Journal of Feline Medicine and Surgery (2002) 4, 27–42doi:10.1053/jfms.2001.0148, available online at http://www.idealibrary.com on

CASE REPORT

Gastroduodenal ulceration in cats: eight cases and areview of the literature

JM Liptak†, GB Hunt‡, VRD Barrs, SF Foster, PLC Tisdall, CR O’Brien,R Malik

University Veterinary CentreSydney, Faculty of VeterinaryScience, The University of Sydney,NSW 2006, Australia

Date accepted 12 September 2001

Gastroduodenal ulceration (GU) and blood loss was diagnosed in eight cats andcompared with 25 previously reported cases of feline GU. Cats with GU presentedin a critical condition. Clinical signs consistent with gastrointestinal bleeding wereinfrequently identified although anaemia was a common finding. Non-neoplasticcauses of feline GU tended to have a shorter clinical course with ulcers confined tothe stomach. Conversely, cats with tumour-associated GU usually had a moreprotracted clinical course, weight loss, and ulcers located in the stomach for gastrictumours and the duodenum for extra-intestinal tumours. In this series, definitivediagnosis was possible for cats with neoplasia (gastric tumours and gastrinoma),however, it was difficult to precisely identify the underlying aetiology in cats withnon-neoplastic GU. Prompt stabilisation with a compatible blood transfusion,surgical debridement or resection, antibiotic and antiulcer therapy, and treatmentof the underlying disease, if identified, was successful in the majority of cases. Theprognosis for cats with appropriately managed GU depended on the underlyingaetiology, but even cats with neoplasia could be successfully palliated forprolonged periods. © 2002 ESFM and AAFP

Introduction

Gastroduodenal ulcers (GU) are mucosaldefects which expose the submucosa ordeeper layers of the stomach to gastric

acid (Guilford & Strombeck 1996b). Any con-dition which compromises the normal physio-logical defence mechanisms of the gastricmucosa, such as increased secretion of hydro-chloric acid, reduced mucosal blood flow andalteration of the mucus-bicarbonate barrier, canresult in GU (Guilford & Strombeck 1996a,1996b, Hall 2000).

Ulcers of the stomach and duodenum are un-common in cats, with less than 30 cases reported(Seawright & Grono 1964, Schalm et al 1975,Wrigley 1977, Hasler & van den Ingh 1978, Liskaet al 1979, Weller & Hornof 1979, Evans &

1098–612X/02/01027+16 $35.00/0

Biery 1980, Gordon 1980, Jones & Hunt 1983,Middleton et al 1983, McEwen et al 1985, Sheikh-Omar & Abdullah 1985, van der Gaag et al 1988,Holmberg et al 1989, Thilgar et al 1989, Aoki et al1990, Bortnowski & Rosenthal 1992, Eng et al1992, Jergens et al 1992, Curtsinger et al 1993,Twedt 1994, Mai & Bouhoula 1998, Muller et al1998, Runk et al 1999). Cats with GU frequentlypresent with life-threatening gastrointestinalhaemorrhage. However, definitive diagnosis canbe difficult as clinical signs identifying the gas-trointestinal tract as the site of blood loss, such ashaematemesis and melaena, are often inapparentor obscured by hypovolaemia, sepsis or moreobvious signs referable to anaemia.

In dogs, neoplasia, non-steroidal antiinflam-matory drugs (NSAIDS), hepatic disease andinflammatory bowel disease (IBD) are commoncauses of GU (Stanton & Bright 1989, Hall 2000).The aetiology of GU in cats, however, has notwell characterised. The aim of this report, bypresenting a series of eight cats with GU and

†Present address: Animal Cancer Center, Colorado StateUniversity Veterinary Teaching Hospital, 300 West Drake Road,Fort Collins, CO 80526, USA.‡Author for correspondence: E-mail: gbhunt@mail.usyd.edu.au

© 2002 ESFM and AAFP

28 JM Liptak et al

Materials and methodsGastric and/or duodenal ulcers were diagnosedin eight cats at the University Veterinary CentreSydney (UVCS) between February 1998 andJanuary 2001. A definitive diagnosis of GU wasmade at either surgery or necropsy and con-firmed histologically. Signalment, clinical andlaboratory findings, treatment, ulcer location andoutcome were determined from case records. Theliterature was reviewed for cases of feline GUand the findings from these reports were tabu-lated when sufficient information was available,otherwise the diagnosis only was recorded.

Results

Case reports

Details of these cases are summarised in Table 1.

Case 1. A 2-year-old, castrated domestic short-hair (DSH) (4.4 kg) presented to the UVCS with a6-day history of vomiting, malaena and polydip-sia. The cat was tachycardic [260 beats per min(bpm)] and had pale mucous membranes. Hae-matology, biochemistry and urinalysis revealed apoorly regenerative, macrocytic, normochromicanaemia [packed cell volume (PCV) 0.09 l/l,mean corpuscular volume (MCV) 50 fl, meancorpuscular haemoglobin (MCH) 15 pg/l, reticu-locytes 63×109/l], marked azotaemia [urea52.2 mmol/l, creatinine 580 �mol/l and urinespecific gravity (USG) 1.012], hypokalaemia(2.3 mmol/l) and hyponatraemia (127 mmol/l)(reference ranges; Table 2). The total plasmaprotein concentration was 59 g/l. A blood leadconcentration (0.09 �mol/l) was within normallimits. Abdominal radiographs revealed disten-sion of the stomach and some loops of smallintestine with gas. A fresh, cross-matched wholeblood transfusion was administered and anexploratory celiotomy performed.

Abnormalities detected at surgery includedgastric serosal discolouration at the angular in-cisure, reflux of bile into the pancreatic ducts andoedema of the portal lymphatics. Gastrotomyrevealed a 10 mm diameter ulcer in the pyloricantrum. The ulcer was resected and the resultantdefect sutured. The bile duct was catheterisedand flushed with saline through a duodenotomy.

Firm, dark faeces were removed through a col-otomy. There was no evidence of hair or bones inthe faeces. The small intestine, colon, pancreas,liver and a mesenteric lymph node werebiopsied.

Histologically, the gastric ulcer consisted ofa layer of fibrin, cellular debris and necroticmaterial. There was coagulative necrosis andneutrophilic infiltration of the hepatic paren-chyma compatible with either acute hypoxia orexposure to a toxin. The pancreas, small intes-tine, colon and lymph node were unremarkable.

Initially, the cat was fasted for 36 h and treatedwith cimetidine [(Tagamet; SmithKline Beecham)44 mg subcutaneously (SC) every 8 h] and enro-floxacin [(Baytril; Bayer) 20 mg SC every 12 h].Two days post-operatively, oral feeding wascommenced and the medication changed tocimetidine [50 mg per os (PO) every 8 h], sucral-fate [(Carafate; Hoechst Marion Roussel) 250 mgPO every 12 h] and enrofloxacin (25 mg POevery 12 h) for 14 days.

A cause for the gastric ulcer was not foundalthough a toxic agent may have been respon-sible for both the gastric ulcer and hepatic necro-sis. Acute renal failure could not be excluded butchronic renal failure was considered an unlikelyexplanation for the gastric ulcer, due to theabsence of ulcerative stomatitis and continuingpolyuria and polydipsia, but could not beexcluded. The azotaemia and inappropriatelydilute urine may have been secondary tohyponatraemia and/or hypokalaemia as bothcan interfere with normal urine-concentratingmechanisms (DiBartola 2000; DiBartola & DeMorais 2000) and the hypovolaemia may havecontributed to reduced mucosal perfusion.

Case 2. An 11-year-old, castrated Manx (8.7 kg)presented with a 9-day history of respiratorydistress and coughing, followed by vomiting. Ithad received aggressive frusemide therapy fromthe referring veterinarian. The cat was obese andlethargic with bruising over venepuncture sites(cephalic and jugular veins), a grade II/VI sys-tolic heart murmur, increased inspiratory effortwith an expiratory stridor, and marked abdomi-nal pain. Haematology revealed a poorly regen-erative, macrocytic, normochromic anaemia(PCV 0.16 l/l, MCV 54 fl, MCH 16.6 pg/l, reticu-locytes 90×109/l), leucocytosis with neutrophilia(17.75×109/l) and lymphocytosis (7.83×109/l). Acoagulation profile was not performed but plate-let numbers were adequate on examination ofa blood smear. Lymphocyte morphology was

reviewing 25 cases reported in the literature, is tofurther elucidate the aetiology and managementof cats with GU.

Gastroduodenal ulceration in cats 29

Tab

le1.

Sum

mar

yof

cats

with

gast

rodu

oden

alul

cers

seen

atth

eU

nive

rsity

Vet

erin

ary

Cen

tre

Syd

ney

from

1998

to20

01

12

34

56

78

Bre

edD

SHM

anx

cros

sA

byss

inia

nD

SHD

SHD

SHD

SHC

hinc

hilla

Age

(yea

rs)

211

0.6

1014

713

12Se

xM

NM

NM

NFS

FSFS

FSFS

Dur

atio

n(w

eeks

)0.

861.

30.

078

523

0.14

35V

omit

ing

YY

YY

YY

YH

aem

atem

esis

YY

Mel

aena

YY

YIn

appe

tenc

eY

YY

YY

Wei

ght

loss

YY

YY

YPo

lyd

ipsi

aY

YY

Abd

omin

alpa

inY

YY

Ana

emia

YY

YY

YY

YY

Hyp

opro

tein

aem

iaY

YY

Lym

phop

aeni

aY

YY

Neu

trop

hilia

YY

YY

YL

eft

shif

tY

YH

ypok

alae

mia

YY

YU

lcer

loca

tion

Pylo

rus

(1)

Pylo

rus

(3)

Fund

us(1

)Py

loru

s(1

)D

uod

enum

(1)

Fund

us(N

R)

Pylo

rus

(NR

)Fu

ndus

(1)

Pylo

rus

(1)

Duo

den

um(2

)Py

loru

s(N

R)

Perf

orat

edY

YY

Trea

tmen

tSu

ture

Non

e/D

ied

Sutu

reSu

ture

Sutu

reB

illro

thI

Bill

roth

IE

utha

nasi

aC

ause

Unk

now

nU

nkno

wn

Unk

now

nG

astr

inom

aPa

ncre

atic

AC

Gas

tric

LSA

Gas

tric

LSA

Gas

tric

AC

Surv

ival

(mon

ths)

>16

0>

3018

12>

20>

130

DSH

,dom

esti

csh

ort

hair

;MN

,mal

ene

uter

;FS,

fem

ale

spay

ed;Y

,yes

;AC

,ad

enoc

arci

nom

a;L

SA,l

ymph

osar

com

a;N

R,n

otre

cord

ed.

30 JM Liptak et al

atypical. Total plasma protein level was normal.Biochemistry revealed a moderately increasedcreatine kinase (5253 u/l) and total bilirubin(18.0 �mol/l), mildly increased alanine ami-notransferase [(ALT) 310 u/l], moderateazotaemia (urea 24.2 mmol/l and creatinine225 �mol/l), hypokalaemia (2.5 mmol/l), hy-ponatraemia (131.3 mmol/l) and hypochlorae-mia (100.1 mmol/l). Abdominal radiographyand ultrasonography were unremarkable.

The cat died unexpectedly. Necropsy revealedthree strips of ulceration (4 mm by 10–30 mm)in the pyloric antrum with numerous smallererosions on the mucosal surface of the stomach.Histologically, the gastric lesions were character-ised by deep ulceration, fibroplasia and infiltra-tion with inflammatory cells. The stomach andcolon were filled with digested blood while thesmall intestine contained a large amount of freshblood. Ulceration was not detected in either thesmall or large intestine. Other findings includedmyocarditis, adrenocortical necrosis and chronicinterstitial pancreatitis. Toxoplasmosis was con-sidered a diagnostic possibility although zoites

were not detected. The precise aetiology of thegastric ulceration was not determined althoughstress secondary to severe illness, hypovolaemiaand azotaeima due to frusemide administrationand poor cardiac output associated with myocar-ditis may have compromised gastric mucosalperfusion (Vleet & van Ferrans 1986, Kiss &Szilagyi 1988).

Case 3. A 7-month-old, castrated Abyssiniancross (3.2 kg) presented with a 12 h history ofvomiting and lethargy 36 h after eating part of acooked chicken carcass. The cat had marked,generalised abdominal pain. Haematology,serum biochemistry and urinalysis were per-formed. Abnormalities included neutrophilia(17.38×109/l) with a left shift (1.15×109/l) andincreased creatine kinase (2580 u/l) and ALT(308 u/l) activities. Abdominal radiographswere considered normal, however, barium-impregnated polyethylene spheres (BIPS,Chemstock Animal Health) were administereddue to the suspicion of an intestinal foreignbody. The cat initially responded to supportive

Table 2. Reference ranges for haematology, biochemistry, analytes, thyroxine and lead

Parameter Reference range

Packed cell volume (l/l) 0.30–0.45Mean corpuscular volume (fl) 40–45Mean corpuscular haemoglobin (pg) 13–17Reticulocytes (×109/l) <60Total plasma protein (g/l) 59–78Leucocytes (×109l) 8–14Lymphocytes (×109l) 1.6–7.0Neutrophils (×109l) 3.76–10.08Bands (×109l) 0.0–0.42Monocytes (×109l) 0.08–0.56Urea (mmol/l) 7.2–10.7Creatinine (mmol/l) 90–180Inorganic phosphate (mmol/l) 1.3–2.3Urine specific gravity 1.035–1.080Alanine aminotransferase (u/l) <60Alkaline phosphatase (u/l) <50Aspartate aminotransferase (u/l) <40Total bilirubin (�mol/l) 2.5–3.5Creatine kinase (u/l) <200Potassium (mmol/l) 4.0–4.6Sodium (mmol/l) 147–156Chloride (mmol/l) 115–130Bicarbonate (mmol/l) 17–21Thyroxine (nmol/l) 15–45Lead (�mol/l) <0.50Gastrin (pg/ml) 44–64

Note that the reference range for gastrin was based on the results of six clinicallynormal cats assayed simultaneously with cases 3 and 4.

(a)

(b)

Fig 1. Lateral (A) and ventrodorsal (B) abdominal radio-graphs of a cat with perforated gastric ulcers of undeter-mined cause (case 3). Note the loss of serosal detailindicative of peritoneal fluid accumulation secondaryto generalised peritonitis. Retention of the barium-impregnated polyethylene spheres in the stomach 36 h afteradministration was suggestive of delayed gastric emptyingor a pyloric outflow obstruction.

32 JM Liptak et al

treatment with intravenous crystalloids[Hartmann’s Solution (Baxter Healthcare)] andfasting. However, vomiting and lethargy re-curred following cessation of intravenous fluidtherapy and resumption of feeding. Abdominalpain and an equivocal mass were detected dur-ing palpation of the cranial abdomen. Repeatabdominal radiographs revealed retention ofBIPS in the stomach and generalised loss ofserosal detail (Fig 1). The PCV had dropped from0.39 l/l to 0.23 l/l and an exploratory celiotomywas therefore scheduled to investigate the acuteabdomen and occult blood loss.

During preparation for surgery, subcutaneousbruising of the ventral abdomen was noted.Exploration of the abdominal cavity revealedperforated ulcers in the gastric fundus and py-loric antrum. Ingesta was present in the perito-neal cavity. The perforated ulcer in the funduswas associated with adhesions to the visceralsurface of the liver. Adhesions and an abscesshad formed between the ulcer in the pyloricantrum and the left limb of the pancreas. Thegastric ulcers were debrided and sutured, andthe abscess debrided, lavaged and omentalised.The abdominal cavity was copiously lavagedwith warm isotonic saline and closed routinely.

Histologically, the gastric ulcer consisted ofhaemorrhage, fibrinous exudate and immaturegranulation tissue with erythrophagocytosis inthe submucosa and interstitium of the musclelayers. Areas of necrosis were associated withhair and foreign material. The lamina propriacontained low to moderate numbers of neu-trophils with occasional eosinophils. Furtherblood tests were performed. Gastrin concen-tration (45 pg/ml) was within the referencerange and blood lead levels were suggestive ofexposure but not toxicity (0.53 �mol/l). A defini-tive cause was not determined although in-creased creatine kinase activity and bruising ofthe ventral abdomen was compatible with atraumatic aetiology.

Initial treatment consisted of cimetidine [32 mgintravenously (IV) every 6 h], cephazolin[(Kefzol; Eli Lilly) 100 mg IV every 6 h] andgentamicin [(Gentapex-50; Apex Laboratories)6.4 mg IV every 8 h] until oral feeding resumed48 h post-operatively. The cat recovered un-eventfully and was treated successfully withenrofloxacin (50 mg PO every 24 h), metronida-zole [(Metrogyl; Alphapharm) 25 mg PO every12 h], amoxycillin [(Apex Laboratories) 50 mgPO every 12 h], ranitidine [(Zantac; Glaxo-Wellcome) 18.75 mg PO every 12 h] and sucral-

fate (250 mg PO every 12 h) for 14 days. Thirtymonths after surgery, the cat remains in excellenthealth.

Case 4. A 10-year-old, spayed DSH (3.3 kg) pre-sented to the UVCS with an 8-week history ofvomiting and polydipsia. The cat vomited darkbrown fluid daily, unrelated to eating, andwas losing weight despite a normal appetite.Vomition was unresponsive to medical manage-ment with cimetidine and dietary manipulation.

The cat was emaciated with palpably enlargedthyroid glands. Haematology demonstrated amacrocytic, normochromic anaemia (PCV 0.16 l/l, MCV 52 fl, MCH 16 pg/l), neutrophilia(13.2×109/l) with a left shift (bands 1.1×109/l)and monocytosis (1.1×109/l). Serum biochemis-try showed marginal hypoproteinaemia (52 g/l),mildly increased aspartate aminotransferase[(AST) 70 u/l] and ALT (267 u/l) activities, hy-pokalaemia (2.0 mmol/l), and urea and creati-nine within the reference range. The plasmathyroxine concentration (37 nmol/l) was withinthe upper limits of the reference range.

Abdominal ultrasonography revealed mildthickening of the stomach and small intestineand enlargement of the aortic and mesentericlymph nodes. Barium-impregnated polyethylenespheres were administered to evaluate gastro-intestinal motility and the possibility of a lumi-nal obstruction. During the BIPS study, there wasradiographic evidence of free abdominal gas.

The blood type was determined (type B) andan exploratory celiotomy performed. Pneu-moperitoneum was confirmed. The liver waslarge and infiltrated by fat. The common bileduct was tortuous and dilated proximal to alobulated mass in the body of the pancreas. Aperforated ulcer, 20 mm in diameter, was foundin the pyloric antrum. Two additional perforatedulcers were detected in the proximal duodenum.The ulcers were debrided and sutured. The liver,stomach, mesenteric lymph node and mass in thebody of the pancreas were biopsied. The cat washypotensive throughout surgery and receivedinotropic support [continuous rate infusion ofdopamine (David Bull Laboratories) at 6 �g/min] and an intraoperative transfusion of fresh,type B blood.

Histology demonstrated necrosis and granula-tion of the pyloric and duodenal ulcers withhelicobacter-like organisms in moderate num-bers in the crypts surrounding the duodenalulcers. However, the relative lack of an inflam-matory response adjacent to the ulcers suggested

Gastroduodenal ulceration in cats 33

that a non-infectious process caused the ulcers.The liver showed moderate fibrosis and conges-tion and the mass obstructing the bile duct wasconsidered a normal lymph node.

The cat was treated with cimetidine (30 mg IVevery 6 h), enrofloxacin (20 mg SC every 12 h)and amoxycillin-clavulanic acid [(Clavulox;Pfizer) 50 mg SC every 12 h] until oral feedingwas resumed 48 h post-operatively. The cat re-quired a second fresh, typed blood transfusionthree days after surgery as the PCV had droppedfrom 0.18 l/l to 0.11 l/l. A fasting serum gastrinlevel was performed on the basis of exploratoryceliotomy findings and on-going gastrointestinalblood loss. The marked increase in gastrin(404 pg/ml), in the absence of azotaemia, wassupportive of a diagnosis of gastrinoma. Thepancreatic mass and enlarged mesenteric lymphnode may have been the primary gastrinomawith lymph node metastases as the samplessubmitted for cytological and histological analy-sis, respectively, may not have been represen-tative of the disease process.

Treatment was changed to omeprazole [(Losec;Astra) 10 mg PO every 24 h] and ranitidine(18.75 mg every 12 h) for four weeks. Omepra-zole was continued for 18 months. The cat had

gained weight and was clinically normal duringthis time. However, the cat died three days afterthe owner discontinued omeprazole therapy.Necropsy was not permitted but, followingdeath, fluid collected by abdominocentesisconfirmed haemoperitoneum.

Fig 2. Lateral abdominal radiograph of a cat with a perforated duodenal ulcer and pancreatic carcinoma (case 5).Pneumoperitoneum (arrows) and loss of serosal detail is suggestive of gastrointestinal perforation and generalisedperitonitis.

Case 5. A 14-year-old, spayed DSH (3.9 kg) pre-sented with a 12-month history of vomiting,inappetence, weight loss and polydipsia. Vomit-ing occurred daily and was unrelated to eating.The cat was emaciated but no other abnormalphysical findings were detected. Haematology,serum biochemistry and plasma thyroxine con-centration were unremarkable. Managementwith dietary manipulation was unsuccessful andthe cat returned six weeks later with continuedvomiting. The cat was then anaemic (PCV 0.25 l/l) and hypoproteinaemic (50 g/l) and a proximalgastrointestinal obstruction was suspected as thecat was hyponatraemic (136 mmol/l), hypochlo-raemic (93 mmol/l) and alkalotic (bicarbonate27.8 mmol/l).

Abdominal radiography showed free perito-neal gas, gastric dilation and loss of serosaldetail of the abdominal viscera (Fig 2). A thick-ened pancreas surrounded by fluid, gas and

34 JM Liptak et al

hyperechoic fat, and moderate thickening of thegastric and small intestinal wall were notedduring abdominal ultrasonography. Cytologicalexamination of fluid collected by abdomino-centesis was diagnostic for septic peritonitiswith 90% neutrophils and intracellular bacteriasuch as Gram-positive rods and cocci and Gram-negative rods.

A ventral midline exploratory celiotomy wasperformed. There was a large amount of turbidperitoneal fluid and the stomach was distended.A tube was passed to decompress the stomach.A perforated ulcer, 8 mm in diameter, on theserosal surface of the proximal duodenum sur-rounded by gastrointestinal contents and in-flamed, discoloured omentum. The duodenalulcer was debrided and enlarged to examine theduodenal papilla and mucosa. The papilla ap-peared normal although the mucosal surface ofthe antimesenteric duodenal border was poly-poid. The debrided ulcer was sutured. Tissuesamples of the gastric fundus, duodenal mucosa,liver and right pancreatic limb were obtained formicroscopic examination. The abdomen wascopiously lavaged and closed routinely.

The most significant histological finding was aductal carcinoma of presumed pancreatic origin.The epithelial cells on the pancreatic biopsyshowed moderate pleomorphism and mitosisand were arranged in tightly packed papillarystructures. There was no evidence of extension ofthe tumour into the duodenum or stomach. Theduodenal ulcer was characterised by densegranulation tissue with necrotic edges. Therewere non-specific changes in the liver.

The cat was initially treated with cimetidine(10 mg IV every 8 h), enrofloxacin (20 mg SCevery 12 h) and flucloxacillin [(Flucil; Rhone-Poulenc Rorer) 80 mg IV every 6 h]. The catstarted eating three days post-operatively andwas discharged with instructions to administerranitidine (18.75 mg PO every 12 h), clindamycin[(Antirobe; Pharmacia & Upjohn) 25 mg POevery 12 h] and enrofloxacin (25 mg PO every24 h). Long-term management with ranitidinewas effective although vomiting resumed ninemonths post-operatively and the cat was eutha-nased 12 months after surgery. Necropsy was notperformed.

Fig 3. A gastroduodenal anastomosis (Billroth I) performedafter resection of a gastric lymphosarcoma (case 6).

Fig 4. The mucosal surface of a gastric adenocarcinoma(case 8). Note the extensive ulceration.

Case 6. A 7-year-old, spayed DSH (2.5 kg) pre-sented with a 3-week history of inappetence andintermittent vomiting. Blood tests revealed amicrocytic, hypochromic anaemia (PCV 0.12 l/l,MCV 39 fl, MCH 9.0 pg/l). An occult faecal

blood test was positive. The cat improved clini-cally and haemodynamically following an un-matched, fresh whole blood transfusion and wasreferred to the UVCS.

On physical examination, the cat was thin,tachycardic (210 bpm) and tachypnoeic (60breaths per min). The poorly regenerative, micro-cytic, hypochromic anaemia (PCV 0.17 l/l, MCV41 fl, MCH 12.1 pg/l, reticulocytes 67×109/l)was confirmed on repeat blood tests. The cat wasobserved for 6 days and treated with cimetidine(19 mg PO every 12 h). During this period, shebecame progressively inappetent and developedmelaena and haematemesis. As a result, the catwas scheduled for exploratory surgery and herblood type determined (type A).

At celiotomy, the caudal fundus and antrum ofthe stomach were thickened and a mesenteric

Gastroduodenal ulceration in cats 35

lymph node was enlarged. Crush preparations ofthe thickened gastric mucosa and lymph nodewere suggestive of gastric lymphosarcoma (LSA)and a reactive hyperplasia, respectively. A partialgastrectomy and gastroduodenal anastomosis(Billroth I) were performed (Fig 3). Histopathol-ogy confirmed the diagnosis of gastric LSA withno evidence of LSA in the mesenteric lymphnode. Fresh, type A blood was administeredpre- (20 ml) and intra-operatively (80 ml).

The cat was treated with antibiotics(amoxycillin-clavulanic acid, 0.5 ml SC every12 h; gentamicin, 5 mg every 12 h) for 48 h, cime-tidine (19 mg every 8 h) for seven days, andrecovered uneventfully from surgery. A sequen-tial, multiagent chemotherapy protocol (Maliket al 2001) was administered for six months. Thecat is alive and well 20 months after surgery withno evidence of recurrent gastric LSA.

Case 7. A 13-year-old, spayed DSH (4.3 kg) pre-sented with an acute onset of lethargy and in-appetence. A mass was palpable in the cranialabdomen. Serum biochemistry was within nor-mal limits but a regenerative normocytic, hy-pochromic anaemia (PCV 0.14 l/l, MCV 44 fl,MCH 11.3 pg/l, reticulocytes 333×109/l) andlymphopenia (0.3×109/l) were detected. Ab-dominal ultrasound revealed a 30×40 mm massin the cranioventral abdomen with anechoicmaterial in the gastric lumen. Blood type wasdetermined (type B) and an exploratory celi-otomy performed. The cat received a fresh trans-fusion of type B blood (100 ml) during theperioperative period. At celiotomy, a mass wasdetected in the pyloric antrum of the stomach.The pylorus and proximal duodenum wereresected and a gastroduodenal anastomosisperformed. The gastric lymph node was alsobiopsied.

Histopathology revealed gastric LSA withinvolvement of the regional lymph node. Themucosal surface of the tumour was extensivelyulcerated. The cat was maintained on intra-venous fluids [0.45% sodium chloride and 2.5%glucose (Baxter Healthcare) with an additional20 mmol/l potassium chloride], cimetidine(8.5 mg IV every 8 h), amoxycillin-clavulanic acid(0.5 ml every 12 h) and gentamicin (10 mg every8 h). All treatment was ceased when the catresumed eating two days after surgery. Thesequential multiagent chemotherapy protocolwas begun at suture removal 10 days post-operatively and continued for a total of sevenmonths. The cat is currently doing well 13 months

post-operatively with occasional vomiting but noultrasonographic evidence of recurrence.

Case 8. A 12-year-old, spayed Chinchilla cat(5.4 kg) had a 4-day history of inappetence, poly-dipsia and haematochezia. She had presentedtwice in the preceding eight months with vomit-ing, diarrhoea and weight loss (0.4 kg). Physicalfindings included tachycardia (250 bpm), palemucous membranes and caudal abdominal pain.Haematology, serum biochemistry and urinalysiswere performed. Abnormalities included a re-generative, macrocytic, normochromic anaemia(PCV 0.14 l/l, MCV 47 fl, MCH 14.0 pg/l, reticu-locytes 300×109/l), neutrophilia (32.7×109/l)and lymphopenia (0.79×109/l).

Abdominal ultrasonography revealed an intra-mural gastric mass with thickening of thestomach wall in the body and pyloric antrumand anechoic material in the gastric lumen. Ananechoic cystic structure (20 mm×30 mm), con-taining echogenic particles, was detected in theright kidney.

The cat was euthanased and a necropsy per-formed. A 30×30 mm mass, with an extensivelyulcerated mucosal surface, was present along thelesser curvature of the stomach (Fig 4). Thecontents of the stomach and proximal smallintestine were dark-coloured and voluminous.Histologically, the gastric mass was a poorlydifferentiated adenocarcinoma. Polycystic kid-ney disease, with haemorrhage into a large cystin the right kidney, was also confirmed.

Literature review

A review of the literature revealed a further 25cases of GU in cats. Gastroduodenal ulcers wereassociated with neoplasia in 11 cases with mastcell tumour (n=7) (Seawright & Grono 1964,Schalm et al 1975, Hasler & van den Ingh 1978,Liska et al 1979, Gordon 1980, Jones & Hunt1983, Bortnowski & Rosenthal 1992, Mai &Bouhoula 1998) the most common diagnosis fol-lowed by gastrinoma (n=3) (Middleton et al1983, van der Gaag et al 1988, Eng et al 1992) andLSA (n=1) (Weller & Hornof 1979). Zwahlen et al(1998) described two additional cases of intesti-nal perforation associated with alimentary LSAalthough the location of perforation were notrecorded and hence were not included in thismetanalysis.

A variety of other causes for GU were diag-nosed in the remaining cats. Two cases referableto parasitic disease, Aonchotheca putorii (n=1)

36 JM Liptak et al

(Curtsinger et al 1993) and Toxocara cati (n=1)(Aoki et al 1990), have been reported. Inflamma-tory bowel disease has been reported as a causeof gastroduodenal erosion and ulceration in cats(Jergens et al 1992). Gastroduodenal ulcerationhas also been associated with hypereosinophilicsyndrome (McEwen et al 1985), staphylococcalgranuloma (Sheikh-Omar & Abdullah 1985), tox-icity to Dieffenbachia leaves (Muller et al 1998),carprofen administration (Runk et al 1999),and following surgery (Evans & Biery 1980,Holmberg et al 1989). One case of gastric rupturewas excluded from review as the presentationwas not consistent with gastric ulceration andhistopathology of the gastric lesion was not per-formed (Wright 1983). Interestingly, a cause forulceration was not identified in the remainingfour cases (Wrigley 1977, Gordon 1980, Thilgaret al 1989, Twedt 1994).

Detailed information was available for 14 ofthe reviewed cases (six with neoplasia and eightwith non-neoplastic causes of GU). Table 3 liststhe causes of GU and Table 4 summarises thepertinent clinical findings of neoplastic and non-neoplastic causes of feline GU in the presentseries and previously recorded cases. The lo-cation of ulcers was almost exclusively pyloroan-tral or fundic in cats with non-neoplastic GU.Only one cat with non-neoplastic GU, due tocarprofen administration, had a duodenal ulcer(Runk et al 1999). Conversely, duodenal ulcer-ation was more common in cats with extra-intestinal neoplasia. There was a relatively equaldistribution of single and multiple ulcersirrespective of the aetiology.

Table 3. Causes of gastric and duodenal ulcers reported in cats

Causes of ulcers Types

Drugs Nonsteroidal antiinflammatory drugsPrimary gastric disease Neoplasia (lymphosarcoma and adenocarcinoma),

inflammatory bowel diseaseStress SurgeryGastric hyperacidity Systemic mastocytosis, gastrinomaSystemic disorders Renal failure, hypovolaemiaMiscellaneous Endoparasites, bacterial granuloma, hypereosinophilic

syndrome, toxicity, pancreatic adenocarcinoma

DiscussionGastroduodenal ulceration is uncommonly re-ported in cats. The present series describes theclinical features of eight cats with gastrointestinaldisease and blood loss due to GU. By including a

further 25 cases from the literature, a greaterrange of causes for feline GU were detected(Table 3). Gastroduodenal ulceration was arbi-trarily divided into neoplastic and non-neoplastic causes, however, a definitive aetiologycould not be identified in some cats with non-neoplastic GU. Most cats responded well to ap-propriate management, including several caseswith neoplasia, despite often presenting in, orprogressing to, a critical condition.

The presenting signs, physical findings andlaboratory results in cats with GU were eithernon-specific or consistent with upper gastro-intestinal disease. The duration of clinical signswas notably greater in cats with tumour-associated GU and these cats were more likely topresent with weight loss due to prolonged inap-petence or cancer cachexia. Haematemesis andmelaena provided evidence for blood loss intothe gastrointestinal tract but were present in lessthan a third of cats with GU (Table 4). Examina-tion of the oral cavity is important in the inves-tigation of cases with occult gastrointestinalblood loss as it may reveal a linear foreign bodyanchored to the base of the tongue or ulcerativestomatitis as an accompaniment to uraemic gas-tritis. Furthermore, bleeding palatine ulcers(Wildgoose 1990, Menrath & Miller 1995), whichmay mimic GU, can be excluded.

Anaemia was detected in all cats with GU inthe present series. Thus, GU should be consid-ered in any cat presenting with anaemia in whichthe cause of blood loss cannot be readily ident-ified. Other laboratory findings were non-specific and reflected changes associated withvomiting, blood loss, inflammation and stress(Guilford & Strombeck 1996b).

A variety of imaging techniques have beendescribed in the diagnosis of GU includingendoscopy, ultrasonography, plain and contrastradiography, and scintigraphy (Guilford &Strombeck 1996b, Penninck & Tidwell 1997, Hall

Gastroduodenal ulceration in cats 37

Tab

le4.

Sum

mar

yof

sign

alm

ent,

pres

entin

gsi

gns,

phys

ical

exam

inat

ion

and

labo

rato

ryfin

ding

s,an

dul

cer

char

acte

ristic

sin

cats

with

gast

rodu

oden

alul

cers

from

the

Uni

vers

ityV

eter

inar

yC

entr

eS

ydne

yan

dlit

erat

ure

revi

ew

Tum

our

UV

CS

Non

-tum

our

UV

CS

Tum

our

revi

ewN

on-t

umou

rre

view

Tum

our

tota

lN

on-t

umou

rto

tal

Tota

l

Bre

ed80

%D

SH(4

/5)

33%

DSH

(1/

3)60

%D

SH(3

/5)

83%

DSH

(5/

6)70

%D

SH(7

/10

)67

%D

SH(6

/9)

68%

DSH

(13/

19)

Age

(yea

rs)

11.2

4.5

9.7

9.1

10.4

7.2

9.1

Sex

100%

F/FS

(5/

5)0%

F/FS

(0/

3)50

%F/

FS(3

/6)

60%

F/FS

(3/

5)73

%F/

FS(8

/11

)38

%F/

FS(3

/8)

58%

F/FS

(11/

19)

Dur

atio

n(w

eeks

)19

.60.

725

.41.

522

.51.

312

.4V

omit

ing

80%

(4/

5)10

0%(3

/3)

100%

(5/

5)29

%(2

/7)

90%

(9/

10)

50%

(5/

10)

70%

(14/

20)

Hae

mat

emes

is40

%(2

/5)

0%(0

/3)

25%

(1/

4)17

%(1

/6)

33%

(3/

9)11

%(1

/9)

22%

(4/

18)

Mel

ena

40%

(2/

5)33

%(1

/3)

0%(0

/4)

33%

(2/

6)22

%(2

/9)

33%

(3/

9)28

%(5

/18

)In

appe

tenc

e80

%(4

/5)

33%

(1/

3)60

%(3

/5)

60%

(3/

5)70

%(7

/10

)50

%(4

/8)

61%

(11/

18)

Wei

ght

loss

100%

(5/

5)0%

(0/

3)10

0%(4

/4)

29%

(2/

7)10

0%(9

/9)

20%

(2/

10)

58%

(11/

19)

Poly

dip

sia

40%

(2/

5)33

%(1

/3)

0%(0

/4)

0%(0

/7)

22%

(2/

9)10

%(1

/10

)16

%(3

/19

)A

bdom

inal

pain

20%

(1/

5)67

%(2

/3)

0%(0

/3)

29%

(2/

7)13

%(1

/8)

40%

(4/

10)

28%

(5/

18)

Ana

emia

100%

(5/

5)10

0%(3

/3)

50%

(2/

4)40

%(2

/5)

78%

(7/

9)63

%(5

/8)

71%

(12/

17)

Hyp

opro

tein

aem

ia60

%(3

/5)

0%(0

/3)

0%(0

/4)

40%

(2/

5)33

%(3

/9)

25%

(2/

8)29

%(5

/17

)Ly

mph

opae

nia

60%

(3/

5)0%

(0/

3)0%

(0/

4)40

%(2

/5)

33%

(3/

9)25

%(2

/8)

29%

(5/

17)

Neu

trop

hilia

60%

(3/

5)67

%(2

/3)

25%

(1/

4)20

%(1

/5)

44%

(4/

9)38

%(3

/8)

41%

(7/

17)

Lef

tsh

ift

20%

(1/

5)33

%(1

/3)

25%

(1/

4)40

%(2

/5)

22%

(2/

9)38

%(3

/8)

29%

(5/

17)

Hyp

okal

aem

ia20

%(1

/5)

67%

(2/

3)0%

(0/

4)20

%(1

/5)

11%

(1/

9)38

%(3

/8)

24%

(4/

17)

Ren

alfa

ilure

0%(0

/5)

0%(0

/3)

0%(0

/3)

0%(0

/5)

0%(0

/8)

0%(0

/8)

0%(0

/16

)H

epat

icfa

ilure

0%(0

/5)

0%(0

/3)

0%(0

/3)

0%(0

/5)

0%(0

/8)

0%(0

/8)

0%(0

/16

)U

lcer

loca

tion

30%

Fund

us17

%Fu

ndus

17%

Fund

us69

%Fu

ndus

23%

Fund

us54

%Fu

ndus

39%

Fund

us40

%Py

loru

s83

%Py

loru

s0%

Pylo

rus

19%

Pylo

rus

18%

Pylo

rus

36%

Pylo

rus

27%

Pylo

rus

30%

Duo

den

um0%

Duo

den

um83

%D

uod

enum

13%

Duo

den

um59

%D

uod

enum

9%D

uod

enum

34%

Duo

den

umPe

rfor

ated

40%

(2/

5)33

%(1

/3)

50%

(2/

4)44

%(4

/9)

44%

(4/

9)42

%(5

/12

)43

%(9

/21

)Su

rviv

al(m

onth

s)12

.214

.76.

82.

39.

26.

48.

0

UV

CS,

Uni

vers

ity

Vet

erin

ary

Cen

tre

Syd

ney;

DSH

,dom

esti

csh

ort

hair

;F,f

emal

e;FS

,fem

ale

spay

ed.

38 JM Liptak et al

2000). In the present series, simple imaging tech-niques, such as abdominal radiography andultrasonography, provided pertinent informationrapidly and without the need for chemical re-straint. In cats with a perforated ulcer, evidenceof pneumoperitoneum or peritonitis on plainabdominal radiographs signalled the need forurgent exploratory surgery. Abdominal ultra-sonography was performed if plain radiographywas unrewarding. In dogs, the ultrasonographicfeatures of gastric ulceration include local muralthickening, loss of the five-layer structure, pres-ence of a defect or crater in the gastric wall, fluidaccumulation in the lumen of the stomach anddiminished gastric motility (Penninck & Tidwell1997). However, of the seven cases in whichabdominal ultrasonography was performed inthis study, these findings were only recognisedin the three cats with gastric tumours. Althoughendoscopy is the preferred imaging modality fordetecting gastric and duodenal ulcers (Guilford& Strombeck 1996b, Hall 2000), the majority ofcats with GU presented in a critical conditionwhich precluded its use due to time constraints,anaesthetic risk and possibility of iatrogeniculcer perforation.

The management of cats with gastrointestinaldisease and blood loss can be complicated bytheir critical nature and lack of specific clinicalsigns and physical findings. In general, followingblood tests and abdominal imaging, cats withGU were stabilised with a transfusion of fresh,whole blood. All cats receiving blood trans-fusions in the present series were either cross-matched or blood-typed to ensure compatibility.Transfusion reactions are common in cats, rang-ing from decreased erythrocyte survival time intype A cats receiving type B blood to life-threatening incompatibility reactions in type Bcats receiving type A blood (Hohenhaus &Rentko 2000). Hence, cross-matching or blood-typing is mandatory prior to administration offresh, whole blood, especially in Australia whereapproximately 25% of DSH are type B (Auer &Bell 1981).

In the present series, surgery was performedin all cases that subsequently survived. Life-threatening-haemorrhage, failure to respond tomedical management and perforation are indica-tions for surgical intervention (van Sluys 1993,Hall 2000). In humans, non-surgical manage-ment of peptic ulcers is common as prospectivestudies comparing conservative and surgicaltreatment of perforated peptic ulcers show nosignificant difference in morbidity and mortality

(Zittel et al 2000). However, in our experience,prompt surgical intervention is preferred as catswith GU often present in a critical condition withperforation and spillage of intestinal contentsand bacteria into the peritoneal cavity.

A thorough exploration of the abdominal cav-ity should be performed as extra-intestinal neo-plasms may cause GU and unperforated ulcerscan be difficult to locate (Hall 2000). Intraopera-tive endoscopy or ultrasonography has beenrecommended to localise unperforated ulcers(Hall 2000). However, in the present series, un-perforated GU was easily identified as the ulcerswere associated with either adhesions or a gas-tric mass. Since multiple lesions are relativelycommon in cats with either neoplastic and non-neoplastic GU, a complete examination of thegastrointestinal tract should be performed(Gordon 1980, Middleton et al 1983, van der Gaaget al 1988, Aoki et al 1990, Jergens et al 1992).

In humans, conservative management of hy-peracidity with H2-receptor antagonists and pro-ton pump inhibitors has replaced the need forradical surgery (Guilford & Strombeck 1996b,Hall 2000, Zittel et al 2000). The current recom-mendation for surgical management of GU, asemployed in the majority of the present cases, isdebridement and suturing of the ulcer (Zittelet al 2000). The risk of disruption to the majorduodenal papilla is minimised by using suchconservative surgical techniques in the treatmentof duodenal ulcers. However, more extensivesurgery, such as a Billroth I, may be required forthe resection of gastrointestinal masses causingGU (van Sluys 1993).

Extra-intestinal tumours that can cause GU incats include systemic mastocytosis, pancreaticadenocarcinoma and gastrinoma (Seawright &Grono 1964, Schalm et al 1975, Hasler & van denIngh 1978, Liska et al 1979, Jones & Hunt 1983,Middleton et al 1983, van der Gaag et al 1988,Eng et al 1992, Mai & Bouhoula 1998). Splenec-tomy is recommended in cats with GU secondaryto systemic mastocytosis with splenic involve-ment (Vail 1996). Partial pancreatectomy shouldbe performed in cats with resectable pancreaticmasses (Simpson & Dykes 1997). However, tu-mours of the pancreas may either be inapparent,such as the suspected gastrinoma in case 4, ordiffuse, as illustrated by the adenocarcinoma incase 5, and hence not amenable to partial pan-createctomy. In dogs with Zollinger-Ellison syn-drome, resection of the right limb of the pancreashas been recommended if the pancreatic mass isnot visible grossly (Simpson & Dykes 1997) but

Gastroduodenal ulceration in cats 39

this should not be extrapolated to cats as littleinformation is available on the distribution ofgastrinomas in the feline pancreas due to apaucity of reported cases (Eng et al 1992, van derGaag et al 1988, Middleton et al 1983).

Adjunctive medical therapy is essential in themanagement of cats with GU. Antibiotics havesignificantly reduced the morbidity and mor-tality associated with perforated ulcers in hu-mans (Zittel et al 2000). The oral cavity is themost common source of gastric bacteria andrecent studies have shown that healthy cats har-bour high numbers of gram-positive cocci, coli-forms, and facultative and strict anaerobes in theproximal small intestine (Guilford & Strombeck1996a, Papasouliotis et al 1998, Johnston et al2001). Hence, a broad spectrum antibiotic, suchas amoxycillin-clavulanic acid, or combination ofantibiotics, such as amoxycillin-clavulanic acid,enrofloxacin and metronidazole, is recom-mended.

Antisecretory agents, such as H2-receptor an-tagonists and proton pump inhibitors, are im-portant in the management of cats with GU. Inthe present series, H2-receptor antagonists, suchas cimetidine and ranitidine, were used in theimmediate post-operative period to aid the heal-ing of sutured gastroduodenal defects as theywere the only preparations available in bothparenteral and oral preparations at the time.Ranitidine is considered superior to cimetidineas it results in greater suppression of gastric acidsecretion and a longer duration of action, thusrequiring less frequent administration (Hall2000, Guilford & Strombeck 1996b). Omeprazole,a proton pump inhibitor, is preferred for catswith unremitting gastric hyperacidity, such aswith systemic mastocytosis and gastrinoma, as ithas a more profound suppression of gastric acidsecretion than H2-receptor antagonists, inhibitsgastric acid secretion regardless of the secreta-gogue, and only requires once daily admin-istration (Guilford & Strombeck 1996b). In thepresent series, one cat with duodenal ulcerationdue to a suspected gastrinoma (case 4) survived18 months with once daily omeprazole admin-istration. Other possible treatments includesucralfate, which protect ulcers from gastricacid, and misoprostol, a prostaglandin E1 ana-logue, which is preferred for the prevention andtreatment of NSAIDS-induced GU (Hall 2000).

Causes of GU were divided into neoplastic andnon-neoplastic in the present series and literaturereview. Non-neoplastic GU tended to have ashort clinical history, minimal weight loss

and ulcers located in the gastric fundus, body,antrum or pylorus. However, diagnosing theunderlying cause of GU was difficult in these cases.Gastroduodenal ulcers in cats do not appear to bestrongly associated with renal or hepatic dysfunc-tion. Hepatic disease, although a common cause ofGU in dogs (Stanton & Bright 1989), was not ident-ified in cats with GU. Renal dysfunction may havecontributed to GU in case 1, but has not beenidentified as a potential cause in previous reports.However, a strong association has been reportedbetween chronic renal failure and iron deficiencyanaemia, presumably due to gastrointestinal bloodloss (Cowgill et al 1998). Gastric erosions and ul-ceration have been diagnosed in cats with IBD,however, these lesions are usually subclinical andrarely cause significant gastrointestinal blood loss(Jergens et al 1993, Baez et al 1999, Willard 1999).The administration of NSAIDS is a common causeof GU in dogs (Stanton & Bright 1989), however,despite numerous experimental reports of the ul-cerogenic effects of NSAIDS in cats (Twedt 1994),NSAIDS-induced GU has only been reported inone clinical case (Runk et al 1999). The incidence ofNSAIDS-induced gastric ulcers may increase asmore NSAIDS are registered for management ofpain and treatment of osteoarthritis in cats (Runket al 1999). Hypovolaemia or stress may also play arole in the development of GU as perforated gastriculcers have been reported in two cats followingsurgery (Evans & Biery 1980, Holmberg et al 1989)and either could have contributed in case 2 of thepresent series.

Parasitic infestation, bacterial infection, toxinsand foreign bodies are reported causes of local-ised, non-neoplastic GU in cats (Sheikh-Omar &Abdullah 1985, Aoki et al 1990, Curtsinger et al1993, Muller et al 1998, Hall 2000). Parasitesassociated with feline GU include Toxocaracati (Aoki et al 1990) and Aonchotheca putorii(Curtsinger et al 1993). Ollulanus tricuspis andGnathostoma spp also have the potential to causegastric ulceration (Trueman & Ferris 1977,Guilford & Strombeck 1996b, Hall 2000). Infec-tion with Helicobacter spp is the most importantcause of chronic gastritis, peptic ulceration andgastric neoplasia in people (Neiger & Simpson2000). The role of Helicobacter spp in the patho-genesis of feline GU is uncertain, especially asHelicobacter-like organisms are commonly foundin normal cats (Guilford & Strombeck 1996b,Neiger & Simpson 2000). Spiral-shaped bacteriawere not considered to be the primary causativeagent in any of our cats with GU. Other potentialcauses of feline GU include external trauma and

40 JM Liptak et al

intraluminal trauma from a foreign body ortrichobezoar. However, identification of a defini-tive cause of non-neoplastic GU was uncommonin this series and previously reported cases(Wrigley 1977, Gordon 1980, Thilgar et al 1989,Twedt 1994). Regardless of the cause, the prog-nosis is good for non-neoplastic GU followingprompt stabilisation and surgical intervention.

Tumour-associated GU tended to present witha protracted history of vomiting, inappetenceand weight loss. A number of different tumourshave been reported to cause GU (Seawright &Grono 1964, Schalm et al 1975, Hasler & van denIngh 1978, Liska et al 1979, Weller & Hornof1979, Jones & Hunt 1983, Middleton et al 1983,van der Gaag et al 1988, Eng et al 1992, Mai &Bouhoula 1998). Gastric tumours, such as LSAand adenocarcinoma, cause gastric ulceration byaltering mucosal integrity and blood flow (vanSluys 1993, Hall 2000). However, ulceration isapparently rare in cats with proximal gastroin-testinal tumours (Weller & Hornof 1979, Mahonyet al 1995, Zwahlen et al 1998, Cribb 1988,Kosovsky et al 1988, Turk et al 1981, Patnaik et al1976). Gastric LSA may behave differently toother types of feline alimentary LSA as survivalgreater than 12 months was reported in both ofthe present cases following surgical resectionand a brief but intensive course of adjunctivemultiagent chemotherapy. This survival time isgreater than typically reported for alimentaryLSA (Mahony et al 1995, Zwahlen et al 1998) and,although case numbers are too low for a mean-ingful comparison, similar conclusions havebeen made by other investigators (Willard2000).

Systemic mastocytosis is the most frequentlyreported cause of neoplastic GU in cats(Seawright & Grono 1964, Schalm et al 1975,Hasler & van den Ingh 1978, Liska et al 1979,Jones & Hunt 1983, Bortnowski & Rosenthal1992, Mai & Bouhoula 1998). Intestinal mast celltumours have not been reported to cause ulcer-ation in cats (Alroy et al 1975), despite being acommon cause of GU in dogs (Takahashi et al2000), although a perforated gastric ulcer wasreported in one cat with a gastric mast celltumour (Bortnowski & Rosenthal 1992).

Gastrinomas are functional non-islet cell tu-mours of the pancreas resulting in hypergastri-naemia, hypersecretion of gastric acid and pepticulceration (Zerbe & Washabau 2000). A gastri-noma was suspected in case 4 on the basis ofmarkedly elevated serum gastrin levels. Theprognosis is guarded for cats with gastrinoma, as

metastases are frequently detected at diagnosis,although surgical resection of the primary lesionand adjunctive treatment with antisecretorydrugs, including omeprazole, may result insurvival times greater than 12 months (Eng et al1992).

Pancreatic adenocarcinoma has not previouslybeen reported to cause GU. Ulceration may havebeen caused by either local invasion or the localrelease of activated pancreatic enzymes (Steiner& Williams 1997). Pancreatitis may also havecontributed in case 2. The prognosis for pancre-atic adenocarcinoma is usually poor due to re-gional extension, distant metastases at the timeof diagnosis or the development of paraneoplas-tic syndromes (Pascal-Tenorio et al 1997, Steiner& Williams 1997), although case 5 in the presentseries survived 12 months following surgery.

ConclusionCats with GU often presented in a critical con-dition. Clinical signs consistent with gastro-intestinal bleeding were uncommon althoughanaemia was a frequent laboratory finding. Ap-propriate management of cats with GU involvesprompt stabilisation with a compatible bloodtransfusion, surgical debridement or resection ofthe ulcer, antibiotic and antiulcer therapy, andtreatment of the underlying disease, if identified.

Non-neoplastic causes of feline GU tended tohave a shorter clinical course with ulcers con-fined to the stomach. The causative factor wasdifficult to identify. However, with appropriatemanagement, cats with non-neoplastic GU hadan excellent prognosis.

Cats with tumour-associated GU usually had amore protracted clinical course, weight loss, andulcers located in the stomach for gastric tumoursand the duodenum for extra-intestinal tumours.In both the present series and previously pub-lished case reports, the prognosis for cats withGU secondary to gastric LSA, gastrinoma andsystemic mastocytosis is good.

AddendumSince writing this report a 20-year-old, spayedDSH died acutely in our hospital. Necropsyrevealed proximal duodenal ulceration with sig-nificant intraluminal haemorrhage, generalisedsplenomegaly and mild hepatomegaly. A diagno-sis of duodenal ulceration secondary to systemic

Gastroduodenal ulceration in cats 41

mastocytosis was made on the basis of splenicand hepatic histopathology.

AcknowledgementsThe authors would like to thank clinicians,anaesthetists and technical staff at theUniversity Veterinary Centre Sydney, and refer-ring veterinarians for their assistance with casemanagement.

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