Hypokalaemia

Introduction

Hypokalaemia occurs most commonly in cats secondary to Chronic Renal Failure and is the most common electrolyte abnormality seen in small animal practise. Potassium is important for nervous and muscle conduction, especially in cardiac muscle. It also has metabolic functions. The classic clinical sign is ventroflexion of the neck, with the cat unable to raise its head properly. It is also reported in calves following dehydration and diarrhoea. The consequence is cardiac arrest following ventricular dissociation.

Aetiology

Low potassium levels in the blood can be due to:

• Decreased uptake

This is normally the result of prolonged low-potassium fluid therapy (Hartmanns) administration in the anorexic cat. It does not usually cause disease in itself, instead exacerbating signs of existing hypokalaemia.

• Increased loss

Potassium can be lost from the gastrointestinal tract or urinary system. Diarrhoea results in the direct loss of potassium in the faeces. Vomiting results in both direct loss and excretion of potassium from the kidneys secondary to metabolic alkalosis. Hypokalaemia is also a common consequence of chronic renal failure, it is caused by increased loss of potassium in the urine coupled with polyuria, anorexia and low dietary intake. Low levels of potassium can be a primary cause of kidney dysfunction, this condition is known as 'potassium depletion nephropathy'. Clinical signs normally improve following dietary supplementation. The excessive or long-term use of non-potassium sparing diuretics (frusemide) can also increase loss of potassium into the urine. Rarely, the endocrinopathy known as hyperaldosteronism aka Conn's syndrome may also cause potassium loss by increasing secretion from the distal convoluted tubule in the kidney.

• Trans-cellular shift

Shifting of potassium from the extracellular fluid into the intracellular fluid in high quantities or for prolonged periods can cause low serum levels and hypokalaemia. This is caused by an metabolic or respiratory alkalosis and the subsequent compensation, insulin therapy, hyperthyroidism and hypokalaemic polymyopathy in the Burmese cat.

• Drug-induced

Insulin therapy, fluid therapy, bicarbonate therapy, B2-agonists, laxatives and nephrotoxic drugs can all cause low serum potassium levels.

It should be noted that hyperproteinaemia or hyperlipaemia cause a false hypokalaemia by 'diluting' the serum potassium. This is not clinically significant.

Clinical Signs

The severity of clinical signs is normally proportional to the severity of hypokalaemia.

• Ventroflexion of the neck
• Lethargy and fatigue
• Crouched gait and reluctance to walk
• Muscle pain
• Hindlimb stiffness progressing to weakness and ataxia

Onset of clinical signs may be acute or chronic, demonstrable when serum levels of potassium drop below 2.5-3.0 mmol/L.

Diagnosis

History and clinical signs and the results of a thorough neurological exam should be suggestive of hypokalaemia. Diagnosis can be confirmed by standard biochemistry. Further adjunct tests include; renal function tests, fractional excretion of potassium calculations, creatinine kinase measurements, ECG, and blood gas analysis.

Treatment

Treatment involves potassium supplementation, either orally or intravenously.

Oral supplementation is more suitable for mild or chronic cases, it is quite unpalatable and therefore not suitable for some anorexic or vomiting cats. Improvement of clinical signs should be evident after 1-3 days. Potassium levels should be measured approximately every two weeks until serum levels stabilise.

Intravenous supplementation is more suitable in acute or severe cases. IV potassium preparations are not licensed in small animals therefore potassium chloride administration with IVFT is the treatment of choice. As a result of the fluid therapy, hypokalaemia may worsen before improving (as the existing potassium is diluted down), therefore acute cases require very close monitoring during treatment (severe muscle weakness and subsequent respiratory arrest can occur). The maximum rate of potassium infusion should not be exceeded. Treatment should take effect within hours and at this point oral supplementation should be used if possible.

There should be no concurrent administration of glucose or insulin therapy as this reduces serum potassium levels by increasing uptake into the intra-cellular fluid.

Hyperkalaemia should always be avoided. This is achieved by closely monitoring potassium levels, administering potassium slowly and at the correct dose, and by checking renal function prior to treatment. Treatment with ACE-Inhibitors and potassium-sparing diuretics should also be avoided.

Prognosis

Hypokalaemia is common in small animals, and following appropriate treatment and identification of the underlying cause, prognosis should be good.

Hypokalaemia Learning Resources
Flashcards Test your knowledge using flashcard type questions	Feline Medicine Q&A 05

References

Hodson, S (1998) Feline hypokalaemia In Practice 1998 20: 135-14

Sparks, AH & Caney, SMA (2005) Self-Assessment Colour Review Feline Medicine Manson