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

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: FR-PO033

Osmotic Demyelinating Syndrome and COVID-19

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Vasquez Espinosa, William Andres, Saint Peter's University Hospital, New Brunswick, New Jersey, United States
  • Joshi, Aditi Ashok, Saint Peter's University Hospital, New Brunswick, New Jersey, United States
  • Puri, Megha, Saint Peter's University Hospital, New Brunswick, New Jersey, United States
  • Toquica Gahona, Christian C., Saint Peter's University Hospital, New Brunswick, New Jersey, United States
  • Vasquez Espinosa, Carla F., Universidad UTE, Quito, Pichincha, Ecuador
  • Dwivedi, Shaunak A., Saint Peter's University Hospital, New Brunswick, New Jersey, United States
Introduction

Osmotic demyelination syndrome (ODS) is a dreaded complication of rapid sodium correction in high-risk hyponatremic patients. Predisposing factors include chronic alcoholism, malnourishment, severe hyponatremia. SARS-Cov2 infection may also be a risk factor as it is linked with multiple patterns of brain injury, renal damage and hyponatremia.

Case Description

Patient is a 48-year-old female with history of alcohol use disorder who presented with malaise, vomiting, diarrhea for 3 days. On admission, the patient was stuporous and confused. She was clinically hypovolemic. Initial labs demonstrated severe hyponatremia (102 mmol/L), hypokalemia (2.2 mmol/L), HCO3 of 35mmol/L, lactic acid of 4 mmol/L, no EtOH, preserved GFR. SARS-CoV2 PCR was positive. She was not hypoxic, her chest X-ray was clear. The patient was resuscitated with 1L of isotonic saline, potassium correction was attempted. Her bloodwork 4 hours later showed Na of 113 mmol/L and K of 2.4 mmol/L. At this point patient had prominent diuresis, UNa was 13mmol/L, Uosm 175mOsm/kg and U spec gravity 1.006. Immediately DDAVP and D5W were started. She had a poor response to this therapy and her sodium continued raising even at maximal doses. At 24h her sodium was 118 mmol/L and at 48h it was 125mmol/L with stabilization at this level. She had clinical improvement and was more responsive on day 3. On the following days, sodium gradually drifted toward 132 mmol/L. On day 5 she developing worsening mental status. She was found poorly responsive with fixed gaze, aphasia, minimally removing extremities from pain, able to blink when asked. Brain MRI revealed signal abnormalities in the central pons, bilateral thalami, caudate, basal ganglia, subinsular regions consistent with ODS. Intensive treatment was restarted with D5W and DDAVP. Na of 124mmol/L was achieved at 24h. Over the course of the following days, she had partial recovery. She was discharged to rehab, able to smile, move her head and partially move her extremities.

Discussion

SARS-Cov2 causes hyponatremia through several mechanisms. Poor oral intake, gastrointestinal loses, kidney injury and SIADH have been described. All of them may occur at the same time and cause hypovolemic/euvolemic states with high ADH. Volume replacement rapidly shuts off the ADH drive predisposing patients to get sodium overcorrection.