Equine pastern leukocytoclastic vasculitis

Josepha DeLay, Meegan Larsen, Teresa Reitz

Animal Health Laboratory, University of Guelph, Guelph, ON (DeLay, Larsen), Rideau St. Lawrence Veterinary Clinic, Prescott, ON (Reitz)

AHL Newsletter 2022;26(4):20.

Pastern leukocytoclastic vasculitis is an uncommon but distinct histologic entity in horses, and contributes to the clinical syndrome of pastern dermatitis in this species.  Frequent involvement of non-pigmented skin, and occurrence of many cases in summer months has spurred speculation that vascular injury is aggravated by sunlight.  However in some studies, pigmented skin may also be affected, and lesions may also develop in other seasons.  The lesions may be painful, resulting in lameness.

Between January 1, 2010 and November 1, 2022, AHL pathologists have diagnosed pastern vasculitis in 10 horses, with 3 cases identified in 2022.  All horses were >2 years of age, as is typical for this condition.  Lesions may affect 1 or more limbs.  The diagnosis relies on histologic identification of vasculitis or vasculopathy in biopsies from affected skin, in addition to the clinician’s description of compatible skin lesions; these include lesion characteristics, distribution and targeting of non-pigmented skin. 

A recent case diagnosed at the AHL involved a 16-year-old gelding with chronic recurrent hindlimb pastern dermatitis.  Lesions primarily, but not exclusively, affected non-pigmented skin, and consisted of erosions and ulcers with serous exudate (Fig. 1).  The lesions typically developed in summer and were non-responsive to various topical antibiotic, antibacterial, and anti-inflammatory therapies.  In biopsies from affected skin, small blood vessels in the superficial dermis had thickened walls expanded by fibrin, small clumps of necrotic cellular debris, and rare neutrophils, consistent with leukocytoclastic vasculitis (Fig. 2).  Fibrin thrombi filled lumens of a few blood vessels.  Fibrin and free intact or fragmented erythrocytes surrounded some affected blood vessels, indicative of vessel compromise.  Concurrent epidermal injury included hydropic degeneration of some basal epithelial cells, erosion and ulceration, reflecting ischemic injury resulting from vascular damage. 

The cause of pastern vasculitis is unknown.  The condition is thought to represent an immune complex disease and, as discussed above, may be exacerbated by exposure to sunlight.  Secondary bacterial dermatitis is common due to epidermal injury and breach of the skin barrier.

As for many dermatologic conditions, knowledge of the anatomic distribution and appearance of clinical lesions is very important for correlation with histologic lesions and in reaching a working diagnosis.  In cases of pastern leukocytoclastic vasculitis, communicating the lesion distribution to the veterinary pathologist is especially important, as this particular condition often involves distal limbs, and especially white-haired regions.  A clear description of the primary skin lesions will aid in interpretation of histologic lesions, and in reaching a diagnosis.  Biopsies should include acute lesions, if possible.  Assessment of potential bacterial, fungal, or parasitic contribution to pastern dermatitis is also important in biopsy evaluation.

Therapeutic interventions are multifaceted and include management efforts to keep skin of the distal limbs clean and dry, preventing exposure to ultraviolet light by wrapping the distal limbs, and potential use of systemic or topical immunosuppressive and immunomodulatory medications.   AHL  

Figure 1. Multifocal erosive to ulcerative pastern dermatitis, mainly involving non-pigmented skin. Note that biopsies were taken at the margin of lesions to include both affected and surrounding unaffected skin, as indicated by suture placement.

Figure 1. Multifocal erosive to ulcerative pastern dermatitis, mainly involving non-pigmented skin.  Note that biopsies were taken at the margin of lesions to include both affected and surrounding unaffected skin, as indicated by suture placement.

Figure 2. Superficial dermal blood vessels with mural thickening, perivascular fibrin and fragmented erythrocytes (black arrows).  H&E.

Figure 2. Superficial dermal blood vessels with mural thickening, perivascular fibrin and fragmented erythrocytes (black arrows).  H&E.

 

References

1. Psalla D, et al. Equine pastern vasculitis: A clinical and histopathological study. Vet J 2013;198: 524-530.

2. Yu AA. Equine pastern dermatitis. Vet Clin Equine 2013;29: 577-588.