Question 21.3

A 46-year-old male from a foreign fishing vessel presents unconscious to the Emergency Department. He complained of visual disturbance prior to his deterioration.

The following blood results are obtained:

Parameter	Patient Value	Normal Adult Range
Sodium	144 mmol/L	135 – 145
Potassium	4.0 mmol/L	3.5 – 5.0
Chloride	102 mmol/L	95 – 110
Bicarbonate	8.2 mmol/L*	22.0 – 30.0
Urea	6.4 mmol/L	3.0 – 7.0
Creatinine	127 μmol/L*	44 – 97
Glucose	5.0 mmol/L	3.5 – 7.8
Calcium (ionised)	1.10 mmol/L	1.03 – 1.23
Lactate	4.1 mmol/L*	0.6 – 2.4
Osmolality	324 mOsm/kg*	275 – 295

a) What is the most likely diagnosis? (10% marks)

b) What is the pathophysiology of the visual disturbance? (20% marks)

c) List three specific treatments you would institute. (15% marks)

[Click here to toggle visibility of the answers]

College Answer

Methanol toxicity

Methanol - > formaldehyde - > formate which is neurotoxic (especially retina and basal ganglia)

Sodium bicarbonate

ADH inhibition with Ethanol (or fomepizole if available)

Dialysis

Cofactor therapy with either folic or folinic acid

Discussion

So as to be fair to the other no-less-toxic alcohols, here is a table of the common alcohol toxidromes

Disorder	Toxin	Clinical and Laboratory Abnormalities
Alcoholic ketoacidosis	β-hydroxybutyric acid Acetoacetic acid	Metabolic acidosis
Methanol intoxication	Formic acid Lactic acid Ketones	Metabolic acidosis hyperosmolality retinal damage with blindness Basal ganglia (putamen) damage
Ethylene glycol intoxication	Glycolic acid Calcium oxalate	Cardiovascular collapse Myocardial damage Cerebral damage Renal failure Metabolic acidosis Hypocalcemia
Diethylene glycol intoxication	2-Hydroxyethoxyacetic acid	Neurological damage Rrenal failure Metabolic acidosis
Propylene glycol intoxication	Lactic acid	Metabolic acidosis
Isopropyl alcohol intoxication	Isopropanol	Coma hypotension No acidosis! Only acetone is the metabolic product

Management of toxic alcohol poisoning:

Decontamination

Activated charcoal is useless. Absorption is too rapid.

Enhanced elimination

Haemodialysis: toxic alcohols and their metabolites are rapidly cleared in this manner
Thiamine enhances metabolism of ethylene glycol to alpha-hydroxy-beta-ketoadipate
Pyridoxine enhances metabolism of ethylene glycol to glycine (and ultimately hippuric acid).
Folate and leucovorin enhance the clearance of formate
Alkalinization of urine with a bicarbonate infusion promotes dissociation of formic acid (it is less toxic in its ionised state) and improves its clearance by ion trapping in the urine

Specific antidotes

Alcohol - the precise use of this substance in overdose is discussed in the chapter on ethylene glycol and its toxic acid metabolytes.
In brief, one should sustain a blood ethanol concentration of 20 to 30 mmol/L (100 to 150 mg/dL) - this equates to a blood alcohol level of 0.1-0.15%.
Fomepizole as it is known, is basically a competitive antagonist to alcohol dehydrogenase. It does what ethanol would do, except it does so with great expense, and without ethanol intoxication. The advantage of using it is its lack of CNS effects - if the patient is confused already you do not want to add alcohol into the mix.

Supportive management

Boring supportive care is all that is required.
Airway control and mechanical ventilation: the patient may be uncooperative and with a foul manner.
Circulatory support in case of significant haemodynamic collapse
Sedation and analgesia with short acting substances

References

Kraut, Jeffrey A., and Ira Kurtz. "Toxic alcohol ingestions: clinical features, diagnosis, and management." Clinical Journal of the American Society of Nephrology 3.1 (2008): 208-225.

Henderson, William R., and Jeffrey Brubacher. "Methanol and ethylene glycol poisoning: a case study and review of current literature." Cjem 4.1 (2002): 34-40.

[Submit a comment or correction]