Articles: brain-injuries.
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Randomized Controlled Trial Clinical Trial
The effect of hypothermia on the incidence of delayed traumatic intracerebral hemorrhage.
Hypothermia has been shown to cause coagulation abnormalities, primarily related to platelet dysfunction. We reviewed coagulation function and the incidence of delayed traumatic intracerebral hemorrhage in a series of 36 patients with severe head injuries (Glasgow Coma Scale 3-7) enrolled in a prospective, randomized, clinical trial of therapeutic moderate hypothermia. Patients were randomized to a normothermic group (n = 16) or to a group cooled to 32 to 33 degrees C within 6 hours of injury (n = 20). ⋯ Three patients in the hypothermic group and one in the normothermic group developed thrombocytopenia (a platelet count of less than 100,000). There were no significant differences between the two groups in the incidence of delayed traumatic intracerebral hemorrhage, in measured coagulopathy, or in the mean values of measured coagulation parameters. Although the possibility of a hypothermia-induced coagulopathy has not yet been excluded, the short-term use of hypothermia does not appear to increase the risk for intracranial hemorrhagic complications in head injuries.
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Intensive care medicine · Jan 1994
Comparative StudyA new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation.
To evaluate a new therapy of posttraumatic brain oedema, with the main concept that opening of the blood-brain barrier upsets the normal brain volume regulation, inducing oedema formation. This means that transcapillary fluid fluxes will be controlled by hydrostatic capillary and colloid osmotic pressures, rather than by crystalloid osmotic pressure. If so, brain oedema therapy should include reduction of hydrostatic capillary pressure and preservation of normal colloid osmotic pressure. ⋯ The results indicate that the therapy should focus on extracellular rather than intracellular oedema and that ischemia is not the main triggering mechanism behind oedema formation. We suggest that our therapy is superior to conventional therapy by preventing herniation during the healing period of the blood-brain barrier.
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Cerebral lesions of variable severity lead to systemic and intracranial reactions. These create secondary brain damage due to hypoxia and ischemia. The causes as well as the sequelae of secondary brain damage necessitate long-term intensive care treatment with high technical and personal expenditure. ⋯ The decision to limit treatment should be based on the numerous national and international statistical models and discussed on an individual basis, excluding even a 5% chance of survival. Early information of the family on the probable prognosis is useful. Their participation in the process of decision can be assessed only on an individual basis.
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J Neuropsychiatry Clin Neurosci · Jan 1994
The prevalence of traumatic brain injury and co-occurring disabilities in a national household survey of adults.
This original point prevalence study provides sociodemographic characteristics and Canadian household prevalence rates of adults (15 years and older) with disability who have survived a traumatic brain injury (TBI) and the type, number, and prevalence rates of co-occurring disabilities. This report is based on the Health and Activity Limitation Survey, a national survey conducted by Statistics Canada in 1986-87. ⋯ Rates are highest in the 45-64 age range, 3 times those in the 15-24 age group. Eighty-four percent of adults with TBI have co-occurring disabilities (median = 2), the most prevalent being limited mobility and agility.