Acute electrolyte disorders that cause seizures typically present with rapidly progressive neurologic symptoms and signs, and therefore require emergency treatment. In general, the short-term prognosis for seizure control and neurologic recovery is related to the correction of the specific metabolic derangements; the long-term prognosis depends on correction of the underlying condition.
Water homeostasis and disorders of electrolytes, particularly sodium, are interrelated. Intracellular fluid (ICF) and extracellular fluid (ECF) are the two components of total body water.4 The ECF is further divided into the intravascular compartment (plasma water) and the extravascular compartment (interstitial water).
The concentrations of particles (osmoles) in the ECF and ICF determine their osmolalities, expressed in milliosmoles (mOsm) per kilogram water. Because water moves along osmolality gradients and can pass freely across cell membranes, the osmolality of each compartment of the ECF equilibrates. Secondarily, the osmolality of the ECF equilibrates with the ICF. Because the ECF compartment has a considerably larger volume than the ICF compartment, ECF osmolality determines the volume of ICF once osmotic equilibrium is achieved.
Although water freely passes across cell membranes, some solutes may not because of active transporters or pumps that maintain different solute concentrations between the inside and outside of cells. These solutes determine the effective osmolality (also referred to as tonicity) of the compartment in which they are concentrated. Sodium is mainly confined to the ECF and hence largely determines the effective osmolality of the ECF (and, in turn, the ICF volume). Consequently, the main cause of serum hypoosmolality is hyponatremia.
The normal range of plasma osmolality is 275–290 mOsm/kg, which is maintained as long as the volume of water absorbed equals the volume of water excreted. Water excretion occurs predominantly through the kidneys but also through insensible water loss (e.g., sweat, respiration) and stool. Renal water excretion is regulated by antidiuretic hormone (ADH; also called arginine vasopressin), which acts on the kidney to reabsorb water. The secretion of ADH from the posterior pituitary in healthy subjects depends on serum osmolality or tonicity, which is sensed by hypothalamic osmoreceptors as a function of cell volume.5
In healthy subjects, a water load causes plasma osmolality to fall. The release of ADH is suppressed, resulting in the rapid excretion of water from the kidneys as dilute urine. Conversely, circulatory volume loss, such as through bleeding, vomiting, diarrhea, and use of diuretics, or in association with edematous states (e.g., nephrotic syndrome, congestive heart failure) elevates ADH secretion. Absorption of water from the kidneys is increased and the urine becomes concentrated.4
Adapted from: Schachter SC and Lopez MR. Metabolic disorders. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;195–208.
With permission from Elsevier (www.elsevier.com).
