Central pontine myelinolysis associated with ethylene glycol intoxication

March 4, 2014, 6:04 pm

central pontine myelinolysis, MRI

central pontine myelinolysis, MRI


Massive Ethylene Glycol Poisoning Triggers Osmotic Demyelination Syndrome. Ahmed A et al. J Emerg Med 2014 Mar;46(3):369-74


Central pontine myelinolysis has long been associated with too rapid correction of subacute hyponatremia. Although the pathophysiologic mechanism has not yet been fully elucidated, it appears to involve stress from relative serum hyperosmolality and loss of water from brain cells. Endothelial damage and injury to the blood-brain barrier may also play a role. Recently, this process has been renamed osmotic demyelination syndrome (ODS) with recognition that  neuropathological damage is not limited to the pons.

In addition, some cases of ODS have been associated with other forms of osmotic stress, such as hyperglycemia. This interesting report describes a case in which ODS apparently was caused by ethylene glycol intoxication and its treatment.

A 64-year-old woman was brought to the emergency department following a massive ingestion of ethylene glycol. The initial plasma ethylene glycol level was 1055.5 mg/dL, the plasma osmolality was 535 mOsm/kg, and the osmolal gap was 218 mOsm/kg. She was treated with fomepizole and hemodialysis. However, her neurological status did not improve as expected with elimination of the toxic alcohol and correction of acidosis. She remained somnolent, with hyperreflexia and symmetric muscle weakness. MRI (not the one pictured above) showed findings consistent with ODS. Her condition improved over several days and she returned to baseline neurological status.

Although neurological sequelae of ODS — including quadriparesis, cognitive changes, tremor and weakness — may be persistent, the few reported cases involving hyperosmolar stress seem to have had relatively good outcomes. It is certainly reasonable to assume that the rapid development of hyperosmolality caused by massive ethylene glycol ingestion, and then rapid decrease in osmolality as a result of treatment, were responsible for the clinical and MRI findings in this case. Certainly ODS is something to consider when the neurological status of a patient being treated for toxic alcohol poisoning does not follow the expected script.

[MRI of central pontine myelinolysis from wikipedia.org]



  1. Josh King Says:

    A small point to make – it is probably the case that the initial plasma hyperosmolality was more likely to cause ODS than treatment of ethylene glycol. The differential between plasma and brain osmolality is what is thought to cause ODS; usually (as in the case of hyponatremia) both are low, but plasma osmolality goes up before brain osmolality can adjust. If anything, theoretically, rapid treatment of acute hyperosmolality in this case would reduce the risk of ODS (analogous to reintroduction of hyponatremia in patients that overcorrect, which has some animal studies backing it up). Either way, certainly ODS could be a consideration in cases where mental status doesn’t improve after treatment of a toxic alcohol ingestion.

  2. Leon Says:


    Thank you for your comment. I agree, the rapid increase in osmolality from massive acute EG ingestion would be expected to cause intracellular water loss — and thus mirror the mechanism causing ODS when chronic hyponatremia is rapidly reversed.