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Kamila Gliriska-Suchocka, Krzysztof Kubiak, Urszula Paslawska, Marcin Jankowski, Jolanta Spuzak, Pawel Jonkisz, Jakub Nicpori, Krzysztof Simon* ®
Department of Internal and Parasitic Diseases with Clinic for Horses, Dogs and Cats, Wroclaw University of Environmental and Life Sciences, Poland.
*Department of Infectious Diseases Wroclaw Medical University, Poland.
PORTAL RADIOGRAPHY IN A DOG WITH PORTOSYSTEMIC SHUNTS -
CASE REPORT
Abstract
One of the most frequently described diseases of the liver vascular system is a portosystemic shunt [PPS].
Key words: dog, portosystemic shuts, portography
Introduction
Portosystemic shunts are abnormal vascular connections between the hepatic portal vein (the blood vessel that connects the gastrointestinal tract with the liver) and the systemic circulation. Such anomalies cause blood in the gastrointestinal track to be diverted past the liver, there by limiting the liver's vital functions in metabolism and detoxification of compounds and the body's defenses against intestinally derived pathogens. Congenital shunts occur more commonly in purebred dogs than in mixed breeds; miniature schnauzers, Yorkshire Terriers, and Irish Wolfhounds appear to be at increased risk. Extrahepatic shunts are most common, accounting for 61% to 94% of congenital shunts, and are typically seen in small breeds of dogs, such as the Miniature Schnauzer and Yorkshire Terrier. Intrahepatic shunts represent between 6% and 40% of congenital shunts and are more common in large and giant breeds of dogs such as Irish Wolfhounds and Golden Retrievers. Dogs with congenital portosystemic shunts are typically less than 1 year old. The severity of clinical signs varies and is related to the anatomic position of the shunt and the fraction of portal blood that is shunted past the liver. The basic examination allowing the determination of a portosystemic shunt location and type is a contrast examination of the liver vascular system - angiography, portography.
Task, the aim of the article
This report describes the diagnosis of a portosystemic shunt in yorkshire terrier with episodes of hyperactivity, weakness, vomiting and loss of appetite.
Material and methods
This study is the case presentation of the female yorkshire terrier marked aged 11 months. The examinations were performed as follows: the history and clinical examination, abdominal USG, blood examination (erythrocyte count, hematocrit value, hemaglobin concentration, leucocyte count with leucogram, thrombocyte count and erythrocyte indices, urea and creatinine concentration, activity of alanine aminotransferase [ALP], asparagine aminotransferase [AST], alkaline phosphatase
® Kamila Glinska-Suchocka, Krzysztof Kubiak, Urszula Paslawska, Marcin Jankowski, Jolanta Spuzak, Pawel Jonkisz, Jakub Nicpon, Krzysztof Simon, 2008
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[AP], y-glutamylotransferase [GGT], amylase and lipase concentration of total bilirubin, ammonia, total protein and albumins). Next dog underwent the angiography of the liver vascular system. Prior to the examination the animals were subject to 24 hour fasting. The dogs was premedicated (xylasine-1mg/kg b.w. and nalbufine-0.1mg/kg) and was induced with propofol (2-4mg/kg b.w.). A catheter 18-20G was inserted into the mesentenic vein, through which the contrast material [UROGRAFIN 76%] in dose 1-2ml/kg b.w. was injected. Next the flow of blood in the liver vascular system was recorded with the aid of a fluoroscope for intraoperative X-ray examinations.
Results of research
The dog presented with episodes of hyperactivity, weakness, vomiting and loss of appetite. Central nervous system signs are the most common and may be vague and subtle. One important function of the liver is to clear toxins, many of which are by-products of protein digestion, from the blood. In PSS, these toxins are not cleared, and circulate in the body.
The laboratory blood tests showed leukocytosis, hiperamonemmia, hypoglycemia and decrease in the urea level. Ammonia production results from deamination of dietary amino acids by intestinal bacteria, and endogenous amino acid catabolism. Hyperammonaemia and reduced urea concentrations are common in PSS cases, due an inadequate conversion of ammonia to urea. Hypoglycaemia probably resulted from portal shunting and hepatic functional insufficiency. Intestinal endotoxin release into systemic circulation due to reduced hepatic extraction, could also be a potential cause of hypoglycemia.
The ultrasound examination showed a decreased liver and both enlarged kidneys. The contrast examination of the liver vascular system in the dog revealed an extrahepatic portosystemic shunt. A connection of the splenic vein with the caudal vena cava in the form of a short loop between the portal vein branching off and the jejunal vein was observed. Contrast dye is injected into one of the blood vessels going into the liver. In a normal liver, the contrast material disperses into the many blood vessels in the liver, but in congenital PSS, a large portion of the contrast bypasses those vessels and goes directly to the caudal vena cava, the large blood vessel that carries blood to the heart. Contrast radiography also helps in assessing the chances of successfully tying off the shunt surgically. The more contrast that is apparent in the liver, the higher the likelihood of success. Contrast radiography will also identify whether the shunt is intra- or extra-hepatic.
Conclusion
Generally the diagnosis of congenital PSS is suspected based on the history, clinical signs, and laboratory features. Typically an affected dog is young, of a breed with a predisposition for PSS, with clinical signs and laboratory findings relating to liver dysfunction. A special radiographic tool, contrast portal radiography, is the best way to confirm the diagnosis. Treatment of PSS includes medical management (lactulose, neomycin, metronidazole), dietary therapy (high carbohydrate, low protein) and surgical intervention (ameroid ring contrictor, suture attenuation). Complete surgical ligation of the shunt has an excellent prognosis.
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Reference
1. Benoit J., Granger N.: Splanchic hemodynamics in chronic portal hypertension. Sem .Liv. Dis.1986, 6, 287-294.
2. Boothe H.W., Howe L.M., Edwards J.F., Slater MR.: Multiple extrahepatic portosystemic shunts in dogs: 30 cases (1981-1993). J. Am. Vet. Med. Assoc. 1996, 208, 1849-54.
3. Dial S.M.: Clinicopathologic evaluation of the liver. Vet. Clin. North Am. Small Anim. Pract. 1995, 2, 257-273.
4. Ferrell E.A., Graham J.P., Hanel R., Randell S., Farese J.P., Castleman W.L.: Simultaneous congenital and acquired extrahepatic portosystemic shuts in two dogs. Vet. Radiol. Ultrasound 2003, 44, 38-42.
5. Griffon D.: What is your diagnosis? Multiple portosystemic shunts, acquired or congenital. J. Small Anim. Pract. 1998, 39, 61-98.
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Summary
In animals with a portosystemic shunt (PSS) there is abnormal blood flow in the liver. Blood should flow from the digestive tract to the liver via the portal system into the blood vessels of the liver, and then to the caudal vena cava which is the large blood vessel carrying blood back to the heart. Most animals with congenital portosystemic shunts show clinical signs before 6 months of age. Generally the diagnosis of congenital PSS is suspected based on the history, clinical signs, and laboratory features. While medical treatment will improve the clinical signs temporarily, surgery to tie off the shunt is required to correct the condition for the long term.
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