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Jae Hong Lee, Daniel F. Kelly, Matthias Oertel, David L. McArthur, Thomas C. Glenn, Paul Vespa, W. John Boscardin and Neil A. Martin

Object. Contemporary management of head-injured patients is based on assumptions about CO2 reactivity, pressure autoregulation (PA), and vascular reactivity to pharmacological metabolic suppression. In this study, serial assessments of vasoreactivity of the middle cerebral artery (MCA) were performed using bilateral transcranial Doppler (TCD) ultrasonography.

Methods. Twenty-eight patients (mean age 33 ± 13 years, median Glasgow Coma Scale score of 7) underwent a total of 61 testing sessions during postinjury Days 0 to 13. The CO2 reactivity (58 studies in 28 patients), PA (51 studies in 23 patients), and metabolic suppression reactivity (35 studies in 16 patients) were quantified for each cerebral hemisphere by measuring changes in MCA velocity in response to transient hyperventilation, arterial blood pressure elevation, or propofol-induced burst suppression, respectively. One or both hemispheres registered below normal vasoreactivity scores in 40%, 69%, and 97% of study sessions for CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.0001), respectively. Intracranial hypertension, classified as intracranial pressure (ICP) greater than 20 mm Hg at the time of testing, was associated with global impairment of CO2 reactivity, PA, and metabolic suppression reactivity (p < 0.05). A low baseline cerebral perfusion pressure (CPP) was also predictive of impaired CO2 reactivity and PA (p < 0.01). Early postinjury hypotension or hypoxia was also associated with impaired CO2 reactivity (p < 0.05), and hemorrhagic brain lesions in or overlying the MCA territory were predictive of impaired metabolic suppression reactivity (p < 0.01). The 6-month Glasgow Outcome Scale score correlated with the overall degree of impaired vasoreactivity (p < 0.05).

Conclusions. During the first 2 weeks after moderate or severe head injury, CO2 reactivity remains relatively intact, PA is variably impaired, and metabolic suppression reactivity remains severely impaired. Elevated ICP appears to affect all three components of vasoreactivity that were tested, whereas other clinical factors such as CPP, hypotensive and hypoxic insults, and hemorrhagic brain lesions have distinctly different impacts on the state of vasoreactivity. Incorporation of TCD ultrasonography—derived vasoreactivity data may facilitate more injury- and time-specific therapies for head-injured patients.

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Matthias Oertel, Daniel F. Kelly, David McArthur, W. John Boscardin, Thomas C. Glenn, Jae Hong Lee, Tooraj Gravori, Dennis Obukhov, Duncan Q. McBride and Neil A. Martin

Object. Progressive intracranial hemorrhage after head injury is often observed on serial computerized tomography (CT) scans but its significance is uncertain. In this study, patients in whom two CT scans were obtained within 24 hours of injury were analyzed to determine the incidence, risk factors, and clinical significance of progressive hemorrhagic injury (PHI).

Methods. The diagnosis of PHI was determined by comparing the first and second CT scans and was categorized as epidural hematoma (EDH), subdural hematoma (SDH), intraparenchymal contusion or hematoma (IPCH), or subarachnoid hemorrhage (SAH). Potential risk factors, the daily mean intracranial pressure (ICP), and cerebral perfusion pressure were analyzed. In a cohort of 142 patients (mean age 34 ± 14 years; median Glasgow Coma Scale score of 8, range 3–15; male/female ratio 4.3:1), the mean time from injury to first CT scan was 2 ± 1.6 hours and between first and second CT scans was 6.9 ± 3.6 hours. A PHI was found in 42.3% of patients overall and in 48.6% of patients who underwent scanning within 2 hours of injury. Of the 60 patients with PHI, 87% underwent their first CT scan within 2 hours of injury and in only one with PHI was the first CT scan obtained more than 6 hours postinjury. The likelihood of PHI for a given lesion was 51% for IPCH, 22% for EDH, 17% for SAH, and 11% for SDH. Of the 46 patients who underwent craniotomy for hematoma evacuation, 24% did so after the second CT scan because of findings of PHI. Logistic regression was used to identify male sex (p = 0.01), older age (p = 0.01), time from injury to first CT scan (p = 0.02), and initial partial thromboplastin time (PTT) (p = 0.02) as the best predictors of PHI. The percentage of patients with mean daily ICP greater than 20 mm Hg was higher in those with PHI compared with those without PHI. The 6-month postinjury outcome was similar in the two patient groups.

Conclusions. Early progressive hemorrhage occurs in almost 50% of head-injured patients who undergo CT scanning within 2 hours of injury, it occurs most frequently in cerebral contusions, and it is associated with ICP elevations. Male sex, older age, time from injury to first CT scan, and PTT appear to be key determinants of PHI. Early repeated CT scanning is indicated in patients with nonsurgically treated hemorrhage revealed on the first CT scan.

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Paul M. Vespa, W. John Boscardin, David A. Hovda, David L. McArthur, Marc R. Nuwer, Neil A. Martin, Valeriy Nenov, Thomas C. Glenn, Marvin Bergsneider, Daniel F. Kelly and Donald P. Becker

Object. Early prediction of outcomes in patients after they suffer traumatic brain injury (TBI) is often nonspecific and based on initial imaging and clinical findings alone, without direct physiological testing. Improved outcome prediction is desirable for ethical, social, and financial reasons. The goal of this study was to determine the usefulness of continuous electroencephalography (EEG) monitoring in determining prognosis early after TBI, while the patient is in the intensive care unit.

Methods. The authors hypothesized that the reduced percentage of alpha variability (PAV) in continuous EEG tracings indicates a poor prognosis. Prospective continuous EEG monitoring was performed in 89 consecutive patients with moderate to severe TBI (Glasgow Coma Scale [GCS] Scores 3–12) from 0 to 10 days after injury. The PAV was calculated daily, and the time course and trends of the PAV were analyzed in comparison with the patient's Glasgow Outcome Scale (GOS) score at the time of discharge.

In patients with GCS scores of 8 or lower, a PAV value of 0.1 or lower is highly predictive of a poor outcome or death (positive predictive value 86%). The determinant PAV value was obtained by Day 3 after injury. Persistent PAV values of 0.1 or lower over several days or worsening of the PAV to a value of 0.1 or lower indicated a high likelihood of poor outcome (GOS Scores 1 and 2). In comparison with the combination of traditional initial clinical indicators of outcome (GCS score, pupillary response to light, patient age, results of computerized tomography scanning, and early hypotension or hypoxemia), the early PAV value during the initial 3 days after injury independently improved prognostic ability (p < 0.01).

Conclusions. Continuous EEG monitoring performed with particular attention paid to the PAV is a sensitive and specific method of prognosis that can indicate outcomes in patients with moderate to severe TBI within 3 days postinjury.

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Matthias Oertel, Daniel F. Kelly, Jae Hong Lee, David L. McArthur, Thomas C. Glenn, Paul Vespa, W. John Boscardin, David A. Hovda and Neil A. Martin

Object. Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP.

Methods. Thirty-three patients with a mean age of 33 ± 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 ± 5 to 27 ± 5 mm Hg and in ICP from 20 ± 11 to 13 ± 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 ± 5 mm Hg and ICP increased from 16 ± 9 to 19 ± 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 ± 10 to 16 ± 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression.

Conclusions Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

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Matthias Oertel, W. John Boscardin, Walter D. Obrist, Thomas C. Glenn, David L. McArthur, Tooraj Gravori, Jae Hong Lee and Neil A. Martin

Object. The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients.

Methods. Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA > 120 cm/second); B (VMCA > 120 cm/second and a Lindegaard ratio [LR] > 3); C (spasm index [SI] in the anterior circulation > 3.4); D (VBA > 90 cm/second); and E (SI in the posterior circulation > 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate.

Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA—Criterion D or E—was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF.

Conclusions. The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.

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Edson Bor-Seng-Shu and Manoel Jacobsen Teixeira

Object.

The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients.

Methods.

Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA > 120 cm/second); B (VMCA > 120 cm/second and a Lindegaard ratio [LR] > 3); C (spasm index [SI] in the anterior circulation > 3.4); D (VBA > 90 cm/second); and E (SI in the posterior circulation > 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate.

Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA—Criterion D or E—was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF.

Conclusions.

The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010