Journal of medical toxicology : official journal of the American College of Medical Toxicology
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Intravenous lipid emulsion (ILE) has been demonstrated to be an effective treatment for systemic toxicity associated with local anaesthetics and increasingly non-local anaesthetic agents of high lipophilicity. Effect for ILE has been demonstrated in animal models of propranolol poisoning; however, any benefit for ILE in more hydrophilic β-blockers remains uncertain. We determined to examine the effect of ILE on haemodynamic recovery following induction of hypotension with the relatively hydrophilic β-blocker, metoprolol. ⋯ No statistically significant difference between ILE and saline-treated groups was observed in MAP, or pulse rate, at any time point following rescue therapy. ILE was not effective in reversal of metoprolol-induced hypotension in this rabbit model. These findings lend inferential support for the 'lipid sink' as principal mechanism for the beneficial effect observed with ILE administration in other models of lipophilic β-blocker-induced toxicity.
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Liver aminotransferases are elevated with rhabdomyolysis in the absence of significant liver injury.
Rhabdomyolysis is an uncommon finding in the emergency department. However, the clinical implications of rhabdomyolysis are important, with a significant minority of patients developing acute renal failure and multiorgan failure. When present, the cause of elevated aminotransferases in the setting of rhabdomyolysis is often unclear. ⋯ Furthermore, AST concentrations (and not ALT) fall in parallel with CPK during the first 6 days of hospitalization for patients with rhabdomyolysis. Aminotransferase abnormalities, particularly AST, are common in the setting of rhabdomyolysis. AST concentrations decrease in parallel to CPK, suggesting skeletal muscle may be a significant source of AST elevation in these patients.
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Salicylates are common exposures. We report an unusual case of salicylate ingestion, as salsalate, with resolution of symptoms and return of salicylate levels to non-toxic values, with a subsequent, unexpected recrudescence to toxic levels requiring reinstitution of therapy. A 31-year-old man ingested unknown amounts of salsalate, hydroxyzine, and a benzodiazepine. ⋯ He was treated with sodium bicarbonate and charcoal, which resulted in decreased serum salicylate to therapeutic levels. Salicylate ingestions are known to exhibit unusual toxicokinetics and absorption in overdose; however, this is the first case we are aware of that shows a return to toxic concentrations after apparent resolution of toxicity. Recrudescence of salicylate concentrations to a degree that would dictate reinstitution of therapy for overdose is unusual and may warrant prolonged monitoring of serum salicylate concentrations in salsalate ingestions.
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Case Reports
Acute chloroform ingestion successfully treated with intravenously administered N-acetylcysteine.
Chloroform, a halogenated hydrocarbon, causes central nervous system depression, cardiac arrhythmias, and hepatotoxicity. We describe a case of chloroform ingestion with a confirmatory serum level and resultant hepatotoxicity successfully treated with intravenously administered N-acetylcysteine (NAC). A 19-year-old man attempting suicide ingested approximately 75 mL of chloroform. ⋯ Previous reports describe survival after treatment with orally administered NAC, we report the first use of intravenously administered NAC for chloroform ingestion. Acute oral ingestion of chloroform is extremely rare. Our case illustrates that with appropriate supportive care, patients can recover from chloroform ingestion, and intravenously administered NAC may be of benefit in such cases.
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Levosimendan (Levo) increases sensitivity of troponin-C to calcium, thus increasing myocardial contractility. It is also a vascular K+-ATP channel agonist producing peripheral vasodilation. Previous research with levosimendan revealed an increase in cardiac output (CO) but not blood pressure (BP) in experimental verapamil poisoning. ⋯ Levosimendan moderately improved CO but not BP in verapamil poisoning. The hypotensive effects of levosimendan were not overcome by coadministration of either 4-AP or CaCl₂. Levosimendan may not be an appropriate agent to use in the treatment of verapamil poisoning.