Medycyna Wet. 2008, 64 (9)1112

Praca oryginalna Original paper

Diseases of the liver vascular system constitute a com-mon clinical problem in veterinary practice. One of the mostfrequently described diseases of the liver vascular systemis a portosystemic shunt (PPS) (2, 4, 6-8). A portosystemicshunt in dogs was for the first time described by Hickam in1949 (3). It may also occur in cats, foals, calves, miniaturepigs and humans (3). The diagnostics of liver vascular sys-tem diseases is conditioned by a veterinary doctor�s know-ledge of anatomy. Blood reaches the liver via two mainvessels: the hepatic portal vein (delivers about 75% ofblood) and the hepatic artery (25% of blood) (9). Theportal vein originates from the connection of the splenicvein and common mesenteric vein. It supplies the liver withblood rich in substances absorbed in the oesophagus

lumen, among others: waste products, toxins (ammonia,phenols, indols, biogenic amines, etc.), enterohormones andother compounds originating in the oesophagus lumenunder the influence of bacterial flora (5, 9). It is calleda public vessel (vas publica) since the blood it supplies isused by the whole organism. The hepatic artery is a branchof the visceral artery branching off the aorta. It is calleda private vessel (vas privata) since it supplies the liver withnutritious blood.

A portosystemic shunt is most often diagnosed inMiniature Schnauzers, Yorkshire Terriers and Irish Wolf-hounds (6). In terms of their location, portosystemic shuntsare divided into intrahepatic and extrahepatic. Extrahepa-tic portosystemic shunts account for 60% to 94% of clini-

Portography in dogsKAMILA GLIÑSKA, PIOTR SKRZYPCZAK*, URSZULA PAS£AWSKA,

JÓZEF NICPOÑ, KRZYSZTOF SIMON**

Katedra Chorób Wewnêtrznych i Paso¿ytniczych z Klinik¹ Chorób Koni, Psów i KotówWydzia³u Medycyny Weterynaryjnej UP, pl. Grunwaldzki 47, 50-366 Wroc³aw

*Katedra i Klinika Chirurgii Wydzia³u Medycyny UP, pl. Grunwaldzki 51, 50-366 Wroc³aw**Katedra i Klinika Chorób Zaka�nych, Chorób W¹troby i Nabytych Niedoborów Odporno�ciowych AM,

ul. Koszarowa 5, 51-149 Wroc³aw

Gliñska K., Skrzypczak P., Pas³awska U., Nicpoñ J., Simon K.Portography in dogs

SummaryThe aim of the study was to assess the usefulness of vascular angiography in the diagnostics of liver vascular

system diseases. The study was conducted on 3 dogs: Yorkshire terrier marked C1, German Shepherd �C2 and Airedale Terrier � C3, aged 11 months, 9 and 5 years respectively. The examinations were performedas follows: the history and clinical examination, abdominal USG, morphological examination, urea andcreatinine concentration, AlAT, AspAT, ALP, GGT, amylase and lipase, the concentration of total bilirubin,ammonia, total protein and albumins. All animals underwent the angiography of the liver vascular system.Additionally, in laparotomy, an oligobiopsy of the liver was performed during which liver samples werecollected for histopathological examinations. Results: Dogs C1 and C3 manifested leucocytosis. Only in dogC2 the morphological examination revealed thrombocytopenia. The biochemical examinations of bloodserum in dog C1 showed a decrease in the urea level. Dog C2 demonstrated an increase the activity of AspAT,AlAT, ALP and GGT, as well as hyperbilirubinemia, hypoproteinemia and hypoalbuminemia. Dogs C1 andC2 had hyperammonemia. The histopathological examination of liver samples collected during diagnosticlaparotomy in dog C1 revealed a slight fibrosis of single portal spaces and dilation of central veins and sinuses,which suggested passive hyperemia. Additionally, diffuse micro- and macrofollicular lipidosis of the wholebioptate was recognized. The histopathological examination of the collected liver bioptate in dog C2 showedmacro- and micronodular cirrhosis of the liver. In dog C3 a venous congestion of the liver without signs ofinflammation, fibrosis or lipidosis was diagnosed. The contrast examination of the liver vascular system indog C1 revealed an extrahepatic portosystemic shunt. A connection of the splenic vein with the caudal venacava in the form of a short loop between the portal vein branching off and the jejunal vein was observed. DogC2 had multiple intrahepatic portosystemic shunts. In addition, a characteristic spiral course of intrahepaticbranches was observed, which suggested liver cirrhosis. The examination of the liver vascular system indog C3 revealed no abnormalities in the structure of the liver vascular system. Clinical signs and results oflaboratory tests suggest the disease but the basic examination enabling the final diagnosis and location ofa shunt is portography. This method is widely used in the diagnostics of liver vascular system diseases.However, it is an invasive method and should be performed in large specialist centres.

Keywords: dog, portography, liver

Medycyna Wet. 2008, 64 (9) 1113

cal cases and are most frequently diagnosed in small breeddogs. Intrahepatic portosystemic shunts account for 6-40%of all cases and are commonly diagnosed in large breeddogs (3). The basic examination of a portosystemic shuntlocation and type is a contrast examination of the livervascular system: angiography, portography (9). The angio-graphy is a modern technique of imaging of the livervascular system, which enables detection of obstructionsin the flow through these vessels as well as detection ofcongenital and acquired anomalies in their structure. Theaim of the study was to evaluate the usefulness of vascularangiography in the diagnostics of liver vascular systemdiseases.

Material and methodsThe study was conducted on three dogs: Yorkshire terrier

marked C1, German Sheperd � C2 and Airdale Terrier � C3, aged:11 months, 9 and 5 years, respectively. The examinations wereperformed as follows: the history and clinical examination, abdo-minal USG, morphological examination (erythrocyte count,hematocrit value, haemoglobin concentration, leucocyte countwith leucogram, thrombocyte count and erythrocyte indices (ureaand creatinine concentration, activity of alanine aminotransfera-se (ALP), asparagine aminotransferase (AST), alkaline phospha-tase (AP), y-glutamylotransferase (GGT), amylase and lipase, con-centration of total bilirubin, ammonia, total protein and albumins).Next, the animals underwent the angiography of the liver vascu-lar system. Prior to the examination the animals were subjectedto 24-hour fasting. The dogs were premedicated with xylasine �1 mg/kg b.w. and nalbufine � 0.1 mg/kg. Both preparationsmixed in one syringe were given intramuscularly. After 10-15 min.a catheter was inserted into vena cephalica antebrachii. Theanimals were induced with propofol in dose 2-4 mg/kg b.w., andnext intubated. Anaesthesia was maintained by a continuous in-fusion of propofol (0.4 mg/kg/min.). During the entire procedurepassive oxygenotherapy and monitoring of basic life functionswere performed by means of pulsoxymetry and capnometry.A catheter 18-20 G was inserted into the mesentenic vein toinject the contrast material (urografin 76%) in dose 1-2 ml/kgb.w. Next, the flow of blood in the liver vascular system wasrecorded with the aid of a fluoroscope for intraoperative X-rayexaminations. Additionally, during laparotomy an oligobiopsy ofthe liver was performed to collect liver samples for histopatho-logical examinations. The obtained preparations were stained withhematoxylin-eosin (HE), Giemsa method, according to Malloryand for the presence of reticulin fibres.

Results and discussionThe clinical history revealed seizures in all the exami-

ned dogs. In one dog marked C1 the neurological signsintensified after eating. Blood carried to the liver by theportal vein contains many substances that in normalphysiological conditions are metabolized in the liver. Inanimals with a portosystemic shunt these substances arenot metabolized in the liver. Instead, they penetrate intothe systemic circulation and cause toxic damage to thecentral nervous system (3, 6, 8, 9). The concentration ofammonia, mercaptans, B-hydroxylic biogenic amines, sub-stances of benzodiazepine activity and other metabolites(GABA) rises. An increase in the concentration of thesesubstances in CNU causes an impairment of synapticstimuli transmission, the damage of neurons membrane andimpairment of metabolism in the nervous tissue whichleads to the emergence of encephalopathy symptoms (6).

The clinical signs accompanying a portosystemic shunt areconditioned by an increase in intoxication of the organism:apart from seizures other non-specific neurological dis-orders may occur in animals, i.e. no response to externalstimuli, purposeless walking, walking in circles, hallucina-tions, motor ataxia, dementia, metabolic tremor (characte-rized by occasional contractions of some muscle groups),and in more severe cases � coma (3, 9).

The animal with a portosystemic shunt may also expe-rience gastroenterological disorders caused by an impair-ment of the liver synthesizing function (7). The clinicalexamination of the dog marked C2 revealed an enlarge-ment of the abdomen outline. Additionally, on palpation,an increased tension of the abdominal muscles was notedand shifting dullness was heard on percussion. Ultra-sound examination of dog C1�s abdominal cavity revealeda decreased liver of homogeneous hyperechogenic structu-re with no focal changes and both kidneys enlarged. Ultra-sound examination of dog C2�s abdominal cavity showedfluid in the peritoneal cavity as well as a significantly de-creased liver of heterogeneous echostructure and irregularmargins. The dog marked C3 did not manifest any changesof the abdominal cavity organs in ultra-sound examination.Laboratory blood examinations in animals with a porto-systemic shunt show in some cases microcyte anemia, whichwas not observed in the performed study (tab. 1). Dogs C1and C2 manifested leucocytosis. Only in dog C2 morpho-

rtemaraP 1C 2C 3C

)l/t(etycorhtyrE 10.7 97.6 47.7

)l/l(tircotameH 94.0 24.0 35.0

)l/lomm(nibolgomeaH 9.9 8.8 7.01

)l/f(VCM 07 26 96

)lom/f(HCM 15.1 3.1 93.1

)l/lomm(CHCM 2.12 9.02 5.02

)l/g(etycocueL 4.81 9.31 2.22

)%(etycofmiL 2.11 6.4 0.51

)%(etyconoM 6.4 1.2 1.11

)%(etycolunarG 2.48 3.39 9.37

)l/g(etycobmorhT 954 331 023

)l/lomm(aerU 6.2 5.4 2.21

)l/lomµ(eninitaerC 911 38 421

)l/U(TApsA 33 131 32

)l/U(TAlA 0.62 5.921 0.26

)l/U(PLA 12 5.711 22

)l/U(TGG 01 53 01

)l/lomµ(ainommA 101 34 1

)l/lomµ(niburiliblatoT 7.1 0.23 7.1

)l/g(nietorplatoT 86 43 56

)l/g(nimublA 53 81 43

)l/U(esalymA 1311 895 946

)l/U(esapiL 896 152 086

Tab. 1. Test results of chosen morphological and biochemicalparameters in blood of dogs C1, C2, C3

Medycyna Wet. 2008, 64 (9)1114

logical examination revealed thrombocytopenia, which isa typical sign of coagulation disorders in the course of liverdiseases. The biochemical examinations of blood serum indog C1 showed a decrease in the urea level. Dog C2demonstrated an increase in AspAT, A1AT, ALP and GGTactivity (tab. 1). In dogs with a portosystemic shunt a slightincrease in alanine and asparagine aminotransferase isnoted in some cases, yet the observed increase in hepaticenzymes in dog C2 suggested a serious liver damage (5). Inaddition, dog C2 demonstrated an increased concentrationof total bilirubin and a decreased concentration of totalprotein and albumins, which is a specific sign of liver andbile duct diseases. Dogs C1 and C2 had hyperammonemia.Ammonia is a basic proteine catabolite in the intestines.The main location where ammonia originates as a result ofproteolytic enzymes and bacterial ureases is the large inte-stine (2, 4, 7). In normal conditions ammonia originatingin the intestines is metabolized in the liver into urea in theso-called Kreb�s cycle. An increase in the concentration ofammonia in blood serum occurs in the course of chronicliver parenchyma diseases and also in cases of anomaliesin the liver vascular system. The histopathological exami-nation of liver samples collected in diagnostic laparotomyin dog C1 revealed slight fibrosis of single portal spacesand a dilation of central veins and sinuses, which sug-gested passive hyperemia. Additionally, diffuse micro- andmacrofollicular lipidosis of the whole bioptate (20-25%hepatocytes) was recognized. The histopathological exa-mination of the collected liver bioptate in dog C2 showedmacro- and micronodular cirrhosis of the liver (Cirrhosismacro- et micronodularis hepatis).

In dog C3 fibrosis, lipidosis and a venous congestion ofthe liver without signs of inflammation were diagnosed.The contrast examination of the liver vascular system in dogC1 revealed an extrahepatic portosystemic shunt (fig. 1).A connection of the splenic vein with the caudal vena cavain the form of a short loop between the portal vein branchand the jejunal vein was observed. Dog C2 had multipleintrahepatic portosystemic shunts (fig. 2). In addition,a characteristic spiral course of intrahepatic branches wasobserved in this dog, which suggested liver cirrhosis. Inthe examination of the liver vascular system in dog C3no abnormalities were found in the structure of the liver

vascular system. In intra-uterine life there is a con-nection between the portalvein and jejunal vein throughthe umbilical vein. Thisconnection closes sponta-neously within 3 days afterbirth under the influence oftrombosan A2 released bythe epithelium of blood ves-sels and the liver. If it failsto close, a permanent con-nection between the portalvein and systemic veins isformed and a portosystemicshunt is originated.

A portosystemic shuntis found primarily in largebreed dogs. An acquiredportosystemic shunt results

from chronic liver diseases leading to portal hypertension.Numerous diseases that may initiate portal hypertensioninclude, among others, chronic liver inflammation, livercirrhosis, an arterio-venous shunt, portal vein thrombosis.Haemodynamic disorders in the portal system are usuallysecondary to the basic disease, yet in some cases they mayoccur spontaneously e.g. idiopathic portal hypertension inpuppies. An increase in pressure in the portal system leadsto its spontaneous relief through opening normally inacti-ve connections between the portal system and the venoussystem of the systemic circulation. The portosystemic con-nections are subject to mutual hemodynamic relationshipsand constitute a natural way of collateral circulation regu-lating haemodynamic disorders in the liver vascular sys-tem. The number of originating connections depends onthe duration of the primary disease and the location of theobstruction causing portal hypertension. Clinical signs andresults of laboratory tests may suggest the disease but thebasic examination that enables the final diagnosis and de-termination of shunt location is portography. This methodis widely used in the diagnostics of liver vascular systemdiseases. However, it is an invasive method and should beperformed in large specialist centres.

References1.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 M. R.: Multiple extrahepatic

portosystemic shunts in dogs: 30 cases (1981-1993). J. Am. Vet. Med. Assoc.1996, 208, 1849-1854.

3.Dial S. M.: Clinicopathologic evaluation of the liver. Vet. Clin. North Am. SmallAnim. Pract. 1995, 2, 257-273.

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5.Gliñska K., Nicpoñ J., Hildebrand W.: Kwas ursodeoksycholowy w terapiichorób w¹troby psów. Medycyna Wet. 2005, 61, 911-913.

6.Griffon D.: What is your diagnosis? Multiple portosystemic shunts, acquired orcongenital. J. Small Anim. Pract. 1998, 39, 61-98.

7.Grose R., Hayes P.: Review article: the patophysiology and pharmacologicaltreatment of portal hypertension. Aliment. Pharmacol. Ther. 1992, 6, 521.

8.Hunt G. B., Youmans K. R., Sommerlad S., Swinney G., Nicholson A., Melvil-le L., Hoffman K. L., Allan G. S.: Surgical management of multiple congenitalintrahepatic shunts in two dogs: case report. Vet. Surg. 1998, 27, 262-267.

9.Knapik Z.: Postêpy diagnostyki chorób w¹troby i dróg ¿ó³ciowych. Pol. Arch.Med. Wewn. 1984, 72, 65-68.

Adres autora: dr Kamila Gliñska, pl. Grunwaldzki 47, 50-366 Wroc³aw;e-mail: kamilaglinska@o2.pl

Fig. 2. Multiple portosystemic shunts in dogwith liver cirrhosis (C3)

Fig. 1. Extrahepatic portosystemic shunt inYorkshire Terrier (C1)