The underlying cause of ischemic dermatopathy should be identified and treated if possible. In drug-induced cases, future administration of the drug should be avoided. If rabies vaccination is the trigger, the risks and benefits of vaccination versus avoiding vaccination should be assessed. If medically appropriate, local jurisdictions may accept a letter stating it is medically unwise to vaccinate a patient for rabies—this is a serious decision because of the zoonotic risk for rabies.
When planning treatment, severity of disease versus adverse effects of treatment should be considered. Therapeutic options include pentoxifylline, glucocorticoids, oclacitinib, and/or other immunosuppressive agents (eg, mycophenolate, modified cyclosporine, sulfones, sulfasalazine).
Pentoxifylline (15-25 mg/kg PO every 8-12 hours) should be included as first-line therapy because of its safety, positive effects on microcirculatory blood flow, and rheologic and immunomodulatory effects.1,8-11 There may be a 30- to 90-day lag before the patient demonstrates full clinical response.
Pentoxifylline and its metabolites improve the flow properties of blood by decreasing viscosity, although the mechanism of action and sequence of events leading to clinical improvement are still undefined. In patients with chronic peripheral arterial disease, blood flow is increased to the affected microcirculation and enhances tissue oxygenation. Pentoxifylline administration has been shown to produce dose-related hemorrheologic effects, lower blood viscosity, and improve erythrocyte flexibility.1,8-11 Leukocyte properties of hemorrheologic importance have been modeled in veterinary and in vitro human studies. Pentoxifylline has been shown to increase leukocyte deformability and inhibit neutrophil adhesion and activation.8 Tissue oxygen levels have been shown to be significantly increased by therapeutic doses of pentoxifylline in patients with peripheral arterial disease.12
Vitamin E (dogs <55 lb [25 kg], 400 IU PO every 12 hours; dogs >55 lb [25 kg], 800 IU PO every 12 hours)2 and essential fatty acids are used for their anti-inflammatory properties and antioxidant activity; however, there have been no studies evaluating the efficacy of this therapeutic modality in canine ischemic dermatopathy.2,13 When prescribing vitamin E, the author recommends alpha-tocopherol,* as it is preferentially absorbed and accumulated in humans. Vitamin E should be given with a small amount of fatty food to increase absorption.
Topical therapy (ie, glucocorticoids) may initially be used to treat focal lesions to minimize adverse effects associated with systemic glucocorticoid administration. A potent topical glucocorticoid (eg, desoximetasone 0.25%) can be applied every 12 hours until clinical remission (not to exceed 21 days), and then tapered slowly over the next few months.
Although topical steroids are used to avoid systemic adverse effects, systemic signs consistent with steroid administration are possible but rare. If adverse effects occur, or if the lesions fail to respond to topical steroids, topical tacrolimus (0.1%) can be given every 12 hours for 30 days, and then tapered.2 Of note, topical tacrolimus may initially cause transient focal erythema that will resolve as the lesions resolve. Pet owners should wear gloves when handling topical steroids or tacrolimus.
Systemic steroids have historically been the mainstay of therapy for ischemic dermatopathy and are the author's drug of choice for more severe forms of disease; however, oclacitinib has been reported as rapidly effective for resolution of active lesions (eg, erosions, ulceration, crusting).3,14 For mild to moderate cases of ischemic dermatopathy, the author administers oclacitinib (0.4-0.6 mg/kg PO every 12 hours for 30 days [extra-label]) rather than using glucocorticoids.
If the patient is in remission (ie, crusts are in the hair coat or are easily removed from the skin and all ulcers are healed) after 30 days, the author decreases the frequency to once every 24 hours for 30 days, and then to once every 48 hours for 30 days; treatment is then stopped. If treatment every 12 hours for 30 days is ineffective, oclacitinib should be discontinued and oral glucocorticoids should be dispensed.
If clinical relapse occurs during a medication taper, the drug should be increased to the last effective dose and frequency.
In cases of severe, generalized disease, systemic steroids are used as follows:
- Prednisone (1 mg/kg PO every 12 hours for 4 days, then 0.5 mg/kg PO every 12 hours for another 10 days), with recheck every 14 days.
- If the disease is in remission, the dose should be decreased by 25% every 14 days and not tapered too quickly.
- If lesions recur during tapering, a steroid-sparing agent should be added to the treatment regimen.
At 14-day recheck:
- If systemic steroids are administered but the disease has not improved, a steroid-sparing agent should be added and the prednisone dose should be increased back to 1 mg/kg PO every 12 hours for 14 days.
- If lesions have improved but are not in remission, the dose can be continued and rechecked after 14 days.
At 28-day recheck:
- If the disease is still not in remission, a steroid-sparing agent should be added and prednisone should be maintained at the current dose (0.5 mg/kg PO every 12 hours).
- If the disease is in remission, the prednisone dose should be decreased by 25%.
Rechecks should be performed every 14 days to determine the effectiveness of the medications, and adjustments should be made based on clinical assessment of lesions (Figure 4).
For patients receiving a steroid-sparing agent in addition to prednisone, prednisone should be tapered first, as it is typically associated with overt adverse effects. Once prednisone has been discontinued or is at its lowest dosage, the steroid-sparing agent can be tapered by 25% every 30 days (other than oclacitinib, as previously described).
In cases in which ischemic dermatopathy does not respond to prednisone, other immunosuppressive agents (eg, mycophenolate, modified cyclosporine, sulfones, sulfasalazine) can be added to therapy. A food trial should also be initiated, as food can trigger ischemic dermatopathy.2 The author only begins a food trial if the disease is unresponsive to additional drugs (eg, steroid-sparing agents). Diet should be maintained until the dose and frequency of all drugs are stable; diet can then be changed to determine if disease is exacerbated.
CBC, serum chemistry profile, and urinalysis should be performed every 6 months in dogs receiving glucocorticoids for a prolonged period.