Abstract: TH-PO334
Exploring the Cause of Acute Severe Hyponatremia: Cytarabine vs. Suspected Brain Lesion Due to Acute Myeloid Leukemia
Session Information
- Sodium, Potassium, and Volume Disorders: Clinical
October 24, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Vazquez Morales, Emily, Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Adams Chahin, Juan J., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
- Ocasio Melendez, Ileana E., Universidad de Puerto Rico Recinto de Ciencias Medicas, San Juan, Puerto Rico
Introduction
Hyponatremia is a serious electrolyte disorder associated with life-threatening neurological complications with a 47% prevalence in cancer patients. This case involves a patient diagnosed with acute myeloid leukemia (AML) and suspected central nervous system involvement, presenting with hyponatremia.
Case Description
A 54-year-old female with a history of AML was admitted to the Oncology ward for suspected AML relapse. A brain MRI revealed a homogenously enhancing lesion, lymphoproliferative in nature. Due to worsening leukocytosis (increasing from 61K to 126K), cytoreductive therapy with Cytarabine was initiated. After therapy was started, the patient developed an acute symptomatic hyponatremia of 120 mEq/L and Nephrology service was consulted. On examination, the patient was disoriented and lethargic with moist oral mucosa and no signs of volume overload. Serum osmolality was 253 mOsm/kg, and TSH levels were within normal limits. Urine spots were ordered, and 3% saline bolus was administered for a stated sodium correction goal of 4-6 mEq/L in 24 hours. The patient’s hyponatremia was attributed to the syndrome of inappropriate antidiuretic hormone (SIADH) secretion, potentially precipitated her intracranial lesion or Cytarabine infusion. After 3% saline bolus administration, sodium level improved to 123 mEq/L, but case was complicated by spontaneous ICH and fur further workup for the patient’s hyponatremia was not able to be ined due to the patient’s untimely death.
Discussion
Although laboratory evidence identifying SIADH as the primary cause of patient’s hyponatremia was insufficient, clinical suspicion was high. While cytarabine-induced SIADH is a rare occurrence, it has been documented in medical literature. Furthermore, in cases involving an intracranial lesion that may predispose a patient to SIADH, should we avoid the use of alkylating agents such as cytarabine, or should we instead implement closer monitoring if such agents are administered?