|Symptoms||What happens||Possible causes||Treatment||First Aid Treatment|
This is a condition which occurs mostly in large and giant breeds of dog, in which there is a build-up of gas in the stomach and in which in many cases the stomach twists, closing it off from the oesophagous and the intestines, which leads to pain, shock, pressure on the heart/circulatory system, necrosis of stomach tissue, and death. It is an absolute emergency that requires instant veterinary attention/surgery. A delay of only twenty minutes can be too long for survival.
The symptoms are: retching with no vomiting of stomach contents but frequently with thick white froth (like whipped egg white) produced. The dog is restless and uncomfortable, either standing or pacing about and unwilling to lie down. If he does finally lie down it is not a sign that the condition is improving but that shock has set in and death is imminent. The stomach area is usually (but not always obviously) enlarged and hard. The cause/s are not yet known but possibilities have been suggested as vaccines (particularly multivalent modified live virus vaccines), processed foods, feeding only once a day, exercising too close to a meal, giving calcium supplementation to puppies, or rearing puppies on low calorie or poor quality complete foods, foodstuffs infected with gas forming organisms such as clostridia, feeding foods high in saponins, and air swallowing. There is ongoing research into this disorder in the U.K. and in the U.S.A.
The official list of symptoms are 1) after midnight; 2) excessive salivation; 3) unproductive retching; 4) rapid swelling of abdomen; 5) appears in discomfort; 6) breathing difficulty; 7) collapse of circulation; 8) pale gums, mucus membranes in mouth, tongue; 9) rapid heart rate; 10) weak pulse.
One of the major problems is the spleen, which is attached strongly to the stomach and so moves with the stomach if that organ rotates. This may tear blood vessels, which causes necrosis of areas of the stomach wall. This leads to peritonitis. In the early days of GDV, it was thought that the spleen was the cause of the stomach twisting and so the spleen was nearly always removed. It was then discovered that the spleen was carried with the stomach, not the propulsive force, and so it is now left whenever possible. Especially since it has been realised that the spleen is an important part of the immune system and not the unnecessary appendage it was previously thought to be.
A breeder in the USA of Standard Poodles ran into major problems with GDV in the early 1980s, when vaccines were produced in modified live virus form rather than the killed form previously used. When she stopped using the multivalent mlv vaccines and went on to killed vaccines given separately (as suggested by Dr. W. Jean Dodds), the episodes of GDV stopped.
One suggestion for a possible cause of GDV is soya, found in large amounts in many commercial feeds. Another is dry food expanding in the stomach; another is the large amounts of carbohydrates from grain products (as well as such fillers as sugar beet pulp) in commercial feeds which slows down digestion and allows fermentation to take place, and may cause dietary intolerance. Saponins are contained in common dog food ingredients such as soya beans, beet pulp, alfalfa, peas, beans, and oats. When mixed with water and shaken saponins create a dense foam with a very high surface tension - like shaving cream - which traps the gases produced by normal fermentation of the food during digestion. Saponins are also toxins which suppress the vomiting reflex and can paralyze the gastrointestinal tract.
Because of the large size of their molecules, saponins are not readily absorbed from the intestines and usually only produce local effects such as irritation and inflammation of the intestines, although this can be severe enough to lead to death. Stool hardeners added to commercial foods, such as beet pulp, sodium bentonate, or cellulose flour, could compound the risk of bloat caused by saponins because they slow the passage of food and fibre through the large intestine.
Research has been carried out into the possibility of the feeding of calcium supplements to puppies predisposing them to getting GDV later in life. It has been shown that calcium stimulates the production of a hormone called gastrin which has the effect of decreasing gastric emptying and, via a knock-on effect, interferes with the tone of the sphincter muscles at either end of the stomach, thereby upsetting proper stomach emptying and belching to release gas build-up. It has been shown that dogs that bloat have too much gastrin present quite some time before they bloat and not just afterwards. This suggests that excess calcium in the diet increases the risk of bloat.
Note that the suggestion is only that calcium supplementation increases the risk, not that it is the main cause, and there are many experts who feel that no one cause is likely to be found, either because there are different causes for the condition in different dogs, or that the cause is multi-factorial.
Another possible cause for GDV that has been put forward is the feeding to puppies of a diet of low caloric value such as a complete feed intended for maintenance of adults, or a feed of poor quality which results in excessive stools and gastric distension because the puppy has to eat larger quantities in order to increase its energy intake. Gastric distension in conjunction with the puppy's normal physical activity stretches the gastrohepatic ligament resulting in laxity of the stomach's suspension which is a necessary prerequisite for bloat/torsion and could predispose the puppy to the disorder later in life.
The usual procedure for treating GDV is to first decompress the stomach, usually by passing a stomach tube. If the tube cannot be passed into the stomach, then the stomach has twisted (torsion, or the volvulus of the main title), but even if the tube can be passed it does not necessarily mean there is no torsion. Gas (and fluid and any food) is released from the stomach by means of the tube, or, if the tube cannot be passed, a hollow needle is put into the stomach from the side in order to release the gas and other stomach contents and allow time for the hound to be stabilised. The second priority is to treat for shock and stabilise the system as much as possible. Shock therapy involves giving a large volume of fluid, also steroids and antibiotics, and treating the heart.
In a trial at Ohio State University, funded by Morris Animal Foundation, William Muir DVM PhD found that hypertonic saline solution showed great promise in treating shock in dogs with GDV. The treatment originally was used on burn victims and wartime casualties to replace fluids. It had dramatic results on the dogs in the trial, enabling them to be taken to surgery more quickly than when given the usual lactated Ringer's Solution, and the sooner surgery can be carried out, the better the chances of survival. Dr. Muir says that 99% of the time it is shock that kills a dog affected with GDV, and being able to improve the treatment for shock has made an enormous difference in the mortality rates, which used to be 60% but are now less than 25%.
SURGERY IS NO SUBSTITUTE FOR INADEQUATE SHOCK THERAPY!
If the stomach is twisted then surgery has to be carried out to untwist it and put it back in its normal position, to remove any necrosed tissue, and to stitch the stomach on both sides. This procedure is called gastropexy. It has been found that if the stomach is only stitched to the abdomen on one side, in time the attachment stretches and the stomach can twist again. Performing gastropexy has been found to increase survival rates from a median of 188 days for dogs not given this treatment to 547 days for those that are.
It has to be said that many dogs do not survive GDV, and that most who do will have another episode.
Some researchers believe that many dogs which get GDV die not from the initial shock and blood-flow stoppage, but from reperfusion injury. This is the term for chemical damage that occurs in a tissue when oxygen-rich blood returns to tissues that have been temporarily deprived of a blood supply, as in a dog being treated for bloat/gastric torsion. When the dog's blood flow is re-established and the oxygen-rich blood returns to the blood-starved tissues, poisons known as toxic oxygen radicals are released, resulting in reperfusion injury.
It is of major importance to get any dog which even may be starting with GDV to the vet immediately, as proper treatment as soon as possible is essential. It is sensible to telephone the vet to say you are on your way, so they can carry out any necessary preparations before you get there so as to avoid any delay in starting the treatment.
However, if possible while on the way to the vet it could help to carry out the following procedures:
There is an acupressure point that has been found to work very well on dogs caught early in the GDV sequence, i.e. when they first start bloating. See here for more information - http://www.iwane.org/acp_point_v2.htm
Spraying the dog with Rescue Remedy, and taking some yourself, can help deal with the stress.
We had only one incident where an Irish wolfhound started showing signs of developing GDV. Having 'phoned the vet to tell him I was bringing her in immediately, I gave her a dose of the two homeopathic remedies suggested to me by homeopathic vet George MacLeod and which I kept in my First Aid pack, which were Colchicum and Colocynthis. I gave her a second dose on the way to the surgery and a third as I got her out of the car when we arrived. By the time we got into the surgery the obvious symptoms - bloated abdomen, arched back, moving wide in the rear with short steps, and so on - had disappeared and the vets could find nothing wrong, although they kept her in for a few hours to make sure she was okay. This was before I'd even heard of acupressure, so I didn't know about the acupressure point.
So is there any way to prevent it? As with heart disease and many other health problems, the skeletal system plays a major role in the proper function of the digestive system, so having your dogs checked regularly for skeletal misalignments with therapies such as McTimoney Chiropractic could be a major step in preventing GDV. An interesting article can be seen here - http://peterdobias.com/community/2011/05/stomach-bloat-gdv/. The website for the McTimoney Animal Association in the U.K. can be found here - http://www.mctimoney-animal.org.uk/
Certainly it is sensible not to exercise after feeding (although some dogs have developed GDV when they have not eaten for a day or longer) but to allow at least two hours between feeding and exercising. It is not considered necessary not to exercise before a meal, but it would probably be more sensible not to feed immediately following strenuous exercise, as stress has certainly been found to be at least a trigger for GDV in some cases. It would also be sensible to feed dogs of breeds prone to GDV at least two meals a day to avoid over-stretching the stomach.
It is also considered by some researchers that gulping food down very quickly predisposes to GDV, as it can lead to air swallowing. This is apparently particularly common in the Irish Setter. Suggestions were that any dog that does this should have its bowl raised to shoulder joint height and a brick or two put into its bowl so that it has to pick out its food from around the brick and cannot gulp it down.
However, after several years of more people with at-risk breeds feeding their dogs from raised bowls, what has come up in the statistical research is that a large proportion of dogs that get GDV are fed from raised feed bowls, which has now brought about the suggestion that raised feed bowls are a cause of GDV. To my mind, it would seem more sensible to view it that raising feed bowls has no [or few] benefits in preventing GDV, because, if you take it that anything that is done in many cases has to be a cause, then the main cause would have to be being fed by a human.
Purdue University research in 2009 found that giving dry food containing fat among the first four ingredients, and dry food listing citric acid as a preservative, especially if such food was moistened prior to feeding, brought about an increased risk of GDV. They also stated that water should not be restricted, as dogs that were so restricted before and after meals were more likely to develop bloat/gastric torsion.
When we first started in wolfhounds in 1968, we did hear about cases of bloat but only rarely and then it always seemed to be the dog that had raided the horse nuts or the chicken feed. In those days most people fed raw meat/tripe and table scraps and wholemeal biscuit or bread. It does seem that the disorder has increased alarmingly since the vast majority of dogs are fed on commercial foods, especially the dry foods. Giving digestive enzymes with each meal or snack could help, and giving live yoghurt (preferably sheep's or goat's milk yoghurt, as these are more easily dealt with by dogs than is cow's milk) or some other form of probiotic on a regular basis could also be helpful. However, some dogs do well on dry complete foods, so it really is a case of finding out what is best for each individual animal.
Unfortunately there is no one diet that is going to be best for all dogs. Some dogs will benefit from the raw diet, some from other types of diet. But, the inclusion of cheap fillers, and stool hardeners in commercial foods should be avoided as much as possible.
It seems very possible that food intolerance could play a part in the causation of GDV, and it has been found that many dogs that have an adverse reaction of some sort to meat can eat raw meat without any problem. Avoiding diets that contain soya would also be sensible.
Studies have been made of various foods given to dogs that have suffered episodes of GDV but nothing has really come of this so far, except that dry food has a question mark over it. However, it does seem that in all cases the diet was based on either canned, dry, or homecooked food. No researcher I have questioned has been able to tell of a dog fed a raw food diet which has developed GDV, although I have heard of one dog (a GSD) which did get bloat/torsion after starting on the raw diet, but following a meal in which he was given quite a large quantity of green beans. Beans are very gas forming.
What of vaccination being a cause, or part of the cause? It is impossible to tell, but is a possibility. See under vaccination. There was a breeder in the U.S.A. of Standard Poodles who had major problems with bloat in her dogs when multiple modified live virus vaccines started to be given as a matter of course. When she stopped giving these vaccines and followed Dr. W. Jean Dodds' vaccine protocol of giving only single killed vaccines she stopped getting bloat in her Poodles.
|The Irish Wolfhound Health Group (UK) page on bloat|
|Purdue University's bloat page|
|Detailed page on GDV with list of emergency bloat links|
|The Whole Dog Journal feature on bloat|
|The Healthypets.mercola.com page on GDV|
|The site for Canine Health Concern|
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The common term for this condition is night blindness, because that is the first thing that happens with this condition - that the dog cannot see at night. There are two types of PRA - early onset and late onset and Irish wolfhounds are affected by the early onset type, which means that they start to go blind at around two years of age. They end up totally blind.
In 2005 there had only been six known cases of PRA in the breed in the UK but breeders have been providing blood samples for research into the genetic marker for the disorder, and having breeding stock eye tested in an effort to deal with the problem before it becomes more widespread.
First signs are often a change in behaviour, with the hound becoming nervous and jumpy. They can be especially twitchy about other animals, people, and so on coming upon them from behind, because one of the earliest degenerative effects in the eyes is to cut out peripheral vision. Thus they don't see approaches from the side or behind until they can feel/hear the presence. The sight gradually deteriorates over a period of months until they cannot see at all. Some hounds are totally unable to cope with this and have been euthanased as the kindest option.
The British Veterinary Association and the Kennel Club have a joint testing scheme, but, although having breeding stock tested is a sensible course, it will only find affected animals not carriers. A search is being made for the genetic marker for the condition so that carriers can be discovered by a blood test. The genetic marker has been found in other breeds, such as the Corgi, but appears to be different for each breed.
The following report was made in March, 2001 to the Irish Wolfhound Club by Dr. David Sargan & J. Aguirre Hernandez of University of Cambridge Centre for Veterinary Science:
Early onset Progressive Retinal Atrophy in the Irish Wolfhound appears to have emerged quite recently. The disease shows clear autosomal recessive inheritance. Individuals affected are members of two related pedigrees. We have 5 affected and 4 obligate carrier individuals in a total of 102 samples, most of which are related to these two central pedigrees.
To find the cause of PRA in the breed we have first used "the candidate gene approach". This has allowed us to rule out 9 genes which cause PRA in other breeds or retinitis pigmentosa (RP) in man. This work is continuing. We have also investigated the possibility of performing 'parametric linkage analysis' to use microsatellites to identify the gene. Because of the family structures involved, this technique will not work. Instead we are beginning a study using 'homozygosity analysis' to which the samples lend themselves better.
As yet we do not have the cause of the defect.
We have 102 blood samples from Irish wolfhounds, of which 41 have come in the last two years. We have 5 affecteds: Bokra Dixie, Bokra Hope, Bokra Honesty, Foresight Diva, and Westmount Clint-Axel, 4 obligate carriers and many sibs of both affecteds and obligate carriers.
2. Candidate genes
We have surveyed the following genes for mutation:
|Opsin (mutated in many human retinitis pigmentosa families||Method GC heteroduplex and SNP|
|Transducin alpha (occasionally mutant in RP)||Method SSCP|
|PDE alpha (mutant in corgi PRA)||Method SSCP and microsatellite|
|PDE beta (mutant in Irish setter and Sloughi PRAs)||SSCP in progress|
|PDEG (mutant in a gene knock out mouse model)||Method - sequence|
|CNGC alpha (mutant in some RP)||Method SSCP|
|Peripherin/rds (mutant in rds mouse model and some RP)||Method SSCP|
|Rom-1 (mutant in some RP)||Method SNP|
|SAG (mutant in human congenital stationary nightblindness)||Method sequence|
|Phosducin (mutant in some schnauzer PRA)||Method SSCP (incomplete dataset)|
So far all of these attempts have resulted in exclusions. That is to say that we know that the disease is not caused by mutation in these genes. (For phosducin and PDEB the work is still incomplete).
Fortunately the work on human RP has proceeded fast and given us other genes to look at.
3. Parametric linkage analysis.
Originally we hoped to use this method in which polymorphic markers are followed through pedigrees to see if any are always found with the disease. In order to detect such a linkage and to prove that it has not occurred by chance, we calculate a probability known as the LOD (likelihood of disequilibrium) score. We can perform computer simulations within pedigrees from which individuals are missing to see whether we would be able to detect linkage between a marker and a disease locus, assuming that it was present. This is possible when LOD scores above 3 can be generated within the pedigree. JAH has performed a total of 1200 simulations done this way on the Irish wolfhound PRA to see whether we could find linkage given the small number of obligate carriers which we have sampled. This has shown that the dataset has crucial gaps. It can only perform exclusions (showing that a marker is not linked to the defect) and then only when the marker is quite close to the disease locus. It cannot prove linkage, since a LOD score of three cannot be reached by the data set. Hence we have abandoned this technique for this disease.
4. Homozyogisity analysis
This works on a different principle. The markers are not followed within families. Instead, all affected animals are grouped and analysed together and all other non-affected are also grouped and analysed. The principle works well in this case because all dogs affected by the disease are closely related and hence will share a region of DNA around the mutation site whch is said to be "identical by descent". They are homozygous (have two copies of the same DNA) at the mutation site if affected by the disease but, if not, may be normal or carriers and hence will have more than one type of DNA present. We simply use polymorphic markers and look for those which are homozygous in affected animals but heterozygous in normal/carrier animals. These define regions of the DNA in which to look for candidate genes. The number of candidates is thus restricted. This method needs very polymorphic markers at frequent intervals on the chromosomes, and hence requires work on the map.
Much of our current work is in this direction.
|The Irish Wolfhound Foundation page on PRA|
|The PetEducation site PRA page|
|Candidate Gene Studies in Canine Progressive Retinal Atrophy|
|The Animal Eye Care page on PRA|
|The Canine Genetic Diseases page on PRA|