Vol. 22, No.
9 September 2000
CE Refereed Peer Review
FOCAL POINT
★ Cats with hepatic lipidosis (HL)—
a common, reversible cause of
icterus in cats—should be
systematically evaluated for
concurrent underlying diseases
that could alter prognosis,
treatment, and recovery.
KEY FACTS
■ Experimentally, dietary energy
must be restricted 50% to 75%
for at least 2 weeks to induce HL
in cats.
■ HL frequently occurs secondary to
other underlying diseases, most
commonly cholangiohepatitis,
inflammatory bowel disease, or
chronic pancreatitis.
■ Serum biochemical profiles
of cats with HL reveal marked
elevations in bilirubin and alanine
aminotransferase, dramatic
increases in alkaline phosphatase,
and normal to mild increases in
γ-glutamyltransferase.
■ Nearly half of all cats with HL
have at least one coagulation
abnormality, most commonly
vitamin K deficiency.
■ Coagulation abnormalities are
positively correlated with the
magnitude of increase in serum
alkaline phosphatase.
Feline Hepatic Lipidosis:
Pathophysiology,
Clinical Signs, and
Diagnosis
Auburn University
Brenda Griffin, DVM, MS
ABSTRACT: Feline hepatic lipidosis is a common form of hepatobiliary disease in domesticat-
ed cats. Typical clinical findings include anorexia, weight loss, muscle wasting, icterus, hep-
atomegaly, and increased serum liver enzyme activities. Although the cause of the disorder re-
mains undetermined, its pathogenesis likely involves the unique pathways of protein and lipid
metabolism in cats. Diagnosis is based on history, physical examination, clinical pathology,
radiography, abdominal ultrasound, cytology of fine-needle liver aspirates, and liver biopsy.
When hepatic lipidosis is suspected, a clinical investigation into predisposing conditions
should be made.
F
eline hepatic lipidosis (HL) is a syndrome characterized by severe hepato-
cellular lipid accumulation, intrahepatic cholestasis, and impaired liver
function. First described in 1977 by Barsanti and colleagues,1 HL is one of
the most common liver diseases in cats, representing 49% of 175 feline liver
biopsies in one recent study.2 It occurs primarily in middle-aged to older cats.
The cause of HL is unknown. Its pathogenesis likely involves the unique path-
ways of protein and lipid metabolism in cats. Feline HL may occur either as a
primary event (idiopathic feline HL) or secondary to another disease process.
This article discusses the pathophysiology, clinical signs, and diagnosis of fe-
line HL. A companion article will discuss the treatment of this important feline
disease.
PATHOPHYSIOLOGY
The lipid concentration in the liver increases after ingestion of a high-fat meal,
as a result of mobilization of fat stores during fasting, or because of hepatic syn-
thesis of lipids from carbohydrates.5,7 Lipid is typically oxidized within mito-
chondria or secreted as part of a very-low-density lipoprotein. If lipid buildup
occurs, lipid is stored in vacuoles within hepatocytes. HL occurs when lipid ac-
cumulation becomes severe. In most species, lipid accumulation is innocuous; in
Small Animal/Exotics Compendium September 2000

cats, however, metabolic de- weight. Histologic examina-

rangements and liver dysfunc-
tion appear to occur in re-
sponse to hepatocellular lipid
accumulation.
The mechanisms of hepatic
fat accumulation include in-
creased delivery of fatty acids
to the liver, decreased release
of very-low-density lipopro-
teins, and decreased oxidation
of fatty acids within mito-
chondria. 5,7 Increased fatty-
acid mobilization to the liver
occurs during starvation. Cats
with HL usually have a peri-
od of anorexia that leads to
severe protein restriction and
adipose tissue mobilization to
the liver, resulting in excessive
hepatic triglycerides. In addi-
tion, starvation may reduce Figure 1—Although hepatic lipidosis most commonly af- did not accumulate in the liv-
the synthesis of the proteins fects obese housecats, obesity is not the only factor in- ers of six cats fed 60% of their
required for very-low-density volved in its pathogenesis.
lipoprotein formation, which
in turn makes the liver unable
to remove excess triglycerides.
Transmission electron microscopy reveals that the hep-
atocytes of cats with HL have reduced quantities of per-
oxisomes, endoplasmic reticulum, Golgi complexes, lyso-
somes, and mitochondria.8 These organelles all perform
metabolic functions necessary for hepatic lipid metab-
olism and fatty-acid oxidation. Electron microscopy
studies also demonstrate that lipid-distended bile canali-
culi collapse, resulting in intrahepatic cholestasis. As a se- dicative of HL.11 Based on this study, the degree of en-
quela, both serum and tissue concentrations of bile acids
increase and hepatotoxic bile acids accumulate, further
damaging the liver parenchyma.
Although the precise pathologic mechanism(s) of fe-
line HL remains a mystery, most researchers believe that
multiple factors associated with cats’ unique metabolism
of proteins and lipids are involved. Proposed pathophysi-
ologic mechanisms include metabolic changes associated
with starvation and obesity, protein and nutrient defi-
ciencies, relative carnitine deficiency, and insulin resist-
ance.
One study confirmed that long-term fasting may in-
duce clinical HL in obese cats.9 Voluntary fasting oc-
curred when obese cats were offered a purified, nutri-
tionally complete but unpalatable diet. Clinical signs and
laboratory results consistent with HL were observed in
12 of 15 cats after 5 to 7 weeks of fasting and were asso-
ciated with a 30% to 35% reduction in initial body
tion of weekly liver biopsy
specimens revealed that obesi-
ty was not associated with liver
parenchymal lipid accumula-
tion but that fasting resulted
in HL in all 15 cats beginning
at 2 weeks. Histologic exami-
nation of successive liver biop-
sies revealed progressive hepa-
tocyte lipid accumulation
in all 15 cats. These findings
suggest that clinical HL should
not develop in otherwise
healthy obese cats after only a
few days of fasting.
Laboratory models have
been developed to define the
degree of food restriction re-
quired to induce HL in cats.
One author found that lipid
calculated maintenance ener-
gy requirements for 14 weeks
but did accumulate in the liv-
ers of six other cats fed only 25% of their calculated
maintenance energy requirements for the same amount
of time.10
In another study, weight loss was induced in six obese
and six non-obese cats by feeding them 50% of their
calculated maintenance energy requirements for 29
days; none of the cats developed apparent changes in
physical, hematologic, or serum biochemical values in-
ergy restriction needed to induce HL was defined to be
between 50% and 75%. No differences between obese
and non-obese cats in terms of their responses to food
restriction were observed in either of these models.
Thus it appears that near-total anorexia, restriction of
an essential nutrient, significant weight loss, or factors
other than obesity are required for the development of
HL (Figure 1).
Another proposed pathophysiologic mechanism of
feline HL involves carnitine, an amine synthesized from
methionine and lysine. Carnitine is required for trans-
port of fatty acids through hepatic mitochondrial mem-
branes for oxidation and removal. Plasma, liver, and
skeletal muscle carnitine concentrations are higher in
cats with HL than in control cats,12 suggesting that in-
creased carnitine synthesis may be a metabolic response
to HL to facilitate fatty-acid oxidation.7 If the demand
for carnitine exceeds its synthesis, a relative deficiency

ANOREXIA ■ OBESITY ■ DIETARY ENERGY RESTRICTION ■ CARNITINE

Compendium September 2000
of carnitine would exist despite the increased concen-
trations.7
This theory of relative carnitine deficiency is support-
ed by a study that assessed the effects of increased di-
etary carnitine in an HL model in cats.13 In cats fed
25% of their required energy needs, hepatic lipid accu-
mulation was minimal in cats given supplemental carni-
tine compared with control cats. This finding implies
that carnitine requirements are much higher for cats
with increased mobilization of fat to the liver than for
normal cats. Carnitine supplementation may thus be a
rational and beneficial treatment for cats with HL.
Insulin resistance is another theory to explain the
cause of HL. Breakdown of stored body fat (lipolysis)
normally occurs when insulin function is inadequate.
Both glucose tolerance and insulin response to glucose
infusion were decreased in healthy cats undergoing se-
vere restriction of calorie intake and weight loss, and the
cats subsequently developed HL.14 When cats were re-
turned to a positive nutritional plane, glucose tolerance
and insulin response normalized and HL resolved. This
phenomenon suggests that once energy restriction oc-
curs, poor insulin function may set up a cycle for con-
tinued lipolysis and ultimately the development of HL.
CLINICAL SIGNS
Feline HL is a disease of middle-aged to older cats of
either sex; no known breed predilections exist. One ret-
rospective study of 77 cats with severe HL showed that
female cats were affected nearly twice as often as males.15
A second retrospective study of 96 cats by some of the
same authors, however, revealed approximately equal
numbers of affected male and female cats.3 Most cats
that develop HL are obese housecats.5
Illness is usually preceded by anorexia of a few weeks’
duration.1 Some cats become anorectic after a stressful
event (e.g., a move to a new home, separation from an
owner) or a change to a less-palatable (e.g., weight-re-
duction) diet. Owners often note a progressive onset of
anorexia and depression accompanied by intermittent
vomiting over several weeks. Median duration of illness
before diagnosis was 4 weeks in one study.15
As liver function worsens, cats may develop icterus,
severe loss of muscle mass, and such signs of hepatoen-
cephalopathy as severe depression and ptyalism. Icterus
can be detected on the soft palate first, followed by yel-
low tinting of the sclera, mucous membranes, and skin.
Neurobehavioral signs indicative of hepatoencephalopa-
thy other than ptyalism and depression are rare.15 Physi-
cal examination findings usually include obvious hep-
atomegaly, jaundice, dehydration, and a loss of at least
25% of body weight.
Retrospective studies indicate that 49% to 76% of
INSULIN RESISTANCE ■ PTYALISM ■ CONCURRENT ACUTE PANCREATITIS
Small Animal/Exotics
cats have secondary HL.3,15 According to the authors of
these studies, this range may reflect increased motiva-
tion to identify underlying or initiating diseases. Disor-
ders associated with secondary HL include liver diseases
(cholangiohepatitis, extrahepatic bile duct obstruction,
portosystemic vascular anomalies), neoplasia (urinary
bladder transitional cell carcinoma, intestinal adenocar-
cinoma, intestinal lymphosarcoma, metastatic carcino-
ma), renal diseases (pyelonephritis, chronic interstitial
nephritis), hyperthyroidism, gastrointestinal diseases
(eosinophilic enteritis, lymphocytic–plasmacytic enteri-
tis), diabetes mellitus, and pancreatitis.15 Retrospective
studies have demonstrated an increased incidence of in-
flammatory bowel disease and chronic pancreatitis in
cats with cholangiohepatitis.16 In fact, cholangiohepati-
tis, inflammatory bowel disease, and chronic pancreati-
tis are the most common diseases associated with sec-
ondary HL.3
One recent study characterized the incidence of acute
pancreatitis in cats with HL.17 Five (38%) of 13 cats
histologically diagnosed with HL also had acute pan-
creatitis. Cats with HL alone were indistinguishable
from those with concurrent acute pancreatitis in terms
of signalment, history, physical examination, and clini-
copathologic features, except that cats with acute pan-
creatitis were more likely to be cachectic and have peri-
toneal effusion and coagulation abnormalities. The
recovery rate was 20% for cats with concurrent acute
pancreatitis compared with 50% for cats with HL
alone. Because of the rate of disease coincidence, the
difficulty in identifying cats with concurrent acute pan-
creatitis, the opposing therapies of the two diseases, and
the significant prognostic differences, cats with HL
should be rigorously evaluated for concurrent acute
pancreatitis (see Pancreatitis in Cats17,18). Feeding a cat
with HL may exacerbate acute pancreatitis, whereas
fasting a cat with acute pancreatitis may worsen HL.
DIAGNOSIS
Diagnosis of feline HL should be based on history,
physical examination, clinical pathology, radiography,
abdominal ultrasonography, and cytology of fine-nee-
dle aspirates of the liver. Definitive diagnosis is based
on liver biopsy; HL is present when more than 50% of
hepatocytes in an acinus have vacuolar lipid accumula-
tion.15
When HL is suspected, a clinical investigation into
predisposing conditions for secondary HL should be
made. Serum total thyroxine concentrations, feline
leukemia virus and feline immunodeficiency virus test-
ing, and chest radiography should be used to rule out
primary diseases and screen for metastasis (neoplastic
disease may be an underlying condition). Additional
Small Animal/Exotics Compendium September 2000

diagnostic tests (e.g., toxoplas- assess liver function is obtained

mosis titers, heartworm tests) Pancreatitis in Cats17,18 by collecting paired fasting and
may be indicated based on re- postprandial samples of serum
Feline acute pancreatitis is an infrequently
sults of other tests or geo- bile acids. 19 Elevations in
graphic location. recognized disease; it is characterized by acute serum bile acids indicate the
inflammation of the pancreas, and clinicopathologic presence of cholestasis and are
Clinicopathologic findings are consistent with extrahepatic more sensitive than is bilirubin
Features 17
cholestasis. Peripancreatic fat necrosis and acinar for the detection of cholestasis.
Clinicopathologic features cell necrosis and inflammation are common Bilirubinuria, which pre-
are characterized by hyperbili- cedes the development of bili-
rubinemia and at least a two- findings. Lethargy and anorexia are the most rubinemia, is another useful
fold increase in the activities common clinical signs of pancreatitis in cats; marker of cholestasis (or other
of serum alanine aminotrans- vomiting and abdominal pain are reported only cause of hyperbilirubinemia) in
ferase, aspartate aminotrans- occasionally.18 Causes of acute pancreatitis in cats cats. Although dogs may nor-
ferase, and alkaline phospha- have not been definitively established. Antemortem mally have small quantities of
tase (ALP), with only a small, diagnosis is difficult. Prognosis is poor, and cats bilirubin in concentrated urine
if any, increase in γ-glutamyl- samples, bilirubinuria in cats is
transferase activity.15 The most with acute pancreatitis have a worse prognosis always abnormal and is a pre-
dramatic increases usually in- compared with cats with chronic pancreatitis. lude to hyperbilirubinemia.
volve ALP concentrations, with Chronic pancreatitis is often an incidental Other results of serum bio-
over half of the cats in one large finding at necropsy in cats and is characterized by chemical profiles in cats with
study having fivefold or greater interstitial fibrosis, acinar atrophy, and lymphocytic HL include normal concentra-
increases.15 The near-normal infiltrates.17 The cause of chronic pancreatitis is tions of total protein, normal
values of serum γ-glutamyl- or mildly subnormal albumin
transferase activity contrast also unknown. concentrations, normal to sub-
with the substantial increases in normal blood urea nitrogen as-
γ-glutamyltransferase activity that develop in other forms sociated with a normal creatinine concentration, normal
of acquired feline hepatobiliary disorders (e.g., cholangio- or mildly increased total cholesterol concentration, and
hepatitis).15 euglycemia to hyperglycemia.15 Electrolyte concentra-
Evaluation of serum globulin concentrations can tions vary, with hypokalemia being the most frequent
also be helpful in distinguishing HL from other serious and significant abnormality15; signs of severe hypokal-
15
cholestatic disorders. Most diffuse hepatobiliary dis- emia include profound weakness and ventroflexion of
eases are associated with an acute-phase inflammatory the neck.
response and hyperglobulinemia. Serum biochemical Decreased blood urea nitrogen concentration associ-
profiles of cats with primary HL are typically character- ated with HL may be caused by chronic anorexia or in-
ized by normal globulin concentrations. sufficient urea-cycle function.15 Hypercholesterolemia is
Evaluation of serum total bilirubin concentration usually seen in cats with extrahepatic cholestasis caused
and serum ALP activity may be useful in differentiating by bile-duct obstruction. The mechanism for hyper-
between primary (idiopathic) and secondary HL. In cholesterolemia in feline HL is unknown. Hypergly-
one large retrospective study of feline HL, the median cemia may be associated with stress (catecholamine re-
total bilirubin concentration of cats with primary HL sponse) or changes in glucose tolerance and/or insulin
was 4.8 mg/dl compared with 1.9 mg/dl in cats with response. Other laboratory changes may reflect dehydra-
secondary HL.15 Serum ALP concentrations reflected a tion, electrolyte abnormalities, and chronic illness.
median 6.9-fold increase above maximum normal refer- Baseline hematologic test results of cats with HL are
ence range values in cats with primary HL versus a 3.8- characterized by a normal packed cell volume or mild to
fold increase in cats with secondary HL. moderate nonregenerative anemia, the presence of poik-
Although the majority of cats with HL are icteric, the ilocytes, and a normal leukocyte count.15 The cause of
absence of hyperbilirubinemia does not exclude a diag- poikilocytosis in cats with HL and liver disease is
nosis of HL. Elevations in serum liver enzymes develop unknown. It has been suggested that alterations in cell-
before hyperbilirubinemia, and histologic evidence of wall lipid may induce conformational changes in ery-
severe HL precedes development of cholestasis.15 Hepat- throcytes or that altered liver function may compromise
ic function should be evaluated in any nonicteric cat erythrocyte metabolism, leading to loss of membrane
with suspected HL. The best diagnostic information to integrity.

BIOCHEMICAL PROFILES ■ BILIRUBINURIA ■ HYPOKALEMIA ■ POIKILOCYTOSIS

 Small Animal/Exotics Compendium September 2000
COMPENDIUM
ON CONTINUING EDUCATION
F O R T H E P R A C T I C I N G V E T E R I N A R I A N ®
Coagulopathies
Coagulopathies are common in cats with a variety of
Veterinary Technician reprints also available liver diseases, including HL. One study found the
prevalence of coagulation abnormalities in 22 cats with
2001 PRICE SCHEDULE* naturally occurring liver disease to be 82%.20 Approxi-
2 4 8 12 16 mately 45% of cats with HL have one or more coagula-
Quantity pages pages pages pages pages
tion abnormalities.3,15
Black & White Clinical bleeding tendencies, as evidenced by bruising,
100 $ 108 $ 204 $ 416 $ 604 $ 784 overt bleeding, or excessive bleeding from venipuncture
500 152 296 616 896 1,156
1000 208 412 868 1,260 1,628 sites, were noted in 20% of cats in the largest retrospective
5000 636 1,264 2,828 4,076 5,160 study of felines with HL.3 Clinical bleeding tendencies
10,000 1,172 2,332 5,280 7,596 9,572 were noted in 50% of cats with one or more coagulogram
Color abnormalities. This finding suggests that lack of clinical
100 $ 972 $1,408 $2,856 $4,180 $5,380 bleeding tendencies does not exclude the presence of a co-
500 1,152 1,612 3,112 4,704 6,040
1000 1,264 1,840 3,428 5,260 6,852 agulopathy. All cats with HL should be evaluated for coag-
5000 2,328 3,600 7,140 10,672 12,168 ulopathies by performing a platelet count and coagulation
10,000 3,280 5,792 10,640 16,704 18,812 profile (activated partial thromboplastin time, prothrom-
*Price includes UPS Ground Shipping to one location.
bin time, fibrinogen, and fibrin degradation products).
ORDER FORM Abnormal coagulation test results may reflect vitamin
Quantity _____________ ❏ Black & White ❏ Color K deficiency, decreased production of clotting factors
❏ With Review Questions ❏ Without Review Questions by the liver, or consumptive coagulopathies. The most
common abnormality is prolongation of the prothrom-
Author _________________________________________
bin time consistent with vitamin K deficiency.3,15 Cats
Title of Article ___________________________________ with HL may develop vitamin K depletion secondary
______________________________________________ to anorexia and malabsorption of vitamin K as a result
From Vol. _________________ No. ______________ of severe cholestasis; this is because vitamin K is a fat-
❏ Compendium ❏ Veterinary Technician soluble vitamin and thus requires bile excretion into the
intestines for fat absorption.
❏ Payment Enclosed (All payments must be in US funds drawn
on a US branch of a US bank.)
Hypofibrinogenemia is another common coagulo-
gram abnormality in cats with HL.3,15 It may corre-
❏ Purchase Order Attached
spond to hepatic synthetic failure and absence of an
Contact Person ___________________________________ acute phase response.
Phone __________________________________________ Increased serum ALP activity showed significant sta-
tistical correlation with coagulation abnormalities in a
SHIP TO: study of 22 cats with naturally occurring liver disease.20
NAME Vitamin K deficiency, which occurred in 50% of these
cats, was the most common coagulation abnormality.
COMPANY OR PRACTICE
These findings suggest that hepatic diseases resulting in
ADDRESS marked cholestasis and marked increases in serum ALP
activity (such as HL) are likely to be associated with de-
CITY STATE ZIP
rangements of vitamin K absorption and may increase
BILL TO: the risk for coagulopathies and bleeding.
NAME
Diagnostic Imaging
COMPANY OR PRACTICE
Radiography and abdominal ultrasonography can be
ADDRESS helpful in diagnosing feline HL. These imaging tech-
niques often reveal hepatomegaly and assist in exclud-
CITY STATE ZIP
ing other disease processes potentially associated with
Detach and Mail to: Reprints Department secondary HL. Abdominal ultrasonography is particu-
Veterinary Learning Systems larly useful because it can help rule out biliary obstruc-
275 Phillips Boulevard tion, focal masses, and acute pancreatitis. In addition, it
Trenton, NJ 08618
No telephone calls accepted. can be used to guide biopsies of the liver and/or other
structures as indicated based on findings.

VITAMIN K DEFICIENCY ■ HYPOFIBRINOGENEMIA

Compendium September 2000
Ultrasonography is perhaps the best noninvasive tool
for evaluating the pancreas. As mentioned, cats with HL
should be rigorously evaluated for concurrent acute pan-
creatitis. However, diagnosing pancreatitis in cats is ex-
tremely challenging because clinical signs and clinico-
pathologic features are vague and nonspecific. In addition,
serum amylase, lipase, and trypsinlike immunoreactivity
concentrations are frequently normal.21,22 Such radio-
graphic changes as decreased contrast in the cranial ab-
domen, dilated and gas-filled small intestine, and trans-
position of the duodenum are sometimes present but
may be subtle. Experienced ultrasonographers, howev-
er, can usually locate and visualize the pancreas where it
lies dorsomedial to the duodenum. An acutely inflamed
pancreas frequently appears as a hypoechoic mass.21,23 Vari-
able amounts of free abdominal fluid may be present as
well23; if so, abdominocentesis to obtain fluid for cyto-
logic evaluation is indicated and may yield valuable di-
agnostic information.
Ultrasonography reveals the lipidic liver to be diffuse-
ly hyperechoic. Ultrasonographic diagnosis has classical-
ly been based on evaluation of the relative echogenicity
of the liver compared with that of falciform fat (i.e., the
liver appears hyperechoic compared with falciform fat in
cats with HL).24 Although this criterion was initially be-
lieved to be a highly sensitive and specific diagnostic in-
dicator of HL, a recent prospective study revealed that
the liver is diffusely hyperechoic compared with falci-
form fat in clinically normal obese cats.25 Additionally,
both lymphosarcoma and cirrhosis have been described
as diffusely hyperechoic diseases of the liver.26 The pres-
ence of a hyperechoic liver, therefore, is neither a specif-
ic finding nor a sensitive indicator of HL in cats.
Hepatobiliary scintigraphy is a noninvasive diagnos-
tic imaging technique that has been recently evaluated
for diagnosis of feline hepatobiliary diseases. Although
this technique can be useful in assessing the severity of
hepatic dysfunction and determining whether extrahep-
atic biliary obstruction is present, it cannot differentiate
specific disease entities.27
Fine-Needle Aspiration
Although laboratory testing and diagnostic imaging
can identify a high likelihood of HL, evaluation of hep-
atocellular morphology is required to make a definitive
diagnosis. Fine-needle aspiration of the liver may reveal
vacuolar changes typical of HL (Figure 2) but should be
interpreted with caution because it cannot rule out such
concurrent liver diseases as cholangiohepatitis with cer-
tainty and may miss focal lesions.
Fine-needle aspirates can usually be collected with no
or only minimal sedation, and complications are ex-
tremely rare (see Fine-Needle Aspiration of the Feline
ABDOMINAL ULTRASONOGRAPHY ■ ABDOMINOCENTESIS ■ CYTOLOGY ■ HISTOPATHOLOGY
Small Animal/Exotics
Figure 2—Cytology of a fine-needle aspirate from the liver of
a cat with hepatic lipidosis. The severe cytoplasmic vacuoliza-
tion of the hepatocytes represents fatty infiltration.
Liver). Hepatic cytologic samples are most useful in di-
agnosing diffuse diseases that readily exfoliate cells,
such as HL or lymphosarcoma.
Liver Biopsy
Definitive diagnosis of feline HL requires histopatho-
logic evaluation of a liver biopsy specimen. Liver biop-
sies offer the advantage of evaluating both hepatocellu-
lar morphology and liver lobule architecture. Cats
should be evaluated for coagulopathies before undergo-
ing liver biopsy. Pretreatment with subcutaneous vita-
min K1 (1 mg/kg 12 hours before biopsy) is advised.3,4
Techniques for obtaining liver tissue include ex-
ploratory celiotomy and percutaneous needle biopsy
(blind, ultrasound-guided, or laparoscopic methods).
The technique selected largely depends on the condi-
tion of the cat and the skill and experience of the sur-
geon. Because of metabolic derangements and impaired
liver function, cats with severe HL are often poor surgi-
cal candidates,3,4,7 and major surgery should be avoided
before the initial stabilization phase of their therapy.3,4
Advantages of exploratory surgery include the ability to
visually inspect the liver, select biopsy sites, control
bleeding, and obtain biopsies from other organs.
Both impression smears of biopsy specimens and
histopathologic evaluation are recommended. In a ret-
rospective study of 56 hepatic cytology specimens, cy-
tologic evaluation of impression smears concurred with
histopathologic diagnosis in 83% of specimens.28 Re-
sults of cytology may be obtained rapidly and may aid
practitioners in making treatment decisions while they
await results of histopathology. In cats with HL,
histopathology reveals the presence of swollen vacuolat-
ed hepatocytes and canalicular bile stasis. Vacuoles stain
with oil red-o, confirming the presence of lipid. Little
Small Animal/Exotics
Fine-Needle Aspiration of the Feline Liver
■ Place the cat in dorsal recumbency with the body tilted
so that the thorax is slightly higher than the abdomen. In
this position, the liver moves caudally, usually allowing
palpation of an enlarged liver.
■ Use a 10-ml syringe and a 1-inch, 22- or 23-gauge
needle to perform fine-needle aspiration. A 1.5-inch
needle may be needed in obese cats (selection of needle
length can be aided by reviewing abdominal radiographs
to identify the thickness of the falciform fat pad through
which the needle is to be inserted to reach the liver).
■ Shave and sterilely prepare the cranioventral abdomen
between the costal arches.
■ If the liver cannot be palpated, perform blind aspiration
by inserting the needle midway between the midline and
the left costal arch at a level 1 cm caudal to the end of
the xiphoid process (see figure). (Care should be taken
to avoid entering the right side of the liver to prevent
accidental aspiration of the gall bladder.)
■ Aiming cranially, insert the needle at an 80˚ to 90˚ angle.
(Care should be taken to avoid the use of longer needles
or narrower insertion angles to prevent penetration of
the diaphragm.)
■ Advance the needle approximately 1 inch. Briskly
aspirate two or three times, applying 3 to 6 ml of suction
each time. A brisk linear advancement of the needle
followed by a return to its original position while suction
is maintained may aid in sample retrieval. (Care should
be taken to avoid excessive motion of the needle during
to no inflammation is present. On gross examination,
the liver appears yellow and mottled. Its cut surface is
often greasy, and sections float in water or formalin.
SUMMARY
Feline HL is a common hepatobiliary disease in do-
mesticated cats and results in severe impairment of liver
function. All cats with HL need thorough systematic
evaluation to rule out primary underlying diseases. Per-
sistent anorexia should be avoided, particularly in obese
cats. Cats that are anorectic for less than 1 week, how-
ever, are unlikely to develop HL.9
The pathogenesis of feline HL is multifactorial, and
studies are needed to focus on the unique pathways of
hepatic metabolism leading to lipid accumulation and
clinical disease. Results of such studies should be useful
in the development of methods to prevent and treat fe-
Compendium September 2000
aspiration to prevent trauma to the liver and
contamination of the sample with peripheral blood.)
■ Release all pressure and withdraw the needle. If blood
appears in the hub of the needle at any time during
aspiration, discontinue aspiration, select an adjacent
site, and reaspirate.
■ Immediately eject aspirated material onto slides: Remove
the needle, fill the syringe with air, and expel the air
through the needle. Grossly, liver aspirates appear
reddish brown.
■ Place a second glass slide on top of the sample and
gently slide it off the lower slide (i.e., make a “squash
prep smear”). Air-dry slides as rapidly as possible to
preserve cellular morphology.
■ Examine one slide to determine whether the sample is
adequate. Multiple aspirations often improve diagnostic
yield.
line HL. Current therapeutic recommendations will be
discussed in a future article.
ACKNOWLEDGMENTS
The author thanks Drs. D. S. Spano, DVM, PhD, Dip-
lomate American College of Veterinary Practitioners,
and D. K. Macintire, DVM, MS, Diplomate American
College of Veterinary Internal Medicine and American
College of Veterinary Emergency and Critical Care,
College of Veterinary Medicine, Auburn University, Al-
abama, for their encouragement in writing this article.
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2. Gagne J, Weiss DJ, Armstrong PJl: Histopathologic evalua-
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3. Center SA, Warner K: Feline hepatic lipidosis: Better defin-
ing the syndrome and its management. Proc 16th Annu
ACVIM Forum:56–58, 1998.
4. Norsworthy G: Improving survival in cats with hepatic lipi-
dosis. Proc TNAVC:285, 1998.
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About the Author
Dr. Griffin is affiliated with the Scott-Ritchey Research
Center, College of Veterinary Medicine, Auburn Universi-
ty, Alabama. She is a Diplomate of the American College
of Veterinary Internal Medicine.