Intravenous lipid emulsion (ILE) has been demonstrated to be effective in amelioration of cardiovascular and central nervous system sequelae of local-anaesthetic and non-local-anaesthetic drug toxicity in animal models. Sequestration of lipophilic toxins to an expanded plasma lipid phase is credited as the predominant beneficial mechanism of action of ILE. Systematic review of published human experience is however lacking. We determined to report a comprehensive literature search of all human reports of ILE application in drug poisoning. Forty-two cases of ILE use (19 local-anaesthetic, 23 non-local-anaesthetic) were identified, with anecdotal reports of successful resuscitation from cardiovascular collapse and central nervous system depression associated with ILE administration in lipophilic toxin overdose. Although significant heterogeneity was observed in both agents of intoxication, and reported outcomes; case report data suggest a possible benefit of ILE in potentially life-threatening cardio-toxicity from bupivacaine, mepivacaine, ropivacaine, haloperidol, tricyclic antidepressants, lipophilic beta blockers and calcium channel blockers. Further controlled study and systematic evaluation of human cases is required to define the clinical role of ILE in acute poisonings.
Objective: Recent case reports of successful amelioration of lipid-soluble drug toxidromes with Intralipid infusion have prompted interest in the scope of lipid emulsions as antidotal therapy. Propranolol is a highly lipid-soluble, nonselective beta-blocker with additional local-anaesthetic properties. We explored the hypothesis that propranolol toxicity may be similarly attenuated by Intralipid infusion in a rabbit model.Methods: Twenty sedated, invasively monitored, and mechanically ventilated New Zealand White rabbits underwent propranolol infusion at 4.2 mg/min to a target mean arterial pressure (MAP) of 60% baseline MAP. Animals subsequently received 6 ml/kg 20% Intralipid, or 6 ml/kg 0.9% saline solution over a 4-minute period. Pulse rate and MAP were recorded at 2.5-minute intervals to 15 minutes.Results: MAP was greatest in the Intralipid group (median 69 mmHg, interquartile range [IQR] 17.5 mmHg Intralipid vs. median 53 mmHg, IQR 12.75 mmHg saline; p ϭ 0.029) at 15 minutes. No difference was observed in first derivative of MAP, or pulse rate between groups.Conclusions: Propranolol-induced hypotension is ameliorated by Intralipid infusion in this intact rabbit model. The mechanism of action remains to be elucidated.
Intralipid treatment prolongs survival and doubles median lethal dose in a rat model of verapamil toxicity. The mechanism of action remains to be elucidated.
The use of intravenous lipid emulsion (ILE) as an antidote has prompted significant academic and clinical interest. Between August 2009 and August 2012, data from cases of ILE use in intoxicated patients in different hospitals on different continents were voluntarily entered into a registry based on the world wide web (www.lipidregistry.org). Here, we report data from this project. Participating centers were given access to the registry following institutional subscription. Specifically sought were details of the individual patients' presenting condition, indications for ILE use, ILE administration regimen, potential complications, and of clinical outcome. Forty-eight uses of ILE were reported from 61 participating centers. Ten cases of local anesthetic systemic toxicity were reported; all (10/10) survived. Thirtyeight cases of intoxication by other agents were reported [30 decreased conscious state, 8 cardiovascular collapse (3 deaths)]. There was an elevation in GCS (p<0.0001) and increased systolic blood pressure (p=0.012) from immediately prior to ILE administration to 30 min after use. One serious and two minor adverse effects of ILE use were recorded in 48 reported cases (one case of bronchospastic reaction, one case of hyperamylasemia and one case of interference with laboratory testing). In this series of cases reported to the registry, improvements were seen for GCS in patients with central nervous system toxicity and in systolic blood pressure in shocked patients over a short time frame after the injection of ILE. Few adverse effects were recorded. Clinical trials and the reporting of drug concentrations after ILE use are necessary to further elucidate the role of ILE in clinical toxicology.
Objectives: Drug sequestration to an expanded plasma lipid phase has been proposed as a potential mechanism of action for lipid emulsions in lipophilic cardiotoxin overdose. The authors set out to document plasma and peritoneal diasylate clomipramine concentration after resuscitation with lipid emulsion in a rabbit model of clomipramine-induced hypotension.Methods: Twenty sedated mechanically ventilated New Zealand White rabbits were allocated to receive either 12 mL ⁄ kg 20% Intralipid or 12 mL ⁄ kg saline solution, following clomipramine infusion to 50% baseline mean arterial pressure (MAP). Hemodynamic parameters and serum clomipramine concentration were determined to 59 minutes. Peritoneal dialysis with 20% Intralipid or saline solution was evaluated for clomipramine concentration.
Inadvertent ingestion of sodium nitrite is known to precipitate metheamoglobinaemia. No cases exist, however, of intentional suicide by methaemoglobinaemia following self-poisoning with sodium nitrite. A 76-year-old man collapsed and rapidly developed brady-asystolic cardiac arrest 25 min following self-poisoning with an unknown quantity of crystalline sodium nitrite. On arrival in the ED the patient was asystolic with cardiopulmonary resuscitation in progress. Haemoglobin concentration was 110 g/L, arterial methaemoglobin measured 82.6% and serum lactate 9.6 mmol/L. Antioxidative treatment was undertaken with total 5 mg/kg intravenous methylene blue administered in divided aliquots. Despite prolonged resuscitative efforts the patient died. Resuscitation from methaemoglobinaemia-induced asystole following self-poisoning presents a unique therapeutic challenge. Treatment of methaemoglobinaemia-induced cardiovascular instability and overt cardiopulmonary arrest are discussed.
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