toXXX Flashcards by Caroline Mak

Q

Poison control #

A

1-800-222-1222

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Q

What information to collect when a patient calls or presents with substance poisoning

A

Age, weight
PMH
Time of exposure and route
Present s/s
Exact name of product, formulation, strength
- How much has been ingested
Occupation
Were there suicide notes?

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Q

General management to a patient with substance poisoning

ABCDE

A

Airway
Breathing
Cirulaation
Dextrose/Decontamination
EKG/Elimination

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Q

Non-pharm for substance poisoning

A

If the agent was inhaled: remove pt from the exposure area
If agent is topical/derm: irrigate with soap and water
If agent is ingested: can consider orgogastric (“stomach pumping”)
hemodialysis can also be considered for specific situations

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Q

When to use orgogastric methods in substance poisoning

stomach pumping

A

Ingestant has potential for serious toxicities
No antidotes exist
Time window gives reason to believe agent may still be in stomach

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Q

When to use hemodialysis in substance poisoning

A

Other elimination strategies not effective or are contraindicated
Ingestant has potential to produce serious ADR
Agent is able to be removed through filtration
EXTRIP is a good source to find out if hemodialysis would work

ex: ASA and tox alcohols

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Q

GI decontamination methods (pharm-ish) for substance poisoning

A

do NOT use Ipecac
Can consider activated charcoal: enhances gastric dialysis of certain drugs and prevents prolonged absorption or enterhepatic recirculation
Can consider PEG3350 with electrolytes (whole bowel irrigation)
- golytely, nulytely, colyte, NOT miralax

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Q

When to use activated charcoal in substance poisoning

A

Most benefit if used within an hour of ingestion (doesn’t mean you can’t use it if it’s been mmore than an hour)
- It helps prevent absorption
No benefit if the ingested substance is
- Ionized metals: lithium, iron
- Alcohols
- Gasoline

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Q

Activated charcoal dosing

A

sometimes the first dose is formualted with sorbitol to improve palatability tho no big evidence for benefit of sorbitol
- 1g/kg
pediatric dosing
- 0.5-1g/kg OR
- multiple dose: loading dose of 1g/kg followed by 0.5g/kg Q4-6H up to 24 hrs

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Q

Activated charcoal AE

A

vomitting, black tarry stools
- Do NOT want pt to vomit this up and have it in their airways

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Q

When to use whole bowel irrigation in substance poisoning and dose

A

Goal is to minimize time that ingestant is in GI tract for absormption
Beneficial for XR products, metals (Fe), and body packers (people who store packets of illicit drugs in their GI system to smuggle across borders)
1-2 L/hr or until rectal effluent is clear
peds: NG is easier to use
- 0.5L/hr in small children Q4-h H
- 1.2-2L/hr in older chilren/adolescants Q4-6 H

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Q

Toxidrome defininiotn

A

s/s that point to a class of toxin based on understanding of pharmacology

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Q

Drug(s) that have adrenergic/sympathomimetic toxidrome

A

Cocaine
Amphetamines
Bathsalts
Pseudoephedrine
Nootropics
Bupropion

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Q

Drug(s) that have cholinergic toxidrome

A

Organophosphates
Pesticides

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Q

Drug(s) that have anticholinergic toxidrome

A

TCAs
antihistamines (like benadryl)

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Q

Drug(s) that have sedative/hypnotic toxidrome

A

Benzos
EtOH

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Q

Drug(s) that have opioid toxidrome

A

opioids
heroin
morphine
loperamide (need 30-200mg → cross BBB and PGP can’t kick it out)

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Q

Adrenergic/sympathomimetic toxidrome S/S

A

Enlarged pupils
Increased BP
Increased HR
Increased RR
Increased temp
Bowel sounds
Tremor
Seizures

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Q

Cholinergic toxidrome S/S

A

Salivation
Lacrimation
Urination
Defecation
Gastric cramps
Emesis
Bradycardia
Bronchorrhea
Bronchospasm
Pinpoint pupils
Bowel sounds

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Q

Anticholinergic toxidroe S/S

A

Blind as a bag
Hot as a hare
Dry as a bone
Red as a beet
Mad as a hatter (agitated)
Enlarged pupils
Increased BP
Increased HR
Increased RR
Increased temp
Urinary retention
Tremor
Seizures

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Q

Sedative/hypnotic toxidrome S/S

A

Sleepy with normal vitals
- bp, hr, rr may be a little decreased

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Q

Opioid toxidrome S/S

A

Unresponsive to painful stimuli
Pinpoint pupils
Low RR
Low BP
Low HR
Low temp
Hyporeflexia
Decreased mental status

Loperamide can cause arrhythmias

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Q

Treatment for pts with cholinergic toxidrome

A

Atropine: inhibits muscarinc actions of ACh
- 1mg IV titrated to effect, no MDD

Pralidoxime: reactivates cholinesterase
- 30mg/kg IV load
- 8-10mg/kg/hr continuous infusion

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Q

Treatment for pts with anticholinergic toxidrome d/t antihistamine overdose

A

Physostigmine: ACh inhibitor
- 0.5 - 2 mg IV

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Treatment for pts with benzo overdose

Benzos alone aren’t that bad, can be handled with monitoring, supportive care; intuation if needed - NOT LETHAL

The problem with flumazenil and when to use it

Can send someone who is benzo overdosed (not lethal) into withdrawal (lethal) _ So when to use flumazenil? - procedural sedation - in peds accidental overdose who are not benzo dependent - Z-drug overdose (not really tho)

Flumazenil dosing

competitivte antag at benzo receptor site - 0.2mg IV over 15 seconds - peds: 0.01 mg/kg IV - onset: 1-2 min | idk if this is just for benzo overdose or in general

Opioid overdose treatment

IV naloxone dose - 0.4mg for non-opioid dependent - 0.04mg for opioid dependent pt - titrate to effect (ideally) - continuous inf: 1/2 of initial effective dose as bolus then 2/3 of effective dose/hr Protect airway or breath for them

Naloxone IV vs. nasal

- IV: quick onset, quick wear off - IN: longer onset and duration - IM: somewhere inbetween

Naloxone AE

- **flash pulmonary edema:** treat with nitroglycerin, diuretic, and positive pressure ventilation - **runny nose**

Loperamide overdose treatment

- Naloxone - IF CARDIAC DISTURBANCE - IV Mg - Sodium bicarb - IV isoproteronol or transcutaneous pacer

What drug levels do we like to draw in patients who present with overdose/substance poisoning?

- Digoxin - Vanco - Phenytoin - Lithium - APAP - no toxidrome - ASA - unique toxidrome

Polysubstance overdose approach

- Eliminate: activated charcoal - Admin antidotes: naloxone, NAC - Supportive care: benzos

Benzo withdrawal s/s

- Severe sleep disturbance - Irritability - Increased tension and anxiety - Panic attacks - Sweating - Difficulty in concentration - Dry retching and nausea - Palpitations - Headache - Psychotic reaction - **Seizures** - **Death**

Which is deadlier? benzo overdose or benzo withdrawal

WITHDRAWAL

OTC that can cause asa/ salicylates overdose

- Peptobismol - Alkaselzter - Oil of wintergreen: 98% methyl salicyalte (98g/100ml) - Icy hot - Bengay - ASA

ASA/salicylate toxic levels (adults)

- Toxic at >150mg/kg - Life threatening at >500mg/kg

ASA/salicylate mechanism of tox

metabolic acidosis and uncoupled oxidative phosphorylation (can’t produce ATP and excess H+)

ASA/salicylate overdose S/S

- **Resp**: tachypnea/hyperpnea - **GI**: disrupt nucosal barrier, N/V, hemorrhagic gastritis, bezoar formation - **CNS**: neuoronal energy depletion, hypoglycorrachia (hypoclycemia in brain only), AMS, tinnitus, hyperpyresxia, tachycardia, fever, coma, seizures - **Non-cardiogenic pulmonary edmea** - **Renal and hepatic injury**

ASA/salicylate overdose acid/base labs

- Early on in overdose: resp alkalosis - Middle of overdose: mixed metabolic acidosis and resp alkalosis - Late/preterminal overdose: metabolic and resp acidosis - Body can no longer compensate and you can’t even compensate by breathing hard

What is a bezoar formation

concrete ball of salicylate in stomach that can break off and release more drug into system

ASA/salicylate overdose *electroytes* presentation

- Hypo or hyperglycemia - Increased fluid and electrolyte losses - Increased anion gap - Urine: ketones in urine

ASA/salicylate overdose treatment

- Airway, breathing, circulation (do NOT ventilate) - Enhance elimination - Multiple doses of activated charcoal (1g/kg) - Urine alkalization (we want a pH >7.5) - Can consider hemodialysis - Dextrose (even if normal glucose levels): 0.5-1g/kg - Fluid maintenance - Serum pH 7.45-7.55 - 150 mEq of sodium bicarb in D5W at twice maintenance rate (alkalinize urine) - Treat spefic AE too (seizures, edema, etc.)

ASA/salicylate overdose monitorng

Monitor Q2H - Mental status - Urine and blood pH - Salicylate levels - Fluid and electrolytes - Maintain K (often low)

ASA/salycylate overdose: if pt is on hemodilaysis for the overdose, when to stop

Stay on hemodilaysis until clear inprovement in pt AND salicylate level <19mg/dL - Or 4-6 hrs if you can’t get labs

ASA/salicylate overdse: who qualifies for hemodialysis

- Serum level >100mg/dL in pts with acute - Serum level >60mg/dL in pts with chronic - Neurologic deterioration - Seizures - Intractable acidosis (pH <7.2) - Renal failure - Pulmonary edema

Purpose of urine alkalinzation in asa/salicylate overdose

shift salicylate into un-ionized form → move across barriers → more excretion

If you overdose on an antidepressant, will it present as serotonin syndrome?

Very unlikely, usually only see serotonin syndrome if polypharmarcy with multiple serotenergic agents or with drug specific for 5HT2A or 5HT1A

Serotonin syndrome presentation

- Spontaneous clonus - Agitation - Diaphoresis - Hyperthermia - Tremor - Hyperreflexia - Diarrhea - AMS - Incoordination

SSRI overdose presentation

Seroternergic features - AMS - Tachycardia - Myoclonus - Tremors - Diarrhea

Serotonin syndrome antidone

cyproheptadine but it is very anticholinergic, so not used often - Can use benzos and propranolol for symptom treatment

Serotoin overdose treatment

- Supportive care - Monitoring - Escitalopram and citalopram are most likely to cause seizures and QTc prolongation

List the TCAs

- amitriptyline - nortriptyline - doxepin - imipramine - desipramine

TCAs MOA and related overdose S/S

- Catechol reuptake inhibitior: hypotension - Alpha adrenergic blocker: hypotension - GABA antag: seizure - Sodium channel blocker: dysarrythmias → lethal ## Footnote initial increase in BP and HR and then quick drop; anticholinergic toxidrome

TCA and EKG/ECG

- If there’s an R wave in aVR: there was some exposure to TCA (not necessarily a TCA overdose, but it is present) - Elevated QRS → increased risk of seizure - Bigger R wave amplitude → higher incidence of seizure

TCA overdose treatment | don't worry about the treatments for specific s/s for this card

- If pt came in early enough; can consider - orogastric lavage (GI flush) or activated charcoal - hypertonic sodium bicarb 1-2 mEq/kg bolus and then 150 mEq in 1L D5W at twice maintenance rate (150-200 ml/hr); give until - Do this until QRS narrows - We would also like to see blood pH go back to normal (<7.5) but fixing QRS is more important

Hypertonic sodium bicarb MOA in TCA overdose

- Sodium (hypertonic sodium like 3% NaCl) → prevents lethal sodium channel blockade - Alkalinzation (via hyperventiliation) may also be effective

TCA overdose: additional treatment if pt is experiencing seizures

- Benzos - Barbituates - do NOT give phenytoin: can increase frequency and duration of VT - do NOT give flumazenil: prevents benzo protection against seizure and can worsen seizures

TCA overdose: addition treatment if dysrhythmias aren't going away

- Mg - Lidocaine (replace TCA with a more benign sodium channel blocker)

TCA overdose: additional treatment if pt is hypotensive

- Ne, E, vasopressin, phenylephrine - Methylene blue, lipid emulsion, high dose insulin

Bupropion overdose S/S

- May be asymptomatic until like 24 hrs later when they suddenly have a seizure -> hold pt until certain no seizures - Widening of QRS complex but does NOT respond to sodium bicarb - Sympathomimetic crisis - Cardiogenic shock - Status epilepticus - Lazarus effect (pronouced dead but then randomly wakes up later) - Death

Bupropion overdsoe treatment

- Supportive care - *Maybe* lipid emulsion and ECMO - *Maybe* orogastric lavage or activated charcoal or whole bowel irrigation - IF HTN, can try benzos

Antihypertensive overdose general presentation

Toxidrome: bradycardia, hypotension - Cardiac: AV blocks and CHF - Sotalol can cause torsades - CNS: depressed LOC - Propranolol can cause seizures

Differentiation dx between CCB and BB overdose

CCB has elevated glucose

CCB specific overdose presentaiton

- Alert initially - Elevated blood sugar - Hypotension (d/t vasodilation) - **non-DHP** CCBs: - decreased ventricular contratility - sinus node depression - AV node depression -> various blocks

CCB and BB overdose treatment

1. GI decontamination if applicable 2. fluids: isotonic crystalloids (0.9 NaCl, LR) 2. atropine: 0.5-1mg Q5min 3x 3. calcium - CaCl (can cause sclerosing): 1-3g IV - Ca gluconate: 3-9g IV 4. high dose insulin (HIET) - 1 U/kg bolus then 1-10 U/kg/hhr - give glucose to counteract insulin - maintain glucose >100 mg/dL - 30-60 min onset 5. potassium prn to maintain 2.8-3.5 mg/dL | Same as BB

Other than the normal treatment steps, what other agents might you use in the setting of CCB and BB overdose?

- vasopressors: NE and E - can be used as monotherapy in mild overdose - can also be used as bridge insulin - inotropes: dobutaminne (CCB), milrinone (BB) - cardiac pacing - intralipid: - pull toxin off of site - modulate myocardial energy - ECMO - **BB ONLY**: glucagon 3-5mg bolus then 3-5mg/hr + zofran (n/v)

Why can glucagon be considered in BB overdose but not CCB?

it’s like a beta agonist that bypasses the beta receptor

Glucagon AE

vomiting (zofran ppx) - avoid use in pts wtih AMS

Alpha agonist specific overdose s/s

* Decreased mental status * Small pupils * No delay in onset * **CLONIDINE SPECIFIC** - transient HTN and tachycardia before suddenly going to bradycardia and hypotension - CNS depression - Respiratory depression

Alpha agonist overdose treatment

- Suportive care - **Clondine**: naloxone for respiratory depression - 5-10mg bolus - can start an infusion if response

Acute digoxin toxicity s/s

- Predistribution - N/V - *Hyperkalemia*: guaranteed death if K >5.5 - Post distribution (6 hrs) - Hypotension - Bradycardia - Dysrhythmias - Death

Chronic digoxin toxicity S/S

less typical and K level is unhelpful

Digifab indication in *chronic* digoxin tox

- Post-distribution (>6 hrs after ingestion) level of >6 mcg/L - Progressing or severe signs of tox

Digifab dosing in practice

2 vials and then titrate to effect - Give every hr if no response is seen

Acute digoxin tox treatment

- GI decontamination: activated charcoal, repeat doses needed in renal failure - Digifab if appropriate - K >5 - Digoxin level >20 mg/dL - Progresing signs of tox - Temporizing measures: Ca if patient is looking bad (high K+) ## Footnote But too much calcium induces “stone heart” = irreversible contraction of heart Data says still give calcium too

MUDPILES

- *M - Methanol* - U – Uremia - D – DKA, SKA, AKA - P – Phenformin (metformin), Paraldehyde - I – Isoniazid, INH - L – Lactate, CO, CN, MetHb - *E – Ethylene Glycol* - S – Salicylates | Causes of anion gap metabolic acidosis

Anion gap calculation

Calculating anion gap: gap = Na - (Cl + HCO3) | normal = 4-12

Clinical presentation after ingestion of toxic alcohols

- Early: - AMS - like they’re drunk - GI distress - Late: - High anion gap metabolic acidosis - Specific differences between EtOHs - Methanol: visual changes "blind" - Ethylene glycol: nephrotox, hypocalcemia

Toxic alcohols

- Methanol: high volatility - in gasline antifreeze and windshield washer fluid - Ethylene glycol: low volatility - in engine fluid

What labs to look at in pts who present for ingestion of toxic alcohol

- Electrolytes - and treat where needed - Arterial blood gas - Ethanol level - Methanol and ethylene glycol levels - The labs won’t return until the next day, so for the first day that they present, you don’t really know which they have - Measured osmolality

Management/treatment of ingestion of toxic alcohols

- **GI decontamination: useless** - alcohol dehydrogenase (ADH) inhibitor: ethanol OR 4-methylpyrazole-fomepizole (4-MP, Antiol: preferred agent) - Supplementation - ethylene glycol - B6 pyroxidone IV 100mg QD - B1 thiamine IV 100mg QD - methanol - folic acid: 1mg/kg Q4-6H for 24hrs - Mg - Sodium bicarb: to correct acidosis | supplement doses are from peds lecture, idk what adult doses are

Ethanol dosing in ingestion of toxic alcohols

- adults:1g/kg to maintain a BAC of ~100 mg/dL - peds: loading dose of 8 ml/kg over 1 hr → 0.8 ml/kg/hr IV - Goal serum [ ]: 100-150 mg/dL - Goal [ ] of toxic alcohols: <25 mg/dL

Ethanol formulations

- IV 10% soln - PO: shots x 4

Ethanol AE

- CNS inebriation - thrombophlebitis (IV) - GI symptoms

4-MP (fomepizaole) AE

- HA - Dizziness - Minor allergic reactions

4-MP (fomepizaole) dosing in ingestion of toxic alcohols

- 15 mg/kg load, then 10mg/kg Q12h x4, then 15mg/kg Q12H - Dilute in NS or D5W and infuse over 30 min - Lower then re-up dose d/t autoinduction - Dose increased during hemodialys - peds: same dosing as adults - goal toxic alcohol [ ]: <25 mg/dL

Who needs hemodilaysis in pts who have ingested toxic alcolhols

- Methanol or ethylene glycol level 25-50 mg/dL - High osmal gap (>10) without aother cause - A normal gap could mean pt is doing well or tthat pt is doing trash, not super specific or helpful - End organ manifestations of tox (renal, vision) - Severe metabolic acidosis

CB1 receptors

- CNS - GPCRs - Motor activity - Thinking - Pain perception

CB2 receptors

- Periphery - GPCRs - Immune modulation - Anti-inflammatory

Unwanted effects form phytocannabinoids

- Short term memory difficulties - Agitaion - Feeling intense - Anx - Dizziness - Lightheadedness - Confusion - Loss of coordination

Phytocannabioids

- natural cannabis - THC parital agonism at CB1 receptor

Sythetic cannabinoids

- Full agonist (act on CB1 AND CB2) - Higher receptor affinity - Longer half lives

Synthetic cannabinoids tox clincal presentation

- CNS depression - Disorientation - Restlessness/agitation - Hallucinations - Seizures - Comativeness - Anx - Mydriasis - Tachycardia - Vomitting

Synthetic cannabinoids tox labs

- Hypokalemia - Increased blood glucose - Increased SCr - Increased WBC - Increased Creatinine kinase

synthetic cannabinoids tox treatment

- Agitation: treat with benzos - Seizures: treat with benzos - Dehydration: treat with IV crystalloids - HTN/tachycardia: treat with benzos ad if benzos don’t work, IV antihypertensives

synthetic cannabinoids n/v moa and dx

- excessive vomitting d/t dysregulation of endocannabinoid system and alteration in TRPV2 receptor - dx - Hx of regluar cannabis use - Cyclic N/V - Generalized diffuse abdominal pain - Compulsive hot showers with symptom improvement

synthetic cannabinoid n/v presentation: pre-emetic phase

- months-years - diffuse abdominal dyscomfort - feelings of agitaiton or stress - morning nausea - fear of vomiting - Often pts will self treat with more marijuana

synthetic cannabinoid n/v presentaito: hyperemetic phase

- 24-48 hrs - Cyclic episodes of N/V - Diffuse, severe abdominal pain

Synthetic cannabinoid n/v presentation: recovery phsase

- Only upon cessation of cannabis (may take a month for full resolution) - Bowel regimens - Fluids - Electrolyte replacement

synthetic canabinod n/v treatment

- Activate TRPV1 - Hot showers - Caapsaicin topical cream - Anti-nausea - Haloperidol - better opiton - Ondansetron - Benzos: inhibitory effect on medullary and vestibular nuclei associated with n/v - Supportive care - Fluids - Electrolytes

Cocaine specific tox s/s

- euphoria - seizures - dysrhythmias - HTN - coronary artery spasm MI

cocaine speific tox treatment

- benzos - supportive care

amphetamines specfic tox s/s

- agitation - seizures - hyperthermia - HTN - delirium | longer acting than cocaine

Amphetamine specific tox treatment

- benzos or barbituates - anti-htn - supportice care

Bath salts specific tox s/s

- agitation - tachycardia - insomnia - paranoia - seizures - violent unpredictable behavior

Bath salts specific tox treatment

supportive care

sympathomimetic (general) treatment

- Elimination strategies (charcoal) - Clinical effects: Benzos - Airway protection: intubation - Hyperthermia: Ice baths, benzos, antipyretics - Dysrrthmias: Sodim bicarb, lidocaine - Rhabdo: Fliuds - Antihypertensives - Anti-psych - Electrolyte management

Peds poisoning labs to get

- Lab evals as is relevant to the H&P and pt presentation - but almost always at least serum chemistries and acid-base - s**trong consideration for serum APA**P (also salicylates, ethanol, iron) d/t easy access/OTC status

toxic APAP doses in peds

>200mg/kg PO or >60mg/kg IV

Peds apap overdose treatment

- GI contamination with activated charcoal if it has been less than an hr - NAC dosing - PO: 140mg/kg x1 → 70mg/kg Q4H x17 - IV (more often used): 150mg/kg over 1 hr → 50mg/kg over 4 hrs → 100mg/kg over 16 hrs - To prevent hypoNa, product should be diluted to a [ ] of 40mg/dL

household cleaners/caustic exposures: possible causes and treatment

- Cleaners: bleaches, detergents, soaps - Caustics: toilet cleanere, drain cleaner, oven cleaner - JUST SUSPPORTIVE CARE - If GI injury can consider PPIs - do NOT use GI decontamination

Foreign body ingestion treatment

GI decontamination: manual removal if esophagaeal impact suspected

Peds cough and cold: overdose/tox treatment

- Products should be avoided in pts < 6 per FDA 2017 - **Use activated charcoal** - Symptomatic management - HTN: labeatol, nicardipine - Arrhythmias: amiodarone - Seizures: benzos | Fatalities due to pseudoephedrine