TOPIC DISCUSSION: METHANOL and TOXIC EFFECTS

A nice feature in AJKD , the acid base teaching case this month presents the lack of toxic effects of methanol in someone with HIV.  Why does that matter? Like detectives, they figured this out in this case.  Methanol toxicity usually presents with anion gap and an osmolar gap.  The levels of methanol might take some time to come back but the AG is what you want to aim for. But in this case, there was no anion gap noted with this methanol ingestion.  Without a clinical history, this overdose can be overlooked especially, if there is an inhibitor of alcohol dehydrogenase present already doing its job such as ethanol.
Certain populations express lower levels of endogenous alcohol dehydrogenase :- infants, young women, cirrhotic patients, and certain racial groups.
Ethanol ingestion, or other alcohol such as isopropanol can competitively inhibit the metabolism of methanol and give this false impression of no methanol on board
Medications that can block this enzyme can also do it- fomepizole and in this case they presented was abacavir.

Great case and nice review of methanol kinetics and metabolism and the role of dialysis in removal of the toxin.

CONSULT ROUNDS: METHANOL and the EYE?

Methanol toxicity increases formic acid and causes an anion gap and osmolar gap and classic optic findings.
WHY the eye and not other organs like liver, other small vessels? anyone ever wondered? Even as little as 10ml can destroy the optic nerve.
Methanol is a CNS depressant and can cause same effects as alcohol. It also gets metabolised to formic acid via formaldehyde in a process by an enzyme called alcohol dehydrogenase in the liver.
Formic acid can inhibit mitocondrial cytochrome c oxidase leading to hypoxia and anerobic changes leading to acidosis.

The eye has Vitamin A and needs it for functioning. Apparently Vitamin A is metabolized by alcohol dehydrogenase ( the same enzyme), since there is a place for that enzyme there, its possible that the optic nerve becomes a target for methanol's toxication. and not other organs specifically.

ANION GAP ACIDOSIS: GOLD-MARK makes a MARK:

GOLDMARK  is the new MUD PILES

A new mnemonic has been created in the last few years for anion gap acidosis. 

Glycols( ethylene glycol, propylene glycol)
Oxoproline
L- lactate
D-lactate
Methanol
Aspirin
Renal failure
Ketoacidosis

Two popular mnemonics were often used to remember the major causes of the high-gap metabolic acidoses. The first is KUSMALE which represents Ketoacidosis, Uremia, Salicylate poisoning, Methanol, Aldehyde (paraldehyde), Lactate, and Ethylene glycol. 

The second is MUD PILES( most popular), spells out Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Iron (and Isoniazid), Lactate, Ethylene glycol, and Salicylate.

Why GOLDMARK then? The causes have changed in the 21^st century. We barely see any more paraldehyde any more, neither we see that much Iron and INH related causes.

Newer causes: D-lactate: seen with short gut syndrome( especially after sugary drinks), diabetes can lead to d-lactate as well. Other new causes is pyroglutamic acid ( oxoproline) seen with chronic Tylenol use. Finally, propylene glycol infusion that is usually found in lorazepam, phenobarb and banana bags.

Initially this was proposed in LANCET

Consult Rounds: Toxic alcohol ingestions

A summary of all potential alcohol toxicities ( Renal perspective)

Name	Metabolic Acidosis	Osmolar Gap	Anion Gap	Ketones	Ca Oxolate Stones	Reduced Vision
Alcohol	Yes	Yes	Yes( lactate also)	Yes	No	No
Methanol	Yes	Yes( earlier on and then disappears)	Yes	No	No	Yes
Ethylene Glycol	Yes	Yes	Yes	No	Yes	No
Isopropyl Alcohol	No	Yes	No	Yes	No	Yes
Propylene Glycol	Yes	Yes(initially)	Yes(converted to lactate)	No	No	No

TOPIC DISCUSSION: Alcohol Poisonings, gaps and osmoles

This weeks Kidney International's Whats your diagnosis section discusses a case of Diethylene glycol poisoning. ( image courtesy on left: Precious Body Fluids Blog)
Of all the alcohol poisonings, its important to distinguish which one you are dealing with. The article has a nice table that shows the similarities and differences of them.
Methanol poisoning usually has acute renal failure, met acidosis ( part of MUDPILES), and increased or normal osmolar gap; there is some neurological and visual disturbances.
Propylene glycol is usually seen with ativan drips, is seen with acute renal failure, metabolic acidosis and sometimes an osmolar gap but other findings are negative.
Ethylene glycol, another cause of metabolic acidosis and increased osmolar gap, you see with renal failure and + calcium oxalate crystals.
The Diethylene glycol poisoning is more rare but can happen as in this case. Its usually seen with acute renal failure, + metabolic acidosis and sometimes an osmolar gap but very frequently as noted in this article with neurological facial nerve pals and mild hepatitis.
Isopropyl alcohol is a classic one that has an elevated osmolar gap but no anion gap.
There is always something hiding in the gap. Even a low osmolar gap is abnormal.
take a look at this table I saw in Canadian medical association journal. I think that this table is a nice review.
Says it all.

TOPIC DISCUSSION: Mnemonic for toxins that are removed by hemodialysis

Toxins that are removed by hemodialysis

Here is a mnemonic I found online

I   STUMBLE

I = Isopropanol
S= Salicylates
T = Theophyline
U = Uremia
M= Methanol
B= Barbituates, beta blockers (water soluble ones such as atenolol)
L= Lithium
E= Ethylene glycol

Source: http://crashingpatient.com/toxicology/general-toxicology-random-drugs.htm/