Transcript Antidote Toxin/Drug - Med Student Workshops

THE APPROACH TO THE
POISONED PATIENT
Toxicology Skills Workshop
Regions Hospital Emergency Medicine Program
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Develop a Systematic Approach
Look for Toxidromes (“Talkingdromes”)
Attention to ABCs and need for Antidote
Know the Indications for Decontamination
Procedures
Enhance when possible and appropriate
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A – Antidote
B – Basics ; ABCs
C – Change catabolism
D – Distribute differently; Decontamination
E – Enhance elimination
Antidote
Toxin/Drug
Oxygen
Naloxone
CO, CN, H2S
Narcotics/Opiates
NAC
APAP, Carbon tet
Atropine, Pralidoxime
Organophosphates
Calcium
DMSA
HF, Fl, Oxalates
As, Lead, Hg
Sodium Bicarbonate
TCA
Antidotes
Toxin/Drug
Ethanol, 4MP
EG, (methanol)
Digoxin-specific Fab Digoxin
Glucose
Hydroxocobalamin*
Insulin
CN
Physostigmine
Pyridoxine
Anticholinergics, central
INH, hydrazines
Glucagon
Beta-blockers
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Airway
Breathing
Circulation
Do the DONT
 Dextrose
 Oxygen
 Naloxone
 Thiamine
Reduce Adsorption
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Vomiting (Ipecac)
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Activated Charcoal
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Generally not indicated or used in an ED setting
Contraindicated in patients < 6 mos old, caustic ingestions, actual or potential
loss of airway reflexes, need to give oral antidote
Most effective if given within one hour
Caution in the patient with altered mental status (need a protected airway)
Not effective for hydrocarbons, metals (Lead, Iron, Lithium)
Gastric Lavage
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Rarely used
Consider in large, potentially life threatening ingestions not amenable to
activated charcoal
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Hemodialysis
STUMBLE(D) - Dialysis
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Salicylates
Theophylline
Uremia
Methanol
Barbiturates, Bromide
Lithium
Ethylene Glycol
Depakote (high levels)
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Focused History and Brief Tox Exam
History: what-when-how much
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Reliability factor, relatives, paramedics
Exam
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Vital signs
Mental status
Pupillary response
Skin changes, Odors/other prominent features.
M
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Exam
 Vital
signs
 Pulse
up or down or normal
 BP up or down or normal
 Temp up or down or normal
 Resp up or down or normal
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Bradycardia (PACED)
Propranolol or other Beta blockers,
Poppies (opiates)
 Anticholinesterase drugs
 Clonidine, CCBs, Ciguatera
 Ethanol or other alcohols, Ergotamine
 Digoxin
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Tachycardia (FAST)
Free base or other forms of cocaine
 Anticholinergics, antihistamines,
amphetamines
 Sympathomimetics (ephedrine,
amphetamines), Solvent abuse
 Theophylline, Thyroid hormone
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Hypothermia (COOLS)
Carbon monoxide, Clonidine
 Opiates
 Oral hypoglycemics, Insulin
 Liquor
 Sedative-hypnotics
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Hyperthermia (NASA)
 Nicotine,
Neuroleptic malignant
syndrome
 Antihistamines
 Salicylates, Sympathomimetics
 Anticholinergics, Antidepressants
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Hypotension (CRASH)
Clonidine, CCBs (and B-blockers)
 Reserpine or other
antihypertensives
 Antidepressants, Aminophylline,
Alcohol
 Sedative-hypnotics
 Heroin or other opiates
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Hypertension (CT SCAN)
Cocaine
 Thyroid supplements
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Sympathomimetics
 Caffeine
 Anticholinergics, Amphetamines
 Nicotine
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Rapid Respiration (PANT)
PCP, Paraquat, Pneumonitis
(chemical)
 ASA and other salicylates,
Amphetamines
 Non-cardiogenic pulmonary edema
 Toxin-induced metabolic acidosis
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Slow Respirations (SLOW)
 Sedative-hypnoptics,
Strychnine, Snakes
 Liquor
 Opiates, OPs
 Weed (marijuana)
 Other
causes: Nicotine,
Clonidine, Chlorinated HC
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Seizures?
Hallucinations?
CNS depressed?
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WITH LA COPS
 Withdrawals
(alcohol, benzos)
 INH, Insulin, Inderal
 Tricyclics, theophylline
 Hypoglycemics; Hemlock, water; Haldol
 Lithium,
Lidocaine, Lead, Lindane
 Anticholinergics, Antiseizure
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WITH LA COPS
 Cocaine,
Camphor, CN, CO, Cholinergics
 Organophosphates
 PCP, PPA, propoxyphene
 Sympathomimetics, Salicylates, Strychnine
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Miosis (COPS)
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Cholinergics, Clonidine
Opiates, organophosphates
Phenothiazines, pilocarpine
Sedative-hypnotics, SAH
MydriASis (A3S)
Antihistamines,
Antidepressants, Atropine
 Sympathomimetics
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Diaphoretic (SOAP)
 Sympathomimetics
 Organophosphates
 ASA
or salicylates
 Phencyclidine (PCP)
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Dry Skin
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Antihistamines, Anticholinergics
Bullous Lesions
Barbiturates and other sedativehypnotics
 Carbon monoxide
 Tricyclics (personal case series)
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www.acponline.org/graphics/bioterro/bullous.jpg
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Flushed
 CO
(rare)
 Anticholinergics
 Boric acid
 CN (rare)
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Cyanosis
 Phenazopyridine
 Aniline
dyes
 Nitrates
 Nitrites
 Ergotamine
 Dapsone
 Any agent
hypoxia, hypotension
 MetHb
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Bitter Almonds
Carrots
Fruity
Garlic
Gasoline
-Cyanide
-Cicutoxin (water hemlock)
-DKA, Isopropanol
-OP, As, DMSO, selenium, thallium,
phosphorus
-Petroleum distillates
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Mothballs
Pears
Pungent aromatic
Oil of wintergreen
Rotten eggs
-Naphthlene, camphor
-Chloral hydrate
-Ethchlorvynol
-Methylsalicylate
-Sulfur dioxide, hydrogen
sulfide
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Toxicology Screens
Urine Stat
 Urine vs Serum
 Acetaminophen level
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Routine Tests
CBC
 SMA-7
 Anion Gap
 ABGs
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Drug
Hrs Post-Ing
Pos Interv
APAP
4
NAC
COHgb
ASA
Immed*
6-12*
HBO
Dialysis
Iron
2-4*
Antidote
Dig
2-4*
Fab
Alcohols
1/2 - 1*
Antidote
*Clinical Symptoms may dictate treatment, not level.
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A MUD PILE CAT
 ASA
 Methanol
 Uremia
 DKA
 Paraldehyde,
Phenformin
 INH, Iron, Ibuprofen
 Lactic acidosis
 Ethylene Glycol
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A MUD PILE CAT
 CO,
CN, Caffeine
 AKA
 Theophylline,
Toluene
 Others
 Benzyl
alcohol
 Metaldehyde
 Formaldehyde
 H2 S
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Decreased Anion Gap
 Bromide
 Lithium
 Hypermagnesemia
 Hypercalcemia
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Calculated
 2(Na)+[Glu/18]
+ [BUN/2.8] + EtOH(mg/dL)/4.6
Osm Gap = measured - calculated
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Significant if >10
Really significant if >19
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Increased Osmolar Gap
 MAD
GAS
 Mannitol
 Alcohols
(met, EG, Iso, eth)
 Dyes, Diuretics, DMSO
 Glycerol
 Acetone
 Sorbitol
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A 40 year old man collapsed at work while
moving his car. He has a hx of depression.
He had recently attended his mother’s funeral
the day before.
He was found slumped over the steering wheel
of his car, lethargic and incoherent. A coworker left the patient and went to call
medics. He was intubated and transferred to
Regions Hospital.
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Examination
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BP 130/88, P90, R-vent, T 1012
Pupils 6mm unreactive but equal.
Skin warm, red, dry
Absent bowel sounds
Labs were unremarkable
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ABG:pH 7.50, 32, 140
EKG - QRS 102, occasional PVC
Is there a Toxidrome?
 A. Opioid
 B. Anticholinergic
 C. Delayed Exercise Syndrome
 D. Cholinergic poisoning
Is there an antidote?
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Anticholinergic (antihistamines, cyclic
antidepressants, Jimson weed)
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Hot as a hare (hyperthermia)
Red as a beet (flushed)
Dry as a bone (dry skin, urinary retention)
Blind as a bat (mydriasis)
Mad as a hatter (hallucinations, delirium, myoclonic
jerking)
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Also with anticholinergic
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Mydriasis
Tachycardia
Hypertension
Hyperthermia
Seizures
How do you treat it?
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Supportive care
TCAs – Sodium Bicarb for widened QRS
Benzodiazepenes for agitation, seizures
Consider physostigmine for pure anticholinergic overdoses
(contraindicated in TCA overdose or with dysrhythmias)
Toxidromes: Case #2
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A 19 year old male presents after from a party
after his friends noted he was “acting funny.” He
was “out of control” and not making sense, so they
decided to bring him into the Emergency Room.
The patient is agitated on arrival
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Examination
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BP 180/114, P120, R20, T 101
The patient is agitated and appears to be
hallucinating
Pupils 6mm sluggish but equal.
Skin warm, red, very diaphoretic
Labs were unremarkable
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EKG – sinus tachycardia
Toxidromes: Case #2
Is there a Toxidrome?
A. Opioid
B. Anticholinergic
C. Sympathomimetic
D. Cholinergic
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Sympathomimetics (cocaine, amphetamines,
ephedrine)
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Mydriasis
Tachycardia
Hypertension
Hyperthermia
Seizures
Diaphoresis
Treatment
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Supportive care
Benzodiazepines as needed
Toxidromes: Case #3
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A 40 y/o female is brought by medics. A family
member called after a suicide note was found and
the patient was found unresponsive.
On medic arrival the patient was noted to be very
somnolent. She was transported to Regions
Hospital.
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Examination
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BP 100/65, P50, R6, T 98.6
The patient is arousable only to sternal rub.
Pupils 2mm sluggish but equal.
Skin cool, dry
Labs were unremarkable
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EKG – sinus bradycardia
Toxidromes: Case #3
Is there a Toxidrome?
A. Opioid
B. Anticholinergic
C. Sympathomimetic
D. Cholinergic
Is there an antidote?
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Narcotic (heroin, methadone, other opioids)
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Miosis
Bradycardia
Hypotension
Hypoventilation
Coma/CNS depression
Treatment
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Naloxone
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Clonidine
 Hypotension
usually more profound
 May require HIGH dose naloxone to see any effect
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Tetrahydrozaline
 Periodic
apnea in kids
 Kids should be admitted if symptomatic in ED
Toxidromes: Case #4
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A 50 y/o male is brought in after being found in his
garage. According to paramedics, there were
several containers of liquids in glass jars near the
patient. They also noted a large amount of emesis.
He was noted to have altered mental status and
some respiratory distress prior to arrival. He was
intubated prior to arrival and transported to
Regions Hospital.
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Examination
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BP 110/65, P50, R - intubated, T 98.6
The patient is obtunded, intubated
Pupils 2mm sluggish but equal.
There are copious secretions in the patient’s mouth and
in the endotracheal tube
Incontinent of both urine and stool
Skin is cool, diaphretic
Labs were unremarkable
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EKG – sinus bradycardia
Toxidromes: Case #4
Is there a Toxidrome?
A. Serotonin Syndrome
B. Anticholinergic
C. Sympathomimetic
D. Cholinergic
Is there an antidote?
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Cholinergic (DUMBELS or SLUG BAM)
Salivation
 Lacrimation
 Urination
 GI complaints (nausea, vomiting, diarrhea)
 Bradycardia, Bronchoconstriction
 Abdominal cramping
 Miosis, Muscle fasciculations
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Treatments: Pralidoxime (2PAM), Atropine
MORE TALKINGDROMES
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Salicylates (ASPIRIN)Harris
 Altered
MS (lethargy to coma)
 Sweating
 Pulmonary edema
 Increased
 Ringing
ventilation, temp, heart rate
in ears
 Irritable
 Nausea and vomiting
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Serotonin Syndrome
 VS:
T, HR, BP (unstable)
 MS: Agitation, coma
 Pupils: Mydriasis
 Skin: Diaphoresis
 Other: LE rigidity, myoclonus, hyperreflexia, seizure
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MAOI and other drug
Idiosyncratic reaction
Alteration in MS
 Autonomic instability
 Neuromuscular abnormality
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Treatment is supportive
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Symptoms resolve 24-72 hrs
Lactic acidosis, rhabdo, hyperthermia
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Specific drugs
 SSRIs
(i.e., Prozac)
 Dextromethorphan
 Demerol
 Ecstasy (MDMA): hallucinogenic amphetamine
 Cocaine
 L-tryptophan
Acetaminophen Toxicity - Metabolism
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Metabolized in the liver primarily to nontoxic
glucoronide and sulfide conjugates, however small
amount is converted via cytochrome P450 to
potentially toxic NAPQI
Normally, NAPQI is conjugated with glutathione to
nontoxic metabolites
In significant overdose, glutathione stores are
depleted
NAPQI destroys hepatocytes leading to liver failure
Acetaminophen Toxicity – Clinical
Presentation
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First few hours
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18 – 24 hours
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Non-specific signs and symptoms
Nausea, vomiting, pallor, diaphoresis
Even severely poisoned patients may remain symptomatic
Asymptomatic phase
No laboratory evidence of hepatotoxicity
After 24 – 36 hours
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Aminotransferases begin to rise
Signs and symptoms of hepatotoxicity
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72 – 96 hours
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N, V, RUQ pain, hepatic enlargement, jaundice
Peak hepatotoxicity
Although massive liver necrosis can occur, recovery is the rule and
usually complete if the patient survives
Acetaminophen Level
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Levels are important
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Check levels in all cases of
suspected overdose or polydrug
overdose
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Antidotal therapy is most effective
if started within 8 – 10 hours
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Signs and symptoms are delayed
for 18 – 36 hours
Rumack-Matthew nomogram
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Used to predict the severity of
toicity and need for antidotal
therapy
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4 hour level
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Levels above the line require
antidotal therapy
Acetaminophen Toxicity - Antidote
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N-acetylcysteine (NAC)
 Glutathione
precursor and glutathione substitute
 Increases substrate supply for the non-toxic sulfate
conjugation pathway
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Available as oral and IV form
Extremely effective if initiated within 8 hours
Standard of care to treat patients up to 24 hours
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ABCs - Antidotes
Decontaminate - Special Treatments?
Toxidromes?
Investigate - look closely
REASSESS, MONITOR, SUPPORT