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Veterinary Focus

Issue number 28.1 Other Scientific

Cutaneous vasculitis in dogs

Published 01/10/2020

Written by Elizabeth Goodale

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The vasculature of the skin plays a vital role in ensuring various homeostatic mechanisms function as normal, but when disease strikes, the effects can be dramatic. Elizabeth Goodale takes an analytical look at what can go wrong.

Vascular skin disease

Key Points

Cutaneous vascular diseases most commonly affect the skin over pressure points and distal extremities such as the footpads, tail, pinnae and scrotum.

True vasculitis often causes epidermal necrosis and ulceration, and patients are frequently systemically unwell.

Ischemic dermatopathy, or cell-poor vasculitis, usually causes epidermal lesions of ischemia such as alopecia and collagen changes.

Several unique familial vasculitis and vasculopathy syndromes have been reported in various breeds of dog.


As the largest organ in the body, the skin has a variety of anatomical and physiological functions. The vasculature of the skin is important for thermoregulation, immune function, endocrine function and wound healing, and the hair follicle cycle and normal epidermal turnover are dependent on adequate blood supply. The skin receives about 4% of the total cardiac output, and the cutaneous vasculature is a complex network of plexuses of arteries and veins. The deep plexus contains the major arteries and supplies the subcutaneous tissues, the dermis, the lower portion of the hair follicles and the sebaceous glands. The middle plexus is at the level of the sebaceous glands and supplies the arrector pili muscles, the mid portions of the hair follicles, and the sebaceous glands. The superficial plexus supplies the upper portion of the hair follicles and the epidermis 1. The external ears, footpads, nipples and mucocutaneous junctions (eyelid, lip, nostril, prepuce, anus and vulva) are exceptions to this, which may explain why some vascular diseases affect these locations more commonly.

Without an adequate blood supply, skin lesions can range from alopecia to complete ulceration and necrosis, depending on the size of vessel affected and the severity. Most vascular diseases affecting companion animals primarily affect the smaller vessels.


Vasculitis is inflammation that specifically targets blood vessels and it is generally regarded as a reaction pattern, rather than a definitive diagnosis. Any diagnosis of vasculitis should therefore prompt a thorough investigation into possible triggers 2 3.

Patients with true vasculitis are often systemically unwell; pyrexia, anorexia and lethargy are common. Pain is also frequently reported, but can be variable. The cutaneous lesions of vasculitis vary depending on the severity of vascular compromise and subsequent tissue hypoxia. Mild cases may show alopecia, erythema, edema and urticaria 2 3. More severe acute vasculitis can cause sharply demarcated ulcerations (Figure 1) or eschars (devitalized skin that is hard and cold to the touch). The pinnae, footpads, tail tip, scrotum, oral cavity and pressure points are most commonly affected, but lesions can also be generalized (Figure 2) (Figure 3a) (Figure 3b) 2 3

Severe, sharply demarcated oral ulceration due to vasculitis triggered by a drug reaction to cephalexin.
Figure 1. Severe, sharply demarcated oral ulceration due to vasculitis triggered by a drug reaction to cephalexin. © Elizabeth Goodale
The pinnae are often affected in vasculitis cases. This dog with neutrophilic vasculitis presented with vesicles on the concave aspect of its ears.
Figure 2. The pinnae are often affected in vasculitis cases. This dog with neutrophilic vasculitis presented with vesicles on the concave aspect of its ears. © Elizabeth Goodale
A case of neutrophilic vasculitis showing ulcerations and erythema in the axilla.
Figure 3a. A case of neutrophilic vasculitis showing ulcerations and erythema in the axilla. © Elizabeth Goodale
A case of neutrophilic vasculitis showing ulceration of the lip margins and oral cavity.
Figure 3b. A case of neutrophilic vasculitis showing ulceration of the lip margins and oral cavity. © Elizabeth Goodale
Drugs (e.g., cephalosporins, sulfonamides, itraconazole) 
Bacterial, viral, protozoal and vector-borne infections
Insect bites
Food hypersensitivity
Immune-mediated diseases (e.g., systemic lupus erythematosus)

Table 1. Potential triggers of vasculitis.

There are many reported triggers of vasculitis and it is important to try to identify the etiology for every case (Table 1). It is especially important to identify patients with septic vasculitis (including vasculitis caused by deep pyoderma, endocarditis or cellulitis), because immunosuppressive treatments are contraindicated 3. A thorough history – including details of diet, supplements, topical therapies, vaccination history and any medications given – is critical. Patients should undergo a general physical exam in addition to a dermatological exam. A complete blood count (CBC), serum biochemistry profile, urinalysis and titers for tick-borne diseases should be evaluated in every case.

The diagnosis of vasculitis is made on skin biopsy, which should be collected from acute lesions (erythema and petechiae) rather than completely ulcerated or necrotic skin. Biopsies must be down to the subcutaneous tissue, because the lesions are often very deep. Histopathological lesions essentially show damage to the vascular walls associated with inflammation; there is often microhemorrhage, leukocytoclasia (fragmented granulocyte nuclei) and necrosis. The most common inflammatory cell type is neutrophils, and small vessels are most frequently affected 2.

Treatment options

Given the wide range of severity and clinical signs, treatment protocols should be tailored to the individual patient (Table 2). If a drug reaction is suspected the offending medication should be discontinued. Infectious diseases and neoplasia should be treated where possible. Food hypersensitivity can also be a trigger (especially if a generalized urticarial vasculitis is present) and an elimination diet trial may be considered appropriate 2

Pentoxifylline 15-30 mg/kg q8-12H
Doxycycline 5 mg/kg q12H
Niacinamide 250 mg q8H <10 kg, 500 mg q8H >10 kg
Prednisone/prednisolone 0.5-1 mg/kg q24H
Ciclosporin 5-10 mg/kg q24H
Azathioprine 2.2 mg/kg q24H for 14 days, then q48H
Mycophenolate mofetil 10-20 mg/kg q12H
Sulfasalazine 20-40 mg/kg q8H
Dapsone 1 mg/kg q8H
Vitamin E 200IU q12H small breeds, 400IU q12H medium breeds, 600IU q12H large breeds

Table 2. Commonly used medications and oral dosage for vasculitis and ischemic dermatopathies.

Very mild idiopathic cases are often managed with pentoxifylline or a combination of doxycycline and niacinamide 2. Pentoxifylline is a methylxanthine derivative that increases red blood cell flexibility, decreases blood viscosity and has anti-inflammatory effects. It is generally well tolerated, but clinical response can take 1-3 months. Doxycycline (a tetracycline antibiotic) and niacinamide (a B-vitamin) used in conjunction have immunomodulatory effects, although the exact mechanisms are not fully understood. Hepatotoxicity with doxycycline has been reported, but is rare. This drug combination also has a very slow onset of action; if a rapid response is necessary, both pentoxifylline and doxycycline/niacinamide can be combined with corticosteroids. Vitamin E has also been used alongside doxycycline/niacinamide.

More severe cases will need more aggressive therapy with a faster onset of action. Glucocorticoids can provide very rapid improvement in clinical signs, but must be used cautiously in patients with extensive ulcerations because they delay wound healing. Anti-inflammatory doses (0.5-1 mg/kg/day) are often sufficient 3.

Secondary immunosuppressive agents (i.e., steroid-sparing drugs, such as ciclosporine or azathioprine) can also be used. Ciclosporin has been used to treat atopic dermatitis and a variety of immune-mediated conditions including vasculitis 2 3 4, although the cost can be prohibitive. Branded microemulsified products have better absorption than generic formulations and are to be preferred 4. Maximal effect is generally seen after 4 weeks, with transient gastrointestinal upset (vomiting and diarrhea) the most common side effect. Freezing the capsules and administering while frozen has been anecdotally reported to decrease the incidence of vomiting 4 and does not appear to impact the bioavailability 5. There are many drugs that interact with ciclosporin, so its use should be evaluated carefully when multiple medications are being administered.

A less expensive option as a secondary immunosuppressive agent would be a purine antagonist such as azathioprine or mycophenolate mofetil 3 4 5 6. Azathioprine can cause hepatotoxicity and bone marrow suppression, as well as an increased risk of pancreatitis, so frequent bloodwork is required 3. A serum biochemistry profile and CBC is generally recommended prior to initiating therapy and should be repeated after 2, 4, 8 and 12 weeks of treatment; if the drug is well tolerated at this point, the tests are then typically repeated every 4 months. A clinical response can take 3-6 weeks. Hepatotoxicity is most likely to occur within the first 2-4 weeks, while bone marrow suppression may occur with chronic usage 7.

Mycophenolate mofetil has not been as extensively employed as azathioprine until recently because of its cost, but generic products are now available and its use is increasing 6. It has fewer side effects when compared to azathioprine, although diarrhea can occur; bone marrow suppression is uncommon. Again baseline CBC and biochemistry are recommended, but intensive monitoring is not generally required. Clinical response can take 3-8 weeks.

Sulfonamides (e.g., sulfasalazine and dapsone) have been recommended for cases of neutrophilic vasculitis that have not responded to other therapies 2 3. They interfere with the neutrophil myeloperoxidase system, but their exact mechanism of action is not fully understood. Sulfasalazine is generally better tolerated but can cause reversible keratoconjunctivitis sicca (KCS). Dapsone has been associated with bone marrow suppression, hemolytic anemia, hepatotoxicity, neurotoxicity and hypersensitivity reactions. Baseline CBC and biochemistry is recommended and testing should be repeated every 2-3 weeks for the first 4 months, then every 3-4 months.

As with other immune-mediated skin diseases, the secondary agents are used at the full dose with or without corticosteroids until remission is achieved. The corticosteroid is then generally tapered, aiming to reduce the dose by 25% every 2-4 weeks. Ideally, the goal is to discontinue the corticosteroid before tapering the secondary agent, again by 25% every 4 weeks until the lowest effective dose is achieved or the drug is discontinued. In some cases low doses of both corticosteroid and the secondary agent may need to be maintained.

Ischemic dermatopathies

These are a group of clinical conditions whereby ischemic tissue damage results in lesions without significant visible vasculitis 8. Often termed “cell-poor vasculitis“, common clinical signs include alopecia, hyper- or hypopigmentation, skin thinning, scale and erosions or ulcers that are slow to heal. These lesions are typically seen at pressure points and the distal extremities. The most common histological lesions are follicular atrophy, pale-staining mucinous collagen and clefting at the basement membrane zone.

Post rabies vaccination panniculitis 

An area of alopecia that developed after rabies vaccination. Notice the drip pattern ventrally.
Figure 4. An area of alopecia that developed after rabies vaccination. Notice the drip pattern ventrally. © Dr. Stephen White

This ischemic dermatopathy presents as a focal area of alopecia with hyperpigmentation and occasionally a swelling or plaque at the site of a rabies vaccination (Figure 4) 9. It is most commonly seen in Miniature Poodles and other small breed dogs 8 9. The signs typically occur 2-6 months after vaccination and the lesions are non-painful. The diagnosis is often made simply on clinical signs, but biopsy shows a cell-poor vasculitis with follicular atrophy and dermal pallor; inflammation in the subcutaneous tissues (panniculitis) may be present 9. Amorphous blue material, thought to be vaccine components, can sometimes be seen, and rabies-specific immunofluorescence has been identified within the walls of blood vessels. These lesions are mainly cosmetic and rarely necessitate therapy, but pentoxifylline may be used if the lesions are expanding. Repeat vaccination should be done with caution as progressive disease is possible.

Pinnal margin vasculopathy

Sometimes referred to as proliferative thrombovascular necrosis of the pinnae, this is a fairly common ischemic dermatopathy that targets the ear margins. Lesions begin as an area of thickening and scale, often wedge-shaped, on the concave surface of the pinnae, and can progress to ulceration and necrosis of the tips (Figure 5a) (Figure 5b) 8. Lesions are generally bilateral and can deform the ear margin. Many cases are idiopathic but there may be an association with recent vaccination or with cutaneous adverse food reactions 8. Since the lesions have a very striking appearance, and because the location is difficult to biopsy, diagnosis is often on clinical signs alone. Biopsy shows ischemic tissue damage with or without a cell-poor vasculitis that can have severe thickening of the arteriole walls. Pentoxifylline, doxycycline/niacinamide and/or vitamin E are the most commonly used treatments. For cases that are ulcerated or bleeding, anti-inflammatory doses of corticosteroids are often required, but must be used cautiously because they can delay healing 8. Tacrolimus 0.1% ointment has a similar mechanism of action to ciclosporin and can be applied topically in these cases, although irritation and pruritus at the site of application has been reported in dogs (and humans). If a cutaneous adverse food reaction is suspected then an elimination diet trial should be performed. For cases that have not responded to medical management surgical removal of the pinnae can be curative, but this should be done cautiously. 

Pinnal margin vasculopathy causing ulcerations and a defect in the pinnal margin.
Figure 5a. Pinnal margin vasculopathy causing ulcerations and a defect in the pinnal margin. © Elizabeth Goodale
Pinnal margin vasculopathy causing thickening of the pinna.
Figure 5b. Pinnal margin vasculopathy causing thickening of the pinna. © Elizabeth Goodale
Elizabeth Goodale

Vasculitis often causes a severe clinical syndrome with systemic signs, with ulcerations and necrosis of the skin, while ischemic dermatopathy is typically much milder with lesions resulting from epidermal hypoxia.

Elizabeth Goodale

Generalized ischemic dermatopathy 

Adult onset generalized ischemic dermatopathy with significant muscle atrophy of the temporalis muscles in a Welsh Pembroke Corgi.
Figure 6. Adult onset generalized ischemic dermatopathy with significant muscle atrophy of the temporalis muscles in a Welsh Pembroke Corgi. © Elizabeth Goodale

These cases present with widespread lesions of ischemic tissue damage, especially over bony prominences of the face and extremities (i.e., distal limbs, ears, pinnal folds, and tail) 8 9 10. Lesions often begin as alopecia, scale and crusting, and progress to erosions and ulcers with eventual scarring. The nailbeds can be involved and sloughing of the claws may be seen. There can also be a prominent myopathy causing severe muscle atrophy (Figure 6) 10. Clinically these cases are often indistinguishable from familial canine dermatomyositis (see below). Skin biopsies are consistent with a cell-poor vasculitis and show the typical ischemic epidermal and dermal changes. This condition can occur in juvenile or adult animals and has been associated with vaccination, although it is often idiopathic 8 9 10. Secondary bacterial infections can cause pruritus which can result in these cases being mistaken for allergic animals. Treatment options include pentoxifylline, vitamin E, doxycycline/niacinamide or ciclosporin, depending on the severity, but corticosteroids are often avoided because they can exacerbate the epidermal and muscle atrophy. If triggered by a vaccine, repeat vaccinations should be avoided as they can cause a relapse.

Familial vasculitis and vasculopathy

Several unique familial vasculitis and vasculopathy syndromes have been reported, and they are briefly discussed below.

Familial canine dermatomyositis

This is a familial generalized ischemic dermatopathy that has been reported in the Border Collie, Shetland Sheepdog, Beauceron Shepherd, Australian Kelpie, Portuguese Water Dog and Belgian Tervueren Shepherd 11 12 13 14 15 16. Signs typically occur in dogs under 6 months of age, although adult onset has been reported, and signs can vary in severity from mild to severe 8 11 12 13 14 15 16. These cases are clinically and histologically indistinguishable from generalized ischemic dermatopathy, and the treatment is the same for both conditions.

Cutaneous vasculopathy of German Shepherd Dogs

Affected dogs usually develop signs between 4-7 weeks of age and often within 7-10 days of their initial vaccination 17. The signs typically include swelling, depigmentation and ulceration of the footpads, ulcers on the pinnae, tail tip and nasal planum, swelling on the bridge of the nose, and nasal depigmentation. Repeat vaccination causes a recurrence or worsening of signs. Affected dogs are usually lethargic, febrile and can be lame with swollen joints. There are no consistent laboratory abnormalities in these cases, and patients generally recover by 5-6 months of age; no treatment has been shown to be effective. Biopsies show subtle vasculopathy and panniculitis with inflammation centered around degenerate collagen bundles 17.

Leukocytoclastic vasculitis of the nasal planum in Scottish Terriers

Clinical signs start at 3-4 weeks of age with a clear nasal discharge and ulceration of the nasal planum, and progressively worsen with destruction of the planum and nasal mucosa 18. Biopsies show pyogranulomatous inflammation, neutrophilic leukocytoclastic vasculitis and epidermal necrosis. No effective treatment has been reported and all affected dogs have been euthanized.

Cutaneous vasculitis of the Parson Jack Russell Terrier

The most common clinical signs are alopecia, crusting and ulcerations over bony prominences, wedge-shaped necrosis of the pinnae tips, and ulceration of the footpads 19. Reports note that vaccinations were given 2-3 weeks prior to the onset of lesions in 60% of cases. Histopathology shows leukocytoclastic vasculitis, apoptotic keratinocytes and ischemic degeneration of hair follicles. The clinical and histological appearance is similar to dermatomyositis. Cases have been managed successfully with prednisone, dapsone and/or vitamin E 19.

Dermal arteritis of the nasal philtrum

Nasal arteritis in a Saint Bernard.
Figure 7. Nasal arteritis in a Saint Bernard. © Elizabeth Goodale

A proliferative vasculitis affecting the dermal arteries and arterioles underlying the nasal philtrum has been described primarily in Saint Bernards, but also in Giant Schnauzers and Basset Hounds 20 21. The primary lesions consist of an ulceration affecting only the nasal philtrum that hemorrhages (Figure 7). The bleeding can be severe enough to cause anemia and require hospitalization. This condition has been successfully medically managed with prednisone acutely and doxycycline/niacinamide, fish oils and/or topical fluocinolone in dimethyl sulfoxide 20. Surgery to resect the affected tissue, ligate the vessels and reconstruct a new “philtrum” has also been successful 21.

Cutaneous and renal vasculopathy of Greyhounds

This condition most commonly affects Greyhounds between the ages of 1 and 4 years 22. Lesions occur most commonly on the tarsus, stifle or thigh and begin as bruising that progresses into sharply demarcated ulcers; these extend into the subcutaneous tissue and heal slowly. Azotemia, polyuria, polydipsia, vomiting, dark or tarry stools, salivation, pyrexia and distal limb edema develops in some cases. Skin biopsies show thrombosis and necrosis of arteries, arterioles, venules and capillaries which cause large areas of tissue necrosis. Renal biopsies show peracute glomerular necrosis involving afferent arterioles, with thrombi in glomerular capillaries. When signs of renal failure are present, aggressive fluid therapy and supportive care is required, but these cases often die. There is some suggestion that this may be similar to hemolytic uremic syndrome in humans, which is caused by a Shiga-like toxin produced by Escherichia coli 22.

Environmental vascular diseases

Solar vasculopathy

Chronic sun exposure can cause damage to the vessels in the superficial dermis. This most commonly affects non-pigmented and lightly haired skin on the dorsal muzzle and nasal planum. Acute clinical signs are erythema, swelling, erosions or ulceration, and with chronic sun exposure this can lead to scarring and further depigmentation. Treatment is mainly through sun avoidance.

Cryofibrinogenemia and cryoglobulinemia

This is a very rare disease whereby cold temperatures cause either fibrinogen or globulins in the blood to form thrombi or immune complexes which precipitate and induce vasculitis. The end result is disruption of blood flow to the extremities, resulting in pain, erythema, purpura, acrocyanosis and necrosis. The cryoglobulins can also target erythrocytes and cause a hemolytic anemia, renal disease or peripheral polyneuropathy. These conditions may be primary in nature or can be secondary to infection or lead poisoning. Diagnosis is by demonstrating agglutination of blood at cold temperatures, a Coombs test, or measuring cryoprecipitate levels. Management involves avoiding a cold environment, correcting the underlying cause, and occasionally medical management with corticosteroids or pentoxifylline.

Vascular diseases of the skin most commonly affect the skin over pressure points and distal extremities, such as the footpads, tail, pinnae and scrotum. Vasculitis often causes a severe clinical syndrome with systemic signs, with ulcerations and necrosis of the skin, while ischemic dermatopathy is typically much milder with lesions resulting from epidermal hypoxia. In all instances the underlying triggers should be identified whenever possible, and whilst treatment for both vasculitis and ischemic dermatopathies employ similar medications, the therapy should always be tailored to the severity of disease.


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  2. Nichols PR, Morris DO, Beale KM. A retrospective study of canine and feline cutaneous vasculitis. Vet Dermatol 2001;12:255-264.
  3. Innera M. Cutaneous vasculitis in small animals. Vet Clin Small Anim 2013;43: 113-134.
  4. Forsythe P, Paterson S. Ciclosporin 10 years on: indications and efficacy. Vet Rec 2014;174:13-21.
  5. Bachtel JC, Pendergraft JS, Rosychuk RA, et al. Comparison of the stability and pharmacokinetics in dogs of modified ciclosporin capsules stored at -20C and room temperature. Vet Dermatol 2015;26:228-e50.
  6. Ackermann AL, May ER, Frank LA. Use of mycophenolate mofetil to treat immune-mediated skin disease in 14 dogs – a retrospective evaluation. Vet Dermatol 2017; 28:195-e44.
  7. Wallisch K, Trepanier LA. Incidence, timing and risk factors of azathioprine hepatotoxicosis in dogs. J Vet Intern Med 2015;29:513-518.
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  11. Hargis AM, Haupt KH, Hegreberg GA, et al. Familial canine dermato-myositis – initial characterization of cutaneous and muscular lesions. Am J Pathol 1984;116:234-244.
  12. Hargis AM, Prieur DJ, Haupt KH, et al. Postmortem findings in a Shetland sheepdog with dermatomyositis. Vet Pathol 1986;23:509-511.
  13. Guaguere E, Magnol JP, Cauzinille L, et al. Familial canine dermatomyositis in eight Beauceron shepherds. In: Kwochka KW, Willemse T, Von Tscharner C, (eds). Advances in Veterinary Dermatology. New York: Pergamon Press 1996;527-528.
  14. Rothig A, Rufenacht S, Welle MM, et al. Dermatomyositis in a family of working kelpies. Tierärztl Prax Ausg K Kleintiere Heimtiere 2015;43:331-336.
  15. Campbell KL, Lowe AD, Lichtensteiger CA. Dermatomyositis in three Portuguese water dog littermates [abstract]. Vet Dermatol 2008;19:69.
  16. Guaguere E, Degorce-Rubiales F, Muller A. Familial canine dermatomyositis in six Belgian shepherds (Tervueren) [abstract]. Vet Dermatol 2008;19:70.
  17. Weir JA, Yager JA, Caswell JL, et al. Familial cutaneous vasculopathy of German Shepherds: clinical, genetic and preliminary pathological and immunological studies. Can Vet J 1994;35:763-769.
  18. Pedersen K, Scott DW. Idiopathic pyogranulomatous inflammation and leukocytoclastic vasculitis of the nasal planum, nostrils and nasal mucosa in Scottish Terriers in Denmark. Vet Dermatol 1991;2:85-89.
  19. Parker WM, Foster RA. Cutaneous vasculitis in five Jack Russell Terriers. Vet Dermatol 1996;7:109-115.
  20. Torres SM, Brien TO, Scott DW. Dermal arteritis of the nasal philtrum in a Giant Schnauzer and three Saint Bernard dogs. Vet Dermatol 2002;13:275-281.
  21. Pratschke KM, Hill PB. Dermal arteritis of the nasal philtrum: surgery as an alternative to long-term medical therapy in two dogs. J Small Anim Pract 2009;50: 99-103.
  22. Carpenter JL, Andelman NC, Moore FM, et al. Idiopathic cutaneous and renal glomerular vasculopathy of Greyhounds. Vet Pathol 1988;25:401-407.

Further Reading

  1. Muller & Kirk’s Small Animal Dermatology 7th ed. Miller WH, Griffin CE, Campbell KL (eds). St. Louis: Elsevier Mosby, 2013

  2. Skin diseases of the dog and cat 2nd ed. Gross TL, Ihrke PJ, Walder EJ, et al (eds). Oxford: Blackwell Science Ltd, 2005

  3. Plumb’s veterinary drug handbook 8th ed. Plumb DC. Wisconsin: PharmaVet Inc 2015

Elizabeth Goodale

Elizabeth Goodale

Dr. Goodale qualified from the Ontario Veterinary College and followed a small animal rotating internship at the Western College of Veterinary Medicine Read more

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