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 don’t 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
Don’t 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 – doesn’t 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

21. August 21,
2013 Sarin
was used in
the attack in
the Ghouta
region of
Damascus in
Syria.

22. 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

23. 23
Mini Presentations

24. 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)

25. 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

26. Clinical Manifestations
Excess AChE at muscarinic and nicotinic
receptor – predominant findings are based
upon the specific agent

27. Muscarinic:
SLUDGE & KILLER B’s
• 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)

28. Nicotinic:
Autonomic Ganglia
• Diaphoresis
• Mydriasis (dilated eye)
• Tachycardia
• Hypertension
Neuromuscular Junction
• Fasciculations
• Muscle weakness
• Paralysis

29. 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

30. 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

31. 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.

32. 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

33. Mini Presentations

34. Initial ED Management
• Airway
• Breathing
• Circulation
• Other signs of trauma
• Smells
• EKG
• Antidote

35. 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

36. 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

37. 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

38. 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 ½ had vent. dysrhythmias

39. 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%

40. 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

41. 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

42. 6 yo boy brought by
mother who is
convinced that he was
bit by a spider last
weekend while at her
ex-husband’s house.
He is a no good...

43. Brown Recluse Spider
• Little spider with tiny violin on
thorax, legs are as long as 1-5 cm,
but body is <1cm
• South central US
• Prefer dry, dark sheltered areas
(shoes)
• Evolution of lesion: Necrotic Arachnidism
• 2-6 hrs – pruritus, tenderness, erythema,
edema
• 6-12 hrs – irregular area of erythema
surrounded by ischemic pallor
• 1-7 days – slow healing ulcer
• Venom is cytotoxic
• Hyaluronidase, lipase, ribonuclease,
deoxyribonuclease
• Sphingomyelinase D: involved in
complement activation, tissue
necrosis, red blood cell lysis
• Treament: hyperbaric oxygen,
dapsone, antihistamines, antibiotics,
dextran, glucocorticoids,
vasodilators, heparin, nitroglycerin,
electric shock, antivenom
• There is NO concensus
• No clinical trials

44. Poison Control

45. Further Resources