Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Toxicology 1st Year Handwritten Notes, 2nd Year Handwritten Notes, 3rd Year Handwritten Notes & Final Year Handwritten Notes (Lecture Notes)
NReduce exposure
NReduce absorption
NIncrease elimination
NKnow when to intervene
NGive supportive care
NGive specific therapy and
antidotes when appropriate
2
THE COMA COCKTAIL
NDEXTROSE
NNALOXONE
NTHIAMINE
NFLUMAZENIL (NO)
3
4
5
Hypoglycemia
NSalicylates
NAcetaminophen
NInsulin
NAlcohol
NOral hypoglycemic
Check glucose in all patients with ODs
and those with altered mental status
6
Gastric Decontamination Overview
NThe vast majority of patients are unlikely to
benefit from gastric decontamination:
?They have ingested nontoxic
substances
?They have ingested nontoxic amounts of
toxic substances
?They present long after
decontamination would
be expected to be
of any benefit
7
Gastric Decontamination Overview
NPatients who theoretical y may benefit from
decontamination:
?Present early after ingestion (within 1 hour)
?Have taken a delayed-release product
?Are symptomatic before ful absorption is
likely to have occurred
?Have taken potential y
life-threatening overdoses
NNo prospective studies have
demonstrated outcome benefits
with gastric decontamination
8
9
Syrup of Ipecac
NBecause of many limitations,
not recommended in emergency
departments
NPossible role in remote or long transport
time settings
NContraindications
?Caustics, low viscosity hydrocarbons
?Bleeding disorder, seizures, < 6 months
?Altered mental status, unprotected airway
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Gastric Lavage
NNow uncommonly used
NPossible Indications
?Recent (<1hr) life-threatening
ingestion
?Agent not bound by charcoal
NMethod
?Large-bore orogastric tube
?Left lateral decubitus position
?Protect airway
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Gastric Lavage
NContraindications
?Unprotected airway
?Caustics
?Nontoxic agents
?Hydrocarbons (unless they
contain a dangerous additive)
NComplications
?Aspiration / esophageal tears
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13
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Activated Charcoal
NDose: 1-2 g/kg (max 100 g)
NThe optimal ratio of charcoal to toxin is
10:1
NIn massive overdoses, may require extra
doses of charcoal
NAdministration of oral charcoal is associated
with little risk, a low threshold for use is
reasonable unless ful absorption of the drug
has occurred
15
Activated Charcoal
NEnhanced elimination
?Direct binding, enterohepatic recirculation,
"gut dialysis"
NPoorly bound: Lithium, iron, caustics, cyanide,
hydrocarbons, alcohols, alkali, acid
NContraindications: Caustics, ileus, obstruction
NMultidose: Sustained release drugs, theophylline,
phenobarbital, salicylates, carbamazepine
Avoid multidose cathartics (sorbitol,
magnesium citrate) due to dehydration,
electrolyte problems
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17
Drug Elimination (1)
NCharcoal hemoperfusion
? Protein-bound
?Theophylline, phenobarbital, carbamazepine
NWhole bowel irrigation
?Sustained release preparations, bezoars
?Iron, lithium, drug packers, lead
?Contraindications
? Ileus
? Obstruction
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19
Drug Elimination (2)
Avoid urine acidification and forced diuresis
NUrine alkalinization: Salicylates, phenobarb, INH
?Urine pH goal is 7-8
?Need to replace K+ to alkalinize urine
NHemodialysis: Salicylates, lithium, methanol,
isopropanol, ethylene glycol, theophylline,
phenobarbital
?Low protein binding, low molecular weight
?Smal volume of distribution
?Water-soluble
20
Agent / Antidote (1)
Agent
Antidote
Acetaminophen
Acetylcysteine (NAC)
Arsenic
BAL, DMS
Aspirin
Alkaline diuresis, hemodialysis
Beta-blocker
Glucagon, intralipids
Barbiturate
Alkaline diuresis, hemodialysis
Calcium channel blocker
Calcium, glucagon, gluc/insulin,
intralipids
Carbamate
Atropine
Carbon monoxide
100% O2, hyperbaric O2
Warfarin
FFP / Vit K / PCCs
Cyanide
Sodium nitrite, sodium thiosulfate,
hydroxycobalamine
Digitalis
Digibind (fab antibodies)
21
Agent / Antidote (2)
Agent
Antidote
Ethylene glycol
Bicarbonate, ethanol, dialysis, 4-MP
Heparin
Protamine
Hydrofluoric acid
Calcium, magnesium
Iron
Deferoxamine
Isoniazid (INH)
Pyridoxine (Vit B-6)
Lead
BAL, DMS, EDTA
Mercury
BAL, DMS
Methemoglobin
Methylene blue
Methanol
Bicarbonate, ethanol, dialysis, 4-MP
Nitrites
Methylene blue
Opiates
Naloxone
Organophosphates
Atropine, 2-PAM
Oral hypoglycemic agents
Glucose, glucagon, octreotide
TCA
Sodium bicarbonate, intralipids
22
Formulas (1)
NAnion gap metabolic acidosis
(Na) - (Cl + CO
2), normal < 12
NIncreased
M Methanol, metformin, massive ingestions
U Uremia
D DKA
P Paraldehyde
I Iron, INH
L Lactic acidosis (CO, CN)
E Ethylene glycol
S Salicylates
23
Formulas (2)
NOsmolal gap = (measured) ? (calculated)
NNormal gap <10
Calculated (nl 285-295) = 2 Na + BUN + Glu + EtOH
2.8 18 4.6
NIncreased gap: Acetone, isopropanol,
methanol, ethylene glycol, mannitol,
ketoacidosis, ethanol (most common)
24
Toxicology Screens
NQuantitative urine specimens are superior to
blood specimens since drug metabolites can
be detected 2-3 days after exposure
NUrine screens are specifical y designed for
drugs of abuse
NA positive or negative screen
does not necessarily rule in or
rule out an overdose
25
Toxicology Screens
NFalse positives:
?Amphetamines: Pseudoephedrine
?TCAs: Cyclobenzaprine, carbamazepine,
phenothiazines, diphenhydramine
?PCP: Ketamine,
dextromethorphan
NFalse negatives:
?Dilute urine
?Methadone: Opioid screens
?MDMA: Amphetamines
?Rohypnol: Benzodiazepines
26
Specific Drug Levels
NQuantitative blood tests should be limited to
those drugs for which levels can predict
subsequent toxicity or guide specific therapy
(e.g. iron, lithium, acetaminophen, ASA,
theophylline, digoxin)
27
TOXIDROMES
NAnticholinergic
NSympathomimetic
NCholinergic
NOpioid
NWithdrawal
28
Anticholinergic (1)
NAtropine, tricyclic antidepressants,
phenothiazines, antihistamines,
antiparkinsonian drugs, Jimsonweed
N"Hot as hel , blind as a bat, dry as a bone, red
as a beet, mad as a hatter"
NDry, flushed skin, dry mucus membranes,
mydriasis, decreased bowel sounds, urinary
retention
NHOT / DRY / RED / BLIND / MAD
29
Anticholinergic (2)
NConfusion, agitation, delirium, seizures
?Treatment: Benzodiazepines
?Avoid phenothiazines (e.g., prochlorperazine) and
butyrophenones (e.g., haloperidol)
NWide-complex tachycardia
?Treatment: Sodium bicarbonate
NVentricular dysrhythmias
?Treatment: Lidocaine, amiodarone
?Avoid procainamide
NTorsades de pointes
?Treatment: Magnesium sulfate, overdrive pacing
30
Anticholinergic (3)
NPhysostigmine: Consider if unresponsive to
benzodiazepines; refractory seizures,
ventricular dysrhythmias, hyperthermia
malignant hypertension, hypotension
?Contraindicated in TCA overdose, heart block
31
Sympathomimetic
NAmphetamines, cocaine, PCP
NCNS excitation, seizures, hypertension,
tachycardia, sweating, dilated pupils,
hyperthermia
NTreatment: Benzodiazepines
Anticholinergic: Dry skin
Sympathomimetic: Diaphoresis
32
Opioids
NCodeine, morphine, heroin, demerol,
diphenoxylate (Lomotil), propoxyphene
(Darvon), hydrocodone (Vicodin), etc.
NRespiratory depression,
ARDS, hypotension, coma
NPinpoint pupils (not always seen)
NClonidine can mimic opioid OD
NTreatment: Naloxone
33
Cholinergic
NOrganophosphates, insecticides, some
mushrooms, chemical warfare agents
NInhibit cholinesterases increase acetylcholine
NMuscarinic effects: SLUDGE + Killer "B"s
?Salivation, Lacrimation, Urination, Diarrhea,
Gastrointestinal upset, Emesis
?Bradycardia, Bronchospasm,
Bronchorrhea
?Miosis (pinpoint pupils)
34
Organophosphates
NNicotinic effects: Muscle weakness,
fasciculations, respiratory failure
NCholinesterase levels helpful in diagnosis
but not helpful in management
NTreatment: Atropine (until secretions dry),
Pralidoxime
(2-PAM)
Mark-1 Autoinjection Kit
35
ATROPINE and 2-PAM
36
Withdrawal Syndromes
? Alcohol, barbiturates, benzodiazepines,
cocaine, clonidine
? Diarrhea, mydriasis, hypertension, tachycardia,
insomnia, cramps, diaphoresis, agitation,
piloerection
? Treatment: Benzodiazepines,
clonidine
37
ACETAMINOPHEN
38
Acetaminophen (1)
NToxic metabolite causes liver injury
?Saturation of glucuronidation and sulfonation
pathways (major metabolic pathways)
?Metabolism shifts to minor pathway
(cytochrome P450)
?Cytochrome P450 metabolism requires
glutathione, which depletes rapidly
?Toxic metabolite NAPQI (n-acetyl-p-
benzoquinoneimine) accumulates
? Is a free radical
?Direct hepatocel ular toxicity
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40
Acetaminophen (2)
NFour clinical stages
Stage I GI symptoms (N/V)
Stage II GI symptoms resolve
Hepatic and renal dysfunction begins
Stage III Peak LFTs, GI symptoms return
Stage IV Recovery phase
41
Acetaminophen (3)
NToxic ingestion: 140 mg/kg (7-10 g in adults)
N4 hour level >140: Potential y toxic
NN-acetylcysteine (NAC)
?Prevents binding of NAPQI to hepatic macromolecules
?May also reduce NAPQI back to acetaminophen
NAC provides a cofactor needed to make inert metabolites
of APAP
Lack of this cofactor results in the production of
hepatotoxic intermediary metabolites
?Oral and IV preparations available
?Safe in pregnancy
?Charcoal does not inhibit effectiveness
?Still indicated in late presentations >24hrs
NHepatotoxicity is rare in children
42
Alcohol (1) - Ethanol
NEthanol intoxication should not give acidosis
NSearch for other causes of altered MS (CNS)
Withdrawal
N"The shakes" (6-8 hours) / hal ucinations (visual)
NAlcohol withdrawal seizures (6-48 hours)
?Treat with benzodiazepines; no role for phenytoin
NDelirium tremens: Confusion, fever, tachycardia
NTreatment: Fluids, thiamine (B1), multivitamins,
Mg++, folic acid, benzodiazepines
Wernicke's encephalopathy: Oculomotor crisis
CN VI palsy (lateral rectus), nystagmus, ataxia, global
confusion
Korsakoff's psychosis: Retrograde amnesia, confabulation
44
45
Alcohol (2) - Methanol
NPaint thinner, window washer solvent, wood alcohol,
gas tank additive
NAnion gap acidosis, increased osmolal gap
NDisc hyperemia (visual symptoms common)
NMethanol itself is nontoxic but alcohol dehydrogenase
forms the toxic metabolite
?Formaldehyde
?Formaldehyde is then broken down by formaldehyde
dehydrogenase into another toxin = formic acid
NSymptoms (often delayed 12-18hrs): Seizures,
respiratory failure, N/V, pancreatitis, visual changes
or blindness
46
Alcohol (3) - Methanol
NTreatment
?Fomepizole (4-methylpyrazole) (Antizol)
?An alcohol dehydrogenase inhibitor
?Allows methanol to be excreted intact via the kidneys
without being broken down into its toxic metabolites
?Ethanol
?Occupies alcohol dehydrogenase to limit breakdown
of methanol into its toxic metabolites
?Ethanol is preferential y metabolized by alcohol
dehydrogenase over methanol and ethylene glycol
?Dialysis and bicarbonate if severe acidosis
refractory to 4-MP or ethanol therapy
47
Alcohol (4) - Ethylene Glycol
NAntifreeze, paint, solvents / has a sweet taste
NCNS depression, intoxication (without alcohol
odor), anion gap acidosis, anuria, osmolal gap
NMetabolized by alcohol dehydrogenase to the
toxic intermediate glycoaldehyde which is then
broken down to:
? Oxalic acid (precipitates in urine and blood with
calcium to form calcium oxalate crystals)
? Glycolic acid (causes profound acidosis)
NRenal failure, hematuria, hypocalcemia
48
Alcohol (4) - Ethylene Glycol
NTreatment:
?Fomepizole to inhibit the activity of alcohol
dehydrogenase, or IV alcohol to preferential y
consume alcohol dehydrogenase
? Treatment al ows the renal excretion of intact
ethylene glycol
?Requires supplemental pyridoxine and thiamine
(both consumed in metabolism of ethylene glycol)
?Bicarbonate for acidosis
?Dialysis if severe acidosis or high blood levels
49
CALCIUM OXALATE CRYSTALS
50
4-Methylpyrazole (ANTIZOL)
51
TOXIC ALCOHOL THERAPY
52
Alcohol (5) - Isopropyl Alcohol
NRubbing alcohol
NCNS depression greater than ethanol
NMetabolism: In liver > 50% metabolized to acetone;
renal & pulmonary excrete unchanged isopropyl
alcohol
NHemorrhagic gastritis, pulmonary edema,
hypoglycemia
Ketosis but no acidosis / normal anion
N
gap / increased osmolal gap
Severe hypotension
NSupportive care, don't give alcohol. Hemodialysis (if
severe)
Increasing alcohol toxicities:
ethanol < isopropyl alcohol <
ethylene glycol < methanol
53
SYMPATHOMIMETICS
54
ECSTACY (MDMA)
55
Amphetamines / Cocaine (1)
NCause sympathomimetic syndrome
?Hypertension, tachycardia, seizures, dilated
pupils, hyperthermia, agitation, diaphoresis
NTreatment: Benzodiazepines, decrease
stimulation (dim room), cooling
NBeta blockers are contraindicated (cause
unopposed alpha stimulation: hypertension,
ischemia, vasoconstriction)
Cocaine: Abruptio placentae, prematurity,
status epilepticus, strokes, MI, rhabdomyolysis
56
57
Amphetamines / Cocaine (2)
NCocaine is metabolized by plasma
pseudocholinesterase and liver enzymes
metabolites excreted in urine
NPsychiatric complaints are common
Chest pain: Usually noncardiac - consider
PE, endocarditis, pneumothorax, pneumonia
NBody packer usual y has positive plain film
NFormication: "Cocaine bugs"
NDesigner agents: MDA, Ecstasy, MMDA, etc.
58
Antabuse (Disulfiram) Reaction
N Alcohol + metronidazole (Flagyl)
? Flushed face, neck, trunk
? Marked diaphoresis
? Nausea, vomiting, headache
? Severe
?Hypotension
?Seizures
?Dysrhythmias
59
Anticholinergics / Antihistamines (1)
NAtropine, scopolamine, diphenhydramine, TCAs
NTachycardia, dryness, ileus, urinary retention,
dilated pupils, fever
NTreat agitation with benzodiazepines; avoid
phenothiazines
Wide QRS >100 msec?
Terminal R wave axis
rightward?
Consider TCA
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61
Anticholinergics / Antihistamines (2)
NPhysostigmine
?Inhibits acetylcholinesterase, increases
acetylcholine
?Not first-line drug (benzodiazepines preferred)
?Consider in: Seizures, coma, arrhythmia,
agitation
?Contraindicated in TCA (may cause asystole)
62
Arsenic
NCommon heavy metal exposure
NWood preservatives, weed kil ers,
pesticides
NGastroenteritis, hypotension, muscle
twitches, delirium, hepatic and renal
failure, death
NDiagnosis: 24 urine
NTreatment: Chelation (BAL, DMSA)
NChronic effects: Anemia, metal ic
taste, neuropathy, horizontal Mees'
lines in nails (nonspecific ? also
seen with thal ium, other heavy
metals and renal failure), alopecia
63
Barbiturates
NShort-acting
? Pentobarbital, secobarbital
? High lipid solubility
? Hepatic degradation
NLong-acting
? Phenobarbital
? Renal excretion, dialyzable
NMiosis, hypotension, CNS depression
NCutaneous bullae (bad prognosis)
NTreatment: Lavage, charcoal, urine
alkalinization: long-acting agents, hemodialysis
64
Benzodiazepines
NRespiratory depression, ataxia, hypotension,
hypothermia, coma
NTreatment: Supportive
Flumazenil may cause intractable seizures:
chronic users, seizure disorders, seizure-causing
co-ingestants, increased ICP
65
Beta Blockers
NHypotension, bradycardia, AV block
NAntidotes:
?Glucagon 5-10mg IV, (avoid phenol diluent)
?Insulin + dextrose therapy
?Intralipids
NOther : Atropine, pressors, pacemaker
NTimolol eye drops can cause systemic toxicity
66
Calcium Channel Antagonists
NMost common: Verapamil, diltiazem, nifedipine
NBradycardia, hypotension, conduction delay
NAntidotes
?Calcium gluconate
?Glucagon
?Insulin + glucose rescue therapy
?Intralipids
NOther treatments: Fluids, pacemaker, pressors
Leading cause of death from cardiovascular drugs
67
Carbamazepine (Tegretol)
NClassic triad
? Severe symptoms
?Dizziness
?Coma
?Ataxia
?Seizures
?Nystagmus
?Arrhythmia
NMild symptoms
? Treatment
?Ataxia
?Multidose charcoal
?Drowsiness
?Hemoperfusion
?Slurred speech
?NaHCO3 for QRS
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Carbon Monoxide (CO) (1)
NLeading cause of toxic death
NBinds Hgb, cytochrome A3, myoglobin
NCOHgb affinity for O is 250 times more than
2
Hgb
NShifts oxyhemoglobin dissociation curve to left
(inhibits release of oxygen from hemoglobin)
NHeadache, nausea, confusion, coma, seizures,
no cyanosis (may be mistaken for "flu")
NAlso suspect cyanide toxicity with smoke
exposure and profound acidosis
Levels do not always correlate with toxicity
70
Carbon Monoxide (CO) (2)
NCO crosses the placenta and fetal Hgb has
high affinity for CO
NDiagnosis: COHgb level (pulse ox not reliable)
NHalf life of CO
?320 min (air)
?90 min (100% O )
2
?20 min (HBO)
NDelayed neuropsychiatric syndrome
NHBO may prevent delayed CNS injury
NTreatment: 100% oxygen, HBO (controversial)
71
72
Carbon Monoxide (CO) and ABGs
NCarboxyhemoglobinemia
?Pulse Ox is normal (oximeter mistakes
carboxyhemoglobin for oxyhemoglobin)
?PaO2 on ABG is normal (oxyhemoglobin is
calculated from measurement of dissolved O2,
which is normal)
Key point:
Need to measure carboxyhemoglobin
73
Caustic Ingestions
NAcids
? Coagulation necrosis
? Eschar formation stops progression
NAlkali
? More common
? Liquefaction necrosis facilitates progression
? Ful thickness injury
Pr esence of oropharyngeal burns in alkali ingestion
is not predictive of esophageal injury
74
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Caustic Injuries
Treatment
NCharcoal and lavage are contraindicated
NBlind nasotracheal intubation contraindicated
NHydrofluoric acid: Give milk, Mg citrate by NGT
NSolid alkali ingestion: Dilute with water or milk
NOther caustic ingestions: Dilution is
contraindicated, as it may induce vomiting
NUpright CXR
NEndoscopy within first several hrs of ingestion
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Chlorine
NWidely available (labs, paper manufacture,
pool chemicals, cleaning products)
NYel ow-green gas, pungent odor
NFormation of acid and oxidants on moist
membranes
NImmediate ocular and upper airway irritation
NCan lead to pulmonary edema
in severe exposure
NSupportive care, humidified O2
78
Clonidine
NAlpha-adrenergic agonist
NCentral effects: Hypotension, bradycardia
NPeripheral effects: Hypertension fol owed by
hypotension
NCNS: Lethargy, apnea, miosis, decreased reflexes
NCardiac: Bradycardia, hypotension, AV block
Can mimic opiate OD
coma, miosis, respiratory depression
NTreatment: Fluids, atropine, pressors
NCan mimic opioid OD; Naloxone may be beneficial
NWithdrawal: Hypertension, tachycardia, anxiety,
diaphoresis
79
Cyanide (1)
NBinds cytochromes, causes anaerobic
metabolism and lactic acidosis
NJewelers, chemical labs, apricot pits, smoke
inhalation (burning plastic)
NSuspect in lab worker, suicide, coma with
acidosis, use of artificial nail remover, ICU
patient on nitroprusside
NAbdominal pain, nausea, coma, bradycardia,
acidosis, sudden CV collapse
NDistinctive odor (bitter almonds)
NNo cyanosis
NNormal PaO2 and O2 sat; acidosis
80
Cyanide (2)
N Lab: Lactic acidosis (with anion gap)
N Treatment goal is to create a control ed state of
methemoglobenia to compete for CN
? CN + metHgb cyanometHgb
N Nitrites create metHgb that binds CN
? Amyl nitrite (inhaled)
? Sodium nitrite IV
? Sodium thiosulfate IV
? Sodium thiosulfate + CN = thiocyanate (renal
excretion)
N Hydroxocobalamin (Cyanokit) is a B12 precursor
that combines with cyanide to form
cyanocobalamin (B12) which is cleared renal y 81
Cyanide Antidotes
82
Digitalis (1)
NInhibits Na-K ATPase pump
NK+ leaks extracel ularly; Na+ and Ca++ leak
intracel ularly
NHyperkalemia, AV blocks, arrhythmias
NAntidote: Digibind (Fab fragments)
?Each vial binds 0.5 mg digoxin
? 20 vials should treat any life-threatening
toxicity
?Acute ingestion: Start with 10 vials if dig level is
unknown and life threatening dysrhythmia
?Chronic toxicity: Start with 6 vials
83
84
Digitalis (2)
NClass 1A antiarrhythmics are contraindicated
NLow K+, Low Mg, High Ca increases toxicity
NHigh K+ indicates severe OD
NPathognomonic: PAT with AV block
NCalcium administration contraindicated if
digoxin toxicity suspected or confirmed
Most common dig toxic
dysrhythmia is PVCs
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Gamma Hydroxybutyric Acid (GHB)
NA natural y occurring analog of the
neuroinhibitor gamma-aminobutyric acid
(GABA)
NStreet names: Grievous bodily harm,
Georgia home boy, Liquid X
N"Date rape" drug / "rave" drug
NTypical y ? white male,
mid- to late 20s, nightclub,
present to ER after midnight
NAlso used by body builders
87
Gamma Hydroxybutyric Acid (GHB)
NNot routinely detected on drug screens
NCNS depressant, rapid onset, lowered gag
reflex, severe respiratory depression
NTreatment: Airway control, no role for
naloxone, flumazenil, or physostigmine
NUsual rapid resolution within 8 hours
NIf co-ingestion of ETOH observe longer
NWithdrawal from chronic use is similar to
ethanol or sedative/hypnotic withdrawal
88
Hallucinogens
NLSD, mushrooms, mescaline, morning glory
seeds, designer drugs
NSerotonin antagonism
NPsychosis, anxiety
NSympathomimetic signs
? Tachycardia
? Hyperthermia
? Dilated pupils
NTreatment: Sedation, benzodiazepines,
haloperidol (Haldol), minimal stimulation
NAmanita mushrooms account for most deaths
89
90
Hydrocarbons (1)
NIncreased toxicity with
?Halogenated hydrocarbons or other toxic additives
?Low viscosity
?High volatility
?Low surface tension
NAspiration pneumonitis (coughing, tachypnea)
?Do not induce vomiting
Exposure (sniffing, huffing) can sensitize myocardium
dysrhythmias (catecholamines contraindicated)
NLavage if halogenated (carbon tet, PVC) or aromatic
(benzene, toluene, xylene)
NCXR: Deceptively clear- delayed findings (4-6 hours)
NSteroids and prophylactic antibiotics are not indicated
91
Hydrocarbons (2)
NThe general rule is NOT to empty the stomach,
unless the hydrocarbon solution contains a
toxic substance such as: (CHAMP)
Camphor
Halogenated (carbon tet, PVC, vinyl chloride)
Aromatic (benzene, toluene, xylene)
Metals (leaded gas)
Pesticides
NKwel (lindane)
? Chlorinated hydrocarbon
? CNS toxicity, seizures
? Avoid in young children, pregnancy
92
Hydrogen Fluoride
N Used in glass etching
N One of the strongest inorganic acids
N Can cause deep cutaneous injury, systemic
hypocalcemia
N Skin may appear normal despite significant
burn ? causes significant delayed injury
N Treatment
? Calcium gluconate (infiltration, gel, or intra-
arterial infusion) / avoid intradermal CaCl
? Calcium binds with fluoride ion stops pain
? If pain returns, repeat treatment
93
94
Hydrogen Sulfide (H S)
2
NOil refinery, hot asphalt, sewage, mines
NRapid knockdown agent with rotten egg odor
NInhibits cel ular respiration, blocks cytochrome
oxidase (leading to anaerobic metabolism)
NHas higher affinity for methemoglobin than
cytochrome oxidase, increase elimination by
production of methemoglobin
NTreatment: Remove from source, increase
elimination using methylene blue in cyanide
antidote kit to generate methemoglobin (do not
use the thiosulfate)
95
Isoniazid (INH)
NOverdose
- vitamin B6 (required for GABA synthesis)
- seizure threshold (can present in status)
? Coma
? Metabolic acidosis
NConsider in pediatric seizures (unintentional OD)
NConsider in populations likely to be on INH
NLittle role for bicarbonate therapy in acute toxicity
Antidote: Pyridoxine (vitamin B6)
96
Iron (1)
Common cause of poisoning death in children
NFree circulating iron damages blood vessels
?Direct GI corrosive effect
?Inhibits aerobic metabolism
?Vasomotor col apse, hepatorenal failure
NToxic dose is 30-40 mg/kg elemental iron
?0-6 hrs
- Gastroenteritis, dehydration, shock
?6-48 hrs - Quiescent phase
?12-48 hrs - Acidosis, coma, hepatic injury
?2-6 weeks - Recovery, GI scarring,
obstruction
97
Iron (2)
GI symptoms suggest significant exposure
N4 hour serum Fe level (TIBC not reliable)
NAvoid bicarb lavage
NCharcoal doesn't bind Fe
NLabs suggestive of OD: gap, glucose, WBC
NLiver has greatest injury due to portal circulation
NAbdominal X-ray: Bezoar
NAntidote: Whole bowel irrigation,
deferoxamine (chelating agent)
NDeferoxamine indications
?Severe GI symptoms, acidosis, shock
?Serum iron > 500, significant history
98
VIN ROSE URINE
99
Lead (1)
NCommon cause of chronic poisoning
NSuspect in children with headache,
encephalopathy, anorexia, abdominal
pain, paint exposure, lead lines
NCombines with sulfhydryl (SH) groups,
interferes with
enzyme activity
NCNS, GI tract, hematologic
100
101
Lead (2)
NPeripheral neuropathy (classic - wrist drop)
NDiagnosis: Serum level (>50 mcg/dL is
severe), basophilic stippling on blood smear
NTreatment: Chelation (BAL, DMSA, EDTA)
NIf KUB shows lead paint chips, whole bowel
irrigation
102
103
Lithium (1)
NMost patients under long-term treatment develop
toxicity at some point
NRenal elimination
NHyponatremia and hypovolemia increase toxicity
NIn acute ingestion, toxicity may be delayed (lags
rise in serum levels).
NMay be toxic at low levels (chronic ingestion)
NSerum levels do not predict CNS levels
NClinical: Tremor, vomiting, diarrhea, confusion,
slurred speech, coma, arrhythmias
NSeizures: Use benzodiazepines, phenobarbital
?Dilantin decreases excretion of Li+
104
Lithium (2)
Clinical status more important than Li+ level
NTreatment: Hold drug, no diuretics, lavage,
Kayexalate
NAggressive hydration with normal saline
NHemodialysis (severely toxic patient)
?Best based on clinical indications: : Coma,
seizures, myoclonus, hemodynamic col apse
?Consider if acute ingestion level > 3.5 mEq/L
?High risk in renal failure, rapidly increasing
levels, sustained release ingestion
105
Mercury
NToxicity depends on dose, form, and route of
exposure (elemental, organic, inorganic)
NCNS, GI, renal toxicity
NMetal ic mercury is benign if ingested, but very
dangerous when inhaled or injected
NDiagnosis: 24 hour urine col ection
NTreatment: Lavage, chelation (BAL, succimer)
Mercury from thermometer is inert
(not absorbed by GI tract)
106
Monamine Oxidase Inhibitors
(MAOI)
NBlock degradation of catecholamines
(norepi, epi, serotonin)
NDelayed symptoms 6-12hrs post-ingestion:
Headache, HTN, tachycardia
NHypertensive crisis: Amphetamines, cheese,
wine, fava beans (tyramine)
Meperidine and dextromethorphan are
contraindicated
with MAOI (can cause severe hyperthermia)
107
Methemoglobinemia (1)
NResults from the oxidation of normal Fe++ state
to Fe+++
NMethemoglobin is unable to bind oxygen
NCauses: Nitrites, nitrates, benzocaine,
dapsone, phenazopyridine (Pyridium)
NPresents often with vague symptoms
NMay present with signs and symptoms of
hypoxia, including cyanosis at metHgb levels
>15%
108
Methemoglobinemia (2)
NCyanosis unresponsive to O2
NChocolate brown blood (also seen with
SO Hgb)
4
NPulse ox unreliable, arterial PaO2 normal
NDefinitive identification with co-oximetry
Cyanosis reversible with methylene blue
(Reduces Fe+++ to Fe++)
Methylene blue is contraindicated in G6PD
deficiency
109
METHEMOGLOBINEMIA
110
Mushrooms
NIf lethal, usual y Amanita species
NNausea, vomiting, diarrhea, hepatic failure,
renal failure
NTime from ingestion to symptom onset
helps determine risk of significant toxicity
?Symptoms within 2 hours of ingestion indicate
benign course if only one type of mushroom
ingested
?Symptoms delayed more than 6 hours indicate
a toxic ingestion with risk of hepatic and renal
failure
111
Amanita Phalloides "Death Cap"
Liver
toxicity
Mushrooms
Amanita Phalloides
NNausea, vomiting and diarrhea 12 hours post-
ingestion, then latent period
NGI symptoms return in 24-48 hours with liver
necrosis and renal failure
NToxin kil s GI epithelial cel s, hepatocytes
NSupportive care, liver transplantation
113
Amanita muscaria
Mushrooms
Amanita Muscaria / Pantherina
NToxin is GABA agonist
NMental status changes
(delirium, hal ucinations,
seizures)
NNo hepatic toxicity
Psilocybin
NHal ucinations, euphoria,
nausea
NSupportive care
115
False Morels (Gyromitrin)
Good
Bad
116
MUSHROOMS (Gyromitrin)
NSpecies: Gyromitrin (false morels)
NToxin: Monomethylhydrazine (rocket
fuel... real y!)
NClinical effects: Gastroenteritis
(delayed), headache and seizures
NTreatment: Pyridoxine (Vitamin B6)
117
Neuroleptics / Phenothiazines
NClinical effects
?Dystonic (extrapyramidal) reactions
?Tremor, torticol is, rigidity, facial grimacing, dysphagia,
oculogyric crisis
?Akathesia (inability to sit stil )
?Tardive dyskinesia (involuntary lip and tongue
movements)
?Anticholinergic symptoms
?Quinidine-like, anticholinergic, peripheral alpha-blockade,
antihistaminic , prolonged QT, cardiac dysrhythmias
?Other: Heat stroke, hypotension, sedation, psychosis,
urinary retention, seizures
NTreatment: Benzotropine (Cogentin), diphenhydramine
(Benadryl), benzodiazepines, lavage, bicarbonate
118
Neuroleptics / Phenothiazines
NNeuroleptic malignant syndrome (NMS)
- Rare, not dose-related (idiosyncratic)
- Slow onset (hours to days)
- Altered mental status, severe hyperthermia,
lead-pipe rigidity, opisthotonos, hypertension,
tachycardia
- Elevated creatine kinase
- Treatment: Fever control, benzodiazepines,
dantrolene, paralysis, bromocriptine
119
Opioids
NComa, apnea, pinpoint pupils (hypoxia can cause
dilated pupils), hypotension
NCan cause noncardiogenic pulmonary edema
NNaloxone: Duration of action 30-60 minutes
NDiphenoxylate (Lomotil): slow onset of symptoms
NIncreased dose of naloxone
? Propoxyphene
? Methadone
? Fentanyl
? Codeine
? Pentazocine
120
Naloxone
NDose: 0.2-2mg IVP
NReflexive large doses discouraged
?Wil precipitate withdrawal
?Smal er doses, titrating to effect preferred
NContinuous drip may be required
NOther routes of administration
?IM, IO, SC, ET, Neb
121
Oral Hypoglycemic Agents (1)
NSulfonylureas cause prolonged hypoglycemia
?Glyburide (Micronase), glipizide (Glucotrol),
glimepiride (Amaryl), chlorpropamide (Diabinese)
?Increase release of insulin from pancreatic cel s
?Risk factors for toxicity: Extremes of age, poor
nutrition, EtOH, hepatic and renal insufficiency, beta
blockers
?Particularly dangerous in children
NNon-sulfonylureas do NOT cause hypoglycemia
?Metformin [Glucophage], acarbose [Precose],
repaglinide [Prandin], rosiglitazone [Avandia],
pioglitazone [Actos]
122
Oral Hypoglycemic Agents (2)
NMetformin can cause lactic acidosis
?IV contrast wil not induce lactic acidosis unless renal
failure/insufficiency develops
NAdmit symptomatic patients with sulfonylurea or
metformin overdose
NTreatment of sulfonylurea overdose
?Glucose bolus and drip
?Glucagon (not used as empiric therapy)
?Octreotide (refractory sulfonylureas overdose)
NAccidental ingestion without risk factors for toxicity can
be observed in ED
? If hypoglycemia does not occur, may discharge home
(does not apply to pediatric patients)
123
Organophosphates
NInsecticides, pesticides
NInhibit cholinesterases. Increase acetylcholine
(cholinergic toxidrome)
NMuscarinic effects: pinpoint pupils, SLUDGE +
Killer "B"s ? Bradycardia, Bronchospasm,
Bronchorrhea
S ? Salivation
L ? Lacrimation
U ? Urination
D ? Diarrhea
G ? Gastrointestinal upset
E ? Emesis
124
Organophosphates
NNicotinic effects: Muscle weakness,
fasciculations, respiratory failure
NAvoid use of succinylcholine with
neuromuscular blockade
NTreatment: Atropine (until secretions dry)
NPralidoxime (2-PAM)
?Not indicated with carbamates
125
Phencyclidine (PCP)
NFindings
?Rotatory nystagmus
?Agitation, seizures
?Hyperthermia, rhabdomyolysis
NTreatment
?Hydration, cooling
?Benzodiazepines
Do not acidify urine
?Haloperidol
?Ketamine toxicity similar
(without violent presentation)
126
Phenytoin (Fosphenytoin)
NSide effects are related to dose and rate of
infusion
?Nystagmus, ataxia, vomiting, slurred speech,
dystonias, lethargy, coma
?Paradoxical seizures are rarely seen
?Too-rapid infusion can cause dysrhythmias and
hypotension due to propylene glycol diluent
NTreatment: Lavage, multidose charcoal
NHemodialysis and hemoperfusion are NOT
useful
127
Poisonous Plants (1)
NPits of apricot, cherry, peach and plum
?Contain hydrocyanic acid (CN)
?Cyanide toxicity, supportive care, cyanide kit
NAnticholinergic plants
?Deadly nightshade (bel adonna) berries
?Henbane (seeds in pod)
?Jimsonweed (dried leaves and seeds)
NDigitalis toxic plants (FOLLY)
?Foxglove, Oleander, Lilly of the Val ey
128
Cyanide
129
Jimsonweed Datura stramonium
Anticholinergic
Digitalis toxic plants (FOLLY)
Foxglove, Oleander, Lilly of the Valley
Lilly of the Valley
Digitalis Toxicity
Poisonous Plants (2)
NHol y (bright red berries)
?GI toxicity: N/V, abdominal cramps
NPhilodendrons
?Common house plants
?Immediate pain or burning in mouth and throat
?GI irritation
NPoinsettia
?Vomiting, cramps, contact dermatitis
133
134
Poisonous Plants (3)
NPokeweed (purple and black berries)
?Minor toxicity: Nausea, vomiting, cramps
and diarrhea
?Severe toxicity: Respiratory depression,
seizures, hemorrhage gastritis, hemolytic
anemia
NDiffenbachia
?GI mucosal membrane
irritation
?Calcium oxylate crystals
135
Pokeweed
Poisonous Plants (4)
NTobacco
?Pediatric ingestion of cigarettes
?Dermal exposure in tobacco workers
?Cholinergic symptoms: Salivation, N/V/D,
miosis, confusion, seizures in children
?Lavage, charcoal, benzodiazepines for seizures
137
Morning Glory - LSD
138
Poison Hemlock
139
140
Rodenticides -Anticoagulants
NWarfarin
?PT increases over 8-24 hrs, peaks at 32 hrs,
lasts as long as 5 days
NSuper warfarin (rat poison)
?Duration as long as 6-8 weeks with significant
suicidal ingestions
?Pediatric "tastes" usual y benign
NBlock synthesis of vitamin K-dependent
clotting factors (II, VII, IX, X)
NTreatment: Lavage, activated charcoal, vitamin
K, FFP, PCCs
141
142
SALICYLATES
143
Salicylates (1)
NUncouple oxidative phosphorylation, causing
metabolic acidosis
NTachypnea, coma, seizures, pulmonary
edema, fever, tinnitus, tachycardia
NAcute poisoning: GI symptoms, level correlates
better with toxicity - suspect in unknown OD
NChronic poisoning: Fewer GI and more CNS
symptoms, level may not correlate with toxicity
?Consider in elderly pt with ALOC
NChildren: Hyperventilation, diaphoresis,
behavioral changes - caution oil of wintergreen
Anion gap metabolic acidosis
and respiratory alkalosis
144
Salicylates (2)
NHypoglycemia common; check glucose
NMay see hypokalemia, T3/T4 levels
NDone nomogram no longer recommended
?Doesn't apply to enteric-coated forms
?Absorption is erratic
?Treat the patient, not the level
NTreatment: Urine alkalinization, fluids,
glucose, potassium; hemodialysis for severe
cases
Oil of wintergreen contains high
concentrations of salicylates (very toxic)
145
Serotonin Syndrome
NSSRI (selective serotonin reuptake inhibitors)
?Fluoxetine (Prozac, Sarafem)
?Sertraline (Zoloft)
?Citalopram (Celexa)
?Escitalopram (Lexapro)
?Paroxetine (Paxil)
NCombination of 2 or more drugs increases
serotonin levels
?SSRI, MAOI, meperidine, dextromethorphan,
cocaine, amphetamines, St. John's wart
146
Serotonin Syndrome
NClinical syndromes (rapid onset)
?CNS (altered mental status, coma, seizures)
?Autonomic (hyperthermia, tachycardia,
hypertension)
?Neuromuscular (myoclonus, hyperkinesia)
NTreatment: Cooling, cyproheptadine (Periactin)
NDistinguish from NMS
?NMS: Slow onset, lead pipe rigidity
?Serotonin syndrome: Rapid onset,
myoclonus
147
Strychnine Toxicity
NHighly toxic alkaloid
NBlocks inhibition of postsynaptic brainstem
glycine receptors and spinal cord motor neurons
NResults in CNS hyperstimulation
NMuscle twitching, facial grimacing,
extensor spasm, opisthotonos
(back muscle spasm, body arched)
NPatient remains conscious
NMedul ary paralysis and death occur
NTreatment: Airway, benzodiazepines,
may require paralytics
148
Tricyclic Antidepressants (1)
NSigns of serious toxicity manifested within 6
hours of ingestion - often earlier
NAnticholinergic effects
?Flushed skin, dry mouth, mydriasis, decreased
bowel sounds, urinary retention
NCNS effects
?Drowsiness, confusion, ataxia, delirium,
seizures, coma
NCardiovascular effects
?Hypotension, tachycardia, wide QRS, V-tach,
torsades
?Right axis deviation (negative S in I, positive R
in aVR)
149
Tricyclic Antidepressants (2)
NTreatment
?Lavage, multidose charcoal (avoid ipecac &
flumazenil)
?Hypotension: IV saline, bicarbonate,
norepinephrine
?Wide QRS, ventricular dysrhythmias:
Bicarbonate, lidocaine (avoid procainamide)
?Torsades: Magnesium sulfate, overdrive pacing
?Delirium, seizures: benzodiazepines
(avoid phenytoin and physostigmine)
Sodium bicarbonate decreases
cardiac toxicity
150
151
Xanthines
NInhibits breakdown of cyclic AMP (the adrenergic
transmitter) causing excess adrenergic excess
NTheophylline, caffeine
NTachycardia (also multifocal atrial tachycardia = treat
with IV Mg), vomiting, seizures
NIncreased theophylline levels caused by erythromycin,
ciprofloxacin, cimetidine, CHF, liver failure
NAcute ingestion: Hypokalemia, acidosis 2o to seizures.
Levels usual y correspond to toxicity
NChronic ingestion: Toxicity seen with lower serum levels
NLab: Metabolic acidosis, K, Mg, PO4
NTreatment: Multidose charcoal, phenobarbital, beta
blockers, Mg++, dialysis, hemoperfusion
152
Toxicology Pearls (1)
NBradycardia
P Propranolol (beta blockers), poppies (opioids)
A Anticholinesterase drugs
C Clonidine, calcium channel blockers
E Ethanol, other alcohols
D Digoxin
NTachycardia
F Freebase (cocaine)
A Anticholinergics,
antihistamines, amphetamines
S Sympathomimetics, solvent abuse
153
T Theophylline
Toxicology Pearls (2)
NHyperthermia
N NMS, nicotine
A Antihistamines
S Salicylates, sympathomimetics
Serotonin syndrome
A Anticholinergics, antidepressants
154
Toxicology Pearls (3)
NHypothermia
C Carbon monoxide
O Oral hypoglycemics, insulin
O Opioids
L Liquor
S Sedatives, hypnotics
NHypotension
C Clonidine, calcium channel blockers
R Reserpine (antihypertensive agents)
A Antidepressants, aminophylline
S Sedatives, hypnotics
H Heroin (opioids)
155
Toxicology Pearls (4)
NHypertension
C Cocaine
T Thyroid supplements
S Sympathomimetics
C Caffeine
A Anticholinergics, amphetamines
N Nicotine
NHypoventilation
S Sedatives, hypnotics
L Liquor
O Opioids
W Weed (marijuana)
156
Toxicology Pearls (5)
NHyperventilation
P PCP, pneumonitis (chemical)
A ASA (salicylates)
N Noncardiogenic pulmonary edema
T Toxic metabolic acidosis
NMiosis
C Cholinergics, clonidine
O Opioids, organophosphates
P Phenothiazines, pilocarpine, pontine bleed
S Sedatives, hypnotics
157
MYDRIASIS
158
Toxicology Pearls (6)
NMydriasis
A Antihistamines
A Antidepressants
A Anticholinergics, atropine
S Sympathomimetics (cocaine, amphetamines)
NDiaphoretic skin
S Sympathomimetics
O Organophosphates
A ASA (salicylates)
P PCP
159
Toxicology Pearls (7)
Skin Findings
NRed skin:
Anticholinergics, boric acid,
carbon monoxide
NBlue skin:
Cyanosis, methemoglobinemia
(nitrates, nitrites, aniline dyes,
dapsone, phenazopyridine)
NBlistering:
Barbiturates, CO,
spider bites, snakes envenomations
160
Toxicology Pearls (8)
Seizures
? O Organophosphate
? T Tricyclic antidepressants
? I INH, insulin
? S Sympathomimetics
? C Cocaine, camphor
? A Amphetamines
? M Methylxanthines (theophylline)
? P Phencyclidine (PCP)
? B Benzo withdrawal, botanicals
? E Ethanol withdrawal
? L Lindane, lidocaine
? L Lead, lithium
162
Toxicology Pearls (9)
Odors
NBitter almonds or "silver polish": Cyanide
NMothbal s: Camphor
NGarlic: Arsenic, organophosphate, DMSO
NRotten eggs: Sulfur dioxide, hydrogen sulfide
NWintergreen: Methyl salicylate
NPeanuts: Vacor (rat poison)
NCarrots: Water hemlock
NGasoline: Hydrocarbons
NFruity: DKA, isopropanol
NPears: Chloral hydrate
163
Toxicology Pearls (10)
NRadiopaque Drugs
C Chloral hydrate
Cocaine packets
O Opiate packets
I Iron
(Heavy metal: Pb, As, Hg)
N Neuroleptic agents
S Sustained release
products, enteric coated
preparations
164
Toxicology Pearls (11)
NNoncardiogenic pulmonary edema
M Meprobamate, methadone
O Opioids
P Phenobarbital, propoxyphene
S Salicylates
165
Toxicology Pearls (12)
NCharcoal Not Useful NMultidose Charcoal
?Alcohols
?Theophylline
?Cyanide
?Sustained release
?Iron
drugs
?Lithium
?Phenobarbital
?Arsenic
?Salicylates
NCharcoal
NWhole Bowel Irrigation
Contraindicated
?
?Sustained release drugs
Caustics
?Not absorbed by charcoal
?Body packer
166
Toxicology Pearls (13)
NDialysis
NNondialyzable
?Methanol
?CN
?Isopropyl alcohol
?TCAs
?Ethylene glycol
?Iron
?Lithium
?Benzodiazepines
?Salicylate
?Phenothiazines
?Theophylline
?Hal ucinogens
?Phenobarbital
167
Toxicology Pearls (14)
NDelayed toxicity
? Acetaminophen
? Digoxin
? Ethylene glycol
? Heavy metals
? Methanol
? Mushrooms
? Narcotics
? Iron
? Salicylates
? Slow release compounds
168
TOXICOLOGY QUESTIONS
169
A 24 y/o patient presents with an unknown
ingestion 2 hours prior to arrival. Which of the
following statements is true?
A. Regardless of the method, gastric emptying
is always 100% effective
B. Too much time has elapsed in this case for
gastric emptying to have any benefit
C. If the patient has a normal mental status at
presentation, syrup of ipecac is indicated
D. Sorbitol should be routinely administered
with activated charcoal
E. Activated charcoal administration may stil be
indicated and has the fewest adverse side
effects
TO 1
A 32 y/o dialysis patient presents to the ED
following an overdose. Which of the following
agents can be eliminated via hemodialysis?
A. Secobarbital
B. Lithium
C. Digoxin
D. Phenytoin
E. Iron
TO 2
Regarding whole bowel irrigation, which of the
following statements is true?
A. Should not be utilized in drug packers
B. Has been shown to be clinical y effective in
wel designed clinical trials
C. May be utilized for iron ingestions with a
positive abdominal radiograph
D. Is contraindicated in lead ingestions since it
may exacerbate encephalopathy
E. Can be used cautiously in patients with bowel
obstructions
TO 3
Regarding antidotes, which statement
is correct?
A. Warfarin toxicity is treated with protamine
B. Beta blocker toxicity is treated with glucagon
C. Cyanide toxicity is responsive to methylene
blue
D. Calcium channel blocker toxicity is not treated
with glucagon
E. Carbamate toxicity should always be treated
with 2-PAM
TO 4
A 17 y/o patient presents following an unknown
ingestion. His electrolytes are as follows: Na+ =
145, Cl- = 92, CO2 = 13. What toxin did this
patient most likely ingest?
A. Acetaminophen
B. Phenobarbital
C. Salicylates
D. Isopropanol
E. Mercury
TO 5
Which of the following therapies is likely to be
most efficacious in the previous patient's
management?
A. N-acetylcysteine
B. Urinary alkalinization
C. Urinary acidification
D. 4-Methylpyrazole
E. BAL chelation
TO 6
A 15 y/o patient presents with confusion,
agitation, mydriasis and dry, flushed skin.
Which is the most likely etiology?
A. MDMA toxicity
B. Amanita phal oides mushroom ingestion
C. Methadone toxicity
D. Jimson weed exposure
E. Cannabis exposure
TO 7
A 44 y/o patient presents 30 hours after an acute on
chronic acetaminophen ingestion. He reports abdominal
pain, vomiting and is jaundiced. Which of the following
statements is true regarding the proper management?
A. The acetaminophen nomogram can stil be used
to plot serum levels to guide therapy
B. The antidote indicated in this scenario can only
be administered oral y
C. The patient's hepatotoxicity unlikely to be due to
acetaminophen toxicity
D. N-acetylcysteine is stil indicated and may have
clinical benefit in this delayed setting
E. N-acetylcysteine therapy is contraindicated after
24 hours post ingestion
TO 8
A 29 y/o female presents to the ED complaining
of nausea, vomiting and headache. She is
flushed and diaphoretic. She reports being
seen & treated 24 hours ago for a vaginal
discharge. Which is the most likely cause of her
symptoms?
A. Hypersensitivity reaction to doxycycline
B. Subarachnoid hemorrhage
C. Viral meningitis
D. Jarisch-Herxheimer reaction
E. Disulfiram reaction
TO 9
A 25 y/o patient presents with headache, vomiting and
somnolence. She reports using 2 gas space heaters for
warmth last night. You order a carbon monoxide level
which is measured at 25%. Which statement is true?
A. The patient's pulse ox wil be low
B. CO shifts O2 saturation curve to the right
C. HBO is always indicated in this case due to
CO neurotoxic effects
D. If the patient is pregnant, the fetal
hemoglobin has a high affinity for CO
E. Administration of the cyanide antidote kit
should also be considered in this case
TO 10
A 39 y/o alcoholic male presents with nausea,
vomiting and visual disturbances. His CO2 = 5.
His osmolal gap = 40. What is likely to improve
this patient's condition ?
A. Intravenous 4-methylpyrazole
B. Intravenous octreotide
C. Intravenous methylene blue
D. Intravenous N-Acetyl cysteine
E. Intravenous physostigmine
TO 11
Which of the following entities
causes a normal anion gap acidosis?
A. Isoniazid toxicity
B. Salicylates
C. Renal tubular acidosis
D. Uremia
E. Metformin
TO 12
An 18 year old patient presents to the ED comatose with
midrange pupils following a rave party on a Saturday night
at 2am. After no response to D50 and naloxone therapy, the
patient is orally intubated without complications. At 6am
the patient suddenly becomes agitated and extubates
himself. What drug of abuse is this scenario most
consistent with?
A. LSD-laced psilocybe mushrooms
B. Ketamine
C. Gamma hydroxybutyric acid
D. Ecstasy MDMA
E. Fentanyl
TO 13
A 47 y/o patient presents with an altered mental
status following an ingestion of an unknown
quantity of clonidine. Which of the following is
true?
A. This patient's symptoms wil be similar to an
anticholinergic overdose
B. The patient wil experience hypotension,
fol owed by hypertension
C. The patient will be agitated with dilated pupils
D. Naloxone may be beneficial
E. This overdose does not share any similarities
with a opiate toxicity
TO 14
A 23 y/o fire fighter was involved in a extinguishing
a large 5 alarm factory fire. He presents to the ED
comatose with profound metabolic acidosis despite
high flow oxygen therapy. What is the most
appropriate intervention?
A. Sodium thiosulfate and hydroxycobalamine
B. Methylene blue
C. Pyridoxine therapy
D. Pralidoxime therapy
E. Emergent hemodialysis
TO 15
A 78 y/o patient is hyperkalemic with a digoxin
level = 8.5. Her ECG shows PAT with AV block.
Which of the following would be most
appropriate?
A. Administer Digibind
B. Administer CaCl for this patients hyperkalemia
C. Withhold further digoxin awaiting clearance of
the patient's toxicity
D. Cardiovert the patient with 50 Joules
E. Administer procainamide
TO 16
A 45 y/o patient was working with a liquid while
etching glass. He was not wearing his gloves.
He is complaining of intense hand pain. Which
of the following is indicated?
A. Copious irrigation with copper sulfate
B. Intradermal calcium chloride
C. Topical calcium gluconate
D. Intravenous potassium phosphate
E. An immediate surgical intervention
TO 17
A 36 y/o migrant worker presents in status
epilepticus despite benzodiazepines, phenytoin
and phenobarbital administration. His ABG pH is
6.8 on high flow oxygen therapy. What is the
next most appropriate therapeutic step?
A. Vitamin B6 pyridoxine therapy
B. Vitamin B12 hydroxycobalamine
C. Vitamin B3 niacin
D. Vitamin B1 thiamine
E. Bicarbonate drip
TO 18
Which of the following agents causes
miosis?
A. Cocaine
B. Jimson weed
C. Atropine
D. Methamphetamine
E. Fentanyl
TO 19
A 39 y/o Type II diabetic presents following an
overdose. He is unresponsive with a GLC = 25
mg/dl. Which therapy may be indicated if this
patient's hypoglycemia persists despite
aggressive dextrose administration?
A. Octreotide
B. Cyproheptadine
C. Insulin rescue therapy
D. Metformin administration
E. Emergent pancreatectomy
TO 20
Toxicology Answer Key
1. E
11.A
2. B
12.C
3. C
13.C
4. B
14.D
5. C
15.A
6. B
16.A
7. D
17.C
8. D
18.A
9. E
19.E
10.D
20.A
This post was last modified on 24 July 2021