HIPPOCRATES once stated that “Healing is a matter of time.” Generally, wounds will heal given time and as veterinarians we hope that our intervention aids wound healing.
Wounds over tendons
Firstly, wounds to tendons, although very serious, can be managed and the prognosis may be better than traditionally believed. In a study by Jordana (2010) in Veterinary Surgery, 82% of horses with surgically treated flexor tendon and ligament lacerations survived more than one year after initial injury, with 55% returning to an equal level of performance and 27% to a lower level of performance.
It is well established that extensor tendon injuries largely heal successfully once afforded appropriate time and treatment. A septic focus or foreign body movement and a fistula secondary to a septic synovial infection are the common reasons why wounds associated with tendons don’t heal.
It is imperative to establish why wound healing has not occurred. It is prudent to ultrasonographically assess the tendon for an area that would benefit from debridement or identify a foreign body that was not evident previously.
Generally I do not suture tendons, as it is common for equine wounds to be grossly contaminated.
On occasion, a septic focus can be associated with a tendon suture and this should be remembered during your investigations.
Distension of the synovial structure should be carried out if a fistula is suspected. The prognosis is generally believed to be poor with such injuries; however, there was a study by Turlough McNally (2012) that used tenosynoviotomy as a treatment for infection of the digital flexor tendon sheath and this resulted in five of seven returning to intended use with two horses requiring euthanasia.
Interestingly, three of the horses that survived had a time from injury to treatment of three weeks to nearly two months.
Is this technique a suitable salvage procedure for horses with synovial fistula and long-standing digital flexor tendon sheath infection?
A thorough investigation is required when presented with a synovial fistula associated with a tendon sheath. Usually the fistula is within an area of proud flesh. Is there a foreign body or septic focus/necrotic tendon and has a bacterial culture been obtained?
Often an affected horse is nonpainful or at least less painful when the synovial structure is discharging via the fistula and becomes painful when distension of the tendon sheath occurs as the wound closes.
Debridement of proud flesh followed by closure of the wound and immobilisation (usually with a bandage cast) is my treatment of choice coupled with appropriate antimicrobial treatment both locally (e.g. intravenous regional perfusion and by intrathecal injection on alternate days) and systemically.
Similar treatment is required for those wounds that don’t involve a tendon sheath but are associated with a tendon such as mid-cannon injuries of the flexor tendons. Immobilisation with a bandage cast is my favoured option. In time the cast can be split length-ways to form a distal limb splint; however, it is not uncommon for further bandage rubs to occur and for the splint bandage to be only partially effective.
A good team of people and organisation is required to ensure that a bandage cast can be placed properly. Casts are notorious for cast rubs. This new injury may well be associated with the flexor tendons and can be worse than the original wound and so there is understandable consternation from a horse’s owner when it is suggested that further immobilisation using another cast is required! Close monitoring is required and removal at the first sign of discomfort is advisable.
It is surprising how well midcannon flexor tendon lacerations heal; however, patience is required as two years from injury is often the required convalescence time. Beware of communication via the wound in the tendon to the digital flexor tendon sheath by propagation of infection through torn tendon fibres.
Furthermore, when the cast is removed there will be purulent material present and there will be proud flesh. I foolishly (through lack of experience) attempted debridement of these wounds.
It must be remembered that the proud flesh has been laid down in an attempt to cover the tendon and its removal will often result in the tendon being exposed or the granulation tissue weakened so that it will subsequently break down.
I favour medical treatment of these proud flesh wounds after immobilisation has established a covering layer of proud flesh. It is difficult to recommend chemical debridement (such as copper sulfate) as it results in indiscriminate cell damage of the epithelial cells. I have found Vulketan gel (Elanco) to be a very useful treatment in these cases following cast removal, although the manufacturer does not have evidence on use in this way.
Wounds in high motion areas
Heel bulb lacerations are the classic “movement” proud flesh wound. Similarly, the dorsal aspect of the fetlock, the calcaneal bursa/point of hock wound and extensor tendon carpal wounds often have prolonged healing and proud flesh formation due to movement of the associated joint.
My advice is to keep an open mind as there may be another reason why the wound is not healing such as bone involvement, a septic focus within a tendon or foreign body or wound infection.
Ideally, always culture and perform a radiographic examination and ultrasonographic examination before the presumption that it is movement alone that is preventing healing. A bandage cast is generally the treatment of choice for movement. Box rest and a Robert Jones bandage are alternatives but are sometimes not sufficient.
Wounds over bone
Sequestrum formation associated with the cannon (e.g. secondary to wire wounds) is common. My general rule when dealing with sequestrum formation is: if it is not discharging (i.e. a fistula is not present) then it is likely the wound will resolve without surgical treatment.
On occasion the sequestra that do not discharge have recurrent localised swelling and it can be difficult to tell if this is just inflammation or infection/ cellulitis.
Often there is a visible fistula surrounded by proud flesh and this tract allows for the sequestrum to be identified and removed more easily.
An ultrasonographic examination of the affected bone edges is useful as it allows for the sequestered bone edges to be defined as they may well extend beyond the area of proud flesh. Splint bone fractures can result in sequestrum formation.
Many splint bones don’t require removal to allow the wound to heal but, on the other hand, case management can be frustrating with displaced bone fragments.
Generally their removal can be achieved as a standing procedure under sedation and local anaesthesia in a placid and amenable animal.
The risk of splint bone luxation/ destabilisation or catastrophic fracture is not insignificant with splint bone fracture injuries and this should be contemplated when making decisions as regards a treatment plan and the need for general anaesthesia. Remember that ideally the proximal portion of a splint bone should not be removed and the integrity of the inside splint bone should be respected, most especially but not exclusively with regards to the medial splint bone of the forelimb because of its joint supporting function.
Furthermore, always check for suspensory ligament involvement as it may be a traumatic injury to this structure that is causing the horse’s lameness and not the more obvious sequestrum and associated proud flesh.
Similarly, a splint bone fracture as far distal as the mid cannon can communicate with the lower/middle carpal joint, so keep this in mind during your investigations.
Once the sequestrum is removed, the wound and proud flesh will dramatically improve within a few weeks. I am generally aggressive with surgical debridement of the proud flesh present, and leave the wound to develop a confluent granulation tissue bed before removing bandaging. I then start twice-daily treatment with Vulketan gel to assist the healing process.
Proud flesh associated with “infected” wounds
There are occasions where despite antimicrobial treatment and acceptable wound management, chronic infection occurs resulting in proud flesh.
Stashak and Theoret’s book entitled Equine Wound Management outlines the reasons why wound infection prevents healing. These include separation of wound edges, accumulation of exudate, a reduction in vascular supply by microthrombus formation, prolongation of the inflammatory phase, digestion of collagen by proteolytic enzymes, the binding of bacteria to matrix proteins preventing mesenchymal cells from binding and the release of endotoxins inhibiting growth factor and collagen production.
I tend to keep an open mind with these cases. Firstly (as previously outlined), rule out bone, tendon involvement or the presence of a foreign body. Identifying the causative organism and the correct antimicrobial treatment is generally the key to successful treatment.
A histopathological sample can also be useful to identify more rare causes of non-healing wounds such as a fungal or parasitic infection or the presence of a tumour (most commonly sarcoid).
Pythiosis, an oomycete parasite is a pyogranulomatous infectious disease that grossly causes striking plaques of granulation tissue; thankfully not present in the UK but beware of horses that have travelled from South America among other warm and humid foreign climes.
Achieving an effective concentration of appropriate antimicrobial is important – check dosage regimes and compliance and instigate an intensive course of intravenous regional perfusions until infection is controlled.
Debridement is useful as is topical antibiotic therapy. Manuka honey has positive effects as regards the treatment of infection and debridement. Vulketan gel was reported by Engelen et al (2004) to reduce development of infection associated with hypergranulation tissue in an article in the Canadian Veterinary Journal (45: 144-149).
A new licensed treatment
Vulketan gel (ketanserin) is a potent serotonin-S2-receptor antagonist and has a stimulating effect on fibroblast proliferation and collagen synthesis. It also results in improvement of the microcirculation by local effects on vasculature.
Improved blood supply and subsequent oxygen and nutrients to the wound could play a part in reducing formation of exuberant granulation tissue.
Ketanserin has no antibacterial activity in vitro but indirectly contributes to controlling infection by antagonising the serotonin-induced suppression of macrophages (further details on request from Elanco).
In summary, Vulketan gel is an adjunctive treatment for prevention of exuberant granulation tissue and to encourage wound healing in the horse. It is not a panacea and it will not heal sequestra or wounds where there is movement of a tendon beneath a wound, thus underlying issues need to be diagnosed and appropriately managed.
In my experience it has produced positive results, helping to reduce infection and proud flesh formation and encouraging wound healing.
- The information in this article reflects the opinion of the author and has been independently written; supported by Elanco animal Health, manufacturer of Vulketan.
Engelen, M., Besche, B., Lefay, M.-P., Hare, J. and Vlaminck, K. (2004) Effects of ketanserin on hypergranulation tissue formation, infection, and healing of equine lower limb wounds. The Canadian Veterinary Journal (La Revue Vétérinaire Canadienne) 45 (2): 144-149.
Jordana, M., Wilderjans, H., Boswell, J., Dewulf, J., Smith, R. K. W. and Martens, A. (2011) Outcome after Lacerations of the Superficial and Deep Digital Flexor Tendons, Suspensory Ligament and/ or Distal Sesamoidean Ligaments in 106 Horses. Veterinary Surgery 40 (3): 277-283.
McNally, T. P., Slone, D. E., Hughes, F. E. and Lynch, T. M. (2012) Tenosynoviotomy for Sepsis of the Digital Flexor Tendon Sheath in Nine Horses. Veterinary Surgery 42 (1): 114-118.
Stashak, T. S. and Theoret, C. L. (2011) Equine Wound Management. John Wiley & Sons.