So, in about 9 months, our whole life is going to change. I am pregnant!!! I'll have more information after my trip to the OB tomorrow. Actually, I am quite terrified and simultaneously really excited. Anyone with words of advice about parenthood, pregnancy, or being an ER veterinarian mother (or just a veterinarian mother) - feel free to drop by. I feel like I know nothing!

Stars burn brightest before they burn out...

My frustration cup once again runneth over. That didn't take long. Ha.

Without getting into specifics, I will try and explain. Being an emergency veterinarian is a lot like being a goldfish. You exist in your own little bowl. Unfortunately, the whole world can see into your bowl all the time. You have to deal with clients who have never met you and automatically don't trust you. Those clients come with their own veterinarians, who go over the records with a fine tooth comb to determine if everything was done perfectly "right" (as if there is such a thing). If you have to send a complicated case to the referral/specialty hospital, you have those specialty doctors and technicians poring over the records and everything you did.

Why is that a bad thing, you wonder?

In and of itself, it's not. There are many checks and balances as an ER doctor. Mistakes are much more visible, and it makes it easier not to repeat them - especially when everyone else sees them.

On the other hand, it opens us up to nit-picking from other veterinarians, other clinics, and clients. How I handle one emergency might not be how another veterinarian would have handled it and vice versa. Does this make me (or them) wrong? No. Does everyone see it that way? No.

I am beyond frustrated at the moment because I am still trying to learn balance. Keep in mind, I have only been out of veterinary school for 2.5 years. I work in a poor area in North Carolina, thus I see many people with very limited means. As a result, I am striving to find the ground between malpractice and "Ivory Tower" medicine. I still want to do everything exactly "right" - I want to check serial blood pressures on hospitalized patients, I want to monitor electrolytes, PCV/TS, and blood glucose at least once a day on sick patients, I want to make sure my diabetic ketoacidotic patients get exactly the kind of TLC and monitoring they need (which is expensive and involved). On the other hand, many people can't afford this.

I am afraid I have alienated some local veterinarians because I am doing the best medicine that I know how to do and that is not always a cheap thing.

It's so hard to learn balance - balance between doing what is "right" as I was taught in school and in textbooks and what is "best" for the patient (sometimes what is best for the patient is what is best for the owner's wallet). On top of that, I put enormous pressure on myself to be perfect. From the simplest dislocated elbow to the most complex polytrauma post-hit-by-car...I constantly question myself, my medicine, my abilities. I go back, review cases again and again, looking for the key that would unlock the mystery, give me answers, help me treat better. I spend hours on the Veterinary Internetwork (VIN), posting about cases I've seen, questions I've thought of. I read my journals. I talk to colleagues. I work when I'm not at work. I love my job. Yet I feel like I'm constantly failing...all the time, every day.

In short, I do everything I can to be better, and yet every day, I feel like a quack. My best friend told me that if you don't feel like a quack at least once a week, you're not doing your job well.

Sometimes I tell myself to just lighten the hell up, and don't take it all so seriously. Then I think of the anguished owners, the emotional euthanasias, the animals I couldn't save, and the look in their owners' eyes when I told them, and I realize that lightening up would be doing a grave disservice to my clients, my patients, and myself.

I need to find a bit of work/life balance. I'm joining the gym tomorrow. Sometimes I'm very afraid that my time in the veterinary field will be limited, because how can I keep going at this pace and not just burn out?

The weight

So before I tell this story, I would like to temper it with the fact that my whipworm/pseudo-Addisonian patient from this weekend is doing extremely well. Tonight, she ate on her own, and she is walking well and wagging her tail.

A month or so ago, I was confronted with a nightmare ER case. The doors burst open, and my techs wheeled in a 100+ pound Labrador. She'd been spayed earlier that day at her veterinarian's office. She was in heat during the spay, and she was morbidly overweight. The vet that did her surgery was very experienced (30+ years), and when I spoke to him, he expressed no concerns about how the surgery went.

When she came to me, she was lateral, her gums were muddy and pale, her pulses were weak, her heart rate was sky-high, and her abdomen was severely distended. We started standard aggressive shock treatment with IV fluids while I went about ensuring that she was bleeding into her abdomen.

Sure enough, about 3 liters of blood were present in her abdomen. Her clotting times were normal, so this didn't appear to be a clotting disorder. Thus, I was left to decide if she was still actively bleeding, or if I could maybe stabilize her with IV fluids. When it comes to this decision, it is never, ever an easy one. Many patients that are bleeding post-surgically will eventually clot on their own without surgical intervention. Some will not. Thus, deciding who is who can be difficult. The standard approach is to try and stabilize the patient with IV fluids - get the blood pressure up, get improvement in vitals (heart rate, gum color, capillary refill time, and mentation), and try to keep the patient that way. If that cannot be successfully done, then surgery is usually indicated.

The bleeding patient is a trick in and of itself. The first line of stabilizing a bleeding patient is getting fluids into the body to make up for the blood that is being lost. Crystalloids (which are fluids similar to the composition of blood), colloids (synthetic fluids with very high molecular weight that say in the bloodstream better), and blood products such as packed red blood cells and fresh frozen plasma are all choices. Knowing which one to choose in the bleeding patient can be a really, really big challenge.

In this case, my patient needed blood cells. She also needed regular fluids. Unfortunately, we can only keep 1 unit of packed red blood cells around. We set about warming it. While waiting, we started crystalloids. Using the right amount is crucial - too little, your patient doesn't get better, too many, and they start bleeding worse because of a spike in blood pressure. Further, when you give a large amount of fluids into the bloodstream, you're diluting out the blood. Everything in the blood gets diluted out too - including clotting factors. Thus, if you are not careful with your fluids, the patient will develop a clotting problem (called a "dilutional coagulopathy"). Colloids work better for increasing blood pressure, but the one we use (Hetastarch) has been associated with possibly causing bleeding problems at high doses. Not the best choice in a bleeding patient.

In the end, I used all 3 to no avail. Her condition did not improve, indeed she started to deteriorate. Her anemia worsened, and her clotting times were off the chart high (secondary to blood loss and dilution from all the fluids). I had to take her to surgery.

Of course, in surgery, I found no active bleeding - just a grapefruit sized clot sitting on the uterus. Three technicians assisted me. One was scrubbed in, one was monitoring anesthesia, and one was auto-transfusing my patient's blood as I handed it to her. We were shoving it into her as fast as we could. We closed her up after placing extra sutures on all the blood vessels.

After surgery, she continued to bleed into her abdomen (now due to her inability to clot from a combination of massive fluids and losing all of her clotting factors into her belly). We put a giant needle into her abdomen, sucked out the blood, and auto-transfused her as fast as we could. We bolused her plasma, as fast as we could (plasma will supply the body with clotting factors that it needs), and yet, she looked worse and worse.

Finally, I called the owners and told them I thought we weren't catching up. The bill was already at $3500. They made the call to euthanize her.

I feel terrible about this case. To be fair to myself, I was behind the curve well before that dog hit our doors. Yet part of me feels that if I'd managed the IV fluids better, gotten the plasma and packed blood cells in faster, used less crystalloids and Hetastarch, and waited on surgery, maybe I could have pulled her through. I know - woulda, coulda, shoulda. The case made me feel like a big fat failure, even though I know that's not true. It's been weighing on me heavily since it happened, and I think about it at least once a day. Not in a "let's beat yourself up" kinda way, but in a "what could I have done better, or done differently" sort of way. I've talked to numerous colleagues - specialists and non-specialists about this, and while they have made me feel better, I still wish I could go back in time and do some things very differently.

Hi guys, a request...(i.e. shameless self-promotion)

I'm trying to interest our local newspaper in hiring me as a pet columnist - sort of like a Dear Abby for pets. It would be really helpful if you who follow me regularly but haven't done so yet would join my blog. I'm including this information in my "resume" of sorts. Also, if you have a blog with links that include pet blogs, please add me! Thanks to anyone who can help out in any way!

Hazards around the home

Animals injure themselves in the most unlikely ways. This little guy came in last night, whimpering and bleeding. Thankfully with heavy sedation and a little maneuvering, as well as a few sutures, we fixed him up really nicely.

In other news, my weird anaphylaxis patient is doing ok. At our urging, her owners took her to the specialty clinic for continued care. She has not improved fully, but she is much better than she was. She's been able to maintain her blood glucose and blood pressure, and sepsis has not occurred. She is still "not right" mentally, but she's alive. I'm grateful for that.

Holy WTH, Batman??

Yowza, what a draining weekend. No surgeries, but plenty of difficult, confusing cases that left me wishing I was smarter, more capable, and perhaps board-certified in emergency and critical care. The "last" case of the day was a humdinger.

I was presented with 6 year old, unspayed female terrier type dog. She'd been perfectly normal that day, no health problems, UTD on her vaccines, and otherwise healthy. The owners let her out into the backyard for about a half hour. The yard is fenced, and there are no chemicals, plants, or anything else the dog could have ingested.

When they found her 30 minutes later, she was unable to walk, she was drooling profusely, and she was covered in a mucoid diarrhea. She was barely responsive and had absolutely no palpable femoral pulses.

By the time she got to me, her temperature was 94.2 degrees, her heart rate was a whopping 20 beats per minute (normal 90-150). Her blood pH was 6.99 (normal 7.35-7.5) - indicating a horrible acidosis that was almost incompatible with life. Her blood glucose was elevated at 400, and she had very high amylase and lipase values (enzymes secreted by many organs in the body including the GI tract, pancreas, and kidneys). Initially, I was concerned about diabetic ketoacidosis, but the more I examined this dog, the more convinced I became that she was suffering anaphylactic shock or (less likely) organophosphate toxicity.

I gave her a dose of atropine to bring her heart rate up, and she responded beautifully. We bolused her fluids, and she responded very well. Blood pressure up, blood glucose came down to normal (105), and her blood pH normalized at 7.36. She began to sit up and take interest her in her surroundings.

She was suffering a syndrome I had never heard of until I went to NAVC this past week. It's called "stress of death" hyperglycemia. In cats, it is very normal for the blood sugar to spike when they are stressed or ill. I have seen cats with a blood glucose of 400 simply due to stress. This is a very unusual response in a dog, however. If you see a hyperglycemia in a critically ill animal that is not diabetic, it is called a "stress of death" hyperglycemia, is secondary to massive catecholamines (epinephrine, norepinephrine, etc), and is an indicator of impending cardiac arrest.

When I saw this hyperglycemia in a patient that I didn't suspect was diabetic, my mind immediately jumped to that - and I started treating aggressively.

She has responded much better than I expected, given the severity of her condition. She has developed "mucosal diarrhea." She is losing the lining of her intestines. Why? The GI tract acts as the shock organ in the dog. When there is hypoxemia, low blood pressure, and other shock factors, the gut bears the brunt of it. Hence, the elevated amylase and lipase.

To further my case, I did a brief abdominal ultrasound (also to rule out a weird pyometra manifestation) and found gallbladder wall edema, a very common marker in anaphylaxis.

Unfortunately, my patient is very, very ill. She went to the brink of death, and we brought her back. I don't know if she will make it though. Her blood pressure is stable, her electrolytes, pH, and blood glucose are normal...but she is mentally damaged to some extent. We'll see how it goes. Keep your fingers crossed for her, she is a very sick girl.

Phew

Busy first day back at work, but everything moved along fairly smoothly. I was stuck there until 7:30pm, 2 hours past the end of my shift, as often happens. A late, complicated case came in and I stayed long after my shift trying to work it all out. It was an interesting day with several very interesting/complicated cases.

Earlier in the day, a cat with acute onset of neurological signs and Horner's syndrome presented. Horner's syndrome describes a condition in which one side of the face looks paralyzed. The 3rd eyelid becomes elevated and covers the eye, the pupil becomes tiny (miotic) on the one side, and the eyelid starts to droop (ptosis). This condition is usually caused by interruption of the innervation to the side of the face where it is observed. Differentials for this are numerous and somewhat surprising as they include a mass in the chest. Why a mass in the chest? Part of the nerve runs through the chest, so compression with a mass can lead to Horner's syndrome. Other causes are severe middle to inner ear infections, tumors in the inner ear, trauma to the shoulder/shoulder area, tumor in the shoulder area, idiopathic (no underlying cause), trauma to the cervicothoracic area, sinus infections, etc. Unfortunately, given the cat's age (15), and the severity of the other signs (including staggering and ataxia), he did not want to pursue either diagnostics or treatment. I ended up euthanizing kitty. I didn't feel good about it, as the cat was oriented and talkative otherwise, but I understood the decision.

Following that came a 9 year old, severely lethargic, unable to stand Golden Retriever mix. She'd been treated at her rDVM for a severe whipworm infestation. They had sent her home that morning, but the owners were concerned, as her condition seemed to be worsening. No bloodwork or xrays had been done. The patient had been diagnosed with severe whipworm infestation and discharged home. When I saw her, I was immediately suspicious of a condition called 'pseudo-Addison's disease' secondary to her whipworms. Addison's disease is a condition in which the body cannot or does not produce natural steroids (needed for every small function of the body, practically). As this worsens, this lack leads to weakness, lethargy, vomiting, diarrhea, a drop in blood glucose, electrolyte imbalances (potentially life-threatening), and eventual collapse. For some reason that I cannot remember pathophysiologically, dogs will develop a pseudo-Addisonian crisis when infested with whipworms.

When I ran my bloodwork, my suspicions were confirmed - high potassium, very low sodium and chloride - indicative of an Addisonian crisis. She has improved markedly already with fluids and is able to stand and walk outside.

And then there was the puzzler at the end of the day. An 11 year old, intact male dog that became acutely lethargic and feverish (104.9). When he came in, he walked with a very hunched posture. His temperature was elevated, and he was very dehydrated. He was also very lethargic, although he managed a slow tail wag when I talked to him. Bloodwork showed possible infection/inflammation. His urine was a horrifying muddy brown color with tons of white blood cells but few bacteria. At this point, I am thinking he is suffering prostatitis - inflammation and/or infection of the prostate gland. This is much more common in intact dogs (virtually unheard of in neutered dogs). Prostatic neoplasia is possible, as is prostatic abscessation. Treatment of prostatitis requires long-term antibiotics and eventual neutering. I hope that I am right about his diagnosis and that I'm not missing something else. That's the scary thing about medicine. You just never know. I've spent some time on VIN tonight cruising articles to determine if I'm missing something...

Sprinkled liberally throughout were the usual frustrations: a woman with a Rottweiler (3 years old) that had never been vaccinated and now had parvovirus. This was her 5th dog with parvovirus, and yet she still refuses to vaccinate. Oh, and said dog has puppies at home. Splendid, eh? Then the Boxer puppy in severe, severe respiratory distress (I suspect electrocution or choking injury) with bloody fluid coming out of its nose. The "breeder" (I use the term loosely) had no finances at all, not even enough to pay for the exam fee. Given the severity of the puppy's condition, I offered free euthanasia. It sucked, as well.

Despite that, I was happy to be back at work, refreshed and interested and in a much better mood. I'm not sure where the mental resolution and cheerfulness came from - perhaps just time in Florida near my grandparents, but it was there!

Home again

and pleased to be here. I was exhausted yesterday when I arrived, due to the fact that I had to be up at 4:30am to catch my flight. We got back around 12:30 (after having breakfast together), and collectively crashed on the couch for a Lost marathon, as well as pizza and gyros for dinner. It was decadent. Today, I have a list of things to accomplish before heading back to work tomorrow.

In the meantime, a few pearls I picked up at NAVC:

-Unlike dogs, if a cat does not have a heart murmur, it is highly unlikely that they have heart disease. Dogs can have heart disease in the absence of a murmur.

-Pimobendan (Vetmedin) is being used in cats with heart failure now, although the dose is extrapolated from dogs, and there are no scientific studies to support its use.

-Long term use of albuterol inhaled in cats may worsen the inflammation associated with feline asthma. It should be used infrequently and only as a rescue therapy.

-Approximately 90% of proptosed eyes (eyes popped out of the head) will likely need to be removed at some point. They commonly develop problems after being fixed such as ulcers, blindness, and suture loosening.

I'll have to leave you with that for now.

Greetings from NAVC

The first day of NAVC has been underwhelming. The ER talks I attended this morning were EXTREMELY rudimentary. The first was titled "Common Mistakes to Avoid in the ER." I was very excited, because the speaker is a very dynamic, interesting woman, and I picked up many pearls of wisdom from her last year. The talk however, was geared toward GPs, not ER practitioners. So, I was already aware of all the pratfalls she discussed and gleaned nothing new from it (nor the next 6 hours of lecture).

The day did not improve from there. The only bright side was seeing friends from vet school and having dinner with my internmate, 2 doctors from my internship, and some other friends. It's lovely to hang out and be social.

And, further on the bright side, I'm attending the VECCS (Veterinary Emergency and Critical Care) conference this year (in September), so at least I'll be learning new and fascinating stuff. I'm very excited about that!

Our day started at 6:00am, and it is now 11pm. I think I need to collapse, as I am EXHAUSTED.

Whoo

For those of you who don't know this about me, I loathe taking medications. I'm notoriously bad about finishing antibiotics, for instance. I do rely heavily on NSAIDs and tramadol during my period, but otherwise, I stay away from medications at all costs. I can't tell you the last time I've been to the doctor for an illness or even a physical exam.

Flying makes me panicky. I've overcome the mental panic associated with it, and I can stay calm and mentally focused. There's no more crying or thoughts of death running through my head. On the other hand, I have never learned to control the physical aspects of anxiety - lightly sweating (palms mainly), moderate tachycardia (heart rate shoots up to 120-150), and dizziness. No matter how mentally relaxed I am about flying, I just cannot control these symptoms. Thus, I generally arrive at my destination bathed in a light sweat, clammy, and exhausted. Oddly enough, I love planes and flying.

When we flew to Hawaii, I finally decided to cave in and take a medication for the anxiety.

Let me tell you folks, I will NEVER fly without chemical enhancement again. I've just accepted the fact that while I can control the mental aspects of fear of flying, the physical reaction is beyond my capability. My flight or flight response is activated by the mere sound of jet engines and continues running at high throttle until the plane touches down. With a touch of medication, I can listen to my Ipod, look out the window at the ocean, and generally enjoy the experience of being conveyed to my destination by FLYING 500mph 25,000 feet in the air.

Florida is cold, by the way. We landed, and I got off the plane fully expecting to ditch my scarf. No dice. It was 50 degrees with a light, COLD breeze. Tonight, it promises to drop down to freezing. Oh well, so much for the warm Florida vacation. At least the day itself was beautiful!

The conference starts on Saturday, my friends arrive tomorrow afternoon. I'm very excited to go to CE, see friends, and generally have a great time. I'll get to reconnect with 2 of my internmates, as well. Whoo!

AWOL

Sorry that I've been AWOL - work and all. I leave for Florida in about 24 hours for the North American Veterinary Conference. This is my third year in a row. My 2 best friends from vet school are joining me again, so fun should abound.

Things have been amusing here. Work has been dreadfully slow, so there's not much to say on that subject. The snowy weather has been beautiful, but it has wreaked havoc on the roads. I had to drive 20mph on the interstate to get home yesterday morning, and there were cars in the ditch and wreckers everywhere. For some reason, the minute snow hits the ground, everyones' brains shut down. Semi trucks were passing me at 60+ mph. I watched an Isuzu Trooper nearly roll itself right in front of me.

Sometimes, I hate that I have a job that requires my presence no matter what. Some of my techs called in and said they couldn't make it (they live deep in the country). Unfortunately, I have no such option and must risk life and limb to get to the clinic. Fortunately, my hand-me-down Mercedes SUV drives like a total champ in the snow (other than one hitting the curb incident at 3mph). Today, it is cold, but the sun is out - so the roads are clear. No hindrance to getting to the airport in the morning.

I'll keep you posted from Florida (if I can).

Sadness

I am very sad this morning. McGregor (my black foster kitten) had to be euthanized last night.

He stayed at the clinic while I was gone, and he was fine while I was away. I picked him up Monday, and he was his usual spunky self, up from 1.5 pounds to almost 3 pounds. Over the course of the next 2 days, he became progressively more lethargic, and his appetite dropped off. I didn't think much of it, because I related it to stress from being at the clinic, then coming home. On the 3rd day, I realized that he had most definitely not eaten in 24 hours and then alarm bells started to go off. Keep in mind, I'm working - so gone all night, sleeping all day. I realized something was definitely amiss Thursday morning, but I had just gotten home from work.

I offered him some wet food, as well as dry and Kitten Milk Replacer, made sure his heating pad was on, and then elected to sleep and bring him into work with me Thursday night. When I woke up, he was even more lethargic and weak, and I knew it was bad.

Bloodwork showed a profoundly low blood sugar (43), he was extremely cold despite being on his heating pad all day, and his white blood cell count was low. His weight - in 2 days - had dropped 11 ounces. All fitting classically with panleukopenia (feline parvovirus). I had not vaccinated McGregor yet, because when I got him, he was very sick with a feline upper respiratory tract virus. Vaccines should not be administered to sick animals, so I was waiting until he was fully recovered before giving him his first FVRCP (the P standing for panleukopenia).

He was so sick that I couldn't see putting him through panleukopenia treatment. Unlike canine parvovirus, which we treat with a high level of success here, feline parvovirus is much harder to treat. We've had 2 confirmed cases in the last month here, and they both died - one after SIX days of intensive care. I felt much like most of my clients must feel when faced with this kind of decision. Cost versus outcome versus prolongation of suffering. Sure, I get a discount at work, but I still would have ended up spending $700-1200 on his treatment with a 50/50 prognosis at best. Further, I didn't want him to languish in the hospital for days, only to die or be euthanized later.

Of course, I'm now torturing myself - why didn't I notice he was dumpy earlier? Why didn't I turn around and take him back to work with me on Thursday morning? Why didn't I give him the panleukopenia vaccine right before I left for Christmas (he was likely healthy enough at that point to stand it, though still underweight). Did I do the wrong thing euthanizing him? Should I have treated and hoped for the best?

I loved that little kitten, and though I would have adopted him out, it did not diminish my feelings toward him. I feel terrible, as if I failed him. There were so many places along the way I could have been more alert and prevented this or at least treated him before he got so bad. It made me very empathetic to owners who - without medical knowledge - are faced with the challenge of knowing when an animal is truly sick. They can decline so rapidly.

Rest in peace little McGregor. I'm so sorry I didn't do better for you.

Heart disease (part 3: HCM)

Let me take a moment to briefly point out that heart disease in dogs and cats just plain sucks. We know what the diseases are, how to identify them correctly, and how to manage the end-stage result (congestive heart failure) - but as for preventing them or curing them, nope. We can do nothing. These diseases, once identified, are progressive. What course they will take often depends on breed of the animal, other disease processes occurring at the time, age, and genetics.

Cats being what they are, must have their own weird brand of heart disease. As I said in the last post, they can have DCM, just like dogs. The more common type of heart disease in cats however is hypertrophic cardiomyopathy (HCM). Maine coon cats are in particular prone to developing HCM. It is known to be a genetic trait - autosomal dominant for those hardcore nerds out there.

In HCM, the left ventricle of the heart and the wall that separates the ventricles start to thicken. As those walls thicken, the chamber becomes smaller and smaller, with less and less room for blood to fill the heart. Blood flow becomes turbulent, and a murmur can be heard.

Concurrently with this heart thickening, there is often something called SAM of the MV. This acronym stands for systolic anterior motion of the mitral valve. What it means in normal person speak is that one of the little leaflets of the mitral valve gets sucked into the outflow tract of the heart. It causes worsening turbulence and may contribute to blood clot formation in the heart.

There are some notable differences in cat heart disease that are important for all veterinarians to know. First and foremost, murmurs in cats are often much more difficult to hear. They are usually very focal - meaning that they can only be heard in one place on the chest (dog murmurs are often heard easily - unless they are very soft). Thus, very careful cardiac auscultation is absolutely necessary to make sure that cat murmurs are not missed. On top of that, cats often develop an unusual arrhythmia. It is called a gallop rhythm. It is so named because of the sound it makes. A traditional heart beat sounds like a lub-dub, lub-dub. A gallop rhythm sounds like a horse galloping - a tallot, tallot, tallot, tallot...

If a gallop rhythm is ausculted, this IS ABSOLUTELY A SIGN OF DISEASE. A gallop rhythm in a cat is ALWAYS pathogenic, bar none. If your veterinarian hears an abnormal rhythm in your cat, further investigation is warranted.

Like heart disease in dogs, there is no prevention, and there is no cure. Some cardiologists use ACE inhibitors like enalapril or benazepril presumptively, but there has been no proof that this helps with the heart disease.

Diagnosis is the same - careful auscultation of heart and lungs, xrays of the chest, and echocardiogram. Progression of the disease can follow a similar course as dogs (to congestive heart failure), but there are notable differences in cats. Cats are often asymptomatic up until they develop heart failure. Whereas dogs will often have a steadily worsening cough, possible exercise intolerance, and syncopal episodes, cats may be totally normal until they develop a severe problem (heart failure or a blood clot or both).

Cats tend to develop blood clots in the heart as a result of the turbulent blood flow. These clots will eventually break free from their moorings and enter into the bloodstream. These clots choose to lodge in one of two places - either at the blood supply to the front leg (usually one) or at the place where the aorta splits to the rear limbs. Classic signs of this include paralysis in the rear limbs. The legs will be cold, the muscles hard/rigid, and the condition is extremely painful. Often cats will present screaming in pain. There is no satisfactory or effective treatment for this, and often veterinarians will recommend euthanasia at this point.

The clots can break down with time, so sometimes supportive care with pain medications and monitoring can give the patient some time. The downside is that the clots will always recur - sometimes in a matter of days, sometimes not for months; but it will happen again. Thus, when cats throw clots, it is a very, very grim prognosis. It is ultimately fatal. Less commonly, the clots can lodge in the blood supply to one of the front legs, leading to limping and pain, as well as death of that leg. Like the back legs, the clots can break up with time, and the prognosis is slightly better, although still grim long-term.

These clots form in the absence OR presence of congestive heart failure. If heart failure is also present, the prognosis is absolutely bleak.

Cats also like to be unusual in that they develop pleural effusion with their congestive heart failure. Dogs develop pulmonary edema (fluid IN the lungs). Cats develop that AND fluid AROUND the lungs. Thus, managing them is a much more challenging situation. No one knows exactly why cats do this and dogs do not. There are several theories, but at this time, the reason is not known.

HCM in cats can be primary/idiopathic, related to breed (Maine coon cats), or secondary to metabolic disease such as hyperthyroidism and hypertension. Elucidating a cause is important. If the HCM is secondary to hyperthyroidism, it cannot be cured or fixed, but the thyroid can be managed, hopefully stopping the progression of heart disease.

Other than HCM, cats also develop unclassified cardiomyopathies, arrhythmogenic cardiomyopathies, and restrictive cardiomyopathies, but these are less common.

Heart conditions (part 2: DCM)

Dilated cardiomyopathy is near and dear to my heart, as it affects approximately 50% or more of Dobermans. This is a condition of large breed dogs and occasionally cats. There is thought to be a genetic component because there are very specific breed tendencies. Breeds typically affected include the *Doberman Pinscher, Irish wolfhounds, Great Danes, Newfoundlands, Dalmations, German shepherds, Portuguese water dogs, *Boxers, *Cocker spaniels, and other large or giant breed dogs.

*These have special tendencies to be discussed later.

As with most animal heart diseases, we do not know what starts the disease process or why some breeds seem particularly affected. The heart muscle becomes less efficient at pumping, blood pools, and the left ventricle and left atrium start to dilate. The walls becomes thin, and eventually forward blood flow cannot be maintained. As a result, heart failure occurs (much in the way as with mitral valve disease).

Diagnosis is very similar to that of MVD. Thorough auscultation with concurrent pulse evaluation (usually the femoral pulse), xrays with a VHS, and referral for echocardiogram.

As with MVD, there is no cure for this disease. Treatment is aimed at controlling the signs of heart failure once they occur. Prognosis actually varies with breed.

Some of the specifics:

Cocker spaniels: an association between DCM and taurine levels was found in Cockers. Taurine is an amino acid that is necessary for many important body functions. It was found that supplementing this specific breed with taurine (and L-carnitine, as well) improved contraction of the heart muscle. If you have a cocker spaniel that has been diagnosed with DCM - blood should be submitted to a labratory to have these levels checked, and your pet should be receiving taurine and L-carnitine supplements.

Cats were also found to have a taurine responsive DCM - sometimes due to poor diet. It can be related to canned food diets or homemade diets. Feeding dog food to cats can also cause this. As with dogs, there is an idiopathic form (unknown cause) that takes much the same disease course.

Doberman pinschers: a breed that I love, obviously. Unfortunately, they are the most represented breed to suffer DCM. Also, the course it takes is much nastier in Dobies. They tend to only survive about 2.5 months once heart failure has occurred. Further, they can die quite suddenly and without any advance warning. This is usually due to a fatal arrhythmia. This can occur even if they have never been in heart failure before. Some books and cardiologist recommend yearly screening with a Holter monitor . As with all dogs, there is no preventing or curing this disease. Once heart failure occurs, there are some management options, but Dobies do not do well with this disease.

Boxers: it was recently discovered that Boxers have their own variation of cardiomyopathy that was previously lumped with DCM. It is actually called arrhythmogenic right ventricular cardiomyopathy and also occurs in humans (I think women are more predisposed). It is a totally different disease process and presents usually as syncopal episodes (fainting/collapse). The heart does not necessarily become enlarged, a murmur may be absent, and the only sign might be these fainting episodes. Prognosis is highly varied according to the individual dog.

As a sidenote, there are also secondary dilated cardiomyopathies - specific to some cause. These include chemotherapy induced DCM (notably the drug adriamycin/doxorubicin), nutritional DCM (related to taurine as noted above, also noted in some dogs on Hill's u/d diet for stones), familial DCM in Portuguese water dogs (occurs at a young age and progresses rapidly to death), and infectious DCM (related to tryapanosomiasis (a blood parasite). With the exception of the chemo induced DCM, there are fairly rare. Adriamycin is a very commonly used chemotherapeutic used in the treatment of lymphoma in dogs. As a result, cardiac auscultation and echocardiograms are routinely conducted on dog's undergoing lymphoma treated with adriamycin.

Heart conditions (part 1: mitral valve disease)

Cardiology was not a favorite subject of mine in vet school. This was not due to the subject matter. I'm fascinated by the heart and find it be to more logical than some subjects (neurology, for example). Unfortunately, it was a 5+ inch stack of notes, only 2 exams, and a high level of stress. Now that I'm finished with school, I deal with the real aspects of cardiology and still find it fascinating (although challenging at times).

Animals, as people, develop heart conditions as they age. Unlike people, true myocardial infarction/heart attack is rare. It is much more common for dogs, as they age, to go into congestive heart failure due to pre-existing heart disease. MI is practically unheard of. I am going to talk about the heart disease that occurs in dogs and cats below. We'll start with conditions that develop as pets age rather than congenital conditions.

Understanding blood flow in the heart is relatively easy and necessary in the discussion of heart disease. The heart is an efficient pump. It takes blood from the body that has already been "used" (de-oxygenated) back into itself via the vena cavas. This blood flows into the right atrium, through the tricuspid valve, into the right ventricle. From there, it is pumped into the pulmonary artery (via the pulmonic valve) to the lungs. Here it receives a fresh load of oxygen. From the lungs, it goes into the left side of the heart via the pulmonary veins, into the left atrium, through the mitral valve into the left ventricle, and out the aortic valve/aorta to the rest of the body.



With that understanding, let us discuss diseases.

The most common that I see is probably mitral valve insufficiency (75-80% of heart disease in dogs). This typically occurs in small breed dogs as they age - Schnauzers, Shih-Tzus, Lhasas, Dachshunds, etc. Large breed dogs can be affected, but this is not as common.

The hallmark is an older dog abruptly developing a heart murmur. For some reason that we fail to understand, the body starts to produce thicker layers (fatty) within the leaflets of the valves that separate heart chambers. This is called myxomatous valvular disease (also endocardiosis and degenerative valvular disease). This is very rare in cats.

The mitral valve separates the left atrium from the left ventricle. As the fatty deposits build up, the leaflets of that valve pull apart, causing improper blood flow between the chambers (regurgitation of fluid from the left ventricle backwards into the left atrium). Blood should flow forward - from the lungs to the pulmonary veins to the left atrium to the left ventricle out through the aorta. When the gates between chambers become weak, blood becomes turbulent, flows improperly, and the patient will develop a heart murmur.

As this problem worsens, the left atrium will become enlarged and thin-walled. This happens due to back pressure of the improper blood flow and turbulence. As the atrium becomes thin, it becomes unable to do its job properly. Blood starts to back up, as it is not being pumped forward correctly. The blood backs up into the lungs causing changes in the pressure gradient there. Eventually, fluid starts to leak into places it shouldn't and pulmonary edema ("fluid in the lungs") develops. This is congestive heart failure.

So, what should you do if your older, small breed dog is diagnosed with a new heart murmur (this link will let you listen to a normal heart versus a heart murmur)?

First and foremost, your veterinarian should thoroughly and carefully listen to all areas of the heart - both the right and left sides of the chest. By just listening carefully, a veterinarian can often determine where the murmur originates and thus, what the most likely cause is. They can also determine if any degree of heart failure is present by listening for crackling and wheezing in the lungs.

Then xrays of the chest should be conducted. These will help evaluate heart size and for the presence of pulmonary edema and heart failure. A vertebral heart score should be determined. This is the only objective way to identify heart enlargement on xrays. Your veterinarian will measure the width and height of the heart, compare those numbers to a specific vertebrae, and come up with a number. Normal VHS in dogs is 10-10.5. Anything greater indicates an enlarged heart.

Next, your veterinarian should recommend an echocardiogram performed by either a cardiologist or a specialist with ultrasound training. This will help determine what is causing the murmur. Many owners balk at this point due to cost. It is understandable, but an echo is the only way to know for sure where the murmur originates. If owners cannot pursue an echo, the veterinarian should treat based on the most likely cause of the murmur. (The murmur itself is not a disease, it is a symptom, and as such, it is not specifically treated.)

If mitral valve disease is determined to be present, your veterinarian will likely recommend xrays to re-evaluate heart enlargement every 3-6 months. Your vet will also discuss monitoring for signs of impending heart failure such as exercise intolerance, weakness, fainting/collapse, and coughing or wheezing. Some veterinarians will start an ACE inhibitor at that time (enalapril/Enacard or benazepril/Lotensin). It is important to know that at this point, there is NO way to prevent progression of heart disease. In people, valvular replacement can be done, but this is not done (or only done extremely rarely) in animals. The cost is prohibitively expensive.

There is no way to tell how each individual dog will progress. Some will live years with a heart murmur and no heart failure, some will live months and then go into heart failure. It is individual to each dog. If your older, small dog has a heart murmur, your veterinarian should be monitoring closely at 3-6 month check ups for changes in lung sounds, severity of the heart murmur, and clinical signs.

Questions?

Christmas pictures

Nothing new in my life to report. I go back to work Wednesday night, so stories will abound, I have no doubt. In lieu of a medically themed post (I'm being lazy, ya'll)...some pictures of my Christmas (starting with the view from my in-laws' back patio)...

Hopes for the New Year

I don't make New Year's resolutions, I stopped doing that when I was still an optimistic youth. The Christmas tree has been taken down, the bags unpacked, and we are home again (at least, temporarily). It was a lovely belated Christmas. I was lucky to spend 5 days packed with activity with my family and friends. We saw a great concert in Asheville and celebrated New Year's Eve out and about with friends (the first time we've gone out on NYE in a long time).

As I sit here and think about the year to come, I have no resolutions, but I do have some hopes.

I hope that I continue to love my job and everything about it - that this peaceful time in my life continues.

I hope and am going to work towards undoing some of the cynicism my job has instilled in me the last year. I want to remain realistic without making assumptions before having anything to base them on.

We hope to be adding to our family in a big way - new dog, new bird, new baby? We shall see what the year brings.

I hope that this year, I will continue to unlearn my long entrenched ways of self-centeredness and become a more outwardly focused person - especially wife, sister, and daughter.

Most of all, I hope that everyone I know and love will have a productive, happy year, that everyone will stay healthy, and that we will all be here to celebrate 2012 together.