Inservice Review: Toxicology
Gerry Maloney, DO
Attending Physician, Emergency
Medicine and Medical Toxicology
CWRU/MetroHealth Medical Center
Analgesics
• APAP
• 140 mg/kg toxic dose for
single acute ingestion (200
mg/kg peds)
• Rumack-Mathews
nomogram only for single
acute ingestion
• NAC can be given with
charcoal (no need to adjust
dose)
• PO NAC: 140 mg/kg load,
then 70 mg/kg q 4 h for 72 h
• IV NAC: 150 mg/kg LD,
then 50 mg/kg over 4 h,
then 100 mg /kg over 16 h
• APAP
• Liver injury usually takes 24
h to develop for acute OD
• Elevated AST & detectable
APAP treat with NAC
• Refer for transfer: elevated
INR, encephalopathy,
acidosis, renal failure
Analgesics
• ASA
• Toxic dose 140 mg/kg
• See respiratory alkalosis first, then mixed
metabolic acidosis/resp alkalosis
• Cause of AGMA
• Treatment is IV bicarb
• HD for: level > 60 chronic or > 90 acute,
esp if mental status changes
Opiates
• Heroin: short-acting
• Methadone: long-acting
• Narcan: lasts approx 25-45 min
• Can see seizures from
demerol/propoxyphene
• Wide QRS and hypotension with
propoxyphene
• Pulmonary edema can be seen with all
Alcohols
• EtOH: zero-order kinetics
• IsoOH: osmole gap, may be serum/urine ketones, gastritis, no
metabolic acidosis
• MeOH: blindness, severe acidosis; windshield-washer fluid
• Ethylene Glycol: antifreeze; Ca Ox crystals in urine, flourescent
urine; renal failure, metabolic acidosis
• If double gap (osmole and anion) is present, think MeOH or EG
• MeOH/EG treated with IV EtOH or fomepizole; hemodialysis
for acidosis, levels > 25 mg/dL
• Anion: Na-Cl + HCO3; Osmole: 2(Na) + BUN/2.8 + Glu/18 +
EtOH/4.6
Anesthetics
• Know the dose and effects of your procedural
sedation drugs (versed, ketamine, fentanyl,
propofol) and when not to use them
• Classic question is lidocaine allergic pt who
need local anesthesia; what can you use?
• Lidocaine is an amide; amides have 2 i’s
• So look for the answer with one i, or can also use
benadryl
Autonomic Agents
• Know cholinergic, anticholinergic,
sympathomimetic toxidromes
• Cholinesterase inhibitors (OP agents,
nerve agents)
• Treatment is atropine 1st (endpoint is
secretions, not heart rate or atropine dose)
• Then 2-PAM (to prevent aging, ie
irreversible binding of OP to cholinesterase
enzyme)
• DUMBELS is mnemonic
Autonomic Agents
• Anticholinergic
• Dry skin/mouth or decreased bowel sound
is clue
• Treatment is benzo first; can consider
physostigmine (though NOT if tricyclic on
board)
• Jimson weed or benadryl are classic agents
Autonomic Agents
• Sympathomimetics
• HTN, tachy, dilated pupils, moist skin
• Cocaine can cause Na channel blockade
and wide QRS
• Treatment for all sympathomimetics is lots
of benzos
• Avoid β blockers in cocaine
• Ecstasy-see bruxism and hyponatremia
Anticoagulants
• Most children with rat poison
(brodifacoum) asymptomatic
• FFP is first-line for severe bleeding
• IV vitamin K is associated with allergic
reactions
• Make sure you give K1 (activated vit K)
Anticonvulsants
• Dilantin
• Iv infusion: hypotension (from propylene
glycol) that is rate-related, necrosis if IV
infiltrates
• PO: OD sees ataxia/nystagmus, may be
obtunded late
• Normal level is 10-20
• Load is 17 mg/kg IV
Anticonvulsants
• Carbamazepine
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•
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Level is 4-12
Has active metabolite that is also toxic (10,11 epoxide)
Can cause seizure in OD, cross react with TCA on urine tox
Treat with multi-dose AC
• VPA
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Hyperammonemia in absence of toxic level or abnl LFT
Need serial levels in OD (irregular absoprtion)
Normal is 50-100
Can use MDAC, hemodialysis (level >1000) or carnitine
Antidepressants
• TCA: hypotension, seizure, anticholinergic sx;
wide QRS on EKG (look at aVR); treat with
bicarb
• QRS > 120 predicts increased risk of szr
• Trazodone: priapism, orthostatic hypotension
• Buproprion: wide QRS, seizure, SND
reuptake
• Citalopram: cardiotoxic
• SSRI or MAOI think serotonin syndrome,
may be delayed if MAOI involved
Antipsychotics
• Can see QT prolongation and orthostatic
hypotension with all
• EPS/akathisia decreased with use of
benadryl/cogentin
• NMS vs SS: NMS has slow onset, lead pipe
rigidity, hyperthermia; SS rapid onset,
reflexes and muscle tone LE>UE
• Stop offending agent, benzos, may consider
cyproheptadine (SS) or dantrolene (NMS)
CO
• Know half life of CO (RA 3-4 h, 100% 90
min, HBO 23 minutes)
• Know classic presentation (HA,
vomiting, winter, whole family sick)
• Refer for HBO: level > 40% (15% if
pregnant), syncope, MI, mental status
change, neuro deficits
• CNS lesion: bilat globus pallidus
Cardiac Meds
• Digoxin
• Level > 2 ng potentially toxic
• Classic EKG is bidirectional VT or PAT
with block
• Most common finding is PVC’s
• K > 5 serious toxicity
• Digibind: empiric treatment is 5-10 vials
(acute OD), 3-5 vials (chronic OD)
• Can calculate if level is known (dig level x
wt in kg/100= # of vials)
Cardiac Meds
• Beta blockers
• Glucagon is antidote
• Propranolol causes seizures
• CCB
• See metabolic acidosis and hyperglycemia (DKA like
picture)
• Most ER so need prolonged observation
• “pill can kill” in kids
• Treatment: calcium, pressors, HIE
• Clonidine
• Looks like opioid, narcan sometimes reverses effects
Caustics
• No vomiting, no charcoal
• Alkali: liquefactive necrosis deeper
burn
• Acid: coagulation necrosis stops burn
• Can have severe esophageal injury w/o
intra-oral injury
• Steroids not generally helpful
CN/HS
• CN: rapid BP fluctuations, metabolic acidosis
(elevated lactate)
• Affects Cytochrome aa3
• Treatment: amyl nitrate/sodium nitrite, then
sodium thiosulfate
• See “arterialization” of venous blood (high
venous O2 sat)
• HS: rapid knockdown with rotten egg smell
Metals
• AC binds poorly to all metals (works for strychnine)
• Li: causes ataxia; HD if level > 2.5 (chronic) or 4
(acute); can treat with IVF/WBI
• As: see vomiting early, then neuropathy/multi-organ
failure/prolonged QT, Mee’s lines
• Lead:
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•
•
•
level > 70 needs parenteral chelation.
Give BAL and EDTA.
Peanut allergy is contraindication to BAL.
> 10 is action level
Herbicides/pesticides/rodenticides
• Many are arsenical
• Also see superwarfarins or
organophosphates
• Paraquat: need to decrease FiO2
Hydrocarbons
• Determinants of aspiration risk:
• Surface tension
• Viscosity
• Volatility
• Never induce vomiting
• May see delayed pneumonitis (esp in kids)
• Sniffers/huffersmyocardial sensitization to
catecholamines, can have sudden death
Hypoglycemics
• Insulin: not much
• Sulfonylurea: prolonged hypoglycemia;
octreotide is antidote
• May be delayed in kids, generally need 24
hour OBS
• Metformin: lactic acidosis, esp in renal
failure
Inhalational
• Water solubility determines toxicity
• High-immediate irritation to eyes/MM
• Medium (like Cl) some upper and lower
airway stuff
• Low: all the way into the lungs, delayed
pulm edema (phosgene)
• Bleach + acids/ammoniachlorine or
chloramine gas
• CS: riot control agent
Iron
• See phases (Phase 1: immediate GI sx;
phase 2: quiescent; phase 3: acidosis,
liver injury, GI bleed; phase 4: recovery)
• Know different preps have different
amounts (FE
fumarate>sulfate>gluconate)
• Deferoxamine (DFO)is antidote
• Vin rose urine is sign DFO is working
INH
• Inhibits pyridoxal phosphateprevents
creation of GABA
• Clinical picture is intractable sz
• Causes profound lactic acidosis (“I” in
MUDPILES or METALACIDGAP)
• Treatment is pyridoxine (1 g of B6 for
every G of INH ingested, or 5 g empiric
dose)
Methemoglobin
• Change in oxidation of iron in heme molecule
(Fe++ to Fe+++ )
• Chocolate brown coloration of blood
• Also the MOA of nitrates in the CN antidote
kit
• Treatment (if levels >20% or severe sx) is
methylene blue 1 mg/kg
• High-risk persons include those susceptible
to oxidative stress (G6PD)
Shrooms/Plants
• Shroom you most need to know: amanita phalloides
• Delayed GI sx (>4 h) after ingestion is associated with
toxic mushrooms (delayed sx bad)
• Liver failure is result of A. phalloides
• coprinus antabuse reaction
• Gyromitra (false or brain morel) intractable sz
(INH-like, treated like INH)
• Amanita muscaria (red shroom)-anticholinergic
• Psilocybin (little brown shroom)-hallucinogen
Shrooms/Plants
a. phalloides
gyromitra
coprinus
a. muscaria
psilocybin
Shrooms/Plants
• Plants
• Cardiac glycosides (yew, oleander, lily of
the valley, foxglove) dig-like toxicity
• Can treat with digibind
• Poison Ivy: 3 shiny leaves; blistering rash;
type IV allergic reaction
• Jimson weed: anticholinergic
• Castor bean: ricin; inhibits RNA, MOSF
Shrooms/Plants
jimson
foxglove
ricin
Poison ivy
Neuroleptics
• EPS responds to cogentin/benadryl
• Can decrease EPS when giving
phenothiazines by pretreating with benadryl
• NMS: gradual onset, hyperthermic, AMS,
lead pipe rigidity, rhabdo; treat with benzos,
+/- dantrolene, stop agent
• SS: more rapid onset, similar clinical picture
except LE more rigid than UE; consider
cyproheptadine
Nonprescription drugs
• Cough & cold preps
• Dextromethorphan: can x-react with PCP on U
Tox; see nystagmus and AMS/ataxia
• Pseudoephedrine: sympathomimetic,
methamphetamine precursor
• Vitamins: know Fe content
• Imidazolines (afrin): look like clonidine
• Oragel: benzocaine, can cause methemoglobin
• Lido patches: seizures
Recreational Drugs
• Cocaine
• Sodium channel blockade
• Sympathomimetic toxidrome, may see
widened QRS
• Metabolite in urine: benzoylecgonine
• EtOH + coke cocaethylene, which may
be more toxic than plain coke
• Treat with benzos, avoid β-blockers
Recreational Drugs
• Heroin-already covered
• Ecstasy hyponatremia
• GHB: comatose, then wakes up
suddenly and yanks out ETT
• Ketamine: dissoc anesthetic, emergence
reactions, intact airway reflexes
• PCP: hallucinations, rotary nystagmus
Sedative-hypnotics
• Benzos
• Dec LOC, generally need to mix with EtOH to
have sig toxicity
• Rohypnol: ultra rapid metabolizer, does not xreact on standard U Tox
• Barbiturates
• Skin bullae, coma, hypothermia; can treat
phenobarb with MDAC/urinary
alkalinization/HD
• Soma
• Meprobamate, may cause bezoar/radio-opague
Strychnine
• Increase in excitatory
neurotransmission
• Pseudo seizure activity (rigid,
opisthotonus, awake)
• Marked lactic acidosis
• Rat poison is culprit
Toxicology in the Core
Curriculum
Environmental Toxicology
• Arthropods
• Black Widow
• Presentation is severe abd cramping mimicking acute
abd with normal labs
• Key: may have been working in garage/reaching into
pile of lumber
• Treatment: supportive, may try calcium gluconate;
antivenin not generally available
• Brown recluse
• Small wound that develops into ulcer
• Treatment: wound care; dapsone has been advocated
before but not used widely d/t risk of MetHb
Environmental Toxicology
• Scorpions
• Centuroides only significantly venomous
species in US
• Neurotoxin that cause
paresthesias/vomiting/cramping,
treatment is supportive
• Tick
• Tick paralysis= neurotoxin by dermocentor
sp usually
Environmental Toxicology
• Marine
• Scombroid: large fish (tuna, mahi-mahi,
swordfish), excess histamine in flesh;
flush/cramping/diarrhea/hypotension
• Ciguatera: also larger fish, hot/cold
reversal in extremities
• Jellyfish: treat with ammonia or urine (not
fresh water)
• Lionfish: hot water immersion
Environmental Toxicology
• Snakes
• Pit viper: diamond shaped head, pits anterior to
eyes, fangs
• Crofab: used instead of Wyeth antivenin; less risk
of anaphylaxis/serum sickness
• Pit vipers (rattlers, cottonmouth, copperhead)
have hemotoxin (low plt, coagulopathic) and
cause tissue swelling +/- compartment syndrome
• Elapids (coral snake, cobras) are neurotoxic
• Mojave rattler is only NA pit viper with primary
neurotoxin
Environmental Toxicology
• Snakes
Good Luck!