Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2000
Continuous assessment of cerebral autoregulation--clinical verification of the method in head injured patients.
Previously, using transcranial Doppler ultrasonography, we investigated whether the hemodynamic response to spontaneous variations in cerebral perfusion pressure (CPP) provides reliable information about cerebral autoregulatory reserve. In the present study we have verified this method in 166 patients after head trauma. Waveforms of intracranial pressure (ICP), arterial pressure and transcranial Doppler flow velocity (FV) were captured daily over 0.5-2.0 hour periods. ⋯ Mx depended on outcome following head injury stronger than the Glasgow Coma Score on admission (ANOVA, F values 18 and 15 respectively; N = 166). In patients who died, cerebral autoregulation was disturbed during the first two days following injury. These results indicate an important role for the continuous monitoring of autoregulation following head trauma.
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Acta Neurochir. Suppl. · Jan 2000
The role of decompressive craniectomy in the treatment of uncontrollable post-traumatic intracranial hypertension.
The benefit of decompressive craniectomy for the treatment of uncontrolled post-traumatic intracranial hypertension seems to be encouraging if medical management fails. We present our experience in 22 cases of cerebral edema due to head trauma. The edema alone was rarely the direct consequence of head trauma. ⋯ In our series 41% of patients had a good recovery, 18% a severe disability, 23% a vegetative state and 18% died. The findings showed that the bony decompression must be performed early before the situation becomes irreversible. We suggest that if intracranial pressure values remain greater than 30 mmHg with cerebral perfusion pressure below 70 mmHg, despite vigorous anti-edema therapy, decompressive craniectomy should be considered.
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Acta Neurochir. Suppl. · Jan 2000
Thrombin preconditioning, heat shock proteins and thrombin-induced brain edema.
Intracerebral injections of high concentrations of thrombin cause brain edema but, in vitro, low concentrations of thrombin may be neuroprotective. This study investigated whether a low dose of thrombin might induce tolerance to subsequent large doses of thrombin (thrombin preconditioning; TPC) in a manner analogous to ischemic preconditioning. The study involved five parts. ⋯ TPC also induced HSP32, but this effect occurred earlier than the effect on edema formation. TPC had no effect on HSP70. These results suggest that thrombin-induced brain tolerance may be related to HSP27 induction.
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Acta Neurochir. Suppl. · Jan 2000
Diffuse axonal injury with or without an evacuated intracranial hematoma in head injured patients. Are they different lesions?
The general classification of head injury proposed by Marshall et al., based on admission CT scan findings, might mask a group of patients who have Diffuse Brain Injury (DI) in addition to intracranial haematomas. The aim of this study was to assess possible differences in outcome with respect to the level of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) between a group of patients with DI: III-IV (Marshall's classification) after the evacuation of an intracranial haematoma (group A) and another group with DI: III-IV in the absence of a mass lesion (group B). We prospectively studied 129 patients with isolated and closed severe head injury (GCS < 9). ⋯ In group B (n = 68), median values of 20 and 5.5 hours were obtained for ICP > 20 and CPP < 70 respectively, whilst 39 (57.3%) survived with favourable outcomes. When we analysed the effects of the DI: III-IV in both groups of patients, we found that the differences in percentage of time with ICP > 20 and CPP < 70 were statistically significant (p < 0.01) and patients in group A had a higher morbidity and mortality (p < 0.05). This study has demonstrated that the levels of ICP, morbidity and mortality in patients with DI: III-IV and an evacuated mass lesion were higher than in patients with DI: III-IV without a mass lesion.
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Acta Neurochir. Suppl. · Jan 2000
The use of decompressive craniectomy for the management of severe head injuries.
The aim of Neurosurgical care is to minimise the secondary brain damage that occurs after a severe head injury. This includes the evacuation of an intracranial space occupying haematoma, the reduction of intracranial volume, external ventricular drainage with hydrocephalus, and conservative therapy to reduce intracranial pressure (ICP) and to maintain tissue oxygen p(ti)O2. When conservative treatment fails, a decompressive craniectomy might be successful in lowering ICP. ⋯ The prognosis after decompression depends on clinical signs and symptoms on admission, patients' age and the existence of major extracranial injuries. Our guidelines for decompressive craniectomy after failure of conservative intervention and evacuation of space occupying hematomas included: a patient's age below 50 years without multiple trauma or a patient's age below 30 years in the presence of major extracranial injuries; severe brain swelling on CT scan (primary brainstem injuries were excluded). In 8 patients conservative 1TU treatment had failed.