More information about Canine Megaesophagus: Much of this was placed by a veterinarian in answering questions from owners, but is ONLY for informational purposes.

All of us wonder why some cases are more easily managed than other. After being on this board for several years, some theories have come to me. I don’t think that megae is just ONE disorder, but, rather, that it can be a syndrome, meaning that there may be several “pieces” to this disorder. Some of the co-existing disorders seem to be pharyngeal achalasia (difficulty swallowing), poor gastric motility, IBD (Inflammatory Bowel Disease) +/- Helicobacter pylori, esophagitis, pancreatitis, dietary intolerance (aka food allergy), LES (Lower Esophageal Sphincter) dysfunction, pyloro-spasm, GERD (GastroEsophageal Reflux Disease), hiatal hernia as well as some other disorders. We should probably cause this “megaesophagus syndrome,” rather than just megaesophagus.

The point of the article was to let people know euthanasia is not their only choice when they are faced with a ME and/or MG diagnosis for their pup. I had several calls from people who had euthanized their pups unneccessarily because their DVM did not know how to treat ME/MG. I also received 2 calls from people whose dogs were having symptoms of ME/MG and they had no idea what was wrong. Both said they were going to print out the article and take it to their vet for review. One person even said they were going to start the vertical feeding before the vet visit.

Megaesophagus is a disorder which affects many species – people, dogs, cats, ferrets, etc. It involves the partial or complete paralysis of the esophagus, the “food tube,” which normally propels the food into the stomach. In general, the esophagus becomes a flaccid (reduced or no muscle tone) tube, which is
incapable of squeezing the food/water/medications into the stomach, allowing anything swallowed to just “sit” in the food tube. When food does not pass into the stomach there is a chance of it “refluxing” (backing up) into the back of the throat and pass out of the mouth (regurgitation) or down into the trachea (windpipe). When it passes into the lungs, aspiration pneumonia can develop. Symptoms include regurgitation (sudden throwing up without any warning; versus vomiting, which usually is associated with retching), weight loss, loss of appetite, aspiration pneumonia and lethargy. Death results from starvation or development of aspiration pneumonia. Most of these symptoms can be controlled and treated if addressed quickly, and DOGS CAN LEAD TOTALLY NORMAL LIVES, with some management techniques. These dogs must be held in a vertical position after eating, drinking or receiving medications, to take advantage of gravity, allowing whatever is swallowed to actually FALL into the stomach. They usually need to be held vertically for at least 15-30 minutes. Dogs with megaesophagus cannot be allowed to eat or drink anything (ie. no treats, no rabbit or goose poop, no surfing the table) without the benefit of sitting vertically.

Megaesophagus has been identified as being genetic in a number of breeds, with the mode of inheritance (recessive or dominant) identified in a number of these. Recessive (as expected) seems to be the most common form, though a few are dominant, which implies different genes are involved in at least
some of these breeds.

Simple recessiveness or dominance are the primarily modes of inheritance for simple traits, and each mode has some specific features, with specific probabilities of inheritance for each, and features that make tentative determination of the mode possible. For a recessive trait, both parents have to have the gene for any offspring to show the trait. If only one parent has the gene, no offspring will show the trait, but some (probably about half) will likely carry the gene, which may then be expressed in some of their offspring (if mated to another carrier of the gene). If two parents both have a recessive gene for a trait (like megaesophagus), then on average, about 1/4 of the offspring will have 2 of the gene and have the trait, about 1/2 of the offspring will have just 1 of the gene and not show the trait but still be able to pass it on, and about 1/4 of the offspring will have none of the gene, will not have the trait, and cannot pass it on. These fractions can vary widely with a single litter, especially a small litter, but are averages for many offspring from many litters. For a dominant trait, one only parent has to have the gene for some offspring to show the trait. In this case, assuming one parent has one of the gene and the other parent has none, about half the offspring will have 1 of the gene and have the trait, and about half will have none of the gene and not have the trait (again, on average, over many litters). Generally speaking, for a dominant trait, the parent with the gene will show the trait (especially if it is a trait that normally shows up shortly after birth). For a dominant gene, if an individual does not show the trait, then the individual probably does not have the gene (unless the trait only shows up later in life, which does happen with some genes). This means that if neither parent shows the trait but some offspring do (especially when the trait normally shows up when very young), then the gene is most probably recessive, which means both parents have the gene, about half their offspring will not have the trait but still be carriers for it, about 1 in 4 will have the trait, and about 1 in 4 will be completely free of it. So the message is this: If neither parent has megaesophagus but some of the pups do (typically about 1 in 4, though this is variable), which seems to be a common case, it is safe to assume a recessive gene. This in turn means both parents and about 3/4 of the offspring carry the gene. The implication of this is that neither parent should be bred again, and both probably should be fixed to prevent any accidental litters. Also, none of the pups should be bred, and hence all should probably be fixed as well. A few of the pups will likely be free of the gene, but until a genetic test is available, there is no way to tell which ones, so the safest thing is just to fix all of them. Also, if the grandparents are around and potentially breeding, they probably should not be bred again either, because probably at least 1 of each pair of grandparents has the gene as well. In this particular case, you may get lucky. If a sister of your dog had megaesophagus, your dog may be just a carrier if it is not displaying megaesophagus, or may not have the gene at all. But even if your dog is a carrier, unless the other parent is also a carrier, presuming a recessive gene (which seems most likely), you will probably have no pups with megaesophagus. Some of the pups could be carriers, which means it might be wise to fix your dog and the pups to prevent spread of the gene, but you may get lucky and not have any pups with megaesophagus.

Megaesophagus can be congenital (born w/ it), genetic (passed from either parent), or acquired (develop later in life). There are some breeds in which it seems to be more prevalent, but, we see it here in all breeds, as well as “mutts.” We usually suggest to consider not breeding either the sire or dam, again. Unfortunately, there are no genetic tests that can be done in most (if any) breeds, at this time, and no way we can provide percentages.

The short answer to your question about surgery to restore function to a megaesophagus is “No.” There are exceptions but they are not for primary, idiopathic mega-e. The reason is that the problem is the ennervation. You can’t fix nerves with an operation, to oversimplify. The exceptions to “no surgery” generally concern when a vascular ring anomaly entraps the esophagus (if done early enough, some dogs regain function), and certain strictures (the latter is generally very risky because once over-dilated, the dog has little hope of survival). Idiopathic mega-e is sadly way too common in GSDs and their mixes, but most dogs are very manageable and with some careful vigilance by their humans, have an excellent chance of a good, long quality life.

In humans, we have an Upper Esophageal Sphincter (UES) and a Lower Esophageal Sphincter (LES). The UES dilates and opens once food passes thru the oropharynx so that it can go into the esophagus. The peristalsis movement of the esophageal muscles then move the food down to the LES. Once the food get to the LES, it relaxes to allow food to pass into the stomach then constricts to prevent food and acid from traveling back up the esophagus. Now if the LES is not working properly, there are surgeries that can be done (however, they are not always permanent). If the LES won’t relax so food can pass thru, causing stasis in the esophagus, then thru surgery the LES can be stretched (or even cut in some patient’s that I’ve known). The other issue with the LES is if it’s too dilated and stomach contents are not able to stay down. Surgery is then sometimes considered to tighten the sphincter muscle. So I’m thinking that if the issue in Barrett is more structural in nature (LES dysfunction rather than true esophageal), then surgery might be an option?!?

The esophagus normally moves food to the stomach by muscular contractions (peristalsis). In ME dogs, the esophagus is enlarged and there are little or no muscular contractions. If the dog is eating on all 4 feet, the esophagus is horizontal, and with no peristalsis, that’s why the food stays in the esophagus and doesn’t get into the stomach. The upper and lower esophageal sphincters keep food and digestive enzymes from coming back up the esophagus from the stomach. During eating the sphincters are supposed to be relaxed but should be contracted when not eating.

Actually as the dog regurgitates and reswallows the food, it gradually becomes more liquified and would eventually make it to the stomach. Chances are good that the dog could also aspirate it and get pneumonia.

The idea for feeding the dog in an upright position is that gravity makes up for the esophagus not functioning as it should. Gravity pulls the food to the stomach. Maybe your dog had an issue with the sphincters not relaxing as they should while eating. I would think the dog would still need to be fed upright to allow the food to reach the stomach. It is possible due to an object causing injury to the esophagus and nerves Esophageal trauma, from foreign bodies or post anesthesia reflux or stomach acid, have been implicated as causes for megae. Most are idiopathic, but, mechanical damage can either cause it, or precipitate
it in predisposed patients.

Basically, the esophagus is a smooth muscle whose function is to move food from the mouth to the stomach. When a dog, person, horse, cat, etc., has ME, the esophagus muscles don’t work as they should. In some they do not work at all and in others there are varying degrees of function. Since the esophagus is not pushing the food down to the stomach, the food simply sits in the esophagus until it “plops” back out. )Please note that there is a big difference between regurgitation and vomiting. Regurgitation is a non-active process, there’s no warning, it’s just there. With vomiting, you generally have some forewarning that something is coming up, the sides tend to heave in and out and the body may rock back and forth before the stomach contents exit with some force.) Without the esophagus pushing the food down into the stomach, the dog is always hungry, eating more and more and more. This results in the esophagus (because of lack of muscle tone) simply stretching out in order to accommodate the food that is going nowhere.

Is there medical literature on the inheritability of this condition? there are a number of dog breeds where it has been verified that megaesophagus is genetic. I don’t know if specific genes have been found yet, but statistical analysis can pretty much verify it in many cases. I do know that some work is being done to find specific genes in some breeds. It is entirely possible that different genes are involved in some of the different breeds, which would probably account for differences in severity and onset shortly after birth or later in life. My personal suspicion that most idiopathic megaesophagus (i.e., without obvious cause, such as trauma or toxins) is genetic in origin. If it is suspected that a particular dog (such as yours) has megaesophagus (any other condition) that is probably genetic, then there are some definite things that can be said, even without having identified specific genes. This is because most genetic traits come in two types, called recessive and dominant. There are occasional cases that are something of a mix of these two types, but the vast majority seem to be one or the other of these two types, so with lack of other data, it is reasonable to assume one of these two types. First, a bit needs to be said about inheritance in general. In any sexually reproducing species on Earth, which includes most higher vertebrates (including ourselves and dogs) and many plant species, an individual will possess two genes for any simple trait, one of these having been taken randomly from the pair the mother had, and the other being taken randomly from the pair the father had. Thus half the genetic make up comes from the mother, and half from the father. However, not all genes contribute equally. The normal condition in Earthly genetics (it might well be different on some alien planet) is that only one of the two genes for a simple trait gets used. There are often different variants of the genes for a particular simple trait, which are technically referred to as alleles. For many types of genes in a species, there will be no variants, because these define the species. But for others, by random mutation, different variants sometimes arise. If some are deleterious, they will tend to be weeded out in time, replaced by more beneficial mutations. So an individual may inherit different variants of a gene type from its parents. As I mentioned earlier, one of these will normally take precedence over the other, so that only this one gets used, and the other is effectively ignored. As I also mentioned earlier, there are rare cases where the effect is some blend of the two different variants. Anyway, a gene variant that takes precedence over another variant is said to be dominant with respect to the other, and the other is said to be recessive with respect to the dominant one. For a dominant variant, you only need to inherit it from one parent to get the effect of the gene (which may be for a positive trait, or something bad, like megaesophagus). Dominant genes are pretty easy to spot, because if one offspring has the condition, then one of the parents should also have the condition. If neither parent has the condition, then the gene responsible is probably recessive. So if a dog has megaesophagus for which a gene is responsible and neither parent has megaesophagus, then the gene is very likely to be recessive. Recessive genes are much harder to spot, because if you only have one copy of a recessive gene, you will not show the trait (such as megaesophagus), but you can
still pass it on. Recessive genes can easily skip generations, which can fool you into thinking things are fine. The nature of recessive conditions is that to have the condition, you have to inherit the gene for it from both parents, so that you have two copies of it. If you have a recessive condition, that also means that both parents carry the gene and can pass it on. If you have two parents, each of which has just one copy of a recessive gene, then statistically about 1 in 4 of their offspring will have 2 of the gene and have the condition, about half will have 1 of the gene and not show the condition but still be able to pass it on, and about 1 in 4 will be free of the gene. However, in a small litter of dogs, for instance, if both parents possess a single gene for megaesophagus, then by random chance any mix of the genes is possible. That is, you might have all carriers, or all free of the gene, or all with megaesophagus, or any combination of the 3, though certain combinations are less likely (like all free of the gene or all with megaesophagus). The point here is, if you have a puppy with megaesophagus which is suspected to be genetic (given no obvious environmental causes), if neither parent has megaesophagus, then the gene is probably recessive, which means that both parents have to be carriers, and about half the litter will be carriers. And, by the luck of the genetic draw, sometimes from breeding these two parents, you might have no pups with megaesophagus, but still many of the pups probably would be carriers. The result is that just because most or all the pups do not have megaesophagus does not mean you are safe. In this case, for safety, neither parent should be bred again. Also, at least until genetic testing is available (hopefully in not too many more years), none of the pups should be bred either, to prevent passing on the gene. Also, if you know the grandparents, at least one of each set of grandparents have to have the gene as well, so for safety, they probably should not be bred again either if they are still around.

The esophagus normally moves food to the stomach by muscular contractions (peristalsis). In ME dogs, the esophagus is enlarged and there are little or no muscular contractions. If the dog is eating on all 4 feet, the esophagus is horizontal, and with no peristalsis, that’s why the food stays in the esophagus and doesn’t get into the stomach. The upper and lower esophageal sphincters keep food and digestive enzymes from coming back up the esophagus from the stomach. During eating the sphincters are supposed to be relaxed but should be contracted when not eating. Actually as the dog regurgitates and reswallows the food, it gradually becomes more liquified and would eventually make it to the stomach. Chances are good that the dog could also aspirate it and get pneumonia. The idea for feeding the dog in an upright position is that gravity makes up for the esophagus not functioning as it should. Gravity pulls the food to the stomach. Maybe your dog had an issue with the sphincters not relaxing as they should while eating. I would think the dog would still need to be fed upright to allow the food to reach the stomach.