You are on page 1of 5

CASE 1

Case History and Clinical Examination


A 13-year-old female neutered domestic shorthair cat
presented to the referring veterinarian after the owners
had noticed blood on furniture and on the cats food
bowl. The cat had a history of excessive grooming that
was attributed to flea allergy. The cat was being treated
every three weeks with topical fipronil
1
. Ulcers on the
hard palate were identified and the cat was referred to the
Valentine Charlton Cat Centre. Further physical
examination findings were pale mucous membranes, a
heart rate of 240 beats per minute, a grade IV/VI systolic
heart murmur and alopecia over the ventral abdomen. A
linear ulcer (2 x 0.5cm) was present on the left side of the
hard palate midway between the midline and the dental
arcade (Fig 1a). A second, circular (0.8cm diameter)
ulcer on the right side of the hard palate was noted caudal
to the central incisors (Fig 1a).
Diagnostic Tests
Blood tests revealed a mild elevation in glucose and a
regenerative anaemia (Table 1). The cat was blood
typed
2
(blood type A) and a 50mL type A blood
transfusion was given prior to surgery.
Treatment
At surgery, the cat was placed in dorsal recumbency with
the jaws taped open for maximal exposure of the hard
6 Aust Vet Practit 37(1) March 2007
CASE STUDIES
Use of a Bipedicle Mucoperiosteal
Flap to Treat Arterial Haemorrhage
from Palatine Ulcers in Three Cats
CJ Bailey, PLC Tisdall
a
, JA Beatty
b
, A Lingard
b
and VR Barrs
b
North Shore Veterinary Specialist Centre
64 Atchison Street, Crows Nest, NSW 2065
a
Veterinary Specialist Centre
PO Box 307, North Ryde, NSW 1670
b
Valentine Charlton Cat Centre
Faculty of Veterinary Science, University of Sydney, NSW 2006
Aust Vet Practit 37(1) March 2007 6
ABSTRACT
Anovel surgical treatment for palatine arterial haemorrhage secondary to hard
palate ulceration is described in three cats. The owners first noticed external
haemorrhage in all cases. Determination of the exact site of haemorrhage was
not always possible on visual inspection because bleeding was intermittent.
Severe anaemia was present in all cats and two cases required blood
transfusion. Surgery was performed to ligate the palatine arteries and cover
the ulcerated regions of hard palate with sliding bipedicle mucoperiosteal
flaps. The flaps remained viable and stopped ongoing haemorrhage from the
erosive lesions successfully in all cases. [Bailey CJ et al (2007) Aust Vet
Practit 37:6]
Ph: 02 9436 1213. Fax: 02 9906 5710
Email: cjbailey@iprimus.com.au
1
Frontline, Merial
2
Rapid Vet-H Feline desk-top blood typing kits, Agrolab,
Switzerland (Australian distributor IDEXX laboratories)

PALATINE ULCERS
palate. Both palatine arteries were ligated blindly at the
caudal extent of the hard palate with simple interrupted
3/0 poliglecaprone 25
3
sutures (Fig 1b). An incision was
then made along the lateral margin of the palatine
mucosa immediately adjacent to the left dental arcade.
The lateral edge of the ulcer was incised to enable
elevation of the mucoperiosteum with a periosteal
elevator, leaving the caudal and rostral bases intact to
create a bipedicle mucoperiosteal flap. This flap was
transposed over the linear ulcer deficit then sutured to
the incised medial edge of the ulcer using simple
interrupted 4/0 poliglecaprone 25 sutures
3
(Figs 1c &
1d). The lateral palatine bone was left to granulate. A
short unipedicle mucoperiosteal flap was elevated and
transposed to cover the circular ulcer on the right side
(Fig 1e). Amoxycillin-clavulanic acid
4
was administered
(8.75 mg/kg sc) at the time of surgery followed by a
seven-day course (12.5 mg/kg po bid). An Elizabethan
collar was applied post-operatively to prevent
overgrooming. Excess salivation was noted in the first 24
hours but no further haemorrhage was observed.
Analgesia was provided with buprenorphine
5
0.01mg/kg
sc qid and soft food was introduced 24 hours after
surgery. Two weeks after surgery the mucoperiosteal flap
appeared intact and viable, the exposed hard palate had a
bed of granulation tissue and the PCV was 0.34L/L. In
addition to flea control, a food elimination diet was
recommended to further investigate the overgrooming.
Three months post-operatively the mouth had
completely healed.
CASE 2
Case History and Clinical Examination
A 14-year-old female neutered domestic shorthair cat
was presented to the referring veterinarian because the
owners noticed profuse bleeding from the cats mouth. A
palatine ulcer was identified extending longitudinally for
2cm on the right side of the hard palate and crossing the
midline at the rostral aspect (Fig 2). Haemorrhage
appeared to originate from the linear part of the ulcer. At
initial presentation blood tests (Table 1) revealed mild
anaemia and pre-renal azotaemia (urine specific gravity
>1.055). Twenty-four hours later the PCV had decreased
to 0.19L/L and the cat was referred to the Veterinary
Specialist Centre, North Ryde. Abnormalities noted on
physical examination were the ulcer, a grade II/VI
systolic heart murmur and the presence of flea dirt in the
coat.
Aust Vet Practit 37(1) March 2007 7 7 Aust Vet Practit 37(1) March 2007
HAEMATOLOGY AND BIOCHEMISTRY
Parameter Case 1 Case 2 Case 3 Reference Range
Haematocrit (L/L) 0.15 0.270.19 0.10 0.30-0.45
Total Plasma Protein (g/L) 71 74 84 59-78
Red Cell Count (x10
12
/L) 3.55 n/a 2.60 6.0-10.0
Hb (g/L) 50 n/a 27 80-140
MCV (fl) 42.3 n/a 38.5 40-45
MCH (pg) 14.1 n/a 10.4 13-17
MCHC (g/L) 333 n/a 270 310-350
Platelets (x10
9
/L) n/a 478 634 200-700
Uncorrected Reticulocytes % 3.6 n/a 9 0-1.0
Absolute reticulocyte count (x10
9
/L) 128 n/a 234 50
White Blood Cell count (x10
9
/L) 18.2 n/a 12.2 8.0-14.0
Neutrophils (x10
9
/L) 9.65 n/a 11.71 3.76-10.8
Lymphocytes (x10
9
/L) 6.01 n/a 0.24 1.6-7.0
Monocytes (x10
9
/L) 0.18 n/a 0.24 0.08-0.56
Eosinophils (x10
9
/L) 1.82 n/a 0.00 0.16-1.4
Basophils (x10
9
/L) 0.36 n/a 0.00 0-0.14
Bands (x10
9
/L) 0.18 n/a 0.00 0-0.42
Urea (mmol/L) 6.92 37 13.7 7.2-10.7
Creatinine (mol/L) 126 167 214 90-180
Glucose (mmol/L) 10.4 9.4 8.90 3.6-6.6
ALT (IU/L) 25 43 47 <60
ALP (IU/L) 23 37 76 <50
FIV status n/a n/a Negative
TABLE 1: Haematology and biochemistry. n/a = not available.
3
Monocryl, Ethicon
4
Clavulox, Pfizer
5
Temgesic, Reckitt Benckiser

PALATINE ULCERS
Aust Vet Practit 37(1) March 2007 8 8 Aust Vet Practit 37(1) March 2007
FIGURE 1b: Ligation of the left and right major palatine
arteries in the region where they exit the palatine foramina
of the hard palate.
FIGURE 1a: Erosive lesions on hard palate of Case 1.
L=left, R=right. Arrow points to smaller lesion.
FIGURE 1c: Elevation of a bipedicle
mucosal flap.
FIGURE 1d: Mucosal flap transposed
medially and sutured to cover the
palatine ulcer.
FIGURE 1e: Short unipedicle mu-
cosal flap covering smaller ulcer.
Arrows point to exposed areas left to
granulate.
FIGURE 2: Erosive lesions on hard
palate of Case 2, appearing as mirror
image of Case 1.
FIGURE 3a: Erosive lesions on hard
palate of Case 3, similar to Case 2.
FIGURE 3b: Healed mucosal flap in
Case 3, 11 months post-operatively.

PALATINE ULCERS
Diagnostic Tests and Treatment
The cat was blood typed on admission (blood type A).
The PCV had increased to 0.24L/L before surgery (TPP
76g/L). Since the cat was clinically stable, blood
transfusion was not performed. At surgery, a biopsy was
taken from the cranial edge of the linear ulcer and
submitted for histopathology. A similar surgical
technique to that used in Case 1 was performed:
horizontal mattress sutures using 4/0 polydioxanone
6
were placed at the caudal aspect of the ulcer to ligate the
right palatine artery. The bipedicle mucoperiosteal flap
was transposed over the linear ulcer deficit on the right
side and sutured to the incised medial edge of the ulcer,
using simple interrupted 4/0 polydioxanone sutures.
Post-operative care, including analgesia, antimicrobial
therapy, feeding and provision of an Elizabethan collar,
was similar to Case 1. Monthly topical flea control with
fipronil was prescribed.
On histopathology the biopsy tissue was composed of
hyperplastic stratified squamous oral epithelium with
underlying dense connective tissue. Within the
connective tissue there was interspersed granulation
tissue. There was no evidence of a neoplastic process,
haemosiderosis or an ischaemic cause such as a
thrombosed vessel.
The cat re-presented four days after discharge because
the owner had noticed bleeding from the mouth. The
mucoperiosteal flap was intact and viable with no
evidence of haemorrhage from that site. However, a
small focal point of haemorrhage appeared to originate
from a small ulcer on the left side of the rostral hard
palate. Blood tests revealed a PCV of 0.26L/L and TPP
of 76g/L. Surgery was performed to ligate the left
palatine artery and appose the ulcer edges with 4/0
polydioxanone horizontal mattress sutures. At
examination four weeks later, the mouth had completely
healed. No recurrence of the ulcer occurred. The cat
developed an invasive mandibular lesion two years later
and was euthanased.
CASE 3
Case History and Clinical Examination
A seven-year-old male domestic short hair cat presented
for lethargy and inappetence. The owner had noticed a
small amount of blood on the cats lips and firm black
faeces had been observed. Physical examination
revealed a heavy flea burden, very pale mucous
membranes and ulceration of the hard palate in an
L-shape (3 x 0.5cm on right side of hard palate with a
short narrow extension across to the left side at the
rostral margin; Fig 3a).
Diagnostic Tests
Severe regenerative anaemia was identified on
haematology with results consistent with iron deficiency
anaemia secondary to chronic blood loss (Table 1).
Treatment
The cat was typed, treated with fipronil and given a
50mL type A blood transfusion before surgery. Both
palatine arteries were ligated and the linear ulcer was
covered with a sliding bipedicle mucoperiosteal flap as
described for the previous cases. The short narrow ulcer
on the right side was small enough to have the edges
apposed using horizontal mattress sutures without
creating excessive tension. Post-operative care was the
same as for Case 1 with the addition of ferrous sulphate
81.5mg po sid and topical imidocloprid
7
every four
weeks. The PCV 10 days post surgery was 0.26L/L and
the mouth was healing well. Eleven months post-
operatively there had been no recurrences of palatine
ulceration but the residual healed areas were still visible
(Fig 3b).
DISCUSSION
Palatine arterial haemorrhage in the cat was first reported
in 1990 (Wildgoose 1990). In that case, a small erosion
was located on the hard palate level with the anterior
aspect of the second premolar tooth, 4 to 5mm from the
midline. Profuse haemorrhage was identified from the
erosion which overlaid the right major palatine artery.
Haemorrhage was controlled with electrocautery
(Wildgoose 1990). Menrath & Miller (1995)
subsequently reported a cat with a bleeding palatine
erosive lesion that resulted in severe blood loss anaemia.
They postulated that the pathogenesis of these lesions
was excessive licking/grooming as a result of a pruritic
skin condition. The cat was given a blood transfusion
and horizontal mattress sutures were placed across the
width of the erosion (Menrath & Miller 1995).
Many aetiologies can cause ulcerative lesions in the oral
cavity of the cat but, typically, these do not result in
significant oral haemorrhage. Aetiologies of oral
ulcerative lesions in the cat include eosinophilic
granuloma complex (Frost & Williams 1986, von
Tscharner & Bigler 1989, Pedersen 1992), Calicivirus
infection (Hoover & Kahn 1975, Pedersen 1992),
neoplasia such as squamous cell carcinoma (Frost &
Williams 1986, Pedersen 1992), immune-mediated
diseases such as pemphigus vulgaris and systemic lupus
erythematosus (Manning et al 1982, Pedersen 1992),
ingestion of caustic substances and trauma (Pedersen
1992).
The three cases in the current series all presented with
evidence of bleeding from the mouth that was detected
by the owners. However, if the cat has been repeatedly
swallowing the blood, external haemorrhage may not be
apparent and the extent of blood loss anaemia may be
profound by the time the cat is presented to the
veterinarian. Therefore, lethargy, inappetence and/or
melaena may be the main presenting signs and a full
physical examination should be performed on all cases to
detect ulcerative lesions of the hard palate and the
initiating cause of pruritis.
The clinical appearance of all three lesions was similar,
demonstrating longer linear erosions with defined edges
on one side of the hard palate and smaller, short erosions
at the rostral aspect on the opposite side. Case 2
demonstrated that haemorrhage was not limited to the
larger lesion, as a second procedure was required to
cover the smaller erosion. This highlights the difficulty
associated with identification of the exact site of
haemorrhage. Also, at the time of presentation many of
these cases do not display active haemorrhage.
Aust Vet Practit 37(1) March 2007 10 10 Aust Vet Practit 37(1) March 2007
6
PDS II, Ethicon
7
Advantage, Bayer
PALATINE ULCERS
Therefore, diagnosis is often made by pattern-
recognition, in which cats presented with a regenerative
anaemia and a palatine ulcer are assumed to be bleeding
from the ulcer. The consistent finding was that the
erosions overlay the major palatine arteries in the hard
palate. The right and left major palatine arteries, which
are branches of the maxillary arteries, are the main blood
supply to the hard palate (Evans & Christensen 1979).
They exit the palatine foramina of the hard palate at the
level of and medial to the distal cusp of the upper fourth
premolar (Orsini & Hennet 1992) and course forward in
the palatine sulcus just medial to midway between the
dental arcade and the midline (Bezuidenhout 2003).
They become more superficial as they course rostrally to
lie closely under the oral mucosa. Asmall branch passes
through the oval palatine fissure between the canine
teeth before the artery travels to the back of the incisor
teeth where the vessel anastomoses with its fellow
(Evans & Christensen 1979).
An understanding of the regional anatomy was important
for performing the surgical procedure, especially
because the major palatine arteries are not directly
visible. Ligation of the bases of the major palatine
arteries was attempted with the dual aim of reducing
intra-operative haemorrhage whilst elevating the
mucoperiosteal flap and to stop ongoing haemorrhage
from the palatine erosions. The mucosa of the hard palate
remained viable and healed in all three cases indicating
that sufficient collateral circulation exists after ligation
of the major palatine arteries.
Abipedicle mucoperiosteal flap was transposed over the
larger ulcerated regions to provide a robust coverage of
the ulcerated area. Electrocautery had been previously
described in the treatment of palatine arterial
haemorrhage (Wildgoose 1990) but that case involved
only a small lesion and the extensive use of
electrocautery in the oral cavity can be detrimental to
wound healing (Fossum 2002). The use of tightly-
approximated broad horizontal mattress sutures placed
across the width of the erosion has also been described
for the treatment of this condition (Menrath & Miller
1995). However, for larger lesions, it is not possible to
appose the mucosal edges with sutures as the mucosa is
not compliant and undue tension may result in wound
dehiscence (Fossum 2002). The mucoperiosteal flap
used in the current study for the closure of the longer
linear erosive lesions was bipedicle because it supplied a
better blood supply than that which would be provided
from a narrow single base. The flap needed to be
undermined sufficiently to allow enough mobility to be
transposed medially without tension. The principles of
atraumatic tissue handling were adhered to reduce the
chance of dehiscence (Fossum 2002). The exposed area
of the hard palate immediately adjacent to the dental
arcade was left to heal with granulation tissue.
Histopathology was performed on Case 2. The
microscopic appearance of the tissue was consistent with
the previously proposed pathogenesis of repetitive
trauma from excessive licking/grooming in this
particular case (Menrath & Miller 1995). The feline
tongue has numerous well-developed harsh conical
papillae that provide an effective rasping action for
grooming and prehension (Dyce et al 1987, Menrath &
Miller 1995). In the process of licking/grooming, the
tongue is thought to repeatedly impinge on the hard
palate in a backward rasp-like fashion with the cross-
sectional shape of the tongue preferentially contacting
either side of the midline over the regions of the major
palatine arteries (Menrath & Miller 1995). The continual
abrasion of the epithelium may result in the eventual
erosion into the major palatine arteries and cause
substantial haemorrhage (Menrath & Miller 1995). A
possible explanation for the asymmetrical appearance of
the lesions is the cats preferentially grooming to the left
or right. It is unclear as to why so few feline cases with
pruritis or overgrooming develop bleeding palatine
ulcers and why the condition was not recognised in the
literature prior to 1990 (Wildgoose 1990). Affected cats
may be those that overgroom constantly. Another
possible explanation for the disease pathogenesis is
extension of the inflammatory process secondary to
trauma-induced mucosal ulceration to involve the
palatine arteries and surrounding tissues, resulting in
arteritis or periarteritis of the palatine arteries. The
histopathology for Case 2 was consistent with repetitive
trauma rather than arteritis/periarteritis but histo-
pathological anlayisis of biopsies from a larger number
of cases would be useful.
The haemorrhage from the palatine ulcers may be severe
enough to warrant a blood transfusion as in two of the
present cases. Whilst a definitive pathogenesis is not
proven for these three cases, the surgical technique
described proved effective in arresting ongoing
haemorrhage in cats with significant anaemia. The
presence of fleas or flea dirt and/or the history of
overgrooming in the present case series were consistent
with the previously proposed pathogenesis of repetitive
abrasion from the tongue. Therefore, the authors
recommend that subsequent to the surgery, an
Elizabethan collar is applied to stop overgrooming in the
short-term. Cats should be treated with effective flea
parasiticides and other causes of pruritic skin disease
should be investigated (e.g. dietary elimination trials and
intradermal allergen skin testing).
REFERENCES
BEZUIDENHOUT, AJ (2003) Textbook of Small Animal Surgery, Ed
Slatter, 3
rd
edn, pp2630-2627, Saunders, Philadelphia
DYCE, KM, SACK, WO & WENSING, CJG (1987) Textbook of
Veterinary Anatomy, 1
st
edn, pp100-101, Saunders,
Philadelphia
EVANS, HE & CHRISTENSEN, GC (1979) Millers Anatomy of the
Dog, 2
nd
edn, pp141-675, Saunders, Philadelphia
FOSSUM, TW (2002) Small Animal Surgery, 2
nd
edn, p275,
Mosby, St. Louis
FROST, P & WILLIAMS, CA (1986) Feline dental disease, Vet Clin
Nth Am Small Anim Pract 16:851
HOOVER, EA & KAHN, DE (1975) Experimentally induced feline
calicivirus infection: clinical signs and lesions, J Am Vet Med
Assoc 166:463
MANNING, TO, SCOTT, DW, SMITH, CA & LEWIS, RM (1982)
Pemphigus diseases in the feline: seven case reports, J Am
Anim Hosp Assoc 18:433
MENRATH, VH & MILLER, R (1995) The repair and prevention of
bleeding palatine erosive lesions in the cat, Aust Vet Practit
25:202
ORSINI, P & HENNET, P (1992) Anatomy of the mouth and teeth
of the cat, Vet Clin Nth Am Small Anim Pract 22:1265
PEDERSEN, NC (1992) Inflammatory oral cavity diseases of the
cat, Vet Clin Nth Am Small Anim Pract 22:1323
VON TSCHARNER, C & BIGLER, B (1989) The eosinophilic
granuloma complex, J Small Anim Pract 30:228
WILDGOOSE, WH (1990) Palatine arterial haemorrhage in a cat,
Vet Rec 126:273
Aust Vet Practit 37(1) March 2007 11 11 Aust Vet Practit 37(1) March 2007