Joseph G. Verbalis*
Hypoosmolality and hyperosmolality are relatively common clinical problems (1). Many different factors contribute to the morbidity and mortality known to occur during states of altered osmotic homeostasis. The most serious complications are associated with pathological changes in brain volume: brain edema during hypoosmolar states and brain dehydration during hyperosmolar states. This chapter will summarize what is known about the changes that occur in brain fluid and solute composition during hypoosmolar and hyperosmolar states, which are responsible for the compensatory process of brain volume regulation. Most experimental and clinical studies have used serum sodium concentration as an indicator of osmolality, and throughout this chapter the terms hyponatremia and hypoosmolality are used interchangeably, as are hypernatremia and hyperosmolality.
Hypoosmolality is well known to cause a variety of neurological symptoms, including disorientation, confusion, obtundation, seizures and death from tentorial herniation, called hyponatremic encephalopathy (4,5), but the incidence and severity of such symptoms in hyponatremic patients is quite variable (6). It is not unusual to find patients with low serum sodium concentrations ([Na+]) who are relatively asymptomatic, while others exhibit severe neurological dysfunction at equivalently low levels of serum [Na+]. Such clinical observations indicate that the brain can successfully adapt to even severe degrees of hypoosmolality in many cases. Knowledge of how the brain regulates
* Georgetown University Medical Center, 4000 Reservior Rd., Washington DC 20007. USA Phone: 202-6872818, Email: [email protected].
its volume in response to hypoosmolality has been crucial to understanding this sometimes perplexing spectrum of clinical presentations of hypoosmolar patients.
Was this article helpful?