Today's Veterinary Practice

MAR-APR 2018

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PEER REVIEWED 54 FLUID THERAPY: PART 2 Patients with chronic hyponatremia often have no clinical signs, although those with a rapid onset of hyponatremia may present with seizures, ataxia, weakness, lethargy, nausea, or vomiting. Acute hyponatremia results in movement of water from the extracellular to the intracellular space, causing cerebral edema. Patients with chronic hyponatremia are typically not clinically affected because loss of potassium and organic osmolytes from neurons adjusts brain volume. 1 Treatment As with hypernatremia, hyponatremia is commonly considered chronic unless a recent baseline sodium measurement is available or the patient exhibits clinical signs to suggest an acute change. If hyponatremia is chronic, sodium should not be raised more than 10 to 12 mEq/L in a 24-hour period. A rapid correction of sodium may result in central pontine myelinolysis, in which neurons shrink away from the myelin sheath. Clinical signs of myelinolysis, such as lethargy, weakness, ataxia, hypermetria, and tetraparesis, occur several days after rapid sodium correction and can be treated with free water administration, although the damage may be irreversible. IV fluid choice should depend on the degree of hyponatremia. If the patient has no clinical signs and is normally hydrated, water restriction is indicated. In patients that have a sodium concentration <130 mEq/L and need IV fluids, the commercially available fluid with the lowest sodium, lactated Ringer's solution (130 mEq/L), should be used. Sodium concentration should be measured at least every 4 hours during the beginning of therapy and adjustments to fluid made as needed. Typically, patients transition from solutions containing lower sodium concentrations (eg, lactated Ringer's solution) to solutions with higher concentrations (eg, Plasmalyte-A [ baxter.com ]) as their sodium concentration slowly rises. Hypochloremia Hypochloremia may result from a net loss of chloride but is also associated with changes in water balance. Changes in sodium and chloride secondary to water loss or gain are frequently concurrent because chloride tends to follow sodium. True hypochloremia is seen with chloride loss, but the effect of water balance must be eliminated to determine the actual (corrected) chloride. To calculate the corrected chloride, the following equation can be used: Corrected Cl = Cl measured × (Na normal /Na measured ) In small animals, hypochloremia is commonly caused by gastrointestinal obstruction, but it can also be secondary to administration of loop and thiazide diuretics. 1 Loss of chloride and concurrent hypovolemia result in retention of bicarbonate to maintain electroneutrality, and metabolic alkalosis will persist if the hypochloremia goes untreated. The fluid of choice to correct hypochloremia is 0.9% NaCl because it has the highest chloride concentration of the isotonic crystalloid solutions available. Once volume status has been corrected with 0.9% saline, the metabolic alkalosis will resolve. Hypokalemia Hypokalemia is a common finding in small animal patients and may result from increased potassium loss through the gastrointestinal or urinary tract, decreased potassium intake, intracellular shifting of potassium due to alkalemia or insulin administration, catecholamine release, hyperaldosteronism, and administration of loop or thiazide diuretics. 3 Hypokalemia can result in muscle weakness, cervical ventroflexion, rhabdomyolysis, hypoventilation, cardiac conduction abnormalities, and refractory hypomagnesemia. TABLE 1 Effect of Serum Abnormalities on Measured Sodium 1 ABNORMALITY INCREASE DECREASE IN SODIUM (MEQ/L) Hyperproteinemia Each g/dL >8.0 0.25 Hypertriglyceridemia 1000 mg/dL 2 Hyperglycemia 100 g/dL* 1.6 *Correction factor is 2.4 mEq/L if blood glucose >440 mg/dL. 50

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