Ketamine anaesthesia for burns surgery

Sage, Michael R.; Laird, S. M.

doi:10.1136/pgmj.48.557.156

Cited by 13 publications

(4 citation statements)

References 5 publications

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“…demonstrated in 1972 that ketamine had distinct advantages, namely, superior cardiovascular stability profile and reduced respiratory depression when compared with other anesthetic agents. This study reported complications including emergence delirium or hallucinations, hypotension in one child (who responded to cortisone), and uncontrolled limb movements, more often seen in patients with epilepsy [20]. An article published in 1976 by Ward et al.…”

Section: Discussionmentioning

confidence: 81%

A Systematic Review of Ketamine as an Analgesic Agent in Adult Burn Injuries

McGuinness

Wasiak²,

Cleland³

et al. 2011

Pain Med

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Section: Discussionmentioning

confidence: 81%

A Systematic Review of Ketamine as an Analgesic Agent in Adult Burn Injuries

McGuinness

Wasiak²,

Cleland³

et al. 2011

Pain Med

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“…(bolus) or 4-11 mg/kg administered i.m. (Sage and Laird, 1972;Sussman, 1974;Dachs and Innes, 1997;Weber et al, 2004;Green et al, 2011;Gao et al, 2016). Peak ketamine plasma concentrations of approximately 1200-2400 ng/ml, or 5-10 mM, are necessary to induce dissociative anesthesia (Little et al, 1972;Idvall et al, 1979;Grant et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Ketamine and Ketamine Metabolite Pharmacology: Insights into Therapeutic Mechanisms

et al. 2018

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Ketamine, a racemic mixture consisting of ()- and ()-ketamine, has been in clinical use since 1970. Although best characterized for its dissociative anesthetic properties, ketamine also exerts analgesic, anti-inflammatory, and antidepressant actions. We provide a comprehensive review of these therapeutic uses, emphasizing drug dose, route of administration, and the time course of these effects. Dissociative, psychotomimetic, cognitive, and peripheral side effects associated with short-term or prolonged exposure, as well as recreational ketamine use, are also discussed. We further describe ketamine's pharmacokinetics, including its rapid and extensive metabolism to norketamine, dehydronorketamine, hydroxyketamine, and hydroxynorketamine (HNK) metabolites. Whereas the anesthetic and analgesic properties of ketamine are generally attributed to direct ketamine-induced inhibition of -methyl-D-aspartate receptors, other putative lower-affinity pharmacological targets of ketamine include, but are not limited to, γ-amynobutyric acid (GABA), dopamine, serotonin, sigma, opioid, and cholinergic receptors, as well as voltage-gated sodium and hyperpolarization-activated cyclic nucleotide-gated channels. We examine the evidence supporting the relevance of these targets of ketamine and its metabolites to the clinical effects of the drug. Ketamine metabolites may have broader clinical relevance than was previously considered, given that HNK metabolites have antidepressant efficacy in preclinical studies. Overall, pharmacological target deconvolution of ketamine and its metabolites will provide insight critical to the development of new pharmacotherapies that possess the desirable clinical effects of ketamine, but limit undesirable side effects.

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“…4 These symptoms are less frequent in children of less than 10 years old and seen commonly in elderly patients of fourth of fifth decades of life. 5 Beyond emergent reactions, ketamine produces a number of side effects that influence major body systems. The drug stimulates the cardiovascular system, producing increases in heart rate and blood pressure by 20%, immediately after injection and this effect may persist throughout the period of anaesthesia.…”

Section: Discussionmentioning

confidence: 99%

“…The drug stimulates the cardiovascular system, producing increases in heart rate and blood pressure by 20%, immediately after injection and this effect may persist throughout the period of anaesthesia. 5,6 These effects are indirect and are most likely mediated by inhibition of both central and peripheral catecholamine reuptake. Ketamine has direct negative inotropic and vasodilating activity, but these effects usually are overwhelmed by the indirect sympathomimetic action.…”

Section: Discussionmentioning

confidence: 99%

Oral Ketamine. Is it safe?

Joshi¹,

Awale²,

Lee³

2011

jgpeman

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Introduction: Safety of use of ketamine by the oral route has not been verified. Methods: Randomized controlled trial involving 30 patients in each group, comparing effects of oral ketamine and intravenous morphine on vital signs and oxygen saturation. Results: Significant change in Systolic blood pressure was noted after administration of oral ketamine (p < 0.05), which normalized after 2 hours of administration of the drug but change in Diastolic blood pressure, Mean Arterial pressure and oxygen saturation was insignificant (p>0.05). Conclusion: Use of Oral Ketamine can be considered a safe method for conscious sedation.

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Ketamine anaesthesia for burns surgery

Cited by 13 publications

References 5 publications

A Systematic Review of Ketamine as an Analgesic Agent in Adult Burn Injuries

A Systematic Review of Ketamine as an Analgesic Agent in Adult Burn Injuries

Ketamine and Ketamine Metabolite Pharmacology: Insights into Therapeutic Mechanisms

Oral Ketamine. Is it safe?

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