Aspirin Poisoning 2013
Aspirin Poisoning
Introduction
Aspirin is considered by many people to be an old-fashioned
drug, but although it’s no longer as popular in the United
States as it once was, it is a drug that is still commonly used
and abused. The American Association of Poison Control
Centers (AAPCC) collects exposure data from all the poison
control centers in the United States. In one year, the AAPCC
recorded over 15,000 toxic exposures to aspirin, either alone
or in combination with other drugs, and there were 44
fatalities. All of the fatal cases involved adults 17 or older.
This fatality rate - 0.3% - may not seem too alarming. However, the basics of treating an
aspirin overdose are well outlined, and years of clinical experience clearly show that
with timely, appropriate intervention, patients with an aspirin overdose should survive.
Aspirin overdoses can be successfully treated but to do so, it’s absolutely critical that
the healthcare team understand the pathophysiology of aspirin poisoning and the
rationale for the standard therapy.
Pathophysiology
Aspirin (salicylic acid) is a non-steroidal anti-inflammatory. It is one of the most popular
drugs in the world today, and with good reason. It is effective as an analgesic, as an
anti-inflammatory, and as an antipyretic. It also acts to inhibit platelet aggregation (a
significant contributor to thrombus formation) and is widely used prophylactically for
patients at risk for developing coronary thrombi. It is also used acutely for patients
experiencing myocardial infarction. Although the popularity of aspirin has diminished
because of its association with Reye’s syndrome in children and because of the
development of newer, non-steroidal anti-inflammatory drugs that have a longer
duration of action and fewer side effects, aspirin is still in common use today. Given its
effectiveness for a variety of conditions and its low cost, that’s not surprising. Aspirin is
found in a variety of over-the-counter products, alone or in combination with other
drugs. Less well-known sources are Pepto- Bismol liquid (8.7 mg/mL of salicylic acid)
and tablets (118 mg of salicyclic acid per tablet), some analgesic salves, and
concentrated oil of wintergreen (1.4 grams of salicyclic acid per mL.).
Aspirin works by inhibiting the formation of prostaglandins, compounds that help
initiate and sustain the inflammatory process. Aspirin in therapeutic doses is rapidly
absorbed from the stomach and the small bowel, although aspirin can form bezoars
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Aspirin Poisoning 2013
(large, insoluble masses of the drug) and induce pylorospasm, both of which can delay
emptying of the drug from the stomach. The peak serum level is usually one hour after
ingestion, and therapeutic blood levels are 15-30 mg/dL. The half-life of aspirin is 2-4
hours. Most of a dose is eliminated in the kidneys and elimination is dependent on urine
pH. The absorption of salicyclic acid through skin is very limited unless the skin surface
is compromised.
Aspirin-Containing Products










Excedrin
Pepto-Bismol
Topical analgesics, eg, Icy Hot
Alka-Seltzer
Aspergum
Percodan
Fiorinal
Doan’s pills
Darvon compound
Ecotrin
Pharmacokinetics of Aspirin Poisoning
The absorption, metabolism and elimination of aspirin in overdose are very different
than the pharmacokinetics of aspirin in therapeutic doses.

Absorption: When taken in large amounts, the absorption of aspirin can be
delayed by bezoar formation in the stomach and pylorospasm. Ingestion of large
amounts of enteric-coated tablets can also delay absorption.

Peak serum level: In therapeutic doses, the peak serum level is reached in
approximately one hour. However, in overdose, the peak serum level can be
dramatically delayed. Again, this decreased absorption can be due to bezoars,
pylorospasm or ingestion of enteric-coated tablets.

Distribution: Normally, aspirin has a low volume of distribution (this indicates
that much of an ingested dose does not enter tissues, but is circulating in the
serum), and it is highly protein-bound (this prevents the aspirin from entering
tissues.) The volume of distribution is not changed in overdose, but in aspirin
poisoning the supply of protein is quickly saturated and protein binding is
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Aspirin Poisoning 2013
decreased, effectively creating a large amount of free salicylic acid that can enter
the tissues.

Metabolism: In therapeutic doses, aspirin is metabolized using first-order
kinetics; the drug is metabolized at a rate that is proportional to the dose, so
metabolism is increased in response to larger doses. In overdose, the normal
metabolic pathways become saturated and aspirin is metabolized by zero-order
(Michaelis-Menten) kinetics; a constant amount of drug is metabolized per unit
of time regardless of the dose. If a large amount of aspirin is ingested, the levels
can soon become toxic because metabolism does not speed up to accommodate
the extra drug. This is important because metabolism converts the drug to an
ionized form that cannot pass through tissue membranes (more on this later.)

Elimination: In normal doses, hepatic elimination is primary. But in overdose,
renal excretion becomes more active and this depends on urine pH.
So when aspirin is taken in toxic amounts,
absorption is delayed (at times, considerably),
the time to peak serum level is significantly
delayed (at times, considerably), there’s more
free, circulating aspirin that can enter into
tissues, and elimination depends on kidney
function and urine pH.
Instant feedback: When aspirin is taken in large amounts, the peak serum level is
greatly delayed. Why?
Answer: Bezoars and pylorospasm can delay gastric emptying, and the metabolism
changes from first-order to zero-order kinetics.
Instant feedback: A patient with an aspirin
overdose has serum levels, taken two hours
apart, of 36, 45, 57, 31, 56 (the units are mg/dL).
Is this a laboratory error?
Answer: No, it is not. Although it is not common,
the serum levels of aspirin in patients that have
taken an overdose can rise, decline, then rise again.
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Aspirin Poisoning 2013
Pathophysiology of Aspirin Poisoning
Understanding aspirin poisoning is not easy. Aspirin is a “multi-system” poison and it
has many complicated effects. The pathophysiology will be discussed here and the
specific clinical effects in the next section.

Acid-base: Aspirin poisoning can cause profound derangements in the patient’s
acid-base balance. Aspirin in toxic amounts stimulates the respiratory center,
increasing the rate and depth of respirations and eliminating carbon dioxide.

Acid-base/glucose metabolism: Aspirin in toxic amounts also affects acid-base
status by interfering with glucose metabolism and a review of this process will be
useful.

The first step of glucose metabolism is glycolysis in
which the glucose molecule is converted to pyruvic
acid.

The next step is the Krebs cycle. Here, the
pyruvic acid is converted to acetyl
coenzyme A.

The final step is oxidative phosphorylation;
here, the hydrogen ions that were liberated
in the first two steps are oxidized to create
energy – ATP – that is needed by the cells
to survive.
Aspirin interferes with the Krebs cycle. When this process can’t function, pyruvic
acid builds up. This would stop glycolysis and ATP production. The body
responds by converting the excess pyruvic acid to lactic acid, a compound that
can be used for energy. Unfortunately, lactic acid can only be used for energy
for a brief period of time, and then it starts to build up. Aspirin also interferes
with oxidative phosphorylation, and this also causes a buildup of pyruvic acid
and lactic acid. Interference with the Krebs cycle and oxidative phosphorylation
and the resulting decrease in ATP production increases the use of lipids for
energy and causes a buildup of ketone bodies, and metabolism of ketones
produces an acid.

Fluid and electrolyte: Fluid and electrolyte abnormalities are caused by (1) an
increased metabolic rate (due to the interference of ATP production) with excess
heat production, (2) water lost through the increased respiratory rate, and (3)
decreased fluid intake and vomiting. In the early stages of poisoning, the kidneys
are excreting bicarbonate and as a result, potassium is excreted.
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Aspirin Poisoning 2013

Pulmonary effects: An aspirin overdose can
increase pulmonary capillary permeability.

Central nervous system effects: Aspirin
poisoning causes the ionized aspirin to be
converted into a non-ionized form. This
allows the aspirin molecules to pass through
tissue membranes, specifically the brain and
other CNS tissue.

Otic effects: Aspirin causes increases
pressure in the inner ear and may affect
nerve transmission in the ear.

Gastrointestinal: Aspirin is directly irritating
to the gut.
It’s clear then that aspirin poisoning affects multiple body systems in complex ways that
are not easy to understand and remember. However, a basic knowledge of these
mechanisms is necessary to understand the clinical effects of aspirin toxicity.
Instant feedback: Aspirin can interrupt the Krebs cycle and oxidative phosphorylation.
What acid-base disturbance can occur as a result?
Answer: Metabolic acidosis.
Instant feedback: Patients who have taken an overdose of aspirin can be dehydrated.
Why?
Answer: Aspirin causes nausea and vomiting and fluid intake is decreased because of
the nausea. The Krebs cycle and oxidative phosphorylation are interrupted, decreasing
the amount of ATP that is produced, so the body’s metabolic rate is increased to
produce more ATP and excess heat is produced. Also, tachypnea can increase water
loss.
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Aspirin Poisoning 2013
Clinical Effects of Aspirin Poisoning
There are a myriad of clinical effects that can be seen in aspirin poisoning, but
remember that not all of them will be present, they can take time to develop and their
presentation, at times, can be subtle and difficult to detect.

Acid-base disturbances, respiratory
alkalosis: Stimulation of the respiratory
center causes hyperventilation and a
respiratory alkalosis. This usually occurs
early, within several hours of the
overdose. In most cases, it isn’t clinically
important, but if it lasts for a long time,
pulmonary “fatigue” is possible.

Acid-base disturbances, metabolic acidosis: Interruption of the Krebs cycle and
oxidative phosphorylation causes a buildup of lactic and pyruvic acid and a
metabolic acidosis. Also, because these methods of ATP production are
blocked and the body is using fats for energy, ketones are produced and these
are another source of acids. Metabolic acidosis generally develops after the
respiratory alkalosis, but in severe cases it may occur soon after the ingestion.

Metabolic effects: Fever (usually low-grade fever) is commonly seen. A high
fever is an ominous clinical sign.

Neurological effects: The acidemia caused by aspirin poisoning converts aspirin
into a non-ionized form that can leave the serum, cross the blood-brain barrier
and enter CNS tissue. Agitation, dizziness, lethargy and stupor are possible.
Coma is possible. The exact mechanism by which aspirin causes CNS
depression is not known. Neurological changes should be considered to be very
serious. They indicate that aspirin is entering the brain. Death from aspirin
poisoning is caused by coma and seizures and is preceded by central nervous
system depression.

Metabolic effects: Because of the disruption of glucose metabolism, the body
responds by mobilizing stored glucose (glycogenolysis) and by producing
glucose from fats (gluconeogenesis.) The initial effect is hyperglycemia. Later,
as the clinical course continues, glycogen stores are depleted, gluconeogenesis
cannot keep up with the body’s metabolic demands and hypoglycemia can be
seen.
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Aspirin Poisoning 2013

Pulmonary effects: An increase in pulmonary capillary permeability can cause
pulmonary edema. The exact incidence of this in aspirin poisoning is not known.

Fluid and electrolyte effects: The increased metabolic rate and the resulting
increase in body temperature, the water loss from the lungs due to
hyperventilation, and vomiting all contribute to the dehydration that is
common in aspirin poisoning. In the initial stages of poisoning, respiratory
alkalosis causes the kidneys to excrete bicarbonate,
and potassium is excreted with it. Later, when the patient becomes acidotic,
Potassium shifts from the extracellular space to the
intracellular space.

Gastrointestinal effects: Aspirin is directly irritating to
the gut and nausea and vomiting are common.
Gastrointestinal bleeding has been reported, but it is rare.

Otic effects: Tinnitus (ringing in the ears) is common.
The description above may seem to indicate that patients’ aspirin poisoning will be
profoundly and obviously sick – and occasionally that is true. But for every aspirin
poisoned patient that is stuporous, hyperventilating, diaphoretic and febrile, there are
many more that are slightly drowsy, afebrile and just a bit nauseous. A patient with an
aspirin overdose must be frequently and carefully assessed, and even “mild” changes in
acid-base status and neurological status must be treated with great caution.
Instant feedback: You are caring for a patient with an aspirin overdose. Their
respiratory rate is 32. Why are they tachypneic?
Answer: There are three possible reasons: (1) aspirin stimulates the respiratory center,
(2) the patient has a metabolic acidosis and is trying to compensate by excreting carbon
dioxide, and (3) aspirin increases pulmonary capillary permeability and can cause
pulmonary edema.
Instant feedback: You are caring for a patient with an aspirin overdose and over a
period of hours, the patient has become increasingly drowsy. Why is this happening?
Answer: Aspirin poisoning can cause metabolic acidosis. As the serum pH decreases,
aspirin is converted from an ionized to a non-ionized form. The non-ionized form is able
to cross cell membranes, and because there is a high amount of aspirin in the serum and
a low amount in the CNS tissue, the aspirin will move (to establish an equilibrium) from
the serum to the CNS tissue and cause drowsiness.
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Aspirin Poisoning 2013
Nursing Care of the Patient with an Aspirin Overdose
Good nursing care of the patient with an aspirin overdose is absolutely critical. These
patients have the potential to become very sick and die, and as mentioned earlier, the
clinical presentation can be subtle, even in patients that are very ill. Nurses must
understand the pathophysiology of aspirin overdose, they must know the signs and
symptoms of aspirin overdose, understand why these happen, and they must perform
appropriate, frequent and careful assessments; this cannot be stressed enough. The
following is an assessment checklist that can be used. How often these assessments be
done depends on the patient’s clinical condition and the serum salicylate levels.

Neurological: Neurological assessments should initially be done every two hours.
Orientation to time, place and person should be evaluated. Check the patient
carefully for any signs of central nervous system depression and if they are
present, report these to the physician immediately. Remember, these are
indicators that aspirin is entering the brain and CNS tissue.

Acid-base: Obtain arterial blood gases and electrolytes as needed to check for
acidosis and an anion gap. Remember, aspirin is normally present in large
amounts in the serum and very little crosses the blood-brain barrier. When the
patient develops an acidosis the aspirin is changed to a non-ionized form that
can enter CNS tissue. The lower the serum pH, the more aspirin will enter the
brain. Frequent assessment of the acid-base status is crucial

Pulmonary: The rate and depth of the patient’s respirations must be carefully
checked, every hour, if the patient is very sick. You must auscultate the lungs to
look for pulmonary edema, and perform pulse oximetry as needed to check
oxygen saturation.

Vital signs: The patient’s temperature must be checked regularly and fever
should be reported to the physician.

Serum glucose: Hyperglycemia can be present initially. In the later stages of the
poisoning the patient can become hypoglycemic. Check the glucose frequently.

Serum potassium: The patient should be monitored for hypokalemia.

Urine output/urine pH: A good hourly urine output is essential for the patient
with an aspirin overdose, and the urine pH must be maintained at 7.5 or greater
(this will be explained in the treatment section).
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Instant feedback: You are caring for a patient with an aspirin overdose. You need to
assess the patient’s neurologic, pulmonary and acid-base status. How often should this
assessment be performed?
Answer: There is no definite answer to this
question. It is more important to know that the
frequency of the assessment should depend on the
patient’s salicylate level and their clinical status at
any given time. The higher the level and the more
symptomatic the patient is, the more frequently the
assessment should be performed. Patients with
high serum salicylate levels who are acidotic and
drowsy should be assessed every hour.
Instant feedback: You are caring for a patient with an aspirin overdose and over the
past few hours the patient has become increasingly drowsy. Is this important, and if so,
why? What should you do in this situation?
Answer: CNS depression indicates that aspirin is concentrating in the brain, and death
from aspirin poisoning is caused by CNS depression and intractable seizures. Any signs
of CNS depression should be reported immediately to the physician.
Treatment of the patient with an aspirin overdose
The goal of treatment of the patient with
an aspirin overdose is to prevent the aspirin
from moving from the serum into the brain
and CNS tissue. Patients who die from an
aspirin overdose die from coma and
intractable seizures.
ABCs
When assessing the ABCs (airway, breathing, circulation) in a patient with aspirin
poisoning, pay close attention to the respiratory rate. Tachypnea indicates either the
beginning stage of aspirin poisoning (respiratory alkalosis) or the late stage (metabolic
acidosis.), or pulmonary edema. Unless the patient is comatose, there should be no
issues of a patent airway. Tachycardia is possible. Hypotension is possible but it is
unusual.
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Gastric decontamination
Gastric decontamination refers to efforts made to prevent absorption of a drug or a
toxic material. There are five basic methods of gastric decontamination:

syrup of ipecac

activated charcoal

gastric lavage

whole bowel irrigation

cathartics
Each has benefits and risks, and a discussion
of those is beyond the scope of this article.
The current consensus is that activated charcoal is the best method of gastric
decontamination for an aspirin overdose. Activated charcoal acts by adsorbing drug
molecules to its surface. The charcoal-drug complex is very stable and is (1) excreted in
the stool, (2) taken up by macrophages, (3) or dissociates slowly enough so that the
amount of drug released and the rate at which it is released are not toxic. Activated
charcoal is most effective if a patient presents 1 to 2 hours after ingestion. However, in
cases of aspirin overdose, this can be extended to 4 hours after the ingestion. Aspirin
can cause pylorospasm and bezoars are possible (especially if an enteric-coated product
was ingested), so there may be aspirin in the stomach for hours after the ingestion.
Activated charcoal is typically packaged in 50 gram bottles, and this amount is sufficient
for almost all cases of aspirin poisoning.
Instant feedback: Should a patient that has taken an
aspirin overdose be lavaged? Should they receive
multiple doses of activated charcoal?
Answer: Lavage is reserved for patients who have
taken a large amount of a dangerous drug (eg,
verapamil) and present to the hospital within an
hour of the ingestion. The consensus of practicing
clinical toxicologists is that multiple doses of
activated charcoal are not useful for treating aspirin
overdose.
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Laboratory
The basic laboratory tests needed are
salicylate level, acetaminophen level,
electrolytes, BUN, creatinine, glucose
and arterial blood gas. These tests will
tell you how high the salicylate level is,
whether or not the patient ingested
acetaminophen as well (it’s not uncommon
for people to confuse one for the other),
if they have an anion gap, if they have normal renal function (this is important to know;
the reasons will be covered later), if they are alkalotic or acidotic, and if they are
hyperglycemic or hypoglycemic. The salicylate level, electrolytes and arterial blood gas
should be repeated; how often to repeat these tests and the amount of time between
repeats will depend on the patient’s clinical status and the results of the previous tests.
A salicylate level of > 30 mg/dL indicates the need for treatment. A level > 100 mg/dL in
an acute ingestion or > 60 mg/dL in a chronic ingestion is considered an emergency.
Note: Normally, peak serum salicylate levels are seen at six hours post-ingestion.
However, after an acute overdose it is not uncommon for the peak level to occur eight,
12 or even 16 hours post-ingestion. Also, salicylate levels can go down – giving the
impression that the patient is not in danger - and then rise. When monitoring salicylate
levels, it is crucial to obtain at least three levels to make sure that the level is going
down.
Alkalinization
Alkalinization of the urine is one of the
mainstays of treatment for salicylate
poisoning. Gastric decontamination with
activated charcoal may be useful, but it
cannot always be depended on to absorb
a significant amount of ingested drug.
Raising the pH of the urine increases the
renal excretion of salicylates, and it is
important to understand how this works.
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Salicylic acid is a weak acid. In an alkaline solution, it will ionize and ionized molecules
do not easily cross cell membranes. As pH increases, the degree of ionization increases
and urinary alkalinization takes advantage of this fact. Sodium bicarbonate is given IV,
raising the serum pH. Aspirin in the serum becomes ionized and will not cross the
blood-brain barrier. In addition, as the blood is filtered through the kidneys into the
kidney tubules, the ionized salicylic acid
cannot be reabsorbed so it is excreted in
the urine. Keeping the urine pH > 7.5 will
dramatically increase the renal excretion
of aspirin, and keep aspirin from entering
the brain and CNS tissue. Also, as serum
levels fall, aspirin will move out of the brain
to establish equilibrium.
Note: This is one the common ways of
administering sodium bicarbonate to a
patient with an aspirin overdose. You may read about others; the exact method of
alkalinization is less important than achieving the goal of the therapy.
Put 50-100 mEq of sodium bicarbonate into a liter of 5% dextrose/0.25% normal saline.
Infuse at 2-3 mL/kg/h. Maintain the urine pH at 7.5 or higher.
Hemodialysis
Gastric decontamination and urinary alkalinization may
not be sufficient treatment for some cases of aspirin
overdose, and hemodialysis is the third method of
treatment. It is used if the serum salicylate level is >
100 mg/dL in an acute overdose or > 60 mg/dL in a
chronic overdose. Dialysis should also be considered if
the patient is acidotic and has a large anion gap or has
significant CNS depression.
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Summary
Aspirin is a common non-steroidal anti-inflammatory. It is effective as an analgesic, as
an anti-inflammatory, and as an antipyretic. It is also used prophylactically for patients
at risk for developing coronary thrombi. The popularity of aspirin has decreased
because of its association with Reye’s syndrome in children and because of the
development of newer, non-steroidal anti-inflammatory drugs. However, it is still
commonly used. Aspirin is found in a variety of over-the-counter products, alone or in
combination with other drugs. Examples include Excedrin, Pepto-Bismol, Alka-Seltzer,
Aspergum, etc.
When aspirin is taken in toxic amounts, absorption is delayed, the time to peak serum
level is significantly delayed, there’s more free, circulating aspirin that can enter the
tissues, and elimination depends on kidney function and urine pH.
Aspirin is a “multi-system” poison and it has many complicated effects. Clinical effects
include hyperventilation and respiratory alkalosis, metabolic acidosis, and low-grade
fever. Agitation, dizziness, lethargy and stupor as well as coma are possible. Initially
hyperglycemia is evident and later after glycogen stores are depleted, hypoglycemia can
be seen. Nausea and vomiting are common as is ringing in the ears.
Good nursing care of the patient with aspirin
poisoning is absolutely critical. There is a
potential for the patient to become very ill and
die. The clinical presentation can be very subtle,
even in patients that are very ill. Performing
appropriate, frequent, and careful assessments
cannot be stressed enough.
The goal of treatment is to prevent the aspirin
from moving from the serum into the brain and
CNS tissue. Gastric decontamination using
activated charcoal is thought to be the best
method for preventing the absorption of aspirin.
Laboratory tests are done to determine how high
the salicylate level is. This in turn indicates the
need for treatment. Also alkalinization of the urine
is one of the mainstays of treatment for salicylate
poisoning. Raising the pH of the urine increases
the renal excretion of salicylates. Finally, dialysis may be considered if the patient is
acidotic and has a large anion gap or has significant CNS depression.
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Aspirin Poisoning 2013
Suggested Reading
Flomenbaum, N.E. (2002). Salicylates. In: Goldfrank, L.R., Flomenbaum, N.E., Lewin,
N.A., Howland, M.A., Hoffman, R.S., Nelson, L.S., eds. Goldfranks’s Toxicologic
Emergencies. 7th ed. New York: McGraw-Hill; 2002:507-527.
Krenzelok, E.P., Kerr, F., Proudfoot, A.T. Salicylate Toxicity. In: Haddad, L.M., Shannon,
M.W., Winchester, J.F., eds. Clinical Management of Poisoning and Drug Overdose. 3rd
ed. Philadelphia: W.B. Saunders; 1998:675-686.
Kim, S.K. Salicylates. In: Olson, K.R., Anderson, I.B., Benowitz, N.L., Blanc, P.D., Clark,
R.F., Kearney, T.E., Osterloh, J.D., eds. Poisoning and Drug Overdose. 3rd edition.
Stamford, Conn: Appleton & Lange; 1999:284-286.
Bibliography
1. AJEM Vol 21, No. 5, September 2003, p 403, p 373-374, Watson, Williams, et al
2002 annual report of the AAPCC toxic exposure surveillance system.
2. Brunton, L.L., Lazo, J.S., Parker, K.L., Buxton, I.L.O., Blumenthal, D., eds.
Goodman & Gilman’s The Pharmacological Basis of Therapeutics, 11th ed. New
York: McGraw-Hill; 2006.
3. Haddad, L.M., Shannon, M.W., Winchester, J.F., eds. Clinical Management of
Poisoning and Drug Overdose. 3rd ed. Philadelphia: W.B. Saunders; 2008.
4. Goldfrank, L.R., Flomenbaum, N.E., Lewin, N.A., Howland, M.A., Hoffman, R.S.,
Nelson, L.S., eds. Goldfranks’s Toxicologic Emergencies. 7th ed. New York:
McGraw-Hill; 2002.
5. Dart, R.C. ed. Medical Toxicology, 3rd ed. Lippincott Williams & Wilkins: 2003.
6. Aspirin Poisoning, accessed April 2010.
http://en.wikipedia.org/wiki/Aspirin_poisoning.
7. Aspirin Poisoning Symptoms, accessed April 2010.
http://www.emedicinehealth.com/aspirin_poisoning/page3_em.htm
8. Aspirin and Other Salicylate Poisonings, accessed April 2010.
http://www.merck.com/mmpe/sec21/ch326/ch326d.html
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