GLAUCOMA - "Glaucoma is a painful, often blinding and more common than is essentially known eye disorder" says Dr. Kerry Ketring, a Cincinnati-based veterinary opthamologist and public relations chairperson of the American College of Veterinary Opthamologist.
The eye maintains its turgid, spherical shape because natural processes within it produce a fluid called 'aqueous' which nourishes ocular tissues, absorbs waste products and then drains off, creating a relatively constant innocular pressure (IOP)
When metabolic and mechanical processes interfere with its drainage, that pressure can rise, causing extreme pain, damaging the retina and optic nerve, and causing blindness.
Signs of glaucoma include sudden blindness, a cloudy cornea which obscures the iris, dilated and non-responsive pupils, inflammation of the sclera with large elevated vessels, and frequently, a visibly enlarged eye. Animals suffering from glaucoma will likely squint or hold the eye closed, and behave lethargically because of the discomfort associated with the disorder.
Animals suffer from two broad categories of glaucoma, primary and secondary, and successful management depends upon the proper differentiation of these two categories:
Primary glaucoma, the most common, is an inherited disorder which occurs when the 'drainage angle' becomes clogged and fails to drain the eye properly. Primary glaucoma often affects both eyes, but usually not at the same time or to the same extent. Using special examination techniques, veterinary opthamologists can further classify primary glaucoma into narrow, closed and open-angle glaucoma.
Secondary glaucoma is an increase in pressure which occurs as a result of another abnormality of the eye such as a tumour, severe trauma, an uncontrolled inflammation, or a shifting of the lens that blocks the outflow of aqueous.
Differentiating between primary and secondary glaucoma is critically important since the treatments for each are almost opposite," says Dr. Ketring. "A mistake at this point can result in irreversible blindness". Most vets diagnose glaucoma on the basis of observing the 'cardinal signs', but since many of these signs are also associated with other eye disorders, it is frequently mis-diagnosed or missed. The only way to accurately diagnose gaucoma is by demonstrating an increase in intraocular pressure. Veterinary opthamologists measure that pressure with an instrument called an electronic tonometer. When a dog's pressure exceeds the normal range of 15-25 mm of mercury, it is time to act - sustained pressures of 60 or greater for a day or longer can result in irreversible blindness.
With the exception of some procedures, glaucoma is treated the same in animals as in humans. Treatments are formulated based on the animals prognosis for vision and the proper classification of the glaucoma. And, Dr. Ketring says, treatments always seek to reduce the extreme pain associated with the disorder. The success of medical and surgical treatments depends upon when the disorder is diagnosed. If you diagnose it early enough, treatment can be very successful. If you catch it late, the chances for success are reduced."
Medical treatments include the administrations of oral drugs intended to reduce the amount of aqueous produced by the eye; and in some cases, may reduce the production of aqueous. An animal with glaucoma must take medication for the rest of its life. Surgical treatments are also useful. Veterinary opthamologists may perform cyclocryosurgery, which freezes the aqueous-producing tissues; filtering procedures, which improve fluid drainiage; or in cases of secondary glaucoma, correct the displaced lens or other abnormality causing the drainage problem. A new technique which involves implanting a device to aid in the drainage of aqueous is still in the developmental stages, according to Dr. Ketring.
Because the disease is frequently undetected, many animals are often in advanced stages by the time they are referred to a board certified veterinary opthamologist. In these cases removing the irreversibly blind eye to eliminate the pain and carefully evaluating the other eye for signs of glaucoma may be the best treatment.
Many vet opthamologists elect to implant intraocular protheses. While these 'artificial eyes' do not restore vision, they are popular with clients for cosmetic reasons.
Dogs adapt more easily to blindness than people, according to Dr. Ketring; eliminating the pain often creates a happier, more lively animal. People don't realize that their dog has been suffering from chronic pain. Many can't believe how active the dog becomes after the surgery. New techniques for treating glaucoma in people may eventually prove useful in dogs. But for now, Ketring says, early detection and prompt referral to a board-certified veterinary opthamologist is the best response to glaucoma.
CATARACTS - Cataracts: When there is an eye defect - this is the most common one found in Min Pins. Cataracts that develop before the age of two have the potential to cause the dog to go blind. There are three main types of cataracts:
Congenital Cataracts: This type of cataract is present when the dog is born. They can occur in one eye or both. The cause is usually from illness, infection or toxins while the dog is still developing in the uterus.
Developmental Cataracts: This type typically occurs early on in a dog's life. The cause can include illness, infection or trauma.
Senile Cataracts: This type of cataract is more commonly found in dogs over 6 years of age.
If you would like to know more about cataracts in dogs please follow the links below.
http://www.animaleyecare.com/catarctsurg.htm (shows pictures of dog's eye)
PROGRESSIVE RETINAL ATROPHY - Commonly referred to as P.R.A., progressive retinal atrophy is an inherited form of blindness which, in the dog, occurs in two forms, generalised and central. By way of explanation, the retina is the light sensitive membrane at the back of the eyeball. Atrophy infers degeneration. Hence P.R.A. leads to gradual loss of retinal sensitivity, impaired function and progressive loss of vision.
Early in the disease, affected dogs are nightblind, lacking the ability to adjust their vision to dim light; later their daytime vision also fails. As their vision deteriorates, affected dogs will adapt to their handicap as long as their environment remains constant, and they are not faced with situations requiring excellent vision. At the same time the pupils of their eyes become increasingly dilated, causing a noticeable "shine" to their eyes; and the lens of their eyes may become cloudy, or opaque, resulting in a cataract.
No effective method of treatment exists. However, curtailment and/or eventual elimination of the disease is possible by careful selection of blood lines used for breeding.
HEPATIC VASCULAR DISORDER - Portosystemic shunts (PSSs) are vascular communications between the portal and systemic venous systems that allow portal blood to reach the systemic circulation without first passing through the liver. Decreased hepatic blood flow and lack of hepatotropic factors such as insulin, glucagon, and nutrients result in hepatic atrophy. Urate urolithiasis, an important complication of PSSs, occurs because of increased urinary excretion of ammonia and uric acid. Renal, cystic, or urethral calculi (kidney stones) may occur. Urolithiasis may be a complication in as many as 50 per cent of animals with congenital PSS.
PSSs in dogs and cats can be either congenital or acquired. The congenital form is most commonly recognized. Congenital PSSs are anomalous embryonal vessels that usually occur as single shunts (either intrahepatic or extrahepatic) and are not associated with portal hypertension. The genetic basis for congenital PSS is unknown, although affected lines have been recognized in Miniature schnauzers, Irish wolfhounds, Old English sheepdogs, Cairn terriers, and Miniature Pinschers An autosomal polygenic mechanism is suspected in Irish wolfhounds. Acquired PSSs, which form in response to portal hypertension, are typically multiple extrahepatic shunts that connect the portal system and the caudal vena cava.
Single intrahepatic PSSs provide a communication between the portal vein and the caudal vena cava. Intrahepatic shunts can be classified as left, central, or right divisional . The morphology of the left divisional shunt (via the left hepatic vein) is consistent with failure of the fetal ductus venosus to close. The ductus venosus, a fetal vessel that allows oxygenated blood to be shunted from the umbilical vein directly into the caudal vena cava, normally closes within the first few days after birth. The underlying mechanisms associated with failure of the ductus to close are unknown. The pathogenesis of intrahepatic PSSs that occur in the right medial (central divisional) or right lateral (right divisional) liver lobes is unknown. Single intrahepatic PSSs are most common in large breed dogs. Single extrahepatic PSSs usually connect the portal vein or one of its tributaries (often the left gastric or splenic vein) with the caudal vena cava cranial to the phrenicoabdominal veins. Less frequently, the anomalous vessel enters the azygos vein or other systemic vessel. Single extrahepatic PSSs represent a developmental abnormality of the vitelline system. Single extrahepatic PSSs are most common in cats and small breed dogs.
In dogs and cats with congenital PSS, the liver is grossly small and often mottled in appearance. Liver biopsy most consistently reveals hepatocyte atrophy with small or absent portal veins and arteriolar hyperplasia, although biopsy abnormalities may be subtle. Congenital PSSs occur more commonly in purebred than in mixed breed dogs. Breeds at increased risk include Miniature schnauzers, Yorkshire terriers, Irish wolthounds, Cairn terriers, Maltese, Australian cattle dogs, Golden retrievers, Old English sheepdogs, and Labrador retrievers. A slight predilection for female dogs has been suggested and affected male dogs are commonly cryptorchid. Age is an important diagnostic clue because most animals develop signs by 6 months of age. A congenital PSS should still be a diagnostic consideration in middle-aged or older dogs, because signs may be subtle and some dogs with congenital PISS go undiagnosed until as late as 10 years of age. This is especially true for dogs with urate urolithiasis who may not have an obvious history of HE.
Clinical signs of congenital PSS are referable to the central nervous system, gastrointestinal system, or urinary tract. Signs of HE usually predominate. The most consistent signs of HE are often subtle, such as anorexia, depression, and lethargy. Other common findings indicative of diffuse cerebral disease include episodic weakness, ataxia, head pressing, disorientation, circling, pacing, behavioral changes, amaurotic blindness, seizures, and coma. Hypersalivation is also a prominent sign in cats but also occurs in dogs. Clinical signs of HE tend to wax and wane and are often interspersed with normal periods, reflecting the variable production and absorption of enteric products that are neurotoxic. Signs of HE may be exacerbated by a protein-rich meal; gastrointestinal bleeding associated with parasites, ulcers, or drug therapy; or administration of methionine-containing urinary acidifiers or lipotropic agents. Clinical improvement of HE after fluid therapy is common and most likely attributed to correction of dehydration and promotion of urinary excretion of ammonia and other toxins. Improvement with broad-spectrum antibiotic therapy reflects the effect of antibiotics on the toxin-producing intestional flora. Gastrointestinal signs of intermittent anorexia, vomiting, and diarrhea are common nonspecific features of hepatic dysfunction and are not necessarily accompanied by overt signs of HE. Many affected animals have a history of stunted growth, failure to gain weight compared with unaffected littermates, or weight loss.
A history of prolonged recovery after general anesthesia or excessive sedation after treatment with tranquilizers, anticonvulsants, or organophosphates can be attributed to impaired hepatic metabolism of these substances. Other less consistent clinical findings include polyphagia, pica (eating stool) and foreign body ingestion, intermittent fever, and intense pruritus in dogs. Physical examination may be unremarkable except for -small body stature or weight loss. The neurologic examination is normal, or if overt signs of HE are present, neurologic findings are consistent with diffuse cerebral disease. Hypoglycemia, especially after a prolonged fast, is most likely in affected toy breeds of dogs such as Yorkshire terriers. Ultrasonography is a useful noninvasive method for evaluating animals with a suspected congenital PSS. Intrahepatic PSSs are more reliably detected with this procedure than are extrahepatic PSSs. It is a rapid technique that can be performed without sedation or anesthesia but is highly dependent on the experience of the operator. Ultrasonographically, the liver usually appears small, there is a consistent decrease in the number and size of intrahepatic veins, and the shunting vessel may be identified. The kidneys and bladder should also be routinely scanned to detect urate urolithiasis. In normal animals, the portal blood (and injected dye) flows to the liver, outlining the portal vein and its multiple intrahepatic branches. With a single congenital PSS, the shunting vessel is outlined as blood is diverted directly into the lower pressure systemic venous system.
Medical management of HE in dogs with congenital PSS is indicated before anesthesia and definitive surgical correction. The cornerstone of therapy is a diet that is moderately protein restricted with the bulk of calories derived from carbohydrates and fat (soy protein) and dairy (cottage cheese, yogurt) proteins are preferred. Meat and egg proteins are poorly tolerated. The recommended dietary protein intake on a dry matter basis for patients with HE is 18 to 22 per cent. The short-term response to therapy for HE in dogs with congenital PSS is often dramatic. Most dogs are clinically normal with therapy, even before surgical shunt ligation. If surgical shunt correction is not feasible or is declined by the owner, long-term medical management can adequately control clinical signs for as long as 2 to 4 years in some dogs. However, most dogs managed medically on a long-term basis are not clinically normal. and eventually have refractory neurologic signs. The treatment of choice for dogs with a congenital PSS is surgical attenuation or ligation of the anomalous vessel." On occasion, seizures and status epilepticus are a complication of surgical shunt ligation. The prognosis in dogs for resolution of signs after total surgical ligation of the shunt is excellent if the dog survives the immediate postoperative period. In dogs with partial shunt ligation, the prognosis is not as good. Although clinical signs may resolve after surgery and the response appears favorable in the first few years, long-term follow-up (more than 3 years) suggests that signs recur in 40 to 50 percent of dogs with partial shunt legations. On the basis of this information, dogs who have previously undergone a partial ligation should be reevaluated by transcolonic scintigraphy. If shunting persists, surgical exploration to perform complete suture ligation or ameroid constrictor placement is indicated.
TUBE FEEDING - Many studies have been made about Fading Puppies, and scientists have isolated several causes for that phenomenon. However, the main trouble starter seems to be the lack of milk intake by puppies. Sometimes, the puppies are very busy around the mother, but they take too long to learn how to suck. They get weaker and weaker, until they can do nothing, and nothing can help. Were they unable to suck, because they were already sick? Or did they become sick because they were unable to suck? That is an important question for which it is not always necessary to know the answer. Experience has proven that if puppies are fed the proper quantity of the proper formula right from the start, the great majority of them will pull through.
WAYS TO FEED
Bottle & Nipple: if the puppies do not suck on the mother, chances are they will not suck on the bottle either. Of course, you can enlarge the hole in the nipple of the bottle; you can squeeze a little bit of milk into the puppy's mouth; but if the temperature of the formula is not perfectly right, the puppies will not suck anyhow. You will end up putting some formula into the puppy's mouth all the time and risk sending some of it into the lungs! That reduces your chances of success tremendously. Naturally, with great skill, and 1 hour of work a day, for each puppy, it can be done.
With A Dropper: chances are that sooner or later, you will send some formula into the lungs. Newborn pups do not have the swallow instinct when it comes to putting fluids on their tongue!
Syringe & Tube: This is the easiest, the less dangerous, the fastest and the most precise way of feeding puppies. In our opinion, it is the only practical method for a kennel. Best of all, it is the Key to Success
THE REGULAR FORMULA
More than one has been designed. Some include milk, oil & Vitamins. Some include milk & egg yolks. Some are ready made by companies. A formula consisting of approximately 5 parts of homogenized milk and 1 part of 35% homogenized cream is adequate. However, additional comments are in order: less cream makes the more digestible for newborns, and more cream, when the puppies are 'started' permits feeding less often without losing weight gains. Too much cream can induce diarrhea. Some research and experimentation could improve the results, but always remember, it is usually better to feed even plain milk, than nothing at all. A short cut to a highly studied and highly reliable formula would be to use a powder bitch milk (Esbilac). In addition to the required nutrients, it contains important Vitamins & Minerals. Needless to say, ALL formulas should be fed WARM. You can use the back of a finger or the back of your arm to test the proper temperature, just as you would for a baby. The correct temperature should be approx. 100 degrees F.
When a puppy has the tendency to stay cold despite a warm environment, or when it's digestion is poor, any formula will only make things worse. The digestive tract does not want to work while the puppy's other systems are zeroing in on trying to keep the heart, lungs, kidneys etc functioning. In other words never feed a formula to a cold puppy. Warm sugared water should be fed until the condition is under control. One measure of sugar mixed thoroughly with 9 measures of water is adequate (1:9). In some cases a formula of glucose and special proteins are indicated. Paedialyte liquid for children is available in most drug stores and is one I recommend for even just a bit of dehydration seen in some pups.
Measuring for tube feeding is as follows : First, on the outside mark the feeding tube by using tape or marking pen at a point 3/4 of the distance from the puppy's nose to it's last rib. This indicates the depth of insertion of the tube into the esophagus to assure delivery of the formula directly into the stomach. NOTE: Have an experienced vet or breeder show you how to feed the first few times, until you are relaxed with doing it yourself.
HOW TO INSERT A FEEDING TUBE
For this operation a person alone is definitely capable of doing a perfect job. A table is necessary.
1. Attach the tube to the top of the syringe and draw up the required amount of water/formula through the tube.
2. Put the filled syringe on it's side on the table.
3. Do not wipe the tip of the tube dry, as the remaining milk will serve as a lubricant going down the throat. If a drop forms, it will stay on the puppy's tongue, and will not impair the operation.
4. Make sure that the tip of the tube is straight.
5. Pick up the puppy in your left hand, just as you would for bottle feeding, then slightly open the puppy's mouth, insert the tube just over the tongue, and gently pass the tube over the tongue towards the throat, inserting the tube up to the mark. Sometimes you have to backup several times and push forward again until it goes easily past. The angle of the pup's head is what makes the tube go into the stomach, instead of the lungs.
The throat of some puppies is easier to get past than others. Therefore, in order to get the feel of it, try many puppies, until you find a real easy one. After the throat is passed correctly, you push the tube GENTLY until you touch the bottom of the stomach. Still holding the pup in position, slowly empty your syringe, withdraw the tube, refill and proceed with the next puppy. It is at this point that should the fluid be going into the lungs, you will be happy it is only water, which can be absorbed by the body, whereas a formula would lead to infection! At this point too, we must reassure you. If the tube starts to engage in the windpipe, the pup will show very evident signs of distress. It will struggle much more than usual and it's abdominal muscles will contract. In such an event, pull the tube away, let the puppy rest for 2 minutes, then try again. As long as you are gentle and alert, no damage will result. While practising, always remember that with the tube, you have more to gain than to lose.
Sometimes, a small amount of air gets into the syringe while you introduce it. This does not necessarily mean that you are in the lungs. It can mean that some gases already in the stomach have been evacuated thru the tube. In such a case, however, it is reasonable to believe that digestion is not perfect, and sugared water should be used instead of the regular formula for the first tube feeding.
Feed a very small amount for the first meal, like ½ cc. Then 1 cc should be sufficient for the next meal. After that, you will have to decide according to the rules outlined below. If you feed too much at the beginning, the puppy, not used to digesting your formula, will become rigid and hard, after a few hours. However, the amount fed can be increased relatively fast. When you hold the puppy in your left hand, you can always feel the stomach, and be ready to stop if it gets hard. Also when the pup cries, it usually has enough. Overfeeding is less dangerous after three or four days, and naturally, you cannot expect success if you do not feed enough. To give you some idea, a puppy of a small breed usually can take approximately 3 cc each meal, after four days. However, you must keep in mind that you are competing with the mother for nursing. Some pups do not get any milk from the mother, some get a little but not enough, and some get enough. Therefore, in the last analysis, you must learn to decide on the amount of formula, according to the feel of the puppies. Usually after a while, the litter can rely on the mother alone. If you really exaggerate in overfeeding your pup, it will vomit the whole contents of the stomach immediately. That reaction is not a real indigestion, and you can feed a small amount 30 minutes later. However, as soon as you realize that a pup is getting ready to vomit, turn it upside down for two minutes, in order to make sure that no formula gets into the lungs, then wipe the nose carefully. When the puppies take too long to learn how to suck, it is advisable to milk the mother daily, to insure that her milk production does not stop.
WHEN TO FEED
When pups are born, it is recommended to wait 4 hours before the first meal, but it is also recommended NOT to wait much more than 7 hours before that first meal. Then the ideal frequency of feedings would be every 4 hours. However, to be practical, 5 feedings at 4 hour intervals during the day, and nothing during the remaining 8 hours, gives completely good results. Four feedings at 5 hour intervals is also satisfactory, as soon as the pups are a few days old. Later, this can be reduced even to 3 feedings a day. The formula must be adjusted accordingly (more cream, or if powdered bitch milk is used, a little less water).
This following amounts have been used successfully for Min Pins and Poms 6 CC PER OZ. OF BODY WEIGHT DIVIDED INTO AT LEAST 3 FEEDINGS. ( A 4 oz pup X's 6 cc's = 24 cc's. 24 divided by 3 feedings = 8cc's per feeding).
STERILITY OF SYRINGE & TUBE
A laboratory would probably use a new tube for each puppy for each feeding. Of course that method would be very good, except for the cost. If your kennel is healthy, using the same tube for all the pups saves many of them also. If you do that, thoroughly rinse your syringe and tube with cold and then hot water, before and after each session. You could also have many tubes that you sterilize before each session, and use them over and over. That is naturally the best way to do things. In any event, you will have to decide for yourself HOW close to perfection you want to get.
Sooner or later, you are bound to come across puppies that cannot be saved, tube or not, and some that are hard to save. We highly recommend the reading of all articles on Fading Puppies to keep abreast of new developments in that field.
Some Pups Fail To Grow: Often, because of being born immature; for example: the liver can be too small in proportion to the brain. With the tube, you can sometimes bring these puppies to maturity.
Some Pups: bloat, cry, and get colder and harder. In addition: when they have a protruding red rectum, it is possible that there is incompatibility between the milk and the pups, in other words, the pups get intoxicated by the milk, or allergic to it. In a case such as this, affected puppies must be separated from the mother, and given a glucose formula for a while. If the condition gets better, different regular formulas can be tried gradually. If this occurrence was due to a sickness of the mother, and if she can be treated successfully, the pups can be returned to her later on. Kindly note that when young pups are separated from the mother, you must periodically rub the rectum, penis, and the vagina of these pups in order to insure elimination.
When Pups Have Blue Coloration of The groin: This can mean navel infection, oral antibiotics can be tried in such a case.
A Very Frequent Occurrence is: A generalized infection (Septicemia) antibiotics can be tried, but chances of success are remote.
For All Sick Pups: it is important to recognize the trouble at a very early stage, otherwise it gets out of hand.
In a kennel, the success of the feeding tube is based more on the Prevention, than on the Correction. The main point is that it prevents the puppies from getting weak, with the consequence that they are less vulnerable to different diseases. All this looks complicated on paper, but in reality it is easy. You will quickly discover that you are an expert at tube feeding. Within a day or so of three or four feedings of three or four pups, you will become quite experienced. Every litter you have can benefit from a day or two of tube feedings, if for nothing else, but to just get pups started on the right foot. They'll soon look for it. Mom too!
1 can Carnation Evaporated milk.
2 cans of cooled boiled water.
1 TBSP of liquid honey.
1 TBSP of heavy cream
2 egg yolks
1 envelope of gelatin (optional)
1 dropperful of Vetamino 4X
To Heat: I place a small amount in a small glass or plastic nursing bottle, then place the small glass bottle in another larger bowl filled with hot water. Draw up the necessary amount into syringe and feed your babies. This recipe raised two orphaned Weeskelf Min Pin babies It Works! I also use this formula when weaning pups off the mother.
NOTE: I have the written authorization of the (past) Decary Enterprises out of Quebec to print this Copyrighted information from a booklet that they put together along with the Tube & Syringe kits that they once sold from their Kennels - Sue Caillier - Weeskelf Miniature Pinscher Kennel.
|Heart / Hematology
Causes and controls of cardiac disease by Kim Campbell Thornton © First published in "YOUR DOG", Tafts University School of Veterinary Medicine., Aug 2000. Reprinted w/ permission of the Author.
Lup-dup, lup-dup, lup-dup. That's the sound of a normal heartbeat. As most of us learned in school, the heart operates with a pumplike action. Divided into four chambers-right atrium, right ventricle, left atrium, left ventricle-the heart has four valves that work to keep blood flowing in one direction. The valves open and close, letting blood in and then pumping it out. That lup-dup sound is created from the movement of the valves and the flowing of the blood.
But what happens when valves become diseased or worn? Often, they fall to close completely with each heartbeat, resulting in a backwash of blood. The effect is an abnormal sound called a heart murmur.
The sound a murmur makes depends on when it occurs in the cardiac cycle. A murmur that occurs when the ventricles are beating is called a systolic murmur. A murmur that occurs when the ventricles are relaxed-a period called cardiac diastole-is called a diastolic murmur. Instead of going lup-dup, lup-dup, the heart with a systolic murmur goes lup-shh-dup; a heart with a diastolic murmur makes the sound lup-dup-shh.
LISTENING TO LEARN
Murmurs are graded in severity from 1 to 6, with 1 being the softest murmur that can be heard and 6 being loud enough that it's evident before the stethoscope even touches the chest. Murmurs graded at 4 to 6 can often be felt if the hand is placed at the right spot on the chest. Most murmurs are diagnosed by auscultation, which simply means that the veterinarian listens to the heart with a stethoscope. Although auscultation can indicate the presence of a murmur, further tests are needed to determine its cause and severity. Your veterinarian is likely to refer you to a veterinary cardiologist for these tests.
Depending on the breed, age, and predispositions of your dog, the cardiologist will want to take thoracic radiographs (chest X rays), if the referring veterinarian hasn't already taken them, and run an electrocardiogram and an echocardiogram (ultrasound). The radiographi indicate overall heart size and enable the cardiologist to see the pulmonary vessels in the lung. This allows him to judge the degree of normalcy or abnormalcy resulting from the heart disease. An electrocardiogram shows the heart's rate and rhythm and is useful if abnormal rhythms are detected through auscultation. An echocardiogram provides a precise measure of the thickness of the various chamber walls of the heart and a look at each of the cardiac valves. This test allows the cardiologist to determine the state of the valves and to calculate overall cardiac performance, which is helpful in deciding whether therapy is necessary. Follow-up echocardiograms tell the veterinarian whether or not the therapy is working.
The cardiologist may also check your dog's kidney function. "Renal disease is the most frequent cause of high blood pressure in dogs and cats," says James Ross, DVM, professor of cardiology at Tufts University School of Veterinary Medicine. "The presence of renal disease adds a greater workload onto the heart and can make some cardiac conditions much worse much quicker unless the hypertension is brought under control.
"So it's often advisable to do some screening of blood for buildup of waste products, take a look at some urine, and make sure there's nothing going on there-and maybe check some enzymes that are associated with liver disease and congestion that sometimes develops as the heart falls."For more info, please check out:
von Willebrands Disease
Taken from the September 1994 issue of the Weimaraner Magazine Inherited and acquired von Willebrand's Disease is now recognized as secondary to familial auto-immune thyroid disease. Presently 47 of the 59 dog breeds known to have von Willebrand's also transmit this form of thyroid disease which results in hypothyroidism. The prevalence of both diseases has increased rapidly over the last decade despite the collective efforts of conscientious breeders to test and screen out carriers from their breed programs.
Inherited or Congenital von Willebrands Disease.
This is the primary inherited problem from one or both parents. Carriers of this genetic defect may show no symptoms until some other stress event further comprises the ability of the body to form clots. The most common form of Willebrands is classified as Type 1, and is autosomal or non-sex linked incomplete dominant trait. This means it has variable expression within affected families. Both homozygotes who have inherited a double dose of the gene, one from each parent, and heterozygotes that carry a dose from either parent can manifest a bleeding tendency. Homozygosity is rarely seen because affected puppies usually die during fetal development or shortly after birth. The other types of Willebrands are type II which is rare and usually seen in German Shorthaired Pointers, and type III which is an autosomal recessive disease seen in Scottish Terriers, Chesapeake Bay Retrievers, and occasionally Shetland Sheepdogs (usually when two dogs effected with type I).
Willebrands affects many animals, although few develop severe problems and even fewer die. The bleeding episodes become worse from physical, emotional and physiological stresses and other diseases. Typical clinical signs include: recurrent gastrointestinal hemorrhage (with or without diarrhea); bleeding from the gums, vagina or penis; lameness that mimics eosinophilic panosteitis; still-births or neonatal deaths with evidence of bleeding at necropsy; prolonged bleeding at estrus or after whelping; bruises or blood-filled lumps on the surface of the body, limbs, or head; excessive umbilical cord bleeding at birth; excessive bleeding from toenails cut too short, after elective procedures such as ear cropping and dewclaw removal. Affected dogs may even bleed to death from surgical procedures. Diagnostic tests require specialized assays as routine screening coagulation tests are non-diagnostic. Affected individuals have long bleeding times. Definitive diagnosis is made by finding reduced levels (less than 50%) of the Willebrand factor antigen (vWF:Ag).
Because the production of Willebrands disease in the body arises almost exclusively from the endothelial cells lining blood vessels, any disease process altering the endothelial metabolism and protein synthesis can affect Willebrands levels. Auto-immune disease, especially thyroid disease, can disrupt Willebrands production and function. The disruption causes a secondary, acquired form of Willebrands. A classic situation arises when an animal develops auto-immune thyroid disease later in life. Platelets are small cells involved in helping the body form clots and Willebrands acts on the platelet surface, making it more sticky or adhesive. The disease acts on the platelets, impairing their clotting function. In dogs with the congenital form of Willebrands disease, their bleeding tendency becomes clinically severe when hypothyroidism is present. Frequently, dogs developing thyroid disease have lower levels of Willebrands. Hypothyroid dogs also may exhibit low platelet counts (thrombocyopenia) which can cause mucosal bleeding. Finding low or low-normal levels of Willebrands and/or platelet numbers may be early indications of thyroid dysfunction in your stock.
It is generally impossible with currently available techniques to distinguish between the inherited and the acquired types of Willebrands disease in an individual patient.Therefore, it is important to screen for both Willebrands disease and thyroid function to assess susceptibility to these interrelated disorders.
Recommendations to Breeders
The following recommendations are offered to reduce the prevalence of Willebrands disease.
Blood test animals for Willebrands disease that are related to those bloodlines known to have the problem.
Ideally, all dogs affected by Willebrands disease and carriers of the genes should not be used for breeding purposes. It may not be feasible, however, to remove all carriers from a breeding program. If breeding a Willebrands disease carrier is necessary to preserve important bloodlines or type, breed symptom-free disease carriers to normal mates and blood test the puppies. On average, one half of the litter should be normal and the other half will be carriers.
Do not mate carries of Willebrands disease together. One quarter of the litter on average will be affected "bleeders".
Never breed an affected animal as its puppies are likely to be carriers of Willebrands disease. Also, severely affected females may not survive pregnancy or the postpartum period. Several commercial veterinary testing laboratories offer testing and use validated methods based on the Laurell eletroimmuno assay, radioimmuno assay, or enzyme-linked immunosorbent assay (ELISA) techniques.
Legg, Calve, and Perthes, in 1910, simultaneously and independently described a disease of the hip joint that affected young children and was characterized radiographically by flattening of the femoral head. They speculated that the lesion was a non-inflammatory, aseptic necrosis, possibly caused by trauma. The disease soon became known as Legg-Calve-Perthes disease (LCPD).
Earlier, Waldenstrom mistakenly thought the disease was a tuberculous lesion. He used the term 'coxa plana' to describe the flattened femoral head. Other common synonyms are aseptic necrosis, -avascular necrosis,- and osteochondrosis of the femoral head. LCP disease and coxa plana are the terms most commonly used today.
Schnelle and Moltzen-Nielsen are given credit for describing the first cases of LCPD in dogs having described 12 cases, all in Wirehaired Fox Terriers. Since the early reports, the disease has been in dogs of miniature and toy stature found between three and ten months of age. Some larger breeds are now known to have it but it is more rare.
Affected dogs are presented during the first year of life, usually between 5 and 8 months of age. Lameness in one rear leg, with an insidious onset over several weeks, is the usual history. In some dogs, however, the onset may be sudden. Six to eight weeks may pass before lameness progresses from intermittent limping to continuous carrying of the leg. Pain is easily elicited in the hip joint when the leg is abducted. Mild to severe muscle atrophy, (as in smaller muscle) shortening of the affected leg, and restricted joint movement, especially on abduction of the leg, are common physical findings. The diagnosis must be confirmed by x-ray of the joint.
The age range for the disability was 3 to 13 months with a peak at about seven months from the onset of clinical signs. All the dogs tested were of small breeds usually less than 20 pounds with the following being over represented (for the clinic at the time of testing) Miniature Pinschers, Poodles, Lakeland Terriers, West Highland Terriers, and Cairn Terriers. The right and left legs appeared to be involved equally often and in only 12% to 16% of the dogs were both hips simultaneously affected.
A compromise of the blood supply to the femoral capital epiphysis leads to the necrotic changes that occur with LCPD. Infection, trauma, metabolic and hormonal imbalances, and vascular abnormalities have all been suggested as possible causes for the ischemia. A genetic predisposition must also be considered a factor in the pathogenesis because of the exclusive occurrence in miniature and toy breeds.
ORTHOPEDIC FOUNDATION FOR ANIMALS writes:
Legg-Calve-Perthes Disease (LCP) is a disorder of hip joint conformation occurring in both humans and dogs. In dogs, it is most often seen in the miniature and toy breeds between the ages of 4 months to a year.LCP results when the blood supply to the femoral head is interrupted resulting in avascular necrosis, or the death of the bone cells. Followed by a period of revascularization, the femoral head is subject to remodeling and/or collapse creating an irregular fit in the acetabulum, or socket. This process of bone cells dying and fracturing followed by new bone growth and remodeling of the femoral head and neck, can lead to stiffness and pain.LCP is believed to be an inherited disease, although the mode of inheritance is not known. Because there is a genetic component, it is recommended that dogs affected with LCP not be used in breeding programs.
Breeds at risk for Legg-Calve-Perthes:
Affenpinscher, Australian Terrier, Bichon Frise, Border Terrier, Boston Terrier, Cairn Terrier, Chihuahua, Cocker Spaniel, Dachshund, Fox Terrier, Jack Russell Terrier, Lakeland Terrier, Manchester Terrier, Miniature Schnauzer, Miniature Pinscher, Pomeranian Pekingese, Poodle, Pug, Schipperke, Scottish Terrier, Shetland Sheepdog, Silky Terrier, Welsh Terrier, West Highland White Terrier, Yorkshire Terrier
Legg-Calve-Perthes Treatment Options
The degree of clinical severity of LCP varies, and treatment can vary accordingly. In mild cases, the dog may occasionally resist bearing weight on the affected leg or may exhibit periodic lameness. In these cases, limited activity and treatment with non-steroidal anti-inflammatory drugs (NSAIDs) may be sufficient. In more severe cases as the pain and discomfort experienced increase, the dog may become totally lame and avoid all use of the affected leg. Furthermore, the leg muscles may begin to atrophy after extended periods of non-use. In severe cases, treatment often resorts to excision of the femoral head and neck. By removing the femoral head and neck, the bone on bone contact that is the source of the pain and discomfort is eliminated. Later, through the healing process and with therapy, a new false joint is formed by muscle and tissue, and the dog may have a complete recovery.
MORE INFO AT: http://www.offa.org/lcptreat.html
The patella, or kneecap, is part of the stifle joint (knee). In patellar luxation, the kneecap luxates, or pops out of place, either in a medial or lateral position. Bilateral involvement is most common, but unilateral is not uncommon. Animals can be affected by the time they are 8 weeks of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can be seen to twist laterally as weight is placed on the limb.
Patellar luxations fall into several categories:
Medial luxation; toy, miniature, and large breeds
Lateral luxation; toy and miniature breeds
Lateral luxation; large and giant breeds.
Luxation resulting from trauma; various breeds, of no importance to the certification process.
Numbers 1, 2 and 3 are either known to be heritable or strongly suspected.
Medial Luxation in Toy, Miniature, and Large Breeds - Although the luxation may not be present at birth, the anatomical deformities that cause these luxations are present at that time and are responsible for subsequent recurrent patellar luxation. Patellar luxation should be considered an inherited disease.
Three classes of patients are identifiable:
1) Neonates and older puppies often show clinical signs of abnormal hind-leg carriage and function from the time they start walking; these present grades 3 and 4 generally.
2) Young to mature animals with grade 2 to 3 luxations usually have exhibited abnormal or intermittently abnormal gaits all their lives but are presented when the problem symptomatically worsens.
3) Older animals with grade 1 and 2 luxations may exhibit sudden signs of lameness because of further breakdown of soft tissues as result of minor trauma or because of worsening of degenerative joint disease pain.
Signs vary dramatically with the degree of luxation. In grades 1 and 2, lameness is evident only when the patella is in the luxated position. The leg is carried with the stifle joint flexed but may be touched to the ground every third or fourth step at fast gaits. Grade 3 and 4 animals exhibit a crouching, bowlegged stance (genu varum) with the feet turned inward and with most of the weight transferred to the front legs.
Permanent luxation renders the quadriceps ineffective in extending the stifle. Extension of the stifle will allow reduction of the luxation in grades 1 and 2. Pain is present in some cases, especially when chondromalacia of the patella and femoral condyle is present. Most animals; however, seem to show little irritation upon palpation.
Lateral Luxation in Toy and Miniature Breeds - Lateral luxation in small breeds is most often seen late in the animal's life, from 5 to 8 years of age. The heritability is unknown. Skeletal abnormalities are relatively minor in this syndrome, which seems to represent a breakdown in soft tissue in response to, as yet, obscure skeletal derangement. Thus, most lateral luxations are grades 1 and 2, and the bony changes are similar, but opposite, to those described for medial luxation. The dog has more functional disability with lateral luxation than with medial luxation.
1) In mature animals, signs may develop rapidly and may be associated with minor trauma or strenuous activity. A knock-knee or genu valgum stance, sometimes described as seal-like, is characteristic.
2) Sudden bilateral luxation may render the animal unable to stand and so simulate neurological disease. Physical examination is as described for medial luxation.
Lateral Luxation in Large and Giant Breeds - Also called genu valgum, this condition is usually seen in the large and giant breeds. A genetic pattern has been noted, with Great Danes, St. Bernards, and Irish Wolfhounds being the most commonly affected. Components of hip dysplasia, such as coxa valga (increased angle of inclination of the femoral neck) and increased anteversion of the femoral neck, are related to lateral patellar luxation. These deformities cause internal rotation of the femur with lateral torsion and valgus deformity of the distal femur, which displaces the quadriceps mechanism and patella laterally.
1) Bilateral involvement is most common. Animals appear to be affected by the time they are 5 to 6 months of age. The most notable finding is a knock-knee (genu valgum) stance. The patella is usually reducible, and laxity of the medial collateral ligament may be evident. The medial retinacular tissues of the stifle joint are often thickened, and the foot can often be seen to twist laterally as weight is placed on the limb.
Diagnosing Patellar Luxation - Examination and Certification
The dog is examined awake (chemical restraint is not recommended) and classified by the attending veterinarian according to the application and general information instructions. The veterinarian then completes the application form indicating the the results of the dog's patella evaluation. The application and fee can then be mailed to OFA. The attending veterinarian and owner is encouraged to submit all evaluations, whether normal or abnormal, for the purpose of completeness of data. There is no OFA fee for entering an abnormal evaluation of the patella in the data bank. A breed database number will be issued to all dogs found to be normal at 12 months of age or older. The breed database number will contain the age at evaluation and it is recommended that dogs be periodically reexamined as some luxations will not be evident until later in life.Information obtained with permission from OFA.
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