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Canadian Anaesthetists' Society journal 1981-May

Cerebrospinal fluid cyanide after nitroprusside infusion in man.

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
P A Casthely
J E Cottrell
K P Patel
A Marlin
H Turndorf

Atslēgvārdi

Abstrakts

Sodium nitroprusside (SNP) is frequently used as an hypotensive agent for clipping of intracranial aneurysms, repair of arteriovenous malformations and resection of vascular tumours. Cyanide (CN), which is its main metabolic product, has been recovered from the cerebrospinal fluid (CSF) of the rat after intravenous administration of CN, but recovery of CN from CSF after SNP has not been reported in man. Seven consenting adults were studied. Adequate premedication was provided with pentobarbitone 2 mg x kg-1 and atropine 0.4 mg one hour before operation. Anaesthesia was induced with thiopentone 8 mg x kg-1 and maintained with nitrous oxide 60 per cent with oxygen and supplemental fentanyl 0.05 mg and pancuronium 0.5-1 mg as needed. Lumbar subarachnoid, radial artery, central venous, and Foley urinary catheters were inserted. Arterial carbon dioxide tension (PaCO2) was maintained between 4.6-5.32 kPa (35-40 torr) with an Air Shields ventilator. Red cell, plasma and CSF cyanide were measured using a digital ionanalyzer before and at 30 minutes interval after infusing SNP at a rate sufficient to maintain the blood pressure at two thirds of the pre-operative level. Average total dose of SNP was 0.51 mg x kg-1. CN concentration in the red blood cells increased from 9.5 +/- 2.05 to 75.12 +/- 17.12. Plasma CN increased from 0.54 +/- 0.05 to 1.09 +/- 0.14 micrograms per cent. CSF CN increased from 0.11 +/- 0.04 to 0.72 +/- 0.07 micrograms per cent. Significant increase in red cell, plasma and CSF CN occurred five minutes after the start of SNP and returned to the preoperative level 19 hours later. Conclusion CN crosses the blood-brain barrier. Large doses of SNP in patients with neurovascular brain disorders warrants caution because cytotoxic cerebral oedema and CN encephalopathy have been described in rats after intravenous injection of sodium cyanide or exposure to hydrogen cyanide.

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