Fat, Fluffy or Just Big Boned?

Fat, fluffy or just big boned?


August 7, 2014


From the desk of Dr. Voorheis



As promised before I went hiking (and yes I am proud to say I did finish my 36 year journey on the John Muir Trail!), I said the next blog was to be on obesity. Some of you were kind enough to share your success stories of your pet’s weight loss with me and I have included some of those below. All puns aside, this is a huge topic and one I will not be able to completely address in the confines of this blog. It is not a simple subject as you can probably imagine. Yet in both people and our pets it is a sensitive subject that is usually ignored or minimized. It is also not well addressed by the veterinary community, either in treatment or acknowledgement that some of what we do as veterinarians can contribute to obesity. I’ll share more on that later.

 I’m a veterinarian, and this is a veterinary blog but I would venture to guess that everyone who reads this knows there is an obesity problem with people in this country. The causes are multi factorial and it is a significant problem for society as a whole and for individuals. We can point to sedentary lifestyles, poor eating habits and food preparation, the ease of the fast food drive thru, portion size (which has increased by 30% plus in the past 50 years) and genetic predisposition.

Whatever we may blame or point to as an excuse, obesity is the result and the same factors also affect our pets.

 The simple fact is that fat cells once thought to be benign storage cells with no metabolic activity are now known to be active. They are critically involved in a number of metabolic processes such as angiogenesis (blood vessel formation) fat cell recruitment, dissolving and reforming structures around fat tissue, generation, storage and release of fat, growth factor production, glucose metabolism, production of factors that affect blood pressure, cholesterol metabolism, enzyme production, steroid metabolism, blood clotting, and immune response. Fat cells produce pro-inflammatory compounds such as leptin, interleukins, tumor necrosis factor alpha, c-reactive proteins and on and on. If fat cells release too many pro-inflammatory compounds, the net pro-inflammatory response can contribute to metabolic disease. That metabolic disease contributes to inflammation in joints, type 2 diabetes, hypertension, reduced HDL levels and elevated triglycerides. The challenges for people dealing with obesity  are significant. The same is true for our pets.   

 In veterinary medicine, obesity is defined as a clinical syndrome involving the excess accumulation of body fat. Obesity is considered the most common form of malnutrition in small animal practices like WBAH. National surveys suggest that 25 to 40% of all pets presented to a veterinarian are overweight or obese. I think those numbers are low. I believe the numbers are much closer to 50% or more.  Obesity is associated with an increased risk of arthritis, diabetes mellitus, hepatic lipidosis, feline lower urinary tract disease, urine incontinence in spayed female dogs, constipation, dermatitis, heart problems, and respiratory problems. There is more cruciate injury in dogs that are obese than their non-obese counterparts. Obese animals are also anesthetic risks. There is a 3 fold increased risk of death in obese middle aged cats compared with lean middle aged cats. Dogs that are lean live almost two years longer than littermates that are overweight.


Obesity develops when energy intake consistently exceeds energy expenditure. That is the bottom line. This is true for animals and humans. Think calories – if you consume more calories than you burn, you gain weight. So do our pets. Here are some risk factors that enable this to happen so easily and so gradually that you don’t even notice. 

  1. Decreased daily exercise due to confinement of the pet in the house and overfeeding of the pet in those circumstances.

 Let’s talk about overfeeding for a minute. The guidelines of how much to feed your dog or cat   were developed for intact (i.e. not spayed/neutered) maximally working dogs. Maximally working dogs are dogs running 8 hours per day. For example, if the back of the dog food bag says to feed the dog 1 cup twice a day for its weight, bear in mind that if your dog is not running 8 hours a day, and instead is confined in a house, then its caloric needs are markedly less than what the dog food bag says to feed. The dog food bag is not the end all, be all. Again, you are your pet’s biggest and most important health care advocate. That’s right, YOU not me.  YOU live with your pet.  You are ultimately responsible for keeping your eyes and ears open and making sure that your pet is acting normal, eating and drinking normally, pooping normally etc.  Your pet depends on YOU first and foremost for their well being. So the next time you look into the cute face of your dog or cat and think to yourself “oh you are so cute – here have a treat” or worse yet “here have a bite of my burger or a piece of my bacon”, think again. A better way to think in that situation is “oh you are so cute… and I want you to live longer and be healthy so I WON’T stuff you full of treats and table scraps”. And then maybe take Fido for a walk or throw the ball for a while. Grab a cat toy and engage your cat in some good play time.  This is a much better reward for both of you.  Need a visual on this?

    Food Chart                      

In addition, I alluded earlier to the veterinary community’s role in obesity in our pets. We promote spay and neuter. Remember my blog on that? It’s important because pet overpopulation leads to millions of dogs and cats being euthanized in shelters across the country every year. So it is correct and appropriate to recommend spay and neuter. However, we need to bang on the drum once we have spayed/neutered your pet. Its caloric requirement will change. It becomes much easier to gain weight when spayed/neutered than when intact. The bottom line is the day after your pet is spayed you can probably start feeding less food. How much less? I’d start with 10 to 20% less and make adjustments from there. Again, you live with your pet, I don’t. So watch and see. If they start to pack on the pounds, decrease another 10% until you see a better result.  For our cats, many if not most of our cats are now indoors and spayed/neutered. They are indoors for a reason because we don’t want them to be exposed to the dangers of cars, aggressive dogs, feral cats, and coyotes. So they are not out hunting which is their nature. They are lolling around free feeding on dry food all day. Obesity is a consequence.

2. Owners may overfeed their pets because a good appetite is perceived as a sign of good health, they may use food as a palliative (comfort) agent when they leave for work- they replace exercise with food and begging behavior is “endearing”

By far and away, the number one cause of obesity in our animals is overfeeding. Only about 5% of overweight or obese animals have a medical problem such as hypothyroidism, hyperadrenocorticism, hyperinsulinism, acromegaly or hypopituitarism. Again, the overwhelming reason is too many calories consumed for too little energy expenditure.

In practice, the diagnosis of overweight or obesity is done in the exam room. Every animal examined is assigned a body condition score (BCS). We use a scoring system on a scale of 1-9, with 5 being ideal and 8 or 9 being obese. Animals with 6 and 7 are considered overweight.  BCS’s have the advantage of being fairly quick and easy to perform.  Another system, developed by Hill’s which has a terrific app for your smart phone that allows you to calculate ideal body weight using a system called BFI calculator. Using your smart phone, search for Hill’s HWP weight management app. Using a measuring tape, you can quickly make 4 measurements and calculate your dog’s ideal weight. The BFI system is something you can do at home, and/or we can show you and we can quickly develop your pet’s ideal weight. If you don’t happen to have a smart phone, you can also go to the website where there is an instructional video to help show you how to get the proper measurements. You can click here:  http://www.hwp.hillsvet.com/resources/resources.html

 Pet Chart

So, how do we get to an ideal weight once we have arrived at the decision that our pet is too heavy? First, we determine who feeds the dog or cat.  Does the animal free feed or do you feed them? Write down all the calories (everything that crosses the animal’s lips in a twenty four hour period). We can choose to make a diet change, i.e, move to a prescription diet designed to have an animal lose weight. By far and away, the best weight loss diet to come about in recent years is a prescription diet by the Hill’s/Prescription diet company. This is a better food than their original weight loss diet called r/d. The new diet is called Metabolic Diet. Again, the app or the link I provided will help you decide how much to feed in a 24 hour period. There are even treats for dogs and cats in the Metabolic line, so they have covered everything!


 Metabolic Food  Metabolic Dog Treats  Metabolic Cat Treats

There are other methods of feeding, designed for weight loss. Adherence to these methods will also result in weight loss. Feed less. Don’t change the food you are feeding but instead feed 25% less. Cut treats in half, literally. Your pet just wants the treat. They don’t know that you cut it in half. Then, instead of giving 6 treats per day, give 3. They can still have 6 treats per day, but once you cut the treat in half, they are actually getting half the treats there were originally getting. And they won’t know the difference. This way, you aren’t the big meanie that took the treats away.  Re-weigh and re-measure in one month. If no weight loss or no significant weight loss, feed 25% less and cut treats in half again.  Re-weigh in one month. There is no question that if you decide to commit to getting weight off of your dog or cat, you will succeed. You see, they can’t sneak candy bars and stop at the drive through like we can. They don’t have to deal with self control and cravings like we do. Getting weight off your pet is not brain surgery. It just takes commitment and patience on your part. Don’t we wish we had someone to this for us? Let me say this another way, if I could promise you that I had a pill in my pharmacy that would guarantee two extra years with your dog or cat, would you not ask for it? That magic pill is a body condition score of 4/9 for a dog and 5/9 for a cat. Believe it. For some cats, the easiest way to weight loss is to stop free feeding and instead feed a measured amount of food. Or feed canned food twice daily and give no dry food.

As promised, here are some client comments on diet and weight loss:

“Very good results with Sasha (cat) on Hill’s Diet you prescribed for him a few months ago. There were struggles at first, but we learned together how to make it work.” ……Nancy A.

“My cat has been fat all of her life… I free fed her for years…. Now she is 11. 4 lbs (down from 16) and she is more energetic at 11 year of age than she was at 6.   ¼ cup measured metabolic diet two times a day. I feed dry food only”. – Nelson V.

“You provided perfect advice for the weight problem our Akita (Tika) had. She was something in the 100 lb range. You wanted her at 88 lbs. Your solution was simple… reduce the feedings by 25%. Easy enough… I used a ¾ measuring cup using Wellness Core brand food. And I fed her treats with a minimum protein content of 70% and kept up the daily walks. We weighed her monthly as the weight came down about 1-2 lbs a month. With all that success, we kept her on the diet and stopped monthly weighings. Big mistake. After several months, we checked her on a Petsmart scale that read 82 lbs. WBAH recorded her weight at 83 lbs. I have since increased her food and she is now 88 lbs and I am working to find the right balance to maintain her here .. expect experience will find that level. Essence of story… your solution was easy and very effective.” – Glenn and Carole M.

“Red is a really sweet boy who likes to sit at the table while we eat our meals (A habit that started since the day he was found on our doorstep). This is a really “adorable” way of begging in my opinion but needless to say, we let him join us. Everyone thought it was cute to give him a “bite” of people food. That was when we began our first effort to control Red’s weight. We stopped giving him bites, or “just a taste” of our meals. His health became more important than his participation at the dinner table. Also, since Red was growing in years we switched his food to a “senior” product of the same food.  I don’t know how much difference “age appropriate nutrition” factored into his weight loss but I believe it was significant. We also cut the mixture of wet/dry food and opted only for “dry only”, which I’m guessing is better for his oral health as well, but that is only a guess. Red still joins us at the table and is very polite given he is denied the little “treats” that were contributing to his obesity. -Toni M.
A HUGE thank you to those clients who provided me with some feedback on this topic! Your input is invaluable because, once again, YOU are your pet’s biggest health advocate.

Until next time…..

Dr. Voorheis

Short Blog? What’s That?!

Short Blog? What’s that?


July 24, 2014


From the Desk of Dr. Voorheis


“What’s this Dr. Voorheis, a short blog?” I can only imagine some of you thinking that as you read this title. I bet you didn’t think I was capable of writing a short blog. I continue to be full of……..surprises. This one is more of me straying from the medical arena and into the personal and WBAH reporting arena.

For one thing, I’ve been writing and preparing a blog about every two weeks now. I was not able to keep up the once a week pace and I finally admitted it to myself …and now I admit it to all of you. Apparently, I am not Superman.  I wrote one last week, so shouldn’t the next one be due in another week? Yes it should. However…..next week I’ll be in Yosemite National Park finishing the John Muir Trail; a journey I began 36 years ago. Remember my blog about this back in April? I am quite excited with the thought of finishing it, so hopefully if everything goes well, I will be able to say I finished it. As of this writing, the only thing I am aware of that could prevent me from finishing the hike is permits. Usually I get a permit several months in advance and I tried every day for two weeks a few months back but was not able to get a permit. My game plan is to show up and get that permit for the Yosemite backcountry as a “walk up”. If that doesn’t work, I will shoot for a long weekend at the end of September. Wish me luck! 

Onward and upward! If you are wondering what to do this Saturday, July 26, take a short drive into La Habra Heights for some good old fashioned family fun. There is an all day event happening called “Dog Days of Summer” which is put on by the Pet Prescription Team and the City of La Habra Heights. The Pet Prescription Team, founded on the principle of “To Touch People’s Lives Through Pets”, is a volunteer organization dedicated to helping pet owners train their family pet to become therapy animals. The work they do is phenomenal and “yours truly” is honored to be the Grand Marshall of the event this year. I actually prefer “Grand Poo Bah” but I suppose Grand Marshall will have to do. This fun event is held at “The Park” 1885 Hacienda Road, La Habra Heights. The official flyer is offered below so take a look for all the details. I hope to see you all there.

 Two weeks from now, I will be writing a blog on obesity in our pets. Yup, this one is way overdue. I will write on the science of obesity. The hint of the topic is this; the actual science behind obesity has exploded in the past 15 years or so, there is much to write about. In addition, I am hereby reaching out to those of you who have had an obese pet and through team effort have had success in having your pets lose weight. For example, the diets you have used and the restrictions on those foods. Who is using Hill’s Metabolic Diet? Other means? More exercise? Please share your story with me by sending me a quick email at drvoorheis@wbanimalhospital.com

 This doesn’t have to be long or fancy, just a few words on your experience with this topic. I’m really looking forward to your feedback! Who knows, some of you may be co-authors of that blog!

 And now what you have all patiently been waiting for since I first mentioned in January in my first blog….the new WBAH building. Below is an artist’s rendering of what the new Washington Blvd. Animal Hospital will look like. This was an idea that first started at a dinner meeting in July of 2012 between Dr. Throgmorton, our attorney and myself. Certainly, when this kernel of an idea started, I had no idea of the immensity of a project of this size, nor did I have any idea of how long the process could take. Slowly, the kernel took root as hundreds of questions were asked and answered. We have employed one of the country’s top architects specializing in veterinary hospitals. The plans were drawn, torn apart and redrawn again and again as we developed a hospital specific for our needs and the needs of the community WBAH serves. There have been multiple meetings with the planning department and more “studies” than I care to talk about. Traffic studies, soil studies, water drainage studies, etc. At this point, it is our hope to be under construction in the fall. Much more detail will be sent out as the construction timing is firmed up. The construction of a new building on our existing lot, while working in our current building will be challenging to say the least. We think we have come up with solutions for those challenges and more will be written about those solutions as we firm up a date for the start of construction. For now, I hope you all enjoy the artist rendering of the new building and I hope that you are all as excited as we are. This has been, is and will continue to be a true labor of love us and it is all for our clients and their critters. It causes sleepless nights and many headaches but at the end of the day, you all deserve to have it…..the best state of the art animal hospital in the area and we want to give it to you!


Until next time……


Dr. Voorheis







Internal Parasites – Part Deux

Internal Parasites – Part Deux


July 17, 2014


From the Desk of Dr. Voorheis


 Who’s up for the sequel about the creepy, crawly parasites that live in our precious pets? Two weeks ago we talked about worms. As a reminder, that was an incomplete discussion as I kept it to the most common worms of the alimentary (gastrointestinal) tract. We talked about big worms and small worms that are visible to the naked eye. The little stinkers we are talking about today are tiny one celled organisms. They might be little, but they are mighty and sometimes their effects are devastating. If I limit the discussion to common culprits, we would be talking about just two organisms. But for you, my avid and loyal readers, I’ll offer two or three more.  

Protozoa (Coccidia)

 Coccidia are one celled organisms that cause disease in animals. There are multiple types of Coccidia; Isospora, Eimeria, Toxoplasma, Cryptosporidium and Neospora. Toxoplasma, Cryptosporidium and Neospora deserve “special topic status”. An entire blog could be devoted to these Coccidia and given how serious it is, I probably will write one. I will confine this discussion to Isospora. There are two types that affect our pets. Isospora canis and felis. They don’t cross over. Cat Coccidia is cat Coccidia and dog Coccidia is dog Coccidia. Eimeria is found in the feces of rabbits and deer, so dogs that eat deer and rabbit poop may be affected. Yet another reason to dissuade the poop eating.  

 Isospora primarily affects puppies and kittens. When found in the stool of an adult dog, it might not even be causing disease. It causes watery to mucoid and sometimes blood tinged diarrhea. It can be a cause of weak puppies and kittens. Infected puppies and kittens will contaminate the environment with oocyts. Occasionally, a puppy or kitten can even be anemic from coccidiosis. How are they diagnosed? A fecal exam is done. I cannot stress the importance of an annual fecal examination enough. It is a crucial tool. Treatment is relatively straight forward. If a puppy or kitten is healthy, we treat as an outpatient. If the animal is dehydrated or otherwise debilitated, fluid and other supportive care is indicated. Sulfa drugs are the treatment of choice. We usually treat for a period of ten to fourteen days. The sulfa drug does not eradicate the Coccidia but inhibits it so that body defense mechanisms can reestablish control.



Protozoa (flagellate)



Giardiasis is caused by a protozoan, Giardia sp. Animals are infected when they ingest cyst shed from infected animals, often via shared water. Giardia live in the small intestine, specifically the duodenum, where they interfere with digestion through unknown mechanisms. The cysts are immediately infective when shed in feces. This is a common disease. It wasn’t always as common as it is now. In our hospital setting, Giardia is the most common intestinal parasite diagnosed, outpacing roundworms. It is more common in young animals and signs vary. In some animals this means acute diarrhea while in others it means intermittent and even transient diarrhea. It also can become a chronic disease and can cause a malabsorption syndrome leading to debilitation. It is transmitted when ingested cysts from contaminated feces are ingested through water, food, environment or fur. Indirect water borne transmission is most common and cool moist conditions favor survival. Lest you think by living in our Southern California desert allows us to escape all of this, let’s think of the microenvironment we create in our backyard.  Sprinklers that go off daily or every other day keep the microenvironment in the grass and shrubbery in your backyard cool and moist. The survival of Giardia cysts in the backyard are no problem either. There is a definite higher risk and higher numbers of Giardia in dogs and cats that come from high density populations such as kennels, pet-shops, catteries and animal shelters. Of course a dog or a cat doesn’t come in with a sign that says “Hi, I’ve got Giardia”. Giardiasis diarrhea can resemble either a large or small bowel diarrhea, it can look like IBD (inflammatory bowel disease) or it can look like maldigestion and malabsorption too. In cats it can be confused with another protozoan, Tritrichomonas fetus.


How do we diagnose it? Again, a fecal exam is our number one tool. Routine fecals can find it, cysts can be found on flotation, direct examination of stool will sometimes yield trophozoites and there is a highly specific ELISA test that uses special techniques to test for the Giardia surface antigen. Sometimes two or three tests in succession will be used to both diagnose the disease and/or confirm it is clear. When we treat Giardia, we treat the animals as out-patients in the vast majority of cases. There are cases where Giardia is so severe and so debilitating that the animals require hospitalization. It is recommended that drug therapy such as metronidazole or fenbendazole be combined with environmental cleaning using quaternary ammonia disinfectants plus bathing of the patient to prevent re-infection. There is a Giardia vaccine available, however many internists do not believe this is an efficacious vaccine.                 


There are some animals that do not clear as puppies or kittens. This may be due to resistance of the organism to the medication being used to treat it. Immunodeficiency or a slow maturing immune system may also make it difficult to eliminate the organism. They continue to shed and test positive for Giardia until their immune systems mature, even after a year of age of more. Re-infection is easy because Giardia cysts are resistant to environmental influences and relatively few are needed to reinfect a dog or person. In addition, and this is not common, there are dogs that have chronic Giardia, that either through re-infection or persistent infection develop chronic signs of bowel disease. Fortunately, this is rare.

 The above two organisms, the Coccidia Isospora, and the protozoa, Giardia are by FAR the most common of the one celled organisms affecting the dog and cat.  There are a few others worth mentioning. Trichomoniasis (caused by Tritrichomonas foetus) is another protozoa of interest. The coccidial organisms, toxoplasma, cryptosporidium, and neospora are also worth mentioning.


Protozoa (flagellate)


 Trichomoniasis in cats is caused by Tritrichomonas foetus. Animals are infected by the fecal oral route. Cats with trichomoniasis have signs of a foul smelling large bowel diarrhea which rarely contains blood or mucus. It is more commonly seen in exotic cat breeds such as  Somalis, Ocicats, Bengals and Abyssinians. This may be due to the fact that these cats are commonly “show cats” and the environment where exposure may take place is cat shows where an individual animal is potentially exposed to many other individuals. The disease is diagnosed by either finding motile trophozoites in fresh stool specimens, fecal culture, or the much more accurate PCR testing. In our practice, testing is limited primarily to PCR testing.

Treatment frequently involves testing the entire cattery and separating infected from non-infected, treating the positives and then retesting. Eventually, a cattery with trichomoniasis can be cleared. Some cats have either resistant strains or cannot clear the organism. These cats eventually clear, but may test positive for one or two years.



Protozoa (Coccidia)


 Toxoplasmosis, is caused by the coccidial organism Toxoplama gondii, and is by far too complex a topic to be covered in this short blog. I think I stated earlier an entire blog could be devoted to Toxoplasmosis. Toxoplasmosis can be acquired transplacentally (across the placenta), ingestion of tissues containing encysted organisms such as when a cat eats a mouse with encysted organisms in its muscle or through ingestion of food or water contaminated by cat feces containing oocysts. And toxoplasmosis does not just affect dogs and cats. Marine mammals such as sea lions and sea otters and others are particularly sensitive to toxoplasmosis. It is felt by most wildlife biologists that the feral cat population has a role in shedding the toxoplasma organism into storm runoff channels where it find its way into the food chain that eventually affects sea lions and sea otters. What can we do? Trap, neuter and release feral cat programs. Do not use flushable litter or if you do use flushable litter, don’t flush it. Dispose of it in a way it ends up in the landfill rather than in our water ways. In kittens, toxoplasmosis can cause signs affecting liver, lung, brain and the eye. In older cats, it can be in the lung, the brain, muscle, liver, pancreas, heart and eye. In dogs, lung CNS and muscle infections predominate. We treat toxoplasmosis using a number of different antibiotics but clindamycin is considered the most effective.                           


Protozoa (Coccidia)


 Neospora caninum is a protozoal parasite that causes neuromuscular disease in dogs. Domestic dogs and coyotes are the definitive hosts. They shed the organism in their stool after ingesting the cysts in the muscle from the intermediate hosts like deer and cattle. Another way they get it is to be infected across the placenta, which can cause infection in puppies or subclinical infection causing encystment in neural and muscular tissue. This is another reason to NOT feed raw foods. The organism can encyst in cattle muscle. Neospora can cause a wide variety of signs from the vague, lethargic and muscle sore dog, to a dog showing severe neurologic and muscular signs. Treatment is available, but sometimes the signs are too severe to be reversed. “C’mon Dr. Voorheis have you diagnosed this disease?” No, I have not. However, I am currently treating a dog with suspicion for this disease. Suspicion does not equal diagnosis. But the disease is pretty devastating. So why risk it by feeding raw meat? Remember my nutrition blog from so many months ago? I think I addressed the problems associated with raw diets in that blog. Add this scenario to that list of reasons not to feed raw food to your animals.


 Well, that’s enough of that.  I hope you’ve all enjoyed your tutoring session on internal parasites. Don’t worry, there won’t be a test!


Until next time………


Dr. Voorheis

A Whole New Can Of Worms

A whole new can of worms


July 3, 2014


From the desk of Dr. Voorheis



It is always a little uncomfortable to consider that intestinal parasitism exists in our pampered pets. We’d all like to think that is a more common problem in some other country, or that it happens to animals that aren’t as well cared for as yours. Well, to some extent that is true. It is helpful to remember however that there are a number of organisms whose only job is to survive, and your dog and cat are their hosts. The best way to combat the creatures that invade the gut is through knowledge. Knowing their life cycles and what you can do to keep your pet safe is key. So, what do I mean by intestinal parasites? In general, they come in two types; worms and protozoa. Let’s start with worms. To limit this discussion even further, I’m going to stick with the worms we see the most in our practice. Those would be Roundworms and Tapeworms. Neither is a dog or cat’s best friend. Pardon the graphic pictures, but I thought it a good idea to give examples so that you know what to watch for. Mind you, in the Tapeworm picture below, the worm is the small white rice looking object in the brown pile of ….well you are all familiar I’m sure. 



Roundworms are common in dogs and cats. Two types affect dogs and two types affect cats. In dogs you have Toxacara canis and Toxascaris leonine and in cats you have Toxacara cati and Toxascaris leonine. Fancy names but at the end of the day, still parasites that are no good for your pets.

Dogs and cats can become infected by ingesting ova (worm eggs) or by using an intermediate host. Toxacara canis, the most common roundworm in the dog, is often obtained transplacentally from the mother. Yes, the puppies are actually born with them. Toxacaris cati uses transmammary passage (in mother’s milk). Toxascaris leonina can use an intermediate host.

 The immature stages of roundworms migrate and can cause liver fibrosis and pulmonary lesions. Immature worms will encyst in “somatic tissues – i.e. body tissues” and won’t start migrating again until they are under the influence of certain pregnancy hormones. Then they will migrate to the uterus and into the fetus. The adult stages live in the small intestine and migrate against the flow of ingesta (nourishment taken in by mouth). They can cause inflammatory infiltrates in the wall of the intestine. Sometimes they will migrate into the stomach and are vomited up. A heavy worm load can cause intestinal obstruction, although this is uncommon.

 Zoonotic potential

 This is the potential for an animal disease to cause disease in people. According to the Centers for Disease Control in Atlanta (CDC), roundworms make up part of a group of five parasitic diseases that are targeted for public health action. Close to 14% of the population of the United States have antibodies to roundworms indicating exposure. In people, the disease can cause one of two syndromes, ocular larval migrans and visceral larval migrans. There are 70 cases of ocular larval migrans per year in this country. They can cause permanent blindness. Children are at increased risk because they will sometime ingest dirt during outdoor play. Below is a diagram of the life cycle of the roundworm:




Diagnosis, treatment and prevention

Diagnosis is easy as ova are produced in large numbers and are readily found by fecal flotation. In some neonatal puppies the worms obtained transplacentally are in such high numbers that the puppies get sick before the worms mature enough to lay eggs.

 The CDC recommends treatment of all puppies, regardless of positive or negative fecal results, beginning at age 2, 4, 6, and 8 weeks of age. Newborn puppies can be treated with fenbendazole (100 mg/kg x 3 days) – this treatment can be repeated in 2 to 3 weeks. High dose fenbendazole can be given daily (50 mg/kg/day) to the pregnant dog at day 40 of gestation and continued daily until two weeks post partum. For kittens, deworming at 6, 8 and 10 weeks of age is the proper protocol. Lastly, monthly treatment can be given to adult dogs, usually also given in the form of their heartworm preventative or monthly flea preventative. Two specific products come to mind. The first is Revolution which kills fleas, ticks and heartworm and is also effective against roundworms and scabies. The second product is Sentinel Spectrum which is a heartworm preventative and IGR + monthly deworming medication. For cats, use Revolution. No cat should be without it. I don’t want to be seen as putting one product up against another but Revolution is a very effective products for our cats and kittens and it is my responsibility to relay that information to my clients.

 Here’s the bottom line on roundworms. It is a treatable zoonotic disease that we could and should do a much better job of getting rid of. Roundworms are a big part of the reason why a yearly fecal examination is so important.



Tapeworms are hands down the most common worm we deal with. I see dogs and cats infected with tapeworms every day. That is not an exaggeration – every day. Tapeworms have an indirect life cycle as the dog or cat is infected when it eats an infected intermediate host. Fleas and lice are intermediate hosts for D. caninum, wild animals such as rabbits are intermediate hosts of Taenia spp. Tapeworms are by far the worm that gets the most reaction from our clients. They are offensive to look at and nothing is more gross than cuddling with your favorite pet and ending up with motile tapeworm segments on your lap. Tapeworms rarely cause disease in our dogs and cats. The most common sign in infested dogs and cats is anal irritation (just another reason for our dogs to scoot on their behinds) associated with the shed segments crawling on the area. Tapeworms are usually diagnosed when the owner reports seeing segments (that are about the size of a motile grain of rice) either in the perineal area or in the feces. See picture above.

 Treatment is with any drug or combination of drugs that contains praziquantal. Prevention of tapeworms involves controlling the intermediate hosts (i.e. fleas). Said another way… if your dog or cat has tapeworms, they have fleas. Period, end of story. So it cycles back to flea control. Remember my flea blog? It’s the circle of life.


There are three other intestinal worms to consider. These thre are far less common in Southern California. I have seen all three, but they are rare. They are Hookworms, Whipworms and Strongyloides. Whipworms should be investigated IF a dog has signs of colitis or large bowel disease. Whipworms may cause an unusual electrolyte disturbance that resembles that of Addison’s disease, but this is rare. Hookworms are not common in this part of the country. They can cause severe anemia as they are blood feeders. Strongyloides are also uncommon but should be looked for in puppies and kittens from pet stores and animal shelters. It too can cause large bowel signs.




Well, that’s enough gross worm business for today. Next time I will delve into one cell causes of parasitism such as Giardia, Coccidia and Tritrichomonas. Something to look forward to. (Gulp)

Until next time……

Dr. Voorheis

Musings, Coyotes and Snakes

Musings, Coyotes and Snakes

June 19, 2014

From the Desk of Dr. Voorheis


As I sit here typing and wondering about writer’s block, I am also reflecting at the success of the blog over these first six months. The blog has (so far) accomplished exactly what I intended for it to do. I will acknowledge it is still a work in progress and I haven’t exactly been consistent with it over the past few weeks, but overall I am pleased with the effort. Some topics I have tackled have been a bit more intense than I had originally planned, but I think most have been right on target. I’ve also been able to get a little more personal and invite you all to get a glimpse of a different side of Dr. Voorheis. Those entries seem to be the most popular. So I’m reminded of Sally Field……you like me…you really, really like me! I crack myself up!

Looking forward, upcoming topics will include pain management, gastrointestinal disease with a focus on IBD, pancreatitis, gastric dilatation-volvulus, physical rehabilitation, diabetes mellitus and an extra special one on cancer. On a personal note, look for an upcoming topic on “aquaponic gardening” which is another passion of mine. I will also update everyone very soon on the progress of our new building, a project which has been two years in the planning and is getting closer and closer to fruition. Of course, this does take a great deal of my time and thus the delayed blogs of late. I can’t blame all the delays on critter care. I will say that the new building will be something to behold and I know you will all enjoy it a great deal!

 This week I have a shorter blog than those of recent weeks. I actually have a couple of warnings for all the WBAH pet parents. As you know, we are in the midst of a drought here in Southern California. This will not be a blog to lecture you about conserving water. I will leave that to your own common sense. So I won’t mention things like switching to native landscapes and sweeping the driveway instead of washing it down etc. No, this blog is a reminder that we share our suburban lives with wild animals. How does that tie in with a blog written by a veterinarian? Well, the wild animals that normally do not impact us too much are leaving the hills in search of water and food. Sadly, cats and dogs qualify as a food source. This week alone, we have had 4 animals attacked by coyotes. It is beginning to feel like coyote attacks are coming close to outnumbering dog bite wounds. Coyotes do not attack to win a fight and wander off. They attack with the intent to make a meal of your dog or cat. I suspect we have only seen the tip of the iceberg. As I drive through Whittier, there is always a sign or two about a missing dog or cat. Sadly, a significant number of these missing cats and small dogs have probably fallen victim to being carried off by a coyote. Coyotes are primarily nocturnal hunters but MANY daytime attacks have been documented as well. In fact, a rather old documentary shown on public television many years ago showed that coyotes around Griffith Park in Los Angeles have long adapted their lifestyle to suburban life in the communities surrounding the park. They begin their hunt as people leave for work. Most of our Whittier area coyote attacks are in the evening and over night, but not all of them are.


Prevention of coyote attacks:

1. Cats – Keep your cats inside – this one is foolproof. Indoor cats do not get eaten by coyotes. For those cats that must go outside or remain indoor/outdoor cats, please understand there is a risk. I’m not saying all cats must be kept inside. I’m saying that there is risk for a cat to be outside. The longer the cat is outside, the risk will of course increase. Cats that spend the night outside are in the highest risk group. In Whittier, the risk is greatest up near the hills. The neighborhoods surrounding Uptown Whittier, Friendly Hills and La Serna HS are probably at the highest risk. However, we have seen coyote attacks in neighborhoods below Whittier Blvd as well. Coyotes are not adverse to trotting down our streets. They can easily use the green beltway as a conduit to cross busy streets and access neighborhoods you would not think they can get to.

2. Dogs – the smaller the dog, the greater the risk. The highest risk dogs are dogs under 20 to 25 lbs. Small dogs might think they are tough, but are no match for a coyote. Most coyote attacks on dogs are small dogs being attacked in their backyard at night. Coyotes have no difficulty hopping a 5 foot fence. Many clients think their dogs are safe in their own backyard but that is where most attacks occur.  Keep an eye on your small dogs when they are out in the backyard. On that final trip outside at night to go potty, go with your dog. Don’t leave food outside, pet or human. If you feed outdoors, feed only what the dog can eat in a few minutes then pick up the uneaten food. If your dog is leaving food in the dish, you may be feeding too much. That’s a subject for another blog which I believe I have already written. Remember the nutrition blog? The point is that uneaten food will attract wildlife. Everything from ants to possums, raccoons and coyotes. Always leash walk all dogs. Don’t let small dogs walk off leash.  As a matter of fact, don’t let big dogs walk off leash either.

A number of years ago, we had clients who lived just off a golf course. They enjoyed strolling in the evening with their small dogs on the fairway that was near their home. As the two small dogs scampered ahead of them, no more than 100 feet from the owners, a coyote dashed out from the bushes lining the fairway, grabbed one of the dog’s and took off. They never saw their dog again. Don’t let this happen to you. If a coyote grabs your pet and you witness it, do all possible to make a lot of noise. Yell, scream and give chase because there is a chance that the animal will drop your pet. We have had a number of clients save their dog’s lives by chasing the coyote off. Now, I am not advocating getting into a physical confrontation with a coyote but sometimes startling the coyote will make them drop their prey. Treatment is obviously based by what and where the damage is on your critter.



This spring has also produced the greatest number of rattlesnake bites we have seen in a number of years.  It is estimated that about 150,000 dogs and cats are bitten by snakes each year in this country. The vast majority of these snake bites (99%) are bites by Crotalidae. By what? Pit vipers. The family Crotalidae includes rattlesnakes, copperheads and water moccasins. In our neck of the woods, it’s the Western Diamondback rattlesnake.

The venom is a complex mix of bioactive enzymes and peptides. Some of these enzymes aid in spreading the venom through the tissues. Other enzymes in the venom lead to coagulopathies (clotting problems) and tissue necrosis. The venom damages small blood vessels called capillaries and causes them to leak red blood cells and plasma. This accounts for the swelling and bruising. Snake bitten dogs suffer from clotting problems (coagulopathies), low platelet numbers (more bleeding problems), pain (snake bites are PAINFUL), and renal failure. If the dog is unfortunate enough to be bitten by the Mohave Green rattlesnake we can add neurotoxicity to the mix as well.

The severity of the signs directly correlates to the amount of venom introduced into the dog or cat. Snakes have control over how much venom they release. The more they feel threatened the more they release. Most snake bites occur on the head and face. Dogs frequently investigate with their nose. Curiously, cats will often be bitten either on the face or the front feet, because they also investigate with their feet. The symptoms include fang marks (sometimes hidden under the hair coat), swelling, edema and considerable pain. We will also see redness and bruising. Did I mention pain? Swelling worsens with time. Upon presentation at the animal hospital, we will run laboratory work, including clotting profiles. These may need to be repeated depending on response to therapy. Treatment includes treatment for shock, fluid support, and pain management. The cornerstone of treatment is antivenin which works by neutralizing venom. The sooner it is administered the better. That is not to say a dog that doesn’t receive antivenin won’t survive. Many still do survive, but the best chance for survival is administering antivenin as soon as possible. Other medication may be used at the discretion of the treating veterinarian depending on severity of signs.

copperheadsnake                     diamondbackrattlesnake

Copperhead Snake                                                                       Diamondback Rattlesnake


Water Moccasin Snake

Prevention of Snake Bites:

Keep dogs on leashes and closely supervised when in or near known or prime snake habitats. Cats are safest inside if you live in areas of high snake density. If you hunt with your dog in areas where rattlesnakes are known to be in abundance, enroll in a snake avoidance class. There is also a rattlesnake toxoid vaccination. Two doses are given about one month apart. We still don’t know just how effective this vaccination is. By that I mean if your dog has been vaccinated and gets bitten by a rattlesnake, I would not take that to mean you don’t have to rush your dog to a veterinarian. I would still advise immediate emergency treatment. The hope with the vaccination is that the dog would have less severe symptoms than one who had not received the vaccination.

 Well, that’s all I’ve got for this week’s blog. Certainly shorter reading than the renal failure treatise I wrote. Until next time……..

 Dr. Voorheis

The Ailing Kidney

The Ailing Kidney


May 29, 2014


From the desk of Dr. Voorheis



Two weeks ago, I devoted an entire blog to one of the most fascinating and hard working organs in the animal or human body – the kidney.  We talked about what it does and how it functions when all is well with the world.  Now, even though it may have seemed quite detailed, I assure you that we only just touched on the topic. I say “touched on” because the real detail is enough to make my eyes spin so I can only imagine that complete detail would probably make you all hit the delete button rather quickly.  And I certainly don’t want that, so this week I will attempt to provide an interesting peek into the world of the sick kidney without sending anyone into a comatose state.

To cover all aspects of renal disease in tremendous detail is beyond the scope of this blog and really is too much information to absorb in one sitting. Or several sittings for that matter. Rather, it is a better idea to share some basic terms and knowledge in an effort to educate and inform my clients so that you are all armed with the knowledge needed to keep your eyes open and watch for signs and symptoms and be aware of when it may be time to get Fido or Fluffy into the office for a visit.

 As with most diseases, renal disease is most treatable and manageable when it’s caught early.   Statistically speaking, the number one killer of cats is renal disease. Sad, but true. A quick side note: that information (afore mentioned renal disease statistics), known almost intuitively to any small animal clinician, was published in a huge study in Sweden. The numbers were gleaned from Swedish insurance companies and published in 2009 in the Journal of Veterinary Internal Medicine. Nearly 50,000 cats were looked at to determine common causes of death. What I thought was most interesting was that most dogs and cats in Sweden are insured for veterinary care. Remember my insurance blog?  In older dogs, renal disease is a significant player in cause of death, but it is not the most common. Dog statistics are greatly influenced by breed, size of animal etc. The most common cause of death in older dogs is neoplasia (abnormal growth of cells, which may lead to a neoplasm or tumor).

 So, on to the educational part of our session. I’ll start with some terminology that is basic and necessary to understand what we’ll cover this week. First, some terms and then some brief descriptions of the various stages of renal disease. Later, we will talk about signs and symptoms and what to watch for as well as treatment options.

Ÿ  Renal – pertaining to the kidney

Ÿ  Renal disease – implies the existence of renal lesions; it does not qualify the cause, severity or distribution of the lesions or the degree of renal function

Ÿ  Chronic Kidney Disease – refers to a loss of nephrons associated with a prolonged (usually two months or longer) and progressive disease process.

Ÿ  Renal reserve – think of the percentage of extra nephrons available, i.e. those not necessary to maintain normal renal function. Although it probably varies from animal to animal, it is greater than 50% in most dogs and cats.

Ÿ  Renal insufficiency – begins when the renal reserve is lost. Animals with renal insufficiency outwardly appear normal but have a reduced capacity to compensate for stresses such as infection and dehydration and have a reduced capacity to concentrate urine.

Ÿ  Azotemia – is the increased concentration of urea nitrogen (BUN), creatinine and other nonproteinaceous nitrogenous waste products in the blood. There can be non renal causes for azotemia (pre-renal, e.g. dehydration and shock and post renal – lower urinary tract obstruction).

Ÿ  Renal Azotemia – denotes azotemia caused by renal parenchymal issues, i.e. – nephron nonfunction.

Ÿ  Uremia – is the presence of all urine constituents in the blood. It may occur secondary to renal failure or post renal disorders, including urethral obstruction and bladder rupture.

Ÿ  Uremic Syndrome – is the constellation of signs that occurs secondary to uremia. These include oral cavity ulceration, gastroenteritis, acidosis, pneumonitis, osteodystrophy, and encephalopathy).

Ÿ  Renal failure – is a state of decreased renal function that allows persistent abnormalities (azotemia and inability to concentrate urine) to exist; it refers to a level of organ function rather than specific disease entity. Occurs when approximately 3/4 of the nephrons from both kidneys cease to function. That is nephron disease (remember our new friend the nephron from the last blog?) – anything from the glomerulus to the collecting ducts.

Ÿ  Acute renal failure (ARF) – results from an abrupt decline in renal function and is usually caused by an ischemic, toxic or infectious insult to the kidneys. In some instances this can be reversible if we get to the case in time.

Ÿ  Chronic renal failure (CRF) – In contrast, the nephron damage associated with chronic kidney disease (CKD) is usually irreversible, regardless of whether the underlying disease primarily affects the glomeruli, the tubules, the interstitium or the renal vasculature. Irreversible damage to any portion of the nephron renders that nephron nonfunctional. Irreversibly damaged nephrons are replaced by fibrous connective tissue. It is difficult to determine the specific cause once end stage kidney damage is present. CKD occurs over a period of weeks, months, or years and, as stated above is a leading cause of death in both dogs and cats. Once advanced stage CKD has occurred, improving renal function is not possible, but many times it is possible to alleviate the signs. The goal of CKD treatment is 3-fold:

  1.  If possible, identify and correct the primary disease process
  2.  Monitor and slow disease progression
  3.  Alleviate patient clinical signs

So, as you can see there are various stages of renal disease. As I mentioned, catching it early gives your critter the best chance at survival. So, how do we know that renal disease is developing in our dog or cat?  We will go over signs and symptoms in a moment, but first we should talk about the disease itself in a bit more detail.

 Sick kidney 1

The Glomerulopathies

I had thought to basically divide this blog into a discussion on Acute Renal Failure and Chronic Renal Failure. Glomerular disease was going to be included in those topics. I’ve since decided to devote a bit more time to glomerular disease as its own separate topic. Although it is primarily seen as a chronic kidney disease, it deserves mention by itself.  Glomerulonephritis (GN), or inflammation of the glomeruli and tubules, is the most common type of glomerulonephropathy and it is caused by immune complexes within the glomerular capillary walls. It is one of the major causes of chronic kidney disease in dogs. There are other causes of glomerular disease such as amyloidosis (a type of protein – think SharPei dogs, Abyssinian cats) and hereditary glomerular diseases (seen in male Cockers, Samoyeds).

 The disease is characterized by the appearance of proteins in the urine, principally a protein called albumin. The amount of protein in the urine is a direct indicator of the severity of the disease and can be used as a marker of progression as well. Immune complexes present in the glomerular capillary wall are usually responsible for initiating the glomerular damage and subsequent protein loss. Immune what? Immune complexes are circulating antigen (think foreign protein) + antibody (immune response) molecules that may be deposited or trapped in the glomeruli. They can also occur when circulating antibodies react with glomerular antigens (proteins) within the wall of the glomeruli. Finally, sometimes foreign proteins (such as antigens associated with heartworm disease) become trapped in glomeruli capillary wall and attract antibody. Once these guys are trapped in the capillary wall, they attract other inflammatory components and a cascade of events takes place. The result of this dance is a damaged or destroyed glomerulus.  There are a host of conditions associated with glomerulonephritis in dogs and cats and far too many to list here. Some you may be familiar with are Dirofilariasis (heartworm), Pyometra (from my spay/neuter blog), Pancreatitis, Cushing’s disease, and Diabetes in dogs and Feline leukemia virus, Neoplasia, Diabetes and Pancreatitis in cats.

  Sick kidney 2                                         

Signs and Symptoms

There are often no signs associated with low level proteinuria (protein loss through the kidneys). If signs are present, they are often non-specific and mild such as lethargy and weight loss. If protein loss is severe and serum albumin drops to <1.5, we may see edema or ascites (fluid buildup in the abdomen). If the glomerular disease causes more than ¾ loss of the nephrons, then we will see the signs that we typically see with advanced stage CKD (chronic kidney disease). Those signs will be increased thirst, increased urination, poor to no appetite, nausea, vomiting and weight loss. Occasionally, the clinical signs will be associated with one of the underlying infectious, inflammatory, endocrine or neoplastic conditions mentioned above and we will discover the glomerular disease as a faucet of one of those diseases.

 Persistent proteinuria can lead to something called “nephrotic syndrome” which is a constellation of signs. The combination includes proteinuria (excess protein in urine), hypoalbuminemia (low blood albumin), ascites or edema (fluid in abdomen or in tissues), and hypercholesterolemia (high blood cholesterol). In addition, systemic hypertension (high blood pressure) and hypercoagulability are frequent complications in dogs with nephrotic syndrome. Systemic hypertension is common in dogs with GN. Some of these dogs will become blind as hypertension can cause retinal detachment. Most of the time we think the high blood pressure is secondary to kidney disease rather than a primary cause. A word about blood pressure measurement in dogs and cats; it is not as easy and simple as we might think it should be. A consistent and accurate measurement of blood pressure in our small animal patients is frustrating to say the least. Doppler ultrasound can give a systolic measurement but not a mean arterial pressure or diastolic measurement. Breed size of dog or cat and temperament of animal all influence the accuracy of measurement. Oscillometric (indirect) uses an automated system for processing pressure cuff oscillation signals.

 The diagnosis of glomerular disease is made with persistent, severe proteinuria within an otherwise normal urine sediment. The urine protein:creatinine ratio is used to measure the magnitude of protein loss.


Since immune complexes usually cause GN, the primary treatment objectives would include finding and eliminating the cause of the immune complex and reduce the glomerular response to those immune complexes. Elimination of the source of antigenic stimulation is the treatment of choice. An example of this is the proteinuria associated with heartworm disease. Treat the heartworm and the glomerular disease goes away.

Unfortunately, elimination of the antigen source or underlying disease is not always possible, either because we cannot identify the antigen source or we cannot eliminate the antigen source. Immunosuppressive agents, such as cytoxan, imuran or prednisone are not generally recommended in the dog for treatment of GN. Aspirin therapy, ACE inhibitors (benazepril, enalapril), dietary sodium restriction, high quality-low quantity protein diets. Each case is individual and treatment is tailored to that individual. Remember, we do not practice cookie cutter medicine at WBAH. Now, on to the world of ARF.

Acute Renal Failure

As we now know from above, renal failure occurs when approximately 3/4’s of the nephrons of both kidneys cease to function. Acute renal failure results from an abrupt decline in renal function and is usually the result of an ischemic (lack of blood, i.e oxygen supply to tissues) or toxic insult to the kidneys. It is important to remember that the kidneys are highly susceptible to the effects of ischemia and toxicants because of their unique anatomic and physiologic features. The kidneys receive 20% of cardiac output directly which makes them sensitive to blood borne toxicants. Ischemic or toxicant induced injury results in damage to the epithelial cells of the proximal tubules and thick ascending loop of Henle. Huh? Nephrotoxicants interfere with essential tubular function and cause cellular injury, swelling and death. Renal ischemia causes cellular hypoxia, swelling and death. Sometimes tubular lesions from toxic insults and ischemia are reversible if addressed in a timely fashion. Many factors may predispose the kidney to ischemia and toxicant induced injury. Those factors would be the following: 
  • The kidneys receive 20% of cardiac output. The kidney cortex receives 90% of that flow.
  • Glomerular capillaries have a large surface area
  • Proximal tubule and thick ascending loop of Henle cells have high metabolic rate and are susceptible to hypoxia and nutrient deficiency
  • Tubular secretion and resorption may concentrate toxicants within cells
  • Countercurrent multiplier system may concentrate toxicants with the medulla area of kidney
  • Xenobiotic (substance foreign to body) metabolism may generate toxic metabolites. For example, the metabolites of ethylene glycol (radiator fluid) are more toxic than the ethylene glycol is.


Acute renal failure

In some cases, ARF inadvertently develops in the hospital setting in conjunction with the performance of diagnostic or therapeutic procedures. Fortunately, these are not common. An example might be the ARF case caused by hypotension (low blood pressure) and decreased renal perfusion associated with anesthesia and surgery. Another example is the use of vasodilators or non-steroidal anti-inflammatory drugs (NSAIDS). Prolonged anesthesia with inadequate fluid therapy in older dogs and cats with preexisting, subclinical renal insufficiency is a cause of renal ischemia and ARF in the hospital setting. The setting where I see the most potential for this kind of injury is during a teeth cleaning. This is where we have the potential for poor communication when discussing cleaning Fluffy’s teeth. It is normal and reasonable for a client to think of their older dog needing his/her teeth cleaned in terms of how that procedure works when they themselves go to the dentist and lay in a chair for an hour while their hygienist cleans their teeth. They get their teeth cleaned; they get up, and walk out and go about their day. This client may also have the feeling that, wow, cleaning my dog or cat’s teeth is expensive; and then the vet wants to do blood work and put the animal on IV fluids? Is this really necessary? The short answer is absolutely! The longer answer is if an animal is placed under an anesthetic, the potential exists for alteration of blood pressure (hypotension – which contributes to poor renal blood flow), for hypothermia (which contributes to poor renal blood flow), and for vasodilation (which contributes to poor renal blood flow). That does not mean you shouldn’t have your dog or cat’s teeth cleaned even at an advanced age. By having the teeth cleaned, you are removing or preventing painful teeth and eliminating one of the sources of immune complex disease that can cause GN.

 In our hospital setting it is recommended that animals undergoing surgery and dental procedures are wrapped in a warm water circulating blanket, assessed for pre-existing renal disease, and receive IV fluid support before, during and after the procedure. This is recommended because of the need to support those nephrons. Most of our clients understand that when these recommendations are made for elective procedures they are made with the pet’s safety in mind. Sometimes, a client will decline IV fluid support without the knowledge of why it was recommended or knowing the added risk that this adds to their pet. This blog attempts to address just one of the reasons for IV fluid support. In addition, even though this is the renal blog, it may be a timely reminder to revisit the insurance blog and the dental blog. If we take a good look at our young dog’s and cat’s mouths (those critters in the 1 to 3 year old age brackets), that’s a good time to not only clean teeth at home, but have those animals brought in for the sedation and hand scale dental prophy. Not only is it way cheaper, it is a way to keep their mouths healthy for life. This young animal dental prophy is only available for those dogs and cats that have grade 1 dental disease.

 As I write this blog, I am grateful to my colleagues, associates and clients at WBAH. We really see very few cases of acute renal failure; much of that is due to the preventative steps my colleagues take when presented with the dog who has a rising red count and diarrhea. I have gratitude to the client who allows us to take the aggressive steps to treat something before it gets so bad that we have to deal with two problems, the initial disease and the secondary acute renal failure.

 The biggest risk factors for acute renal failure in our hospital setting are something I would call “acute on chronic”. Animals with renal insufficiency have a reduced renal concentrating ability. When any hypovolemic event happens, most commonly dehydration caused by vomiting or diarrhea or perhaps a dietary indiscretion, then “bingo” – a critter who was able to handle their renal insufficiency can no longer do so because they are volume depleted.

 There are at home toxins that can lead to acute renal failure and death as well. I covered most of these in the blog entitled “Dangers Lurking in Your Home”. The most common one we see is ethylene glycol toxicity commonly known as anti-freeze toxicity. Just a tiny amount can be fatal to an animal. We see this every year. There is an antidote, but it must be administered quickly or we won’t be successful in preventing fatal renal failure.  Another cause of acute renal failure worth mentioning is the ingestion of pet food containing contaminated wheat and corn gluten and rice protein concentrates. The investigation has focused on melamine and cyanuric acid as the major contaminants; however melamine related substances may also be involved in the toxicity. It is thought that a chemical reaction between melamine and cyanuric acid produces insoluble crystals that form in the distal tubules of affected animals, compromising renal function. There is a pet food recall resource at http://www.petpoisonhelpline.com/category/product-recalls/feed/ . Fortunately, this problem is on the marked decline. There are medications that will cause renal issues as well. Generally speaking, certain antibiotics are avoided in known dehydrated animals. For the arthritic dog who develops vomiting and diarrhea we will avoid giving his non steroidal anti-inflammatory medications until he is properly hydrated again.


In general the treatment of ARF is to establish renal perfusion and correct dehydration. In the ARF animal, hydration needs are corrected quickly (rehydrate within 6 hours) as opposed to rehydrating over 24 hours. Treatment priorities are fluids, phosphate binders, anti-emetics, acid blockers and sometimes judicious use of diuretics and ACE inhibitors. Electrolyte monitoring is also key. In some cases animals are referred for peritoneal dialysis or hemodialaysis.

 Chronic Kidney Disease

 The cause of CKD is usually difficult to determine because by the time an animal has CKD the endpoint of irreversible glomerular and tubular damage is the same. Nevertheless, recent studies have shown that primary glomerular disorders are a major cause of CKD in the dog. Because glomerular filtration is uniformly reduced, CKD may be considered a single pathologic entity, although diverse pathways can lead to this end point.  Below is a tablet that highlights potential causes of chronic kidney disease in dogs and cats.

  • Potential Causes of Chronic Kidney Disease in Dogs and Cats
  • Immunologic Disorders – Systemic Lupus Erythematosus, Glomerulonephritis, Vasculitis (e.g. Feline Infectious Peritonitis)
  • Amyloidosis
  • Neoplasia
  • Nephrotoxicants
  • Renal Ischemia
  • Inflammatory or Infectious Causes – Pyelonephritis, Leptospirosis, Renal Calculi

  • Hereditary and Congenital Disorders – Renal hypoplasia or dysplasia, polycystic kidneys, Familial Nephropathies (Lhasa Apsos, Shih Tzus, Norwegian Elkhounds, Rottweilers, Bernese Mountain Dogs, Chow Chows, Newfoundlands, Bull Terriers, Pembroke Welsh Corgis, Chinese Shar-Peis, Doberman Pinschers, Samoyeds, Golden Retrievers, Standard Poodles, Soft Coated Wheaten Terriers, Cocker Spaniels, Beagles, keeshonds, Bedlington Terriers, Cairn Terriers, Basenjis, Abyssinian cats
  • Urinary Outflow Obstruction
  • Idiopathic

 At the level of the kidney, the fundamental pathologic change that occurs is a loss of nephrons and a decreased GFR. Reduce the GFR and that results in an increase in plasma concentrations of substances normally eliminated by the kidney. Uremic syndrome is the constellation of signs thought to occur as a result of these substances accumulating.  These signs affect sodium and water balance, red blood cell count (anemia), carbohydrate intolerance, neurologic disturbances, gastrointestinal tract disturbances, osteodystrophy, immunologic incompetence and acid base disturbances. As I have mentioned before, the kidneys also function as endocrine organs. When they fail, hormonal disturbances will occur.

 Kidney Vs Kidney                                     

Signs and symptoms

CKD develops over a period of months to years and the signs are often mild at first. These signs include a history of weight loss, polydipsia-polyuria, poor body condition, non-regenerative anemia and small and irregularly shaped kidneys. The diagnosis is made based on compatible history, physical examination and laboratory findings. Radiographs and ultrasound can be performed to identify or rule out potentially treatable causes of CKD, such as pyelonephritis and renal urolithiasis (stones). The International Renal Interest Society has come up with a staging system to help better diagnose, understand and treat feline and canine kidney disease.

 Serum creatinine concentrations must always be interpreted in light of the patient’s urine specific gravity and physical examination findings to rule out prerenal and postrenal causes of azotemia. The CKD stages are further classified by the presence of absence of proteinuria and systemic hypertension.


 In general, characterization of the renal disease and its stability is most important in early stages of CKD when appropriate treatment has the greatest potential to improve or stabilize renal function. In the later stages of CKD, most therapeutic efforts are directed at treating the problems such as inappetence, vomiting, acidosis, potassium depletion, hypertension, anemia and other signs that come up.

 For example, many of these cats and dogs may have dietary changes to reduce their serum phosphorus, and ACE inhibitors to normalize systemic and intraglomerular pressures. Very often, especially with cats, we will have owners administer fluids subcutaneously several times a week. Potassium supplementation is often used and both dogs and cats with CKD are often potassium depleted. Bacterial UTI’s are tested for and treated. Phosphate binding agents are fed to try to reduce serum phosphorus and control secondary renal hyperparathyroidism. Non-regenerative anemias can be managed by use of injectable erythropoietin (EPO). We are fairly conservative with the use of EPO in dogs and cats as the only available EPO is a human variety and over time dogs and cats build up antibodies to it.

 So, that is the ailing kidney in a nutshell. I really did try to simplify it as much as possible. I realize it was a bit heavy this week so I think it’s terrific that you read this all the way to the end. Thank you! As always, keep a watchful eye on your critters and bring them in if you notice anything abnormal. Early detection is key to helping our furry friends.  

 Until next time,

 Dr. Voorheis

A Day In The Life Of A Kidney

A day in the life of the kidney

May 15, 2014

From the Desk of Dr. Voorheis


A quick apology for not having a blog for you all to read last week. It was another busy week and Dr. Voorheis was knee deep in critter care. And as we all know by now, the critters come first. However, I did allude to a kidney blog that I had in the works and as promised a couple of weeks ago, I have finally finished the piece on the kidney. I have wrestled with this topic for a couple of weeks now and finally decided to do what I should have done in the first place. The intent is to write a blog that is both interesting and informative but as I reviewed current veterinary literature and current available information for clients (handouts, Dr. Google etc.), most of what I found was lacking substance. Most literature is only vaguely informative of what a kidney does, why is it so vital, and why protecting it is so important. We could start answering that last question right away. Any organ that receives 20% of cardiac output directly has got to be pretty important, right? That also makes the kidney exquisitely sensitive to toxic insult.  It seems that the only thing most people know about the kidney is that it acts as a filter.  Well, it does that but it also does so much more.  I’m going to try to tackle this topic in two parts. Part one being the healthy kidney and part two being the sick kidney. This week it’s important to start by laying some ground work and giving you all a good sense of what the kidney actually does for the body. We’ll talk about the sick kidney next week and I will divide that blog into two parts as well. Those parts being acute and chronic renal failure.

Most information regarding kidney function mentions excretion of metabolic waste products as the only function of the kidney, a.k.a “a filter“. What most literature available to the lay person fails to mention is that an equally important function is the regulation of the volume and composition of extracellular fluid, i.e. the body’s internal environment. You can think of it this way – the composition of bodily fluids is determined NOT by what the mouth takes in but what the kidneys retain. In addition, the kidneys have a critical role in red blood cell production and calcium/phosphorus balance (homeostasis).

In most mammals, the kidneys are paired, bean shaped organs located near the top of the back in the dorsal lumbar region. They are bean shaped in the dog and cat but interestingly heart shaped in a horse. They are separate from the rest of the abdomen because they are covered with peritoneum, the lining of the abdomen. That makes them referred to as “retroperitoneal”. Blood is carried to the kidneys by renal arteries which arise directly off the aorta. As stated above, 20% of cardiac output reaches the kidneys with each beat of the heart.


 If I were to slice a kidney open along its long axis, it would be immediately apparent they are two distinct areas, the outer area called the cortex and the inner area called the medulla. The striations (lines) that are seen are formed by an arrangement of the nephron which is the functional unit of the kidney. The kidney’s currency if you will. I’ll explain later.

The concave portion of the kidney is where blood vessels enter and leave through the renal artery and renal vein. Also exiting from this area is the ureter which is the tube that collects urine and transports it to the bladder. Not shown in the diagram above are things like renal lymphatics and renal nerves.

Ok, now back to those nephrons I mentioned above. As I said, the functional unit of the kidney is the nephron. In dogs, each kidney has about 415,000 nephrons. In cats, each kidney has about 190,000 nephrons. Humans have about a million nephrons in each of our kidneys. Ok, I can‘t resist. Here comes the classic rocker in me. As I was typing this up, I thought about the Beatles song “A Day in the Life”. Maybe they got the same guy to count nephrons as counted holes in Blackburn, Lancashire. So here is some trivia for you – how many holes does it take to fill the Albert Hall? All I can say is that guy’s job was easy compared to the job of “counting nephrons”.



The functional unit of the kidney is pictured above. That’s our new friend the nephron. This guy makes all the magic happen. This guy is also responsible for weeding out more pre-veterinary and pre-medical students from those lucky ones who make it.  I suppose renal physiology must take its place next to organic chemistry as a major challenge in undergraduate curriculum. The point being that this is complex stuff and I’m only going to skim the surface in this week‘s blog.

Here is where we dive deeper and get our hands dirty so to speak. Prepare for medical vocabulary. In actuality, there are two types of nephrons. They are named for their location in the kidney and for how “deep” their “Loops of Henle” penetrate into the medulla. The exception is the cat whose nephrons are always “juxtamedullary” with 100% long looped nephrons. The juxtamedullary nephrons are those nephrons that develop and maintain the osmotic gradient from low to high. Huh? The what? The concentration gradient. Ok, we are halfway home so stay with me. The glomerulus is the “tuft” of capillaries (tiny blood vessels) through which filtration takes place. Branches of arteries become important here because certain drugs act on them which can help treat some types of kidney disease. The “afferent arteriole” is a tiny branch of the kidney artery that feeds blood directly to the glomerulus and the “efferent arteriole” is a tiny branch of the kidney artery that takes blood away from the glomerulus. This blood leaving through the efferent arterioles goes into another bed of capillaries called peritubular capillaries which supply the nephron tubules. The vasa recta are capillary branches from the peritubular capillaries associated with the long looped nephrons. After perfusion of the kidneys, blood is returned to the caudal vena cava by the renal veins. Filtrate from glomerulus is collected by the Bowman’s capsule and is subsequently directed through the proximal tubule, loop of Henle, and distal tubule. The distal tubule then empties into a cortical collecting tubule. A cortical collecting tubule is not unique to a single nephron because it receives tubular fluid from the convoluted portion of several distal tubules. When the collecting tubule turns away from the cortex and passes down into the medulla, it is known as a collecting duct. The tubular fluid is subjected to reabsorption and secretion. Successive generations of collecting ducts unite to form progressively larger collecting ducts. The tubular fluid is finally discharged from the larger collecting ducts into the pelvis of the kidney and is conveyed from there by ureters to the urinary bladder for storage until discharge through the urethra.

We now enter the phase of renal physiology that causes pre-vets to drop out and decide to do something else. The statement highlighted in bold is the one that holds some very complex physiology (how things normally work) and even more complex pathophysiology (what happens when things go wrong).

I don’t intend for this blog to be too complex and teach renal physiology (I know, I know…too late!).  So I’m going to try to summarize some important points in an effort to demonstrate that the kidney is more than a filter.  Some of you have had a CBP (complete blood profile) done for your dog or cat and therefore some of you have heard me mention BUN and Creatinine.  Have you ever wondered what those are? Well, here’s where you find out. There are some terms that will need explanation so I’ll start there. Renal blood flow (RBF) is the rate at which blood is delivered to the kidneys. Another term is renal plasma flow and this refers to the liquid part of the blood.  As long as there is renal blood flow, (except in some disease circumstances) there will be a glomerular filtrate formed. Remember it’s at the glomerulus that the filtrate starts. All of these components are measured at milliliters per minute. So that allows us to compute a ratio, we can compute something called filtration fraction. The filtration fraction is that value that we get when we divide GFR by RPF. In reality, in clinical medicine we are most interested in GFR. So we measure two compounds that because of their usual even production and filtration, allow us an assessment of glomerular filtration rate. Those two compounds are blood urea nitrogen (BUN) and creatinine (Cr). Elevations in those two substances usually mean that there is a decrease in glomerular filtration rate. GFR can be decreased due to dehydration, renal disease or post renal obstruction. Probably a bit complicated but interesting none the less I think.

The kidney uses some complex mechanisms to try to keep GFR constant. It can sense decreases in volume of blood being provided to it and it will immediately begin to act. The afferent renal arteriole will open and the efferent renal arteriole will narrow and this acts to increase the flow rate at the glomerulus. In addition, in the glomerulus there are cells called the macula densa. If these cells sense a decreased volume of filtrate to distal tubules, they act to increase sodium and chloride ions in the ascending loop of Henle. They also increase the release of an enzyme called rennin. Rennin increases the formation of angiotensin which is converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II acts to constrict the efferent arteriole and thus increases GFR. Angiotensin II also stimulates the production of a hormone called aldosterone. Aldosterone causes reabsorption of sodium – all of which assist the kidneys to regulate volume.  So you see, the kidney has a big job to do. Actually, many big jobs.

The amazing miracle of kidney function continues as we follow the filtrate into the proximal convoluted tubule, the descending loop of Henle and the ascending loop of Henle and on into the collecting ducts. There is a vast network of capillaries right next to these tiny tubules. Through a mechanism called “Countercurrent exchanger” and “Countercurrent multiplier”, essential substances that the body needs to conserve are conserved. Glucose and amino acids are absorbed along with sodium in a rather complex dance that allows for concentration of urine, the excretion of toxic nitrogenous wastes, secretion of potassium and hydrogen and conservation of water.

The two illustrations below show the glomerulus in a little more detail and also show a pretty good diagram the countercurrent exchange and multiplier system. Fascinating stuff!  



 What about hormones? Don’t they play a part in all this too?Yes they do! I briefly mentioned the hormone aldosterone above. Aldosterone is produced by the adrenal gland.  Aldosterone increases sodium absorption in the tubule and is critical in regulation of potassium by promoting the secretion of potassium.

ADH and Osmoregulation

Anti-diuretic hormone (ADH) is a hormone secreted by the pituitary gland that acts on the collecting tubules and ducts to affect their permeability for water. The degree of hydration of extracellular fluid is detected by receptor cells in the hypothalamus. When the cells of the hypothalamus detect and increase in plasma osmolality (concentration), they stimulate the posterior pituitary to secrete more ADH. The secreted ADH is circulated by blood to the kidney tubules where the water permeability change takes place. The thirst center is also located in the hypothalamus and is stimulated by hyperosmolality.  A water deficit requires water intake for correction and these guys will seek water.

Parathyroid Hormone (PTH)

PTH is secreted by the parathyroid glands and acts on the kidney tubules to increase reabsorption of calcium, while at the same time promoting the excretion of phosphorus. PTH hormone is secreted in response to low concentrations of calcium in the ECF. Another role of the kidney in response to decreasing calcium involves the formation of the active form of Vitamin D, also known as calcitriol. Active vitamin D promotes Ca absorption from the intestine. PTH controls the formation of active vitamin D by the kidney.

Erythropoietin (EPO)

EPO is a hormone produced in response to the tissue need for oxygen and stimulates the production of new erythrocytes by its activity in the bone marrow. The kidney is the major site, and the only site in dogs, of EPO production in adult mammals. EPO is produced by peritubular interstitial cells located within the inner cortex and outer medulla of the kidney. Extrarenal EPO production in certain animals and humans helps to maintain erythropoiesis during anemia caused by severe kidney diseases. Anemia is a common side effect of chronic interstitial nephritis in dogs because of the lack of an extrarenal source of EPO.

For any given molecular size, positively charged molecules are more readily filtered than negatively charged ones. This happens because the glomerular membrane has a load of negatively charged proteins in it that attract positive charges and repel negative charges. Hang with me I’m trying to make a point. Plasma albumin is a relatively small protein as compared to globulins, and might be filtered through; however, they have a negative charge. So they generally escape being lost into the urine. In kidney disease, in which poor perfusion may become a factor, the electrostatic charge of the glomerular membrane can change and molecules previously restricted from filtration can be filtered and gain entrance to the capsular space. My point – in some kidney diseases proteins are lost in the urine.

Other kidney diseases affect other parts of the nephron. Some toxins attack and affect the proximal convoluted tubule or transport of critical ions due to membrane damage along the loop of Henle. We’ll talk more about that next week.

Well, that is the kidney in as small a nutshell as I could manage to put it in. Now, to give credit where credit is due. Much of the work of this week’s blog and my understanding of renal physiology must go to the classic textbook, Functional Anatomy and Physiology of Domestic Animals, by Dr. William O. Reece, D.V.M. Ph.D. Dr. Reece is a Professor of Biomedical Sciences at the College of Veterinary Medicine, Iowa State University of Science and Technology, Ames, Iowa. It is gratitude that I have for those teachers who make difficult subjects understandable. I have tried to that here for all of you.

So, now you’ve all got one week to absorb this day in the life of the kidney. Next week we will talk about what happens with a sick kidney when all the fascinating components aren’t playing nicely with each other. Team work is certainly required for the kidney to do all of its jobs properly and when the team work goes down the tubules (joke), it isn’t pretty.

Until next week,

Dr, Voorheis

Perineal Hernia – Viewer discretion is advised!

Perineal Hernia – Viewer discretion is advised!

May 1, 2014

From the desk of Dr. Voorheis


For days now, I have been working on this week’s blog and intended a focus on all facets of renal disease beginning with an explanation of what the kidney does, what goes wrong in acute renal failure, and what goes wrong in the more common chronic renal failure. This was to be followed with information on treatment of both conditions. So, how did I jump from renal function and disease to perineal hernias?  Well, there is a very special dog in the hospital at the moment who brought us to this topic today. His condition and surgery took a great deal of my writing time, so I decided to dedicate this week’s blog to him instead.  Like I’ve said before, the critters come first. And second, third and forth for that matter. So, this will be a short one.

Before I get into this topic though, I will let you know that a thorough topic on the kidneys is coming. After all, any organ that gets 20% of the blood flow directly from the heart has got to be pretty important! Now one disclaimer as my title indicates – pictures in this blog are graphic, so readers beware.


Perineal hernias occur when the muscles of the perineum separate, allowing the rectum, pelvic or abdominal contents to displace perineal skin. This occurs when the muscles of the pelvic diaphragm fail to support the wall of the rectum, allowing persistent rectal distension and impaired defecation. This condition is most commonly seen in “intact” (un-neutered) male dogs. The causes of perineal herniation are poorly understood but it is known to be associated with male hormones, straining (to defecate) and congenital or acquired muscle weakness or atrophy. The pelvic diaphragm is stronger in female dogs. In some cases this muscle weakness is associated with other nerve weakness as well. Other conditions that seem to predispose the animal to perineal herniation include prostatitis, bladder infections, urinary tract obstructions, colorectal obstructions, rectal deviation, perianal inflammation, anal sac inflammation and diarrhea or constipation. In other words, anything that causes additional straining or pushing of those pelvic muscles can cause them to herniate.

Herniation can be unilateral or bilateral which means on one side or on both sides. The hernias occur between the levator ani, external anal sphincter and internal obturator muscles. They can occur between the sacrotuberous ligament and the coccygeal muscles. There are other muscle groups that can be affected as well.  Is your head spinning yet?

The hernia may contain pelvic or retroperitoneal fat, deviated or dilated rectum, a rectal diverticulum, prostate, or urinary bladder, or small bowel. Organs that become displaced into the hernia may become obstructed or strangulated. This can be associated with rapid decline of the animal, who may have had the condition for several months before the negative outcome arises. Sometimes, the retroperitoneal fat that is in the hernia changes over time and becomes thickened. Sometimes these contents adhere themselves to the wall of the rectum and that tissue has to be broken down for the hernia to be repaired.

So you might be wondering how you would know if your dog (or cat) has a perineal hernia. Well, most of these critters are older, intact male dogs. About 93% of affected animals fall into that category. The condition is rare in female dogs and even more rare in cats. Most owners will bring the dog to see the vet because the dog for is having trouble defecating. Sometimes the owners will notice a swelling lateral to the anus. Again, photos are quite graphic:

Hernia1 Hernia2

Occasionally these animals present as emergencies due to bladder or intestinal entrapment which is not good. The diagnosis is most often made by a rectal examination. Radiographs can be utilized to visualize bladder entrapment and sometimes contrast is used to document that condition. The veterinarian must consider some other causes for perineal swelling such as perianal cancer, perianal gland hyperplasia, anal sac disease or infection or anal sac cancer.

Most often, this is a surgically correctable disease. Occasionally, we treat conservatively with stool softeners, enemas, dietary changes and manual rectal evacuation. But surgery is usually recommended in these cases. We also generally recommend castration at the same time as castrated dogs have a recurrence rate nearly 3 times less than non castrated dogs. When the herniation is bilateral, the hernias are often repaired one at a time.  For those unfortunate dogs with bilateral disease, they are usually repaired in two procedures. Sometimes we repair both sides at the same time with a one to two month time frame in between procedures, but that is not the norm.

Infection is common with this type of surgery, so close attention must be paid after surgery to increase the chance of success.  The most common surgical complications can include infection, fecal incontinence, recurrence, and full or partial paralysis of the nerve endings surrounding the surgical site.

A word about prevention; this disease is extremely rare in neutered dogs. Full castration is certainly a preventative measure. No other means of prevention are currently known.

Well, as I said….this was a short one. I’m headed back in to surgery!

Until next week,

Dr. Voorheis

It’s the journey that matters the most

It’s the journey that matters the most


April 24, 2014


From the desk of Dr. Voorheis


When I first started to write this blog I said that some weeks would be about veterinary medicine and some weeks would be more personal. So far, I have given you one personal introduction and the rest have been about medicine. The medical topics are vast, so much so that I could pick a new topic every week for years and never run out of topics. But this week I’ve decided to switch it up a bit and talk about something near and dear to me. Not that veterinary medicine isn’t near and dear to me mind you, but it’s time for something more personal. So I’m going to share with you one of my greatest journeys in life….hiking.

 I have been hiking and backpacking periodically most of my life. I say periodically because I don’t do it every day or every week. As I started to write this, I thought I better give some credit to where credit is due, to my parents. Some of my earliest childhood memories were spending summers and weekends in Big Bear Lake, Ca. My parents initially took us to an old vacation lodge where they rented a small cabin. We used it as a “base camp” for all kinds of mountain adventures like fishing, hiking and miniature golf. Lots of childhood memories that I still carry with me today. I was not privy to their grand plans at that time as I was only about 6 years old. In the summer of 1961 or 1962 (foggy memory), my parents purchased a lot in the Moonridge area of Big Bear. Shortly after that, my Dad started construction on his project. He built a vacation home for us (mostly all by himself) working weekends and spending all his free time there. All the Voorheis kids had jobs to do associated with the cabin. Mine was picking up nails I think. I’m sure my older brothers had other jobs that were more important. It was there I developed a love for the mountains that has never ended. My mom used to “make us” go for a walk with her every night. At that age, maybe 6 or 7, the main features of those walks were chasing and trying to catch lizards.  It was also at that age that I took one of my first long hikes. Without telling my parents where I was going, I walked to the gas station to buy a soda. That station was on the main street that travels around Big Bear Lake. The house in Moonridge was probably about 2 miles from that location one way. I was walking back home savoring my orange soda when the family station wagon screeched to a halt in front of me. Seems my parents were quite concerned about my whereabouts. I got my hide tanned for that one. Later adventures included me climbing to the top of a fire lookout station located on the mountains surrounding the Moonridge area. That lookout station is/was  in or near the Bear Mountain Ski Resort area, although it wasn’t there then.

 When I started to write this particular blog I looked for a quote by someone who could sum up my love of hiking and the mountains better than I could. After a long search, I found it. “There is no exercise so beneficial, physically, mentally, or morally, nothing which gives so much of living for so little cost, as hiking our mountain and hill trails and sleeping under the stars”. – Will Thrall (explorer, historian, and author)

 I started hiking and backpacking in earnest in the early to mid 1970’s. My oldest brother Jeff was also into hiking and backpacking and many of my hikes were done with him. It enabled brothers to forge a bond that is still strong today. As an avid reader (some things don’t change) I stumbled across two books that influenced my enthusiasm for hiking tremendously. Written by the same author, John W. Robinson, these two guidebooks, “Trails of the Angeles” and “San Bernardino Mountain Trails” were guidebooks for hiking our local mountains. These books were and still are far more than instructions for where to find the trailhead and which direction to turn at the fork in the trail a mile from the start. Mr. Robinson often gives a brief history of the area you are hiking in and then proceeds to describe the trails in ways that make you want to experience it. These discussions of the history, the flora (plant life) and fauna (animals) hooked you into wanting to walk it. I got hooked and if John Robinson thought a place was worth visiting, I tried to walk it. Most of my early hikes and frankly most of my hikes today are still in the same places. I have visited or walked most of the eastern range of the San Gabriel mountains. Most of my early hikes were spent trying to hike to the top of one of the local mountains. I have hiked almost all of them from Cucamonga Peak at the easternmost part of the range located in the Cucamonga Wilderness to Iron Mountain rising almost straight up from the eastern fork of the San Gabriel River. I’ve hiked Mt Baldy many times in all seasons and even once at midnight where we timed the hike so that we would arrive at Mt Baldy to see the sunrise from the top. I’m not recommending a midnight hike up to the top of Mt. Baldy by any means as there are too many chances for a mis-step or getting off trail. But my brother and I did it back in the days when we were younger and more foolish. Our local mountains hold a treasure of plant and animal life that we just don’t expect or are unaware of,  living safely in our suburban homes. The Cucamonga Wilderness is home to a herd of Nelson Bighorn Sheep. If you’re lucky, when you hike that part of the range you will see one or two, scampering away from you because they saw you long before you saw them.

 … In 1877, naturalist John Muir sampled our local San Gabriel mountains and described the range as “more rigidly inaccessible… than any other I ever attempted to penetrate”

 Fortunately, today we have good trails to hike into our local mountains, but they can be rather tough work at times. I still like to walk to the top of a hill or a mountain, but I don’t have to do that to enjoy the mountains. In fact, the most pleasant hike I take on a regular basis is the walk up IceHouse Canyon. The trailhead is literally 20 minutes from my house and within a few minutes I can be walking up a canyon I have walked dozens of times. The hike “ends” at the top of a saddle (amazingly called Icehouse Saddle), where you can sit and have a sandwich, or continue along one of 4 different trails to 4 different mountain peaks or canyons. I think the thing I like about this hike is that it feels so comfortable and it is so close. Yet very quickly, you forget about cell phones and all other trappings of civilization.  The first half of the hike is under the cover of alders and pines with a creek making noise on the right almost the entire first half of the hike. Then you enter the Cucamonga Wilderness where a permit is required and you hike up a south facing slope to the saddle. This hike is 7 miles round trip.

 I was in college for most of the 70’s and a portion of the early 80’s as well. As an undergraduate, studying like crazy to try to get the grades to become a veterinarian, my breaks from studying were often hiking with my brother. I should also mention the third member of our group, our friend Howard Boyd. Howard, a quiet man and dear friend of my older brother would hike everywhere with us. He too, never lost his love for the mountains. He passed away a couple of years ago, and I don’t venture into the San Gabriels without thinking of him.    


 Gradually, I began to accumulate some hiking gear, a day pack, a backpack and a good sleeping bag. This was the time of external frame backpacks, and I bought a JanSport external frame backpack which I used until about 5 years ago. I also met like minded friends in college who also hiked. It was with these friends that I was first introduced to hiking in the Sierras. We would take some weekend trips or spring break trips and go hiking into the Sierras. My brother and I would also begin to make the much longer drive into the southern end of the Sierra’s to hike and backpack. At one point, we hiked to the top of Mt Whitney. My biggest memory of that hike? I was cold, didn’t have proper gear, and wore socks on my hands for warmth. I look back on that now and see some poor choices.

 I completed undergraduate work in 1977 and had applied and been rejected from veterinary school. In those days California students had only one school in the country they could apply to at that time. It was UC Davis or nothing. I began work on an MS in Radiation Biology in 1977. I also reapplied to UC Davis for the fall of 1978. I made a deal with a dear friend. If we made it into veterinary school we would take the time and hike the John Muir Trail (JMT). Dr. Phil Solter and Dr. Dennis Voorheis received their acceptance letters into UC Davis in early May of 1978. The plans for hiking the JMT went into effect immediately.

 Some of you may not know just what the John Muir Trail is and since the rest of this blog is devoted to it, a brief description is in order. The JMT runs 212 miles from the top of Mt. Whitney to the floor of Yosemite Valley. The trail passes through some of the most dramatic scenery in the country starting at the highest point in the continental United States and traveling up and down mountain pass after mountain pass, through meadows, past pristine alpine lakes while walking at dizzying elevations. Since one cannot just start at the top of Mt. Whitney, we can add the 10.3 hike from Whitney Portal to the top of Mt Whitney, making the total distance of the JMT hike 222 miles.

 There were four of us that undertook that hike in late July and August of 1978. Phil, his wife Leellen, her cousin (whose name escapes me at the moment), and myself all started the journey together. We carried heavy packs and gear. All of the food for a 22 day hike. It was meticulously planned.  We started in great spirits as all hikes of this magnitude do. We made great time, and the early hike was marked by two significant events. The the first was about 40 miles into the trip with a night spent at Rae Lakes. Phil and I had caught our limit of trout that night. We cooked it and I will say to this day that it was the best fish I have ever eaten. It was that meal that brought unwelcome visitors to our campsite that night. We were relatively experienced backpackers so the meal was cooked about 50 to 100 yards from our campsite. In the days before bear canisters, we hung our food in between trees. Nonetheless, the odor of that fish drew the attention of a bear and he visited us that night. There is nothing like the feeling of a bear outside your tent at 2:00 am. Lots of yelling and screaming and noise drove our friend off with no damage to any of us other than elevated heart rates. The second event came about another 40 miles into the hike. So now we are considering ourselves pretty experienced long distance trekkers. This event was planned. My brother and I had calculated where we would be on that particular day. He hiked up one of the lateral trails and met us to spend a night or a weekend with us. My apologies as my  memory is kind of vague on this one. I think he even hauled up a steak or two amongst other refreshments. We did manage to cook this without a visit from a bear. We parted after the allotted time for the visit and our next plan was for him to meet me at Happy Isles at the floor of the Yosemite Valley.

 So what happened next? What happened ended up being an influence on me for much of my life. I got homesick. Two or three days after he left, after hiking 123 miles, I was so homesick I decided to walk out of the trail and go home. I left and I did not finish the trail. My other 3 friends finished the entire trail. I had to walk another 10 miles on a lateral trail to reach any kind of settlement and then hitchhiked my way to Fresno and hopped a bus home to Southern California. My brother was surprised, and I think a little disappointed, when I showed up at his door. For a while (months, years?) I continued to justify my leaving the trail and then I began to realize that sometimes a few more hours or days of perseverance changes a perspective. A changed perspective will sometimes allow me to complete a task that I otherwise wouldn’t complete. Had I known that or been willing to stick to it, who knows what a few more hours would have done and I would perhaps have had a changed perspective. Nowadays a changed perspective will sometimes allow me to look at a case a little differently. That different look allows me to solve problems that  maybe I wouldn’t solve otherwise. Walking off the JMT changed my life. Changed how I view challenges.    After the JMT, I was presented with a whole series of life challenges. Veterinary medical school, marriage, employment and partnership, kids, divorce…. life happens. I continued to hike but often thought my long distance hiking was done; I had no time to take a couple of weeks off and finish the trail.

 Yet, the JMT continued to loom in the back of my mind. I had not finished it. A few years ago I was sharing this with my wife Suzy and my daughter Grace. Both encouraged me to try to finish the hike I began so long ago. I had some 100 plus miles to complete.

My daughter Grace and her boyfriend Mike accompanied me on the hike to restart the JMT. I had tried to get myself ready for a long hike but hiking long distance in your mid 50’s is a little different that hiking long distance in your twenties. We decided to hike the exact trail I had walked out on, 30 some years earlier. A rather ambitious game plan was curtailed almost immediately as on the second day of the hike I fell and injured my hip. We still hiked but made less time than we would have otherwise. We hiked out of the JMT at Reds Meadow, which as it turns out, was an ideal place to leave the JMT as it allowed for easy re-entry the next time.                                                                      


Last summer my daughter and I, plus a new hiking partner, veterinarian Dr. Bob Dufort, from Idexx laboratories, re-entered the trail at Reds Meadow in Mammoth and hiked to Tuolumne Meadows in Yosemite. This was last September during the big fire; we were unable to hike into the valley, because roads into the valley were closed.

 So as of this posting, I have a mere 22 miles left to complete a journey that started in 1978. This summer I will take a long weekend and complete the hike. I think I have learned a little bit along the way. Perhaps it really is the journey that matters the most.

Until next week………………….


Dr. Voorheis


The dangers that lurk in our homes

The dangers that lurk in our homes

April 10, 2014

From the desk of Dr. Voorheis


Some of you may be familiar with the term “baby proof your home”. But have you ever heard of “pet proofing” your home? Same concept really, it’s all about providing a safe environment for those that cannot protect themselves. Children and pets often get into many of the same “things” around the house and suffer from similar consequences. But sometimes, pets offer up a completely unique set of challenges. So guess what we’re talking about his week…..the dangers that lurk in our homes! Some of this you may already know, but I guarantee there will be some new and valuable information as well.

By definition, this cannot be an all inclusive list or discussion of things that can harm your pets. The number of things that dogs and cats get into never ceases to amaze me. We can attempt to get a handle on it by dividing things into categories. But let’s understand something. There are 114 chapters in my latest Small Animal Emergency and Critical Care text book. Of those, 26 chapters would be included in the topic of Household Poisons and Emergencies. I’m not even going to attempt to be “all inclusive” this week.  As usual, I will attempt to discuss the things that I see and the things that interest me and hopefully interest you. A word up front: if you don’t know whether or not something will harm your pet, Google it or better yet, ask your veterinarian. Better safe than sorry.

So what are the main culprits in our homes that negatively affect our pets? Things we see most often at WBAH are adverse reactions to:

 •      Common household and yard plants that can cause illness

 •      Drugs – prescription, over-the-counter, and otherwise

 •      Insecticides and insect control products

 •      Chemical bait products – rat, mice bait

 •      Household cleaners

 •      Food and food like products

Let’s break this down. I will go in the order of the most frequently seen here at the hospital. I’m including photos so you know what to watch for in your yards and when out on walks, hikes or on vacation.


Household and Yard Plants

Sago Palm – It’s often found in your back or front yard. They are beautiful, commonly sold at Lowes, Home Depot or your local nursery.  All parts of the Sago Palm are poisonous but especially the seeds or “nuts” which contain the largest amount of the toxin. The ingestion of just one or two seeds can cause serious effects including vomiting, diarrhea, depression, seizures and acute hepatitis culminating in liver failure. As a clinician you don’t forget these cases. I think these plants should be equipped with a warning label prior to purchase. They are heartbreaking cases to treat. Even if you don’t have them at your house, watch your dogs closely when you’re out on walks as your neighbors may have one accessible in their front yard.

  sago1           sago2                                 

Lillies – the Easter Lilly in particular, but all lillies belonging to genus Lillium are highly toxic to cats (Easter Lilly, Tiger Lily, Rubrum Lily, Japanese Show Lily and certain species of daylily).

Ingestion of small amounts of the plant can cause kidney failure and ultimately death.

     lilles2   lilles3   lillies1       

Marijuana – the incidence of marijuana intoxication is on the rise. For whatever reason, we used to see a few cases a year. We now see- more than one case a month.  It is the number one plant/drug toxicity seen at WBAH. The signs vary from depression of the Central Nervous System and lack of coordination to vomiting, diarrhea, drooling, increased heart rate, seizures and coma.

The signs are dose related. In other words, the more of the drug consumed, the more severe the signs. In addition, the form that the drug is ingested in seems to make a difference in the symptoms. Most deaths related to marijuana in dogs are due to the ingestion of cannabis butter. Apparently the drug is more highly concentrated in butter.  Now- a word about your veterinarians and staff at WBAH. We are not the police. We are here to help you and your pets. It is far more helpful to your pet that you are honest about the possibility of marijuana ingestion. Withholding that information does not allow us to do our job properly and save lives.

 mj1 mj2 mj3                              

Oleander – I was raised by my mom to be scared to death of this plant yet we had a backyard full of it at one point – hmmmm. All parts of the plant are toxic and contain cardiac glycosides that have the potential to cause serious side effects such as gastrointestinal irritation, abnormal heart function, hypothermia and death.

  ole1 ole2 ole3             

Tulip/Narcissus bulbs – The bulb portion of Tulipa/Narcissus spp. contain toxins that can cause intense gastrointestinal irritation, drooling, loss of appetite, depression of the central nervous system, convulsions and cardiac abnormalities.

tup1 tup2                    

Azalea/RhododendronMembers of the Rhododendrum spp. contain substances known as grayantoxins which can produce vomiting, drooling, diarrhea and weakness and depression of the central nervous system in animals. Severe azalea poisoning could ultimately lead to coma and death from cardiovascular collapse.

 aza1 aza2 aza3   

Castor Bean – The poisonous principle in Ricinus communis is ricin which is a highly toxic protein that can produce severe abdominal pain, drooling, vomiting, diarrhea, excessive thirst, weakness and loss of appetite. Severe cases of poisoning can result in dehydration, muscle twitching, tremors, seizures, coma and death.

bean1                    bean2                                

Cyclamen – Cyclamen species contain cyclamine and the highest concentration of this toxic component is typically located in the root portion of the plant. If consumed, cyclamen can produce significant gastrointestinal irritation, including intense vomiting. Fatalities have been reported.

cyc1 cyc2 cyc3                

Yew – Taxus spp. contains a toxic component known as taxine which causes central nervous system effects such as trembling, lack of coordination and difficulty breathing. It can also cause significant gastronintestinal irritation and cardiac failure which can result in death.

 yew1 yew2 yew3          

Kalanchoe This plant contains components that can produce gastrointestinal irritation as well as those that are toxic to the heart and can seriously affect cardiac rhythm and rate.

 pot1 pot2 pot3        

Pothos – Pothos belongs to the Araceae family. If chewed or ingested, this popular household plant can cause significant mechanical irritation and swelling of the oral tissues and other parts of the gastrointestinal tract.

green1 green2 green3       


Holiday Plants

Poinsettias – generally overrated in toxicity. If ingested, poinsettias can be mildly irritating to mouth and stomach and may cause mild vomiting and/or nausea. “But wait Doc, I’ve always heard they are deadly”.  This information is out there on the internet and even some veterinarians claim it’s true but it’s just not so. It is felt to have come from plants of the same family as poinsettia being labeled as poinsettia.


pont1 pont2 pont3 


Mistletoe – usually causes gastrointestinal upset if ingested. If enough is ingested, it can cause cardiac arrhythmias. If you pet eats Mistletoe it should be seen by a veterinarian immediately.

 toe1 toe2


Holly – ingestion can cause vomiting, nausea, diarrhea and lethargy.

 holly1 holly2                                      

Christmas trees & decorations And while I’m on the subject of holiday hazards. Put water in the Christmas tree bowl – don’t add the packet of “fertilizer”. Some of these packets contain fertilizer that if ingested are toxic. Just better and easier to avoid adding packets of unknown composition to the water the tree is sitting in. Cats love to drink this water. So let’s make it safe, ok?

Electric light cords – hide them and protect them because your dogs and cats like to chew on them. Electrical shock injury ranges in severity from burns to lips and tongue to pulmonary (lung) edema and death.

Ribbons and tinsel – the presents under the tree at my house- long ago stopped having ribbon on them. One of our cats is crazy about ribbons. Both ribbons and tinsel have HIGH potential to cause the worst type of foreign body injury. It’s called linear foreign body and it is often fatal. A linear foreign body occurs when some part of something linear like a cloth, ribbon or string gets stuck in the stomach or base of tongue. The rest of the linear foreign body tries to pass or move along. The result is a bunching up of the gut. Think of trying to pass an elastic waistband through sweat pants, or elastic through the tops of curtains. Hmmmm, not sure what that’s called but you have to bunch up the material to get it to pass, right? The foreign body that is stuck remains as an anchor and the stuff that tries to pass literally saws through the intestine. The result may be as many as 30 or 40 holes in the intestinal tract. These pets die. It’s much easier to stop wrapping with ribbons and stop using tinsel if you have pets, especially cats!

 decor1 decor2 decor3


Medications – prescription and over-the-counter

Keep medications (yours and your pets) out of the reach of your animals. Dogs and cats both can be very clever about getting into medication. Keep the medications that you take and that you give to your dog or cat in a closed cabinet, preferably with a child/pet safe lock on the door. It can be more of a pain to keep them hidden that way but it is so much safer for the pets.  Things even happen at my house.  Many of you have heard me talk fondly of my Labrador, Milo. That dog has gotten himself in more trouble than almost any client’s dog I have ever worked with. Several years ago, he ingested more than 100, 75 mg non flavored Rimadyl tablets. They were kept on top of the refrigerator. One of my cats jumped on the counter and then on to the top of the refrigerator, knocking down the bottle. Milo ate every single pill. It happened in the wee hours of the morning.  I remember hearing a sound in the kitchen which I ignored and went back to sleep.  At 6 am, I found the empty bottle and rushed him in to work. Massive over dosages of non-steroidal anti-inflammatory drugs could have and maybe should have put him into renal failure, caused gastric ulceration or caused severe liver damage. He spent a few days in the hospital but never developed the failure that was expected. He did get sick but the point is he should have died and he didn’t. I never expected that my animals would tag-team to get into trouble but it happens. It happens more than you think.  All pet and human medications should be kept safe and out of reach in a cabinet.  Pain killers, cold medicines, anti-cancer drugs, anti-depressants, diet pills, are all examples of human medications that can be potentially lethal to pets.

There are two common medications that deserve special mention. The first is Acetaminophen better known as Tylenol. This drug is found in over 200 different over the counter and prescription medications. This medication can be fatal to cats, even in small doses. Cats lack glucuronyl transferase which decreases their ability to metabolize the drug. A toxic metabolite build up causes severe damage to red blood cells by causing the oxidation of hemoglobin from hemoglobin to methemoglobin, a compound which DOES NOT carry oxygen. Do not give your cat Tylenol or acetaminophen in any form.  Dogs, especially small dogs, can get sick from Tylenol. There are appropriate dosages for using Tylenol in dogs, especially in combination with a narcotic for pain relief, but it is my belief that we have plenty of other and much safer drug combinations to reach for than to risk the misuse of Tylenol in dogs.  Best not to go there.

The second special mention drug is Ibuprofen.  Ibuprofen belongs to a class of drugs called non steroidal anti-inflammatory drugs (NSAIDS). These drugs inhibit an enzyme called cyclooxygenase. This enzyme is involved in the production of inflammatory chemicals called prostaglandins. When the inflammatory cascade is active, cells use their cyclooxygenase enzymes to begin to convert fats from their cell membranes into prostaglandins. NSAIDs put a stop to this.  There are several types of cyclooxygenase. Some types are involved in producing inflammatory prostaglandins and others involved in producing prostaglandins needed for normal body functions. Ibuprofen is what is called a non-selective cyclooxygenase inhibitor which means it inhibits all types of cyclooxygenase, not just the ones that produce inflammatory mediators. Ibuprofen inhibits prostaglandins involved in the blood supply to the stomach as well as blood supply to the kidneys. In humans, these effects are minor enough that they do not preclude approval for over-the-counter use but in dogs and cats, these issues are life threatening. It turns out that dogs and cats are more sensitive to these issues. Prescription NSAIDs in the dog are more sparing of COX-1 effects on the stomach and kidneys. Ibuprofen is too toxic for safe use in dogs or cats at any dose. If a pet is lucky, exposure will not have reached toxic dose but it may not take much given that the typical non-prescription pill contains 200 mg. The first level of toxicity involves ulceration of the stomach which leads to vomiting with or without blood, appetite loss, and/or stools that are black from digested blood. The worst case is rupture of the stomach leading to death. Repeated use of ibuprofen will increase the risk of toxicity even at doses that are not toxic in single exposures. Ibuprofen inhibits production of prostaglandins needed for normal blood circulation to the stomach. Without normal blood flow, the stomach cannot produce a proper protective layer of mucous to protect its tissues from the harsh digestive acid it contains. That is the cause of the stomach ulceration. Treatment involves IV fluids and medications to heal the ulcer or ulcers. At higher doses, we see kidney failure. Toxins that the kidneys normally filter out are not filtered. Depending on the dosage administered or ingested and the amount of time between ingestion and presentation at the vet’s office, that damage may or may not be permanent. Treatment involves IV fluids, medications to try to open up kidney blood flow, and other supportive measures. High doses of Ibuprofen can cause coma and death.

 It’s time to add to a statement I make often which is “Remember, cats are not small dogs”. By that I mean that cats are a completely different species with different metabolic requirement and different ways of metabolizing medications, etc. To this I will now add “Dogs and cats are not small people”. Don’t use your medications on them without consulting a veterinarian first. Never ever. 

Insecticides and Insect Control Products

Organophosphates – these are insecticides. Not as commonly used around the house as they once were. Some of you may know them by the names malathion, parathion, diazinon, fenthion, dichlorvos, chlorpyrifos, ethion. Exposure in our type of practice is rare. They inhibit or inactivate an enzyme which causes excessive amounts of a neurotransmitter to accumulate resulting in muscle over stimulation. I still remember the mnemonic we used in veterinary medical school to remember the signs… SLUDGE (salivation, lacrimation (tearing), urination, defecation, gastrointestinal-movement, emesis).

We don’t see this much in an acute type of ingestion or exposure. Chronic low level exposure is beyond the scope of this blog as we don’t live in an agricultural area where low level exposure might take place. Diagnoses of this type would require testing for level of acetylcholine esterase activity in the blood.  Treatment is atropine which works for the majority of signs of high level exposure. Less is known about its efficacy with low level exposure.

Pyrethrins and Permethrin – pyrethrins are a pair of natural compounds produced by the Chrysanthemum cinerariifolium that have potent insecticide activity. They are often combined with piperonyl butoxide which is a synergist and prevents the insect’s detoxification of the pyrethrin. These are used in products such as Ovitrol or Adams flea spray. These are safe for use in dogs and cats. They rapidly breakdown in sunlight and air. So they don’t last a long time, with applications needing to repeat usually daily.

Permethrin is different. This is a synthetic product which can be used as flea and tick control ONLY FOR DOGS. Every year we see cat’s that are poisoned because someone applied a topical flea product for DOGS onto their cat. If the flea product that you are about to put on your cat says DOGS, please don’t use it. 

Here are some over the counter dog products that are potentially fatal to your cat:

1. Happy Jack DuraSpot

2. Liberty 50

3. Omnitrol

4. K9 Advantix

5. K9 Advantix II

6. Pronyl OTC Max

7. FiproGuard Max

8. SpectraSure Plus

9. Vectra 3D

10. Zodiac Spot On Groomer’s Pack

There are two labeled for cats that I personally would stay away from:

1. Biospot Defense

2. Vet-Kem Ovitrol X-tend

Both have the synthetic pyrethroid “etofenprox + methoprene” in them. They appear to be safe for cats. However, etofenprox is a synthetic pyrethroid that is metabolized by liver and cats lack that liver enzyme system. Remember the acetaminophen we talked about earlier? I would not use these products on a cat because there are safer products available such as Revolution and Comfortis.  

Bait products

Rat and Mouse bait products can be a problem. In our suburban environment, we have loads of rats and mice. There are two main types of rat and mouse bait.  Those that cause brain swelling and hyperkalemia and those that inhibit vitamin K and therefore the synthesis of clotting factors. These are factors involved in forming a blood clot and what keeps the blood inside vessels and not leaking into tissues.  Those that inhibit Vitamin K such as Warfarin, Diphacinone, Brodifacoum and Bromadiolone are actually easier to treat.  But don’t get me wrong, both types can be fatal. But at least there is an antidote to the vitamin K inhibitors.

Here is the important take home point. Most of these cases that are presented to us are presented days after ingestion of the rat bait. Often the owners were aware that the dog ate the product but because no signs developed right away, they thought they were “in the clear”. Then the dogs begin to bleed out. If your dog eats any kind of poison, especially the rat and mouse baits, bring the dog and the bait or its box to the hospital right away. Do not delay. Treatment for rat bait toxicity depends on how quickly we get to the dog. We may induce vomiting and inject with Vitamin K and send home with oral vitamin K. Or we may have to hospitalize, give blood or plasma transfusions, and other supportive measures.

Snail bait

What about those pesky snails? They are often controlled with molluscicide (Antimilice, Ariotox, Blitzem, Deadline, Halizan, Limatox, Limeol, and Slugit).  The active ingredient is Metaldehyde. Metaldehyde was popular in the 70’s when it was sold as slug bait that was “non-toxic” to dogs. We would see dog after dog, seizuring after exposure. This stuff is still being sold. Even the water runoff from an area that has been treated can be toxic. If ingested, signs follow quickly such as drooling, muscle tremors and restlessness progressing to seizures. The seizures will not stop until treated or until death happens. It also is hepatotoxic. Treatment is to stop the seizuring, control hyperthermia and provide lots of IV fluid support. Survival is possible if we get to them in time.

Household/Garage products

Ethylene Glycol – This is the greenish-yellow fluid that you put in your car’s radiator otherwise known as Anti-freeze. It is a sweet tasting fluid and it will kill your cat or dog. The absolute best way to avoid the problems associated with ethylene glycol toxicity is to address any radiator leak immediately and professionally. Do not allow dogs or cats assess to radiator fluid or under cars with a radiator leak. It is rapidly absorbed from the gastrointestinal tract and rapidly transformed in the liver by alcohol dehydrogenase to glycoaldehyde, glyoxalic acid and oxalic acid. This leads to severe metabolic acidosis and renal (kidney) damage.  A lethal dose is only 1.4 ml/kg in cats which is one teaspoon for average sized cat. A lethal dose in dogs is 6.6 ml/kg.  Two organ systems are affected. One is the nervous system where it appears as though they are drunk. The other is the kidneys. Rapid kidney failure occurs. Ethylene glycol has the highest fatality rate of all poisons. Animals present depressed, vomiting and initially increased thirst progressing to kidney shut down. Neurologic signs progress from lethargy, coma, seizures and then death. Kidneys are often swollen and painful, especially in cats. If we get the case within 5 hours and confirm ethylene glycol poisoning, it is treatable. If we get to the patient more than 5 hours post ingestion, we treat with a drug called fomepizole. Still worth trying if diagnosis is within 12 to 24 hours. Peritoneal dialysis may be beneficial. Kidney transplantation has been performed at University referral centers for cats with this problem. If fomepizole is not available, ethanol can be used.  I don’t however want to write about this poison as if it is highly treatable. We always try because that’s who we are and that’s what we do. But most cats and dogs die from ethylene glycol toxicity. It’s sad but true.


Before I talk about individual problem foods, a particular food category should be addressed and that would be fatty foods. Things like bacon and/or bacon drippings.  fat from your steak, chicken or turkey skin and butter. High fat foods contribute to gastrointestinal signs and especially a condition called pancreatitis. Pancreatitis is going to be a subject of a different upcoming blog because it is a rather complicated discussion. One of the risk factors for pancreatitis is high fat diets. We certainly do our dogs and cats no favors by feeding high fat table scraps. They are not small people and cannot handle the level of fat in the diet that people can.

 Now let’s talk about some individual foods and food ingredients that may act as toxins that many people may not be aware of.

 Macadamia nuts – ingestion of this item causes a syndrome of tremors, weakness, agitation, vomiting, diarrhea and paralysis in dogs.  Clinical signs develop when 2.4 to 62.4 gram/kg of macadamia nuts have been ingested. The symptoms can develop within 12 hours of ingestion. Mechanism of toxicity is unknown. The neurologic signs include tremors, ataxia (drunken gaits), weakness and ascending paralysis primarily of the rear limbs. Treatment is symptomatic. If we get to the animals within 3 hours of ingestion we will induce vomiting. Recovery generally happens within 48 hours.

 Chocolate toxicity ingestion of chocolate (methylxanthine alkaloids) in sufficient quantity can cause gastrointestinal, neurologic and cardiac abnormalities. Methylxanthine alkaloids = theobromine and caffeine from the cocoa bean.


Type Theobromine (mg/oz) Type Theobromine(mg/oz)
Cocoa Shell Mulch 400-857 Semi Sweet Chocolate 150-257
Cocoa Beans 314-1228 Milk Chocolate 44-63
Cocoa Powder 150-742 Hot Chocolate Powder 11-14
Baker’s Chocolate 390-457 White Chocolate 0.26-1.4
Range of theobromine per ounce of chocolate      
MilkChocolate44mg/oz 5 kg 10 kg 20 kg 30 kg 50 kg 70 kg
1 oz 9 mg/kg 4.5 mg/kg 2.2 mg/kg 1.5 mg/kg < 1mg/kg < 1mg/kg
8 oz (1 c) 71 mg/kg 35 mg/kg 18 mg/kg 12 mg/kg 7 mg/kg 5 mg/kg
16 oz (2 c) 141 mg/kg 70 mg/kg 35 mg/kg 23 mg/kg 14 mg/kg 10 mg/kg
32 oz (4 c) 282 mg/kg 141 mg/kg 71 mg/kg 47 mg/kg 28 mg/kg 20 mg/kg
Semi SweetChocolate(150 mg/oz) 5 kg 10 kg 20 kg 30 kg 50 kg 70 kg
1 oz 30 mg/kg 15 mg/kg 8 mg/kg 5 mg/kg 3 mg/kg 2 mg/kg
8 oz (1 c) 240 mg/kg 120 mg/kg 60 mg/kg 40 mg/kg 24 mg/kg 17 mg/kg
16 oz (2 c) 480 mg/kg 240 mg/kg 120 mg/kg 80 mg/kg 48 mg/kg 34 mg/kg
32 oz (4 c) 960 mg/kg 480 mg/kg 240 mg/kg 160 mg/kg 96 mg/kg 69 mg/kg
Bakers Chocolate 390mg/oz 5 kg 10 kg 20 kg 30 kg 50 kg 70 kg
1 oz 78 mg/kg 39 mg/kg 20 mg/kg 13 mg/kg 8 mg/kg 6 mg/kg
8 oz(1 c) 624 mg/kg 312 mg/kg 156 mg/kg 104 mg/kg 62 mg/kg 45 mg/kg
16 oz (2 c) 1248 mg/kg 624 mg/kg 312 mg/kg 208 mg/kg 125mg/kg 89 mg/kg
32 oz (4 c) 2496 mg/kg 1248 mg/kg 624 mg/kg 416 mg/kg 250 mg/kg 178 mg/kg
Chocolate dose based on weight (kg) of the patient and type of chocolate  
Red numbers indicate a dose greater than or near 100 mg/kg    

 Systems affected by ingestion of chocolate products are gastrointestinal (vomiting and diarrhea), urologic , nervous system (hyperactivity), CNS stimulation, seizures. Musculoskeletal (tremors, increased reflexes) and cardiovascular (tachycardia). Treatment involves inducing vomiting if they have recently ingested the chocolate. Otherwise it will be fluid support, activated charcoal to try to block absorption, placement of a urinary catheter because the active ingredient is absorbed back into circulation through the bladder wall. Seizures are controlled and drugs to slow the heart rate down. Expect two to three days of treatment.

 Grapes and Raisins –

This topic is poorly understood. Symptoms are vomiting, diarrhea and Acute Renal Failure secondary to the ingestion of raisins or grapes. Ingestion also causes acute tubular necrosis of the kidney tubules and little urine to no urine is produced. Signs start within 24 hours of ingestion of raisins or grapes. Vomiting and diarrhea come first and renal signs follow. Treatment includes induction of vomiting followed by administration of activated charcoal and lots of IV fluids. Damage to kidneys may be permanent.

 There are many food and beverage items that cause problems for dogs and cats and far too many to list here. To name just a few of the common offenders we have coffee, alcohol, artificial sweeteners in food items, onions, garlic, avocados, walnuts, yeast dough, any pit fruit like cherries/apricots/peaches etc. With pit fruits, the actual pit is the problem.  For a longer list of food and chemicals/drugs that are poisonous to pets, please visit:


http://www.petpoisonhelpline.com/    or      http://www.aspca.org/pet-care/animal-poison-control


Another tool to get familiar with is CPR for pets. There is a handy guide below.

 Well, I think that’s enough doom and gloom for today. Pet proof your home and yard and keep your critters out of harm’s way.  Give it the old college try!

Until next week,


Dr. Voorheis