Case Study

Suspected Hepatic Arteriovenous Malformation (HAVM) Shunt in a 3-year-old, intact M, Yorkshire Terrier

History: presented for evaluation of abdominal effusion, parasitism (flea infestation), anemia, low albumin, and elevated liver enzymes.

PE: Abdomen- Distended with fluid but not overly tense, unable to palpate individual organs. 648 ml clear fluid via abdominocentesis first visit; fluid continued to accumulate and approximately 650 ml removed a week later. Fleas and mild alopecia. Has been given drontal, Capstar, Revolution.

Labwork: CBC–HCT 19.1%, retics 209K, monos 1.87. Chem–ALT 282, GGT 5, Alb 2.2. Nexus:

Chem- Alt 242, GGT 5, Amylase 286. CBC- RBC 5.62, Hematocrit 31.4, Hemoglobin 10.5, MCV 55.9, MCH

18.7, Reticulocytes 159.0, Reticulocyte Hemoglobin 20.3, Monocytes 1.50, Platelets 570, Plateletcrit 0.60

Brief AUS: large volume of anechoic effusion, large nest of dilated blood vessels seen in liver consistent with HAVM.

Sonographic Differential Diagnosis

suspect HAVM or other complex hepatic shunting

Image Interpretation

The liver in this patient presented minimal parenchymal volume with tortuous, irregular, complex intrahepatic shunting. The portal vein was followed to its branching which appeared to terminate into a central divisional intrahepatic shunt. However, the left liver revealed a complex intrahepatic shunt with a nest of multiple tortuous vessels suggestive for arterial venous malformation. Complex and multiple congenital intrahepatic shunting is evident. The gallbladder and common bile duct were unremarkable.

DX

HAVM

Comments

Multiple, complex intrahepatic shunting, suspect HAVM or other complex hepatic shunting with minimal hepatic parenchyma and secondary portal hypertension. Minimal normal hepatic parenchyma. Given the ascites present I am strongly concerned for hepatoarterial venous malformation, which is the only intrahepatic shunt that causes secondary portal hypertension. However, this should be confirmed by CT. The clinical issue in this patient, primarily, in addition the ascites formation is the minimal amount of subjectively normal hepatic parenchyma. Therefore, prognosis is extremely guarded to poor depending on further diagnostics. If this is a patient belonging to a breeding line the genetically related line should be evaluated for potential related disease.