Student study notes from paramedic coursework (2023 to 2024), not medical advice. Verify clinical values against current references and your local protocols.
| EMS etiologies | Setting: ER |
Poisoning occurs when harmful substances are ingested, inhaled, or absorbed, overwhelming the body’s ability to detoxify or eliminate them. Each toxin has a distinct pathophysiology:
Treatment varies widely depending on the substance involved. Activated charcoal is sometimes given to adsorb the toxin for removal but there are associated risks of aspiration and GI upset. Symptoms can include nausea, vomiting, abdominal pain, confusion, respiratory distress, seizures.
Some common toxins and their treatments:
Acetaminophen: Toxicity occurs when excess NAPQI, a toxic metabolite, builds up due to glutathione depletion, leading to liver damage. The antidote, N-acetylcysteine, replenishes glutathione and is administered either orally or intravenously based on the patient’s condition.
Organophosphates: Treatment involves three key drugs: Atropine (to counter acetylcholine buildup), pralidoxime (to regenerate acetylcholinesterase), and diazepam (for seizures). Atropine is titrated until respiratory symptoms improve.
Warfarin: Reversal includes Vitamin K (slow-acting), fresh frozen plasma (FFP), or prothrombin complex concentrate (PCC) for immediate clotting factor replacement.
Digoxin: Antidote involves anti-digoxin Fab for patients with life-threatening toxicity (e.g., arrhythmias, hyperkalemia). The dose is calculated based on digoxin levels or amount ingested.
Ethylene glycol and methanol: Toxic alcohols are metabolized to harmful byproducts. Antidotes include fomepizole (preferred) or ethanol, both of which inhibit alcohol dehydrogenase and prevent toxic metabolite formation.
Tricyclic Antidepressants (TCA): Sodium bicarbonate is the treatment for dysrhythmias or hypotension in TCA toxicity, with repeated dosing as needed.
Beta-blockers/Calcium channel blockers: Treatment includes calcium, glucagon, high-dose insulin, and, in refractory cases, IV lipid emulsion therapy.
Heavy metals: Chelation therapy with dimercaprol, succimer, or other agents is used to bind heavy metals like lead, mercury, and arsenic for renal excretion.
Iron: Deferoxamine is the chelation agent used to treat severe iron overdose, helping excrete iron via the kidneys.
Cyanide: Antidotes include hydroxocobalamin (preferred), sodium nitrite, and sodium thiosulfate, each acting to neutralize or excrete cyanide.
Benzodiazepine overdose Symptoms: excessive sedation with unremarkable vital signs and anterograde amnesia. Larger doses can cause coma and respiratory depression. Treatment: maintaining airway, respiration, and hemodynamic support. Intubation or assisted ventilation may be necessary. Flumazenil, a specific benzodiazepine antagonist, is useful in reversing the sedation and respiratory depression. It carries the risk of seizures (or of not being able to treat coincidental seizures).
Opioid overdose is caused by various factors, including: Chronic use of opioids, leading to tolerance and higher doses; accidental excessive intake or deliberate misuse; incorrect dosing during medical treatment.
Opioids act on the brain’s opioid receptors, causing euphoria and pain relief, but overdose suppresses the respiratory system, leading to potential death from respiratory failure. Risk factors include escalating doses, returning to opioid use after cessation, existing medical conditions or psychiatric conditions, and combining opioids with other sedative medications. Opioid overdoses often present with the “opioid overdose triad” of pinpoint pupils, respiratory depression, and reduced consciousness. Naloxone, a competitive opioid receptor antagonist, is the primary treatment for reversing opioid toxicity.