Feline Hypokalemic Polymyopathy

Feline hypokalemic polymyopathy is a generalized metabolic muscle-weakness disorder in cats secondary to hypokalemia.

Most cats develop this polymyopathy secondary to chronic kidney disease and the subsequent loss of potassium through urination. However, feline hypokalemic polymyopathy has been associated with hyperthyroidism, dietary potassium deficiency, hyperaldosteronism, excessive fluid administration, chronic vomiting or diarrhea, and the use of potassium-wasting diuretics.

Feline hypokalemic polymyopathy has been reported in cats receiving ophthalmic dorzolamide (1) and in Burmese kittens with episodic hypokalemic myopathy (2).

Extracellular hypokalemia causes muscle cell membrane hyperpolarization and secondary excessive permeability to sodium. This makes the muscle cell membrane refractory to depolarization and subsequent contraction.

Clinical signs of feline hypokalemic polymyopathy are typically acute in onset and include the following:

• generalized weakness

• ventroflexion of the neck (see cervical ventroflexion image)

• stiff, stilted gait

• anorexia

• muscle pain

Severe hypokalemia can result in respiratory paralysis and rhabdomyolysis.

Historically, diagnosis has relied on demonstration of hypokalemia. Serum biochemical analysis in cats with hypokalemic polymyopathy typically reveals low potassium concentrations—a median potassium concentration of 2.45 mmol/L (2.45 mEq/L) was reported in one study (3)—and possibly increased creatinine concentration and CK activity (4). PCR assay provides a straightforward means of diagnosis in Burmese and related breeds with familial episodic hypokalemic polymyopathy.

Abdominal ultrasonography is recommended to evaluate for an underlying adrenal tumor that may be causing hyperaldosteronism. Hyperaldosteronism is definitively diagnosed by measuring serum aldosterone concentration in a properly hydrated patient.

Feline hypokalemic polymyopathy, cervical ventroflexion

Image

Courtesy of Baye Williamson, DVM, DACVIM (Neurology).

Treatment of feline hypokalemic polymyopathy is potassium supplementation (5–8 mEq/cat, PO, every 24 hours or divided every 12 hours) (5). Normal potassium concentrations are typically achieved in 1–3 days.

In cats with profound hypokalemia, potassium can be administered parenterally (0.5 mEq/kg/h, IV) (5); electrolytes should be checked every 4 hours, and supplementation can be decreased once potassium concentration returns to normal.

Once normokalemia is achieved, most cats with conditions that cause hypokalemia will require long-term potassium supplementation (2 mEq/cat, PO, every 12 hours) (5). Treatment of the underlying cause, such as managing hyperthyroidism or lowering the diuretic dose, may also be required.

The prognosis for cats with feline hypokalemic polymyopathy is excellent when the condition is diagnosed and treated early.

For other metabolic myopathies in small animals (dogs and cats), see the Overview for this chapter.