Lameness is regarded as the second most common condition by horse owners, with nearly one-fifth of clinical cases of lameness attributed to laminitis. Laminitis is generally seen as a result of endocrinopathic disease (approximately 90 percent of cases) and is linked to insulin dysregulation. Laminitis is most commonly found bilaterally in the forelimbs and is often signified by weight shifting and a reluctance to walk. It is characterised by a number of stages, with the initial prodromal stage occurring up to 72 hours prior to the onset of clinical lameness, which marks the start of the acute phase.
The best medical care for laminitis is widely regarded to be prevention and early recognition. Hoof wall temperature and palmar digital artery pulse pressure have been identified as potential indicators of the stages of laminitis onset. In a normal horse, the digital arterial pulse is faint or absent. In acute laminitis, it often presents as a “bounding” pulse, making it a universally recognised diagnostic criterion.
Whilst radiography and venogram methods are current diagnostic possibilities for laminitis, both veterinarians and horse owners would benefit from the identification of reliable, non-invasive methods of laminitis recognition. What evidence is there to suggest that hoof wall temperature and digital pulse pressure could be utilised for detecting laminitis in the early prodromal stage?
Five papers were identified; four were experimental case studies documenting changes in hoof wall temperature and/or digital pulse pressure throughout induced pathological onset. The fifth paper, an epidemiological study, was considered as it investigated the current use of diagnostic indicators of acute laminitis episodes in the UK.
Two of the studies (where laminitis was induced through carbohydrate overload or hyperinsulinaemia) reported an increase in hoof wall temperature. In these studies, a significant increase in hoof wall temperature occurred approximately six to 24 hours prior to laminitis onset. The hyperinsulinaemia-induced study also described a significant increase in palpated digital pulse pressure, estimated to occur up to nine hours before the clinical appearance of laminitis. In the carbohydrate overload study, this increase occurred approximately eight hours before laminitis onset.
In another carbohydrate overload study, a decrease in hoof temperature was observed eight to 12 hours prior to the onset of lameness. However, this was only significant when normalised to the onset of lameness, and the scale of change was unlikely to be palpably detected by an owner or veterinarian.
A further study mimicked endotoxaemia-induced laminitis. An initial hoof cooling occurred, before an increase in hoof wall temperature between six and 12 hours post-induction. A palpable increase in digital pulse pressure occurred at seven to 12 hours post-administration and decreased 13 to 23 hours post-administration. However, given the short laminitis onset time (10.22 hours versus an average of 36.5 hours in the other studies) and likeness to sepsis-associated laminitis, it is uncertain whether the results relate to the typical endocrinopathic case.
The epidemiological study showed that whilst 99.1 percent of horse owners used raised hoof wall temperature in their assessment of laminitis, only 58.3 percent reported it as a diagnostic sign. Given that the experimental data considered indicates that a rise in temperature is consistently associated with the onset of lameness, this discrepancy may be due to hoof temperature being recorded at inappropriate times by horse owners.
These observations should only form a crude diagnostic indicator
Considering the time-points associated with changes in hoof wall temperature and digital pulse pressure across these studies, a maintained bilateral increase in forelimb hoof temperature may indicate that the horse is approximately one day from acute laminitis onset. A period of increased digital pulse pressure occurring approximately half a day prior to the onset would be expected, potentially disappearing at the onset of clinically apparent laminitis. Whilst these observations should only form a crude diagnostic indicator, in at-risk animals these changes may be sufficient to warrant removal of the inciting factor, ie high carbohydrate intake, encouraging a more favourable clinical outcome.
The method of laminitis induction differed between the studies, depending on the agent used and the time course of induction. The clinical patient is unlikely to be the subject of induced laminitis, and the horses used in the experimental studies were not typically representative of the classic endocrinopathic case. Further studies are therefore needed to investigate changes in the true-risk population for endocrinopathic laminitis.