Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Oct 1999
ReviewRecovery from anesthesia and postoperative extubation of neurosurgical patients: a review.
The most feared complications after intracranial surgery are development of an intracranial hematoma and major cerebral edema. Both may result in cerebral hypoperfusion and brain injury. Arterial hypertension via catecholamine release or sympathetic stimulation and hypercapnia may be predisposing factors. ⋯ It is, however, often possible to perform a brief awakening of the patient without extubation to allow early neurological evaluation, followed by delayed emergence and extubation. Close hemodynamic and respiratory monitoring are mandatory in all cases. The availability of ultrashort intravenous anesthetic agents and adrenergic blocking agents has added to the flexibility in the immediate emergence period after intracranial surgery.
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J Neurosurg Anesthesiol · Oct 1999
Cerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure.
Early impaired cerebral blood flow (CBF) after severe head injury (SHI) leads to poor brain tissue oxygen delivery and lactate accumulation. The purpose of this investigation was to elucidate the relationship between CBF, local dialysate lactate (lact(md)) and dialysate glucose (gluc(md)), and brain tissue oxygen levels (PtiO2) under arterial normoxia. The effect of increased brain tissue oxygenation due to high fractions of inspired oxygen (FiO2) on lact(md) and CBF was explored. ⋯ The PtiO2 response to 100% FiO2 (oxygen reactivity) was inversely correlated with outcome (P < .01). Monitoring PtiO2 after SHI provides valuable information about cerebral oxygenation and substrate delivery. Increasing arterial oxygen tension (PaO2) effectively increased PtiO2, and brain lact(md) was reduced by the same maneuver.
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J Neurosurg Anesthesiol · Oct 1999
Monitoring brain PO2, PCO2, and pH during graded levels of hypoxemia in rabbits.
Brain ischemia and hypoxia are of concern when they occur following traumatic brain injury because they frequently result in potentially preventable secondary brain damage. In this study, we examined the ability of an implantable catheter (Paratrend 7; Diametrics Medical, St. Paul, MN) to continuously measure brain tissue pH, PCO2, and PO2 during graded levels of hypoxia. ⋯ As expected, there was a good correlation between the changes in pH, PCO2, and PO2 in brain tissue and sagittal sinus blood. Brain tissue PO2 was numerically lower than sagittal sinus blood at all inspired levels of oxygen. These data suggest that the Paratrend 7 may be useful in monitoring brain tissue oxygen tension in patients at risk for regional cerebral ischemia and hypoxia.
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J Neurosurg Anesthesiol · Jul 1999
Administration of hypertonic (3%) sodium chloride/acetate in hyponatremic patients with symptomatic vasospasm following subarachnoid hemorrhage.
A retrospective study was carried out to evaluate the effect of hypertonic (3%) saline chloride/acetate on various hemodynamic parameters in mildly hyponatremic patients with symptomatic vasospasm following aneurysmal subarachnoid hemorrhage (SAH). We identified 29 hyponatremic (serum sodium < 135 mEq/L) patients who received hypertonic (3%) sodium chloride/acetate as a continuous infusion. Administration of hypertonic (3%) sodium chloride/acetate resulted in higher central venous pressures and positive fluid balance, with a concomitant increase in serum sodium and chloride concentrations without metabolic acidosis. ⋯ We conclude that hypertonic (3%) sodium chloride/acetate can be administered to patients with mild hyponatremia in the setting of symptomatic vasospasm following SAH without untoward effects. Sample size and limitations of a retrospective analysis preclude conclusions about safety and efficacy of hypertonic (3%) sodium chloride/acetate administration in this patient population. However, our results support justification for a prospective, randomized, double-blind trial of hypertonic (3%) sodium chloride/acetate versus normal saline in patients with symptomatic vasospasm following SAH.
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J Neurosurg Anesthesiol · Jul 1999
Randomized Controlled Trial Clinical TrialEffects of clonidine on human middle cerebral artery flow velocity and cerebrovascular CO2 response during sevoflurane anesthesia.
The present study was designed to evaluate the effects of clonidine on human middle cerebral artery flow velocity and the cerebrovascular CO2 response during sevoflurane anesthesia using transcranial Doppler ultrasonography. The subjects were nine awake volunteers (group A) and 18 patients receiving oral preanesthetic medication of clonidine, 3-4 mcg/kg, (group C), or placebo (group S). In groups C and S, anesthesia was induced with inhalation of sevoflurane-nitrous oxide. ⋯ The Vmca value of group C was significantly lower than that of group S in hypercapnia, but not in hypocapnia or normocapnia. The CO2 response slope of group C was significantly lower than those of groups A and S. The results indicate that clonidine, administered as an oral preanesthetic medication, reduces Vmca in hypercapnia but not in hypocapnia or normocapnia, and reduces the cerebrovascular CO2 response during sevoflurane anesthesia.