Introduction

• Cause: reduced potassium intake due to inappetence or anorexia coupled with concurrent (external or internal) losses; redistribution.
• Signs: muscle weakness, S-shaped neck position, gastrointestinal stasis, anorexia.
• Diagnosis: history, clinical signs, serum potassium concentration.
• Treatment: oral potassium supplementation, correct underlying disease process.
• Prognosis: dependant on cause.

Pathogenesis

Etiology

• Decreased potassium intake alongside concurrent loss.
• Internal redistribution.

Pathophysiology

• The main source of potassium is the diet. Moderate hypokalemia is therefore common among cattle which have a reduced appetite or total anorexia, eg due to an underlying/pre-existing condition.
• Alone this hypokalemia is not generally associated with clinical signs. Combined with potassium loss, however, overt clinical hypokalemia can occur. Such losses might be caused by: 
  • Reduced gastrointestinal absorption, eg due to diarrhea.
  • Increased renal excretion, eg due to:
    • Mineralocorticoid effects of eg isoflupedrone actetate.
    • Chronic renal failure.
    • Post-urinary obstruction diuresis.
    • Diuretic therapy.
• Potassium levels can also be relative rather than absolute, and hypokalemia caused by altered distribution of potassium across the intracellular and extracellular fluid spaces, eg due to:
  • Alkalosis.
  • Insulin therapy.
• The transmission of action potentials and therefore electrical signaling and muscular contractions are highly dependent on the resting membrane potential of cells. This, in turn, is dependent on the gradient between ICF and ECF potassium concentrations. This explains why, even in the absence of significant muscle necrosis, severe hypokalemia results in muscular weakness and cardiac electrical instability. 

Diagnosis

Treatment

Prevention

Outcomes