Patients with severe hyponatremia ([Na+] < 120 mEq/L) can present with altered mentation, seizures, lethargy, and even coma. After identifying the likely cause(s), treatment is centered around a combination of sodium replacement (usually with 3% hypertonic saline, HTS) and volume correction depending on if the patient is hypo-, eu-, or hyper-volemic. The goal correction rate is 4-6 mEq/L in 24 hours (no more than 8 mEq/L); however, overcorrection is a concern and can result in devastating consequences like osmotic demyelination syndrome (ODS) in the central nervous system.
In particular, patients with hypovolemic hyponatremia (poor intake, vomiting, diuretics, etc.) can present an interesting challenge. These patients usually have an appropriate excess of antidiuretic hormone (ADH) to conserve volume; however, ADH levels rapidly decrease, leading to diuresis after resuscitation. This loss of free water, coupled with the administration of HTS, can result in an undesirable overcorrection in serum sodium.
Desmopressin (DDAVP), a synthetic analog of arginine vasopressin (ADH), promotes free water retention through aquaporin mobilization via V2 receptor activation in the nephron’s collecting duct. To be proactive, I’ll limit enteral water intake and immediately start DDAVP (2 mcg q6h IV) with 1 cc/kg HTS over 6 hours. These doses can be adjusted based on the rate of sodium correction and water loss (diuresis, vomiting, insensible losses, etc.). By “clamping” the kidneys with DDAVP while simultaneously administering HTS, the correction rate tends to be at goal.
If sodium increases too quickly, I’ll continue DDAVP and slow down HTS. If patients have already overcorrected, I’ll continue DDAVP and replace HTS with free water (e.g., D5W). When I decide to wean the clamp (DDAVP and HTS), I closely monitor the urine output and serum sodium, restarting the clamp if needed.