Page 950 - Small Animal Internal Medicine, 6th Edition

922 PART VII Metabolic and Electrolyte Disorders

of hypokalemia include hypokalemic nephropathy, which
BOX 53.5 is characterized by chronic tubulointerstitial nephritis,
VetBooks.ir Causes of Hypokalemia in Dogs and Cats impaired renal function, and azotemia and manifests clini-
cally as polyuria, polydipsia, and impaired urine concen-
trating capability; hypokalemic polymyopathy, which is
Transcellular Shifts (ECF to ICF)
Metabolic alkalosis characterized by increased serum creatine kinase activity
Hypokalemic periodic paralysis (Burmese cats) and electromyographic abnormalities; and paralytic ileus,
which manifests clinically as abdominal distention, anorexia,
Increased Loss vomiting, and constipation. Hypokalemic nephropathy and
Gastrointestinal fluid loss (vomiting, diarrhea)* polymyopathy are most notable in cats.
Chronic kidney disease, especially in cats*
Diabetic ketoacidosis* Diagnosis
Diet-induced hypokalemic nephropathy in cats Measurement of the serum potassium concentration iden-
Distal (type I) renal tubular acidosis
Proximal (type II) renal tubular acidosis after sodium tifies hypokalemia. Once it has been identified, a careful
bicarbonate treatment review of the history, physical findings, CBC, serum bio-
Postobstructive diuresis chemistry panel, and urinalysis usually provides clues to the
Primary hyperaldosteronism cause (see Box 53.5). If the cause is not readily apparent
Chronic liver disease after review of this information, other less likely causes for
Hyperthyroidism hypokalemia should be considered, such as renal tubular
Hypomagnesemia acidosis, or another renal potassium-wasting disorder,
primary hyperaldosteronism, and hypomagnesemia. To
Iatrogenic Causes* help differentiate renal from nonrenal sources of potas-
Potassium-free fluid administration (e.g., 0.9% saline) sium loss, the clinician may need to determine the frac-
Parenteral nutritional solutions tional excretion of potassium on the basis of a single urine
Insulin- and glucose-containing fluid administration
Sodium bicarbonate therapy and serum potassium and creatinine concentration or may
Loop (e.g., furosemide) and thiazide diuretics need to evaluate 24-hour urine potassium excretion (see
Low dietary intake Chapter 39).
Pseudohypokalemia Treatment
Hyperlipidemia (dry reagent methods; flame photometry) Therapy is indicated if the serum potassium concentration is
Hyperproteinemia (dry reagent methods; flame less than 3.5 mEq/L, if clinical signs related to hypokalemia
photometry) are present, or if a serum potassium loss is anticipated (e.g.,
Hyperglycemia (dry reagent methods) insulin therapy in diabetic ketoacidosis [DKA]) and the ani-
Azotemia (dry reagent methods) mal’s ability to compensate for the loss is impaired. The goal
of therapy is to reestablish and maintain normokalemia
ECF, Extracellular fluid; ICF, intracellular fluid.
*Common causes. without inducing hyperkalemia.
Modified from DiBartola SP, Autran de Morais H: Disorders of Potassium chloride is the compound most commonly
potassium: hypokalemia and hyperkalemia. In DiBartola SP, editor: used for parenteral potassium supplementation, in part
Fluid, electrolyte, and acid-base disorders in small animal practice, to help promote chloride as well as potassium repletion.
ed 4, St Louis, 2012, Saunders Elsevier. IV administration is preferred, although potassium chlo-
ride can be given subcutaneously as long as the concentra-
tion of potassium does not exceed 30 mEq/L. In dogs and
most common clinical sign of hypokalemia is generalized cats with normal renal function, the maintenance amount
skeletal muscle weakness. In cats ventroflexion of the neck of potassium supplementation is approximately 20 mEq/L
(see Chapter 67), forelimb hypermetria, and a broad-based of fluids. The amount of potassium first added to fluids
hindlimb stance may be observed. The timing of onset of depends on the animal’s serum potassium concentration
hypokalemia-induced weakness is extremely variable among (Table 53.3) and the amount of potassium already present
animals. Cats seem more susceptible than dogs to the del- in the fluids (see Table 53.1). The rate of IV potassium
eterious effects of hypokalemia. In dogs, signs may not be administration should not exceed 0.5 mEq/kg/h. The rate
evident until the serum potassium concentration is less than of potassium administration can be increased cautiously to
2.5 mEq/L, whereas in cats signs can be seen when the serum 1.0 mEq/kg/h in patients with profound hypokalemia and
potassium concentration is between 3 and 3.5 mEq/L. normal or increased urine output. Close ECG monitoring is
Cardiac consequences of hypokalemia include decreased recommended.
myocardial contractility, decreased cardiac output, and dis- It is difficult to estimate the amount of potassium required
turbances in cardiac rhythm. Cardiac disturbances assume to reestablish normal potassium balance on the basis of the
a variable clinical expression, often evidenced only by elec- serum potassium concentration because potassium is pri-
trocardiography (see Box 53.4). Other metabolic effects marily an intracellular cation. As such, serial measurement