Juan Carlos Ayus spoke last week at the American College of Physicians annual meeting on hyponatremic encephalopathy, as reported by DB’s Med Rants. Having heard Dr. Ayus speak on this topic before, I wish I could have heard the talk. Ayus has talked and written extensively on the dangers of hyponatremia and believes they are underemphasized, perhaps due to concerns about osmotic myelinolysis which can follow correction of hyponatremia. He co-authored this article from Nature Clinical Practice Nephrology (via Medscape, linked in DB’s post) in which he recommends a much more aggressive approach to the prevention of hyponatremia and the treatment of hyponatremic encephalopathy than is currently popular.
Hyponatremic encephalopathy is a dire emergency and must be treated rapidly. Reluctance to do so may stem from confusion between this condition and the more commonly encountered chronic hyponatremia which carries the greater risk of osmotic myelinolysis.
Of note, from the article:
In contrast with healthy persons who have a normal renal and neuron-humoral milieu, virtually all hospitalized patients are susceptible to hyponatremia. Elevated vasopressin levels can be taken for granted, as they have been associated with most hospital diagnoses.
Unless there is a special situation requiring hypotonic IV fluids, normal saline should be used in all patients requiring IV fluid. Ringers lactate, by the way, often considered isotonic, is actually hypotonic.
If the hyponatremic symptoms are severe (active seizures, respiratory arrest) the article recommends a 100 ml 3% saline bolus over 10 minutes. Elsewhere Ayus recommended this same regimen for marathon runners suffering from severe symptoms of hyponatremic encephalopathy. Milder symptoms of acute hyponatremic encephalopathy (nausea, vomiting, confusion, single resolved seizure) can be treated with the traditional 3% saline slow infusion. I was never taught to bolus patients with 3% saline. I did a quick search of UPtoDate and the new editions of Harrision’s and Cecil Medicine, none of which mentioned the bolus regimen. Though it seems extreme it makes sense in the situations described---the patient is about to herniate.
With respect to the risk of osmotic demyelination the overall rate of correction at 24-48 hours is more important than the hour to hour rate during the first few hours of treatment of hyponatremic encephalopathy. The article describes counter-measures and precautions to help prevent excessively high sodium concentrations at 24-48 hours.
The article mentions the relationships between hyponatremic encephalopathy and respiratory disturbances. These relationships are complex and exist on several levels. Hyponatremic encephalopathy causes two forms of respiratory failure: hypercapnic respiratory failure and non-cardiogenic pulmonary edema. The pulmonary issues associated with hyponatremic encephalopathy are discussed in greater detail in this paper co-authored by Ayus.