Abstract: PUB151
Hypertonic Pseudohyponatremia with Seizures: A Treatment Dilemma
Session Information
Category: Trainee Case Report
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Jaju, Neelam, Bhaskar Medical College and Bhaskar General Hospital, Yenkapally, Telangana, India
- Agraharkar, Mahendra L., The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
Introduction
Hyperosmolar hyperglycemic non ketotic syndrome (HHS) with seizures can cause brain damage and rapid correction of plasma sodium (pNa) and plasm glucose (pGL) can cause osmogenic demyelination (OD). If untreated it causes death due to cerebral edema. We lack guidelines for fluid and the rate of correction of hyponatremia in HHS. We describe a patient with hyponatremic seizure due to very high plasma glucose (pGL). Hyponatremia occurs with extracellular water shift and corrects as pGL improves as water shifts intracellularly. The seizures in HHS are due to high plasma osmolarity (pOsm) from high pGL. The protocols for HHS mandate saline infusion to repleat volume and simultaneous insulin infusion for pGL. Each infusion alone can correct pNa and pGL. We present a case of pseudohyponatremia with seizures and the dilemma we faced.
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Case Description
A 55-yr-old female diabetic unwell for a few days had a seizure. She received levetiracetam on the way to the hospital where she was unconscious and volume depleted. Her pGL was 1452 mg/dl, pNa 115 mEq/L, HCo3 of 21 mg/dl and a pH 7.37. HHS was diagnosed as the plasma osmolality (pOsm) was 320 mOsm/kg. Her urine sodium was 42 mg/dl, osmolality was 448 mOsm/kg and no ketones. With infusion of saline and insulin her pNa was 123 mEq/L and 128mEq/L in 3 and 6 hours while pGL was 1158 and 709 mg/dl and pOsm 315 and 302 mOsm/Kg respectively. A 0.225% saline was infused to reduce correction rate and pNa was 128 mEq/L for 2 days while pGL continued to fall. She made a complete recovery in 6 days.
Discussion
HHS has greater mortality than DKA. HHS with seizures may get treated with vasopressin receptors antagonists (VRA) or hypertonic saline causing an acute rise in the pNa and pOsm enhancing OD. There are no guidelines for correcting HHS seizures with pseudohyponatremia. In our case we used hypotonic saline to slow down the correction rate. We feel that saline infusion alone corrects volume depletion and reduces pGL and pNa merely by the dilutional effect. Simultaneous infusion of saline and insulin may be unnecessary and can be harmful due to a precipitous drop. There is no role for VRA, hypertonic saline or medications in the management peudo hyponatremic seizures. We propose that pOsm should guide the correction rate rather than pNa or pGL and only saline may be used initially to avoid rapid correction and OD. The mortality may be due to rapid correction.