Toxic alcohol includes Methanol, Ethylene Glycol, Isopropyl alcohol. The toxicokinetics, clinical features are explained separately. Pathophysiology of toxic alcohols explained using diagrams. diagnosis can be done using HAGMA, High osmolar gap, UFR and ECG. Management is determined by block metabolism, correct pH and eliminate toxic metabolites.

1. TOXIC ALCOHOL
Dr KTD PRIYADARSHANI
REGISTRAR IN EMERGENCY MEDICINE
TEACHING HOSPITAL PERADENIYA
2023/04/11

2. SCOPE
 OVERVIEW
 TOXIC ALCOHOLS
 PATHOPHYSIOLOGY
 DIAGNOSIS
 MANAGEMENT

3. Toxic alcohols
OVERVIEW
 group of substances containing a hydroxyl group
 not meant to be ingested
 significant number of accidental and non-accidental exposures
 associated with a significant degree of morbidity and mortality if not promptly
recognized and treated
 readily available in common hardware and household materials
 patient with an altered mental status or concerning history warrants
consideration of this potentially deadly ingestion.

4. Methanol
Ethylene
glycol
Isopropyl
alcohol

5. Methanol
 industrial solvent and synthetic precursor
 windshield fluid, antifreeze, paint, paint removers, gasoline,
adhesives, glass cleaner, a solvent/cleaner.
 highly variable lethal dose
 in itself if is not very toxic, however metabolized to formaldehyde -
> formic acid (neurotoxic – retina and optic nerves)

6. Clinical features
Stage 1
0-6 hours
• mimics ethanol
intoxication
• Inebriation (dizzy,
ataxic, confused)
• Gastric irritation
(pain, nausea,
vomiting)
Stage 2
6-30 hours
• latent phase may
occur
• Inebriation resolves
• Can be asymptomatic
Stage 3
6-72 hours
• Visual symptoms
(blurred vision,
blindness)
• Seizure, coma,
cerebral edema,
herniation
• Cardiac failure,
respiratory arrest can
occur

7. Ethylene glycol
 slightly oily, sweet-to-taste clear liquid without color and odor
 Worldwide, about two thirds of ethylene glycol is used as a
 chemical intermediate,
 in the automotive antifreeze,
 brake fluid
 anti-corrosion additives
 Solvent
 Polish, paints
 cosmetics
 Ethylene glycol itself is relatively no toxic > metabolites are extremely toxic

8. Toxicokinetic
 The minimum lethal dose of ethylene glycol for adults is 1.4-1.6 ml/kg
 weight of 80 kg it is 200-220 ml (according to other data, 90-100 ml)
 Absorption
 Rapid - gastrointestinal tract
 its vapor or aerosol is absorbed through the respiratory tract
 In the liver and kidneys, undergoes enzymatic metabolism
 Excretion of ethylene glycol occurs through exhaled carbon dioxide and
excreted in the urine of ethylene, glycol and glycolic acid.
 T ½ - 2.5-8.4 hours.

9. Clinical features
Stage 1
30 min-12 hours
• mimics ethanol
intoxication
• Gastric irritation
(pain, nausea,
vomiting)
• Acting drunk
(ataxia, nystagmus)
• May see CNS
depression,
cerebral edema,
seizure
Stage 2
cardiopulmonary
stage
• 12-24 hours
• Tachycardia
• hyperventilation
• Myocardial
dysfunction
• Shock
• Tachypnea, ARDS
• Heart failure
Stage 3
renal stage
• 24-72 hours
• Renal failure is the
primary problem
Stage 4
Neurological
• 5-20 days
• Late neurologic
sequelae can occur
• coma
• seizures
• meningism
• muscle spasms
• external ocular
paralysis

10. Inhalation
• concentration in the air up to 140-200 mg / cc.
• within five minutes
• a strong irritation of the upper respiratory tract,
including a burning sensation in the trachea and cough
chronic ethylene glycol poisoning
• feeling of weakness, dizziness, irritation of the mucous
membranes of the nose and eyes, increased heart rate
and blood pressure, and immunosuppression.

11. Isopropyl alcohol
 can cause morbidity and mortality
 more commonly ingested
 presents similarly to ethanol poisoning only more severely with coma and
cerebellar signs
 hemorrhagic gastritis and pancreatitis
 Isopropyl alcohol is about twice as inebriating as is ethanol (for any
particular load or blood level) and lasts twice as long.

12. Toxicokinetics
 used in industry and clinical laboratory diagnostics as a solvent.
 less toxic than methanol and ethylene glycol.
 Ingestion
 rapidly absorbed
 metabolized by alcohol dehydrogenase to form acetone, CO 2, and
water.
 T ½ - 3 hours
 lethal dose - 250 ml

13. Clinical Features
 dizziness,
 greased speech,
 headache,
 nausea,
 vomiting,
 abdominal pain
 hemorrhagic gastritis,
 diarrhea,
 ataxia,
 arterial hypotension,
 stupor
 Coma
 Later
 bradycardia,
 Rhabdomyolysis
 hemolysis

14. The concentration of isopropanol in the blood
• above 40 mg% is regarded as severe intoxication,
• above 100 mg% coma develop,
• a lethal concentration above 350 mg%.
severe metabolic acidosis and a high anion gap
Lactic acidosis and high concentration of acetone in blood and urine are
characteristic.
The presence of acetone in blood and urine, especially in high
concentrations, in patients in a coma suggests poisoning with isopropanol.

16.  methanol and
ethylene glycol get
metabolized into
acids
 isopropyl alcohol
gets metabolized
into acetone
Pathophysiology

19. Diagnosis
 Most toxic alcohol ingestions are recognized by
 History
 anion gap metabolic acidosis
 Early signs of both methanol and ethylene glycol toxicity are the
same as for ethanol
 The symptoms usually develop over 6-24hrs but can be delayed up
to 4 days if ethanol is congested

20. HAGMA
 Anion gap >12
 Both methanol and ethylene glycol may cause an elevated
lactate
 Ethylene glycol may cause renal failure with an elevated
creatinine contributing to the AG metabolic acidosis
 Absence of an anion gap metabolic absence does not rule out
toxic alcohol poisoning

21. High Osmolarity +/- Osmolar gap
 Osmolar gap calculation [2 x (Na)] + [glucose] + [urea] + [1.2 x ethanol] mmol/l
[2 x (Na)] +(glucose / 18) + (urea / 2.8) + (ethanol/4.1) mg/dl
 osmolality decreases with time
 the osmolar gap has poor positive and negative predictive value for toxic alcohol
poisoning
 High osmolar gaps are generally only seen early after toxic alcohol ingestion
 >10-25 mOsm
 »» acidosis and osmolality - inversely related
»» normal osmolar gap does not rule out toxic alcohol poisoning

23. UFR
 very poor sensitivity and specificity for ethylene glycol
toxicity
 But if present- pathognomonic for ethylene glycol
poisoning
 rarely helpful in the ED
 wood’s lamp examination of urine to detect fluorescein
is rarely helpful in detecting ethylene glycol poisoning

24. Ethanol level
 Low ethanol level in intoxicated patient
 The patient with a decreased LOC with a negligible ethanol concentration
must be investigated for other pathology.
 the serum ethanol must be taken into account when calculating the osmolar
gap.
 Pearl: The triad of acidosis, high osmolality and low or zero
ethanol level is highly suspicious for a toxic alcohol ingestion.

25. Hypocalcemia with prolonged QT
 Ethylene glycol toxicity - calcium is bound to oxalate
and deposits
in the kidneys - renal failure
in the brain - the late findings of parkinsonism and
basal ganglia hemorrhages.
 Bilateral basal ganglia hemorrhages on CT (late
finding) with ethylene glycol ingestion.

26. Goals of management
1. Block the toxic metabolites with fomepizole or
ethanol
2. Correct pH with bicarb
3. Eliminate toxic metabolites with dialysis (especially
methanol)
 A delay in initiating treatment of toxic alcohol poisoning leads
to worse outcomes.
 Do not wait for serum toxic alcohol levels to initiate treatment

27. Resuscitation
• RSI with ketamine (aspiration risk)
• beware of the acidosis;
• match the pre-intubation respiratory rate with
post intubation respiratory rate
• consider bicarbonate boluses to avoid worsening
acidosis and cardiovascular collapse.
Modify airway management for severe
acidosis:
Call ( local poison control center +/-
nephrology early)

28. GI Decontamination
 Not routinely recommended
 NG suction may be considered within 30
minutes of ingestion
 rapid gastric absorption

29. Antidote
 Ethanol
 Fomepizole

30. Indication for fomepizole or ethanol
 Serum concentration of methanol/ ethylene glycol >20
mg/dL
 Confirmed or suspected methanol / ethylene glycol
ingestion and two of the following
 Osmolar gap >10 mOsm
 Arteral pH <7.3
 Bicarbonate <20 mmol/L
 Presence of urinary oxalate crystals

31. • Consider fomepizole ideally within 30 minutes.
• If fomepizole N/A, consider ethanol.
Prevent toxic metabolites:
• loading dose of 15mg/kg,
• then 10mg/kg q12h for the first 48 hours,
• after which the dose is increased to 15mg/kg q12h
Fomepizole dosing:
• oral ethanol to target serum ethanol level = 22-23 mmol/L.
• if the patient comes in having co-ingested ethanol, they will
not require fomepizole or additional ethanol as long as their
serum ethanol remains above 22-23 mmol/L.
Ethanol dosing:

32. Ethanol
 Enteric (oral/NG)
 Loading dose
 1.8 ml/kg of 43% ethanol or
 4 * 30 ml Shots of Vodka in 70kg adult
 Maintenance
 0.2-0.4 ml/kg/h of 43% ethanol, or
 40 ml shot each hour
 IV (10% By 100% 100ml + 5% dextrose 900ml)
 Loading dose- 8ml/kg
 Maintenance – 1-2 ml/kg/hr
 Blood or breath ethanol level every 2 hrs
 Target 100-150 mg/dL or 22-33 mmol/L

33. Supportive management
• Methanol;
• Folic acid (50mg IV q4-6h) or
• folinic acid (1-2mg/kg IV q4-6h)
• Ethylene glycol
• thiamine (100mg IV q6h) and
• pyridoxine (100mg IV q6h)
Replenish cofactors:
• bicarbonate infusion if pH<7.3
Correct acidosis
• In isopropyl alcohol poisoning- hemorrhagic gastritis
PPI

34. Indication for dialysis
1. Metabolic acidosis pH <7.25-7.3
2. Evidence of end organ damage
1. Visual abnormalities
2. Renal failure
3. Electrolyte abnormalities not responsive to conventional
treatment
4. Hemodynamic instability refractory to ICU treatment
5. Serum concentration >50 mg/dL

35. Hemodialysis:
• may not be required if fomepizole is started early in ethylene glycol
poisoning assuming there is no acidemia or renal dysfunction.
• Methanol is eliminated too slowly for antidotal treatment alone to be
effective and so usually requires dialysis.
Pitfall: A delay to dialysis in methanol poisoning is a common
pitfall leading to poor outcomes. Call nephrologist early!

36. Disposition
 Toxicologically clear
 Methanol or ethylene glycol level <20 mg/dL
 Normal anion gap and osmolar gps
 Normal blood pH
 No evidence of end organ dysfunction or hemodynamic instability
 ICU admission
 Acidemia
 Signs of end organ dysfunction

37. References
REFERENCES
 Life in the Fast Lane
 Tinitinali’s Emergency Medicine- 9th edition
 Helman, A, Thompson, M, Austin, E. Toxic Alcohols – Minding the Gaps. Emergency Medicine
Cases. January, 2018. https://emergencymedicinecases.com/toxic-alcohols.
 Gallagher N, Edwards FJ. The Diagnosis and Management of Toxic Alcohol Poisoning in the
Emergency Department: A Review Article. Adv J Emerg Med. 2019 May 22;3(3):e28. doi:
10.22114/ajem.v0i0.153. PMID: 31410405; PMCID: PMC6683589.
 Borron SW, Mégarbane B, Baud FJ. Fomepizole in treatment of uncomplicated ethylene glycol
poisoning. Lancet. 1999 Sep 4;354(9181):831. doi: 10.1016/S0140-6736(99)80015-4. PMID:
10485727.
 Ashurst JV, Nappe TM. Methanol Toxicity. 2021 Jun 26. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2021 Jan–. PMID: 29489213.