D Feline Dermatophytosis: An Update on Diagnosis and Treatment

Volume 1, Issue 7
j
November/December 2011
Feline Dermatophytosis: An Update on
Diagnosis and Treatment
Jeanne B. Budgin, DVM, DACVD
Animal Specialty Center
D
ermatophytosis, or “ringworm,” is a superficial infection of the
keratinized tissues including the claws, hair, and outer layer
of the skin. The fungus that causes most infections in the
cat is Microsporum canis (M .canis). It is an important zoonotic agent;
approximately 60% of human household members are likely to develop
lesions. Young, immunosuppressed, and previously unexposed animals are
most susceptible; this implies a role of protective immunity in the disease.
Clinical Signs
The lesions in cats consist of the “classic” circular expanding alopecic
lesions with or without inflammation, scale, crusts, and widespread patchy
hair loss (fig 1). Miliary dermatitis, kerion reaction, onychomycosis,
eosinophilic plaques, and an unapparent carrier state may also be
observed. These clinical presentations are extremely variable and may
closely mimic other common dermatoses including allergies. Persian
and Himalayan breeds are more susceptible to infection.
Diagnosis
Wood’s lamp examinations frequently yield false positive and negative
reactions and should not be relied upon for a definitive diagnosis.
Approximately 30-50% of M. canis strains will fluoresce. Fungal
culture is the diagnostic procedure of choice. Skin biopsy may also be
helpful in reaching a definitive diagnosis, but is not usually necessary
nor is it as sensitive as fungal culture.
Dermatophyte test medium (DTM) is used most commonly for fungal
culture. Dermatophytes produce a red color change simultaneously with
observable colony growth, whereas non-pathogenic fungi begin to utilize
the protein in the medium only after the carbohydrate source has been
exhausted, resulting in a later color change. False positive DTM results
occur if this late color change is incorrectly interpreted. Malassezia sp. may
also produce an early color change with growth on DTM.
Fungal culture may be performed by several different techniques. A
hemostat may be used to pluck hairs along the advancing edge of active
lesions, or hair that fluoresces on Wood’s lamp examination. If the cat has
more generalized lesions, or a carrier state is suspected, a sterile toothbrush
should be brushed through the entire coat to collect scale and hair. The
tips of the bristles are then embedded in the media.
Figure 1 : Classic lesions associated with M. canis infection: circular
areas of alopecia, erythema, and peripheral crust.
The fungal culture plates should be incubated for four weeks. And while
specific conditions for incubation have been recommended in the past,
Moriello et al. determined that colony growth and sporulation were not
influenced by light and temperature. Under all experimental conditions,
consistent sporulation was evident on all plates at five days. Growth
may be delayed in patients who are already receiving treatment. Daily
examination for white to off white, fluffy growth with a simultaneous color
change is recommended. The importance of microscopic examination of
the fungal hyphae cannot be over emphasized to prevent a false positive
report. This is easily accomplished by grasping a piece of clear acetate tape
Feline Dermatophytosis
Figure 2 : Spindle or canoe shaped macroconidia
of M. canis.
with a hemostat and touching the sticky side of
the tape to the culture growth. A drop of new
methylene blue or lactol phenol cotton blue
is placed on a slide and the tape is then stuck
to the slide and examined at 40x. Spindle or
canoe-shaped macroconidia, with thick walls, a
terminal knob, and compartments with greater
than 6 cells are consistent with M. canis (fig 2).
Rational selection of therapy for dermatophytosis
depends on several factors including the severity
of the infection, the age of the patient, and the
possible presence of underlying concurrent
disease. Currently topical treatments for
dermatophytosis are only recommended when
combined with systemic therapy. The endpoint
of treatment is at least two negative consecutive
fungal cultures collected at bi-weekly intervals.
A combination of oral therapy, clipping of the
hair coat (especially for cats with long hair and/
or generalized infection), topical rinses (lime
sulfur dips every 5-7 days), and environmental
decontamination is necessary for effective
treatment. Fungal cultures should be performed
every 2-4 weeks until mycological cure, as
clinical cure (the resolution of lesions) often
occurs before mycological cure.
Systemic antifungal therapy is the treatment
of choice for dermatophytosis. Itraconazole,
griseofulvin, fluconazole, and terbinafine
are all effective systemic antifungal agents.
Ketoconazole is considered contraindicated in
cats due to the high incidence of side effects;
25% of patients may experience anorexia, fever,
depression, vomiting, diarrhea, hepatopathy, and
cholangiohepatitis.
Itraconazole (Sporanox®, Janssen Pharmaceutica
and generic) is not labeled for use in animals in
the United States. However, it is considered the
2
Continued from page 1
treatment of choice for dermatophytosis in cats
and is dosed at 5-10 mg/kg orally every 24 hours.
Itraconazole is available as a 100 mg capsule and
a 10 mg/ml solution; compounding the drug
renders it less effective. Long tissue half-life
and high levels in the skin, hair follicles, and
glandular structures makes this drug amenable
to “pulse” dosing regimens. Several dosing
schedules are recommended including (1) daily
dosing; (2) combined continuous/pulse therapy:
daily dosing for 28 days, then on an alternate
week regimen; and (3) cycle therapy: daily
dosing for 15 days, followed by fungal cultures
10-15 days post treatment. The cycle is repeated
until the cat is cured. Finally, treatment for two
consecutive days per week is useful in preventing
infection for long haired cats in contaminated
environments, since relapse is common under
these circumstances. Side effects of itraconazole
include anorexia, depression, vomiting, weight
loss, elevated ALT activity, jaundice, and
hepatotoxicity. The drug should not be used
in cats with pre-existing liver disease. Hepatic
enzymes should also be monitored monthly
during treatment.
Griseofulvin (Fulvicin-U/F®, Schering-Plough)
is available in two formulations: microsize dosed
at 50 mg/kg orally every 24 hours or divided
every 12 hours, and ultramicrosize dosed at
10-15 mg/kg orally every 24 hours or divided
every 12 hours. Side effects include bone
marrow suppression, increased liver enzyme
activity, anorexia, vomiting, depression, ataxia,
and pruritus. As a potent teratogen, griseofulvin
must not be used in pregnant animals. Cats
should also test negative for feline leukemia
and feline immunodeficiency virus due to the
potential for immunosuppressive side effects.
Kittens may be more susceptible to side effects
and should be monitored very closely.
Fluconazole (Diflucan®, Roerig and generic)
may be used effectively at a dose of 50 mg/cat
orally every 24 hours or 5 mg/kg orally every 1224 hours. Fluconazole appears to be relatively
safe with inappetence most commonly reported.
Because it is primarily eliminated through renal
excretion, doses or dosing intervals may need to
be adjusted in patients with renal impairment.
Terbinafine (Lamisil®, Novartis and generic)
is the newest systemic agent and is available in
a 250 mg size tablet. Based on pharmacologic
data, a dose of 30 to 40 mg/kg orally every 24
hours is appropriate for therapy. At this dose,
significantly higher concentrations are found in
hair, therefore resulting in potential for pulse or
cycle therapy similar to itraconazole. The drug
appears to be well tolerated with gastrointestinal
side effects most commonly reported.
The clinical efficacy of lufenuron (Program®)
has been disappointing, thus its use in
the treatment of dermatophytosis is
not recommended. Vaccination with a
commercial vaccine, currently off the market,
was also not recommended for prophylaxis or
treatment, as sterile abscesses were observed
at the injection site, and lesions often resolved
but cats remained positive for disease, thus
complicating treatment duration.
Environmental decontamination must be
emphasized in every case. Fungal spores
are highly resistant and may survive in the
environment for 18 months. Animals in the
household may be asymptomatic carriers
harboring spores on their coat without clinical
signs. All animals should be tested and/or
treated. All brushes, beds, leashes, collars, and
other sources of infection should be thoroughly
cleaned or discarded and replaced. Current
recommendations for cleaning the environment
include thoroughly vacuuming, cleansing, and
disinfecting all surfaces, floors, and tolerant
fabrics with a 10-20% bleach solution. Steam
cleaning may also be beneficial, but professional
steam cleaning should be utilized, as high water
temperature is very important. In households
with many animals or in breeding situations,
infected animals and those that test positive on
fungal culture should be isolated for the duration
of treatment. Owners should be advised to
avoid direct contact with the lesions or hair
of the infected animal by wearing protective
clothing and gloves. Hand washing should
occur after every encounter. Confining the
infected animal(s) to one room or to a cage/crate
will help prevent spread of infection to other
animals, people, and environments.
Effective diagnosis, treatment, and client
education is essential for the successful
management of dermatophytosis. j
References:
Moriello KA. Treatment of dermatophytosis in dogs
and cats: a review of published studies. Vet Dermatol
2004;15:99-107.
Scott DW, Miller WH, Griffin CE. Small Animal
Dermatology. 6th ed. Philadelphia: WB Saunders
Co.; 2001.
Moriello KA, Verbrugge MJ, Kesting RA. Effects
of temperature variations and light exposure on the
time to growth of dermatophytes using six different
fungal culture media inoculated with laboratory
strains and samples obtained from infected cats. J
Feline Med Surg 2010;12(12):988-990.
Full Circle Forum
Attacked by a Snake:
A Case Report
Danna M. Torre, DVM, DACVECC
VCA Shoreline Veterinary Referral & Emergency Center
“G
riffin,” a 10-year-old castrated male
Brussels Griffon, presented to VCA
Shoreline Veterinary Emergency
and Referral Center as a referral from Dr. James
St. Clair at Meriden Animal Hospital. Two days
prior to being transferred to VCA Shoreline,
Griffin had been bitten by a venomous snake,
which his owners suspected was a Copperhead,
as they had seen Copperheads on their property.
Griffin had been treated with intravenous
steroids, antibiotics, pain medications, and fluids,
however he had become progressively more
anemic and was transferred to VCA Shoreline
for more intensive treatment.
On presentation, Griffin was quiet but alert and
responsive. His heart rate and temperature were
within normal limits, however he was panting
excessively and had pale mucous membranes. He
was hypotensive with a systolic blood pressure
of 70 mmHg. Griffin had several bite wounds
generalized over his body. His right front leg
was swollen and he had necrotic bite wounds
in the axilla and antebrachium (medial aspect).
Two puncture wounds were noted on the ventral
thorax with a small area (about 1 cm in diameter)
of necrotic black skin adjacent to wounds. Initial
diagnostic evaluation included a venous critical
care and blood gas analysis, a coagulation panel,
and a CBC/mini chemistry panel (performed
by the referring hospital that morning). The
critical care panel showed a hyponatremia (135.4
mmol/L, reference range 142 -150 mmol/L), a
mild hypokalemia (3.75 mmol/L, reference range
3.80-4.90 mmol/L), a mild hyperlactatemia (3.5
mmol/L, reference range 0.3-1 mmol/L), and
mild azotemia with a BUN of 40 mg/dL (reference
range 7-28 mg/dL) and a creatinine of 1.7 mg/
dL (reference range 0.5-1.3 mg/dL). The CBC
showed anemia and thrombocytopenia (HCT
18%, platelets 48,000). The mini chemistry panel
from that morning showed hypoproteinemia (4.7
g/dL), hyperglycemia (158 mg/dL), an increased
BUN (45 mg/dL), and an increased alkaline
phosphatase (174 U/L, reference range 20-150
U/L). The prothrombin time (PT) was normal
at 17 seconds (reference range 12-17 sec). The
activated partial thromboplastin time (PTT) was
out of range (reference range 71-102 sec).
Griffin was admitted to the hospital.
November/December 2011
An
intravenous catheter was placed for the
administration of medications/fluids. He was
started on broad spectrum antibiotic coverage
(ampicillin and enrofloxacin). Hydromorphine
was given intravenously for pain management
every 4 hours. A wet to dry bandage was placed
on the right front leg. Our goal was to have
the bite wounds declare themselves in order to
determine how much of the skin was going to
need to be debrided. He was given a single unit
of packed red blood cells over 4 hours. He was
also given a single unit of fresh frozen plasma
over 2 hours. Crystalloid therapy was instituted
to maintain Griffin’s fluid requirements after the
blood transfusions were complete.
By day 2 of Griffin’s hospitalization, his
coagulation profile had normalized (PT 14 sec,
PTT 113 sec). His PCV/TS was 27%/4.3 g/
dL. A fentanyl patch was placed for continued
pain management. Hetastarch was started to
minimize his crystalloid fluid requirement
and, given his low protein levels and suspected
decreased oncotic pressure, to help with oncotic
pressure. The remainder of the treatments
remained unchanged throughout the duration
of hospitalization. The wet to dry bandage
was replaced, as debridement was not deemed
necessary yet. Later in the day, Griffin started to
eat for the technical staff.
and a nonadherent bandage was placed over the
medial aspect of the antebrachium.
On day 5 of hospitalization, Griffin’s vital
signs were stable, his PCV/TS was holding
(31-33%/5.4 g/dL), and he was eating
intermittently on his own. The wet to dry and
nonadherent bandages were replaced and no
further debridement was necessary at that time.
The decision was made to discharge Griffin
with frequent follow up examinations. He was
discharged on Clavamox, Baytril, and tramadol.
Over the next month, Griffin had frequent recheck
examinations. He had two additional surgeries
to debride necrotic tissue over his ventral thorax
and right axilla. He continued to get stronger and
gain weight. His laboratory values continued to
improve. After two months, he was reevaluated
and was found to have made a full clinical recovery.
Case Discussion
North American venomous snakes are divided
into two major taxonomic groups. The first is
the Crotalidae, or pit vipers, which contains the
rattlesnakes (genera Crotalus and Sistrurus) and
moccasins (genus Agkistrodon), the latter genus
containing the Copperhead (Agkistrodon contortix)
and the Cottonmouth. The second major group
On day 3 of hospitalization, Griffin’s PCV fell
to 19% (TS 4.4 g/dL) and he appeared clinical
for his anemia. A re-check coagulation was
normal (PT 13 sec, PTT 92 sec). After crossmatching, he was given a second packed red
blood cell transfusion. His recheck PCV/TS was
36%/4.8 g/dL. Griffin ate for his owner after the
transfusion was complete.
On day 4 of hospitalization, Griffin was placed
under general anesthesia to assess his wounds. The
wound on his thorax was still declaring itself so it
was left alone. About 40% of the medial surface
of the right antebrachium was deemed nonviable
tissue. The skin was debrided until bleeding was
noted. The subdermal muscle layer/fascia was
healthy viable tissue. The skin was closed in a
simple interrupted pattern. The skin in the right
axilla had questionable viability, and the decision
was made to continue to assess the region daily. A
wet to dry bandage was placed in the right axilla
Griffin and his family pictured with Dr. Holahan
and Dr. Torre.
Continued on page 4
3
Attacked by a Snake
of venomous North American snakes contains
representatives of the family Elapidae, the eastern
(Micrurus fulvius) and western (Micruroides
euryxanthus) coral snakes. This review will focus
on the first group, the Crotalidae. Although each
type of snake venom has its own level of virulence,
the clinical sequelae of bites are similar.
The Pathogenesis of Venom
Crotalid venom consists of 90% water, numerous
enzymes, and peptides. Hyaluronidase and
collagenase aid in spreading venom through
interstitial spaces, proteases can lead to
coagulopathies and necrosis, and phospholipases
cause cytotoxic effects that lead to both endothelial
cell damage and resultant inflammation. Crotalid
venom increases the permeability of capillary
cell membranes, which allows the venom to
spread within the prey.1 Polypeptides cause
capillary endothelial cell damage, which leads
to endothelial cell swelling and rupture. The
resultant gaps in the microvasculature allow third
spacing of plasma and erythrocytes, leading to
both edema and ecchymosis.2 This process occurs
in any capillary exposed to venom, including
skeletal muscle, kidneys, myocardium, and
endothelium. The cardiovascular effects manifest
as hypotension secondary to an increase in vascular
permeability causing third spacing of fluid out
of the intravascular space. Hypotension can also
occur secondary to fluid losses from vomiting
and hemorrhage. Skeletal muscle can become
necrotic due to a myotoxin within the venom that
causes increases in intracellular calcium leading
to activation of damaging enzymes. Acute
renal failure is occasionally reported and the
pathogenesis includes hypotension, circulatory
collapse, intravascular hemolysis with resultant
hemoglobinuria, myoglobinuria, direct toxic effects
to the kidney and thromboembolic events. The
hematological effects of venom can be classified
into four categories: procoagulants, anticoagulants,
fibrinolytic enzymes, and thrombocytopenia.
Although all areas of the coagulation cascade
appear to be targeted, the net effect of venom on
hemostasis is an anticoagulative state.
Diagnosis
The diagnosis of envenomation is often based on
the owner’s observation as well as clinical signs.
Toxicity depends upon several variables including
the volume of venom injected, the depth of the
bite, and the size of the victim. If there has
been little or no envenomation, clinical signs
will consist of minor swelling. With moderate
to severe envenomation, immediate and
progressive pain is noted.3 Clinical signs usually
develop within 10 to 30 minutes. Ecchymosis,
4
Continued from page 3
with resultant tissue necrosis at the site of
injury, is a common clinical finding. Common
signs include lethargy, weakness, hypotension,
arrhythmias, ataxia, bleeding, vomiting, diarrhea,
respiratory distress, and shock. 3
Patients that present with suspected or known
envenomation should have complete bloodwork
and a urinalysis and coagulation profile performed.
Throughout the duration of hospitalization, a
patient’s electrolytes, renal parameters, hematocrit,
platelet count, protein level, and coagulation
status should be continuously monitored. Typical
bloodwork abnormalities include echinocytosis,
spherocytosis, thrombocytopenia, anemia,
leukocytosis, and prolonged clotting times.4
Echinocytosis are erythrocytes with uniform,
regularly spaced membrane projections.Echinocyte
formation is thought to be caused directly by the
venom itself, is dose dependent, and is self-limiting
with changes resolving within 48 hours. Common
chemistry profile abnormalities include azotemia,
hypoalbuminemia, hypoproteinemia, and elevated
levels of creatinine kinase, alkaline phosphatase,
alanine transaminase, g-glutamyl transferase, and
aspartate transaminase.4
First Aid Treatment
Although safe and rapid transport to a veterinary
emergency center is recommended, owners can
institute some initial first aid treatment en route.
First they should be instructed to slow the spread
of venom. This can be performed by limiting
the patient’s activity level or immobilizing the
bitten area. If signs of envenomation occur,
a constricting band applied tightly enough to
impede lymph flow can be applied. Lymphatic
outflow is the main dissemination route for
envenomation.2 In addition, the owner should
monitor their pet very closely on the way to
the veterinary hospital. The owner can be
very helpful to the veterinarian in providing an
assessment of the initial clinical course of the bite.
In-Hospital Treatment
The treatment for snakebite envenomation is
multi-faceted and depends upon the individual
patient’s clinical presentation, laboratory
abnormalities, and wound care requirements.
Initial emergency treatment should consist of
stabilization of the cardiovascular and respiratory
systems. At least two large bore intravenous
catheters (or a multiple lumen central catheter
if the patient is not coagulopathic) should be
established for the administration of either
crystalloids, or a combination of crystalloids and
colloids, and intravenous medications. Clinical
parameters, such as mucous membrane color,
capillary refill time, pulse quality, blood pressure,
urine output, and improvement in the degree
of lactic acidosis, can all be used as a guide to
gauge appropriate fluid therapy. If respiratory
compromise is observed, initial treatment
with oxygen via a facemask or nasal cannula is
recommended. Thoracic radiographs and arterial
blood gas analysis are indicated if respiratory
compromise continues despite supportive
measures as acute lung injury (ALI) or adult
respiratory distress syndrome (ARDS) are known
sequelae of envenomation. Although anemia and
coagulation abnormalities are common, the use of
blood products for envenomation is controversial.
Coagulopathy associated with envenomation is
consumptive and unresponsive to either heparin
or blood products while unneutralized venom is
circulating.1 Providing coagulation factors and
blood products adds substrate for unneutralized
venom, which leads to potential thromboembolic
events.1 Current recommendations emphasize
neutralization of venom with antivenin.1 In
the current case, the decision was made to give
Griffin blood products as we did not feel there was
circulating venom to neutralize and he was clinical
for his anemia and coagulopathy.
Antivenin administration is recommended for
cases in which there is worsening local injury,
clinically significant coagulopathy, or systemic
signs (i.e. hypotension).1 Antivenin should
ideally be administered within the first 4 hours
after envenomation.1 The benefits of antivenin
decrease if administration is delayed, but antivenin
can still have clinically positive effects for up to 24
hours after envenomation.1 When administered
early, antivenin binds to the venom itself,
subsequently neutralizing it, reversing some clinical
manifestations of envenomation, and preventing
further progression.
Local tissue necrosis,
unfortunately, cannot be stopped by antivenin
administration.1 There are two commercially
available antivenins for animals in the United
States. Antivenin (Crotalidae) Polyvalent (ACP;
Fort Dodge Animal Health) and Crotalidae
Polyvalent Immune Fab (ovine; CroFab, FabAV,
Protherics, Nashville, TN). The use of the ACP
antivenin is considered more favorable due to less
clinical side effects and its reasonable price.
Acutely, the area of the snakebite should be clipped
of fur and cleaned using aseptic scrub and kept
dry. The circumference of the swelling should
be measured and recorded every 15 minutes to
help determine progression and requirements for
antivenin administration.1 If the wound progresses
and local necrosis occurs, the affected area should
be treated like an open wound until a healthy
granulation bed forms. Surgical debridement may
Full Circle Forum
be needed for necrotic tissue after several days.1
renal compromise due to their side effects.
Additional treatment should consist of broad
spectrum antibiotic therapy as numerous
pathogenic bacteria have been isolated
from the mouths of crotalid species.4 The
administration of pain medication is an
essential part of treatment. Opioids, as
intermittent injections or as a continuous
rate infusion, should be instituted as early as
possible in the course of treatment. The use
of nonsteroidal anti-inflammatory drugs are
contraindicated in hypotensive patients with
Prognosis
The mortality rate of envenomation in dogs has
reportedly been as low as 3.7% with treatment.4
Snakes bites have a variable prognosis, with the
more important parameters being time from
envenomation to presentation, the number of
bites (as well as the areas bitten) and the degree
of hematologic abnormalities.
Aggressive
therapy with intravenous fluids, antibiotics, pain
medications, and antivenin (when appropriate)
should be considered. It is not uncommon to have
extensive necrotic wounds from snake bites which
will require surgical attention. j
References:
Gold B, Dart R, Barish R. Bites of venomous
snakes. N Engl J Med 347(5): 347-356, 2002.
2
Walter FG, Bilden EF, Gilby RL. Envenomations.
Crit Care Clin 15(2): 353-386, ix, 1999.
3
Hudelson S, Hudelson P. Pathophysiology of snake
envenomation and evaluation of treatments, part 1.
Compend Contin Educ Pract Vet 17(7):889-897, 1995.
4
Hudelson S, Hudelson P. Pathophysiology of
snake envenomation and evaluation of treatments,
part II. Compend Contin Educ Pract Vet 17(8):10351041, 1995.
1
The Use of Ultrasound for Diagnosis
of a Gastric Foreign Body
Joseph D. Stefanacci, VMD, DACVR
VCA Veterinary Referral & Emergency Center
“B
ailey,” a 10 year old, spayed female
Puli, presented to Dr. Christian
Benyei at Schulhof Animal
Hospital in Westport, CT, with a clinical
history of difficulty walking, weakness,
ataxia, chronic anemia, and (most recently) a
significantly decreased appetite bordering on
complete anorexia. Bailey had been medicated
since April of the same year with a tapering
dose of prednisone for a previous bout of nonspecific ‘back pain.’ The patient had been seen
Figure 1
Figure 2
November/December 2011
at that time by Dr. Heather Galano, VCA
Shoreline’s neurologist, but despite a thorough
workup (including MRI), no definitive cause
was found and empirical treatment with
prednisone was successful in resolving clinical
symptoms. Upon current examination Bailey’s
neurological status was determined to be within
normal limits so Bailey was referred to Dr.
Larry Berkwitt, internal medicine specialist for
VCA Shoreline, for anemia and inappetence.
Dr. Berkwitt determined that the anemia was
likely related to chronic corticosteroid therapy
but was unable to find a cause for the anorexia.
Bailey was then referred to me for an abdominal
ultrasound examination.
During Bailey’s abdominal ultrasound
examination I noted that the wall of the
stomach was symmetrically, abnormally
thickened (fig 1). The wall layers were intact
but the outer rim of the wall was diffusely
hypoechoic (dark). Also, within the lumen
of the fundus there was a solid appearing,
hyperechoic curvilinear ‘band’ beyond
Figure 3
which an intense shadow was noted. This
structure moved independently within the
gastric lumen, and was not attached to any
portion of the gastric wall. It continued to
cast a dark shadow regardless of the angle of
insonation (the direction of the ultrasound
beam). Gastric motility was decreased. No
other abdominal abnormalities were noted.
My differential diagnoses for this abnormal
ultrasonographic finding included: intraluminal
gastric foreign body, inspissated food ball,
Figure 4
Figure 5
5
Ultrasound for Diagnosis of a Gastric Foreign Body
and atypical gastric wall mass, i.e. a neoplasm,
granuloma, or large polyp. The patient was
then returned to VCA Shoreline in Shelton,
CT, for endoscopy. During endoscopy a large
trichobezoar (hairball) was discovered in the
fundic lumen (fig 5). The large size of this
foreign object made removal via endoscopy
impossible; a decision to take Bailey into
surgery for an exploratory laparotomy and
gastrotomy was then made. At surgery a single
gastrotomy incision was made over the fundus
and the hairball and other debris was removed
(fig 3). Bailey recovered uneventfully from this
surgery and is currently doing well at home. His
appetite returned almost immediately following
and he continues to eat well to this day.
Gastric foreign bodies are often easily
recognized in animals on survey abdominal
radiographs, CT examination (fig 2) and with
abdominal ultrasound evaluation. Survey
radiographs of a patient with a suspected
gastric foreign body, however, can look
normal depending on the amount of gas and
fluid present within the gastric lumen and the
type and size of the foreign body present.
Case Discussion
Ultrasound examination of the gastrointestinal
tract is a safe and noninvasive imaging
modality that can provide important diagnostic
information for animals with GI disease.
Despite the potential limitations imposed by
intraluminal gas, which can result in lesionmasking artifacts, this imaging procedure can
still be performed prior to any other diagnostic
test by employing minimal patient preparation,
i.e. overnight fasting. Also, ultrasound imaging
can follow screening survey radiography to
help confirm a diagnosis when a suspicion
of GI pathology exists. Gastric distention,
excessive small bowel dilatation, intraluminal
abnormalities (such as foreign bodies or masses),
bowel wall thickness and GI motility can all
be assessed using ultrasound. Based on any or
all of these abnormal findings, the decision
as to which diagnostic direction to then take,
i.e. endoscopy, exploratory laparotomy, guided
sampling procedures (aspiration, biopsy), can
be made with confidence. Also, any suspicious
findings can be re-evaluated during additional
examinations. Because of its usefulness in
evaluating the GI tract, ultrasound has generally
replaced the gastrointestinal contrast study.
However, if choosing to perform a contrast
study, the ultrasound examination should be
done prior to giving barium because this contrast
medium will effectively stop transmission of the
sound beam. When performing an ultrasound
examination of the GI tract, it is important
to slowly and methodically evaluate the entire
system from stomach to colon. The walls of the
stomach and intestines have a distinctive 5-layer
Continued from page 5
appearance of alternating echogenicities (fig 4).
The innermost layer visible with ultrasound is the
mucosal-luminal interface, which is hyperechoic
(bright). This is followed from the inside out
by a hypoechoic (dark) mucosa, a hyperechoic
(bright) submucosa, a hypoechoic muscularis and
a hyperechoic serosa-subserosa. The thicknesses
of the different parts of the GI tract vary from
3-5 mm in the stomach, 2.5-3.5 mm in the small
bowel, and 1-2 mm in the colon.
A bezoar, by definition, is a hard, indigestible,
mass of material such as hair, vegetable fibers or
seeds and skins of fruits; trichobezoars are a mass
of hair, i.e. excessive grooming. When in the
stomach, the size and density of these structures
can make passage through the pylorus into the
duodenum impossible, often causing chronic
patient nausea and anorexia and abdominal
discomfort. Also, the size and shape of the
foreign body may require an invasive procedure
such as gastrotomy to remove it. The density of
this material and its often large size (by the time
it is usually diagnosed), a trichobezoar presents
a strongly attenuating surface to the ultrasound
beam. The beam is completely absorbed
and reflected by this highly acoustic interface
giving the described appearance of a classic, or
pathognomonic, hyperechoic curvilinear ‘band’
with a strong acoustic shadow deep to this band
(see fig 1). j
Osteoma on the Forelimb of a Cat
Kate Margalit, DVM, DACVS
Fifth Avenue Veterinary Specialists
“G
ordo” is a six-year-old male
neutered domestic shorthair
that was referred to the surgery
service at Fifth Avenue Veterinary Specialists
by Dr. Eric Dougherty of The Cat Practice
in New York City. Gordo initially presented
for right carpal swelling and right thoracic
limb lameness that his owner first observed
three days prior to examination.
On presentation, Gordo was bright and
alert. Physical examination revealed a grade
1 lameness of the right thoracic limb. There
was a firm, affixed 3 x 3 cm mass on the cranial
aspect of the distal radial and carpal region.
6
The mass was nonpainful on palpation, but
there was mildly decreased range of motion of
the right carpus. Gordo had a body condition
score of 8/9. The remainder of the physical
examination was unremarkable.
Bloodwork performed by Dr. Dougherty
just prior to referral revealed: mild
thrombocytopenia with evidence of platelet
clumping at 132 103/μL (reference range
200-500 103/μL), mild basophilia at 166
109/L (reference range 0-150 109/L),
mild hyperalbuminemia at 4.1 g/dL
(reference range 2.5-3.9 g/dL), and mild
hypertriglyceridemia at 204 mg/dL (reference
Dr. Dougherty of The Cat Practice, NYC
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occur more frequently in horses and cattle.
There are rare reports of osteomas in cats in
the veterinary literature.
The largest case series reports 7 cats with
osteomas in the oral and maxillofacial
regions.1 Two distinct patterns of osteoma
were characterized on CT scan: compact (or
cortical) and cancellous. Compact osteoma
was well marginated and smooth, while
cancellous osteoma was more irregular and
expansile with some destruction of adjacent
bone. Due to the small sample size of this
study, no conclusion can be drawn as to the
significance of this distinction.
Figure 1
Figure 2
range 25-160 mg/dL). The remainder of his
complete blood count and chemistry panel
was unremarkable. FeLV and FIV retroviral
testing was negative.
radius and carpus. The mass was elevated from
its attachment of the distal radius and proximal
aspect of the joint capsule with a Freer elevator.
An osteotome and mallet were utilized to
smooth the cranial surface of the distal radial
cortex. Histopathology was submitted and
reconfirmed the initial diagnosis of osteoma.
A soft padded bandage was placed on the right
thoracic limb.
Orthogonal right carpal radiographs were
completed under sedation at The Cat Practice
(figs 1, 2). Surrounding the distal radius, a
large, smoothly margined mineralized mass
was detected. The mass protruded distally and
was seen slightly overlaying the radiocarpal
joint, however the carpal bones did not appear
to be involved. No evidence of bone lysis was
visible. Three view thoracic radiographs were
completed at the time of consultation at FAVS
prior to anesthesia and were unremarkable.
Incisional biopsy of the right carpal mass
was completed. The outer surface of the
mass appeared to have a smooth contour.
A biopsy was obtained with use of a
Jamshidi biopsy instrument and curette.
Histopathology revealed branching and
interconnecting osseous trabeculae that
formed spaces containing fibrous tissue.
Lacunae were irregularly clustered. Cells in
lacunae and intertrabecular spaces had small
nuclei with condensed chromatin and a low
mitotic index. There were no significant
inflammatory cell infiltrates. The mass was
diagnosed as an osteoma.
One week after the incisional biopsy was
completed, the owners elected a more definitive
surgery. An excisional biopsy was performed by
making a cranial approach over the distal right
November/December 2011
Gordo recovered uneventfully from his
surgery and was discharged with sublingual
buprenorphine. Two weeks post-operatively,
Gordo’s sutures and bandage were removed.
Gordo had subtle lameness and appeared
more comfortable at home. Two months
post-operatively, a follow up phone call was
completed. The owner had not noted any
recurrence of the carpal mass and he was
ambulating normally at home.
Case Discussion
Differential diagnoses for an osseous mass
involving the distal radius or carpal joint
include: osteochondroma (either solitary or
as part of multiple cartilaginous exostoses),
synovial
osteochondroma,
osteoma,
chondroma, chondrosarcoma, osteosarcoma,
or metastatic neoplasia.
An osteoma is a benign bone tumor that
is generally slow growing. Some believe
that an osteoma is not a true neoplasm,
but a developmental anomaly that occurs
secondary to trauma or infection. It can
occur in all domestic species, but tends to
The mandible was the most common
location. Of the three biopsy samples
that were cultured, only one grew E.
cloacae; however this was believed to be a
contaminant rather than a true infection.
Only one cat underwent a debulking surgery
of the mass and was reported to do well
one year after surgery. Mandibulectomy
or maxillectomy were pursued in three cats.
Overall, the cats that underwent surgical
intervention had follow up at 1 to 9 years
after diagnosis and had a good quality of life
and no signs of recurrence.1
There is one case report of extraskeletal
osteoma in the cat.2 The mass was within
the subcutaneous tissue adjacent, but not
attached to the olecranon. The mass was
easily excised and no recurrence was noted
3.5 months post-operatively.
In Gordo’s case, give the benign nature of the
mass, an amputation was mentioned, but not
recommended. CT scan would have been a
helpful imaging to modality to characterize
the extent of the mass and bony involvement.
At this time, Gordo is doing well with
no observable lameness or recurrence two
months post-operatively. While an osteoma
is considered benign, early intervention is still
recommended. Debulking surgery as opposed
to aggressive resection can be a viable option to
address osteomas. While there is no evidence
in the literature that malignant transformation
occurs, recurrence is possible. j
References:
Fiani N, Arzi B, Johnson EG, Murphy
B, Verstraete FJ. Osteoma of the oral and
maxillofacial regions in cats: 7 cases (1999-2009).
J Am Vet Med Assoc 2011;238(11):1470-1475.
2
Jabara AG, Paton JS. Extraskeletal osteoma
in a cat. Aust Vet J 1984;61(12):405-407
1
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Upcoming Events
November 15, 2011 — Fifth Avenue Veterinary Specialists will host an evening of CE at the Union
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DACVECC, presenting a critical care lecture, and Mary Buelow, DVM (practice limited to dentistry),
presenting “Recognition of Oral Pathology.” Please contact Monica Dunn at (212) 924-3311 or monica.
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h
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