19% for stroke evaluation, 21% for medical management, and 7% for acute rehabilitation therapies. Sixteen percent were admitted to an intensive care unit. Length of stay accounted for 43% of the variance in total cost. Other independent predictors of cost included stroke severity, heparin treatment, atrial fibrillation, male sex, ischemic cardiac disease, and premorbid functional status. CONCLUSIONS: We conclude that the major predictors of acute hospital costs of stroke in this environment are length of stay, stroke severity, cardiac disease, male sex, and use of heparin. Room charges accounted for the majority of costs, and attempts to reduce the cost of stroke evaluation would be of marginal value. Efforts to reduce acute costs should be monitored for potential cost shifting or a negative impact on quality of care.