Visiting Vet


One of the fun parts of writing my column is naming the animals. For hypothetical cases, I might choose something silly. Sweetie Pie, the diabetic cat. Polly Dipsia, the dog who drinks excessive water. When reporting about actual pets, I use pseudonyms to protect the privacy of the owners. Dogs don’t seem to care much. Cats like to read about themselves in the paper, but they know my pseudonym choice is irrelevant as it is never their true “deep and inscrutable singular name.”

Sometimes I go obvious. Tom, the cat, becomes Dick or Harry. The dog Grover becomes Elmo. Sometimes I take a more circuitous route. Leopold becomes Kinshasa. (Know your African history?) Charlotte becomes Currer. (Check out pen names of the Bronte sisters.)

When I write about patients, it is often in the midst of caring for them. Researching the latest helps me keep current medically while simultaneously gathering information for the column. The upshot, however, is that I often don’t know how things are going to turn out when we go to press. A gentleman recently left me a message inquiring about the outcome of one story. “What happened to Thunderbolt? Please call back.”

I was happy to reply, but being a pseudonym, I had no idea who Thunderbolt was or what problem he had. I racked my brain. I checked my old articles about thunderstorms. I thought about dogs named Zeus or Thor. I searched my data base for various terms. I finally gave up. I couldn’t remember. Here at the office we have computerized reminders for follow-up calls. I plug in data when a pet goes home, and later my staff calls owners and gets updates. You don’t have that option, so today here are progress reports about some cases you may have read about in these pages.

Isaac, the overweight golden retriever who went acutely blind soon after starting weight loss medication was diagnosed by MRI with immune-mediated meningitis of unknown cause. The neurologist does not think it was related to the diet medication, though we opted not to use it again with him. He has been on corticosteroids for a year. His vision returned quickly, though when we first tried to lower his cortisone dose he relapsed slightly until we bumped it back up. He’s doing great now, though still plump, and we are very, very slowly weaning down his medication.

Tunny, the border collie cross with autoimmune hemolytic anemia received multiple blood transfusions and other treatment at the specialists but then had to come home a little before the doctors would have liked. He’s doing well on a variety of long-term immunosuppressants as well as medications to protect his gastrointestinal tract from side effects and anticoagulants to lower the risk of blood clots. I was a little concerned about how long it has been taking for

his blood counts to normalize. In my 30 years of practice, all the AIHA cases I have seen either got completely better or passed away by this point, but I check in with the specialists regularly and they reassure me everything is on track.

Don Quixote, the big lab with neck pain who was collapsing and virtually unable to walk, had an MRI that revealed a large lesion in his spine. At first we thought it might be cancer, but it turned out to be a ruptured disc that was removed surgically. Don is dancing around now almost as though nothing ever happened.

Sylvester, the diabetic Maine coon cat, had less definitive results. The special diet did not get his blood sugar under control. Before starting insulin, we decided to send him to the neurologist, who noticed abnormalities in his front legs as well as his hind. She is concerned he may have a primary problem with his muscles or nerves, unrelated to his diabetes, but recommended regulating his blood sugar with insulin first. If he doesn’t improve, the next steps may be MRI, muscle biopsies, or other specialized tests to evaluate his neuromuscular function.

Piglet was the cat with the recurrent urinary tract blockage who needed the penile amputation surgery called a perineal urethrostomy. Surgery went well, after which, on the advice of some specialists, I stopped his antibiotics. Big mistake. Piglet’s kidney failure worsened dramatically soon thereafter. We obtained a urine sample, and cultured a nasty bacteria that turned out to be susceptible to only a very limited number of antibiotics. I prescribed one available at the local human pharmacy. His owners gave it to him faithfully, as well as daily subcutaneous fluids at home. The renal failure turned out to be completely the result of bacterial pyelonephritis, i.e., a kidney infection, which resolved with a month of treatment. He has gained two pounds, his kidney function is normal, and he’s peeing beautifully. It’s funny the things that make me happy.

Maya, the rottie who I was afraid might have the uterine infection called pyometra that is life-threatening without emergency surgery, happily survived to bark another day with just oral antibiotics. But her problem is likely to recur with each heat so her owner is thinking about having her spayed despite her senior age.

Blanche, the cat with feline infectious anemia, and Coal, the kitten with anaplasmosis, both recovered completely with antibiotics, though sadly Coal passed away from other causes. Zev was the cockapoo with the cardiac problem called AV block. The cardiologists suggested a pacemaker, but Zev was not a young dog, so his owner decided to just enjoy whatever time he had left. We had hoped he might live for many months, but he passed away peacefully in his sleep soon after his diagnosis.

I’ve scanned back through years of articles to glean these follow-ups. Still haven’t found Thunderbolt. And now I’ve misplaced the message slip with the caller’s name and number. Perhaps it will come to me, suddenly, like a bolt of lightening. Or maybe you will call and remind me. Please. I promise to report how things turned out.


You know you’re getting old when women your own age, or even younger, start showing up with Little Dogs. We’re talking dogs that fit in your pocketbook — Yorkshire terriers, teacup poodles, Chihuahuas.

As a teenager, my family had a diminutive cocker spaniel I adored, but by college I youthfully dismissed any canine under 50pounds as Not A Real Dog. I longed for a statuesque Irish wolfhound, but settled for an Irish setter husky cross (who, sadly, ended up having the worst traits of both breeds). As an adult I adopted Heidi, a Labrador with diabetes and cataracts, then Sadie, a Samoyed with glaucoma. Both were blind, but both were big. Then when my kids came along, we got Flower, a mixed breed pup who grew large enough to be a passable substitute for the often requested pony. My younger daughter inherited my penchant for large dogs, yearning for a great dane or Swiss mountain dog, both of which I tell her she can have when she has her own house, hopefully bigger than the one we live in now. But the older I get, the more I understand about owning Little Dogs.

Animals intentionally bred for extreme physical characteristics, like being extra big or extra small, are at greater risk for medical problems. Giant breed dogs have notoriously short life spans, as well as a predisposition for problems like bloat. Pug-faced dogs are known for respiratory difficulties from their smooshed-in snouts. Little Dogs…well, they have their own list.

Take Amigo, the Chihuahua, who came in recently for an introductory examination. At six months old, he weighed less than four pounds. “I can’t let him outside unattended,” his mom said. “A big hawk buzzed him the other day. It just came out of nowhere.” I nodded.

Another Chihuahua owner I know was walking her wee one on a Vineyard beach when a red-tailed hawk swooped down, grabbed her pup by the head, lifting it several feet into the air. Whether it was the weight of the dog, or the effect of an hysterical woman screaming and waving her arms frenetically, the big bird lost its grip and the Chihuahua tumbled to the ground. Miraculously, except for several puncture wounds from the talons, the pup was uninjured. Yup. Better not let Amigo run around outside taunting the local raptors.

Examining young dogs always includes checking for congenital defects, i.e., abnormalities they were born with. Amigo looked fine. Eyes, ok. Teeth, no overbite or underbite. I opened his mouth to look for cleft palate. Nope. I ran my hands over the top of his domed head, gently feeling where the various skull bones join across the crown. Except Amigo’s skull bones didn’t all join in the middle. Instead there was a central area about the size of a nickel that was soft and squooshy.

It’s called a fontanel — a membrane-covered opening between the bones of a young skull. If you’ve raised a baby, you know those “soft spots” on an infant’s head that allow it to squeeze through the birth canal. In people, fontanels close gradually between the age of three months up to two years. In dogs, the fontanel on top of the head should close by 12 weeks of age. But in Chihuahuas, as well as several other toy breeds, the fontanel often doesn’t close. Ever.

Chihuahua fanciers call it a “molera,” saying that it is normal for the breed, and it is not considered a defect by the American Kennel Club Breed Standards. In fact, for many years, the presence of a molera was considered proof of the purity of a dog’s Chihuahua blood line. Here’s where breeders and veterinarians may be at odds. Many veterinarians consider any fontanel that does not close by 12 weeks to be an inherited defect and advise that the dog in question not be used for breeding.

There is also some controversy as to the health implications of persistent fontanels. (A brief aside about grammar. Many people call this condition an “open fontanel.” Technically speaking, that is redundant: by definition, a fontanel is open.) Some veterinarians believe that persistent fontanels are associated with greater risk of hydrocephalus — increased accumulation of cerebral spinal fluid inside the ventricles of the brain. This puts pressure on the brain and can lead to seizures, blindness, pressing of the head into corners, and extreme difficulty in house training. Hydrocephalic dogs may also exhibit the “setting sun sign” in which the eyes point downward and sometimes to the outside. They can be treated temporarily with medications to reduce the pressure, but eventually a shunt should be placed surgically to drain the excess fluid. In their “Molera Statement,” the Chihuahua Club of America cites several studies and veterinarians stating that there is “adequate medical evidence” that a molera does not predispose a Chihuahua to hydrocephalus. But I think the jury is still out on this one.

Amigo was well past the 12-week mark for closure of the fontanel, but some Chihuahua sites claim moleras may continue to get smaller until a dog is up to three years old. I do not know if this is true. I do know that since Amigo appeared neurologically normal there was nothing else we needed to do. If he ever showed signs of hydrocephalus, an ultrasound of the brain could be done via the fontanel, but he has a perfectly good chance of leading a perfectly normal life and never having any problems. I advised his owner to take extra care with his head and to never press the soft spot. If she wanted, there were even places she could purchase a tiny helmet for him. I wondered if Amigo would tolerate such headgear. Then I thought how cute he would look and imagined myself toting around a four-pound dog wearing a mini-bike helmet. That could be as cool as having an Irish wolfhound.

The older I get, the more I understand the charm of Little Dogs.

— Photo courtesy of

Every year at his physical exam, I gaze into Bingo’s big brown eyes. Being a pug, those eyes — well — they bug out a bit, but that’s part of his charm. Adopted from the shelter at the age of two, he’s eight now and handsome as ever. This year, however, I noticed a change. “Let me get the big light,” I said, rolling the lamp around the table and shining the beam at Bingo’s face, giving me a better look at his corneas.

The cornea is the outer transparent surface of the eyeball — at least it’s supposed to be transparent, but in Bingo’s case it looked as though someone had splashed a blotch of brown paint on each eye at the inner corner closest to the nose. Bingo has pigmentary keratitis, a condition that can occur in response to a variety of different stimuli that irritate the eye, leading to the appearance of these brown opacities in the corneas. It is most common in brachycephalic dogs. That’s a fancy word that literally means “short-headed” and refers to breeds such as bulldogs, Pekinese, Shih tzus, Lhasa Apsos — and pugs. A recent study showed that as many as 82 percent of all pugs are affected with some degree of pigmentary keratitis.

So what are the different stimuli that may be irritating all these eyes? And why are our smoosh-faced friends so frequently affected? Here’s why I love ophthalmology — all the great words: buphthalmos, exophthalmus, lagophthalmos, distichiasis, trichiasis, keratoconjunctivitis sicca, entropion, to list a few. Let’s start with simple anatomy. Pugs tend to have unusually large eyeballs. That’s buphthalmos. Because of how their faces are pushed in, they also have shallow eye sockets, resulting in bulging eyeballs. That’s exophthalmos. Large, bulging eyeballs may mean that when they close their eyelids, the lids may not completely cover the globes. That’s lagophthalmus. Taken all together, what do you get? Chronically exposed corneas, irritation, and pigmentary keratitis.

“Does he sleep with his eyes open? I asked. “Or do his eyes not close all the way when he shuts them?” His owner responded that Bingo slept with eyes closed and she thought the lids covered the globes fully.

What else could lead to his corneal irritation? Looking closely, I could see that a small bit of Bingo’s lower eyelids curled inward, rubbing ever so slightly on the corneas. This is called entropion. Bingo also had very pronounced nasal folds — those adorable rolls of furry skin on his face. Bingo’s nasal folds were prominent enough that when he moved in certain ways, the fur on the folds touched his corneas. This is called trichiasis, when normally occurring hair touches the eye. Both his entropion and trichiasis could be contributing to his keratitis.

There were two more similar conditions I needed to rule out — distichiasis in which aberrant hairs grow out of little glands that line the eyelid, and ectopic cilia, abnormal eyelashes growing from the inside of the lids. Using a magnifying headset and then an ophthalmoscope, I scrutinized the margins of Bingo’s lids but could not see any evidence of these.

Now it was time to check for keratoconjunctivitis sicca. Commonly known as KCS or “dry eye,” in this condition the dog does not produce adequate tears to lubricate the eye. Constant dryness results in irritation and inflamation. We measure tear production by tucking a small strip of special calibrated paper in the corner of the eye for exactly one minute. Bingo was not thrilled with this procedure, but we were able to determine that he appeared to be making a normal amount of tears.

Some dogs, however, make sufficient quantity of tears yet still have poor “tear film quality.” In other words, they have an inherent deficiency in the viscosity of the tears, so the fluid breaks up too fast, not keeping the eye properly protected. I put a drop of fluorescein stain in each of Bingo’s eyes. This non-irritating, water-soluble dye, starts out as orange, then turns day-glo green. It is used primarily to check for corneal ulcerations but can also be used to evaluate tear film quality. With normal tear film, a drop of dye placed on the eye should take 20 seconds to evaporate, if the dog is not allowed to blink. With tear film deficiency, dry spots may appear almost immediately. Bingo was not keen on our attempts to prevent him from blinking, and I did not have much experience with this test, making it hard to assess his tear film quality. But since many ophthalmologists automatically assume that all pugs with pigmentary keratitis probably have some degree of deficiency, I did the same. There were no corneal ulcers and his intra-ocular pressure was fine.

“Optimal treatment is to correct any underlying causes,” I advised, and I offered referral to a veterinary ophthalmologist who could evaluate Bingo more thoroughly and make sure I hadn’t missed anything. Then the entropion and trichiasis could be surgically corrected. If warranted, there is also an eyelid surgery that can be done to improve coverage of the cornea. In the past, surgeons sometimes removed the pigment by shaving off the corneal surface, but this is no longer recommended as the pigment recurred in most cases.

Bingo’s owners opted to try medical treatment, as some dogs improve without surgery. I prescribed two ophthalmic ointments. The first, cyclosporine, promotes increased tear production and better film quality and also has pigment-reducing properties. The second was a combination antibiotic and anti-inflammatory steroid. Although pigmentary keratitis is not painful, it definitely affects an animal’s vision, even causing complete blindness in severe cases.

Bingo’s owners have recently noticed him being less active and having trouble going down stairs. We ruled out Lyme disease and put him on arthritis medication, but I suspect the main reason for his inactivity is that he has trouble seeing where he is going. We hope medical treatment will stop the progression of the disease or even reverse it. If not, then it’s time to see the ophthalmologist.


This has been one of those weeks when I really wish my patients could talk. I’ll tell you a secret. Some days, after innumerable appointments with extremely chatty human beings, I appreciate the nonverbal reticence of the animals.

Don’t get me wrong. A master gabber myself, I love conversing with folks about everything from parenting to politics. But today, I wish it were Sylvester who was talking. During 30 years of practice I’ve gotten pretty good at “listening” to cats and dogs. The wince of a sore back. The hunched demeanor of belly pain. The happy bounce of the limping dog saying he’s just sore from playing hard. All those little cues they give me. But this week, with my friend Sylvester, not so much.

Sylvester is a big guy — almost 20 pounds of taciturn Maine coon cat. At home he has often expressed himself with what we delicately call Feline Inappropriate Elimination (FIE.) Like when we put him on a reducing diet and he immediately began urinating and defecating on the rugs. Message received. We changed from the low-calorie approach to a low-carb diet instead, and he stopped misbehaving. Temporarily.

The behavior would recur sporadically, especially when his owners had to leave him in the care of pet sitters. Over the years, we discussed various things that can cause FIE — medical conditions like feline idiopathic cystitis and inflammatory bowel disease versus behavioral issues like litter box aversion or territory marking. As Sly got older he also began pulling out the hair on his tummy and acting nervous and grumpy. We discussed allergies, anxiety-related overgrooming, hairballs. His owners coped with Sly’s foibles and I depended on their astute interpretations of his actions.

But this week, when Sylvester started seeming unhappy, even his owner was unsure what he was trying to tell us. “He’s limping on his left hind leg,” she said. “His coat seems different. See these big matts? He never used to have them, and he’s vomiting hairballs. He’s urinating and defecating outside the box again…and today he was crying pitifully at the top of the stairs and was very slow to come down. When he did come down, he didn’t finish his breakfast, which is very unusual.” Sly stared at me, inscrutable, and didn’t say a word.

Examining the big cat, I searched hard for explanations for his symptoms. Was his lower back a little tender? Was that left knee puffy? Why was he crying and not eating well? He had lost a little weight. Was there some kind of metabolic disease going on? We put him on the floor to observe the limp, but Sly would only take a step or two, then sit down. All attempts to nudge him into motion were met with regal disdain.

“Let’s run blood work to get some more information,” I suggested. “But it may just be back pain, or arthritis, or an injured knee,” I concluded lamely, sending them home with a prescription for TLC while awaiting lab results.

All the tests were normal except a moderately elevated blood glucose, technically called hyperglycemia. If his glucose had been much higher, I would have immediately thought “Diabetes,” but his was in a gray zone.

“We can’t conclude too much from this blood sugar,” I told his owner. “He hadn’t been fasted before we drew the sample, and normal cats can get hyperglycemia just from stress.”

Definitive diagnosis of feline diabetes requires three things — a persistently elevated fasting blood glucose, glucose in the urine, and clinical signs consistent with the disease such as excessive drinking and urination, or excessive appetite combined with weight loss. We scheduled to fast Sylvester overnight, recheck his blood glucose, do an additional test called a fructosamine level which would provide a ballpark idea of where his blood sugar had been over the last few weeks, and, finally, take radiographs of his hind end to look for other explanations for his reluctance to move.

When Sly arrived for the second visit, I put him on the exam room floor again. This time he shuffled around a bit, enough that I could clearly see his “plantigrade” stance. That means his hocks were dropped down abnormally until they almost touched the floor as he walked. This “dropped hock” gait can occur if a cat has ruptured tendons in the hind leg, but it can also indicate something else — diabetic peripheral neuropathy. That’s right. Sylvester’s funny walk might be a sign of diabetes.

We don’t know exactly why, but the hyperglycemia that occurs with diabetes will sometimes lead to functional, structural, and/or biochemical abnormalities of the peripheral nerves, especially the hind legs. Symptoms in cats include difficulty jumping, difficulty getting in and out of the litter pan, inappropriate elimination, change in attitude or behavior, irritability, pain on palpation of joints or limbs, and a plantigrade stance. Sound familiar? Diabetic people may also get peripheral neuropathy. In humans, symptoms may include extreme sensitivity to touch, tingling, burning or sharp jabbing pain, or numbness in the extremities, especially the feet.

So was Sly diabetic, or had he just hurt himself? If only Sylvester could tell me “I landed wrong jumping off the bed and hurt my leg,” or “I’m thirsty all the time and my feet are tingly and numb.”

His fasted blood sugar and fructosamine level both came back elevated Urinalysis confirmed the presence of sugar in his pee. Putting it all together, we concluded Sly was indeed diabetic, with peripheral neuropathy.

Because his blood glucose is not too high, we are first going to see if a prescription diet can control his disease. If not, he will need insulin injections. For the neuropathy, there is no specific cure. If we get their blood sugar well-regulated, a certain percentage of diabetic cats will regain normal hind leg function. Others do not, but they seem to adjust to getting around with the altered gait and do not appear to be in pain. Perhaps they’re just stoic. Sylvester isn’t saying.


Piglet, a nine-year-old tabby cat, looked me right in the eye. It was midnight. I don’t usually offer nighttime care, but Piglet had arrived on emergency 24 hours earlier for a urinary tract blockage and I’d been checking his bladder repeatedly ever since. Feline Lower Urinary Tract Disease is a common syndrome encountered in veterinary medicine, a catchall name encompassing a multitude of problems that all result in inflammation of the bladder and/or urethra.

We call it FLUTD (pronounced fluted) for short. Although it occurs in both sexes, in tomcats FLUTD can be life-threatening. It’s all about anatomy. In female cats, the urethra (the tube which carries urine from the bladder out of the body) is short, ending in a relatively wide opening inside the vulva. In male cats, the urethra travels farther. The last inch becomes very narrow and makes an “S” shaped curve before reaching the tip of the penis.

In FLUTD, urine from the inflamed bladder may contain mucous, crystals, red and white blood cells, bladder epithelial cells, even tiny bladder stones. This material can get stuck in that narrow male urethra causing an obstruction. With the urethra blocked, urine backs up. The bladder becomes excessively distended and tense. Clinical signs can include non-productive straining to urinate, abdominal pain, licking the genitals, loss of appetite, vomiting, acute kidney failure, severe electrolyte imbalances, possible bladder rupture, and eventually collapse, and death.

When Piglet arrived, the first thing we needed to do was relieve the obstruction by putting in a urinary catheter. Easier said than done. Sedation or even general anesthesia is often needed. My friend, Piglet, was feeling pretty badly, however, leaving him sufficiently apathetic that I was able to start placing the urinary catheter without knocking him out. As expected, within a centimeter from the tip of his penis, the catheter encountered resistance — the obstruction. What we do then is simple. We try to flush the junk out of the way by pulsing blasts of sterile saline through the catheter with a syringe, then advance the catheter farther and farther until it reaches the bladder.

Piglet’s case was tough, requiring multiple flushes but we eventually got the catheter in and were able to empty out the urine. Once the catheter is in place, sometimes we just flush the bladder, then pull out the catheter. Other times we sew it in place for a day or two, allowing time to treat the FLUTD without having to worry about our patient reblocking. Ah, there’s the rub. Cats with urethral obstruction have a high risk of blocking again in the first few days to weeks after the initial episode.

Piglet was one of those cats. In fact, Piglet seemed to have almost every complication possible. The night he first presented, he was in kidney failure due to the length of time he was blocked. Luckily, relieving the obstruction, followed by several days of intravenous fluid, returned his renal function to nearly normal. Then there was the issue that his bladder had been distended so long it had lost its ability to contract well. I knew by keeping his bladder emptied and using medication to stimulate muscle contraction, it would most likely regain contractility.

That’s where things stood that Saturday night. I had pulled the catheter earlier, hoping he could now pee on his own. But he couldn’t. With no one around to hold him for me, I had worked on developing a rapport with him. I petted him. I talked to him. “Let me help you,” I said soothingly, placing one hand on either side of his belly and gently squeezing out the urine. It hadn’t been coming in a good stream, but at least it was coming out, and he was letting me do it every few hours.

Then, at midnight, I squeezed him and nothing came out. His bladder was tense and distended again. Now I pride myself on being good with cats. Piglet and I understood each other, right? Such hubris. Piglet suddenly had enough. He turned without warning and sank his fangs deep into my arm. I think it hurt my feelings almost as much as my arm. So there we were. I had to sedate him and relieved the blockage. Again. Sew the catheter in place. Again. And add an Elizabethan collar to keep him from chewing it all out.Over the next few days Piglet proved to be a Houdini, pulling out every catheter I put in, despite sutures, despite the E-collar. I put on a bigger collar. He managed to get it off overnight. And he kept reblocking. Each time he needed sedation to replace the catheter. Urine culture showed a bacterial infection, resistant to all the usual antibiotics. Radiographs revealed multiple small bladder stones. By the end of a week it was apparent Piglet needed a perineal urethrostomy, often simply referred to by vets as a P.U.

Perineal urethrostomy is surgery intended to prevent the recurrence of obstruction by creating a wider outlet for the urine flow. The surgeon actually removes the penis, which contains that narrow S-shaped portion of the urethra, and makes a new opening, more like a female cat’s. Sounds bad, I know, but without that P.U. surgery, Piglet can’t pee. If he can’t pee, he can’t survive. As many as a third of all cats presented for urethral obstruction are eventually euthanized due to repeated blockage. Cats with P.U.s are still susceptible to FLUTD, but it is no longer life-threatening.

Piglet’s surgery went well. The stones were removed. The specialists were not overly concerned about the bacterial infection. Now we just have to hope he heals well, his bladder contracts normally, and that there is not too much residual kidney dysfunction.

Me? When my arm started to swell up and turn bright red, I saw the doctor and got some antibiotics. But I don’t hold a grudge. I’m one of Piglet’s biggest fans, despite that momentary lapse when he forgot how good I am with cats.


Hunter is a seven-month-old Bernese Mountain Dog. Just a puppy, he already weighs 76 wiggly pounds. If you haven’t had the pleasure of meeting a Bernese, this breed is one of several varieties of Swiss Mountain Dogs with an ancient heritage. Their ancestors are thought to have developed two thousand years ago from crossbreeding between mastiffs brought to the region by Roman invaders and local farm dogs that worked driving cattle, pulling carts to market, and being both watchdogs and companions.

These beautiful animals had many names including Farmer’s Dog, Gelbackler (Yellow Cheeks), Vierauger (Four Eyes, because of the facial markings), and my particular favorite, Cheese Factory Dog. In the early 1900s, dog fanciers pronounced them one breed, dubbing them “Durrbachlers,” after the Durrbach region in the canton of Bern. In 1908, Dr. Albert Heim, a professor, geologist, and canine researcher, introduced the name “Berner Sennenhund,” which means “Bernese Alpine Herder’s Dog.” This has remained the breed’s official name in Switzerland to this day, though they are often referred to affectionately as simply “Berners.”

Berners are sturdy, powerful dogs with long, silky black coats highlighted by dramatic rust and white markings. Bred to work, they need both exercise and interesting activity to stay healthy. They do best when exposed to many people when young. Berners are not for everyone. They’re big. They’re hairy. They like to be an integral part of the family and may not do well if left alone long or cooped up in a kennel or small space.

Our friend, Hunter, had plenty of company and exercise, his owners being well aware of a Berner’s needs, especially since his mom is my longtime assistant, Elise. She also knows that Berners have a notoriously short life expectancy, often only seven to eight years, although some lines may live longer and that purebred dogs have a higher risk of genetic disorders than mutts.

There is an old Swiss saying about Berners and related breeds. “Three years a young dog, three years a good dog, three years an old dog.” But the heart wants what the heart wants, and Elise and her husband, Daniel, wanted a Berner.

Last week Hunter spent the day playing at a relative’s house. He seemed fine that evening but next morning woke up lame on his left front leg. Hunter was so thrilled to visit Elise and me at work that day that it took two helpers just to take his temperature as he danced and squirmed on the table. His temperature was a bit elevated, but this is not uncommon in excited, active dogs. After a quick look at his general demeanor I went right to the gimpy leg, beginning with the foot. Owners frequently bring in limping dogs, saying “Maybe he has a thorn in his paw.” This is what comes from making school children read Aesop’s fable of Androcles and the lion. In 30 years of practice, and thousands of limping dogs, I have only seen an actual thorn (or any other foreign body) in a paw a handful of times. Nonetheless, I always check that first.

Hunter’s paw was fine. Working my way up I palpated each bone, and flexed and extended each joint while Elise tried to hold him still. Metacarpals, check. Carpus, check. Radius, ulna, check. Elbow, check. Humerus, check. Shoulder, ch… YOW. Hunter let out a sharp yelp when I hyperextended his shoulder. I let him relax a minute, then tried again. YOW.

I wasn’t being mean. I needed to confirm the reaction was repeatable, indicative of a real problem, not just a fluke. “It’s his shoulder,” I concluded. “Let’s watch him walk.” Hunter’s gait supported my findings. He placed his foot firmly on the ground, without hesitation. Dogs with paw injuries put the foot down tentatively, if at all. But as Hunter moved to bear more weight on that side, it hurt, so he shifted quickly back to the other leg. Voila. Limping Berner. Maybe he sprained it playing, but there was another more serious possibility.

Osteochondrosis dissecans (OCD) is a developmental problem affecting the cartilage that covers the ends of certain bones inside certain joints. Shoulders are most frequently affected, but OCD may occur in elbows, knees, or hocks. Most common in rapidly growing, large breed male dogs between four and ten months of age, no one knows the exact cause, but factors implicated include genetics, over-nutrition, hormones, excessive calcium intake, and trauma.

Imagine the shoulder joint. The top of the big arm bone, the humerus, is shaped like a ball and is coated with a smooth cartilage surface that allows the joint to rotate unimpeded. Now imagine a small area of that coating is abnormal — hard, thickened, and rough. It is more susceptible to injury and inflammation and eventually creates a small flap. Bits may even break free, creating tiny foreign bodies called “joint mice,” and leaving a divot in the surface of the humeral head. The degree of lameness varies with the severity of the lesion and may fluctuate with activity. Definitive diagnosis requires radiographs.

Treatment for OCD can start with conservative medical approach. Mild cases may do fine with just rest and medication, but, depending on the severity, untreated dogs are at risk for ongoing lameness and crippling. These require surgery, the earlier the better, to remove loose fragments, curette the defect, and try to stimulate healing. If one shoulder is affected, the other may be too. It is important to check both sides. Prognosis post-surgically is good, with 75 percent of patients eventually returning completely to normal. Since Hunter would barely hold still for an exam, properly positioned X-rays were going to require sedation.

“Let’s start with rest and pain medication. It may just be a sprain, “I said, optimistically. “If he doesn’t improve, we’ll anesthetize him for radiographs, check for OCD, and send you to the orthopedic specialist if necessary.” Hunter agreed with enthusiasm, wagging his whole body so hard he almost knocked me over. Three years, a young dog. Yup.


Dog Quixote is an 85-pound, senior Labrador retriever. We’ve known for a while about his hip dysplasia and arthritis, but one morning he took a dramatic turn for the worse. He just couldn’t get up. At all. I get millions of calls about old dogs who “can’t get up.” The majority are jauntily trotting around by the time they arrive at my office.

Many geriatric dogs simply get so stiff and achy they have trouble hoisting themselves up and getting their footing and balance, especially after lying down for a long time, after excessive exercise, or on slippery floors. Often all they need is a rubber-backed carpet for traction, a little assistance getting up, and arthritis medications.

But Quixote could barely lift his head. His owners carried him in on a homemade stretcher. When we tried using a sling to help him stand, he collapsed to the floor. His size and the degree of weakness made it hard to effectively evaluate his reflexes, but he did have feeling in all his limbs, and the ability to move them. He cried out when I touched various places, but it seemed more from anxiety than actual pain. Otherwise Quixote was bright-eyed and alert, eagerly eating the liver treat I offered.

Collapse is defined as the inability to support weight and walk without assistance. There is a long list of possible causes. We immediately ruled out respiratory and cardiac disease, and heat stroke, since he was breathing well, heart and lungs sounded fine, temperature was normal. Blood tests quickly ruled out metabolic disturbances that alter neuromuscular function such as low calcium, blood sugar, or potassium levels. That left us three categories of disease that could cause Quixote’s infirmity — orthopedic, neuromuscular, or neurological.

Orthopedic collapse is simply failure of the skeleton and/or joints to support an animal’s weight. In Quixote’s case there were pre-existing problems in his hips and knees, but we had never seen such severe symptoms, nor had his front legs ever been affected.

“His joint disease could certainly be contributing to his difficulties,” I said, “but it’s unlikely that’s the sole cause.” We needed to look further.

Neuromuscular collapse occurs when there is dysfunction in nerve conduction, in transmission of signals from nerve to muscle, or in the muscles’ ability to respond. This includes odd diseases like tick paralysis, myasthenia gravis, and polyradiculoneuritis, a.k.a. coonhound paralysis. Tick paralysis is caused by a neurotoxin in the saliva of certain ticks. It comes on fast, starting with the hind legs and rapidly progressing forward until the dog is completely paralyzed. Diagnosis is made by finding and removing the tick, and seeing if the patient improves. Without removing the tick, dogs may die from respiratory failure. Just what we need, huh? One more tick disease to worry about.

Polyradiculoneuritis is a similar progressive paralysis and is often linked to exposure to raccoon saliva, hence the alternate name “coonhound paralysis,” although many cases have no known initiating cause. Diagnosis is made on history and clinical signs. Most affected dogs spontaneously improve within three weeks and recover completely in two to four months.

One final neuromuscular disease to consider was acquired myasthenia gravis, an autoimmune disease affecting the receptors at the junctions between nerves and muscles, causing extreme muscle weakness.

But Quixote’s presentation did not fit any of the neuromuscular disorders exactly, so our diagnostic process went on to consider neurological diseases in which nerve impulses in the brain or spinal cord either fail to generate or are not communicated properly to the body. “Probably not in his brain,” I thought, since his mental status and cranial nerve functions were all normal. It was time to consider various spinal cord diseases.

Fibrocartilaginous embolism (FCE) occurs when a bit of gelatinous material from inside an intervertebral disc extrudes into an artery supplying the spinal cord. Exact symptoms depend on the exact location of the embolism, though classic presentation is sudden onset of weakness, without pain, often affecting only one side of the body. Definitive diagnosis requires MRI. FCE is most common in large breeds, like Quixote, although it typically affects younger dogs. Treatment is simply supportive care and most dogs improve with time. FCE is usually painless, and not progressive, but by Day Two, Quixote was a bit worse and clearly painful when I gently flexed his neck side to side. Probably not FCE. We were narrowing things down to intervertebral disc disease ( IVD).

Intervertebral discs are little cushions that sit between the vertebrae acting like shock absorbers. As animals age, these discs become less flexible and can push out into areas they shouldn’t, putting pressure on the spinal cord and/or nerve roots. Radiographs can help support a diagnosis, but MRI is often needed for a definitive answer and helps rule out other things like spinal cord tumor. Again, exact symptoms depend on exact location, as well as the severity of the disc herniation. Our radiographs showed an area in Quixote’s neck consistent with IVD. We also saw spondylosis deformans in his back, a non-inflammatory condition in which new bone forms bridging vertebrae together. This is fairly common in older dogs and is often of minimal clinical significance, although Quixote’s was quite extensive. With a presumptive diagnosis of IVD, we gave Quixote intravenous corticosteroids to reduce spinal cord swelling, emptied his bladder with a catheter since we weren’t sure he could urinate, then sent him home with oral steroids, analgesics, and antibiotics to cover for diskospondylitis, a bacterial infection of the intervertebral discs. His mom and I emailed back and forth constantly. Day Three Quixote heaved himself up, ran outside, urinated and defecated, then collapsed again. Same thing next day. His owner sent me video. His hind end staggered. His left front foot knuckled under. But he walked. Quixote is on his way now to an appointment with the neurologist. We hope an MRI and the specialist’s expertise will confirm a definitive diagnosis and treatment plan in hopes that Dog Quixote will soon get his feet solidly back under him.


Just past dawn Saturday, a call from my answering service rouses me. Coal, the cat, is not moving. His owners are afraid he has been poisoned. I shake myself awake, collecting my thoughts.

Being finicky, cats are less prone to eating strange substances than dogs, so true cases of toxicity are infrequent in felines. There are always worrisome items like antifreeze or lilies, but, more often than not, what a cat owner thinks is poisoning is something more common, like a fever.

Sure enough, when Coal arrived at my office he had a temperature of 104.5, well over the normal 101-102.5. I examined him. No wounds. No abscesses. Heart and lungs sounded fine, though his breathing was rapid and shallow. His tail twitched when I squeezed his abdomen, but he didn’t seem like it hurt. His third eyelids were up. He was slightly dehydrated, but his gums were a healthy pink.

“It’s a UFO,” I said, my standard stupid joke. Actually, it’s an FUO — Fever of Unknown Origin. “We see a lot of these in cats. There are many possible causes.”

Fever in a previously healthy young cat is usually caused by a viral or bacterial infection. If viral, it could be one of the big, bad viruses, like Feline Leukemia or Feline Immunodeficiency virus. Or it could be a milder disease, some nonspecific virus we can’t test for but that will pass on its own with time and TLC. Bacterial infections can also range from mild to something potentially deadly, like tularemia.

“Does he hunt?” I asked. Knowing an outdoor cat’s preferred prey can help steer us in the right diagnostic direction. Cats who prefer bunnies to birds or mice have a greater risk of contracting tularemia. Coal did hunt occasionally, but they had not seen him with any rabbits.As we continued talking, I observed Coal, flat on his side on the table, eyes half closed. Not good.

Even with a fever, most cats stay at least marginally alert in strange surroundings like the vet’s office. Coal was really down and out. What’s going on? I wondered, patting him gently and gazing into his face. Tell me, little guy, what’s wrong? Coal stared back limply, and purred.

“I’m worried,” I said. “He’s so spiritless. We should run some tests.” His owners agreed.

We quickly ruled out Feline Leukemia and Immunodeficiency Viruses, then ran an in-house screen for tick-borne diseases. “This is designed specifically for dogs, ” I explained, “but I do occasionally use it for cats. It’s fast and may help us figure out what’s going on.”

Soon after, two bright blue spots appeared in the results window. Coal was positive for antibodies to the organism called Anaplasma.

Anaplasma phagocytophilum (previously known as Ehrlichia equi) is a bacterium transmitted by deer ticks. Depending on the strain, susceptible species include deer, coyotes, mountain lions, horses, llamas, people, dogs, and — rarely — cats. Clinical signs of illness usually occur one to two weeks after the tick bite. In dogs, typical symptoms are fever, lethargy, depression, anorexia, muscle pain, stiffness, lameness, and reluctance to move. Occasionally dogs may also exhibit vomiting, diarrhea, coughing, labored breathing, swollen lymph nodes, and/or central nervous system signs such as incoordination or seizures. There are few documented cases of anaplasmosis in cats but symptoms reported in kitties are similar — primarily fever, lethargy, depression, and anorexia.

Coal certainly fit that picture, but our positive in-hospital test only meant he had been exposed to the organism and made antibodies. It didn’t necessarily confirm a current infection. Definitive diagnosis of anaplasmosis can be made in two ways. The bacteria infect white blood cells, forming little microcolonies called morulae.

Seeing these morulae on a blood smear under the microscope is one way to confirm diagnosis. I made slides of Coal’s blood, stained them, and searched in vain for morulae, but the fact that I couldn’t find them didn’t rule out anaplasmosis. Even in confirmed cases, morulae are only rarely found in feline blood. The second way to confirm would be to send out blood for a moderately expensive test called polymerase chain reaction (PCR) assay. But Coal was too sick to wait for results. He needed treatment now.

The drug of choice for many tick-borne diseases, including anaplasmosis, is doxycycline. For cats, this presents a dilemma as they can have a quirky reaction to this antibiotic when it is given in tablet or capsule form — inflammation of the esophagus. This may lead to a permanent stricture that can interfere with normal passage of food from mouth to stomach. To avoid this problem, we ordered a liquid doxy preparation from a compounding pharmacy, and to cover our bases for other infections, such as tularemia, prescribed an additional antibiotic called enrofloxacin. I sent him home that first night, hoping I had correctly communed with Coal and interpreted the clues he was giving us.

Returning several days later for a recheck, his mom confided that she had phoned her “animal communicator” about Coal’s case. She knows I am a bit of a skeptic when it comes to things like over-the-phone divining of an animal’s medical condition, but, hey, who am I to say? People didn’t use to believe in bacteria or viruses.

“The animal communicator says Coal has a headache,” she said, then asked “Why would he have a headache?” Well, the CDC page on anaplasmosis in people lists headache as the second symptom, right after fever.

“Your animal communicator’s reading is consistent with my presumptive diagnosis,” I laughed.

Coal’s mom laughed too. “Know what she says cats call you veterinarians?” I couldn’t wait to hear. “The Smelly Humans.” I considered the appellation. I suppose it fit. We veterinarians spend our days among multiple animals, bodily fluids, disinfectants, and other odoriferous items.

Coal looked at me from where he sat on my exam table. He was clearly feeling better, no longer laid out flat as a pancake. “That’s Doctor Smelly Human to you,” I thought.

Coal just looked smug, and purred.


When Maya was young, her owner thought he might let the big Rottweiler have a litter of pups. I gave my spiel about pet overpopulation, and the increased risk of mammary and uterine cancer as well as urogenital infections in unspayed dogs, then launched into my spiel about responsible breeding. So when Maya was four years old, we took radiographs to evaluate her hips for dysplasia. We discovered her conformation wasn’t great, making her a dubious candidate for breeding. It seemed she might be infertile anyway, as her heats were erratic and unusually mild. “You should have her spayed,” I suggested regularly.

But somehow the years slipped by. Maya had a bout of tick-borne disease, an unfortunate encounter with a fishhook, a case of “dry eye,” but she remained unspayed. More time passed. Now she was an old lady, with an old lady’s share of lumps and bumps, not surprisingly including several in her mammary area.

Spaying a dog before their first heat reduces the risk of mammary tumors to less than one percent compared to intact females. After one heat, the odds are eight percent. After two heats, 26 percent. By the third, spaying does not significantly reduce the incidence of mammary cancer. The good news is that as many as half of canine mammary tumors are benign. Due to her age, and the reasonable chance the masses were benign, Maya’s owner opted against surgical removal, and since it seemed silly to make a fuss at this late stage, I lightened up about urging him to spay her.

Then this July, during that awful heat wave, Maya started drinking and urinating excessively. At first, her owner didn’t think much of it. It was so stinking hot, of course she was drinking more. Then her appetite waned. “She’s barely eaten for a day and a half,” he told me. “Though she did eat a biscuit from the bank.”

I examined her. Temperature, weight, heart, lungs, all fine. Abdomen — well, at almost 100 pounds, she was too big for me to palpate much. I advised blood work and a urinalysis. Excessive urination and drinking are technically called polyuria and polydipsia, abbreviated as PU/PD. A chemistry profile would help evaluate for kidney failure, Cushing’s disease, diabetes, and other metabolic conditions that cause PU/PD. A complete blood count (CBC) would determine if she was anemic, or if there was an infection lurking. A urinalysis might reveal a urinary tract infection, and give us other useful information. I sent Maya home on broad-spectrum antibiotics, pending test results.

Back in the lab, I noted that the urine was pale, almost straw color. Using a refractometer, I checked the specific gravity. The urine was unusually dilute, almost like water. After spinning the sample in the centrifuge, I poured off the supernatant, added stain, then examined this sediment on a slide under the microscope. (If you don’t know supernatant from precipitate, go back to high school chemistry class!) Not much exciting. None of the inflammatory cells expected if this was a simple urinary tract infection.

Moving on to blood tests, her kidney, liver, blood sugar, and electrolytes were all normal. She was mildly anemic. Her white blood cell count was moderately elevated. Hmmmm. I put on my thinking cap. She was the right age range for a splenic tumor. That could cause anemia. She might have pyelonephritis — an infection up in the kidneys. She might have… Oh, drat! She might have a pyometra.

Pyometra literally means pus-filled uterus. When a dog goes into heat, the cervix relaxes to allow sperm to enter. Sometimes bacteria can invade instead. In older unspayed females, long-term hormone influences cause a pathological change in the uterine lining called cystic endometrial hyperplasia. This abnormal uterine lining is especially conducive to bacterial growth and massive infection can result.

Pyometra usually occurs one to two months after a heat cycle. If the cervix remains open, pus may drain from the dog’s vulva, but if the cervix closes, purulent material stays sequestered inside. The uterus can become extremely distended with pus. Toxins and bacteria may leak into the bloodstream making the dog extremely sick, the uterus may even rupture, but clinical signs of pyometra can be fairly nonspecific and vague, especially in the early stages. Symptoms may include depression, lethargy, poor appetite, PU/PD, vomiting, abdominal distension, vaginal discharge, and/or occasionally fever.

In some cases, the enlarged uterus can be felt by palpating the belly (taking care not to press too hard and risk a rupture), but radiographs, or even ultrasound, are often required for definitive diagnosis. Laboratory abnormalities may include anemia and elevated white blood cell count, as noted on Maya’s tests, as well as others we didn’t see with our patient, such as kidney dysfunction, low blood sugar, and electrolyte imbalances.

Pyometra is a life-threatening disease, especially if the cervix is closed. Recommended treatment is immediate surgical removal of the infected uterus. Risks of surgery include rupture of the pus-filled uterus into the abdomen, peritonitis, sepsis, kidney failure, disseminated intravascular coagulation, even aspiration pneumonia. The surgery can be difficult, and expensive, usually requiring several days of hospitalization.

Occasionally, if it is a valuable breeding animal, medical management with antibiotics and hormones can be attempted, but this is risky, and the problem tends to recur with each subsequent heat. Reviewing Maya’s previous history, I noted she had experienced similar symptoms last year and had recovered with oral antibiotics. This year seemed worse. Without definitive diagnosis by X-ray or ultrasound, I couldn’t say for sure, but pyometra was certainly a possibility, in which case, her life was in danger. As is often the case in veterinary medicine, age, prognosis, other ailments, and finances all had to be considered when deciding whether to pursue further diagnostics and surgery.

For now, we are hoping it’s not pyometra, and that she will again respond to medical treatment. But her case is a cautionary tale about some of the serious problems that may affect an unspayed female dog.


Retronym. I thought I had made it up but learned that the term was coined by a guy named Frank Mankiewicz in 1980. You know, those words we didn’t need back when all clocks were analog, all phones were land lines, and all documents were hard copy? Now although I love my computerized vaccination reminders and my cell phone, I still cling to a faux-leather, spiral-bound, paper appointment book where we scrawl our schedule in number two pencil. “10:00 Smith, K-9, Tunny, ADR. ” That’s “Ain’t Doin’ Right,” our catchall abbreviation for animals with nonspecific malaise.

This time of year, many ADRs turn out to be tick-borne diseases, so when Tunny, a middle-aged border collie cross, first arrived, that is what I expected. Until I checked his color. Not his coat color. The color of his gums. Unless pigmented black, these mucous membranes should be a healthy pink, but Tunny’s were pale, almost white. I glanced up, catching the eye of my assistant, Elise. She had seen it too and knew Tunny was in trouble.

“I just want to do a little test,” I explained, palpating Tunny’s tummy. Many things can cause pallor — but the most common in middle-aged dogs is a bleeding tumor of the spleen. I didn’t feel any unusual masses but could check quickly for internal bleeding by abdominocentesis, a five-second procedure tapping the belly with a needle and syringe. “No blood,” I reported, relieved, but still mightily concerned. It was time for further diagnostics.

Radiographs revealed an enlarged spleen but no obvious tumors. Blood tests showed severe anemia.When an animal is this anemic, there are three things that could be happening. He could be losing red blood cells through bleeding. Tunny had no visible source of blood loss — no nosebleeds, no bloody vomit or stool, no trauma. The abdominocentesis had not found blood in his abdomen, but I still couldn’t completely rule out a small tumor on the spleen, or even his heart, that didn’t show on x-ray. Referring Tunny for an ultrasound could help determine this.

The second possible cause for anemia is lack of red blood cell production. This happens with things like bone marrow cancer. The third is red blood cell destruction. When the body recognizes an abnormal blood cell, such as one infected with a blood parasite like Babesia, that cell is removed from circulation and broken down by the immune system. But red blood cell destruction can also happen spontaneously (and excessively) in a disease called autoimmune hemolytic anemia (AIHA).

AIHA occurs in dogs of both sexes and all ages, though some studies suggest middle-aged spayed females are at greatest risk. Breeds predisposed to the syndrome include cocker spaniels, springer spaniels, collies, miniature schnauzers, Dobermans, bichon frises, and Old English sheepdogs. Almost half of reported cases occur in the spring, especially May and June. Owners may notice progressive lethargy and weakness, poor appetite, vomiting, and discolored urine.

On physical exam, a veterinarian may find pale mucous membranes, elevated heart and respiratory rates, enlarged spleen or liver, heart murmur, and/or jaundice. Mortality rates can run as high as sixty percent.

Tunny’s family had difficult decisions to make. He needed an ultrasound to definitively rule out bleeding tumors. He needed further diagnostics to determine the precise cause of his anemia. He needed a blood transfusion while these tests were being pursued. Tunny’s situation was precarious. Hospitalization at a facility with ICU, specialists, blood bank, and round-the-clock care would optimize his chance of survival.

It is a particularly tough decision for Islanders, as this level of intervention requires a burdensome trip to the mainland. When I first came to the Vineyard, thirty years ago, few people opted to make that trek, and the standard of care for animals was far different. In those days we might make our best guess and send Tunny home with a handful of pills and a prayer. We might give Tunny a transfusion, using our own pet as a donor, without anything but the most rudimentary cross-matching to check compatibility. Sick animals often spent the night alone in unattended hospital cages. On the other hand, owners rarely ended up with huge veterinary bills.

Tunny’s owners lovingly opted to go to the specialists, but before leaving we had a heart-to-heart about prognosis and cost. “They won’t be able to tell if he is going to make it right away,” I said. ” They’ll probably advise several days of intensive care, maybe longer.” We discussed pragmatic options. The reality was that if Tunny was so sick that he needed more than one transfusion, his odds of recovery dropped dramatically, and the cost of more than a brief stay would be very high.

Over the next twenty-four hours Tunny was definitively diagnosed with AIHA. He was given a special transfusion of several units of packed red blood cells, kept in an oxygen cage, and started on an aggressive medical protocol. As anticipated, the specialists wanted him to remain hospitalized, but his owners were prepared. They had thought it through and made rational choices — emotional, medical, and financial. If Tunny was going to respond to the current protocol, we would know in a few days, whether he stayed hospitalized or not. Constant monitoring might give us more information, but wouldn’t necessarily change the outcome. And if he wasn’t responding well, his owners didn’t want heroic measures, nor did they want him spending his last days in a hospital cage, no matter how fancy.

Together we modified Tunny’s regimen to one we could manage here on Island as an outpatient. It’s a gift to have access to state-of-the-art medical care, but it is also both wise and compassionate to set limits. Maybe we need a retronym for the old-school, common-sense approach to veterinary medicine. Tunny received the initial benefits the specialists could provide, but now he needed to come home. Maybe that’s the retronym. Home care. Home, where he could be with the people who loved him, regardless of what lay ahead.