Transcript A 47 yo male schizophrenic, noted by his mother to be breathing

Introduction to the Poisoned
Patient
Department of Emergency Medicine
The Ottawa Hospital
Outline
• Directed toxicology history
• Toxidromes
• Cases/Treatment
Toxicology - Objectives
-Determine whether poisoning has occurred, the
substance involved, how severe the exposure was, how
toxic it is likely to become, and the causticity of
substance.
-Perform supportive care, decontamination or
prevention of further absorption, give antidote where
indicated, and enhance elimination of the poison.
- Discuss special considerations in the management of
poisoning with aspirin, acetaminophen, tricyclic
antidepressants, and methanol.
Clinical Timeline
History
Toxidrome
Treatment
Laboratory
Confirm or refute
Reassess
Directed Tox History
• When (most NB)
• What
• How
– How much?
– Method?
• Whose?
– Compliance
• Coingestants?
– Access
– Specifics
• Self treatment?
– Ipecac
– Induced emesis
– Ethanol
• Intent?
• Symptoms
Work hard to get it, then be suspect!
Toxidrome
What it is:
– a clustering of symptoms and/or signs
– consistent with a class of drugs/medications
What it isn’t:
– a way to identify a specific substance
– a way to discriminate well among
“contradictory agents” until repeated over time
Common Toxidromes
•
•
•
•
•
•
•
•
Narcotic (coma resp depression, miosis)
Anticholinergic (mad as a hatter …)
Cholinergic (DUMBELS)
Sedative/Hypnotic (pupillary rxn spared)
Stimulant or Sympathomimetic
Hallucinogens
Extrapyrimidal
Serotonergic
Anticholinergics
• TCA’s, atropine, scopolamine, antihistamines
– Mad as a hatter (delerium)
– Hot as a hare (fever)
– Blind as a bat (mydriasis)
– Dry as bone (dry mucous membrane, urinary retention,
decreased BS)
– Red as beet (flushing)
– Bowel and bladder lose tone and heart goes on alone)
• Difference with adrenergics =
– Bowel sounds present
– Diaphoresis
Cholinergics
• Pheostigmine, organophosphtes (insecticides), and
nerve gas (DUMBELS)
–
–
–
–
–
–
–
Diaphoresis, diarrhea, decreased BP
Urination frequent
Miosis
Bronchospasm, bronchorrhea, bradycardia
Emesis, excitation of skeletal muscle
Lacrimation
Salivation / seizures
Sympathomimetics
• Amphetamine, cocaine
–
–
–
–
–
Resemble paranoid schizophrenic
CNS stimulation
Seizures
Psychosis
Increased BP, pulse, Temp
Hallucinogens:
•
•
•
•
•
Hallucinations
May be oriented to time / place / person
Tachy
HTN
mydriasis
Opioids
• Coma
• Resp depression
• Miosis (not with demerol)
Sedatives
• Barbituarates, ethanol, benzo’s, ethanol,
GHM (gamma hydroxybutyric acid)
–
–
–
–
CNS depression
Resp depression
Coma
Pupil rxn usually spared
Extrapyramidal
• chlorpromazine, stemetil, halodol,
metocloperamide
– Dystonia (occulogyric crisis, laryngospasm,
torticollis)
– Akithesia
– Parkinson like sx (tremor, ridgidity, akinesia,
postural instability)
– Dyskinesia (tic, spasm, chorea, myoclonus)
Seratonergic
• Mimics NMS (neuroleptic malignant syndrome) of increased BP,
increased pulse, increased temp, increased resp rate (onset within 24
hours, hyperactive, clonus, hyperreflexic, clonus)
• NMS (due to massive dopamine blockade) (FARMERS)
–
–
–
–
–
–
–
–
Fever
Autonomic changes (increased bp, pulse, sweating) / acidosis (rare)
Rigidity of muscles / rhabdomyolyis
Mental status changes (eg. Confusion)
Elevated BP, HR, pulse, RR
Rhabdomysolysis
Seizures
Onset days to weeks
Case
A 78 yo F presents with agitation and
confusion. BP 180/105, P 110 RR 16
T 38.2 C. Physical exam reveals an
acutely agitated pt, pupils 6 mm,
CVS/resp normal except tachycardia.
Is a toxidrome present?
What are the treatment priorities?
What tests do you want to order?
Investigations
• Serum levels
–
–
–
–
acetaminophen (4 hour level)
ASA
Ethanol
ingestion specific (eg phenytoin, digoxin level)
• Electrolytes, BUN/Cr
• EKG
• Serum osmolarity
What about a “Tox Screen”?
• Urine immunoassays
– lab determines which tests to include on the
“screen”
• Often clinically irrelevant
– confuse the clinical picture
• positive cocaine in a patient with an opioid
toxidrome
• “toxic” TCA level in a cyclobenzaprine (Flexeril)
overdose
Treat the patient, not the test!
Case
A 78 yo F presents with agitation and
confusion. BP 180/105, P 110 RR 16
T 38.2 C. Physical exam reveals an
acutely agitated pt, pupils 6 mm,
CVS/resp normal except tachycardia.
Is a toxidrome present?
What are the treatment priorities?
What tests do you want to order?
Supportive treatment of the
poisoned patient is the
cornerstone of management
A 20 yo F comes to the ED saying she
just took a whole bottle (1.5 grams) of
Elavil (amitriptylline). Her vital signs
are normal. She is alert and exam is
normal.
Treatment considerations?
Treatment
Elimination:
-Activated Charcoal
-Whole Bowel Irrigation
Removal:
-Gastric Lavage
Antidotes
Treatment
Elimination:
-Activated Charcoal
-Whole Bowel Irrigation
Removal:
-Gastric Lavage
Antidotes
Activated Charcoal
• Ingestion < 1 hr
– upto 2 hrs if delayed emptying, bad toxin
• 1 g/kg or 10 g for each gram of OD drug
• Ineffective
–
–
–
–
–
–
Pesticides
Hydrocarbons
Alcohols
Iron
Lithium
Alkali’s / acids (contraindicated)
Activated Charcoal
• CX
– Aspiration
• Gastric content aspiration worse than charcoal
aspiration
• But a lot worse if dump charcoal into lungs
– Perforation if bowels not moving
Cathartics
• Sorbitol
– available premixed with charcoal
• can use for first dose
– contraindicated if < 2 years
• electrolyte problems
– Used with charcoal to counteract its
constipating effect
To Give or Not to Give...
An alert 36 year old M 2 hours post
accidental ingestion of antifreeze
To Give or Not to Give...
An alert 36 year old M 2 hours post
accidental ingestion of antifreeze
A: Not indicated; 2hrs is too late (esp
for liquid) and alcohols bind poorly
To Give or Not to Give...
A somnolent 45 yo F with ingestion of
olanzapine (Zyprexa) and venlafaxine
(Effexor) at an undetermined time.
To Give or Not to Give...
A somnolent 45 yo F with ingestion of
olanzapine (Zyprexa) and venlafaxine
(Effexor) at an undetermined time.
A: Not indicated; undetermined time
(likely greater than 1 hr for toxicity to
develop from these agents) and risk of
aspiration given altered mental status.
To Give or Not to Give...
An intubated 37 yo F 30 min after
collapsed after metoprolol OD.
To Give or Not to Give...
An intubated 37 yo F 30 min after
collapsed after metoprolol OD.
A: Indicated; recent ingestion, (very)
bad drug and airway is protected.
Treatment
Elimination:
-Activated Charcoal
-Whole Bowel Irrigation
Removal:
-Gastric Lavage
Antidotes
Decontamination
• Gastric Lavage
–
–
–
–
–
–
–
recent (< 1hr)
Life threatening ingestion
no antidote
not adsorbed by AC
sustained release
concretions
no emesis
EasyLav
Gastric Lavage
• Large hose with blunt end (need this for
tablets to pass)
• LL decubitus position with pylorus pointing
upwards
• Has to have airway protected either
intubated of fully conscious
• Have bucket of warm water and bucket on
floor
Gastric Lavage
• Give warm water through funnel / tube
above pt … Percuss stomach … move tube
below level of head to drain into bucket …
repeat
• Prevents drug from getting into small
intestine as drain directly from stomach
Treatment
Elimination:
-Activated Charcoal
-Whole Bowel Irrigation
Removal:
-Gastric Lavage
-Dialysis
Antidotes
Whole Bowel Irrigation
• Polyethylene glycol (eg. Golytely)
– 1-2 L/hr via NGT until clear effluent
– Do for 4 to 6 hours until clear effluent via rectal
tube
• SR preps, Lithium, iron, sustained release
drugs
• Body packers/stuffers
A 20 yo F comes to the ED saying she
just took a whole bottle (1.5 grams) of
Elavil (amitriptylline). Her vital signs
are normal. She is alert and exam is
normal.
Treatment considerations?
Tricyclic Antidepressants - Sx
• Block sodium channels
• Neuro:
– mental status changes
– anticholinergic toxicity
– seizures
• Cardiac:
– (lethal) arrhythmias
– AV blocks
– hypotension
• QRS > 120 ms and ‘R” in aVR > 3mm predicts seizures/
arrhythmias
Tricyclic Antidepressants - Mgmt
• Activated Charcoal (no role for dialysis)
• Alkalinization of blood (7.45 – 7.50) with
sodium bicarbonate
– Abolishes dysrhythmias and improves
hypotension
– Use if QRS > 100 msec
– Administer as 1 – 2 mEq/kg IV push then 20
mEq / hr drip
Enhanced Elimination
• Diuresis
– Alkaline
• 3 amps NaHCO3 in 1 L D5W with 40 mmol KCl at
250 mL/hr
• goal: urine pH 7.5-8
• E.g Salicylates, Phenobarbital
– Neutral
• Lithium
Tricyclic Antidepressants - Mgmt
- Seizure mgmt:
- avoid dilantin (increases dysrhythmias)
- Diazepam/lorazepam/ phenobarbitol
- Hypotension
- Crystalloid and alkalinization
- Vasopressors if no response
- Dysrhythmias unresponsive to bicarb
- Lidocaine
- Consider pacemaker insertion for blocks
A 34 yo M presents 4 hours after
ingesting 100 regular ASA pills.
He complains of tinnitus, is
vomiting and has an ASA level of
6 mmol/L. His vital signs are BP
132/78 P 85 RR 28 T 37.5° C
Decontamination?
Other treatment considerations?
Commonly Dialysable Drugs
•
•
•
•
•
•
•
•
Isopropanol
Salicylates
Theophylline
Uremia
Methanol
Barbiturates
Lithium
Ethylene Glycol
Salicylates - Symptoms
• Causes metabolic acidosis .. Initially resp
alkalosis as stimulates resp centre
• Mild = ototoxicity (tinnitis, vertigo)
• Severe = CNS stimulation followed by
depression (confusion, delerium, seizures_
– Cardiac dysrhythmias, noncardiogenic
pulmonary edema, renal failure, hemorrhage
Salicylates – Treatment
• Treatment is not dependant on specific
serum level; it is a CLINICAL diagnosis
• Done nomogram USELESS
• Draw levels to ensure declining
Salicylates – Evaluation
• Decontamination with Activated charcoal
• Consider gastric lavage if < 60 min
• Alkaline diuresis with bicarb increases elimination
of ASA (goal of urine pH 5 – 8)
– See TCA OD for bicarb dosing
• Hemodialysis is most effective means
– Indications include renal failure, severe cardiac tox,
rising ASA levels despite alkalinization, pulm edema,
severe acidbase imbalance
Case
A 42 yo M presents after ingesting 30
grams of acetaminophen. He is
asymptomatic. A serum level 4 hours
after ingestion is 1625 mol/L.
Antidotes
Acetaminophen
N-acetylcysteine
Atropine
Carbon monoxide
Cyanide
Physostigmine
oxygen
Amyl nitrite +
sodium nitrite +
sodium thiosulfate
Ethanol / fomepizole
Ethylene glycol /
Methanol
Iron
Lead
Deferoxamine
EDTA (calcium
disodium edetate)
Antidotes
Nitrites
Methylene Blue
Organophosphate
Opiods
Isoniazid
Digoxim
Benzodiazepines
Atropine
Naloxone
Pyridoxine
Digibind
Flumazenil
Acetaminophen
• Delayed hepatoxicity
• Consider activated charcoal
• Rumack-Matthew nomogram
– predicts toxicity 4 hrs after acute ingestion
– No use less than 4 hours before
• N-acetylcysteine antidote
– Minimum 300 mg/kg IV over 20 hrs
• Goal of therapy is administration of NAC within 8
hrs of ingestion
Methanol
• Found in windshield washing fluid, paint
thinners, solvents
• Converted by alcohol dehydrogenase to
formaldehyde (liver) to formic acid
– Formic acid – toxic product
– Causes high anion gap and osmole gap
– Affects optic nerve fxn causing papillitis and
retinal edema – “blind drunk”
High Anion Gap
•
•
•
•
•
•
•
•
•
•
•
C (carbon monoxide, cyanide)
A (Arsenic)
T (toluene)
M (methanol, metformin)
U (uremia)
D (DKA)
P (paraldehyde, phenformin)
I (INH, iron)
L (Lactic acidosis)
E (ethylene glycol (antifreeze), everything
S (salicylates, strychtnine)
Anion and osmole gap
– AG = Na – Cl – HCO3
– Osmole Gap = 2Na + BUN + glucose + ETOH( 1.25)
• Osmole gap causes:
– Ethanol, Isopopanol, Methanol, Ethylene glycol,
Acetone, Glycerol, Mannitol, Uremia, Ketocacidosis
• Isopropanol causes high osmole but not anion gap
• Peraldehyde and isoniazide cause high AG but not
high osmole gap
Methanol
• 8 hour – 30 hour latent period followed by onset
of abdo pain, nausea, vomiting, blurred vision,
metabolic acidosis
– Often dilated pupil with photophobia
• High anion gap acidosis
– Na – Cl – HCO
3
• Osmole gap may be high but can be normal
– 2Na + BUN + glucose + EtOH (1.25)
– Normal is 280 – 295 mosm
Methanol
• Supportive measures
• Consider bicarbonate with severe acidosis
• ADH inhibitor
– Fomepizole – inhibits alcohol dehydrogenase
– Ethanol (BEER!) – ethanol infusion as alcohol
dehydrogenase preferentially metabolizes ethanol (keep
at 22 – 33)
• Hemodialysis
– If symptomatic or methanol level > 8 mmol / L
– Severe acidosis
TOXICOLOGY AXIOMS
• The most important aspect of the history is the time
of ingestion and coingestants
• The most critical therapy varies with the time course
of the patient’s presentation
• No evaluation is complete until repeated over time
• Toxidromes can help identify classes of drugs
• It is often not important to determine the exact drug
taken within a class
• Supportive tx is the cornerstone of tx