Page 947 - Small Animal Internal Medicine, 6th Edition

CHAPTER 53 Electrolyte Imbalances 919

must be differentiated from pseudohyponatremia (discussed paresis, ataxia, dysphagia, and obtundation and often do not
in a previous section). Hyponatremia is not a diagnosis per manifest until several days after treatment of hyponatremia.
VetBooks.ir se but rather a manifestation of an underlying disorder. As The prognosis for recovery is guarded.
such, a diagnostic evaluation to identify the cause, as well as
appropriate therapy to correct the hyponatremia, should be
initiated. In most dogs and cats the cause of hyponatremia HYPERKALEMIA
is readily apparent after evaluation of the history, physical
examination findings, CBC, serum biochemistry panel, and Etiology
urinalysis findings, but further diagnostic tests may be nec- Hyperkalemia is present if the serum potassium concen-
essary. Careful assessment of urine specific gravity and tration exceeds 5.5 mEq/L (although reference ranges may
plasma osmolality and of the hydration status of the animal vary between laboratories) and is considered severe and
will help to localize the problem (see Box 53.2). potentially life-threatening when it exceeds 7.5 mEq/L.
Hyperkalemia can develop after increased potassium intake
Treatment (uncommon) or translocation of potassium from the intra-
The goals of therapy are to treat the underlying disease and, cellular to the extracellular space (uncommon), or as a result
if necessary, to increase serum sodium concentration and of impaired potassium excretion in the urine (common; Box
plasma osmolality. The goals of treatment directed at the 53.3). Impaired urinary excretion of potassium is usually
hyponatremia are to correct body water osmolality and caused by chronic kidney disease or hypoadrenocorticism.
restore cell volume to normal by raising the ratio of sodium Iatrogenically induced hyperkalemia is also common in dogs
to water in ECF using IV fluid therapy, water restriction, or and cats, typically resulting from excessive IV administra-
both. The increase in ECF osmolality draws water from cells, tion of potassium-containing fluids. Generally the IV rate
thereby reducing their volume. The approach to treatment of potassium administration should not exceed 0.5 mEq/
and the type of fluid used depend on the underlying cause, kg body weight per hour. Pseudohyperkalemia refers to an
the severity of the hyponatremia, and the presence or absence increase in potassium in vitro and can occur in the setting of
of clinical signs (see Table 53.1). Chronic hyponatremia in severe hypernatremia (if dry reagent methods are used), leu-
an asymptomatic animal is best treated conservatively. Lac- kocytosis (white blood cell count >100,000/µL), or throm-
6
tated Ringer’s or Ringer’s solution can be used for mild hypo- bocytosis (>1 × 10 /µL), and in the setting of hemolysis in
natremia (serum sodium concentration >130 mEq/L) and Akitas (and possibly Shiba Inus and Kindos) and in English
physiologic saline solution for more severe hyponatremia Springer Spaniels with phosphofructokinase deficiency. Col-
(serum sodium concentration <130 mEq/L). Physiologic lection of blood in heparinized tubes rather than in clot
saline solution is typically used in symptomatic animals with tubes and prompt separation of plasma from cells help to
severe hyponatremia. prevent pseudohyperkalemia. Obtaining blood from fluid
Fluid and electrolyte balance should gradually be restored lines or catheters contaminated with potassium-containing
over 24 to 48 hours, with periodic assessment of serum elec- fluids may yield falsely increased potassium concentrations.
trolyte concentrations and the patient’s CNS status. The
general goal is to increase the serum sodium concentration Clinical Features
slowly toward the lower end of the reference range at a rate The clinical manifestations of hyperkalemia reflect changes
no greater than 0.5 to 1.0 mEq/L/h. The more acute and in cell membrane excitability and the magnitude and rapidity
severe the hyponatremia, the more slowly the serum sodium of onset of hyperkalemia. Mild to moderate hyperkalemia
concentration should be corrected. A rapid increase in the (serum potassium concentration <6.5 mEq/L) is typically
serum sodium concentration to levels greater than 125 mEq/L asymptomatic. Generalized skeletal muscle weakness devel-
is potentially dangerous and should be avoided in animals ops as the hyperkalemia worsens. Weakness occurs after a
with acute, severe hyponatremia (serum sodium concentra- hyperkalemia-induced decrease in resting cell membrane
tion <120 mEq/L) and neurologic signs. For these animals, potential to the level of the threshold potential, thereby
the serum sodium concentration should be gradually impairing repolarization and subsequent cell excitation. The
increased to 125 mEq/L or higher over 6 to 8 hours. Because most prominent manifestations of hyperkalemia are cardiac
loss of brain solute represents one of the compensatory in nature. Hyperkalemia causes decreased myocardial excit-
mechanisms for preserving brain cell volume during dilu- ability, an increased myocardial refractory period, and
tional states, an increase in serum sodium concentration slowed conduction—effects that may cause potentially life-
toward normal is relatively hypertonic to brain cells that are threatening cardiac rhythm disturbances (Box 53.4).
partially depleted of solute as a result of hyponatremia. Con-
sequently, raising the serum sodium concentration rapidly Diagnosis
to greater than 125 mEq/L can cause CNS damage. Measurement of serum potassium concentration or evalua-
The major complication of treatment of hyponatremia is tion of an electrocardiogram (ECG) can identify hyperkale-
myelinosis, which results from neuronal shrinkage away mia. Once it has been identified, a careful review of the
from the myelin sheath as water moves out of the neuron history, physical findings, CBC, serum biochemistry panel,
during correction of hyponatremia. Clinical signs include and urinalysis usually yields clues to the cause. The most