What to Do About Hypokalemia: Recognition & Management
ACVIM 2008
Joe Bartges, DVM, PhD, DACVIM, DACVN
Knoxville, TN, USA

Introduction

Potassium (K+) is the major intracellular cation and sodium (Na+) is the major extracellular cation with approximately 140 mEq/L of K+ and 10 mEq/L of Na+ located intracellularly. These concentrations are reversed from extracellular fluid. Total body K+ is regulated primarily by the kidneys because it is nonselectively absorbed by the intestines, although increased intestinal excretion can occur in some instances. Obligatory renal losses of K+ occur proportional to renal tubular flow rate; however, aldosterone is the major modifier of renal K+ excretion. Aldosterone stimulates active Na+ reabsorption and K+ and hydrogen excretion in the distal nephron. External K+ is maintained by matching output (primarily renal) to input (primarily from diet via the intestinal tract) while internal K+ balance is maintained by translocation of K+ between the intracellular and extracellular fluid compartments. Insulin, β2-adrenergic receptor stimulation, and alkalosis in the extracellular fluid compartment promote translocation of K+ from the extracellular fluid compartment to the intracellular fluid compartment.1

Potassium functions in many metabolic processes, but its major role is in generation of the normal resting cell membrane potential. The normal relationship between the extracellular fluid and intracellular fluid K+ concentrations is maintained by the Na+-K+-ATPase pump, which pumps Na+ out of the cell and K+ into the cell at a ratio of 3:2. This results in greater intracellular K+ concentration when compared with extracellular K+ concentration. The result of this relationship is that a net negative charge develops within the cell and a net positive charge develops outside of the cell, and, therefore, a potential difference exists across the cell membrane. Disorders of potassium are often manifested as consequences of alterations of a change in this potential difference.

Definition

Hypokalemia exists when the measured serum or plasma K+ concentration is less than normal. Normal values for serum or plasma K+ concentration in dogs and cats vary slightly among laboratories, but are usually between 3.5 and 5.5 mEq/L. Serum concentration exceeds plasma concentration because K+ may be released from platelets during clot formation. This difference may be substantial in animals with thrombocytosis.2 Although red blood cells in dogs and cats have K+ concentrations similar to that of plasma and serum, red blood cells from adult Akitas contain higher K+ concentrations.3

Clinical Signs

Many dogs and cats with hypokalemia have no clinical signs. Muscular weakness and polyuria/polydipsia, are the most likely recognized clinical signs. Hypokalemic polymyopathy occurs when the serum K+ concentration is < 3.0 mEq/L and can result in overt muscle damage with increased creatine kinase activity and overt rhabdomyolysis when < 2.0 mEq/L.4 Polymyopathy characterized by ventroflexion of the neck occurs more commonly in cats than in dogs and is usually associated with renal failure5, although this seems to be observed less frequently. In cats with chronic renal failure, mild hypokalemia may be associated with decreased activity, which owners assume is due to advancing age.

Whole body potassium depletion produces functional and morphological renal abnormalities. Polyuria/polydipsia associated with hypokalemia results from impaired renal responsiveness to ADH. Disruption of proximal renal tubular cell function in rats can result in tubular dysfunction and vacuolization; this has been observed to occur in dogs.6 Furthermore, in rats, potassium depletion results in increased renal ammoniagenesis that may activate complement and contribute to tubulointerstitial disease.7 Renal disease and lesions (lymphoplasmacytic interstitial nephritis and interstitial fibrosis) occurred in a small group of cats fed a diet containing 42% protein and 0.32% potassium (dry matter basis) over a 2 year period.8

Causes

Hypokalemia in dogs and cats occurs typically from one of three basic mechanisms that are not mutually exclusive: 1) decreased intake, 2) translocation from extracellular fluid to intracellular fluid, and 3) increased loss.1 Usually the cause or causes of hypokalemia are obvious; however, determination of the fractional clearance of potassium may help differentiate renal and non-renal losses. Fractional clearance of potassium is expressed as a percentage and is calculated by determining the urine and serum/plasma concentrations of K+ and creatinine. Divide the urine K+ by the serum/plasma K+ and divide the urine creatinine by the serum/plasma creatinine; then divide the resultant K+ quotient by the resultant creatinine quotient and multiply the answer by 100 to give a percent. With urinary K+ loss, the fractional clearance of K+ will be > 4-6%, and with non-renal loss, it will be < 4-6%.9

Decreased Intake

Decreased K+ intake by diet alone is unlikely to occur; however, administration of low K+ or K+ free fluids to patients occurs commonly. Ingestion of clay litter containing bentonite, which binds K+ in the gastrointestinal tract, has been associated with hypokalemia in a cat.10

Translocation

Translocation of K+ from extracellular fluid to intracellular fluid occurs with alkalemia, administration of insulin or glucose containing fluids that stimulate insulin release11, endogenous catecholamine release or exogenous catecholamine administration, ingestion of a β2-adrenergic receptor agonist12, and as a familial disorder in Burmese cats < 1 year of age.13

Increased Loss

Increased loss of K+ may be either through the urinary or gastrointestinal tracts; urinary loss occurs more commonly. Vomiting may result in hypokalemia due to urinary potassium excretion in exchange for sodium and water reabsorption14, although K+ can be lost with diarrhea. Urinary K+ loss occurs with chronic renal failure in cats15, diet-induced nephropathy in cats8, distal renal tubular acidosis16, post-obstruction diuresis17, mineralocorticoid excess18, and with certain drugs (primarily diuretics).

Management

Potassium repletion and management of the primary cause for hypokalemia are the goals in managing dogs and cats with hypokalemia. Potassium chloride is the additive of choice for parenteral treatment because chloride repletion is also important if hypokalemia occurs in association with vomiting or diuretic administration. When administered intravenously, K+ should not be infused at a rate > 0.5 mEq/kg/hr because arrhythmias may occur at higher administration rates.9 Consider adding K+ to parenteral fluids to patients receiving glucose in the fluids or beginning on insulin for management of diabetes mellitus (Table 1).

Because cats, in particular, with chronic renal failure appear to have risk for developing hypokalemia, measuring serum/plasma K+ concentration should be part of the monitoring of these patients with the goal of maintaining the concentration at or above the middle of the normal reference values for the laboratory. Commercially available diets formulated for patients with renal failure contain additional K+ to help manage the potential hypokalemia. If supplementation is required, K+ gluconate or K+ citrate can be used.

If hypokalemia occurs due to other causes, such as vomiting, diarrhea, diuretic administration, etc., then management of the primary disease or discontinuation or modification of drug administration should be attempted. In patients requiring diuretic therapy that develop hypokalemia, use a potassium-sparing diuretic, such as spironolactone, to help prevent development of hypokalemia.

Table 1. Guidelines for routine intravenous supplementation of potassium in dogs and cats.9

Serum/plasma K+ concentration
(mEq/L)

mEq KCL to add to
250 mL of fluid

mEq/KCl to add to
1 L of fluid

Maximal fluid infusion rate
(mL/kg/hr)

< 2.0

20

80

6

2.1-2.5

15

60

8

2.6-3.0

10

40

12

3.1-3.5

7

28

18

3.6-5.0

5

20

25

References

1.  DiBartola SP, de Morais H. Disorders of potassium: Hypokalemia and hyperkalemia In: DiBartola SP, ed. Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice. 3rd ed. St. Louis: Saunders Elsevier, 2006;91-121;

2.  Reimann KA, Knowlen GG, Tvedten HW. Factitious hyperkalemia in dogs with thrombocytosis. The effect of platelets on serum potassium concentration. J Vet Intern Med 1989;3:47-52;

3.  Degen M. Pseudohyperkalemia in Akitas. J Am Vet Med Assoc 1987;190:541-543;

4.  Knochel JP, Schlein EM. On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest 1972;51:1750-1758;

5.  Dow SW, LeCouteur RA, Fettman MJ, et al. Potassium depletion in cats: hypokalemic polymyopathy. J Am Vet Med Assoc 1987;191:1563-1568;

6.  Abbrecht PH. Effects of potassium deficiency on renal function in the dog. J Clin Invest 1969;48:432-442;

7.  Nath KA, Hostetter MK, Hostetter TH. Pathophysiology of chronic tubulointerstial disease in rats: Interactions of dietary acid load, ammonia, and complement component C3. J Clin Invest 1985;76:667-675;

8.  DiBartola SP, Buffington CA, Chew DJ, et al. Development of chronic renal disease in cats fed a commercial diet. J Am Vet Med Assoc 1993;202:744-751;

9.  DiBartola SP. Management of hypokalaemia and hyperkalaemia. J Feline Med Surg 2001;3:181-183;

10. Hornfeldt CS, Westfall ML. Suspected bentonite toxicosis in a cat from ingestion of clay cat litter. Vet Hum Toxicol 1996;38:365-366;

11. Bruskiewicz KA, Nelson RW, Feldman EC, et al. Diabetic ketosis and ketoacidosis in cats: 42 cases (1980-1995). J Am Vet Med Assoc 1997;211:188-192;

12. Vite CH, Gfeller RW. Suspected albuterol intoxication in a dog. J Vet Emerg Crit Care 1994;4:7;

13. Lantinga E, Kooistra HS, van Nes JJ. [Periodic muscle weakness and cervical ventroflexion caused by hypokalemia in a Burmese cat]. Tijdschr Diergeneeskd 1998;123:435-437;

14. Willard MD. Disorders of potassium homeostasis. Vet Clin North Am Small Anim Pract 1989;19:241-263;

15. DiBartola SP, Rutgers HC, Zack PM. Clinicopathologic findings associated with chronic renal disease in cats: 74 cases (1973-1984). J Am Vet Med Assoc 1987;190:1196-1202;

16. Bartges JW. Disorders of renal tubules In: Feldman EC, Ettinger SJ, eds. Textbook of Veterinary Internal Medicine. 5th ed. Philadelphia: WB Saunders, 1999;96-99;

17. Bartges JW, Finco DR, Polzin DJ, et al. Pathophysiology of urethral obstruction. Vet Clin North Am Small Anim Pract 1996;26:255-264;

18. Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;7:173-182.

Speaker Information
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Joseph Bartges, DVM, PhD, DACVIM, DACVN
University of Tennessee
Knoxville, TN


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