Page 94 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Musculoskeletal system: 1.3 The foot 69

VetBooks.ir 1.112 1.113

Fig. 1.113 Cross-section of a foot post laminitis
rotation. Note the wedge of damaged tissue dorsally
underneath the hoof wall and the beginning of
Fig. 1.112 Cross-section of a foot with acute laminitis bending of the tubules at the coronary band.
before it has displaced. Note that the dorsal epidermal
lamellae have been damaged and started to pull away.

phases is somewhat arbitrary and is not associated that the PPID induces insulin resistance. Pasture-
with marked changes in approach, either diagnosti- associated laminitis is associated with grazing on
cally or therapeutically. grasses with high non-structural carbohydrates.
How this causes laminitis is unclear, but in some
Aetiology/pathophysiology cases it may lead to weight gain and insulin resis-
There are several known pathophysiological entry tance, while in others pasture-associated laminitis
pathways identified in the pathogenesis of lamini- without evidence of insulin resistance develops.
tis. Broadly speaking, these are sepsis-related lami- Laminitis may also follow prolonged weight bear-
nitis, endocrinopathic laminitis, supporting limb ing on one limb or occur as a spontaneous event
laminitis, corticosteroid-associated laminitis and with no known cause. Anecdotal evidence impli-
traumatic laminitis. Of these, sepsis-related lami- cates systemic or intra-articular steroid administra-
nitis is associated with diseases such as grain over- tion, particularly administration of triamcinolone,
load, colic, colitis, pleuropneumonia and metritis, as a cause of laminitis, but this is not supported by
which are frequently accompanied by clinical signs controlled data in the literature.
of endotoxaemia. However, in the experimental The pathophysiology of chronic laminitis is less
models of sepsis-related laminitis, detection of well documented. Depending on the severity of
circulating endotoxin is not a feature. That said, the tissue necrosis within the lamellae, the stresses
experimentally induced laminitis is associated of weight bearing and movement cause displace-
with the expression of inflammatory mediators in ment of the distal phalanx in relation to the hoof
the lamellae during the prodromal stages of the capsule. The necrotic tissue can subsequently be
disease, consistent with a systemic inflammatory repaired and in severe cases this forms a wedge of
response caused by one of the aforementioned dis- hyperplastic epidermal tissue between the parietal
eases. Endocrinopathic laminitis is typically asso- dermis and the hoof capsule (Fig. 1.113). In chronic
ciated with pars pituitary intermedia dysfunction laminitis the hoof wall grows faster at the heels than
(PPID) and insulin resistance. Recent evidence at the toe. The presence of the lamellar wedge and
suggests that PPID alone may not be an inciting the abnormal growth give rise to the characteristi-
cause and that most horses with PPID that develop cally deformed hoof, with a concave dorsal wall, high
laminitis have concurrent insulin resistance or heels and flattened sole.