Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Apr 1997
Case ReportsCerebral oximetry during circulatory arrest for aneurysm surgery.
A patient underwent surgical clipping of a complex giant intracranial carotid aneurysm with the aid of extracorporeal circulation and complete hypothermic circulatory arrest. During the entire procedure, cerebrovascular oxygen saturation (ScO2) was spectroscopically measured. The patient experienced circulatory arrest for 34 min; for 15 of the 34 min ScO2 was < 34% (minimum 32%). The patient tolerated the procedure without new neurological deficit, thus demonstrating that the previously suggested "critical" level of 35% ScO2 is not absolute.
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J Neurosurg Anesthesiol · Apr 1997
Jugular venous bulb oxygen saturation monitoring in arteriovenous malformation surgery.
We describe a case in which jugular venous bulb oxygen saturation (SjvO2) monitoring proved useful during the surgical resection of an intracranial arteriovenous malformation (AVM). Surgical resection of large intracranial AVMs may be followed by normal perfusion pressure breakthrough with brain swelling, hyperemia, and subsequent problems in achieving hemostasis. ⋯ In the case discussed, SjvO2 monitoring enabled assessment of the risk of postresection hyperemia preoperatively and permitted the degree and completeness of surgical AVM resection to be followed intraoperatively. During the normal perfusion pressure breakthrough bleeding which followed complete AVM resection, SjvO2 monitoring helped with safe management of the controlled hypotension that finally permitted hemostasis to be achieved.
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J Neurosurg Anesthesiol · Apr 1997
Case Reports Comparative StudySensitivity to vecuronium after botulinum toxin administration.
When used to treat focal dystonias, botulinum toxin may cause a transient impairment of neuromuscular transmission in muscles distant from those injected. These systemic effects are not clinically evident, but should not be ignored when patients are exposed to other drugs or conditions that also impair neuromuscular transmission. ⋯ Compared with that observed in 24 individuals who were free from neuromuscular problems, the patient's sensitivity to vecuronium was low 90 days after the seventh treatment with toxin and normal 8 days after the ninth. The possibility is considered that repeated treatments with the toxin may cause continuous remodeling of neuromuscular junctions and may cause the patient to develop some tolerance to the action of neuromuscular blockers.
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J Neurosurg Anesthesiol · Apr 1997
Case ReportsHyperalgesia induced by high-dose intrathecal sufentanil in neuropathic pain.
The patient had lower lumbar arachnoiditis as part of a failed back surgery syndrome. Two years after discectomy, she still suffered from left lumbosciatic pain despite various invasive treatments. Psychologic impairment could be excluded. ⋯ Increasing the dose to 50 mg daily could only be supported for 3 h. Sufentanil was stopped and saline started, after which the evoked hyperalgesia disappeared. It is concluded that relatively high doses of sufentanil may induce hyperalgesia in patients with arachnoiditis and neuropathic pain.
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J Neurosurg Anesthesiol · Apr 1997
Comparative StudyThe influence of acute and chronic alcohol treatment on brain edema, cerebral infarct volume and neurological outcome following experimental head trauma in rats.
The aim of this study was to determine the influence of acute and chronic ethanol treatment on neurological outcome following head trauma in rats. Eight-two Sprague-Dawley rats were divided into 10 groups. Four groups received sham head trauma (surgical incision of the scalp but no trauma) and were treated with (A) nothing, (B) chronic ethanol (6% ethanol in drinking water for 40 days), (C) acute ethanol 1.5 g/kg, intraperitoneally (IP) and (D) acute ethanol 3 g/kg IP. ⋯ Specific gravity was also lower in the acute ethanol-treated groups compared with no ethanol, chronic ethanol, and acute ethanol plus ketamine groups (p < 0.03). Based on these observations, we conclude that in this rat head trauma model acute ethanol treatment increases mortality, neurological deficit, hemorrhagic necrosis volume, and brain edema. On the other hand, chronic ethanol treatment has no apparent effect and ketamine treatment does not counteract the effect of acute ethanol treatment.