Page 98 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

88 ELECTROLYTE DISORDERS

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No information was provided about whether the cats in identified in sled dogs anticipation of exercise, and during
66
this report had vomited. In at least one ketoacidotic prolonged endurance exercise. However, corrected chlo-
dog, corrected hypochloremia also was found. 100 ride concentration did not change in sled dogs during high
Patients with hypoadrenocorticism and hypoaldos- intensity sprint exercise of extended (>10 miles) dura-
teronism have chloride retention and hyperchloremic tion. 95 Corrected hyperchloremia also was observed in
metabolic acidosis because of the lack of mineralo- dogs during and after agility competition. 85
corticoids. These patients typically have decreased serum Treatment of corrected hyperchloremia should be
sodium and chloride concentrations caused by lack of directed at correction of the underlying disease process.
aldosterone. The hyponatremia is more pronounced than The effects of fluid therapy on chloride concentration

the hypochloremia, and Cl (corrected) is increased. 17 should be anticipated, especially in patients with diabetes
Well-hydrated dogs with mineralocorticoid deficiency mellitus or abnormal renal function. Special attention
that are able to maintain serum sodium concentration should be given to plasma pH because patients with
usually have a mildly increased serum chloride corrected hyperchloremia tend to be acidotic. Bicarbon-
concentration. ate therapy can be instituted whenever plasma pH is less
Drugs that cause chloride retention also can cause than 7.2 or bicarbonate concentration is less than
hyperchloremia. Potassium-sparing diuretics such as 12 mEq/L in patients with hyperchloremic metabolic
spironolactone act by decreasing the number of open acidosis.
aldosterone-sensitive sodium channels in the principal
cells of the cortical collecting tubules. 81 Inhibition of CONCLUSION
sodium reabsorption at this site leads to hyperkalemia
and hyperchloremic acidosis. Acetazolamide inhibits car- Although it is the major anion in ECF, chloride has not
bonic anhydrase in the proximal tubule, resulting in received much attention in the clinical setting. It should
bicarbonaturia, urinary alkalinization, and in rats, but be remembered that the chloride ion also is important
not in dogs, reduction in renal ammoniagenesis. 32,44 in the metabolic regulation of acid-base balance.
Chloride reabsorption proceeds normally in the ascend- The kidneys regulate acid-base balance by changing
ing loop of Henle, resulting in chloride retention, 58 the amount of chloride that is reabsorbed with sodium.
and use of acetazolamide is associated with Chloride is important in determining the patient’s SID,
hyperchloremia and metabolic acidosis. 51,81,83 Parenteral and therefore changes in chloride concentration will
nutrition can cause hyperchloremia, because some reflect the patient’s acid-base status. Corrected hypo-
solutions have high concentrations of cationic amino chloremia is associated with increased SID and metabolic
acids (e.g., lysine-HCl, arginine-HCl) that release chlo- alkalosis. Chloride is the only anion in ECF that can con-
ride and generate hydrogen ions. 52 tribute to a substantial increase in SID. Administration of
Fluid therapy is another important cause of chloride is necessary for correction of hypochloremic
hyperchloremia in hospitalized patients. Administration metabolic alkalosis. Corrected hyperchloremia is
of isotonic saline, lactated Ringer’s solution, or isotonic associated with decreased SID and metabolic acidosis.
saline with 5% dextrose has been associated with Treatment with sodium bicarbonate should be carried
corrected hyperchloremia in dogs. 11,82 Hyperchloremia out in hyperchloremic patients with a pH of less than 7.2.
can be exacerbated by intravenous infusion of 0.9%
sodium chloride. 57 Isotonic sodium chloride solution
supplemented with 20 mEq/L of KCl has a final sodium REFERENCES
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