No abstract

Hyponatremia frequently complicates the care of neurosurgical patients and requires prompt effective therapy. These patients commonly fulfill the laboratory criteria of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or cerebral salt wasting; the classification depends on the volume status of the patient. The authors have been dissatisfied with the standard therapy of fluid restriction for the critically ill neurosurgical patient because of 1) slow rates of sodium correction; 2) poor applicability in patients requiring multiple intravenous medications and/or nutritional support; and 3) possible dangers of inducing or enhancing cerebral ischemia in patients who already may be fluid-depleted. Reported successes in the treatment of hyponatremia due to SIADH by administration of urea and normal saline led to the authors' routine use of this therapy for hyponatremic neurosurgical patients. A retrospective review of an 18-month period revealed 48 patients (3% of all neurosurgical inpatients) with hyponatremia from various causes who received 62 treatments of urea and normal saline. Treatment consisted of 40 gm urea dissolved in 100 to 150 ml normal saline as an intravenous drip every 8 hours and an intravenous infusion of normal saline at 60 to 100 ml/hr for 1 to 2 days. The mean pretreatment serum sodium level (+/- standard deviation) was 130 +/- 3 mmol/liter (range from 119 to 134 mmol/liter). There was a significant mean posttreatment elevation to 138 +/- 4 mmol/liter (range 129 to 148 mmol/liter) (p less than 0.001, Student's t-test). Average daily fluid intake and output on treatment days were 2719 +/- 912 and 2892 +/- 1357 ml, respectively. There were no treatment complications in this group. It is concluded that urea and saline administration results in a rapid, safe, and effective correction of hyponatremia, making this method superior to fluid restriction in many neurosurgical patients.

Centrally released arginine vasopressin (AVP) has been implicated in the regulation of intracranial pressure (ICP) and brain water, and is elevated in the cerebrospinal fluid (CSF) of some patients with pseudotumor cerebri or subarachnoid hemorrhage. The authors have examined the relationship of AVP levels in CSF to ICP and brain water content in three experimental groups of cats with and without cold-induced vasogenic edema. With the cats under general anesthesia, a cold lesion was made and cannulas were placed in the cisterna magna, lateral ventricle, and aorta. Subsequent central and systemic measurements were made while the animals were awake and free-roaming. In Experiment 1, endogenous AVP levels in CSF were measured every 12 hours over a 48-hour period by radioimmunoassay in cats with sham craniotomy, mild edema, or moderate edema; no significant difference was found between groups although a diurnal variation was seen (range 2 to 18 pg/ml). In Experiment 2, either carrier solution or AVP, in doses of 1.5 or 30 ng, was administered via a lateral ventricle every 2 hours over 24 hours in unlesioned cats. In Experiment 3, cats received 2 or 35 ng of carrier solution or AVP in a similar manner, but coupled with a cold lesion. The CSF AVP levels ranged from an average of 100 to 681 pg/ml and 1.4 to 11.9 ng/ml in the two dose groups in both experiments. Neither the low nor the high dose had an effect on brain water content in normal white matter (Experiment 2), but both doses increased brain water content in edematous white matter (p less than 0.05 in Experiment 3), as determined by wet and dry weight measurements of standardized pieces of white matter. The ICP was decreased by high-dose AVP in normal cats (p less than 0.01 at 24 hours), but in lesioned cats was unchanged by low-dose and increased by high-dose AVP (p less than 0.05 at 18 hours). The authors conclude that pharmacological doses of central AVP facilitate the production of vasogenic edema.

Increasing knowledge of the neurochemical aspects of central nervous system function raises the possibility of treating neurological disease by the appropriate manipulation of neurotransmitters, neuromodulators, and neurohormones. Clinical application of this knowledge has been inhibited, however, by long-standing problems with drug delivery to the central nervous system (CNS). The availability of implantable drug infusion pumps and stereotactic catheter placement techniques may overcome many of these problems. The problems of drug delivery to the brain and the present and potential uses of implantable drug pumps for neurological disease are discussed. In addition, the relationship between CNS drug infusion and neural tissue transplantation is briefly reviewed.

Hypothesis:The North American Symptomatic Carotid Endarterectomy Trial and the European Carotid Surgery Trial demonstrated that a greater benefit from carotid endarterectomy (CEA) was seen in elderly compared with younger patients. However, no patients older than 89 years were included in either study. We hypothesized that CEA is safe and effective in patients 89 years and older.Design and Setting: This is a retrospective review of 3 neurosurgeons' CEA experience with nonagenarian patients.Participants and Interventions: Of our 1800 patients who underwent CEA, 26 were 89 years or older. Twenty-three patients had had cerebral ischemic symptoms (unilateral hemispheric symptoms in 21 and 2 dizzy spells associated with bilateral high-grade stenosis). Cerebral angiography was performed in 3 patients. Twentythree patients underwent noninvasive imaging. Four patients had bilateral high-grade stenosis and underwent staged bilateral CEA. All procedures were performed after the induction of general anesthesia with electroencephalographic (and, more recently, transcranial Doppler) monitoring and etomidate-induced burst suppression for cerebral protection during cross-clamping.Results: Unusual technical difficulties were frequently noted, including high bifurcations, looping rotated internal carotid arteries, and marked adherence of surrounding soft tissues. In 3 of the 30 procedures, a shunt was used. There were no perioperative cerebral ischemic or cardiac events. The mean hospital stay was 2 days. One patient had a transient vocal cord paresis. Twentytwo patients were alive and well 24 months following the procedure. Four patients died of non-stroke-related causes.Conclusions: Carotid endarterectomy was successfully performed without perioperative cerebral or cardiac complications in our series of 26 patients 89 years and older undergoing 30 CEAs. Extrapolating from reported results from the North American Symptomatic Carotid Endarterectomy Trial and the European Carotid Surgery Trial, we believe CEA should be considered in nonagenarian patients with high-grade symptomatic carotid stenosis who are otherwise well medically. Our recommendations are less certain in the case of asymptomatic disease.