Friday, February 26, 2010

2/26/2010 Friday - More on Flash's lameness

Vet tip of the Day: Understanding the lameness exam
Key Words: splint bone, cannon bone, fracture, sclerosis, lysis

Today I’m going to continue following the trail of Flash’s lameness which remains unsolved. A quick review of the initial findings: an acutely grade 4 lame 11 year old gelding with history of trauma to the medial  left front mid-metacarpus . There was hot painful swelling mid-way down the splint bone, no other pertinent findings on physical examination.

The American Association of Equine Practitioners has established a uniform grading system to describe equine lameness. If you Google - AAEP lameness - you can read more on how veterinarians evaluate lameness. Here is the scoring system:

0: Lameness not perceptible under any circumstances. 1: Lameness is difficult to observe and is not consistently apparent, regardless of circumstances (e.g. under saddle, circling, inclines, hard surface, etc.). 2: Lameness is difficult to observe at a walk or when trotting in a straight line but consistently apparent under certain circumstances (e.g. weight-carrying, circling, inclines, hard surface, etc.). 3: Lameness is consistently observable at a trot under all circumstances. 4: Lameness is obvious at a walk. 5: Lameness produces minimal weight bearing in motion and/or at rest or a complete inability to move.

While this grading system is useful, it does not specifically describe the characteristics of an individual horse’s lame gait. When watching Flash move, what concerned me was not only the degree of lameness – clearly visible at the walk, but the inconsistency of the lameness. When turning, or stepping onto uneven ground Flash would occasionally take steps that were almost non-weight bearing. The veterinary vernacular for this type of gait is “fracture lame”. When walking carefully on a flat surface Flash’s gait would improve to a fully weight bearing walk.

When evaluating a lame horse it is important not to develop tunnel vision. While Flash had obvious evidence of trauma to the splint bone area of the forelimb, the character of the lameness was not characteristic of that produced by a splint bone fracture. I was immediately concerned that there might be a non-displaced fracture (a crack, more or less) of the cannon bone or first pastern bone, although these injuries are uncommon. Also the occasional “bad steps” suggested pain in the hoof. Flash wore shoes with full pads, making it impossible to apply hoof testers to his foot reliably to check for a signs of pain originating from the foot.

A second concern when examining a horse with a grade 4 lameness is making a bad situation worse. If a diagnostic nerve block is performed which eliminates the pain, the horse may no longer protect the injured area and in bearing full weight, cause a non-displaced fracture to become unstable, or comminuted, with disasterous consequences. So, on my first examination of Flash I broke the rules of lameness evaluation that you learned in yesterday’s blog. I skipped the diagnostic nerve blocks and only evaluated the gait at a walk. I completed a careful examination of the limb and went straight to x-rays to rule out a fracture.

Radiographs of the medial splint bone and cannon bone ( MCII and MCIII – see blog archive from Feb 7th for review) did not reveal a fracture, although there was obvious enlargement of the splint bone at the swelling site. So what to do? Small, fresh, non-displaced fractures are not always immediately apparent on radiographs, even with excellent quality digital x-rays. Keeping the veterinary code of “above all else, do no harm” foremost, I decided to treat Flash conservatively and repeat the x-rays in two weeks. There were no open wounds or swollen joints, so the chance of infection requiring immediate treatment was minimal, and if there was a non-displaced fracture present that I had failed to detect, it was best treated with stall rest and observation at this point.

I prepared an anti-inflammatory “sweat” containing furacin, glycerin and DMSO and instructed the trainer to apply it daily to the swelling under a bandage. I prescribed a low dose of phenylbutazone to decrease pain and inflammation. The dosage was very conservative because I did not want Flash to feel too comfortable and not protect his leg. I instructed the trainer to call me immediately if the lameness worsened or did not improve somewhat over the next 2-4 days, and scheduled a recheck in two weeks barring complications.

Hopefully the past two blogs have helped illustrate some of thought processes we employ when approaching lame horses. The take home message: for chronic, low grade lamenesses, we use a systematic approach:

Step 1: physical examination

Step 2: gait evaluation

Step 3: diagnostic nerve blocks

Step 4: Diagnostic imaging

When evaluating acute, severe lameness, additional concerns come into play which may alter this plan. Two important things to keep in mind: 1: Do No Harm, 2: Don’t get tunnel vision.

More on Flash on Monday – what do you think the answer is?

Enjoy your weekend – the 4th chapter of Veterinary Tales will be ready next week, introducing one of my favorite clients, getting Sticky’s histopathology results, and treating a horse with a mysterious swelling!

2/26/2010 - Nerve Blocks

My apologies for this late posting - problems connecting with Internet prevented uploading for the past 2 days!

Vet tip of the Day: Diagnosing Lameness with Nerve Blocks

Key Words: Peripheral nerve, intra-articular, neurovascular bundle, lameness, imaging, posterior digital nerve block, medial, lateral, palmar, plantar

I’ve been scratching my head over a horse with a challenging lameness for the past 2 weeks. He inspired Wednesday's blog concerning veterinary specialists, since I’ve sent his x-rays off to three different ACVS (American College of Veterinary Surgeons) Diplomates for their opinions. This gelding became acutely lame after an accident during training. While working in a round pen, the trainer observed the horse hit the inside of his left front cannon bone with the opposing front foot. The horse began limping immediately and was brought back to the barn. The area of impact became warm, swollen and painful to touch in under an hour. I was called and scheduled an appointment to see the horse that afternoon. Today’s vet tip will explain how we evaluate and diagnose lameness with an emphasis on understanding nerve blocks. Tomorrow we will return to the case and how it is progressing.

Lameness diagnosis and treatment composes a large part of practice with performance horses. There are four main parts to lameness diagnosis: physical examination, gait evaluation, localization with nerve blocks, and diagnostic imaging. These four tools form layers of information which when combined, should each complement the other, allowing your veterinarian to confirm the cause of your horse’s lameness. Often a client will call me and ask to have their horse "x-rayed".  However, because horses cannot tell us where they hurt, it is necessary to use the first three diagnostic tools before obtaining diagnostic images. It is a mistake to jump to diagnostic imaging, such as x-rays, before performing an exam and nerve blocks.

Here’s the problem: let’s say I see a horse limping on its right front foot. It is a 15 year old Quarter horse with narrow heels and upright pasterns. I assume it has navicular disease and x-ray the front feet. Sure enough, there are radiographic changes consistent with navicular disese. End of story, right? Wrong. Without evidence from physical examination and regional nerve blocks, I cannot prove that the abnormalities on the x-rays are responsible for the horse’s lameness. What if he also has a bone chip in his knee with associated arthritis and this in fact is the source of his lameness? Because horses cannot describe their pain to me, in order to localize lameness to a particular anatomical location, it is critical that I use peripheral and articular “blocks” to localize the pain. The theory is simple: if I have pain in the big toe on my left foot causing me to limp and somehow that big toe loses its sensation, my limp would be gone

A systematic approach is used to localize a lame horse’s pain. The lower limb is blocked in sequential regions, progressing from the foot upward, until the lameness resolves. There are two types of nerve block: the peripheral block, and the intra-articular block. Peripheral nerve blocks involve the subcutaneous instillation of a small amount of local anesthetic into the tissue immediately surrounding a particular nerve. These blocks are performed after a brief surgical prep, typically the veterinarian does not wear gloves, and the risk of complication is extremely low. Intra-articular blocks refer to the injection of sterile local anesthetic directly into a joint space. Intra-articular blocks must be performed very carefully under aseptic conditions, because of the risk of introducing infection into a synovial structure. A careful surgical prep is performed, the veterinarian always wears sterile gloves and follows strict aseptic technique.

The body is a complex highway of neurovascular bundles that supply blood and innervation to precisely mapped regions. These bundles consist of a vein, an artery, and a nerve. They are uniformly constructed, with the nerve lying along the back of the bundle, preceded by the artery and vein, respectively. In the leg, there are two long neurovascular bundles that run along the inside and outside of the limb from the knee to the ground , along the back of the cannon bone. The nerves in this bundle are called the medial and lateral palmar or plantar nerves . Medial: inside, lateral: outside, palmar: front leg, plantar:back leg. When “working up” a lameness of unknown origin, we begin by blocking the horse’s heel region using a posterior digital peripheral nerve block.

One milliliter of lidocaine or carbocaine is infiltrated just beneath the skin low in the pastern along the medial and lateral axial planes. It is very easy to palpate the neurovascular bundle in this location. Pick up your horse’s left front leg and hold the foot in your left hand, facing your horse’s head. Press your right thumb firmly against the back (palmar aspect) of the pastern just lateral to midline, then slide your thumb laterally (toward the outside of the pastern), continuing to press firmly. You will feel a rubbery cord slip beneath your thumb. This is the neurovascular bundle. It also is easy to palpate at the base of the fetlock, along the medial and lateral palmar borders.

After the anesthetic is instilled, and an amount of time passes appropriate for the block performed (this varies a bit from one anatomical location to another, but generally is between 5 and 10 minutes), the horse’s gait is re-evaluated. If the gait has improved 80% or more, the block is considered diagnostic. This means that the pain causing the lameness originates from a structure that lies below (distal to) the location of the nerve block. In the case of the heel block, or posterior digital block, the source of the pain must be in the back one third of the foot. This includes the navicular bone, navicular bursa, the ligaments which support the navicular bone (there are a bunch of these), the digital cushion (the pad-like structure that supports the heel region of the foot), and the sole in the heel region. Once localized to this area, further diagnostic tests such as x-rays, ultrasound, or in complex cases, MRI can be performed. The trick is then to correlate imaging abnormalities with the information derived from the nerve block response and physical examination.

In tomorrow’s Vet Tip of the Day we will return to the horse with the challenging lameness I’ve been looking at for the past 2 weeks and begin peeling back the layers of his diagnostic work up in an effort to determine the source of his problem. See you then.

Tuesday, February 23, 2010

2/23/10 - Veterinary Specialists

Vet Tip of the Day: Understanding your Veterinarian's Training
Key Words: Diplomate, Board Certification, Residency, Internship

I've been looking at a horse with a challenging lameness problem for a couple of days.  This weekend I examined another horse with an unusual neck problem.  I obtained radiographs of both horses.  Tonight I will e-mail the x-rays of the lame horse to a board certified large animal surgeon for his opinion.  Yesterday I mailed a disc of the neck films to the radiology department at UC Davis where they will be reviewed by a board certified radiologist.  Last week a colleague of mine called me to ask for a consult on a horse with pleuropneumonia.  He was seeking my opinion on treatment options because I am board certified in Large Animal Internal Medicine.

What do you know about your veterinarian's training and post-doctoral experience?  All of us practicing veterinary medicine have completed a 4 year graduate veterinary degree program after our undergraduate college years.  When we graduate from veterinary school we receive a doctoral degree: DVM or VMD (if you graduate from the University of Pennsylvania your veterinary degree is awarded in latin so it ends up VMD instead of DVM).  In order to practice veterinary medicine we also have to pass the day long National Board Exam as well as an exam in any state in which we intend to practice.  With a DVM and passing scores on the National Board and state exams, we are licensed to practice all aspects of veterinary medicine according to the laws of the veterinary practice act in the state in which we work.

Unlike human medicine, veterinary medicine does not require an internship or residency after vet school.  However, many individuals choose to complete such post-doctoral training.  Most Colleges of Veterinary Medicine offer rotating small and large animal internship programs which provide a year of experience in medicine, surgery and reproduction under the supervision of experienced faculty members.  Many private practices also offer internship programs, but many of these programs do not fall under the guidance of any governing body.  While some private practice internships are of excellent quality and value, some are not.

After completing an internship, the final phase of advanced clinical training available to veterinarians is residency programs.  Most of these programs take place in a University setting, but there are private practice residency programs as well.  All residency programs must comply with rules and regulations set down by the Specialty College under which they operate.  The three main specialty colleges are the American College of Veterinary Internal Medicine (ACVIM),  the American College of Veterinary Surgeons (ACVS), and the American College of Theriogenology (ACT, reproduction).  There are many subspecialties in the Medicine college.  These include neurology, cardiology, oncology, and large and small animal internal medicine. There are also specialty colleges of Emergency Medicine, Exotic and Zoo Animal Medicine and Critical Care.

As you can see, there are many opportunities for advanced training after the Doctor of Veterinary Medicine is obtained.  My list above is far from complete.  All ACVIM and ACVS residency programs are at least 3 years long.  Some combine their clinical residency with a Masters or PhD program in a basic science.  My Large Animal Internal Medicine Residency was completed at the University of Georgia and was combined with a PhD degree program.  This combination training took 5 years to complete, and offered a great complementary combination of basic research and clinical training which in my case had a strong emphasis on colic, or equine gastrointestinal diseases.  It is important to remember that while we are completing residency programs, not only are we becoming highly skilled experts in our specialty field, but we also are working as practicing veterinarians in a teaching hospital, and so are interacting on a daily basis with other services, including surgery, lameness, reproduction, etc.

At the end of a residency program, the resident candidate's credentials must be approved by their resident mentor, and then they have the priviledge of taking a monster exam.  To give you an idea of how stringent our veterinary specialty residency programs are, when I took the ACVIM Large Animal Internal Medicine exam, the pass rate was 23%.  That means that only 1 of every 5 people who sat for the exam that year received board certification.    

If your veterinarian is a general practicioner, he or she may choose to consult with a specialist from time to time concerning certain issues with your horse, or in some circumstances may choose to refer you and your horse directly to a specialist.  As veterinarians, we have a strict code of referral ethics.  I encourage you to  follow your primary care veterinarian's advice, consult with the specialist, and return to your primary care veterinarian for follow up care.  It is important that specialist referral centers maintain open lines of communication both with their clients and with the referring veterinarians in order to provide the best care to your horse while maintaining continuity of service.

Now that you know a little bit about specialization within the veterinary profession, take advantage of your knowledge and ask your veterinarian any questions you may have about our profession.  Don't be afraid to ask any professional about their credentials and experience.  And if you do take your horse to see a specialist for any reason, be sure that that person is in fact a Diplomate of the Specialty College of Veterinary Medicine in which they are practicing.

To learn more about our specialty colleges, log on to or

I am your Vet Tip of the Day Blogger,
Chrysann Collatos VMD (Veterinariae Medicinae Doctoris), PhD (Doctor of Philosophy in Physiology), DACVIM (Diplomate American College of Veterinary Internal Medicine)

Monday, February 22, 2010

2/22/2010 - Omega-3's & Colic

Vet Tip of the Day: The role of Omega-3 Fatty Acids in Colic prevention
Key Words: Colic, Polyunsaturated fat, fatty acid, cell membrane, endotoxin

Since you are now budding experts on the subject of endotoxemia and its devastating effects on horses with gastrointestinal disease, I thought we would conclude this segment on colic with a discussion of Omega-3 fatty acids.  You've may have heard a lot of buzz about these special fats; following are some facts about Omega-3's and how they can help protect your horse from some of the terrible consequences of endotoxemia.

Omega fatty acids - What are they?

This part is pretty dry, but it will only last a few sentences, so hang in there. Our bodies derive four types of fat from food:cholesterol, saturated fat, monounsaturated fat, and polyunsaturated fat. Omega-3 fatty acids are polyunsaturated fats. They are called omega-3 because a certain chemical bond between two carbon atoms occurs at the third carbon in this fatty acid chain of carbons. The other major polyunsaturated fat in our diet is Omega-6 fatty acid (first double bond at the sixth carbon).

Omega-3 and Omega-6 fatty acids are considered “essential” fatty acids, because neither horse nor human can construct these substances internally. They must be obtained in our diets. While both O-3 and O-6 are necessary for good health, we and our horses eat diets that are relatively high in Omega-6 fatty acid and deficient in Omega-3. As we will see, it appears that an ideal ratio of dietary O-3 to O-6 is about 2:1, while most of us are eating these fatty acids in a ratio more like 1:10 or even 1:20.

Omega fatty acids - What is their function?

Consider the building blocks of our bodies. We and our horses are amazing machines, composed of a group of organ systems that works in harmony to create life. Each of our organs is a mass of cells, and each organ has its own distinctive cell type. Liver, kidney, skin, nervous tissue, brain, blood vessel walls - each has its own unique cellular architecture. However, all of these cell types are encased in the same basic cell membrane. Guess what our cell membranes are made of? You’re right - they are made of fat!

Cell membranes are composed of a double layer of phospholipid, a complex fat containing Omega-3 and Omega-6 fatty acids. The cell membrane is like a telegraph system; signals from outside the cell are communicated to the inside through the cell membrane. The composition of the cell membrane determines in large part how signals are translated from outside to inside; the cell membrane makeup greatly influences the cell’s response to a given stimulus. Specifically, a cell membrane enriched in Omega-3 fatty acids is protected from many of the inflammatory responses to injury that are produced by an Omega-6 enriched membrane. 

If your horse experiences a serious colic in which gut motility is disrupted, remember that this leads to a die off of bacteria normally present within the bowel.  Some of these bacteria contain endotoxin, which is absorbed into the blood stream through the compromised gut wall of your colicky horse.  This endotoxin attaches to cell membranes in your horse's system, sending a series of telegraph signals across cell membranes and from cell to cell that lead to the production of many small molecules responsible for inflammation, shock, and cardiovascular collapse.  If your horse's cell membranes are enriched with Omega-3 fatty acids, the severity of the inflammatory response to these signals is dampened, resulting in less devastating effects on your horse's circulatory system.

Omega-3 Fatty Acids - Where do we find them?

Omega-3 fatty acids are relatively abundant in oily, cold water fish such as tuna, salmon, and mackerel. These fish contain large amounts of two Omega-3's, eicosapentaenoic acid (EPA) and docosahexanoic acid (DHA). Vegetable sources of Omega-3's include kelp, as well as flaxseed, canola, walnut, and soy oils. The latter 4 oils contain alpha-linolenic acid (ALA) the third major Omega-3 fatty acid. One should remember that all of these sources of Omega-3 fatty acid also contain Omega-6 fatty acid. Once ingested, the Omega-3 and Omega-6 fatty acids compete for the same processing sites in the body, emphasizing the importance of the balance of O-3 and O-6 in the diet.

For us, consumption of Omega-3's is easily achieved by eating fish. Since 2000, the American Heart Association’s dietary guidelines have recommended that healthy adults eat at least two servings of fish per week. Alternatively, there are many encapsulated fish oils available: people with existing cardiovascular disease are encouraged to take 1 gram of EPA and/or DHA daily.

For our horses, there are an increasing number of supplements and concentrate feeds on the market that are enriched with flaxseed oil to supply Omega-3 fatty acids. Unfortunately, we have no good information on how much a horse should eat to achieve a beneficial result. Therefore, while there is mounting evidence that dietary enrichment with Omega-3 fatty acids will improve your horse’s overall well-being, we are still guessing with our dietary supplementation. One positive note concerning flaxseed oil, the primary source of Omega-3 for horse consumption: flaxseed oil contains three times more Omega-3 than Omega-6 fatty acid, making it likely to shift the overall dietary balance of O-3 to O-6 in the right direction, toward 2:1.

How will Omega-3's help my horse?

We may not know how much to feed, but we do have some experimental evidence concerning the beneficial effects of Omega-3 fatty acids in horses. In the laboratory setting, researchers have looked at the effects of Omega-3 fatty acids on various equine cell types. Cells from joint linings, or cells from the abdominal cavity, for instance, can be grown and maintained in the lab. The cell cultures, as they are called, represent miniatures of the whole horse. Each cell type can be “fed” diets containing varying amounts of Omega-3 fatty acids. Then, cells can be subjected to an experimentally induced injury and the cell’s response to this injury can be measured. In fact, a beneficial effect of Omega-3 fatty acids on equine intestinal cells has been demonstrated in this experimental setting.  The presence of Omega-3 fatty acids in the cell membrane reduces the cell's inflammatory response when exposed to endotoxin.
There is much left to be learned concerning the role of Omega-3 fatty acids in our overall health plan, for our horses and our selves. However, early evidence weighs in strongly in favor of a beneficial effect with no apparent associated dangers. Educate yourself more about the world of Omega-3 fatty acids and make an informed decision concerning the inclusion of an increased amount of this essential fatty acid in your horse’s diet.

A bit of trivia: who remembers the heart-rending movie Lorenzo’s Oil? The story of a child with a degenerative nerve disorder. Guess what the magic oil was? Right again - Lorenzo’s Oil was an Omega-3 fatty acid.

Friday, February 19, 2010

Fri 2/19/10 - Colic - Clinical Case

Vet Tip of the Day: Fatal Colic
Key Words: Ischemia, Shock, Banamine, Heart Rate, Pain

My assistant Jessie and I had a hectic day - three emergencies, each in a different geographic area, on top of scheduled calls.  Our third emergency was the horse pictured here, who had an acute onset of abdominal pain.  Unfortunately, the outcome was not positive.  I am going to share this case with you so that perhaps by learning from this lovely old horse we can give some small value to his death.  The education he provides will be his last gift to us.

Chance was a 23 year old gelding.  His nutrition and preventive health care were excellent, and he was in very good condition.  He was used as a school horse for beginning riders and had no previous history of colic.  He was normal this morning, but suddenly around 2 PM began to look back at his abdomen  and paw at the ground.  Within 20 minutes these signs had progressed to the point that Chance would crumple to the ground and roll unless one person led him forward while a second person encouraged him to stay up with a longe whip.  We arrived 30 minutes after the onset of signs.

Chance's behavior is classic for acute, severe colic.  Mild signs of abdominal pain include looking back at the abdomen,  standing in a stretched out posture as if trying to urinate, loss of appetite, occasional pawing and spending unusual amounts of time lying down.  Moderate pain is characterized by persistent pawing, and frequent lying down and getting up.  As pain becomes severe, signs include falling suddenly to the ground and rolling violently.

When we arrived, it was impossible to perform a physical examination on Chance because as soon as he stood still he would attempt to throw himself down.  I administered a mild sedative intravenously as he was walking.  After 10 minutes this medication had had no effect so a second, more powerful sedative/analgesic combination was given.  Five minutes later Chance would stand without trying to roll, but was heavily sedated and not normally responsive to stimuli.  At this time his heart rate was moderately elevated (52 beats per minute/normal range 28-40), he had no gut sounds, and his gums were pale pink.  On rectal examination I could palpate an increased quantity of heavy ingesta in the large colon, which was displaced from its normal position.  A stomach tube was passed through the nose into Chance's stomach, and when a siphon was applied it was determined that there was no build up of fluid in the stomach.

Although I had not felt anything too alarming on rectal exam, at the time of our initial evaluation Chance has only been showing signs of discomfort for 30 minutes.  And in this time his degree of pain had escalated rapidly.  At this point my assessment was that Chance was suffering from an acute, severe colic.  Based on the severity of pain (which was only controlled temporarily by a very potent pain relieving injection) and the rapid progression of signs I was suspicious of a strangulating obstruction, or a twist in the bowel that had cut off blood supply to a section of the intestine.  These sudden strangulating lesions cause the most immediate, severe, and unrelenting pain of all forms of colic.  The strangulation can occur in either the large or small intestine.  Eventually the normal bowel becomes very distended in front of the strangulation, but this takes a few hours to develop, and during this time the rectal exam may be deceptively normal.  Unfortunately I couldn't accurately assess Chance's heart rate because I had to sedate him before I could listen to his heart and the sedative lowers heart rate significantly.  To answer one of yesterday's questions, of all the information we can gain from a colic, including sophisticated laboratory data, the two most sensitive indicators of the severity of the situation are heart rate and degree of pain.

At this point, Chance becomes a surgical candidate.  The only hope for horse's with strangulating lesions is rapid surgical intervention.  Once a significant portion of bowel looses blood supply,  endotoxic shock (see yesterday's blog) sets in very rapidly. Cardiovascular collapse and death can occur within 4-6 hours in the most severe cases. Because of Chance's age and economic constraints, surgery was not an option.  The only hope was that my assessment was incorrect.  I gave Chance a dose of flunixin meglumine (Banamine), a powerful anti-inflammatory medication which relieves gastrointestinal pain and combats the effects of endotoxemia, and we waited.

Within 30 minutes, when the sedative/pain killer was wearing off, Chance became very painful again.  With the recurrence of pain now Chance also exhibited an elevated heart rate (80 beats per minute), muscle tremors, a continued abscence of gut sounds, and deteriorating mucous membrane color.  His gums took on a grey/purple hue, which is hallmark indicator of cardiovascular compromise, or shock (see picture).

Euthanasia was performed 3 hours after the onset of Chance's colic.  Within that short time he had progressed from a healthy horse to one with multiple signs of severe endotoxic shock, the result of a strangulating intestinal lesion.

Long term (over 1 year) survival of horses with severe strangulating lesions after surgery ranges from 30 - 60%, depending on what study you read.  Estimated cost of surgery and hospitalization for these severe cases is 7,000 to over 10,000 dollars.  These are the worst case scenario colics, and they are by far the least common.  Colics requiring surgery that do not involve dead bowel, such as simple large colon displacements, have 85 - 90% long term survival rates, with cost estimate around 6,000 dollars.  And while Chance's story is a tragic one, remember that the vast majority of colics do not require surgery, and respond well to medical therapy.

The key to preventing colic is regular preventive health care, excellent quality diet, and a regular exercise program.  Unfortunately, colic can be an  indiscriminant killer, and as Chance showed us today, even horse's receiving the best of care can be stricken.  Chance was a wonderful horse, and will be sorely missed.  Hopefully by sharing his story he will help bring veterinary assistance to another horse with the chance for a better outcome.

Thursday, February 18, 2010

Thurs 2/18/2010 - Colic

Vet Tip of the Day: What is Colic?
Key Words: gastrointestinal, endotoxin

I had a special visitor today.  Dr. James Moore, from the University of Georgia, was in Reno speaking at the AERC National Convention.  Dr. Moore was my major professor when I completed my doctoral research back in the early 90's.   He is a brilliant surgeon and researcher, and has spent much of his career investigating the factors that make colic such a deadly disease in horses.  As we ate pizza and swapped old stories this evening, I thought I would use his visit as inspiration for today's Vet Tip of the Day.

Colic is a very general term that refers to pain originating from the abdominal region.  In horses, colic has been associated with any disease of the gastrointestinal (GI) system that causes clinical signs of  GI pain.  The most common mechanisms of GI pain are distension and loss of blood supply.  Both of these occur when a section of bowel shifts into an abnormal position, or rotates on its own access.  The equine gastrointestinal system is composed of the esophagus, stomach, small intestine, cecum, large colon, small colon and rectum. The large colon is divided into 4 sections, which lie folded on each other, running along either side of the abdominal cavity. The intestinal tract of an adult horse, from stomach to rectum, is over150' in length!  Here's the most amazing part: the vast majority of the intestinal tract is free to move all over the abdomen,  only the cecum is attached at its base to the body wall.  Therefore, whenever the horse's complex intestinal motility pattern is upset, loss of coordination in progressive motility can lead to displacement of portions of the small intestine, or any of the colons.  When this occurs food material cannot move in an organized manner through the GI system.  When food transit is slowed, the bowel wall becomes distended.  This distension causes pain and further disrupts motility.  If the bowel rotates on itself (torsion or volvulus), a complete obstruction occurs, with loss of blood supply and severe distension, which can rapidly lead to death.

What kills horses with severe colic?  When a piece of the intestinal tract loses motility, becomes distended, or has reduced blood supply, several things happen.  First, the contents of the intestine stop moving. Second, the wall of the intestine begins to lose integrity as its oxygen supply is cut off due to lack of blood supply.  The intestinal contents are normally rich in bacteria which aid digestion.  However, when gut contents stop moving, the chemical environment in the gut contents is altered, resulting in bacterial death.  The dead bacteria decompose, and are absorbed across the now unhealthy gut wall into the blood stream.  One of the components of the bacterial cell wall is called endotoxin or lipopolysaccharide.  Endotoxin is a very powerful toxin to which horses are exquisitely sensitive.  Very small amounts of endotoxin in the equine blood stream cause severe inflammation, which leads to shock, cardiovascular collapse, and ultimately death.  So horses which die due to colic are actually poisoned by the contents of their own gastrointestinal tract.

Less serious colics, caused by temporary delay of transit through parts of the gut, such as large colon impactions, often respond to conservative treatment including anti-inflammatory analgesic medication such as flunixin meglumine (Banamine) combined with administration of fluid, and mineral oil via a naso-gastric tube.  When a complete obstruction occurs, however, surgical intervention is necessary to empty the affected bowel and return it to a normal position.  In the most severe cases, where segments of bowel have had severe compromise to their blood supply, surgical resection (removal of the affected bowel) may be necessary.

Can you list 5 signs of colic (gastrointestinal pain) in order or increasing severity?
Do you know what the 2 most reliable indicators are to determine whether a horse with colic requires surgery?

Answers in tomorrow's Tip of the Day.

Wednesday, February 17, 2010

2/16/10 All Vaccines are Not Equal

Vet Tip of the Day: How Vaccines Vary
Key Words: Antibody, Cell Mediated, Immune System, Virus, Bacteria, West Nile, DNA

We've looked at the factors that help you decide whether or not to vaccinate your horse against a certain disease.  Now let's examine how vaccines work.

All vaccines work by stimulating the immune system in some fashion.  We think most simply of a vaccine as something that stimulates the production of antibodies.  These antibodies then prevent invasion by either a bacterial or viral disease causing organism.  In fact, there are many different classes of antibodies in the equine immune system, and certain classes of antibody are more effective than others in fighting particular diseases.  For instance, IgA antibodies are very effective in fighting off infections that begin in the upper respiratory tract, such as Strangles.  Therefore, the intranasal Strangles vaccine was designed to stimulate a strong protective IgA reponse.  It does this by physically depositing live, chemically altered Strep Equi bacteria onto the back of the horse's pharynx when the vaccine is injected through the nasal passages.  This live bacteria mimics the actual Strangles organism and causes the horse to produce IgA antibodies in the upper airway which then combat the actual Strangles organism when your horse is exposed to it.  The protection is not absolute, and the antibody response to the vaccine is variable.  In addition, because the vaccine contains live, chemically altered organisms, there is a small risk of inducing a vaccine strain case of Strangles in response to the vaccine itself.

In addition to antibody production, the body has is a second, non-antibody dependent arm of the immune system.  It is called cell mediated immunity and is very important in the body's ability to fight viral diseases.  You may have read about the new technologies being used in some of the equine West Nile vaccines.  Instead of using an altered form of the disease causing organism to directly stimulate antibody production, these vaccine use a variety of technologies involving the actual genetic material (DNA) of the disease causing organism.  DNA based vaccines are more effective in stimulating all aspects of the immune system, thereby providing a stronger, more broad based protection against viral organisms, such as West Nile
Virus.  The Intervet DNA chimera vaccine is a fascinating cutting edge product with excellent safety and efficacy against the West Nile Virus.  To learn more about it, Google: Prevenile, Intervet, West Nile.

Finally, while the ideal vaccine will stimulate all arms of the immune system and prime it to rapidly eliminate an invading pathogen, it can only work if the organism causing disease can be consistently identified by the body.  For instance, the West Nile Virus is a very stable, unchanging organism that looks exactly the same to the horse in Massachusetts and the horse in California.  Influenza, on the other hand, is a viral organism that is constantly changing its appearance.  In exactly the same way our human flu produces new strains all the time, equine influenza undergoes small changes in its viral structure that allow it to evade the defenses of horses vaccinated with products produced using older strains of the virus.  So in the case of equine influenza, not only are we dealing with a viral disease, which challenges both the antibody and cell mediated arms of the horse's immune system, but we also are dealing with a disease that frequently alters its appearance, thereby posing one of the greatest challenges to researchers whose goal is to develop highly effective vaccines.

The subject of vaccines, the immune system, and disease prevention is extremely complex.  Luckily, those diseases which our horses may contract which are most deadly, are also the diseases against which it is possible to develop excellent, safe, and effective vaccines.  The prime examples of these are Tetanus and West Nile Virus.  Therefore, these are diseases against which ALL horses should be vaccinated.

The decision whether or not to vaccinate against influenza, rhinopneumonitis, and Strangles, should be made based on your individual horses risk of disease, and the impact that disease is likely to have on your horse's performance and well-being.  Refer to this past Saturday's blog to review the information that will help you make this decision, and then consult with your veterinarian as well.

Tuesday, February 16, 2010

Tuesday, 2/16/10 - Veterinary Tale Chapter 3 - A Man of Few Words

Sorry for no post yesterday - internet and telephone service to my valley were out for 48 hours. A transformer burned out and a new one had to be shipped in from who knows where before service could be restored.  That's the bad news - the good news is today's post is the latest chapter in Veterinary Tales.  I hope you enjoy it.   In case you missed the first two Veterinary Tales, you can find them in the blog archives from January 31st, and February 4th.  More on vaccinations and the immune system on tomorrow's Vet Tip of the Day.

Veterinary Tale Chapter 3 - A Man of Few Words
I excel in emergency situations. Throughout my life I’ve espoused the theory that there are basically two types of people. The ones who step forward toward crisis, and the ones who step back. Years ago a horse trailer pulled up in front of the large animal clinic at the University of Georgia where I was the resident on duty accepting emergencies. The driver jumped out of the truck, shouting over her shoulder as she rushed to the back of the trailer.

“It’s a really bad colic, and I think he just went down,” she said as she opened the door of the stock trailer before I could stop her.

I was standing about 6 feet away and what I saw was this woman standing there holding the door with her right hand, facing the open trailer. In the trailer, inches away from her face, was a horse in the process of throwing itself over backwards, its head and flying front feet coming directly at the woman. Without hesitation I jumped forward, shoving the gal to the side with my right arm while reaching up with my left arm and grabbing the horse’s lead rope. The rope was sailing through the air just ahead of the horse’s nose, following the trajectory caused when it snapped loose from the tie ring at the front of the trailer. As the horse’s owner went stumbling off to the right, I yanked the lead rope as hard as I could to the left, lunging in the same direction. The horse came tumbling out the back of the trailer, all 4 feet flying in the air, and hit the pavement left shoulder first. The owner was unhurt, the horse scrambled to his feet, and without pausing I headed into the clinic leading the horse to get emergency treatment started. James Bond eat your heart out.

This is the kind of thing I’m really good at – acting during a crisis. But the mass I’d discovered in my dog Sticky’s mouth was another matter all together. This was something I had time to think about, worry about, plan about – something that wasn’t going to be over and done within a short time, something that wasn’t going to go away. So I acted accordingly: I ignored it, just blocked it out, and when I did think about it, tried to convince myself that the mass was scar tissue that had formed at a tooth extraction site. I knew it had not been present 4 months ago, because Sticky had had her teeth cleaned by Dr. Mark Altman, my local small animal veterinary buddy, and a tooth had been extracted at that time. My denial continued for 5 days, and then I realized I had to face the music.

Here’s the thing. I’m a veterinarian, and while I don’t treat small animals, I am board certified by the American College of Veterinary Internal Medicine, and I’ve been practicing medicine for 22 years. I’ve seen my fair share of neoplasia (cancer) in large animal species, and I knew that the horrible thing growing in my dog’s mouth was not benign. On day 6, when Fern arrived at the office in preparation for the day’s calls, I asked for her help.

“Hey, Fern, I think we need to biopsy this thing in Sticky’s mouth,” I said, sounding all unconcerned.

“I was wondering what you were doing about it. I didn’t want to say anything, but it looks pretty bad, don’t you think?” Fern asked. Bless her heart; Fern is the soul of discretion. She’d come to work for 5 days without mentioning Sticky’s condition, even though I knew she’d been as upset by the discovery as I had. All nineteen year olds should have a fraction of her maturity and compassion.

Fern’s been one of my assistants since she was fifteen. She’s never wanted to be anything but a veterinarian, and I’ve been taking care of her horses since I met her family when Fern was eight. She announced she was ready to begin working for me when she was ten, and her mother and I struggled to dissuade her, pledging that if she was patient, she could start working at fifteen. Her intention never wavered, and for the past four years she’d been with me every summer and on weekends during the school year. We knew each other well, and worked in easy companionship most of the time. After all, I taught Fern early on my number one rule for employees: whatever goes wrong, it’s their fault. Once they get this down, the road smoothes right out.

I looked at Fern and nodded, “My small animal medicine is pretty rusty, but I do remember that oral tumors in dogs tend to be aggressive and malignant. But before we make assumptions, we need to submit a biopsy to be sure. They did pull a tooth right where the mass arises, so we cannot rule out that it is a mass of granulation tissue and not neoplastic.”

Fern gently held Sticky’s lip back while I took a scalpel blade and sliced off a small piece of the mass. My little PCD sat quietly, staring at me with absolute trust, without sedation or local anesthesia, as I performed the biopsy. She was just that kind of dog – she never made a big deal about anything. I knew the tumor would not have a nerve supply, so there would be no pain associated with the small biopsy, but most dogs would object to the restraint, especially around the mouth. But not Sticky, she didn’t move a muscle, just let Fern hold her lip back and wagged her tail slowly.

The biopsy safely stored in a submission jar filled with formalin, Sticky licked her bloody lips and jumped into the truck, ready to start the day. Fern and I looked at each other, hesitated a moment and then both burst out laughing.

“Sticky says, ‘come on you guys, let’s get going!’ “Fern said, her eyes shining with tears even as she smiled. “They just aren’t like us humans are they? No worries, just another day to live and enjoy. I don’t know, Dr. C, sometimes I’m just overwhelmed by how brave animals are.”

I climbed in and started the truck, motioning to Fern to join me. “I know, Fern, they teach us every day how to be better than ourselves, if we would just pay attention.” Sticky put her head in my lap, assuming her travel position. “Hand me a towel, will you – I’m going to have Sticky blood all over my pants for the rest of the day.”

“Here you go, Dr. C,” Fern said, handing me a blue surgical towel for my lap. “Maybe we should stop at the Frosty on the way to Roger & Barb’s and get her a soft cone – I bet that would feel good.”

“Good idea,” I agreed, “Today, whatever Sticky wants, Sticky gets.”

By the time we arrived at Roger Carlson’s cutting horse barn Sticky had lapped up her ice cream cone and was observing the world with her usual aura of ancient wisdom. Fern and I greeted Roger’s wife Barb and began preparations for the day’s procedure: castration of a two year old stallion.

Roger and Barb Carlson have been training cutting horses for over 30 years, almost as long as they’ve been married. They were high school sweet hearts, Barb the daughter of a local ranching family and Roger a Paiute Native American. They managed a training barn just over the California line, about 20 miles west of my office, in Sierra Valley. This was a picturesque area, located right at the transition elevation where desert and sage merged into aspen and pine stands peppering the steep Sierra Nevada foothills. I loved coming into this valley and had been excited about gaining the Carlson barn as an account. I inherited the work about a year previously from my friend Mark Altman when his small animal practice became so busy he no longer could provide adequate coverage to this area.

Mark was a real cowboy, a man’s man, a Deacon in the Church of the Latter Day Saints and one hell of an equine veterinarian. Guys like Roger Carlson and guys like Mark were born speaking the same language. When I first began working for the Carlson’s Roger’s wife Barb did all the talking, while Roger just watched me. I don’t think he said more than three consecutive words over the first year I came regularly to the barn. When he did finally begin talking to me, his dry humor and rare warm smile bowled me over. Roger had rich red skin, deep set dark eyes and a face etched by years riding outdoors in the high desert.

Today we were gelding one of his best young prospects. Roger brought the colt out into the center of the indoor arena and held him while I administered the first of two injections used for short term equine anesthesia. When my left hand closed around the colt’s neck to occlude the jugular vein I could feel his heart hammering through the skin against my thumb. I glanced at his eye to catch him glaring at me, his left ear cocked back and his expression saying loud and clear, “One wrong move and you are breakfast”. If only Sticky could talk to these young stallions and pass along some of her peaceful karma.

The first sedative successfully injected without incident, the colt began to relax, his head dropped, his lower lip drooped and he became wobbly. Ralph spoke to know one in particular,

“I guess this is the nicest colt I’ve ever raised.”


“He certainly is a beauty, Roger,” I agreed. “Look at that hip, and the shoulder isn’t half bad either.” I added, thinking to myself – just lie down quietly and stay down until I’m done, you little monster.

Just as I pushed the plunger on the second syringe containing the ketamine that would cause the colt to drop, Ralph spoke again,

“You know when Dr. Mark used to do my colts he was done in no time at all.”


“He’s quite a guy, that Dr. Mark” I mumbled, planning to wring his neck the next time I saw him.

“Why don’t you let me hold him while he goes down, Roger, “ I said, taking the lead rope into my left hand just as the youngster sank quietly to the ground with a deep groan. “How’s that for a smooth induction, oh Marvelous Mark?” I mentally complimented myself.

Fern moved in to tie up one hind leg, cover the colt’s eyes with a towel and scrub the scrotum while I gloved up and opened the emasculator and scalpel blade. I removed the first testicle and looked up to see where Sticky was. Don’t be too disgusted, but Sticky always knows when we are gelding a colt, and she is always sitting intently by the horse’s flank, waiting for her special treats. Soft ice cream cones are great, but they don’t compare to this. I spot her watchful eye and prepare to toss her the prize.

“Hold on there, doc!” Roger’s voice is actually raised a few notches, a new experience for me.

“I’m sorry Roger, I usually give these things to Sticky as a treat, but if you don’t want me too, that’s fine.”

“ I don’t care what happens to the damn things, but you move that dog up here by the colt’s head and throw ‘em forward to her – don’t you know that if you toss them over his head he’ll never look back?”

“Um, OK, no problem, come here Sticky,” I called, cursing Mark for not giving me a head’s up on this old western horseman’s tradition I’d certainly never heard before.

Sticky finished her hors d’oeuvres with relish, the colt recovered uneventfully from anesthesia, and Fern cleaned up and packed the truck while I stood with the now young gelding and Roger. More silence, but I figured I was better off saying nothing than trying to make conversation and sounding like an idiot. As I saw Fern finishing, I checked the colt’s incisions for bleeding and turned to Roger.

“Everything looks good Roger; he can go back to his stall now.”

Roger led the colt from the arena without a word and put him in his stall. I wrote up the bill and went out front to the travel trailer that served as an office to give it to Barb. We chatted as she wrote out the check and said thanks and good bye. I went out to the truck to leave. As I was pulling away from the barn Roger walked out. He spoke just loudly enough for me to hear.

“I guess Dr. Mark was right when he said you were OK.”

After a year, I was still thankful for small mercies.

Saturday, February 13, 2010

Sat. Feb 13, 2010: Vaccination Protocols

Vet tip of the Day: Selecting Appropriate Vaccines
Key Words: West Nile, Tetanus, Influenza, Rhinopeumonitis, Encephalitis, Rabies, Strep Equi

Diseases are like brush fires.  Some smolder for awhile and are easily extinguished, others flare up and have devastating effects.  Choosing vaccinations for your horse has a lot to do with the nature of each disease we are attempting to prevent.  Toward this goal, here are the answers to yesterday's questions.  

Note: The answers about likelihood of exposure are only pertinent to horses in Northern Nevada.  Consult your veterinarian for other geographic regions.

1.     How likely is it that this horse will be exposed to Disease A?
  • West Nile:  Likely
  • Tetanus: Unlikely
  • Influenza: Very Likely
  • Rhinopnuemonitis: Very Likely
  • Encephalitis: Very Unlikely
  • Rabies: Very Unlikely
  • Strangles: Likely
2.     Is Disease A a deadly disease, such as Tetanus? (this assesses risk to this horse)

  • West Nile: Yes, 40% mortality
  • Tetanus: Yes, 80+& mortality
  • Influenza: No
  • Rhinopneumonitis: No, but high risk abortion in pregnant mares
  • Encephalitis: Yes, 85+% mortality
  • Rabies: Yes, uniformly fatal
  • Stangles: No, 10% complication rate, with fatality uncommon
3.     Is Disease A highly contagious, such as Influenza? (this assesses risk to neighboring horses)

  • West Nile: No, is not transmitted horse to horse. Disease is transmitted from infected bird, to mosquito, to horse
  • Tetanus: No, is not transmitted horse to horse. Tetanus bacteria lives in soil and usually gains access to horse through deep puncture wound that creates an oxygen free environment where bacteria can proliferate.
  • Influenza: Yes! Transmitted directly horse to horse by aerosole (cough) and direct contact.
  • Rhinopneumonitis: Yes! As for influenza.
  • Encephalitis: Moderately, disease is not transmitted directly horse to horse, but is carried from horse to horse by a "vector", which for this disease is the mosquito.
  • Rabies: No, is not transmitted horse to horse
  • Stangles: Yes! Primarily transmitted by direct contact horse to horse AND by contact with contaminated "fomites": halters, lead ropes, hands, feet, water buckets, etc.
4.     Is the vaccine used to protect against Disease A highly effective?

  • West Nile: Yes, Intervet DNA vaccine extremely safe and effective with minimal side effects
  • Tetanus: Yes, killed vaccine 95+% safe and effective
  • Influenza: Vaccines against influenza currently available are moderately effective, with relatively short lasting immunity provided. 
  • Rhinopneumonitis/Equine Herpes type I and IV: There are 2 main Equine herpes viruses that cause upper respiratory disease in horses. They are also responsible for abortion and a neurologic disease which can be fatal.  Currently available vaccines are very effective in preventing abortion, moderately effective in preventing upper respiratory disease, and of questionable efficacy against the neurologic form of herpes virus.  More discussion on this in a later vet tip post.
  • Encephalitis: Yes, killed vaccine very safe and effective
  • Rabies: Yes, killed vaccine very safe and effective
  • Stangles: The intranasal vaccine against Strep equi bacteria is moderately effective, and of all the vaccines discussed here has the highest complication rate.  We will discuss Strangles in more depth in a later vet tip post.

5.     What is the cost vs. effectiveness vs. safety value of the vaccine for Disease A?

  • West Nile: Excellent
  • Tetanus: Excellent
  • Influenza: Moderate
  • Rhinopneumonitis: Moderate, except very good against Equine Herpes induced abortion
  • Encephalitis: Very Good
  • Rabies: Excellent
  • Stangles: Fair

 With this information, consider the following:
Your horse's age: the young and the old are always more susceptible to disease
Your horse's lifestyle: travel, stress of competition, and exposure to other horses always increase the risk of disease

Now decide which vaccines you think are appropriate for your horse.

More on Monday.  Have a wonderful weekend.


Friday, February 12, 2010

Friday, Feb 12, 2010 - Vaccination

Vet Tip of the Day: Vaccination
Key Words/Phrases: Immunity, West Nile Virus, Influenza, Encephalitis, Veterinary Consultation

It is mid-February, almost time to begin gearing up for spring, which means administration of spring vaccinations.  For the next few vet tips, I would like to discuss some of the theory behind the practice of vaccination, in order to give you the tools to make informed decisions about appropriate vaccination strategies for your particular horses.  Rule #1: never be afraid to ask your veterinarian the basis for choosing your horse's vaccination program.  You deserve this attention.  However, I am as guilty as anyone else in this regard - the words "hectic" and "springtime" are virtually synonymous for equine practicioners.  We are usually scrambling to keep our heads above water during the months of March, April and May, from gelding colts, to getting mares in foal, to welcoming new babies into the world, to preparing performance horses for upcoming show seasons our days (and nights!) are already full, so we tend to be on the go when it comes time to administer routine vaccinations.

You may want to try this strategy: avoid trying to slow your veterinarian down to talk in the spring when they are most likely to be distracted.  Instead, talk to your veterinarian about routine health strategies such as vaccination during the quiet winter months.  Schedule a consultation appointment and let your vet know the topics you would like to discuss ahead of time.  This approach allows your veterinarian to sit down and focus on your questions in a relaxed fashion that will lead to a more thorough, rewarding information exchange.

To begin our discussion of vaccination strategies, let's determine how we decide whether a horse should receive a certain vaccine.  Consider vaccinating a horse against Disease A.  I ask myself the following questions:
1.     How likely is it that this horse will be exposed to Disease A?
2.     Is Disease A a deadly disease, such as Tetanus? (this assesses risk to this horse)
3.     Is Disease A highly contagious, such as Influenza? (this assesses risk to neighboring horses)
4.     Is the vaccine used to protect against Disease A highly effective?
5.     What is the cost vs. effectiveness vs. safety value of the vaccine for Disease A?

With these questions answered, I then can make an informed decision whether or not to recommend vaccinating this horse against Disease A.

The diseases against which we routinely vaccinate horses in the Western United States are listed below.  Test your own knowledge and try to answer the questions above for each of them - I will post the answers in tomorrow's Vet Tip of the Day.

West Nile Virus
Influenza, Rhinopneumonitis
Eastern & Western Encephalitis
Strep Equi (Strangles)

Our new and improved website if coming on line.  It is like a fledgling chick pecking its way out of the egg - if you want to watch it emerge, then keep checking in over the next week or so.  If you'd rather just see the final product, wait a couple of weeks and then look.  Either way, you can now get to this blog through the website - it's an easier address to remember and the link to the blog is on the home page.  Just log on to

There is quite a bit of information on the website as well for your education. 

Finally, for my local clients, the spring vaccination clinic schedule will be posted by Monday, February 15th.


Wednesday, February 10, 2010

Wednesday, Feb 10, 2010 Face Lacerations

Vet Tip of the Day: Facial Lacerations
Key Words/Phrases: Wound healing, primary closure, golden period

We've been hammering limb anatomy and lameness for over a week, so I think it's time to take a break and look at something entirely different. Facial lacerations are a relaxing break out topic because while they often start with a horrified horse owner and a gaping wound such as this one, they are simple to treat and usually end with an excellent outcome.

The tissues of the face have a tremendous blood supply, and because blood is what carries all the magical factors necessary for wound healing to the site of injury, lacerations on the face have a healing advantage not present in other areas of the body.

The first six hours after a skin laceration occurs is called the "golden period" in wound healing.   In general, sutures placed in a wound more than 6 hours after its occurrence are likely to fail, no matter how carefully the wound is prepared and how correctly the sutures are placed.  With every minute that passes after a laceration is sustained, exposure to external factors increases the risk of infection while at the same time the lack of blood supply to exposed tissues decreases the chance that tissue will remain alive and reattach when sutured.  The one anatomical exception to the "golden period" rule applies to facial lacerations, where wounds often heal uneventfully when sutured 24 hours or more after they occur.  Even large wounds filled with debris that involve skin flaps with wide areas of exposed underlying bone usually heal well, due to the excellent blood supply to tissues of the face.

The horse pictured here sustained a high impact injury involving a rigid metal object. Following sedation with 10 mg of intravenous detomidine, and subcutaneous placement of a local anesthetic around the wound margins, this horse's wound was carefully cleaned with dilute betadine, then flushed copiously with sterile saline.   Skin staples were used to hold the skin flap back in position.  The staples were removed 14 days later and as you can see, the wound healed without any skin loss.  Even if you find a severe face laceration that is over 12 hours old (the thunderstorm during the night is a classic for this), don't despair - primary closure may still be possible and successful.

Horses that sustain lacerations to the face and have concurrent nose bleeds should always receive antibiotics.  The presence of bleeding at the nose indicates that the concussive force may have been severe enough to cause bleeding into one of the sinuses that underlie much of the space beneath your horse's forehead and nose.  Because the sinus cavities communicate with the nasal passages, bacteria in the nasal passages can gain access to the sinus.  If there are broken blood vessels in the sinus, bacterial infection (sinusitis) can set up housekeeping in the sinus cavity.  Treating a well established bacterial sinusitis is difficult, and the need to do so can be avoided by initiating antibiotic treatment at the time of facial trauma.  So don't forget - face lacerations accompanied by nose bleeds should be seen by your veterinarian, even if the laceration itself is not severe.

I'm late writing the Veterinary Tale for this week, so it may not get posted tomorrow, but I'll do my best to get it to you soon.  The practice website is being updated this week.  I really like the new look and will let you know as soon as it is on line so you can check it out and give us your opinion.

The sun was out today in Reno - halleluiah! We used to take it for granted, but after this winter, no longer.


Tuesday, February 9, 2010

February 9, 2010 - Injectable Joint Therapies

Vet Tip of the Day: Injectable Joint Therapies
Key Words: Adequan, Legend, PSGAG, Hyaluronic Acid

To finish our segment on the hock, here is a brief discussion of the two FDA licensed injectable agents to improve joint health.  The first, Adequan, is used more commonly for osteoarthritis of the hock (bone spavin).  Adequan is a large molecule with the chemical name polysulfated glycosaminoglycan (PSGAG) which cannot be absorbed when given orally and so is administered by intramuscular injection.  Adequan has been shown repeatedly in controlled clinical trials to improve lameness associated with chronic degenerative joint disease, however, on an individual animal basis, it's effectiveness is quite variable.   Its mechanism of action is similar to chondroitin and glucosamine.  Remember that these oral supplements are building blocks used by the body in the construction of cartilage.  Adequan is a very large molecule, more complex than either chondroitin or glucosamine, and is further along the construction pathway in the formation of cartilage matrix.  The PSGAG molecule is incorporated into cartilage, giving it elasticity and shock abosorbing capacity.

I use the brand name Adequan, although there are generic PSGAG products available, as well as compounded products.  However, as with oral supplements, the molecular construction of the generics and compounded products are not necessarily equivalent to Adequan, and have not stood the test of clinical or experimental study.  In fact, Luitpold Pharmaceuticals, the manufacturer of Adequan, has spent quite a bit of money conducting quality research on their product, and in the comparison studies performed to date, Adequan has outperformed generics.  Once again, you get what you pay for.

Legend is injectable hyaluronic acid (HA).  And yes, just like PSGAG,  hyaluronic acid comes in many molecular weights and qualities, and so far, for intravenous administration, Legend is the gold standard.  While Adequan is used most commonly for hock arthritis, it is not uncommon to combine Adequan and Legend as joint therapies.  In the joint environment, hyaluronic acid and PSGAG have complex actions.  In addition to acting as structural components of joint fluid and cartilage, both HA and PSGAG have anti-inflammatory effects within the joint.  On top of that, when used together, each component enhances the activity of the other, so 1+1=3!  Therefore, in performance horses with joint issues, it may be advisable to use combination therapy. 

There is a standard protocol for initiation of Adquan therapy, established by the manufacturer.  The recommendation is to give 1 vial every 4 days for 28 days followed by one vial every 2-4 weeks thereafter. Legend is often given once monthly intravenously as maintenance therapy, with additional doses given around the time of competition.

Oral and injectable chondroprotectant agents are widely used in treating osteoarthritis of the hocks.  They often are used in conjunction with intra-articular (directly into the joint space) injections of similar products in combination with corticosteroids, as well as oral adminstration of non-steroidal anti-inflammatories such as phenylbutazone.  Finally, a topical anti-inflammatory cream is now available which provides local, temporary pain relief and can be effective to control hock pain during exercise.  This product is Surpass, or diclofenac acid.

We've covered a lot of information on the hock.  If you are interested in learning more,  use the key words provided as Search words in Google and you will find LOTS more to read.

Have a great day,

Monday, February 8, 2010

Monday, Feb 8 2010 - Winding up the Hock

Vet Tip of the Day: Oral Joint Supplements
Key words: chondroprotectant, synovial fluid, cartilage, joint capsule

Osteoarthritis is only one of many conditions that affect the hock; in the future we will come back and discuss other disease processes that affect tarsal joints.  But to conclude this introduction to hock anatomy and bone spavin, the most common cause of hock lameness, there will be two final Vet Tips of the Day: today we will look at oral joint supplements, how they work, and IF they work.  Tomorrow we will consider injectables.

It is important to distinguish between oral and injectable agents administered as chondroprotectants.  "Chondro" refers to cartilage, "protectant" is self-explanatory.  Chondroprotectant joint supplements are substances which claim to enhance the health of joints by improving the the quality of joint fluid and joint cartilage.  Cartilage is the spongey substance which lines the surface of bones within joints.  The cartilage is bathed in synovial fluid, or joint fluid, which is contained within the joint space by the joint capsule.  The joint capsule is lined by synovium, the site of joint fluid production.  In the simplest terms, the joint fluid and cartilage act as shock absorbers to diminish the force transmitted to bones when joints are compressed by weight bearing.

You've almost certainly heard of glucosamine and chondroitin.  These are two of the most common ingredients in oral chondroprotective joint supplements.  These substances are two of the primary building blocks the body uses in the construction of cartilage.  Theoretically, by increasing the amount and quality of glucosamine and chondroitin in the diet, the body is better able to produce and maintain healthy cartilage.  There are three major problems with this theory.  First, there are many structural varieties of glucosamine and chondroitin, and their absorption across the gut wall is widely variable.  Second, and perhaps more importantly, there are few government regulations regarding the manufacture of oral joint supplements, which are considered "neutraceuticals".  Therefore, the amount and quality of ingredients listed on the label vary widely from product to product, and there is not even any guarantee that the label claims of a given product are true.  Therefore, when buying an oral joint supplement, you are completely at the mercy of the manufacturer's ethics regarding the actual contents of the product.

Finally, the third problem is, assuming the product you buy is excellent quality and your horse absorbs the ingredients, there is very limited research availabe indicating what an appropriate dosage is for a given combination of chondroprotective ingredients.  In addition to glucosamine and chondroitin, additional additives found in many joint supplements include cetyl myristoleate (an anti-inflammatory) , hyaluronic acid (a major components of joint fluid), as well as various herbal extracts such as devil's claw, boswellia and avocado extract, just to name a few.

Before you throw in the towel, be comforted in knowing that, while limited, there are a few well designed clinical studies indicating that the oral administration of chondroprotective agents can improve lameness in horses with chronic osteoarthritis.  The bottom line is, at this time there is more unknown than known about these products, so if you choose to give one to your horse, buy a recognized brand manufactured by a company with a longstanding reputation.  Be sure the product is clearly labelled with respect to ingredients, amounts of ingredients, and recommended dosage.  It should be easy to calculate the actual amount of each ingredient you will be giving your horse by reading the label.  The product should have a lot number and expiration date easily identifiable, and there should be clearly printed information telling you how to contact the manufacturer.  Finally, if the product claims to cure everything from laminitis to navicular disease to hock pain in 30 days, don't buy it.  Remember, you get what you pay for, and if it sounds too good to be true, it probably is.

Sunday, February 7, 2010

Fri & Sat Feb 4,5. More on the hock

Vet tip of Two Days!
Key words: osteoarthritis, hock,chondoprotective, joint therapy, glucosamine, chondroitin

My apologies for this late vet tip. It's actually Sunday morning, but it is snowing again and I've get an hour before I go out to do a couple of calls this morning. One of them is to inject the carpus of an older rope horse with chronic osteoarthritis. Do you remember how many joints there are in the carpus and which joint on your body is similar anatomically to this equine joint? (for review see last Wednesday's blog).

Osteoarthritis of the lower hock joints (bone spavin) is the most common cause of chronic lameness that I see in my practice, with forelimb heel pain a close second. Bone spavin occurs in every type of athletic horse, and unfortunately it is not uncommon to see horses develop sore hocks at a relatively early age. The 3 or 4 year old cutting horse is the extreme example, but jumpers, dressage horses, foxhunters, endurance horses, and other western sport horses may have degenerative changes in their hocks before 10 years of age.

Why are these joints predisposed to arthritis more than other joints of the body? Probably because of their unique position of high stress and low motion. Watch your horse's hocks closely as he trots on the longe line. Most of the flexion that occurs is due to motion of the large tibiotarsal joint, which has a large joint space and round, ball bearing like sliding surface where the tibia sits on the knuckle shaped talus. This joint is an uncommon site for osteoarthritis secondary to athletic activity.

Now look at the radiograph from Thursday's blog (the normal hock), then look at this radiograph which demonstrates osteoarthritis in the distal intertarsal and tarsometarsal joints. These are the joints at the bottom of the hock that are complex and relatively rigid in construction. The joint space is the thin black line between the rows of tarsal bones. Imagine the force that flows through these joints when your jumper throws his thousand plus pound body into the air to clear an obstacle or your barrel horse digs in to accelerate out of the turn around the last barrel or your dressage horse sucks it up to sit back on his hocks and put that tremendous effort into a canter pirouette. There isn't much room for error in these joints, because there is very little room for movement, so over time, the stress of high force through tightly packed bone results in chronic inflammation.

Joint fluid lubricates and cushions the cartilage that lines bone surfaces. The inflammatory process causes this fluid to becomes thin and less able to absorb repeated impact. The cartilage, in turn, looses its flexibility and ultimately the bone is left to take up too much of the load of activity. It's response is to say "Hey, I'm working too hard, maybe if there is more of me this job will be easier." Unfortunately, the production of extra bone simply destroys the smooth architecture of the carefully constructed joint anatomy with the end result: pain.

That's how the process starts, now how do we treat it?

Many of the key words for this vet tip are related to the huge topic of joint therapies. Tomorrow's vet tip will be devoted to the subject of oral and intra-articular therapies, and trying to separate fact from fiction. To close today's entry, here is the bottom line: there is sound, repeatable scientific evidence that certain oral and injectable chondroprotective agents can help to alleviate the inflammation, and therefore the pain, associated with osteoarthritis of the hock. The efficacy of these products is variable, and the products themselves are variable. We will look at them in more detail tomorrow.

I hope you are enjoying these vet tips - we are in the process of updating the practice website - the blog name is probably going to change (high brow internet search engine stuff that is GREEK TO ME). I promise to keep everyone up to date as the High Desert Veterinarian continues to explore cyberspace in order to share the knowledge and wonderful life of a practicing veterinarian with you all.

Thursday, February 4, 2010

Thursday, Feb 4 - The Hock and a Veterinary Tale

Vet Tip of the Day:  The Hock
Key Words: Equine tarsus, horse hock anatomy, bone spavine, degenerative joint disease

Today we will look at the hock, which is the hind limb joint that sits above the cannon/splint bones.  It corresponds anatomically to your heel.  There are 4 joints in the hock (identify them on the radiograph).  From top to bottom they are the tibotarsal joint, the proximal and distal intertarsal joints, and the tarsometatarsal joints.

The two distal intertarsal and tarsometatarsal joints are low motion joints that are very common sites for arthritic changes (degenerative joint disease or bone spavin) in all athletic horses.  This is a very common, and very treatable condition. Most horses with bone spavin continue in full work with maintenance veterinary care in the form of intra-articular injections with corticosteroids and hyaluronic acid in conjunction with a regimen of oral or injectable chondoprotectant agents such as Adequan, Legend, or oral chondroitin sulfate/glucosamine products.

The hock is a complex joint and is the site for many different problems that can cause lameness.  We will spend a few days looking at it in more depth, but since today is a Veterinary Tale day, this is the end of this Vet Tip - here's the story - hope you enjoy it.

Chapter 2 Good News Bad News

Thursday was a good news/bad news day. In the truck, my cell phone in its normal position, wedged between my head and left shoulder, in what I consider my personal “hands free” mode, I’m speeding of course, steering with my left hand while rubbing my dog Sticky behind her ears with my right hand. Sticky is in her favorite spot, curled up beside me with her shoulder pushing into my right hip and her head in my lap. This pretty much describes how I spend the majority of my life – motoring from one appointment to the next, multi-tasking on the phone, and rubbing my dog’s ears because I don’t have time to meditate. One of my two veterinary hopeful college student assistants completes our travelling circus, doing her best to keep me on track as I zoom around trying to protect the well-being of the equine population of northern Washoe County. On this particular day I was on the phone with a third year medicine resident from UC Davis who was telling me that Brandy was on her way home, fully recovered after her experience dancing with a T-post. Good news.

Sticky has been my constant companion for the past 8 years – she is much cuter than me, with better manners and a distinctly more endearing personality. She’d been in the truck when I treated Brandy, but she knew better than to get into the middle of that mess, and slept through the drama on the front seat. My clients, without exception, adore Sticky, and there is an ongoing debate among them whether or not she is part coyote. The physical resemblance is remarkable, but her disposition is so quiet, consistent and loving that it is hard to imagine she is related to those conniving rascals that lure puppies out into the desert and rip them to shreds. I tell everyone Sticky is a PCD, or Prostitute Companion Dog, descended from the gentle dogs that were friends to the girls in Julia Bouillet’s Bordello in Virginia City at the turn of the century. Some folks find this confusing, but it works for me.

I met sticky 8 years ago while responding to a call from a new client. Tanya Buckman was a cowgirl with a lame foal. Tanya was about 40 years old, 5’7”, with hair so blond, teeth so white, breasts so perky and jeans so tight if I wasn’t in Nevada I wouldn’t have believed it possible. When I first moved west these women were a real challenge to me, and I still look at them with some puzzlement and more than a little envy. They all are so beautiful, and so NICE, and SO TOUGH, they belong in movies. Every one of them wears their womanhood like a ship’s flag: the big belt buckles, the white cowgirl hats, the long stride and the high heeled Ropers. How they get their Levi’s to bunch up just so over the tops of their boots is beyond me. I’m a Yankee, I grew up in New England, I wear a string of pearls every day and my idea of risque is leaving the top button on my polo shirt open.

I’m going to digress for a minute here, but just to give you an example of what these gals are like, here’s what happened when I volunteered to draw blood for pseudorabies testing from a 4-H project pig belonging to one of my cowgirl client’s daughters. When I arrived the pig was loose in a large pen and since my generosity stopped short of chasing it around like a lunatic I asked the daughter to catch Charlotte for me. I watched her futile attempts to contain the pig until my head was about to explode then announced my impending departure if the pig wasn’t under control within 5 minutes. The daughter pulled out her cell phone and made a quick call.

The next thing I know, a bright red 1 ton Dodge diesel pickup comes screaming down the driveway from the house to the barn where we waited with the pig. The truck stops in a cloud of dust, the driver’s door flies open and Raquel Welsh in skin tight Levi’s gets out, struts over the to the pig enclosure, climbs the fence, grabs the pig by a back leg so fast I never saw her move, and hollers over her shoulder at me, “Hurry up and bleed this damn thing, I’ve got to get my nails done at three o’clock.” That was my client, the cowgirl mom, and I guarantee you that when she sashayed away from that pig pen she smelled just as fresh as a daisy.

Tanya Buckman was one of these Nevadan women, and like so many of them she was a savvy hand with horses. She had a buckskin quarter horse mare which had foaled 2 weeks previously. Everything was fine, until yesterday when the filly’s leg became swollen and it began to have trouble walking. Tanya easily cornered the wary 100 pound youngster and held her while I began my examination, questioning her as I did.

“ Has the mare ever foaled before, Tanya?” I asked as I took the foal’s temperature.

“No, this is her first, and she was real nervous about letting it suckle for the first couple of days,” she replied. “Does she have a fever?”

“Her temp’s 102.5, which is a little higher than I’d like to see. Maybe she didn’t get enough colostrum when she was born.”

Colostrum is the special milk that mares only produce for a few days after the birth of a foal. Horses are born with what is called a “na├»ve” immune system. They have no antibodies to protect them against infection, and must drink enough antibody rich colostrums within the first 24 hours of life or they are at high risk of developing serious infections. One of the most common ways for such infection to manifest is as a septic joint, which causes severe lameness and can be life threatening if the infection invades the bone or spreads to other organ systems.

After palpating the fluid in the foal’s fetlock joint and asking a few more questions, I was certain that the most likely cause of the lameness and fever was a bacterial infection in the joint that needed immediate attention. Tanya was clear that she wanted the foal treated there on the farm, so we began preparations to flush the joint. Needles are inserted in 2 locations, one to allow delivery of sterile fluid that lavages the joint space, the second to provide an exit route for the infected joint fluid and bacteria. This procedure is ideally performed under sterile, or aseptic, conditions. This presents a challenge in a field setting. The trick is not to make matters worse by introducing more bacteria into the joint than already are present.

The best environment Tanya could offer was a 3 sided shed with manure rich shavings covering a dirt floor. On our side was the fact that there was very little wind. In general I love the climate in northern Nevada – we enjoy over 300 sunny days a year and while winter is winter, the sun and 5,000 foot elevation usually melt snow within a few days to weeks. The climate is very dry, so the summer heat, typically 85 to the rare 100+ degree days, is very tolerable. Our one weather detractor is the wind. We have it frequently, and when it blows it is not unusual to experience gusts in excess of 45 mph. But this was a clear, quiet days, so it was unlikely we’d have chunks of windswept manure and sand landing on our sterile field.

We laid down some fresh shavings and put a clean sheet on the ground. Fern held the foal in a classic “foal grip” with one hand grapsing the base of the tail, her other arm looped under the foals neck, holding the head snuck against her chest. I sedated the foal using 50 milligrams of intravenous xylazine. Within three minutes she was a wet noodle, and we laid her down on the sheet, Tanya sitting at her head and my assistant Fern holding the affected leg in elevation. After wrapping the hoof in clean gauze and performing a sterile prep of the leg from well above the joint to hoof, I donned sterile gloves and quickly inserted the needles into the joint on either side. We were half-way through the flush procedure using a 1 litre bag of lactated ringers solution when a coyote stuck it’s head around the corner of the shed and stared at us.

“Chloe, you git!” snarled Tanya.

“My God, Tanya, is that a coyote?” I asked, trying not to lose my concentration.

“Heck no, that’s Chloe, she came from the pound in San Diego. My husband says he’s gonna divorce me if I don’t get rid of her, we’ve got so many dogs. You want her? “

“No thanks. Hey, let’s pay attention here, this foal is going to wake up soon.”

The foal responded well to a series of three joint flushes and systemic antibiotics. Her x-rays showed no evidence of invasion of the infection into the bone, and a sample of joint fluid obtained after the third lavage procedure indicated that the infection was resolving. What didn’t resolve was Chloe’s fascination with veterinary medicine, and on our last visit to see the foal the little coyote dog hopped into my truck and made it very clear that she belonged there for better or worse. I changed her name to Sticky after a few weeks because she stuck to me like a little flea, and over the years she became as much a part of my practice as my stethoscope.

Eight years later, as I’m speeding along, speaking with the UC Davis resident about Brandy and rubbing Sticky’s ears, my fingers discover a lump under Sticky’s jaw. When we arrive at our next call I take a closer look at my little dog with the piercing topaz eyes. Not only can I palpate an enlarged lymph node at the base of her neck, when I examine her oral cavity I discover a dense mass of tissue covering the floor of her mouth between her lower canines.

“Oh shit, Fern, look at this - I think Sticky has cancer,” I say quietly.

Bad news.

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