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Toxicological Emergencies
Dr. Shahid Aziz MBBS, MRCP (UK), MCEM (London)
Assistant professor and consultant emergency medicine, DEM
King Khalid University Hospital
Objectives
History and Physical Examination
Toxicology Screening
Three gaps are important in toxicology
Treatment
ICU Admission
History and Physical Examination
Difficulties
 No reliable history in patients with profoundly
altered metal status
 Focused treatment decisions quite difficult.
 Multiple substances
History and Physical Examination

Separating patients who have suspected
poisoning into broad categories that are
based on vital signs, eye findings, mental
status, and muscle tone, that helps to
determine drug or toxin class
i.e.“toxidromes.”
Diagnosing toxicity from vital signs
Bradycardia (PACED)
Propranolol (beta-blockers), poppies
(opiates), propoxyphene, physostigmine
Anticholinesterase drugs, antiarrhythmics
Clonidine, calcium channel blockers
Ethanol or other alcohols
Digoxin, digitalis
Tachycardia (FAST)
Free base or other forms of cocaine, freon
Anticholinergics, antihistamines, antipsychotics,
amphetamines, alcohol withdrawal
Sympathomimetics (cocaine, caffeine, amphetamines,
PCP), solvent abuse, strychnine
Theophylline, TCAs, thyroid hormones
Hypothermia (COOLS)
Carbon monoxide
Opioids
Oral hypoglycemics, insulin
Liquor (alcohols)
Sedative-hypnotics
Hyperthermia (NASA)
Neuroleptic malignant syndrome, nicotine
Antihistamines, alcohol withdrawal
Salicylates, sympathomimetics, serotonin syndrome
Anticholinergics, antidepressants, antipsychotics
Hypotension (CRASH)
Clonidine, calcium channel blockers
Rodenticides (containing arsenic, cyanide)
Antidepressants, aminophylline, antihypertensives
Sedative-hypnotics
Heroin or other opiates
Hypertension (CT SCAN)
Cocaine
Thyroid supplements
Sympathomimetics
Caffeine
Anticholinergics, amphetamines
Nicotine
Rapid respiration (PANT)
PCP(phencyclidine), paraquat, pneumonitis (chemical),
phosgene
ASA and other salicylates
Noncardiogenic pulmonary edema, nerve agents
Toxin-induced metabolic acidosis
Slow respiration (SLOW)
Sedative-hypnotics (barbiturates, benzodiazepines)
Liquor (alcohols)
Opioids
Weed (marijuana)
COMA
L: Lead, lithium
E: Ethanol, ethylene glycol, ethchlorvynol
T: Tricyclic antidepressants, thallium, toluene
H: Heroin, hemlock, hepatic encephalopathy, heavy metals, hydrogen
sulfide, hypoglycemics
A: Arsenic, antidepressants, anticonvulsants, antipsychotics,
antihistamines
R: Rohypnol (sedative hypnotics), risperidone
G: GHB
I: Isoniazid, insulin
C: Carbon monoxide, cyanide, clonidine
Agents that cause seizures (OTIS CAMPBELL)
Organophosphates, oral hypoglycemics
Tricyclic antidepressants
Isoniazid, insulin
Sympathomimetics, strychnine, salicylates
Camphor, cocaine, carbon monoxide, cyanide,
Amphetamines, anticholinergics
Methylxanthines (theophylline, caffeine), methanol
Phencyclidine (PCP), propranolol
Benzodiazepine withdrawal,bupropion, GHB
Ethanol withdrawal, ethylene glycol
Lithium, lidocaine Lead, lindane
Agents that affect pupil size
Miosis (COPS)
Cholinergics, clonidine, carbamates
Opiates, organophosphates
Phenothiazines (antipsychotics), pilocarpine)
Sedative-hypnotics
Mydriasis (SAW)
Sympathomimetics
Anticholinergics
Withdrawal
Agents that cause skin signs
Diaphoretic skin (SOAP)
Sympathomimetics
Organophosphates
Acetylsalicylic acid or other salicylates
Phencyclidine
Dry Skin
Antihistamines, anticholinergics
Bullae
Barbiturates and other sedative-hypnotics,
Bites: Snakes and spiders
Acneiform rash
Bromides
Chlorinated aromatic hydrocarbons (dioxin)
Flushed or red appearance
Anticholinergics, niacin
Boric acid
Carbon monoxide (rare)
Cyanide (rare)
Cyanosis
Ergotamine
Nitrates
Nitrites
Aniline dyes
Phenazopyridine
Dapsone
Any agent causing hypoxemia,
hypotension, or
methemoglobinemia.
Agents causing an elevated anion gap
(METAL ACID GAP)
Methanol, metformin, massive overdoses
Ethylene glycol
Toluene
Alcoholic ketoacidosis
Lactic acidosis
Acetaminophen (large overdoses)
Cyanide, carbon monoxide, colchicine
Isoniazid, iron, ibuprofen
Diabetic ketoacidosis
Generalized seizure-producing toxins
Acetylsalicylic acid or other salicylates
Paraldehyde, phenformin
Drugs causing pneumonitis or pulmonary edema
(MOPS)
Meprobamate, methadone
Opioids
Phenobarbital, propoxyphene, paraquat, phosgene
Salicylates
Common toxidromes
Cholinergic (Examples: organophosphates,
carbamates, pilocarpine)
(DUMBELLS)
Diarrhea, diaphoresis
Urination
Miosis
Bradycardia, bronchosecretions
Emesis
Lacrimation
Lethargic
Salivation
Nicotinic (recalled by the days of the week)
Monday: Miosis
Tuesday: Tachycardia
Wednesday: Weakness
Thursday: Tremors
Friday: Fasciculations
Saturday: Seizures
Sunday: Somnolent
Anticholinergic (Examples: antihistamines, cyclic
antidepressants, atropine, benztropine, phenothiazines,
scopolamine)
Hyperthermia (HOT as a hare)
Flushed (RED as a beet)
Dry skin (DRY as a bone)
Dilated pupils (BLIND as a bat)
Delirium, hallucinations (MAD as a hatter)
Tachycardia
Urinary urgency and retention
Sympathomimetic (Examples: cocaine,
amphetamines, ephedrine, phencyclidine,
pseudoephedrine)
Mydriasis
Tachycardia
Hypertension
Hyperthermia
Seizures
Opioid (Examples: heroin, morphine, codeine, methadone, fentanyl,
oxycodone, hydrocodone)
Miosis
Bradycardia
Hypotension
Hypoventilation
Coma
Agents responsive to multiple doses of activated charcoal
Substances adsorbable by activated charcoal (ABCD)
Antimalarials (quinine), aminophylline (theophylline)
Barbiturates (phenobarbital)
Carbamazepine
Dapsone
Substances not adsorbable by activated charcoal (PHAILS)
Pesticides, potassium
Hydrocarbons
Acids, alkali, alcohols
Iron, insecticides
Lithium
Solvents
Table -- Antidotes and their indications
Antidote
n-acetylcysteine
Ethanol/fomepizole (4-MP)
Oxygen/hyperbarics
Naloxone/nalmefene
Physostigmine
Atropine/pralidoxime (2-PAM)
Methylene blue
Nitrites
Deferoxamine
Dimercaprol (BAL)
Succimer (DMSA)
Fab fragments
Glucagon
Sodium bicarbonate
Calcium/insulin/dextrose
Dextrose, glucagon, octreotide
Indication (agent)
Acetaminophen
Methanol/ethylene glycol
Carbon monoxide
Opioids
Anticholinergics
Organophosphates
Methemoglobinemia
Cyanide
Iron
Arsenic
Lead, mercury
Digoxin, colchicine, crotalids
Beta-blockers
Tricyclic antidepressants
Calcium channel antagonists
Oral hypoglycemics
Toxins accessible to hemodialysis (UNSTABLE)
Uremia
No response to conventional therapy
Salicylates
Theophylline
Alcohols (isopropanol, methanol)
Boric acid, barbiturates
Lithium
Ethylene glycol
Enhanced elimination by charcoal hemoperfusion
Theophylline
Barbiturates
Carbamazepine
Paraquat
Glutethimide
History and Physical Examination
Toxidrome Yes
Treat
No
ovital signs
oocular findings
omental status
omuscle tone
determine drug
or toxin class
History and Physical Examination
Physical examination
A rapid but careful physical examination of
the patient is performed in stages.

Initially, a rapid survey for ABCs & life-threatening nature

Then, a more focused examination for





Signs of trauma
Neurologic findings
Skin changes
Odors
Eyes
History and Physical Examination
Physical examination
Patients may present with
 hypotension or hypertension
 bradyarrhythmias or tachyarrhythmias.

The pathogenesis of hypotension varies and may
include




Hypovolemia
Myocardial depression
Cardiac arrhythmias
Systemic vasodilation.
Urine Drug Screens

Detect only natural opiates

Do not detect synthetic or semisynthetic products
o
o
o
o
o
o
Oxycodone
Hydrocodone
Fenanyl
Propoxyphene
Meperidine
methadone.
o morphine
o codeine
o heroin
Laboratories Investigation
Most hospital laboratories have the capability to
rapidly identify and quantify only a small fraction of
the substances commonly encountered in clinical
practice.

Toxicology Screening
Check acetaminophen levels in all cases
of suspected intoxication
Supportive serum toxicology assays
Acetaminophen
Lithium
Salicylate
Valproic acid
Carbamazepine
Co-oximetry (carboxyhemoglobin,
methemoglobin)
Digoxin
Phenobarbital
Iron
Ethanol
Methanol
Ethylene glycol
Theophylline
Data from Wu AH, McKay C, Broussard LA, et al. National Academy of Clinical Biochemistry
Laboratory Medicine practice guidelines: recommendations for the use of laboratory tests to
support poisoned patients who present to the emergency department. Clin Chem 2003;49:357–79.
Skelton H., Dann L.M., et al. Drug screening of patients who deliberately harm themselves
admitted to the emergency department. Ther Drug Monit (1998) 20 : pp 98-103.
GENERAL TREATMENT

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ABCs.
Protection of the cervical spine (unless trauma has
been excluded).
A rapid assessment of the need of endotracheal
intubation
Attention to any abnormalities of the vital signs.
Discontinuing the offending
Any life-threatening abnormalities
A 12-lead EKG is obtained along with continuous
cardiac monitoring.
ABG
Initial supportive measures
Endotracheal intubation is indicated



when there is concern regarding airway
protection and clinical deterioration
acute respiratory failure.
the need for high levels of supplemental
oxygen
It decreases (but does not eliminate) the risk of aspiration
(which is approximately 11% in the comatose patient with drug overdose).
Initial supportive measures


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Rapid IV normal saline solution infusion is
indicated in most instances.
Vasopressors may be required for refractory
hypotension.
The vasopressor of choice depends on the
type of intoxication
Hypertension-induced (reflex) bradycardia
generally should not be treated.
Coma Cocktail

Initial supportive measures
Dexrtrose, flumazenil, naloxone, thiamine.
.
Coma Cocktail
Initial supportive measures
There is no evidence that dextrose should be withheld
until thiamine is administered.
Reuler
JB, Girard DE, Cooney TG. Wernicke's encephalopathy.
N Engl J Med 1985; 312:1035–1039
Coma Cocktail
Initial supportive measures
Naloxone

rapidly reverses coma, respiratory depression, and
hypotension induced by opioids.

An initial dose of 0.2 to 0.4 mg is administered IV
(or endotracheally).

If there is no response after 2 to 3 min, repeated
up to 10 mg as required.

lack of response to 10 mg of naloxone generally
excludes opioid toxicity.
Coma Cocktail
Initial supportive measures
Naloxone


a higher dose may precipitate large
cardiovascular changes in opioid
dependent patients.
Observe for
 acute pulmonary edema
 opioid withdrawal
 seizures
Coma Cocktail
Initial supportive measures
Flumazenil

Its use in undifferentiated ED patients is not
recommended

Withdrawal seizures in mixed overdoses or in patients
with long-term use of benzodiazepines.
Hoffman R.S., Goldfrank L.R., The poisoned patient with altered
consciousness: controversies in the use of a coma
cocktail. JAMA (1995) 274 : pp 562
Spivey W.H., Flumazenil and seizures: analysis of 43 cases. Clin
Ther (1991) 14 : pp 292-305.
Coma Cocktail
Initial supportive measures
Flumazenil



Case reports have cautioned clinicians of the
risk of precipitating seizures with flumazenil
when there is a suspicion of benzodiazepine
plus TCA overdose
0.2 mg of IV flumazenil over 30 s followed
by another 0.3-mg dose if necessary.
Doses beyond 3 mg generally do not
provide additional benefit.
GASTRIC LAVAGE


Decontamination
Patients must be able to maintain their airways or
be intubated.
Should not be performed on patients who have
ingested medications that may cause seizures or
abrupt central nervous system deterioration.
GASTRIC LAVAGE

Decontamination
There is no clear definition of when to
end the procedure.
GASTRIC LAVAGE

Decontamination
One study using radiographic markers suggested
that GL may actually propel gastric contents past
the pylorus, moving the poison into the small
intestine, where most of the drug will be
absorbed
Saetta J.P., March S., Gaunt M.E., et al. Gastric emptying procedures
in the self-poisoned patient: are we forcing contents beyond the
pylorus?. J R Soc Med (1991) 84 : pp 274-276.
GASTRIC LAVAGE

Decontamination
three clinical trials have failed to demonstrate
improved outcomes when GL is added to AC for the
management of undifferentiated symptomatic
poisoning patients.
Kulig K., Bar-Or D., Cantrill S.V., et al. Management of acutely poisoned patients
without gastric emptying. Ann Emerg Med (1985) 14 : pp 562-567.
Pond S.M., Lewis-Driver D.J., Williams G.M., et al. Gastric emptying in acute
overdose: a prospective randomised trial. Med J Aust (1995) 163 : pp 345-349.
Saetta J.P., March S., Gaunt M.E., et al. Gastric emptying procedures in the selfpoisoned patient: are we forcing contents beyond the pylorus?. J R Soc Med (1991)
84 : pp 274-276
GASTRIC LAVAGE
Decontamination
Complications associated with GL include
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GI tract perforation
hypoxia
aspiration.
esophageal perforation
Arterial oxygen tension dropped 17%
during GL
pneumothorax
GASTRIC LAVAGE

Decontamination
Based on the available data, the
American Academy of Clinical Toxicology
does not recommend gastric lavage
unless a patient has ingested a
potentially life-threatening amount of a
poison and the procedure can be
undertaken within 60 minutes of
ingestion
ACTIVATED
CHARCOAL



Decontamination
Current consensus recommendations are that
adult overdose patients receive 25 to 100 g
The efficacy of charcoal is time dependent.
A recent consensus statement suggests that
charcoal should be administered within 60
minutes of ingestion
Laine K., Kivisto K.T., Neuvonen P.J., Effect of delayed administration of
activated charcoal on the absorption of conventional and slow-release
verapamil. J Toxicol Clin Toxicol (1997) 35: pp 263-268
ACTIVATED
CHARCOAL
Decontamination
CLINICAL EFFICACY OF ACTIVATED CHARCOAL
 A study evaluated AC versus supportive care alone
in asymptomatic pt.
 231 patients were assigned to observation and 220
were assigned to AC.

No patient in either group deteriorated, suggesting
that AC provided no benefit in the management of
asymptomatic poisoning patients.
Merigian
K.S., Woodard M., Hedges J.R., et al. Prospective
evaluation of gastric emptying in the self-poisoned patient.
 Am J Emerg Med (1990) 8 : pp 479-483.
ACTIVATED
CHARCOAL


Decontamination
a large study was published comparing AC with
supportive care for symptomatic and asymptomatic
overdose patients.
This study is described as a randomized controlled
trial (RCT) where 1479 patients were assigned on
an alternating-day basis to either AC or supportive
care.
Merigian
K.S., Blaho K.E., Single-dose oral activated charcoal in the
treatment of the self- poisoned patient: a prospective, randomized,
controlled trial. Am J Ther (2002) 9 : pp 301-308.
ACTIVATED
CHARCOAL

Decontamination
One additional RCT with Preliminary results
suggest that the patients who were given AC
had a trend toward longer ED stay and no
change in mortality
Cooper
G.M., Le Couteur D.G., Richardson D., et al. A
randomised controlled trial of activated charcoal for the routine
management of oral drug overdose. J Toxicol Clin Toxicol (2002)
40 : pp 313-.
ACTIVATED
CHARCOAL
Decontamination
The major complications of AC are



Vomiting
intestinal obstruction
aspiration.
ACTIVATED
CHARCOAL

Decontamination
Clinical benefits remain unproved
American Academy of Clinical Toxicology and
European Association of Poison Centers and
Toxicologist. Position paper: single-dose activated
charcoal. J Toxicol Clin Toxicol (2005) 43 : pp 6187
ACTIVATED
CHARCOAL
Decontamination
Complication
pneumonia
bronchiolitis obliterans
ARDS
death.
ACTIVATED
CHARCOAL
Decontamination
Toxins and Drugs Not Adsorbed by Activated Charcoal
Alcohols
Hydrocarbons
Organophosphates
Carbamates
Acids
Potassium
Dichloro diphenyl trichloroethane (DDT)
Alkali
Iron
Lithium
Extracorporeal
Removal of Toxins
Three methods
 (1) dialysis (usually hemodialysis
rather than peritoneal dialysis)
 (2) hemoperfusion
 (3) hemofiltration.
Hemodialysis
Toxins Characteristics


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low molecular weight (< 500 d)
water soluble
low protein binding (< 70 to 80%)
small volume of distribution (< 1 L/kg).
It can especially be effective in correcting concomitant electrolyte
abnormality and metabolic acidosis.
I,e:
 methanol,
 ethylene glycol,
 boric acid,
 Salicylates
 lithium.
Hemoperfusion


Hemoperfusion is defined as direct contact of blood with an
adsorbent system
drug clearance is not limited by low water solubility, high
molecular weight, or increased protein binding, but on the
ability of the adsorbent to bind to the drug/toxin.

toxin needs to be present in the central compartment for
hemoperfusion to be effective.

used to enhance elimination of theophylline, phenobarbital,
phenytoin, carbamazepine, paraquat.
Hemofiltration



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application of this technique has not been vigorously studied in
poisoned patients
there are increasing numbers of case reports of extracorporeal
intoxicant removal by either the continuous arteriovenous or
venovenous hemofiltration methods
Hemofiltration is potentially useful for removal of substances with a
large volume of distribution, slow intercompartmental transfer, or
extensive tissue binding.
combined digoxin-Fab fragment complexes, or desferoxamine
complexes with iron or with aluminum.
ICU Admission
Initial supportive measures
Criteria for Admission of the Poisoned Patient to the ICU
•Respiratory depression (PaCO2 > 45 mm Hg)
•Emergency intubation
•Cardiac arrhythmia
•Seizures
•SBP < 80 mm Hg
•Unresponsiveness to verbal stimuli
•Glasgow coma scale score < 12
•Need for emergency dialysis, hemoperfusion, or ECMO
•Increasing metabolic acidosis
•Pulmonary edema induced by toxins (including inhalation) or
drugs
ICU Admission
Initial supportive measures
Criteria for Admission of the Poisoned Patient to the ICU
•Hypothermia or hyperthermia including neuroleptic malignant
syndrome
•Tricyclic or phenothiazine overdose manifesting anticholinergic
signs, neurologic abnormalities, QRS duration > 0.12 s, or QT >
0.5 s
•Body packers and stuffers
•Emergency surgical intervention
•Administration of pralidoxime in organophosphate toxicity
•Antivenom administration
•continuous infusion of naloxone
•Hypokalemia secondary to digitalis overdose (or need for
digoxin-immune antibody Fab fragments)
ICU Admission
Initial supportive measures
In this retrospective study, if a poisoned patient did not
exhibit any of the eight characteristics, no ICU interventions
(intubation, vasopressors or antiarrhythmics, and dialysis or
hemoperfusion) were required.
(1) PaCO2 > 45 mm Hg,
(2) need for intubation,
(3) toxin-induced seizures,
(4) cardiac arrhythmias,
(5) QRS ≥ 0.12 s,
(6) sBP < 80 mm Hg,
(7) 2nd or 3rd degree AV block,
(8) unresponsiveness to verbal stimuli.

• Brett AS, Rothschild N, Gray R, et al. Predicting the clinical course in intentional drug overdose:
implications for the use of the intensive care unit. Arch Intern Med 1987; 147:133–137
•Mokhlesi B, Leikin JB, Murray P, et al. Adult toxicology in critical care: part I: general
approach to the intoxicated patient. Chest 2003;123(2):577-92.