Nicotine toxicity

(Redirected from Nicotine Poisoning)


  • Nicotine is an alkaloid. Alkaloids are a group of compounds that are typically produced by plants to discourage animals from eating them.
  • Nicotine commonly comes from the tobacco plant
  • There are 66 other plants from which nicotine can be obtained.
  • These plants are apart of the nightshade family (include eggplant, tomato, potato, green pepper)
  • Free-base nicotine is used as an insecticide since it is highly poisonous and reactive with oxygen and other chemicals, destroying cells and tissues.

Delivery Mechanisms

  • Inhalation
  • Cigarettes (~1.0mg)
  • Vaporization
  • Nasal spray
  • Oral Chew
  • Gum
  • Lozenges
  • Tablets
  • Transdermal Patch
  • Oral bioavailability is 30-40% because of presystemic metabolism and spontaneous vomiting

Receptor Activity

  • There are 2 types of neuronal nicotinic receptors, cns and pns (α-bungarotoxin). These are ligand gated ion channels.
  • Nicotine binds to these receptors that are located on nerve terminals or on axons on cell bodies, α-bungarotoxin, polypeptide that binds irreversibly to nicotinic receptors with a high binding affinity
  • Nicotinic acetylcholine receptors are made up of α and beta subunits that form a pentameric motif
  • Different combinations of these subunits have different effects in the body.
  • Interferes with the binding of acetylcholine, binds to the receptor which then opens the ion channel releasing sodium into the cell.
  • Nicotine’s most important effect is the activation of the reward pathway which is caused by dopamine release.

Clinical Features

Postive Negative
Anxiolysis Gastrointestinal Distress
Congnitive Enhancement Hypothermia
Cerebrovasodilation Emesis
Neuroprotection Hypertension
Analgesia Seizures
Antipscyhotic Respiratory Distress

Eye pain

  • Nicotine is also an irritant and eye pain is a frequent complaint


  • Due to the neuromuscular nicotinic activation


At high doses nicotine will activate muscarinic receptors

Differential Diagnosis

SLUDGE Syndrome


If there are also muscarinic effects then strongly consider an broader treatment for Cholinergic Syndrome



  • Providers should wear appropriate PPE during decontamination.
    • Neoprene or nitrile gloves and gown (latex and vinyl are ineffective)
  • Dispose of all clothes in biohazard container
  • Wash patient with soap and water

Supportive Care

  • IVF, O2, Monitor
  • Aggressive airway management is of utmost importance.
    • Intubation often needed due to significant respiratory secretions / bronchospasm.
    • Use nondepolarizing agent (Rocuronium or Vecuronium)
    • Succinylcholine is absolutely contraindicated
  • Benzodiazepines for seizures


  • Dosing with atropine and pralidoxime are time dependent and provides ability to reverse symptoms while awaiting agent metabolism
  • For exposure to nerve agents, manufactured IM autoinjectors are available for rapid administration:
    • Mark 1
      • Contains 2 separate cartridges: atropine 2 mg + 2-PAM 600 mg
      • Being phased out with newer kits
    • DuoDote
      • Single autoinjector containing both medications
      • Same doses as Mark 1: atropine 2 mg + 2-PAM 600 mg



  • Competitively blocks muscarinic sites (does nothing for nicotinic-related muscle paralysis)
  • May require massive dosage (hundreds of milligrams)
  • Dosing[1]
  • Adult: Initial bolus of 2-6mg IV; titrate by doubling dose q5-30m until tracheobronchial secretions controlled
    • Once secretions controlled → start IV gtt 0.02-0.08 mg/kg/hr
    • Child: 0.05-0.1mg/kg (at least 0.1mg) IV; repeat bolus q2-30m until tracheobronchial secretions controlled
    • Once secretions controlled → start IV gtt 0.025 mg/kg/hr
  • No max dose, doses >400mg have been reported[2]


  • AKA 2-PAM
  • For Organophosphate poisoning only - reactivates AChE by removing phosphate group → oxime-OP complex then excreted by kidneys.
    • This must be done before "aging" occurs - conformational change that makes OP bond to AChE irreversible[3]
    • Pralidoxime can actually bind and inhibit AChE once all AChE enzymes have aged, and can make the toxicity worse
    • Window to aging depends on the agent, and is a matter of debate, but pralidoxime within 1-2 hours of exposure is the goal
  • Dosing[1]
    • Adult: 1-2gm IV over 15-30min; repeat in 1 hour if needed or 50 mg/hr infusion.
    • Child: 20-40mg/kg IV over 20min; repeat in 1 hour if needed or 10-20 mg/kg/hr infusion.


  • Depending on severity of symptoms patients can be admitted for continued aggressive supportive care or discharged if symptoms all resolve in the ED

See Also

Electronic cigarettes


  1. 1.0 1.1 Agency for Toxic Substances and Disease Registry, Case Studies in Environmental Medicine, Cholinesterase Inhibitors: Including Pesticides and Chemical Warfare Nerve Agents. Centers for Disease Control (CDC). PDF Accessed 06/21/15
  2. Hopmann G, Wanke H. Höchstdosierte Atropinbehandlung bei schwerer Alkylphosphatvergiftung [Maximum dose atropin treatment in severe organophosphate poisoning (author's transl)]. Dtsch Med Wochenschr. 1974;99(42):2106-2108. doi:10.1055/s-0028-1108097
  3. Eddleston M, Szinicz L, Eyer P, Buckley, N (2002) Oximes in Acute Organophosphate Pesticide Poisoning: a Systematic Review of Clinical Trials. QJM. 95(5): 275–283.