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478


EQUINE VETERINARY EDUCATION / AE / SEPTEMBER 2017


Clinical Commentary


Loss of the hoof capsule in horses as a consequence of limb ischaemia


B. J. Ahern and A. W. van Eps* School of Veterinary Science, The University of Queensland, Gatton, Queensland, Australia. *Corresponding author email: a.vaneps@uq.edu.au


This edition of EVE contains a case series of three horses with spontaneous hoof capsule loss (Ruzickova et al. 2017). These horses had a history of traumatic injury to the distal aspect of a hindlimb with subsequent hoof capsule loss occurring 10 days after the initial injury. As the authors of this case series state, this condition is poorly described and not well understood in horses; however, there are many similarities in these three cases to acute limb ischaemia (ALI), which is well reported in man (Braun and Lin 2015; Lurie et al. 2015; Wang et al. 2016). In man, ALI is most commonly caused by primary thrombosis (often iatrogenic) or trauma (mostly fractures, dislocations or blunt injuries due to road traffic accidents). Fractures or dislocations can cause secondary arterial thrombosis: stretch of the artery can cause an intimal tear while the tunica media and tunica adventitia layers remain intact because they contain elastin and can stretch. As a result, the underlying thrombogenic collagen is exposed and a thrombus forms at the site. When this affects both the medial and lateral vascular supply to the distal limb of a horse, such as can occur during traumatic disruption of the suspensory apparatus (TDSA) or severe laceration with or without infection (as reported in this case series), then a situation of ALI can occur. In man, the most sensitive tissues to ischaemia (in descending order) are nerves, muscle, skin and bone, hence the early clinical signs in human patients are pain and/or numbness of the affected extremity. Besides pain, which is often already present, the first clinical manifestation of distal limb ischaemia in the horse may be lamellar separation and sloughing of the hoof (as seen in the case series), with the clinical effects of nerve, skin and bone ischaemia likely to appear more slowly and be initially less apparent. Ischaemia is recognised as a cause of sloughing of the nails of the fingers or toes in man (onycholysis) (Cabanillas et al. 2011); however, the phenomenon receives little attention in the literature, probably due to its relative lack of clinical importance. In the horse digit, the distal phalanx is suspended within


the hoof capsule by the lamellae: it is this specialised epidermal tissue that must be damaged both globally and severely enough in order for the hoof to detach circumferentially and slough. The epidermal and dermal lamellae fold and interdigitate to form a large surface area of attachment in each foot that results in a normally very strong bond between hoof and bone, able to withstand the incredible forces associated with locomotion at the gallop. Aside from hoof growth, which occurs almost exclusively at the coronary band and sole dermis, the function of the extensive digital blood supply is to provide nutrients for the cells of the lamellar epidermis whose primary responsibility is to maintain this attachment. The epidermal basal cells (EBCs), located at the junction between lamellar epidermis and dermis, are at the coal face of the attachment and are


© 2016 EVJ Ltd


highly metabolically active. These EBCs, however, do not have a direct blood supply and rely on diffusion of nutrients and oxygen from the lamellar dermis and because there is no means for storage of glycogen locally the EBCs rely on a constant glucose supply via incoming blood: in fact the relative extraction of glucose from the arterial blood of the digit exceeds that of the head in the horse (Pollitt 2016). In order to maintain constant nutrient supply to the lamellar epidermis, components of the vasculature must also overcome potential mechanical compression associated with their course between rigid hoof wall and bone, and between lamellar and sublamellar structures that come under tension during load. Despite this, the very fact that ischaemic sloughing of the hoof is an uncommon occurrence highlights that the lamellar vascular supply is protected and well regulated. The terminal arch of the medial and lateral digital arteries is housed within the bone of the distal phalanx and, like the circle of Willis at the base of the brain, it ensures redundancy in arterial supply to the lamellae if either the lateral or medial digital arterial supply to the foot is lost. This redundancy is supported by other anastomoses including the circumflex arteries proximal to and within the hoof capsule. Therefore, disruption proximal to or affecting both medial and lateral digital arteries is required to cause arterial ischaemia of the foot. The rich lamellar capillary network is drained via lamellar veins into an extensive sublamellar venous plexus, but with the distal limb devoid of muscle, the mechanical effect of cyclic loading of the foot is the only aid to venous return. It follows that venous return could become compromised in cases with severe distal limb swelling and also further compromised if there is limb pain sufficient to cause reduced cyclic loading of the limb: both features are reported in the case series in this issue. Similarly, there is evidence suggesting that reduced cyclic limb loading may lead to supporting limb laminitis by compromising lamellar perfusion (Medina-Torres et al. 2014). As the authors of this case series point out (Ruzickova et al. 2017), the severity of the swelling and inflammation, if extended distally into the hoof capsule, may have been sufficient to impair lamellar capillary perfusion (compartment syndrome), or other factors such as septic arterial thromboembolism could also have contributed to ischaemia in the reported cases, besides purely traumatic vascular damage. In horses with circumferential distal limb wounds, vascular


stretching (e.g. TDSA cases) or severe limb cellulitis (where there is a risk of compartment syndrome), consideration of vascular perfusion should be included early in clinical decision making. Because the early clinical signs of poor vascular perfusion evident in man (pain and numbness) are extremely difficult to assess in horses, contrast arteriography using either radiography or computed tomography should be considered initially, although these procedures will often


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