Page 943 - Small Animal Internal Medicine, 6th Edition

CHAPTER 53
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Electrolyte Imbalances

HYPERNATREMIA maintains adequate skin turgor and gives a false impres-
sion of hydration, even though the animal has experienced
Etiology a detrimental loss of fluid.
Hypernatremia exists if the serum sodium concentration The severity of clinical signs is related to the absolute
exceeds the reference interval, which may vary between increase in serum sodium concentration and especially to
laboratories (in general >160 mEq/L). It most commonly the rapidity of onset of hypernatremia and hyperosmolality.
develops after water loss exceeds sodium loss (Box 53.1). The Clinical signs usually do not develop until the serum sodium
water loss may be pure (i.e., not accompanied by loss of concentration approaches 170 mEq/L. If hypernatremia is
electrolytes, such as that which occurs with diabetes insipi- rapid in onset, clinical signs may develop at a lower sodium
dus), or it may be hypotonic (i.e., loss of both water and concentration and vice versa. With a gradual increase in the
sodium but with the water loss predominating, such as that serum sodium concentration, the cells in the CNS can adapt
which occurs with gastrointestinal fluid loss and chronic by producing osmotically active solutes (idiogenic osmoles)
kidney disease). Insufficient water intake and an abnormal intracellularly within a few hours of cell shrinkage to reestab-
thirst mechanism are usually facets of an excessive water loss. lish osmotic equilibration between extracellular and intra-
Rarely, hypernatremia may occur in animals with hypodipsia cellular compartments, thereby minimizing cell shrinkage.
caused by neurologic disease, an abnormal thirst mecha-
nism, or defective osmoregulation of vasopressin release. Diagnosis
Less commonly, hypernatremia develops after sodium Measurement of the serum sodium concentration identifies
retention, such as that which occurs with iatrogenic sodium hypernatremia. After it has been identified, the underlying
overload or primary hyperaldosteronism. Primary hyperal- cause should be sought. Careful evaluation of the history,
dosteronism is caused by an aldosterone-secreting adrenal physical examination findings, and results of complete blood
tumor or idiopathic bilateral adrenal hyperplasia but is count (CBC), serum biochemistry panel, and urinalysis
uncommon in dogs and cats. Increased serum aldosterone usually yield clues to the cause. Evaluation of the urine spe-
concentrations cause variable hypernatremia, hypokalemia, cific gravity is especially helpful. Hypernatremia and hyper-
and systemic hypertension. osmolality stimulate the release of vasopressin, resulting in
hypersthenuria. A urine specific gravity of less than 1.008 in
Clinical Features a dog or cat with hypernatremia is consistent with central or
Clinical signs of hypernatremia originate in the central nephrogenic diabetes insipidus. A urine specific gravity
nervous system (CNS) and include lethargy, weakness, greater than 1.030 in a dog and 1.035 in a cat implies a
muscle fasciculations, disorientation, behavioral changes, normal vasopressin–renal tubular axis and indicates the
ataxia, seizures, stupor, and coma. Clinical signs typically existence of sodium retention, primary hypodipsia-adipsia,
become apparent when the plasma osmolality exceeds or gastrointestinal or insensible water loss. A urine specific
350 mOsm/kg (serum sodium concentration >170 mEq/L). gravity of between 1.008 and 1.030 (dog) or 1.035 (cat) indi-
Clinical signs are caused by neuronal dehydration. Hyper- cates the presence of partial vasopressin deficiency or
natremia and hyperosmolality cause fluid to shift from the impaired renal tubular response to vasopressin, most likely
intracellular to the extracellular space. As the brain shrinks, secondary to a primary kidney disorder.
meningeal vessels are damaged and torn, causing hemor-
rhage, hematoma, venous thrombosis, infarction of cere- Treatment
bral vessels, and ischemia. This gradient flow of water from The goals in treating patients with hypernatremia are to
the intracellular to the extracellular compartment often restore the extracellular fluid (ECF) volume to normal, to

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