SERUM ELECTROLYTES: WHAT DO THEY MEAN?

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1 SERUM ELECTROLYTES: WHAT DO THEY MEAN? S.P. DiBartola, DVM, DACVIM Emeritus Professor of Medicine, College of Veterinary Medicine, Ohio State University, Columbus, Ohio, USA SUMMARY The kidneys are responsible for regulating the composition of extracellular fluid and consequently play an important role in regulation of serum electrolyte concentrations and acid base balance. The serum concentration of an electrolyte does not necessarily reflect the total body store of the electrolyte in question. SODIUM Dog 145 ( ) meq/l Cat 156 ( ) meq/l The serum sodium concentration is an indication of the amount of sodium relative to the amount of water in the extracellular fluid and provides no direct information about total body sodium content. Patients with hyponatremia or hypernatremia may have decreased, normal, or increased total body sodium content. An increased serum sodium concentration (hypernatremia) implies hyperosmolality whereas a decreased serum sodium concentration (hyponatremia) usually, but not always, implies hypoosmolality. Hypernatremia develops when water intake has been inadequate, when fluid losses have been hypotonic to extracellular fluid, or when an excessive amount of sodium has been ingested or administered parenterally. Hypernatremia is unlikely to occur due to ingestion of large amounts of salt if the thirst mechanism is intact and the animal has access to water. Causes of hypernatremia include pure water loss (e.g., lack of intake), hypotonic fluid loss (e.g., gastrointestinal loss, third space loss, renal loss), and gain of impermeant solute (e.g. salt poisoning, hypertonic fluid administration). Hyponatremia develops when the patient is unable to excrete ingested water or when urinary and other fluid losses have a combined osmolality greater than that of ingested or parenterally administered fluids. In most instances, hyponatremia is accompanied by hypoosmolality. Total body sodium content and extracellular fluid volume in patients with hyponatremia may be increased (hypervolemia), normal (normovolemia), or decreased (hypovolemia). Hyponatremia with hypervolemia occurs in three main situations (severe liver disease, congestive heart failure, and nephrotic syndrome) that share a common pathophysiology characterized by activation of the renin-angiotensin-aldosterone system. Hyponatremia with normovolemia may occur in dogs with psychogenic polydipsia, after administration of drugs with antidiuretic effects, or with administration of hypotonic fluids. Hyponatremia with hypovolemia is this most common clinical situation and may occur with gastrointestinal losses (e.g., vomiting, diarrhea), third space losses (e.g., pancreatitis, peritonitis, uroabdomen, pleural effusion), hypoadrenocorticism, or diuretic administration. The hyponatremia that occurs in these situations is in part a consequence of non-osmotic stimulation of antidiuretic hormone release which occurs with severe volume depletion.

2 CHLORIDE Dog 110 ( ) meq/l Cat 120 ( ) meq/l Chloride is the most abundant anion in extracellular fluid, and Cl - and HCO 3 - are the only important resorbable anions in renal tubular fluid. An alteration in the normal relationship between these ions underlies the pathophysiology of acid base disturbances such as hyperchloremic (normal anion gap) metabolic acidosis and hypochloremic metabolic alkalosis. Causes of hypochloremia include vomiting of stomach contents, overzealous use of diuretics (e.g., furosemide, thiazides), and as compensation for chronic respiratory acidosis. Causes of hyperchloremia include excessive loss of sodium relative to chloride (e.g., diarrhea), excessive gain of chloride relative to sodium (e.g., NH 4 Cl, KCl, 0.9% NaCl, hypertonic saline, salt poisoning), and excessive chloride retention by the kidneys (e.g., renal tubular acidosis, acetazolamide, spironolactone, compensation for chronic respiratory alkalosis). POTASSIUM Dog 4.5 ( ) meq/l Cat 4.5 ( ) meq/l Hypokalemia arises from decreased intake, translocation of potassium from extracellular to intracellular fluid, and excessive loss of potassium by either the gastrointestinal or urinary routes. Decreased intake of potassium alone is unlikely to cause hypokalemia, but it may be a contributing factor. Translocation occurs as a consequence of alkalemia or administration of insulin and glucose-containing fluids. Increased loss may be a result of gastrointestinal disorders (e.g., vomiting of stomach contents, diarrhea) or urinary tract disorders (e.g., chronic renal failure, renal tubular acidosis, postobstructive diuresis, mineralocorticoid excess, diuretics). Hyperkalemia is uncommon if renal excretion of potassium is normal, and increased intake is unlikely to cause hyperkalemia if renal function is normal unless potassium intake is iatrogenic (e.g., infusion of potassium-containing fluids at an excessively rapid rate). Translocation of potassium from intracellular to extracellular fluid can occur with acute mineral acidosis (e.g., NH 4 Cl) or insulin deficiency (e.g., diabetic ketoacidosis). Finally, hyperkalemia can arise from decreased urinary excretion associated with urethral obstruction, ruptured bladder, anuric or oliguric renal failure, hypoadrenocorticism, or certain drugs (e.g., angiotensinconverting enzyme inhibitors, potassium-sparing diuretics). CALCIUM Dog 10.1 ( ) mg/dl Cat 9.2 ( ) mg/dl

3 Serum calcium concentration is closely regulated by the actions of 3 hormones (calcitriol, parathyroid hormone, and calcitonin) working on three organ systems (gut, kidney, and bone). Total serum calcium concentration is composed of three components. Ionized calcium is the biologically active component and represents approximately 50% of the total serum calcium concentration. Complexed calcium is bound to organic and inorganic anions in plasma and represents approximately 10% of the total serum calcium concentration. Protein-bound calcium is bound mainly to albumin and represents approximately 40% of the total serum calcium concentration. The serum calcium concentration reported on routine biochemistry profiles is the total serum calcium concentration. Hypercalcemia may be caused by dehydration, various malignancies (e.g., lymphosarcoma, perirectal apocrine gland adenocarcinoma), hypoadrenocorticism, acute or chronic renal failure, hypervitaminosis D (including cholecalciferol-containing rodenticides), primary hyperparathyroidism, and some skeletal lesions. The HARD IONS mnemonic (popularized by Dr. Dennis Chew) is useful way to quickly recall the causes of hypercalcemia (so-called hard water has a lot of calcium in it): Hyperparathyroidism Addison s disease Renal disease vitamin D excess Idiopathic (in cats) Osteolytic Neoplasia Spurious (lab error, dehydration)

4 Hypocalcemia may be caused by hypoalbuminemia (the most common cause), acute or chronic renal failure, ethylene glycol intoxication, eclampsia, acute pancreatitis, and primary hypoparathyroidism. Low serum albumin leads to a low total serum calcium concentration (despite normal ionized calcium concentration) because of a decreased in the protein-bound fraction of calcium. PHOSPHORUS Dog 4.2 ( ) mg/dl Cat 6.3 ( ) mg/dl Plasma inorganic phosphorus is largely a mixture of H 2 PO 4-1 and HPO 4-2. Since the valence and number of milliequivalents (meq) of phosphate in extracellular fluid are influenced by ph, it is more simple and convenient to discuss phosphate in millimoles (mmol) or milligrams (mg) of elemental phosphorus. Serum phosphorus concentrations are reported by clinical laboratories in terms of the amount of elemental phosphorus present and are expressed as mg elemental phosphorus per dl serum. Phosphorus is located intracellularly, and it is difficult to judge total body stores of phosphorus from evaluating serum phosphorus concentration. Shifting of phosphorus between intracellular and extracellular fluid can result in sudden large changes in serum phosphorus concentration. The kidneys are the main route for excretion of phosphorus from the body and the most common reason for increased serum phosphorus concentration is decreased glomerular filtration rate (renal failure and primary renal azotemia) although pre-renal (dehydration) and post-renal (e.g. ruptured bladder, obstructed urethra) factors also may cause hyperphosphatemia. Compensatory renal secondary hyperparathyroidism maintains serum phosphorus concentration within the normal range until > 85% of the nephron population has become nonfunctional. Thus, hyperphosphatemia is not observed in renal failure until after the onset of azotemia (loss of > 75% of the nephron population). Serum phosphorus concentration often is increased in acute renal failure with severe reduction in glomerular filtration rate (< 15% of normal). Hypophosphatemia may be caused by translocation of phosphate from extracellular to intracellular fluid (maldistribution), decreased renal reabsorption of phosphate, or decreased intestinal absorption of phosphate. Hyperphosphatemia may be caused by translocation of phosphate from intracellular to extracellular fluid (maldistribution), decreased renal excretion of phosphate, and increased intake of phosphate. Mild hyperphosphatemia is a normal physiologic finding in young growing animals. REFERENCES DeMorais HA and Biondo AW, 2012: Disorders of Chloride: Hyperchloremia and Hypochloremia. In: DiBartola SP. Fluid, Electrolyte, and Acid Base Disorders in Small Animal Practice, ed 4, Elsevier, St. Louis, pp DiBartola SP, 2012: Disorders of Sodium and Water: Hypernatremia and Hyponatremia. In: DiBartola SP. Fluid, Electrolyte, and Acid Base Disorders in Small Animal Practice, ed 4, Elsevier, St. Louis, pp

5 DiBartola SP and DeMorais HA, 2012: Disorders of Potassium: Hypokalemia and Hyperkalemia. In: DiBartola SP. Fluid, Electrolyte, and Acid Base Disorders in Small Animal Practice, ed 4, Elsevier, St. Louis, pp Schenck PA, Chew DJ, Nagode LA, and Rosol TJ, 2012: Disorders of Calcium: Hypercalcemia and Hypocalcemia. In: DiBartola SP. Fluid, Electrolyte, and Acid Base Disorders in Small Animal Practice, ed 4, Elsevier, St. Louis, pp DiBartola SP and Willard MD, 2012: Disorders of Phosphorus: Hyperphosphatemia and Hypophosphatemia. In: DiBartola SP. Fluid, Electrolyte, and Acid Base Disorders in Small Animal Practice, ed 4, Elsevier, St. Louis, pp

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