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Salicylate Poisoning

para>Increased risk for chronic toxicity because of decreased renal function
  • Increased risk for bleeding or perforated gastric ulcers in patients >70 years of age

  • � �
    Pediatric Considerations

    Acidosis is often more severe in the very young, particularly in chronic or repeated therapeutic-dose poisonings.

    � �
    Pregnancy Considerations
    • Salicylates may cause premature closure of ductus arteriosus in the fetus.

    • Increased risk of ante- and intrapartum hemorrhage

    � �

    EPIDEMIOLOGY


    Incidence/prevalence in the United States � �
    • >11,100 single-substance ingestions of acetylsalicylic acid or ASA combination products reported by poison control centers in 2011.
    • 22 deaths in 2011, none in children <6 years of age
    • Occurs in children and adults at any age

    ETIOLOGY AND PATHOPHYSIOLOGY


    • Accidental or intentional ingestion of salicylates or salicylate-containing medications (bismuth subsalicylate)
    • Percutaneous absorption of dermatologic medications containing salicylate (such as oil of wintergreen)
    • Breastfeeding by mothers ingesting salicylate-containing medications
    • Teething gels containing salicylates

    RISK FACTORS


    • Dehydration
    • Conditions causing metabolic or respiratory acidosis
    • Extremes of age " �very young and elderly
    • Psychiatric illness
    • History of previous toxic ingestions or suicide attempts
    • Concurrent oral poisoning with other substances
    • Concurrent use of acetazolamide (Diamox)
    • Compromised skin: burns, psoriasis

    GENERAL PREVENTION


    • Patient and parent/caregiver education essential; see "Patient Education " �
    • Emergency telephone numbers (poison control centers): (800) 222 " �1222 (American Association of Poison Control Centers)

    COMMONLY ASSOCIATED CONDITIONS


    • Reye syndrome with salicylate use and varicella or influenza viral infection
    • Bezoars
    • Iatrogenic salicylate toxicity noted in 6 out of 143 children with malaria in Kenya.

    DIAGNOSIS


    PHYSICAL EXAM


    • Signs and symptoms may differ when the intoxication is acute or chronic.
    • Acute intoxication (adults) (1)[C]
      • Symptoms vary with amount ingested, usually begin within 4 to 8 hours of ingestion. Enteric-coated aspirin ingestion may not show systemic symptoms for up to 12 hours. In general, children and elderly will exhibit symptoms more rapidly.
        • 30 to 60 mg/dL mild toxicity
        • 60 to 80 mg/dL moderate toxicity
        • >80 mg/dL severe toxicity
      • Mild toxicity can present with lethargy, nausea, vomiting, and tinnitus.
      • Moderate toxicity can also include tachypnea, fever, sweating, restlessness, and impaired coordination.
      • Severe toxicity notes hypotension, renal failure, metabolic acidosis, and CNS manifestations including hallucinations, stupor, seizures, and coma.
    • Chronic intoxication
      • Onset of symptoms is usually gradual.
      • Signs and symptoms similar to acute intoxication may occur and may be advanced at diagnosis and include severe hypotension and ARDS.
      • Neurologic symptoms often predominate, particularly in the elderly; they include agitation, confusion, stupor, hyperactivity, paranoia, bizarre behavior, dysarthria, and restlessness.

    DIFFERENTIAL DIAGNOSIS


    • All ages
      • Infection
      • Sepsis
      • Diabetic ketoacidosis
      • Other causes of metabolic acidosis
    • In the elderly
      • Delirium
      • Cerebral vascular accident
      • Myocardial infarction
      • Ethyl alcohol intoxication
      • Congestive heart failure

    DIAGNOSTIC TESTS & INTERPRETATION


    Initial Tests (lab, imaging)
    • Serum salicylate levels initially and ≥6 hours after ingestion; then repeat q2h until the levels are declining and patient 's condition has stabilized.
    • Levels are unreliable in chronic toxicity. Acidosis is considered an emergency regardless of the level.
    • Electrolytes, BUN, creatinine, glucose, LFTs, uric acid
    • Arterial blood gases
    • Lactic acid
    • PT/INR
    • Urinalysis: urine pH
    • Stool guaiac testing may be positive.
    • Chest radiograph
      • Noncardiogenic pulmonary edema
      • Variable severity, from mild to ARDS
    • Abdominal plain film: nonspecific bowel gas pattern with retained contrast material in chronic bismuth subsalicylate ingestion
    • Head CT if there are clinical signs of cerebral edema

    Diagnostic Procedures/Other
    None, other than correlating serum salicylate concentration with clinical presentation � �
    • Use of the Done nomogram in managing patients is not recommended.

    Test Interpretation
    • Acid " �base abnormalities common
      • Usually respiratory alkalosis or mixed respiratory alkalosis and metabolic acidosis
      • Metabolic acidosis often predominates in chronic or severe acute poisonings and in poisonings in young children.
    • Increased anion gap, especially in acute poisonings and salicylate-only poisonings
    • Initial hyperglycemia may be followed by hypoglycemia.
    • Electrolyte abnormalities, such as hypernatremia or hyponatremia and hypokalemia, are common.
    • Dehydration findings are common, including an increased BUN: creatinine ratio.
    • Prothrombin time (PT)/international normalization ratio (INR) may be increased.
    • Liver function abnormalities may be present.
    • Proteinuria and renal function abnormalities may be present.
    • Stool guaiac testing may be positive.
    • Occasional hypouricemia
    • Drugs that may alter lab results
      • Diflunisal (Dolobid) may cross-react with assay of salicylate concentration.
      • Medications affecting similar organ systems, including oral anticoagulants and hypoglycemic agents
    • Disorders that may alter lab results: concurrent medical conditions involving similar organ systems

    Other findings � �
    • GI
      • Antral and prepyloric ulcers
      • Small bowel ulcerations with enteric-coated salicylates
    • Renal
      • Interstitial nephritis
      • Acute tubular necrosis
      • Minimal change nephrotic syndrome
    • Pulmonary
      • Noncardiogenic pulmonary edema

    TREATMENT


    MEDICATION


    • Prevent further absorption if the ingestion is felt to be life-threatening.
      • Activated charcoal may be given within 1 hour of toxic ingestion (immediately after gastric lavage if performed) (2,3)[C].
      • Gastric lavage is rarely indicated.
      • Ipecac is no longer recommended for use at home or in health care facilities (4)[C].
    • Emergency facility/hospital
      • Activated charcoal 1 g/kg, single dose, within 1 hour of toxic ingestion (up to maximum 50 g in children, 100 g in adults)
      • Fluid/electrolyte balance: IV fluids to restore intravascular volume and prevent hypoglycemia
      • With hypotension, give isotonic fluid until orthostatic changes are no longer present.
      • Fluids should contain ≥5% dextrose unless hyperglycemia is a problem.
      • Normal saline or a mixture of 0.45% NaCl with 1 ampule of sodium bicarbonate (43 mEq NaHCO3) may be administered at 10 to 15 mL/kg/hr for 1 to 2 hours, depending on the degree of acidosis.
      • When blood pressure is stable, fluid management is directed toward alkalinizing the urine to enhance salicylate excretion, preventing CNS hypoglycemia, and treating fluid and electrolyte abnormalities.
      • Enhance elimination by alkaline diuresis (5)[C]
        • Alkaline diuresis (urine pH >7.5) and prevention of hypoglycemia usually can be accomplished by initial bolus of NaHCO3 1 mEq/kg IV given over 1 hour, followed by infusion of 1,000 mL D5W plus 3 ampules of NaHCO3 (44 mEq NaHCO3/ampule) at 1.5 to 2 times maintenance rate (or, at 2 to 3 mL/kg/hr). Consider adding 40 mEq of potassium chloride to each liter; monitor potassium levels closely.
        • Goal: bicarbonate to alkalinize the urine (pH >7.5) and, when appropriate, to correct severe systemic acidosis (for pH <7.1)
        • Potassium should be added for potassium levels <4 mEq/L.
        • Patients with cardiovascular compromise should be monitored closely for fluid overload.
        • Alkalinization can be discontinued when the salicylate level decreases into the therapeutic range (<30 mg/dL)
      • Serum electrolytes and glucose should be monitored frequently and urine pH checked hourly until stable at >7.5. Arterial blood gases should be monitored every 2 to 4 hours to ensure blood pH ≤7.5.
      • Intermitted hemodialysis (with IV bicarbonate therapy between session) (6)[A] should be considered in poisonings with markedly elevated salicylate levels (>100 mg/dL in acute poisonings, >60 mg/dL in chronic poisonings), acidosis unresponsive to alkalinization and diuresis, renal and/or hepatic dysfunction with impaired salicylate clearance, endotracheal intubation (excluding for coingestants), noncardiac pulmonary edema, and new altered mental status.
      • Dextrose-containing IV solution to prevent hypoglycemia; CNS hypoglycemia may be present despite a normal serum glucose level.
    • Contraindications: medication allergies
    • Precautions
      • Intravascular overload may result from injudicious use of sodium bicarbonate.
      • Dextrose should not be given to patients with severe hyperglycemia.
      • Avoid utilization of acetazolamide (Diamox) to alkalinize urine, as it can worsen metabolic acidosis.
      • Caution is advised in early mechanical intubation in those with depressed mental status, due to the increased metabolic demands and respiratory rate noted in those with severe salicylate poisoning.
      • If intubation is required (e.g., development of pulmonary edema), it is recommended to hemodialyze the patient near simultaneously (7).

    ISSUES FOR REFERRAL


    • Psychiatric and psychological evaluation in emergency department and in close follow-up for intentional overdose
    • Consider referral to obstetrics for pregnant women.

    INPATIENT CONSIDERATIONS


    Admission Criteria/Initial Stabilization
    • Evaluate all patients at a health care facility.
    • Outpatient for nontoxic accidental ingestions
    • Inpatient for toxic and intentional ingestions (4)[C]

    ONGOING CARE


    FOLLOW-UP RECOMMENDATIONS


    Patient Monitoring
    • Fluid, acid " �base, blood glucose, and electrolyte status until stable; urine pH (to enhance elimination of salicylate)
    • Psychiatric follow-up after intentional ingestions

    DIET


    No special diet � �

    PATIENT EDUCATION


    • Education of parents/caregivers during well-child visits
    • Education of patients about chronic salicylate therapy
    • Anticipatory guidance for caregivers, family, and cohabitants of potentially suicidal patients
    • http://familydoctor.org/familydoctor/en/kids/home-safety/child-safety-keeping-medicines-out-of-reach.html
    • Poison control: (800) 222-1222

    PROGNOSIS


    • Complete recovery with early therapy
    • Clinical course and prognosis are worse in the very young and elderly, chronic intoxications, and in patients with concurrent conditions that cause dehydration and/or acidosis.

    COMPLICATIONS


    • Rare following recovery from poisoning
    • Noncardiogenic pulmonary edema
    • ARDS

    REFERENCES


    11 Gaudreault � �P. Activated charcoal revisited. Clin Pediatr Emerg Med.  2005;6:76 " �80.22 Heard � �K. Gastrointestinal decontamination. Med Clin North Am.  2005;89(6):1067 " �1078.33 Chyka � �PA, Erdman � �AR, Christianson � �G, et al. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila).  2007;45(2):95 " �131.44 Proudfoot � �AT, Krenzelok � �EP, Vale � �JA. Position paper on urine alkalinization. J Toxicol Clin Toxicol.  2004;42(1):1 " �26.55 Juurlink � �DN, Gosselin � �S, Kielstein � �JT, et al. Extracorporeal treatment for salicylate poisoning: systematic review and recommendations from the EXTRIP workgroup. Ann Emerg Med.  2015;66(2):165 " �181.66 Dargan � �PI, Wallace � �CI, Jones � �AL. An evidence based flowchart to guide the management of acute salicylate (aspirin) overdose. Emerg Med J.  2002;19(3):206 " �209.77 O 'Malley � �GF. Emergency department management of the salicylate-poisoned patient. Emerg Med Clin North Am.  2007;25(2):333 " �346.

    ADDITIONAL READING


    Bronstein � �AC, Spyker � �DA, Cantilena � �LRJr, et al. 2011 Annual report of the American Association of Poison Control Centers ' National Poison Data System (NPDS): 29th annual report. Clin Toxicol (Phila).  2012;50(10):911 " �1164. � �

    CODES


    ICD10


    • T39.014A Poisoning by aspirin, undetermined, initial encounter
    • E87.2 Acidosis
    • T39.011A Poisoning by aspirin, accidental (unintentional), init
    • T39.012A Poisoning by aspirin, intentional self-harm, init encntr

    ICD9


    • 965.1 Poisoning by salicylates
    • 276.2 Acidosis

    SNOMED


    • Poisoning by salicylate (disorder)
    • Metabolic acidosis due to salicylate (disorder)
    • Accidental poisoning by salicylates (disorder)
    • Intentional salicylic acid salt poisoning (disorder)

    CLINICAL PEARLS


    • Gastric decontamination should not be done in all poisonings, only in potentially life-threatening ingestions.
    • Think of salicylate toxicity with mixed metabolic acidosis and respiratory alkalosis, especially if anion gap.
    • Activated charcoal within 1 hour of toxic ingestion (immediately after gastric lavage, if performed) (2,3)[C]
    • Ipecac is no longer recommended for use at home or in health care facilities.
    • There is a bedside test to evaluate for the presence of salicylates. A few drops of 10% ferric chloride solution added to 1 mL of urine usually will produce a purple color if salicylates are present.
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