Adopted by his current owner three years ago from a New York City shelter, Odysseus is a mix of chow, shepherd, and maybe Labrador retriever. A thickly furred, big beefy adult weighing around 80 pounds, at first I was concerned. Was this the right dog for a senior woman, living alone?
But Ody soon dispelled my reservations, proving himself to be a wonderful, gentle companion. This fall at his annual physical examination, his mom mentioned he had been drinking a lot of water. “It started this summer,” she said. “At first I thought it was just the heat and his heavy coat, but he’s still doing it.”
I asked about urination. ” He’s urinating more, too,” she replied. “He’s actually gone in the house a few times.” This was unusual behavior, but there had been construction going on. Perhaps he was just upset and stressed, she suggested.
Polyuria and polydipsia ( PU/PD) are the technical terms for peeing and drinking excessively. They usually occur together and possible causes include diabetes mellitus, kidney or liver failure, cancer, fever, pain, and behavioral issues, to name just a few.
I suggested we run a urinalysis, so my assistant, Elise, took Ody outside. He obliged immediately, passing a large amount of urine that was very pale yellow, almost clear. Analysis showed a trace of blood, but more significant was the specific gravity — a measure of how concentrated the urine is. This urine was extraordinarily dilute. Was Ody drinking so much to make up for fluid being lost in his urine due to malfunctioning kidneys? Or was he peeing so much because he was drinking excessively (like when we drink too much beer and have to keep going to the restroom)? And if the latter, why was he suddenly drinking an abnormal amount? We needed more tests.
Initial kidney function tests were normal, but two liver enzymes were elevated. One in particular, the alkaline phosphatase, was quite high. Bear with me now. PU, PD, and elevated alkaline phosphatase. This picture is highly suspicious of hyperadrenocorticism, also known as Cushing’s disease. If you read my column faithfully (which I’m sure you do), you have heard about this disease before.
It’s a fairly common endocrine abnormality in dogs caused by excessive production of cortisol by the adrenal glands. Eighty-five percent of cases are the result of benign but hormone-producing pituitary tumors. Fifteen percent are caused by malignant adrenal gland tumors. Either way, excessive cortisol causes thirst. They drink more, then they pee more. Did Odysseus have hyperadrenocorticism? We needed more tests.”The easiest first step is to have his urine tested for cortisol,” I advised.
“That will tell us for sure if he has Cushing’s?” his mother asked.
I shrugged. Maybe. “If there’s no cortisol in his urine, we can rule it out completely. But if he does have cortisol in his urine, well, that is supportive of a diagnosis of hyperadrenocorticism, but could still be something else.”
Two days later, the lab reported a positive for urine cortisol. We needed more tests. Next would be an ACTH stimulation test. I’ll spare you the physiology lecture. Suffice it to say we drew blood, gave a hormone injection, waited an hour, drew more blood, and sent it all off to the lab.
“This will tell us for sure if he has Cushing’s?” his mother asked again. I shrugged. Most of the time. Not always. A small percentage of dogs with hyperadrenocorticism will have a normal ACTH stim. I bet you know what happened next. The ACTH stim was normal. We needed more tests.
The differential diagnosis list was narrowing. It could still be Cushing’s. It could be a quirky psychological syndrome called primary polydipsia. It could be diabetes insipidus (DI). That’s not the kind of diabetes most people are familiar with, diabetes mellitus, which involves insulin and blood sugar regulation. DI is a problem with antidiuretic hormone (ADH).
Getting overwhelmed with all these initials? PU, PD, ACTH, DI, ADH. You’re not alone. But wait, there’s more. There are two types of DI — central (CDI ) and nephrogenic (NDI). CDI is caused by inadequate hormone production by the pituitary. NDI is the result of inadequate response by the kidneys to the hormone.To proceed, I asked Ody’s mom to quantify how much water he drank daily. “Measure a huge bowl,” I advised. “Twenty-four hours later, measure what’s left.” We officially documented that he was drinking excessively, then spoke with an internal medicine specialist, who recommended a modified water deprivation test.
Do not try this at home. We are trained professionals! Seriously. Withholding water from a sick animal, even for short periods, can sometimes be deadly.
Following our instructions, the owner withheld water, then collected urine. The specific gravity showed that his kidneys were able to concentrate his urine at least a little. “That rules out CDI, ” said the specialist, “but it could still be nephrogenic DI.” You’re kidding, right? No. We needed more tests.
“Do whatever he needs,” his mom said patiently, ” but I’m moving into an apartment while they work on the house and I really need him not to urinate inside.” We then started Ody on DDAVP, a synthetic antidiuretic hormone. DDAVP is used for people with diabetes insipidus and sometimes prescribed to children for bed-wetting. Available as oral tablets or intra-nasal spray, veterinarians, being resourceful creatures, have found we can safely use nasal spray with dogs by putting a drop in the eye instead of the nose. It’s effective and less expensive than tablets, but for this owner, administering pills was easier.
Within days of starting DDAVP, Odysseus’s water consumption and urination had returned to normal. Soon after, a low-dose dexamethasone suppression test (LDDS) confirmed our earliest suspicions. He has hyperadrenocorticism. The DDAVP is controlling his PU/PD.
Eventually we may need to treat the Cushing’s disease more directly, but for now, after an epic journey through a sea of medical initials, we are happy to arrive home with a diagnosis and a way to control our hero’s challenging symptoms.