1. Basic Approach to the Poisoned Patient
Damon M. Dell’Aglio, MD
Clinical Assistant Professor
Emergency Medicine/ Medical Toxicology
Emory University School of Medicine
Georgia Poison Center

2. Outline Basic approach Toxidromes Decontamination Diagnostics
APAP basics
Observation
Toxicology consultation

3. What this lecture is not. . .
A comprehensive review of all of toxicology
Though important it will also not cover envenomations, medications like oral hypoglycemics, blood pressure medications, lithium, caustics or carbon monoxide

4. What this lecture is. .
Basic review of the initial approach to the following patient. . .

5. Your patient. . . He is now in your ED 29 year old man found “down”
EMS transports
Reports from scene: “he took something”
No pill bottles on scene
No family with him
Roommates that found him are long gone
He is now in your ED

6. You are never going to know exactly what he took. . .
What do I do with him?
What do I order?
How do I treat him?
How do I decontaminate him?
Do I give him an antidote?
When can he go to psych?

7. You can. . . Start with the basics Get a better history
Airway, breathing, circulation
Get a better history
Get EMS to get pill bottles, tell you what they do know (found outside, inside, garage…)
Call friends, family, neighbors
Call psych or primary MD to see what he is on regularly
Get him to tell you
Always remember that suicidal patients (just like everyone else) can lie so be skeptical of their history

8. TOXIDROME Or. . . Establish a pattern to his symptoms Toxic syndrome
Also known as a:
TOXIDROME

9. Toxidromes Not every drug fits into a broad based category
Lots of meds have unique effects not easily grouped
5 Basic Toxidromes
Sympathomimetic
Opiate
Anticholinergic
Cholinergic
Seditive Hypnotic

10. Toxidromes: Sympathomimetic

11. Sympathomimetics Cocaine Methamphetamine/Amphetamines Ephedrine
Ecstasy (MDMA)
ADHD meds like ritalin, adderal
Ephedrine
Caffeine

12. Why do they do what they do?
Excessive SYMPATHETIC stimulation involving epinephrine, norepinephrine and dopamine
Excessive stimulation of alpha and beta adrenergic system

13. What goes wrong? Tachycardia +/- arrythmias Hypertension +/- ICH
Confusion with agitation
Seizures
Rhabdomyolysis
Renal failure can result

14. What do you do about it? Supportive care
Monitor airway, diagnose ICH, rhabdo
IVF for insensible loses and volume repletion
Benzos, benzos, benzos, benzos
BP mgmt if severe
NEVER GIVE BETA BLOCKERS

15. Toxidrome: Opiate

16. Opiates / Opioids Opiate: derived directly from the opium poppy
morphine and codeine
Opioids: much broader class of agents that are capable of producing opium-like effects or of binding to opioid receptors
Heroin
Methadone
meperidine
Hydrocodone
oxycodone

17. Why do they do what they do?
Primarily bind to the mu, kappa or delta opioid receptor
There are others but these play the biggest role

18. What goes wrong Coma Miosis Respiratory depression
Peripheral vasodilation
Orthostatic hypotension
Flushing (histamine)
Bronchospasm
Pulmonary edema
Seizures (meperidine, propoxyphene)

19. What do you do about it? Competitive opioid antagonist: Naloxone
Goal of return of spontanous respirations sufficient to ventilate the patient appropriately
May have to re-dose as opiates may act longer than antagonist
There are other longer acting opioid antagonists such as nalmefene and naltrexone but these are not often used

20. Toxidrome: Anticholinergic

21. Why do they do what they do?
By definition these agent ANTAGONIZE the effects of endogenous Acetylcholine

22. Mechanism of Action Ach receptors are either nicotinic or muscarinic
The “anti-cholinergic” drugs just block the muscarinic receptors
Some have argued that the “anticholinergic” poisoning syndrome should be called the “antimuscarinic poisoning syndrome” because you do not see anti-nicotinic symptoms

23. What goes wrong? CNS muscarinic blockade:
Confusion
Agitation
Myoclonus
Tremor
Picking movements
Abnormal speech
Hallucinations
Coma
Peripheral muscarinic effects:
Mydriasis
Anhidrosis
Tachycardia
Urinary retention
Ileus

24. Better way to remember it. . .
Hot as Hades - Fever
Fast as a Hare - Tachycardia
Dry as a Bone – Lack of diaphoresis
Red as a Beet – Flushed skin
Mad as a Hatter – Delerium
Full as a Tick – Urinary retention
Blind as a Bat – Mydriasis

25. What do you do about it? Supportive care Benzos to stop agitation
IVF to replace insensible losses from agitation, hyperthermia
Benzos to stop agitation
Physostigmine
Induces cholinergic effects
Short acting
May help with uncontrollable delirium
Do not use if ingestion not known
Danger with TCAs

26. Toxidrome: Cholinergic

27. Why do they do what they do?
Normal
Block acetylcholinesterase from working
End up with excess of acetylcholine in synapses
Leads to excess stimulation of the muscarinic and nicotinic systems
E= Acetylcholinesterase
NA= nerve agent
Ach= acetylcholine
With blockade

28. What goes wrong? D - Diarrhea U - Urination M - Miosis
BBB – Bradycardia, Bronchorrhea, Bronchospasm
E - Emesis
L - Lacrimation
S - Salivation

29. What goes wrong? S - Salivation L - Lacrimation U - Urination
D - Diaphoresis
G - Gasterointestinal upset
vomiting, diarrhea
E - Eye
miosis

30. What else goes wrong? Nicotinic effects M- Mydriasis T - Tachycardia
W - Weakness
(t) H - Hypertension
F -Fasiculations

31. What do you do about it? Antagonize muscarinic symptoms
Atropine
Stop aging of enzyme blockade
2-PAM
Prevent and terminate seizures
Diazepam
Supportive care

32. Toxidrome: Sed-Hypnotic

33. Why do they do what they do?
Different agents have different mechanisms
Many interfere in the GABA system

34. What goes wrong?

35. What goes wrong? CNS depression, lethargy
Can induce respiratory depression
Can produce bradycardia or hypotension

36. What do you do about it? Supportive care
Be wary of the benzo “antidote” Flumazinil
Is an antagonist at the benzo receptor
RARELY INDICATED
If seizures develop either because of benzo withdrawal, a co-ingestant or metabolic derangements, have to use 2nd line agents, barbiturates, for seizure control

37. So back to our patient. . .
Agitated, pupils 8 mm, sweaty, HR 140’s, BP 230/130
Sympathomimetic
Unarousable, RR 4, pupils pinpoint
Opiate
Confused, pupils 8mm, flushed, dry skin, no bowel sounds, 1000 cc output with Foley
Anticholinergic
Vomiting, urinating uncontrollably, HR 40, Pox 80% from bronchorrhea, pupils 2 mm
Cholinergic
Lethargic, HR 67, BP 105/70, RR 12, pupils midpoint
Sedative Hypnotic

38. So basic approach: Airway, breathing, circulation
Establish IV, O2 and cardiac monitor
Consider coma cocktail
Thiamine, D50, Narcan
Evaluate history and a thorough physical exam
Look at vitals, pupils, neuro, skin, bowel sounds. . .
Gives you hints regarding the general class of toxins
Guides your supportive care
Draw blood / urine for testing
Time to consider decontamination options

39. Decontamination or “How do I get the poison out of your body?”
Induce vomiting – Ipecac
Take out pills from the stomach – Lavage
Adsorb the toxins in the gut – Charcoal
Flush out the system – Whole Bowel

40. Ipecac DOES NOT HAVE A ROLE IN ED CARE Emetine and Cephaeline
Induces emesis
Rarely if ever still recommended for HOME use
DOES NOT HAVE A ROLE IN ED CARE

41. Gastric Lavage Can be a brutal procedure
Indication: life threatening ingestions that occurred within one hour
Airway protection is key
Limited indications
Lots of complications
DO not lavage tylenol, do not lavage an SSRI

42. Charcoal Basically, everybody gets a dose
Works to adsorb substances to its matrix
Not for metals, caustics
Generally safe, few contraindications
Aspiration, bowel obstruction
Dosing 1g/kg po dose, +/- single dose of cathartic
Charcoal is made by heating wood pulp, washing then activating it with steam or strong acids. The subsequent network of tiny pores is capable of trapping toxins. Does not bind well to: CN, lead, Li, boron, boric acid, some pesticides, iron, ethanol, strong acids or alkalis. Usually try to achieve a 10:1 ratio – 10 gm charcoal to 1 gm of drug.

43. Whole Bowel
Isotonic polyethylene glycol electrolyte solutions (GoLytely)
Large volumes ingested “wash” the substances through the bowel
Especially useful for metals or other things not well adsorbed by charcoal
Avoid in patients with bowel obstruction or ileus
Dose in volume sufficient to create clear rectal effluent
Not absorbed, isotonic so no risk of dangerous fluid shifts

44. WBI
Dosing:
1-2 LITERS/HOUR
Have to use an NG tube

45. Now you are ready to order diagnostic studies. . .
Want to evaluate
Acid base status
Renal function
Liver function
Cardiac conduction
EKG
Drug levels
Based on history or clinical findings
Any toxin specific findings
CK for cocaine, NH3 for valproate, etc

46. Other common ingestants may have common dx test abnormalities. . .
APAP
APAP level, LFT, coags
Salicylates
ASA level, metabolic acidosis, respiratory alkalosis, renal insufficiency, anion gap
SSRI
Prolonged QTc
Toxic Alcohols
Osmolal. gap with ethylene glycol, methanol and isopropyl alcohol
Anion gap acidosis with EG and methanol but not with Iso OH

47. Basic diagnostic testing
Measured serum osmolality
Especially if unknown ingestion or ANY toxic alcohol is suggested
Osm gap = Measured Osm – Calculated Osm
Calc Osm:
2([Na]) + ([glucose]) + ([BUN]) + ([EtOH])
Chemistry
Evaluate renal function (EG, APAP)
Evaluate liver enzymes (APAP, mushrooms)
Evaluate CO2 and calculate anion gap
CAT MUD PILES

48. CAT-MUD-PILES C cyanide, carbon monoxide A alcoholic ketoacidosis
T  toluene
M  methanol, metformin
U  uremia
D  diabetic ketoacidosis
P  paraldehyde, phenformin
I   inborn errors, iron, INH
L  lactic acid
E  ethanol, ethylene glycol
S  salicylates, starvation ketoacidosis

49. EKG Evaluate QRS and QTC, presence of blocks, rhythm
QTc > 450 and a QRS > 100 can be concerning for toxin induced (eg TCAs) cardiac abnormalities

50. Radiographs Limited usefulness CHIPES Packers/ stuffers Aspiration
Chloral hydrate, Ca
Heavy metals
Iron, iodides
Phenothiazines
Enteric coated
Slow release
Packers/ stuffers
Aspiration

51. Acetaminophen Get an APAP level on every overdose
Use nomogram only if there is a single acute ingestion with a level drawn between 4 hours and 24 hours post ingestion

52. Use the nomogram to help decide who needs treatment
APAP level
Use the nomogram to help decide who needs treatment
Must be between 4-24 hours from single acute ingestion of non-extended release product

53. APAP levels If your patient is toxic on the nomogram
Start NAC
If your patient does not have a known time of ingestion
If your patient took multiple rounds of APAP
If you have any question about the history…

54. Other tox labs. . . Strongly consider an ASA on every overdose
Not as silent as APAP can be but initial signs can be subtle
Urine drug screen
Little benefit but makes consultants feel better
EtOH level
Poor form to miss something as common as too much beer
EG or Methanol levels
CONTACT THE LAB SUPERVISOR BEFORE SENDING THEM TO BE SURE THAT IT GETS DONE RIGHT
Specific drug or toxin levels as indicated
Know what you are looking for and how to order it
There is no such thing as a comprehensive drug screen

55. Observation Period
Normal labs, normal EKG, normal exam, no history of extended release drug
Approximately 6 hours
Extended release medications, buprorion, oral hypoglycemics involved
Depending on agent, hours

56. So back to your patient. . . What do I order Do I give him an antidote
How do I treat him
Good supportive care, good physical examination
How do I decontaminate him
Charcoal as long as he is not an aspiration risk
What do I order
Chem, ASA, APAP, EKG at a minimum
Do I give him an antidote
Coma cocktail, others as indicated by labs
When can he go to psych?
Observe for 6 hours and re-evaluate

57. Now you know what do do with that patient found down

58. If ever in doubt 404-616-9000 24 hours a day
Anywhere in the United States
Poison Specialists and Medical Toxicologists are available
Locally at

59. Thank you