Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 1997
Cerebral vascular response to hypertonic fluid resuscitation in thermal injury.
The purpose of this project was to study the effects of various resuscitation fluid protocols in a systemically thermally injured rat sustaining 70% body surface area third degree burn using the pial window model in rats. The results show that there was a significant albumin leak in the cerebral vessels in both the experimental group which underwent no resuscitation fluid, as well as the experimental group that was resuscitated with Lactated Ringer's solution using the Parkland formula. When this was compared to the control group, as well as to the experimental group which received hypertonic hyperosmotic saline (HMS) boluses every hour, there was little if any leakage seen.
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Acta Neurochir. Suppl. · Jan 1997
Characterisation of brain edema following "controlled cortical impact injury" in rats.
Significance, origin and nature of posttraumatic brain edema are still being debated. Recently, a "controlled cortical impact injury" (CCII) was introduced to model traumatic brain injury. Purpose of this study was to investigate the development and nature of brain edema following CCII. ⋯ A significantly decreased ADC (apparent diffusion coefficient) indicates the cytotoxic (ischemic) component of edema in this model. In conclusion, CCII produces significant posttraumatic brain swelling and edema which is both, of vasogenic and cytotoxic nature. Thus, the CCII models the human cortical contusion more appropriately and opens new avenues for therapeutical studies focussing on cortical contusions.
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Acta Neurochir. Suppl. · Jan 1997
Acute blood-brain barrier changes in experimental closed head injury as measured by MRI and Gd-DTPA.
The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury (CHI) and to what extent BBB is affected by secondary insult. The BBB disruption was quantified using T1-weighted MRI following administration of Gd-DTPA. The maximal signal intensity (SI) enhancement was used to calculate BBB disruption. ⋯ However, the SI increased dramatically upon reperfusion and was equal to that of control after 60 minutes. In conclusion we may consider, that CHI is associated with a rapid and transient BBB opening which begins at the time of the trauma and lasts not more than 30 minutes. It has been also shown that addition of hypoxia and hypotension prolongs the time of BBB breakdown.
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Acta Neurochir. Suppl. · Jan 1997
Clinical TrialHypertonic/hyperoncotic saline reliably reduces ICP in severely head-injured patients with intracranial hypertension.
Hypertonic saline (HS) has been shown to decrease intracranial pressure (ICP) and cerebral water content in experimental models of traumatic brain injury (TBI). 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 therapy-resistant intracranial hypertension in patients with severe TBI. Six patients with severe TBI (GCS < 8) 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 and received between one and ten bolus infusions of maximal 250 ml HS/HHES at a rate of 20 ml/min. ⋯ Plasma sodium normalized within 30 min. Experimental studies from our laboratory indicate that the ICP lowering effect is primarily due to dehydration of brain tissue and that cerebral blood volume remains largely unaffected by HS. In summary, HS/HHES reduces otherwise therapy-resistant intracranial hypertension and improves cerebral perfusion even after repeated administration without negatively affecting blood pressure or causing a rebound ICP increase.