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toxicology pt 2

Cholinergic Toxidrome (Organophosphate exposure and mushrooms with muscarinic effects)

  • Key idea: Cholinergic toxicity arises from excess acetylcholine signaling, most classically via organophosphate pesticides and certain mushrooms with muscarinic properties.

  • Two main exposure sources discussed:

    • Organophosphate poisoning (insecticides/pesticides)

    • Mushroom ingestion with muscarinic activity (not psilocybin mushrooms; some mushrooms have dangerous muscarinic effects even in small quantities)

  • Symptoms (SLUDGE + Killer Beees):

    • S: Salivation

    • L: Lacrimation (tearing)

    • U: Urination

    • D: Destination/Defecation (GI cramping and diarrhea)

    • G: Gastrointestinal upset (cramps, vomiting)

    • E: Emesis

    • Also: Bronchorrhea, bronchospasm, sweating, miosis (pinpoint pupils), bradycardia, sweating, wheezing, and airway secretions

  • Other descriptors discussed:

    • “Sludge” = salivation, lacrimation, urination, defecation, GI cramps, emesis

    • “Dumbbells” mnemonic for diarrhea and urination; “Killer bees” mnemonic for bradycardia, bronchorrhea, bronchospasm

    • Wet/wet-willy description of secretions and sweating

    • Pinpoint pupils indicate cholinergic effect; mydriasis indicates dilated pupils seen with stimulants/anticholinergics; narcotics typically cause miosis as well

  • Differential pupil findings:

    • Pinpoint pupils: cholinergic, narcotics/opioids

    • Dilated pupils: stimulants, anticholinergic

  • Hallmarks of cholinergic toxicity beyond pupils:

    • Excessive secretions, sweating

    • Bronchorrhea and bronchospasm leading to respiratory compromise

    • Diarrhea and incontinence (urination/defecation) due to smooth muscle stimulation

  • Common triggers and settings:

    • Organophosphate poisoning is a common occupational/household exposure

    • Ingestion of certain dried mushrooms with muscarinic toxins

  • Prehospital/clinical management (as discussed):

    • Atropine to counteract muscarinic effects and improve airway/hemodynamics

    • Fluids to support perfusion due to secretions and ongoing loss

    • Benadryl (diphenhydramine) mentioned in the discussion as part of treatment

    • Emphasis on treating early and recognizing the constellation of symptoms (don’t rely on heart rate alone; look for saliva, tearing, urine, stool, GI cramps, emesis, and secretions)

  • Noted caveats:

    • Cholinergic toxidrome can present with bradycardia; heart rate changes may not be the sole clue

    • Miosis is common; mydriasis can occur with other toxidromes, so use constellation clues

    • Poison control is an important resource for mushroom and mixed exposures

    • The speaker emphasized that you can treat based on a constellation of symptoms even if a precise toxin isn’t identified yet

  • Practical implications for prehospital care:

    • Recognize SLUDGE + DUMBELLS + KILLER BEES patterns

    • Initiate atropine and fluids when cholinergic toxidrome is suspected

    • Do not delay treatment awaiting lab confirmation

  • Miscellaneous notes:

    • ChatGPT/mushroom-ID limitations were discussed; mushrooms are not reliably identified by chat tools and should be treated as a constellation of symptoms

    • The term “organophosphate poisoning” is still the canonical reference in exams and practice for cholinergic pesticide exposure

Salicylate (Aspirin) Overdose from Pepto-Bismol and similar products

  • Case context: 3-year-old ingested Pepto-Bismol (contains salicylates) with mother seeking guidance

  • Key symptoms of salicylate toxicity:

    • Hyperthermia (increased body temperature)

    • Hyperventilation (tachypnea) due to metabolic acidosis/respiratory compensation

    • Tinnitus and potential temporary hearing loss

    • Vomiting and possible metabolic acidosis

  • Common non-aspirin salicylates exposure sources:

    • Pepto-Bismol (bismuth salicylate) and wintergreen oil contain salicylates

  • Toxic doses and thresholds discussed:

    • Lethal dose for a 3-year-old discussed as 7{,}500 \, mg (3-year-old example)

    • Toxic dose threshold cited around 500 \, mg (sick threshold in some discussions; context dependent)

    • Example calculation for baby aspirin (81 mg each):

    • Lethal dose for a 3-year-old: 7500 \text{mg}

    • Number of baby aspirin tablets to reach lethal dose:
      rac{7500}{81} \, \approx \, 92 \text{ tablets}

  • Treatment considerations and thresholds:

    • Early activated charcoal can be considered depending on time since ingestion

    • Sodium bicarbonate therapy can be used to alkalinize urine and support acid–base balance

    • Potassium management if prolonged vomiting or electrolyte disturbances occur

    • Supportive care and monitoring, with transfer to ED for closer management

  • Important clinical distinctions:

    • Salicylate overdose often presents with a mixed respiratory alkalosis and metabolic acidosis; profound toxicity can lead to coma and death without timely treatment

    • Hearing symptoms (tinnitus) can be an early clue in adults; in children, the presentation may be more variable

Opioid Overdose and Narcan (Naloxone) Reinforcement Case

  • General opioid overdose triad (as discussed in the session):

    • Decreased respiratory rate and depth

    • Pinpoint pupils (miosis)

    • Altered mental status; can be unresponsive

    • Other notes: temperature changes and variable bowel sounds are not consistently diagnostic in opioids; focus on respiration and mental status

  • Cardiac arrest scenario with opioids:

    • Narcan (naloxone) can be used but not as a primary treatment for arrest without a reversible respiratory component

    • Prehospital priority in arrest is high-quality CPR; Narcan may be layered if airway/respiratory status improves or if opioid exposure suspected with respiratory compromise

  • Narcan dosing and administration in the field:

    • Intranasal naloxone (MAD device): typically start with 2 mg total (1 mg per nostril)

    • Intravenous or intramuscular dosing: starting 0.4–0.5 mg, titrating upward as needed

    • If continuous exposure suspected or high-dose ingestion, re-dose after a short interval due to short duration of action relative to some opioids (rebound respiratory depression possible)

    • Duration of action for naloxone: 20{-}$60 \, minutes; patients can relapse into respiratory depression as the antagonist wears off

  • Dosing considerations and cautions:

    • If active opioid exposure suspected, provide supportive care (ventilation, airway management) and administer Narcan as needed to restore respirations

    • Avoid excessive doses that cause sympathetic surge unless necessary; monitor for withdrawal and agitation after reversal

    • Be aware of mixed overdose scenarios where opioids co-exist with other depressants or stimulants

  • Field approach to suspected opioid overdose:

    • Assess respiratory status and provide ventilation as needed

    • Administer Narcan if respiratory depression is present; titrate to maintain adequate respiration

    • Reassess after each dose; plan for transport and ongoing monitoring

  • Additional notes on opioid toxidromes:

    • Pupillary changes can be pinpoint; not all patients will have classic features

    • GCS and respiratory status are more reliable indicators than pupil size alone

    • Some opioid exposures include methadone or other long-acting opioids, increasing risk of re-depression after initial reversal

Stimulants (Cocaine, Methamphetamine, MDMA, etc.)

  • Common stimulants discussed: cocaine, methamphetamine (and related forms such as MDMA, ecstasy, etc.), caffeine, Ritalin, and others

  • Typical toxidrome features:

    • Tachycardia and hypertension

    • Hyperthermia, agitation, anxiety, and insomnia

    • Vasoconstriction effects can lead to chest pain and potential myocardial ischemia or MI in young patients

    • Affected electrical activity can manifest as wide QRS or STEMI-like patterns on EKG due to sodium channel effects

  • Cocaine-specific considerations:

    • Routes of administration: snorted, smoked (“crack”), injected, topical

    • Can cause QT/QRS widening due to sodium channel effects

    • Chest pain and potential MI risk due to increased myocardial oxygen demand and vasospasm

  • Acute management principles:

    • Benzodiazepines are a first-line treatment to reduce agitation, sympathetic drive, and seizures; acceptable for tachyarrhythmias caused by stimulants

    • Aggressive cooling for hyperthermia; oxygen as needed

    • Maintain airway and ventilation; consider ACLS if necessary

    • If evidence of STEMI, give aspirin; treat as appropriate, but consider underlying stimulant-induced ischemia

  • Arrhythmia considerations:

    • Sinus tachycardia can be a result of stimulants; SVT or other tachyarrhythmias may require different interventions

    • Vagal maneuvers or pharmacologic strategies may be considered; benzodiazepines help reduce sympathetic tone

  • Specific cautions:

    • Avoid using nitroglycerin or beta-blockers as a blanket approach in stimulant-associated chest pain due to potential unopposed alpha-adrenergic activity; benzodiazepines are preferred initially

    • In cases with suspected VT or other complex rhythms, prioritize airway and breathing; avoid improper rhythm-based therapy without confirming the rhythm and underlying cause

  • Ecstasy/MDMA and prolonged exposures:

    • Raves or sustained activity can lead to severe hyperthermia requiring aggressive cooling plus benzodiazepines

  • General notes:

    • Supportive care (IV fluids, cooling, oxygen) is central; benzodiazepines are foundational

    • STEMI pattern due to stimulant use is often physiologic ischemia rather than a fixed coronary blockage, but must be evaluated and treated appropriately

Depressants and Sedative-Hypnotics (Benzodiazepines, Barbiturates, etc.)

  • Overview: Depressants slow CNS activity; barbiturates and benzodiazepines are common examples discussed

  • Key management principles:

    • Support ABCs (Airway, Breathing, Circulation)

    • Consider airway support and ventilation if needed

    • Fludis and electrolyte management as indicated

    • Avoid patient harm from aspiration when intoxicated or unconscious

  • Benzodiazepines in toxidromes:

    • Used to counteract agitation, seizures, and sympathetic overdrive in various stimulant or mixed overdoses; caution in elder patients or polypharmacy cases

  • Barbiturates:

    • Similar depressant effects; provide supportive care; not as commonly used as antidotes in prehospital settings as benzodiazepines

Cannabinoids and Cannabis-related Issues

  • Marijuana overdose is typically not life-threatening, but can be complicated when laced with other substances

  • Cannabinoid hyperemesis syndrome (CHS):

    • Repeated heavy cannabis use can lead to cyclic vomiting and abdominal pain; hot baths/showers can help alleviate symptoms temporarily

  • Practical point:

    • Cannabis alone is less likely to cause severe toxidrome; attention to possible co-ingestions is important

Alcohol (EtOH) Intoxication and Overdose

  • Acute alcohol intoxication increases CNS depression via GABAergic enhancement and glutamate suppression

  • Overdose risks include respiratory depression and aspiration

  • Management approach:

    • Supportive care and ABCs

    • Fluids to manage dehydration and general supportive care

    • Do not rely on a single antidote; focus on airway protection and monitoring

  • Withdrawal considerations (not deeply covered in this episode but mentioned historically):

    • Withdrawal can cause tremors, agitation, autonomic hyperactivity; management discussed in later sessions

Beta-Blocker and Calcium Channel Blocker Overdoses

  • Beta-blocker overdose:

    • Presents with bradycardia, hypotension, and potential shock

    • Reversal strategies discussed: glucagon can increase heart rate and inotropy; consider epinephrine/dopamine infusions as needed

  • Calcium channel blocker overdose:

    • Similar to beta-blocker overdose; management may include calcium administration (calcium gluconate or calcium chloride) and vasopressors/epinephrine drips to support perfusion

  • General principle: Offsets of negative inotropy and chronotropy require dedicated supportive care and often vasoactive support; consider advanced therapies per protocol

Digoxin Toxicity

  • Classic ECG clue: “ice cream scoop” appearance on the ST segment (sagging or scooped ST segment)

  • Symptoms: nausea, vomiting, blurred vision, halos

  • Often seen in patients with atrial fibrillation on digoxin therapy; can have arrhythmias or PVCs

  • Management considerations (briefly noted):

    • Digoxin-specific antibodies (Digibind) may be used in severe overdose; exact dosing guided by serum levels and clinical status

Tricyclic Antidepressant (TCA) Overdose

  • Key cardiac effect: Sodium channel blockade leading to QRS widening on ECG

  • Resulting clinical picture: arrhythmias, seizures, hypotension

  • Main prehospital treatment detail discussed:

    • Sodium bicarbonate therapy is the antidotal/definitive maneuver in TCA overdose: administered as 1 mEq/kg IV bolus and repeated as needed to narrow QRS and stabilize rhythm

    • Dosing guidance mentioned: “1 mEq/kg” per ampoule and repeat until QRS improves and patient stabilizes

  • Associated risks: seizures are a common complication; supportive care and rapid transport are essential

Carbon Monoxide, Cyanide, and Other Hazardous Toxins

  • Carbon monoxide exposure (CO): classic exposure in enclosed spaces; treat with high-flow O2; hyperbaric oxygen therapy in select cases based on protocol

  • Cyanide exposure: often seen in smoke inhalation and certain industrial exposures; treat per local protocol

  • Other toxins listed briefly (for exam familiarity): hydrofluoric acid and related chemical exposures; be prepared to identify exposure routes and immediate safety concerns

Case-based Review and Exam Prep Takeaways

  • Case 1: Acetaminophen overdose

    • Consider acetaminophen-containing products in the patient’s meds; ask about all products used in prior 24 hours and/or days

    • Early NAC administration is crucial; activated charcoal if early and appropriate

    • Toxic dose threshold: 150 rac{mg}{kg} within 24 hours; antidote works best when given early

  • Case 2: Salicylate overdose (Pepto-Bismol exposure)

    • Watch for hyperthermia, tachypnea, tinnitus, and metabolic acidosis

    • Lethal dose in a child example: 7{,}500 \, mg; sick dose around 500 \, mg; calculation example for baby aspirin: rac{7500}{81} \approx 92 tablets

    • Early charcoal and sodium bicarbonate therapy; monitor and consider hospital transfer for intensive support

  • Case 3: Opioid overdose in a pulseless patient with Narcan considerations

    • Do not delay CPR; identify whether Narcan is indicated by respiratory depression rather than solely based on pupil size

    • Initial Narcan dosing: intranasal approx. 2 \, mg\text{ total} (1 mg per nostril); IV/IM dosing: 0.4-0.5 \, mg; duration of effect: 20-60 \, minutes with potential need for repeat dosing

    • Rebarreling of rescue: continue ventilatory support and transport

  • General teaching points:

    • Always check a constellation of signs rather than rely on a single symptom

    • Call poison control for uncertain exposures (e.g., case with Pepto-Bismol) to guide management

    • Prehospital management often includes specific antidotes, timing of administration, and decisions about transport

    • Dosing and durations noted in the lecture reflect guidelines and common practice; confirm with protocol in your region

Quick-reference mnemonics and cues

  • Cholinergic: SLUDGE + DUMBELLS + KILLER BEES; pinpoint pupils; bradycardia; sweating; bronchorrhea

  • Opioids: miosis; bradypnea; hypotonia; respiratory depression; Narcan reversal

  • Salicylates: hyperthermia, tachypnea, tinnitus; mixed acid-base disorders; treat with charcoal and bicarbonate

  • Acetaminophen: hepatotoxic threshold at 150 \, mg/kg$$; NAC antidote; stage-based progression

  • Stimulants: tachycardia, hypertension, hyperthermia, sweating; treat with benzodiazepines and cooling

  • TCAs: QRS widening; sodium bicarbonate therapy

  • Cardiac drugs: beta-blockers/calcium channel blockers – glucagon, calcium, Epi/dopamine infusions as needed; calcium administration is key for CCB overdose

  • CO/CN: high-flow O2; consider hyperbaric O2 for CO in select cases; cyanide management per protocol

Final reminder for exam readiness

  • Focus on recognizing toxidromes by constellation of signs rather than isolated symptoms

  • Remember key antidotes and first-line treatments discussed: atropine for cholinergic; NAC for acetaminophen; Narcan for opioid; sodium bicarbonate for TCA overdose; benzodiazepines for stimulant/sympathetic crises; charcoal for recent ingestions when appropriate

  • Be prepared to perform dose calculations and convert between mg/kg and tablets or total mg

  • Always prioritize airway and ventilation; transport to definitive care when indicated