Acid-base and Electrolyte Disturbances

Acid-base and electrolyte disturbances can result from upper intestinal obstruction, stasis, or other pathology in monogastric animals. Vomiting, in itself, does not usually lead to metabolic alkalosis since bicarbonate rich fluid from the duodenum is lost in addition to hydrochloric acid (HCl) from the stomach. However, if there is selective loss of gastric HCl, metabolic alkalosis will occur. Reasons for this include high intestinal obstruction due to foreign body, neoplasm, or functional/physical pyloric diseases; slow moving foreign body which initially caused high intestinal obstruction; and reduced small intestinal motility from swelling or inflammation. Hypergastrinemia, which is usually caused by a gastrin secreting tumor (gastrinoma), though rare, results in excessive secretion of HCl into the pylorus, vomiting, duodenal ulcers, and metabolic alkalosis.

In ruminants, abomasal stasis, obstruction, or torsion also leads to acid-base and electrolyte abnormalities due to sequestration of HCl in the abomasum, rather than direct loss from the body. Paradoxic aciduria is sometimes found in patients with long-standing metabolic alkalosis, hypovolemia, hypochloremia, and hypokalemia caused by abomasal or upper intestinal disorders (discussed in Chapter 6: Body Water, Electrolytes, and Acid-Base Balance).

Secretory diarrhea can lead to significant losses of sodium, chloride, potassium, and bicarbonate. If a large volume of bicarbonate-rich fluid is lost, metabolic acidosis with a normal anion gap may be seen because the bicarbonate is lost from the body and not used to titrate excess acid.