Articles: brain-injuries.
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Anesthesia and analgesia · Oct 1998
The effect of hyperventilation and hyperoxia on cerebral venous oxygen saturation in patients with traumatic brain injury.
Eighteen head-injured patients undergoing hyperventilation were studied for changes in jugular venous oxygen saturation (SjvO2) and arteriovenous oxygen content difference (AVDO2) in response to changes in PaO2 and PaCO2. SjvO2 decreased significantly from 66% +/- 3% to 56% +/- 3% (mean +/- SD) when PaCO2 decreased from 30 to 25 mm Hg at a PaO2 of 100-150 mm Hg. SjvO2 values returned to baseline (66% +/- 2%) when PaCO2 was restored to 30 mm Hg. Repetition of the study at a PaO2 of 200-250 mm Hg produced a similar pattern. However, SjvO2 values were significantly greater with PaO2 within the range of 200-250 mm Hg (77% +/- 4% and 64% +/- 3%) than SjvO2 measured at a PaO2 of 100-150 mm Hg at PaCO2 values of both 30 and 25 mm Hg. AVDO2 also improved with a PaO2 of 200-250 mm Hg at each PaCO2 (P < 0.001). In conclusion, decreases in SjvO2 associated with decreases in PaCO2 may be offset by increasing PaO2. ⋯ The adequacy of cerebral oxygenation can be estimated in head-injured patients by monitoring jugular bulb oxygen saturation and the arteriovenous oxygenation content difference. Increasing the partial pressure of arterial oxygen above normal offset deleterious effects of hyperventilation on jugular bulb oxygen saturation and arteriovenous oxygenation content difference in head-injured patients.
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J. Nerv. Ment. Dis. · Oct 1998
Posttraumatic stress symptomatology after childhood traumatic brain injury.
The purpose of this study was to quantify and to identify predictors of posttraumatic stress disorder (PTSD) symptomatology after traumatic brain injury (TBI). Fifty children aged 6 to 14 years, hospitalized after TBI, were assessed soon after TBI regarding injury severity and preinjury psychiatric, socioeconomic, family functioning, and family psychiatric history status; neuroimaging was also analyzed. Psychiatric assessments were repeated 3, 6, 12, and 24 months after TBI. ⋯ The presence of an internalizing disorder at time of injury followed by greater injury severity were the most consistent predictors of PTSD symptomatology. It is apparent, therefore, that PTSD and subsyndromal posttraumatic stress disturbances occur despite neurogenic amnesia. These problems should be treated, particularly if symptoms persist beyond 3 months.
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Journal of neurosurgery · Oct 1998
Factors affecting excitatory amino acid release following severe human head injury.
Recent animal studies demonstrate that excitatory amino acids (EAAs) play a major role in neuronal damage after brain trauma and ischemia. However, the role of EAAs in patients who have suffered severe head injury is not understood. Excess quantities of glutamate in the extracellular space may lead to uncontrolled shifts of sodium, potassium, and calcium, disrupting ionic homeostasis, which may lead to severe cell swelling and cell death. The authors evaluated the role of EEAs in human traumatic brain injury. ⋯ The release of EAAs is closely linked to the release of structural amino acids and may thus reflect nonspecific development of membrane micropores, rather than presynaptic neuronal vesicular exocytosis. The magnitude of EAA release in patients with focal contusions and ischemic events may be sufficient to exacerbate neuronal damage, and these patients may be the best candidates for treatment with glutamate antagonists in the future.