We have written about percutaneous coil embolization before; here is a first-hand report from the owner of a Deerhound who has undergone this procedure.
Bile-acid testing for all Deerhound puppies is an SDCA Recommended Health Test so no buyer unknowingly purchases a puppy with a liver shunt. Because there is no genetic (assuming it is genetic) test available for this condition in our breed, for now, Deerhound puppies with liver shunts will still be produced. The good news is there are now several treatment options available, two of which—medical management and percutaneous coil embolization—are discussed in this article. Thanks to these treatments, many Deerhounds with a shunt no longer need to be euthanized and can live happy and healthy lives. – Ed.
By Tara Denholm
The summer of 2017 was the right time to bring a new puppy into my home. My senior dog, a lurcher-setter, was turning ten. I hoped a new pup could join the family while he was still young enough to be a good mentor. I wanted a sighthound and hoped it could be a Deerhound.
Amazingly, there was a litter of Deerhound puppies on the AKC website. I talked to the breeder, got lots of pictures of the pups, mom, and dad. There were three males available. I chose the smallest boy with the big, serious, dark eyes. When he was 13 weeks old, the breeder drove him out to me in Idaho and his brother to a new home in Washington. He was much smaller than his littermate, but he was my perfect puppy.
Rowan was a good, affectionate puppy. He was smart and easy to train, but he was less playful and energetic than I would have expected. When losing baby teeth in November, his lower baby canines persisted and my vet said they needed to be removed. His liver levels were a little elevated, which she said was unusual for a puppy, but not too high to cancel the surgery.
In January he started growing really fast, and I switched to a higher protein large-breed puppy food. That is when his first symptoms occurred. Rowan was pacing, crying, and digging at his bedding. It was Saturday night, so I went to the emergency vet, afraid it was gastric torsion. They took x-rays and there was no sign of bloat or internal injury. They gave him a very small dose of a sedative and we went home. He was drunk-wobbly and restless for a few hours, then symptoms subsided.
It happened again shortly afterward. He had been getting freeze-dried liver training treats and cooked chicken with his supper. I did not know it at the time, but that extra protein triggered a severe episode of hepatic encephalopathy (HE). Rowan woke me up crying and pacing at midnight. He peed the floor. He was biting the kitchen table legs and chewed through the power cord to my computer while I wasn’t looking. He bit my phone and cracked the screen. He kept digging at the floor and circling, following the wall, and pressing his head into the corner. I took him outside to potty and realized he could not see where he was going or hear/understand me. I was terrified he had been poisoned and was going to die on me. It was 6:30 AM Monday. I drove straight to the vet and went in as soon as they unlocked the doors.
My vet saw us right away. She immediately suspected a liver shunt. When they took him in back, I started researching: A liver shunt is an abnormal blood vessel or vessels that allow blood containing waste from the digestive system to bypass the liver and circulate in the body. His HE symptoms were being caused by ammonia from his high-protein diet entering his brain and causing neurological problems. My vet treated for HE with lactulose orally, lactulose enema, subcutaneous fluids, antibiotics, and an anticonvulsant.
The diagnosis was confirmed with a bile acid test: In a healthy body, bile acids are absorbed by the liver after digestion. If bile acids are in the bloodstream in high levels, it indicates shunting. The vet gave me the worst-case scenarios, a grim prognosis of a liver shunt either with or without surgery. She planned a consultation with a specialist at the University of Washington. Rowan was put on lactulose, amoxicillin, metronidazole, and prescription low-protein liver food.
Plans were made for an appointment and CT imaging at UW. I learned more about shunts. I joined a Facebook support group with other people with shunt dogs. Their prognosis was better than the vets’. I learned that many dogs now thrive on medical and nutritional management without surgery. (There are, however, different types and severity of shunts, and not all are treatable with only medical and nutritional management.)
Rowan’s scan showed a very large intrahepatic shunt. The surgeon at UW discussed different surgery options and medical management. I was informed of the dangers and common complications of surgery and the statistical survival rates of each option. We decided that endoscopic coil embolization provided the best chances for Rowan to make a recovery and have a long life.
We had to wait for surgery until Rowan was larger so that the stent being put in his vein would still be the right fit when he was full grown. In the meantime, Rowan was a new dog! He was thriving on the low-protein prescription food and meds. I supplemented with rice, goat yogurt, and milk thistle. He gained nearly 30 pounds in two months, with no more HE episodes and lots more energy and feistiness.
His surgery was two weeks before his first birthday in May. Coil embolization was performed by the UW surgeon under the supervision of Dr. William Culp from UC Davis, who is one of the pioneers of the procedure. Twelve coils were inserted through his jugular vein into the shunt, behind a mesh stent in his vena cava. The procedure only took a few hours, and I was able to spend time with him after he came out of anesthesia. They kept him overnight in the ICU to observe for post-surgery complications.
At home, he remained on keppra and amoxicillin for a few weeks, weaned off of them, and stayed on a lower-protein diet with lactulose and metronidazole for a couple more months. By August he was nearly 80 pounds, running fast, and really becoming quite a dog. We transitioned slowly to a typical diet with no antibiotics over the next couple of months.
In February of the next year, he had another HE episode that was severe and needed a trip to the vet. This meant that although the surgery had gone very well, there was still some shunting—maybe only a small shunt—that still would have to be managed. Instead of prescription food, I consulted with a veterinary nutritionist, and we developed a half homemade, half low-protein kibble diet with lactulose, Sam-e, and milk thistle supplementation.
This is the diet he has been on ever since. He has occasionally had mild HE symptoms but very rarely, and only after eating something he really shouldn’t (e.g., cat litter). As of his last vet visit in 2020, all of his blood levels are in normal range.
I am very grateful for the veterinarians who diagnosed and treated him and saved his life. Rowan is happy, active, and funny. He has completed CGC and therapy volunteer training courses. He is still small, under 80 pounds, and definitely not a show dog. He is perfect in my eyes. It may be possible to have his shunt surgery updated in the future by adding more coils. At this time, I have decided to forego more surgery and continue with a careful diet, supplements, and enormous amounts of love.
Veterinary science has not yet determined whether intrahepatic shunts have a heritable genetic cause, are a developmental defect caused by environmental factors, or a combination of both. My breeder did not have another litter with Rowan’s parents. She was very supportive, reimbursed me for his purchase price, and helped with the cost of his surgery.
I would be happy to talk and share resources with anyone who needs fellowship or support with their own shunt dog. Please contact the page administrator, and she will forward your message.