NEUROLOGY OF COMMON ELECTROLYTE DISORDERS

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CHAPTER 116 NEUROLOGY OF COMMON ELECTROLYTE DISORDERS

Martin A. Samuels, Julian L. Seifter

HYPEROSMOLALITY AND HYPERTONICITY

Normal serum, and therefore body fluid, osmolality is in the range of 275 to 295 mOsm/kg; clinically significant effects are generally seen at levels greater than 325 mOsm/kg. Osmolality may be measured directly by the freezing point depression or calculated as serum osmolarity in milliosmoles per liter with the following formula, which accounts for the millimolar quantities of major serum solutes (where BUN is blood urea nitrogen):

Effective hyperosmolality is called hypertonicity and indicates the effect of increased extracellular osmoles to draw water from cells by osmosis. If hyperosmolality is caused by hypernatremia, cells initially shrink until adaptive mechanisms allow cell volume to recover. Similarly, a diabetic patient with hyperglycemia loses cell water and develops a hypertonic syndrome. In contrast, azotemia (i.e., an elevated BUN level) may cause hyperosmolality but not hypertonicity, because the high permeability of urea allows solute movement into cells so that cell water does not leave by osmosis. The difference between hyperglycemia (glucose cannot enter cells) and azotemia is seen by the effect on the serum sodium concentration. Water leaving cells in the hyperglycemic patient lowers serum [Na], whereas serum sodium [Na] is not altered by a rise in BUN. Addition of extrinsic osmoles such as mannitol, like glucose, causes hyperosmolality, hypertonicity, loss of cell water, and hyponatremia. On the other hand, added alcohols that quickly permeate cells, such as ethanol, ethylene glycol, isopropyl glycol, and methanol, act more like azotemia, causing hyperosmolality but not hypertonicity or hyponatremia. Because measured osmolality is increased with addition of these extrinsic solutes but sodium, glucose, and urea are not, there is an osmolal gap, defined as the difference between measured and calculated osmolality. The osmolal gap should be less than 10 mOsm/L.

Hypernatremia is defined as a serum sodium concentration higher than 145 mEq/L. In all tissues, hypernatremia leads to loss of intracellular water, which in turn leads to cell shrinkage. The nervous system is unique in that it is capable of generating (or accumulating from the extracellular fluid) solutes referred to as idiogenic osmoles, such as amino acids (glutamine, taurine, glutamate), polyols (myoinositol), and methylamines (glycerophosphorylcholine and choline), to minimize cell shrinkage, a process that is complete in 1 to 2 days. When hypernatremia is unusually severe (serum sodium level exceeds 160 mEq/L), these mechanisms fail, which leads to encephalopathy. When hypernatremia occurs, antidiuretic hormone (ADH) is released and thirst increases, which lead to renal retention of ingested water and thereby lower the serum sodium level toward normal. Hypernatremia is thus caused by a defect in thirst or inability to access water, inadequate release or effect of ADH, loss of hypotonic fluid, or addition of concentrated sodium.

Hyperglycemia is nearly always caused by diabetes mellitus, which results from either inadequate insulin production or insulin resistance. In patients with neurological disease, this is often precipitated by stress, infection, or the therapeutic use of glucocorticoids.

Azotemia is caused by renal failure or inadequate renal perfusion (prerenal azotemia).

Hyperosmolar agents such as mannitol or glycerol are often used in patients with neurological disease to treat increased intracranial pressure and may result in hyperosmolality.

Hyperosmolality usually produces a generalized encephalopathy without localizing or lateralizing features, but an underlying focal lesion (e.g., stroke, multiple sclerosis, neoplasm) could become symptomatic under the metabolic stress of a hyperosmolar state. The prognosis of the hyperosmolality itself is good, but the long-term outlook depends on the cause. For unknown reasons, hyperosmolality alone, particularly when caused by hyperglycemia, may lead to continuous partial seizures, and even careful studies may fail to uncover any underlying lesion. These seizures generally respond promptly to lowering of the serum glucose level.

The treatment of hyperosmolality requires calculation of apparent water losses:

1. The normal total body water (NTBW) is calculated as body weight (in kilograms) × 0.6.

2. The total body solute (sodium + potassium) is estimated as NTBW × 140 mEq/L. Note that 140 mEq/L is normal serum [Na] but is approximately equal to intracellular [K] needed to estimate total body solutes.

3. The patient’s body water is calculated as total body solute/patients serum [Na].

4. The patient’s water deficit is calculated as NTBW – patient’s body water.

5. Apart from deficit correction, large ongoing losses in the urine (osmotic diuresis or diabetes insipidus) or sweat (fever) are estimated and replaced.

The water losses are replaced, with water or 5% dextrose in water, so that the serum sodium level falls no faster than 2 mEq/L/hour. In the hypotensive or volume-depleted patient, normal saline may first be needed to correct blood pressure. In patients with renal failure, dialysis may be required. Insulin is administered, with frequent blood glucose testing, if there is hyperglycemia. Intramuscular and subcutaneous insulin may be unpredictably absorbed, particularly in hypovolemic patients, because of poor tissue perfusion. Rapid-acting insulin, 0.1 U/kg by rapid intravenous infusion followed by 0.05 U/kg/hour by continuous intravenous infusion, is usually sufficient to reduce the blood glucose level adequately and safely, but the mainstay of hyperglycemia correction in the patient with hyperosmolar type II diabetes is volume expansion, which leads to urinary glucose clearance. Rapid reduction of extreme elevations of glucose should be avoided.

Diabetes insipidus is recognized as hypernatremia (>292 Osm) with simultaneous submaximal concentration of the urine. A subcutaneous dose of vasopressin and subsequent measurement of serum ADH level help distinguish central from nephrogenic diabetes insipidus. Treatments include deamino-D

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