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 could have participated in the ingestion. In this situation, the

children could have shared equally in the missing medication,

all of the drug could have been fed to one child, or all of the

drug could have been ingested by the oldest or most aggressive

child. When it is unclear how much is missing among a group

of children, each child should be evaluated and managed as if

he or she may have ingested the total missing quantity.

Triage of Call

CASE 4-1, QUESTION 3: M.O. has now determined that a

total of five tablets each containing 325 mg per tablet of

aspirin are missing from the bottle. Because M.O. recalls

having taken two aspirin tablets from this bottle, it is not

likely that her daughter took more than three tablets. M.O.

states that D.O. weighs 36 pounds. What treatment is

needed for this child?

The maximal dose of aspirin ingested by this child is likely to

be much less than the minimal dose required to cause significant

symptoms based on her weight for her age (i.e., 36 pounds or

approximately 16 kg). A dose of 150 mg/kg of aspirin is the smallest dose at which treatment or assessment at a health care facility

is necessary.72,75 D.O. is likely to have ingested a maximum of

975 mg of aspirin (i.e., three 325-mg tablets), which is about

60 mg/kg (975 mg divided by 16 kg). If this child is healthy, takes

no medications, and is not allergic to aspirin, the child does not

require any treatment. With this history of ingestion, the only

adverse effect that might occur is some mild nausea. Providing

information to the mother that her child had not ingested a toxic

or dangerous amount will be reassuring.

For many years, aspirin was the most common cause of unintentional poisoning and poisoning deaths among children.75–77

However, safety closure packaging and reduction of the total

aspirin content in a full bottle of children’s aspirin to approximately 3 g has steadily reduced the frequency of pediatric aspirin

poisoning and deaths.76–78 Although acute aspirin poisoning

remains a problem, the largest percentage of life-threatening

intoxications now results from therapeutic overdose.72 Therapeutic overdoses occur when a dose is given too frequently,

when both parents unknowingly dose the child with the drug, or

when too large a dose is given. Therapeutic overdoses are especially problematic when excessive doses are given for a prolonged

period and the drug is able to accumulate.72

Outcome for M.O.

Follow-up telephone consultation on toxic ingestions is important to identify children who unexpectedly develop symptoms

that might need to be treated. A telephone call to M.O. 6 to

24 hours after her initial call would be appropriate to follow up

on the child. On a call back to M.O., the parent stated that she gave

D.O. lunch at the appropriate time. D.O. then watched cartoons,

took her usual nap, and remained asymptomatic.

Acute and Chronic Salicylism

SIGNS AND SYMPTOMS

CASE 4-2

QUESTION 1: V.K., a 65-year-old, 55-kg woman with a history of chronic headaches, has taken 10 to 12 aspirin tablets

daily for several months. On the evening of admission, she

became lethargic, disoriented, and combative. Additional

history revealed that she ingested up to 100 aspirin tablets

on the morning of admission (about 10 hours earlier) in

a suicide attempt. She complained of ringing in her ears,

nausea, and three episodes of vomiting. Vital signs were

BP 140/90 mm Hg, pulse 110 beats/minute, respirations

36 breaths/minute, and temperature 102.5◦F. V.K.’s laboratory data obtained on admission were as follows:

Serum sodium (Na), 148 mEq/L

Potassium (K), 2.8 mEq/L

Chloride (Cl), 105 mEq/L

Bicarbonate, 10 mEq/L

Glucose, 60 mg/dL

Blood urea nitrogen (BUN), 35 mg/dL

Creatinine, 2.2 mg/dL

Arterial blood gas (ABG) values (room air) were as follows: pH, 7.25; PCO2, 20 mm Hg; and PO2, 95 mm Hg.

A serum salicylate concentration measured approximately

12 hours after the acute ingestion was 88 mg/dL. Her

hemoglobin was 9.6 g/dL with a hematocrit of 28.9% and a

prothrombin time (PT) of 16.4 seconds. Is V.K. at high risk

because of her ingestion?

72 Section 1 General Care

The symptoms and severity of salicylate intoxication depend

on the dose consumed; the patient’s age; and whether the ingestion was acute, chronic, or a combination of the two.77,79,80 This

case illustrates an acute ingestion in someone who has also chronically ingested aspirin. Acute ingestion of 150 to 300 mg/kg of

aspirin is likely to produce mild to moderate intoxication, greater

than 300 mg/kg indicates severe poisoning, and greater than

500 mg/kg is potentially lethal.72,75 V.K., who ingested approximately 600 mg/kg, has taken a potentially lethal dose. Chronic salicylate intoxication is usually associated with ingestion of greater

than 100 mg/kg/day for more than 2 days.72,75 V.K. has been taking

70 mg/kg/day for her headaches in addition to her acute ingestion. V.K. demonstrates many of the findings typical of severe

acute salicylism (see Pathophysiology of Salicylate Intoxication

and Assessment of Toxicity sections). V.K.’s prognosis is potentially poor because she is elderly and has taken a potentially lethal

overdose of aspirin.

Pathophysiology of Salicylate

Intoxication

CASE 4-2, QUESTION 2: Describe the pathophysiology and

clinical features of acute and chronic salicylism.

Toxicity from salicylate exposure results in direct irritation of the GI tract, direct stimulation of the CNS respiratory center, stimulation of the metabolic rate, lipid and

carbohydrate metabolism disturbances, and interference with

hemostasis.72,75,77,79,80 Toxic doses of salicylate directly stimulate the medullary respiratory center leading to nausea, vomiting, tinnitus, delirium, tachypnea, seizures, and coma, and

influence several key metabolic pathways.72,77–81 Direct stimulation of the respiratory drive increases the rate and depth

of ventilation, which can result in primary respiratory alkalosis. The respiratory alkalosis causes increased renal excretion

of bicarbonate, resulting in decreased buffering capacity. The

patient usually presents with a partially compensated respiratory alkalosis.72,78,79,81 Hypokalemia can result from increased

GI and renal losses of potassium, as well as from systemic

alkalosis.72,79,80

Although marked metabolic and neurologic abnormalities

are most commonly observed in young children with advanced

salicylate intoxication, adolescents or adults acutely poisoned

with a large dose of salicylates can exhibit these symptoms as

well.72,78,79 Acute salicylism in a young child often takes a more

severe course than that typically seen in adults. After acute ingestion, children quickly pass through the phase of pure respiratory

alkalosis. Renal bicarbonate loss secondary to respiratory alkalosis reduces the buffering capacity more profoundly in a child

and facilitates the development of metabolic acidosis.72,77,79,81

Salicylates have toxic effects on several biochemical pathways

that contribute to metabolic acidosis and other symptoms.72,79–81

Mitochondrial oxidative phosphorylation is uncoupled and

results in an impaired ability to generate high-energy phosphates, increased oxygen use and carbon dioxide production,

increased heat production and hyperpyrexia, increased tissue glycolysis, and increased peripheral demand for glucose. Salicylates

also inhibit key dehydrogenase enzymes within the Krebs cycle,

resulting in increased levels of pyruvate and lactate. The increased