Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 1997
Morphologic analysis of the cerebral microcirculation after thermal injury and the response to fluid resuscitation.
Using the pial window model, we have previously demonstrated that there is a disruption of the blood brain barrier with distal thermal injury [1-3]. Our laboratory has shown that treatment with Lactated Ringer's Solution did not improve labeled albumin leakage. ⋯ The results show that there was significant progressive arterial dilatation over six hours in the thermally injured animals treated with HHS. There was also a significant increase in leukocyte number if the animals were thermally injured and had no resuscitation fluid or if the animals were thermally injured and underwent resuscitation fluid with Lactated Ringer's compared to either the control group or the group that was treated with HHS after thermal injury.
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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.