WORKUP	Section 5 of 10
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Lab Studies:

• Obtain measurements of serum electrolytes, blood urea nitrogen (BUN), creatinine, calcium, magnesium, and glucose.

• Repeat these tests at least every 12 hours until the salicylate level falls and the acid-base disturbance improves. If hemodialysis is required, testing is needed more frequently.

• Monitor serum potassium concentrations; normal levels may be difficult to obtain during alkalinization therapy.

• Serum salicylate level

• If managing an acute or acute-on-chronic ingestion, repeat this test every 2 hours until the salicylate level falls.

• If the levels increase, consider the possibility that a sustained-release preparation was ingested or that a concretion in the GI tract has formed.

• In general, the Done nomogram (noted in numerous emergency medicine and toxicology textbooks) is not as useful in salicylate ingestions as other nomograms are in other ingestions. The Done nomogram has not been proven valid in the following instances:
  • Acute ingestions when other salicylates have been taken within the past 24 hours

  • Acute overdoses when salicylates have been ingested over several hours

  • Chronic salicylate ingestions

  • Ingestions of enteric-coated or sustained-release preparations

  • Renal failure patients

• Many toxicologists suggest avoiding the use of the Done nomogram. The Done nomogram assumes complete absorption by 6 hours postingestion; 6-hour postingestion levels may be correlated with the following degrees of toxicity:
  • Less than 50 mg/dL - Asymptomatic

  • 51-110 mg/dL - Mild-to-moderate toxicity

  • 110-120 mg/dL - Severe toxicity

• Serum levels determined less than 6 hours postingestion (acute overdose) do not rule out impending toxicity because salicylates are in the absorption-distribution phase. Likewise, in cases of chronic salicylism, measured toxic levels may be only 30-40 mg/d.

• Urinalysis

• Monitor and maintain an alkaline urine pH every 2 hours during alkalinization therapy.

• Maintain a urine pH of 7.5-8 (monitor the serum pH rather than the urine pH). Excessive sodium bicarbonate induces severe alkalemia and/or hypernatremia. Consider obtaining a urine specimen for a qualitative toxicology screen.

• Obtain hepatic, hematologic, and coagulation profiles for patients with clinical evidence of moderate-to-severe toxicity (eg, those that need to be admitted for inpatient care).

• Arterial blood gas

• Repeat approximately every 2 hours until metabolic acidosis improves.

• During urinary alkalinization therapy, the arterial pH should remain between 7.3 and 7.5.

Imaging Studies:

• A chest x-ray is indicated if evidence of severe intoxication, pulmonary edema, or hypoxemia is present.

• Consider an abdominal x-ray if an aspirin concretion is suspected. For better sensitivity, this should be performed before administration of activated charcoal.

• Other methods of identifying gastric salicylate pharmacobezoars include the following:

• Ultrasonography

• CT scan of the head

• Endoscopy

Other Tests:

• ECG

• The ferric chloride test and the Ames Phenistix test are sensitive but nonspecific screening tests that may be available in the ED. However, these tests are currently almost never performed because of the availability of rapid and accurate quantitative serum assays.

• If acetylsalicylic acid is present, combining 1 mL of urine and a few drops of 10% ferric chloride causes a purple color change.

• The Phenistix turns brown if salicylates are present in the urine, but this test lacks specificity.

	TREATMENT	Section 6 of 10
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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 employs a single IV bolus of NaHCO3 at 1-2 mEq/kg. Follow this with a constant infusion of D5W with NaHCO3 100-150 mEq/L and KCl 20-40 mEq/L at 1.5-2.5 cc/kg/h to produce a urine flow of 0.5-1 cc/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	Section 7 of 10
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Drug therapy includes activated charcoal, sodium bicarbonate, and polyethylene glycol solution.

	MISCELLANEOUS	Section 9 of 10
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Medical/Legal Pitfalls:

• Failure to diagnose salicylate toxicity in a patient presenting with vague signs and symptoms, such as anxiety, tachypnea, agitation, delirium, tinnitus, or a combined respiratory alkalosis and metabolic acidosis

• Failure to initiate GI decontamination in a patient with acute salicylate ingestion who, subsequently, has recurrent toxicity from a salicylate bezoar

• Failure to hyperventilate a patient with severe salicylate poisoning who has just been intubated (when acid-base status had been maintained previously by the patient's own hyperventilation) to prevent lethal acidemia

• Failure to remove any possible ingestants from a patient's access when presentation follows an intentional ingestion, such as a suicide attempt

• Failure to diagnose and treat concomitant hypoglycemia in the salicylate-intoxicated patient; more common in children than in adults

• Failure to diagnose and treat hypoxemia caused by salicylate-induced pulmonary edema

• Failure to consider co-ingestions or other diagnoses

• Failure to consider recurrent or delayed toxicity from sustained-release preparations or from an unrecognized medication bezoar