Plasma volume, electrolyte, and endocrine changes during onset of laminitis hypertension in horses.
Authors: Clarke, Garner, Hatfield
Journal: American journal of veterinary research
Summary
# Editorial Summary: Plasma Volume and Electrolyte Changes in Experimental Laminitis Clarke, Garner and Hatfield induced acute laminitis through controlled carbohydrate overloading in 12 horses, establishing a standardised model to investigate the physiological cascade underlying this devastating condition. Obel grade 3 lameness developed within approximately 40 hours, allowing researchers to map sequential changes in plasma volume, electrolytes, and endocrine markers before and after clinical onset. The most striking finding was a significant reduction in plasma volume by the time clinical lameness appeared (P<0.005), accompanied by hyponatraemia that developed early and persisted throughout the acute phase, followed by hypokalemia and elevated aldosterone concentrations once lameness was established. Transient spikes in cortisol and renin activity, alongside hypochloremia, further demonstrated a coordinated neuroendocrine and fluid-electrolyte response to the systemic insult. These results suggest that laminitis onset involves genuine hypovolaemia and compensatory activation of the renin-angiotensin-aldosterone system, which has implications for understanding why aggressive fluid therapy and electrolyte monitoring remain cornerstone interventions in acute cases, and why electrolyte disturbances themselves may perpetuate the pathophysiology if not corrected promptly.
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Practical Takeaways
- •Carbohydrate overloading triggers a predictable cascade of physiological changes leading to laminitis within ~40 hours; strict feed management is critical for prevention
- •Plasma volume depletion and electrolyte imbalances (particularly sodium and potassium) accompany acute laminitis development and may require fluid and electrolyte therapeutic support
- •Monitoring serum electrolytes and understanding the endocrine response (renin-aldosterone axis activation) can help guide clinical management during the acute phase
Key Findings
- •Obel grade 3 lameness developed 40 hours (±3.5 SEM) after carbohydrate overloading in all 12 horses
- •Plasma volume significantly decreased at onset of OG3 lameness (P<0.005) compared to baseline
- •Hypokalemia and increased plasma aldosterone concentration occurred persistently after OG3 lameness establishment
- •Transient increases in plasma cortisol and renin activity occurred during the syndromal phase, interpreted as homeostatic responses to fluid and electrolyte imbalances