{"id":30708,"date":"2022-04-11T20:29:58","date_gmt":"2022-04-11T20:29:58","guid":{"rendered":"https:\/\/todaysveterinarypractice.com\/?p=30708"},"modified":"2022-04-12T18:05:30","modified_gmt":"2022-04-12T18:05:30","slug":"evaluation-and-management-of-the-hyperkalemic-patient","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/internal-medicine\/evaluation-and-management-of-the-hyperkalemic-patient\/","title":{"rendered":"Evaluation and Management of the Hyperkalemic Patient"},"content":{"rendered":"

Hyperkalemia is defined as a plasma or serum potassium concentration (i.e., [K]) in excess of the established reference range and is commonly encountered in companion animal practice. The causes of hyperkalemia are generally classified as (1) increased potassium input, (2) decreased potassium excretion, and (3) translocation from intracellular to extracellular compartments.<\/span><\/p>\n

Clinically significant hyperkalemia is most often the result of impaired potassium excretion, usually due to compromise to the kidneys\/urinary tract or to hypoaldosteronism.1<\/sup> Mild hyperkalemia (i.e., [K] above the reference range but <6 mmol\/L) may be noted in patients with third spacing of fluids (e.g., pleural effusion, ascites, pregnancy) or colonic parasitism (primarily Trichuris vulpis<\/i><\/a>); this is thought to reflect systemic volume loss, increased secretion of antidiuretic hormone, and decreased fluid delivery to the distal convoluted tubules of the kidneys.2<\/sup> Because more than 95% of the body\u2019s potassium is located within the intracellular compartment, serum concentrations may be increased by disorders that impact intracellular translocation, such as insulin deficiency, or by the release of potassium from damaged cells, particularly myocytes.3<\/sup> Excessive dietary intake is not a recognized cause of hyperkalemia because healthy patients can tolerate significant amounts of oral intake.<\/span><\/p>\n

The potassium gradient between the intra- and extracellular compartments plays a key role in action potential generation by excitable cells. The impact of hyperkalemia is most clearly evident on the heart, ultimately resulting in disruption of cardiac muscle excitation and conduction followed by cessation of all electrical activity. Although the cardiac effects of increasing [K] are fairly predictable in experimental models, this is not the case in clinical patients wherein electrocardiogram (ECG) changes correlate poorly with serum [K].4<\/sup> Mild hyperkalemia (<6 mmol\/L) is usually of little clinical consequence, but [K] \u22656 mmol\/L should be investigated, and values >7 mmol\/L often require emergent intervention.<\/span><\/p>\n

Causes of Hyperkalemia<\/h2>\n

Spurious<\/h3>\n

Increased [K] may be noted in serum samples with increased platelet counts (i.e., thrombocytosis), as potassium is released during aggregation.5<\/sup> Alternatively, contamination of the serum or heparin tube with EDTA may cause marked increases in reported [K]; this is predictably accompanied by substantial hypocalcemia. Excessive hemolysis during sample collection or processing can also impact measured [K]; this may be more likely to occur in the Japanese breeds.<\/span><\/p>\n

Compromise to the Kidneys\/Urinary Tract<\/h3>\n

Surplus potassium is continuously excreted by the kidneys, and urine concentrations are severalfold higher than those of serum. Compromised excretion will predictably result in both hyperkalemia and azotemia. The magnitude of these changes is variable and depends on the underlying etiology:<\/span><\/p>\n