What complications of treatment of SIADH can occur?
Neurons, in response to hypotonic hyponatremia, expel electrolytes and organic osmolytes to reduce intracellular tonicity and limit brain swelling.
When the serum sodium concentration rises too fast for the cells to reverse the prior compensation by regaining or regenerating osmolytes, water flows down its osmotic gradient and out of the cells into the newly relatively hypertonic interstitium causing cell shrinkage and, potentially, demyelination of neurons.
This condition, termed osmotic demyelination syndrome (ODS), is characterized by an array of often irreversible neurologic manifestations including dysarthria, dysphagia, movement disorders (particularly spasticity), quadriparesis, behavioral abnormalities, seizures, delirium, and coma. In more severe cases, patients can become “locked in”—that is, conscious but unable to move, speak, or swallow. This complication occurs several days after the rapid correction, and the findings may be permanent. The classic presentation is a patient who initially becomes more alert as serum sodium concentration is corrected, then deteriorates a few days later.