A 58 year old man with altered mental state, low GCS with tachycardia and hypotension requiring airway control and resuscitation
1.Compensated high anion gap metabolic acidosis due to high lactate (very high, therefore consider other spurious cause ie. another compound being interpreted as lactate by the gas machine)
mild elevation of chloride
Normal renal function (borderline Creat unlikely to account for acidaemia0
Normal glucose, no ketones
negative blood alcohol
low calcium
2.
Causes:
Must consider toxicological cause – especially toxic alcohols, paracetamol, Salicylate, CO/CN, Iron (low Calcium, bordeline elevation in Creatinine and low GCS imply likely toxic alcohol ingestion)
Seizure
CNS
sepsis /shock – CNS, abdo, other – no vitals given
3.Osmolar gap
Measured osmolality – in this patient was 323
Calculated – 298.5
Osmolar gap = 25 –> high and indicates toxic alcohol ingestion
If you dont have a high index of suspicion for the diagnosis, you may miss it leading to catastrophic effects on the patient
Temporizing treatment is po (NGT) alcohol, best with 3X40ml shots of vodka as a loading dose and then 1-2 shots hrly aiming for a blood alcohol of >0.1% (inhibits the enzyme in the metabolism of toxic alcohols)
Some gas machines record glycolic acid as lactate, which may explain the very high lactate level.
Ethylene glycol is a parent compound that exerts most of its toxicity by conversion to metabolites. Ethylene glycol itself may cause some alteration of mental status but it is a relatively nontoxic compound before it is metabolized. The metabolites cause the distinctive toxicity associated with this compound.
Knowing the pathway of ethanol metabolism is necessary to understand ethylene glycol toxicity properly. Ethanol is metabolized by the enzyme alcohol dehydrogenase (ADH) pathway, which is located in the liver and gastric mucosa, and by the cytochrome P-450 mixed function oxidase (MFO) system in the liver. The mixed function oxidase component is subject to greater inducibility than alcohol dehydrogenase.
As with ethyl alcohol and methanol, ethylene glycol is metabolized by the enzyme alcohol dehydrogenase. In this step it forms glycoaldehyde. Through interaction with aldehyde dehydrogenase, ethylene glycol is then metabolized to glycolic acid (GA). A profound acidosis often ensues with this intoxication which is attributable to the glycolic acid in circulation. This glycolate is then transformed into glyoxylic acid. At this point, the molecule may be transformed into the highly toxic oxalate or the safer glutamate or α-ketoadipic acid metabolites.
Calcium oxalate crystals may form and accumulate in blood and other tissues. The precipitation of calcium oxalate in the renal cortex results in decreased glomerular filtration and renal insufficiency. The formation of these crystals consumes circulating calcium, and hypocalcaemia may occur.
The rate-limiting step of ethylene glycol metabolism is the alcohol dehydrogenase–catalyzed step. Common ethyl alcohol (ethanol) binds much more easily to alcohol dehydrogenase than ethylene glycol or methanol does. Because ethanol is the preferred substrate for alcohol dehydrogenase, the presence of ethanol may essentially block metabolism of ethylene glycol. In addition, this enzyme is blocked by the administration of fomepizole (4-methylpyrazole [4-MP]). Not available in Australia.
Upon oral ingestion, serum levels of ethylene glycol peak within 1-4 hours. The elimination half-life (assuming preserved renal function) is 3 hours.