PATIENT: Rocky Hays
HISTORY: ?severe primary hepatopathy – marked elevation in liver enzymes and bile acids 250, jaundiced, anorexia
The findings confirm the suspicion of a severe primary hepatopathy and despite the elevation in coagulation times (PT 40 – 2.5 upper limit of reference range, APTT 152 0.5x upper limit) ultrasound guided biopsy was performed (4x upper limit is a contra-indication to guided biopsy). There is no evidence of congenital portosystemic shunt although turbulent flow surrounding the renal vessels, elevated portal vein flow (0.5M/S), urinary sediment and splenorenomegaly – are suggestive of acquired portosystemic shunting due to portal hypertension.
LIVER: Abnormal: significantly small, coarse hypoechoic exchotexture, regular margins
BILIARY TRACT: Abnormal: thickened gallbladder wall consistent with primary hepatopathy
SPLEEN: Normal to mildly enlarged
LEFT KIDNEY: Normal to mildly enlarged 7cm length
RIGHT KIDNEY: Normal as above
LEFT ADRENAL: Normal
RIGHT ADRENAL: Normal
URINARY BLADDER: Abnormal: moderate quantity of urinary sediment
ILIOSACRAL LYMPH NODES: Normal
VISCERAL LYMPH NODES: Normal
SMALL INTESTINES: Normal
LARGE INTESTINES: Normal
GENITAL TRACT: Prostate small and hypoechoic
3x biopsies from liver
Three sections of liver are examined and there is no normal liver present. There is severe degeneration vacuolar swelling and necrosis of hepatocytes (particularly periacinar to midzonal hepatocytes) with moderate to marked expansion of portal tracts with hyperplasia and duplication of biliary epithelia/ducts and moderate to marked neutrophilic to plasmacytic portal infiltrates. Multifocally, there are aggregates of erythroid and myeloid precursors (extramedullary haematopoiesis). There is a moderate increase in macrophages/Kupffer cells that often contain large amounts of yellow-gold pigment (bile/haemosiderin). Multifocally, small arterioles and biliary ducts display endothelial/epithelial necrosis.
Sever acute to subacute necrotising neutrophilic hepatitis
This is a severe and inflammatory liver disease and in my opinion, is consistent with an infectious process. There is some chronicity in this lesion suggested by the biliary proliferation although there is also a significant active inflammatory and necrotising component. I could not entirely exclude infectious canine hepatitis although specific viral inclusion bodies are not evident. My main differential is a severe subacute bacterial cholangiohepatitis.
BVSc, MVSc, MACVSc, DipACVP, MRCVS