Definitions

1. Clinical toxicology: Focuses on the eff ects of substances

in patients caused by accidental poisonings
or intentional overdoses of medications, drugs of abuse,
household products, or various
other chemicals
2. Intoxication: Toxicity associated with any chemical
substance
3. Poisoning: A clinical toxicity secondary to accidental
exposure
4. Overdose: An intentional exposure with the intent of
causing self-injury or death
5. Toxidromes: A group of signs, symptoms, and laboratory
findings that suggest a specific
ingestion

General Management

A. Supportive care and ABCs: Evaluating and supporting

the vital functions (airway, breathing, and circulation
[ABCs]) are the mandatory first steps in the initial
management of drug ingestions. After the patient is stabilized,
the specific issue(s) of poison management should be
addressed.

B. Treatment for patients with depressed mental status

includes the following:
1. To rule out or treat hypoglycemia, 50 mL of 50% dextrose
in adults and 1 mL/kg in children intravenously (IV).
2. Thiamine 100 mg IV push (glucose can precipitate the
Wernicke-Korsakoff syndrome in thiamine-deficient
patients).
3. Naloxone (Narcan) 0.4 to 2 mg IV push, if opiate ingestion
is suspected. Naloxone may also be administered by the
following routes: inhalation, intramuscular, and intranasal.

C. Obtaining a history of exposure

1. Identify the substance(s) ingested, the route of exposure,
the quantity ingested, the amount of time
since ingestion, signs and symptoms of overdose, and any
associated illness or injury. Corroborate history and other
physical evidence (e.g., pill containers) from prehospital
providers.
2. Neurological examination evaluates any seizures,
alterations in consciousness, confusion, ataxia, slurred
speech, tremor, headache, or syncope.
3. Cardiopulmonary examination evaluates any syncope,
palpitations, cough, chest pain, shortness of breath, or

5. Past medical history should include

a. Medications, including nonprescription (over-the-counter
[OTC]) substances
b. Use of herbal medications
c. Alcohol or drug abuse
d. Psychiatric history
e. Allergies
f. Occupational or hobby exposures
g. Travel
h. Prior ingestions
i. Social history with potential for domestic violence or

D. Routine laboratory assessment

1. Complete blood cell (CBC) count
2. Serum electrolytes
3. Blood urea nitrogen (BUN); serum creatinine (SCr)
4. Blood glucose
5. Urinalysis
6. Electrocardiogram (ECG)
7. Chest roentgenogram and/or kidneys, ureters, and bladder
(KUB) x-ray

E. Toxicology laboratory tests

1. Advantages
a. Confirm or determine the presence of a particular agent
b. Predict the anticipated toxic eff ects or severity of exposure
to some poisons
c. Confirm or distinguish diff erential or contributing
diagnosis
d. Occasionally help guide therapy

2. Disadvantages
a. These tests cannot provide a specifi c diagnosis for all
patients.
b. All possible intoxicating agents cannot be screened.
c. In critically ill patients, supportive treatment is needed
before laboratory results of the toxicology screen are
available.
d. Laboratory drug-detection abilities differ.
e. In general, only a qualitative determination of a substance
or substances is necessary; however, quantitative levels of the
therapeutically monitored drugs may be necessary to guide
therapy. Consult with your local laboratory for the
availability of specific drug assays.

F. Skin decontamination should be performed when

percutaneous absorption of a substance may result
in systemic toxicity, or when the contaminating substance
may produce local toxic effects (e.g., acid burns).
The patients clothing is removed, and the areas are irrigated
with copious quantities of water.
Neutralization should not be attempted. For example,
neutralizing acid burns with sodium bicarbonate will produce
an exothermic chemical reaction, thereby exacerbating the
patients condition.

G. Gastric decontamination may be attempted when

supportive care is begun.
GI decontamination involves removal of the ingestant with
emesis or lavage, the use of activated charcoal potentially to
bind any ingestants, and the use of cathartics to hasten
excretion and thereby limit absorption.

1. Emesis
a. Contraindications
(1) Children younger than 6 months of age
(2) Patients with central nervous system (CNS) depression or
seizures
(3) Patients who have ingested a strong acid, alkali, or a sharp object
(4) Patients with compromised airway protective reflexes (including
coma and convulsions)
(5) Patients who have ingested some types of hydrocarbons or
petroleum distillates
(6) Patients who have ingested substances with an extremely rapid
onset of action
(7) Patients with emesis after the ingestion

b. Syrup of ipecac: Owing to concerns of safety, efficacy,

and the delay of antidote administration, syrup of ipecac is no
longer recommended for general use.
Ipecac may be administered within 30 mins of ingestion and
only on the advice of a poison control center.

2. Gastric lavage
a. Use: Gastric lavage is infrequently used in patients who are not
alert or have a diminished gag reflex.
This procedure should also be considered in patients who are seen
early after massive ingestions.
This procedure is contraindicated in patients who have ingested
acids, alkalis, or hydrocarbons. In addition, patients should not
receive gastric lavage if they are at risk for GI perforation or if
they are combative.

3. Activated charcoal adsorbs almost all commonly ingested

drugs and chemicals and is usually administered to most
overdose patients as quickly as possible (ideally, within 1 hr
of ingestion). Commonly ingested substances not adsorbed
include ethanol, iron, lithium, cyanide, ethylene glycol, lead,
mercury, methanol, organic solvents, potassium, strong acids,
and strong alkalis.
a. Dosage: Activated charcoal (Actidose with sorbitol) is
available as a colloidal dispersion with water or sorbitol. In
adults, the dose of activated charcoal is 25 to 100 g; the dose
in children1 to 12 years of age is 25 to 50 g; the dose in

Constipation has not been observed after the administration of a

single dose of activated charcoal.
Multiple doses of any cathartics should be avoided because they
can cause electrolyte imbalances and/or dehydration.
Toxic ingestions with drugs having an enterohepatic circulation
(e.g., carbamazepine, theophylline, phenobarbital, tricyclic
antidepressants, phenothiazines, digitalis) generally require that
the charcoal be readministered every 6 hrs to prevent reabsorption
during recirculation.

b. Adverse effects:
Charcoal aspiration and empyema have been reported in the
literature. As such, charcoal should be withheld if patients are
vomiting.
Bowel obstruction may occur with multiple doses of activated
charcoal and/or patients who are receiving concomitant
therapy with neuromuscular-blocking drugs.

H. Whole bowel irrigation has been shown to be effective

under certain conditions, particularly when activated charcoal
lacks efficacy.
An isosmotic cathartic solution such as polyethylene glycol
(GoLYTELY, Colyte) is used. The dosage is 1 to 2 L/hr given
orally or by nasogastric tube until the rectal effluent is clear.

Forced diuresis and urinary pH manipulation may be used to enhance the

elimination of substances, whose elimination is primarily renal, if the
substance has a relatively small volume of distribution with little protein
binding. However, the use of these methods is associated with fluid and
electrolyte disturbances.
Alkaline diuresis promotes the ionization of weak acids, thereby
preventing their reabsorption by the kidney, which facilitates the
excretion of such weak acids. This procedure has been used in the
management of patients who have ingested long-acting barbiturates such
as phenobarbital or salicylic acid. Patients are given 50 to 100 mEq of
sodium bicarbonate IV push, followed by a continuous infusion of 50 to
100 mEq of sodium bicarbonate in 1 L of 0.25% to 0.45% normal saline,
maintaining a urine pH of 7.3 to 8.5. Urine output should be 5 to 7
mL/kg/hr. Complications include metabolic alkalosis, hypernatremia,
hyperosmolarity, and fluid overload.

J. Dialysis: In patients who fail to respond to the measures of

decontamination already outlined, hemodialysis, and to a lesser
extent peritoneal dialysis, may enhance drug elimination. Substances
that are removed by hemodialysis generally are water soluble, have
a small volume of distribution ( 0.5 L/kg), have a low molecular
weight ( 500 Da), and are not significantly bound to plasma proteins.
Hemodialysis usually is indicated for life-threatening ingestions of
ethylene glycol, methanol, or paraquat. This technique also has been
used to enhance the elimination of ethanol, theophylline, lithium,
salicylates, and long-acting barbiturates.

K. Hemoperfusion is a technique in which anticoagulated blood is

passed through (perfused) a column containing activated charcoal or
resin particles. This method of elimination clears substances from
the blood more rapidly than hemodialysis, but it does not correct
fluid and electrolyte abnormalities as does hemodialysis.
Hemoperfusion, although more effective in removing phenobarbital,
phenytoin, carbamazepine, methotrexate, and theophylline than
hemodialysis, is less eff ective in removing ethanol or methanol.
Complications of hemoperfusion include thrombocytopenia,
leukopenia, hypocalcemia, hypoglycemia, and hypotension.

III. MANAGEMENT OF SPECIFIC INGESTIONS

A. Acetaminophen (Tylenol) is an antipyretic-analgesic that can
produce fatal hepatotoxicity in untreated patients through the
generation of a toxic metabolite.
1. Available dosage forms: Acetaminophen is available in a
variety of OTC and prescription drug products.
2. Toxicokinetics: Acetaminophen is well absorbed from the GI
tract and has a half-life between 2 and 3 hrs. Less than 5% is
excreted unchanged in the urine; the remainder is metabolized in
the liver by the cytochrome P450 system.

3. Clinical presentation
a. Phase I (12 to 24 hrs postingestion). Nausea, vomiting,
anorexia, and diaphoresis
b. Phase II (1 to 4 days postingestion). Asymptomatic
c. Phase III (2 to 3 days in untreated patients). Nausea,
abdominal pain, progressive evidence of hepatic failure, coma,
and death.

4. Laboratory data
a. Serum acetaminophen levels: Patients with levels greater than
150, 70, or 40 mg/mL at 4, 8, or 12 hrs after ingestion require
antidotal therapy with N-acetylcysteine (NAC) according to the
Rumack-Matthews nomogram.
b. Baseline liver function tests should be done in all patients.
c. Renal function tests, including a BUN and SCr, should be done.
d. Coagulation studies include prothrombin time (PT), partial
thromboplastin time (PTT), and bleeding time.

5. Treatment
a. Adult patients who have ingested 10 g or children who have
ingested 200 mg/kg require treatment. Elderly and alcoholic
patients have an increased susceptibility to acetaminophen
hepatotoxicity.
b. The recommended treatment is GI decontamination with
activated charcoal.
c. Antidotal therapy with NAC is indicated for patients with toxic
blood levels of acetaminophen.
(1) NAC dosage is 140 mg/kg as a loading dose followed by 70
mg/kg every 4 hrs for a total of 17 doses. NAC is administered
either orally or via a nasogastric tube. NAC (Mucomyst) 20%

Each dose must be diluted 1:3 in either cola or fruit juice to

mask the unpleasant taste and smell. The dose of NAC should
be repeated if the patient vomits within 30 mins of
administration. Patients with severe nausea secondary to
NAC may be pretreated with IV metoclopramide (Reglan) 10
mg every 6 hrs. Metoclopramide acts as an antiemetic while
increasing the rate of NAC absorption.
(2) IV NAC (Acetadote)
(a) Loading dose: 150 mg/kg over 60 mins
(b) Maintenance dose: 50 mg/kg over 4 hrs followed by 100
mg/kg over 16 hrs
(c) Anaphylactoid reactions are observed in approximately
20% of patients. Caution should be exercised in patients with
a history of asthma.

B. Alcohols
1. Ethylene glycol
a. Available forms: Ethylene glycol commonly is used in
antifreeze and windshield de-icing solutions. This form is
sometimes colorless and has a sweet taste.
b. Toxicokinetics: Ethylene glycol is hepatically metabolized by
alcohol dehydrogenase to glycolaldehyde,which is metabolized
by aldehyde dehydrogenase to glycolic acid. Glycolic acid is
converted to glyoxylic acid, whose most toxic metabolite is
oxalic acid.

c. Clinical presentation
(1) Stage I (0.5 to 12 hrs postingestion). Ataxia, nystagmus, nausea
and vomiting, decreased deep tendon reflexes, and severe acidosis
(more severe overdoses: hypocalcemic tetany and seizures, cerebral
edema, coma, and death)
(2) Stage II (12 to 24 hrs postingestion). Tachypnea, cyanosis,
tachycardia, pulmonary edema, and pneumonitis
(3) Stage III (24 to 72 hrs postingestion). Flank pain and
costovertebral angle tenderness; oliguric renal failure
d. Laboratory data may reveal severe metabolic acidosis,
hypocalcemia, and calcium oxalate crystals in the urinalysis.

e. Treatment
(1) Gastric lavage is performed within 30 mins of ingestion.
(2) IV ethanol (EtOH) is used in situations in which fomepizole
is not available.
(a) Indications include an ethylene glycol level 20 mg/dL,
suspicion of ingestion pending
level, or an anion gap metabolic acidosis with a history of
ingestion, regardless of the level.
(b) EtOH dosage
(i) An EtOH level of at least 100 mg/dL should be maintained.
(ii) Loading dose is 7.5 to 10 mL/kg of a 10% ethanol in dextrose
5% in water (D5W) over 1 hr, followed by a maintenance infusion

(3) Fomepizole (Antizol) is a potent inhibitor of alcohol

dehydrogenase that can prevent the formation of the toxic
metabolites of either methanol or ethylene glycol.
(a) Administer a loading dose of 15 mg/kg (up to 1 g) in 100
mL of D5W or 0.9% sodium chloride (NaCl) infused over 30
mins.
(b) Maintenance doses: 10 mg/kg every 14 hrs for four
doses, then increase to 15 mg/kg (to off set autoinduction
phenomenon) until methanol or ethylene glycol levels are 20
mg/dL.

(4) Pyridoxine (100 mg IV every day) and thiamine (100 mg

IV every day) are cofactors that may convert glyoxylic acid
to nonoxalate metabolites.
(5) Sodium bicarbonate is used as needed to correct the
acidosis.
(6) Hemodialysis Fomepizole must be continued, and the rate
of administration may need to be increased. Indications
include ethylene glycol level 50 mg/dL, congestive heart
failure, renal failure, and severe acidosis.

2. Methanol
a. Available forms include gas-line antifreeze, windshield
washer, and some sterno.
b. Toxicokinetics: Alcohol dehydrogenase converts methanol
to formaldehyde, which is then converted to formic acid.
c. Clinical presentation
(1) Stage I. Euphoria, gregariousness, and muscle weakness
for 6 to 36 hrs, depending on the rate of formation of formic
acid
(2) Stage II. Vomiting, upper abdominal pain, diarrhea,
dizziness, headache, restlessness, dyspnea, blurred vision,
photophobia, blindness, coma, cerebral edema, cardiac and

e. Treatment
(1) Gastric lavage. Charcoal has not been shown to absorb
alcohols.
(2) IV EtOH (used in situations in which fomepizole is not
available)
(a) Indications include any peak methanol level 20 mg/dL, a
suspicious ingestion with a positive history, or any symptomatic
patient with an anion gap acidosis.
(b) Administration is the same as per ethylene glycol (see III.B.1).
(3) Folic acid administered at 1 mg/kg (maximum 50 mg) IV every
4 hrs for six doses increases the metabolism of formate.
(4) Fomepizole (Antizol)
(5) Sodium bicarbonate is used for severe acidosis.
(6) Hemodialysis is used for methanol levels 50 mg/dL, severe and
resistant acidosis, renal failure, or visual symptoms.

C. Anticoagulants
1. Heparin/Low-Molecular-Weight Heparin (LMWH)
a. Available dosage forms include parenteral dosage forms
for IV and subcutaneous administration.
b. Toxicokinetics. Heparin has a half-life of 1 to 1.5 hrs and
is primarily metabolized in the liver. The newer LMWHs
enoxaparin (Lovenox), dalteparin (Fragmin), tinzaparin
(Innohep)have a longer half-life, especially in patients with
renal failure.
c. Clinical presentation. Look for any signs or symptoms of
bleeding or bruising.

e. Treatment
(1) Stopping heparin administration for 1 to 2 hrs
and restarting therapy at a reduced dose can reverse
mild over-anticoagulation.
(2) Severe overdoses may require the administration
of protamine.
(a) Protamine combines with heparin and neutralizes
it: 1 mg protamine neutralizes 100 U heparin.
(b) Protamine should be administered slowly,
intravenously over 10 mins. The maximum dose of
protamine is 50 mg in any 10-min period.

(c) Considerable controversy exists about the method of

reversing the over-anticoagulation with LMWHs. Some
sources recommend the administration of protamine to
neutralize part of the effects of these anticoagulants, whereas
case reports reported successes with recombinant factor VII
(NovoSeven).
(d) These overdoses should be referred to a hematologist
and/or the poison control center

2. Warfarin (Coumadin)
a. Available dosage forms include oral tablets and a solution for
parenteral administration.
b. Toxicokinetics. Warfarin is well absorbed after oral
administration. Its mean half-life is 35 hrs; protein binding is 99%,
with 5-day duration of activity. Vitamin K-dependent clotting
factors begin to decline 6 hrs after administration, but therapeutic
anticoagulation may require several days.
c. Clinical presentation includes minor bleeding, bruising,
hematuria, epistaxis, and conjunctival hemorrhage. More serious
bleeding includes GI, intracranial, retroperitoneal, and wound site.
d. Laboratory data include PT, international normalized ratio
(INR), and bleeding time.

e. Treatment
(1) If PT or INR is slightly elevated, withhold warfarin for 24
to 48 hrs, then reinstitute therapy with a reduced dosage.
(2) If PT or INR is elevated and bleeding, administer 10 mg
of phytonadione (vitamin K) over 30 mins. Patients who are
bleeding may require the administration of blood products
that contain clotting factors.
(3) For mild over-anticoagulation, follow American College
of Chest Physicians (ACCP) guidelines.
(4) For patients with life-threatening bleeding or intracranial

3. Pradaxa (dabigatran)
a. Available dosage forms include oral capsules.
b. Toxicokinetics. Dabigatran is poorly absorbed following
oral administration, but it has a half life of 12 to 17 hrs in
healthy subjects with normal renal function.
c. Clinical presentation includes minor bleeding, bruising,
hematuria, and epistaxis. More serious bleeding includes GI,
intracranial, retroperitoneal, and wound site.
d. Laboratory data specialized hematologic monitoring may
be required such as thrombin clotting time and ecarin clotting
time.

e. Treatment
(1) Mild bleeding. Local treatment and withholding one dose
(2) Moderate bleeding. Consider blood product transfusion
and/or hemodialysis
(3) Severe bleeding. As noted earlier with the additional
consideration of charcoal filtration along with either
recombinant factor VII or prothrombin complex concentrates.
Dabigatran is the fi rst FDA-approved oral direct-acting
thrombin inhibitor. Many more compounds are in clinical
trials and due to the paucity of overdose data with these
drugs, consultation with a hematologist and/or a poison
information specialist is highly recommended

D. Antidepressants
1. Tricyclic antidepressants (TCAs)
a. Available forms include amitriptyline (Elavil),
nortriptyline (Aventyl), imipramine (Tofranil), desipramine
(Norpramin), doxepin (Sinequan), protriptyline (Vivactil),
and clomipramine (Anafranil).
b. Toxicokinetics. The compounds are hepatically
metabolized, undergo enterohepatic recirculation,
are highly bound to plasma proteins, and have an elimination
half-life of approximately 24 hrs.

c. Clinical presentation. Anticholinergic eff ects include

mydriasis, ileus, urinary retention, and hyperpyrexia.
Cardiopulmonary toxicity exhibits tachycardias, conduction
blocks, hypotension, and pulmonary edema. CNS
manifestations range from agitation and confusion to
hallucinations, seizures, and coma.
d. Laboratory data. Blood level monitoring does not
correlate well with clinical signs and symptoms of toxicity.
Some authors suggest that electrocardiographic monitoring is
a better guide to assessing the severity of ingestion.

e. Treatment
(1) GI decontamination. Syrup of ipecac is not recommended because
patients may quickly become comatose, increasing the risk of aspiration.
Activated charcoal is given every 6 hrs.
(2) Alkalinization with sodium bicarbonate 1 to 2 mEq/kg to maintain an
arterial pH of 7.45 to 7.55 decreases the free fraction of the absorbed
toxins, while reversing some of the cardiac abnormalities.
(3) Phenytoin (Dilantin) and/or benzodiazepines may be required to
control seizures. Phenytoin must be administered at a rate not exceeding
25 mg/min because of hypotensive side effects. (Fosphenytoin [Cerebyx]
may be used because it has a lower incidence of hypotension than
phenytoin.)
(4) Physostigmine 2 mg IV over 1 min may be used to reverse severe
anticholinergic toxicity owing to these drugs. Because this antidote may
cause asystole, the use of this antidote for TCA overdoses is declining.

2. Selective serotonin reuptake inhibitors (SSRIs)

a. Available forms (nontricyclic agents) include fl uoxetine
(Prozac), sertraline (Zoloft ), and paroxetine (Paxil).
b. Toxicokinetics. SSRIs are well absorbed aft eroral
administration. Peak levels occur within 2 to 6 hrs. SSRIs are
hepatically metabolized with a half-life between 8 and 30 hrs.
c. Clinical presentation includes mild symptomatology.
Patients may become agitated, drowsy, or confused. Seizures
and cardiovascular toxicity are rare.
d. Laboratory data. ECG monitoring is recommended.
Blood level monitoring is not recommended.

E. Benzodiazepines
1. Available forms include chlordiazepoxide (Librium), diazepam
(Valium), fl urazepam (Dalmane), midazolam (Versed), lorazepam
(Ativan), alprazolam (Xanax), and triazolam (Halcion).
2. Toxicokinetics. These drugs are hepatically metabolized.
3. Clinical presentation includes drowsiness, ataxia, and
confusion. Fatalities are rare.
4. Laboratory data. Drug level monitoring is not indicated.

5. Treatment
a. Supportive treatment includes gastric emptying, activated
charcoal, and a cathartic.
b. Flumazenil (Romazicon) is given 0.2 mg IV over 30 secs;
repeat doses of 0.5 mg over 30 secs at 1-min intervals for a
maximum cumulative dose of 5 mg.
(1) Flumazenil has a short elimination half-life.
(2) Careful observation for resedation is necessary,
especially for ingestions of long-acting benzodiazepines.
(3) Flumazenil is contraindicated in mixed overdose patients
(particularly involving tricyclic antidepressants) in whom
seizures are likely.

F. -adrenergic antagonists
1. Available dosage forms. Class examples include
propranolol (Inderal), metoprolol (Lopressor), and atenolol
(Tenormin). Oral and parenteral dosage forms are available.
2. Toxicokinetics. All of the members within this class differ
in regard to renal versus hepatic elimination, lipid solubility,
and protein binding. Patients may become toxic owing to
changes in organ function.
3. Clinical presentation includes hypotension, bradycardia,
and atrioventricular block. Bronchospasm may occur,
particularly with noncardioselective agents.
4. Laboratory data include serum electrolytes and blood

5. Treatment
a. GI decontamination includes gastric lavage and activated
charcoal.
b. Glucagon is given 50 to 150 mcg/kg as a loading dose over 1
min, followed by a continuous infusion of 1 to 5 mg/hr.
c. Epinephrine should be used cautiously in -blocker overdoses.
Unopposed -receptor stimulation in the face of complete -receptor
block may lead to profound hypertension.
d. Calcium salts (see Calcium Channel Antagonists)
e. High-dose insulin dextrose (see Calcium Channel
Antagonists)

G. Calcium channel antagonists

1. Available forms include verapamil (Calan), diltiazem
(Cardizem), and the dihydropyridine class (nifedipine
derivatives [Procardia]).
2. Toxicokinetics. Onset of action is approximately 30 mins,
whereas the duration is 6 to 8 hrs. Several compounds are
available as sustained-release dosage forms, which may
contribute to prolonged toxicity.
3. Clinical presentation. Hypotension is common to all
classes. Bradycardia and atrioventricular block are more
commonly seen with ingestions of verapamil or diltiazem.
Pulmonary edema and seizures (verapamil) have been

5. Treatment
a. GI decontamination includes gastric lavage, activated charcoal, and
whole-bowel irrigation (especially for ingestions with sustained-release
products).
b. Calcium. Calcium chloride 10% (10 to 20 mL) IV push is given for the
management of hypotension, bradycardia, or heart block.
c. Glucagon dosage is the same as for -blocker overdose.
d. Combined insulin and dextrose administration has been used in
selected cases. The insulin dosages used are as follows: regular insulin 1
U/kg and a loading dose along with IV dextrose 0.5 g/kg. This should be
followed with a continuous infusion of insulin at a rate of 0.5 to 2 U/kg/hr
along with continuous dextrose infusions of 0.5 g/kg/hr to maintain serum
glucose levels within a 100 to 250 mg/dL range. Insulin dosages are
titrated to appropriate hemodynamic indices in an intensive care
environment. This should be used only in consultation with a poison

H. Cocaine
1. Available forms include alkaloid obtained from
Erythroxylon coca.
2. Toxicokinetics. Cocaine is well absorbed aft er oral,
inhalational, intranasal, and IV administration. Cocaine is
metabolized in the liver and excreted in the urine.
3. Clinical presentation includes CNS and sympathetic
stimulation (e.g., hypertension, tachypnea, tachycardia,
nausea, vomiting, seizures). Death may result from
respiratory failure, myocardial infarction, or cardiac arrest.
4. Laboratory data include cocaine and cocaine metabolite
urine screens.

I. Corrosives
1. Available forms include strong acids or alkalis.
2. Toxicokinetics. Corrosives are well absorbed aft er oral
and inhalational administration.
3. Clinical presentation. These compounds produce burns on
contact.
4. Laboratory data. Arterial blood gases (ABGs), chest
radiographs, and at least 6 hrs of observation are required for
inhalation exposure.
5. Treatment is decontamination. Exposed skin must be
irrigated with water. Neutralization should be avoided
because these reactions are exothermic and will produce

J. Cyanide
1. Available forms include industrial chemicals and some
nail polish removers.
2. Toxicokinetics. Th e drug is rapidly absorbed aft er oral or
inhalation exposure.
3. Clinical presentation includes headache, dyspnea, nausea,
vomiting, ataxia, coma, seizures, and death.
4. Laboratory data include cyanide levels, ABGs,
electrolytes, and an ECG.

5. Treatment
a. Cyanide antidote kit
(1) Amyl nitrite. Pearls are crushed and held under the
patients nostrils.
(2) Sodium nitrite 10 mL IV push. Converts hemoglobin to
methemoglobin, which binds the cyanide ion.
(3) Sodium thiosulfate 50 mL of a 25% solution IV push.
May be repeated if there is no response.
b. Oxygen
c. Sodium bicarbonate. As needed for severe acidosis
d. Hydroxocobalamin (Cyanokit) adult dose is 5 g IV over 15
mins. Dose may be repeated for a total dose of 10 g. No data

K. Digoxin (Lanoxin)
1. Available dosage forms include oral and parenteral.
2. Toxicokinetics. Digoxin is well absorbed, is primarily
renally eliminated, and has a half-life of 36 to 48 hrs. Its
volume of distribution is 7 to 10 L/kg. Equilibration between
serum level and myocardial binding requires 6 to 8 hrs.
3. Clinical presentation includes confusion, anorexia,
nausea, and vomiting in mild cases. In more severe cases,
cardiac dysrhythmias are seen.
4. Laboratory data include serum digoxin levels,
electrolytes, particularly serum potassium levels,
and an ECG.

5. Treatment
a. Decontamination with activated charcoal is
recommended.
b. Supportive therapy includes managing hyperkalemia or
hypokalemia and inotropic support as needed.
c. Digoxin-specifi c Fab antibodies (Digibind). To
determine the dosage, use the following formula:
Dose (mg) [(serum digoxin concentration [ng/mL] weight
(kg)/100]) (mg/vial)
Digibind 38 mg/vial or Digifab 40 mg/vial

L. Electrolytes
1. Magnesium
a. Available dosage forms include oral, rectal, and
parenteral. Magnesium-containing cathartics (e.g.,
magnesium citrate) have been reported to produce
hypermagnesemia in patients receiving repetitive doses with
activated charcoal.
b. Toxicokinetics. Magnesium is found intracellularly and is
renally eliminated.
c. Clinical presentation
(1) Mild. Deep tendon refl exes may be depressed; lethargy
and weakness

d. Laboratory data
(1) Mild: 4 mEq/L
(2) Severe: 10 mEq/L
e. Treatment is 10% calcium chloride 10 to 20 mL to
temporarily antagonize the cardiac effects of magnesium. In
severe cases, hemodialysis may be required.

2. Potassium
a. Available dosage forms are oral and parenteral.
b. Toxicokinetics. Potassium is primarily an intracellular
cation. Changes in acidbase balance produce shift s in serum
potassium values (e.g., a 0.1 U increase in serum pH produces
a 0.1 to 0.7 mEq/L decrease in serum potassium values).
c. Clinical presentation includes cardiac irritability and
peripheral weakness with minor increases. Cardiac
dysrhythmias, including bradycardia, may progress to
asystole.
d. Laboratory data. ECG data include peaked T waves and
prolongation of the QRS complex.

e. Treatment
(1) Calcium. Administer calcium chloride 10% 10 to 20 mL
to antagonize the cardiac effects of hyperkalemia.
(2) Sodium bicarbonate. 1 to 2 mEq/kg IV increases serum
pH and causes an intracellular shift of potassium.
(3) Glucose and insulin. 50 mL of 50% dextrose and 5 to 10
U of regular insulin are administered via IV push to shift
potassium from the extracellular fl uid into the cells.

(4) Cation exchange resins bind potassium in exchange for

another cation (sodium). Sodium polystyrene sulfonate
(Kayexalate) is given 15 g/60 mL with 23.5% sorbitol in doses 15
to 30 g by mouth every 3 to 4 hrs as needed until the hyperkalemia
resolves.
Alternatively, 50 g of sodium polystyrene sulfonate can be given
rectally in 200 mL of sodium chloride as a retention enema. Th ere
have been reports of colonic necrosis and other GI events. Some
authors recommend other treatments before utilizing exchange
resin therapy.
(5) Hemodialysis is reserved for life-threatening hyperkalemia that
does not respond to the aforementioned measures.

M. Iron (Fe)
1. Available dosage forms. Numerous OTC products are
available. Toxicity is based on the amount of elemental iron
ingested: sulfate salt 20% elemental Fe; fumarate salt 33%
elemental Fe; and gluconate salt 12% elemental Fe.
2. Toxicokinetics. Iron is absorbed in the duodenum and
jejunum.
3. Clinical presentation
a. Phase I. Nausea, vomiting, diarrhea, GI bleeding,
hypotension
b. Phase II. Clinical improvement seen 6 to 24 hrs
postingestion

4. Laboratory data include serum Fe levels, total ironbinding capacity (TIBC; is controversial), ABGs, liver
function tests (LFTs), hemoglobin, and hematocrit.
Radiological evaluation of the abdomen notes the presence of
radiopaque pills.
5. Treatment
a. Decontamination. For ingestions 40 mg/kg. Gastric
lavage using sodium bicarbonate is of questionable efficacy.
Whole-bowel irrigation is used for large ingestions.
b. Supportive treatment
c. Deferoxamine (Desferal) is used to chelate iron.
Administer at a rate of 15 mg/kg/hr up to a maximum dose of

N. Isoniazid (INH)
1. Available dosage forms include oral and parenteral.
2. Toxicokinetics. INH is well absorbed orally. Peak levels
are within 1 to 2 hrs postingestion. Isoniazid is hepatically
metabolized.
3. Clinical presentation includes nausea, vomiting, slurred
speech, ataxia, generalized tonicclonic seizures, and coma.
4. Laboratory data include severe lactic acidosis,
hypoglycemia, mild hyperkalemia, and leukocytosis.

5. Treatment
a. Decontamination. Avoid emesis because patients are at
high risk for developing seizures; for severe ingestions, use
activated charcoal gastric lavage.
b. Pyridoxine, which reverses INH-induced seizures, is given
in gram doses equivalent to the amount of isoniazid ingested.
Pyridoxine is mixed as a 10% solution in D5W and infused at
0.5 g/min until seizures stop, with the remainder infused over
4 to 6 hrs (maximum adult dose: 5 g).
c. Sodium bicarbonate corrects the acidosis.

O. Lead
1. Available forms include lead-containing paint or gasoline
fume inhalation.
2. Toxicokinetics. Lead has slow distribution, with a half-life
of approximately 2 months.
3. Clinical presentation includes nausea, vomiting,
abdominal pain, peripheral neuropathies, convulsions, and
coma.
4. Laboratory data include anemia and an elevated bloodlead level.

5. Treatment
a. Edetate calcium disodium (Calcium Disodium Versenate)
is given 50 to 75 mg/kg/day intramuscularly (IM) or via slow
IV in four divided doses.
b. Dimercaprol (BAL) is given 4 mg/kg IM every 4 hrs for 3
to 5 days. Dimercaprol therapy is administered fi rst.
Following the second dose, concomitant edetate calcium
disodium is initiated and both therapies are continued for up
to 5 days. Oral chelation therapy is used for less severe cases.

P. Lithium (Eskalith)
1. Available dosage forms include liquid, capsules, and
tablets (immediate and sustained release).
2. Toxicokinetics. Lithium is well absorbed aft er oral
administration. It is not appreciably bound to plasma proteins
and has a small volume of distribution (Vd) of 0.5 L/kg.
Elimination is renal, with a half-life of 14 to 24 hrs.
3. Clinical presentation
a. Mild. Polyuria, blurred vision, weakness, slurred speech,
ataxia, tremor, and myoclonic jerks

5. Treatment
a. Supportive care, including basic life support and fl uid and
electrolyte replacement
b. Decontamination
(1) Syrup of ipecac not recommended
(2) Activated charcoal ineffective
(3) Sodium polystyrene sulfonate has been eff ective in
experimental models. Need to monitor potassium levels.
(4) Whole-bowel irrigation for large ingestions, especially those
involving sustained-release products
(5) Hemodialysis for severely symptomatic patients with acute
exposure levels 2.5 mEq/L or chronic levels 1.5 mEq/L. Note:
Lithium levels may rise aft er dialysis owing to a rebound eff ect.

Q. Opiates
1. Available dosage forms include oral immediate-release
and sustained-release preparations as well as parenteral
agents.
2. Toxicokinetics. Some agents have prolonged elimination
half-lives (e.g., heroin, methadone).
3. Clinical presentation includes respiratory depression and
a decreased level of consciousness.Rare effects include
hypotension, bradycardia, and pulmonary edema. Seizures
have been reported in patients with renal dysfunction in
individuals who are receiving meperidine owing to
the accumulation of the metabolite or meperidine.

5. Treatment
a. Naloxone is given 0.4 to 2.0 mg every 5 mins up to 10 mg
and 0.03 to 0.1 mg/kg in pediatric patients. Naloxone has a
very short half-life, and resedation is a concern in patients
overdosing on long-acting opioids or sustained-release
dosage forms.
b. Nalmefene (Revex) has a half-life of 4 to 8 hrs. Initial
dosages are 0.5 mg/70 kg. A follow-up dose 2 to 5 mins later
is 1 mg/70 kg.

R. Organophosphates
1. There are several available forms; they are usually
pesticides or chemical warfare agents.
2. Toxicokinetics. Organophosphates are absorbed through
the lungs, skin, GI tract, and conjunctiva.
3. Clinical presentation includes excessive cholinergic
stimulation.
4. Laboratory data include red blood cell
acetylcholinesterase activity.
5. Treatment
a. Decontamination
b. Atropine is given 0.5 to 2.0 mg IV to reverse the

S. Salicylates
1. Available dosage forms include several OTC products:
oral, rectal, and topical.
2. Toxicokinetics. Salicylates are well absorbed aft er oral
administration. The half-life is 6 to 12 hrs at lower doses. In
overdose situations, the half-life may be prolonged to more
than 20 hrs.
3. Clinical presentation includes nausea, vomiting, tinnitus,

4. Laboratory data for the following 6-hr postingestion

levels are:
a. 40 to 60 mg/dL: tinnitus
b. 60 to 95 mg/dL: moderate toxicity
c. More than 95 mg/dL: severe toxicity
d. With the presence of acidemia and aciduria, evaluate
ABGs.
e. In addition, laboratory evaluation may show leukocytosis,
thrombocytopenia, increased or
decreased serum glucose and sodium, hypokalemia, and
increased serum BUN, creatinine,
and ketones.

5. Treatment
a. Decontamination. Repetitive doses of activated charcoal
every 6 hrs, with one dose of cathartic for patients who
ingested 150 mg/kg. Whole-bowel irrigation for large
ingestions.
b. Alkaline diuresis is given as noted in decontamination
section to enhance salicylate excretion.This is indicated for
levels 40 mg/dL.
c. Hemodialysis is used for severe intoxications when serum
levels are 100 mg/dL. This method of decontamination is
much better than repetitive doses of activated charcoal.

T. Snake bites
1. Types. There are numerous species of snakes found
worldwide. The venomous snakes found in North America
include the following: rattlesnake, cottonmouth, copperhead,
and coral. Because patients may be exposed to more exotic
snakes, a herpetologist should be consulted for a more defi
nitive identifi cation.
2. Toxicokinetics. Onset of symptomatology depends on the
species of snake and the patients underlying medical
condition.

4. Laboratory data
a. CBC and platelet count
b. Coagulation profi le
c. Fibrin degradation products
d. Electrolytes
e. BUN, SCr, and urinalysis

5. Treatment
a. Supportive. Move the patient away from striking distance
of the snake. Ideally, the patient should be transported to a
medical facility as soon as possible. Constrictive clothing,
rings, watches, etc. should be removed. Tetanus immunization
should be assessed, and surgical intervention may be
necessary for severe cases.
b. Antivenoms
(1) Antivenin (Crotalidae) polyvalent is a horse-derived
product that has been reported to produce allergic reactions.
For mild bites, the recommended dose is 5 to 10 vials;
moderate,1020; and severe envenomations may require 20

U. Theophylline
1. Available dosage forms include liquid, sustained-release
tablets, and capsules as well as parenteral forms.
2. Toxicokinetics. Well absorbed orally with a Vd of
approximately 0.5 L/kg. Th eophylline is hepatically
metabolized and has a half-life of 4 to 8 hrs. Theophylline
clearance depends highly on age, concomitant disease states,
and interacting drugs.
3. Clinical presentation includes nausea, vomiting, seizures,
and cardiac dysrhythmias. Chronic toxicity carries a poorer

5. Treatment
a. Supportive therapy includes maintaining an airway and
treating seizures and dysrhythmias as they occur.
b. Decontamination. Syrup of ipecac not recommended.
c. Activated charcoal (repetitive doses) to enhance
elimination. Whole-bowel irrigation for massive ingestions
(especially with sustained-release products). Charcoal
hemoperfusion is used in unstable patients who are in status
epilepticus. Hemodialysis is used when hemoperfusion
is unavailable.
d. -adrenergic antagonists (e.g., esmolol, Brevibloc) are