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Jaundice
British Small Animal Veterinary Association , 256 (2013); https://doi.org/10.22233/9781910443149.5.22
/content/chapter/10.22233/9781910443149.chap5_22
Jaundice
- Author: Andrea Harvey
- From: BSAVA Manual of Feline Practice
- Item: Chapter 5.22, pp 256 - 258
- DOI: 10.22233/9781910443149.5.22
- Copyright: © 2013 British Small Animal Veterinary Association
- Publication Date: January 2013
Abstract
Jaundice may be caused by pre-hepatic, hepatic and post-hepatic disorders. This chapter looks at clinical approach, empirical treatment pending investigations/results, when to refer and if finances are limited.
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/content/figure/10.22233/9781910443149.chap5_22.ch5_22fig1
5.22.1
A diagnostic approach to differentiate pre-hepatic, hepatic and post-hepatic causes of jaundice. a Tissue jaundice will only generally be evident when serum bilirubin exceeds approximately 50 µmol/l (reference range 0–15 µmol/l). The degree of hyperbilirubinaemia is also important in interpretation. There are no hard and fast rules but, generally, with pre-hepatic jaundice serum bilirubin is rarely above 50–100 µmol/l. FIP, pancreatitis, amyloidosis and sepsis also rarely result in serum bilirubin concentrations >100 µmol/l. When serum bilirubin is >200 µmol/l, this is most often caused by either hepatic lipidosis or post-hepatic obstruction, which may be a surgical emergency. Hepatic lipidosis may frequently result in serum bilirubin concentrations >200–300 µmol/l but, generally, the higher the serum bilirubin, the more likely that complete post-hepatic biliary obstruction is present. b Haemolysis needs to be acute and severe (typically PCV<13%) to cause clinically evident jaundice, and caution should therefore be taken in over-interpreting a mild anaemia to be the cause. Cats will frequently have mild to moderate anaemia associated with chronic or inflammatory disease in hepatic and post-hepatic disorders. The degree of anaemia needs to be carefully interpreted with the degree of hyperbilirubinaemia, together with other clinicopathological features. c If serum bilirubin is >100 µmol/l, abdominal ultrasonography is critical in identifying whether extrahepatic biliary duct obstruction is present. Where abdominal ultrasonography is not immediately available, if serum bilirubin is <100 µmol/l, other clinical features (see
Figure 5.22.4
) can be evaluated first to assist in identifying the most likely cause. Detecting early or partial extrahepatic biliary duct obstruction may require expertise in ultrasonography, and referral may need to be considered. For the practitioner, the priority is to know whether the case is a surgical emergency, and in this case the bilirubin is frequently >250 µmol/l and the gall bladder and common bile duct are grossly distended (see
Figure 5.22.2
). © 2013 British Small Animal Veterinary Association
10.22233/9781910443149/fig5_22_1_thumb.gif
10.22233/9781910443149/fig5_22_1.png
5.22.1
A diagnostic approach to differentiate pre-hepatic, hepatic and post-hepatic causes of jaundice. a Tissue jaundice will only generally be evident when serum bilirubin exceeds approximately 50 µmol/l (reference range 0–15 µmol/l). The degree of hyperbilirubinaemia is also important in interpretation. There are no hard and fast rules but, generally, with pre-hepatic jaundice serum bilirubin is rarely above 50–100 µmol/l. FIP, pancreatitis, amyloidosis and sepsis also rarely result in serum bilirubin concentrations >100 µmol/l. When serum bilirubin is >200 µmol/l, this is most often caused by either hepatic lipidosis or post-hepatic obstruction, which may be a surgical emergency. Hepatic lipidosis may frequently result in serum bilirubin concentrations >200–300 µmol/l but, generally, the higher the serum bilirubin, the more likely that complete post-hepatic biliary obstruction is present. b Haemolysis needs to be acute and severe (typically PCV<13%) to cause clinically evident jaundice, and caution should therefore be taken in over-interpreting a mild anaemia to be the cause. Cats will frequently have mild to moderate anaemia associated with chronic or inflammatory disease in hepatic and post-hepatic disorders. The degree of anaemia needs to be carefully interpreted with the degree of hyperbilirubinaemia, together with other clinicopathological features. c If serum bilirubin is >100 µmol/l, abdominal ultrasonography is critical in identifying whether extrahepatic biliary duct obstruction is present. Where abdominal ultrasonography is not immediately available, if serum bilirubin is <100 µmol/l, other clinical features (see
Figure 5.22.4
) can be evaluated first to assist in identifying the most likely cause. Detecting early or partial extrahepatic biliary duct obstruction may require expertise in ultrasonography, and referral may need to be considered. For the practitioner, the priority is to know whether the case is a surgical emergency, and in this case the bilirubin is frequently >250 µmol/l and the gall bladder and common bile duct are grossly distended (see
Figure 5.22.2
).
/content/figure/10.22233/9781910443149.chap5_22.ch5_22fig2
5.22.2
This ultrasound image of a 10-year-old male neutered DSH cat that had been presented with vomiting and acute-onset jaundice shows dilatation of the common bile duct (CBD) consistent with extrahepatic biliary tract obstruction. The normal diameter of the CBD in cats is <4 mm; in this case it measured up to 9 mm. On laparotomy the obstruction was found to be due to a cholelith in the CBD at the level of the duodenal papilla. Neutrophilic cholangitis was identified on hepatic histopathology, and this was thought to be the cause of the cholelithiasis. © 2013 British Small Animal Veterinary Association
10.22233/9781910443149/fig5_22_2_thumb.gif
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5.22.2
This ultrasound image of a 10-year-old male neutered DSH cat that had been presented with vomiting and acute-onset jaundice shows dilatation of the common bile duct (CBD) consistent with extrahepatic biliary tract obstruction. The normal diameter of the CBD in cats is <4 mm; in this case it measured up to 9 mm. On laparotomy the obstruction was found to be due to a cholelith in the CBD at the level of the duodenal papilla. Neutrophilic cholangitis was identified on hepatic histopathology, and this was thought to be the cause of the cholelithiasis.