Articles: brain-injuries.
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Because hyperventilation is often associated with a rapid fall in intracranial pressure, it has been assumed to be effective in the treatment of severe head injury. Hyperventilation reduces raised intracranial pressure by causing cerebral vasoconstriction and a reduction in cerebral blood flow. Whether reduced cerebral blood flow improves neurological outcome however, is unclear. ⋯ The data available are inadequate to assess any potential benefit or harm that might result from hyperventilation in severe head injury. Randomised controlled trials to assess the effectiveness of hyperventilation therapy following severe head injury are needed.
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Forensic medical experts are offered a set of morphological signs which help identify the gunshot origin of a skull injury, identify which of the injuries is the inlet and which is the outlet, specify the direction of the shot and succession of formation of injuries in cases with several shots. The author suggests evaluating a gunshot wound in the head with due consideration for the mechanisms of its formation. From a complex of signs of a gunshot injury to the brain skull he singles out the tissue defect with a conical channel and the edge of bone defect, additional injury to the external compact plate near the inlet, and type, number, and location of the radial and concentric cracks. Analysis of the morphology of the above listed signs of gunshot injuries to the skull notable extends the potentialities of forensic medical expert evaluation in cases with gunshot injuries.
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The authors conducted a study to determine the value of transcranial Doppler (TCD) ultrasonography in evaluating the outcome of severely head injured patients and to correlate the TCD values with those obtained from intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring. The authors conducted a prospective study of 125 patients with severe head injury (Glascow Coma Scale scores of less than 9) who underwent TCD ultrasonography according to the standard technique of insonating the middle cerebral artery (MCA) and measuring the mean blood flow velocity and pulsatility index within the first 24 hours of admission. The ICP and CPP values, as well as other clinical, analytical, and neuroimaging data, were also recorded. ⋯ The mean PI in cases of good outcome was 1 whereas in poor outcome was 1.56 (p < 0.0001). The correlations of ICP and CPP to PI were statistically significant (r2 = 0.6; p < 0.0001). When performed in the first 24 hours of severe head injury, TCD ultrasonography is valid in predicting the patient's outcome at 6 months and correlates significantly with ICP and CPP values.
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Clinical Trial
Bedside microdialysis for early detection of cerebral hypoxia in traumatic brain injury.
The authors evaluated the use of bedside cerebral online microdialysis for the detection of impending and present cerebral hypoxia in patients who had sustained traumatic brain injury. ⋯ The authors conclude that a PtiO2 below 10 mm Hg is critical to induce metabolic changes seen during hypoxia/ischemia. Early markers of cerebral hypoxia are increased levels of glutamate and lactate. Regional hypoxia is not always associated with anaerobic cerebral metabolism. In the future, this technology of bedside monitoring may allow optimization of the treatment of severely head injured patients.
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Disturbed ionic and neurotransmitter homeostasis are now recognized to be probably the most important mechanisms contributing to the development of secondary brain swelling after traumatic brian injury (TBI). Evidence obtained from animal models indicates that posttraumatic neuronal excitation via excitatory amino acids leads to an increase in extracellular potassium, probably due to ion channel activation. The purpose of this study was therefore to measure dialysate potassium in severely head injured patients and to correlate these results with intracranial pressure (ICP), outcome, and also with the levels of dialysate glutamate, lactate, and cerebral blood flow (CBF) so as to determine the role of ischemia in this posttraumatic ionic dysfunction. ⋯ The simultaneous increase of potassium, together with dialysate glutamate and lactate, supports the hypothesis that glutamate induces ionic flux and consequently increases ICP due to astrocytic swelling. Reduced CBF was also significantly correlated with increased levels of dialysate potassium. This may be due to either cell swelling or altered potassium reactivity in cerebral blood vessels after trauma.