Clinical Case Scenario

A 70-year-old man, known hypertensive managed on telmisartan and thiazide diuretic was brought to the hospital by her family due to confusion and lethargy. For the last week, he had been complaining of low oral intake. He seemed disoriented during inspection, but his hemodynamics were stable. His symptoms started around two days ago and the plasma sodium level  was found to be 120 mmol/L. He experienced convulsions at the emergency room after an hour of arriving at ER and was given 3% saline to treat it. Within the following 12 hours, his blood sodium level quickly returned to 136 mmol/L. His neurological condition then worsened. An urgent MRI brain showed the following image as shown in figure 1.

Figure 1: T2 weighted imaging showing hyperintensities in basis pontis (white arrow)

(Case courtesy of Frank Gaillard, Radiopaedia.org, rID: 2598)

Wrong Answer: A. Cerebral edema due to acute osmotic influx of water into neurons

Wrong Answer: B. Activation of vasopressin in response to poor oral intake.

Right Answer: C. Demyelination due to rapid correction of chronic hyponatremia and opening of the blood-brain barrier

Explanation
Since the patient's hyponatremia persisted for more than 48 hours, it is termed as chronic. Brain cells adjust to persistent hyponatremia by exporting osmoles (such as K⁺ and organic solutes) in order to lessen swelling.
In this situation, rapid sodium correction can cause demyelination, including central pontine myelinolysis, decrease cerebral endothelial cells, and interfere with the blood-brain barrier. The pathogenesis includes oligodendrocyte destruction, microglial activation, and immunological agents (lymphocytes, cytokines) entering the brain.

The following are the six therapeutic tenets:
1) If the symptoms are mild to severe and acute, treat right away with hypertonic saline (about 3% saline).
2) Regardless of the corrective technique, make moderate corrections if the patient is chronic, asymptomatic, or very slightly symptomatic.
3) Stop using any drugs that affect natriuresis or renal free water excretion.
4) Except in acute/symptomatic (moderate-to-severe) situations, individuals at high risk of developing osmotic demyelination syndrome (ODS) should adhere to the maximum correction limit.
5) Re-lower to low serum [Na+] using 5% dextrose (D5W) and/or desmopressin in carefully chosen patients if corrected too quickly.
6) Following the start of therapy, do routine blood tests and track urine output.