Today's Veterinary Practice

MAR-APR 2018

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51 MARCH/APRIL 2018 ● TVPJOURNAL.COM FEATURES As a result, intravascular volume depletion is uncommon with pure water loss. With hypotonic fluid loss, the water loss is not proportional, and both a greater reduction in extracellular fluid and a greater chance of intravascular volume depletion occur. As the tonicity of the fluid lost increases, the degree of hypovolemia increases. Sodium gain is not as common as water loss in small animal medicine but may result from administration of isotonic replacement crystalloids to patients with renal dysfunction; ingestion of salt, homemade salt–flour mixes, or seawater; hyperaldosteronism; or administration of hypertonic saline, sodium phosphate enemas, or sodium bicarbonate solutions. 1,2 A rise in extracellular sodium results in movement of water out of cells, leading to dehydration of all body cells. Neurons are the least tolerant of cellular dehydration, and clinical signs of obtundation, head pressing, seizures, or coma are seen if the rise in sodium is rapid or severe (>180 mEq/L). 2 A rapid decrease in brain volume may also cause rupture of cerebral vessels and focal hemorrhage. 1 To compensate for increased extracellular osmolality, neurons produce idiogenic osmoles, which accumulate intracellularly and draw water back into the cell. The production of idiogenic osmoles begins within a few hours of cell volume loss but may not reach peak effects for 2 to 7 days ( FIGURE 1 ). 2 Treatment In cases of acute hypernatremia (<12 hours), sodium can be restored to baseline quickly; however, in most patients that present with hypernatremia, the duration of hypernatremia is unknown and must be presumed to be chronic. Because of the presence of idiogenic osmoles in patients with chronic hypernatremia, rapid restoration of a free water deficit (FWD) results in fluid shifts into the intracellular space and cerebral edema. It is therefore recommended that sodium be decreased by no more than 10 to 12 mEq/L over 24 hours ( BOX 1 ). In cases of severe hypernatremia, this decrease may take days. If volume depletion is present, the extracellular volume should be restored with a fluid that has a sodium concentration similar to that of the patient's FIGURE 1 . In acute hypernatremia, excess sodium molecules ( green ) result in an increase in the osmolarity of the extracellular fluid compared with intracellular fluid, resulting in a net movement of water out of the intracellular space ( arrows ) and dehydration of the neurons. To combat fluid loss during chronic hypernatremia, neurons produce idiogenic osmoles ( red ). BOX 1 Calculating Free Water Deficit and Replacement Rate Free water deficit (FWD) is calculated using the following equation: FWD (L) = 0.6 × weight (kg) × [(Na patient /Na normal ) − 1] In hypernatremic patients, the FWD should be replaced at a rate that reduces the sodium concentration (Na) by no more than 0.5 mEq/L per hour. Because the "normal" sodium concentration may vary depending on the analyzer used, this number may vary slightly between individual clinics. For example, if a patient weighs 20 kg and has a sodium concentration of 180 mEq/L, its FWD is 2.9 L. 0.6 × 20 × [(180/145) − 1] = 2.9 L To find the amount by which sodium needs to be reduced in this patient: Na patient − Na normal = 180 − 145 = 35 mEq/L To find the time required to safely reduce the sodium concentration: 35 mEq/L × 0.5 mEq/L/h = 70 hours To find the rate of free water replacement: (2.9 L × 1000 mL)/70 h = 2900 mL/70 h = 40 mL/h of free water

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