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Updated: May 1 2021

Poisons and Treatments

  • Overview
      • Poisons and Treatments
      • Treatment
      • Poison(s)
      • Notes
      • Iron
      • Used for aluminum poisoning in renal failure
      • Used in repeat transfusions that can cause iron overload (thalassemia)
      • Used in iron overdose
      • Deferasirox
      • Iron
      • Used for aluminum poisoning in renal failure
      • Used in repeat transfusions that can cause iron overload (thalassemia)
      • Used in iron overdose
      • Prussian blue
      • CesiumThallium
      • Used in the case of a radioactive incident
      • Penicillamine
      • Copper (Wilson's disease)
      • Water-soluble form of penicillin
      • Avoid in patients who have penicillin allergy
      • Weak association with improve outcomes in scleroderma
      • Lead
      • Can chelate and deplete calcium ions
      • Only needed in moderate to severe lead poisoning
      • Dimercaprol (BAL)
      • Arsenic
      • Lead
      • Mercury
      • Used in conjunction with EDTA for lead poisoning
      • Arsenic
      • Lead
      • Mercury
      • Chelation therapy more commonly used in children
      • N-acetylcysteine
      • Acetaminophen
      • Best if given with 8-10 hours
      • Also a mucolytic
      • Best next step in management if you suspect acetaminophen intoxication yet have no lab results (it is a benign treatment)
      • Sodium bicarbonate
      • Salicylates
      • Tricyclic antidepressants (TCA)
      • First sign of OD is hyperventilation and respiratory alkalosis
      • Do not give with physostigmine
      • First do an EKG, if wide QRS (in TCA overdose) then try sodium bicarbonate
      • Deprotonation of drugs causes improved urinary excretion
      • Potassium iodide
      • Radioactive iodine (I-131)
      • Given to prevent the uptake of I-131
      • Can also be used in thyroid storm as iodine initially decreases thyroid hormone production
      • Ammonium chloride (NH4Cl, acidic)
      • Amphetamines (basic)
      • Eliminates amphetamines by acidifying urine which results in a charged amphetamine molecule which is excreted
      • Atropine
      • Pralidoxime
      • Hyoscyamine
      • Anticholinesterases
      • Organophosphates
      • Sarin (nerve gas)
      • Atropine blocks Ach receptors decreasing the effect of these drugs.
      • Hyoscyamine is second line if atropine is not available
      • Pralidoxime, if given in a timely manner, regenerates acetylcholinesterase reversing the initial pathology
      • Physostigmine
      • Antimuscarinic
      • Anticholinergic agents
      • Do not give if patient may have TCA OD as it may lead to heart block or asystole
      • Tertiary amine that can cross the BBB and reverse CNS symptoms of atropine
      • Naloxone/naltrexone
      • Opioids
      • Precipitates withdrawal symptoms in chronic opioid users
      • Not indicated in neonates who may be withdrawing
      • Indicated particularly in adult patients who have respiratory depression
      • Naltrexone decreases alcohol cravings
      • Flumazenil
      • Benzodiazepines
      • May cause seizures in addicted benzodiazepine users
      • Not routinely used, better to let the patient "sleep off" their benzodiazepine overdose
      • Ensure patient maintains respiratory effort and airway
      • Ethanol IV infusion
      • Antifreeze (ethylene glycol)
      • Methanol
      • Think antifreeze when ingested substance is said to be sweet and individual appears "drunk without the typical smell of alcohol"
      • Glucagon
      • β-blockers
      • IM glucagon is best initial therapy
      • β-blockers (propranolol, esmolol)
      • Theophylline
      • OD symptoms are due to β2activation: hypotension, tachycardia, hypokalemia, hyperglycemia
      • Digitalis antibody, lidocaine, Mg2+
      • Digitalis
      • GI disturbance and visual halos classic in overdose
      • Amyl and sodium nitrite
      • Sodium thiosulfate
      • Hydroxycobalamin
      • Cyanide found in rodenticides "gopher goitter",released in burning of plastics and wool, and plants such as cassava
      • Cyanide binds Fe3+ of cytochrome c in the electron transport chain and blocks cellular respiration
      • Nitrites generate methemoglobin, which can save the ETC by binding up the cyanide
      • Methylene blue
      • Vitamin C
      • Methemoglobin
      • Iron in the heme molecule is Fe3+ which cannot bind oxygen until it is reduced to Fe2+by treatment
      • 100% O2 (consider hyperbaric O2)
      • Carbon monoxide (CO)
      • CO binds with much greater affinity than O2
      • Aminocaproic acid
      • tPA
      • Streptokinase
      • -
      • Vitamin K
      • Plasma infusion
      • Warfarin
      • Bridge with heparin
      • If patient suddenly has increase in PT/PTT look for other medications that are P450 inhibitors
      • Protamine
      • Protamine is a highly positively charged peptide which strongly binds to the negatively charged heparin
      • Antivenin
      • Rattlesnake bite
      • -
  • Iron Poisoning
    • Most deaths due to iron poisoning (ingestion of iron tablets) occur in children between 12 - 24 months of age
    • Symptoms occur within 30 min to several hours
      • abdominal pain, diarrhea, vomiting
      • cyanosis, drowsiness, hyperventilation resulting from acidosis
    • Death can result in six hours, but an apparent recovery may happen from 6 - 12 hours with death ensuing in the next 12 hours
    • If not treated early, damage to the stomach can lead to pyloric stenosis or gastric scarring
    • Early treatment with deferoxamine can reduce mortality significantly from 45% to 1%
    • Mechanism of action of iron related damage
      • iron overdose results in the peroxidation of membrane lipids leading to cell death
      • the Fenton reaction produces dangerous free radicals
  • Methanol and Ethylene Glycol Toxicity
    • Each are competitive substrates for alcohol dehydrogenase (ADH)
    • Methanol
      • metabolized by ADH to formaldehyde followed by aldehyde dehydrogenase to form formic acid which is toxic to the optic nerve
        • early toxicity of formic acid is metabolic acidosis by formic acid itself
        • formic acid also binds to cytochrome oxidase blocking oxidative phosphorylation
        • resulting in lactic acidosis which is the latter and leading cause of the metabolic acidosis
      • signs and symptoms appear within 12 - 24 hours after ingestion
        • CNS depression
          • methanol acts similarly as ethanol as a CNS depressant
        • metabolic acidosis
        • visual changes
          • blindness occurs with as little as 30 mL and death at 100 mL ingestion
    • Ethylene glycol
      • colorless, odorless, sweet-tasting liquid
      • toxicity derives from the hepatic oxidation of ethylene glycol to oxalic acid
        • degraded by same pathway as methanol
          • the glycolic acid produced by aldehyde dehydrogenase is converted in oxalic acid
        • oxalic acid binds calcium and forms calcium oxalate crystals that damage the heart, brain, lungs, kidneys
      • signs and symptoms develop in stages after ingestion
        • first stage: 0.5 - 12 hours
          • stronger inebriant than methanol and ethanol causing mild depression of CNS resulting in seizures and coma
          • patients appear "drunk without smelling like alcohol"
          • within 4 - 12 hours, calcium oxalate crystals deposit in the brain causing CNS toxicity, cerebral edema, meningismus (nuchal rigidity, photophobia, headache without infection or inflammation)
          • hypocalcemia occurs due to binding of calcium by oxalic acid and can cause prolonged QT, arrhythmias, myocardial depression
        • second stage: 12 - 24 hours
          • tachypnea occurs to offset the metabolic acidosis due to the toxic metabolites produced
          • multiorgan failure (CHF, lung injury, myositis) due to widespread crystal deposition
          • NOTE: most deaths occur in the second stage
        • third stage: 24 - 72 hours
          • acute anuric renal failure from crystal deposition but full recovery occurs within weeks to months
    • Treatment
      • IV ethanol: competitive substrate for ADH and has greater affinity for ADH than methanol and ethylene glycol
      • fomepizole: inhibits ADH preventing production of toxic metabolites
    • Tetrodotoxin
      • Highly potent toxin that binds to fast voltage-gated Na+ channels, preventing depolarization
      • Presents with nausea, diarrhea, paresthesias, weakness, dizziness, and loss of reflexes
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