Healthy Pet Network

Portions of this article appeared in a two-part series in GREAT SCOTS MAGAZINE, Aug. - Sept., Vol. 13, No. 4 , and in Oct.-Sept. Vol 3., No. 5: "A Stone's Throw: Ripples Across Time with Scottish Terriers."

Bonnie Sue: One Scottish Terrier's Experience with Adrenal Exhaustion and SARDS

By Russie McDement-Fogarty

Page 7

Who Gets What

I wanted to try to determine which dogs would receive steroid therapy for SARDS or IMR at Iowa State and how that was decision was made. Grozdanic and his colleagues write:

"SARDS has been considered an untreatable canine-blinding disease because of the complete lack of therapeutic response to anti-inflammatory, antimicrobial or immunosuppressive medications. Antibody-mediated retinopathy in human beings is frequently described as poorly responsive to medical treatment; however, high-dose steroids, plasmapheresis, and IVIg therapies have been described to reverse symptoms of blindness partially."

Grozdanic SD, Harper MM, Kecova H Antibody-mediated retinopathies in canine patients: mechanism, diagnosis, and treatment modalities. Vet Clin North Am Small Anim Pract 2008 Mar; 38(2):361-87; pp.384.

However, Grozdanic indicated in a March 26, 2008, e-mail to me that the current "general recommendation" is to initiate steroid and doxycycline therapy in SARDs and IMR dogs as a first step if there are no other associated organ problems. If the dog has liver disease, kidney failure, heart insufficiency or infectious disease, systemic steroids are thought to be contraindicated.

According to Dr. Grozdanic, Bonnie and at least one other dog with SARDS had a positive response to steroid treatment, results he would expect to see in dogs with IMR instead of SARDS. His paper reflects that dogs receiving IVIg treatment for IMR will need long-term steroid/doxy treatment because a "decrease in the medication dose (especially steroids) can rapidly result in severe visual disturbances within 24 hours." So, IMR dogs are treated with steroids and doxycycline, sometimes for a lifetime. But SARDS dogs in the past did not get steroids after IVIg treatment.

Bonnie was a lucky exception, I guess. She got the steroids she needed in the beginning and because she responded, did not need IVIg treatment.

Featured in Dr. Grozdanic's research are two photos of Bonnie, one showing her lack of menace response, the other in the visual maze, with the quote: "(A) Lack of menace response after treatment in a patient that has SARDS. (B) Excellent visual maze navigation is present despite the lack of a menace response (this patient did not have any detectable ERG activity before or after treatment)."

Ibid., p.370

I was delighted to see her memorialized in this research, but her picture is directly under the heading "Iowa State University Sudden Acquired Retinal Degeneration Syndrome Intravenous Immunoglobulin Treatment Protocol." It seems important to note that Bonnie did not receive IVIg therapy as might be misinterpreted; her only treatment consisted of prednisone and doxycycline, and her vision was sustained through continued treatment with prednisone (originally prescribed by ISU) and thyroid supplementation.

It may be quite unfortunate that dogs with pre-existing organ problems are often unable to receive any kind of cortisol replacement therapy because of its supposed contraindication. These might be the very dogs who could most benefit from simple steroid treatment. This would only be true if those dogs were tested for and found to be in adrenal exhaustion-and if (1) you accept that adrenal exhaustion plays a role in the development of SARDS, and (2) that non-treatment of this imbalance results in other serious diseases, and (3) that steroid therapy is necessary in addressing this imbalance. Owners with dogs suffering from these debilitating diseases and SARDS will have to find a sympathetic veterinarian willing to test for adrenal exhaustion and treat accordingly.

This is difficult because conventional wisdom would hold that long-term steroid treatment is harmful, that it is immunosuppressive. Even my own vet was somewhat resistant. So, it is indeed ironic that dogs who might truly need steroid treatment to address not only their SARDS, but also their other metabolic symptoms, are denied it because veterinarians and specialists might not completely understand the way in which these steroids could have a restorative instead of harmful effect.

This is one of the main problems for animals with adrenal exhaustion or SARDS in receiving treatment. Vets just don't recognize the disorder. My own vet told me it wasn't anything he'd studied in school and of course, that placed the burden of seeking treatment on us, the owners. Valuable time can be wasted convincing your veterinary professional of the existence of this disorder and then acquainting them with the recommended treatment and assuring them of its validity. My advice is that if your vet doesn't get it, move on. Your pet's health depends on it.

What About the Metabolic Symptoms of SARDS?

Many of the metabolic symptoms of SARDS are not tracked at ISU, but excessive hunger, thirst and urination are mentioned as sometimes resolving after SARDS of long duration. This finding is reinforced in Levin's work and is also probably part of the "stress adaptation response" written about by Dr. Hans Seyle, the father of endocrinology. But other abnormalities are present in dogs that are brought to ISU, even if they are not chosen to be completely addressed.

"Retrospective studies and the author's personal experience is that all symptoms of abnormal metabolic activity (eg, polyphagia, polydypsia, polyuria) resolve within 3 to 6 months after the onset of blindness in most patients. The results of the general physical examination are usually unremarkable, and serum analysis frequently shows the presence of elevated liver enzyme values, lipid abnormalities (predominantly increased cholesterol levels), increased levels of vitamins A and E, increased serum protein fractions . . . and increased levels of cortisol and sex hormones."

Ibid, p.362

Dr. Grozdanic's work is aimed at showing how IVIg therapy works to restore vision, but is of course, shown through the lens of SARDS being an antibody-mediated process which must be suppressed. And make no mistake, his work is a big deal to Iowa State University, so they are promoting the IVIg therapy as much as possible, and it would seem, downplaying the abnormal metabolic involvement. By their own admission, they are not tracking these issues after IVIg treatment.

As I understand the role of adrenal exhaustion in SARDS as seen through the work of Plechner and Levin, restoring the hormonal and cortisol balance through hormone replacement puts the immune response back to normal, which in turn stops the degenerative process going on within the retina. But if through IVIg injection, the inflammatory response is reduced, isn't hormone therapy aimed at doing exactly the same thing, but using a different reasoning and less expensive method? In dogs that are given both IVIg and long-term steroid therapy (both before and after treatment), how can you know which therapy is working its magic? Perhaps both are working together, but in a different way than those at ISU might propose.

Dr. Plechner writes of some of his more critical cases such as patients with cancer, malabsorption issues and viral diseases as needing more than an oral form of steroid treatment. He uses it in cases where he suspects the medications might not be absorbed properly or which could take weeks or months of oral treatment to correct. He then turns to intramuscular injections or, if the patient is hospitalized, a soluble cortisone preparation, along with certain vitamins, and if needed, an antibiotic. This in turn quickly restores normal levels of estrogen and cortisol, which then returns the immune system to its normal function. The administration of IVIg that ISU offers may actually be doing the same thing, just coming at it from another direction.

Dr. Grozdanic states the following:

"In these diseases, however, it is not clear if the antibody production precedes the retinal disease or if the immune reactivity is a consequence of the retinal degenerative process."

Ibid. p. 381

Wondering if my questions about the cause of SARDS had any merit, I turned to the co-author of at least three studies Grozdanic cites in his research, Dr. Kenneth L. Abrams, DVM, DAVCO. Dr. Abrams is a board-certified veterinary ophthalmologist, practicing for the last 15 years in his own private referral ophthalmology practice, Veterinary Ophthalmology Services, Inc. He completed his small animal medicine and surgery internship at Angell Memorial Animal Hospital in Boston. He then pursued advanced training in his residency in comparative ophthalmology at the University of Tennessee but left the south to return to Boston, where he was the staff Ophthalmologist at Tufts School of Veterinary Medicine and Angell Memorial Animal. He is a past president of the American College of Veterinary Ophthalmologists and has authored several scientific articles and textbooks. However, from my perspective, his most valuable background comes through in his strong clinical interest in retinal disease, including SARDS.

Dr. Abrams co-authored a study that evaluated the blood of thirteen dogs affected by SARDS and five dogs with normal ocular examinations to determine the presence of antiretinal autoantibodies. The conclusion of this study was that "no antiretinal autoantibodies were identified in the serum of dogs affected by SARDS as compared to normal canine patients."

Keller RL et al. Evaluation of canine serum for the presence of antiretinal autoantibodies in sudden acquired retinal degeneration syndrome. Veterinary Ophthalmology 2006;9:195-2001

In his own practice, Dr. Abrams sees about 50 dogs a year with SARDS, and observes that Schnauzers, Brittany Spaniels and Dachshunds are the most affected breeds. He often sees a loss of the sense of smell in dogs with SARDS, but has not noticed the hearing loss that Bonnie experienced. He has also observed that stress is a precursor to this disease: "groomer, boarding, new house, new-born children." Both his research and personal experience point toward a corresponding hormonal imbalance. He indicated to me several theories had been put forth to explain the development of SARDS, including glutamate toxicity and autoimmune disease, but he did not believe these to be correct. "Many patients (70%) have an associated problem where they will drink lots of water, eat aggressively, and gain a lot of weight in recent times. These signs hint at a hormone disorder called Cushing's disease, a similar disease to diabetes. However, when patients are tested for Cushing's disease, the results are usually normal or borderline, therefore indicating that SARDS patients probably don't have true Cushings disease."

Common Eye Diseases, Sudden Acquired Retinal Degeneration

Clearly, the debate about whether IMR and SARDS are truly auto-immune diseases will persist, just as blindness in affected dogs will continue to occur. Even though it is helpful for owners of affected pets to understand the origin of these diseases and the factors which predispose pets toward them, it is perhaps far more important that we seek appropriate testing and demand proper treatment for any pet that might display the symptoms of adrenal exhaustion, SARDS or IMR.

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