Вы находитесь на странице: 1из 8

Vol. 22, No.

9 September 2000

CE Refereed Peer Review

Feline Hepatic Lipidosis:

FOCAL POINT Pathophysiology,
★ Cats with hepatic lipidosis (HL)—
a common, reversible cause of
icterus in cats—should be
Clinical Signs, and
systematically evaluated for
concurrent underlying diseases
that could alter prognosis,
treatment, and recovery.
Auburn University
Brenda Griffin, DVM, MS
■ Experimentally, dietary energy ABSTRACT: Feline hepatic lipidosis is a common form of hepatobiliary disease in domesticat-
must be restricted 50% to 75% ed cats. Typical clinical findings include anorexia, weight loss, muscle wasting, icterus, hep-
for at least 2 weeks to induce HL atomegaly, and increased serum liver enzyme activities. Although the cause of the disorder re-
in cats. 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,
■ HL frequently occurs secondary to radiography, abdominal ultrasound, cytology of fine-needle liver aspirates, and liver biopsy.
other underlying diseases, most When hepatic lipidosis is suspected, a clinical investigation into predisposing conditions
should be made.
commonly cholangiohepatitis,
inflammatory bowel disease, or
chronic pancreatitis.

eline hepatic lipidosis (HL) is a syndrome characterized by severe hepato-
■ Serum biochemical profiles cellular lipid accumulation, intrahepatic cholestasis, and impaired liver
of cats with HL reveal marked function. First described in 1977 by Barsanti and colleagues,1 HL is one of
elevations in bilirubin and alanine the most common liver diseases in cats, representing 49% of 175 feline liver
aminotransferase, dramatic biopsies in one recent study.2 It occurs primarily in middle-aged to older cats.
increases in alkaline phosphatase, The cause of HL is unknown. Its pathogenesis likely involves the unique path-
and normal to mild increases in ways of protein and lipid metabolism in cats. Feline HL may occur either as a
γ-glutamyltransferase. primary event (idiopathic feline HL) or secondary to another disease process.
This article discusses the pathophysiology, clinical signs, and diagnosis of fe-
■ Nearly half of all cats with HL line HL. A companion article will discuss the treatment of this important feline
have at least one coagulation disease.
abnormality, most commonly
vitamin K deficiency. PATHOPHYSIOLOGY
The lipid concentration in the liver increases after ingestion of a high-fat meal,
■ Coagulation abnormalities are as a result of mobilization of fat stores during fasting, or because of hepatic syn-
positively correlated with the thesis of lipids from carbohydrates.5,7 Lipid is typically oxidized within mito-
magnitude of increase in serum chondria or secreted as part of a very-low-density lipoprotein. If lipid buildup
alkaline phosphatase. 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 of weekly liver biopsy
tion appear to occur in re- specimens revealed that obesi-
sponse to hepatocellular lipid ty was not associated with liver
accumulation. parenchymal lipid accumula-
The mechanisms of hepatic tion but that fasting resulted
fat accumulation include in- in HL in all 15 cats beginning
creased delivery of fatty acids at 2 weeks. Histologic exami-
to the liver, decreased release nation of successive liver biop-
of very-low-density lipopro- sies revealed progressive hepa-
teins, and decreased oxidation tocyte lipid accumulation
of fatty acids within mito- in all 15 cats. These findings
chondria. 5,7 Increased fatty- suggest that clinical HL should
acid mobilization to the liver not develop in otherwise
occurs during starvation. Cats healthy obese cats after only a
with HL usually have a peri- few days of fasting.
od of anorexia that leads to Laboratory models have
severe protein restriction and been developed to define the
adipose tissue mobilization to degree of food restriction re-
the liver, resulting in excessive quired to induce HL in cats.
hepatic triglycerides. In addi- One author found that lipid
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. calculated maintenance ener-
lipoprotein formation, which gy requirements for 14 weeks
in turn makes the liver unable but did accumulate in the liv-
to remove excess triglycerides. ers of six other cats fed only 25% of their calculated
Transmission electron microscopy reveals that the hep- maintenance energy requirements for the same amount
atocytes of cats with HL have reduced quantities of per- of time.10
oxisomes, endoplasmic reticulum, Golgi complexes, lyso- In another study, weight loss was induced in six obese
somes, and mitochondria.8 These organelles all perform and six non-obese cats by feeding them 50% of their
metabolic functions necessary for hepatic lipid metab- calculated maintenance energy requirements for 29
olism and fatty-acid oxidation. Electron microscopy days; none of the cats developed apparent changes in
studies also demonstrate that lipid-distended bile canali- physical, hematologic, or serum biochemical values in-
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 ergy restriction needed to induce HL was defined to be
increase and hepatotoxic bile acids accumulate, further between 50% and 75%. No differences between obese
damaging the liver parenchyma. and non-obese cats in terms of their responses to food
Although the precise pathologic mechanism(s) of fe- restriction were observed in either of these models.
line HL remains a mystery, most researchers believe that Thus it appears that near-total anorexia, restriction of
multiple factors associated with cats’ unique metabolism an essential nutrient, significant weight loss, or factors
of proteins and lipids are involved. Proposed pathophysi- other than obesity are required for the development of
ologic mechanisms include metabolic changes associated HL (Figure 1).
with starvation and obesity, protein and nutrient defi- Another proposed pathophysiologic mechanism of
ciencies, relative carnitine deficiency, and insulin resist- feline HL involves carnitine, an amine synthesized from
ance. methionine and lysine. Carnitine is required for trans-
One study confirmed that long-term fasting may in- port of fatty acids through hepatic mitochondrial mem-
duce clinical HL in obese cats.9 Voluntary fasting oc- branes for oxidation and removal. Plasma, liver, and
curred when obese cats were offered a purified, nutri- skeletal muscle carnitine concentrations are higher in
tionally complete but unpalatable diet. Clinical signs and cats with HL than in control cats,12 suggesting that in-
laboratory results consistent with HL were observed in creased carnitine synthesis may be a metabolic response
12 of 15 cats after 5 to 7 weeks of fasting and were asso- to HL to facilitate fatty-acid oxidation.7 If the demand
ciated with a 30% to 35% reduction in initial body for carnitine exceeds its synthesis, a relative deficiency


Compendium September 2000 Small Animal/Exotics

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


Small Animal/Exotics Compendium September 2000
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 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.
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-
rangements of vitamin K absorption and may increase
BILL TO: the risk for coagulopathies and bleeding.
Diagnostic Imaging
Radiography and abdominal ultrasonography can be
ADDRESS helpful in diagnosing feline HL. These imaging tech-
niques often reveal hepatomegaly and assist in exclud-
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.


Compendium September 2000 Small Animal/Exotics

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- Figure 2—Cytology of a fine-needle aspirate from the liver of
able amounts of free abdominal fluid may be present as a cat with hepatic lipidosis. The severe cytoplasmic vacuoliza-
tion of the hepatocytes represents fatty infiltration.
well23; if so, abdominocentesis to obtain fluid for cyto-
logic evaluation is indicated and may yield valuable di-
agnostic information. Liver). Hepatic cytologic samples are most useful in di-
Ultrasonography reveals the lipidic liver to be diffuse- agnosing diffuse diseases that readily exfoliate cells,
ly hyperechoic. Ultrasonographic diagnosis has classical- such as HL or lymphosarcoma.
ly been based on evaluation of the relative echogenicity
of the liver compared with that of falciform fat (i.e., the Liver Biopsy
liver appears hyperechoic compared with falciform fat in Definitive diagnosis of feline HL requires histopatho-
cats with HL).24 Although this criterion was initially be- logic evaluation of a liver biopsy specimen. Liver biop-
lieved to be a highly sensitive and specific diagnostic in- sies offer the advantage of evaluating both hepatocellu-
dicator of HL, a recent prospective study revealed that lar morphology and liver lobule architecture. Cats
the liver is diffusely hyperechoic compared with falci- should be evaluated for coagulopathies before undergo-
form fat in clinically normal obese cats.25 Additionally, ing liver biopsy. Pretreatment with subcutaneous vita-
both lymphosarcoma and cirrhosis have been described min K1 (1 mg/kg 12 hours before biopsy) is advised.3,4
as diffusely hyperechoic diseases of the liver.26 The pres- Techniques for obtaining liver tissue include ex-
ence of a hyperechoic liver, therefore, is neither a specif- ploratory celiotomy and percutaneous needle biopsy
ic finding nor a sensitive indicator of HL in cats. (blind, ultrasound-guided, or laparoscopic methods).
Hepatobiliary scintigraphy is a noninvasive diagnos- The technique selected largely depends on the condi-
tic imaging technique that has been recently evaluated tion of the cat and the skill and experience of the sur-
for diagnosis of feline hepatobiliary diseases. Although geon. Because of metabolic derangements and impaired
this technique can be useful in assessing the severity of liver function, cats with severe HL are often poor surgi-
hepatic dysfunction and determining whether extrahep- cal candidates,3,4,7 and major surgery should be avoided
atic biliary obstruction is present, it cannot differentiate before the initial stabilization phase of their therapy.3,4
specific disease entities.27 Advantages of exploratory surgery include the ability to
visually inspect the liver, select biopsy sites, control
Fine-Needle Aspiration bleeding, and obtain biopsies from other organs.
Although laboratory testing and diagnostic imaging Both impression smears of biopsy specimens and
can identify a high likelihood of HL, evaluation of hep- histopathologic evaluation are recommended. In a ret-
atocellular morphology is required to make a definitive rospective study of 56 hepatic cytology specimens, cy-
diagnosis. Fine-needle aspiration of the liver may reveal tologic evaluation of impression smears concurred with
vacuolar changes typical of HL (Figure 2) but should be histopathologic diagnosis in 83% of specimens.28 Re-
interpreted with caution because it cannot rule out such sults of cytology may be obtained rapidly and may aid
concurrent liver diseases as cholangiohepatitis with cer- practitioners in making treatment decisions while they
tainty and may miss focal lesions. await results of histopathology. In cats with HL,
Fine-needle aspirates can usually be collected with no histopathology reveals the presence of swollen vacuolat-
or only minimal sedation, and complications are ex- ed hepatocytes and canalicular bile stasis. Vacuoles stain
tremely rare (see Fine-Needle Aspiration of the Feline with oil red-o, confirming the presence of lipid. Little


Small Animal/Exotics Compendium September 2000

Fine-Needle Aspiration of the Feline Liver

■ Place the cat in dorsal recumbency with the body tilted aspiration to prevent trauma to the liver and
so that the thorax is slightly higher than the abdomen. In contamination of the sample with peripheral blood.)
this position, the liver moves caudally, usually allowing ■ Release all pressure and withdraw the needle. If blood
palpation of an enlarged liver. appears in the hub of the needle at any time during
■ Use a 10-ml syringe and a 1-inch, 22- or 23-gauge aspiration, discontinue aspiration, select an adjacent
needle to perform fine-needle aspiration. A 1.5-inch site, and reaspirate.
needle may be needed in obese cats (selection of needle ■ Immediately eject aspirated material onto slides: Remove
length can be aided by reviewing abdominal radiographs the needle, fill the syringe with air, and expel the air
to identify the thickness of the falciform fat pad through through the needle. Grossly, liver aspirates appear
which the needle is to be inserted to reach the liver). reddish brown.
■ Shave and sterilely prepare the cranioventral abdomen ■ Place a second glass slide on top of the sample and
between the costal arches. gently slide it off the lower slide (i.e., make a “squash
■ If the liver cannot be palpated, perform blind aspiration prep smear”). Air-dry slides as rapidly as possible to
by inserting the needle midway between the midline and preserve cellular morphology.
the left costal arch at a level 1 cm caudal to the end of ■ Examine one slide to determine whether the sample is
the xiphoid process (see figure). (Care should be taken adequate. Multiple aspirations often improve diagnostic
to avoid entering the right side of the liver to prevent yield.
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, line HL. Current therapeutic recommendations will be
the liver appears yellow and mottled. Its cut surface is discussed in a future article.
often greasy, and sections float in water or formalin.
SUMMARY The author thanks Drs. D. S. Spano, DVM, PhD, Dip-
Feline HL is a common hepatobiliary disease in do- lomate American College of Veterinary Practitioners,
mesticated cats and results in severe impairment of liver and D. K. Macintire, DVM, MS, Diplomate American
function. All cats with HL need thorough systematic College of Veterinary Internal Medicine and American
evaluation to rule out primary underlying diseases. Per- College of Veterinary Emergency and Critical Care,
sistent anorexia should be avoided, particularly in obese College of Veterinary Medicine, Auburn University, Al-
cats. Cats that are anorectic for less than 1 week, how- abama, for their encouragement in writing this article.
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 REFERENCES
1. Barsanti JA, Jones BD, Spano JS, et al: Prolonged anorexia
hepatic metabolism leading to lipid accumulation and associated with hepatic lipidosis in three cats. Feline Pract
clinical disease. Results of such studies should be useful 7:52–57, 1977.
in the development of methods to prevent and treat fe- 2. Gagne J, Weiss DJ, Armstrong PJl: Histopathologic evalua-
Small Animal/Exotics Compendium September 2000

tion of feline inflammatory liver disease. Vet Pathol 33:521– Med 7:205–209, 1993.
526, 1996. 18. Hill RC, Van Winkle JJ: Acute necrotizing pancreatitis and
3. Center SA, Warner K: Feline hepatic lipidosis: Better defin- acute suppurative pancreatitis in the cat: A retrospective study
ing the syndrome and its management. Proc 16th Annu of 40 cases (1976–1989). J Vet Intern Med 7:25–33, 1993.
ACVIM Forum:56–58, 1998. 19. Center SA, Erb HN, Joseph SA: Measurement of serum bile
4. Norsworthy G: Improving survival in cats with hepatic lipi- acid concentrations for diagnosis of hepatobiliary disease in
dosis. Proc TNAVC:285, 1998. cats. JAVMA 207:1048–1054, 1995.
5. Dimski DS, Taboada J: Feline idiopathic hepatic lipidosis. 20. Lisciandro SC, Hohenhaus AE, Brooks M: Coagulation ab-
Vet Clin North Am Small Anim Pract 25:357–373, 1995. normalities in 22 cats with naturally occurring liver disease. J
6. Jacobs G, Cornelius L, Allen S, Greene C: Treatment of id- Vet Intern Med 12:71–75, 1998.
iopathic hepatic lipidosis in cats: 11 cases (1986–1987). 21. Williams DA: Feline pancreatic disease. Proc 15th Annu
JAVMA 195:635–638, 1989. ACVIM Forum:407–408, 1997.
7. Dimski DS: Feline hepatic lipidosis. Semin Vet Med Surg 22. Swift NC, Marks SL, MacLachlan NJ, et al: Serum-like im-
(Small Anim) 12:28–33, 1997. munoreactivity in the diagnosis of feline pancreatitis [abstract].
8. Center SA, Guida L, Zanelli MJ, et al: Ultrastructural hepa- Proc 17th Annu ACVIM Forum:699, 1999.
tocellular features associated with severe hepatic lipidosis in 23. Nyland TG, Mattoon JS, Wisner ER: Ultrasonography of
cats. Am J Vet Res 54:724–731, 1993. the pancreas, in Nyland TG, Mattoon JS (eds): Veterinary
9. Biourge VC, Groff JM, Munn RJ, et al: Experimental in- Diagnostic Ultrasound. Philadelphia, WB Saunders Co,
duction of hepatic lipidosis in cats. Am J Vet Res 55:1291– 1995, pp 85–94.
1302, 1994. 24. Yeager AE, Mohammed H: Accuracy of ultrasonography in
10. Armstrong PJ: Feline hepatic lipidosis. Proc 7th Annu the detection of severe hepatic lipidosis in cats. Am J Vet Res
ACVIM Forum:335–337, 1989. 53:597–599, 1992.
11. Dimski DS, Buffington CA, Johnson SE, et al: Serum 25. Nicoll RG, O’Brien RT, Jackson MW: Qualitative ultra-
lipoprotein concentrations and hepatic lesions in obese cats sonography of the liver of obese cats. Proc 1996 Annu Sci
undergoing weight loss. Am J Vet Res 53:1259–1262, 1992. Meet Am Coll Vet Res:7–10, 1996.
12. Jacobs G, Cornelius L, Keene B, et al: Comparison of plas- 26. Newell SM, Selcer BA, Cornelius LM: Imaging techniques
ma, liver, and skeletal muscle carnitine concentrations in cats for evaluating feline hepatobiliary disease. Vet Med 9:859–
with idiopathic hepatic lipidosis and in healthy cats. Am J 868, 1994.
Vet Res 51:1349–1351, 1990. 27. Newell SM, Selcer BA, Roberts RE, et al: Hepatobiliary
13. Armstrong PJ, Hardy EM, Cullen JM, et al: L-carnitine re- scintigraphy in the evaluation of feline liver disease. J Vet In-
duces hepatic fat accumulation during rapid weight reduc- tern Med 10:308–315, 1996.
tion in cats. Proc 10th Annu ACVIM Forum:810, 1992. 28. Kristensen AT, Klausner JS, Weiss DJ, Hardy RM: Liver cy-
14. Biourge V, Nelson RW, Feldman EC, et al: Effect of weight tology in cases of canine and feline hepatic disease. Compend
gain and subsequent weight loss on glucose tolerance and in- Contin Educ Pract Vet 12(6):797–809, 1990.
sulin response in healthy cats. J Vet Intern Med 11:86–91,
15. Center SA, Crawford MA, Guida L, et al: A retrospective About the Author
study of 77 cats with severe hepatic lipidosis: 1975–1990. J
Vet Intern Med 7:349–359, 1993. Dr. Griffin is affiliated with the Scott-Ritchey Research
16. Weiss DJ, Armstrong PJ, Gagne J: Inflammatory liver dis- Center, College of Veterinary Medicine, Auburn Universi-
ease. Semin Vet Med Surg (Small Anim) 12:22–27, 1997. ty, Alabama. She is a Diplomate of the American College
17. Akol KG, Washabau RJ, Saunders HM, Hendrick MJ: of Veterinary Internal Medicine.
Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern