All club members please remember if you are going to get your Dogue heart certified before breeding you can get a discount on the the procedure by stating when you make the appointment, which does not require a referral, that you are a DDB Club member, and on presentation of your membership card , at VSG in Auckland.
Veterinary Specialist Group
97 Carrington Road,
Mt Albert, Auckland
Phone 09 845 5455
the club highly recommends all breeding parents be certified to avoid breeding heart issues into the potential pups ...especially now breeders can be taken to court should there be a problem , better to lessen your chances of this happening ...plus it is such a small investment of around $300 to have done.
LATEST HIP / ELBOW SCORES FOR NZ
Here are the breeds latest Hip scores as at January 2010
Dogs tested Average Score
Nov 2008 67 18.1
Jan 2010 80 17.9
It is always advisable to stay under the breed score especially if you are new to breeding and to get a pup from a breeder who uses dogs under these scores to lessen your chance of getting a pup with Dysplasia ...we do not recommend you get a pup from any dogs that are unscored.
# Dogs Tested Accredited Dysplasia
Gd 1 Gd 2 Gd 3
Nov 2008 46 15 18 10 3
Jan 2010 56 19 22 12 3
Grading of elbows for elbow dysplasia is divided into five grades.
No evidence of elbow dysplasia. This is the optimum grade.
Subtle changes are seen on the elbow radio graphs which are suggestive of elbow dysplasia but are of insufficient severity to be conclusive. A Borderline grade is a good score.
Obvious osteophytes indicating arthrosis of the joint. In the high risks breeds this score currently represents a better than average score. In breeds with a low risk of osteochondrosis, a Grade 1 score is less than desirable.
As too many dogs have proved to fall into this category it was decided to split the grade into 1a and 1b. 1a is the more desirable grade.
More severe arthrosis is present. A grade 2 score is a poor score, and breeding with dogs with this grade is not recommended. This recommendation is especially true in low risk breeds. Breeding from grade 2 dogs can be justified only if the dog has other genetic traits that would be advantageous to the gene pool of that breed as a whole.
Severe arthrosis and we recommend that in no circumstances should these dogs be used for breeding.
Dogs that are scored either 0-0, 0-B or B-B in both elbows and are between 1-2 years of age at the time of radiography are eligible for a re-check when more than two years of age. Any dog with a score of 0-0, 0-B or B-B when older than two years old is given ACCREDITATION status (i.e. accredited free of elbow dysplasia by radiographic examination).
Thanks to the NZVA for making this information available.
*** Pennhip scoring is now the preferred choice when scoring as dogs can be done as young as 3 months of age. ****
Hip dysplasia (HD) is the most common heritable orthopaedic condition seen in veterinary practice, affecting virtually every breed. There is no effective cure for this condition, and treatment consists mainly of palliation.
Traditional methods for diagnosing HD have been associated with disappointing progress in reducing the incidence of the disease. Some of the schemes also had a voluntary submission policy, in other words xrays of really bad hips were never sent for scoring, which resulted in breed scores being better than they should have been.
The only practical means of eliminating or reducing the incidence of HD is through selective breeding, based on well-defined objective phenotypic (physical make up, such as xray appearance) criteria. In theory, these phenotypic criteria will identify those dogs that lack the genetic predisposition for HD, and therefore will be suitable for breeding.
Most traditional screening systems looked at a single view of the hips, with the hips fully extended. Since this method underestimates true hip laxity, it cannot effectively predict the dog’s susceptibility to HD later in life. In one study, 55% of dogs scored normal by a hip extended radiograph, went on to develop osteoarthritic hips later in life. It is likely that the prevalence of HD in a breed is 2-3 times higher that is actually started from traditional hip-extended scoring schemes.
Therefore, using the extended hip method for selecting breeding dogs will retain a high level of HD in the offspring.
There is also considerable variation in scores when using the hip extended views, both between examiners and from the same examiner.
Hip laxity (looseness) is a measurable objective component that can be used to predict an animal’s susceptibility to develop HD and the osteoarthritis (OA) of HD later in life. Hip laxity, combined with rapid growth and weight gain, increases the risk of OA in the hips.
PennHIP testing measures hip laxity.
PennHIP involves two radiographic views: a compression view with the femoral heads compressed deeply into acetabula (sockets), and distraction view obtained by levering a custom-designed device between the legs to maximally displace the femoral heads from the acetabula.
This is then read by a panel of experts in Pennsylvania to give a distraction index (DI), defined as a measure of how much the femoral head is distracted from the acetabulum when under stress. DI of 1.0 = full distraction. 0.5 = 50% distraction.
Distraction xray revealed 2.5 times more laxity than the hip extended xray, and is therefore much more sensitive at detecting laxity in hips, the prime phenotypic factor in predicting a dog’s susceptibility for developing OA of HD.
Lax hips on PennHIP more highly correlated with OA than lax hips on extended view.
Tight hips on PennHIP are extremely unlikely to develop OA.
Hips with DI < 0.29 are very unlikely to develop OA.
DI > 0.3 is termed hyperlaxity. These hips are at risk of OA, with an increasing risk as DI increases further. In one study 98% of Labrador Retrievers with DI > 30% developed OA later in life.
DI of 0.3 can be thought of as a biological threshold, separating normal disease-free hips from OA prone hips.
DI can be measured from 4 months of age, and is a good predictor of susceptibility to OA, but the strength of the prediction improves at 6 months and again at 1 year. As DI increases over 0.3, the risk of OA increases, but rate of OA risk increase is breed related. Some breeds such as the German Shepherd Dog, are much more likely to develop OA as their laxity increases beyond 0.3. Other breeds are much less likely.
Majority of dogs certified suitable for breeding by hip extended radiographic scheme were found under PennHIP to have hip laxities corresponding to OA susceptibility, showing the prevalence of hip dysplasia to be far higher than previously thought.
Heritability denotes the reliability of the phenotype in predicting the genotype. In other words, it indicates how reliable measuring a physical characteristic is (such as hip laxity) in predicting the genetic make up of that individual.
High heritability means all the variation in phenotype is explained by the genes, and no environmental component exists. So, if a factor was found to have a high heritability, its measurement would give a clear indication of the genetic make up, and there would be no influence from other factors such as diet.
The higher the heritability of a selected trait and the stricter the selection criteria chosen, the more rapid the genetic change per generation of breeding. So, a highly heritable trait, which then is very strictly chosen for when selecting dogs for breeding, will lead to a very rapid change in the breed.
However, given the extremely high incidence of hip laxity, if we were to select dogs for breeding which had very good scores only (<0.3) we would be left with a very small population of dogs to breed from. As an example, Golden Retrievers with distraction index less than 0.3 constitute less than 5% of the population. To avoid problems associated with inbreeding caused by breeding from such a small group, a more moderate approach has been taken.
In is therefore prudent to choose breeding stock from those in the breed who have a distraction index less than the median score for the breed. This then represents the “tightest half” of the breed.
This will then apply continuous selection pressure while maintaining genetic diversity. In time, the breed median will steadily change and the breed scores will improve.
More rapid genetic change could be achieved by applying stricter selection pressure, which individual breeders are more than welcome to do.
PennHIP does not evaluate dogs in a pass/fail manner, it just gives a measure of hip laxity that a breeder can use to make an informed choice about whether to breed from that individual dog. We will not advise whether the individual is suitable for breeding or not, since there are obviously many other factors taken into consideration when selecting a dog for breeding than its hip score alone.
It is the owner’s responsibility to decide whether to breed from individual dog or not.
As a guiding principle, tighter hips are better hips, and a good starting point would be to accept for breeding any dog with a DI less than the breed median for the preceding year. Breed medians are updated continuously.
All xrays taken are submitted for evaluation, even ones that are obviously dysplastic.
When taking PennHIP xrays, there is a risk of cavitation risk. This is due to bubbles of nitrogen gas forming in joint fluid as the joint is stretched, as happens when we crack our knuckles. Cavitation causes no harm, but can make scoring the hip laxity difficult or impossible. 4% of hips will have cavitation when distracted, which may increase joint laxity artificially. DI can be measured if only one hip cavitates, but cannot be done if both cavitate. This happens in less than 1% of cases. In such a case, the procedure would need to be repeated.
Phil Macleod and Paul Eason have both now been accredited to perform PennHIP testing. This means we can offer this effective means of testing the susceptibility of a dog developing OA from HD later in life, at both our Papakura and Pukekohe clinics.
Testing involves a full anaesthetic, and a day stay in the clinic. Results are normally available in a few weeks, since they have to be sent to the USA for reading.
HEALTH ISSUES EFFECTING THE BREED
HEALTH ISSUES EFFECTING THE BREED
Here are a few conditions, in brief , full details will follow below of each condition .
Gastric torsion -volvulus is also known as bloat or twisted stomach , it is an extremely serious condition and should always be considered a life threatening .Because the Dogue is a deep chested dog they are prone to this condition , so it is always wise to feed them split there daily meal into two ,as dogs fed once a day are more likely to get bloat , and to avoid exercise after eating for at least an hour with limited water intake. Some people fed there dogs using raised feeders to reduce the risk of bloat , but there is no scientific evidence to confirm it lessens a dogs risk.
Gastric Torsion Video
Hip / Elbow Dysplasia
Hip and Elbow dysplasia these are a major problem with the breed mainly because they are a large breed they grow very fast and if care is not taken when they are young this can have a disastrous effect on them as they get older , it is always wise to make sure any breeding dogs are hip and elbow scored before breeding to reduce this in the breed and also avoid young ones from using stairs and jumping up and down off things until at least 6-8 months of age . ...because they have large chests there is a lot of weight on those elbows.
Hip dysplasia Video
Heart disease is becoming more of a health issue with the breed ,especially Dilated Cardiomyopathy ,Pulmonary Stenosis, ASA and Mitral Dysplasia, so again always a good idea to health check any potential breeding dogs on a cardiograph as a stethoscope is not thorough enough .....this is a very heartbreaking and financially draining disease to have to deal with and sometimes can go undiagnosed until the dog dies suddenly.
The thyroid gland has a number of functions in the body , but is most well known for regulating the metabolism . If you have a dog that has trouble gaining weight ,is obese and suffer from Skin and hair conditions a quick blood test can check out the various levels of thyroid hormones including T 3 and T 4. Most dogs once diagnosed respond really well to treatment.
Demodectic mange is the most common skin condition in the breed and can be easy treated if got onto when the signs first appear , hair loss, skin irritation , crustiness ,scabbiness and possible itching....skin infections from scratching can become another issue is left can become life threatening . Ivormec is usually the choice of treatment under vet supervision only ,advantage multi can be used as a preventative treatment but is not a remedy for the condition.
The latest treatment being used is the Bravecto tablet but we do urge you to do your research before opting to use this drug.
Boosting your dogs immune system by way of natural supplements is also necessary as it is generally caused by a lowered immune system.
This breed can suffer from allergies so they are best fed a well balanced raw diet or a grain free dry food.
\Also known as wandering lameness or pano , it is most commonly seen between the age of 5 – 12 mths and is the result of excessive bone production on the long bones.....growing pains i guess you could say. Diet is thought to be a contributing factor in pano as a puppy diet contains a high protein levels it also increases growth rate and can increase the chance of pano so it can sometimes be a good idea to pup your pup if they suffer pano on an adult diet earlier . Pano is usually outgrown by the age of 18 mths old.
Entropian ( rolling inward ) eyelids and Ectropian ( drooping or rolling outward) eyelids are the most common eye problems . Ectropian ,unless very pronounced, does not generally lead to severe disease of the eye itself ,however a drooping eyelid can catch dust and debris which will cause irritation and possible eye infections .Entropion on the other hand frequently causes ocular pain and corneal disease. If the eyelid is rolled inward sufficiently so that the hairs of the eyelid rub on the eye, much damage may be done. Dogs with entropion usually squint and have watery eyes. If the entropion is not corrected and the rubbing continues, ulcers often develop on the cornea and the cornea becomes pigmented. Vision may be lost. Dogs that have had entropion correction surgery cannot be shown.
Epilepsy & Seizures
A seizure is a convulsion caused by abnormal bursts of electrical activity in the brain. They may last from seconds to minutes. Some characteristics of seizures will include jerking of the limbs, anxiety, salivation, vocalizing, and loss of bodily functions (urination/defecation). Epilepsy can be caused by metabolic disorders, infectious diseases, brain injury, toxins, or brain tumors. A genetic seizure condition can occur in dogs called idiopathic (of unknown cause) or inherited epilepsy. Since a dog with idiopathic epilepsy shows no recognizable abnormalities, it is assumed to be an inherited condition in most breeds and demonstrated to be heritable in some breeds. Treatment of seizures is usually two-fold which includes treatment of the underlying problem (infection, tumor, injury) and reducing or eliminating the seizure episodes with anticonvulsant medication.
We highly recommend doing health checks on any breedin stock you may be going to use ,together we should be trying to help eliminate some of the health issues that our breeds have ...if people just keep breeding without health testing the health issues will only get worse and never better .....and it will greatly increase your chances of ending up with a very sick dog or appearing in court.
THOSE ARE SOME CONDITIONS IN BRIEF PLEASE SEE BELOW FOR FULL ARTICLES FOR MORE DETAILED INFORMATION
STOMACH TORSION ARTICLE
by Dudley E. Johnson, M.V.Sc.
Professor of Surgery, University of Pennsylvania
Torsion of the stomach in the dog is characterized by life-endangering distension of the stomach with gas; the stomach is usually found to be severely dilated and congested, and often to have rotated about an axis in the plane of the esophagus.
There are many unknown features of this disease. Even the correct mane for the disease is not known. It is commonly called torsion of the stomach; however, many veterinarians, including the author, believe the primary condition is not torsion, but distension or dilation of the stomach with gas. This distension may or may not be followed by torsion or twisting of the stomach.
Torsion of the stomach is seen most commonly in large breeds including that are Large breed deep chested breeds including the Great Dane and Bloodhound, as well as some of the intermediate size breeds. Most people agree it is a serious problem in the first-two named breeds. There does not appear to be any association with the sex or the age of the animal. It has been reported in young adults as well as fully mature dogs. There is no doubt it can occur suddenly after eating in a previously healthy dog.
The Cause of Torsion of the Stomach
A commonly expressed explanation is that the disease is purely a mechanical twist of the stomach. The stomach, containing some comparatively heavy food material, is pictured as swinging in a pendulum-like fashion. Then, as a result of a sudden jump from a high bench or from rolling or playing, the pendulum is swung completely around the point of fixation of the stomach, the point where the esophagus passes through the diaphragm, giving rise to a twist. This occludes both the entrance to and the exit from the stomach so that gas, which is produced in the stomach, cannot escape, giving rise to the distension. As stated previously, there is considerable doubt concerning the validity of this explanation.
In criticism of this mechanical theory, several objections can be raised. In many cases, there is no evidence that a sudden or vigorous movement of the dog after feeding has occurred. In addition, the contents of the stomach are not such that would facilitate a pendulum-like movement. In the normal, tightly packed, abdominal cavity of the dog, the tonicity of the abdominal muscles, the shortness of the gut, and the normal absence of much gas or fluid, tend to preclude the free mobility visualized for the stomach.
In addition, it has been shown experimentally if the stomach of the dog is distended with air by means of a stomach tube, the stomach eventually twists in either a clockwise or counter-clockwise direction, depending on the position of the spleen at the onset of distension. If the previous theory is correct, there must be some factor which causes the initial distension of the stomach. This factor is not known, but it is probably due to a condition which causes atony or paralysis of the wall of the stomach associated with a large meal and then gas production. Much of the gas found in the stomach could be caused by swallowing air.
The Development of the Disease in the Dog
According to the theory that distension is the primary condition, following distension with gas, the stomach rotates in a clockwise or counter-clockwise direction. The dog is usually severely ill, and can die within one or two hours. The stomach is severely distended, the wall of the stomach is congested, and may even be deprived of blood. The spleen is also twisted and enlarged.
A second situation can occur which is not so serious, but is still a good idea to get the dog checked, the condition is more chronic, and may last several days. Some dogs eventually become severely distended, and may die.
What Causes the Death of the Dog?
This condition in the dog has a sudden onset, usually within one to two hours of eating a large meal. The dog is first breathless and, if examined closely, the abdomen is excessively large.
The dog will stand, lie still, or move only with caution. He will generally pass feces and gas so that eventually the entire gut with the exception of the stomach has been emptied. There are often attempts at vomiting although these attempts are rarely successful. In a period varying from one-half to three hours, the stomach becomes grossly distended, and there is severe dyspnea, or difficulty in breathing. The dog may live up to 36 hours but many will die within one to two hours.
There are several explanations for the rapid onset of severe signs and rapid death. It has long been suggested one of the important aspects is the stomach pressing forward on the diaphragm thus compressing the lungs so that the animal has difficulty in breathing. There is experimental and clinical evidence, however, that the rapid development of severe signs can be better explained by the pressure of the enlarged stomach on the vena cava, the large vein which carries blood to the heart from the abdomen and hind legs. As a result of this pressure, there is an inadequate amount of blood returning to the heart, which cannot function effectively as a pump, and therefore, the blood pressure of the animal falls. This produces shock and rapid death. Other factors contribute to a lessor degree to the development of the clinical signs. There is a loss of fluids and electrolytes from the body into the distended gut, and there probably is some pressure by the distended stomach on the lungs, interfering with their function.
It can be seen from this discussion of the cause of death in torsion of the stomach, that the first priority in the treatment of torsion of the stomach must be relief of the distension.
Management of the Dog with Torsion of the Stomach
This is one of the true emergencies in veterinary medicine, and treatment must be instituted immediately if the animal is to survive. If the dog cannot be treated immediately by a veterinarian, the owner may be forced to render first aid to his dog. This is difficult, and there is no uniformly successful method to relieve the distension. In some dogs, a stomach tube can be passed. This can be done by the owner. Unfortunately, it is not possible to do this in dogs with major torsion of the stomach since the entrance into the stomach is obstructed by the twist in the esophagus. Some owners puncture the stomach with a large-bore needle so that the gas will escape. It is probably best to do this on theright side of the dog over the point of greatest distension. Again, unfortunately, this is not always successful. The needle can become obstructed by stomach contents, and there maybe a leakage of fluids and gas into the abdominal cavity with risk of peritonitis. If the animal is severely affected, the owner may have no choice but to attempt one of these methods to relieve the distension. The dog should be treated by a veterinarian as soon as possible. Unfortunately, there has been insufficient experimental work done by veterinarians on the treatment of torsion of the stomach, and opinions vary on the correct form of therapy.
Many veterinarians advise immediate anesthesia and surgery to relieve the distension and the twist of the stomach. If large volumes of fluids and electrolytes are given by intravenous injection before and during the operation, reasonably good results can be expected.
More satisfactory results have been obtained by a method in which the distension is relieved by a simple surgical procedure. This is later followed by correction of the torsion when the dog is no longer in shock and better able to withstand anesthesia and surgery. This is the method recommended by this author. A small opening is made into the stomach using a local anesthesia. The wall of the stomach is sutured to the skin so that leakage into the abdominal cavity with subsequent peritonitis cannot occur. Fluid and electrolytes are given by intravenous injection; surgery is performed later to close the hole in the stomach and reposition the stomach, if necessary. Strict control of food and water intake for many days after surgery is needed to avoid a recurrence of the condition.
The treatment of torsion of the stomach is unsatisfactory for two reasons. First, the condition develops so quickly that the animal can die in such a short time that many dogs die before treatment can be instituted. Second, it is not possible to save all animals with any of the presently accepted forms of treatment. Using the method in which the distension is relieved and the torsion corrected at a later date, it is expected that 75 to 80 % of dogs should survive. Some dogs are so close to death before treatment that they cannot be saved, and in others, the stomach wall is severely injured by lack of blood supply so that recovery cannot occur.
Therefore, we should direct our attention to prevention of this condition. Unfortunately, there are not generally accepted methods for prevention, and much investigative work is needed.
In some large populations of dogs, such as those in the armed forces, a high incidence of torsion of the stomach has been seen with certain feeding regimens. In many cases, the condition disappears when these dogs are given food ad lib., that is, the dogs have access to a large amount of food so that the dog may eat a small amount of food on many occasions during the day. Obviously, with this management system, the dog has no incentive to eat one large meal at any given time and he does not eat hurriedly.
The most common advice given to owners of large breed dogs is based on experiences such as the one described previously. If there is a high risk, it is best to avoid one large meal per day. The dog should be fed at least twice daily; he should be discouraged from eating rapidly, and he should not be allowed to play actively before and after feeding. The dog should have access to water continuously so there is less chance he will drink a large amount immediately after eating.
It seems there is a high risk of torsion of the stomach if the animal is given one feeding a day, the dog is allowed to drink and to indulge in vigorous exercise after eating. All these factors should be avoided.
Certain drugs that alter the mobility of the gastrointestinal tract have been advocated to prevent gastric torsion. There is no experimental or clinical evidence that any of the presently available drugs is useful. An operation known as pyloroplasty has been advocated by some to increase the size of the exit opening in the stomach. Again, there are no reports in the scientific literature that this procedure should be used.
Raising the fed bowl can slow down fast eaters , as well as a object in the bowl so they have to eat slower, dry food has also been said to contribute to Bloat as it can be difficult for some owners that forget the food swells once wet so will be much more . Breaking meals into two a day is recommended and Mylanta will give you a larger window to get your dog to the vet should you suspect Bloat. Mylanta IS IN NO WAY a cure for Bloat your dog will still need medical treatment.***
MASTIFFS & ANESTHETICS
By Robin M Smith , DVM
I thought that I would talk about anesthesia concerns and the mastiff since that is the most frequently asked question I get from mastiff owners.
First off, you MUST have a veterinarian that is willing to listen to you and who is not afraid to be questioned about their anesthesia methods and how they monitor the pet once they are under anesthesia. If they do not want to discuss this or if they have a comment like, "well, I have always done it so and so way and I am not going to change", find yourself another veterinarian. I think that the public needs to be aware of exactly what is happening to their dogs and the risks that are possible. ALL anesthesias are putting the dog at risk... BUT there are some that are much safer than others and I will discuss these.
To start, I want to mention a few anesthesias that I would avoid if at all possible. In the past, most of these drugs were used exclusively, but with the advent of the new drugs and safer ones, they should not be used in the mastiff. Mastiffs are not just big chihauhas. The mastiff generally has a slower heart rate than smaller dogs and they also have inherently a lower blood pressure. They also, as you know, have a larger body mass. These things add to the risk of anesthetizing them.
I never use acepromazine anymore as a pre-anesthetic or tranquilizer. Acepromazine lowers blood pressure and dilates blood vessels thereby making the blood pressure even lower. It also is metabolized (gotten rid of by the body) very slowly and tends to accumulate in fatty tissues. Therefore, larger dogs and fatter dogs usually have to be given a larger dose than normal in order to have effect, and because of this, it takes these dogs sometimes days to get back to normal. I have used it a lot in the past... In fact, it was the "gold standard" for pre- anesthetic sedation, but not anymore. Many people have used it in tablet form for tranquilization during stressful periods, i.e. thunderstorms. Again, I used to use it for this, but do not now, especially in giant breeds... It is too unpredictable. Just to let you know, I use Benadryl for thunderstorms at a dose of 1 mg./lb but not to exceed 100 mg. and find it works very well to make the dog tired and rest better.
Xylazine (Rompun) is another drug I avoid. I haven't used it in about 5 years. It makes the heart more susceptible to the effects of epinephrine (adrenalin) that is in the body and therefore, making the dog more susceptible to heart abnormalities. It is a difficult drug to dose in giant breed dogs.
Acepromazine and Xylazine are the two drugs that I try to avoid if possible. If your veterinarian is also a large animal (cow, not mastiff) veterinarian, he may very well use the two drugs as they are used in farm animals a lot.
If for some reason, your veterinarian must use these two drugs, I think it is mandatory that the dog be monitored by an EKG machine during surgery and immediately post-operatively.
Other drugs that I do not use much although they are still used are the thiopentals. These are like sodium pentathol. They work very rapidly to knock the dog down, but are very powerful and stay in the system a long time. Also if the drug gets out of the vein (like if the dogs jump) the thiopentals can irritate the surrounding area and completely slough the area (all the tissue dies).
The drug(s) that I use the most in mastiffs are valium, ketamine, telazol, and propofol.
A combination of valium and ketamine given intravenously will be enough to knock the dog down in order to insert the endotracheal tube. Both of these drugs are very safe and I use them a lot in the older dogs. Neither one effect the heart much.
Telazol is very similar to valium and ketamine and also works well for anesthesia so that an endotracheal tube be place (I use .1 cc/lb and do not exceed 1.5 cc total).
I do use propofol (deprivan) for short procedures, i.e. OFA radiographs. Propofol is a fairly new drug in the veterinary field but has been used for a long time in the human field. It is a milky solution that after opening a vial cannot be stored. It gets contaminated with bacteria very easily. Because it is expensive, the veterinarian may try to cut corners and use old leftover propofol that is sitting in the fridge. It is given to effect or in other words, it is given IV until the dog goes down and then the dog is intubated and put on gas. The GREAT thing about this drug is that as soon as the animal is taken off the gas, the dog is awake and can walk out without assistance. I have also used the drug in C-sections to sedate the dog long enough to insert the endotracheal tube. It is a very top of the line drug. I do find the dosages of propofol to be a lot lower than the manufacturers literature dosage. One added thing: Propofol can lower blood pressure so the pet needs to be monitored while on that.
I also use oxymorphone for sedation and sometimes as the sole sedative for simple procedures like biopsy. It is an opiod and therefore it can cause respiratory depression, which means that the dog needs to be constantly monitored. There is a reversal agent called Naloxone that will reverse the effects of the drug and works quite well.
I will always put the dog on gas for a fairly short procedure. Isoforane is a gas of choice since it has fewer side effects. Halothane is still being used by some veterinarians. I do not use it since it (just like xylazine) sensitizes the heart which can cause irregular beats. But, as long as the dog is properly monitored, there should be no problem.
Prior to ANY anesthesia in any aged animal, I require a pre-anesthetic blood work up. I get a PCV (monitors whether anemic or dehydrated), a BUN (monitors liver and kidney function), Creatinine (monitors kidney function), ALT (monitors liver function), Alkaline phosphates (monitors liver and the biliary system), Total protein (monitors the immune system and hydration status), glucose and the electrolytes (sodium, potassium and chloride). I get these as I said even in young animals... It is just good medicine to know where the dog is prior to surgery and anesthesia so we will know how they will tolerate anesthesia. It is the base line. These test also guide me to my use of anesthesia. For example, if there is kidney damage I know to avoid drugs that have to go through the kidney to be eliminated from the body. The temperature is also monitored along with the heart by an EKG.
Atrophine was a drug that was used all the time as a pre-medication to dry up the saliva in dogs and cats and to keep the heart rate up. It is not used much anymore, or shouldn't be used in large and giant breeds. I don't use it in any breed anymore. Atrophine causes the gut to slow down and this is not good especially in the mastiff. I believe slowing the gut down predisposes the mastiff to bloating.
Routine spay or neuter. I hate the word ROUTINE used here because no surgery is routine. I used valium at .3 mg/kg and ketamine at 10 mg/kg IV and then I put the tube down the trachea and start the dog on isoforane gas anesthetic. I have not had problems with these in the mastiff.
OFA radiographs. I know many of you try to get OFA radiographs while the animal is awake. An unsedated animal is very hard to position correctly, but even more importantly OFA asks you to sedate the dogs. OFA believes that by not sedating the dogs, we're not getting good representative x-rays. I believe if the OFA radiographs are done with sedation, it would be very hard to miss a dysplastic animal. Depending on if the dog is going to go right home or stay in the hospital. I will use 2 anesthetics for each case. If the dog is staying, I use the valium/ketamine mixture and if the dog is not staying, then I use the propofol and then the dog is intubated. Just another added note. I always put an IV catheter in for a quick access to the blood stream in case something does happen and I need to give drugs quickly.
The main goal here is to obtain the least sedation possible in the puppies. For the Ceaserain section, I utilize Propofol at a dose of 3 mg./ lb. or until I can get an endotracheal tube down the dog. If I had to choose a second choice I would give the bitch torbutrol and valium as a preanesthetic as described next and then intubate after masking down. I use torbugesic at .45 mg/kg and give it to the muscle. Then I give valium (.45 mg/kg) intramuscularly. We prep the bitch on the floor by shaving her belly and then when done, we put her on the table and mask her down. We put a large mask over her muzzle and turn the gas all the way until she is asleep enough to put the endotracheal tube in. While masking the bitch down, she may struggle since the dog thinks it is not getting oxygen, even though it is. The trick here is to get in and the puppies out ASAP. Propofol can also be used and I have had good results with it. The bitch is wide awake as soon as the last staple is in. I am comfortable with either one.
By Robin M Smith , DVM
My bitch has dark brown spots on her flanks, what is it? My dog hardly eats anything and she or he is still overweight, why? My bitch does not seem to have normal cycles and I can't get her bred, why? My bitch was bred and confirmed pregnant by ultrasound but on her recheck at 30 days, the ultrasound showed evidence of resorption, why?
Many of you have had these same questions and are looking for answers. I believe there can be a multitude of causes for these problems and by all means your veterinarian is the first one for you to ask about your concerns. One of the causes for all of the above problems can be abnormal thyroid function. While I will talk about the thyroid and the diagnosis of thyroid problems and the treatment, I again prevail to you to seek your veterinarian's advise before doing anything. Sometimes, even if what I talk about is to you what you think is the exact think happening to your dog, you could create more of a problem by not getting it accurately diagnosed.
Hypothyroidism is a syndrome characterized by deficient thyroid hormone secretion that can readily be treated with synthetic thyroxine (T4). Once the diagnosis is established, virtually all clinical signs and related disturbances can be completely reversed by T4 replacement therapy. In a small percentage of cases (5%), however, reduced thyroid function occurs as a result of a more serious condition and recognition of the cause is at least as important as documentation of deficient thyroid hormone secretion.
Hyperthyroidism is rare in the dog and will not be considered here.
Hypothyroidism in most dogs result from progressive loss of functional; thyroid tissue due to a primary problem with the gland. In the dog, there are two distinct mechanisms of thyroid destruction: lymphocytic thyroiditis, which is probably an autoimmune disease, and idiopathic (meaning "unknown") atrophy, in which the thyroid gland is replaced by fat and connective tissue. There are other less common causes which will not be discussed here, since the above accounts for about 95% of the cases.
Although not proven, genetic factors may play a role in the origin of hypothyroidism. In a major study in 15 U.S. and Canadian veterinary teaching hospitals, the mastiff was not among any of the dogs tested. In this test, strong evidence for genetic transmission of thyroid pathology in dogs was found in data from selected groups of laboratory Beagles, in which that cause was lymphocytic thyroiditis. These dogs showed a higher frequency of autoantibodies (antibodies produced against oneself) to some thyroid molecules. Therefore, although good data conclusively demonstrating breed predisposition to primary cause, idiopathic atrophy, has not been linked to being heritable, it is hard to suggest sterilizing a dog unless the thyroid is biopsied and the diagnosis of lymphocytic thyroiditis is obtained. Also, the onset of canine hypothyroidism usually occurs later in life, after producing many puppies. With the advent of new diagnostic techniques, like the testing for autoantibodies, we may be bale to determine without surgical intervention, whether or not one is dealing with lymphocytic thyroiditis or idiopathic atrophy. I will deal more with the diagnostic in a later paragraph.
The clinical signs of hypothyroidism can be subtle to being very overt. Signs include mental dullness (your dog may not be as dumb as you think), exercise intolerance, lethargy, poor hair coats, hair coat color change, hair not regrowing when shaved (especially noticed after a surgery), infertility, irregular estrous cycles, resorption of fetuses after bred, neurological problems, bradycardia (slow heart rate), and cardiac arrhythmias (abnormal heartbeats). Not all of these symptoms will be seen, but whenever a breeder has a problem with reproduction, the thyroid should be examined.
Thyroid function and reproductive function have many interaction, any of which are not fully understood. In dogs, it has been shown that thyroxine (t4) is significantly higher during pregnancy that in any other reproductive rate. We usually think of the females when we speak of reproductive problems, but males are affected also. Affected dogs have decreases testicular size and lower fertility than nonaffected dogs. Poor semen quality has also been reported. Infertility, prolonged anestrus, short estrus, and poor libido are reportedly associated with hypothyroidism in bitches. An increased occurrence of abortion, stillbirth, resorption and mummified fetuses have been reported also. But, it has also been found that reproductive dysfunction is NOT always found in hypothyroid bitches. In human women, hypothyroidism has been shown to cause irregular cycles, including ovulation failure or cessation of cycles. When conception did occur, spontaneous abortion, low birth weight, and fetal death were common. It has been shown that pregnant women with clinical signs of impending spontaneous abortion who later did abort had lower T4 and T3 levels.
Where does all this leave us? Now that we know the thyroid can cause a lot of problems, what do you need to do? My recommendation, as a mastiff breeder whom is a veterinarian, is to have your dogs thyroid tested. The best place to send the thyroid tests at this time is Michigan State University. The reason I recommend testing all your dogs is that we do not have enough information on mastiffs on what is normal or abnormal. I have encountered bitches that have undergone resorption of fetuses, or low fertility tests. I have also had dogs with the typical dark skin patches on the flanks have normal thyroid function tests. In all these dogs, I have explored as many possibilities as I could to find other causes and have found none. After supplementing these dogs with thyroxine, the symptoms disappear and the bitches get bred and maintain their pregnancies. I am not saying we should just arbitrarily put dogs on replacement therapy, but I am saying we need to look at what is "NORMAL" for the mastiff breed. I believe if a particular breed or line of breed has demonstrable signs of thyroid abnormalities, and all other causes have been eliminated, that maybe we need to look at an alteration of "normal range" for thyroid function tests in that breed.
This is not the place to go into the physiological aspects of thyroid function. But I will say that there are more thyroid function tests than just the "T4" that many people test for. The actual thyroid hormone that is active in the body is T3. There is also reverse T3, free T4, bound T4, free T3 and bound T3, and circulating antibodies that can be measures and can help in diagnosing the problem. Michigan State tests all of these and give a good overall view of what is happening. A very important test, the antibodies produced, is important to know since these are often generated in association with lymphocytic thyroiditis, which we spoke of as possibly being hereditary. There is ongoing work to identify other important molecules, as TSH which once identified will lead to a new generation of thyroid diagnostic tests.
When diagnostic tests do not provide a cleat diagnosis, thyroid replacement therapy has been suggested as a valid diagnostic step in an animal suspected to be hypothyroid. Again, every attempt should be made to rule out nonthyroidal illnesses using history, physical examination, routine laboratory, and other appropriate testing before doing this. Your veterinarian is the best judge for this trial.
I believe that we have a lot to learn about the mastiff and the thyroid problems encountered in the breed. I am trying to collect information on as many mastiffs as I can and their thyroid profiles. Again, one must know what the :normal" is before we can diagnose the abnormal. I would appreciate your input and any thyroid test information that you have on your dogs as I am trying to put together information. The more I have, the more valid the information and the more we can all learn from it. If anyone has any questions regarding thyroid problems or would like more information, please feel free to contact me. Again, I am learning also and some of you have had much more experience with the breed and their particular problems.
Tricuspid valve dysplasia
The tricuspid valve is located between the right atrium and right ventricle of the heart. Consisting of three irregularly shaped flaps, the purpose is to control the backflow of blood from the right ventricle into the right atrium during contraction of the right ventricle. When the right ventricle contracts there is some blood, which will flow back into the atrium. It is this flow which pushes against the valvular flaps causing the valve to close.
During normal fetal development the tricuspid valve flaps are adhered to the septa (wall separating atrium from ventricle). As the fetal development progresses under normal circumstances the adhesive bonds holding the valve open will degenerate, allowing the valve flaps to move into their proper position.
One of the primary causes of tricuspid valve dysplasia, is the failure of the adhesive bonds to degenerate. This lack of degeneration can be partial or total in nature, and results in a range of right-side heart murmurs. Dependent upon the severity of the valvular deformation the work of the right-side of the heart is increased. If the malformation is severe enough it can lead to enlargement of the right atrium and ventricle. Eventually congestive heart failure can result.
Symptoms of tricuspid valve dysplasia are dependent upon the extent of the malformation, but some of the most common symptoms are: fluid retention, cool extremities and exercise intolerance (possibly followed by collapse) , pot belly or on going fussy appetite.
Tricuspid valve dysplasia in dogs is usually congenital (present at birth). Due to the fact that this condition (when it occurs) appears in several littermates, and tends to be more prevalent in some family bloodlines than others - it is suspected that the tendency to have this birth defect is hereditary. It is hoped that through screening of breeding stock and their lineage (parents, grandparents, littermates, aunts, uncles, etc.) efforts can be made to eliminate susceptible bloodlines from breeding programs.
CONGESTIVE HEART FAILURE
Heart failure is a condition, caused by an abnormality in the structure or the function of the heart, in which it is unable to pump normal quantities of blood to the tissues of the body. The heart is a pump, and when it fails, it often leads to fluid retention in the lung and the body cavities leading to congestive heart failure.
There are many causes of heart failure in dogs, including:
Birth (congenital) defects of the heart
Degeneration of the heart valves
Heart muscle disease (cardiomyopathy)
Diseases of the pericardium (the lining around the heart)
Irregular electrical rhythms of the heart (arrhythmia)
Dogs of any age and any breed can develop heart failure. There is certainly a predisposition for heart failure caused by cardiomyopathy in giant canine breeds.
Many older, small breed dogs develop heart failure from abnormal function of the heart valves as the valve tissue degenerates.
Heart failure affects your dog by reducing the amount of blood that is pumped to the muscles, leading to fatigue. In addition, most cases of heart failure are associated with the accumulation of fluid in the lungs (pulmonary edema), the chest cavity (pleural effusion), or the abdominal cavity (ascites). This fluid accumulation can lead to shortness of breath and other problems such as coughing and difficult breathing.
What To Watch For
Some of the symptoms of heart failure, and the progression of heart failure in a dog, are related to increased activity of the nervous system and to increased concentrations of circulating hormones (and related chemicals). These include:
Shortness of breath
Difficult breathing (dyspnea)
Unexplained Weight loss
Dilated cardiomyopathy (DCM) is a disease characterized by dilation or enlargement of the heart chambers and markedly reduced contraction. The left ventricle is most always involved. Advanced cases demonstrate dilation of all cardiac chambers.
DCM is very common in dogs, representing the most common reason for congestive heart failure (CHF). This heart disease also can cause heart valve leakage causing heart murmurs or abnormal electrical activity of the heart-producing arrhythmias (irregular or abnormal heartbeats). Large and giant breed dogs, especially males, are predisposed.
The clinical condition of canine DCM can range from overtly healthy (occult disease) to severe heart failure. Some dogs experience primary electrical disturbances (arrhythmia) such as atrial fibrillation or ventricular tachycardia.
The disease is thought to be genetic in Doberman pinschers, Irish wolfhounds, Newfoundlands, boxers, and Portuguese water dogs. The disease is sometimes seen in Dalmatians fed a low protein diet and in cocker spaniels and gold retrievers with taurine deficiency.
The average age of onset is 4 to 10 years, although Portuguese water dogs can acquire the disease when very young.
DCM is very serious and the mortality rate, even of treated cases, is very high.
What to Watch For
Shortness of breath
Loss of appetite
The advent of these problems should alert you that a serious emergency is at hand.
PLEASE GET YOUR DOG CARDIOGRAPHIC SCREENED BEFORE BREEDING AS THESE ARE HEREDITARY CONDTIONS ...WE HIGHLY RECOMMEND YOU CONTACT RICHARD LUCY AT PET PRACTICE IN HAMILTON TO GET YOUR DOG SCREENED & CLEARED OF ANY HEART CONDITION.
Symptoms of SAS
Subvalvular aortic stenosis (SAS) (frequently shortened to aortic stenosis or subaortic stenosis) is the most common type of inherited heart disease in Golden Retrievers, Newfoundlands, and Rottweilers.
The disease is characterized by a narrowing (stenosis) caused by a ridge or ring of abnormal tissue growth that inhibits blood flow from the heart to the aorta. The narrowing is classified as mild, moderate, or severe.
Sadly, seemingly healthy dogs with SAS can die suddenly, in part because even animals with severe stenosis may show no clear signs of illness. And often their owners don’t recognize that episodes of exercise intolerance, or fainting or collapsing from excitement are red flags for SAS.
In mild cases of subvalvular aortic stenosis, there are typically no observable clinical signs of disease.
In some moderate cases, and almost all severe cases of SAS, symptoms include difficulty breathing, weakness, fainting, and in extreme cases, sudden death. According to Cornell University College of Veterinary Medicine, we must “Realize that dogs with subaortic stenosis, even severe subaortic stenosis, may look perfectly healthy and active. These dogs generally do not realize that their hearts are compromised.”3
The median survival time for dogs with severe SAS who do not receive treatment is 19 months. For dogs receiving traditional treatment (beta-blockers), the median survival is 56 months. Most dogs with the severe form of the disease die before they reach 4 ½ years of age. Dogs with mild to moderate SAS usually do much better, with some living a normal lifespan.
Diagnosis involves a thorough physical exam, including using a stethoscope to listen for a heart murmur or irregular heartbeat. Your veterinarian will also want to know if your dog has displayed any of the symptoms typical of SAS.
Chest x-rays will be performed to check for fluid accumulation in the lungs. An electrocardiogram (ECG) may also be done to look at the electrical activity of the heart and check for arrhythmias.
An echocardiogram (cardiac ultrasound) is the diagnostic test of choice for SAS, because it allows your veterinarian or veterinary cardiologist to visualize the inside of the heart to assess the heart valves, blood flow patterns and velocity, extent of blockage, and severity of disease (mild, moderate, or severe), and other details of the heart’s structure and function.
Cutting Balloon Valvuloplasty: A Procedure with Promise for Dogs with Severe SAS
In mild cases of the disease, treatment is not required. However, since subvalvular aortic stenosis can worsen as a young dog matures, animals with moderate to severe disease may require medication. To reduce the workload on the heart and avoid symptoms, these dogs should also be prevented from engaging in sudden bursts of activity or intense physical exertion.
Follow-up appointments with your veterinarian are important to monitor your pet’s progress, adjust treatment as necessary, and to insure your dog is as comfortable as possible. If medications are being given, periodic echocardiograms may be performed to customize the therapy as necessary.
If your dog is having trouble breathing or collapses, it’s important to get to your veterinarian or the local veterinary emergency clinic immediately, even if your dog recovers quickly from the collapse.
Though rare, SAS also occurs in human children, and one treatment option is surgery to remove the ridge or ring of abnormal tissue below the aortic valve. This procedure has been tried with dogs, but has not increased survival rates according to Dr. Stern of UC Davis. In addition, open-heart surgery for dogs is only available at a handful of centers worldwide.
Genetic Testing Is Now Available
Several other types of surgical procedures and balloon catheterization procedures have been performed in dogs with SAS, with inconsistent results. However, more recently veterinarians at the University of Florida Veterinary Teaching Hospital have had some success with a technique using cutting balloon valvuloplasty for dogs with severe disease.
The procedure works like this, according to the Newfoundland Club of America:
“The cutting balloon is customized with four 2-millimeter microsurgical blades that are about five times sharper than conventional surgical blades.
As the deflated balloon is initially inserted through the carotid artery in the neck, the blades do not touch the arterial walls. When the balloon is inflated, the blades are forced open within the stenotic region, which cuts four incision-like slits into the obstruction.
The balloon is then deflated, removed, and replaced with a high-pressure balloon, which is inflated to forcibly dilate the stenotic region. The slits created by the blades are opened up with the high-pressure balloon. This combined technique has been evaluated for effectiveness in dilating the tough stenoses in dogs with severe SAS.”4
The first dog to undergo the procedure in 2009 was a 15 month-old Golden Retriever named Buddy with severe SAS. As of 2011, Buddy had reached a healthy weight and was still going strong, with plenty of energy and a good quality of life. He was also being given beta-blockers and an omega-3 supplement, which he’ll need for the rest of his life.
The UF veterinarians then conducted a study using the procedure with 14 additional dogs with severe SAS, including 4 Boxers, a French Mastiff, a German Shepherd Dog, 6 Goldens, a Rottweiler, and a Swiss Mountain Dog.
Three of the 14 dogs died between 9 and 25 months after the procedure due to SAS-related complications (sudden death or congestive heart failure). The researchers will monitor the remaining 11 dogs for the rest of their lives to evaluate their long-term survival and quality of life.
Veterinary hospitals across the US have started offering cutting balloon valvuloplasty to canine patients with severe SAS. The cost of the procedure ranges from $3,000 to $6,000 depending on the location and clinic, and the cost of follow-up care is not included in those numbers. Part of the expense is the balloons used in the procedure – they are highly specialized, not reusable, and were developed initially for human use.
Genetic testing for presence of the PICALM mutation is available through North Carolina State University’s College of Veterinary Medicine and the Veterinary Genetics Laboratory at the UC Davis School of Veterinary Medicine.
Going forward, now that scientists know one gene is responsible for SAS and which proteins are involved, they will be working to develop novel therapies to help treat dogs with the disease.
The researchers are also now studying the differences in severity of the disease, and the genetic basis of SAS in Golden Retrievers, Rottweilers, and other breeds.
Demodectic mange (Demodex canis), also called Red Mange is a type of skin disease caused by mites, more particularly the demodex canis mites. Veterinarians say that this disease is most common in puppies aged 3 to 9 months old.
Puppies that have acquired the disease may even spontaneously recover from it as they mature and their immune systems get stronger. Then again, the transition from a small puppy to an adult dog may bring about a demodectic mange attack in some breeds of dogs.
The change in a dog's habits may trigger the disease because the dog becomes stressed .It may also occur if there is a need to change from one living area to another. Mange can also be caught at birth by being in close contact with there mother or if there immune system is not up to strength to fight off the mites. These are the instances when the dogs are most prone to demodectic mange. Demodectic mange is not contagious to humans but can be tranferred to other dogs if the infected dog is in very close body contact with another , as in sleep together , for long periods.
Puppies suffering from demodectic mange usually have reddened feet or faces. The actual parts where the skin disorder affects your dog will be exposed. That means that there is total hair loss around those areas , the patch of missing hair maybe very small to start with but they will get more and bigger as time goes by.
Demodectic mange may progress from just a patch in the dog's ear and then cover the entire surface of their skin. This will definitely happen if the proper medications are not provided to the dog immediately. When the disease has spread all over, it becomes much harder for a veterinarian to control it.
The main difference between demodectic mange and sarcoptic mange is itchiness.
Demodectic mange doesn't itch at all. Sarcoptic mange, on the other hand, is very itchy, forcing your dog to scratch all over. Demodectic mange may not be itchy, but it is a discomfort to your dog just the same. Additionally, demodectic mange is not contagious.
Generally speaking, demodectic mange is not a life-threatening disease. However, you still need to take your dog to the vet once you see the symptoms as it can get easy out of control. Demodectic mange is very similar to sarcoptic mange and it is impossible to tell the two diseases apart without your vet doing a simple skin scrapping to confirm which mite it is....then the right course of treatment can be carried out.
This is the best possible thing that you can do for your dog.
Panosteitis is a disease primarily affecting young dogs of large breeds. It is characterized by inflammation within the bones, especially those of the legs. Lameness of one or more legs is often apparent.
The disease may persist for 1-6 months, with the average case lasting 2-3 months. During the course of the disease, periods of pain and lameness are interrupted by intervals of good health. Lameness may switch from one leg to another, and the degree of discomfort may vary. Full recovery is common and is usually expected.
Important Points in Treatment
1. Panosteitis is considered a self-limiting disease. This means recovery occurs after the disease runs its course. The only treatment presently used is oral anti-inflammatory or pain-relieving drugs.
2. Repeated radiographs (x-rays) may be required to evaluate the progress of the disease and to rule out the occurance of other orthopedic conditions which may occur at the same time as panosteitis.
3. Exercise: Inactivity is to be expected during the painful periods of the disease. Limiting exercise during this time is beneficial. There is no need to restrict your pet's activity during the non-painful time.
What is panosteitis?
Panosteitis is a self-limiting, painful condition affecting one or more of the long bones of young, medium-to-large breed dogs. German shepherd dogs, and dogs that are crossbred with German shepherds, are most commonly affected.
What causes panosteitis?
The cause of panosteitis is unknown. Attempts to isolate germs such as bacteria or viruses as the causative agent have not been successful. Theories of nutritional, allergic, endocrine (hormone) or metabolic (involving buildup and breakdown of tissues and energy), causes are also unproven.
What are signs of panosteitis?
Lameness of varying intensity usually starts in the forelegs, but may then affect the hind legs, resulting in a "shifting" leg lameness. Mild depression, loss of appetite, and weight loss may occur in severely affected patients. Affected dogs generally show signs of pain upon deep palpation of the long bones of the affected leg(s). There may also be low-grade fever and muscle wasting (atrophy).
How is panosteitis diagnosed?
Your veterinarian may suspect panosteitis after examining your pet. Radiographs (X-rays) are required to confirm the presence of the disease.
How is panosteitis treated?
Since the cause for panosteitis is unknown, there is no specific treatment for this condition. Treatment of the signs of pain is helpful to the pet, but appears to have no influence on duration of clinical signs. The primary goal of treatment is to minimize pain and inflammation with pain relieving drugs. Although limited activity has not been shown to hasten recovery, it does seem to lessen the pain associated with the condition. Signs of pain and lameness may last for several weeks.
Notify the Doctor if Any of the Following Occur:
* Your dog's legs become swollen.
* Your dog seems unusually uncomfortable.
* There is a change in your dog's general health
What is the prognosis for animals with panosteitis?
The long-term prognosis for a dog with panosteitis is very good. While clinical signs of lameness and soreness may last several weeks, complete recovery is typical. However, recurrence of clinical signs and lameness is common up until two years of age.
Entropion which is a rolling-in of the eyelid. This causes the hair on the surface of the eyelid to rub on the eyeball, which is both painful and often causes corneal ulcers or erosions. The corneal damage can also result in corneal scarring, which can interfere with vision. Usually the dog will squint and tear excessively. However, many flat-faced dogs with medial entropion (involving the inside corner of the eyes) show no obvious signs of discomfort.
Entropion is treated by surgical correction ("blepharoplasty"), which is essentially plastic surgery. Excessive folds and sections of facial skin are removed, and the eyelids tightened. It is uncommon for entropion to recur after surgery unless the entropion is quite involved, particularly in the Shar Pei breed. Very young puppies with entropion will often have "lid tacking" performed (rather than plastic surgery), in which temporary lid sutures are placed to roll out the lids. Often, these puppies do not require permanent plastic surgery once they have matured and "grown into" their facial skin. Permanent plastic surgery is usually not performed in puppies less than 5 or 6 months of age, giving the dog some time to develop its mature head conformation.
Dogs with inherited entropion should not be bred, as they can pass the trait on to their offspring. The Canine Eye Registration Foundation (see CERF information) publishes a list of breed-specific breeding recommendations for purebred dogs with entropion.
If you suspect that entropion is present in your pet, please consult with your family veterinarian. Your doctor may elect to have your pet referred to a veterinary ophthalmologist for further evaluation and possible surgical treatment.
Eyelids of dogs can grow abnormal hairs. These hairs grow from the oil glands (Meibomian glands) of the lids and are called distichia if the hair protrudes from the oil gland opening onto the edge of the eyelid. Distichia are often irritating, especially if the hairs are long and stiff. Ectopic cilia are also hairs growing from oil glands on the eyelid, but the hair protrudes from the inner surface of the eyelid and is very painful, often causing corneal ulcers.
Dogs with distichiasis may or may not show signs of discomfort, ranging from slight intermittent squinting and/or rubbing of the eyes, to severe squinting and discomfort. Dogs with ectopic cilia are always uncomfortable. Most dogs with ectopic cilia are young adult dogs or older puppies. Many breeds have problems with distichia. Both conditions are treated surgically under general anesthesia, with a procedure called cryoepilation. With this procedure, the abnormal hair follicles are frozen using a liquid nitrogen probe, and the hairs then removed.
After surgery, the eyelids are swollen for 4-5 days, and the eyelid margins will depigment and turn pink. Usually, the lid margins will repigment within 4 months. It is important to understand that new abnormal hairs can grow from new sites after surgery, but this is uncommon in dogs older than 3 years old.With cryoepilation, 85-90% of the treated hair follicles will not regrow. Repeat surgical treatment is rarely required, unless the animal is a puppy.
The Dysplastic Joint
Hip Dysplasia is a terrible genetic disease because of the various degrees of arthritis (also called degenerative joint disease, arthrosis, osteoarthrosis) it can eventually produce, leading to pain and debilitation.
The very first step in the development of arthritis is articular cartilage (the type of cartilage lining the joint) damage due to the inherited bad biomechanics of an abnormally developed hip joint. Traumatic articular fracture through the joint surface is another way cartilage is damaged. With cartilage damage, lots of degradative enzymes are released into the joint. These enzymes degrade and decrease the synthesis of important constituent molecules that form hyaline cartilage called proteoglycans. This causes the cartilage to lose its thickness and elasticity, which are important in absorbing mechanical loads placed across the joint during movement. Eventually, more debris and enzymes spill into the joint fluid and destroy molecules called glycosaminoglycan and hyaluronate which are important precursors that form the cartilage proteoglycans. The joint's lubrication and ability to block inflammatory cells are lost and the debris-tainted joint fluid loses its ability to properly nourish the cartilage through impairment of nutrient-waste exchange across the joint cartilage cells. The damage then spreads to the synovial membrane lining the joint capsule and more degradative enzymes and inflammatory cells stream into the joint. Full thickness loss of cartilage allows the synovial fluid to contact nerve endings in the subchondral bone, resulting in pain. In an attempt to stabilize the joint to decrease the pain, the animal's body produces new bone at the edges of the joint surface, joint capsule, ligament and muscle attachments (bone spurs). The joint capsule also eventually thickens and the joint's range of motion decreases.
No one can predict when or even if a dysplastic dog will start showing clinical signs of lameness due to pain. There are multiple environmental factors such as caloric intake, level of exercise, and weather that can affect the severity of clinical signs and phenotypic expression (radiographic changes). There is no rhyme or reason to the severity of radiographic changes correlated with the clinical findings. There are a number of dysplastic dogs with severe arthritis that run, jump, and play as if nothing is wrong and some dogs with barely any arthritic radiographic changes that are severely lame.
Once osteoarthritis is present on a radiograph, dysplastic changes are irreversible and usually continue to progress over time. If a dysplastic dog has secondary arthritis and pain, most owners elect to first treat their dog with medical management. The key to medical management of arthritis is weight control and exercise management. Studies have shown that up to 76% of severely dysplastic dogs with arthritis secondary to HD are able to function and live comfortable quality lives with conservative management.
With weight control, the goal is to prevent the dog from becoming overweight to reduce mechanical stresses applied to the hip joints. In general terms, the ribs should be easily palpated and there should be an indentation in front of the pelvic wings (waist line).
Controlled exercise is indicated to prevent or relieve the inflammatory process that leads to the pain associated with arthritis. The amount and difficulty of the activity is determined on a trial and error basis. Exercise should start with short leash walks and be gradually increased until the dog reaches the desired level of activity. If clinical signs start to reappear, the amount of exercise is scaled back to a level that will not cause clinical signs. Overall, exercise should fit to an individual dog's maximum intensity level with the goal to maintain muscle tone and cardiovascular function without causing pain, stiffness, and inflammation to the joint. The right amount of exercise helps to maintain muscle tone and strength and stabilizes the unstable dysplastic joint. Exercise also improves joint range of motion which in turn, keeps the dog more comfortable. Swimming, because it is a non-weight bearing exercise, can be a very useful means of maintaining muscle tone and range of motion without placing concussive forces on the joint.
Keep the dog in a warm environment. Warmth tends to help control the pain of arthritis from hip dysplasia. As in people, arthritic pain in dogs tends to be worse in the damp and cold of winter. Providing a well-padded and warm bed will help alleviate some of the pain associated with osteoarthritis. An egg-crate foam bed for dogs is commercially available. Applying superficial heat in the form of heating pads may also relieve pain. Care must be taken not to burn the skin especially with an electric heating pad. Heat works best for chronically inflamed joints from arthritis while cold works better to treat acute (sudden) types of joint injury.
OFA's Handling ProceduresWhen a radiograph arrives at the OFA, the information on the radiograph is checked against information on the application. The age of the dog is calculated, and the submitted fee is recorded. The board-certified veterinary radiologist on staff at the OFA screens the radiographs for diagnostic quality. If it is not suitable for diagnostic quality (poor positioning, too light, too dark or image blurring from motion), it is returned to the referring veterinarian with a written request that it be repeated. An application number is assigned.
Radiographs of animals 24 months of age or older are independently evaluated by three randomly selected, board-certified veterinary radiologists from a pool of 20 to 25 consulting radiologists throughout the USA in private practice and academia. Each radiologist evaluates the animal's hip status considering the breed, sex, and age. There are approximately 9 different anatomic areas of the hip that are evaluated (Figure 1).
- Craniolateral acetabular rim
- Cranial acetabular margin
- Femoral head (hip ball)
- Fovea capitus (normal flattened area on hip ball)
- Acetabular notch
- Caudal acetabular rim
- Dorsal acetabular margin
- Junction of femoral head and neck
- Trochanteric fossa
The radiologist is concerned with deviations in these structures from the breed normal. Congruency and confluence of the hip joint (degree of fit) are also considered which dictate the conformation differences within normal when there is an absence of radiographic findings consistent with HD. The radiologist will grade the hips with one of seven different physical (phenotypic) hip conformations: normal which includes excellent, good, or fair classifications, borderline or dysplastic which includes mild, moderate, or severe classifications.
Seven classifications are needed in order to establish heritability information (indexes) for a given breed of dog. Definition of these phenotypic classifications are as follows:
(See What Do Hip Grades Mean for more detail on the classifications)
The hip grades of excellent, good and fair are within normal limits and are given OFA numbers. This information is accepted by AKC on dogs with permanent identification and is in the public domain. Radiographs of borderline, mild, moderate and severely dysplastic hip grades are reviewed by the OFA radiologist and a radiographic report is generated documenting the abnormal radiographic findings. Unless the owner has chosen the open database, dysplastic hip grades are closed to public information.
Numerous drugs are available to control the signs of osteoarthritis secondary to HD. Nonsteroidal anti-inflammatory pain relievers can be used during bouts of lameness. These drugs inhibit prostaglandin release which decreases the inflammatory process and therefore, less pain is produced. These medications can also be given an hour or so before known periods of exercise to decrease inflammation. Side effects may be seen in some dogs which include vomiting, diarrhea, and inappetence.
Various alternative drug therapies known as disease-modifying osteoarthritis agents can be used. According to the manufacturers, these drugs work by providing the raw materials to enhance the synthesis of glycosaminoglycan and hyaluronate that cannot be adequately produced in the diseased arthritic joint. These are the molecules that form proteoglycan, which is an important constituent of the hyaline cartilage that lines the joint. These drugs may also enhance the synthesis of other macromolecules by cartilage cells that inhibit degradative enzymes produced within the arthritic joint. Controlled studies have been reported about the positive effects in people for osteoarthritis. No controlled studies, to date, have been reported on the clinical response when treating arthritis in dogs but clinically most dogs seem to respond.
Oral disease-modifying osteoarthritis agents known as nutraceuticals are now on the market. These drugs take approximately one month to reach therapeutic levels in the blood stream. Minimal to no side effects have been reported with their use.
Injectable disease-modifying osteoarthritis agents can be injected into the joint, vein or muscle and have been shown to be a useful adjunctive treatment for osteoarthritis in dogs. Since these drugs are injected, more rapid therapeutic levels are obtained. They may be initially used with the oral nutraceuticals for a series of injections for one month since the oral agents take approximately one month to reach therapeutic levels. The literature indicates that the earlier these drugs are administered, the more likely it will decrease inflammation and protect against cartilage degradation in osteoarthritis.
The use of these drugs should be tailored for the individual dogs and any improvement noted. If side-effects occur like GI upset, the medication should be given with food or discontinued altogether. If there is persistence of obvious lameness/pain after approximately 6 months using one medication, change the therapy to a different medication from the above choices.Surgical Interventions
In younger dogs usually less than 10 months old with only subluxation caused by dysplasia, a triple pelvic osteotomy (TPO) can be performed to reestablish joint stability and encourage normal joint development and minimize abnormal biomechanical forces on the joint before osteoarthritis occurs. This procedure is not indicated if osteoarthitis is already present. Recovery time is about 6 weeks and a good success rate has been reported with return of normal hip function.
For older dogs (over 10 months) that already have established osteoarthritis and can no longer be medically managed, a total hip replacement is the treatment of choice for reestablishing normal, pain-free limb function and joint mechanics. A high degree of success has been reported with this surgery and like the TPO, post-op recovery is about 4-6 weeks. The main disadvantage to this surgery is the high cost.
An alternative surgery which is more of a salvage procedure when there is significant osteoarthritis and a total hip is cost prohibitive is a femoral head and neck excision. This eliminates hip pain by removing the femoral head and neck and initiating the development of a fibrous false joint that permits ambulation. The false joint is less stable with a reduced range of motion than the normal joint which in turn, causes an abnormal gait. Nevertheless, pain relief with adequate function can be achieved. The procedure can be performed in all dogs of all sizes, but there are usually better long-term success rates in smaller dogs less than 20 kg (about 44 pounds). Preoperative muscle mass and early postoperative physical therapy are two important factors in determining a successful outcome. This surgery is usually not as successful if there is severe disuse muscle wasting (atrophy) present and/or the animal is obese.
Heavier dogs usually require more extensive postoperative rehabilitation to help promote an ambulatory pain-free false joint. Rehabilitation is aimed at preserving and promoting the leg's muscle mass, strength and range of motion through early (3-5 days) postoperative weight bearing ambulation and passive range-of-motion exercises. Early ambulation can be achieved by assisting the dog in getting up and walking. A towel can be placed under the abdomen to make assistance easier to perform in heavy dogs. Leash walks and/or swimming beginning the day of discharge from the hospital should be performed until near normal use of the leg returns. Passive range of motion physical therapy is also necessary to increase muscle strength and flexibility. Dogs that are obese, inactive or have substantial muscle atrophy and have poor owner compliance with physical therapy recommendations are poor candidates for this surgery.
With thanks to the OFA website for making this information
This is why it is a good idea to get your breeding stock hip scored before breeding them it is a very small price to pay but could save a lot of heartache.
The Three Faces of Elbow Dysplasia
Elbow dysplasia is a general term used to identify an inherited polygenic disease in the elbow of dogs. Three specific etiologies make up this disease and they can occur independently or in conjunction with one another. These etiologies include:
- Pathology involving the medial coronoid of the ulna (FCP)
- Osteochondritis of the medial humeral condyle in the elbow joint (OCD)
- Ununited anconeal process (UAP)
Studies have shown the inherited polygenic traits causing these etiologies are independent of one another. Clinical signs involve lameness which may remain subtle for long periods of time. No one can predict at what age lameness will occur in a dog due to a large number of genetic and environmental factors such as degree of severity of changes, rate of weight gain, amount of exercise, etc. Subtle changes in gait may be characterized by excessive inward deviation of the paw which raises the outside of the paw so that it receives less weight and distributes more mechanical weight on the outside (lateral) aspect of the elbow joint away from the lesions located on the inside of the joint. Range of motion in the elbow is also decreased.
Evaluating the Elbow
EPILEPSY & SEIZURES
Epilepsy simply refers to repeated seizures. Seizures may occur as a one time event in an animal from a variety of causes, but only if the seizures repeat again and again over a period of time do we call it epilepsy. Seizures are a sign of brain disease the same way a cough is a sign of lung disease. Saying an animal has epilepsy is like saying it has a chronic cough; it is a sign of a problem which isn't going away. Anything which damages the brain in the right area can cause epilepsy. If we can identify the cause of the seizures, say a brain tumor or a stroke, then we say the pet has symptomatic (or secondary) epilepsy. That is, the seizures are a symptom of a disease process we've been able to identify. If we've looked and can't find the cause, then we call it idiopathic (or primary) epilepsy. The term idiopathic simply means that we don't know the cause. It may be that the cause has escaped our attention; for example, a stroke that is too small to detect with routine brain scans or damage that occurred during whelping.
Many of the idiopathic epileptics have inherited epilepsy: epilepsy caused by a mutation in a specific gene which they inherited from their parents. Dogs with idiopathic epilepsy frequently begin seizing at between one and three years of age, and certain breeds are predisposed to develop epilepsy. A few breeds have proven hereditary epilepsy, while in most it is just a strong suspicion. One of the goals of the Canine Epilepsy Project is to identify genes responsible for epilepsy in dogs. This will allow us to positively diagnose the hereditary form and take steps to decrease the incidence of epilepsy in dogs.
How common is epilepsy?
Epilepsy is one of the most common neurologic diseases in dogs, but no one knows for sure just how common it is. Some studies estimate up to 4% of all dogs are affected. In some breeds, the incidence may be higher and some families may have up to 14% epileptics. Epilepsy occurs less frequently in cats and other pets, presumably because they do not have a hereditary form of the disease.
What determines when my pet will have seizures?
No one knows what it is that determines when an epileptic will have seizures. The only thing we can predict about epilepsy is that it's unpredictable. Some pets appear to have seizures very regularly, while in others, the seizures appear to be precipitated by specific events such as stress, or changes in the weather. However, when we try to use what's happened in the past to predict when the next seizure may occur, we usually aren't very successful. For many epileptics, there is no pattern to their seizures.
Lymphoma is one of the most common cancers seen in dogs. Althought here are breeds that appear to be at increased risk for this disease, lymphoma can affect any dog of any breed at any age. It accounts for 10-20% of all cancers in dogs.
Lymphoma (lymphosarcoma or non-Hodgkin's lymphoma) is a malignant cancer that involves the lymphoid system. In a healthy dog, the lymphoid system is an important part of the body's immune system defense against infectious agents such as viruses and bacteria. Lymphoid tissue normally is found in many different parts of the body including lymph nodes, liver, spleen, gastrointestinal tract and skin. Lymphosarcoma is classified according to the location in the body in which the cancer begins.
- Multicentric form occurs in the lymph nodes.
- Gastrointestinal form occurs in the stomach, intestines, liver and lymph nodes in the abdomen.
- Mediastinal form occurs in the mediastinum, in front of the heart in an organ called the thymus. Hence this form of lymphosarcoma sometimes is called thymic lymphoma.
- Cutaneous form occurs in the skin.
- Acute lymphoblastic leukemia occurs when the disease starts in the bone marrow.
- Miscellaneous forms of lymphosarcoma are less common and include those that begin in the nervous system, nasal cavity or kidneys.
Most of the time, lymphoma in dogs appears as “swollen glands” (lymph nodes) that can be seen or felt under the neck, in front of the shoulders, or behind the knee. Occasionally, lymphoma can affect lymph nodes that are not visible or palpable from outside the body, such as those inside the chest or in the abdomen. Other symptoms include vomiting, diarrhea, loss of appetite, weight loss, lethargy, difficulty breathing and increased thirst or urinations. Cutaneous lymphosarcoma can cause redness or flakiness of the skin, ulceration (especially near the lips and on the footpads), itchiness or lumps in the skin. Clinical signs will vary depending on the stage of the disease, volume of tumor and anatomic location of the lymphoma.
A thorough physical examination of the dog is an important part of the diagnostic work-up as it will dictate which further tests will be required. The work up should always include a complete blood count (CBC), platelet count, biochemical profile, urinalysis and fine needle aspirate or excisional or surgical biopsy of the lymph node. These tests help confirm the diagnosis and determine if the dog is hypercalcemic and/or has normal neutrophil and platelet counts, and assess kidney function so that chemotherapy can safely be administered. Lymphoma can also be diagnosed with x-rays and ultrasound The exact tests
performed will depend on the location of the tumor.
Once a diagnosis of lymphoma has been established, it is necessary that the cancer be staged. Staging is the process by which the veterinarian determines to what extent the lymphoma has spread throughout the animal's body. The degree of spread affects the manner in which a dog is treated.
Stage I Involvement of a solitary lymph node or lymphoid tissue in a single organ (i.e. nasal cavity)
Stage II Several lymph nodes in the same general area involved
Stage III All peripheral lymph nodes involved
Stage IV Involvement of liver and/or spleen, and/or anterior mediastinum in the chest involved
Stage V Involvement of bone marrow (some classifications consider cutaneous involvement in this stage)
Substage a without systemic signs of disease (patient generally has no symptoms)
Substage b with systemic signs of disease (patient does not feel well)
Chemotherapy treatment is considered the gold standard for this aggressive form of cancer and usually consists of a combination of oral and injectable drugs given on a frequent basis. The exact treatment protocol will vary depending on the veterinarian and financial resources of the dog's family. There are several different chemotherapy protocols from which to choose. They usually contain from 3-5 different chemotherapy drugs, each of which works on the cancer cells in a different way. If some of the cancer cells are resistant to one drug, hopefully they will be sensitive to another drug.
The Wisconsin Lymphoma Protocol is a short, but intense chemotherapy regimen currently popular with oncologists as the primary canine lymphoma treatment. This protocol involves weekly chemotherapy for the first 9 weeks and then every 2 weeks until week 25. This chemotherapy protocol uses vincristine, doxorubicin (adriamycin), cyclophosphamide (cytoxan), and 1-asparagnase by IV, along with prednisone and/or cyclophosphamide orally. With the use of the 25 week University of Wisconsin-Madison protocol, average first remission lasts 10-14 months, with 20% 2 year survival.
Doxorubicin alone : The patient is treated with a total of 5 treatments of doxorubicin at 3-week intervals. The average survival time with this approach is 10-11 months.
COP: This protocol involves a combination of cyclophosphamide in tablet form, vincristine and prednisone. 4 weekly intravenous injections of vincristine are given, followed by injections at 3-week intervals to complete 6 months of treatment.
Cyclophosphamide is given over 4 days every 3 weeks (4 days on; 17 days off). Prednisone is given daily for 6 months. The average survival time with this protocol is reported as 8-10 months.
Prednisone alone : This medication is a steroid and can be given in pill form daily at home. The average survival time for patients with lymphoma treated with prednisone only is 60 days.
Some owners choose not to treat dogs that develop lymphoma. The life expectancy of these untreated dogs averages 4 to 6 weeks. Oral prednisone therapy may reduce the swellings and discomfort, but probably will not appreciably extend their life span. It must also be noted that oral prednisone treatment prior to chemotherapy is not recommended and may actually reduce the effectiveness of the chemotherapy.
In dogs that do undergo one of the recommended chemotherapy protocols, life expectancy can be extended. Most dogs with lymphoma develop medium to high-grade lymphoma that is very responsive to chemotherapy. Greater than 75% of dogs with lymphoma are expected to achieve a complete remission with chemotherapy. The duration of the first remission is variable, depending on the chemotherapy protocol used, with median remission times varying from 6 months to 11 months. The second remission is more difficult to achieve, with approximately 40% of dogs with lymphoma achieving complete remission with a second course of chemotherapy. Less than 20% of dogs with lymphoma will achieve a third complete remission. Approximately 40-45% of dogs with lymphoma live one year with treatment. Less than 20% of dogs with lymphoma live 2 years with treatment. Eventually, the cancer will infiltrate an organ to such an extent that organ fails (often this is the bone marrow or the liver). The patient loses his/her appetite, vomits or gets diarrhea, weakens and dies. At some point the tumor becomes resistant to therapy and no further remissions can be obtained.
However, if a dog tolerates chemotherapy (fortunately most dogs do) their quality of life can be quite good during the treatment period. Treatment for lymphoma in the dog is considered one of the more successful cancer treatments and can often be performed by a local veterinarian without the need to travel long distances to veterinary schools or specialty clinics. It helps to remember that one year can equate to almost 10% of a dog's expected life span, therefore, the increased life expectancy with lymphoma treatment is often well worth it.
Thanks to caninecancer.com for this information
JUVENILE HEREDITARY GLOMERULONEPHROPATHY
IN THE DDB
IN THE DDB
August 28th , 2009
Since 2 years, a new disease entity is increasingly recognized in the Dogue de Bordeaux in Europe. Affected dogs present with chronic renal failure before they are 2 years-old. Urinary protein loss and modified kidney structure on ultrasound are other characteristics of this newly recognized entity in the Dogue de Bordeaux breed called juvenile hereditary glomerulonephropathy. At least 30 cases have been diagnosed or strongly suspected in Belgium, France and Italy during the last 2 years. All affected dogs were genetically related. Most frequently reported clinical signs are polyuria-polydipsia, excessive thinness, chronic gastrointestinal signs (inappetence, vomiting, diarrhea) and seizures.
Several studies on this condition have been conducted during the last few months. Histopathological studies have all been made at the University of Utrecht. These studies have revealed similar lesions in all affected dogs but the degree of severity of the lesions varied with the severity of clinical signs and renal failure. Well-described canine juvenile nephropathies have been excluded such as renal dysplasia, hereditary nephritis (found in the English Cocker Spaniel among other breeds) or glomerulonephritis (inflammatory disease caused by immune dysregulation). However, as histopathological examination has been only made in advanced cases, primary lesions (found in the early course of the disease) have not yet been identified.
Genotyping studies have confirmed that this disease is hereditary. Simple modes of inheritance have been excluded and it seems that the disease is transmitted with a complex mode of inheritance (possibility of implication of multiple genes). This implies that DNA from more affected and related unaffected dogs is needed in order to better define the mode of inheritance of juvenile hereditary glomerulonephropathy in the Dogue de Bordeaux and the potential mutation(s) at the origin of the disease.
Any help that you could provide us with is of the upmost importance. We ask any breeder or owner of Dogue de Bordeaux dogs potentially concerned by this disease to contact us either directly or via the breed clubs in order to report the clinical signs and pedigree data but also to provide us with some blood for DNA studies. We hope t o improve the diagnosis and treatment of this affection to help your dogs to live longer and in a better condition when affected with this disease. We also aim to make genetic tests available in order to eradicate this disease from the Dogue de Bordeaux breed.
Dr Rachel LAVOUE,
DMV, Résidente ECVIM-CA
Département des sciences cliniques des animaux de compagnie
Université de Liège, Belgique
Prof. Dominique PEETERS,