Toxicology 101

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  • 1. Toxicology 101 Case Based Learning The Emergency Medicine approach to the poisoned patient Nikita Joshi MD Emergency Department Academic Fellow njoshi8@GMAIL.COM @njoshi8

2. Rules of Today VERY interactive If you dont know what something is, raise your hand, we will learn all the facts together I will call on you You will be doing multiple mini presentations There are no wrong questions/answers 3. We love tox! Vietnam War Ricin poisoning Dont drink the Kool Aid Indian school children Bulgarian Dissident Writer James Town Massacre Kool Aid laced with cyanide inhibits cytochrome C oxidase Organophosphates inhibition of acetylcholinesterase Ricin inhibits protein synthesis Dioxin defoliant form of organophosphate 4. This is our specialty! Immediate intervention with antidotes Control of airway Multiple patients Multisystem involvement Hyperbaric Chamber Toxicology Fellowship EMS training Hazmat Disaster Medicine 5. Definition Study of adverse effects of chemicals on living organisms Study of symptoms, mechanisms, treatment & detection of poisoning (wikipedia) 6. A good toxicologist Pathophysiology Biochemistry Pharmacology Organic Chemisty 7. Approach to Patient Scene Safety Decontamination Airway Breathing Circulation Physical Exam Labs Antidotes Disposition 8. Toxicology Physical Exam Vital Signs: HR BP RR O2 Sat T Neuro Eye Cardiac Respiratory Abdominal Bladder Skin 9. Toxidromes Sympathomimetics Cholinergic Anticholinergic Opioids Narcotics 10. 5 yo boy is the victim of a massive apartment building fire. He was found by police unconscious and with scorch marks on his body. His clothes have been scorched. His family are on their way by another ambulance. 11. Considerations in Fire Victims Emergency Department Management Initial approach Medications administered Emergency interventions Consults Carbon Monoxide Poisoning Clinical manifestations Diagnostic tests Antidote Carbon Monoxide Poisoning Epidemiology Pathophysiology Hyperbaric Chamber How does it work Special considerations How do you know if it is successful Transfer indications 12. Mini Presentations 13. Emergency Department Management Airway inhalation injury inflammation, edema Breathing burned skin preventing chest rise Circulation volume loss Other related trauma: broken bones, chemical exposure, parkland formula for fluid 14. Carbon Monoxide Majority of exposure are fire victims Incomplete combustion of carbonaceous fossil fuel (complete combustion leads to CO2) Poor outcomes: extremes of age, pregnant women (fetus), preexisting coronary artery disease, respiratory disease 15. CO Binds Hemoglobin Platelet hemoproteins Myoglobin Cytochrome oxidase 16. Hemoglobin doesnt allow blood to bind with oxygen, decreases the amt of oxygen in the body Myoglobin muscle cell hypoxia Cytochrome oxidase impairs mitochrondrial utilization of oxygen Brain causes lipid peroxidation 17. Clinical Symptoms Brain: headache, dizziness, nausea, vomiting, blurred vision, altered mental status, seizure, coma Cardiac: exertional dysnea, weakness, angina, palpitations, tachycardia, tachypnea, hypotension, myocardial ischemia Lungs: ARDS, pulmonary edema 18. Tests Carbon Monoxide Blood Levels Normal 1-2% Smokers: 5-10% 10-20 flu like symptoms 30 headaches, confusion 40-50 loss of consciousness 60-70 seizure, cardiac collapse, death 80- rapidly fatal 19. Antidote = Oxygen! Hyperbaric Chamber When to transfer? Evidence of end organ damage CO level > 25, >15 if pregnant/child Mechanism: Decreases half life of CO Displaces CO from myoglobin and cytochrome oxidase in tissue Increases O2 concentration in blood 20. August 21, 2013 Sarin was used in the attack in the Ghouta region of Damascus in Syria. 21. Considerations in Organophosphate Poisonings Emergency Department Management Initial approach Role of decontamination Clinical Manifestions of Organophosphates Muscarinic Nicotinic Organophosphate Poisoning Epidemiology Pathophysiology Treatment: Atropine, 2-PAM How does it work Special considerations How do you know if it is successful Transfer indications 22. 23 Mini Presentations 23. Emergency Department Management All personnel must wear protective equipment: organophosphates are absorbed by all routes (inhalation, skin, oral, ocular, parenteral) Some OP are lipophilic and can penetrate latex and vinyl gloves Patients must have clothing removed and discarded in well ventilated area Leather is a great absorbent for OP 90% of toxin is absorbed from skin Do NOT transport pt with clothing (if possible) 24. Mechanism of Toxicity OP binds to cholinesterase enzymes (AChE), preventing breakdown of released acetylcholine with resultant accumulation of AChE at muscarinic and nicotinic receptors Leading to overstimulation and cholinergic excess 25. Clinical Manifestations Excess AChE at muscarinic and nicotinic receptor predominant findings are based upon the specific agent 26. Muscarinic: SLUDGE & KILLER Bs S Salivation, Sweating, Seizures L Lacrimation U Urination Defecation, Diarrhea G Gastric Emptying (Vomiting), GI Upset (Cramps) E Emesis M Muscle Twitching or Spasm B Bradycardia B Bronchorrhea B Bronchoconstriction B ? Miosis (pupil constriction) 27. Nicotinic: Autonomic Ganglia Diaphoresis Mydriasis (dilated eye) Tachycardia Hypertension Neuromuscular Junction Fasciculations Muscle weakness Paralysis 28. Atropine Competitive antagonist of Ach at muscarinic (M1, M2, M3) receptors in CNS and periphery No effect on nicotinic receptors End point to treatment is drying of secretions Give 0.5mg, keep doubling dose until bronchorrhea is controlled every 2-3 minutes 29. Pralidoxime (2-PAM) Forms complex with OP bound AChE Then the OP-2PAM breaks off, leaving the AChE to be free for metabolism Unfortunately may not be helpful in all cases of poisoning 30. EMS brings a 20 yo woman who is a college student at Stanford. After failing her final test and being ridiculed at the football game, she went to her dorm room, wrote a suicidal note, and ingested the entire bottle of Amitriptyline that she had just refilled earlier today. Her roommate found her somnolent but arousable. Her current vitals: HR 120 BP 100/60 RR 10, FSG 130. 31. Considerations in TCA Poisonings Emergency Department Management Initial approach Airway management Important questions to ask EMS EKG as Screening Tool Describe important EKG findings Describe pathophysiology of EKG findings Explain biochemistry of the findings Clinical Manifestations of TCA poisoning Mechanism of action of TCA Physical exam findings Treatment: Sodium Bicarbonate Mechanism of action How to administer How to know if it is successful 32. Mini Presentations 33. Initial ED Management Airway Breathing Circulation Other signs of trauma Smells EKG Antidote 34. TCA MOA Depression State Block reuptake of norepinephrine, dopamine, and serotonin at the central presynaptic terminals This increases synaptic catecholamines Overdose State Initial release of catecholamine can induce transient hypertension followed by catecholamine depletion and relative hypotension 35. TCA Effects Anticholinergic (Anti Muscarinic) Central effects: agitation, lethargy, hallucinations, hyperthermia, ataxia, choreoathetoid movements, seizure, coma Peripheral effects: dilated pupils, dry, flushed skin, decreased bowel sounds, urinary retention. Sodium Channel Blocker EKG Findings Alpha 1 adrenergic receptor blocker Vasodilation leads to hypotension Antihistamine Sedation and seizure 36. Physical Exam Sinus tachycardia Hypotension refractory hypotension is likely the most common cause of death from TCA overdose Hyperthermia antimuscarinic effect Decreased respiratory rate CNS depression Anticholinergic: dilated pupils, tachycardia, dry, hot/flushed skin, decreased bowel sounds, urinary retention 37. EKG as a Screening Tool 1985 Landmark Study Boehnert and Lovejoy: 49 pts, QRS duration is better predictor of effects than TCA concentration QRS < 100 msec no significant toxicity QRS > 100 msec 1/3 had seizures QRS < 160 msec had vent. dysrhythmias 38. EKG as a Screening Tool Niemann and Bessen 1986: Right axis deviation between 130-270 degrees were noted in pts poisoned with TCA RAD + QRS prolonged + QT prolonged + tachycardia = PPV of 66% and NPV 100% of TCA poisoning Efficiency of EKG as diagnostic test was 97% 39. EKG Block fast inward sodium channels. Type 1A antidysrhythmic effects on myocardial conduction system. Phase 0 depolarization is prolonged with resultant QRS widening and characteristic wide complex dysrhythmia 40. Therapy Sodium Bicarbonate Start if QRS > 100, bolus 1-2mEq/kg If the QRS narrows while giving NaBicarb, then you have a winner, and can start a drip 3 amps NaBicarb in 1L D5W, infuse 2X maintainence 41. 6 yo boy brought by mother who is convinced that he was bit by a spider last weekend while at her ex-husbands house. He is a no good... 42. Brown Recluse Spider Little spider with tiny violin on thorax, legs are as long as 1-5 cm, but body is