EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014


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ligaments, although the accessory ligament of the suspensory ligament was smaller and had better alignment of linear echoes. Despite a slowly progressive rehabilitation programme over the next 6 months, hindlimb lameness recurred.


Discussion


Fig 3: Longitudinal ultrasonographic image of the distal aspect of the hock and proximal metatarsal region of the left hindlimb of Case 3. Dorsal is to the left and proximal to the top. The accessory ligament of the suspensory ligament is diffusely hypoechoic (arrows), with loss of parallel alignment of the linear echoes, which are shorter than normal.


images. The suspensory ligament appeared normal in the nonlame hindlimbs. Injury of the accessory ligament of the suspensory ligament was characterised by marked decrease in echogenicity of the ligament and loss of parallel alignment of the linear echoes, which were shorter than normal in longitudinal images (Figs 3 and 4). Injuries of the accessory ligament of the suspensory ligament were identified in 6 of 8 lame hindlimbs, unilaterally in 4 horses (Cases 1, 2, 3 and 5) and bilaterally in one horse (Case 4). In one horse (Case 2), with dynamic extension of all 4 fetlocks, there was enlargement in a cross-sectional area of both suspensory branches of both hindlimbs, with low-grade generalised loss of echogenicity and severe injuries of the medial and lateral suspensory branches in one forelimb. The causes of concurrent forelimb lameness are summarised in Table 1. Four horses (Cases 1–4) had complex clinical presentations


and 3 were retired without treatment. One horse (Case 4) underwent neurectomy of the deep branch of the lateral plantar nerve and plantar fasciotomy and medication of the sacroiliac joint regions using methyl prednisolone acetate. When re-examined 2 months post operatively, the accessory ligaments of the suspensory ligament were much more uniform in echogenicity than previously. However persistent forelimb lameness subsequently prohibited this horse’s return to work. Case 5 also underwent similar surgery and injection of the accessory ligament with platelet-rich plasma (E-Pet)2. When re-examined 2 months post operatively there was little change in the ultrasonographic appearance of the suspensory


To the author’s knowledge, this is the first description of injuries of the accessory ligament of the suspensory ligament, which to date have only been seen in association with proximal suspensory desmopathy. The sequence of events is difficult to determine. Retrospectively, the riders of the 3 horses with saddle slip had recognised saddle slip before any other clinical signs. We have previously documented that saddle slip may be a manifestation of subclinical hindlimb lameness (Greve and Dyson 2013). Two of these 3 horses had palpable oedematous swelling in the region of the accessory ligament of the suspensory ligament suggesting that the injury of this structure may have been recent and thus secondary to pre-existing proximal suspensory desmopathy. Alternatively, it is conceivable that there was acute reinjury of the accessory ligament of the suspensory ligament which may have been the primary injury, with secondary proximal suspensory desmopathy. The coexistence of suspensory ligament injuries in the forelimbs of 3 of the 5 horses, 2 of which were only 5 years of age, suggests that there may be some common unidentified underlying cause of multilimb suspensory ligament injury. One horse, 12 years of age, had long-term dynamic hyperextension of all 4 fetlocks which could result in biomechanical overload of the suspensory apparatus. Alternatively, fetlock hyperextension may have been the result of suspensory ligament malfunction. None of the horses showed increased lameness after


proximal limb flexion. It has previously been suggested that the reason why some horses with proximal suspensory desmopathy have a positive flexion test is because of the anatomical relationship between the suspensory ligament and tarsus via the accessory ligament of the suspensory ligament (Schulze and Budras 2008). That hypothesis is not supported by the observations in this case series. The need to perform a tibial nerve block in 2 horses does


suggest that at least in these horses the injury of the accessory ligament of the suspensory ligament was contributing to pain and lameness. However, it must be recognised that abolition of lameness by perineural analgesia of the deep branch of the lateral plantar nerve is not specific for proximal suspensory desmopathy and more proximal sources of pain may be abolished, presumably because of proximal diffusion of the local anaesthetic solution (Labens et al. 2010; Dyson 2012, 2013; Claunch et al. 2013; Contino et al. 2013; Davis et al. 2014). In addition, entheseous pathology in the third metatarsal bone at the origin of the suspensory ligament may cause pain which is not abolished by perineural analgesia of the deep branch of the lateral plantar nerve, but which is resolved after a tibial nerve block. The complexity of the injury presentations in 4 of the 5


horses makes it impossible to comment about potential treatment and the influence on outcome for horses with injuries of the accessory ligament of the suspensory ligament in addition to proximal suspensory desmopathy. However, this case report serves to emphasise the need to perform a systematic ultrasonographic examination of all the soft tissue structures on the plantar aspect of the tarsus and metatarsal region in horses which show improvement in lameness after


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