More on hyponatremic encephalopathy

In a recent post on this topic I mentioned differing expert opinions on the aggressiveness of treatment of hyopnatremic encephalopathy. Traditional teaching suggests the use of an infusion of 3% saline with treatment selection based at least in part on the absolute value of the serum sodium concentration. In recent years a more aggressive approach (which I originally cited here) has been suggested by Dr. Juan Carlos Ayus and others. That approach, along with some other aspects of hyponatremia in hospitalized patients, was recently discussed in a nice review in ACP Hospitalist. Key points, along with a few observations of my own:

Menstruant women are at greatest risk, followed by postmenopausal women, followed by men. Estrogen impairs brain adaptation to hyponatremia.

Conceptually it is the rate of fall of the serum sodium (relative to the speed with which the brain can adapt) rather than the absolute concentration of sodium which determines the risk of encephalopathy. This is often not known in practice, so clinical assessment coupled with the serum sodium level must govern treatment.

Hyponatremic encephalopathy is often missed in post operative patients because it resembles ordinary post operative nausea and vomiting.

Hospitalized patients, by virtue of their illnesses and circumstances, have multiple stimuli for vasopressin secretion. It can virtually be taken for granted that a hospitalized patient has elevated vasopressin levels.

In the face of elevated vasopressin levels hypotonic fluid will predictably lower the serum sodium concentration. For this reason the authors advocate that isotonic fluids be used in all hospitalized patients. There may be exceptions to this rule but it is safest in terms of preventing hyponatremic encephalopathy.

For treatment of hyponatremic encephalopathy the authors advocate small (100 ml) boluses of 3% saline rather than continuous infusions.

Concern about osmotic demyelination syndrome due to over correction has been a barrier to effective treatment of hyponatremic encephalopathy. But if the patient really has hyponatremic encephalopathy the risk of under treatment is greater than that of over treatment.

Osmotic demyelination remains a concern. After initial treatment of hyponatremic encephalopathy intervention may be necessary to blunt further rise in serum sodium. The Δ [Na+] at 24-48 hours is a frequently cited risk factor for demyelination.

Neurogenic pulmonary edema and hypercapnic respiratory failure are regular but under appreciated features of hyponatremic encephalopathy. Neurogenic pulmonary edema as a complication of hyponatremic encephalopathy is now known as Ayus-Arieff syndrome, and is treated with hypertonic saline.