Authors Posts by Michelle Gerhard Jasny V.M.D.

Michelle Gerhard Jasny V.M.D.

Michelle Gerhard Jasny V.M.D.
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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.

Walter the beleaguered beagle.

Walter was a beagle-springer cross, so I was not surprised that he had an ear infection. Those breeds are both prone to otitis externa, the technical term for an ear infection. You know — when the canal gets all red and oozes that smelly, gooey discharge. Otitis may be caused by yeast or bacteria — sometimes both — and often is initiated by underlying issues such as allergies, frequent swimming, or problems with the anatomical conformation of the ear canals. We treated Walter with a standard ointment, a combination of antifungal, antibiotic, and anti-inflammatory medications. The otitis resolved but then quickly recurred.

“Let’s see what organisms are in there,” I suggested, smearing the green goop I had extracted from Walter’s ear onto a slide, which my assistant heat-fixed and stained. “Lots of cocci bacteria,” I concluded, examining the slide on the microscope. A pretty routine staph infection. Walter also happened to be diabetic, making him more susceptible to infections in general. We dispensed a second ear medication. The otitis got better . . .  then recurred . . .   again. This time as I tried to clean it, the canal began to bleed, and Walter was too tender to let me look down with my otoscope.

When faced with a stubborn case of otitis, there are several things we can try. We could take a culture and see exactly what organisms were growing in Walter’s ear. The laboratory could then run an antibiotic-sensitivity panel to determine the most effective drugs. But some specialists say that culturing an ear is like culturing the inside of a garbage can. You’re going to grow a lot of stuff, but not all the information you get will be useful. Instead, we decided to try a special brew many veterinarians mix up for such situations.

We start with a liquid called trizEDTA, which breaks down bacterial cell walls, allowing antibiotics to then penetrate into the organisms and fight the infection more effectively.  Adding liquid antibiotic to a big bottle of trizEDTA, I instructed Walter’s mom to fill his ears liberally with the fluid twice daily for two weeks. “This should fix him up,” I said confidently. Then, almost as an afterthought, I suggested a recheck in a few weeks. Six weeks later, Walter was back. Once again, the infection had responded, only to rapidly recur when the owner stopped the medication. “OK, let’s see what’s going on,” I sighed, thinking it was time to take a culture, and wheeling over my bright exam light to get a good look. I pulled up Walter’s ear and gazed carefully into the canal. Oh, my. I hadn’t seen that before. A small, red, cauliflower-like mass deep in his ear. “He’s got a growth in there,” I said. At past visits a combination of tenderness, blood, and discharge had made it difficult for me to see what was probably a small growth back then, which had now grown and was easily visible. (Or maybe I just hadn’t looked hard enough.)

Ear tumors are relatively uncommon in dogs, occurring primarily in middle-aged or senior pets. They can affect the flap, canal, or middle or inner ear, and can grow out of the skin, connective tissue, or various glands. They can be benign or malignant. Often there are no obvious clinical signs, depending on where the tumor is, what kind it is, and how fast it grows. If the tumor occurs in the middle or inner ear, neurological and balance problems may occur, resulting in walking problems, facial-nerve paralysis or head tilt. As they did with Walter, ear tumors may lead to secondary infection as they occlude the canal, hindering air flow and trapping debris and wax.

“A lot of times with ear tumors, it’s impossible to remove the whole cancer without removing large portions of the ear canal,” I told his mom. But we needed to start somewhere, so we scheduled surgery to remove as much as we could without being too invasive, and sent out a biopsy.  My hope was that it would be benign and thus not a big problem, even if we had to leave a little behind.

No such luck. Walter’s biopsy came back as ceruminous adenocarcinoma, a malignant cancer originating in the wax glands lining the ear canal. Although in dogs these tumors have only about a 10 percent chance of metastasis (i.e., spreading to other places such as lungs or lymph nodes), they tend to be locally invasive and aggressive. After consulting with a veterinary oncologist, Walter’s mom and I discussed the bad news.  “If you decide to pursue treatment, we start by taking chest x-rays and a lymph-node aspirate to make sure it hasn’t metastasized,” I said. “Then a CT scan gets done off-Island at the specialists’ to determine how far it has spread inside the ear.”  Then, more surgery. Although benign tumors can be removed with less extensive procedures, for this malignant cancer the oncologists advise total ear-canal ablation (TECA), which essentially removes all the ear structures while leaving the flap intact. In about one-quarter of cases, such cancers extend into the tympanic bulla on the skull, in which case the surgeon would also open this area and remove any abnormal tissue in a procedure called a bulla osteotomy. Postoperative complications might include facial-nerve paralysis, healing difficulties, and, of course, deafness on one side.

Walter is not a young dog, and his diabetes increases the potential for poor healing. There are only limited studies tracking the prognosis for dogs in Walter’s situation. Expected survival time for dogs with ceruminous adenocarcinoma who have the TECA surgery is reported to range from one to three years, but these statistics are based on very small numbers of cases. Without treatment, the oncologist says, Walter may develop trouble with his balance as the tumor spreads, and become severely uncomfortable within one year. His mom is considering their options, weighing all these factors . . . and I am taking a good long look down the ears of every dog who comes in with recurrent otitis.

“She’s in the spare bedroom, hiding under the bed,” the owner said when we arrived on our house call.  A recently adopted rescue from down South, this 40-pound bundle of terrified canine is a Louisiana Catahoula Leopard Dog. I had to look that one up. The breed is purportedly descended from crosses of wolves, Native American dogs, and the dogs of  Spanish conquistadors. Some say Catahoula is derived from Choctaw, a regional tribe. As for “leopard,” some have spotted markings, though they actually come with many coat colors and patterns. The Catahoula is the official state dog of Louisiana, and has been widely used to hunt game — everything from bobcats to wild hogs to bears. Knowing timorous Rachel, it’s hard to imagine her hunting bobcat. Today our mission was to give a Lyme booster and trim her toenails without totally freaking her out. “Can we just lift the mattress and work with her on the floor where she is?” her mom suggested.  “We can try,” I said dubiously.

When your pets needs to see their doctor, whether at a clinic, mobile facility, or at home on a house call, let’s face it. Some animals get nervous. Others get downright terrified.  Let’s talk about ways to lessen the stress on Fraidy Cat and Panicky Pup. If you think Panicky will do better at home, ask your veterinarian about house-call options, but most folks travel to the vet’s office, so let’s start there. Be sure Pan has a comfortable, well-fitted collar that he can’t slip out of. Harnesses and head collars are ideal. Occasionally dogs trot up to our door, then put the brakes on and back right out of their collars when they realize where they are. Happily, most run right back to their cars, but occasionally we end up with the dangerous situation of a frightened runaway dog.

For cats, use carriers. Period. I know. Fraidy hates the carrier. You can fix that.  It’s called desensitization and counterconditioning. Choose a well-ventilated carrier with enough room for Fraidy to stand up and turn around. Take the carrier out. Now. Not the day of your appointment. Now. Leave it on the floor with the door open. Let Fraidy explore. Feed her nearby. Gradually move the food bowl closer and closer to the carrier.  Put special treats and toys in or near the carrier. Eventually see if she will eat inside, with the door open. It may take months, but once she is adjusted, leave the carrier out and continue feeding occasional meals or treats inside. You have now turned the carrier from a terrifying instrument of torture to just another fun place to hang out.

So you arrive at the clinic. Now what? In cool weather, anxious pets may do better left in the car until the doctor is ready for you. Check with the receptionist. Larger practices may have separate waiting rooms for dogs and cats. Boy, would I love that. The best we can do at my place is good traffic control, keeping cats and dogs apart as much as possible. If needed, we bring certain pets in through the back door.  It kills me when a client exclaims “Oh, my dog loves cats!” as their Rottweiler sniffs Fraidy’s box in the waiting room. Well, the feeling ain’t mutual. Keep your animal away from others at the vets, please.

In the exam room, we try to greet pets quietly and help them acclimate. Treats. Pats. Soft, soothing tones. A slow approach.  You can help by also staying calm. Owners often use the right words but the wrong tone.”You’re OK, Pan!” they shout repeatedly in a loud, anxious voice. That doesn’t help.  Relax. If there is a chair provided, sit. Some behaviorists think that seeing you or the doctor seated tells Pan that he, too, can relax. Feeding treats throughout the visit helps too.  Of course, most dogs are not used to standing on tables, so the exam table can be daunting. This brings up the question of when to work on the floor versus the table. Usually the advantages of having Pan on the table outweigh the disadvantages. The assistant can use proper restraint techniques that are safe and gentle. The doctor has optimum lighting and easy access for a thorough exam. On the other hand, certain dogs do so much better on the floor, it’s worth the logistical challenges. Discuss it with your veterinarian. (And help me up off the floor. )

For cats, once they’re in the office, we need to help them out of the carriers thoughtfully. For most, it’s fine to simply reach in and take them out gently, but if Fraidy is hissing and cowering in the back of the box, she’s not bad. She’s scared.  Having a carrier that can open from the top or otherwise disassemble easily is helpful. If we take the top off and let Fraidy stay in the bottom half, often that makes her feel safe enough we can proceed.  Because of liability issues, and because we don’t want anyone hurt, it’s generally not smart to have owners restrain their own pets while we work, but sometimes it’s good to let cats and small dogs acclimate first for a while by sitting in their owners’ laps.

If Fraidy or Panicky are still basket cases, talk to your veterinarian about antianxiety drugs or sedatives to give at home prior to future appointments. It can take a while to find the right medication and the right dose, but our goal is always to have your pet have the most positive experience possible. As for Rachel, it was immediately apparent we couldn’t hold her safely on the floor. Instead, we stayed in that bedroom, where she felt a little safer, and her mom scooped Rachel up in her arms. We added a soft muzzle, so the people would be safe too.  While my assistant gently held her head and her mom patted her and made quiet, soothing sounds, I did my vet thing.

I still think we’re often flying by the seat of our pants when it comes to diagnosis, treatment, and long-term implications of tick-borne diseases.

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.

Yaretzi, a handsome eight-year-old golden retriever, had a pretty typical history for an Island dog when it comes to tick-borne diseases. Lyme-vaccinated as a puppy, he still got infected as a young dog, but we caught it early and treated him. At five, he once again tested positive for Lyme and also for another tick-borne disease, Anaplasmosis. Additional tests indicated he had been exposed, and made antibodies, but was probably not actively infected with organisms.

“We don’t really know what we’re talking about when it comes to these diseases,” I admitted to his owner. Maybe I exaggerate our ignorance. There’s plenty of erudite information published in veterinary journals and textbooks, but I still think we’re often flying by the seat of our pants when it comes to diagnosis, treatment, and long-term implications of tick-borne diseases.

The important thing was by eight years old, Yaretzi was testing negative again and feeling great. Except for one thing. “He drinks an awful lot of water,” his mom said.

Excessive drinking is technically called polydipsia. Excessive urination is polyuria. The two often go together. Medical folks just say “PU/PD.” When owners report polydipsia, the first thing we do is document it, by having them measure their pet’s water for 24 hours. A normal dog drinks between 20 and 70 milliliters per kilogram body weight per day. For a 30-kilo dog like Yaretzi, that’s roughly three to nine cups. Water consumption varies with exercise, salty foods, and hot weather. We don’t consider it true PD until a dog consistently drinks more than 100 milliliters per kilo daily. For Yaretzi, that’s almost 13 cups. Measuring total daily urine output, well, that’s harder to get owners to do. With true polyuria, urine is usually abnormally dilute.

Yaretzi’s daily water consumption measured borderline high. His urine, unusually dilute. His owner, exceptionally dedicated.

The list of possible causes for PU/PD is enormous. We began running tests. We ruled out diabetes and kidney failure. Endocrine tests ruled out underactive thyroid and the adrenal gland disorder called Cushing’s disease. His liver function proved normal with a bile acids test. Urine cultures ruled out bacterial infection. His white blood cell count was consistently low but we found no explanation for this. Yaretzi went to a specialist who repeated some tests, and added others. Ultrasound showed a few small nodules on his spleen, but the specialist thought these benign and unrelated to his PU/PD. More samples were collected to determine serum sodium level and osmolality, urine sodium fractional excretion and osmolality, and a urine protein: creatinine ratio.

Huh? What? Wait! Don’t turn the page! No more big words, I promise. Okay, maybe just a few. Protein-losing nephropathy (PLN) and diabetes insipidus (DI.)  You need classes in pathophysiology and endocrinology to fully understand, but since you probably want to get to the beach, here’s the short version.

Kidneys are made up of thousands of tiny units called nephrons that filter the blood. The parts that do the filtering are called the glomeruli. These work like strainers, letting little molecules like electrolytes pass through, while keeping cells, and bigger molecules like proteins, in the blood. Other portions of the nephron then balance electrolytes and pH. When the glomeruli get injured, the holes in the strainer get too big. Stuff that is supposed to stay in the blood, like protein, leaks out into the urine. A little protein in the urine can be normal, which is why special tests beyond standard urinalysis are needed. Yaretzi had an elevated urine protein: creatinine ratio, confirming abnormal protein loss via the kidneys, i.e., PLN. Over time, dogs with PLN become protein-depleted. Usually this is evident on basic blood tests, but Yaretzi’s was apparently in the very early stages, and his blood protein levels still normal.

What causes PLN? Most cases are thought to be the result of chronic inflammation or infection. Here’s your short course in immunology. The immune system makes antibodies against foreign proteins (called antigens.) Antibodies stick to antigens. These antibody-antigen complexes get trapped in the glomerular membranes. The immune system attacks those trapped complexes, inadvertently damaging the glomeruli. This inflammatory condition is called glomerulonephritis (Oops, another big word). Underlying diseases that produce the antigens can be anything from chronic dental disease, to Lyme, to cancer. Another disease that can also damage glomeruli and lead to PLN is called amyloidosis.  Definitive diagnosis of the cause of a case of PLN requires kidney biopsy, but we rarely recommend going to these lengths. Instead we treat any underlying problems identified and then just treat the symptoms.

“It sounds counterintuitive,” I said, “but he needs a low protein diet. I’m prescribing a medication that reduces protein loss through the kidneys, and low-dose aspirin to minimize risk of blood clots. Omega-3 fatty acids are also helpful. They’re already in the recommended prescription diet.”

Our last question was whether Yaretzi also had diabetes insipidus (DI), a rare disorder that occurs when the pituitary gland doesn’t make enough antidiuretic hormone (ADH)  or when the kidneys themselves are unable to respond properly to ADH. Dogs with diabetes insipidus pass huge quantities of very dilute urine, then drink excessively to compensate. Once the specialist has all the final laboratory results back, we will test for DI by giving Yaretzi a small dose of synthetic ADH. If his kidneys are able to respond, his urine should become more concentrated, and he should drink and pee less, confirming the problem to be inadequate pituitary ADH production. We suspect, however, that the problem is in his kidneys, that whatever is causing his PLN also interferes with his kidneys responding properly to ADH.

A complicated case. We don’t have all the answers yet. Are those past episodes of tick-borne disease exposure implicated? Golden retrievers have a high incidence of cancer. Is there a tumor hiding somewhere? Maybe he has some unidentified genetic abnormality? It’s a puzzle we hope to solve. In the meantime, his mother just keeps filling his bowl with water, and his days with love.

So let’s all keep our cool this summer. Understand the limitations of Island life. And don’t leave Tamale panting in the car. Seriously.

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.

Yup. It’s summer. Here’s how I can tell. Over the last few days I have seen three panting dogs sitting in parked cars with the windows cracked. Several people have just shown up at my door with animals after hours and continued knocking until I answered. Others stop me at the grocery store and the beach for advice about everything from ticks and skunks to diarrhea and cataracts. Did I mention the three panting dogs in parked cars? So once again, here are some veterinary reminders for summer on the Vineyard.

Number one. I can’t believe I have to say this again. Don’t leave your dog in the car! Seriously, don’t you people ever go on Facebook? Even my rare forays into social media tell me that FB is plastered with posters about the dangers of hot cars. Do you think your dog is immune? I know, I know. You’re just running in for a minute. Uh-huh. Is there really such a thing as “running in for a minute” on the Vineyard in July? Have you seen the lines at the Black Dog counter?  It only takes a few minutes for a car to become an oven. Dogs who are older, overweight, pug-faced, and those with heart and respiratory problems are at greatest risk, but pets of all sizes and ages succumb to heat stroke.

I’m going to be blunt. There is simply no excuse for leaving your dog in the car in the summer. If Tamale, the terrier, has separation anxiety, talk to your vet about treatment. If you’re worried he might pee on the rental carpets, use a crate. If his potty schedule interferes with your tennis time, change your game. Heat stroke is a potentially fatal condition that is completely avoidable. If Tamale cooks in the car, it is your fault. No excuses.

Heat stroke can also occur just being outside or from excessive exertion. Don’t take Tamale to the beach during the hottest part of the day. Most Island beaches don’t allow dogs during summer anyway. Check local regulations. If you do have access to a dog-friendly bit of shoreline, provide a water bowl and shade for Tamale.  Don’t let him bother wildlife or other visitors. If he poops, clean it up. That doesn’t mean burying it in the sand for the next toddlers with plastic shovels to discover or leaving it trailside in a plastic bag. Take that doggy bag home to the trash.

Don’t ask Tamale to run alongside your ten-mile noon bike ride. Remember: he doesn’t get to “coast.”  While you’re gliding downhill catching your breath and a breeze, Tamale is still running. If he is already fit, it may be okay to exercise during cooler hours, but plenty of vacationing dogs end up with heat exhaustion, injured joints, pulled muscles, or severely blistered feet from overdoing it. Dogs will run their hearts out to follow you. The fact that Tamale can run that far doesn’t mean he should.

Speaking of exhaustion, let’s talk veterinarians. If you’re not a year-rounder, you may not realize that a handful of small town veterinarians here goes from providing service to a local population of fewer than 20,000 people to five times that in summer. And, yes, many of those hundred thousand summer folks bring pets. Unlike New York, Boston, Los Angeles, or wherever you’re from, we have no 24-hour emergency clinics or referral specialty practices. The docs seeing patients all day are the same ones seeing emergencies all night.

If you come here often with a pet, establish a relationship with a local practice. Bring vaccination history and medical records, especially if Tamale has chronic problems. Learn the veterinarian’s office hours and emergency policy. No matter which practice you use, always telephone first. Please, don’t just show up unannounced. This is for your benefit as well as ours. Many local practices are small. There is no guarantee a doctor will be available if you arrive without notice. They might be on a farm treating a colicky horse or in surgery spaying a dog. It might even be the doctor’s day off and some practices only provide emergency care for regular clients. Call first.

After hours, most Island veterinarians forward their calls to an answering service. You may hear one short ring, then a long pause. Don’t hang up. That’s your call being transferred. It will ring again momentarily. Since my practice is home-based, I often hear people call five or six times in a row, hanging up during that pause instead of waiting for the call to forward. You won’t reach anyone that way. Be patient. After it forwards successfully, let it ring. Answering services try their best but sometimes take a while to pick up. Once you get through, make sure you leave the correct phone number, then stay off the phone so the doctor can get through. Make sure your ringer is on. If you don’t hear back within 20 minutes, call again. This all sounds obvious, but I can’t tell you how often one of these necessary steps eludes an owner seeking emergency veterinary care.

Although we do our best to take care of Tamale’s medical needs, if round-the-clock care, elaborate diagnostics, or specialized surgery or treatments are indicated, be prepared to go off Island. Don’t blame the local docs. You don’t expect your family physician to perform appendectomies or MRIs right in her office, right? We won’t always have the necessary equipment, staff, or specialty skills. What we can do is help with referral and travel information — the ferry, the Patriot boat, taxis on the mainland. A few owners have even chartered small planes. Cape Cod Veterinary Specialists in Buzzards Bay have a van that in certain situations may be able to meet you right in Woods Hole.

So let’s all keep our cool this summer. Understand the limitations of Island life. Reserve after-hours calls for true emergencies. Always phone ahead. And don’t leave Tamale panting in the car. Seriously.

We may never have a definitive answer. We’re just glad she’s back on her feet and hope she stays that way.

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.

Stormy is an Australian shepherd in the prime of her life. Last winter at her annual physical examination, her owner mentioned she had been limping recently. Watching her walk, she was a little gimpy on her right front leg, but I couldn’t find any obvious explanation. “Probably a strain or sprain,” I said. Stormy was also significantly overweight, an extra stress on her joints and muscles. “Try to get a few pounds off her,” I advised, sending home pain medication and instructions to rest.

The foreleg lameness resolved quickly, but three months later, Stormy returned. She  had lost three pounds (though still more than pleasantly plump) but there was another issue. She had suddenly developed marked weakness in her hind end. “She just flops over while she’s walking,” her owner said.

Stormy was bright, alert, and responsive. She’d pull herself to her feet and walk willingly, but then her caboose would start swaying and finally she’d drop to the floor. Her temperature was normal and other than the gait abnormality everything looked fine.

“She seems a little tender here,” I said tentatively, palpating her lower back, but it wasn’t definitive. Could be fibrocartilaginous embolism ( a neurological deficit caused by a little plug of stuff occluding the blood supply to the spinal cord) or intervertebral disk disease (a disease in which the little shock absorber between two vertebrae protrudes and presses on the spinal cord.) “She seems stable,” I concluded. “Let’s try rest and anti-inflammatories.”

Two days later, Stormy’s mom called. The dog was no better. Should we be doing something more?

“We can take X-rays,” I offered, though neither of the two diseases on our differential would necessarily show up on radiographs. “Really an MRI would be the next best test, but maybe she just needs a little more time,” I suggested.

I was wrong. Stormy’s condition continued to deteriorate. By the next day she could barely stand, her front legs now almost as weak as her hind.  She spent most of her time lying flat on her side unless her owner hoisted her up with a sling, then she would try to ambulate. Stormy came for a recheck. Dr. Buck did a careful neurologic exam. Stormy could still move all four legs, but that was the only good news. Some of her reflexes were exaggerated while others were diminished. She was trembling all over and had severe neck pain. It was now clear the location of the lesion was not in her lower back. It had to be either in her neck, or even her brain. It was time to consult a neurologist.

Up at VCA South Shore Animal Hospital, Stormy underwent a battery of tests. Blood work, urinalysis, chest X-rays, abdominal ultrasound, then finally MRI and a spinal tap under anesthesia. The MRI confirmed meningomyelitis in her neck. This means there was  inflammation of the spinal cord and surrounding membranes, but it does not identify the cause. She was started on corticosteroids, called prednisone.

Many readers may have taken prednisone yourselves if you’ve ever had a bad allergic reaction, like to poison ivy, or any significant inflammatory disease or auto-immune issues.

She also got gabapentin, a medication currently in vogue for animals with “neuropathic” pain.  But what was causing the problem? The specialists listed possible diagnoses including Steroid-Responsive Meningitis Arteritis (SRMA) and Granulomatous Meningioencephalomyelitis (GME.) Wow. Those are some big words.

Let’s start with SRMA, a disease of unknown cause, thought to be immune-mediated. In other words, for some reason Stormy’s immune system starts attacking her own nervous system. There are two reported forms, acute and chronic. The acute form comes on fast with a stiff neck, pain, fever, and characteristic changes found in the cerebral spinal fluid. The chronic form has a more protracted course with more neurological deficits.

SRMA strikes young adult dogs, like Stormy. Breeds thought to be predisposed to the condition include Bernese mountain dogs, boxers, German short-hair pointers, Norwegian duck tolling retrievers, and beagles. In fact another name for SRMA is Beagle Pain Syndrome.   There is no way to make a definitive diagnosis in a living dog. Basically, if an individual fits the clinical picture and no other explanation can be found, then it’s time to try corticosteroids. If the dog gets better, Bingo! It’s “steroid-responsive.”

GME is an “aseptic inflammatory disease of the central nervous system.” Just like SRMA, the cause is unknown, it can be acute or chronic, and definitive diagnosis is only made on postmortem, although MRI and CSF taps can be helpful in ruling out other disorders. GME has three forms — focal ( affecting one location in the nervous system), disseminated (involving many locations in the nervous system), and ophthalmic (affecting the optic nerve and eye). Symptoms vary depending on location and severity of lesions. Progressive loss of use of the legs is frequently seen. Other signs may include seizures, head tilt, lethargy, blindness, facial abnormalities, walking in circles, and balance disorders. Middle-aged,small breeds, especially terriers and toy poodles, are most commonly affected. GME also may respond to corticosteroids, but sadly, most dogs do not survive more than one to five months, even with treatment.

The neurologists admitted that Stormy did not exactly fit the picture for any one disease. Her CSF tap did not show the changes typically seen with SRMA. On the other hand, she is not a breed in which GME is usually reported. Another possibility was cancer lurking somewhere in the central nervous system, but none could be found on any of the tests. We know so little about these types of progressive neurological diseases, that it can be both frustrating and heartbreaking for owners, but Stormy responded well to the prednisone and within a few weeks was walking almost completely normally. She will be on steroids for several months, gradually weaning down the dose and watching closely for signs of relapse.

We may never have a definitive answer. We’re just glad she’s back on her feet and hope she stays that way.

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.

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.

“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.