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Module 20 • Toxicology
Toxicology
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Toxicology
Kyle Weant ~3 min read Module 20 of 20
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Toxicology

Patient Case

Questions 2 and 3 pertain to the following case.

A 42-year-old woman (height 66 inches, weight 79.2 kg [176 lb]) presents to the ED with the chief concern of

flu-like symptoms. Her symptoms include headache, congestion, severe nausea and vomiting, abdominal pain,

and some confusion. She has been taking acetaminophen 500-mg caplets as needed for her symptoms, but she

just ran out of the bottle she purchased yesterday. On presentation, she is alert and oriented. Her vital signs are as

follows: BP 135/90 mm Hg, HR 83 beats/minute, RR 18 breaths/minute, and temperature 101.8°F (38.8°C). An

acetaminophen concentration on admission was 100 mcg/mL, AST 560 IU/L, and ALT 310 IU/L. The physician

wants to begin general management.

2Which general management strategy is most indicated for this patient?
A.10% magnesium citrate 240 mL per tube once
B.Continued stabilization of the patient and good supportive care
C.Gastric lavage
D.Charcoal 50 g once
3

Which is the most appropriate treatment for her acetaminophen toxicity?

A.Give acetylcysteine 11,200 mg oral bolus, followed by 5600 mg orally every 4 hours for 17 doses.
B.Give acetylcysteine 11,200 mg intravenous bolus, followed by 5600 mg intravenously every 4 hours

for 12 doses.

C.Give acetylcysteine 12,000 mg intravenously over 1 hour, followed by 4000 mg intravenously over 4

hours; then 8000 mg intravenously over 16 hours.

D.Acetylcysteine therapy is not indicated in this patient.
V.SALICYLATES
A.Background
1

Salicylates as a single agent (not in combination with other agents) accounted for 6595 overdoses and

18 deaths in 2022. These numbers, which include overdoses of both adult and pediatric formulations

of acetylsalicylic acid, are often underreported because these products are not typically recognized as

a potential cause.

2However, because of the development of child-resistant containers, aspirin overdose causing accidental
death in children has reduced drastically. (Lancet 1977;2: 289-90)
B.Clinical Presentation
1

The mechanism of toxicity for salicylates is through the interference with aerobic metabolism owing

to the uncoupling of mitochondrial oxidative phosphorylation, leading to increases in anaerobic

metabolism, which causes a significant lactic acidosis (Emerg Med Clin North Am 2007;25:333-46).

This also leads to hypoglycemia because of glycogen depletion, gluconeogenesis, and catabolism

of proteins and free fatty acids. Salicylates also directly stimulate the respiratory center, leading to

hyperventilation and respiratory alkalosis. Secondary complications from hyperventilation include

dehydration and compensatory metabolic acidosis.

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