Page 949 - Small Animal Internal Medicine, 6th Edition

CHAPTER 53 Electrolyte Imbalances 921

TABLE 53.2
VetBooks.ir Treatment Options for Hyperkalemia in the Dog and Cat

TREATMENT DOSAGE ROUTE OF DURATION OF EFFECT
ADMINISTRATION
Physiologic saline ≥60-100 mL/kg/day IV Hours
Dextrose 5%-10% in IV fluids IV, continuous Hours
or
1-2 mL of 50% dextrose/kg IV, slow bolus Hours
Regular insulin and 0.5-1 U/kg in parenteral fluids IV Hours
dextrose plus
2 g dextrose/U insulin administered IV Monitor blood glucose
Sodium bicarbonate 1-2 mEq/kg IV, slow bolus Hours
10% Calcium gluconate 0.5 mL/kg to 1.5 mL/kg over 5-10 IV, slow bolus 30-60 minutes
minutes with ECG monitoring Monitor heart
β 2 adrenergic agonist Terbutaline 0.01 mg/kg IV slowly 2 hours

IV, Intravenous.

life and death. The goals of symptomatic therapy are to more conventional therapy (i.e., IV fluids) has the time to
reverse the cardiotoxic effects of hyperkalemia and, if pos- become effective.
sible, to reestablish normokalemia. Asymptomatic animals For more chronic, mild to moderate hyperkalemia due
with normal urine output and chronic hyperkalemia to kidney disease, especially those with proteinuria and/or
(<7 mEq/L) may not require immediate treatment, but a on ACE inhibitors, a potassium-restricted homemade diet
search for the underlying cause should be initiated. can be effective in controlling serum potassium concentra-
IV fluid administration in amounts designed to correct tions. In these cases, consultation with a board-certified vet-
fluid deficits and to cause volume expansion rehydrates the erinary nutritionist should be pursued to ensure a balanced
animal, improves renal perfusion and potassium excretion, and appropriate diet (see www.acvn.org or www.esvcn.eu/
and dilutes the blood potassium concentration. Physiologic college).
saline solution is the fluid of choice for this purpose.
Potassium-containing fluids (e.g., lactated Ringer’s solution)
can be used if physiologic saline solution is not available HYPOKALEMIA
because the low potassium concentration in these fluids (see
Table 53.1) in relation to that in blood will still have a dilu- Etiology
tional effect on the blood potassium concentration. Dextrose Hypokalemia is present when the serum potassium concen-
can be added to the fluids to make a 5% to 10% dextrose- tration is less than 3.5 mEq/L, although reference ranges
containing solution, or 1 to 2 mL/kg of 50% dextrose can be may vary between laboratories. Hypokalemia can develop
administered by slow IV bolus. Dextrose stimulates insulin after decreased dietary potassium intake (uncommon),
secretion, which in turn promotes the movement of glucose translocation of potassium from the ECF to the intracellu-
and potassium from the extracellular to the intracellular lar fluid (common), or increased potassium loss in urine or
space. Fluids containing more than 5% dextrose should be gastrointestinal secretions (common; Box 53.5). Iatrogenic
given into a central vein to minimize the risk of phlebitis. hypokalemia is also common in dogs and cats. Pseudohy-
Rarely, additional therapy may be required to block the pokalemia is uncommon and depends on the method used
cardiotoxic effects of hyperkalemia (see Table 53.2). Sodium to measure the serum potassium concentration. Hyper-
bicarbonate and regular insulin given with dextrose act to lipidemia, hyperproteinemia (>10 g/dL), hyperglycemia
shift potassium from the extracellular to the intracellular (>750 mg/dL), and azotemia (urea nitrogen concentration
space. IV calcium infusions block the effects of hyperkalemia >115 mg/dL) can potentially cause pseudohypokalemia.
on cell membranes but do not lower the blood potassium
concentration. β 2 adrenergic agonists (e.g., albuterol, terbu- Clinical Features
taline) can be administered as an adjunct treatment, driving Most dogs and cats with mild to moderate hypokalemia (i.e.,
potassium intracellularly by increasing sodium and potas- 3.0-3.5 mEq/L) are asymptomatic. Clinically severe hypoka-
sium adenosine triphosphatase (ATPase) activity. These lemia primarily affects the neuromuscular and cardiovascular
therapies constitute aggressive, short-term, life-saving mea- systems owing to hypokalemia-induced initial hyperpolar-
sures that can reestablish normal cardiac conduction until ization followed by hypopolarization of cell membranes. The