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Basic Approach to the Poisoned Patient

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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

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