- 1 Background
- 2 Clinical Features
- 3 Differential Diagnosis
- 4 Evaluation
- 5 Management
- 6 Antidotes
- 7 Disposition
- 8 See Also
- 9 References
- 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.
- Cigarettes (~1.0mg)
- Nasal spray
- Oral Chew
- Transdermal Patch
- Oral bioavailability is 30-40% because of presystemic metabolism and spontaneous vomiting
- 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.
- 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
- Anticholinergic Toxicity
- Organophosphate Toxicity
- Sympathomimetic Toxicity
- Neuroleptic Malignant Syndrome (NMS)
- Serotonin Syndrome
- Carbamate toxicity
- Mushroom toxicity, especially:
- Organophosphate toxicity
- Nerve agent
- Nicotine toxicity (look alike)
- Acetylcholinesterase inhibitor overdose (e.g in myasthenia gravis or post anesthesia reversal)
- 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
- IVF, O2, Monitor
- Aggressive airway management is of utmost importance.
- 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
- Single autoinjector containing both medications
- Same doses as Mark 1: atropine 2 mg + 2-PAM 600 mg
- Mark 1
- Competitively blocks muscarinic sites (does nothing for nicotinic-related muscle paralysis)
- May require massive dosage (hundreds of milligrams)
- 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
- 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
- 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
- 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
- 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
- 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
- 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.