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Toxicity, Salicylate: Treatment & Medication

Author: Lance W Kreplick, MD, MMM, FAAEM, FACEP, Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC
Contributor Information and Disclosures

Updated: Jul 11, 2008

Treatment

Prehospital Care

  • Stabilize the airway, breathing, and circulation.

Emergency Department Care

Therapeutic objectives include cardiopulmonary stabilization, prevention of absorption, correction of fluid deficits, correction of acid-base abnormalities, and enhancement of excretion and elimination.

  • Endotracheal intubation may be required for several reasons.
    • Ventilatory support in patients with severe hypoxemia from aspirin-induced pulmonary edema
    • Maintenance of hyperventilation (as compensation for metabolic acidosis)
    • Protection of patients who are too agitated and delirious for central line placement, hemodialysis, and other necessary medical procedures without therapeutic sedation
    • Protection of the airway against aspiration during lavage or activated charcoal administration or in obtunded patients who cannot protect their own airway.
  • Large-bore vascular access catheters may be required to facilitate emergent hemodialysis.
  • Methods to prevent absorption involve emesis, gastric lavage, multidose activated charcoal, and cathartics.
    • The use of ipecac syrup is controversial and many studies indicate that it does not alter clinical outcome. It is most effective if given within 30 minutes of ingestion; however, it is relatively contraindicated in the presence of a severe aspirin ingestion because of the risk of seizures from aspirin.
    • Gastric lavage may be beneficial, unless contraindicated, up to 60 minutes after salicylate ingestion. Warmed (38°C) isotonic sodium chloride solution may be used. Protect the airway before gastric lavage.
    • Administer activated charcoal unless contraindications are present. Current literature does not support the administration of multidose activated charcoal. A cathartic agent may be given with the first charcoal dose; however, repeat cathartic dosing generally should be avoided because of concern over resultant electrolyte imbalances.
  • Provide treatment for correction of fluid deficits and enhancement of excretion and elimination
    • Administer lactated Ringer or isotonic sodium chloride solution for volume expansion at 10-20 cc/kg/h until a 1-1.5-cc/kg/h urine flow is established.
    • Provide maintenance fluids to maintain urinary alkalinization.
    • Forced diuresis is not recommended.
    • The greater the urine flow, the more difficult it is to alkalinize the urine.
    • Be cautious of excessive fluid volumes in cases of salicylate-induced pulmonary edema.
  • Perform urinary alkalinization for symptomatic patients and patients with rising salicylate levels or acid-base abnormalities. Consider this treatment if the salicylate level is higher than 35 mg/dL.
    • One method to initiate urinary alkalinization uses a single IV bolus of NaHCO 3 at 1-2 mEq/kg. Follow this with a constant infusion of D5W with NaHCO 3 100-150 mEq/L and KCl 20-40 mEq/L at 1.5-2.5 mL/kg/h to produce a urine flow of 0.5-1 mL/kg/h. Closely monitor the serum electrolytes and urine pH, and maintain the urinary pH between 7.5-8.
    • The urinary excretion of salicylic acid is dependent upon hydrogen ion gradients, which are, in turn, dependent on adequate serum potassium. Alkaline urine facilitates salicylate ion trapping and excretion but can only be accomplished if adequate potassium is present.
  • Monitor glucose levels closely. Initial hyperglycemia may give way to hypoglycemia and worsening CNS symptoms. Tissue glucose levels may be lower than plasma glucose levels.

Consultations

Consult with the regional poison control center or a local medical toxicologist for additional information and patient care recommendations. Consultation with nephrology department personnel is required if hemodialysis is indicated. This decision should be made in conjunction with the medical toxicologist.

  • Hemodialysis is the best method for enhanced elimination. Advantages of hemodialysis are increased salicylate clearance, correction of acid-base disturbances, and correction of fluid and electrolyte abnormalities.
  • Recommendations for hemodialysis include the following:
    • Severe manifestations of intoxication (eg, persistent neurological symptoms, pulmonary edema, renal failure)
    • Refractory or profound acidosis (ie, progressive deterioration despite conservative efforts)
    • Serum levels higher than 100 mg/dL after acute overdose or serum levels higher than 40-50 mg/dL in chronic salicylism

Medication

Drug therapy includes activated charcoal, sodium bicarbonate, and polyethylene glycol solution.

GI decontaminants

Limits absorption of ingested substance.


Activated charcoal (Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.
For maximum effect, administer within 30 min of ingesting poison.

Adult

1 g/kg PO; may repeat in 2-4 h at one-half original dose

Pediatric

Administer as in adults (typical 12.5-25 g)
<2 years: Cathartic not recommended

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix with sherbet, milk, or ice cream (decreases adsorption)

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administration; after emesis with ipecac syrup, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; protect airway in patients with depressed level of consciousness; if using multiple dose charcoal, monitor for presence of bowel sounds to minimize risk of charcoal ileus and vomiting with subsequent pulmonary aspiration


Polyethylene glycol (GoLYTELY, Colyte)

Laxative with strong electrolyte and osmotic effects that has cathartic actions in GI tract. Consider whole bowel irrigation when sustained-release products are involved. Remember that this agent does not adsorb anything but merely pushes things through the GI tract at a faster rate.

Adult

2 L/h PO/NG

Pediatric

20 mL/kg/h PO/NG

Reduces effectiveness and absorption of oral medications

Documented hypersensitivity; colitis, megacolon, bowel perforation, gastric retention or GI obstruction; unprotected airway

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in ulcerative colitis, hot loop polypectomy; caution in obtunded, comatose, or seizing patients

Alkalinizing agent

Alkalinization of the urine enhances elimination of salicylates through ion trapping in the renal tubules.


Sodium bicarbonate (Neut)

Alkalinizes urine, causing excretion of salicylate to increase.

Adult

1-2 mEq/kg IV push, then begin infusion; add 2-3 amps (available in 44 mEq/amp and 50 mEq/amp) of sodium bicarbonate and KCl 20-40 mEq/L in 1 L D5W; infuse at 1.5-2.5 mL/kg/h

Pediatric

Administer as in adults

Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Documented hypersensitivity; alkalosis, hypernatremia, hypocalcemia, severe pulmonary edema, and unknown abdominal pain

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Only use to treat documented metabolic acidosis and hyperkalemia-induced cardiac arrest; can cause alkalosis, decreased plasma potassium, hypocalcemia and hypernatremia (ensure serum pH does not exceed 7.55); caution in electrolyte imbalances such as CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation because can cause tissue necrosis

More on Toxicity, Salicylate

Overview: Toxicity, Salicylate
Differential Diagnoses & Workup: Toxicity, Salicylate
Treatment & Medication: Toxicity, Salicylate
Follow-up: Toxicity, Salicylate
References

References

  1. Acetylsalicylic Acid. National Library of Medicine, TOXNET, Hazardous Substances Data Bank. Available at http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~yiK5GU:1.

  2. Brenner BE, Simon RR. Management of salicylate intoxication. Drugs. Oct 1982;24(4):335-40. [Medline].

  3. Chan TY, Chan AY, Ho CS, Critchley JA. The clinical value of screening for salicylates in acute poisoning. Vet Hum Toxicol. Feb 1995;37(1):37-8. [Medline].

  4. Chapman BJ, Proudfoot AT. Adult salicylate poisoning: deaths and outcome in patients with high plasma salicylate concentrations. Q J Med. Aug 1989;72(268):699-707. [Medline].

  5. Chiaretti A, Schembri Wismayer D, Tortorolo L, et al. Salicylate intoxication using a skin ointment. Acta Paediatr. Mar 1997;86(3):330-1. [Medline].

  6. Danel V, Henry JA, Glucksman E. Activated charcoal, emesis, and gastric lavage in aspirin overdose. Br Med J (Clin Res Ed). May 28 1988;296(6635):1507. [Medline].

  7. Dargan PI, Wallace CI, Jones AL. An evidence based flowchart to guide the management of acute salicylate (aspirin) overdose. Emerg Med J. May 2002;19(3):206-9. [Medline].

  8. Done AK, Temple AR. Treatment of salicylate poisoning. Mod Treat. Aug 1971;8(3):528-51. [Medline].

  9. Dugandzic RM, Tierney MG, Dickinson GE, et al. Evaluation of the validity of the Done nomogram in the management of acute salicylate intoxication. Ann Emerg Med. Nov 1989;18(11):1186-90. [Medline].

  10. Gabow PA, Anderson RJ, Potts DE, Schrier RW. Acid-base disturbances in the salicylate-intoxicated adult. Arch Intern Med. Oct 1978;138(10):1481-4. [Medline].

  11. Gilman AG, Goodman LS, Gilman A, eds. The Pharmacological Basis of Therapeutics. 6th ed. New York: McGraw-Hill; 1980.

  12. Gittelman DK. Chronic salicylate intoxication. South Med J. Jun 1993;86(6):683-5. [Medline].

  13. Johnson D, Eppler J, Giesbrecht E, Verjee Z, Rais A, Wiggins T. Effect of multiple-dose activated charcoal on the clearance of high-dose intravenous aspirin in a porcine model. Ann Emerg Med. Nov 1995;26(5):569-74. [Medline].

  14. Krause DS, Wolf BA, Shaw LM. Acute aspirin overdose: mechanisms of toxicity. Ther Drug Monit. Dec 1992;14(6):441-51. [Medline].

  15. O'Malley GF. Emergency department management of the salicylate-poisoned patient. Emerg Med Clin North Am. May 2007;25(2):333-46; abstract viii. [Medline].

  16. Proudfoot AT. Toxicity of salicylates. Am J Med. Nov 14 1983;75(5A):99-103. [Medline].

  17. Teece S, Crawford I. Best evidence topic report. Gastric lavage in aspirin and non-steroidal anti-inflammatory drug overdose. Emerg Med J. Sep 2004;21(5):591-2. [Medline].

  18. Temple AR. Acute and chronic effects of aspirin toxicity and their treatment. Arch Intern Med. Feb 23 1981;141(3 Spec No):364-9. [Medline].

Further Reading

Keywords

aspirin overdose, aspirin, aspirin poisoning, aspirin ingestion, salicylate toxicity, salicylate ingestion, salicylate overdose, salicylate poisoning

Contributor Information and Disclosures

Author

Lance W Kreplick, MD, MMM, FAAEM, FACEP, Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC
Lance W Kreplick, MD, MMM, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives
Disclosure: Nothing to disclose.

Medical Editor

Mark S Slabinski, MD, FACEP, FAAEM, Vice President, EMP Medical Group
Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, Chair, Department of Emergency Medicine, Director of Medical Toxicology, Department of Emergency Medicine, Associate Professor, Allegheny General Hospital
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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