Hepatic Arteriovenus Malformation in a Canine
Emily Evans BVM&S
Age: 14 weeks
Presented for lethargy, inappetence, vomiting and intermittent diarrhea. Radiographs and barium study showed no gastrointestinal obstruction. There was concern for a portosystemic shunt.
Liver- The overall liver size is enlarged but there is little normal parenchyma remaining. The vasculature of the liver is severely abnormal, tortuous and dilated measuring up to 2.7cm in diameter. The vasculature has a moderate to severe amount of hyperechoic "smoke" and irregular blood flow patterns. The gallbladder is moderately enlarged and rounded with gravity dependent, mineralization in the neck of the gallbladder. The common bile duct appears torturous.
Kidneys- Both kidneys were found to mild-moderately enlarged.
Urinary Bladder- A few hyperechoic suspended particles were identified in the urinary bladder.
A mild amount of ascites was present throughout the abdomen.
ABDOMINAL ULTRASOUND INTERPRETATION:
Vascular changes - the findings are severe- hepatic arteriovenous malformation(HAVM) vs. congenital intrahepatic shunt +/- congenital extrahepatic shunt vs. other vascular anomaly vs. portal hypertension vs. venous congestion(unlikely)
Biliary calculi - the findings are mild-moderate - cholithiasis(non-obstructive vs obstructive)
Tortuous CBD- the findings are mild-moderate- bilary obstruction secondary to choleliths vs. hepatocellular swelling vs. malformation of the bilary system
Kidneys- the findings are mild-moderate- DDx: normal variation in size for this breed vs. enlargement secondary to HAVM/ PSS.
Bladder - the findings are mild - DDx: cellular debris vs. struvite vs. calcium oxalate vs. other urolith
Ascites-this finding is mild - DDx: Transudate vs. exudate vs. hemorrhagic
Formerly known as "arteriovenous fistula (AVF)", hepatic arteriovenous malformation (HAVM) is a rare (typically) congenital vascular anomaly. This malformation results in multiple communications between the portal vein and hepatic artery. These communications cause increased portal pressures (portal hypertension) which leads to the development of multiple acquired extrahepatic shunts.
Some cases can benefit from therapies such as nutrient artery ligation, surgical resection (liver lobectomy or lobectomies), or transarterial embolization (TAE) with glue. There is limited data on outcomes of these patients and case work up( portovenography, ultrasonography, scintigraphy, computed tomography (CT), or magnetic resonance imaging (MRI) ) and surgical case selection is imperative.
Other changes found in the abdomen of this patient were likely secondary to the HAVM.
The patient was referred to an out of state veterinary teaching hospital with a hepatic specialist.
Bile acids test was run; Pre meal - 100, Post meal 164
Urinalysis showed numerous ammonium biurate crystals(frequently found with liver dysfunction and PSS)
Turbulent blood flow could be auscultated over the liver.
A vascular study was performed and the findings were consistent with HAVM. Abnormal vascular connections were also identified elsewhere in the abdomen.
Given the severe degree of vascular change in the liver and abdomen, surgery was not recommended.
Humane euthanasia was elected as the prognosis for this patient long term was grave.
Special thanks to Patterson Veterinary Hospital of Richmond, Virginia and Dr. Bayer for allowing us to collaborate on this case.