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salicylate poisoning


  • salicylate (eg. aspirin (acetylsalicylic acid), teething gels) poisoning has steadily declined over the past 10-15 yrs in parallel with the declining use of aspirin particularly in children, and the use of child resistant packaging. However, parents should still be warned of the potentially lethal dangers of aspirin.


  • for single dose, non-enteric coated acute salicylate ingestions:
    • <150mg/kg ⇒ none or mild toxicity
    • 150-300mg/kg ⇒ mild-mod toxicity
    • 300-500mg/kg ⇒ serious toxicity
    • >500mg/kg ⇒ potentially lethal toxicity
  • As repeated doses may cause accumulation, particularly in infants, aspirin should not be given at all to children under 1 yr old.
  • Aspirin is rapidly absorbed from GIT ( peak levels 2-4 hrs), but in OD, tends to form concretions in GIT which are absorbed slowly over many hours.
  • Factors affecting absorption rate, and hence the timing of peak serum levels, are:
    • formulation: effervescent > buffered preparation (salts formed at disintegration aid absorption) > enteric-coated (peak 4-6 hrs),
    • gastric emptying
    • stomach ph
    • stomach contents
    • concurrent ingestions
  • Aspirin (acetylsalicylate, pka 3.5) is quickly hydrolysed to salicylic acid (pka 3.0) which is further metabolised by enzymes that are readily saturable and thus in OD the metabolites are eliminated slowly;


  • Toxic effects are complex and include:
    • acid-base disturbances
      • severe metabolic (ketolactic) acidosis with compensatory respiratory alkalosis
      • paradoxical aciduria with the depletion of sodium bicarbonate and potassium.
      • respiratory alkalosis with a compensatory (high anion gap) metabolic acidosis defines the next stage in moderate-to-severe intoxication.
    • tachypnoea secondary to direct stimulation of the respiratory centre generates respiratory alkalosis; respiraory acidosis may intervene with severe intoxication due to either CNS depression, pulmonary oedema, or effects of coingestants,
    • uncoupling of oxidative phosphorylation with inhibition of production of high energy phosphates;
    • disordered glucose metabolism;
    • paradoxical CSF hypoglycaemia

clinical features

  • Symptoms and signs may not become apparent for many hours;
  • There may be:
    • nausea, vomiting, abdominal pain, tinnitus, deafness;
    • excitability, tremor, sweating, flushed skin;
    • hyperventilation, disturbed consciousness, coma;
    • initial resp.alkalosis then metabolic acidosis;
    • dehydration;
    • Less commonly:
      • fever, hypoprothrombinaemia, hypoglycaemia;
      • pulmonary oedema, renal failure, hepatotoxicity;


  • avoid sedatives and delay intubation if possible
  • failure to maintain adequate hyperventilation and serum alkalosis in potentially lethal overdoses by giving sedatives or performing intubation without hyperventilation may result in cardiac arrest due to acidosis allowing redistribution of salicylate into CSF! If possible commence haemodialysis PRIOR to intubation
  • consider single dose activated charcoal if possible toxic dose in previous 60 minutes;
  • Take blood for initial salicylate level, U&E, FBE, Glucose, LFT's, serum paracetamol, APPT, and ABG's;
  • plasma salicylate levels:
    • serum levels determined less than 6 hours postingestion (acute overdose) do not rule out impending toxicity because salicylates are in the absorption-distribution phase.
    • in cases of chronic salicylism, measured toxic levels may be only 300-400 mg/L.
    • for single acute ingestions > 6hrs post-ingestion:
      • moderate toxicity: 300 - 750 mg/L;
      • potentially lethal: >750 mg/L;
      • serious poisoning:
        • >800 mg/L after rehydration;
        • >1000 mg/L before rehydration;
  • IV line and fluid replacement if dehydrated or needs correction of hypokalaemia or hypoglycaemia
    • aim for urine output of 1-1.5ml/kg/hr
    • consider urinary alkalinisation if rising salicylate levels above 350mg/L or acid-base disturbance:
      • sodium bicarbonate 1-2mEq/kg iv bolus, then
      • 5% dextrose + 100mEq/L sodium bicarbonate + KCl 30mEq/L at 1.5-2.5ml/kg/hr to give urine output 0.5-1.0ml/kg/hr, aiming for a urinary pH of 7.5-8.
      • closely monitor blood gases and urinary pH.
  • early haemodialysis if:
    • massive ingestion > 500mg/kg
    • likely to need intubation as altered mental state or seizures
    • severe acidaemia with pH < 7.3
    • end-organ damage - ARF, APO
    • rapidly rising salicylate level or clinical deterioration despite optimal treatment
    • serum salicylate > 5.8 mmol/L (80mg/dL)
  • If initial plasma level < 300 mg/L, a repeat level should be done in further 4-6 hours and if this level is lower than the first then the patient may be considered for discharge otherwise admission for further observation and management is indicated.
  • vitamin K may be necessary;
  • forced alkaline diuresis is NOT currently recommended because:
    • inadequately monitored use may cause hypokalaemia and pulm. oedema
    • it is not the rate of urine flow that is important in optimising salicylate excretion but rather a urine pH of between 8 and 8.5.
    • the greater the urine flow, the more difficult it is to make it alkaline.
    • Most other NSAID's are less toxic than aspirin in OD but some notable exceptions are:
      • benorylate(not Aust.) : paracetamol poisoning as well;
      • mefenamic acid (Ponstan): convulsions;
      • phenylbutazone, oxyphenbutazone :
        • haematemesis, coma, convulsions, renal & liver failure;


  • admit if either:
    • major signs of toxicity (preferably to an ICU)
    • minor signs (eg. tinnitus, nausea) - possibly to an ED observational unit
    • infants and elderly regardless of serum levels
    • those with chronic salicylism
    • ingestions of sustained release preparations
  • potentially discharge other patients with 24hr review by LMO if:
    • ingestion < 150mg/kg, and asymptomatic 6 hours after ingestion, and,
    • issues of self-harm are adequately addressed.
odsalicylates.txt · Last modified: 2012/06/27 15:57 by

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