Approach to the Jaundiced Cat

W S A V A W C P , 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

Age

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

(typically 1–5 years)

Young to middle-aged Pancreatitis, neutrophilic cholangitis, hepatic lipidosis

(typically 2–8 years)

Middle-aged to older Neutrophilic cholangitis, hepatic lipidosis, pancreatitis,

(typically > 8 years) neoplasia

Breed
Siamese/Oriental FIP, amyloidosis

Persian FIP, lymphocytic cholangitis

Pedigree FIP

History/clinical signs

Overweight with recent Hepatic lipidosis

weight loss

Weight loss despite a good Lymphocytic cholangitis

appetite

Any current medications Consider possible hepatotoxicity

Abdominal pain Pancreatitis, acute neutrophilic cholangitis, cholecystitis

Physical examination

Pyrexia FIP, neutrophilic cholangitis, sepsis

Hepatomegaly Lymphocytic cholangitis, hepatic lipidosis, neoplasia

Ascites Lymphocytic cholangitis, FIP, neoplasia, haemoabdomen

associated with amyloidosis

Respiratory compromise Could be associated with pleural effusion - FIP, neoplasia

Laboratory test results

Anaemia Haemolysis, anaemia of chronic inflammatory disease

Neutrophilia FIP, sepsis, neutrophilic cholangitis, pancreatitis

Left shift/toxic neutrophils Acute neutrophilic cholangitis, sepsis

More marked increase in Hepatotoxicity, amyloidosis, hepatic neoplasia

ALT compared to ALP

Mild hyperbilirubinaemia FIP, pancreatitis

with normal ALT and ALP

More marked increase in Post-hepatic jaundice, cholangitis, hepatic lipidosis

ALP compared to ALT
Extremely elevated ALP Hepatic lipidosis
with only mildly elevated
GGT

Marked Lymphocytic cholangitis, FIP

hyperglobulinaemia

Hypocalcaemia Pancreatitis, sepsis

Diagnostic imaging

Radiopaque area in gall Cholelithiasis

bladder

Hepatomegaly Lymphocytic cholangitis, hepatic lipidosis, neoplasia

Ascites Lymphocytic cholangitis, FIP, neoplasia, haemoabdomen

associated with amyloidosis, biliary tract rupture
(uncommon)

Thickened gall bladder Cholecystitis/acute neutrophilic cholangitis

wall/sludge in gall bladder

Marked hyperechoic Hepatic lipidosis, lymphoma (less common)

hepatic parenchyma

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.
Analgesia
If abdominal pain present, or if neutrophilic cholangitis or pancreatitis suspected.
Buprenorphine 0.01 mg/kg sublingual or slow IV q 8 h.
Anti-Emetics
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.
Antibiotics
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.

S I
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Andrea Harvey, BVSc, DSAM (Feline), DECVIM-CA, MRCVS, MANZCVS (Assoc)

Small Animal Specialist Hospital
Sydney, NSW, Australia

URL: https://www.vin.com/doc/?id=7259263