insussusception --i have the pup 1 week now this - Page 4

My pup had an intrasussception at 7 months, she had not ingested anything nor had she parasites, the veterinary surgeon felt it was the food she was eating that caused the inflammation that led to the telescoping of the bowel into itself. The surgeon then plicated her bowel after correcting the intrasussception, stapled the entire length of her bowel to the lining of her gut, because as he was fixing the initial intrasussception, he said he could see it starting again in a different spot. Then he kept her on plain rice & a little boiled chicken for a week, & kept her sedated on tramadol for 7 days, to SLOW the motility of her gut. If you go to the site of the American College of Veterinary Surgeons, they list statistics for reoccurrence; if you follow the route of plication, very conservative feeding, keeping the dog on a limited activity while on sedation, & the 7 days of sedation to slow the bowel down.....the risk of re occurrence is almost nil. Yes, a major & very expensive surgery. Heritable? I don't know, but I won't breed her anyway, because of it. And the irritating dog food? The ingredient that the surgeon stated was "very poorly tolerated by some dogs" is beet pulp. Read your labels, it's in some very costly foods. Also, the surgeon said that young dogs, under 1 year of age, do poorly if the bowel has started to necrose, even if that section is removed. The reason he stated was that the bowel's dying tissues release an enzyme that start a cascade of events that challenge the dog's immune system the same way sepsis or a heart attack would, & younger dogs are less equipped to deal with that situation. He recommended that my girl be put to sleep should her bowel be necrotic, but we were lucky. Her bowel was just starting to turn purple, once straightened out, it pinked back up immediately, thus limiting the damage done. Still, we really couldn't afford the $4000.00+ this cost us. I'm sure no one who buys a puppy expects to have to ante up this kind of money days to months after bringing home a puppy.
Wouldn't it be great if you could predict these things? I know no breeder wants to breed a puppy that brings such heartbreak.....we sure didn't! Our puppy was from our own litter. Hopefully we will be able to know if this is heritable someday soon, & have some sort of screening for it. I think it has to do with the ratio of depth of chest to narrowness of waist.
But, anyway, this is long winded, but I want to get the word out on BEET PULP in dog kibble, & on the route of care that best treats intrasussception, so that fewer must go through this, & those that do have better outcomes!
jackie harris

Ok, so the vet suspected intussusception, but the ultrasound showed the problem was ME. That makes sense. I'm sure the necropsy will validate the diagnosis of ME.  I sure hope the breeder will replace Kotch with another pup of equal quality when your cousin is ready. Of course we can never truly replace a precious much loved pup :( , but I think you know what I mean.

Intussusception — In very young pups (and other animals including humans) the intestine can invaginate (one part slips inside another). The condition, also referred to as “telescoping intestines”, also occurs in adults, but not as frequently. Most common immediate causes include worms, obstruction by indigestible materials, garbage, or toxic substances. The German Shepherd seems to experience a high incidence of this disorder and I believe there is a genetic propensity, a familial trait, in certain bloodlines.

 Esophagus Affliction— Congenital esophageal achalasia is also known by many other names such as cardiospasm, megaesophagus, dilated esophagus, and ectasia. The disorder appears to be caused by a simple autosomal recessive in German Shepherds, although it is highly variable in expression. After briefly consulting me, genetics worker Danielle LaGrave wrote an article for the November 2002 GSDCA Review on this subject, and concluded, “I had hoped to have a definitive answer as to how megaesophagus in the GSD is inherited. But regrettably, I was unable to.” My example of a pedigree study in “The Total German Shepherd Dog” (www.hoflin.com) apparently was not convincing enough for her. While reportedly only about one percent of the dog population may be involved, mortality rate in pups is fairly high. Even when PRAA (Persistent Right Aortic Arch) has been ruled out as the cause, I believe the percentage in German Shepherds is quite a bit higher than that reported one percent. Correspondents in the late 1990s have given me testimonial comments that they believe the incidence is on the rise, but this, too, may be more a matter of greater awareness. This abnormally large and flaccid “food-pipe” between the mouth and the stomach can be found in adults, but the most heartbreaking and serious cases are in pups early in the weaning and solid-food stage. The ballooning out reminds one of the extensibility of a pelican’s pouch. The more severe the expression, the earlier it manifests itself.

GSDs, Goldens, and Irish Setters seem most at risk, and if a pup survives to adulthood, the condition often causes or is associated with other esophagus problems, peripheral neuropathies, gastric dilation with or without torsion, and especially myasthenia gravis. Even in adults, many are euthanized or asphyxiate, due to progressive malnutrition, aspiration pneumonia, vomitus obstructing the air passage, and owner frustration over the regurgitation. Most adult cases that are presumed to be acquired have no cause discovered, which leads me to believe it is simply a milder form of the genetic problem that causes death by starvation in most pups between 5 and 8 weeks of age. Some veterinary references, however, stoutly consider these genetically/environmentally different disorders. A loss of peristaltic action is probably due to a disorder of the afferent nerves. This is why there is no successful medical, pharmaceutical, or surgical treatment. There may be a connection with other nerve disorders, even giant axonal neuropathy, which mimics HD and GSD myelopathy. Some have gone so far as to hint that a general immune system deficiency is at the root of this problem, as it appears to be in so many disorders: pannus, Demodex susceptibility, DM, and more.

Symptoms of megaesophagus include slow or halted growth, weight loss, dehydration, water in the lungs, and persistent and progressively worse vomiting of food minutes after swallowing. The disorder usually is detected at or