Articles: brain-injuries.
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Critical care clinics · Jan 1997
ReviewThe use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury.
Traumatic brain injury is a common occurrence in the United States, leading to approximately 190,000 deaths or long-term disabilities. Following the primary insult, secondary disturbances in cerebral blood flow (CBF) and metabolism may have deleterious effects on potentially viable neurons. ⋯ Aggressive hyperventilation produces a marked reduction in CBF, which may give rise to or exacerbate cerebral ischemia, thus enhancing rather than reducing secondary injury. This article reviews the role of hyperventilation in the treatment of increased ICP and its impact on cerebral ischemia following traumatic brain injury.
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Acta Neurochir. Suppl. · Jan 1997
Biphasic pathophysiological response of vasogenic and cellular edema in traumatic brain swelling.
The objective of this study was to quantify the temporal water content changes and document the type of edema (cellular versus vasogenic) that is occurring during both the acute and the late stages of edema development following closed head injury. Adult Sprague rats (n = 50) were separated into two groups: Group I: Sham (n = 8), Group II: Trauma (n = 42). The measurement of brain water content (BWC) was based on T1, whereas the differentiation of edema on the measurement of the random, translational motion of water protons (apparent diffusion coefficients-ADC) by MRI. ⋯ This transient increase; however, was followed by a continuing decrease in ADC beginning at 45 minutes post injury and reaching a minimum at days 7-14 (-103%). Since the BWC continued to increase during the next day (10.3%), it is suggested cellular edema formation started to develop soon after injury and became dominant between 1-2 weeks post injury. In conclusion we may consider, that there is a predominantly vasogenic edema formation immediately after injury and later a more widespread and slower edema formation due to a predominantly cellular swelling.
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Comparative Study
Treatment of refractory intracranial hypertension in severe traumatic brain injury with repetitive hypertonic/hyperoncotic infusions.
Rapid resuscitation of clinical and experimental traumatic brain injury (TBI) with hypertonic saline (HS) has been shown to improve neurological function and decrease intracranial pressure (ICP). The purpose of the present study was to test the efficacy of administration of HS (7.5%) combined with 6% hydroxyethyl starch (molecular weight 200,000/0.60-0.66; HHES) for the treatment of intracranial hypertension refractory to standard therapy in patients with severe TBI. With approval of the Institutional Ethics Committee six consecutive patients with severe TBI (GCS < 8) between 22 and 47 years of age (mean 32) who met the inclusion criteria (therapy resistant ICP > 25 mmHg, cerebral perfusion pressure (CPP) < 60 mmHg, plasma-Na+ < 150 mOsm and > 4 hours since the last HS/HHES treatment) were prospectively enrolled in the study. ⋯ Plasma sodium normalized within 30 min. HS/HES might become an interesting addition to conventional treatment maneuvers currently used for ICP therapy. It reduces otherwise therapy-resistant intracranial hypertension without negatively affecting blood pressure, blood gases and cerebral perfusion.
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Critical care clinics · Jan 1997
ReviewNutritional management of the critically ill neurologic patient.
To summarize, the event of severe neurologic injury results in significant metabolic changes. These changes cause increased requirements for protein and nonprotein calories, micronutrients, and small bowel feedings or TPN. Early feeding has been shown to improve survival. ⋯ Provide 40% to 70% above basal needs as total calories, with 30% to 40% of calories as lipid to minimize hyperglycemia. Provide protein as small peptides to improve tolerance, absorption, utilization, and gut integrity. Provide a lipid source with 50% to 70% medium-chain triglycerides and an omega-6 to omega-3 ratio of 2:1 to 8:1 to minimize negative effects of omega-6 fatty acids and provide an easily absorbed and utilized source of lipid.
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Acta Neurochir. Suppl. · Jan 1997
Comparative StudyBlood-brain barrier breakdown occurs early after traumatic brain injury and is not related to white blood cell adherence.
The time course of blood-brain barrier (BBB) breakdown after traumatic brain injury (TBI) has important implications for therapy. This study was conducted in order to test post-traumatic BBB dysfunction in a model of fluid-percussion induced TBI in rabbits at 1 and 6 hours after TBI and relate it to white blood cell (WBC) activation. Ten anesthetized rabbits had chronic cranial windows implanted three weeks prior to experimentation. ⋯ We conclude that after fluid-percussion injury the BBB is damaged at 1 h post-trauma and that its function is restored 6 h later. Increased WBC sticking at 6 h is not associated with BBB breakdown. Whether WBCs may cause vascular permeability changes at a later point needs further investigation.