Poisonings - salicylates
Red flags
Salicylate poisoning is a dynamic poisoning - the patient who looks stable at 4 h can be dying at 8 h.
- Altered mental state, agitation, confusion, seizure, coma - CNS salicylate penetration; the single most ominous sign
- Falling pH / loss of the compensatory respiratory alkalosis - acidaemia drives non-ionised salicylate into the CNS
- Hyperthermia - uncoupled oxidative phosphorylation; a pre-terminal sign
- Pulmonary oedema (non-cardiogenic) and hypoxia
- Salicylate level >6.5 mmol/L (90 mg/dL) acute, or >5.8 mmol/L (80 mg/dL) with renal impairment
- Rising level on serial measurement - ongoing absorption (enteric-coated, bezoar, pylorospasm)
- Any need for intubation - see Traps: peri-intubation apnoea kills these patients
- Chronic salicylism in an older person - toxic at much lower levels, often misdiagnosed as sepsis or delirium
Differential by mechanism
The metabolic signature - mixed respiratory alkalosis + high anion gap metabolic acidosis
- This combination in an unexplained unwell patient is salicylate until disproven
| Also produces both | Discriminator |
|---|---|
| Sepsis | Fever, source, lactate - and salicylate is regularly misdiagnosed as sepsis |
| Hepatic failure | LFT, encephalopathy, jaundice |
| Pregnancy + another acidosis | Context |
| Iron poisoning | Vomiting, haematemesis, radio-opaque tablets |
Causes of raised anion gap acidosis - the working list
- Lactate, ketones (DKA, alcoholic, starvation), renal failure (urate/phosphate), toxic alcohols (methanol, ethylene glycol), salicylate, metformin, isoniazid, paracetamol (5-oxoproline), cyanide, CO
Mimics of the clinical syndrome
- Sympathomimetic toxidrome (amphetamine, cocaine) - mydriasis, hypertension; salicylate has tinnitus and hyperventilation
- Serotonin syndrome / NMS / malignant hyperthermia - hyperthermia + altered mental state; clonus and rigidity absent in salicylism
- Thyroid storm - tachycardia, fever, tremor
- Theophylline toxicity - vomiting, tachyarrhythmia, hypokalaemia, seizures
- Meningitis/encephalitis, intracranial haemorrhage
- Anticholinergic toxidrome - dry, flushed, urinary retention
Focused history
- Dose, time, formulation, co-ingestants
- Enteric-coated or sustained-release aspirin -> delayed and erratic absorption; peak may be >12 h
- Oil of wintergreen (methyl salicylate) - 1 mL = ~1.4 g aspirin; a teaspoon can kill a child
- Topical keratolytics, bismuth subsalicylate, liniments
- Acute vs chronic - the key branch point
- Chronic/therapeutic excess: elderly, on regular aspirin, intercurrent illness or dehydration; presents as confusion, fever, tachypnoea, non-cardiogenic pulmonary oedema with a deceptively low level
- Toxic dose (acute): >150 mg/kg produces symptoms; >300 mg/kg severe; >500 mg/kg potentially lethal
- Symptoms: tinnitus, deafness, vertigo (early and reliable), nausea, vomiting, sweating, hyperventilation
- Renal function, volume status, diuretic use
Focused examination
- Respiratory rate and depth - hyperpnoea is often read as "anxiety"; count it and document it
- GCS and repeated neurological assessment - deterioration is the trigger for dialysis
- Temperature - hyperthermia
- Volume status - these patients are profoundly dehydrated (vomiting, tachypnoea, sweating, osmotic diuresis)
- Tinnitus / hearing (ask directly)
- Chest - crackles of non-cardiogenic pulmonary oedema
- GI bleeding, epigastric tenderness
- Fundi, pupils, tone and clonus - to exclude the mimics
Investigation strategy
Immediate
- Salicylate level - and repeat every 2-4 h until clearly falling
- A single level is uninterpretable; the trend is the investigation
- Australian labs report mmol/L; therapeutic <2.2 mmol/L (30 mg/dL)
- VBG/ABG with pH, pCO2, bicarbonate - and repeat
- UEC - potassium must be normal before alkalinisation will work
- Glucose - CNS hypoglycaemia occurs with normal serum glucose; keep BSL 5-10
- Paracetamol level (every deliberate self-poisoning)
- FBE, coagulation, LFT, lactate, ketones
- ECG - QT, hypokalaemia
- CXR if hypoxic - non-cardiogenic pulmonary oedema
Interpreting the gas
- Early: respiratory alkalosis (direct medullary respiratory centre stimulation)
- Then mixed respiratory alkalosis + high anion gap metabolic acidosis
- Late/severe: acidaemia - pH falling toward normal or below is deterioration, not improvement
- Children and late adults present acidotic from the outset
Abdominal imaging
- Not routine; consider if massive enteric-coated ingestion and levels still rising (pharmacobezoar)
Management
Three levers: stop absorption, enhance elimination, protect the brain by keeping the blood alkalotic.
1. Resuscitation
- Aggressive IV crystalloid - correct profound dehydration first; alkalinisation fails in a hypovolaemic, hypokalaemic patient
- Correct hypokalaemia vigorously - the kidney will exchange K+ for H+ and acidify the urine otherwise
- Dextrose for any altered mental state regardless of BSL
- Call the Poisons Information Centre 13 11 26
2. Decontamination
- Activated charcoal 50 g if within 2 h of ingestion and airway safe
- Extend the window, and consider repeat doses, for enteric-coated or sustained-release preparations (large, slowly dissolving, may form bezoars)
- Whole bowel irrigation - occasionally for massive enteric-coated ingestion
3. Urinary alkalinisation - the mainstay
- Sodium bicarbonate 1-2 mmol/kg IV bolus, then an infusion (e.g. 150 mmol NaHCO3 in 1 L 5% dextrose) at ~2x maintenance
- Target urine pH 7.5-8.0; serum pH up to 7.55 is acceptable
- Add potassium to the infusion (20-40 mmol/L) - hypokalaemia defeats alkalinisation
- Monitor urine pH hourly, serum K+ and gases 2-4 hourly
- Mechanism: ion trapping - alkaline urine keeps salicylate ionised in the tubule, preventing reabsorption; alkaline serum draws salicylate out of the CNS
4. Haemodialysis - know the thresholds
- Intermittent haemodialysis is the preferred modality
- Indications (EXTRIP):
- Salicylate >6.5 mmol/L (90 mg/dL) regardless of symptoms
- >5.8 mmol/L (80 mg/dL) with impaired kidney function
- Altered mental state
- pH <=7.20
- Hypoxaemia requiring supplemental oxygen
- Failure of standard therapy, or inability to tolerate the fluid/bicarbonate load
- Any patient requiring intubation
- Salicylate is small, water-soluble and poorly protein-bound at toxic levels -> dialyses extremely well
- Continue bicarbonate during and after dialysis - rebound occurs as salicylate redistributes from tissue
5. Supportive
- Benzodiazepines for seizures and agitation; treat seizures aggressively - they worsen acidosis
- Active cooling for hyperthermia
- Avoid: acetazolamide (worsens acidaemia), loop diuretics as a substitute for alkalinisation, and routine forced diuresis
- Glucose-containing fluids as the default carrier
Traps
- *Intubating a salicylate-poisoned patient without a plan. They are maintaining an enormous minute volume to stay alkalotic. Apnoea during RSI -> abrupt fall in pH -> salicylate floods the CNS -> cardiac arrest.*
- If intubation is unavoidable: bicarbonate bolus before induction, minimal apnoeic time, and set the ventilator to match their pre-intubation minute ventilation (often >20 L/min) - and dialyse
- *Reading a normalising pH as improvement.* Loss of the respiratory alkalosis is exhaustion and deterioration
- *Relying on a single salicylate level.* Enteric-coated aspirin peaks late; the level must be falling before you relax
- *Missing chronic salicylism. An elderly patient with confusion, tachypnoea, fever and pulmonary oedema on regular aspirin - toxicity occurs at levels that look almost therapeutic. "Sepsis of unknown source" is the usual misdiagnosis*
- *Failing to replace potassium* - the commonest reason urinary alkalinisation does not work
- *Waiting for hypoglycaemia on the glucometer. CSF glucose can be low with normal serum glucose - give dextrose for any altered mental state*
- *Giving acetazolamide to alkalinise the urine* - it causes a systemic acidosis and increases CNS salicylate
- *Attributing the tachypnoea to anxiety or a "panic attack"* in a young overdose patient
- *Forgetting the paracetamol level* on a deliberate self-poisoning
Talk track
1. Recognise the metabolic fingerprint
- "The pattern that flags salicylate is a mixed respiratory alkalosis and high anion gap metabolic acidosis, usually with tinnitus and hyperpnoea. In an unwell patient with an unexplained acidosis and no obvious source, I check a salicylate level."
2. Explain the pathophysiology, because it drives every treatment
- "Salicylate directly stimulates the medullary respiratory centre, producing the alkalosis, and uncouples oxidative phosphorylation, producing lactate, ketones and heat. Crucially, only non-ionised salicylate crosses into the CNS - so as the pH falls, CNS penetration rises, and that is what kills the patient. Everything I do is aimed at keeping the blood alkalotic."
3. Say that it is a dynamic poisoning
- "I do not act on a single level. I repeat the salicylate and the blood gas every two to four hours until the level is clearly falling, particularly with enteric-coated preparations where the peak may be beyond twelve hours."
4. Sequence the treatment
- "Volume resuscitation and potassium replacement first, because alkalinisation fails without them. Then activated charcoal if the timing allows, then a bicarbonate infusion targeting a urine pH of seven and a half to eight."
5. Be explicit about dialysis thresholds
- "I escalate to intermittent haemodialysis for a level above 6.5 mmol per litre, or above 5.8 with renal impairment, for altered mental state, a pH of 7.2 or below, hypoxaemia, or failure of standard therapy. Salicylate is small and poorly protein bound at toxic concentrations, so it clears very effectively."
6. Flag the airway trap unprompted
- "The one thing I would avoid is intubating this patient casually. Their hyperventilation is compensatory and protective; a period of apnoea drops the pH and drives salicylate into the brain. If they need an airway, I would give bicarbonate first, minimise apnoeic time, match their minute ventilation on the ventilator, and arrange dialysis at the same time."
7. Mention the chronic presentation
- "And I would keep chronic salicylism in mind in an older patient on regular aspirin with confusion, fever and pulmonary oedema - the level is often unimpressive but the toxicity is not."
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