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Abstract: TH-PO339

Rapid Correction of Measured Sodium Levels Despite Relatively Stable Corrected Sodium Levels Can Lead to Osmotic Demyelination Syndrome

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Salvi, Dhairya, Ascension Providence Rochester Hospital, Rochester, Michigan, United States
  • Pineiro De Jesus, Pedro Alberto, Ascension Providence Rochester Hospital, Rochester, Michigan, United States
Introduction

Hyperglycemia causes osmotic shift of water from the intracellular to the extracellular space, causing a dilutional hyponatremia. We refer to the sodium level corrected for hyperglycemia in such situations. We present a case that stresses the importance of measured sodium levels (NaM) rather than corrected sodium levels for hyperglycemia(NaG).

Case Description

A 59-year-old well-nourished, non-alcoholic male presented with polyuria, polydipsia, and generalized weakness for 2 weeks. On admission, he was dry with an unremarkable neurological exam. His labs suggested Hyperosmolar Hyperglycemic state (HHS) with blood glucose 844 mg/dL, NaM 129 mmol/L (NaG 141), bicarbonate 24 mmol/L, anion gap 14, blood urea nitrogen 29 mg/dL and a normal beta-hydroxybutyrate level. HbA1c was >14%. He received 2 liters of normal saline bolus and 15 units of regular insulin. Four hours later, glucose improved to 464 mg/dL with NaM 137 mmol/L (NaG 143). He was further started on a basal-bolus insulin regimen. Approximately 16 hours from arrival, he had a transient episode of dysarthria and right hemiplegia. Labs then showed glucose 178 mg/dL and NaM 139 mmol/L (NaG 140). CT scan of the head did not show any acute findings. MRI brain showed abnormal restricted diffusion and abnormal increased T2 signal intensity in the pons concerning for osmotic demyelination syndrome (ODS). The patient was later discharged safely without any residual neurological deficits.

Discussion

ODS develops as a result of relative hypertonic insult. Patients with HHS are particularly susceptible to a rapid rise in sodium levels, as the relative lack of insulin allows the development of higher glucose and thus lower sodium levels over a longer course as opposed to DKA patients which present more acutely. In this case, the corrected sodium levels were relatively stable, however, there was a rapid rise in the measured sodium levels, which most likely precipitated the event. Rapid lowering of blood glucose has also been proposed as a triggering factor for ODS in HHS. However, it is refutable as it causes a relatively hypotonic insult. This raises the question of whether we are being falsely reassured by relatively stable corrected sodium levels(NaG) even when the measured sodium levels(NaM) fluctuate and have the potential to lead to deleterious consequences.