Felis ISSN 2398-2950

Hypokalemia

Contributor(s): Rosanna Marsella, Severine Tasker

Introduction

  • Common syndrome characterized by persistently low serum potassium levels.
  • Clinical signs are seen when serum [potassium] falls below 2.5-3.0 mmol/l.
  • Cause: excess loss or reduced intake of potassium.
  • Signs: weakness, lethargy.
  • Diagnosis: sings, laboratory tests.
  • Treatment: correct underlying disorder, potassium supplementation.
  • Prognosis: generally good - depends on underlying disease process.

Pathogenesis

Etiology

  • Decreased potassium intake alone does not usually result in severe hypokalemia unless there is concurrent loss of potassium occurring.
  • Increased renal loss of potassium, seen with:
  • Increased gastrointestinal loss of potassium, seen with:
  • Transcellular shift of potassium from ECF to ICF leads to hypokalemia, even if total body potassium levels are normal, seen with:
  • Iatrogenic hypokalemia, seen with:
    • Diuretic therapy.
    • Insulin Insulin.
    • Some nephrotoxic drugs (aminoglycosides and out-of-date tetracyclines Tetracycline).
    • Bicarbonate.
    • Laxatives.
    • Some B2 agonist drugs.
  • Pseudohypokalemia, seen with:
    • Lipemia.
    • Severe hyperproteinemia.

Predisposing factors

General

  • High prevalence in sick cats (37% in one study).

Specific

Pathophysiology

  • Hypokalemia can develop as a result of:
    • Decreased potassium intake.
    • Excessive loss of potassium via the kidneys or gut.
    • Movement of potassium from the extracellular fluid (ECF) to the intracellular fluid (ICF) compartment.
    • Iatrogenic or drug-induced.
    • Pseudohypokalemia due to laboratory error.

Regulation of potassium concentrations

  • Potassium is the major intracellular cation:
    • 90% is in intracellular fluid (ICF) due to the action of the sodium/potassium ATPase pumps within cell membranes.
    • 2% is in extracellular fluid (ECF).
    • Remainder is transcellular, within connective tissue and bone.
  • Regulation of body potassium levels is primarily controlled in the distal convoluted tubules (DCT) of the kidneys, by the mineralocorticoid aldosterone.
  • Aldosterone release is stimulated by:
    • Hyperkalemia  →   aldosterone release from adrenal cortex   →   action in DCT   →   sodium reabsorption and potassium secretion   →   loss of potassium in urine   →   lowering of serum potassium.
    • Hypovolemia  →   reduced renal blood flow   →   release of renin from kidney   →   angiotensinogen release   →   converted to angiotensin I then angiotensin II   →   aldosterone release from adrenal cortices   →   action in DCT   →   sodium reabsorption and potassium secretion   →   reduction in serum potassium and increase in serum sodium.
  • Only a small amount of potassium is lost via the gut, in feces.
  • In the DCT hydrogen ions can take the place of the potassium ions during the exchange process with sodium, to maintain electrical neutrality.

Acid-base status

  • Acid-base status also influences translocation of potassium between the ICF and ECF.
  • Acid-base status has a great influence on potassium levels:
    • Acidosis  →   secretion of hydrogen ions in preference to potassium in DCT required   →   potassium conserved   →   hyperkalemia.
    • Alkalosis  →   reabsorption of hydrogen ions in DCT required, in favor of potassium reabsorption   →   potassium secreted   →   hypokalemia. Alkalosis promotes movement of potassium from ECF to ICF   →   hypokalemia.

Renal dysfunction

  • Metabolic alkalosis (diuretics, chronic vomiting, chronic liver disease, excessive bicarbonate treatment)   →   renal loss of potassium and movement for potassium from ECF to ICF   →   hypokalemia.
  • Respiratory alkalosis (hyperventiliation due to severe anemia, fever or pain and reduced pulmonary function due to asthma or other lung disease)   →   hypokalemia.
    Metabolic acidosis can be associated with paradoxical loss of potassium in the urine in chronic renal failure.
  • Chronic renal failure; increased urinary potassium loss and ongoing polyuria +/- decreased intake   →   hypokalemia.
    Potassium depletion itself can   →   renal dysfunction (potassium depletion nephropathy). Diets high in protein and acid, but marginally low in potassium can result in this syndrome.Affected cats do not always show muscular weakness.
  • Diuretics   →   loss of sodium   →   aldosterone release   →   potassium secretion   →   hypokalemia.
  • Hyperaldosteronism   →   excessive release of aldosterone from adrenocortical tumor   →   retention of sodium and secretion of potassium   →   hypokalemia.
  • Correction of urinary obstruction   →   post-obstruction diuresis   →   urinary potassium loss   →   hypokalemia.

Gastrointestinal dysfunction

  • Chronic or severe diarrhea   →   loss of potassium in feces   →   hypokalemia.
  • Vomiting   →   loss of hydrogen ions (and some potassium) in vomit   →   development of metabolic alkalosis   →   hydrogen ions reabsorbed in DCT in favor of potassium ions   →   excessive urinary loss of potassium   →   hypokalemia.
  • Vomiting or diarrhea may   →   hypovolemia   →   aldosterone release via reninangiotensin system   →   potassium secretion   →   hypokalemia.

Other factors influencing potassium regulation

  • Movement of potassium from extracellular to intracellular space   →   hypokalemia in young Burmese.
  • Insulin Insulin (treatment of diabetes mellitus, especially ketoacidosis) and adrenaline Epinephrine (in hyperthyroidism)   →   movement of potassium from ECF to ICF   →   hypokalemia.
  • Hyperthyroidism Hyperthyroidism. Sudden onset of muscular weakness due to hypokalemia has been reported but cause of hypokalemia not confirmed. May be due to increased adrenergic stimulation   →   movement of potassium from ECF to ICF   →   hypokalemia.

Timecourse

  • Onset of muscular weakness is often quite acute.
  • Life-threatening if respiratory muscles involved.
  • Lethargy and fatigue may be on-going for several weeks.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Skelly B (2002) Causes, consequences and control of potassium imbalances in small animals. In Practice 24 (10), 596-604 VetMedResource.
  • Phillips S L & Polzin D J (1998) Clinical disorders of potassium homeostasis. Hyperkalemia and hypokalemia.​ Vet Clin N Am Sm Anim Pract 28 (3), 545-564 PubMed.
  • DiBartola S P, Buffington C A, Chew D J et al (1993) Development of chronic renal disease in cats fed a commercial diet. JAVMA 202 (5), 744-751 PubMed.
  • Dow S W, Fettman M J, Curtis C R et al (1989) Hypokalaemia in cats - 186 cases (1984-1987)​. JAVMA 194 (11), 1604-1608 PubMed.
  • Dow S W, Fettman M J, Curtis C R et al (1989) Hypokalemia in cat - 186 cases (1984-1987). JAVMA 194 (11), 1604-1608 PubMed.
  • Fettman M J (1989) Feline kaliopenic polymyopathy/nephropathy syndrome. Vet Clin N Am Small Anim Pract​ 19 (3), 415-32 PubMed.
  • Jones B R, Swinney G W, Alley M R et al (1988) Hypokalaemic myopathy in Burmese kittens. N Z Vet J 36 (3), 150-151 PubMed.

Other sources of information

  • Hodson S (1998) Feline hypokalemia. In Practice 20 (3), 135-144.
  • Gruffydd-Jones T (1996) Presentation on hypokalemia. The Burmese cat club news 12, 17-21.
  • Senior D F (1995) Fluid therapy, electrolytes and acid-base control. In: Textbook of Veterinary Internal Medicine. Eds: Ettinger S J & Feldman E C. W B Saunders. pp 294-312.
  • DiBartola S P (1994) Hypokalemic nephropathy. In: Consultations in Feline Internal Medicine 2.Ed: August J R. W B Saunders. pp 319-324.


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