Tox: Alcohols

Question 1

Products that contain ethanol

Answer 1

Mouthwash, perfumes, vanilla extract, aftershave, cold/allergy medications, glass cleaners

Question 2

Acute conditions associated with alcohol use

Answer 2

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

Question 3

Lab findings with ethanol intoxication

Answer 3

+osmolar gap but no anion gap (make sure this is right)

Question 4

How to account for ethanol when calculating osmolar gap (to ensure there is not another toxic alcohol contributing to gap)

Answer 4

Osmolar gap = measured osm - [2Na+sugar+BUN+ 1.2xEtOH level]

Question 5

Sources of methanol

Answer 5

windshield wiper fluid, antifreeze, photocopier fluid, solid fuels (e.g. sterno)

Question 6

Methanol pathophys

Answer 6

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.

Question 7

Symptoms of methanol intox

Answer 7

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

Question 8

When to consider methanol poisoning

Answer 8

AMGA, +/-osmolar gap depending on timing, acute onset visual changes

Question 9

Diagnosis of methanol poisoning

Answer 9

Gold standard = direct measurement.

Generally dx’d based on clinical suspicion and osmolar gap >10 (not present if late), AGMA and visual symptoms.

Question 10

Tx of methanol poisoning

Answer 10

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).

Question 11

Indications for hemodialysis in methanol poisoning

Answer 11

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)

Question 12

Long term complications of methanol toxicity

Answer 12

permanent vision loss, parkinsonian motor dysfunction

Question 13

Causes of osmolar gap

Answer 13

ethanol, mannitol, sorbitol, recent contrast administration, toxic alcohols (isopropyl alcohol, ethylene glycol, methanol)

Question 14

normal osmolality, normal osmolar gap

Answer 14

Normal osmolality: 275-295

Normal gap: 10-14 mOsm/L

Question 15

Sources of ethylene glycol

Answer 15

engine coolants (antifreeze), deicing fuel, latex paints, brake fluid, cleaning products.

Question 16

Pathophys of ethylene glycol toxicity

Answer 16

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.

Question 17

4 stages of ethylene glycol toxicity

Answer 17

1) Acute neurological (0.5-12hrs)
2) Cardiopulmonary (12-24hrs)
3) Renal (24-72hrs)
4) Delayed neurologic sequelae (6-12days)

Question 18

Symptoms of ethylene glycol toxicity

Answer 18

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

Question 19

Ethylene glycol poisoning diagnosis

Answer 19

1. Gold standard: direct measurement.
2. Suspect when: osmolar gap, AGMA, ++lactate, acute renal failure.
3. Presence of oxalate crystals in the urine (not sense or specific )
4. Fluorescent under Woods lamp (UV light) with some brands.

Question 20

Treatment of ethylene glycol poisoning

Answer 20

1. Fomepizole: ADH blockade
2. Ethanol: ADH blockade
3. Thiamine (B1): converts glycolic acid to nontoxic metabolite.
4. Pyridoxine (B6): as per B1
5. HD for some

Question 21

Long term complications ethylene glycol poisoning

Answer 21

Renal failure may or may not be reversible

Question 22

Indications for HD in ethylene glycol poisoning

Answer 22

1. Renal failure
2. Severe acidosis (pH<7.25)
3. Electrolyte disturbances

Question 23

Isopropanolol (isopropyl alcohol) typical presentation

Answer 23

‘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

Question 24

Isopropyl alcohol sources

Answer 24

rubbing alcohol, perfumes, hand sanitizers.

Most often ingested as an ethanol substitute

Question 25

Pathophys of isopropyl alcohol

Answer 25

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

Question 26

Diagnosis of isopropanolol poisoning

Answer 26

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)

Question 27

Tx of isopropanolol poisoning

Answer 27

Supportive