Management of hypokalemia and hyperkaemia (Proceedings)


Management of hypokalemia and hyperkaemia (Proceedings)

Nov 01, 2010

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.

Clinical signs

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.

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