Abomasal Displacement and CO₂ Holdup
Abomasal displacement is one of the clearest examples of ruminal buffer system disruption, or CO₂ holdup. I previously reviewed the pathogenesis of this disease (Laporte-Uribe, 2016), but recent experimental data allow an important update (Laporte-Uribe, 2023).
It remains uncertain whether CO₂ holdup originates primarily from:
Dietary effects, where rich carbohydrate diets directly disrupt the ruminal buffering system (Fay et al., 1980), or
Microbial responses, where bacteria exposed to high-carbohydrate diets generate a dCO₂-rich environment.
For instance, high dCO₂ levels stimulate lipopolysaccharide (LPS) production, and LPS is known to increase rumen fluid viscosity (Cheng et al., 1976; Cheng et al., 1979). Likely, both mechanisms interact. Importantly, during SARA, CO₂ holdup was observed to be independent of feed intake (Laporte-Uribe, 2023). Even when cattle had depressed intake, spikes in dCO₂ concentrations persisted for extended postprandial periods under rapidly digestible starch (RDS) diets.
Once CO₂ holdup is established, both dCO₂ and HCO₃⁻ accumulate, making the ruminal fluid a non-ideal solution where CO₂ gas cannot effervesce freely (Laporte-Uribe, 2024). As this dCO₂-enriched liquor passes into the abomasum, enzymatic digestion disrupts the matrix retaining liquid CO₂, causing a sudden release of CO₂ gas. This rapid degassing generates stable foam, leading to displacement — a hallmark of this disease.
Thus, CO₂ holdup and stable foam are two phases of the same phenomenon: CO₂ holdup occurs within the liquid, while stable foam forms at the fluid surface.
Preventive Insight
By continuously monitoring ruminal dCO₂ concentrations, it is possible to detect the onset of CO₂ holdup in real time. This enables proactive adjustments in feeding management to prevent clinical cases of abomasal displacement — as well as many other nutritional disorders linked to CO₂ holdup.
