16
46TH
ANNUAL
CONGRESS
OF
THE
SAEVA
SKUKUZA
16-‐20
FEBRUARY
2014
Unfortunately, there is still much debate regarding the significance of the poor blood
supply, with studies indicating that even with iatrogenic occlusion of the sesamoidean
arteries, causing disruption to a large part of the PSBs, that lameness was always mild
and resolved relatively rapidly. Histopathology and radiographs also demonstrated
little major change in these cases. These findings are in contradiction to the oftensevere chronic and insidious onset lameness seen in axial osteitis with marked
radiographic changes. The chronic nature of axial osteitis affords ample time for
collateral circulation to develop and thus appreciable bony pathology should not
occur (B. P. M. Cornelissen et al. 2002). This collateral circulation of the PSBs is in
part thought to be due to an “arterial shift”, where a usually insignificant basal
sesamoid blood supply takes over with damage to sesamoidean artery. This is usually
only seen in bones that have new bone development along their abaxial margins,
which is again is not a feature of axial osteitis (B. P. Cornelissen et al. 1996). It
remains that more research needs to be done into the importance of blood supply
with regards to ISL damage and axial osteitis.
Trauma, specifically hyperextension of the metacarpo/tarsophalangeal joints, with
excessive stresses on the PSB and tearing or avulsion of ISL, has also been implicated
in the pathogenesis of axial osteitis (Sherman et al. 2006; Dabareiner et al. 2001).
Barclay (1985), in his report on axial sesamoid injuries occurring concurrently with
lateral condylar fractures, described 2 horses with obvious axial sesamoid fractures
and 2 horses with more progressive axial demineralisation. These axially located PSB
injuries had a poor outcome for future performance, with persistent lameness.
Rotation of the palmar aspect of the metacarpal condyles against a stationary P1, first
from medial to lateral and then from lateral to medial during maximal
hyperextension, is suggested to put severe strain on the ISL and PSBs (Barclay et al.
1985).
Infectious causes of axial osteitis primarily consist of bacterial septic arthritis, which
is associated with more severe lameness and joint effusion. There may also be
extension of infection from a septic digital flexor sheath tenosynovitis, or extension
from the primary site of axial osteitis to the DFTS (Sherman et al. 2006). In the
majority of cases of septic axial osteitis, neither a traumatic wound nor other cause
of introduction for the infection is ever identified (Formston & Serth 1968; Wisner
et al. 1991).
In Wisner et al.’s (1991) study of seven horses with axial osteitis, three horses had
septic tenosynovitis of the DFTS, and two of those horses also had concurrent septic
arthritis. Unfortunately not all horses in his study had arthocentesis, synoviocentesis
of the DFTS or post-mortem studies performed. A study of eight horses by
Dabareiner et al. (2001), revealed that three out of eight horses had evidence of
sepsis of the fetlock joint and digital sheath.
A single case report describes the catheterisation of dorsal metatarsal artery, for
blood pressure monitoring during general anaesthesia, leading to axial osteitis in
three horses, with septic thrombosis of the microvasculature of the PSB thought to
play a role (E. D. Barr et al. 2005). This case differs from other described cases due
to the lack of involvement of t he ISL and the variation in location of the PSB lesions.
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