Tox Flashcards
3 types of GI decontamination
Gastric lavage
Activated charcoal
Whole bowel irrigation
How to do gastric lavage
Put NG/OG, +/- intubate
Irrigate with 250 mL saline at a time (10mL/kg in kids) in aliqouts until fluid runs clear and nothing comes out
Indications for gastric lavage
Not many now. Maybe if can’t give charcoal and pt intubated
Dose of Activated charcoal
50-100 g in adults
1g/kg in kids
Indications of AC
Within 2 hrs of ingestion of toxin (reasonable to stretch to 4 if ongoing symptoms/toxicity)
Substance that will bind AC
LOC appropriate
Substances where AC shouldn’t be given
PHAILS
Pesticides
Heavy metals
Alcohols/acids/alkali
Iron
Lithium
Solvents
When to do multitude activated charcoal
When there is eneterohepatic circulation
Eg carbemazepine, phenobarbital
Contraindications to activated charcoal
-Dec LOC/unprotected airway (can tube first)
-more than 2 hours from ingestion (can stretch it, esp if massive or sustained release product)
-PHAILS
Common indications for whole bowel irrigation
Body packers,
Sustained release meds
Metals
How to do WBI , what are the endpoints
Instill PEG solution at a rate of 1L/h until clear rectal effluent or 10L has been used
3 methods for enhanced elimination of a toxin
Mdac
Urinary alkalinization
HD
Toxins where mdac is indicated
Carbamazepine
Phenobarbital
Dapsone
Theophylline
How to do urinary alkalinization
150 meq (3 amps) sodium bicarbonate in 1L D5W infuse at 2X maintenance rate
Toxins that urinary alkalinization works
Aspirin
Methotrexate
Phenobarbital
Aka weak acids
4 drug characteristics for HD to work
4 main drugs that can be removed with HD
Alcohols
Aspirin
Lithium
Metformin (not dialyzable, but helps with severe acidosis)
Pathognomonic ECG finding for sodium channel blockade
Terminal R wave in avr
4 types of toxins that cause bradycardia
beta blockers are the top one
3 toxins classes that cause tachycardia
3 toxins/types of toxins that cause QRS widening
4 main alcohols to know
ethanol, methanol, ethylene glycol, isopropyl alcohol
how and why does fomepizole work?
blocks ADH (alcohol dehydrogenase) preventing toxic metabolites from methanol and ethylene glycol from forming
where is methanol found?
what is the toxic metabolite?
wiper fluid, antifreeze
formix acid is metabolite
anion gap vs osmolar gap in methanol and ethylene glycol ingestion?
osmolar gap is initially elevated, then decrease as anion gap rises in “X” like pattern, this happens as parent compounds (osmoles) get converted to metabolites (anions)
correcting osmolar gap for etoh
add ethanol level*1.25
osmolar gap formula, what is eleavted gap?
measure osmoles - (Na + Na + glc + urea)
>10 is abn
3 times to suspect methanol ingestion
visual symptoms (“blind drunk”), WAGMA, osmolar gap >10
treatment of methanol, when to consider HD
-fomepizole (15 mg/kg loading dose) or ethanol
-consider HD if serum level >50, renal -failure, visual symptoms, severe acidosis
can give folate
other causes of elevated osmolar gap that aren’t toxic alcohols
ethanol, mannitol, sorbitol, recent contrast administration
where is ethylene glycol found?
what are its toxic metabolites?
antifreeze, brake fluid
oxalic acid, glycolate
General symptoms/signs of methanol
which alcohols cause osmole gap, which one cause anion gap
all of them
only methanol and ethylene glycol
mgmt of ethylene glycol
fomepizole or ethanol
HD is renal failure, severe acidosis,
when to suspect ethylene glycol
WAGMA, osmole gap >10, RENAL FAILURE (the renal failure is to e glycol as the blindness is to methanol)
isopropyl alcohol (aka isopropanol) presentation
twice as drunk, twice as long
++ intoxication and GI Sx (N/V/hematemesis (from )gastritis
why is the mgmt supportive for isopropyl alcohol (aka isopropanol)
bc it is metabolized to acetone (not toxic)
it will have osmole gap, will not have WAGMA
most commonly used TCAs now
amitriptyline
nortriptyline
-biggest toxidrome
-worst ECG change with tricyclics
-other main signs/cmplication
anticholinergic
QRS widening (>100 ms) –> WCT (most common is qrs >160), can also prolong qtc
seizure (risk if qrs >100)
3 ECG changes in TCA OD
wide QRS (>100)
terminal R wave in AVR (bc of sodium channel blockade
long qtc
what is pathophys of terminal R wave in avr and qrs prolongation
Na channel blockade
how to mix a bicarb infusion or give boluses
3 amps (each 50 meq) in 1L of D5W (remove 150 mL from the bag), then run at a rate (eg 100 mL/hr) or in weight based boluses
or give it clean ie just amps boluses OR run “clean amps” as a 1 amp/hr infusion
triad of serotonin syndrome?
altered mental status
autonomic instability (fever)
increased neuromusclar activity (clonus, seizure)
in the setting of serotonergic trigger
What does terminal R avr look like
Mgmt of TCA overdose
mgmt of serotonin syndrome including antidote
benzos for agitation, neuromuscular hyperactivity, seizure
cyproheptadine –> consider in moderate SS that is refractory to other supportive measures (only available po).. its kinda shit
SUPPORTIVE STUFF: eg bicarb for qrs or Mg for qtc
2 types of MAOi and what their toxicity is like
Amantidine (PD med) and St John’s wart
SS and life threatening excessive sympathetic activity
hallmark of wellbutrin OD
seizure
some classes of meds that cause serotonin syndrome
SSRI, SNRI, trazodone, mirtazepine
trazodone toxicity?
SS, priapism, hypotension
diagnostic criteria for SS
seizures refractory to benzos, think…
hyponatremia, isoniazid
antidote to isoniazid toxicity?
pyridoxine (vit B6)
anticholinergic meds, name some
anticholinergic vs sympathomimetic
AC will be dry, sympathomimetic will be diaphoretic
anticholinergic toxidrome
cant see, cant pee, cant spit, cant shit
treatment of anticholinergic toxidrome, including antidote
cholinergic toxidrome
fluids from every orificie and killer B’s
common cholinergics
mgmt of cholinergic toxicity
supportive care
atropine to dry up secretions and treat bradycardia (often need high doses)
benzos for seizure or agitation
**doses so high you will un out in hospital. start with 2 mg IV and double q5 min until secretions dry
two reversal options for a warfarin
Vitamin K: po or IV –> takes hours to work
PCC (aka octaplex) 2000 units –> works almost immediately
use octaplex if life threatening or serious bleed.
reversal for heparin/LMWH
protamine (works better for heparin than LMWH)
reversal for DOACs
reversal for dabigatran
PCC (octaplex)
praxbind (or PCC)
timeline of HIT
within 5-10 days of starting or up to 3 weeks after stopping
lab sign to look for with HIT
platelets down >50%
carbamezepine toxicity is similar to what anti depressant?
-what is one feature of carbamazepine that makes it stand out?
TCA
enterohepatic circulation
what lab abn can valproic acid OD cause, what is the antidote?
hyperammonemia,
L- carnitine
why is phenytoin a more potent toxin than fosphenytoin
phenytoin is mized with propylene glycol, which is a potent diluant (can cause hypotension, bradycardia and cardiac arrest if injected quickly)
What are the 4 types of EPS
Akathisia
Acute dystonia
Parkinsonism
Tardive dyskinesia
onset, reversibility, symptoms, mgmt of:
Akathisia
onset, reversibility, symptoms, mgmt of:
drug induced parkinsonism
onset, reversibility, symptoms, mgmt of:
acute dystonia
onset, reversibility, symptoms, mgmt of:
tradive dyskinesia
NMS vs serotonin syndrome
history
but also NMS is severe rigidity, where as SS can rigidity but is also clonus and tremors
NMS is FARM (fever, autonomic changes, rigidity, mental status changes)
SS is FARM + clonus/twitching/seizure and GI upset
mgmt of NMS
stop offending med, benzos, intubate/paralyze/cool as needed.
mgmt of torsades
unstable = cardiovert
pulseless = defibrillate
- Mag 2g then infusion
or overdrive pacing –> use TVP to pace at rate of 100-120, this shortens qtc and prevents recurrence/can terminate torsades
classes of antidysrhythmics?
Some Block Potassium Channels
1: Sodium channel blockers (most of them)
2: beta blockers
3: Potassium channel blockers :amiodarone, sotalol
4: calcium channel blockers
a/e or contraindication to amiodarone
QTc prolongation or long QTc
stepwise approach to BB and CCB overdose
- GI decontamination wit AC if appropriate
- IVF, atropine, vasopressors (nor epi or epi) for hypotension/bradycardia
- supplement calcium–> increase contractility
- glucagon (don’t really use it b/c ppl vomit)
- high dose insulin –> 1unit/kg bolus insulin R, then 0.5-1 unit/kg/hr AND D50 amp then infusion of 1 amp/hr titrating to normoglycemia
** note insulin acts as an inotrope in this case
how to distinguish BB vs CCB overdose
CCB OD are often hyperglycemic
whereas BB are usually euglycemic
which BB can cause CNS toxicity in absence of cardiovascular effects
propranolol (bc non-cardioselective)
4 meds for your “low and slow” ddx
BB, CCB, digoxin, clonidine
ACEi/ARB toxicity: symptoms, seriousness, mgmt
mild hypotension/hyperkalemia
rarely serious as a single agent
supportive Tx with IVF/pressors
clonidine OD: symptoms mgmt
intiial hypertension, then hypotension/bradycardia
also causes dec LoC, miosis and hypoventiliation
it is a mix of “low and slow” + opiod toxidrome
mgmt is supportive with IVF and rarely pressors
Antidote for sulfonyurea overdoses(eg gliclazide, glyburide etc) why does it work?
Ocreotide! Stops insulin production from pancreas
Treatment of metformin overdose?
Supportive, AC, bicarbonate infusion or HD if severe lactic acidosis
Most dangerous diabetic med for a young child?
Sulfonyureas. One pill can kill, can causes severe hypoglycaemia
2 digoxin MOA and why too much is toxic
acute vs chronic dig toxicity
dig toxicity mgmt
don’t usually tx hyperK in the usual fashion, treat the dig OD
should you use charcoal with caustic ingestion?
nope
acidic vs alkalotic burns
acidic: coagulation necrosis
alkalotic: liquefaction necrosis, slower and deeper process
what are hydrocarbons
any chemical with both hydrogen and carbon
hydrocarbon toxicity?
depends on exact compound and systemic involved. pneumonitis/ARDS common for resp exposure/aspiration
what does hydrogen fluoride do to calcium. what is the antidote?
binds it, causes hypocalemia systemically and locally (ie on skin)
calcium gluconate or calcium chloride
Think of some common nontoxic household chemicals
timeline of lead toxicity?
usually chronic, but has the potential to be acute
antidote for lead, mercury and arsenic poisoning?
chelators: eg BAL (British anti-Lewisite), DMSA, Ca-EDTA
acute aresenic exposure is characterized by?
violent gastroenteritis
what are Mees lines
transverse white lines on nails that appear in chronic arsenic toxicity
sources of CO? what does it smell like
vehicle exhaust, ovens, house fires, furnaces.
it is odorless and colorless
pathophys of CO poisoning
it binds HgB with greater affinity than O2, creating carboxyhemoglobin which doesnt deliver O2 to cells –> cellular hypoxia and lactic acidosis
symptoms of CO poisoning?
vague and non-specific , can cause pretty much everything
elimination of CO at room air, 100% fio2 and hyperbarics
300 mins room air
90 mins 100% fio2
30 mins Hyperbarics
normal pulse oximetry, ABG with metabolic/lactic acidosis and normal PaO2, think?
CO poisoning
what is a norm carboxyhemoglobin level?
< 3-5 in non-smokers
<10 in smokers
mgmt of CO poisoning? dispo in minor toxicity
-apply 100% o2 via NRB immediately
-if minor symptoms, monitor for 4 hours and dc if symptoms resolved.
-assess for hyperbaric indications
indications for hyperbarics in CO poisoning?
-any history of LOC
- level >25%
-coma
-persistent neuro symptoms/cerebellar dysfunction
-prolonged exposure (>24hrs)
-seizure
-pregnancy with signs of fetal distress or > 15%
-severe acidosis
-arrhythmia or MI
sources of cyanide?
burning plastics/wool/synthetics, house fires, industrial processes
cyanide pathophy
disrupts oxidative phospohrylation –> cellular hypoxia and lactic acidosis
cyanide symptoms
coma, shock, severe metabolic acidosis
clues for cyanide poisoning?
metabolic acidosis, marked lactate elevation (>8), arterial appearance of venous blood, elevated venous O2, bitter almond smell
2 antidote options for cyanide toxicity?
- hydroxocobalamin (preferred): 5g IV infusion in adults –> binds cyanide and makes it into vitamin B12 (cyanocobalamin)
- cyano kit (more side effects, dont use all elements in ppl with concomitant suspected CO toxicity)
contains: amyl nitrite pearls (for inhalation), sodium nitrite (IV), sodium thiosulfate (IV)
when to suspect hydrogen sulfide poisoning?
rotten egg smell, sewer or manure exposure,
hydrogen sulfide presentation?
rapid coma, shock and lactic acidosis that improves once removed from exposure
mgmt of hydrogen sulfide poisoning?
mostly supportive, administer 100% O2, observe for a few hours for pulmonary edema,
antidote is sodium nitrite
pitts of bitter almonds, apricots can cause?
cyanide toxicity bc they contain amygdalin, which converts to CN in vivo
methylene chloride (found in solvents), converts to what in vivo?
Carbon monoxide
Local anesthetic toxicity, antidote, and dose
Intralipid: 1.5 mL/kg bolus then infusion of .25 mL/kg/min
Max doses of local anesthetic
Symptoms of local anaesthetic toxicity
Numbness around the mouth, tinnitus, sense of impending doom, other neurotic symptoms, like headache, drowsiness, confusion, etc. Progressing to seizures and at highest doses, haemodynamic collapse/arrhythmia
Two common precipitants of chronic lithium toxicity
Increase in dose, decrease in renal function
Symptoms in acute versus chronic lithium toxicity
Acute equals G.I. symptoms
Chronic equals CNS symptoms ranging from lethargy, confusion,, and seizures
Management of lithium toxicity
Indications and 3 indications for HD
No role for activated charcoal.
IV hydration is essential to increase renal clearance.
Hemodialysis indicated if:
-Anuria/renal failure.
-Inability to handle aggressive hydration (poor EF)
-Severe CNS toxicity/seizures
2 methylxanthines and their general toxidrome
Caffeine
Theophylline (old school copd/asthma med)
Severe n/v + general sympathomimetic
Moa: cause release of more formed catecholamines
Opioid toxicity triad
CNS depression, resp depression, miosis
Narcan infusion dose
2/3 of wake up dose/hr as infusion, titrated to resp rate
Emerg relevant complications of anabolic steroids
Acute MI, VTE, sudden cardiac death
Stages of acetaminophen toxicity
Toxic amount of acetaminophen in single ingestion
10g or 200 mg/kg whichever is smaller ( for all ages)
Toxic amount of Tylenol ingested in repeated supra-therapeutic amounts?
Over 6 years of age: >10 g or 200 mg/kg in 24 hr period
Or >6g/day or 150 mg/kg/day (whichever is less) for >48 hr period
Under 6:
What is the pathophysiology of acetaminophen overdose?
Usually, with nontoxic doses, glutathione stores combined with NAPQI to form non-toxic metabolites. With toxic levels of acetaminophen glut stores become overwhelmed, and NAPQI builds up.
What are Kings College criteria?
pH less than 7.3 after resuscitation
Or all three of: INR greater than 6.5, creatinine over 300, hepatic encephalopathy
Most effective timeframe to give NAC in acetaminophen OD
In first 8 hours
Toxic 4 hour acetaminophen level and iv NAC loading dose:
150 ug/mL
150 mg/kg
When to treat acetaminophen overdose, if time of ingestion is unknown or if there is repeated super therapeutic ingestion
If acetaminophen level is greater than 132 umol/L (20 mcg/mL)
Or AST/ALT are elevated
What is the difference between the toxicity line and the treatment line on the Romac Matthew nomogram? When to use this nomogram?
Treatment line is a 25% lower safety margin.
Only use this in single acute ingestion where time of injection is known
things that contain salicylates
ASA, bismuth subsalicylate (pepto-bismol), 5-ASA, a lot of OTC cold meds
4 pathophys mechanisms of salicylate toxicity
-direct resp stimulation –> hypervent
-uncouples oxidative phosphorylation –> anaerobic metabolism
- stimulation of chemoreceptors –> vomittign
- ototoxicity –> tinnitus/hearing loss
ABG possibilities with salicylate toxicity (3)
- metabolic acidosis (if severe, can lead to CV collapse and death)
- resp alkalosis (if early)
- mixed of the two above (common)
new tinnitus or hearing complaint in older pt? think…
chronic salicylate tox
tx of salicylate toxicity
-activated charcoal
-IV hydration to maintain renal perfusion
- urinary alkalization
- HD if severe acidosis
symptom of NSAID toxicity
gastritis/GIB, at extreme doses can acidosis, AMS or seizures (rare)
toxic dose of ibuprofen
mgmt of OD?
200 mg/kg
symptomatic and supportive
5 stages of iron toxicity
if patient is asymptomatic after ____ hours, they have not had significant iron OD
6
key pahtophys behind iron toxicity
uncouples oxidative phosphorylation –> anaerobic metabolism
mgmt of iron toxicity, including antidote and its indications
-supportive mgmt
-NO ROLE FOR AC
-deferoxamine (chelating agent) = antidote, indications
1. serum iron level >90 umol/L or 500 ug/dl
2. systemic illness (shock, severe acidosis etc)
mechanism of dextromethorphan and mgmt of OD
where is it found?
NMDA receptor antagonist (similar to ketamine),
supportive mgmt
found in OTC cough meds
diphenhydramine (benadryl) action on receptors belwo casues:
H1 receptors
muscarinic receptors
na channels
-leads to sedation
-anticholinergic tox
-wide QRS at high doses
two types of industrial/agricultural insecticides and their main toxidrome?
organophosphates and carbamates
cause cholinergic toxicity
mgmt of organophosphate toxicity, including 2 antidotes
-surface decontamination
-atropine for unstable brady and excessive secretions (start at 1 mg then double q5mins until secretions dry)
-pralidoxime is other antidote (reactivates the inhibited cholinesterase enzymes)
what re superwarfarins, how to manage them
rodenticides
most complications d/t bleeding.
need to monitor INR/PTT for 48 hrs, treat with vit K, PCC etc
what does strychine cause, where is it found? mgmt?
-uncontrolled muscle contractions
-it is a rodenticide but also found in illicit drugs sometimes
- mgmt = benzos, intubation/ventilation prn
Barbiturate MOA
Agonism of GABA channels
Contraindications to flumazenil
- Chronic benzo use
- Congestion of epileptogenic med
- Suspected raised ICP
Flumazenil duration of action, utility?
About 1hr
Not super useful in ED, mainly for reversal of prosed
Mgmt of stimulant OD
Benzos, sodium bicarbonate if wide qrs,
Avoid beta blockers (?unopposed alpha)
Stimulant OD s/s
Sympathomimetic vs anticholinergic
Diaphoresis and hyperactive bowel sounds in sympathomimetic
What is massive acetaminophen toxicity, how is it different from non massive
how to monitor bicarb treatment
do not exceed pH of 7.55 or pCO2 of 55.
should check gas every 6 amps at maximum, more is better.
Sources of carbon monoxide
What test order for query CO poisoning
Co-oximetry (measures oxyhemoglobin, methhaemoglobin and carboxyhaemoglobin)
One specific lesion on CT head that is associated with CO poisoning?
Globus pallidus lesion (usually
Bilateral)
Expected iron toxicity based on elemental iron ingested
