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Abstract: PUB271

True Hyponatremia Secondary to Intravenous Immunoglobulin Infusion

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

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

Authors

  • Shah, Neepa, Marshfield Clinic Health System, Marshfield, Wisconsin, United States
  • Waters, Claudia, Marshfield Clinic Health System, Marshfield, Wisconsin, United States
  • Kattamanchi, Siddhartha, Marshfield Clinic Health System, Marshfield, Wisconsin, United States
  • Blonsky, Rebecca, Marshfield Clinic Health System, Marshfield, Wisconsin, United States
Introduction

Intravenous immunoglobulin infusion (IVIG) is used to treat a number of autoimmune disorders. However, IVIG can cause sodium disorders. Here we present a case of hyponatremia due to IVIG.

Case Description

The patient is a 96 year old female with history significant for chronic hyponatremia and ITP presented following a fall complicated by a displaced femoral neck fracture requiring surgical intervention. Serum sodium at baseline is approximately 130 to 132 mmol/L and at the time of admission sodium was 128 mmol/L. The patient was thrombocytopenic due to underlying ITP, thus was given platelets and IVIG due to need for surgical intervention. Following IVIG her serum sodium fell to a nadir of 113 mmoL/L. Nephrology was consulted for hyponatremia. Based on workup, the patient was diagnosed with true hyponatremia due to increased extracellular water concentrations as a result of the IVIG. The patient was treated with high protein diet, oral sodium chloride 2 grams PO TID, fluid restriction and diuretics. With treatment the patient’s sodium improved and was 126 mmoL/L by discharge.

Discussion

Plasma comprises approximately 93% plasma water and 7% proteins and lipids. Any medical condition causing increased proteins and lipids in the blood will cause automated chemistry to interpret this as a low serum sodium. IVIG can cause post-infusion hyperprotenemia leading to pseudohyponatremia. However, the sucrose used as a carrier in commercial IVIG is osmotically active and can lead to the movement of water from the intracellular compartment to the extracellular compartment causing a true hyponatremia. Patients with impaired free water excretion, such as those with kidney disease can lead to further worsening of this hyponatremia.