PADIS 101 Flashcards
PADIS Services – A simplified explanation
POISON
* Exposure to drugs, chemicals or toxins via
mouth, lungs, skin, eyes (or other
routes!)
* I’ve done something I don’t usually do.
* Have I taken too much? I’m concerned.
Have I poisoned myself?
* How can I prevent poisoning
Medication Advice
* I’m taking a medication or herbal
therapeutically and I have a question
about:
* -Available?/what is it?
* -How does it work?
* -Side effects?
* -Use in Pregnancy and Lactation?
* -Drug Interactions?
* - How to dose or administer it?
Grey area with AE and poisoning (eg/ lithium tox)
The PADIS Team – Who are we
What does the Specialist Training look like?
- PADIS is staffed by specially trained and certified healthcare
professionals - Medical Toxicologists
- Information Specialists (IS)
Pharmacists
Registered Nurses - 4 Month Orientation
- 3 months of Toxicology
- 1 month of Medication Advice training
- Didactic, Role Play and Quiz writing, Preceptored Buddy Shifts
- Focus on:
- Assessment, Documentation, Communication, Resource Navigation,
Pharmacology, Toxico/Pharmacokinetics
Top 10 Categories (2018)
What do we get called about?
- 1) Analgesics (6153)
- 2) Household Cleaning
Substances (3790) - 3) Antidepressants (2870)
- 4) Sedative
Hypnotics/Antipsychotics (2666) - 5) Cosmetics/Personal Care
Products (2349) - 6) Cardiovascular Drugs (1652)
- 7) Hormones and Hormone
Antagonists (1377) - 8) Stimulants and Street Drugs
(1291) - 9) Foreign Bodies/Toys (1148)
- 10) Vitamins (1139)
Top 10 Substances
- 1) Acetaminophen (5226)
- 2) Ibuprofen (4082)
- 3) Atypical Antipsychotics (2865)
- 4) Benzodiazepines (2292)
- 5) Alcohol (1825)
- 6) Antibiotics (1385)
- 7) Diphenhydramine (1244)
- 8) Other Sedative Hypnotics
(1239) - 9) Sertraline (1058)
- 10) Citalopram (940)
national posion data systems (NPDS)
Demographic of pt, nature of poisoning, case hx of what happened
What was ingested, how much
Tx that was recommended for use
Documentation of clinical fx happened during poisoning is mandated
Separated by body systems
Can code for diff symptoms
US - poisons hooked up in real time to data centres (national database)
Can monitor trends like hydroxychloroquine in covid
- False promotion of bleach or hydroxy
- Real time tracking in health care standpoint
Trck new trends and drugs of abuse
General approach
to the toxicology patient
- Airway
- Breathing
- Circulation
- Decontamination
- Elimination
- Find an antidote
- General management
Most can be successfully managed if we anticipate problems with ABC
Take care of ABCs first before doing the stuff below
Decontamination: on skin flush it off, or if on eye flush it
- Swallow tablets, AC to bind it to prevent absorption
If absorption occured, is there a way to enhance elimination
- Dialysis to remove drug
- Change pH of urine and promote elimination like salicylate poisoning
Antidote - very low on list of priorities, not used for everything even if available, service will help determine if needed, not everything has it
General management
- Treat emesis
- Snake bite pain, provide analgesia
Insulin – “I took the wrong insulin”
* At 00:05 call from:
* 42 yo male, on Insulin 25 years
* Usually takes Toujeo 24 units HS and Apidra 8 units with meals.
* Got mixed up, took 24 units of Apidra of instead his Toujeo 15mins ago.
* Staying at a hotel for business trip with co-worker
* BG at onset of call= 7.0 (was 9.0 20 mins ago)
* Ate something, had some sweetened Iced Tea. Blood Glucose rechecked
during call: 6.3
* What to do?
These are PK parameters
If someone takes a lot of insulin, this can be prolonged
Peaks and troughs may not apply in the case
Biggest risk is hypoglycemia
Knowledge - does he knwo what it feels to be hypoglycemic, has it happened before
PADIS involvement in Research
hypoglycemic event early on (blue dots = blood sugar0
Give them dextrose sugar (black diamond)
Saw a yoyo effect
It would go back down very quickly after sugar and would have to give her more
Her pancreas was still making insulin and when they sensed a lot of sugar given they would pump out lots of insulin
Had to artificially shut down pancreas using octreotide
BG normalized after 12 h
Telephone risk assessment
Where do we start?
Current clinical status
Toxin specifics?
* What toxin
* How much
* When exposed
* Route of exposure
* Duration of exposure
* Circumstances (intent)
How is pt doing at the moment?
Vital signs
Assuming no ABC issues
What did they take, how much, how long ago was it
By mouth or injected or other route?
Episodes of self harm are more at risk over accidental OD
Toxicological Exam – What we need from you
CNS
* Level of consciousness/Behavior
Pupils
* Dilated/pinpoint
Vital signs
* HR, BP, RR, Temperature
* ECG (QRS and QTc)
Skin and Mucous membranes
* Diaphoretic/Dry
Muscle tone/reflexes/clonus
* Tremors/stiffness/flaccid
Odors
* Chloral hydrate – pear like odour
Opioid Symptoms - triad
Decreased LOC
Decreased respiratory rate
Pinpoint pupils
Think about ABC
Opioids decrease resp rate
Naloxone may be appropriate
Opioid Management – How does PADIS think?
ABC’s – Severe toxicity risk
D – Potentially useful
E – None
F – Naloxone
* Usual dose is 0.4-2.0 mg IV
* Suspected opioid dependence would start as low as 0.04mg and
titrate up
* Repeat every 2-3 minutes up to 10 mg * Doses of 10-20mg rarely needed except in high potency opioids
* IV infusion – 2/3 dose that worked/hr
G – Supportive care
Do they need O2 to support breathing? Are they so drowsy need intubation?
Could potentially give AC
No role of dialysis
Dose of naloxone depened on pt hx of opioid use
Opioid Naive pt - less risk of naloxone
Longstanding users - withdrawal (agitation, diarrhea)
- Start low and titrate up
- Start with 1/10 of dose
Pt taking longacting opioid
- May need several naloxone doses
- Can give IV infusion easier
- 2/3 of dose needed for pt to wake up given every hour as starting point, then titrate
Anticholinergic Toxidrome
pharmacology
Pharmacology
* Competitive antagonist of M1 and M2 muscarinic cholinergic receptor
* Often referred to as antimuscarinic
TOXICOLOGY
* Extension of the pharmacologic effects, which is due to extensive
antagonism of the central and peripheral muscarinic acetylcholine receptors
Anticholinergic Agents
Antihistamines – diphenhydramine,
dimenhydrinate
Anticholinergic Plants – Jimson weed
TCA’s (Initial phases of toxicity)
Antidepressants and antipsychotics
Others: Atropine, benztropine
Anticholinergic Toxidrome
acronym
Delirium, Hallucinations, “picking”
“Mad as a hatter”
Tachycardia
“Tachy as a polyester suit”
Mild elevation of temp
Mydriasis
“Blind as a bat”
Dry mucous membranes
Dry, warm, flushed skin (including
axilla)
“Dry as a bone”
“Hot as a hare”
“Red as a beet”
Decreased bowel sounds
Urinary retention
“Full as a flask
Tend to see little people, adults picking at sheets
Pupils are large
Anticholinergic Symptoms
CNS
* Sedation
* Agitation, delirium, seizures
* Dilated pupils
CVS
* Tachycardia, hypertension
* Wide qrs (Na channel blocker in
some meds)
GI/GU
* Decreased bowel sounds
* Urinary retention
Skin
* Dry and flushed
Constipation
Urinary retention can drive the delirium
Catheter and drained urine can help pt lighten up a bit
Anticholinergic Management – How does
PADIS think about these cases?
ABC’s – Seizures, widened QRS are possible
D –Activated charcoal effective
E – No role for urinary alkalinization, MDAC, or hemodialysis
F – Physostigmine – Consult with Medical toxicologist –
Potential side effects,
Short duration of action
Special access drug
G –Mainstay of management
Cholinergic Toxidrome
pharmacology
Pharmacology
* Directly stimulate postganglionic cholinergic receptors
* Vary in selectivity for muscarinic receptors and nicotinic sites
Toxicology
* The acetylcholinesterase (AChE) does not adequately metabolize
acetylcholine (ACh) in the synapse
* Leaving an excessive amount of ACh to interact with receptors
Cholinergic Agents
Organophosphate pesticides
Carbamate pesticides
Nicotine
Pilocarpine
Dementia Drugs
Organophosphates and Carbamates
- Cholinesterase Inhibitors
Carbamates - reversible binding - Atropine and Pralidoxime are the
antidotes - Atropine doses may be large
Anticholingeric in atropine to increase HR and dry out secretions of lungs - often need large doses - Secondary contamination:
Protect health care professionals
Working in ED - pesticide poisoings - if exposed to their vomit or clothing you can become a victim of poisoning too
Muscarinic and Nicotinic Effects:
musc
* Salivation
* Lacrimation
* Urinary incontinence
* Diarrhea/Defecation
* GI motility
* Emesis
* Killer B’s: Bradycardia,
Bronchorrhea, Bronchospasm
NICOTINIC – Days of the Week
Mydriasis
Tachycardia
Weakness
tHypertension
Fasciculations
Seizures
Sympathomimetic Toxidrome – Flight or Fight
Pharmacology
* Direct binding at beta and alpha-adrenergic receptors
* OR by indirectly causing an increase of norepinephrine or dopamine
(catecholamines) at the neural junction
Toxicology
* Direct receptor binding or catecholamine increase leads to a
hyperadrenergic physiologic state
Examples: Stimulants and ADHD drugs, Drugs of Abuse, Salbutamol
Sympathomimetic Effects
- Tachycardia
- Hypertension
- Increased Respiration
- Increased temperature
- Agitation, tremor
- Hallucinations
- Mydraisis
- Diaphoresis
Vital signs will go up
Big pupils
Sweating
To differentiate from anticholingeric looking at the skin can be useful
Sympathomimetic Management
ABC’s – severe toxicity risk
D – possibly AC/WBI
E – none
F – none
G – benzodiazepines
* agitation, tremors, tachycardia, hypertension
* the key to preventing severe toxicity
(seizures/hyperthermia/AKI)
* be prepared to provide airway support
ABC problems, heart rhythm
If swallows AC may help
Liberal doses of benzos to sedate pt
Decrease tremors and agitation
Can decrease HR related to pschyomotor agitation
antiseizure
High temp is an ominous sign
Might cool them extenrally w ice packs, cool blankets
