Cardiovascular, acid-base, electrolyte, and plasma volume changes in ponies developing alimentary laminitis.
Authors: Harkema, Robinson, Scott
Journal: American journal of veterinary research
Summary
# Editorial Summary This 1979 study tracked cardiovascular, metabolic and electrolyte changes in 12 Shetland ponies fed a high-starch ration to understand the pathophysiology of alimentary laminitis, with seven animals developing clinical disease approximately 56 hours after overfeeding. The researchers measured heart rate, blood pressure, cardiac output, acid-base status, electrolytes, and plasma volume at regular intervals, identifying measurable changes preceding lameness onset by 24 hours, notably hypokalaemia, increased core temperature and tachycardia, despite stable sodium, chloride and plasma volumes. Interestingly, the blood pressure elevation and increased cardiac output observed at the point of clinical lameness appeared to be a secondary response rather than a causative mechanism, as these values were not predictive of disease development. Of critical concern, three ponies developed fatal shock characterised by severe metabolic acidosis coupled with decreased cardiac output and blood pressure—a distinctly different picture from the surviving laminitic animals. For practitioners, these findings suggest that laminitis development involves complex metabolic derangements beyond simple circulatory changes, and that the presence of metabolic acidosis warrants serious monitoring, as it may indicate either imminent laminitis or progression toward fatal shock rather than serving as a single reliable predictive marker.
Read the full abstract on PubMed
Practical Takeaways
- •High-starch overfeeding in ponies triggers a metabolic cascade including acidosis and electrolyte disturbances; monitor for hypokalemia, fever, and tachycardia 24 hours after suspected overfeeding as early warning signs of impending laminitis
- •Laminitis-associated hypertension in the early clinical phase is a secondary response to lameness, not a causative factor, suggesting vascular changes are consequences rather than primary drivers of disease
- •Some horses progress to shock with cardiovascular collapse rather than laminitis; severe acidosis with hemodynamic compromise (decreased output, increased resistance) indicates life-threatening disease requiring emergency intervention
Key Findings
- •Seven ponies developed laminitis 56 hours (±3.5 SEM) after high-starch overfeeding, preceded by transitory metabolic acidosis, persistent hypokalemia, hyperthermia, and increased heart rate 24 hours before lameness onset
- •At clinical onset of laminitis, cardiac output and blood pressure increased while total peripheral resistance remained unchanged, with hypertension appearing to be a response to rather than cause of lameness
- •Three ponies died of shock 29.3 (±2.7) hours post-overfeeding with severe metabolic acidosis, decreased cardiac output and blood pressure, increased hematocrit and peripheral vascular resistance
- •None of the measured cardiovascular, acid-base, or electrolyte parameters predicted the onset of laminitis in affected ponies