Drowsiness, confusion, stupor, and coma, in conjunction with seizures and sometimes with other neurologic deficits, may have as their basis a more or less pure abnormality of electrolyte or water balance. Only brief reference is made here to some of these, such as hypocalcemia, hypercalcemia, hypophosphatemia, and hypomagnesemia, as they are considered in other parts of the text.
Hyponatremia and Syndrome of Inappropriate Antidiuretic Hormone
Hyponatremia is defined as a serum sodium level below 135 mEq/L. The hyponatremic state may be isotonic, hypertonic, or hypotonic, depending on the mechanism of reduced sodium concentration. The hypotonic variety is most common in neurologic practice but one also encounters cases of pseudohyponatremia caused by hyperlipidemia or hyperproteinemia (isotonic), hyperglycemic or mannitol-induced hyponatremia (hypertonic), and also cases of water intoxication. The last of these may be associated with systemic hypovolemic (blood loss, salt wasting), hypervolemic (edematous states such as renal, hepatic or heart failure), or isovolemic states (retention of free water).
Hypotonic isovolemic hypernatremia is most often a result of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This state is of special importance because it complicates neurologic diseases of many types: head trauma, bacterial meningitis and encephalitis, cerebral infarction, subarachnoid hemorrhage, cerebral and systemic neoplasm, Guillain-Barré syndrome and the effects of certain medications. SIADH is the result of excretion of urine that is hypertonic relative to the plasma.
As the hyponatremia develops, there is a decrease in alertness, which progresses through stages of confusion to coma, often with convulsions. As with many other metabolic derangements, the severity of the clinical effect is related to the rapidity of decline in serum Na. Lack of recognition of this state may allow the serum Na to fall to dangerously low levels, 100 mEq/L or lower.
Treatment Most instances of hyponatremia have developed slowly, allowing for maintenance of brain volume by the extrusion from cells of various osmotic substances. Rapid correction of sodium in these circumstances risks a reversal of osmotic gradient and a reduction in brain volume. This, in turn, is associated with a special type of central nervous system demyelination (“osmotic demyelination” and central pontine myelinolysis) discussed below. One’s first impulse is to administer NaCl intravenously, but this must be done cautiously to avoid these complications. Most cases of SIADH respond to the restriction of fluid intake—to 500 mL per 24 h if the serum Na is less than 120 mEq/L and to 1,000 mL per 24 h if less than 130 mEq/L. Even when the Na reaches 130 mEq/L, the fluid intake should not exceed 1,500 mL per 24 h.
48 h) hyponatremia with stupor or seizures, the mechanisms for maintaining cerebral cellular volume have not yet been engaged and therefore infusion of NaCl is necessary to prevent cerebral edema. The amount of NaCl to be infused can be calculated from the current and the target levels of serum Na by assuming that the infused sodium load is distributed throughout the total body water content (0.6 × weight in kilograms): ([target Na − starting Na] × 0.6) × weight (kg)