Hyperkalemia is defined as a circulating potassium (K) level ≥ 6.5 mEq/L (normal is 4.4 - 6.1).
Serum potassium, the major cation in the intracellular fluid, is normally maintained within a narrow range through an exquisite balance mechanism between cellular potassium efflux and influx. Hyperkalemia may result from both a shift of the ion from the intracellular to the extracellular compartment and a decrease in the renal excretion of potassium. The former may be due to loss of the effects of cortisol upon the sodium-potassium pump, which normally maintains a potassium gradient across the cellular membrane.
Body stores of potassium are intimately related to sodium balances and plasma sodium and potassium concentrations are maintained by balanced intake and excretion, intracellular and extracellular osmotic pressure, and pH. Sodium-potassium (Na:K) ratio has frequently been used as a diagnostic tool to identify adrenal insufficiency. The normal Na:K ratios in dogs range from 27:1 to 40:1, while the values in canine hypoadrenocorticism (Addison’s disease) are often below 27:1 and may be below 20:1 in primary hypoadrenocorticism. However, other disorders including chronic renal disease, intestinal parasites, gastritis, gastric dilation and volvulus and metabolic acidosis can also cause similar electrolyte disturbances classically associated with primary hypoadrenocorticism characterized by hyponatremia and hyperkalemia.
It is particularly important that the signs and symptoms of changes in plasma potassium concentrations should be particularly recognised and quickly treated, because the changes are potentially life threatening, as plasma potassium values are not always a reflection of total body potassium stores - potassium levels can be normal in blood, despite severe deficits in total body potassium.
Hyperkalemia reduces the resting membrane potential of cells, resulting in muscle fasciculation, impaired urine concentrating ability, polydipsia and bradyarrythmia. Severe cardiotoxic effects are evident when the serum potassium concentration is ≥ 8 – 11 mEq/L, often resulting in ventricular fibrillation and death.
Causes of canine hyperkalemia include:
- Renal hypoperfusion
- Chronic renal disease
- Urinary obstruction - urolithiasis, urinary torsion, transitional cell carcinoma
- Hypoadrenocorticism - hyponatremia and hyperkalemia
- Diabetes mellitus with ketoacidosis
- Phosphofructokinase deficiency
- Toxins - potassium bromide overdose
- Pseudohyperkalemia - breed predisposition in Shar Pei, Akitas, Shibas, Jindos
- Sepsis - e.g. pyoderma, pyometra
Pseudohyperkalemia is caused by an increased intracellular RBC potassium concentration and may be accompanied by increased red cell distribution, low MCHC, and increased osmotic fragility with or without mild anemia.
Treatment of hyperkalemia requires intravenous administration of 0.9% NaCl at 60 - 80 mL/kg/hr for 1 - 2 hours. This initial rate of infusion helps to address hypovolemia commonly seen in hyperkalemic dogs, as well as reduced serum potassium levels. The infusion also increases urine production and therefore potassium excretion.
Additional drugs may be required such as sodium bicarbonate, glucose, insulin, and sometimes calcium.
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.
Potassium-low homemade diets have also been effective as a long-term management strategy in dogs with chronic renal disease.
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