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Antidote 9 V3.epub


Toxicology is a complex field where signs and symptoms can be vague and evidence for treatment may be controversial. Blanket use of reversal agents or antidotes in coma can lead to patient harm and is not recommended. Flumazenil, for example, should not be given to patients without sufficient suspicion for benzodiazepine overdose. Pralidoxime, an antidote for organophosphate poisoning, is not used as commonly in other countries that have a higher rate of poisoning. Naloxone administration is not without risk and can potentially cause serious pulmonary edema. Cyanide poisoning is difficult to determine in the pre-hospital setting and can be masked by carbon monoxide poisoning. As with all fields of medicine, toxicology continues to evolve.




Antidote 9 V3.epub



Route & Dosage: 12.5g IV.Onset & Duration: unknown details.Pharmacokinetics: liver metabolism, urine elimination, half-life 3hr (thiosulfate) and 3d (thiocyanate).Indications: cyanide toxicity.Contraindications: no major contraindications.Adverse Effects: hypotension, headache, nausea, salty taste, warmth.Drug Interaction: formal drug interaction studies have not been performed.Sodium thiosulfate serves as a sulfur donor to form thiocyanate, which is far less toxic than cyanide. Cyanide is converted to thiocyanate by the liver enzyme rhodanese. In fire victims with significant carbon monoxide exposure, the nitrite medications can further worsen tissue hypoxia by inducing methemoglobinemia. Sodium thiosulfate does not have this issue and was previously used as the sole agent for suspected cyanide poisoning with significant carbon monoxide levels. Sources disagree on the onset, peak, and duration of sodium thiosulfate. Its use as a sole agent for cyanide toxicity is not well supported (Mégarbane et al, 2003; Gracia et al, 2004). Further, several authors feel the onset is delayed and its half-life too short to be an effective antidote (Gracia et al, 2004; Hall et al, 2007). Further, sodium thiosulfate does not distribute well to the brain where the effects of cyanide could be devastating. Hydroxocobalamin avoids all of these issues.Dosing for sodium thiosulfate in adults is 12.5g IV (50mL of 25% solution) given over 10 minutes. Dosing for children is 400mg/kg IV (1.65mL/kg of 25% solution) given over 10 minutes. If symptoms return, one-half the original dose may be given. Side effects include hypotension, headache, warmth, nausea, and a salty taste. The half-life elimination of thiocyanate is about 3 days and may be doubled or tripled in renal failure. Symptoms of thiocyanate toxicity are increased tendon reflexes (hyperreflexia), pinpoint pupils (miosis), and ringing in the ears (tinnitus).The combination of hydroxocobalamin and sodium thiosulfate has been shown to be effective in severe cyanide toxicity (Hall et al, 1987). The recommended treatment is: Hydroxocobalamin 70mg/kg IV up to 5g + Sodium thiosulfate 400mg/kg IV up to 12.5gIf hydroxocobalamin is not available, the combination of sodium nitrite and sodium thiosulfate can be given. If cyanide toxicity is possible but not certain and hydroxocobalamin is not available, then sodium thiosulfate can be given alone. The preferred treatment for acute cyanide toxicity is hydroxocobalamin.


Naloxone and naltrexone are competitive antagonists at opioid receptors. They block the receptors so that the agonist medication cannot exert its effect. In effect, they are antidotes for opioid overdose. This can trigger acute withdrawal in some patients with severe, distressing symptoms. Additionally, there are some case reports of serious pulmonary edema after bolus administration of naloxone (Lassen et al, 2012; Johnson et al, 1995; Olsen, 1990), with some resulting in death (Wang et al, 1997). Dosing of naloxone should be titrated to effect.


Route & Dosage: 1-6mg IV.Onset & Duration: onset 45-60sec, peak 2min, duration 1-2hr.Pharmacokinetics: liver metabolism, urine elimination, half-life 2-3hr.Indications: symptomatic bradycardia, organophosphate poisoning.Contraindications: narrow-angle glaucoma, prostate hyperplasia, tachyarrhythmias, thyrotoxicosis, routine use during asystole or pulseless electrical activity, hypothermic bradycardia, severe coronary artery disease, severe aortic stenosis.Adverse Effects: tachycardia, palpitation, flushing, drowsiness, dizziness, skin rash, nausea, dry mouth, urinary retention, angle-closure glaucoma, blurred vision, pupil dilation, increased intraocular pressure, blockade of bradycardic response to hypoxia.Drug Interaction: oral potassium.Atropine is an anti-muscarinic agent and therefore is also and anticholinergic and parasympatholytic. The details of this medication were previously discussed. Symptomatic bradycardia secondary to toxicity can be treated with 0.5-1mg IV atropine every 2-3 minutes. Dosing for toxicity-induced symptomatic bradycardia in children is 0.02mg/kg IV every 2-3 minutes, with a minim dose of 0.1mg.In organophosphate poisoning, significantly larger doses of atropine may be needed. Dosing starts at 1-6mg IV and may be repeated every 3-5 minutes (ATSDR, 2011). If the first dose does not provide adequate effect, the next dose may be doubled (Roberts et al, 2007). The goal is atropinization, which is marked by an increased heart rate and reversal of cholinergic effects. Pralidoxime may be given after atropinization is achieved. Once atropinization is achieved, the total loading dose required is divided by 5-10 to get a 10-20% calculation. An IV atropine infusion at 10-20% the loading dose per hour can be started. If an organophosphate antidote kit is being used, atropine should be administered prior to pralidoxime.


Kane-Gill SL, Bellamy CJ, Verrico MM, Handler SM, Weber RJ. Evaluating the positive predictive values of antidote signals to detect potential adverse drug reactions (ADRs) in the medical intensive care unit (ICU). Pharmacoepidemiol Drug Saf. 2009; 18:1185-1191.


9. Novel treatments for snakebite. Snakebite is a neglected tropical disease, killing about 125,000 people in low and middle-income countries each year (see the video here). Current treatment with antivenins are expensive and snake-specific. We collaborate with Ophirex Inc. to understand the mechanisms involved in the benefit of the first near-universal antidote for snake-bite, small molecule inhibitors of venom and endogenous phospho-lipase A2.


2-3 mg of the toxin is lethal to an adult human. No antidote exists though I would try hypertonic sodium bicarbonate for the cardiac dysrrhythmias and appropraite supportive. If the patient survives 24 hrs, the patient will do well without sequelae if appropriately supported.


Hydroxocobalamin is an effective cyanide antidote when administered intravenously. Although intraosseous (IO) access is often used in critically ill patients with difficult or delayed IV access, the efficacy of IO administration has not been investigated until recently.


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