Greta Kaplan, CPDT, CDBC
As part of Companion Animal Solutions, I’m lucky enough to work with Dr. James Ha, Ph.D., CAAB, an ethologist with the University of Washington. This means I can run tricky or unusual cases by his experienced eyes to see what I might be missing in terms of assessment or treatment. Occasionally, Jim mentions the cryptic term: “Addison’s Disease.” Addison’s has always been on my mental list as one of those diseases that can certainly cause behavioral effects; but, as with so many things in life, it took direct personal experience to really bring this home.
My second oldest dog, Cedi (pronounced “Seddie”), is an Australian Shepherd I adopted from Aussie Rescue when she was ten months old, back in 2001. She is now ten years old. She looks great — shiny coat, still slim and athletic-appearing, and no grey showing yet. But she doesn’t feel great. Cedi was my first flyball dog, and she was a star. Around age 6, it seems, she received an injury to one knee (probably during a herding lesson) and it started to interfere with her playing flyball and fetch. Fast-forwarding rapidly over extensive treatment and diagnostics, I now live with a ten-year old dog who has always been a bit anxious around other dogs, resource guards against them, and now lacks her lifelong outlet of vigorous “yahoo” sports to help keep her comfortable. A couple of years ago, working with a local behavior-oriented vet, Cedi was diagnosed with generalized anxiety disorder and placed on fluoxetine. It helped… a little.
About a year ago, she had a major gastric crash. I was unable to stabilize the vomiting and diarrhea at home, but a bag of fluids at the vet’s, fortunately, got her back on track. I discontinued her NSAID at the time, thinking it might have caused the distress. For the last year, she has had no anti-inflammatory for her painful knee, though I’d give her some tramadol if it was bad. (She was receiving a glucosamine/chondroitin supplement.)
But Cedi was still depressed, and over the last 2-3 years, it has gotten worse. She would lie around, except when barking out the window. (She’s always been the house “Sheltie.”) If I talked to her, she would turn her head and droop. She’d perk up for a walk or short game of fetch, then go back to drooping. This formerly affectionate dog didn’t want to sleep in my bedroom. I figured it must have something to do with the increased dog population in my house; she finds it a bit stressful. I talked to vet behaviorists. I said, “she just seems depressed. The anxiety is not worse, but this depressed behavior is much worse. She is anhedonic.” (Anhedonia is the inability to enjoy pleasurable activities, a common symptom of depression in humans.) Although depression is not a permitted diagnosis in dogs because its subjective component cannot be verified, experts said that yes, they sometimes saw what looked for all the world like “major depression.” It probably exists — dogs’ brains have all the same parts and chemicals that participate in human depressive states. But it will be diagnosed as GAD, which is an entirely objective diagnosis.
About six weeks ago, I brought Cedi to a flyball tournament. She used to love flyball, and I usually leave her at home now that she can’t race. I don’t want her frustrated, and her barking in the crate is no fun for anyone. However, petsitting wasn’t available, so she came with me. She stayed in her crate, silent. She didn’t want to come out. If she really had to pee, she’d pee and want to go back in. I moved her to a car crate so she could be in a quieter spot. I also crated Nano in the car, next to her; he was getting a bit too excited about flyball and, not yet being a racing dog, had no outlet for his emotions. On Sunday, I went out to take her for a potty walk. She tried to go into every crate we walked by. She wouldn’t potty, and dragged me back to the car. I offered her a treat; Nano reached for it, a normally suicidal act with my resource-guarding bitch! But Cedi turned her head; she wouldn’t take the treat, and just wanted to be left alone.
I burst into tears. For my dog, this was a flashing red light and siren saying unequivocally, “Something is terribly wrong!” I imagined cancer and autoimmune diseases (she also had a scab mysteriously appear on her muzzle, which looked a bit like discoid lupus, a disease well-known in the breed). When we were back over the border after racing that day, I left a message for my vet.
We got Cedi in a few days later and started testing: bloodwork was normal, and while her midday urine was a bit dilute, a follow-up morning catch was in the normal range. Kicking around the options, my vet finally suggested we could run the definitive test for Addison’s Disease. Apparently, most cases of Addison’s are diagnosed when the patient presents in an Addisonian crisis — very ill, usually with gastrointestinal symptoms, dilute urine, and electrolytes out of whack when bloodwork is done. Cedi’s electrolytes were normal, and she also did not meet the standard profile of a newly diagnosed Addison’s dog (a young to middle-aged female; and Aussies are not among the breeds in which it’s known to be more common genetically). My vet told me that Addison’s is known as “The Great Pretender” and usually takes a long time to diagnose, often being mistaken for renal failure, gastroenteritis, hypothyroidism, or other ailments. I agreed to the test.
It’s an easy test: The dog is fasted overnight and tested in the morning. Blood is drawn; then, synthetic ACTH (adrenocorticotropic hormone) is injected; after an hour, blood is drawn again. Both blood samples are analyzed for cortisol levels. In a typical Addison’s diagnosis, both the before and after levels are zero (undetectable). This is because the adrenal gland has stopped working, so the ACTH, which normally would trigger production of cortisol, does not have this result. It’s similar to diabetes mellitus; normally, sugar intake will cause a pancreas to produce insulin, which starts biochemical processes to metabolize the sugar. If the pancreas stops working, insulin production can’t be stimulated.
Cedi’s results were unusual. Her “before” result was undetectable. The “after” showed a cortisol elevation, but it was only into the normal resting range, not into the normal stimulated range. After doing some research, my vet suggested retesting the resting level after a week. We did this, and even more oddly, that test showed a low, but detectable cortisol level. This produced numerous conversations with the testing lab’s internists. Finally, the chief clinician suggested that the week-later result was probably still slightly elevated from the ACTH stimulation a week earlier. He advised treating with adrenocorticoids only, and testing again a few months later. Technically, since her electrolytes are normal and she is not receiving mineralocorticoid supplementation, her diagnosis is hypoadrenocorticism, not “Addison’s Disease.” (It may progress, though she seems to have a very slow progression and is already rather old.)
We started Cedi on a small dose of prednisone every other day. She’s now been taking it almost one month. I have my dog back! She’s still a bit anxious. She still resource guards. She still barks out the window. But if I talk to her, she pricks her ears up. When I come home, she pushes through to get a greeting scritch on the head. No more drooping, no more avoiding. Occasionally she wiggles her butt. In other words, she’s back to normal — for her.
To me, it all makes sense now. She had been affectionate with friends, but not with me — perhaps this was because seeing them was exciting enough to cause some cortisol production so she felt normal, whereas I was too boring and everyday to trigger this chemical response. Likewise, she was more “normal” if playing a little ball or barking at an intruder. Her sore knee was probably more sore because she was not even getting her body’s own anti-inflammatory effects (cortisol is an anti-inflammatory chemical). No wonder she was depressed.
What I learned:
*I have a great vet. OK, I knew that, but this closed the deal. She thought of doing this test for a dog outside of the profile, not in crisis, with normal electrolytes. It’s a relatively inexpensive test, under $200, and it’s definitive. Turned out to be totally worth it.
*Addison’s can be really vague. I knew something was not right, but honestly, if the most overt symptom was “failed to resource guard a treat from a housemate dog,” what is a vet supposed to do with that?
*From the reading I did that diagnostic week (most of which was so unbelievably medically-Greek as to be incomprehensible), I learned that internists consider atypical Addison’s to be significantly underdiagnosed. Hypoadrenocorticism without electrolyte imbalance is found surprisingly often — it the test is done. But since the test is rarely done until there is electrolyte imbalance, a lot of cases are missed.
*The primary symptoms were behavioral. Droopy, depressed, sad, lethargic. That gastric episode last year may have been related. Hard to know.
Cedi is now drinking more water and having to pee more often… this is normal when a dog takes prednisone. I don’t care and I suspect if I could ask her, she would gladly make the trade. She’s no longer a little puddle of mute, undifferentiated misery. I’m sure she still is sore and misses flyball, but at least she can enjoy me — and I’m who she’s got. She can enjoy walks and a little fetch and training sessions. I bet her knee feels better, too.
I’m seeing it behind every tree right now… though, interestingly, every dog someone tells me about that makes me think of Addison’s turns out to be a young to middle-aged female…. Hmmmm!
I know I’ll be mentioning it more often with behavior clients. I don’t practice veterinary medicine, but I do share observations with clients and sometimes their vets, which they can follow up on if they choose. And it often pans out; my sense of “something being physically wrong” is increasingly keen. Hey, if I think “Addison’s” and it turns out to be Cushing’s, or renal failure, I’m OK with that — at least it got the dog on the way to help for a real problem.