{"id":31022,"date":"2022-06-17T15:36:23","date_gmt":"2022-06-17T15:36:23","guid":{"rendered":"https:\/\/todaysveterinarypractice.com\/?p=31022"},"modified":"2022-07-20T13:15:28","modified_gmt":"2022-07-20T13:15:28","slug":"evaluation-and-management-of-the-hypokalemic-patient","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/internal-medicine\/evaluation-and-management-of-the-hypokalemic-patient\/","title":{"rendered":"Evaluation and Management of the Hypokalemic Patient"},"content":{"rendered":"

Hypokalemia is defined as a plasma or serum potassium concentration (i.e., [K]) that is below the reference range (usually 3.5 to 5.1 mmol\/L). More than 95% of total body potassium is intracellular, where it is the most abundant cation and plays a key role in maintenance of the resting membrane potential.1<\/sup> Changes in [K] within the extracellular fluid are therefore a poor reflection of total body potassium content. Healthy animals consuming adequate quantities of a balanced diet ingest abundant amounts of potassium, and the surplus is eliminated in urine. Renal excretion of potassium is primarily determined by aldosterone from the adrenal glands; this hormone triggers the reclamation of filtered sodium in exchange for potassium in the distal convoluted tubules. A primary driver for aldosterone secretion is a decrease in circulating volume; this triggers the release of renin and the generation of angiotensin II, which in turn stimulates aldosterone synthesis. Complex responses within the cells of the zona glomerulosa allow for the release of aldosterone in response to increases in [K]; conversely, hypokalemia blunts aldosterone secretion.2<\/sup> <\/span><\/p>\n

Acid\u2013base status also impacts serum [K], as protons are moved across cell membranes in exchange for potassium. Serum [K] is therefore increased by acidosis and lowered by alkalosis. In addition, acid\u2013base disorders significantly impact renal potassium handling, with increased kaliuresis in alkalemic patients.3<\/sup> Changes in glycemic status also influence [K], as insulin triggers the intracellular transportation of both glucose and potassium.3<\/sup> The administration of insulin to a hyperglycemic patient with borderline hypokalemia may therefore result in a clinically impactful drop in [K].<\/span><\/p>\n

In most instances, hypokalemia reflects potassium loss (via the kidneys or gastrointestinal tract) or the translocation of potassium into the intracellular compartment.1,4<\/sup> Inadequate potassium intake is unlikely to be a primary cause, although acidifying diets with limited potassium have been associated with clinically impactful potassium depletion in cats.5<\/sup> Mild hypokalemia (3 to 3.5 mmol\/L) is a common electrolyte derangement and is usually of little clinical consequence, although total body stores may be significantly depleted.1,4,6<\/sup> However, serum [K] <<\/span>\u2009<\/span>3\u00a0mmol\/L merits prompt attention, and a value of <<\/span>\u2009<\/span>2.5\u00a0mmol\/L is a medical emergency.<\/span><\/p>\n

Causes of Hypokalemia<\/h2>\n

Gastrointestinal Loss<\/h3>\n

Patients with vomiting and diarrhea are often hypokalemic, as significant amounts of potassium are present in digestive fluids. In patients with a gastric outflow obstruction, the loss of hydrochloric acid and subsequent hypochloremic metabolic alkalosis will further decrease serum [K] as protons are moved out of cells in exchange for potassium. In turn, hypokalemia limits the ability of the kidneys to retain protons, which perpetuates the metabolic alkalosis.<\/span><\/p>\n

Renal Loss<\/h3>\n

Although surplus dietary potassium is routinely excreted via the kidneys, patients with renal dysfunction or other causes of polyuria may experience excessive kaliuresis. Cats with chronic kidney disease are particularly prone to hypokalemia,7,8<\/sup> and life-threatening hypokalemia has been reported in 1 dog with acute leptospirosis<\/a>.9<\/sup> Patients with a postobstructive diuresis may lose substantial amounts of potassium until normal tubular function is restored. Type 1 renal tubular acidosis is also associated with hypokalemia, due to disruption of proton excretion\/bicarbonate generation in the distal convoluted tubule.2<\/sup> Primary hyperaldosteronism is uncommon in cats and very rare in dogs but will cause sustained kaliuresis and may result in significant clinical compromise.10<\/sup><\/span><\/p>\n

Iatrogenic<\/h3>\n

The prolonged administration of fluids with inadequate potassium supplementation is a common cause of hypokalemia; clinicians should routinely add potassium to crystalloids to prevent progressive depletion in anorexic patients. Loop and thiazide diuretics also promote renal potassium loss.11<\/sup> Insulin administration will move potassium into the intracellular compartment. The latter is a particular concern in patients with diabetic ketoacidosis because these animals often present with a substantial total body potassium deficit. Serum [K] may be normal at presentation, due to concurrent hyperglycemia and significant metabolic acidosis, but then drop precipitously following fluid and insulin administration.12<\/sup><\/span><\/p>\n

Toxicity<\/h3>\n

Albuterol\u2014like all <\/span>\u03b2<\/span>-adrenergic agonists\u2014triggers the intracellular movement of potassium. This effect is modest at standard therapeutic doses, but inadvertent overdose or the ingestion of an albuterol inhaler can cause significant hypokalemia.13<\/sup> Severe hypokalemia has also been reported in a dog following the ingestion of organic barium.14<\/sup><\/span><\/p>\n

Hereditary<\/h3>\n

Hypokalemic periodic paralysis\/polymyopathy has been reported in European and Australian Burmese cats. Affected cats are less than 12 months of age and present with acute, episodic, cervical ventroflexion, as well as weakness.15<\/sup><\/span><\/p>\n

Metabolic Alkalosis<\/h3>\n

An increase in the pH of the extracellular fluid triggers the movement of protons out of cells in exchange for potassium. In addition\u2014and perhaps more importantly\u2014alkalemia promotes urine potassium loss by stimulation of renal sodium transporters and increased kaliuresis.3<\/sup> Generous potassium supplementation is therefore necessary in these patients, along with mitigation of the underlying acid\u2013base disturbance.<\/span><\/p>\n

Consequences of Hypokalemia<\/h2>\n

As serum [K] decreases, changes in cell excitability result in muscle weakness. In patients with conditions associated with chronic hypokalemia, such as hyperaldosteronism, this may wax and wane depending on dietary potassium intake. As adequate serum [K] is necessary for effective function of antidiuretic hormone receptors in the collecting ducts, hypokalemia results in compromised renal concentrating ability.16<\/sup> Affected patients are variably polyuric and polydipsic, and urine specific gravity may fall below 1.008.<\/span><\/p>\n

Patients with severe hypokalemia (<<\/span>\u2009<\/span>2.5 mmol\/L) suffer from generalized skeletal muscle weakness caused by instability of muscle cell membranes, resulting in a generalized myopathy. In the cat, a species that lacks a completely developed nuchal ligament, cervical ventroflexion may be noted. Although these findings are not pathognomonic for hypokalemia, potassium status should be determined in any patient with weakness or other evidence of myopathy before administering resuscitative or replacement fluids. Injudicious fluid therapy can quickly drive down serum [K] through simple dilution and lead to further patient deterioration. With progressive hypokalemia, patients will be unable to ventilate due to paralysis of the diaphragm and the other muscles of respiration, resulting in death.<\/span><\/p>\n

In experimental rodent and feline models, chronic hypokalemia has been associated with changes in renal function, generally attributed to impaired renal angiogenesis.17,18<\/sup> However, hypokalemia per se is not recognized as a risk factor for progression in cats with chronic kidney disease.19<\/sup><\/span><\/p>\n

Initial Patient Assessment<\/h2>\n

It is important to try to establish the cause of hypokalemia with a thorough patient history and physical examination, along with a careful review of other routine laboratory data (e.g., complete blood count, serum biochemical profile, urinalysis). Additional diagnostics, such as measurement of systolic blood pressure, muscle enzyme activities (i.e., creatine kinase, aspartate aminotransferase), blood gas analysis, resting aldosterone concentrations, and abdominal imaging, may be necessary to establish a diagnosis.<\/span><\/p>\n

See <\/span>FIGURE 1<\/b><\/span> for an algorithm showing evaluation of the hypokalemic patient.<\/span><\/p>\n

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Treatment of Hypokalemia<\/h2>\n

Serum [K] <\u20093 mmol\/L<\/h3>\n

Potassium should be administered by continuous rate infusion. As a general rule, the rate of potassium administration should not exceed 0.5 mEq\/kg\/hr (0.5\u00a0mmol\/kg\/hr); see below for the calculation. <\/span><\/p>\n

Calculation to determine current rate of potassium administration:<\/span><\/p>\n