Hyperkalemia is common in neonatal ruminants with diarrhea, dehydration, acidemia, and strong ion (metabolic) acidosis. Hyperkalemia often accompanies acidemia because low blood pH results in intracellular acidosis and depression of Na+/K+-ATPase, resulting in leakage of potassium from the intracellular compartment to the extracellular space. Hyperkalemia is common in neonatal foals with uroabdomen secondary to ruptured bladder associated with parturition, and male cats with uroabdomen secondary to obstructive urolithiasis and bladder rupture. Hyperkalemia is rare in steers, wethers, and bucks with obstructive urolithiasis and bladder or urethral rupture, because excess potassium is secreted in adult ruminant saliva and affected animals have a decrease in potassium intake due to illness. Hyperkalemia can be present in horses and ruminants with exertional rhabdomyolysis due to damage to skeletal muscle cells.
Severe hyperkalemia is usually associated with depression, weakness, lethargy, cardiac arrhythmias, and ECG abnormalities, particularly when the serum potassium concentration is >7 mEq/L. Severe cardiotoxic effects are evident when the serum potassium concentration is 8–11 mEq/L.
Serum biochemical analysis is required to confirm a suspected diagnosis of hyperkalemia. As well as measurement of serum potassium concentration, determination of the serum concentrations of sodium, calcium, phosphorus, urea, and creatinine, the serum activities of CK and AST, and blood gas analysis, can be helpful in guiding treatment. ECG may reveal bradyarrhythmias, suppression in P wave amplitude or loss of the P wave, widened QRS complexes, and symmetric T waves (narrowing of T wave duration and “tenting” of the T wave). The ECG effects of hyperkalemia are exacerbated by the presence of hyponatremia, acidemia, and hypocalcemia. The ratio of serum sodium to potassium concentration is important in the development of cardiac arrhythmias; hyperkalemia in the presence of hyponatremia (sodium:potassium ratio <25:1) is commonly associated with the occurrence of cardiac arrhythmias and ECG abnormalities.
Hyperkalemia should initially be treated by the administration of 0.9% NaCl IV to increase the rate of urine production in dehydrated animals with a patent urinary system, and in selected cases by the IV administration of sodium bicarbonate, glucose, insulin, and sometimes calcium. Urine should be removed from the abdomen of animals with obstructive urolithiasis and ruptured bladder, and urethral patency established. Sodium bicarbonate is administered to correct systemic and intracellular acidosis and improve the function of Na+/K+-ATPase. The rationale for IV glucose and insulin administration is that insulin-mediated glucose entry into cells is accompanied by movement of potassium from the extracellular space to the intracellular compartment. Calcium counteracts many of the deleterious effects of hyperkalemia on arrhythmogenesis, and the IV administration of calcium may therefore improve cardiac output. However, hypertonic saline (2,400 mOsm/L) is just as effective as hypertonic sodium bicarbonate in decreasing hyperkalemia and hyperkalemia-associated bradyarrhythmias, probably because of hypernatremia-mediated intracellular movement of potassium, extracellular volume expansion, and increased rate of urine production. The focus of treatment in hyperkalemia should therefore be identification and correction of acidemia, plasma volume expansion to assist in renal excretion of potassium, and increasing the serum sodium concentration. Glucose and insulin do not appear to be routinely needed to correct hyperkalemia.
Hyperkalemia can be prevented by early diagnosis and treatment of its most common causes. Hyperkalemic periodic paralysis can be prevented in horses by feeding a low-potassium diet or the oral administration of acetazolamide.
Last full review/revision July 2011 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM