How do wounds in horses heal?

Stuart Davies BVSc MRCVS, looks how wounds in horses heal, and describes the process

Wounds are responsible for significant morbidity and mortality within the equine world¹. The physiology of wound healing in horses is unique and therefore, wounds pose a particular veterinary challenge. Much evidence, found by extensively studying wound care in human and other veterinary fields, is extrapolated to horses and as such, certain aspects of management develop from anecdotal experience of veterinary professionals.

In addition, new products are continually being created, expanding the market for topical preparations and dressings. Therefore, although wound management can be complicated, understanding normal equine wound physiology can assist in determining when intervention is required.

The efficiency and rate of wound healing differs between equid species. Initially related to body size, when ponies were shown to heal faster when compared to horses², this has later been disproved. It is a possibility that a greater period of domesticated horses has selected for a poorer activity of white blood cells and, the production of chemicals which are vital in driving healing.

The aim of wound management is to optimise healing and restore function to the tissue. While the physiology of wound healing occurs in all tissues, it does differ slightly between different organs and therefore accidental skin injuries are mainly considered. Veterinary advice should be received for all wounds to speed wound healing as much as possible. The appearance of some minor skin wounds can have much more serious consequences, and require a greater degree of veterinary treatment, when associated with damage to an underlying synovial or soft tissue structure.

The phases of healing

There are four horse wound healing stages. They are complex and interlinked phases of skin wound healing with the aim of restoring the tissue barrier with as close a replica of the original cell types as possible.

Haemostasis

Haemostasis – the prevention of blood loss, begins immediately and lasts up to a few hours. Damaged blood vessel linings release chemicals causing blood vessel constriction, termed vasoconstriction, and an increased vessel permeability³. An increase in permeability allows deposition of cells at the site of injury, particularly platelets which form a ‘clot’ stemming blood loss.

Once haemorrhage has been ceased, platelets degrade releasing chemicals, which then reverse the blood vessel changes and draw inflammatory cells to the wound. An increase in the vessel lumen, termed vasodilation, increases blood supply carrying new cells along with oxygen and nutrients to support them. This ‘clot’ will form the matrix for cells to migrate across the wound and overtime will become the scab, overlying the healing wound preventing infection⁴.

 

Inflammation

Inflammation rids the body of foreign or dead material and will prepare the wound environment. The inflam matory stage of healing is proportionate to the wound severity and, correlated to the degree of scar tissue formation. The classic signs of inflammation are redness, heat, swelling, pain, and loss of function.

In the early stages of inflammation neutrophils, a type of white blood cell, debrides the wound of debris and bacteria, peaking 24-48 hours after the original insult. Once the wound bed is clean, these neutrophils then become trapped within the clot and are eventually sloughed. Any remaining neutrophils will be removed by a large white blood cell called a macrophage⁴.

Persistent inflammation will result in dysregulation of wound healing and abnormal scar tissue formation⁴. Therefore, veterinary involvement during the inflammatory stage including, good surgical debridement, irrigation, and drainage, are crucial to achieve efficient wound healing.

The proliferative phase

This is responsible for protecting the underlying healing wound. A granulation tissue bed and surface epithelium forms supported by a vascular network. It is at this stage that the overlying scab is sloughed to reveal the richly vascular red healthy granulation bed. Granulation tissue is composed of macrophages, a white blood cell that debrides material and other cells, blood vessels and fibroblasts, a cell type that secretes collagen. The wound at this point is still weak, with collagen formation being most rapid 7-14 days after injury⁴. The filling in of the wound defect enables adjacent cells to migrate over the wound if conditions are correct. Once a healthy granulation bed is formed that can nourish migrating cells during maturation, blood vessels regress, and fibroblasts denature or change into a type of fibroblasts that have contractile properties⁵. If the signals for this step are delayed improper scar tissue forms rather than healed skin⁶.

Exuberant granulation tissue formation can be an issue in wound healing of equids whereby the skin surface is now below that of the healing wound. Cell migration is impeded and as healing slows the granulation bed becomes less healthy, eventually resulting in a complete cessation of healing and a remaining wound. Veterinary involvement at this stage to remove excessive granulation tissue would involve surgical debridement and possibly topical ointments such as corticosteroids.

Epithelial, skin, tissue moves across the granulation bed from the wound edges and this can occur as quickly as 0.55 millimetres a day², dependant on wound location. Excessive tension in surrounding skin, such as can occur during movement of a limb, will cease cell migration and reduce the ability of the underlying tissue to support new cells. This newly developing surface is still vulnerable to trauma so often requires protection such as dressing and reducing the movement of a limb, for example.

Maturation

Maturation of the wound is the final stage of healing. Up until this stage, at roughly three weeks, the wound has only reached 20% of its optimal strength⁴. The tissue is remodelled by a combination of enzymatic reactions and degradation resulting in improvements of strength, integrity and functionality of the replacement tissue.

When a skin incision is closed surgically with staples or sutures the rate of healing is greater. Therefore, when practically and economically possible, every effort should be made to appose the skin edges. By doing so haemostasis is achieved and if irrigated and debrided adequately the duration of neutrophil debridement is reduced. Unfortunately, surgical repair can fail leaving the wound to heal by secondary intention, following all the processes above.

These include:

• Infection
• Tension on the sutures/ staples due to excessive tensions of wound edges
• Movement of the tissue
• Sequestrum (damaged underlying bone)
• Injury to an underlying structure such as tendon, ligament, joint or other synovial structure

Infection is the most common cause of delayed healing⁷ so therefore topical and systemic antimicrobials may be necessary. However, this should not be as a replacement for correct wound management, and ideally the choice of antimicrobial should be based on culture and sensitivity results. With many topical products available it can be difficult for owners to know whether what they have in their first aid cabinet can be detrimental or beneficial for minor wounds that they encounter. Below is a list of some commonly encountered topical treatments with scientific evidence:

• Antiseptics such as chlorhexidine. However, it should be noted that these can be detrimental to healing cells so should only be used when there is significant bacterial burden on initial presentation. Chlorhexidine is damaging to cells within the cornea (surface of the eye) so use in this area should be avoided⁸
• Silver has a broad-spectrum antibacterial property without the risk of developing resistance. It is available as an active ingredient in aerosols, ointments and impregnated dressings⁹
• Iodine has a broad-spectrum antibacterial property without the risk of developing resistance. However, it is again a chemical that can be damaging to tissues so it should be used with caution¹⁰
• Medical Grade Manuka Honey is both antibacterial and anti-inflammatory. It also contains nutrients for cellular metabolism and is the author’s preferred topical ointment¹¹, however as with all topical preparations it is important to understand what, when and why you are using it.

Wound management can be complicated and with multiple factors to consider. When presented with a wound on your horse initial first aid involves the application of a dressing or pressure to stem blood loss. When possible irrigation of the wound with tap water, can be performed to remove foreign debris. Veterinary advice should always be sought to determine the significance of wound in question and the treatment necessary to optimise healing and recovery.

References

1. Perkins NR, Reid SW, Morris RS. (2005) Profiling the New Zealand Thoroughbred racing industry. Conditions interfering with training and racing. N Z Vet J; 53: 69
2. Wilmink JM, Stolk PWT, van Weeren PR, et al. (1999) Differences in second‐intention wound healing between horses and ponies: macroscopical aspects. Equine Vet J; 31: 53.
3. de Groot PG, Urbanus RT, Roest M. Platelet interaction with the vessel wall. Handb Exp Pharmacol 2012; 210: 87
4. Theoret, C. and Schumacher, J. (2017) Equine wound management. 3rd ed.. John Wiley & Sons, Inc
5. Desmoulière A, Redard M, Darby I, et al.(1995) Apoptosis mediates the decrease in cellularity during the transition between granulation tissue and scar. Am J Pathol; 146: 56.
6. Luo S, Benathan M, Raffoul W, et al. (2001) Abnormal balance between proliferation and apoptotic cell death in fibroblasts derived from keloid lesions. Plast Reconstr Surg; 107: 87
7. Stashak TS. (2008) Management practices that influence wound infection and healing. In: Stashak TS, Theoret CL (eds). Equine Wound Management, 2nd edn. Wiley Blackwell: Iowa,: 85
8. Agarwal S, Piesco NP, Peterson DE, et al. (1997) Effects of sanguinarium, chlorhexidine and tetracycline on neutrophil viability and functions in vitro. J Periodontal Res; 32: 335
9. Ip M, Lui SL, Poon VKM, et al. (2006) Antimicrobial activities of silver dressings: an in vitro comparison. J Med Microbiol; 55: 59
10. Miller CN, Newall N, Kapp SE, et al. (2010) A randomized‐controlled trial comparing cadexomer iodine and nanocrystalline silver on the healing of leg ulcers. Wound Repair Regen; 18: 359.
11. Cooper R, Molan P. (1999) The use of honey as an antiseptic in managing Pseudomonas infection. J Wound Care; 8: 161 Image courtesy of Paul from Flickr Under Creative Commons Licence 2.0