Cyanide and Thiocyanate Concentrations Following Sodium Nitroprusside Infusion in Man

Vesey, C.J.; Cole, P. V.; Simpson, P. J.

doi:10.1093/bja/48.7.651

Cited by 176 publications

(68 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…1~ Vesey, et al, have found in humans that peak cyanide levels had occurred prior to one hour post-infnsion. 5 These results are in accord with current knowledge of nitroprusside pharmacology. In guinea pigs, signs of cyanide poisoning are observed five minutes after sodium cyanide is given, but are delayed 45 to 60 minutes after an equipotent dose of sodium nitroprusside, a2 In vitro, the conversion of the total red cell haemoglobin to cyanmethaemoglobin takes one hour at 37 ~ C. 8 The peak blood cyanide level was closely related to the total nitroprusside administered in this study.…”

Section: Discussionsupporting

confidence: 85%

Cyanide toxicity following nitroprusside induced hypotension

Aitken

West

Smith

et al. 1977

Canad. Anaesth. Soc. J.

View full text Add to dashboard Cite

SODIUM NITROPI:tUSSmE was introduced for the elective induction of hypotension during general anaesthesia because of its apparent pharmacological efficacy. 1 Increased experience with this drug has led to the realization that its toxic potential is greater than previously believed. Several recently reported deaths following use of sodium nitroprusside have been attributed to the accumulation of the nitroprusside metabolite, cyanide. 2,s This has resulted in a series of revisions in the recommended dosage of sodium nitroprusside. Based on clinical experience and theoretical considerations, Davies, et al. "~ recommended that 3.5 mg/kg is the maximum dose of sodium nitroprusside that can be administered safely. Posner, et al.,4 in reporting their studies of nitroprusside-induced cyanide poisoning in baboons, further recommended that the sodium nitroprusside infusion rate be limited to 10/zg/kg/min and that the maximum dose not exceed 3 mg/kg. Most recently, Vesey, et al. '~ recommended that the total dose of sodium nitroprusside should not exceed 1.5 mg/kg during short-term infusions.In this paper the extent of cyanide accumulation and toxicity in patients receiving sodium nitroprusside infusions during intracranial surgery is reported. The doses of sodium nitroprusside employed in these studies fall within the range most recently recommended, that is, less than 1.5 mg/kg. PATIENTS AND METHODSEight female and five male patients (aged 13-66) undergoing surgery for repair of an intracranial aneurysm, were studied. Sodium nitroprusside was infused during the operation to produce hypotension as required by the surgeon. The infusion times and doses are listed in Table I. Five patients undergoing craniotomy without elective induction of hypotension were studied as a control group.Morphine and hyoscine were administered as premedication. All patients were operated on in a horizontal position. Anaesthesia was induced by thiopentone with tracheal intubation under pancuronium and was maintained using 65 per cent nitrous oxide in oxygen and morphine with intermittent pancuronium. A halothane

show abstract

Section: Discussionsupporting

confidence: 85%

Cyanide toxicity following nitroprusside induced hypotension

Aitken

West

Smith

et al. 1977

Canad. Anaesth. Soc. J.

View full text Add to dashboard Cite

show abstract

“…However, its high potency and the use of inadvertently large doses have led, in a few cases, to highly disappointing results (MacRae & Owen 1974 and others) which cannot be overlooked. After its initial clinical trials (Page et al 1955, Moraca et al 1962, Taylor et al 1970, Siegal et al 1971, its metabolic effects have been extensively investigated (Vesey et al 1974(Vesey et al , 1976 and it has been found not to cause any significant changes in cerebral haemodynamics (Griffiths et al 1974). It is thus considered superior to other hypotensive agents (Styles et al 1973, Landauer 1976.…”

Section: Discussionmentioning

confidence: 99%

“…(McDowall et al 1974) has been reduced to 1.5 mg/kg body wt. after comprehensive investigations (Vesey et al 1976). In the study reported herein an average dose of 0.54 mg/kg body wt.…”

Section: Discussionmentioning

confidence: 99%

Controlled Hypotension in Hip Joint Surgery:An Assessment of Surgical Haemorrhage During Sodium Nitroprusside Infusion

Vazeery¹,

Lunde²

1979

Acta Orthopaedica Scandinavica

View full text Add to dashboard Cite

“…11 Second, there is a dose-dependent risk of cyanide and thiocyanide toxicity. 12 Labetalol, an ␣-and ␤-adrenergic blocker, has a slower onset of action with a maximal hypotensive effect within 5 to 15 minutes. 4 Its long half-life of 4 to 6 hours limits the ability to promptly correct hypotension with cessation of the drug.…”

mentioning

confidence: 99%

Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension

et al. 2008

View full text Add to dashboard Cite

Abstract-In patients with malignant hypertension, immediate blood pressure reduction is indicated to prevent further organ damage. Because cerebral autoregulatory capacity is impaired in these patients, a pharmacologically induced decline of blood pressure reduces cerebral blood flow with the danger of cerebral hypoperfusion. We compared the reduction in transcranial Doppler-determined middle cerebral artery blood velocity during blood pressure lowering with sodium nitroprusside with that of labetalol. Therefore, in 15 patients, fulfilling World Health Organization criteria for malignant hypertension, beat-to-beat mean arterial pressure, systemic vascular resistance (Modelflow), mean middle cerebral artery blood velocity, and cerebrovascular resistance index (mean blood pressure:mean middle cerebral artery blood flow velocity ratio), were monitored during treatment with sodium nitroprusside (nϭ8) or labetalol (nϭ7). The reduction in mean arterial blood pressure with sodium nitroprusside (Ϫ28Ϯ3%; meanϮSEM) and labetalol (Ϫ28Ϯ4%) was comparable. With labetalol, both systemic and cerebral vascular resistance decreased proportionally (Ϫ13Ϯ10% and Ϫ17Ϯ5%), whereas with sodium nitroprusside, the decline in systemic vascular resistance was larger than that in cerebral vascular resistance (Ϫ53Ϯ4% and Ϫ7Ϯ4%). The rate of reduction in middle cerebral artery blood velocity was smaller with labetalol than with sodium nitroprusside (0.45Ϯ0.05% versus 0.78Ϯ0.04% cm ⅐ s Ϫ1 ⅐ %mm Hg Ϫ1 ; PϽ0.05). In conclusion, sodium nitroprusside reduced systemic vascular resistance rather than cerebral vascular resistance with a larger rate of reduction in middle cerebral artery blood velocity, suggesting a preferential blood flow to the low resistance systemic vascular bed rather than the cerebral vascular bed. M alignant hypertension and hypertensive encephalopathy are hypertensive emergencies, characterized by a severe elevation of blood pressure (BP) and impaired cerebral autoregulation (CA). 1 CA is defined as the capacity to maintain constancy of cerebral blood flow (CBF) despite changes in mean arterial pressure (MAP). Normally CA is preserved for a range of MAP from Ϸ60 to 150 mm Hg, respectively the lower and upper limits of CA. In patients with moderate hypertension, the autoregulation curve is shifted toward higher BP values, protecting the brain from hyperperfusion. 2 However, in patients with malignant hypertension, 1 BP is supposed to surpass the upper limit of CA with loss of control of cerebral perfusion. Under those circumstances, CBF becomes a function of arterial pressure, socalled pressure dependency. 3 Therefore, the initial reduction in BP is restricted to Ϸ25% of the presenting level to avoid symptomatic hypoperfusion of the brain. 4 -6 Of the therapeutic agents available, sodium nitroprusside (SNP) and labetalol are commonly used for the initial parenteral treatment of malignant hypertension. 5,7 SNP, an arteriolar and venous vasodilator, is widely advocated as a first-line agent in the treatment of malignant hyper...

show abstract

Cyanide and Thiocyanate Concentrations Following Sodium Nitroprusside Infusion in Man

Cited by 176 publications

References 23 publications

Cyanide toxicity following nitroprusside induced hypotension

Cyanide toxicity following nitroprusside induced hypotension

Controlled Hypotension in Hip Joint Surgery:An Assessment of Surgical Haemorrhage During Sodium Nitroprusside Infusion

Cerebral Hemodynamics During Treatment With Sodium Nitroprusside Versus Labetalol in Malignant Hypertension

Contact Info

Product

Resources

About