Metabolic Alkalosis with Paradoxical Aciduria

History. You examine a 3-year-old Holstein-Friesian cow that has been inappetent for 2 to 3 days. The cow recently calved and freshened normally, but milk production has dropped in the last 2 days, and the feces are loose.

Clinical Examination. Physical examination reveals dehydration and an elevated heart rate. Percussion of the abdomen reveals an area of high-pitched resonance on the right side. A distended abomasum is palpable on rectal exam­ination. You diagnose a right displaced abomasum and sus­pect abomasal torsion. Attempts to correct the displacement by rolling the cow fail. The cow is transported to your clinic for surgery, and samples are obtained for a CBC, serum chem­istry profile, and urinalysis. The serum K⁺ level is 2.7 mEq/L (normal, 4.0-5.1 mEq/L)» serum Cl level is 77 mEq/L (nor­mal, 85-103 mEq/L), and total CO₂ concentration (approx­imately the same as serum HCO₃^- concentration) is 35 mEq/L (normal, 24-27 mEq/L). The urine pH is 6.0.

Comment. The cow has hypokalemic, hypochloremic, meta­bolic alkalosis secondary to abomasal displacement. The alkalosis was initialed by continued secretion of HCl by the abomasum and blunted HCO_t secretion by the intestine after the gastro­intestinal obstruction. The hypokalemia is a result largely of intracellular movement of K’ secondary to alkalosis and may not reflect a decrease in total body K' levels.

The expected renal response to alkalosis is the excretion of alkaline urine. However, in this case the volume contraction and hypochloremia prevent the formation of alkaline urine, and the result is paradoxical aciduria. As mentioned, the prox­imal tubule reabsorbs the filtered HCO₃^-, regardless of the plasma pH or serum HCO₃^- concentration. The volume deple­tion enhances Na reabsorption, primarily through the action ofaldosterone, and Cl and H₂O reabsorption are enhanced as a secondary reaction to the increased Na’ uptake.

Renal secretion of HCO₃^- occurs by apical exchange of Cl­in the tubule fluid for intracellular HCLO₃^- in type B inter­calated cells in the collecting duct. Because NaCl is avidly reabsorbed to combat volume depletion, little CΓ remains for exchange with HCO₃^-, and net HCO₃" secretion does not occur. Acid secretion in the collecting duct is known to increase in response to aldosterone and may be enhanced in this volume-depleted animal. Hypokalemia activates the acid-secreting intercalated cells in the collecting duct and thus may contribute to the excretion of acid urine in this case.

Treatment. Treatment involves vigorous volume replace­ment with intravenous normal saline, with KCl added, and surgical correction of the abomasal displacement.