Tox: Alcohols Flashcards
Products that contain ethanol
Mouthwash, perfumes, vanilla extract, aftershave, cold/allergy medications, glass cleaners
Acute conditions associated with alcohol use
Hypoglycemia (poor diet, inability to store glycogen), electrolyte disturbances, vitamin depletion (folate, thiamine, B12), withdrawal, head trauma, hypothermia, other toxin/drug overdose,
alcoholic ketoacidosis, cirrhosis, pancreatitis, GIB, malnutrition, neurological disease
Lab findings with ethanol intoxication
+osmolar gap but no anion gap (make sure this is right)
How to account for ethanol when calculating osmolar gap (to ensure there is not another toxic alcohol contributing to gap)
Osmolar gap = measured osm - [2Na+sugar+BUN+ 1.2xEtOH level]
Sources of methanol
windshield wiper fluid, antifreeze, photocopier fluid, solid fuels (e.g. sterno)
Methanol pathophys
Metabolized by ADH to formaldehyde then by ALDH to formic acid.
Initially just osmolar gap (from methanol), then later on get an AGMA 2* formic acid.
Symptoms of methanol intox
Neuro: similar to ethanol. HA, CNS dep, basal ganglia injury resulting in PARKINSONISM.
Visual: vision changes progressing to possible blindness (‘looking through a snowfield’), hyperemic discs, retinal edema (sluggish, fixed pupils)
Cardio/pulm: Tachycardia, tachypnea.
GI: Abdo pain, n/v, pancreatitis
When to consider methanol poisoning
AMGA, +/-osmolar gap depending on timing, acute onset visual changes
Diagnosis of methanol poisoning
Gold standard = direct measurement.
Generally dx’d based on clinical suspicion and osmolar gap >10 (not present if late), AGMA and visual symptoms.
Tx of methanol poisoning
Fomepizole: blocks ADH so prevents production of formic acid.
Ethanol: preferentially metabolized by ADH.
Folate: improves metabolism of formic acid to CO2.
Hemodialysis
Evaluate response to tx by monitoring HCO3 (should increase with tx).
Indications for hemodialysis in methanol poisoning
1) severe acidosis (pH<7.15) or AGMA>24
2) renal failure
3) visual changes
3) serum level >15.6mmol/L (prior to ADH blockade tx, diff level post-tx)
Long term complications of methanol toxicity
permanent vision loss, parkinsonian motor dysfunction
Causes of osmolar gap
ethanol, mannitol, sorbitol, recent contrast administration, toxic alcohols (isopropyl alcohol, ethylene glycol, methanol)
normal osmolality, normal osmolar gap
Normal osmolality: 275-295
Normal gap: 10-14 mOsm/L
Sources of ethylene glycol
engine coolants (antifreeze), deicing fuel, latex paints, brake fluid, cleaning products.
Pathophys of ethylene glycol toxicity
Ethylene glycol itself minimally toxic.
Metabolized by ADH, ALDH to oxalic acid (direct renal toxin) and glycolate (AGMA).
Oxalic acid falsely read as lactate so often ++high lactate on labs.
4 stages of ethylene glycol toxicity
1) Acute neurological (0.5-12hrs)
2) Cardiopulmonary (12-24hrs)
3) Renal (24-72hrs)
4) Delayed neurologic sequelae (6-12days)
Symptoms of ethylene glycol toxicity
Neuro: intox similar to ethanol. HA, CNS dep. Delayed findings -> CN neuropathy, petechial brain hemorrhage, cerebral edema, papilledema.
Cardiopulm: HTN, tachycardia/ypnea, pulmonary edema, ARDS.
Delayed -> myocardial depression, cardiogenic shock.
GI: abdo pain, n/v
Renal: ARF, hematuria
Electrolytes: symptoms of hypocalcemia
Ethylene glycol poisoning diagnosis
- Gold standard: direct measurement.
- Suspect when: osmolar gap, AGMA, ++lactate, acute renal failure.
- Presence of oxalate crystals in the urine (not sense or specific )
- Fluorescent under Woods lamp (UV light) with some brands.
Treatment of ethylene glycol poisoning
- Fomepizole: ADH blockade
- Ethanol: ADH blockade
- Thiamine (B1): converts glycolic acid to nontoxic metabolite.
- Pyridoxine (B6): as per B1
- HD for some
Long term complications ethylene glycol poisoning
Renal failure may or may not be reversible
Indications for HD in ethylene glycol poisoning
- Renal failure
- Severe acidosis (pH<7.25)
- Electrolyte disturbances
Isopropanolol (isopropyl alcohol) typical presentation
‘twice as drunk for twice as long.’
May have fruity smelly breath 2* acetone
Neuro: similar to ethanol intox, CNS depression, coma.
GI: abdominal pain, n/v, hemorrhagic gastritis
Isopropyl alcohol sources
rubbing alcohol, perfumes, hand sanitizers.
Most often ingested as an ethanol substitute
Pathophys of isopropyl alcohol
NOT converted to organic acid like other alcohols.
Converted to acetone by ADH.
Causes a ketosis (acetone) but NO acidosis (thus NO AGMA).
+osmolar gap, +ketones, NO acidosis/AGMA
Diagnosis of isopropanolol poisoning
Gold standard = direct measurement
Suspect in pts that look ++intoxicated but have negative ethanol levels. May have other clues (osmolar gap, ketones/+serum acetone, no acidosis)
Tx of isopropanolol poisoning
Supportive
