Feline hepatic lipidosis or fatty liver syndrome is
the most common liver disease of cats.
Once initiated, lipidosis sets itself up as a vicious cycle in
which the anorexia or inappetance exacerbates the hepatic lipidosis
further worsening the anorexia. The frustrating aspect of this disease is that the etiology
or pathogenesis is unknown (idiopathic).
Why can certain cats be deprived of food for days to weeks and
start eating once reintroduced to food with no complications and others
become inappetent in the presence of food secondary to external stress
and develop the a severe case of lipidosis in days?
Lipidosis is not always an idiopathic disease.
It can occur secondarily to concurrent disease processes such as
diabetes mellitus, pancreatitis, neoplasia, hepatic disease, renal
failure, hyperthyroidism, inflammatory bowel disease, and starvation.
When another disease process is present, most cases of secondary
lipidosis will spontaneously resolve once the cat begins to eat.
One exception, cats with chronic pancreatitis with secondary
lipidosis have a much worse prognosis.
The idiopathic form most often occurs secondary to some type of
illness or event (upper respiratory tract infection, kenneling, etc)
although many times the initiating event is not known.
Feline idiopathic hepatic lipidosis does not have a
predilection for age, sex or breed. Most cats affected are exclusively indoor animals with many
of those being obese at the time of onset.
Clinical signs include anorexia or inappetance (some cats may
only have a decreased appetite and are not truly anorexic), vomiting and
depression. Early in the
disease, clinical signs may include weight loss, ptyalism, dehydration
and vomiting, while in later stages of the disease many cats present
with severe wasting, icterus and hepatic encephalopathy (circling, head
pressing, etc). (A side
note: ptyalism is often considered an indicator of hepatic disease.)
Diagnostically, a CBC and chemistry profile is
warranted in all suspected cases of feline idiopathic hepatic lipidosis.
Common findings on CBC include a mild non-regenerative anemia but
never severe enough to explain the icterus, and a stress leukogram.
Chemistry profile often reveals a significantly elevated ALP
followed by a hyperbilirubinemia, ALT and AST are commonly elevated but
not to the degree of ALP. In
severe cases of hepatic lipidosis signs of hepatic failure may be
present. These signs include a low albumin, low blood-glucose, low
BUN, and low cholesterol with the low cholesterol being an indicator of
a poor prognosis. CK may
also be elevated secondary to severe muscle wasting.
Urinalysis may show a bilirubinuria, which is always considered
and abnormal finding in cats.
Hepatomegaly in cats with hepatic lipidosis is
considered an inconsistent finding both on palpation and radiographs
making ultrasound and interventional ultrasound the diagnostic tools of
choice. Typical finding on
ultrasound include a diffuse hyperechogenicity of hepatic parenchyma,
decreased visualization of the intrahepatic blood vessels and possibly
an enlarged liver with rounded margins.
Many times, when compared to the falciform fat pad, the liver
parenchyma has a similar or increased echogenicity.
The liver is usually hyperechoic with respect to the spleen and
renal cortices as well. Ultrasound
is also useful for detecting other disease processes which may be
causing a secondary hepatic lipidosis such as pancreatitis and neoplasia.
Feline Hepatic lipidosis is most commonly diagnosed from cytology
obtained by ultrasound-guided fine needle aspirate of the liver.
