ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: FR-PO590

Osmotic Demyelination Syndrome Associated with Acute Severe Hypernatremia and Hyperglycemia

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 902 Fluid and Electrolytes: Clinical


  • Tanemoto, Fumiaki, St. Luke's International Hospital, Tokyo, Japan
  • Nagahama, Masahiko, St. Luke's International Hospital, Tokyo, Japan
  • Ito, Yugo, St. Luke's International Hospital, Tokyo, Japan
  • Nakayama, Masaaki, St. Luke's International Hospital, Tokyo, Japan

The association between hyponatremic osmotic disturbance and osmotic demyelination syndrome (ODS) are well-established and studied. It has been increasingly recognized that ODS can occur in the setting of hypernatremia. In case of hypernatremic ODS, there is no consensus on how rapid or slow to correct plasma sodium. We report a case of ODS accompanied by acute hypernatremia and hyperglycemia.

Case Description

A 63-year-old female with a history of hypertension and dementia was brought to the ER with coma. Laboratory data were significant for plasma sodium of 189 mEq/L, plasma glucose of 629 mg/dL, serum bicarbonate of 22 mEq/L, BUN of 63 mg/dL, and plasma osmolality of 412 mosmol/kg. Head CT did not reveal any abnormalities. She was diagnosed with hyperosmolar hyperglycemic syndrome (HHS) and hypernatremia, and was admitted to ICU. Since there were 2 target components of hypertonicity simultaneously, hypernatremia and hyperglycemia, a great attention was paid to lower the tonicity appropriately to avoid cerebral edema. The upper limit of a correction rate of plasma tonicity during correction of hyperglycemia was set as 3 mosmol/kg per hour and that of plasma sodium was 10 mEq/L per day according to clinical guidelines. Although those correction rates were strictly kept, her neurological symptoms were not improved significantly. Brain MRI was performed to ascertain more precise information on day 6, which was consistent with ODS. With continuation of those correction rates of plasma tonicity and plasma sodium, her neurological symptoms as well as ODS findings in MRIs were improved gradually. The patient was sent to a rehab facility with good condition on day 65.


ODS usually occurs in patients with overly rapid correction of chronic hyponatremia. However, ODS also results from a rapid increase in tonicity in patients with acute hypernatremia or HHS. Since onset of hypernatremia is unclear in most of the cases, serial imaging with different modalities may be warranted for detecting subtle neurological findings associated with hypernatremia, such as cerebral edema or even ODS. Although the appropriate correction rate of plasma sodium with hypernatremic ODS is not known, this case suggests that adhering to clinical guidelines may improve the prognosis of it.