Visiting Vet

Choosing to do “nothing” can be tough, but sometimes it may be the right thing to do.

Michelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury. She can be reached at drjasny@comcast.net.

 

At 11 years old, Nana, the beagle, has been through a lot in her life. A skin condition from demodectic mange mites. A difficult pregnancy with only two of six puppies surviving. A mammary gland infection called mastitis while nursing. A painful infection behind her eye called a retrobulbar abscess. Tick-borne disease. But Nana is a survivor, taking each challenge in stride, still cheerful, still wagging her tail. Then a few years back she developed a lump on her hip.

“It doesn’t feel like a lipoma,” I said, referring to a type of benign fatty growth frequently seen in older dogs. Her owners consented to a “fine needle aspirate,” a quick diagnostic  procedure done in the exam room without anesthesia. Although rarely sufficient for definitive diagnosis, a pathologist can often give a general idea of what we are dealing with from an aspirate like this — in Nana’s case, possibly a malignant tumor.

“The pathologist says it’s probably a kind that doesn’t tend to metastasize,” I reported.  Cancers with high metastatic potential often spread from their original location to distant sites in the body, such as lungs, lymph nodes, or bones. Those with low metastatic rates tend to stay in one place but can be locally invasive and aggressive, causing serious damage. I still advised X-rays prior to surgery, just to be sure there was no evidence the cancer had spread. Her films looked fine so we proceeded to surgery.

Removing the growth, it was hard to tell where tumor ended and normal tissue began. Some masses are well-encapsulated, shelling out easily, but not this one. We cut as wide as possible, and sent it for biopsy. The final diagnosis was nerve sheath tumor, a low-grade malignancy with minimal risk of spread but significant chance of eventual recurrence.

“They can’t say for sure that we got it all,” I explained. “It may never come back, or it may regrow.” I offered options. More surgery. Referral to an oncologist. Radiation therapy.

“Let’s wait and see if it comes back,” Nana’s owners decided.

Time passed. Nana ate rat poison and was treated on emergency. She was okay. Nana binged on a stash of snack food, eating them bags and all — Fritos, Cheetos, Smartfood popcorn. Everything eventually passed. She was okay. Two years after her surgery, Nana started having a series of minor complaints. A swollen eye. Dental tartar. A fatty lump on her chest. A small lump reappearing on her hip. A cough. Addressing one concern after another, we eventually got to the cough. Her heart sounded fine, so not cardiac disease. Her lungs were clear, her temperature normal, so pneumonia was unlikely. Perhaps she had caught an upper respiratory infection, like kennel cough. We prescribed antibiotics, advising a recheck if the cough didn’t improve.

A few weeks later, the cough was better but not gone. A chest X-ray looked normal, and we made a presumptive diagnosis of allergic bronchitis, a common problem in older dogs.

“It’s worse in the mornings,” her mom shared. “Maybe the wood stove is bothering her.”

A logical theory, I agreed. We tried cough suppressants. We tried corticosteroids. The lump on her hip was growing slowly. We wanted to pursue a second surgery, but preferred to wait until the cough resolved.

“I think she’ll improve once spring comes, and we stop using the wood stove,” her mom said. Months passed. April arrived. Nana’s cough did seem better, though not 100 percent.

“It may never clear up entirely,” I sighed, suggesting we start preparing for surgery with preoperative blood tests. We offer two “levels” of screening. Her mom opted for the more comprehensive one. Good call. Everything came back completely normal, except one test. Nana’s calcium levels were elevated.

“It’s called hypercalcemia,” I explained, “but very often it is a spurious finding caused by lab error.” We repeated the test, this time fasting Nana overnight before the blood draw, and sending it to the big reference lab instead of running it here on our little machine. But the retest came back with the same results, confirming the hypercalcemia was real.

“Hypercalcemia of malignancy” is a condition in which a cancer produces a substance similar to the hormone normally responsible for regulating calcium levels. The body gets fooled, thinking it’s supposed to release calcium from the bones into the blood, thus causing the hypercalcemia. Lymphosarcoma and anal gland carcinomas are the most common tumors associated with this problem, not nerve sheath tumors. I checked Nana again. Her anal glands were fine. Maybe we were missing something? Although we had taken X-rays five months previously, we decided to snap more before proceeding with surgery.

There it was. A mass in her chest, just above and in front of her heart in an area called the cranial mediastinum. It was a really large mass, the size of a hefty avocado, compressing her wind pipe and bronchi. Without a biopsy, we couldn’t determine exactly what kind of cancer, but the radiologist doubted it was related to the nerve sheath tumor on her hip. Most likely it was a heart base tumor arising from the aorta or pulmonary artery, hemangiosarcoma, lymphosarcoma, or even a thyroid tumor. The radiologist was frank. “Masses in this location are often quite vascular making successful sampling both difficult and risky. CT or MRI . . . would be very informative but would require anesthesia and is more expensive.”

Definitive treatment requires definitive diagnosis, but was putting Nana through risky and painful procedures in her best interests when the long-term prognosis is very guarded?  We had followed a long trail, through the many maladies of her youth to a tumor on her hip, from a cough to hypercalcemia to a second, far more serious tumor. For now, Nana is still wagging that tail. We are trying various medications in hopes of controlling her cough and keeping her comfortable. Her owners have some difficult decisions to make. Choosing to do “nothing” can be tough, but sometimes it may be the right thing to do.

A leash is a training tool for your dog, and it is a method of giving you control so you can keep everyone safe — you, your dog, other people, other dogs.

Michelle-JasnyMichelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury. She can be reached at: drjasny@comcast.net.

Stopping at SBS for guinea pig bedding, I spotted a handwritten sign on the door. “Please keep your adorable dog on a leash…and please keep the leash in your hand.”  I had to laugh.

We have a similar policy at my office. All dogs must be on a leash. We see many interesting interpretations of what this means. There’s the client who lets Rover jump out of the car loose in my parking lot, then chases the dog through my budding crocuses, trying to connect the leash. Rule number one: attach the leash while you are both still in the car. Next comes Fido. His leash is attached to his collar, but the collar is two sizes too big. As soon as Fido realizes he’s at the vet, he puts on the brakes, backs up, and backs his head right out of the collar. The owner is left looking foolish, holding an empty collar dangling from the leash, while Fido books it, naked, down the drive. Then there’s Goofy, who has a well-fitted collar with a leash attached, but no one’s holding the leash. These clients obviously just came from shopping at SBS.

These may sound funny, but they can lead to serious consequences. Rover may head for the road. Being scared, and in unfamiliar territory, he may lose his street smarts and get hit by a car. Fido may not let us catch him. I remember a big, extremely shy malamute who was what we call a “fear biter.” After slipping his collar on my front steps, and bolting down the dirt road, he would not come to his owner nor let anyone get near him. We tempted him with treats, which he snatched eagerly, but if anyone, including his mom, tried get hold of him, he growled and snapped. Luckily, his dad arrived and persuaded him to jump into his truck before anyone got hurt.

Goofy, on the other hand, will let anyone grab him. Goofy loves everyone. “Oh, he’s very friendly,” his owners say when I admonish them about not holding the leash. Okay. That’s great. But let me tell you something. See Bluto, that big golden retriever, coming out of my office? The one Goofy is running over to greet?  Bluto was here for a behavior consult because he has aggression problems and almost killed another dog recently. If your “very friendly” Goofy runs up to very aggressive Bluto, we’ve got a problem.

A leash has several purposes. It is a training tool for your dog, and it is a method of giving you control so you can keep everyone safe — you, your dog, other people, other dogs. But certain types of leashes can actually be a liability. According to a 2009 article in Consumer Reports in 2007 there were more than 16,000 human injuries associated with leashes serious enough to require medical care. Burns and cuts were the most common injuries but there have also been reports of amputations when a leash got wrapped around a body part like a finger, and retractable leashes are thought to be responsible for many of these. Retractable leashes are extra long cords or sometimes web leashes that automatically retract into heavy plastic handles which have brake buttons and/or release buttons to lock or release them.  These leashes have become extremely popular and although there may be a time and a place for them if used correctly, they often can be bad for both dogs and people.

For dogs, retractable leashes do not foster desirable behavior. Instead of learning to heel and walk politely on his leash, Rover learns that he can pull on the leash, and pull, and pull.  Unless that leash is locked, it really doesn’t provide an owner with any control at all. If Rover decides to bolt, he can get up quite a head of steam before reaching the full length of the leash, at which point he may be suddenly jerked to a halt, sustaining back injuries as severe as intervertebral disc herniation. Or it may be the person on the other end of the retractable leash who bears the brunt of Rover’s momentum. I once had an energetic young Labrador bolt down my porch stairs on his retractable. The owner, an elderly man, stood on the porch holding that plastic handle. When the lab reached the end of her leash, she was going fast enough that instead of stopping, she pulled her owner right off his feet. He sailed down three stairs, landing on his side and breaking his hip. Not a happy day for any of us, and one of the reasons I am so cranky about clients controlling their pups on the porch. I don’t ever want to see you lying in my parking lot surrounded by EMTs.

Another danger is dropping that bulky plastic handle while the leash is still attached to the dog. A fearful dog may be scared by that handle clunking along behind him, leading him to panic, and increasing the risk of injury. In a recent article on the VIN News Service, behaviorist Dr. Laurie Bergman of Villanova, Penn., relates the story of a dog whose retractable leash was dropped in an apartment building stairway. The dog ran away from the handle that was “chasing” him up the stairs to the open roof, where he fell to his death. Admittedly, this is an extreme case, but there are many reported injuries to dogs from retractable leashes getting wrapped around their legs or even their necks.

Maybe a retractable leash is okay if you know how to use it properly, if your dog is already well-trained, and you want to take him for a semi-controlled romp on the beach. But if you are going for a walk in town, or working on obedience, or taking him to the vet, I highly recommend using a traditional nylon or leather leash, no more than six feet in length — and please hold the leash in your hand.

When pets die suddenly owners may attribute it to a “heart attack,” but dogs and cats don’t really get heart attacks.

I got an unexpected crash course in a few aspects of human cardiology recently when I started experiencing tightness in my chest. At first I convinced myself it was asthma, but knowing my family history of heart disease, and knowing the signs of a heart attack can be very vague in women, and knowing too many folks who ignored those warning signs with dire consequences, I eventually went to the emergency room at the Martha’s Vineyard Hospital. Four hours later, my X-rays, ECG, and blood work showed no abnormalities and I felt better, but Dr. Zack was sternly adamant. I could go home now, but must go to Mass General ASAP for a nuclear stress test, an evaluation that involves injecting radioactive dye, then taking images of the heart before and after exercise. These pictures would allow cardiologists to see if any areas of my heart muscle weren’t getting adequate blood flow.

While making travel plans, I thought about cardiac disease in dogs and cats. It’s not uncommon when pets die suddenly for owners to attribute it to a “heart attack.” But dogs and cats don’t really get heart attacks, we tell them. Before we go further, a brief disclaimer.  Damn it, Jim, I’m a veterinarian, not a cardiologist. (Okay, please dismiss all Star Trek references as a side effect of my recent illness.)

Seriously. I’m not a cardiologist, but to the best of my understanding, in human medicine what people refer to as “heart attack,” is an acute myocardial infarction. Acute means it comes on suddenly. Myocardial means “of the heart muscle.” Infarction is tissue damage or death caused by lack of oxygen due to an obstruction of that tissue’s blood supply. So a human heart attack, a.k.a. acute myocardial infarction, is caused by sudden blockage of one or more of the coronary arteries leading to damage or death of part of the heart muscle.

Sudden death. It happens to pets now and then. One day your dog or cat, Valentine,  seems perfectly normal. The next, he keels over and dies. It can be devastating for owners, who urgently want explanations for such unexpected losses. Many people’s thoughts go immediately to poison, especially if Valentine goes outside unattended, but most toxins an animal is likely to encounter around here, such as rat poison and antifreeze, will typically cause clinical signs of illness before an animal dies. “He must have had a heart attack,” is another common conclusion. Wrong. Dogs and cats generally do not get coronary artery disease and thus do not get myocardial infarctions. Perhaps it’s their diet, lifestyle, or just genetics, but they appear to be resistant to this particular cardiac problem. That is not to say there aren’t other conditions that can lead to sudden death.

A sidebar on terminology. The term postmortem is short for postmortem examination, the dissection of a deceased body. It comes from the Latin post, meaning after, and mors, meaning death.  Another term for a postmortem on a human being is autopsy. This word comes from the Greek auto, meaning self, and opsis, meaning sight, or eyes. Thus autopsia meaning eyewitness, or seeing with one’s own eyes. The word autopsy was first used to describe the act of dissecting a cadaver to determine cause of death in around 1670 and is technically reserved for when this is done on human remains. For nonhuman animals, the proper term is necropsy, from the Greek nekros, meaning dead body. The point of all this being that if your pet, Valentine, bites the dust unexpectedly, your veterinarian is probably not going to be able to tell you why without performing a postmortem examination, correctly called a necropsy.

One cardiac condition often proposed to explain sudden death in dogs and cats is ruptured chordae tendineae, fibromuscular cords of tissue inside the heart that connect little mounds called the papillary muscles to the heart valves. They are sometimes poetically referred to as the “heart strings.”  If Valentine ruptures one of these heart strings, it can result in sudden death. Theoretically this occurs primarily when there is underlying disease of the heart valve, but we rarely get the opportunity to do a necropsy and/or postmortem laboratory diagnostics to get definitive answers. Perhaps Valentine died of a ruptured brain aneurysm. An aneurysm is a blood vessel with thinning walls that cause it to bulge abnormally. It can suddenly burst, leading to fatal hemorrhage. Even when we do perform necropsies, we rarely examine the brain, so this is another theory we seldom get to prove.

Other common fatal conditions are easier to demonstrate. Middle-aged large breed dogs are particularly prone to a form of cancer called hemgiosarcoma. There tumors affect the spleen or the heart and can often lead to sudden, fatal internal hemorrhage. Presumptive diagnosis can be made by simply tapping the abdomen, or pericardial sac, depending on the location of the tumor, with a needle and syringe and seeing if there is free blood in these places. Other causes of sudden death can include ruptured spleen from trauma such as being hit by a car, electrocution from biting electrical wires, acute conduction disturbances in the heart causing fatal arrhythmias, electrolytes imbalances from adrenal gland disease, and a variety of genetic problems Valentine might be born with but which don’t cause visible symptoms until he suddenly expires.

By the time I got to Boston, I had fairly constant angina. After an abnormal stress test, they quickly admitted me to the ER, then the cardiac ward. Three days later, I was given what they call “conscious sedation,” and cardiologists placed two stents via an artery in my arm into my coronary arteries, restoring adequate blood flow to the affected part of my heart. Amazing technology. The main thing I remember was the cardiologist yelling at me to stop asking so many questions. I guess I was curious. I know I was lucky. My heart gave me warning. No actual heart attack. No sudden death. Just gratitude.

Michelle-JasnyMichelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury. She can be reached at: drjasny@comcast.net.

The term epulis comes from the Greek word epoulis, meaning gumboil. The word could be used to describe any mass on the gums, but in veterinary medicine, we use it to refer to a specific group of benign tumors that arise from the cells that form the periodontal ligaments.

There are a number of things I find confounding about these oral growths. The first is that the plural of epulis is epulides (pronounced e-pew-li-deez.) That always gets me tongue-tied. The second confounding thing is the fancy nomenclature used to identify the various types of epulides — and they keep changing the terminology.

There are basically three classifications of epulides. Bear with me now. We are about to encounter a whole lot of multi-syllabic words.

A fibromatous epulis (seven syllables) is a smooth pink growth on the gum, often near the upper incisor, canine, or premolar teeth. It may dangle from a stalk, or just be a thick flap protruding down around a tooth. The surface usually looks pretty much like the surrounding gum tissue, and is not irritated or ulcerated.

Next we have peripheral odontogenic fibromas (12 syllables), formerly know as ossifying epulides. These look similar but arise from bone-related cells called osteoblasts and feel more solid.

The third type is acanthomatous ameloblastoma (11 syllables), previously called acanthomatous epulis. These often look very different, having an irregular cauliflower-like appearance, and occur most frequently around the front incisors and canine teeth, on either the upper or lower jaw. Although classified as benign, these epulides are locally aggressive, invading the adjacent bone, and can be quite deforming. All these big words help veterinarians think about the source of the growths and how they should be treated.

Checking the teeth

So let’s take our dog, Gummy Bear. He’s come in for his annual physical exam. Let’s say he’s middle-aged. Most epulides occur in older dogs, with the average age being seven years. Maybe he’s a boxer, or a pug, since short-faced dogs are very prone to epulides, though they can occur in any breed. As part of our routine exam, we check Gummy Bear’s teeth. Maybe his gums are a little swollen or inflamed. Some dogs get a condition called gingival hyperplasia which is simply an exuberant growth of gum tissue that occurs in response to inflamation, trauma (such as a tooth chronically rubbing on the gum), infection, or certain medications.

Maybe he has a lot of dental tartar. We might recommend a dental cleaning, or home care like regular tooth-brushing with a doggy-friendly toothpaste. (Remember dogs don’t “rinse and spit” so dental care products must be safe for them to swallow.) Or perhaps his mouth looks fine except we notice a growth on his gums that looks like an epulis

What do I recommend? There are other tumors besides epulides that may occur in the mouth that can be very serious, such as squamous cell carcinoma, malignant melanoma, or fibrosarcoma.

If your veterinarian is concerned that Gummy Bear’s mass might be a malignant cancer, not a benign epulis, then you will likely be encouraged to authorize a biopsy. Sometimes we can nip off a small piece of tissue  right there in the exam room, but depending on the location, size, and shape of the mass, as well as the temperament of the patient, general anesthesia may be necessary to get a biopsy. In that case, your veterinarian may recommend just going ahead with definitive treatment. For fibromatous epulides and peripheral odontogenic fibromas, recommended treatment involves excising the mass, and often extracting the involved tooth and scraping out the socket (technically called curettage of the alveolus) to try to be sure all abnormal tissue is removed. Acanthomatous ameloblastomas, which invade the bone,  require much more aggressive surgery, actually removing part of the affected upper or lower  jaw bone. It is best to have this done by a board-certified veterinary surgeon. They may advise X-rays of the head to try to determine how invasive the epulis is, and/or chest films to rule out metastasis, though nowadays, more advanced imaging such as MRI or CT scans  can give much more accurate information.

Wait and see?

Most of the time, however, you probably won’t even know Gummy Bear has an epulis, unless it is unusually large or in an area affecting his ability to eat, in which case signs may include drooling, bad breath, and/or facial deformity. In those situations, surgical intervention is clearly advisable. But if a growth looks like a classic fibromatous epulis, is relatively small, and isn’t bothering Gummy or causing clinical symptoms, in my opinion, it is reasonable to take a conservative “wait and see” approach. If I have a dog anesthetized anyway for a dental cleaning, I will sometimes “debulk” an epulis, trimming it back to what looks like the normal gum margins (so it is less likely to be traumatized when the animal chews), but not extracting an otherwise healthy tooth and scraping the socket. And if Gummy doesn’t need anesthesia for other reasons, I will frequently just leave epulides alone, just having owners keep an eye on them. Veterinary oncologists and dentists reading this are now jumping up and down in their seats, yelling at the newspaper in protest, so I must qualify my statement.

I have heard it said by oncologists that “let’s wait and see” are the most dangerous words in the English language. Of course early intervention is often the smart choice, especially with malignant cancer or locally invasive and aggressive tumors. It’s also true that we cannot definitively predict how any growth will progress, so the conventional wisdom of many veterinarians is that all epulides should be removed. But I have seen numerous senior dogs with slow-growing benign epulides that were not removed and that had no significant effect on either their well-being or their longevity. So if Gummy Bear grows a gummy mass, discuss it with your veterinarian. What to do depends a lot on your personal philosophy, your finances, your veterinarian, and Gummy Bear’s exact circumstances.

Michelle-JasnyMichelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury. She can be reached at: drjasny@comcast.net.

“If an orange-faced Oompa Loompa and a grey-faced Oompa Loompa have babies, what percentage of their offspring will have orange faces?” my husband asks. My daughter is studying genetics and her homework is full of chromosomes, genes, dominant and recessive traits.  I smile as my daughter shouts gleefully, “One-fourth orange faces!”

In veterinary medicine, we deal with genetics daily. What’s the difference between Chihuahuas and Great Danes? They’re both dogs, but selective breeding for particular genes makes one huge, the other teensy. Genetics give us the smooshed faces of bulldogs, the wrinkled skin of Shar-Peis. Even behavior and temperament can be driven by genetics — herding behavior, guard dogs, dogs who like water, or retrieve, or track scents. A dog’s breed strongly influences personality and behavior. It also affects predisposition to certain diseases.

“You should review this record before the appointment,” my secretary suggested, the morning after the Oompa Loompas. “Sounds complicated.” The owner had dropped off a list of concerns about his dog, Aberdeen. Difficulty housebreaking. Not responding to commands. Acting like he’s lost. Odd blank stare. Unusual gait. Hypersensitivity to noise. Trouble gaining weight. I then did what every veterinary student is taught to do first. Look at the signalment. That means breed, age, and gender. All these impact the likelihood of various illnesses. Aberdeen was a 15-month-old intact male Llewellin setter. My first thought was that he was so young I should first consider congenital and inherited  problems. My second thought was what the heck is a Llewellin setter? I readily admit I’m kind of lame when it comes to knowing every breed. I have enough trouble remembering where I left my glasses. So I began researching.

The Llewellin setter is a specific “pure” strain of English setter tracing its bloodlines back to a 19th century dog breeder and sportsman named R.L. Purcell Llewellin in South Wales. Ignoring all the doggy politics about whether they are a distinct breed or not, for my purposes the pertinent information was that, medically speaking, they are English setters. Next I researched inherited conditions of English setters. Hip and elbow dysplasia — not relevant. Deafness -— interesting. Hearing-impaired dogs may be hard to train, act lost, not respond to commands. Oh, wait a minute. His owner said Aberdeen was hypersensitive to noise. Scratch deafness.

Then I saw a disease I had never heard of before — neuronal ceroid lipofuscinosis (NCL). An autosomal recessive genetic mutation that causes accumulation of abnormal stuff inside cells in the nervous system, which in turn leads to devastating progressive neurological dysfunction, NCL has been reported in dogs, cats, and humans. (In people it is called Batten disease or Familial Amaurotic Idiocy.) Canine breeds affected include English setters, Tibetan terriers, American Staffordshire terriers and bulldogs, border collies, Australian shepherds, Labrador retriever, Polish Owczarek Nizinnys ( no kidding), and  dachshunds.

Age of onset can span from one year in dachshunds to five years in Tibetan terriers but once NCL begins, it is progressive and typically fatal. Symptoms vary, breed to breed. Most develop vision deficits. Almost all exhibit a change in gait, loss of balance, or incoordination. Dementia with confusion, progressive decline in intelligence, and loss of prior training is common, as is hypersensitivity to sound, touch, and movement. Affected dogs may become withdrawn, fearful, or aggressive. Eventually dogs develop severe seizures and either die or are euthanized by two years of age. There is no cure.

When Aberdeen arrived, I didn’t want to unduly upset his owner. NCL is extremely rare. It was probably something else. Something simple. Something curable. I began my exam. Other than being thin, Aberdeen looked physically healthy. He heard when I made a loud noise. He blinked when I poked my finger at his eyes. His retinas looked fine. He had normal feeling and motion in his legs. Perched on my exam table, he seemed pretty normal, maybe a bit bemused.

“Let me watch him walk,” I said. Aberdeen’s hind legs moved a bit stiffly. His front legs lifted too high with each step as though marching to a drum only he could hear. His dad had mentioned that Aby had recently developed an odd way of cocking his head when offered a treat, so I held out a cookie. Aberdeen slowly extended his neck, tilted his head, then very, very slowly took the treat. I did it again. He did it again. I dropped a treat on the floor. I could tell he had seen and heard it drop, but now couldn’t seem to locate it, searching around an unusually long time before finally finding and eating the tidbit.

“I’d like to record all this and send it to the neurologist,” I said, grabbing my iPad. The owner used treats to entice Aby to walk back and forth as I filmed. Then Aberdeen spontaneously started walking in circles. His owner offered another treat. Aby cocked his head, stretched his neck, and suddenly started spinning in tight circles, like a kid break dancing. He was agitated and growling continually with his head held way up in the air. Dogs with ear infections or balance disorders will frequently have a head tilt and circle, but this was different. There was a weirdness to his behavior that we call “altered mentation,” a kind of dissociation that was clearly neurological. It was time to discuss NCL.

There is a blood test available to screen for the NCL genetic mutation in English setters, so we sent a sample to the researchers in Missouri. The doctors there viewed the video and agreed it might be NCL. If the test comes back negative, Aberdeen still clearly has a problem that should be evaluated by a neurologist who can do further testing and brain imaging. If it turns out to be neuronal ceroid lipofuscinosis, then sadly, there is nothing we can do, other than to alert the breeder that his line of dogs is carrying this rare but fatal genetic condition. If only all genetics were as fun and as easy as orange-faced Oompa Loompas.

Michelle-JasnyMichelle Gerhard Jasny, V.M.D. has been practicing veterinary medicine on the Vineyard since 1982 and writing the Visiting Vet column for more than 25 years. She lives and works in West Tisbury. She can be reached at: drjasny@comcast.net. 

Almost one year old, the playful Bernese mountain dog weighed in at nearly 90 pounds. When he first started behaving as though his back hurt, we weren’t too concerned. “He probably just strained something running around,” we said, prescribing rest and anti-inflammatory pain medication. When that didn’t help, we tried a muscle relaxant, but his symptoms continued. He began to whine and pace at night, sometimes yelping or leaping up suddenly when anyone brushed past him.

Here in the clinic, Bernie walked normally but was anxious, jumping around, and making it hard for us to pinpoint the source of his discomfort. We ruled out Lyme disease with a blood test and added a second pain medication. We discussed radiographs, but since he was so bouncy and would probably need sedation for that, we decided to wait a while longer.

One week later, Bernie slipped and fell on the ice. Immediately after, he developed “posterior paresis,” a weakness in the hind legs resulting in an abnormal gait usually indicative of a spinal cord problem, but we still couldn’t localize any particular place that hurt. “Let’s take those pictures,” I advised.

My main differentials for Bernie at that point included intervertebral disc disease (IVD) or fibrocartilagenous embolism (FCE). In simple English, IVD is a “slipped disc.” FCE is an embolism compromising the blood supply to the spinal cord. It typically affects large breed young dogs. Despite his youth, we also had to consider cancer, as Bernese mountain dogs are very prone to it.  Bernie was now sufficiently subdued to allow us to X-ray without sedation. The films looked normal, but that didn’t rule out anything. It just meant that whatever was causing Bernie’s pain was not visible on plain X-rays.

If it was FCE, there was no rush. FCE is not progressive. There is no specific treatment other than supportive care. The neurological deficits often resolve with time. If it was IVD, that often responds to corticosteroids and rest. As long as he could feel and move his legs, IVD wasn’t urgent, although surgery might ultimately be indicated to relieve pressure on his spinal cord. If it was cancer? Well, that would be a much bigger bridge to cross, should we come to it. We gave Bernie intravenous corticosteroids, prescribed more orally to give at home along with his pain medications, and added tranquilizers to keep him quiet and give his back a chance to heal.

But it was not to be that simple. Bernie’s condition worsened. It was time to consult the specialists.

On initial exam, the neurologist also could not localize Bernie’s pain. That made me feel better. At least I had not missed anything obvious. She and I spoke each day as they gathered information. New radiographs were suspicious for a fracture of Bernie’s third thoracic vertebral body.  No, the fracture wasn’t visible on the films we had taken earlier, and it wasn’t the kind of clean break one would expect from simple trauma. Besides, it would be unlikely for a big healthy puppy to fracture a vertebra just from slipping on the ice — and some of Bernie’s symptoms pre-dated his fall.

The radiologist reported a “moth-eaten” appearance to the bone consistent with either tumor or infection. Either of those might have weakened the bone, resulting in a “pathological fracture” when Bernie slipped. “I’m really concerned it may be a tumor,” the neurologist confided. “Or diskospondylitis, which is almost as difficult to treat.”

Diskospondylitis is a bacterial or fungal infection of the intervertebral disks and adjacent vertebrae. Most often seen in medium to giant breed dogs, especially German shepherds and great Danes, any breed can be affected. It is even occasionally diagnosed in cats. It typically occurs in young to middle-aged individuals, with males being affected twice as often as females. Symptoms vary depending on exact location and severity of the lesion and may develop slowly or suddenly.  Signs may include pain especially when trying to get up, reluctance to jump, a stiff gait, incoordination, weakness, weight loss, poor appetite, lameness, and fever. Radiographs may appear normal for up to a month after the infection starts, but eventually they reveal changes in the intervertebral disk space and adjacent bone. The bacteria are usually spread via the blood, though the primary source of the infection often cannot be determined. It may start as a urinary tract infection, a wound, a foreign body like a grass awn, even dental disease.

Bernie needed more tests — MRI, CT, biopsies, cultures. While waiting for results, the specialists started him on antibiotics. We all held our breath, fingers and toes crossed, that it would not be cancer. The CT confirmed the pathologic fracture and mild spinal cord compression consistent with either diskospondylitis or tumor. The  biopsy showed no cancer.  Urine cultures were negative. Blood cultures, however, were positive for staphylococcus, confirming the diagnosis of bacterial diskospondylitis. The concurrent “sensitivity panel” listed the best antibiotics to combat this specific infection.

Due to the location of his fracture and the presence of infection, surgical stabilization was not advised. We had to depend on Mother Nature to heal the break, and, with our help, to stop the infection. Bernie came home on long-term antibiotics, gradually decreasing corticosteroids, and a cocktail of pain medications. He was outfitted with an elegant vest with handles on the top so his family could easily assist him getting up and walking, though his exercise still needed to be restricted for many weeks as he heals.

This is only the third case of diskospondylitis I have knowingly seen in 30-plus years of practice. We have a saying in medicine — you can’t find something if you don’t look for it. It wasn’t on my initial differential list (that won’t happen again) and it required extensive sophisticated  testing to establish the definitive diagnosis and treatment.

The prognosis for diskospondylitis depends on the degree of spinal cord damage and the organism involved, but Bernie has been improving steadily and we are very hopeful he will make a full recovery.

 

Sipping my morning tea, I was expecting a mellow Monday. January on the Vineyard, not many appointments scheduled. Then the phone rang. Pip, a 12-pound Cairn terrier mix, had found and consumed part of a block of rat poison.

“Bring Pip. Bring the block. Bring the poison container. Now!” I said.

When a dog eats a potentially toxic substance, it sometimes makes sense to do the math to determine if the amount ingested is truly dangerous before rushing to the vet, but in this case, with rat poison, and such a small dog, it was a case of better safe than sorry. When Pip arrived, we instilled a smidgen of apomorphine under her eyelid where it would be rapidly absorbed and tell her brain that she should vomit.

As she deposited multiple piles of bright green barf on strategically placed newspapers, I examined the rat poison container. Most rodenticides are anticoagulants, i.e., they work by interfering with blood clotting. The nice thing is that there is an easy antidote as long as you begin treatment immediately after ingestion, so I wasn’t initially too worried. Then I read the label.

“Drat,” I swore. “It’s not an anticoagulant. It’s bromethalin.” Bromethalin is a potent neurotoxin that works by disrupting nerve function, leading to central nervous system signs and death by respiratory paralysis…and there is no antidote. “Good thing you got here quickly,” I sighed.

The bait had been in a location that the owner thought the dog couldn’t reach, but somehow Pip had managed. Maybe some big rat had dragged it out. Who knows?

We carefully determined the maximum amount of bait Pip could have eaten. I did the math. LD 50 is shorthand for “Lethal Dose 50%,” the amount of a substance that when ingested will kill 50 percent of the animals. Pip’s exposure was probably about half the LD 50, enough to still be worrisome (though from the mess on my exam room floor, it looked like she had thrown up most of it.).

“We’ll give activated charcoal to help prevent further absorption of any poison left in her gut,” I said. “Take her home and watch her like a hawk. Call if you see anything like hyperexcitability, tremors, or seizures.” If Pip did develop clinical signs, all we would be able to do was give supportive care and hope she would survive.

I went on with my day with a constant nagging worry about Pip in the back of my mind, but as each hour passed, I relaxed a bit more. Then, late afternoon, just when I was feeling confident Pip would be fine, the phone rang. Another dog had just eaten a bottle of ibuprofen.

The dog’s name? Pip. I’m not making this up. This Pip, also a terrier mix, was a bit bigger, at 28 pounds. “Bring Pip. Bring the pill bottle,” I said.

The effect of ibuprofen toxicity in dogs is dose dependent. At lower doses it can cause severe gastrointestinal irritation, even ulceration. Moderate doses can lead to kidney failure, and high doses to central nervous system dysfunction. Fatalities are not uncommon. When Pip arrived we gave him apomorphine while I did the math. His owner thought the bottle had only been half full, maybe less, but couldn’t be sure. It sure was empty now. I read the label. 200 mg tabs. Fifty tabs when the bottle was full. For Pip’s size, 11 tabs would put him at risk for fatal kidney damage.

When Pip hurled, we could only find the remnant of two pills in the vomitus. Did that mean he had only eaten two? Or had he eaten 20 and the rest had just moved down into his intestines. Better safe than sorry. We instituted a treatment protocol of activated charcoal, gastric protectants, antacids, and intravenous fluids. It would be three days before we could be sure he was out of the woods. On Tuesday, we continued his intravenous fluids.

Pip One’s mom reported all was well. I went about my day, no longer worried about Pip One, but concerned about Pip Two. That afternoon another client called. Her dog was drooling and his lips were a bit swollen. Yesterday, on their walk, he had eaten something he found in the woods that was red and crumbly and looked kind of like plastic. She had taken it away from him and still had the remains.

Was his name Pip? I joked. No, it was Booley. “Bring Booley. Bring the red stuff,” I said.

When Booley arrived, I examined the remnant of red, waxy, material. It had a ridged surface pattern and bits of bird seed. All the rat poisons I was familiar with were green, but this sure looked and felt like a rodenticide. A little research determined it was, in fact, the anticoagulant brodifacoum. Since Booley had eaten it the day before, it was too late for vomiting or charcoal. He had already absorbed whatever toxin he had consumed.

Anticoagulant rodenticides are tricky as they take three to five days to cause symptoms. People think that because the dog looks fine at first, they will continue to be fine. Not. Once they start bleeding, the prognosis for survival plummets. I did the math. Worst-case scenario, Booley might have consumed one tenth of the lowest reported LD 50. That is right at the cut-off point where specialists advise treatment. Better safe than sorry. We started Booley on the antidote, vitamin K, advising his owners to keep him quiet and watch carefully for any signs of abnormal bleeding.

By Friday, Pip One was fine, his owner planning how to make the rat poison inaccessible in the future. Pip Two’s mother reported he had rolled on a dead fish and was pretty proud of himself. Booley seems okay, but because brodifacoum is a long-acting poison, he will need 30 days of Vitamin K.

I made myself another cup of tea, hoping for a quiet weekend. After all, it’s January on the Vineyard.

The three kittens in the carrier peered out curiously. “We weren’t going to get purebreds again,” one of the owners said. The couple had shared their home for years with a beautiful pair of Burmese cats who were now gone. “Then we read about Tonkinese and couldn’t resist.”

Looking at that trio of exquisite faces peeking through the grate, I understood completely, but I didn’t know much about the breed. To me the word Tonkinese conjured up images, not of cats, but of the musical South Pacific. (“How far away, Philadelphia, P.A….from coconut palms and banyan trees and coral sands and Tonkinese.”) I, too, was curious, so I did a little research.

Tonkin is the name given by the French to the northernmost region of Vietnam. In the 1900s, indigenous people from this area emigrated to work on colonial plantations on the island of Vanuatu (formerly called the New Hebrides). Referred to as “Tonkinese” by westerners, James Michener wrote about them in “Tales of the South Pacific,” on which the famous musical was based. So what about Tonkinese cats? Are they from Vietnam, too?

The breed called Tonkinese was developed in North America in the 1960s by crossing Siamese and Burmese cats, so let’s start there. Siamese cats are thought to date back at least to the 1600s. Their introduction to the West began with a pair named Po and Mia given to a departing British Consul-General by the Siamese king in 1884 (Siam, of course, being modern day Thailand). The Siamese Cat Society of America was founded in 1909. Over the decades Siamese breeders altered their appearance to have a thinner body, elongated head, long, skinny legs, and unusually large ears. The Burmese breed began with a single small walnut-brown cat named Wong Mau brought from Asia by a sailor in 1930 and given to Dr. Joseph Thompson in San Francisco. The doctor bred Wong Mau to Siamese cats and, using selective breeding, developed a consistent coat color called sable. Burmese eventually became recognized as a separate breed, with four officially accepted colors — sable, champagne, platinum, and blue.

In the mid-1960s, two breeders in North America began crossing Siamese and Burmese, working to develop a specific “moderate” breed they agreed to call Tonkinese. So, no, Tonkinese don’t actually come from the Tonkin region of Vietnam, but they are descended from cats that originated in southeast Asia. Tonkinese now come in 12 officially recognized colors with varying levels of contrast between body color and “points.” Most have dramatic aqua eyes. Because they started out as hybrids, theoretically Tonkinese are less likely to have inherited medical issues than breeds like Burmese, which have narrower gene pools.

One of the three kittens had an upper respiratory infection, giving his owners a bit of a scare, but this fairly common condition is rarely serious, and Kitten One soon recovered. Then, at five months old, Kitten Two suddenly began pawing his face. We’re not talking gentle rub-the-face-with-the-paw. Two was having repeated intense episodes of frantically clawing at his mouth. His dad even shot a video for me.

“Let’s take a look,” I said calmly, trying to soothe the owner’s anxiety. Two was acting the way a dog does when a bone or stick gets lodged in the mouth. I expected to find something in Two’s mouth, remove it, and be a hero. But I couldn’t see anything unusual. “Let me check under his tongue,” I continued. Occasionally cats playing with string or thread will get it caught around the tongue causing similar behavior. Nope. Nothing under the tongue. The only thing I could see was Two was teething. His adult canines and premolars were erupting and the associated gums were a bit red.

“We read on the Internet about some kind of serious mouth problem in this breed,” the owner volunteered.

“I think he’s just teething,” I stammered, “but I’m not sure.” We decided I would give Two pain medication and keep him for observation while doing further research.

Who knew? It’s called FOPS. Feline Orofacial Pain Syndrome. First recognized in the 1990s, it is characterized by severe oral pain and self-mutilation. It is most common in Burmese cats. Signs can be intermittent or continuous and can be triggered by eating, drinking, grooming, or stress. Current information suggests that there are two different age ranges when FOPS is likely to occur. The first is around six months of age and is associated with teething.

Bingo. There’s our diagnosis for Two.

The second time it occurs is often between 10 and 12 years old. FOPS is defined as “neuropathic pain,” an exaggerated response to a normally painful stimulus. It appears to be a genetic dysfunction of the processing of information from the trigeminal nerve in the brain. Definitive diagnosis is based on clinical signs and by ruling out everything else. This could mean dental X-rays and referral for expensive tests like MRI. The more I read, the more worried I became. Often multiple drugs are needed to control symptoms, sometimes even anticonvulsants. In one study, 10 percent of cases ended up with unremitting, severe self-mutilation leading to euthanasia.

Luckily, Two responded to the first pain medication we tried. He was still pawing, but much less. One article reported that antibiotics can be helpful in cases with underlying dental infections, so we gave an injection of long-acting antibiotic and sent him home with additional doses of pain medication. In case things got worse, we ordered a second recommended drug in kitten-sized tablets from a compounding pharmacy. But we never needed them: within a few days, Two seemed back to normal. I breathed a cautious sigh of relief.

Seventy percent of FOPS cases recur. All we can do right now is hope that Two is in the other 30 percent. Because of the suspected genetic basis, individuals with the syndrome should not be bred. Two’s owners are fine with that. They just want One, Two, and Three to live long, happy, and healthy lives.

When my daughters were little I read them the Little House On The Prairie series. We loved learning about life on the frontier. The simple pleasures. The ingenuity. The hardships. Sometimes we watched the television show based on the books.

What always struck me was what happened when someone needed a doctor. Pa would hitch up the horse and buggy, then ride as fast as he could into town to find Dr. Hiram Baker, the local physician and veterinarian. When he got to Doc’s office, Pa often found that no one was home. The doctor might be ten miles away, delivering a baby, or tending someone on their deathbed. As far as I remember, there were almost no telephones in Walnut Grove. There were certainly no pagers, no cell phones. Pa couldn’t call, text, or email. If he needed Doc badly enough, he had to physically go track him down. My children couldn’t imagine such a world.

“Well, when I was your age, there were no home computers,” I said while driving them to school. “No wi-fi. No Google. If you wanted to find something out, you had to go to the library, search your subject in a card catalog, find the book in the stacks, look in the index, and see if that book could answer your question.”

They looked aghast. “I love Google,” one sighed. I agreed. It is very cool to have so much information right at our fingertips. Unfortunately, it means we also have a lot of misinformation at our fingertips.

When clients bring me tomes downloaded from “Dr. Google,” I have to wade through all their research, separating the wheat from the chafe. I don’t want to ignore an owner’s efforts. Perhaps there is some new treatment I am not aware of that might be useful. It’s nigh impossible for one lowly veterinarian to keep current with all the advances in medicine these days. But most of the time, I find they are bringing me information about some 21st-century equivalent of snake oil or magic beans.

Then there’s Facebook. I resisted mightily for a long time, but eventually joined in order to find an old friend. Then several old friends found me. That was nice. Then clients started to friend me. Okay. I like my clients. Then people I didn’t know started sending Friend Requests. “Do I know you?” I wanted to ask, but that seemed so rude. Then people started messaging me veterinary questions. All the time.

“It’s bad enough I can’t go to Cronig’s without having to talk about fleas,” I thought grumpily. “Can’t I even waste time on FB reading about everyone else’s perfect lives (children, vacations) without having to play James Herriot!” I longed to move to Walnut Grove where Pa would never hitch up the buggy after dark or on a weekend just to bother Doc about fleas or diarrhea. But in the midst of my Bah Humbugging, I happened to see that one of the animal-focused Facebook folks had shared a link about veterinarians and burnout along with a lovely comment encouraging people to appreciate their veterinarians.

Burnout. Also called compassion fatigue. It is a kind of physical, emotional, and/or mental collapse brought on by overwork, stress, and isolation. Medicine has come a long way since Doc Baker’s day, which is all well and good, but for physicians (and veterinarians) it means a huge amount of ever-burgeoning information to be mastered. This has led to a statistically proven increase in burnout among doctors, often manifested by substance abuse, depression, even suicide.

Doctors on the front lines of health care are at highest risk because they usually work the longest hours for the lowest pay. Primary care docs have a higher rate of burnout than specialists such as dermatologists or pathologists. (Though when you see how busy dermatologists are here on the Vineyard, there’s no doubt they have their share of overwork and stress.). General practice veterinarians are in a similar situation to primary care physicians, facing long hours, hugely diverse demands, and lower pay than their specialist colleagues.

People who are caregivers for the chronically or terminally ill also suffer from the depression associated with burnout. Faced day in, day out with a situation in which a patient doesn’t get better, it is not unusual to succumb to feelings of helplessness and hopelessness.

For veterinarians, because our patients typically have much shorter life spans than human beings, we see an awful lot of death. Probably more than your average primary care physician.

We also play a particularly poignant and personal role, guiding people through decisions about euthanasia, then personally performing the actions that lead to an animal’s passing. Add the loss of control of one’s time that comes with doing emergency work, and technology that now enables us to be available 24/7, and you end up with an emotionally exhausting life. Especially when you consider that most of us went into this business because really, we actually do love animals. Some of us even like the people that own the animals.

And hard as it is for you to lose your beloved pet, it’s hard for your veterinarian too. Hard for us to feel like we couldn’t fix the problem. Hard for us to say good-bye to animals we may have known since they were puppies and kittens. Hard to see you grieve. You, our clients, who often over the years have become our friends.

People in all walks of life suffer from burnout, from depression, from hidden struggles. It’s a good time of year to remember to open our hearts to each other. In the words of Laura Ingalls Wilder, “Christmas Eve was the time when everybody was unselfish. On that one night, Santa Claus was everywhere, because everybody, all together, stopped being selfish and wanted other people to be happy. And in the morning you saw what that had done. ‘If everybody wanted everybody else to be happy, all the time, then would it be Christmas all the time?’ Laura asked, and Ma said, ‘Yes, Laura.'”

Landon has never been a dog who hides his feelings. Adopted from an off-Island shelter six years ago, no one knew for sure how old this sweet beagle was nor much about his medical history, but when anything hurt, Landon let us know loud and clear with a classic hound dog howl. He suffered periodic neck and back pain, yelping in anticipation if his mom went to lift him. As he got older, he developed a heart murmur, a cough, a benign growth inside his eye called an iridociliary cyst, and a case of separation anxiety. He made himself sick eating chicken bones from the trash and chocolate chips off the counter, but his mom adored him, nursing him tenderly through one thing after another.

As his veterinarian, it was often hard to know when something was really wrong, since Landon would scream any time I touched him. Did his leg hurt, or was he just anxious? What about that tooth? It looked fine, but he shrieked whenever I tried to examine his mouth. I was just thankful his owner knew I was not, in fact, torturing her beloved pet when he carried on this way in the exam room. But when he arrived on emergency late one night there was no doubt Landon’s distress was real. Earlier that evening he had been restless and breathing hard. She had called me, but knowing Landon’s propensity for drama, I hadn’t been overly concerned. “Let’s see if he settles down overnight,” I said, suggesting a little Benadryl to calm him, but several hours later his owner decided he truly needed urgent care.

She was right. Landon walked in my door, his breathing rapid and labored, his stomach heaving in and out as he tried to move air. He held his neck stretched forward in his efforts to breathe and had been coughing badly at home. Putting my stethoscope to his chest, I immediately heard loud crackles. “Sounds like fluid in his lungs,” I said. “And that heart murmur is much louder.”

Landon looked like a classic case of acute congestive heart failure (CHF), a cardiac illness that is usually characterized in dogs by sudden onset of fluid in the lungs. The underlying heart problem may vary. Elderly small dogs often have heart valve disease. Certain large breeds such as Doberman pinschers are prone to a genetic condition affecting the heart muscle called cardiomyopathy. Regardless of the initiating cause, the result is often pulmonary edema — fluid in the lungs. Symptoms may include coughing, rapid, labored respiration, and an elevated heart rate. Landon fit the picture and we made a presumptive diagnosis of CHF.

“I’m giving him a diuretic to draw the fluid out of his lungs, and other medications to support his heart,” I said, then explained how to monitor his sleeping respiratory rate (SRR) at home, i.e., the number of breaths per minute when he was fast asleep. “We’ll repeat doses of the diuretic until his SRR is less than 40. Tomorrow we’ll take radiographs. Maybe consult a cardiologist.”

The next day Landon’s SRR was down to 36 and he was feeling fine, but I still wanted X-rays of his heart and lungs. The films surprised me. There was a little fluid in his lungs, but his heart looked pretty normal. His liver and spleen, however, were enlarged.

“Let’s run a few blood tests,” I suggested, beginning to question my late-night diagnosis. A chemistry profile revealed a few abnormalities including elevated liver enzymes. Moving on to a complete blood count (CBC), my in-house machine kept refusing to register a white blood cell count, lights flashing and error messages telling me to make and examine blood smears under the microscope. That’s what we did, and in no time flat realized that something was desperately wrong. There were way too many of the white blood cells called lymphocytes. Way way too many. A sample sent to the pathology lab the next day confirmed our fears. At more than 10 times normal, Landon’s lymphocyte count was consistent with a diagnosis of lymphoid leukemia.

Lymphoid leukemia is cancer of the bone marrow resulting in a huge proliferation of one specific type of white blood cell, the lymphocyte. It is classified as acute or chronic.

Chronic lymphoid leukemia (CLL) often has an insidious onset with virtually no clinical signs initially. It progresses slowly, leading to weight loss and lethargy. Treatment can be delayed until the dog is feeling poorly. Survival times with chemotherapy range one to three years.

Acute lymphoid leukemia (ALL) has a more dire prognosis with less than half responding to chemotherapy and an average survival time of two to four months. It is more common in younger animals, around four to five years old, but older dogs may be affected. Signs may include lethargy, weight loss, poor appetite, nose bleeds, bruising, increased respiratory rate, labored breathing, lameness, and/or enlarged liver and spleen. Sometimes a pathologist can differentiate ALL from CLL on the CBC, but in Landon’s case we would need additional tests — flow cytometry, ultrasound, possibly liver, spleen, and/or bone marrow aspirates.

Landon’s mom was faced with tough choices. The prognosis for ALL was very poor, no matter what we did. CLL might be treatable, but the medications are extremely expensive. While we were still considering the options, Landon suddenly developed another problem, one more consistent with ALL. He went blind in one eye, the eyeball bulging and red. Despite having been surprisingly stoic so far, he now was obviously in pain and his owner was increasingly concerned about his quality of life.

We started oral corticosteroids in hopes of making him feel better, maybe even getting temporary remission, also eyedrops to lower intraocular pressure, and analgesics for pain. Once again, Landon rallied.

We know his time is short, but we’re taking it one day at a time. Landon is not a dog who hides his feelings, and we trust he will tell us when it’s time to say good-bye.