Iron, salicylate and toxic alcohol poisoning

Overview & Definition

A child arrives with vomiting, fast deep breathing and a falling level. The venous gas shows a metabolic acidosis with a wide anion gap. The list of causes is long, but in paediatric toxicology three ingestions dominate this picture because each, by a different route, disables the mitochondrion: iron, salicylate, and the toxic alcohols methanol and ethylene glycol. Holding the three together is not a memory trick; it is how the examiner frames the question, because the resuscitation is shared while the antidote is poison-specific. [3] [10]

The unifying mechanism is impaired oxidative phosphorylation. Free iron catalyses the Fenton reaction, generating hydroxyl radicals that peroxidise mitochondrial membranes. Salicylate directly uncouples oxidative phosphorylation in the same way it does in the mitochondrion of a febrile cell. Methanol and ethylene glycol are harmless until hepatic alcohol dehydrogenase converts them to formic and oxalic acid, which inhibit mitochondrial cytochrome oxidase and precipitate in renal tubules. In every case the cell falls back on anaerobic glycolysis, lactate accumulates, and the child develops a high-anion-gap metabolic acidosis. The organ that fails first differs (the liver in iron, the brain and lung in salicylate, the retina and kidney in the toxic alcohols), but the metabolic signature is shared. [3] [10]

The clinical skill the examiner is testing is whether you can read the poison-specific clues out of the shared acidosis, give the correct weight-based antidote, choose the right decontamination, and avoid the three lethal traps that kill children: discharging during the deceptive iron latent phase, intubating a salicylate-toxic child without maintaining the hypocapnia that has been keeping them alive, and waiting for toxic-alcohol levels before starting fomepizole. Each trap is a failure to understand mechanism, not a failure of memory. [1] [6] [9]

[1] [7] [9]

Classification

The single most useful bedside classification sorts the three by their mechanism and their signature, because this decides the antidote. Iron injures by free-radical catalysis; salicylate by direct uncoupling and respiratory-centre stimulation; the toxic alcohols by enzyme-generated organic acids. Each carries a clue that the others do not. [3] [10]

[1] [6] [10]

A second axis classifies each poison by dose and stage. For iron the decisive number is the elemental iron ingested in mg per kg, not the salt weight; for salicylate the decisive distinction is acute versus chronic salicylism, which changes the dialysis threshold; for the toxic alcohols the decisive axis is the laboratory stage, because the osmolal gap dominates early and the anion gap dominates late. Each axis drives a specific decision, and conflating them is a classic error. [2] [5]

Epidemiology & Risk Factors

These three poisonings have a paediatric face. Iron remains one of the leading causes of accidental poisoning death in young children wherever adult prenatal or iron tablets are stored unsafely; a toddler needs only a handful of ferrous sulphate tablets to reach a lethal elemental dose. Salicylate poisoning in children is most often acute accidental ingestion of adult aspirin or oil of wintergreen, with a smaller burden of deliberate self-harm in adolescents. The toxic alcohols reach children through illicit or contaminated alcohol, windscreen washer, antifreeze, paint thinner and, in recent outbreaks, methanol-contaminated hand sanitiser. [1] [4] [11]

The risk of a severe outcome clusters around three questions for every ingestion: how much was taken (calculated as elemental iron for iron, mg per kg for salicylate, mL per kg for the toxic alcohols), what formulation (immediate-release versus sustained-release), and how quickly the correct antidote was started. A young age and low weight raise the mg per kg burden of even a small number of tablets; sustained-release and enteric-coated formulations delay and prolong absorption, distorting the expected timeline; co-ingestion with paracetamol is common in adolescent self-harm and compounds hepatic injury. [2] [4]

[2] [4] [11]

Pathophysiology

The reason the three poisons share a metabolic signature is that they all disable the mitochondrion, but by three different doors. Following each pathway to its organ target explains every clinical feature and every antidote. [3] [10]

Iron. The body has no excretory route for iron; all balance is at absorption. In overdose, absorbed iron exceeds the binding capacity of transferrin and circulates as free iron. Free iron is directly corrosive to the gastrointestinal mucosa, producing the haemorrhagic gastritis of stage 1. It is then taken up by cells, especially hepatocytes, and catalyses the Fenton reaction: Fe2+ plus hydrogen peroxide yields Fe3+ plus the hydroxyl radical. The hydroxyl radical peroxidises mitochondrial membranes, uncouples oxidative phosphorylation, inhibits aconitase in the Krebs cycle, and inhibits the sodium-potassium ATPase. The cell switches to anaerobic glycolysis and generates lactate; the centrilobular hepatocyte, the most metabolically active cell in the liver, dies first, producing the zone-3 necrosis shared with paracetamol. Free iron also directly inhibits thrombin, which is why the early coagulopathy precedes hepatic synthetic failure. [3]

Salicylate. Salicylate crosses into the mitochondrion and directly uncouples oxidative phosphorylation, increasing oxygen consumption and heat production (the hyperthermia is an uncoupling effect, not a set-point fever, so antipyretics do not help). It also directly stimulates the medullary respiratory centre, producing the primary respiratory alkalosis that characterises the early adult picture. The third effect is disturbance of the Krebs cycle, generating ketoacids and organic acids. The net result is the mixed respiratory alkalosis plus high-anion-gap metabolic acidosis. In children, the metabolic acidosis tends to dominate from the outset, and hypoglycaemia, including cerebral hypoglycaemia with a normal plasma glucose, is a particular threat. [6]

Toxic alcohols. Methanol and ethylene glycol are themselves only mildly intoxicating; the injury is downstream of alcohol dehydrogenase. Methanol is converted to formaldehyde and then to formic acid, which inhibits mitochondrial cytochrome c oxidase in the retina and optic nerve (causing the snowstorm vision and blindness) and injures the basal ganglia. Ethylene glycol is converted to glycoaldehyde, glycolic acid (the main acid load), glyoxylic acid and finally oxalic acid, which chelates calcium and precipitates as calcium oxalate crystals in the renal tubules, causing acute tubular necrosis and hypocalcaemia. Because the toxicity is downstream of one enzyme, blocking alcohol dehydrogenase with fomepizole prevents all of it, which is why fomepizole is started on suspicion and not on a level. [9] [10]

Clinical Presentation

The presentation is built from the shared metabolic acidosis plus the poison-specific clues. The examiner tests whether you can read both layers at the bedside. [1] [6] [10]

Iron follows a stereotyped four-stage course. Stage 1 (0 to 6 hours) is direct corrosive gastrointestinal injury: vomiting, often haematemetic, abdominal pain and diarrhoea, with dehydration and hypovolaemic shock in the significant ingestion. Stage 2 (6 to 24 hours) is the deceptive latent phase: the child looks better while iron is being sequestered by transferrin and is about to spill into tissues. Stage 3 (12 to 48 hours) is systemic toxicity and the killer: high-anion-gap metabolic acidosis, shock, hepatic failure with transaminases over 1000, coagulopathy, renal failure and CNS depression. Stage 4 (4 to 6 weeks) is late gastric or pyloric outlet obstruction from scarring, presenting with post-prandial vomiting and weight loss. [1]

Salicylate presents with tinnitus, deafness, nausea, vomiting and deep rapid breathing (hyperpnoea is the cardinal sign, both rate and depth). The child is often febrile, sweaty and agitated. Severe poisoning brings confusion, seizures, coma and non-cardiogenic pulmonary oedema. The mixed respiratory alkalosis plus anion-gap metabolic acidosis on the venous gas, with tinnitus, is the signature. In chronic salicylism (the child on long-term aspirin), the neurotoxic picture dominates and is easily mistaken for delirium or sepsis. [5] [6]

The toxic alcohols present in two phases. Early there is only intoxication (ataxia, slurred speech, drowsiness) with a high osmolal gap. Hours later the organic acids appear and the child develops Kussmaul breathing from the metabolic acidosis. Methanol then declares itself with visual symptoms: blurred vision, snowstorm vision, photophobia, optic disc hyperaemia or oedema, and progression to blindness; basal ganglia signs may follow. Ethylene glycol declares itself with oliguria and flank pain from acute kidney injury, with calcium oxalate crystals in the urine, hypocalcaemia and a prolonged QT. [9] [11]

[2] [5]

Differential Diagnosis

The differential is the differential of the high-anion-gap metabolic acidosis, built in a fixed order: what can kill now, what is most likely, what is reversible, what is most harmful to miss. [6] [10]

[6] [10]

The key manoeuvre at the bedside is to send iron, salicylate and paracetamol levels together with a measured serum osmolality, and to calculate both the anion gap and the osmolal gap. A normal osmolal gap with radiopaque tablets and a high iron level closes the case for iron; a mixed respiratory alkalosis with tinnitus closes it for salicylate; a dual gap with visual or crystal clues closes it for the toxic alcohols. Always exclude co-ingested paracetamol in the deliberate self-harm ingestion, because paracetamol centrilobular necrosis compounds iron hepatitis and needs N-acetylcysteine. [1] [7]

Clinical & Bedside Assessment

Assess the child as an integrated whole, then layer the poison-specific history and examination on top. The history quantifies risk in minutes; the examination grades severity; together they decide the antidote and the decontamination. [1] [6]

History. Establish the time since ingestion, the agent (iron salt and formulation, aspirin or oil of wintergreen, methanol or ethylene glycol source), the elemental-iron dose or the volume of toxic alcohol, co-ingestants (especially paracetamol and ethanol), the intent (accidental versus self-harm), and the child's weight. Ask specifically about prenatal tablets, sustained-release preparations, and access to adult medications or household chemicals. In suspected toxic alcohol, ask about illicit alcohol, hand sanitiser, windscreen washer and antifreeze. [2]

Examination. Perform a focused ABCDE: heart rate and quality, blood pressure, respiratory rate AND depth (hyperpnoea is the salicylate cardinal sign), capillary refill, temperature, conscious level, and the abdomen for tenderness. In suspected methanol, examine the eyes: visual acuity, colour vision, fields, pupils and fundoscopy for optic disc hyperaemia. In suspected ethylene glycol, look for tetany from hypocalcaemia and feel for flank tenderness. A bedside capillary glucose is mandatory in every salicylate ingestion because cerebral hypoglycaemia can coexist with a normal plasma glucose. [6]

[1]

The bedside assessment closes with a stated synthesis: the agent and the elemental dose, the current stage or severity, the specific antidote and its trigger, the decontamination plan, and the escalation timeline to the poisons centre and PICU. State this aloud to the team; a child with a high-anion-gap acidosis and an unclear history is treated empirically while levels are pending. [9]

Investigations

Stabilise first, then order each test for a named question. The investigation bundle has three layers: the shared metabolic tests, the poison-specific tests, and the rule-out co-ingestion tests. [1] [10]

[1] [10]

Interpret the osmolal gap with the timing caveat firmly in mind. The osmolal gap is the difference between the measured osmolality (by freezing-point depression, because vapour-pressure osmometers miss volatile alcohols) and the calculated osmolality (2 times sodium plus glucose plus urea, all in mmol per L). A normal osmolal gap is roughly minus 10 to plus 10 mOsm per kg; a gap over 20 strongly suggests a toxic alcohol or ethanol, but a normal gap late does not exclude the diagnosis because the parent has been metabolised. The empiric threshold to start fomepizole is a documented ingestion with acidosis, or a high anion-gap acidosis of unknown cause with an elevated osmolal gap, or strong clinical suspicion: do not wait for the methanol or ethylene glycol level. [9] [10]

[10]

Management — Resuscitation

Resuscitation is shared across the three poisons and runs in parallel with the investigations and the first dose of antidote. The aims are to restore perfusion, secure the airway, support the compensatory hyperventilation of salicylate toxicity, take bloods before the antidote, and avoid the useless or harmful interventions. [1] [9]

[1] [7] [9] [1] [6] [9]

Management — Definitive & Stepwise

Once the shared resuscitation is running, definitive management moves to the poison-specific antidote, enhanced elimination, and the cofactors. Each antidote has an explicit weight-based dose and an explicit trigger, and the antidote and dialysis run in parallel where both are indicated. [1] [9]

[1] [9]

Iron: intravenous desferrioxamine and whole-bowel irrigation

Desferrioxamine (deferoxamine) is a siderophore that binds free iron in a stable 1 to 1 complex, ferrioxamine, which is excreted in the urine and gives it the characteristic vin-rose colour. It is the definitive treatment for significant iron toxicity. [1] [3]

[1]

Whole-bowel irrigation with polyethylene-glycol electrolyte solution is the decontamination of choice for iron because activated charcoal does not adsorb a metal. Give it via a nasogastric tube at 20 to 40 mL per kg per hour (around 500 mL per hour in a young child) until the rectal effluent is clear and no tablets remain on a repeat abdominal X-ray. Continue it even after starting desferrioxamine if tablets remain. Activated charcoal is useless and obscures the endoscopic view; this is the single most important negative instruction in iron overdose. [1]

Salicylate: urinary alkalinisation and dialysis

The cornerstone of enhanced elimination in salicylate poisoning is urinary alkalinisation with intravenous sodium bicarbonate, titrated to a urine pH of 7.5 to 8.0. The mechanism is ion-trapping: unionised salicylic acid diffuses into the alkaline tubular urine, is deprotonated to the impermeant salicylate anion, and is trapped for urinary excretion. Renal clearance rises roughly five-fold at urine pH 8 versus pH 5. [6] [7]

[6] [7]

Hypokalaemia prevents urinary alkalinisation from working because the kidney retains potassium by exchanging it for hydrogen, acidifying the tubular fluid; correct the potassium to over 4 mmol per L before and during alkalinisation. Add dextrose to the fluids to prevent cerebral hypoglycaemia. Modern practice has moved away from forced alkaline diuresis (large fluid volumes) toward urinary alkalinisation alone with modest fluid, because the active component is the alkalinisation, not the volume, and large volumes risk pulmonary oedema. [6] [8]

Haemodialysis is indicated for a salicylate level over 700 mg per L in acute poisoning (over 600 in chronic), severe metabolic acidosis with arterial pH under 7.20 to 7.25 unresponsive to bicarbonate, CNS toxicity (confusion, seizures, coma), non-cardiogenic pulmonary oedema, renal failure or an inability to alkalinise the urine, and clinical deterioration despite standard therapy. Use a bicarbonate-based dialysate and a paediatric circuit. After dialysis, continue alkalinisation and recheck the level every 2 to 4 hours for at least 12 to 24 hours because of rebound redistribution from tissue stores. [7] [8]

Toxic alcohols: fomepizole, cofactors and dialysis

The definitive intervention is to block alcohol dehydrogenase. Fomepizole (4-methylpyrazole) is a direct competitive inhibitor of alcohol dehydrogenase with no central nervous system effect, no hypoglycaemia and no monitoring burden, and it is preferred over ethanol in children for all of these reasons. Start it on suspicion, based on a documented ingestion with acidosis, a high anion-gap acidosis of unknown cause with an elevated osmolal gap, or the clinical picture (visual symptoms, calcium oxalate crystals); do not wait for the methanol or ethylene glycol level. [9] [10]

[9] [11]

Give the metabolic cofactors in parallel: folinic acid (leucovorin) 1 mg per kg intravenously (up to 50 mg) every 4 to 6 hours for suspected methanol, because folate-dependent metabolism speeds formate clearance; and thiamine and pyridoxine (vitamin B6) for suspected ethylene glycol, because they divert glyoxylate to non-toxic metabolites. Give intravenous sodium bicarbonate to target a serum pH over 7.20 to 7.30; in methanol this also traps formate in its anionic form and speeds renal clearance. Replace calcium in ethylene glycol only if symptomatic (tetany, seizures, QT prolongation), because over-correction worsens calcium oxalate deposition. Haemodialysis is indicated for a methanol or ethylene glycol level over 50 mg per dL, severe or worsening acidosis, renal failure, visual symptoms, or significant electrolyte disturbance; continue fomepizole through and after dialysis. [9] [10]

[1] [7] [9]

Specific Subtypes & Scenarios

The resuscitation structure stays the same, but the agent, the formulation, the age and the setting change what you watch for, which decontamination you choose, and how early you escalate. [2] [11]

[2] [11]

In pregnancy, maternal outcome determines fetal outcome. Iron overdose in pregnancy typically involves prenatal iron, and intravenous desferrioxamine is indicated for severe maternal toxicity despite placental transfer, because untreated maternal iron toxicity is far more dangerous to the fetus than chelation. Salicylate crosses the placenta and the fetus is acidotic relative to the mother, so salicylate is ion-trapped in the fetal central nervous system; maternal alkalinisation alkalinises the fetus and reduces trapping. Involve obstetrics and monitor the fetus throughout. [1] [6]

Complications & Pitfalls

Most preventable harm in these three poisonings comes from one of three errors: being reassured by the iron latent phase, intubating the salicylate-toxic child without maintaining hypocapnia, or waiting for toxic-alcohol levels before fomepizole. Each is a failure to understand mechanism, not a failure of memory. [1] [6] [9]

[1] [7] [8]

After resuscitation, watch actively for harm from the disease and the treatment: non-cardiogenic pulmonary oedema in salicylate, desferrioxamine lung injury and Yersinia sepsis in iron chelation, ethanol-induced hypoglycaemia if ethanol is used for a toxic alcohol, and acute kidney injury from ethylene glycol. The late complications are gastric or pyloric outlet obstruction at 4 to 6 weeks after iron, permanent visual loss after methanol, and chronic kidney disease after ethylene glycol. [1] [10]

[1] [6] [9]

Prognosis & Disposition

Disposition follows the trend in the level and the response to treatment, not a single reassuring number. Consider the agent and dose, the formulation, the severity and reversibility of organ dysfunction, the local resources, the transport risk, and whether the family can carry the plan forward. [1] [7]

[1] [7]

Modern series report iron mortality under 5 percent with prompt chelation, and acute salicylate mortality under 1 percent when recognised early. The toxic alcohols carry significant morbidity from visual loss and renal failure when treatment is delayed. The strongest modifiable predictor of death in all three is the delay to the correct antidote. Give the family a clear safety net: what change to watch for, how urgently to act, where to return, and how to secure the agent. [1] [4]

Special Populations

Adapt how you assess, dose and escalate, but never lower the standard for recognising the high-anion-gap acidosis. The principles apply across ages and abilities; the differences are in weight, reserve, drug handling and the social context. [1] [11]

[1] [11]

Safeguarding runs in parallel with medical care, and immediate stabilisation comes first. Iron and salicylate poisoning can arise from neglect, unsafe storage of adult medications, induced or fabricated illness, or adolescent self-harm. Ask only necessary open, non-leading questions, document objective findings and spontaneous words, and use the local safeguarding pathway. Reporting thresholds, consent rules and agencies differ by Australian state or territory, UK nation, US state and Canadian province or territory. [2]

Evidence, Guidelines & Regional Differences

What the evidence can and cannot support

The structure of management for all three poisons is strongly endorsed by the major toxicology sources: resuscitate, decontaminate by poison, give the weight-based antidote on its trigger, and enhance elimination with dialysis when indicated. What remains source-specific is the exact threshold for dialysis and the local preference for fomepizole over ethanol, which must be verified against the active regional guideline. [7] [9]

[7]

The Brent 2009 New England Journal of Medicine review established fomepizole as the preferred antidote for ethylene glycol and methanol poisoning, demonstrating efficacy and a far better safety profile than ethanol, particularly in children where ethanol causes CNS depression and hypoglycaemia. Fomepizole has since replaced ethanol as first line wherever it is available. The paediatric case series confirm weight-based dosing and the need for paediatric dialysis circuits. [9] [11]

For iron, the AACT/EAPCCT 2005 consensus (Manoguerra) set the out-of-hospital triage thresholds still in use: refer to the emergency department for any symptoms, any ingestion over 40 mg per kg elemental iron, any sustained-release ingestion over 40 mg per kg, or any intentional ingestion; home observation is acceptable only for asymptomatic ingestions under 20 mg per kg. Whole-bowel irrigation is endorsed by the AACT/EAPCCT as the decontamination of choice for iron, and the 2023 clinical-toxicology consensus reaffirmed that activated charcoal has no role in metal poisoning. [2] [1]

For salicylate, the Prescott 1982 BMJ study established that alkalinisation of the urine, not large fluid volumes, is the active component of enhanced elimination, moving practice away from forced alkaline diuresis toward urinary alkalinisation alone. The rebound phenomenon after dialysis or cessation of alkalinisation is now well characterised and drives serial-level monitoring for 12 to 24 hours. [6] [8]

Jurisdictional implementation

[1] [7] [2] [9]

Exam Pearls

[1] [7] [9]

Viva: why is charcoal useless for iron and toxic alcohols but works for salicylate?

Activated charcoal adsorbs organic molecules by surface binding. Salicylate is an organic acid and binds charcoal well, so it is the one of the three that charcoal helps. Iron is a metal, not an organic molecule, so charcoal does not bind it and is useless; the decontamination of choice for iron is whole-bowel irrigation with polyethylene glycol. The toxic alcohols are small molecules that charcoal does not adsorb in any clinically useful quantity, and they are absorbed rapidly, so charcoal has no role; the intervention that matters is blocking alcohol dehydrogenase with fomepizole. [1] [9]

[1] [9]

Viva: why does a normal osmolal gap late not exclude a toxic alcohol?

Early in toxic-alcohol poisoning the unmetabolised parent alcohol is osmotically active, so the osmolal gap is high. As alcohol dehydrogenase converts the parent to organic acids, the parent disappears (the osmolal gap falls) and the acids accumulate (the anion gap rises). A clinician who measures the gaps only late sees a normal osmolal gap with a high anion gap and may wrongly dismiss the diagnosis. The correct reading is that the two gaps are inversely related over time; treat on the clinical picture and the anion gap, and start fomepizole on suspicion. [10]

[10]

Structured oral: salicylate-toxic child needing intubation

A salicylate-toxic child compensates their metabolic acidosis with hyperventilation; the low PaCO2 is keeping them alive. Intubation removes that compensation: sedation, paralysis and a normally-set ventilator let PaCO2 rise, pH fall, salicylate shift into the central nervous system, and the child can crash within minutes. If intubation is unavoidable, give a bicarbonate bolus and optimise the pH first, pre-oxygenase, use rapid sequence, set the ventilator to a respiratory rate of 20 to 30 with the minute ventilation matched to the pre-intubation hypocapnia, and have haemodialysis ready because the acidosis will worsen. [6] [7]

[6] [7] [1] [6] [9]

References

1. [1]Chang, Timothy P; Rangan, Cyrus Iron poisoning: a literature-based review of epidemiology, diagnosis, and management Pediatric Emergency Care, 2011.PMID 21975503
2. [2]Manoguerra, Anthony S; Erdman, Andrew R; Booze, Laura L; Christianson, George; Wax, Paul M; Scharman, Elizabeth J; Woolf, Alan D; Keyes, Daniel C; Olson, Kent R; Chyka, Peter; Caravati, E Martin; Troutman, William G Iron ingestion: an evidence-based consensus guideline for out-of-hospital management Clinical Toxicology, 2005.PMID 16255338
3. [3]Rafati Rahimzadeh, Milad; Rafati Rahimzadeh, Mahsa; Kazemi, Sara; Moghadamnia, Ali Akbar Iron; benefits or threatens (with emphasis on mechanism and treatment of its poisoning) Human and Experimental Toxicology, 2023.PMID 37526177
4. [4]Chandran, Jeethu; Khanna, Kshitij; Jayashree, M; Gautam, Vikas; Sharma, Aruna; Singh, Meenu Accidental iron poisoning in children - Experience from a teaching institution Journal of Family Medicine and Primary Care, 2023.PMID 38074262
5. [5]Gaudreault, Pierre; Temple, Anthony R; Lovejoy, Frederick H Jr The relative severity of acute versus chronic salicylate poisoning in children: a clinical comparison Pediatrics, 1982.PMID 7122154
6. [6]Snodgrass, Wirt Salicylate toxicity Pediatric Clinics of North America, 1986.PMID 3960612
7. [7]Juurlink, David N; Gosselin, Sophie; Kielstein, Jan T; Ghannoum, Marc; Lavergne, Valerie; Nolin, Thomas D; Hoffman, Robert S; EXTRIP Workgroup Extracorporeal treatment for salicylate poisoning: systematic review and recommendations from the EXTRIP workgroup Annals of Emergency Medicine, 2015.PMID 25986310
8. [8]O'Keefe, Meghan; Stanton, Michele; Feldman, Ruth; Theobald, Jennifer Incidence of rebound salicylate toxicity following cessation of urine alkalinization Clinical Toxicology, 2023.PMID 37427892
9. [9]Brent, Jeffrey Fomepizole for ethylene glycol and methanol poisoning New England Journal of Medicine, 2009.PMID 19458366
10. [10]Kraut, Jeffrey A; Xing, Xuejing Toxic Alcohols New England Journal of Medicine, 2018.PMID 29342392
11. [11]Lin, Po-Yin; Hsu, Chien-Chang; Chen, Chih-Hsien; Huang, Yi-Chun; Lee, Chee-Jen; Chen, Chien-Chang Use of fomepizole in pediatric methanol exposure: the first case report in Taiwan and a literature review Pediatrics and Neonatology, 2016.PMID 24332660