Cerebrovascular Autoregulation Monitoring in the Management of Adult Severe Traumatic Brain Injury: A Delphi Consensus of Clinicians.

BACKGROUND: Several methods have been proposed to measure cerebrovascular autoregulation (CA) in traumatic brain injury (TBI), but the lack of a gold standard and the absence of prospective clinical data on risks, impact on care and outcomes of implementation of CA-guided management lead to uncertainty. AIM: To formulate statements using a Delphi consensus approach employing a group of expert clinicians, that reflect current knowledge of CA, aspects that can be implemented in TBI management and CA research priorities. METHODS: A group of 25 international academic experts with clinical expertise in the management of adult severe TBI patients participated in this consensus process. Seventy-seven statements and multiple-choice questions were submitted to the group in two online surveys, followed by a face-to-face meeting and a third online survey. Participants received feedback on average scores and the rationale for resubmission or rephrasing of statements. Consensus on a statement was defined as agreement of more than 75% of participants. RESULTS: Consensus amongst participants was achieved on the importance of CA status in adult severe TBI pathophysiology, the dynamic non-binary nature of CA impairment, its association with outcome and the inadvisability of employing universal and absolute cerebral perfusion pressure targets. Consensus could not be reached on the accuracy, reliability and validation of any current CA assessment method. There was also no consensus on how to implement CA information in clinical management protocols, reflecting insufficient clinical evidence. CONCLUSION: The Delphi process resulted in 25 consensus statements addressing the pathophysiology of impaired CA, and its impact on cerebral perfusion pressure targets and outcome. A research agenda was proposed emphasizing the need for better validated CA assessment methods as well as the focused investigation of the application of CA-guided management in clinical care using prospective safety, feasibility and efficacy studies.

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.

Neurologic manifestations of major electrolyte abnormalities.

The brain operates in an extraordinarily intricate environment which demands precise regulation of electrolytes. Tight control over their concentrations and gradients across cellular compartments is essential and when these relationships are disturbed neurologic manifestations may develop. Perturbations of sodium are the electrolyte disturbances that most often lead to neurologic manifestations. Alterations in extracellular fluid sodium concentrations produce water shifts that lead to brain swelling or shrinkage. If marked or rapid they can result in profound changes in brain function which are proportional to the degree of cerebral edema or contraction. Adaptive mechanisms quickly respond to changes in cell size by either increasing or decreasing intracellular osmoles in order to restore size to normal. Unless cerebral edema has been severe or prolonged, correction of sodium disturbances usually restores function to normal. If the rate of correction is too rapid or overcorrection occurs, however, new neurologic manifestations may appear as a result of osmotic demyelination syndrome. Disturbances of magnesium, phosphate and calcium all may contribute to alterations in sensorium. Hypomagnesemia and hypocalcemia can lead to weakness, muscle spasms, and tetany; the weakness from hypophosphatemia and hypomagnesemia can impair respiratory function. Seizures can be seen in cases with very low concentrations of sodium, magnesium, calcium, and phosphate.

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.

Reduced cerebral blood flow but intact reactivity to hypercarbia and hypoxia following subarachnoid hemorrhage in rabbits.

Subarachnoid hemorrhage (SAH) was produced in rabbits by four subarachnoid injections of blood (n = 7) or saline (n = 6); a control group (n = 6) had no injections. Basilar artery vasospasm was assessed by serial angiograms. Resting CBF (microspheres) and CBF reactivity to hypercapnia (65 and 85 mm Hg) and hypoxia (fractions of inspired oxygen of 0.15 and 0.10) were determined. Basilar artery vasospasm was seen with SAH. Resting CBF was reduced by 31% (SAH 43 +/- 12, saline 65 +/- 17, control 60 +/- 21 ml 100 g-1 min-1), and resting cerebrovascular resistance was increased (SAH 1.84 +/- 0.30, saline 1.31 +/- 0.49, control 1.39 +/- 0.25 mm Hg ml-1 100 g-1 min-1) after SAH. CBF rose to a similar degree in all three groups in response to hypercarbia and hypoxia. We conclude that resting CBF is reduced in this model of SAH, but vascular reactivity remains intact.

Autoregulatory vasodilation of parenchymal vessels is impaired during cerebral vasospasm.

Impaired CBF autoregulation during vasospasm after aneurysmal subarachnoid hemorrhage (SAH) could reflect impaired capacity of distal vessels to dilate in response to reduced local perfusion pressure or simply indicate that the perfusion pressure distal to large arteries in spasm is so low that vessels are already maximally dilated. Autoregulatory vasodilation can be detected in vivo as an increase in the parenchymal cerebral blood volume (CBV). Regional CBV, CBF, and oxygen extraction fraction in regions with and without angiographic vasospasm obtained from 29 positron emission tomography studies performed after intracranial aneurysm rupture were compared with data from 19 normal volunteers and five patients with carotid artery occlusion. Regional CBF was reduced compared to normal in regions from SAH patients with and without vasospasm as well as with ipsilateral carotid occlusion (P < .0001). Regional oxygen extraction fraction was higher during vasospasm and distal to carotid occlusion than both normal and SAH without vasospasm (P < .0001). Regional CBV was reduced compared to normal in regions with and without spasm, whereas it was increased ipsilateral to carotid occlusion (P < .0001). These findings of reduced parenchymal CBV during vasospasm under similar conditions of tissue hypoxia that produce increased CBV in patients with carotid occlusion provide evidence that parenchymal vessels distal to arteries with angiographic spasm after SAH do not show normal autoregulatory vasodilation.

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.

Does modification of the Innsbruck and the Glasgow Coma Scales improve their ability to predict functional outcome?

BACKGROUND: The accurate prediction of functional outcome requires the development of multivariate models. To enhance their contribution to such models, the predictive power of each component must be optimized. OBJECTIVES: To improve the predictive power of coma scales as the first step in building more sophisticated multivariate models to predict specific levels of functional outcome. DESIGN: Prospective descriptive study. SETTING: Neurology and neurosurgery intensive care unit (NNICU) in a tertiary care academic center. PATIENTS: Eighty-four patients with acute traumatic brain injury, intracerebral hemorrhage, subarachnoid hemorrhage, or ischemic stroke. INTERVENTIONS: None. MAIN OUTCOME MEASURES: The Glasgow Coma Scale (GCS) and Innsbruck Coma Scale (ICS) were administered within 24 hours of admission to the NNICU and then at 48-hour intervals until discharge of the patient from the NNICU. The assessments were performed by 3 occupational therapy graduate students working under the supervision of the medical director of the NNICU. The functional outcome at 3 months after discharge from the hospital was assessed by telephone by the same nurse using the following categories: (1) dead, (2) receiving nursing home or custodial care, (3) home with help, or (4) independent. Cronbach's alpha estimates of reliability for each scale were computed using all scores obtained during the study. The analyses indicated that the verbal response item of the GCS and the oral automatisms item of the ICS were less reliable in this patient population. The scales were modified by deleting those items, and predictive validity for the original and modified scales was computed using a discriminant function of the admission scores. RESULTS: Before modification, both scales were best at predicting independence (GCS and ICS, 71% correct) and mortality (GCS, 60% correct; ICS, 56% correct). The modifications produced a modest improvement in the ability of both scales to better predict levels of outcome (modified GCS: home with help, 33% correct, independent, 71% correct; modified ICS: home with help, 0% correct, independent, 74% correct). CONCLUSIONS: By deleting items with low reliability from the ICS and the GCS we achieved improved reliability and predictive validity. The improvement in predictive power, however, was inadequate to accurately predict functional outcome. Combining clinical scales with other demographic, physiological, functional, and radiographic data will be needed to achieve useful predictions of functional outcome.

Sodium and water regulation in a patient with cerebral salt wasting.

Hyponatremia, in patients with central nervous system disease, can be attributable to impaired free water excretion (syndrome of inappropriate secretion of antidiuretic hormone) or to excessive sodium excretion (cerebral salt wasting). We present a patient with a parietal glioma and hyponatremia characterized by salt wasting and dehydration. Rehydration and sodium repletion corrected the sodium and volume deficits; withdrawal of supplemental sodium resulted in recurrence of dehydration and hyponatremia. We determined sodium and water balance and measured plasma atriopeptin, antidiuretic hormone, and aldosterone. Plasma atriopeptin ranged from 8 to 44 pg/mL (normal, less than 45 pg/mL); antidiuretic hormone was not elevated at 4 to 5 pg/mL, and aldosterone was slightly elevated at 1040.25 pmol/L. The concentrations of these hormones could not directly explain the natriuresis; interactions with neural or other humoral factors may be involved. In evaluating such patients, careful attention to sodium and water balance is important to guide appropriate therapy.

Response to external ventricular drainage in spontaneous intracerebral hemorrhage with hydrocephalus.

We retrospectively reviewed consecutive intensive care unit patients with spontaneous supratentorial intracerebral hemorrhage (i.c.h.) and hydrocephalus who were treated with ventriculostomy to determine intracranial pressure (i.c.p.), Glasgow Coma Scale (GCS) score, and ventricular volume before and after ventriculostomy. Of 22 patients studied, ICP was controlled at < 20 mm Hg in 20. Only one patient had an improvement in both hydrocephalus and GCS. The three patients who survived to 3 months (modified Rankin scores of 0, 0, and 1) were characterized by very small ICH volumes and stable or improving hydrocephalus and GCS.

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.

The effects of mannitol on cerebral edema after large hemispheric cerebral infarct.

OBJECTIVE: To evaluate the effect of a single large dose of mannitol on midline tissue shifts after a large cerebral infarction. BACKGROUND: Theoretically, mannitol use in the largest cerebral infarctions may preferentially shrink noninfarcted cerebral tissue, thereby aggravating midline tissue shifts and worsening neurologic status. To test this theory, we studied patients with hemispheric infarctions using continuous and sequential MRI during administration of a single dose of mannitol. METHODS: Patients with neurologic deterioration from complete middle cerebral artery (MCA) infarctions and CT evidence of at least 3 mm of midline shift were studied using T1-weighted three-dimensional multiplanar rapid acquisition gradient echo image data sets acquired at 5- to 10-minute intervals before, during, and after a 1.5 gm/kg bolus infusion of mannitol. Horizontal and vertical displacements were calculated by previously described methods. Glasgow Coma Scale (GCS) and MCA Stroke Scale (MCASS) were measured before and after mannitol administration. Mean changes in tissue shifts were compared using repeated measures analysis of variance. Clinical variables were compared using paired t-tests. RESULTS: Seven patients were enrolled. The final average change in midline shift compared with the initial displacement was 0.0 +/- 1 mm for horizontal (F = 0.06, p = 0.99) and 0.25 +/- 1.3 mm for vertical displacement (F = 0.06, p = 0.99). Whereas average scores for the group did not change, MCASS improved in two, GCS improved in three, and pupillary light reactivity returned in two patients. No patient worsened. CONCLUSIONS: Acute mannitol used in patients with cerebral edema after a large hemispheric infarction does not alter midline tissue shifts or worsen neurologic status.

Mechanical ventilation for ischemic stroke and intracerebral hemorrhage: indications, timing, and outcome.

OBJECTIVE: To compare the incidence, indication, and timing of intubation and outcome in patients with cerebral infarction (ISCH) and intracerebral hemorrhage (HEM) requiring mechanical ventilation (MV). BACKGROUND: Poor outcomes have been reported for ISCH patients requiring MV. Because the target population, pathophysiology, and management of ISCH and HEM patients differ considerably, we compared the characteristics of patients with ISCH and HEM who required MV. METHODS: A retrospective review of ISCH and HEM stroke patients who underwent MV at a tertiary care academic center from 1994 to 1997 was performed to determine age, sex, type, and location of stroke (anterior or posterior circulation); brainstem dysfunction at intubation (pupillary, corneal, and oculocephalic reflexes); indication for intubation (neurologic deterioration, cardiopulmonary deterioration, or elective intubation for surgery); timing of intubation (on presentation or later); comorbidities; and outcome (hospital disposition). RESULTS: A total of 230 patients, 74 with ISCH and 156 with HEM (mean age, 61 +/- 16 years; male-to-female ratio, 1.15:1), underwent MV. Intubation rates were 6% for ISCH patients and 30% for HEM patients. Two-thirds of the patients required intubation on presentation (84% were intubated for neurologic deterioration) and 131 patients (57%) died (ISCH, 55%; HEM, 58%). Signs of brainstem dysfunction predicted a higher mortality for both groups. Additionally, early intubation and older age predicted mortality for HEM, and male gender predicted mortality in ISCH. Stroke location and comorbidities did not influence outcome. CONCLUSIONS: MV in acute stroke is associated with high mortality. Mortality and outcome were similar for ISCH and HEM; however, the factors predictive of outcome may differ and influence decisions about the use of MV in such patients.

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).

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.

Middle cerebral artery territory infarction and early brain swelling: progression and effect of age on outcome.

OBJECTIVE: To determine the clinical course and outcome in patients with a middle cerebral artery (MCA) occlusion and early computed tomographic (CT) scan findings of infarction, particularly relative to age of the patient. MATERIAL AND METHODS: The clinical and neuroimaging features of 42 consecutive patients with MCA occlusion and early CT signs of swelling (within 24 hours after ictus) were studied. CT scans were graded for displacement of the pineal gland and septum pellucidum as well as compression of the frontal horn of the ventricular system. Young adults, defined as younger than 45 years of age, were assessed separately. RESULTS: Overall mortality was 55% in this patient population at risk for further neurologic deterioration. Of the 42 patients, 33 had deterioration-an impaired level of consciousness ensued in 3, a diencephalic herniation syndrome developed in 19, and uncal herniation occurred in 11. Mortality was 70% in these patients with deterioration. Mortality was significantly lower in younger patients with deterioration in comparison with older patients (3 of 11 patients versus 20 of 22; P = 0.00018, Fisher's exact test). Factors predictive of deterioration and poor outcome were older age (more than 45 years) and the presence of hyperdense clot in the MCA on CT scan, in addition to early swelling. CONCLUSION: Deterioration from further brain swelling is common in patients with MCA occlusion and sulci effacement on early CT scan. The outcome is fatal in most patients who deteriorate. Mortality was significantly higher in deteriorating older patients than in younger patients. Clearly defined criteria for decompressive hemicraniotomy in young patients with complete MCA occlusion are needed, preferably derived from a randomized clinical trial.

Intensive management of severe head injury.

Intensive management of patients with severe head injury offers the best hope of minimizing death and functional disability in a young, working population. Secondary neurologic insult can be decreased by cardiorespiratory support and ICP control from the outset. Rapid neurologic assessment, airway management, and support of circulation are the basis of emergency management for head injury. Patients with severe head injury require intensive care management for two major reasons: management of ICP and management of organ system dysfunction. Care should not be withheld because of initially grim (and inaccurate) prognostic assessment. Newer techniques for assessing the adequacy of cerebral circulation may allow refinement of management strategies in the future.

Relationship between clot location and outcome after basilar artery thrombolysis.

PURPOSE: To identify factors that predict survival and good neurologic outcome in patients undergoing basilar artery thrombolysis. METHODS: Over a 42-month period, 20 of 22 consecutive patients with angiographic proof of basilar artery thrombosis were treated with local intraarterial urokinase. Brain CT scans, neurologic examinations, symptom duration, clot location, and degree of recanalization were analyzed retrospectively. RESULTS: Overall survival was 35% at 3 months. Survival in patients with only distal basilar clot was 71%, while survival in patients with proximal or midbasilar clot was only 15%. At 3 months, 29% of patients with distal basilar clot and 15% of patients with proximal or midbasilar clot had good neurologic outcomes (modified Rankin score of 0 to 2 and Barthel index of 95 to 100). Complete recanalization was achieved in 50% of patients; 60% of those survived and 30% had good neurologic outcomes. Of patients with less than complete recanalization, only 10% survived. Neither duration of symptoms before treatment (range, 1 to 79 hours), age (range, 12 to 83 years), nor neurologic status at the initiation of treatment (Glasgow Coma Scale score range, 3 to 15) predicted outcome. Pretreatment CT findings (positive or negative for related ischemic changes) did not predict outcome or hemorrhagic transformation. CONCLUSION: The single best predictor of survival after basilar thrombosis and intraarterial thrombolysis was distal clot location. Complete recanalization favored survival. Radiologically evident related infarctions, advanced age, delayed diagnosis, and poor pretreatment neurologic status did not predict poor outcome and therefore should not be considered absolute contraindications for intraarterial thrombolysis in patients with basilar artery thrombosis.