Second annual meeting of the Neurocritical Care Society: San Diego, California February 7-8, 2004.
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Biomedical subjects
Publications and source records attributed to Arthur M Lam.
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OBJECTIVE: The aims of this study were to document the incidence of impaired cerebral autoregulation in children with traumatic brain injury using transcranial Doppler ultrasonography and to examine the relationship between autoregulatory capacity and outcome in children following traumatic brain injury. DESIGN: Prospective cohort study. SETTING: Harborview Medical Center (level I pediatric trauma center) in Washington state. PATIENTS: Thirty-six children <15 yrs old with traumatic brain injury: Glasgow Coma Scale score <9 (n = 12, group 1), Glasgow Coma Scale score 9-12 (n = 12, group 2), and Glasgow Coma Scale score 13-15 (n = 12, group 3). INTERVENTIONS: Cerebral autoregulation testing was conducted during extracranial surgery. Mean middle cerebral artery flow velocities were measured using transcranial Doppler as mean arterial pressure was increased to whichever variable was greater: 20% above baseline or a set value (80 mm Hg for <9 yrs and 90 mm Hg for 9-14 yrs). Autoregulatory capacity was quantified by the Autoregulatory Index. Autoregulatory Index <0.4 was considered impaired cerebral autoregulation. Discharge outcome using the Glasgow Outcome Scale score was considered good if the Glasgow Outcome Scale score was > or =4. MEASUREMENTS AND MAIN RESULTS: Twenty-four (67%) of 36 children had an Autoregulatory Index > or =0.4. The incidence of impaired cerebral autoregulation was 42% (five of 12) in group 1, 42% (five of 12) in group 2, and 17% (two of 12) in group 3. Ten (42%) of the 24 children with intact cerebral autoregulation had a good outcome compared with only one of 12 (8%) children with impaired cerebral autoregulation (p =.04). Six of 12 (50%) children with impaired cerebral autoregulation had hyperemia compared with one of 24 (4%) children with intact cerebral autoregulation (p <.01). Hyperemia was associated with poor outcome (p =.01). CONCLUSIONS: The incidence of impaired cerebral autoregulation was greatest following moderate to severe traumatic brain injury. Impaired cerebral autoregulation was associated with poor outcome. Hyperemia was associated with impaired cerebral autoregulation and poor outcome.
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In adults, the lower limit of cerebral autoregulation (LLA) is generally considered to be a mean arterial pressure (MAP) of 60 mmHg. The LLA in healthy children has not been identified. The aim of this report is to describe the LLA in anesthetized children and relate it to age. Static cerebral autoregulation testing was performed in children 6 months to 14 years of age during <1 MAC sevoflurane anesthesia. Mean middle cerebral artery flow velocities (Vmca) were continuously measured using transcranial Doppler ultrasonography. MAP was increased with infusion of intravenous phenylephrine incrementally titrated to the greater of either: 1) 20% above baseline MAP or 2) 80 mmHg (<9 years), 90 mmHg (9-14 years). The LLA was defined by the point where the two linear regression lines fitting the Vmca/MAP crossed. The lower limit reserve (LLR) and autoregulatory reserve (ARR%) were defined as follows: LLR=Baseline MAP-LLA; ARR (%)=(LLR/Baseline MAP)x100. There were 13 subjects <2 years of age (group 1), 13 subjects 2 to 5 years of age (group 2), 14 subjects 6 to 9 years of age (group 3), and 13 subjects 10 to 14 years of age (group 4). Older children (groups 3 and 4) had a higher baseline MAP compared with younger children (groups 1 and 2) (82 +/- 10 mmHg vs. 70 +/- 10 mmHg, respectively; P=0.0001). However, there was no difference in LLA (59 +/- 17 mmHg vs. 60 +/- 8 mmHg; P=0.6) between older and younger children. Consequently, the LLR was greater in older children compared with younger children (25 +/- 12 mmHg vs. 12 +/- 10 mmHg, respectively; P=0.0007). Similarly, the ARR was significantly higher in older children compared with younger children (30% +/- 16% vs. 16% +/- 12%; P=0.002). In this study, we found no age-related differences in the LLA. Older children had a greater LLR and ARR compared with young children. The baseline MAP in young children may rest close to the LLA. These findings may have implications for managing hemodynamics in anesthetized children at risk for secondary brain injury.
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BACKGROUND: The relationship between systolic blood pressure and outcome in children after severe traumatic brain injury (TBI) is unclear. We examined the relationship between age-appropriate systolic blood pressure (AASBP) percentile and outcome after severe pediatric TBI. METHODS: We examined the association between AASBP percentiles and outcome in 172 children younger than 14 years of age with a Glasgow Coma Scale score < 9. Outcome was evaluated using discharge Glasgow Outcome Scale score. Poor outcome was defined as a Glasgow Outcome Scale score < 4. RESULTS: Poor outcome was associated with AASBP < 75th percentile (odds ratio, 4.2; 95% confidence interval, 2.1-8.3). Patients with systolic blood pressure (SBP) > or = 90 mm Hg and AASBP < 75th percentile had a higher odds for poor outcome compared with patients with SBP > or = 90 mm Hg and AASBP > or = 75th percentile (odds ratio, 3.5; 95% confidence interval, 1.7-7.3). CONCLUSION AASBP < 75th percentile was associated with poor outcome after severe pediatric TBI, even when SBP was > or = 90 mm Hg.
The cerebral circulation is tightly regulated to meet the brain's metabolic demands. Although the mechanism is not fully understood, the major physiologic influences on cerebral blood flow have been well documented. In this chapter the basic vascular anatomy, and physiologic control of the cerebral circulation are reviewed. Clinical implications are emphasized.
IMPLICATIONS: Transesophageal echocardiography may be useful in guiding detection and removal of thorax penetrating objects and for the monitoring of complications after removal of such objects.
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BACKGROUND: The potential benefit of propofol dose regimens that use physiologic pharmacokinetic modeling to target the brain has been demonstrated in animals, but no data are available on the rate of propofol distribution to the brain in humans. This study measured the brain uptake of propofol in humans and the simultaneous effects on electroencephalography, cerebral blood flow velocity (V(mca)), and cerebral oxygen extraction. METHODS: Seven subjects had arterial and jugular bulb catheters placed before induction. Electroencephalography and V(mca) were recorded during induction with propofol while blood samples were taken from both catheters for later propofol analysis. Brain uptake of propofol was calculated using mass balance principles, with effect compartment modeling used to quantitate the rate of uptake. RESULTS: Bispectral index (electroencephalogram) values decreased to a minimum value of approximately 4 at around 7 min from the onset of propofol administration and then slowly recovered. This was accompanied by decreases in V(mca), reaching a minimum value of approximately 40% of baseline. Cerebral oxygen extraction did not change, suggesting parallel changes in cerebral metabolism. There was slow equilibrium of propofol between the blood and the brain (t(1/2keo) of 6.5 min), with a close relation between brain concentrations and bispectral index, although with considerable interpatient variability. The majority of the decreases in V(mca), and presumably cerebral metabolism, corresponded with bispectral index values reaching 40-50 and the onset of burst suppression. CONCLUSION: Description of brain distribution of propofol will allow development of physiologic pharmacokinetic models for propofol and evaluation of dose regimens that target the brain.
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