Metabolic alkalosis in animals with upper GI obstruction

If you are presented with an acutely vomiting canine or feline patient who happened to have a metabolic alkalosis on the blood gas analysis, an upper gastrointestinal (GI) obstruction should be suspected. Lozano et al. (Texas A&M University, JSAP 2023) recently published a study that looked at the prevalence of various acid-base and electrolyte disorders in this population of dogs.  A total of 115 dogs were included in the study, with 22% of dogs showing either a simple metabolic alkalosis or a mixed metabolic alkalosis before surgery. While 37% of dogs had a normal acid–base status on presentation. 

Metabolic alkalosis was resolved in nearly all patients post-operatively, with no patients displaying a metabolic alkalosis after surgical or endoscopic treatment of obstruction was performed. A mixed metabolic acidosis and respiratory alkalosis was the most common condition post-operatively, found in 35% dogs. 

With respect to electrolyte derangements, a majority of dogs in this study exhibited hypokalemia (64.4%), hypochloremia (72.8%) and hyponatremia (77.4%) on preoperative venous blood gases, however the majority of these derangements were mild.

Why does metabolic alkalosis occur in animals with upper GI obstruction?

In general, metabolic alkalosis occurs in the body secondary to the loss of acidifying components such hydrogen ions and/or chloride. Profuse vomiting of stomach contents causes a loss of hydrogen ions, potassium and chloride contributing to a hypochloremic (or chloride responsive) metabolic alkalosis (Guilford & Strombeck 1996, Hall & Hall 2021). Continued extracellular fluid depletion caused by GI losses activates renin-angiotensin-aldosterone system (RAAS) that results in secretion of aldosterone leading to hydrogen excretion via urine worsening metabolic alkalosis.

1. Chloride-Responsive Metabolic Alkalosis is characterized by an alkalotic state that can be corrected or improved by increasing chloride levels in the body, typically through the administration of high chloride-containing solutions, such as normal saline (0.9% sodium chloride). In this type of alkalosis, the kidneys respond to the increased chloride levels by reducing bicarbonate reabsorption and promoting bicarbonate excretion in the urine, which helps to lower blood bicarbonate levels and restore the acid-base balance. Therefore, animals presenting with moderate-to-severe metabolic alkalosis secondary to vomiting will usually benefit from intravenous fluid therapy with NaCl 0.9% as opposed to balanced replacement solutions such as LRS or Normosol-R that contain less chloride. In addition, buffers such as lactate or acetate included in these solutions may slow down the resolution of metabolic alkalosis. That said, correction of hypovolemia through administration of appropriate amount of any replacement IV fluids will “shut down” aldosterone secretion resulting in hydrogen reabsorption that is beneficial in these animals.

2. Chloride-Resistant Metabolic Alkalosis: Chloride-resistant metabolic alkalosis refers to an alkalotic state that does not improve significantly or normalize with the administration of chloride-containing solutions. In this type of alkalosis, the underlying cause is not solely related to chloride deficiency or loss, and the response to chloride repletion is limited or ineffective in correcting the acid-base imbalance.

Figure 1. Differentials for metabolic alkalosis. Workbook: Electrolyte and acid-base mastery: certification course (Yankin 2023).

Causes of Chloride-Resistant Metabolic Alkalosis: Mineralocorticoid Excess. Conditions such as primary hyperaldosteronism (Conn’s syndrome) or secondary hyperaldosteronism can lead to excessive aldosterone production, which results in sodium and chloride retention, and potassium and hydrogen ion excretion. This leads to metabolic alkalosis that is not easily reversed by chloride administration.

Treatment for Chloride-Resistant Metabolic Alkalosis: Management of chloride-resistant metabolic alkalosis involves addressing the underlying cause. For example, in cases of mineralocorticoid excess, treatment may include surgical removal of the tumor (if present) or the use of mineralocorticoid receptor antagonists.

The Bottom Line

About 1/5 of all dogs presenting with pyloric or duodenal obstruction may develop metabolic alkalosis. These animals tend to develop chloride-responsive metabolic alkalosis that will resolve in nearly all patients after administration of IV fluids (NaCl 0.9% preferably) and correction of the obstruction.

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Lozano, B. A., Yankin, I., Perry, S., & Rutter, C. R. (2023). Acid-base and electrolyte evaluation in dogs with upper GI obstruction: 115 dogs (2015-2021). The Journal of small animal practice, 10.1111/jsap.13656. Advance online publication. https://doi.org/10.1111/jsap.13656

Electrolyte and acid-base mastery: certification course (Yankin 2023)

Guilford, W. G. & Strombeck, D. R. (1996) Intestinal obstruction, pseudo-obstruction, and foreign bodies. In: Strombeck’s Small Animal Gastroenterology. 3rd edn. Ed W. B. Saunders. Saunders, Philadelphia, PA, USA. pp 487-502

Hall, J. E. & Hall, M. E. (2021) Chapter 31 – acid-base regulation. In: Guyton and Hall Textbook of Medical Physiology. 14th edn. Eds A. C. Guyton, J. E. Hall and M. E. Hall. Elsevier, Philadelphia, PA, USA. pp 403-420