2007
DOI: 10.1080/15563650701365800
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Reversal of salicylate-induced euglycemic delirium with dextrose

Abstract: Salicylate poisoning inhibits Krebs cycle enzymes and uncouples oxidative phosphorylation. Under these circumstances, we hypothesize that CNS glucose supply is sometimes unable to keep up with demand resulting in hypoglycorrhacia and delirium even in the face of serum euglycemia. Supporting this conjecture, we report two euglycemic patients with salicylate-induced delirium who responded to boluses of concentrated dextrose with a prompt improvement in mental status.

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Cited by 3 publications
(2 citation statements)
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“… 22 As the kidney tries to retain potassium, the urine becomes more acidotic and does not favor urinary excretion of the salicylate. Glucose is important to measure because neuroglycopenia can happen at normal glucose level, 14 , 15 and it is preferable for a toxic patient to be normo- to hyperglycemic.…”
Section: Case Discussionmentioning
confidence: 99%
“… 22 As the kidney tries to retain potassium, the urine becomes more acidotic and does not favor urinary excretion of the salicylate. Glucose is important to measure because neuroglycopenia can happen at normal glucose level, 14 , 15 and it is preferable for a toxic patient to be normo- to hyperglycemic.…”
Section: Case Discussionmentioning
confidence: 99%
“…Patients (and providers) may be unaware of hypoglycemia in the absence of objective testing; both the counter-regulatory autonomic response and overt neurological deficit may be absent [233,234]. Additionally, significant neuroglycopenia and hypoglycemia-associated delirium (particularly in salicylism) may occur despite a "normal" peripheral blood glucose [235]. A wide range of clinical presentations have been described, including diaphoresis, nausea, tachycardia, tremor, hypothermia, focal neurological deficits, and CNS agitation, confusion, or depression.…”
Section: Dextrosementioning
confidence: 99%