Acta neurochirurgica. Supplement
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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 permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.
The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). ⋯ Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.
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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.
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Acta Neurochir. Suppl. · Jan 2000
Time profile of neuron specific enolase serum levels after experimental brain injury in rat.
The aim of this study was to investigate the time course of NSE serum levels after traumatic brain injury in rats. 65 male Wistar rats were subjected to severe cortical impact injury (100 PSI, 2 mm deformation). Blood samples were drawn directly after trauma, after 1 h, 6 h, 12 h, 24 h, and 48 h in the trauma group as well as in sham operated animals directly after craniotomy, after 6 h and after 48 h. NSE serum levels were estimated with a commercially available enzyme immuno assay (LIA-mat Sangtec). ⋯ We demonstrated a time dependent release of NSE into the serum after trauma. The highest NSE serum values were detected six hours after trauma (31.5 micrograms/l, mean, n = 10). NSE serum level seems to reflect neuronal damage after cortical contusion in the rat in a time dependent manner.
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Acta Neurochir. Suppl. · Jan 2000
Evidence for lactate uptake after rat fluid percussion brain injury.
Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Glucose declines and lactate increases after TBI as demonstrated in clinical and lab studies, suggesting increased glycolysis. This led us to hypothesize that high extracellular fluid (ECF) lactate may be beneficial after TBI. We measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before & after rat Fluid Percussion Injury (FPI) (2.06 +/- 0.13 atm) with and without i.v. lactate infusion (100 mM x 4.5 hours) to test the hypotheses that arterial lactate determines ECF lactate. 14C-lactate autoradiography was also performed, to demonstrate whether lactate is taken up by traumatized brain. ⋯ Dialysate lactate was always significantly higher than arterial. After lactate infusion, both the dialysate and the arterial lactate were significantly increased (P < 0.0001). Dialysate lactate increased within 10 min. following FPI, with significantly higher values in the lactate infusion group (82% higher with lactate infusion after FPI). Dialysate glucose fell following FPI, with a more severe decline in the saline group (129% lower), suggesting lactate infusion preserves or "spares" glucose in ECF. In our autoradiographic study, i.v. 14C-lactate accumulated at the injury site, with levels 2-4 times higher than in contralateral cortex. In conclusion, arterial lactate augmentation thus increases brain dialysate lactate and results in less reduction in ECF glucose, after FPI. Infused lactate accumulates at the injury site, where metabolism is probably the greatest.