Metabolic acidosis caused by gastrointestinal stasis in rabbits and its treatment approach

Metabolic Acidosis Due to Gastrointestinal Stasis in Rabbits and Treatment Approaches

By Dr. Supawan Sriwiset, DVM (Dr. Bus) and Assoc. Prof. Dr. Somphot Weerakul, DVM, PhD (Ajarn Kaew)

This is a complex and often misunderstood topic. However, it is widely recognized that rabbits can experience metabolic acidosis from various causes. Among these, gastrointestinal (GI) stasis is frequently accompanied by elevated systemic acidity. Without proper understanding, treatment for severe acid-base imbalances is often overlooked, which significantly lowers the survival rate in affected rabbits.

The gastrointestinal tract plays a major role in acid-base regulation, alongside the kidneys, lungs, liver, and other often-overlooked organs. GI disturbances are among the leading causes of acidosis in rabbits. Both acidosis and alkalosis can occur in all animals, but in herbivores—especially rabbits—acidosis tends to be more common and severe. It primarily affects the cecum and large intestine, where nutrient, water, and electrolyte secretion and absorption take place.

Physiological Mechanisms in the GI Tract
In the cecum and large intestine, chloride (Cl⁻) and potassium (K⁺) are secreted into the intestinal lumen through Cl and K channels. Potassium can be reabsorbed into secretory cells via Na⁺/K⁺ ATPase, exchanging three Na⁺ ions out for two K⁺ ions in, using ATP for energy. Bicarbonate (HCO₃⁻) is mainly secreted into the gut, while other electrolytes are absorbed into absorptive cells via Cl⁻/HCO₃⁻ exchangers and Na⁺/H⁺ exchangers. Na⁺ is also absorbed directly through Na⁺ channels, and hydrogen ions (H⁺) are secreted in exchange for potassium via H⁺/K⁺ ATPase, a process influenced by aldosterone.

Unique to this region is the production and absorption of short-chain fatty acids (SCFAs) like acetic, propionic, and butyric acids. These are absorbed through SCFA/HCO₃⁻ exchangers, trading bicarbonate for SCFAs produced by microbial fermentation. This serves as a protective mechanism, helping to buffer acidity and prevent damage to the intestinal mucosa via mucus secretion.

However, when acid production exceeds the body's capacity to neutralize it, the availability of bicarbonate drops while organic acids accumulate. In rabbits, increased levels of lactic, acetic, propionic, and butyric acids are common, especially when fed high-carbohydrate diets. This imbalance is linked to GI stasis, inflammation, and dysbiosis. Despite normal chloride levels and occasionally unchanged blood chemistry (depending on the severity and adaptation), the anion gap typically increases due to lactic acidosis.

Clinically, low bicarbonate and elevated lactate levels serve as indicators. Experimental data also show a correlation between blood histamine levels and acidosis, particularly in rabbits fed inappropriate diets, supporting the use of histamine as a diagnostic marker.

Potassium and Acid-Base Balance
Acidosis causes potassium to shift out of cells in exchange for hydrogen ions. Initially, serum potassium may rise, but total body potassium remains unchanged. Without correction, prolonged acidosis leads to potassium loss via feces and urine, potentially resulting in severe hypokalemia—even when serum potassium appears normal or elevated. Hypokalemia impairs muscle function, exacerbates GI stasis, and hinders recovery.

Treatment includes potassium supplementation, either orally (e.g., Rabbit Oral Fluids or potassium chloride) or intravenously (used cautiously due to dosage sensitivity). Correcting acidosis restores normal potassium balance by promoting intracellular reuptake and reducing excretion.

Compensatory Mechanisms and Liver Function
The body attempts to compensate for bicarbonate loss. Absorbed SCFAs are metabolized in the liver into "potential bicarbonate," contributing to systemic buffering. This process is particularly important in herbivores like rabbits. However, in early or persistent acidosis from improper diet, this compensatory mechanism may be insufficient.

Veterinarians must intervene by administering bicarbonate and managing bacterial overgrowth, particularly lactic acid-producing bacteria. Products like Rabbit Enzyme (Randolph), containing Saccharomyces cerevisiae, help reduce lactic acid accumulation and SCFA overproduction, which may otherwise increase the anion gap and worsen dysbiosis and intestinal inflammation.

Treatment Strategy
The preferred method for treating systemic acidosis is intravenous bicarbonate, especially within the first 1–2 days. Improvement is monitored via the anion gap and GI symptoms. If these improve—even if bicarbonate remains low—further supplementation may be unnecessary, as the liver begins producing potential bicarbonate from absorbed SCFAs.

By days 3–5, acidosis and GI symptoms typically normalize. Oral bicarbonate remains controversial; while well-absorbed, it may alter gastric pH and disrupt fermentation in the cecum, risking alkalosis and microbial imbalance. Thus, its use should be carefully considered, especially in mild cases where correcting GI stasis alone may suffice.

In severe cases with low bicarbonate and signs of weakness or electrolyte imbalance, IV bicarbonate and potassium chloride may be essential.


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