This document discusses salicylate toxicity. It begins by describing the common uses of salicylates as an analgesic, anti-inflammatory, antipyretic, and keratolytic agent. It then outlines the three phases of salicylate toxicity, describing the symptoms in each phase such as hyperventilation, hypokalemia, and metabolic acidosis. The document also covers the pathophysiology, categories of toxicity based on ingestion amount, diagnostic approach including history and physical exam findings, differential diagnosis, and treatment strategies such as gastric lavage, activated charcoal, correcting metabolic abnormalities and providing supportive care.

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3. 
 Salicylate is used as an analgesic agent for the
treatment of mild to moderate pain.
Common use of salycylate

4. 
 Analgesic
 Anti-inflammatory
 Antipyretic
 Keratolytic
 Rubifacient
Therapeutic Uses Of Salicylates

5. 

6. 
 Phase 1 of the toxicity is characterized by hyperventilation resulting
from direct respiratory center stimulation, leading to respiratory
alkalosis and compensatory alkaluria. Potassium and sodium
bicarbonate are excreted in the urine. This phase may last as long as 12
hours.
 In phase 2, paradoxic aciduria in the presence of continued respiratory
alkalosis occurs when sufficient potassium has been lost from the
kidneys. This phase may begin within hours and may last 12-24 hours.
 Phase 3 includes dehydration, hypokalemia, and progressive
metabolic acidosis. This phase may begin 4-6 hours after ingestion in a
young infant or 24 hours or more after ingestion in an adolescent or
adult.
Phases and symptoms of
salicylate toxicity

7. 
 After ingestion, acetylsalicylic acid is rapidly
converted to salicylic acid, its active moiety. Salicylic
acid is readily absorbed in the stomach and small
bowel. At therapeutic doses, salicylic acid is
metabolized by the liver and eliminated in 2-3 hours.
Pathophysiology

8. 
 Less than 150 mg/kg ingested - Spectrum ranges
from no toxicity to mild toxicity
 From 150-300 mg/kg ingested - Mild-to-moderate
toxicity
 From 301-500 mg/kg ingested - Serious toxicity
 Greater than 500 mg/kg ingested - Potentially lethal
toxicity
Categories of toxicity

9. 
 Type of salicylate
 Amount
 Approximate time of ingestion
 Possibility of long-term ingestion
 Potential co-ingestants
 Presence of other medical conditions (eg, cardiac,
renal diseases)
History

11. Based on the Serum level
 Blood level of salicylate should be measured
for at least 6 hours after acute intoxication, or
any time after chronic intoxication.
 Plasma levels should be checked every 2
hours until levels peak. Enteric coated tablets
may take more than 24 hours to be absorbed.

14. 
Physical Examination (1)
 Pulmonary:
 Hyperventilation
(common)
 Hyperpnea
 Severe dyspnea due to
noncardiogenic
pulmonary edema
 Respiratory arrest
 Apnea
 Fever and dyspnea due
to aspiration
pneumonitis
 Cardiovascular:
 Tachycardia , generally
with minimal
hemodynamic or clinical
significance
 Hypotension
 Dysrhythmias
 Asystole - With severe
intoxication
 Electrocardiogram (ECG)
abnormalities
 Sudden hemodynamic
deterioration secondary to
respiratory depression

15. 
Physical Examination (2)
 Auditory:
 Decreased hearing
 Deafness
 Tinnitus
 Neurologic:
 CNS depression, with
manifestations ranging
from somnolence and
lethargy to seizures and
coma
 Tremor
 Blurring of vision
 Seizures
 Cerebral edema - With
severe intoxication
 Encephalopathy

16. 
Physical Examination (3)
 Gastrointestinal:
 Nausea and vomiting,
with are common
 Epigastric pain
 GI hemorrhage - More
common with chronic
intoxication
 Intestinal perforation
 Pancreatitis
 Hepatitis - Generally in
chronic toxicity; rare in
acute toxicity
 Electrolytic:
 Dehydration
 Hypocalcemia
 Acidemia
 Syndrome of
inappropriate
antidiuretic hormone
secretion (SIADH)
 Hypokalemia

17. 
Differential Diagnosis
 Acute respiratory
distress syndrome
 Caffeine toxicity
 Pulmonary embolism
 Schizophrenia
 Septic shock
 Chlorine gas toxicity
 Ethylene glycol toxicity
 Hydrocarbon toxicity
 Iron toxicity
 Organophosphate and
carbamate toxicity
 Theophylline toxicity
 Withdrawal syndromes

18. 
 Principles of treatment include stabilizing the ABCs as
necessary, limiting absorption, enhancing elimination,
correcting metabolic abnormalities, and providing
supportive care. No specific antidote is available for
salicylates.
 Gastric lavage and activated charcoal are useful for acute
ingestions but not for cases of chronic salicylism.
 Patients with accidental ingestions of less than 150 mg/kg
and no signs of toxicity can be discharged 6 hours post
ingestion. Arrange a follow-up for these patients in 24
hours.
Treatment

19. 
Dermal & Eye Exposure
 Dermal exposure
 The skin should be
thoroughly washed
with soap and water;
the patient can be
observed at home.
 Eye exposure
 The eye or eyes should
be irrigated with
room-temperature tap
water for 15 minutes.
If pain, decreased
visual acuity, or
persistent irritation is
reported after
irrigation, referral to
an ophthalmologist is
recommended.

20. 
 No specific antidote for salicylate poisoning is available. Therapy is
focused on immediate resuscitation, correction of volume depletion
and metabolic derangement, GI tract decontamination, and reduction
of the body's salicylate burden. Early consultation with a medical
toxicologist is prudent.
 As previously mentioned, initial treatment should include the use of
oral activated charcoal, especially if the patient presents within 1 hour
of ingestion.
 In a study, whole bowel irrigation (WBI) with polyethylene glycol was
found to be more effective than single-dose activated charcoal in
reducing salicylate absorption. When enteric-coated aspirin has been
ingested or when salicylate levels do not decrease despite treatment
with charcoal, WBI should probably be used in addition to charcoal
therapy.
Medication

21. 
 Medscape Reference www.emedicine.medscape.com
 Departement of Medicine NYU
www.medicine.med.nyu.edu
References