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2011). In early laminitis ischaemia leads to swelling of the endothelial cells, haemoconcentration, capillary congestion and obstruction of small vessels with leucocytes. There is a build-up of extravascular pressure aggravating the compartment pressure (Adam and Southwood 2007). Widespread distal limb thrombosis and associated laminitis have been reported as a complication of lower limb cellulitis in a horse with photosensitivity and bacterial infection (Hanson 2008). However, lymphangitis/cellulitis also frequently occurs in equine lower limbs without hoof capsule loss (Fjordbakk et al. 2008), suggesting that other factors such as reactive vasoconstriction or hypercoaguability, in addition to inflammation and infection, may probably be required to induce spontaneous hoof capsule loss. Septicaemia and a hypercoagulable condition have already been reported to cause acute thrombosis of distal limb arteries and hoof slough in young foals (Brianceau and Divers 2001). One horse in the current series was evaluated for vascular


Fig 3: Lateromedial fistulograph with contrast medium which demonstrates complete detachment of the hoof capsule from the distal phalanx.


and a poor prognosis for a fully functional hoof. The hoof capsule sloughed spontaneously during euthanasia.


Discussion


Novel information is provided on equine hoof capsule loss following distal limb lacerations. This unusual but major complication resulted in hoof slough 10 days after the original trauma in all 3 cases. Lacerations of the distal limb are very common in horses


and are frequently accompanied by partial or total severance of arteries or veins. It is known that collateral vessels develop following injury in the majority of cases and is reported to occur at 2–4 weeks (Keen et al. 2008). In the 3 cases reported herein, there was no history of blood loss, which may indicate that it occurred prior to the horse being observed for the first time or that no vessel rupture occurred. Alternatively, it is possible that the traumatic event caused unidentified vascular injury and thrombosis, without vessel severance, leading to ischaemia in the distal limb. Other factors, in addition to a vascular ischaemia, may


have contributed to the hoof capsule loss. Two of the horses had a very substantial cellulitis on presentation and the third horse (Case 1) progressively developed cellulitis, despite administration of antibiotics. The associated inflammation and oedema in the distal limb could lead to a progressive hoof compartment syndrome and ischaemia of the dermal lamellae in already vascularly compromised tissue precipitating cell necrosis and hoof slough. The extensive cellulitis in the pastern region in the cases


herein precluded an accurate coronary band assessment i.e. concavity that occurs at this site when the third phalanx ‘sinks’ (Cripps and Eustace 1999). We speculate that there could be similarities in the


pathophysiology of the hoof capsule slough and prodromal phase of laminitis (Baxter and Morrison 2008; Percival et al.


compromise by digital vein venography (Redden 2001a,b). Digital arteriography has also been described in horses but requires general anaesthesia (Rosenstein et al. 2000; Walker et al. 2017). In man, computed tomographic angiography (CTA) is the diagnostic entity of choice for identification of a reduction of blood flow to the distal limb after a traumatic event, e.g. gun shot (Gakhal and Sartip 2009). Scintigraphy also allows quantification of vascular flow but does not permit visualisation of single vessels and would not be a practical clinical approach for assessment of limb lacerations (Bell et al. 1995). In human patients with diabetic foot ulcers, distal ankle and toe pressure as well as colour duplex ultrasonography are valuable tools to determine the degree of ischaemia (Falanga 2005). In horses, Doppler ultrasonography also permits the detection of altered digital blood flow (Aguirre et al. 2013). As acepromazine improves digital perfusion and lamellar


blood flow (Baxter and Morrison 2008), its administration early after equine limb trauma could be considered for this purpose. In cases of post-traumatic thrombosis in man, heparin or dalteparin in combination with aspirin is employed to minimise further thrombus propagation (Percival et al. 2011).


Horses were treated orally with enrofloxacin4 as oral


administration of a broad spectrum antimicrobial with activity against Gram-negative bacteria was desired. One 2-year-old horse had bilateral thrombophlebitis of the jugular veins precluding i.v. antimicrobial therapy and synovial culture revealed presence of E. coli sensitive to enrofloxacin4. Risk of cartilage toxicity has been previously reported for enrofloxacin4 (Bertone et al. 2000) but was judged to be minimal in a horse of 2 years old. Measurement of perilesional transcutaneous oxygen


tension has been reported to be important for prognosis in human patients with diabetic ulcers (Fife et al. 2002) and could be considered for evaluation of future cases of equine limb ischaemia. In patients where infection is accompanied by ischaemia and atherosclerosis, vessels may be treated by vascular bypass or angioplasty (Lipsky et al. 2012) but this has not been attempted in equine patients. Euthanasia was elected in all the cases herein. However,


it is possible to treat cases of hoof slough, but the final outcome, following prolonged costly treatment and time investment, is a deformed hoof (de Gresti et al. 2008). The horn of the wall grows from the stratum germinativum of the coronary corium at an average rate of 6–10 mm per month


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