Over 90% of the potassium in the body is located within cells. External balance for potassium is maintained by matching output
to input. Internal balance is maintained by translocation of potassium between intracellular and extracellular fluid. Any
change in plasma potassium concentration must arise from a change in intake, distribution, or excretion.
Decreased intake of potassium alone is unlikely to cause hypokalemia but, in chronically ill animals, prolonged anorexia,
loss of muscle mass, and ongoing urinary potassium losses may combine to cause hypokalemia. Alkalemia contributes to hypokalemia
as potassium ions enter cells in exchange for hydrogen ions. Insulin promotes uptake of glucose and potassium by hepatic and
skeletal muscle cells. A syndrome characterized by recurrent episodes of limb muscle weakness and neck ventroflexion, increased
creatine kinase concentrations, and hypokalemia has been reported in related young Burmese cats.
Gastrointestinal loss of potassium (especially vomiting of stomach contents) is an important cause of hypokalemia in small
animals. Chloride depletion and sodium avidity due to volume depletion contribute to perpetuation of potassium depletion and
metabolic alkalosis by enhancing urinary losses of potassium and hydrogen ions. Urinary loss of potassium is another important
cause of hypokalemia and hypokalemia is common in cats with chronic renal failure. Hypokalemia also may occur in distal renal
tubular acidosis in cats. Finally, hypokalemic nephropathy characterized by tubulointerstitial nephritis may develop in cats
fed diets marginally replete in potassium and containing urinary acidifiers. Hypokalemia commonly occurs during the postobstructive
diuresis that follows relief of urethral obstruction in cats. Mineralocorticoid excess is a rare cause of urinary potassium
loss and hypokalemia in dogs and cats. Administration of loop or thiazide diuretics may cause hypokalemia by increased flow
rate in the distal tubules and increased secretion of aldosterone secondary to volume depletion. Peritoneal dialysis can be
complicated by hypokalemia if potassium-free dialysate is used over an extended period of time.
Muscle weakness may be observed when serum potassium concentration falls below 2.5-3.0 mEq/L. Rear limb weakness and, in
cats, weakness of neck muscles with ventroflexion of the head are commonly observed. Cardiac arrhythmias may develop because
hypokalemia increases automaticity and delays ventricular repolarization. In dogs and cats, the electrocardiographic changes
associated with hypokalemia are inconsistent but ventricular arrhythmias may be observed. Polyuria, polydipsia, and defective
urinary concentrating ability may be observed in hypokalemia.
The clinical history often will provide information about the likely source of potassium loss (e.g. vomiting, diuretic administration).
Determination of the fractional excretion of potassium (FEK as a percentage = UKPCr/PKUCr X 100) may help differentiate renal
and non-renal sources of potassium loss. The FEK should be < 4% for non-renal sources of loss and values > 4% indicate inappropriate
renal loss in the face of hypokalemia. The occurrence of hypokalemia with metabolic alkalosis suggests vomiting of stomach
contents or diuretic administration as likely causes of potassium loss.
Potassium chloride is the additive of choice for parenteral therapy because chloride repletion also is very important if
vomiting or diuretic administration is the underlying cause of hypokalemia. When administered intravenously, potassium should
not be infused at a rate greater than 0.5 mEq/kg/hr. Infusion of potassium-containing fluids initially may be associated with
a decrease in plasma potassium concentration as a result of dilution, increased distal tubular flow, and cellular uptake of
potassium, especially if the infused fluid also contains glucose. This effect may be minimized by using a fluid that does
not contain glucose and by administering it at an appropriate rate. Potassium gluconate is recommended for oral supplementation.
In cats with hypokalemic nephropathy, the initial oral dosage of potassium gluconate is 5-8 mEq per day divided BID or TID
whereas the maintenance dosage can usually be reduced to 2-4 mEq per day.
Careful potassium supplementation is very important when using insulin to treat diabetic ketoacidosis. Chronic potassium
depletion usually is present in affected patients as a result of loss of muscle mass, anorexia, vomiting, and polyuria. Serum
potassium concentrations, however, often are normal or even increased due to the effects of insulin deficiency and hyperosmolality
on serum potassium concentration. As blood glucose concentration falls with insulin treatment, marked hypokalemia may develop
if supplementation is not diligent.