Low threshold for dextrose supplementation if altered mental status
Anion gap calculation
Mixed disorder recognition
Serial trend for deterioration
Salicylate and co-ingestion testing
Concentrations and screening
Salicylate concentration
First level at presentation
Repeat every 2 hours until clear peak and downtrend
More frequent levels for sustained-release or clinical worsening
Acetaminophen concentration
Routine in suspected intentional overdose
Delayed peak consideration
Ethanol concentration
Co-ingestion affecting mental status and acid-base
Urinalysis
Urine pH for alkalinisation target
Ketones
Complication and severity labs
Targeted adjuncts
CBC
Infection assessment
Anaemia in GI bleeding concern
Lactate
Non-specific elevation possible
Persistent rise suggests shock or alternative diagnosis
Creatine kinase
Rhabdomyolysis in hyperthermia or agitation
Liver enzymes
Differential and co-ingestions
Coagulation studies
Bleeding risk assessment
Liver dysfunction marker
Pregnancy test
Management threshold adjustments
Disposition planning
Diagnostic Tests
Scoring Systems
Severity frameworks
Done nomogram
Acute single ingestion of immediate-release aspirin
Not reliable for chronic poisoning
Not reliable for enteric-coated or sustained-release
Not reliable when time of ingestion uncertain
Clinical severity features over concentration alone
Altered mental status
Pulmonary oedema
Persistent acidaemia
Rising concentration on serial testing
MRI
Neuroimaging considerations
MRI brain
Not routine for acute management
Consider if persistent focal deficits after stabilisation
Consider if alternative intracranial pathology suspected
CT
Time-critical imaging
CT head non-contrast
Altered mental status with unclear cause
Seizure with persistent deficit
Trauma concern from collapse
CT abdomen
Not routine
Consider if suspected pharmacobezoar and severe delayed absorption
Ultrasound
Point-of-care applications
Lung ultrasound
B-lines for pulmonary oedema
Pleural effusion assessment
Cardiac ultrasound
Volume status support
Alternative shock causes evaluation
IVC assessment limitations
Tachypnoea reduces reliability
Use alongside clinical context
Disposition
Level of care
ICU or high-acuity admission
Any severe clinical feature
Altered mental status
Seizure
Pulmonary oedema
Need for bicarbonate infusion
Need for ventilatory support
Renal failure or oliguria
Severe acid-base disturbance
pH < 7.30
Worsening anion gap
Salicylate concentration in severe range
Acute ingestion 7.2 mmol/L (1000 mg/L) or higher
Chronic ingestion 4.3 mmol/L (600 mg/L) or higher
Dialysis pathway disposition
Haemodialysis indicated or likely
Transfer to dialysis-capable centre if unavailable
Early initiation planning
Avoid delays for repeat testing if criteria met
Post-dialysis monitoring
Rebound concentration monitoring
Continue alkalinisation until stable downtrend
Discharge suitability
ED observation then discharge only if clearly mild
Asymptomatic after observation
Normal vital signs
Normal mental status
Salicylate concentration low and declining on serial levels
Peak identified
No delayed absorption concern
Normal acid-base status
No metabolic acidosis
No rising anion gap
Reliable follow-up and safe environment
Intentional ingestion addressed
Psychiatric evaluation when indicated
Treatment
Decontamination
GI decontamination options
Activated charcoal
1 g/kg PO or NG
Typical adult 50 g
Typical paediatric 25 g to 50 g based on weight
Repeat dose consideration for sustained-release
Ongoing absorption evidence on serial levels
Enteric-coated ingestion with delayed peak
Contraindications
Unprotected airway with vomiting
Ileus or bowel obstruction
Whole bowel irrigation
Consider for massive enteric-coated ingestion
Severe toxicity with ongoing rise despite charcoal
Pharmacobezoar concern
Polyethylene glycol electrolyte solution
Adult 1.5 L/hour to 2.0 L/hour until clear effluent
Paediatric 25 mL/kg/hour to 40 mL/kg/hour until clear effluent
Alkalinisation
Serum and urine alkalinisation
Sodium bicarbonate IV bolus
1 mEq/kg
Typical adult 50 mEq to 100 mEq
Indications
Symptomatic toxicity
Metabolic acidosis
Rising salicylate concentration
Sodium bicarbonate infusion
Mix 150 mEq sodium bicarbonate in 1 L D5W
Infusion rate 150 mL/hour to 250 mL/hour
Adjust to urine pH goal 7.5 to 8.0
Serum pH target
7.45 to 7.55
Monitoring frequency
Electrolytes every 2 hours initially
Blood gas every 2 hours initially
Urine pH checks every 1 hour to 2 hours
Potassium repletion
Target potassium 4.0 mmol/L to 4.5 mmol/L
Potassium chloride IV or PO as clinically appropriate
Avoid dextrose-free bicarbonate solutions if hypoglycaemic risk
Rationale
Hypokalaemia drives renal H+ secretion
Acidic urine traps salicylate in non-ionised form less effectively
Supportive care
Fluids and temperature control
Isotonic crystalloid
Volume depletion correction
Avoid fluid overload if pulmonary oedema
Dextrose therapy
Altered mental status with normal glucose
Dextrose 10% infusion to maintain euglycaemia
Repeat bedside glucose monitoring
Hypoglycaemia
Dextrose 25 g IV for adults
Dextrose 0.5 g/kg IV for paediatrics
Hyperthermia management
External cooling
Evaporative cooling
Ice packs to axilla and groin
Sedation for severe agitation driving heat production
Seizure and agitation control
Benzodiazepines
Lorazepam IV 0.1 mg/kg
Typical adult 2 mg to 4 mg
Repeat every 5 minutes as needed
Diazepam IV 0.15 mg/kg to 0.2 mg/kg
Refractory seizures
Levetiracetam IV 60 mg/kg
Maximum 4500 mg
Phenobarbital IV 15 mg/kg to 20 mg/kg
Airway and ventilation
Intubation strategy when unavoidable
Pre-intubation preparation
Bicarbonate bolus immediately prior
Maximise pre-oxygenation without suppressing ventilation
Plan for immediate high minute ventilation post-intubation
Post-intubation targets
Maintain pre-intubation PaCO2 or lower
Avoid normalising PaCO2
Avoid permissive hypercapnia
Immediate blood gas check after stabilisation
Paralysis and sedation risk
Apnoea interval minimisation
Avoid long apnoea during induction
Extracorporeal removal
Haemodialysis indications
Severe clinical features
Altered mental status
Seizure
Pulmonary oedema
Shock
Acid-base failure
pH < 7.2 despite bicarbonate therapy
Worsening acidaemia trend
Renal failure
Oliguria
Rising creatinine with inability to alkalinise
Concentration thresholds supporting dialysis
Acute ingestion 7.2 mmol/L (1000 mg/L) or higher
Acute ingestion 5.8 mmol/L (800 mg/L) or higher with symptoms
Chronic ingestion 4.3 mmol/L (600 mg/L) or higher
Lower threshold with any severe clinical feature
Rebound monitoring
Repeat salicylate concentration 2 hours after dialysis ends
Continue alkalinisation until stable downtrend and clinical recovery
Special Populations
Pregnancy
Maternal-fetal considerations
Lower threshold for dialysis
Maternal severe features
Rising concentration despite alkalinisation
Fetal risk physiology
Fetal acidaemia increases salicylate trapping
Placental transfer of salicylate
Consultation
Obstetrics early
Nephrology early
Geriatric
Older adult considerations
Chronic toxicity more likely than acute overdose
Non-specific presentation
Delirium as presenting symptom
Comorbid disease impact
CKD reduces clearance
Heart failure increases pulmonary oedema risk
Medication interactions
Diuretics promote dehydration
Anticoagulants increase bleeding risk
Pediatrics
Paediatric considerations
Higher risk of rapid deterioration
Limited physiologic reserve
Early CNS effects
Weight-based therapy
Activated charcoal 1 g/kg
Bicarbonate bolus 1 mEq/kg
Dextrose 0.5 g/kg for hypoglycaemia
Accidental methyl salicylate exposure
Small volumes can be life-threatening
Early poison centre involvement
Background
Epidemiology
Patterns of exposure
Intentional overdose in adolescents and adults
Often with co-ingestions
Chronic therapeutic misadventure in older adults
Unrecognised progressive toxicity
Topical and household sources
Methyl salicylate products
Multiple salicylate-containing cold preparations
Pathophysiology
Mechanisms of toxicity
Medullary respiratory centre stimulation
Primary respiratory alkalosis
Uncoupling of oxidative phosphorylation
Heat generation
Increased oxygen consumption
Increased CO2 production
Organic acid accumulation
Ketoacids
Lactic acid
Mixed metabolic acidosis
Glucose dysregulation
Increased CNS glucose utilisation
Neurotoxicity with normal serum glucose
Therapeutic Considerations
Rationale for alkalinisation
Increased salicylate ionisation in serum
Reduced tissue penetration
Reduced CNS entry
Increased renal clearance
Ion trapping in alkaline urine
Markedly increased urinary excretion
Rationale for dialysis
Removes salicylate directly
High dialysability at toxic concentrations
Corrects acid-base and electrolytes
Rapid correction of acidaemia
Enables continued alkalinisation
Clinical priority over concentration in severe cases
Pulmonary oedema and CNS toxicity are late markers
Patient Discharge Instructions
copy discharge instructions
Discharge guidance
Medication safety
Stop aspirin and salicylate-containing products unless specifically instructed by clinician
Check labels for salicylates and methyl salicylate
Hydration and monitoring
Maintain oral fluids
Avoid heavy exercise for 24 hours
Return to ED now
Fast breathing or trouble breathing
New confusion, severe agitation, or fainting
Persistent vomiting or inability to keep fluids down
Ringing in ears that is worsening
Fever
Seizure
Follow-up
Primary care within 24 to 72 hours
Mental health follow-up if intentional ingestion
References
Clinical guidelines and consensus
Key guidance documents
American Academy of Clinical Toxicology and American College of Medical Toxicology guidance on salicylate poisoning management
Alkalinisation as first-line enhanced elimination
Early dialysis for severe features
EXTRIP workgroup recommendations on extracorporeal treatment for salicylate poisoning
Haemodialysis criteria based on clinical severity and concentration thresholds
Emphasis on acidaemia and organ dysfunction triggers
Evidence-based sources
Core references
Goldfrank’s Toxicologic Emergencies
Clinical features and treatment algorithms for salicylate toxicity
Standard emergency medicine toxicology texts and poison centre protocols
Serial concentration monitoring and delayed absorption considerations
SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.