Articles: brain-injuries.
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Venous thromboembolism is a major complication associated with traumatic brain injury and is responsible for significant morbidity and mortality. There has been a general reluctance over the years to use anticoagulant prophylaxis for patients with head injury who have suffered intracranial bleeding or for whom intracranial surgery is needed. ⋯ The survey highlighted concern about the failure to implement even the most simple means of prophylaxis. The evidence for the use of the various methods of prophylaxis is reviewed.
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To analyze the prognosis of 2284 cases with acute traumatic brain injury and discuss possible methods to improve the outcome of head injuries. ⋯ To prevent hypoxia, remove intracranial hematoma as soon as possible, use standard large traumatic craniotomy and apply mild hypothermia may be useful means for improving the outcome of severely head injured patients.
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Journal of neurosurgery · Aug 2001
Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study.
Contemporary management of head-injured patients is based on assumptions about CO2 reactivity, pressure autoregulation (PA), and vascular reactivity to pharmacological metabolic suppression. In this study, serial assessments of vasoreactivity of the middle cerebral artery (MCA) were performed using bilateral transcranial Doppler (TCD) ultrasonography. ⋯ During the first 2 weeks after moderate or severe head injury, CO2 reactivity remains relatively intact, PA is variably impaired, and metabolic suppression reactivity remains severely impaired. Elevated ICP appears to affect all three components of vasoreactivity that were tested, whereas other clinical factors such as CPP, hypotensive and hypoxic insults, and hemorrhagic brain lesions have distinctly different impacts on the state of vasoreactivity. Incorporation of TCD ultrasonography-derived vasoreactivity data may facilitate more injury- and time-specific therapies for head-injured patients.
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Brain injury : [BI] · Aug 2001
ReviewFamily carers and the adult head-injured: a critical review of carers' needs.
To appraise recent literature on the topic of perceived needs of family carers of head-injured adult relatives. MEDLINE (1966-2000), EMBASE PSYCHIATRY (1987-1999), CINAHL (1982-January 2000) and PSYCHLIT (1967-1999) databases were searched. ⋯ The design and variation in methodology of most studies reviewed limits the generalization of reported data. Further research is required to fully identify both common and individual needs of family carers of the head-injured.
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Journal of neurotrauma · Aug 2001
Intrathecal levels of complement-derived soluble membrane attack complex (sC5b-9) correlate with blood-brain barrier dysfunction in patients with traumatic brain injury.
It has become evident in recent years that intracranial inflammation after traumatic brain injury (TBI) is, at least in part, mediated by activation of the complement system. However, most conclusions have been drawn from experimental studies, and the intrathecal activation of the complement cascade after TBI has not yet been demonstrated in humans. In the present study, we analyzed the levels of the soluble terminal complement complex sC5b-9 by ELISA in ventricular cerebrospinal fluid (CSF) of patients with severe TBI (n = 11) for up to 10 days after trauma. ⋯ The analysis of the extent of posttraumatic blood-brain barrier (BBB) dysfunction, as determined by CSF/serum albumin quotient (Q(A)), revealed that patients with a moderate to severe BBB impairment (mean Q(A) > 0.01) had significantly higher intrathecal sC5b-9 levels as compared to patients with normal BBB function (mean Q(A) < 0.007; p < 0.0001). In addition, a significant correlation between the individual daily Q(A) values and the corresponding sC5b-9 CSF levels was detected in 8 of 11 patients (r = 0.72-0.998; p < 0.05). These data demonstrate for the first time that terminal pathway complement activation occurs after head injury and suggest a possible pathophysiological role of complement with regard to posttraumatic BBB dysfunction.