Approach to the Jaundiced Cat
World Small Animal Veterinary Association World Congress Proceedings, 2015
A. Harvey, BVSc, DSAM (Feline), DECVIM-CA, MRCVS, MANZCVS (Assoc)
Small Animal Specialist Hospital, Sydney, NSW, Australia

Jaundice may be caused by pre-hepatic, hepatic and post-hepatic disorders. The algorithm below (Figure 1) demonstrates the approach in identifying which of these groups of disorders is the most likely cause. Once the most likely group of disorders has been identified, consideration needs to be given as to what the most common diseases are in each group (Figure 2) and other basic clinical features need to be evaluated to direct the clinician to the most likely cause (Figure 3).

Figure 1. Diagnostic approach to jaundice to differentiate pre-hepatic, hepatic and post-hepatic causes

1. 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.
2. 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 of jaundice. 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.
3. 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 (Figure jaundice.3) 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 if 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 grossly distended.


Figure 2



Figure 3. Most common diagnoses associated with specific clinical features

Clinical features

Most common diagnoses




FIP (typically 6 month–3 years), lymphocytic cholangitis (typically 1–5 years)

Young to middle-aged (typically 2–8 years)

Pancreatitis, neutrophilic cholangitis, hepatic lipidosis

Middle-aged to older (typically > 8 years)

Neutrophilic cholangitis, hepatic lipidosis, pancreatitis, neoplasia




FIP, amyloidosis


FIP, lymphocytic cholangitis



History/clinical signs


Overweight with recent weight loss

Hepatic lipidosis

Weight loss despite a good appetite

Lymphocytic cholangitis

Any current medications

Consider possible hepatotoxicity

Abdominal pain

Pancreatitis, acute neutrophilic cholangitis, cholecystitis

Physical examination



FIP, neutrophilic cholangitis, sepsis


Lymphocytic cholangitis, hepatic lipidosis, neoplasia


Lymphocytic cholangitis, FIP, neoplasia, haemoabdomen associated with amyloidosis

Respiratory compromise

Could be associated with pleural effusion - FIP, neoplasia

Laboratory test results



Haemolysis, anaemia of chronic inflammatory disease


FIP, sepsis, neutrophilic cholangitis, pancreatitis

Left shift/toxic neutrophils

Acute neutrophilic cholangitis, sepsis

More marked increase in ALT compared to ALP

Hepatotoxicity, amyloidosis, hepatic neoplasia

Mild hyperbilirubinaemia with normal ALT and ALP

FIP, pancreatitis

More marked increase in ALP compared to ALT

Post-hepatic jaundice, cholangitis, hepatic lipidosis

Extremely elevated ALP with only mildly elevated GGT

Hepatic lipidosis

Marked hyperglobulinaemia

Lymphocytic cholangitis, FIP


Pancreatitis, sepsis

Diagnostic imaging


Radiopaque area in gall bladder



Lymphocytic cholangitis, hepatic lipidosis, neoplasia


Lymphocytic cholangitis, FIP, neoplasia, haemoabdomen associated with amyloidosis, biliary tract rupture (uncommon)

Thickened gall bladder wall/sludge in gall bladder

Cholecystitis/acute neutrophilic cholangitis

Marked hyperechoic hepatic parenchyma

Hepatic lipidosis, lymphoma (less common)

Other clinical features are also important to take into consideration in interpretation of results, including:

 Cat's age and breed

 Other clinical signs present (e.g., vomiting, abdominal pain, tachypnoea/dyspnoea, inappetence, polyphagia, weight loss) and duration of clinical signs

 Physical examination findings (e.g., body condition score, presence of pyrexia, hepatomegaly, ascites, abnormal/reduced lung sounds, cardiovascular compromise)

 Other laboratory findings (e.g., neutrophilia, presence of left shift/toxic neutrophils, anaemia, degree of ALT/ALP/GGT elevation, hyperglobulinaemia)

 Other diagnostic imaging findings (e.g., radio-opaque choleliths, hepatomegaly, ascites, mesenteric lymphadenopathy, gall bladder wall thickening/sludge, hyperechoic hepatic parenchyma)

Empirical Treatment Pending Investigations/Results

Intravenous Fluid Therapy

0.9% NaCl, usually supplemented with potassium chloride (KCl) depending on serum potassium concentration but if potassium cannot be measured, supplement with 20 mmol/l KCl.

Two–4 ml/kg/h usually an appropriate fluid rate depending on degree of dehydration.

Vitamin K

If clotting times cannot be easily assessed, it is worth treating with vitamin K in case of vitamin K dependent coagulopathy, especially if there is the possibility of surgical intervention.

Assisted Feeding

If inappetent, and vomiting controlled, consider placing naso-oesophageal feeding tube for short-term assisted feeding.


If abdominal pain present, or if neutrophilic cholangitis or pancreatitis suspected.

Buprenorphine 0.01 mg/kg sublingual or slow IV q 8 h.


If vomiting/nausea is a feature: Maropitant (1 mg/kg SQ q 24 h up to 5 consecutive days) and/or metoclopramide constant rate infusion.


If acute neutrophilic cholangitis or sepsis suspected, based on clinical findings.

Broad spectrum (e.g., amoxicillin/clavulanate, cephalexin) initially administered parenterally.

When to Refer

Given the large number of causes of jaundice, the difficulty in reaching a definitive diagnosis without accurate biliary ultrasonography and hepatic biopsy, and the intensive treatment required for many of these disorders, consideration should be given to referral of any jaundiced cat. In particular, referral is appropriate if post-hepatic obstruction is suspected, if liver biopsy is required, if the diagnosis is uncertain or if intensive treatment (e.g., in hepatic lipidosis) is required.


Speaker Information
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Andrea Harvey, BVSc, DSAM (Feline), DECVIM-CA, MRCVS, MANZCVS (Assoc)
Small Animal Specialist Hospital
Sydney, NSW, Australia

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