A 71‐year‐old woman on thiazide treatment for hypertension developed protracted vomiting and diarrhea for several days followed by confusion and lethargy. In the emergency department, serum sodium (SNa) was found to be 107 mEq/L Because of the severity of the hyponatremia, the patient was suspected to have both hypovolemia and SIADH as contributing causes. She received isotonic saline, and over the next 12 hours, she developed polyuria and her SNa rose 21 mEq/L. Because of the rapid rate of correction, she received 5% dextrose in water (D5W) with maintenance of her serum sodium in the 130 mEq/L range. Although at first the patient's mental status improved, on hospital day 3 her neurological condition deteriorated rapidly with development of mutism, increased tone in all extremities, and hyperreflexia. She was transferred to the intensive care unit and was given desmopressin and D5W to lower her SNa back to 115–120 mEq/L, with marked improvement in her neurological status. Thereafter, SNa was slowly uptitrated with desmopressin and 3% (hypertonic) saline. She made a complete neurological recovery.
Osmotic myelinolysis (formerly known as central pontine myelinolysis) is a life‐threatening problem associated with overly rapid correction of subacute or chronic hyponatremia. Current guidelines state that SNa should be corrected at a rate not exceeding 12 mEq/L per day. However, when extracellular volume depletion is the cause, vasopressin suppression after volume resuscitation results in marked production of dilute urine, increasing the risk of overly rapid correction. There is no standard of care that directs treatment once osmotic myelinolysis occurs. We report a case of a patient who developed clinical symptoms of osmotic myelinolysis syndrome who was successfully treated with reinduction of hyponatremia with desmopressin and D5W with complete neurological recovery. To our knowledge, this is one of a handful of case reports of reversible osmotic myelinolysis with reinduction of hyponatremia.1–3
Our case study illustrates several important teaching points in the inpatient management of hyponatremia. (1) Severe hyponatremia can be caused by hypovolemia alone, especially in conjunction with thiazide diuretics. (2) It is very difficult to manage the rate of recovery of hypovolemic hyponatremia. Thus, when it is severe (e.g., SNa < 125), admission to an ICU for very close monitoring is warranted. (3) Osmotic myelinolysis may be reversible with reinduction of hyponatremia and slow titration back to the normal range. (4) The use of desmopressin can rapidly stop the marked free water loss associated with recovery from hypovolemic hyponatremia and, when used in conjunction with D5W and hypertonic saline, allows for controlled adjustment of SNa to desired levels.
1. Oya S, et al. Neurology. 2001;57:1931–1932. 2. Soupart A, et al. Clin Nephrol. 1999;51:383–386. 3. Yamada H, et al. Case Report Neurol Med. 2012;2012:704639.
1. Oya S, et al. Neurology. 2001;57:1931–1932.
2. Soupart A, et al. Clin Nephrol. 1999;51:383–386.
3. Yamada H, et al. Case Report Neurol Med. 2012;2012:704639.