Supporting Limb Laminitis

Most horses will suffer with a severe unilateral lameness at one time in their life, when this is for prolonged periods of time, such as in fractures, synovial infections and tendon injuries (Baxter 2016) the supporting limb becomes more and more predisposed to supporting limb laminitis (SLL) as the time goes on (Peloso et al 1996). Often SLL will be unrecognised until the resolution of the unilateral lameness of the primary injury, however the prevalence of SLL has been stated as ~10% with the severity and duration of primary lameness being large factors in predisposition (Eps et al 2010). Baxter (2016) discussed the contributary factors of the horses’ body weight and length of time in casts, suggesting that increases in both created more likelihood of developing the complication. It also highlighted the importance in monitoring the supporting limb for signs of SLL development, these signs could be similar to the bilateral presentation of laminitis: rocking back on heels; increased digital pulse; wanting the lie down more frequently and a palpable depression in the coronary band. SLL has a high mortality rate of around 50% because of its link to catastrophic break down of the suspensory apparatus of the distal phalanx (SADP) and subsequent sinking of the distal phalanx (DP) within the hoof capsule (Eps et al 2010).

Fig.1 Authors schematic illustration of the SADP. SLL has been attributed to the breakdown of this connection, due to the decreased blood flow of the loaded limb.

Redden (2004) preceeded Baxter (2016) with the same theory of blood occlusion to the SADP being responsible for the onset of SLL. Using venography this study expressed the occlusion of blood to the dorsal laminar vessels with a fully loaded limb.

Fig.2 Redden (2004) used venography to show the reduced vascular filling of the dorsal laminae with a loaded limb.

With this reduction of blood supply to the basement membrane zone and the interdigitation of the horny and sensitive laminae this attachment is at risk of compromise. Orsini (2012) further described the mechanisms mentioned by Redden (2004) of blood occlusion and both studies highlighted the role of the Deep digital flexor tendon (DDFT).

Fig.3 Redden (2004) and Orsini (2012) described how the DDFT caused compression of the vascular structures of the digit creating blood occlusion to the laminal plexus.

The studies on SLL express the importance of restoring blood flow, even in small amounts this can greatly reduce the risk of pathology (Redden 2004, Orsini 2012, Belknap and Durham 2016). The main mechanisms for restoring this blood flow is movement, if movement can be maintained, even in small amounts, the risk factor is reduced. Orsini (2012) expressed that the horse didn’t need to completely unload the hoof, but just small changes in joint angle would allow some returned blood flow. Understanding the mechanisms in this pathology highlight the importance of preventative measures, Baxter (2016) stated that when signs are obvious the process is already well advanced. Redden (2004) outlined two important factors in shoeing intervention, reducing load on the DDFT and providing support. Thompson et al (1993) showed the load on the DDFT reduced by 60% by wedging the heels by 23 degrees, this is the basis for Redden (2004)’s intervention which raised the heels by 10 degrees and set the breakover back enough that the horse transferred its weight onto the toe creating an additional 10 degree elevation of the heels.

Fig.4 Redden (2004) maintained dorsal laminae perfusion by decreasing load on the supporting limb DDFT with a 20 degree elevation.

Redden (2004) emphasised that this shoeing protocol was suitable up until the point at which full weight bearing returned to the primary limb and found a reduction in prevalence from ~10% to ~2%, however considering the load transference onto the suspensory ligament this could cause secondary injury, Redden made no comment on this risk, further research may be appropriate to assess this risk but with the high mortality rate of SLL this intervention could prove to save lives.

A limiting factor in this application and relevant to general risk factor of developing SLL is the individual horses micro conformation, structural elastic modulus and haemodynamic system. Redden (2004) and Orsini (2012) both acknowledge the increased risk in horses with already compromised hoof structure, such as long toe low heel conformations. Considering these feet already have a smaller elastic modulus and are now bearing load for significantly extended periods, their predisposition to increased effects of elastic creep mean they will inherently suffer from collapse and their potentially weaker laminal bond may fail sooner.

This is where solar arch support becomes important, as well as the vascular system coming under pressure, the hoof itself is suffering constant compressive forces.

Fig.5A+B This supporting hoof had suffered considerable collapse, it was provided with frog support padding in an effort to support the failing structures when the primary lame limb was shod with a caudal extension to reduce fetlock drop after an operation on a shattered pastern. This was the first farriery intervention, following the findings of Redden (2004), theoretically it should have had a graduated shoe at the first instance. This horse is now weight bearing on the other limb although not fully.

As you can see from fig.5A+B the supporting foot is significantly flatter then the injured one, although perhaps a secondary consideration, intervention to try and keep the feet as paired as possible for return to work should be considered as high low hoof conformation can play a role in the genesis of later pathologies due to the effects on biomechanics.

Commonly SLL does not manifest till weeks or months after injury, as discussed above this is often because the lameness on the primary limb far outweighs the pain in the supporting foot. Other theories are also suggested, in the presence of constant blood occlusion SLL can be expected imminently, however if the occlusion is partial or intermittent, then a build up of micro damage can accumulate to a point of no return where the SADP fails, this can take longer (Orsini 2012). When the damage is regional this can be the difference between full sinking and phalangeal rotation.

Fig.6 SLL can lead to either sinking or rotation depending on the extent and region of damage to the SADP.

In conclusion, SLL is caused by blood occlusion to the laminae due to increased load. The DDFT plays a significant role in the creation of this occlusion and relieving load of this structure could prove to be a saving grace in mitigating the risks of prolonged unilateral limb loading, however the risks to the suspensory and superficial flexor, as well as the possibility of overloading the heels may still need to be considered. Encouragement of even minimal movement could also play a role increased blood perfusion, Orsini (2012) suggests encouraging transferring load onto the uninjured pair of limbs. Regardless of methods used, farriers should understand the dangers of unilateral loading and can play and encourage an active role in protecting the supporting limb.

References

J.G. Peloso, N.D. Cohen, M.A. Walker, et al.Case-control study of risk factors for the development of laminitis in the contralateral limb in Equidae with unilateral lameness

J Am Vet Med Assoc, 290 (1996), pp. 1746-1749

Supporting Limb Laminitis

van Eps, Andrew et al.

Veterinary Clinics: Equine Practice, Volume 26, Issue 2, 287 - 302

Redden, 2004, Preventing laminitis in the contralateral limb of horses with nonweight-bearing lameness, Clinical Techniques in Equine Practice, Vol 3, issue 1, 57-63

Orsini, 2012, Supporting limb laminitis: The four important ‘whys, Equine Veterinary Journal, Vol 44, issue 6, 741-745

Belknap and Durham, 2016, Overview of laminitis prevention, Equine laminitis, chap 47

Thompson, Cheung, Silverman, 1993, The effect of toe angle on tendon, ligament and hoof wall strains in vitro, Journal of Equine Veterinary Science, vol 13, issue 11, 651-654