8.8A Tox Alcohols Em

Front 1

Regarding ETOH, which is incorrect,
1. features of intoxication include euphoria, nystagmus, aggression, and tachycardia.
2. serum ETOH levels define legal driving limits
3. whole blood concentrations are approximately 10% lower than serum concentrations
4. activated charcoal is not indicated
5. urinary retention may complicate presentation
6. other causes of CNS depression should be considered in the presence of a raised serum ETOH concentration

Back 1

2. incorrect. Whole blood concentrations define legal driving limits

Front 2

Regarding ethylene glycol, true or false:
1. ingestion of greater than 1ml/kg is potentially lethal
2. all deliberate self poisonings should be assumed to be potentially lethal
3. dermal and inhalation exposure can lead to EG intoxication
4. a severe anion metab acidosis may be expected
5. Ca carbonate crystals form in tissues
6. hypercalcaemia may result
7. nephrotoxins include glycolic acid and calcium oxalate

Back 2

1. true
2. t
3. F
4. T
5. F - Ca oxalate
6. F - hypocalcaemia
7. T

Found in - radiator coolants and antifreeze, de-icing solutions, solvents, brake fluids

Front 3

Regarding ethylene glycol, T or F
1. the more important toxic effects are due to the parent compound
2. peak concentrations occurs >10/24
3. toxic metabolites include glyoxylic acid, oxalic acid
4. cranial neuropathies occur up to 20 days later
5. presence of calcium carbonate crystals in urine is pathognomic of EG intoxication

Back 3

1. F
2. F - 1-4 hours
3. T
4. T
5. F - calcium oxalate

Front 4

Regarding mx EG toxicity, T or F
1. intubation with normal ventilatory parameters is essential
2. bolus IV NaHCO3 1-2mmol/kg may be administered to prevent worsening acidaemia
3. correction of hypocalcaemia is always necessary
4. activated charcoal is indicated
5. HD is the definitive mx
6. ETOH is the antidote utilised in Australasia
7. Coingestion of ETOH accelerates onset of clinical features of EG intoxication

Back 4

1. F - HYPERventilation prevents worsening acidaemia
2. T
3. F - only for seizures or prolonged QT
4. F - NOT indicated
5. T
6. T - because Fomepizole (alcohol dehydrogenase inhibitor) is not available; Fomepizole is more easily administrated, has less adverse effects, may reduce need for HD. $$$
7. F - DELAYS (?because ETOH competitively inhibits ADH)

Front 5

Indications for HD in EG toxicity are...

Back 5

1. Hx large EG ingestion with osmolar gap >10 (e.g. any elevation OG)
2. acidaemia with pH <7.25
3. ARF
4. EG level >8mmol/L (50mg/dL) if available

Endpoints - resolution of above, except ARF, EG level <2mmol/L

Front 6

Regarding Isopropanol, T or F
1. the specific antidote is fomepizole
2. marked GI irritation, ketosis and acidosis may directly result
3. coma and refractory hypotension are indications for HD
4. children may develop significant toxicity from dermal absorption
5. a CNS intoxication synd identical to ETOH but more potent and prolonged results
6. acetone fetor may be present
7. elevated osmolality, osmolar gap and severe anion gap acidosis suggest intoxication.
8. serum acetone level is elevated.

Back 6

1. F - no antidote
2. F - acidosis does not directly result
3. T
4. T
5.T
6. T
7. F - elevated osmolality and osmolar gap IN THE ABSENCE of severe anion gap acidosis suggests isopropanol intoxication. ( Cf EG and methanol)

Front 7

Regarding methanol, T or F
1. ingestion >5mL/kg potentially lethal
2. production and accumulation of formic acid produces a nonanion gap acidosis and direct cellular toxicity due to inhibition cytochrome oxidase
3. retinal injury and oedema leads to blindness and in the brain putamenal oedema and cortical WM haemorrhages occur
4. rapidly absorbed - peak levels within 10/60
5. clinical features severe intoxication include drowsiness, blindness, reduced resp rate
6. most patients suffers irreversible visual complications
7. survivors of severe CNS toxicity frequently display extrapyramidal movement disorders

Back 7

1. FALSE - 0.5mL/kg
2. F - ANION gap acidosis
3. T
4. F - 30-60mins
5. F - increased resp rate (because of respiratory compensation for acidosis)
6. F - up to one third
7. T

Found in - solvents, model airoplane fuels, fuel additive, dyes and stains, wood alcohol, wood spirits

Front 8

Methanol intoxication, which is incorrect
1. Venous bicarbonate is a useful surrogate marker of formic acid production in asymptomatic patients where ABGs are not available
2. An ETOH level should be performed to determine coingestion and titrate antidote
3. CTB shows characteristic changes in the thalamic region in patients with temporary neurological sequelae
4. Intubated patients should be hyperventilated
5. pH <7.3 is an indication for bicarbonate administration to prevent formic acid inhibition of cytochrome oxidase

Back 8

3. INCORRECT - CTB shows changes in the BASAL GANGLIA in patients with PERMANENT neuro sequelae

Front 9

RE: Methanol T/F
1. Folinic acid is the antidote at 2mg/kg IV Q6H until poisoning treated
2. ETOH competitively inhibits methanol metabolism to formaldehyde
3. HD is the definitive management via removal of formaldehyde (methanol and formic acid intermediary)
4. Fomepizole and ethanol may be temporizing measures while awaiting HD
5. Australian methylated spirits are a source of methanol
6. asymptomatic patients without deliberate ingestion may be presumed to have insignificant ingestion

Back 9

1. NOT antidote, rather 'cofactor'. Active form of folic acid (cannot substitute folic acid). An adjunctive treatment. Controversial value. Dose is 2mg/kg IV Q6H, rarely causes anaphylaxis and seizures. Hypercalcaemia a cx of rapid administration. Also utilised in methotrextate and trimethoprim poisoning.
2. T
3. F - removes METHANOL and FORMIC ACID
4. T
5. F - but NZ m.spirits may contain up to 5% methanol
6. F - must remain clinically well, have a normal bicarb, and have had an undetectable ETOH level 8/24 prior for admission (e.g. looking for evidence of formic acid production and the absence of ETOH level which will delay onset of clinical features)

Front 10

What are the indications and endpoints for HD for methanol? How do these differ from EG?

Back 10

pH <7.3 (EG - pH 7.25)
OG >10*
ARF*
Visual symptoms
Deterioration vital signs or electrolyte status despite supportive care
Methanol level >15mmol/L (EG >8)

Endpoints
Correction acidosis and OG*
Methanol level <6mmol/L (EG >3.2)

*features that are the same

Front 11

Regarding 'other' toxic alcohols (benzyl alcohol, dipropylene glycol, propylene glycol etc.) T/F
1. AG acidosis, hyperlactataemia and raised OG are surrogate markers of intoxication; venous bicarb is useful if ABG not available
2. Even accidental poisonings cause significant toxicity
3. Effects may include coma, seizures, refractory shock and renal failure
4. Mainstay of severe ingestions is primarily supportive with IVF and diuresis to maintain renal function
5. Fomepizole and ETOH may be useful in glycol ether (EGBE, EGME) poisoning, but role is not established in other toxic alcohols

Back 11

p. 142 Murray
1. T
2. F - accidental do not cause significant toxicity, deliberate poisonings should be assumed to be potentially LETHAL
3. T
4. F - usually require intubation with hyperventilation, sodium bicarbonate, seizure and hypoglycaemia Mx, HD and antidote ETOH
5. T