Page 944 - Small Animal Internal Medicine, 6th Edition

916 PART VII Metabolic and Electrolyte Disorders

decreased at a rate of 1 mEq/L/h. With severe hypernatremia
BOX 53.1 (Na >180), sodium should be corrected at a rate of 0.5 to
VetBooks.ir Causes of Hypernatremia in Dogs and Cats 1 mEq/L/h. Multiple fluid solutions can be used to success-
fully decrease sodium safely (Table 53.1). In the presence of
hemorrhagic shock, whole blood, plasma, or a colloid sus-
Caused by Pure Water Loss
Central diabetes insipidus* pension is the ideal fluid to administer. Serum sodium con-
Nephrogenic diabetes insipidus* centration should be measured frequently (q4-6h) to assess
Hypodipsia-adipsia response to treatment, and the status of the CNS should be
Neurologic disease evaluated frequently to observe for changes in clinical signs.
Abnormal thirst mechanism Worsening neurologic status or sudden onset of seizures
Defective osmoregulation of vasopressin release during fluid therapy is generally indicative of cerebral edema
Inadequate access to water and the need for hypertonic saline solution or mannitol
High environmental temperature (heatstroke) therapy (see Drugs Used in Metabolic and Electrolyte Dis-
Fever
orders, p. 934). Once ECF deficits have been replaced, the
Hypotonic Fluid Loss serum sodium concentration should be reevaluated and
Gastrointestinal fluid loss* water deficits corrected if hypernatremia persists. An
Vomiting approximation of the free water deficit in liters may be cal-
Diarrhea culated using the following formula:
Chronic kidney disease*
] normal
+
Polyuric acute kidney injury* (current [Na ÷ [Na + ]−1 )
Osmotic diuresis × (. × bodyweight in kg ) 2
06
Diabetes mellitus
Mannitol infusion Because the brain adjusts to hypertonicity by increas-
Diuretic administration ing the intracellular solute content via the accumulation
Postobstructive diuresis
Cutaneous burns of “idiogenic osmoles,” the rapid repletion of body water
Third-space loss with ECF dilution causes translocation of water into cells
Pancreatitis and may cause cerebral edema. If slower water repletion
Peritonitis is undertaken, brain cells lose the accumulated intracel-
lular solutes, and osmotic equilibration can occur without
Excess Sodium Retention cell swelling.
Primary hyperaldosteronism Maintenance crystalloid solutions (e.g., half-strength
Iatrogenic causes [0.45%] saline solution with 2.5% dextrose, half-strength
Salt poisoning lactated Ringer’s solution with 2.5% dextrose) or 5% dextrose
Hypertonic saline infusion in water can be used to correct the water deficit in hyperna-
Sodium bicarbonate therapy tremic animals with normal perfusion and hydration, and
Sodium phosphate enemas
Parenteral nutrition can also be used in dehydrated animals with persistent
hypernatremia after fluid deficits have been corrected.
*Common causes. Oral fluid administration is preferable for correcting
Modified from DiBartola SP: Disorders of sodium and water: water deficits, and fluid is administered through an intra-
hypernatremia and hyponatremia. In DiBartola SP, editor: Fluid, venous (IV) route if oral administration is not possible.
electrolyte and acid-base disorders in small animal practice, ed 4, The water deficit should be replaced slowly. Approximately
St Louis, 2012, Saunders Elsevier.
50% of the water deficit should be corrected in the first
24 hours, and the remainder corrected over the following
correct water deficits at a fluid rate that avoids significant 24 to 48 hours. The serum sodium concentration should
complications, and to identify and correct the underlying decline slowly, preferably at a rate of 0.5 to 1 mEq/L/h. The
cause of the hypernatremia. The initial priority is to restore rate of fluid administration should be adjusted as needed
ECF volume to normal. Hypernatremic animals should be to ensure an appropriate decrease in the serum sodium
resuscitated with a balanced electrolyte solution with NaCl concentration. A gradual reduction in the serum sodium
added to the suspension to bring the solution’s sodium concentration minimizes the fluid shift from the extracel-
content up to that of the animal (±6 mEq/L). To achieve this, lular to the intracellular compartment, thereby minimizing
23.4% NaCl can be added to the fluid solution; it contains neuronal cell swelling and cerebral edema and increasing
4 mEq NaCl/mL of solution. In deficit replacement, rapid intracranial pressure. Deterioration in CNS status after
administration of fluids is contraindicated unless signs of the start of fluid therapy indicates the presence of cere-
significant hypovolemia are noted. Any fluid should be bral edema and the immediate need to reduce the rate
administered cautiously at a volume only large enough to of fluid administration. Frequent monitoring of serum
correct hypovolemia. In animals with mild to moderate electrolyte concentrations, with appropriate adjustments
+
hypernatremia ([Na ] <180 mEq/L), sodium should be in the type of fluid administered and the rate of fluid