Aquaponic Gardening

Aquaponic Gardening…….another hobby


October 2, 2014


From the desk of Dr. Voorheis


At the beginning of this year, I said that most of he blog would be about veterinary medicine and every once in a while I would write something a bit more personal for good measure. This week, it’s personal. I’d like to take you all on a gardening and science adventure and tell you all about one of my favorite hobbies….Aquaponic gardening! 

I have always been a gardener. Going back to being a kid in a rural setting, there were always spring and summer gardens. I’ve carried that through my adult life as well. There is nothing quite like home grown vegetables. They actually have flavor because they ripen naturally as opposed to being ripened by exposure to ethylene gas. They still have vibrant flavor as opposed to those selected for toughness of skin and even ripening so they can be picked by automated machines.  As much as I don’t want to sound like someone yearning for the “good ole days”, vegetables used to taste better than they do now, especially tomatoes. Yet I have also had my share of frustration with my traditional gardens. Tilling the soil and pulling weeds is not exactly how I want to spend my  precious time off. Although I will admit to some satisfaction from digging in the dirt, it is not nearly as much fun as I might romanticize it to be. In all honesty, I can gear up to working in the soil only a few times a year. It’s not much fun to have to maintain my backyard garden week in and week out. Really, the time just isn’t there.

I also like to tinker on things, build things. So when I found out a little bit about aquaponics, I thought it sounded pretty darn cool. “Doc – Aqua what?”  Aquaponics is a food production system that combines conventional aquaculture (raising aquatic animals such as fish, crayfish, or prawns in tanks) with hydroponics (cultivating plants in water) in a symbiotic environment. With aquaculture (think most of the fish that we eat or buy in the grocery store), fish are raised in large tanks in a closed system. The waste products of these fish in an intense grow system require that at least 10% of the water needs to be removed and exchanged every day. If the waste products from the fish are not addressed on a daily basis, waste products accumulate and the water becomes toxic and the fish die. A tremendous amount of monitoring has to happen in these tanks where fish are raised for food.  Aquaculture is a very water intensive process. It doesn’t sound attractive to an environment that is in the middle of a drought. 

Hydroponics is the raising of plants in media (soil free, i.e. rocks or hydroton) being fed a nutrient solution (water + needed nutrients) tailored to the requirements of the plant species.

As with aquaculture, hydroponic operations need to carefully monitor the water environment to ensure the highest yield. 

In an aquaponic system, water from an aquaculture system is fed to a hydroponic system where the by-products are broken down by nitrogen-fixing bacteria into nitrates and nitrites. The nitrates are utilized by plants as nutrients. The nitrites are further broken into nitrates by other bacteria. The water is then drained and re circulated back to the fish, oxygenated and void of its toxic nitrogenous waste. There is no need to remove water from the system.

In brief, by combining the two systems, they complement one another perfectly. Fish produce the nutrients that the plants need, bacteria in the grow beds remove the nutrients that kill the fish, and oxygen levels are maintained by the cycling of the water through a natural system similar to that found in nature.

A few years ago, I decided to try this aquaponic thing. Mostly I didn’t know what I was doing, but I read and researched as much as I could on the subject. I found out I would need a few grow beds, a large tank of water for the fish (275 gallons), and a sump tank (also 275 gallons). For a backyard gardener raising fish, I learned tilapia were probably the most resilient fish when it comes to temperature fluctuations and other screw ups by the farmer.  Believe me when I say I screwed things up more than once and tilapia are a very resilient fish.



I built 3 grow beds (3’ x 6’ x 1’). I then lined them with pond liner. I put a large pump in a “sump” tank (a large IBC tote cut to hold 275 gallons of water. I used another IBC tote as a fish tank. Water is pumped continuously to the fish tank and to the grow beds. When the grow bed fills, the water is returned to the sump tank by means of a “Bell Siphon” pictured above.


My pumps (there are two) because of distances of grow beds to sump tank, are powered by solar energy (in fact my whole house is but that is another subject).


The sump tank as it initially filled.


This picture is one of the grow beds a month into the first growth cycle. The grow media is “expanded shale”. It takes about a month, of plants only, for the water to complete the nitrogen cycle. Cycling is really shorthand for the establishment of a biofilter where the nitrogen cycle can take place within your system. The nitrogen cycle is the ongoing process in which bacteria convert ammonia and nitrites into food that your plants can consume. That food is nitrates.


This is another grow bed about a month into the first cycle with strawberries and cilantro. I have grown the following vegetables and herbs with significant success:


  1. Tomatoes – all types
  2. Swiss chard
  3. Onions – yellow and white
  4. Garlic
  5. Basil
  6. Cilantro
  7. Parsley
  8. Brocolli
  9. Cauflower
  10. Peppers – all types
  11. Strawberries
  12. mint
  13. rosemary
  14. Romaine lettuce
  15. leaf lettuce
  16. spinachMy current winter crop is an entire grow bed devoted to lettuce. I also have basil, peppers, and cauliflower started for fall. Tomatoes are still producing too. I’ve got a number of different herbs growing as well. Less success with squash and cucumbers… I still grow those in dirt.Aqua6

    One of the end products was these fish. They were harvested at a BBQ at my house over Labor Day weekend. It was fun because anyone who wanted fish literally had to catch their own fish! These tilapia were about 14 to 15 inches in length and weighed over a pound each.

    I enjoy my aquaponic garden a great deal. I undertook the project because it was challenging, fun, and I wanted to learn more about a different way to garden. It has also given me a lot to think about. I will now jump into some uncharted waters. Whether or not   you think “Global Warming” is real, or that our climate is changing, it is undeniable that we are suffering a significant drought here in the West. It seems rather evident to me that it makes sense to pursue gardening and farming practices that conserve water, and certainly aquaponics uses a fraction of the water of traditional agriculture practices without using any fertilizers or pesticides. This is sustainable gardening at its best.  In some countries of the world, for example Australia, aquaponics has huge support on the government level and on the individual level because of the opportunity to produce a significant amount of food using smaller space and less water. I believe that eventually aquaponic gardening will take off in popularity, simply because it makes sense and it works.

    Next blog in two weeks will be on pancreatitis. Until then………


    Dr. Voorheis

Kennel Cough And Other Canine Cooties

Kennel Cough and other Canine Cooties


From the Desk of Dr. Voorheis


September 4, 2014



The timeliness of this week’s blog is certainly no coincidence. Some of you are already aware of the recent events at Boulevard Grooming and Boarding (the facility behind us that we operate) but for those of you who aren’t, this blog will explain in detail what took place, why it happened and what we did to resolve the situation. It’s important that you all hear this from the horse’s mouth so that details are clear and concise and stories do not evolve with inaccurate facts. Recently, at Boulevard Grooming and Boarding, a number of dogs showed signs of upper respiratory disease. It is not at all uncommon in boarding facilities to have this happen to the occasional dog, but in this circumstance there were more than we (Drs. Voorheis and Throgmorton) were comfortable with. So, PCR testing (DNA) was done on 4 of the dogs and that revealed the reason for the coughing to be a viral disease there was no vaccination against, Pneumovirus. The boarding facility was shut down for a week and all surfaces thoroughly disinfected. Disinfection in both the boarding and hospital facilities is done daily, but what happened during that week was a deep cleaning the likes of which were beyond impressive. I must share with all of you that this has never once happened in the 30+ years that I have been at WBAH. We have never had to shut the boarding facility down.  This decision was inconvenient for clients who had made plans to board their dogs but easily understandable from the point of view of safety for their animals and the other animals scheduled to board. This was absolutely the right decision for us to make. Having said that, we do realize it caused a great deal of annoyance and for that we are truly apologetic. Please know that we will always make the right decision for the health and safety of your animals. They are our absolute first priority.  

Every dark cloud has a silver lining, right? Our silver lining is that this unexpected situation enabled us to review our vaccination policy for boarding and grooming animals even though this “episode” was caused by an organism that there is no vaccination for. We decided to look at diseases that are generally more common and that we do have vaccinations for. Due to the amnestic response (immune memory), dogs who had previously received a booster against bordetella were “ok’d” to get that booster on entering the facility. This policy has now changed. We are now requiring that the bordetella booster to be given one week prior to boarding/grooming. This gives them their absolute best protection against illness. The goal is to prevent any further preventable situations.

As outlined above, it is clear that this episode was caused by a viral infection that there is no vaccination against. It is worth reiterating that there is risk involved when you take your dog to a grooming/boarding facility. There is risk involved when you take your dog to any place where numbers of dogs have gathered. I guess you can say life is a risk. I would ask any client to consider a number of things before making a decision to groom or board their dog. Are vaccinations current? Is my dog coughing now, or recently had a cough? Upper respiratory organisms can be shed for a month following infection. If your dog is recently recovering from an upper respiratory infection, don’t groom or board it. Does your pet have increased risk factors such as existing cardiovascular disease or lung disease? That pet may not be an ideal candidate for boarding. Is your pet on chemotherapy for cancer? This too may not be an ideal candidate for boarding.

Bear in mind that in spite of significant efforts at cleanliness and disinfection, exposure can still take place. The best analogy is sending a child to school or taking an airline flight and then coming down with a cold or flu. “Cooties” are out there for humans and animals. They are airbourne and they attack. Some of them can be vaccinated against and some cannot. Your best defense is vaccinating against what you can and really think about any risk factors that your pet may have and let that guide your decision. This applies to any grooming or boarding facility you may consider as well as places like dog parks or other places where numerous dogs gather. 

So, let’s talk about what is behind all of this, medically speaking.  Canine Infectious Respiratory Disease Complex. Wow! That’s a mouth full.  Let’s talk about this disease, the body’s defense mechanisms, and our current understanding of the diseases involved. It turns out that “kennel cough” is not just one disease. The signs can be caused by a number of different organisms with different severity of signs and different treatments.

Let’s talk about the dog’s defenses against disease first. In the respiratory system, there are three levels of defense. The first level is the mechanical barrier level. Mechanical barriers are things like mucus, enzymes and the mucosa itself. These guys work to inhibit attachment and facilitate clearance of organisms in inspired air. Then there is the second level of defense, an immune response called the innate response. There are circulating white blood cells that move out of the blood into tissues. They recognize certain molecular patterns associated with pathogens. These cells types are phagocytic (engulfing) cells, neutrophils, basophils, mast cells, eosinophils, and natural killer cells (T-lymphocytes). They are what is called non-specific, so they do not have an “immunologic memory”. The third level of defense is an “Acquired Immune Response”. This has to do with lymphocyte development and memory. It is this level of immune response that we are stimulating when we vaccinate. We talked about some of this in my vaccination blog. That blog, at this point, would be an excellent one to go back and refer to.




Allow me to give you a little more detail on the mechanical barrier. The majority of micro-organisms that we inhale every day are handled by anatomical or mechanical barriers. Bacteria, dust, viruses are suspended in inspired air. The conducting airways use turbulence and decreased velocity to accomplish filtering inspired air. This causes these particles to be directed onto mucus-covered walls where they can be easily cleared. These mechanical barriers include the complex turbinate structure of the nose, the changes in angle and direction of the pharynx and larynx, and the multiple branching pathways of the bronchi. In addition, the bronchi and trachea have things called mucociliary escalators. These are the cells that line these airways and are constantly moving to “escalate” the mucus out the bronchi and up the trachea where it can be cleared.

Now for a bit more detail on the innate immune system. That mucus I mentioned? Filled with host defense molecules, defensins, lysozyme, surfactant proteins; these have anti-microbial activity. These substances are secreted by the epithelial cells lining the airways into the mucus. Yes, it turns out someone other than Dr. Egon Spengler studies mucus! Anyone know who that is? Extra credit from me if you do! Anyway, the epithelial cells lining the airways have pattern recognition receptors. These both trigger and amplify the immune response to infection. Then there are patrolling white blood cells that are directed to where the immune response is occurring. These guys engulf the pathogens allowing them to be cleared by expectoration (coughing) or swallowing.

Last, but certainly not least, a little more information on adaptive/acquired immunity. At the same time the above is happening, mucociliary clearance is presenting the organisms to mucosa associated lymphoid tissue (MALT) or bronchial associated lymphoid tissue (BALT). This is lymphoid tissue either in nose, pharynx or nasopharynx (MALT) or trachea and bronchi (BALT). The MALT guys get to work producing an immunoglobulin (IgA). Mucosal antibodies work by immune exclusion or immune elimination. IgA works by immune exclusion. This prevents adherence of bacteria and viruses to epithelial surfaces. IgA is not bactericidal and is fairly short lived. BALT tissues produce IgG, these immunoglobulins are potent activators of destruction of the micro-oganisms by opsonization (the process by which a pathogen is marked by destruction by a phagocyte), and virus neutralization. These guys mediate the immune elimination of the infection by controlling an arm of the immune system called humoral immunity (IgG, IgM and IgE). They get activated if organisms evade IgA and gain access to tissues. They are bactericidal and they have long immunologic memory.  These are the cells that we activate when we give an injectable vaccination.

Now that you have some relevant information on the defense system, let’s talk about canine infectious respiratory disease (CIRD).  Canine infectious respiratory disease (CIRD) is also known as “Kennel Cough” or “Shipping Fever”.  These are a highly contagious group of infections that are spread through respiratory secretions. These secretions are aerosolized when an animal coughs or sneezes, thereby facilitating exposure especially where there are dogs gathered in moderate to large numbers such as dog parks, grooming and boarding facilities, pounds and shelters, rescues and veterinary hospitals. “Fomites” (inanimate objects such as tennis balls, rope toys etc) can be the source of infection as the organisms can survive on inanimate objects for over 48 hours. These pathogens colonize airway epithelium, the nasal cavity, larynx, trachea, the bronchi and bronchioles. They act to disrupt mucociliary clearance. This disruption or dysfunction allows further colonization by other viral and bacterial pathogens. There is a wide range of clinical presentations, from mild self-limiting disease to severe life-threatening disease, although that is fortunately rare.

For years, we have known that the primary agents of CIRD were either Bordetella Bronchiseptica + canine parainfluenza virus (CPV2) or Bordetella Bronchiseptica + canine adenovirus2. These agents can act by themselves or in combination with one another. This knowledge or paradigm is what most veterinarians practiced with for years and years. We know now there are many other causes for CIRD (canine infectious respiratory disease). A more complete list is below. Vaccination is not available for every organism on this list.


  • Bordetella
  • Canine Adenovirus type 2
  • Canine Parainfluenza virus type 2
  • Canine influenza virus
  • Canine respiratory corona virus
  • H1N1 influenza virus
  • Mycoplasma cynos
  • S.Equi zooepidemicus
  • canine pneumovirus
  • canine herpes virus
  • canine reovirus


So what does it look like when you dog is infected with one of these organisms? Signs relate to the degree of respiratory tract damage and range from non-existent to severe. In uncomplicated cases the cough is a dry hacking cough, followed by gagging or expectoration of mucus. Exercise, excitement and pressure of a collar all seem to stimulate cough. Severely affected animals may be inappetant (not interested in food), be lethargic and have trouble breathing. Fortunately, this group is uncommon. The vast majority of dogs with this presentation are treated as outpatients. Antibiotics are used for this group because many of these cases are infected with bacteria, or an organism that is responsive to antibiotic therapy. Cough suppressants may be used to treat these outpatient animals as well. Lastly we will also use bronchodilators to relieve bronchospasm.

There is a subset of dogs that present very ill, with pneumonia. These dogs are treated with IV antibiotics, supportive care including IV fluids, oxygen therapy, nebulization (a process in which antibiotics are put into a small amount of saline and aerosolized into the air the animal breaths. The highest risk dogs for this group are the very young, the very old or dogs with existing heart and lung disease. Animals who are undergoing chemotherapy for cancer would also be an at risk group as mentioned above.



Prevention can be broken into a couple of categories; risk reduction and vaccination.


Studies done at the Western College of Veterinary Medicine, University of Saskatchewan, and published in the Journal of the American Veterinary Medical Association have given us the best information on how to protect dogs against Bordetella.


1. Puppies – who have never been vaccinated.

a. First vaccination – intranasal/oral vaccination

b. 4 weeks later – subcutaneous vaccination


Studies also showed that two subcutaneous vaccinations in puppies spaced 4 weeks apart were nearly as effective as “a” above.


2. Adult dogs – subcutaneous vaccination annually.

                  dogs1                dogs2


Risk reduction:

 Reducing risk is reducing exposure. This would mean don’t take your dog to dog parks, to dog shows, don’t board your dog at a boarding facility. Don’t take your dog to a grooming parlor. Don’t walk your dog through a pet supply store. The lobby of a veterinary hospital is also a place where exposure could take place. Of the list above, boarding is probably the highest risk. Why? Large populations of dogs, stressed because they are not at home, shedding organisms as outlined above and sharing a common air supply. Is the list above realistic? Absolutely not. We cannot have our animals live in a bubble anymore than we ourselves can live in a bubble. We can only educate ourselves and do things that attempt to reduce risk. As I have outlined above, even vaccinated and “protected” dogs can come down with signs of “kennel cough”. There is NOT a vaccination to protect against all organisms that can cause upper respiratory disease in the dog. Sad, but true.

I hope this blog has given you all some solid information and some things to think about. In closing, I want to thank a couple of people for this blog. First, John Barrier from Zoetis.  Zoetis is the pharmaceutical company that was formerly Pfizer Animal Health. John offered me the opportunity to have a two hour long sit down with Dr. Stephan Carey, a respiratory specialist who teaches at Michigan State University. The second person I’d like to thank is Dr. Carey himself. Dr. Carey was visiting the southland in late spring, and was gracious enough to give myself and 4 other veterinarians a couple of hours of his time (and his lecture notes). Most of this blog is a direct carryover of the information he shared. I believe he also shared that his young son was an avid Los Angeles Kings hockey fan. I’d say that young man had a good June.


Until next time,


Dr. Voorheis

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:

 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… 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

 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 . 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