Mastering Hyponatremia: A Physiology Based Approach

Hyponatremia is easier to manage when you understand the physiology. In this Nephrology Notebook lecture, we review a practical approach to hyponatremia using tonicity, effective arterial blood volume, vasopressin physiology, urine osmolality, urine sodium, and correction safety. Topics include hypotonic hyponatremia, pseudohyponatremia, hyperglycemia related hyponatremia, hypovolemic hyponatremia, thiazide induced hyponatremia, hypervolemic hyponatremia, S I A D, low solute intake, emergency hypertonic saline, the SALSA trial, oral urea, vaptans, osmotic demyelination syndrome, correction ceilings, proactive desmopressin clamp, and reactive relowering with dextrose five percent in water. This video is intended for interns, residents, fellows, attendings, and other clinicians. Any patient case discussed is hypothetical and used only for educational purposes. Key Points Serum sodium is a concentration, not a direct measurement of total body sodium. A V P, A D H, and vasopressin refer to the same hormone. Serum osmolality tells you whether hyponatremia is truly hypotonic. Urine osmolality tells you whether vasopressin effect is present. Urine sodium helps infer effective arterial blood volume, but diuretics and kidney disease can confound interpretation. Severe neurologic symptoms require symptom driven three percent hypertonic saline. The initial treatment target is usually a rise of about four to six millimoles per liter, not normalization. Overcorrection often happens when vasopressin turns off and aquaresis begins. Desmopressin can be used proactively to control correction or reactively to halt aquaresis during overcorrection.