Portosystemic shunts in animals

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Congenital portosystemic shunts (PSS) is a hereditary condition in dogs and cats, its frequency varying depending on the breed. The shunts found mainly in small dog breeds such as Shih Tzus, Tibetan Spaniels, Miniature Schnauzers and Yorkshire Terriers, and in cats such as Persians, British Shorthairs, Himalayans, and mixed breeds are usually extrahepatic (outside the liver), while the shunts found in large dog breeds such as Irish Wolfhounds and Labrador Retrievers tend to be intrahepatic (inside the liver). [1]

Contents

Acquired PSS is uncommon and is found in dogs and cats with liver disease such as cirrhosis causing portal hypertension, which is high blood pressure in the portal vein.

Symptoms

Symptoms of congenital PSS usually appear by six months of age [1] and include failure to gain weight, vomiting, and signs of hepatic encephalopathy (a condition where toxins normally removed by the liver accumulate in the blood and impair the function of brain cells) such as seizures, depression, tremors, drooling, and head pressing. Urate bladder stones may form because of increased amounts of uric acid in circulation and excreted by the kidneys.

Pathology

Congenital PSS is caused by an anomaly in fetal liver circulatory system development. Normally, blood from the placenta bypasses the liver and goes into circulation via the ductus venosus, a blood vessel found in the fetus. A failure of the ductus venosus to close causes an intrahepatic shunt. On the other hand extrahepatic shunts usually result from a developmental abnormality of the vitelline veins, which connect the portal vein to the caudal vena cava. [2] Thus in the juvenile and adult animal with PSS, blood from the intestines only partly goes through the liver, and the rest mixes into general circulation. Toxins such as ammonia are not cleared by the liver. Most commonly, extrahepatic shunts are found connecting the portal vein or left gastric vein to the caudal vena cava.

Congenital shunts are usually solitary. Acquired shunts are usually multiple, and are caused by portal hypertension in humans or in dogs with liver disease. This is most commonly seen in older dogs with cirrhosis, but may also be seen in younger dogs with liver fibrosis caused by lobular dissecting hepatitis. [3]

Diagnosis

Initial diagnosis of PSS is through laboratory bloodwork showing either elevated serum bile acids after eating or elevation of fasting blood ammonia levels, which has been shown to have a higher sensitivity and specificity than the bile acids test. [4] Various diagnostic imaging techniques are used to demonstrate PSS. Ultrasonography is a rapid, convenient, non-invasive, and accurate method for diagnosis of PSS. [5] Ultrasonographic diagnosis of congenital PSS depends on finding an anomalous vessel either in the liver or just caudal to the liver in the dorsal abdomen, usually draining into the caudal vena cava. Ultrasonography can also be used to estimate hepatic volume and vascularity, and to identify related lesions affecting other abdominal structures, such as urinary calculi. Computed tomography (CT) may be considered when ultrasound expertise is lacking or ultrasonography is considered sub-optimal (e.g. because of the conformation of the patient). Control of respiration and careful timing of CT acquisition after contrast injection is necessary for optimal depiction of PSS. Rectal portal scintigraphy using 99mtechnetium pertechnetate, a technique of imaging involving detection of gamma rays emitted by radionuclides absorbed through the rectum and into the bloodstream, demonstrates the blood vessel bypassing the liver. In certain institutions, scintigraphy is the preferred diagnostic technique, but this leaves the patient radioactive for 24h, which may be inconvenient depending on nursing needs. Portal venography is the definitive method for demonstrating PSS, but is invasive, hence it is best reserved for animals with a known shunt or those considered highly likely to have a shunt that was not detectable by ultrasonography. [6]

Treatment

Surgical treatment is best, when it can be performed. Pressure within the portal vein is measured as the shunt is closed, and it must be kept below 20 cm H2O or else portal hypertension will ensue. [1] Methods of shunt attenuation should aim to slowly occlude the vessel over several weeks to months in order to avoid complications associated with portal hypertension. These methods include ameroid ring constrictors, cellophane banding, intravascular or percutaneous silicone hydraulic occluders. The most common methods of attenuation used by veterinarians are ameroid ring constrictors [7] and cellophane banding. [8] Both methods have reportedly good outcomes in both cats and dogs, although the true composition of readily sourced cellophane has been found to be made from plastics (inert) and not cellulose (stimulates a fibrous reaction). Recently, a commercial supplier of regenerated cellulose based cellophane for veterinarians has been established for use of cellophane banding for portosystemic shunts in dogs and cats. Complete closure of extrahepatic shunts results in a very low recurrence rate, while incomplete closure results in a recurrence rate of about 50 percent. However, not all dogs with extrahepatic shunts tolerate complete closure (16 to 68 percent). [9] Intrahepatic shunts are much more difficult to surgically correct than extrahepatic shunts due to their hidden nature, large vessel size, and greater tendency toward portal hypertension when completely closed. [10] When surgery is not an option, PSS is treated as are other forms of liver failure. Antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The prognosis is guarded for any form of PSS.

Heredity

The intrahepatic shunts found in large dog breeds are passed on in a simple autosomal recessive way, while the extrahepatic shunts of the small breeds are inherited on a polygenic basis [11]

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References

  1. 1 2 3 Textbook of veterinary internal medicine : diseases of the dog and cat. Stephen J. Ettinger, Edward C. Feldman (4th ed.). Philadelphia: W.B. Saunders. 1995. ISBN   0-7216-6795-3. OCLC   28723106.{{cite book}}: CS1 maint: others (link)
  2. ↑ Miller, Jonathan M.; Fowler, J. David (2006-03-01). "Laparoscopic Portosystemic Shunt Attenuation in Two Dogs". Journal of the American Animal Hospital Association . 42 (2): 160–164. doi:10.5326/0420160. ISSN   0587-2871. PMID   16527918.
  3. ↑ Agg, Emma J. (July 2006). "Acquired extrahepatic portosystemic shunts in a young dog". The Canadian Veterinary Journal. 47 (7): 697–699. ISSN   0008-5286. PMC   1482449 . PMID   16898115.
  4. ↑ Gerritzen-Bruning, M. J.; Ingh, T. S. G. A. M. van den; Rothuizen, J. (2006). "Diagnostic Value of Fasting Plasma Ammonia and Bile Acid Concentrations in the Identification of Portosystemic Shunting in Dogs". Journal of Veterinary Internal Medicine. 20 (1): 13–19. doi: 10.1111/j.1939-1676.2006.tb02818.x . ISSN   1939-1676. PMID   16496918.
  5. ↑ Lamb, Christopher R. (1996). "Ultrasonographic Diagnosis of Congenital Portosystemic Shunts in Dogs: Results of a Prospective Study". Veterinary Radiology & Ultrasound. 37 (4): 281–288. doi:10.1111/j.1740-8261.1996.tb01231.x. ISSN   1740-8261.
  6. ↑ Lee, Karla C. L.; Winstanley, Alison; House, Jacqueline V.; Lipscomb, Victoria; Lamb, Christopher; Gregory, Susan; Jalan, Rajiv; Mookerjee, Rajeshwar P.; Brockman, Daniel J. (September 2011). "Association between hepatic histopathologic lesions and clinical findings in dogs undergoing surgical attenuation of a congenital portosystemic shunt: 38 cases (2000–2004)". Journal of the American Veterinary Medical Association. 239 (5): 638–645. doi: 10.2460/javma.239.5.638 . ISSN   0003-1488. PMID   21879964.
  7. ↑ Falls, Emily L.; Milovancev, Milan; Hunt, Geraldine B.; Daniel, Leticia; Mehl, Margo L.; Schmiedt, Chad W. (November 2013). "Long-term outcome after surgical ameroid ring constrictor placement for treatment of single extrahepatic portosystemic shunts in dogs: Long-Term Outcome After Ameroid Ring Constrictor Placement in Dogs". Veterinary Surgery. 42 (8): 951–957. doi:10.1111/j.1532-950X.2013.12072.x. PMID   24118005.
  8. ↑ Cabassu, Julien; Seim, Howard B.; MacPhail, Catriona M.; Monnet, Eric (January 2011). "Outcomes of cats undergoing surgical attenuation of congenital extrahepatic portosystemic shunts through cellophane banding: 9 cases (2000–2007)". Journal of the American Veterinary Medical Association. 238 (1): 89–93. doi: 10.2460/javma.238.1.89 . ISSN   0003-1488. PMID   21194327.
  9. ↑ Frankel, Daniel; Seim, Howard; MacPhail, Catriona; Monnet, Eric (May 2006). "Evaluation of cellophane banding with and without intraoperative attenuation for treatment of congenital extrahepatic portosystemic shunts in dogs". Journal of the American Veterinary Medical Association. 228 (9): 1355–1360. doi: 10.2460/javma.228.9.1355 . ISSN   0003-1488. PMID   16649938.
  10. ↑ Adin, Christopher A.; Sereda, Colin W.; Thompson, Margaret S.; Wheeler, Jason L.; Archer, Linda L. (December 2006). "Outcome associated with use of a percutaneously controlled hydraulic occluder for treatment of dogs with intrahepatic portosystemic shunts". Journal of the American Veterinary Medical Association. 229 (11): 1749–1755. doi: 10.2460/javma.229.11.1749 . ISSN   0003-1488. PMID   17144820.
  11. ↑ Rothuizen, Jan (2002). "Molecular Genetics-Diseases of the Liver. Proceedings of the 27th WSAVA Conference". Vin.com. Retrieved 2021-08-29.
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