Transcript The Poisoned Patient: A Medical Student Review

William Beaumont Hospital
Department of Emergency Medicine


All chemicals, especially medicines, have the
potential to be toxic
2006 TESS data
 2.7 million exposures
 19.8% were treated in a healthcare facility
 21.6% of those had more than minor outcomes
including death

Over half of poisonings occur in kids < 5 yo








Always consider poisoning in differential diagnosis
IV, O2, monitor
Accucheck
D50 +/- thiamine or naloxone as indicated
Decontamination, protect yourself
Enhanced elimination
Antidotal therapy
Supportive care






Name, quantity, dose and route of ingestant(s)
Time of ingestion
Any co-ingestions
Reason for ingestion – accidental, suicidal
Other medical history and medications
EMS - inquire about scene, notes left, smells,
unusual materials, pill bottles, etc.





Dilated – anticholinergic, sympathomimetic
Constricted – cholinergic
Pinpoint – opiates
Horizontal nystagmus – ethanol, phenytoin,
ketamine
Rotary or vertical nystagmus - PCP





Hyperpyrexia – anticholinergic,
sympathomimetic, salicylates
Hypothermic – opiods, sedative-hypnotics
Dry skin – anticholinergics
Moist skin – cholinergics, sympathomimetics
Color – cyanosis, pallor, erythema

Stimulants – everything is UP
  temp, HR, BP, RR, agitated
 Sympathomimetics, anticholinergics,
hallucinogens

Depressants – everything is DOWN
  temp, HR, BP, RR, lethargy/coma
 Cholinergics, opioids, sedative-hypnotics

Mixed effects: Polysubstance overdose,
metabolic poisons (hypoglycemic agents,
salicylates, toxic alcohols)







Accucheck
EKG
Chemistries (BUN, Cr, CO2)
UA – calcium oxalate crystals in ethylene
glycol poisoning
Drugs of abuse & comprehensive screen
Acetaminophen, aspirin & ethanol levels
ABG, serum osmolality, toxic Alcohol
screen, urine HCG and LFTS if warranted


Remove all clothing
Wash away external toxic substances
 If suspect transmittable contaminant, perform in
decontamination area

If ocular exposure, flush eyes copiously with
until pH 7 – 7.5

Three methods
 Gastric emptying
 Bind the toxin in the gut
 Enhance elimination

Always consider the patient’s mental status,
risk of aspiration, airway security and GI
motility before attempting any method

Indications
 Life threatening ingestions
 Present within one hour of ingestion

Studies show little benefit
 May remove as little as 35% of the substance
 Need secure airway
 Relatively high complication rate



Absorbs toxin within the gut
1 g/kg PO or via NG tube
Contraindications:
 Bowel obstruction or perforation
 Unprotected airway
 Caustics and most hydrocarbons
 Anticipated endoscopy

Not effective for alcohols, metals (iron, lead),
or elements (magnesium, sodium, lithium)





Large doses of toxin
Slow release toxins
Enterohepatic or enterenteric circulation
Toxins that form bezoars
Used for: phenobarbital, theophylline,
carbamazepine, dapsone, quinine




70% sorbitol 1g/kg PO
Administered with charcoal
Decreases transit time of both toxin and
charcoal through the GI tract
Contraindications:
 Children under 5 yo
 Caustic ingestions
 Possible bowel obstruction



Go-Lytely via PO or NG tube at a rate of 2L/hr
(500 mL/hr in peds)
Typically used for those substances not
bound by activated charcoal
Contraindications:
 Potential bowel obstruction

Used for:






Salicylates
Methanol
Ethylene Glycol
Lithium
Isopropyl alcohol
Patients must be hemodynamically stable and
without bleeding disturbances





Acetaminophen N-Acetylcysteine
Anticholinergic agent  Physostigmine
Benzodiazepines  Flumazenil
Beta blockers  Glucagon
Carbon monoxide  Oxygen






Cardiac glycosides  Digoxin-specific Fab
Cyanide  sodium nitrate, sodium
thiosulfate, hydroxycobalamin
Ethylene glycol  Ethanol
Opiates  Naloxone
Organophosphates  Atropine, 2-PAM
Tricyclics  Sodium bicarb
56 y/o male found unconscious in a basement.
He has snoring respirations, frothing at the
mouth, and rales on pulmonary exam. His
pupils are pinpoint. He wakes up swearing
and swinging at staff after a little narcan.
What could it be?


Examples: heroin, morphine, fentanyl
Signs/Symptoms:
 CNS depression, lethargy, confusion, coma,
respiratory depression, miosis
 Vital signs:  temp, HR, RR, +/- BP
 Pulmonary edema, aspiration, resp arrest
 Check for track marks, rhabdomyolysis,
compartment syndrome

Treatment:
 Naloxone 0.4 - 2 mg IV/IM/SC slowly
▪ May result in severe agitation
▪ Monitor closely and re-dose if necessary

Examples: cocaine, amphetamines (speed,
dex, ritalin), phencyclidine (PCP),
methamphetamines (crank, meth, ice),
MDMA (ecstasy, X, E)
 Stimulant: meth > amphetamines > MDMA
 Hallucinogen: MDMA > meth > amphetamines

Signs/Symptoms:
 Agitation,  temp, HR, BP, mydriasis
 Seizures, paranoia, rhabdomyolysis, MI,
arrhythmias, piloerection

Treatment:
 Primarily supportive
▪ Benzo’s, IV hydration, cooling if hyperthermic
 Treat HTN with benzodiazepines or nitrates
 Avoid beta blockers

Bodystuffers (small amt, poorly contained)
 Asymptomatic - AC, monitor for toxicity
 Symptomatic - AC, WBI, treat symptoms

Bodypackers (large amt, well contained)
 Asymptomatic - WBI followed by imaging
 Symptomatic - immediate surgical consult

Organophosphates
 Insecticides, nerve gas (Sarin, Tabun, VX)
 Irreversible binding to AChE – “aging”

Carbamates
 Insecticides (Sevin)
 Reversible binding to AChE – short duration


Examples: physostigmine, edrophonium,
nicotine
All increase ACh at CNS, autonomic nervous
system and neuromuscular junction

Signs/Symptoms:
 SLUDGE Syndrome
▪ Parasympathetic hyperstimulation
▪ Salivation, Lacrimation, Urinary Incontinence,
Defecation, GI pain, Emesis
 Killer B’s
▪ Bradycardia, Bronchorrhea, Bronchospasm
▪ Bronchorrhea and respiratory failure is often the cause
of death
 Miosis, garlic odor,  MS, seizures, muscle
fasciculations, weakness, respiratory depression,
coma


Diagnosis: RBC or plasma cholinesterase level
Management:
 Decontamination – protect yourself
 Supportive therapy
 Atropine - competitive inhibition of ACh
▪ Large doses required
▪ End point is the drying of secretions
 Pralidoxime (2-PAM) - breaks OP-AChE bond
▪ Start with 1-2 g IV over 30 minutes, give before “aging”
▪ Adjust dose based on response, AChE level
22 y/o F presents with decreased urine output.
She is febrile, confused, flushed and has
dilated pupils on exam. You also notice a
linear, vesicular rash on her lower legs.
What do you want to know?

Meds
 She has been using oral benadryl and topical
caladryl lotion for the poison ivy
What is her toxidrome?







Antihistamines
 Diphenhydramine, meclizine, prochlorperazine
Antipsychotics
 Chlorpromazine (Thorazine), thiroidazine (Mellaril)
Belladonna alkaloids
 Jimsonweed, atropine, scopolamine
Cyclic antidepressants
 Amitriptyline, nortriptyline, fluoxetine
OTC’s
 Excedrin PM, Actifed, Dristan, Sominex
Muscle relaxants
 Orphenadrine, cyclobenzaprine
Amanita mushrooms

Signs/Symptoms:






Dry as a bone – lack of sweating
Red as a beet – flushed, vasodilated
Hot as hades – hyperthermia
Blind as a bat – mydriasis
Mad as a hatter – delirium, hallucinations
Stuffed as a pipe – hypoactive bowel sounds,
ileus, decreased GI motility, urinary retention
 VS:  temp, HR, BP

Rule out psychiatric disorders, DTs,
sympathomimetic toxicity

Management:




Sedation with benzodiazepines
Temp control
Treat wide QRS and dysrhythmias with bicarb
Physostigmine
▪ Use only in clear cut cases
▪ Monitor for excess cholinergic response - SLUDGE


Examples: aspirin, oil of wintergreen, OTC
remedies
Signs/Symptoms:






Altered mental status
Tinnitus
Nausea and vomiting
Tachycardia
Tachypnea (Kussmaul respirations)
Hyperthermia

Diagnosis:
 Metabolic acidosis and respiratory alkalosis
 Anion gap
 Salicylate level > 30mg/dL

Treatment:
 Multi-dose AC
 Alkalinize urine
 HD if levels > 100 mg/dl, altered MS, renal
failure, pulmonary edema, severe acidosis or
hypotension

Examples: SSRI’s, MAOI’s, meperidine,
tricyclics, trazadone, mertazapine,
dextromethorphan, LSD, lithium, buproprion,
tramadol

May be caused by any of the above, but
usually occurs with a combination of agents,
even if in therapeutic doses

Signs/Symptoms:
 Altered MS, mydriasis, myoclonus, hyperreflexia,
tremor, rigidity (especially lower extremities),
seizures, hyperthermia, tachycardia, hypo or
hypertension
 Citalopram and escitalopram - prolonged QT and
QRS

No confirmatory test – diagnosis based on
clinical suspicion

Treatment:
 Supportive care
 Single dose AC (ensure airway control)
 Benzodiazepines to treat discomfort, muscle




contractions or seizures
Cooling measures
Treat prolonged QT with magnesium
Treat widened QRS with bicarb
Cyproheptadine (anti-serotonin agent)

Signs/Symptoms:
 Stage I: 0-24 hrs
▪ Nausea, vomiting, anorexia
 Stage II: 24-72 hrs
▪ RUQ pain, elevation of AST and ALT, also elevation of
bilirubin and PT if severe poisoning
 Stage III: 72-96 hrs
▪ Peak of AST, ALT, bilirubin and PT, possible renal failure
and pancreatitis
 Stage IV: > 5 days
▪ Resolution of hepatotoxicity or progression to
multisystem organ failure

Rummack-Mathew
nomogram

Acetaminophen levels vs.
time

Plot 4 hr level

Useful for single acute
ingestion only

Management:
 AC, assume polypharmacy OD
 NAC - N-acetylcysteine (NAC)
▪ Ingested over 140 mg/kg OR toxic level on nomogram
▪ Draw baseline LFTs and PT
▪ IV or PO dose
17 y/o M brought in by family for acting
“drunk.” He is lethargic, confused,
disoriented. Vitals: 130, 90/60, 16, 37 C.
Labs: ETOH 0, CO2 12
What else do you want to know?
Accucheck: 102
Serum osmolality: 330
Na 140, K 4.0, Cl 100, CO2 12, glucose 90
BUN 28, Cr 2.0
UDS, APAP, ASA are all negative
UA has calcium oxalate crystals
What are we hinting at?

Typical Agents




Ethanol
Isopropanol
Methanol
Ethylene glycol (EG)


All toxic alcohols cause an osmolar gap
Methanol, ethanol and ethylene glycol cause an
anion gap acidosis








M – methanol
U – uremia
D – DKA
P – paraldehyde, propylene glycol
I – iron, isoniazid
L – lactic acid
E – ethanol, ethylene glycol
S – salicylates

Anion Gap (mEq/L)
Na - (Cl + HCO3)

Calculated Osmolarity (mosm/L)
2Na + BUN/2.8 + Glu/18 + ETOH/4.6


Examples: rubbing alcohol, antifreeze,
disinfectants
Second most commonly ingested alcohol

Isopropyl alcohol has twice the CNS
depressing potency and up to 4 times the
duration as ethanol

Metabolized by alcohol dehydrogenase to
acetone

Signs/Symptoms:






Fruity breath
Appear intoxicated
Nausea, vomiting, abdominal pain
Hypotension
Respiratory depression  coma
Lab abnormalities
 Ketonuria
 Osmolar gap
 Normal pH, no acidosis
Examples: paint removers, antifreeze,
windshield washer fluid, bootleg liquor
 Metabolized to toxic formaldehyde and formic
acid
 Can cause permanent retinal injury and blindness
as well as parkinsonian syndrome if not treated
promptly
 May have a long latent period (12 to 18 hours),
especially if co-ingested with ethanol


Signs/Symptoms:
 Lethargy, nausea, vomiting, abd pain
 Visual symptoms seen in 50% - blurring, tunnel
vision, color blindness
  HR, RR, BP
 CNS - headache, seizures or coma

Lab abnormalities
 Wide anion-gap metabolic acidosis
 Osmolar gap
 Toxic alcohol screen to confirm





Examples: antifreeze
Seen with alcoholics, suicide attempts and
children
Colorless, odorless and sweet
Is rapidly absorbed and converted to toxic
acids responsible for clinical signs and
symptoms
Treatment similar to methanol

Signs/Symptoms:
 1-12 hours – CNS depression
▪ Inebriation, vomiting, seizures, coma, tetany
(hypocalcemia)
 12-24 hours – cardiopulmonary phase
▪ hypotension, tachydysrhythmias, tachypnea and
ARDS
 24-72 hours – nephrotoxic phase
▪ Oliguric renal failure, ATN, flank pain, calcium
oxylate crystalluria

Lab and EKG abnormalities:
 Hypocalcemia secondary to precipitation with
oxylate, excreted as urinary calcium oxylate
crystals
 Urine may also fluoresce secondary to
fluorescence dye in antifreeze
 EKG: QT prolongation (hypocalcemia) and
peaked T’s (hyperkalemia)
 Myalgias, secondary to acidosis and elevated
CPK
Always consider EG in an inebriated patient
without alcohol breath, with an anion-gap
metabolic acidosis, osmolar gap and calcium
oxylate crystalluria





Supportive, especially airway
Correct acidosis with bicarb, 1meq/kg IV
Benzo’s if seizure
Folic acid 50mg IV q 4 hrs for both
Ca gluconate 10 ml of 10% IV – to correct
hypocalcemia – EG only

Block production of toxic metabolites
 Ethanol – IV or PO
 Fomepizole - preferred method
▪ Has 8000 times the affinity for ADH as ETOH without
CNS depression and hypoglycemia

Hemodialysis indicated if:
 Serum level > 50 mg/dl
 Signs of nephrotoxicity (EG) or CNS or visual
disturbances (methanol)
 Severe metabolic acidosis

Agents:
 Amitriptyline (Elevil), desipramine (Norpramin),
imipramine (Tofranil) and nortriptyline (Pamelor)


Narrow therapeutic index
Have returned to popularity with nondepression indications such as chronic pain,
migraines, ADHD and OCD

Signs/Symptoms:
 CNS – decreased LOC
▪ Confusion, hallucinations, delirium, seizures
 Cardiovascular – arrhythmias and hypotension
▪ QRS > 100 msec, conduction delays
▪ Arrhythmias such as V-tach & torsades may develop as
QRS widens and QT prolongs
 Anticholinergic toxidrome
▪ Tachycardia, mydriasis, hyperthermia, anhydrosis,
urinary retention, decreased bowel sounds
 EKG during TCA toxicity and after treatment
with bicarb. Note wide QRS, prolonged QT
and terminal R’s > 3mm in AVR





AC
Na Bicarb – to treat QRS prolongation > 100
msec and hypotension refractory to IV fluids
Benzo’s to treat seizures and hyperthermia
Magnesium and lidocaine for ventricular
arrythmias refractory to bicarb
Magnesium for QT prolongation or Torsades

Sources:
 Fossil fuel combustion (car exhaust), smoke,
kerosene or coal heaters, steel foundries

CO binds to hemoglobin with 230 times the
affinity to oxygen, decreasing it’s ability to
transport oxygen

Signs/Symptoms:
 Nausea, malaise, headache, decreased mental
status, dizziness, paresthesias, weakness,
syncope
 May progress to vomiting, lethargy, coma,
seizures, CVA , MI or respiratory arrest

Need a high index of suspicion – multiple
family members with flu like symptoms
without fever, winter months



COHb level may not represent the severity of
the poisoning
Pulse oximetry also may be misleading
Half-life of COHb
 4 hours on room air
 60 minutes breathing 100% normobaric O2
 15 to 23 minutes breathing 100% hyperbaric O2

100% O2 via NRB for 4 hrs minimum if mild
symptoms (nausea, heachache, malaise)

100% O2 + HBO if any of the following:








Altered mental status or coma
History of LOC or near syncope
History of seizure
Hypotension during or after exposure
MI
Pregnant with COHb > 15%
Arrythmias
+/- COHb > 25-40%