Something new about ketamine for pediatric anesthesia?

Lois, Fernande; Kock, Marc De

doi:10.1097/aco.0b013e3282f82bde

Cited by 45 publications

(22 citation statements)

References 55 publications

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“…This is based on clinical data published several years ago. The survival rate in intensive care unit of patients with septic shock was improved when they received ketamine as a sedative [23]. …”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Ketamine on Lipopolysaccharide-Induced Microglial Activation

Chang

Lee

Hsieh

et al. 2009

Mediators of Inflammation

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Microglia activated in response to brain injury release neurotoxic factors including nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Ketamine, an anesthetic induction agent, is generally reserved for use in patients with severe hypotension or respiratory depression. In this study, we found that ketamine (100 and 250 μM) concentration-dependently inhibited lipopolysaccharide (LPS)-induced NO and IL-1β release in primary cultured microglia. However, ketamine (100 and 250 μM) did not significantly inhibit the LPS-induced TNF-α production in microglia, except at the higher concentration (500 μM). Further study of the molecular mechanisms revealed that ketamine markedly inhibited extracellular signal-regulated kinase (ERK1/2) phosphorylation but not c-Jun N-terminal kinase or p38 mitogen-activated protein kinase stimulated by LPS in microglia. These results suggest that microglial inactivation by ketamine is at least partially due to inhibition of ERK1/2 phosphorylation.

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Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Ketamine on Lipopolysaccharide-Induced Microglial Activation

Chang

Lee

Hsieh

et al. 2009

Mediators of Inflammation

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“…The degree of dose sparing depends on the chemical properties of the drug, and for more lipophilic opioids such as fentanyl, the difference between equi-effective intrathecal, epidural and systemic doses may be less 96 . Minimal dose sparing has also been demonstrated with ketamine, as 0.5 to 1mg/kg is utilized in caudal studies 97,98 and the same dose systemically provides procedural sedation and analgesia 99–101 , albeit for a shorter duration 102 . Similarly, analgesia was prolonged when comparing caudal and intravenous administration of 2mg/kg tramadol 103 .…”

Section: Clinical Choice Of a Spinal Analgesic: Efficacymentioning

confidence: 99%

Neuraxial Analgesia in Neonates and Infants

Walker

Yaksh

2012

Anesthesia &Amp; Analgesia

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Neuraxial agents provide robust pain control, have the potential to improve outcomes, and are an important component of the perioperative care of children. Opioids or clonidine improve analgesia when added to perioperative epidural infusions; analgesia is significantly prolonged by addition of clonidine, ketamine, neostigmine or tramadol to single shot caudal injections of local anesthetic; and neonatal intrathecal anesthesia/analgesia is increasing in some centers. However, it is difficult to determine the relative risk-benefit of different techniques and drugs without detailed and sensitive data related to analgesia requirements, side-effects, and follow-up. Current data related to benefits and complications in neonates and infants are summarized, but variability in current neuraxial drug use reflects the relative lack of high quality evidence. Recent preclinical reports of adverse effects of general anesthetics on the developing brain have increased awareness of the potential benefit of neuraxial anesthesia/analgesia to avoid or reduce general anesthetic dose requirements. However, the developing spinal cord is also vulnerable to drug-related toxicity, and although there are well-established preclinical models and criteria for assessing spinal cord toxicity in adult animals, until recently there had been no systematic evaluation during early life. Therefore, the second half of this review presents preclinical data evaluating age-dependent changes in the pharmacodynamic response to different spinal analgesics, and recent studies evaluating spinal toxicity in specific developmental models. Finally, we advocate use of neuraxial agents with the widest demonstrable safety margin and suggest minimum standards for preclinical evaluation prior to adoption of new analgesics or preparations into routine clinical practice.

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“…3 Ketamine is specifi cally recommended for use in cases with a high risk of hemodynamic instability 4 and sepsis, 5 and it has been shown to possess novel analgesic and anti-infl ammatory properties. 6 The small intestine is very sensitive to ischemia and hypoxia, leading to severe metabolic and functional alterations. 7,8 Ischemia causes intestinal edema, loss of barrier function, cell necrosis, and bacterial translocation, which causes an endotoxic mediated systemic infl ammatory response, among other alterations, while reperfusion causes additional damage through the activation of the cellular and molecular infl ammatory cascade.…”

Section: Introductionmentioning

confidence: 99%

Ketamine reduces intestinal injury and inflammatory cell infiltration after ischemia/reperfusion in rats

et al. 2010

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Something new about ketamine for pediatric anesthesia?

Abstract: Ketamine has not yet revealed all its interactions in humans. Recent discoveries indicate interesting properties on the one hand and potentially deleterious effects on the other.

Cited by 45 publications

References 55 publications

Inhibitory Effects of Ketamine on Lipopolysaccharide-Induced Microglial Activation

Inhibitory Effects of Ketamine on Lipopolysaccharide-Induced Microglial Activation

Neuraxial Analgesia in Neonates and Infants

Ketamine reduces intestinal injury and inflammatory cell infiltration after ischemia/reperfusion in rats

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