The I },t,.14,my.],,r, al I .q.tlS. 156.

91 - I OIl
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Gastric Disease in the Dog and Cat

M. SLII.I.IVAN and D. A. YO()I,

I)ivi.~iml q~ Sm~tll A,imal Clinical Sludie~. l)epartme,t ~/ ~},le~,m 3' Cli,ical Studies. (;las.~m~, U, iver~il~, 15"terinm7 School,
Brarsden IMad. Beat:w/e,, (;la.~ffow (;61 IQH, Scotland

SUMMARY
The l)hysiolog,3' of the n o r m a l gant,ic d e f e n c e m e c h a n i s m s in tim d o g and cat in reviewed to e m p h a s i z e the
routes by which drugs can be used to protect the gastric mucona. T h e action of the main anti-ulcer and pro-
kinetic drugs are discussed in relation to the diseases that they may be used to treat. (;astric disease in tbe
f o r m o l gastric d i l a t a t i o n / v o h ' u h l s , c h r o n i c v o m i t i n g without o b s t r u c t i o n a n d gastric outflow disease are
desc,'ibed f r o m the point of view o f diagnosis a n d t r e a t m e n t .

KI.:~,~,{)RI)S: Dog; stomach; disease; t r e a t m e n t .

T H E DILEMMA NORMAL DEFENCE MECHANISMS

T h e s t o m a c h is an o r g a n t h a i serw'n to store a n d T h e stomach wall protects its integrity thl'ougb what

partly process ingesta. Digestion in the s t o m a c h is
a i d e d by the s e c r e t i o n o f two c h e m i c a l s , ,lamely
acid and pepsin. T h e p r e s e n c e o f these nvo chemi-
cals ill the l u m e n c r e a t e s an e n v i r o n m e n t that in
p o t e n t i a l l y i n i m i c a l to tile s t o n l a c h ' s own well
being. T h e p r o d i g i o u s g e n e r a t i o n o1: h y d r o c h l o r i c
acid by the timdic parietal cells g e n e r a t e s a pH that
is capable of killing lll~lllV mic,'o-organinmn and con-
t i n u i n g the d i g e s t i v e p r o c e s s s t a r t e d in the oral
cavity. Even on an e m p t y s t o m a c h , acid in continu-
ally p r o d u c e d g i v i n g r i s e to a Imp' b a s a l p H .
Following a meal, d u o d e n a l c o n t e n t s including bile
can rellux into the s t o m a c h and it has b e e n shown
t h a t b i l e is d a m a g i n g to t h e g a s t r i c i n t l c o n a ,
a h h o u g h the induction o t d a m a g e may d e p e n d on
c i r c u n t s t a n c e s o t h e r t h a n t h e p r e s e n c e o f bile
( A d a i r & W l o d e k , 1968; H a p p 6 et al., 1 9 8 3 ) .
Post-prandial d u o d e n o g a s t r i c retlux is of no conse-
q u e n c e as the bile is d i l u t e d by i n g e s t a a n d the
continual, e m p t y i n g o f t o o d boluses to the d u o d e -
n u m t e n d s to clear the retlux ( S o n n e n b e r g el aL,
1982). However, bile retlux can o c c u r on an e m p t y
s t o m a c h a n d in m a n r e a c h e s a p e a k in the early
h o u r s of the m o r n i n g (Borg, 1959).
has been termed the gastric mucosal barrier
w h e r e b y r a p i d i n v a s i o n o f h y d r o g e n ions f r o m
l u m e n to interstitium is prevented. Thin barrier is a
physiological c o n c e p t a n d to date has no definite
a n a t o m i c a l analog,)'. However, the m u c u s layer, sur-
face e p i t h e l i u m a n d the t i g h t j u n c t i o n s m a y be
c o n s i d e r e d to act as a physical barrier. T h e essential
function o f this b a r r i e r is to maintain a high lumi-
nal acid c o n c e n t r a t i o n a n d low p H , a n d in t h e
process avoid autodigestion by the activated e n z y m e
pepsin. Tiffs is a c h i e v e d by the p r e s e n c e o [ a pro-
fuse micvocirculation that delivers b i c a r b o n a t e ions
to b u f f e r h y d r o g e n i o n s d i f f u s i n g t h r o u g h t h e
inucus laver (Allen & (;arner, 1980), with the trans-
p o r t o f b i c a r b o n a t e i o n s b e i n g i n c r e a s e d by a
lowered p H (Flemntr6m & G a r n e r , 1982). T h e con-
trol o f the p r o f u s e m i c r o c i r c u l a t i o n , b i c a r b o n a t e
secretion a n d muctts secretion is t h r o u g h prostag-
landins (Kattf['man el al., 1980). In the m u c u s there
in an a b u n d a n c e of a m p h o t e r i c p h o s p h o l i p i d s that
e n h a n c e the w a t e r r e p e l l e n c y w h e n a d s o r b e d to
n e g a t i v e l y c h a r g e d m e m b r a n e s ( S l o m i a n y el al.,
1978; Hills el aL, 1983). T h u s the m u c u s layer acts as
a partial b a r r i e r p r o d u c i n g a c o n c e n t r a t i o n gradi-
ent so that fewer ions reach the cell. T h e chemical

10.t)0-O233/9~/OSOIIt.I I- 16/$12.00/1} © 1998 Bailli6,'e "l'indall

 92 THE VETERINARY .]()URNAI., 156, 2
and physical p r o p e r t i e s o f tile apical m e m t ) r a n e s
and tight j u n c t i o n s o f the surlace epithelial cells are
such that water soluble substances are very slowly
admitted. This impernlealfility is all i m p o r t a n t fac-
tor in the d e f e n c e o f tile gastric m u c o s a against
inju,'ious agents (Code, 1981 ).
Superficial injury witlmut d e e p e r mucosal dmn-
age and vasctdar inju, T is ,'epaired rapidly by cell
migration, so called mucosal restitution (Pihan el
al., 1986). F o l l o w i n g injury, t h e r e is e x t e n s i v e
nlucus secretion that p r o d u c e s a gelatin,ms l a v e r
with e x f o l i a t e d surface epithelial cells t o r m i n g a
mucus cap, which provides a m i c r o e n v i r o n n l c n t to
aid epithelial h e a l i n g (Wallace & Whittle, 1986).
L o n g e r term recovery from m o r e severe d a m a g e
o c c u r s t h r o u g h m u c o s a l r e g e n e r a t i o n t h a t is
extremeh, rapid and d e e p injury call heal by 5 days
tbllowing insuh (~keomans el aL, 1973).
P H A R M A C O T H E R A P Y OF GASTRIC DISEASES
Drug therapy may be aimed at p r o t e c t i n g the gas-
tric mucosa from the acid and proteolytic
e n v i r o n m e n t that pertains in tile l u m c n when the
n<.-mal d e f e u c e m e c l a a n i s m s are c<m~promised
t h r o u g h disease or surger?'. Prokinetic agents may
also be used to e n c o u r a g e tile aboral m o v e m e n t of
gastric c o n t e n t s ill c o n d i t i o n s o f a l t e r e d gastric
motility. O t h e r the,-apies are aimed at t,'eating the
underlying disease processes.
H 2 Rec#plor anlagonists
This g r o u p of drugs includes cimetidine, ranitidine
alld famotidille, Thev act by p r e v e n t i n g histalnine
from stimulating parietal cells to p r o d u c e gast,-ic
acid. Cimetidine ( 5 - 1 0 m g . k g -I TII)-QII)) has been
the mainstay o f ulcer therapy in animals and is ve D'
effective at r e d u c i n g gastric acidity. It is especially
useful when high circulating levels o f histaulines
cause hyperacidity, tor example, Ilistamine release
from mast cell mmours. Newer I-t2 blockers such as
r a n i t i d i n e ( ( I . 5 - 4 m g . k g - I BID) have f e w e r side
e f f e c t s , are m o r e p o t e n t t h a n c i m e t i d i n e a n d
require less li'equent doses (Ostro, 1987). However,
these drugs are no m o r e effective than cimetidine
at e q u i v a l e n t doses, so a l t e r n a t i v e d r u g g r o u p s
s h o u l d be tried in cases r e f r a c t o r y to c i m e t i d i n e
therapy.
Proton p u m p in hibitors
O m e p r a z o l e ( 0 . 5 - 1 . 5 m g . k g - I SID) is a n e w e r
anti-ulcer d r u g that prevents the u-ansport o f pro-
tons into tile gastric Ittmen [rom the parietal cell
(Wallmark, 1986). h should be effective ill reducing
gastric acidity in all cases o f hyperacidity regardless
o f tile aetiolog~' as it interferes with the COllllllOn
patlaway to parietal cell acid l~roductio,1. A n ~ t h e r
a d v a n t a g e over the H,~ blockers is that, a h h o u g h
o n w p r a z o l e has a ve,y short half-life, it b e c o m e s
t r a p p e d a n d a c c u m u l a t e s in p a r i e t a l cells. T h i s
ineatls that once-a-day Iherapy is effective at reduc-
ing gastric acidity. Experimentally, p , o l o n g e d use
(>8 weeks) has b e e n associated with hypcrgastri-
naenlia and mucosal hyl~ertroplay. A h h o u g h this
l ) h c m m l c , m n has not b e e n r e p o r t e d clinically, a
nlaxinlunl of 4 weeks continual u s e is
recommended.
M u <'osal prolecla n Is
S u c r a l l h t e (<20kg 5 0 0 r a g . d o g - I , > 2 0 k g l g . d o g -I
TI1)) is an a l u m i n i u m sah t o r n l e d f r o m s u c r o s e
o c t a s u l p h a t e and p o l y a h u n i n i u m h y d r o x i d e that
binds selectively to danmgcd areas o f gastric mucosa
and protects it fvom f'urlher d a m a g e by gastric con-
t e n t ( S p i r t ) , 1 9 8 2 ) . It m a y a l s o s t i m u l a t e
prostaglandi,l release. Sucvalfate has virtually no
adverse effecls bul may redl.lCe Ihe abso,'ption o f
certain d r u g s st,oh as tile lllwoquinol<mes. Earh,
work suggested that sucrallate required ;t pH envi-
r o n m e n t of <4 to be effective but this has now been
s h o w l l n o t to 1)e the case a n d s u c r a l f a l e can be
administered at tilt, same lime as H,, blockers.
Proslagla ndin a naloffuc:~
Prostaglandins have a cyt,,protective effect on the
gastric m u c o s a (Robert, 1976) and p r o v i d e resis-
tance against ulcer,ltion regardless o f the level o f
gastric acidity. Misoprostol ( 1 - 5 | N . k g Tll)-Qll)) has
been used clinically as an anti-tdcer agent, particu-
l a r l y in c a s e s a s s ( ) c i a t e d w i t h n ( ) n - s t c r o i d a l
anti-inflanmmtoD, drt,gs (NSAID) use, a l t h o u g h a
good response to o t h e r anti-ulcer drugs shotdd ;list>
be s e e n . Side e f [ e c t s o f pr<~staglandin t h e r a p y
include al)dominal cliscomlin't, d i a r r h o e a and uter-
ine c o n t r a c t i o n so their use s h o u l d be avoided in
p r e g n a n t animals.
M e t o c l o p r a n l i d e ( 0 . 2 - { L 4 m g . k g - I h a l f an hou,"
betore feeding TII)-OII)) is a vital c o m p o n e n t in the
t r e a t m e n t o f delayed gastric emptying. It is a proki-
n e t i c e n c o u r a g i n g gastric e m p t y i n g a n d a b o r a l
m o v e m e n t o f food. Cisapride (0.1-0.5mg.kwl 7"11)),
a n o t h e r prokinetic agent, has been used ill cases o f
 (;:\STRIC DISEASEIN TI IE DOG AND C:\T
delayed gastric e m p t y i n g but may cause w)miting
and abdominal cramping.
Erythromycin mimics motilin at std>therapeutic
doses ( 1 mg.kg -I BII)-TII)) and speeds gastric empty-
ing. It affects the whole intestinal tract and is being
u s e d i n c r e a s i n g l y in t h e m a n a g e m e n t o f gas-
t r o i n t e s t i n a l motility d i s o r d e r s a l t h o u g h it may
c a u s e gastric i r r i t a t i o n a n d v o m i t i n g at h i g h e r
doses. It is particularly effective at r e d u c i n g entero-
gaslric ,-eflux and may be useftd postoperatively in
g a s t r o d t t o d e n o s t o m v and g a s t r o j e j u n o s t o m y
patients. N e i t h e r cisapride n o r e r y t h r o m y c i n are
licenced for use in the dog.
H,~ blockers and mucosal protectants are the first
line o f t r e a t m e n t for gastric u l c e r a t i o n . Ideally,
d r u g dosages and t r e a t m e n t intel-vals a,e ac!justed
to cause continual suppression o f gastric acidity so
that there is no ftv'ther insttlt to the ulcerated areas.
O m e p r a z o l e a n d m i s o p , ' o s t o l are r e s e r v e d for
,-efractm T cases, or where there is a specific indica-
tion [i)r thei," use. In all cases, the inciting cause
must be looked fin" and treated or removed. Simi-
la,ly, in animals predisposed to o," with a histo D' o f
gastric ulceration, care must be taken when using
drugs which are ulcerogenic and anti-ulcer therapy
may have 1o be used prophylactically.
T h e r e are a myriad o f diseases that may affect the
stomach. This article will li)cus on a few o f these and
g r o u p them into syndromes that can be recognized
by the owner or the veterina D' surgeon. ( 1 ) Gastric
dilatation volvuhls (GDV), (2) c h r o n i c v o m i t i n g
without obstruction, and (3) gastric outflow disease.
GASTRIC DILATATION AND V O L V U L U S
K¢q, points
• Abdominal distension, hypersalivation, non-pro-
ductive r e t c h i n g , d y s p n o e a and cardiovascular
col lapse
• Gastric d e c o m p r e s s i o n with lavage and thtid ther-
apy immediately
• Fluid, e l e c t r o l y t e a n d a c i d - b a s e i m b a l a n c e s as
well as c a r d i a c a r r h y t h n a i a s are c o m m o n and
require t r e a t m e n t
• All cases requi,'e gastropexy
• T h e timing o f surgm T d e p e n d s on the cardiovas-
c u l a r status o f the p a t i e n t b u t s h o u l d follow
stabilization
• Patients require careful m o n i t o r i n g in the recov-
e r y p e r i o d as c a r d i a c a r r h y t h m i a s m a y still
develop
93
GDV is seen p r e d o m i n a n t l y in d e e p c h e s t e d ,
large breed dogs, although it has been r e p o r t e d in
small dogs and, ve, T occasionally, in the cat. It is
seen in any age of animal and has no sex predispo-
sition. GDV is c h a r a c t e r i z e d by gastric dilatation
anc[ rotation about its hmg axis. It is widely assumed
that gastric dilatation p r e c e d e s volvulus a l t h o u g h
this is d i f f i c u l t to c o n f i r m . T h e disease p r o c e s s
p r o g r e s s e s rapidly with animals b e c o m i n g mori-
b u n d and dying within a few hours (Glickman el al.,
1994).
T h e aetiolog3, o f (;DV is uncertain and many fac-
tors ( o u t l i n e d in T a b l e I) have b e e n implicated.
Diet and exercise have been t h o u g h t to be central
to the d e v e l o p m e n t of the condition. T h e incidence
of GDV is higher in clogs fed commercial, particu-
larly cereal or soya based diets ahlaough this may
retlect the m a n a g e m e n t o f the b r e e d types r a t h e r
than being a significant contributing factor. Failure
o[ eructation and vomiting have been p r o p o s e d as
initiating factors as the stomach dilates with gas and
f o o d . (;astric h y p o l n o t i l i t y a n d pylo,'ic o u t f l o w
o b s t r u c t i o n have b e e n i m p l i c a t e d as they lead to
gastric r e t e n t i o n a n d c h r o n i c gastric distension.
Cases with pyhwic outflow obstructions that develop
GDV have b e e n r e p o r t e d . Similarlv, gastric hypo-
motilig, has been recognized frequently in animals
which have recovered fl-om GDV'. This is generally
transient and m o r e likely represents an effect of gas-
tric d i l a t a t i o n r a t h e r t h a n an i n i t i a t i n g f a c t o r .
A n a t o m i c a l featttres that have b e e n c o n s i d e r e d
i n c l u d e d e e p chests, typically seen in the l a r g e r
breed clog, and chronic stretching of hepatogastric
and h e p a t o d u o d e n a l ligaments by repeated feeding
o f large meals. Post-prandial exercise and large,
i n f r e q u e n t meals have been implicated for purely
physical reasons.
Table I
Factors implicated in the genesis of gastric dilatation
volvulus (GDV)
l"aclm Reference
(;lickman et al. (1994)
Deep chest
Diet and exercise Hosgood (1994)
l.arge infiequent meals Glickman el al. (1994)
Failu,'e (71eructation and Strmnl~eck & Guiltbrd
vomiting (1991a)
(;astric hyp,mmtility Strombeck & (,uilford
(1991a)
Chronic stretching of hepato- Glickman et al. (1994)
and gastr¢~luodenal ligaments
 94 TFIE VET1-RINARY ]OURNAL, 156, 2
T h e gastric c o n t e n t s in G D V c o n s i s t o f gas (swal-
l o w e d air a n d s o m e f e r m e n t a t i v e g a s e s ) , tluid
(much o f which is due to abnornlal gastric secretion
a r i s i n g froln v e n o u s c o n g e s t i o n c a u s i n g ntural
o e d e n t a and transudation) and toocl (Fox, 1987).
Rising intragastric pressure compromises both res-
piratory and cardiovascuhtr function; hypotensi()n
OCCtlFS rapidly and tile animal enters hypovolaemic
shock. T h e caudal v e n t cava is collapsed by direct
pressure fl*om the dilating stomach and occlusion
o f the portal vein occurs d u r i n g gastric volvuhls.
T h e venous return to tilt" heart is r e d u c e d and fluid
pooling in the al)donlinal viscera leads to a r e d u c e d
c i r c u l a t i n g b l o o d volunle. E n d o t o x i c a n d septic
shock s u p e r v e n e because the , n u c o s a l - b l o o d bar-
rier and hepatic functio,l are severely
contprontised. As tissues b e c o m e ischaemic, cellu-
lar factors, such as ntyocardial d e p r e s s a n t f a c t o r
ti'om the ischaentic pancreas, are released and ntav
c o n t r i b u t e to hypotension by directly affecting the
heart. Myocardial isclmemia and cardiac at-rhyth-
mias also c o n t r i b u t e to the f a i l i n g m y o c a r d i a l
f u n c t i o n . T h e d y s p n o e a , c h a r a c t e r i z e d by rapid
sltallow b r e a t h i n g caused by pressure on the dia-
l ) h r a g m d u e to tile d i l a t i n g st()mach, p r e v e n t s
a d e q u a t e chest m o v e m e n t and will c o n t r i b u t e t,)
hypoxia and respiratory acid()sis in severely com-
promised patients (Mathiesen, 1983).
(;astric voh'uhts about tile longitudinal axis gen-
erally ()ccurs in at clockwise direction. A .90 ° to 360 °
volvulus can occur and, in the vast majority of cases.
resuhs fl-()m tile pyh)rus moving to tile left ()vet tile
ftlll(ltts ;:ISthe fttlldtts llt()ves to tile right, leaving the
ventral aspect o f the s t o m a c h c o v e , e d by g r e a t e r
o n l e n t m n . During volvtdus, the short gastric vessels
b e c o m e stretched or avulsed dmnaging the sert)sal
surface. Mucosal ()edema fronl v e n o u s occlusion
i n d u c e d I)y gastric d i l a t a t i o n leads t() lnuc()sal
hypoxia. Tissue ischaemia and necrosis will eventu-
ally o c c u r with large areas o f gastric wall along the
greater curvature b e c o m i n g necrotic. In advanced
cases, mural necrosis can lead to pertoration and a
g e n e r a l i z e d peritonitis. Stretchi,tg o f the gastros-
plenic ligament also occurs d u r i n g vohadus causing
the s p l e e n to follow the g r e a t e r c u r v a t u r e as it
moves to the ,'ight attd dorsally. This can lead to vas-
c u l a r c o m p r o m i s e o f the s p l e e n which b e c o m e s
c o n g e s t e d as the splenic vessels stretch. Occasion-
all), i n f a r c t i o n , avulsion o f tile splenic vessels or
p r o l o n g e d s p l e n i c t o r s i o n will lead to s p l e n i c
ischaemia (Ellison, 19q3).
Electrolyte and acid-base imbalances are features
o f (,DV b e c a u s e o f p o o r tissue p e r f t , s i t m a n d
a h e r e d h a e m o d y n a n l i c s . Hypokalaemia is the I l l O S [
c o n m m n electrolyte imbalance resulting li'om pool-
i n g o f p o t a s s i u m in tile d i s t e n d e d s t o m a c h .
However, potassium sttpplementation should only
be used when h y p o k a l a e m i a can be c o n f i r m e d as
cell death and acidosis may lead to hyperkalaenfia.
Metabolic acidosis is the most lvequenl acid-base
disturbance but, similarly, bicarl)onate should only
be given w h e n the a c i d - b a s e status can be mea-
sured. (;ardiac arrhvthmias are c o m m o n and resuh
ti-om myocardial ischaemia, electrolvte imbalances
a n d :reid-base {listurbances. R c p e r f u s i t m injury
occurs when ischaemic tissues are repertinsed with
oxygenaled blo()d. T h e oxygen in tile tissues reacts
with tile cellular prt)ducts of ischaemia to p r o d u c e
o x y g e n free radicals (l.antz, 1992). T h e s e cause
d a m a g e to the c e l h , l a r lllenlbranes m a k i n g cells
m o r e p e r m e a b l e and vtdnerable to osmotic factors.
U n f o r t u n a t e l y . tile above are c o m m o n causes o f
death in these patients even in the recovery p e , i o d
(Muir, 19,'q2a,b). O t h e r factors that c o m p l i c a t e
GDV include acl, te renal failu,-e tollowing hypoten-
sion a n d d i s s e m i n a t e d intrawtscular c o a g u l a t i o n
(DIC) tbllowi,lg toxaemia and circulato D, changes.
DI(; will f u r t h e r exacerbate the ischaenlic changes
a n d i n d i c a t e s a very p o o r p r o g n o s i s ( H o s g o o d ,
19q4).
A ,tilling, aids
These patients are critically ill and the clinical find-
i n g s a r e h i g h l y s u g g e s t i v e ()1 (;DV. F u r t h e r
diagn()stic wc)rk-up sh()uld be p()stp()ned until lilt"
patient ]las been stabilized with Iluid therapy and
gast,-ic dec()mpressi()n with lavage. Subsequently,
radi()graphy nlav be used (btll is ll()t e s s e n l i , I ] ) Io
c o n f i r n l the specific diagn()sis o f t()rsi(),l w h e r e
bands ()f tissue sacculating the stomach indicate vol-
v u l u s . H a e , n a t ( ) l o g y , sel'tlnl I ) i ( ) c h e n l i s t r v
(including electr()lytes) and urinalysis are all useful
if the resuhs are inlnlediatelv available. As cardiac
a r r h y t h m i a s are c o m m o n , e l e c t r t ) c a r d i o g r a p h y
should be pertol'med and repeated li'equently dur-
ing patient smbilizati<m, surge D' and aftercare.
MANAGEMENT OF THE G D V PATIENT
Palien! slabilizalion
Fluid lherapy. Peripheral or central i n t r a v e n o u s
access is o b t a i n e d a n d aggressive fluid therapy is ini-
 GASTRIC DISEASE IN T H E D O ( ; AND CAT
tiated using crystalh)ids, l , a c t a t e d R i n g e r s is t h e
lluid o f c h o i c e as a b a l a n c e d i s o t o n i c s o l u t i o n is
n e e d e d . H i g h t a l e s m a y b c necessary in shocked
palients and ,ates up to 90ml..kg. -I.h-I are used ini-
tially. An i m p r o v e m e n l in cardiovascular status may
be seen after gastric d e c o m p r e s s i o n a h h o u g h , if the
p a t i e n t r e m a i n s hyp()tcnsive a n d s h o c k e d despite
high rates of cD'stalloid therapy, the use of colloids
or even wh()le bh)()d may be necessary. H y p e r t o n i c
saline (7%) in (5% ( l e x l r a n ( S m L . k g - l . n a i n -1 f()r
5 r a i n ) in c()njuncti(),l with c r y s l a l l o i d s (0.09%
NaCI) has als()bc'e,l used (Hosgood, 1994).
D()pamine ()r ch)butamine infusions may be imple-
m e n t e d but b o t h are arrhylhm()gel]ic a n d s h o u l d
only be used w h e n the p a t i e n t can be m o n i t ( ) r e d
eleclr()cardi()graph ically. D()pamine
9 - 1 0 [ I g . k g - l . m i n -1 c ( ) n t i n u o u s i n f u s i o n ) is p r e -
t(:wred as it selectively maintains renal perfusion but
it is m()re arrhylhm()genic than d o l m t a m i n e . Over-
perfusio,1 n l n s t be av()ided and m()nitoring central
ven()us i)rcssure f r o m a jugtllar c a t h e t e r is o n e o f
the best indical()rs of the efficacy o f tluid theral)y.
However, i m p r o v i n g pulse quality, c()h)ur, capillm T
relill lilne and bh)()d pressure are also g()od indica-
tors that thfid l h e r a p y is w o r k i n g (l.eib & Martin,
1987).
(;aslric decompression. (;ast,ic d e c o m p r e s s i o n
a n d lax'age are nsuall.v p c r f ( ) r m e d as s()()n as fluid
t h e r a p y has b e e n s t a r t e d . In s e v e r e l y d y s p n o e i c
p a t i e n t s it may be best to perf()rm gastric d e c o m -
pression befo,'e initiating fluid therapy. A
well-lubricated, pliable, large b o r e ( t_) . -a - 4 c m diame-
ter) t u b e , p r e m e a s u r e d to the last , i b to av()id
iatrogenic gaslric perf()rati(m, is passed p r e f e r a b l y
with t h e a n i m a l s i t t i n g ()r with its f ( ) r e q u a r t e r s
raised. T h i s r e d u c e s p r e s s u r e ()n the c a r d i a a n d
facilitates the passage o f the robe. T h e release of gas
will r e l i e v e the d i l a t a t i o n in m o s t cases a n d the
s t o m a c h should be e m p t i e d of s()lid and liquid con-
tents e i t h e r by suction or s i p h o n i n g t h r o u g h the
s t o m a c h tube. T h e gastric l u m e n s h o u l d t h e n be
lavaged several times with w a r m e d water to rem()ve
as m u c h m a t e r i a l as possible r e d u c i n g the likeli-
h o o d o f r e c t l r r e l l t d i l a t a t i o n b e f o r e s u r g e r y . In
s m a l l e r d o g s a m o r e rigid (to aid passage) small
b o r e tube is used with care. T h e success or failure of
p a s s a g e o f a s t o m a c h t u b e is no i n d i c a t o r o f the
p r e s e n c e or a b s e n c e of torsion.
lf a s t o m a c h tube c a n n o t be passed, a t e m p o r a r y
gastrotomy or a tube gastrostomy can be per-
f o r m e d . H o w e v e r , if t h e a n i m a l is in s e v e r e
t.)5
r e s p i r a t o r y distress, p e r c u t a n e o u s n e e d l e d e c o m -
pression of the stomach can be p e r f o r m e d t h r o u g h
the right ttank in a similar area to that used lor tube
gastrostomy. T h e sto,nach is p t m c t u r e d with a 16-
18 g a u g e , 4 - 5 c m n e e d l e , p e r c u s s i n g the a r e a to
e n s u r e t h a t the s p l e e n is n o t o v e r - l y i n g the site
(Leib & Martin, 1987).
If bh)od or necrotic pieces o f m u c o s a are present
in the gastric contents, gastric wall necrosis is occur-
ring and l a p a r o t o m y should be p e r f o , ' m e d as soon
as the p a t i e n t is stable e n o u g h to withstand anaes-
thesia and surgery.
Corticosleroids. T h e use o f c o r t i c o s t e r o i d s in
GDV patients is controversial due to the risk of gas-
tric u l c e r a t i ( ) n . T h e p o t e n t i a l b e n e f i t s in t h e
treaDnent of hypovolaemic and endotoxic shock
p r o b a b l y outweigh the disadvantages and they are
ttsed routinely. D e x a m e t h a s o n e ( 6 - 1 5 m g . k g -1) or
prednis<)h)ne s o d i u m s u c c i n a t e ( 1 0 - 3 0 m g . k g -1)
s h o u l d be given early in the course ()f the disease
(Mathiesen, 1983).
Antibiotics. D u e to t h e risk o f s e p s i s f r o m
muc()sa] d a m a g e and mural necrosis, antibiotics are
indicated, lntraven()us p r e p a r a t i o n s o f ampicillin,
c l a v u h ) n a t e d a m o x y c i l l i n , c e t a t ( ) x a m i n e o r tri-
m e t h r o p , i m s u l p h o n a m i d e s are p r e f e r r e d and may
be c()mbined with metronidazole.
Bicarbonate and potassium. T h e s e s h o u l d only
be s u p p l e m e n t e d w h e n b l o o d gas a n d electrolyte
analysis arc available. Although acidosis and
h y p o k a l a e m i a are the c o m m o n e s t imbalances, both
alkalosis a n d h y p e r k a l a e m i a can occur.
H 2 bloclcer~. T h e early use o f H 2 b l o c k e r s a n d
o t h e r a n t i - u l c e r d r u g s h a s b e e n a d v o c a t e d to
r e d u c e the incidence o f gast,'ic ulceration and per-
f o r a t i o n a l t h o u g h gastric h y p e r a c i d i t y is n o t the
c a u s e o f u l c e r a t i o n in these cases. T h e y are rou-
tinely given to GDV p a t i e n t s as p a r t o f the initial
stabilization t r e a t m e n t a n d must be used p a r e n t e r -
ally ( S t r o m b e c k & Guilford, 1991a).
Cardiac mrhythmias. T h e incidence o f arrhyth-
m i a s at p r e s e n t a t i o n m a y be as low as 10% b u t
increases as the disease p r o g r e s s e s to affect up to
40-50% of" cases. Arrhythmias are frequently diag-
n o s e d for the first time in the recovery period so
f r e q u e n t patient evaluation is necessary to e n s u r e
that d e v e l o p i n g arrhythmias are n o t o v e r - l o o k e d .
The majority of cardiac arrhythmias are vcntricl~lat the fiinclus is pushed hack into its normal position.
in origin such as ventricular premature complexes, Once die stomacli has been tlerotatecl, the gastric
paroxysmal ventricular tacliycardias and continu- wall viability can be assessed using scrosal coloi~r as
ous ventricular tachycarclias. Treatment with the main cletermining factor. Red or haemorrhagic
lignocaine or procainamitle will convert ;i large areas of gaslric wall show veno~~s congestion hut
number, although some will remain refractory. may remain viable. Pale grey, green or black areas
Silpla\‘entl-iculal- arrhythmias also occur and are necrolic ancl should he remoyecl. hlpahlr tliin-
require treatment with chgs such as quinicline sul- ning of the gastric wall indicates impending
pliate. Potential causes of arrhythmias, sllcll as perforation ancl these areas shoulcl also he
acid-base ancl clectrol>~te imbalances, slioulcl be
removed. Acti\re l~aemorrhage from ;I serosal nick
den tilled ancl correctecl (Muir. 19H’La).
indicates good tisstle viability. Vascular patency
slioulcl he assessed as infarctccl or av~~lsccl\~~sscls
!kJRClCXL MANAGEMENT OF GDV mean that the areas of wall suppliecl are not \kihlc.
If it is uncertain whether or not a wsscl is patent, ;I
pulse can be Itill for. If;iny cloubl remains, compro-
Early surgical intewention within I-211 of prcsenta- misecl areas slioi~lcl be left for I .5 min after
tion gives enough lime f’or diagnostic work-up ancl clerot;~tion to see if a healthier coloiir returns to the
initiating stabilization procedures only.. The ach~n- tissue. Necrotic areas arc’ cxcisecl back to the Ic\~l of
tag-es of early surgical intc17.ention are that gastric acti\,c serosal hleccling and the deli-cl closecl using
wall necrosis may be avoiclecl or can be iclentifiecl stanclarcl suture patterns or the areas can be
early and clevitalizetl areas cxcisecl hefore lesions resectecl with a linear stapler. Suspect areas can be
hecc;me cstensive or perforate. A longer delay of up invaginatecl into he gastric lumen by suturing the
to 4811 allows for better stabilization ancl reduced healthy scrosa on one side of the lesion to the
anaesthetic risk hit this can only be clone when gas- serosa on the other sicle. If llie inwginatecl area is
tric decompression is acliie\vecl and maintainccl. viable it will continw lo hnction ancl the potential
The inclicators for early intervention are l~lootl OI complications from gastrectomy will he avoiclecl. If
necrotic mi~cosa in the gastric content, eviclencc of
the area is not \iahle it will sloiigli into the gastric
perilonilis or continuccl splenomegaly ah- clccom-
lumen whilst retaining a serosal seal. This makes
pression (Matliiesen, 19X3; Leih X- Martin, I YXf).
in\3ginalion an attracti\.e dternative to partial gas-
The aims of surgery are gastric clecomprcssion
trectomy in hrcler-line cases. If‘gastric perfi)ration
and la\,age, Cgastric repositioning, assessment of gas-
has occi~rrccl, euthanasia slioulcl he consicleretl as
tric wall viability with p:lrtial gkistrectomy when
necessary, ancl gastropexy Lo pre\‘en t recurrence. the prognosis is cxtrcmely poor (Ellison, 1993).
Gastropcxy proceclures in\folvc anchoring the There are se\feral gastropexy tecl~niques available
pylorus to the abdominal wall to prevent recur- (Table II). Incisional, tube, circrlmcostal and
rence of gaslric vol\ulus. If this is not clone, up to belt-loop gaslropexy procedures have high si~ccess
80% of cases will recur (Ellison, 19%). rates ancl are the techniques of choice. The tube
The rotatecl stomacl~ is decompressed using SLIC- gastropexy has been associatecl with a higher recur-
Lion apparatus ancl he l~imeen la\ugecl to remo\.e rence rate than circumcoslal and belt-loop
any remaining contenLs. The stomach is carefull) gastropexies clue to tube I‘ailure (Ellison, lW3),
clerotatecl by gentle traction on he pylori~s whilst ancl a greater inflammatory response with a smaller
 (;ASTRI(I DISEASF IN THE DO(; AND CAT
area o f a d h e s i o n (Fox el aL, 1988). However, the
ability to c o n t i n u e gastric decolnpression and tube
f e e d the p a t i e n t p o s t o p e r a t i v e l y m a k e this an
e x t r e m e l y valnahle t e c h n i q u e and c o m p e n s a t e for
an increased r e c u r r e n c e rate. Whichever t e c h n i q u e
is chosen, it should be o n e that the surgeon is famil-
iar with to r e d u c e the surgical time.
A new gastropexy t e c h n i q u e has heen described
recently. In tiffs p r o c e d u r e the stomach is d e r o t a t e d
and 5cm o f the wall o f the gastric body is included
in the l i n e a alba s u t u r e p a t t e r n at t h e t i m e o f
abdominal closure. This t e c h n i q u e is quick, simple
and initial reports suggest that it may be nsefifl in
the i n a n a g e m e n t o f GDV (Meyer-Lindenberg et aL,
1995).
S p l e n e c t o m y s h o u l d only be perfk)rmed w h e n
there is evidence of splenic ischaemia or severe vas-
cnlar compromise, for example, avulsion or
tlnombosis o f the splenic vessels. This is best evalu-
ated after careful r e p o s i t i o n i n g o f the spleen and
a f t e r the g a s t r o p e x y p r o c e d u r e s have b e e n per-
f o r m e d to allow time tor splenic revascularization
(Ellison, 1993).
re
Aflerca
Food and water shonld he withheld tor 24--48h fop
l o w i n g s u r g e r y a n d the p a t i e n t m a i n t a i n e d on
intravenous tluids. Oral nutrition is gradually intro-
d u c e d first with fluids and then with bland solids,
but should be stopped if vomiting occurs and rein-
t r o d u c e d a f t e r 2 4 - 4 8 h . T h e use o f a n t i - e m e t i c s
(e.g., m e t o c l o p o r a m i d e ) and p a r e n t e r a l nutrition
may be necessary in some cases. H,2 blockers should
be c o n t i n u e d for 5-7 (lays a11er surgel T. R e c u r r e n t
dilatations without voh, ulus can be seen postopera-
tively and may be due to gastric hypomotility. Small
fi'equent meals c o m p o s e d of low f a t / h i g h carl)ohy-
d r a t e a r e r e c o m m e n d e d a n d w a t e r s h o u l d be
available at all times to p r e v e n t animals d r i n k i n g
excessively large volunaes. M e t o c l o p o r a m i d e and
o t h e r prokinetics can be used to help gastric empty-
ing and o v e r c o m e any residual hypomotility.
Complications
In the initial postoperative period these include car-
diac arrhythmias, sepsis, shock, gastric wall necrosis,
peritonitis, intussusception, pancreatitis,
disseminated intravascular coagulation, b r o n c h o p -
n e u m o n i a a n d i a t r o g e n i c p n e u m o t h o r a x . Rare
complications include intestinal w)l~atlus and aortic
t h r o m b o e m b o l i s m . Gastric h y p o m o t i l i t y may be
seen postoperatively but is usually transient. GDV
97
may recur if the gastropexy p r o c e d u r e fails. Gastros-
tomy sites'may fail to close s p o n t a n e o u s l y or the
s u r r o u n d i n g tissues may b e c o m e infected (Mathie-
sen, 1983).
Progn.osis
T h e prognosis for all cases o f GDV is g u a r d e d with
mortality rates ot" between 33 and 67%. Mortality
rates rise to between 68 and 88% if partial gastrec-
t o m y is r e q u i r e d a l t h o u g h this s h o u l d n o t be
avoided if areas o f the gastric wall are devitalized
(Mathiesen, 1983; Glickman el al., 1994).
CHRONIC VOMITING WITHOUT
OBSTRUCTION
Ke), points
• Vomiting, weight loss and anorexia are c o m m o n
• Volniting is intermittent and often follows eating
or drinking
• Gastric vomiting must be distinguished fi-om sys-
temic Volniting and fi-om regurgitation
• Contrast r a d i o g r a p h y and e n d o s c o p y are useful
diagnostic tools
• Biopsy is necessary to reach a diagnosis and to
plan effective therapy
Presenling signs
Chronic vomiting, weight loss and inappetance are
the most c o m m o n presenting signs in patients with
c h r o n i c gastric disease. Vomiting is usually exacer-
bated by eating or drinking and may contain gastric
juice, food or bilious reflux. The presence of
melaena or haematemesis, either as fi*esh blood or
a l t e r e d b l o o d ( ' c o f f e e g r a n u l e s ' ) indicate gastric
ulceration. Gastric retention due to gastric hypomo-
tility (e.g., in h y p o k a l a e m i c patients) may lead to
VOlniting several h o u r s after e a t i n g even t h o u g h
obstructive lesions are a b s e n t (Hall et al., 1990).
Cranial abdominal pain, such as the adoption o f the
characteristic 'praying' stance and hypersalivation,
may be n o t e d . Small or large intestinal d i a r r h o e a
may be present indicating extensive involvement of
the whole gastrointestinal tract.
It is i m p o r t a n t to rule out non-gastric causes o f
c h r o n i c v o m i t i n g by p e r f o r m i n g a full clinical
examination, serum biochemistry, haematology
and urinalysis. Non-gastric causes o f chronic vomit-
ing include drug therapy (e.g., digoxin,
e r y t h r o m y c i n ) , h e p a t i c , renal, p a n c r e a t i c , e n d o -
c r i n e diseases (e.g., h y p o a d r e n o c o r t i c i s m ) ,
 98 TIlE VETERINARY.IOURNAL,
peritonitis and neurological problems affecting the
vestibular system. Many o f these underlying causes
lead to a secondary gastritis ,'ather than reflecting a
primary gastric disorder.
Clinical examination
Clinical e x a m i n a t i o n o f cases with prima O, gastric
disease is fi'equently unrewarding. A b d o m i n a l dis-
c o m f o r t suggesting gastric u l c e r a t i o n / e r o s i o n or
neoplasia, p a l p a b l e a b d o m i n a l masses o r ascites
d u e to h y p o p r o t e i n a e m i a may be all that is detect-
able. Cases o f c h r o n i c w ) m i t i n g are usually well
h y d r a t e d as, if the animal is v o m i t i n g t i e q u e n t l y
e n o u g h to b e c o m e dehydrated, it will present as an
acute problem.
CHRONIC GASTRITIS
Chronic gastritis is part o f the idiopathic intlamma-
tm T bowel disease g r o u p and is seen in both dogs
and cacs. It may o c c u r in isolation or with enteritis
a n d colitis. T h e a e t i o l o ~ , o f i n f l a m m a t o r y bowel
disease is usnally u n k n o w n . Hypersensitivity reac-
tions (Type 1 to 4) are t h o u g h t to o c c u r to dietary
or intestinal antigens and represent abnormal
r e s p o n s e s by the gut-associated l y m p h o i d tissue.
This may o c c u r due to a h e r e d nmcosal permeahil-
it),, defective mucosal i m m u n e responses, o r may
have a g e n e t i c basis. I n t e s t i n a l p a r a s i t i s m a n d
mechanical irritation (e.g., foreign bodies) are also
t h o u g h t to c o n t r i b u t e in some cases. T h e infiltrate
of inflammatm T cells affects mainly the mucosa and
consists of vmTing p r o p o r t i o n s o f netm'ophils, lym-
phocytes, plasma cells and eosinophils. Eventually,
villous a t r o p h y and fibrosis occu,-. Mucosal hyper-
trophy leading to h y p e r t r o p h i c gastropathies is also
t h o u g h t to be related to this g r o u p o f diseases. T h e
infiltrate present and mucosal changes are used to
classif~¢ the disease allowing m o d i f i c a t i o n o f treat-
m e n t (Magne, 1992; Wolf, 1992).
C h r o n i c gastritis can be d i v i d e d i n t o l y m p h o -
cytic-plasmacytic gastroenteritis, eosinophilic
g a s t r o e n t e r i t i s o r a t r o p h i c gastritis. T h e s e a r e
p o t e n t i a l l y reversible a l t h o u g h a t r o p h i c gastritis
may b e c o m e refl'acto,-y to therapy. As i m m u n e anti-
gens are considered a primary cause of
inflammatory bowel disease and the pathogenesis is
t h o u g h t to be i m m u n e m e d i a t e d ; ( ' h y p o a l l e r -
genic') elimination diets, anti-inflammatories and
cytotoxic drugs are used in the treatment o f these
c o n d i t i o n s . A l t h o u g h clinical r e m i s s i o n is o f t e n
a c h i e v e d , c u r e is rare a n d c o n t i n u e d d i e t a r y
156, 2
m o d i f i c a t i o n , o c c a s i o n a l l y with p e r s i s t e n t d r u g
therapy, is n e e d e d (Strombeck & Guilford, 1991h;
Wolf, 1992).
Chronic gastritis is seen predonfinantly in middle
aged to older animals altlmugh y o u n g animals may
also be affected. T h e r e is no sex or b r e e d predispo-
sition. Melaena and, less fi'equently, haematemesis
are seen if secondm T gastric erosion or ulceration
occurs. Intestinal thickening may be obvious partic-
ularly in cats with inore widespread lesions. Often
inllamlnato, T bowel disease affecting the proximal
s m a l l i n t e s t i n e will also p r e s e n t as w ) m i t i n g
a h h o u g h gast,-ic lesions a,'e not present (|acobs el
al., 1990;Jergens el al., 1990).
Serum bioclaemistJ 3, and I m e m a t o l o ~ , are neces-
sary to rule o u t systemic causes o f v o m i t i n g hut
t h e r e a r e few specitic lindings which positively indi-
cate i n f l a m m a t o r y bowel disease. R a d i o g r a p h y is
usually u n r e w a r d i n g a n d only serves to rule out
o t h e r causes such as obstructive diseases and gastric
foreign bodies. Endoscopy enables direct visualiza-
tion o f lesions althougla t h e r e is p o o r correlatioll
between e n d o s c o p i c and biopsy findings (Gad,
1986). An e x c e p t i o n to this is a t r o p h i c gastritis
which has a characteristic gross a p p e a r a n c e . Com-
mon endoscopic findings include mucosal
e r y t h e m a , friability, g r a n u l a r i t y a n d u l c e r a t i o n .
Faeces should be e x a m i n e d to rule out parasitic or
protozoal (e.g., (;iardia) diseases that may cause or
c o n t r i b u t e to the condition.
In all cases, biopsy is r e q u i r e d to reach a diagnosis
and m u h i p l e biopsy sites are necessa, T as the dis-
ease can have a focal d i s t r i b u t i o n a n d a variable
intiltrate. E n d o s c o p i c biopsies can be diagnostic if
at least 2 r a m e n d o f o r c e p s are used as the main
i n f l a m m a t o r y r e s p o n s e is o f t e n c o n f i n e d to the
mucosa. However, the disease may e x t e n d t h r o u g h
the muscularis mucosa, thus flfll-thickness biopsies
give the most information (Jacobs el aL, 1990).
Lympho~tic-plasma~. tic gast,4tis
Lynlphocytic-plasmacytic gastritis is the most com-
m o n fornl o f c h r o n i c gastritis in clogs (where it is
usually localized to the s t o m a c h ) and cats (where
intestinal i n v o l v e m e n t is c o m m o n ) (Wolf, 1992).
T h e r a p y is based on the use o f e l i m i n a t i o n diets
(such as cottage cheese and rice) with corticoster-
oid therapy ( p r e d n i s o l o n e 0 . 5 - 1 m g . k g BID in dogs
and 0.5-2mg.kg-I BID in cats). If a g o o d response is
seen, corticosteroids can be r e d u c e d slowly over a
n u m b e r o f weeks, b u t r e c u r r e n c e o f clinical signs
may require repeat or continual therapy.
 ( ; A S T R I C D I S E A S E IN T H E D O ( ; A N D ( ; A T
Occasionally, the use of cytotoxic drugs, e.g., azathi-
oprine, concurrently with prednisolone is necessary
to achieve remission. Clinical remission is easily
achieved in most cases and continual dietm T man-
a g e m e n t is necessary to p r e v e n t recttrrence. If a
specific dietm T cause can be identified a complete
cure is possible, althougla, this is vmy rarely the case
(Richter, 1992; Wolf', 1992).
Eosinophilic gastritis
Both d i e t a r y a n t i g e n s a n d parasitic i n f e s t a t i o n s
(including visceral larval migrans) have been cited
as initiating causes of eosinophilic gastritis. This
c o n d i t i o n is recognized less fi-equently than lym-
phocytic-plasnlacytic gastritis and generally
involves several areas of the gastrointestinal tract.
Eosinophilic gastritis has been identified in dogs as
an isolated c o n d i t i o n of the stomach alone (Hay-
den & Fleischman, 1977). Two disease processes
appear to exist in cats. The first is similar to eosino-
philic gastritis in the dog and is very u n c o m n m n
( H e n d r i c k , 1981;Jolanson, 1992). T h e s e c o n d is
part of a laypereosinophilic syndrome where there
is a p e r i p h e r a l e o s i n o p h i l i a with i n v o l v e m e n t of
other organs such as the spleen, liver and I)one mar-
row ( H e n d r i c k , 1981). T h e p r o g n o s i s for this
second group is poor (Moore, 1983) and cytotoxic
drugs are necessat-y. In a p r o p o r t i o n of dogs with
eosinophilic gastritis, there is a peripheral eosino-
philia which, a l t h o u g h it is a nonspecific finding,
can be used to m o n i t o r the response to therapy.
Some animals develop eosinophilic granulomas in
c o n j u n c t i o n with e o s i n o p h i l i c gastritis that may
canse gastric outlet obstruction. Parasitic infesta-
t i o n s s h o u l d be r u l e d o u t w i t h a c o u r s e o f
a n t h e h n i n t i c s such as f e n b e n d a z o l e a n d dietary
therapy instituted. Corticosteroids are used at simi-
lar d o s e s to t h o s e u s e d in t h e t r e a t m e n t o f
C t
lyntplmcytic-plasmacytic gastritis (,Jolmson, 1992).
Atrophic gastritis
Atrophic gastritis is uncomnaon but has been recog-
n i z e d in b o t h d o g s a n d cats. In t h e s e cases,
presumably following a chronic inflammatory pro-
cess, the m u c o s a b e c o m e s inactive a n d fibrosis
replaces n o r m a l g l a n d u l a r structures. Endoscopi-
cally, the m u c o s a is d i s c o l o u r e d a n d thin with
p r o m i n e n t blood vessels. Corticosteroids are used
in h u m a n patients but have not been evahmted in
animals. Antacids a n d o t h e r drugs which r e d u c e
gastric acidity should be avoided as the stomach is
already hyposecretory.
99
Immunoproliferative enteropathy of Basenjis
This is a condition ,affecting Basenjis characterized
by lymphocytic-plasmacytic infiltrate of most areas
of the gastrointestinal tract. Microscopic and gross
a b n o r m a l i t i e s can be d e t e c t e d in the s t o m a c h of
these animals which mimic l y m p h o c y t i c - p l a s m a -
cytic gastritis a l t h o u g h clinical signs are usually
related to small intestinal involvement. T h e prog-
nosis is poor with most cases dying within 2 years of
diagnosis. Some litters of Basenjis are predisposed
to developing clinical disease and there is a strong
breed association (Breitschwerdt, 1992).
GASTPdC ULCERATION AND E R O S I O N
Ulcers are mucosal defects that penetrate through
at least to the level of the muscularis mucosa; ero-
sions involve the mucosa alone. Both occur in the
stomach and d u o d e n u m of cats and dogs, and ani-
mals are o f t e n a s y m p t o m a t i c . T h e p r e s e n c e o f
blood (fi-esh or altered) in the vomitus is more com-
monly associated with gastric ulceration than with
any o t h e r gastric lesion. Animals may lose signifi-
cant vohnnes of blood or develop non-regenerative
anaemias due to iron loss. In these cases, animals
will present with signs of anaemia. Vmy rarely, gas-
tric ulcers perforate and are associated with focal or
generalized peritonitis. Cases with generalized peri-
tonitis have a poor prognosis and usually present in
a collapsed state (Stanton & Bright, 1989).
Serum biochernistl T, haematology and urinalysis
are useftd in identifying systemic causes. Urea may
be falsely elevated due to blood digestion by intesti-
nal flora. H a e m a t o l o g y f r e q u e n t l y shows e i t h e r
regenerative anaenlias or n o n - r e g e n e r a t i v e , iron
d e f i c i e n c y a n a e m i a s (microcytic, h y p o c h r o m i c )
resulting fi'om intestinal blood loss.
Gastroduodenal ulceration is usually secondary to
gastrointestinal or systemic disease although 'stress'
ulceration may occur in animals where no cause is
identified. Causes of gastric ulceration and erosion
i n c l u d e d r u g t h e r a p y , h y p o v o l a e m i c or septic
shock, m a j o r surgery, n e u r o s u r g e r y , h e p a t i c or
renal disease, paraneoplastic syndromes, inflamma-
to W bowel disease, foreign bodies a n d neoplasia.
A l t h o u g h antral spiral bacteria have b e e n recog-
nized in dogs for nearly 100 years (Bensley, 1899),
the recognition of the pathogenic role of Heliobacter
pyloffs in gastritis, peptic ulceration and gastric car-
c i n o m a as has h a p p e n e d in m a n has n o t b e e n
achieved yet in the dog (Hazell & Lee, 1986; Glise,
1990; Maaroos el al., 1991).
 100 THE VETERINARY ]OURNAI., 156, 2
Hepatic and renal disease
Hepatic disease is the most c o m m o n cause of gas-
t r o d u o d e n a l u l c e r a t i o n ( M u r r a y et al., 1977;
Stanton & Bright, 1989). It lnay cause gastric ulcer-
ation by decreased degradation or increased release
o f secretagogues. Ulceration fi'om hepatic disease
affects m a i n l y the d u o d e n u m a l t h o u g h gastric
ulceration will also occur. Uraemia causes changes
in mucosal b l o o d flow and local mucosal hypoxia
leads to gastric u l c e r a t i o n typically a f f e c t i n g tile
fundus (Stanton & Bright, 1989).
LLlcerogenic dru~s"
U l c e r o g e n i c drugs a c c o u n t for many cases o f gas-
t r o d u o d e n a l u l c e r a t i o n in dogs. N o n - s t e r o i d a l
anti-inflammatol T drugs, corticosteroids or c()ml)i-
n a t i o n s o f the two are o f t e n implicated. NSAIDs
h a v e b e e n well d o c u n l e l l t e d its c a u s i n g gas-
t r o d u o d e n a l u l c e r a t i o n at t h e r a p e u t i c d o s e s
(Stanton & Bright, 1989). Ulceration is caused by
inhibition o f prostaglandin synthesis at the gastric
mucosa which leads to r e d u c e d mucosal blood flow,
local hypoxia and r e d u c e d mucus production. T h e
antrtun and pylorus are most c o n m l o n l y affected:
C o n t r a s t r a d i o g r a p h y will infi-equently show the
peptic u l c e r as an o u t p o u c h i n g o f bariunl with a
shallow s h o u l d e r (Fig. 1). Endoscopically the ulcer
is most o f t e n seen at tile i n c i s u r e a n g u l a r i s as a
small (<2cm) ulcer with a p u n c h e d out a p p e a r a n c e ,
tile walls o f which are only slightly raised ti"om the
s u r r o u n d i n g mucosa (Fig. 2). Traditional anti-ulcer
t h e r a p y for 1-2 m o n t h s with w i t h d r a w a l o f tile
NSAID is usually effective ill treating these ulcers
(Fig. 3). Corticosteroids cause ulcers at high doses
and may be tile cause o f gastroduodenal ulceration
associated with neurosurgery. T h e y may also cause
ulceration ill animals with o t h e r predisposing fac-
tors such as those on c o n c u r r e n t NSAID therapy.
Tile p a t h o g e n e s i s o f c o r t i c o s t e r o i d - i n d u c e d ulcer-
ation is u n c l e a r so a n t i - u l c e r t h e r a p y c a n n o t be
specifically chosen to target a particular pathway.
Paraneoplaslic s~ndrom, es
Mast cell t u r n o u t s c a n be a s s o c i a t e d with gas-
t r o d u o d e n a l u l c e r a t i o n f o l l o w i n g tile release o f
histamine fi'om d e g r a n u l a t i n g cells. T h e histamine
binds to H 2 receptors oil parietal cells and leads to
gastric hyperacidity. Prophylactic t r e a t m e n t with H 2
blockers is often o f use in tile t r e a t m e n t o f mast cell
tunlours.
Gastric u l c e r a t i o n s h o u l d be t r e a t e d by with-
d r a w a l o f t h e i n c i t i n g c a u s e , if o n e c a n b e
identilied, coupled with aggressive medical therapy
using antacids and mucosal protectants. Excessive
blood loss and ulcer perforation are indications for
surgical intelwention. Resection of tile ulcer is nec-
essa D, and may also require partial gastric resection
using a Bilh'oth I or II.
BILIOUS VOMITING SYNDROME
Bilious vomiting syndrome, alkaline reflux gastritis
or enterogastric reflux s y n d r o m e is a c,mditi,m o f
dogs characterized by vomiting of bile ,m an empty
StOlnach. Vomiting tends t,, o c c u r th'st tiring in tile
m o r n i n g and there may be a b d o m i n a l cliscomlort.
It is associated with i l l l l a m m a t o r y bowel disease,
d u o d e n i t i s o r a prinlary gastric motility d i s o r d e l
that leads to bilious rellux. Bilious reflux is irritant
to tile empty st<maach and leads to vomiting when
the stomach has been empty for st,me time (Daven-
p o r t , 1968; J o h n s o n , 1972). If tile c o n d i t i o n is
s e c o n d a r y to a n o t h e r disease process tile primary
disease should be treated a h h o u g h a primm T cause
is often not established. Specific therapy includes
f e e d i n g the animal a small fatty meal last thing at
night, anti-ulcer therapy and the use o f prokinetic
agents. El'ythronlycin, at low doses, and metoch)-
pramidc arc both effective.
GASTRIC NEOPLASIA
C a n i n e p r i m a r y gastric t u m o u r s are m l c o m m o n .
T h e y occm- in older animals that generally present
with c h r o n i c vonliting, a n o r e x i a , polydipsia a n d
weight loss. If tile tunlour is ulcerated haematenle-
sis a n d m e l a e n a nlay be s e e n . O n o c c a s i o n
r a d i o g r a p h i c e v i d e n c e o f ascites or loss o f serosal
d e t a i l m a y be s e e n if t h e t u m o u r s i g n i f i c a n t l y
involves tile serosal surface. Gastric tunlours occa-
sionally may cause obstruction o f e i t h e r the lower
oesophageal sphincter (leading to regurgitation) or
tile pylortls (leading to gastric r e t e n t i o n ) . Breeds
that a p p e a r to be p r e d i s p o s e d include the Rough
Collie a n d the S t a f f o r d s h i r e Bull T e r r i e r . Gastric
a d e n o c a r c i n o m a is tile most c o m m o n l y diagnosed
gastric t u m o u r in dogs and carries a vel 7 p o o r prog-
n o s i s d u e to f r e q u e n t , e a r l y m e t a s t a s i s , l o c a l
aggressiveness and a p o o r response to c h e m o t h e r -
apy o r r a d i o t h e r a p y . E n d o s c o p i c a l l y they can be
distinguished fi'om peptic ulcers as there is either a
b l a n c h e d mucosal a p p e a r a n c e d u e to submucosal
infiltrate or the p r e s e n c e o f a large excavating ulcer
that has walls raised above tile mucosal surface with
 ( ;ASTRI(: I)ISEASE IN TI IE Dr)(; AND ( :AI'
a very r a g g e d rim (Sullivan et al., 1987). O t h e r
ttnmours o c c u r less li'equently such as leiomyosarco-
inas, which are m o r e a m e n a b l e to sturgical resection
if d i a g n o s e d early, a n d gast,'ic l y m p h o s a r c o n t a s ,
which r e s p o n d poorly to chemotlaerapy (Figs 4 mtd
5).
Benign gastric ttmtom's may be resectable and, i f
a d e q u a t e margins are attained, the prognosis can
be reasonahle. A d e n o m a t o u s and hyperplastic pol-
yps or leiontyomas are usually asymptomatic. T h e y
can, however, occasionally cause obstruction when
rcgtu'gilation or gastric r e t e n t i o n will be secn and
should he resectcd.
(;als rarely p r e s e n t with gastric t t m t o u r s . T h c
most c o m m o n is gastric l y n t p h o s a r c o m a which is
tlstLallv associated with deposits in o t h e r areas o f the
gastroinlcslintal tract. T h e v can be m a n a g e d with
c h e n t o t h c r a p y a l t h o u g h p o o r responses are SCUll.
These animals are usually Fel. V n egat ire.
GASTRIC OUTLET OBSTRUCTION
K~y points
• Delayed gastric emptying resuhing in wmtiting o f
food several hours after eating
• Contrast radiography and e n d o s c o p y are used to
confirm a diagnosis
• Causes include c h r o n i c h y p e r t r o p h i c gastropa-
thy, p y l o r i c s t c n o s i s , p y l o r i c n e o p l a s m s a n d
polyps, granulontatous gastropathies, gastric lor-
eign bodies and gastric ulceration
• Surgel T is indicated
Presenting signs
Gastric o u t l e t o b s t r u c t i o n is c h a r a c t e r i z e d by a
d e l a y in gastric e m p t y i n g t h a t results in gastric
retention and vomiting of tood seemingly unre-
lated to f e e d i n g , often several hours
post-prandially. In the n o r m a l clog, the s t o m a c h
starts to e m p t y of food within 30rain o f feeding and
is completely e m p t y within 4 - 6 h . In animals with a
gastric outlet obstruction, food remains in the stom-
a c h for l o n g e r l e a d i n g to p y i o r i c a n d f u n d i c
distension. I1, on plain radiography, t o o d is evident
in the stomach 8-10h postoprandially or t h e r e is a
history of vomiting of tbod 8-10h "after feeding, this
is highly indicative of a pathological delay in gastric
emptying (Strombeck & Guilford, 1991b). The pas-
sive regurgitation of f o o d d u e to o e s o p h a g e a l
disease should be ruled out by the history, examina-
tion of the vomitus and radiographic findings.
I 01
Abdominal distension or discomfort may also be
r e p o r t e d iil animals suffering fi'om gastric o u t l e t
obslruction. T h e patient may be in p o o r bodily con-
dition or be stunted if the condition is congenital.
Diffmential dia,ffnoses
Functional and physical ahnormalities can lead to
delayed gastric emptying (Table III). O t h e r factors,
particularly stress and m e d i c a t i o n , can also a h e r
gastrointestinal motility. Some drugs may e n c o u r -
age gastric e m p t y i n g (e.g., m e t o c l o p r a m i d e ) , and
the patient should not receive any medication fi)r
4 8 - 7 2 h prio," to radiography. Benzodiazcpines and
opi()ids, in particular, can p r o f o u n d l y redttce gas-
trointestinal m()tility and sh()tnld be avoided. High
s y m p a t h e t i c t o n e in stressed a n i m a l s can cause
m a r k e d delays in gastric e m p t y i n g and will make
iqterpretation o f contrast studies ve D, diftictth.
/~/orh: slenosis
Pyloric stenosis is an u n c o m m o n disease seen in
yotmg dogs soon after weaning. It causes gastric out-
let obstruction dtte to the h y p e r t r o p h y o f circular
smooth muscle and typically occurs in brachycepha-
lic b r e e d s with m a l e s b e i n g n l o r e f r e q u e n t l y
afl'ected than females (2:1).
T h e acquired disease is known as acqtfired pyloric
antral hypertroplay or c h r o n i c h y p e r t r o p h i c gastr-
opathy. It is seen in m a t u r e dogs, usually between 4
and 7 years o f age. Typically, small b r e e d dogs are
affected with the poodle, Lhasa Apso and Shih Tzu
being r e p o r t e d most commonly. Animals present as
having chronic, intermittent vomiting of weeks to
m o n t h s d u r a t i o n . Often, the c o n d i t i o n is progres-
sive and the animals may have lost weight or show
signs o f i n a p p e t a n c e and anorexia (Dennis el aL,
1987; Walter & Mathiesen, 1993).
Table HI
Causes o f gastric outlet obstruction
('ongenital]~hz6cstenosL~
Hypertrophic gastropathy
Pyhn-ic neoplasms
Inflammatol7 polyps
Foreign bodies
Granulomatous gastropathies
Gastric ulceration
Pancreatic and hepatic abscesses
Post-operative pyloric scar tissue
Stenosis associated with reactive tissue/ollowing
pancreatitis or peritonitis
102 THE VETERINARYJOURNAL, 156, 2
Fig. 1. Dorsoventral abdominal radiograph following
barium administration. The contrast has filled the stom-
ach and on the lesser cOrvature a distinct mushroom
shaped outpouching of barium into a mucosal defect is
evident typical of peptic ulcer (arrows).
Fig. 2. Endoscopic view of antrum. A 2.5cm ulcer filled
with blood is visible. The rim is rounded but not raised
above the gastric surface and no rugae are seen running
onto the rim. Two spots of haemorrhage are seen on
adjacent mucosa. The size and lack of adjacent mucosal
change is suggestive of peptic ulcer.
T h e p a t h o g e n e s i s o f pyloric stenosis is u n c e r t a i n
a n d n o specific cause can usually b e f o u n d . Genetic,
e n v i r o n m e n t a l a n d i n f l a m m a t o r y factors have b e e n
i m p l i c a t e d a n d the excessive s e c r e t i o n o f s o m e gas-
t r o i n t e s t i n a l h o r m o n e s , p a r t i c u l a r l y g a s t r i n , is
t h o u g h t , at least, to c o n t r i b u t e . Gastrin has t r o p h i c
effects on both the pyloric smooth muscle and
m u c o s a . M i l d g a s t r i c d i s t e n s i o n will l e a d to
i n c r e a s e d p r o d u c t i o n o f gastrin a n d this m a y con-
Fig. 3. Endoscopic view of antrum. Following a 1
month course of H 2 antagonist drug, the ulcer has
reduced in size and depth. The healing ulcer disap-
peared following a further one month course of H 2
antagonist.
Fig. 4. Dorsoventral abdominal radiograph following
barium administration. The lumen is narrowed and the
contrast/mucosal interface is very irregular with sharp
outpouching of barium indicative of ulceration and
thickened rugae characteristic of gastric carcinoma.
t r i b u t e to f u r t h e r h y p e r t r o p h y c a u s i n g a positive
loop. Gastrin also stimulates parietal cells to secrete
h y d r o c h l o r i c acid a n d g a s t r o d u o d e n a l u l c e r a t i o n is
f r e q u e n t l y r e p o r t e d in c o n j u n c t i o n with p y l o r i c
stenosis r e q u i r i n g the use o f antacids. In h u m a n s ,
a c q u i r e d pyloric stenosis has b e e n associated with
gastrin-secreting p a n c r e a t i c t u m o u r s . Similar cases
have b e e n seen in dogs a n d cats a l t h o u g h the con-
dition is very r a r e (English et at, 1988).
 GASTRIC DISEASE IN THE DOG AND CAT 10B

p •
', ." ."
e
4

.'o
.a' 411P~41"+
+,ii ii v
.'" • • 41

+"

:
Fig. 5. Endoscopic view of lesser curvature of body on
the stomach. The endoscope has been retroflexed so that
the viewer is looking back towards the cardia. A large 4-
5cm ulcer is raised above the surrounding mucosa. A
large number of thickened rugae run into the visible cir- Fig. 7. Endoscopic view of pylorus. The pylorus has
cumference of the ulcer wall. These changes are been distended with insufflated air and there are a num-
characteristic of neoplasia almost always gastric ber of thickened and fixed folds of mucosa surrounding
carcinoma. the pylorus with one large fold centrally indicative of
chronic hypertrophic gastropathy obstructing gastric
emptying.

Fig. 6. Lateral abdominal radiograph. The abdomen is

distended by a grossly enlarged gastric shadow extending
into the caudal half of the abdominal cavity. The stom-
ach is filled with a large volume of fluid and in the
displaced and dilated pyloric canal there is marked accu- Fig. 8. Endoscopic view of pylorus. Projecting into the
mulation of mineralized material (gravel sign) indicating lumen from the mucosal wall is a pedunculated eroded
pyloric outflow obstruction. polyp that has caused pyloric outflow obstruction.

Pyloric stenosis has also b e e n r e p o r t e d in cats as
b o t h the congenital a n d acquired diseases. Siamese
cats, in particular, have b e e n d e s c r i b e d with con-
g e n i t a l p y l o r i c s t e n o s i s a l t h o u g h this m a y b e a
f u n c t i o n a l r a t h e r t h a n a physical pyloric obstruc-
tion. T h e s e animals c o m m o n l y have a co-existing
megaoesophagus. Acquired pyloric stenosis follow-
ing pyloric muscular hypertrophy has been
r e p o r t e d in domestic cats (Dennis et al., 1987).
O n plain radiographs, gastric distension may be
visible o r the pylorus may be l a r g e r t h a n n o r m a l
a n d c o n t a i n gravel (Fig. 6). If obvious plain film
changes are n o t p r e s e n t t h e n c o n f i r m a t i o n can be
m a d e using contrast, w h e r e a delay in gastric empty-
i n g c o m b i n e d with c o n s i s t e n t n a r r o w i n g o f the
c o n t r a s t c o l u m n at the pylorus is seen. H o w e v e r ,
pyloric a n d fundic distension may overwhelm subtle
c h a n g e in the pylorus. T o o v e r c o m e this p r o b l e m
 104 THE VETERINARYJ()URNAL, 156,
ultrasonography has been used successflflly (Biller
el aL, 1994). Endoscopy will show mucosal hypertro-
phy but will not demonstrate muscular hypertrophy
(Fig. 7). So the relief technique ,nay only be chosen
once the pylorus has heen exposed surgically.
In all cases, the possihility of neoplasia should he
considered a n d eliminated by I)iopsy'ot'ten at the
time of corrective surgery.
Pyloric neoplasia and polyps
Gastric neoplasms occasionally cause gastric outlet
obstructions if they involve the pyloric antruln or
canal. The prognosis for benign polyps is good fol-
lowing resection altlaough, unfi)rtunately, these a,:c
in the minority (Fig. 8) (Happ6 et al., 1977).
Eosinophilic gastT~tis
Severe eosinophilic gastritis can cause hypertrophy
and g r a n u l o m a t o u s changes to the gastric wall. If
this occurs in the pyloric region a gastric o u t l e t
o b s t r u c t i o n can occur. T h e s e g r a n u l o , n a t a are
non-responsive to medical or dietary therapy alone
so surgery is indicated.
MANAGEMENT OF GASTRIC OUTLET OBSTRUCTION
Medical and dietary management
Medical and dietary therapies alone are rarely cura-
tive in cases of gastric outlet obstruction but may
control disease in mildly affected cases. They are
usually used in conjunction with pyloroplasty tech-
n i q u e s . M e d i c a l t h e r a p y s h o u l d a l w a y s be
a t t e m p t e d b e f o r e s u r g e r y in cases o f s u s p e c t e d
pylorospasm or a b n o r m a l gastric motility when a
physical obstruction c a n n o t be found. Dietary ther-
apy consists of frequently feeding small volumes of
semi-liquid food that is low in protein and fat, since
liquid leaves the stomach faster than solid food and
carbohydrate leaves faster than protein or fat (slow-
est). Commercial diets such as Hill's i / d and Hill's
d / d c o m b i n e d with a carbohydrate source such as
pasta (50:50 mix) a n d liquidized with water are
ideal. Metoclopramide, cisapride and erythromycin
can also be used to e n h a n c e gastric emptying.
Surgical therapy
Surgery for gastric outlet obstruction aims to iden-
tify and excise abnormal tissue and restore normal
function. This is achieved either by enlarging or
bypassing the area of obstruction. The procedures
are listed in increasing order of complexity, with
2
three being the teclmiqne preferred hy tile authors
for hyl~ertrophic gastropathy.
1. Heinke-Mikulicz pyloroplasty is similar to Ihc
i)yloromyotomy except that lumen is e n t e r e d and
the l o n g i t u d i n a l incision is sutttred transversely.
This enables visualization and resection of polyps,
tumours o r mncosal hyl~ertropl W and a t e m p , r m T
increase in Imninal diameter.
2. Y-U a n t r a l a d v a n c e m e n t flap p y l . r . l ~ l a s t y
enables direct visualization of the antruln and resc(-
tion of diseased tissue. Its main advantage over the
Heinke-Mikulicz pyloroplasty is that a Ilap of m , -
real pyh)ric a n t r u m is a d v a n c e d into the pyh~ric
canal. This should permanently increase the pyh>ric
diameter and tiffs is the hest procedure for mild or
moder;ttelv affected cases. Scar tissue at the site may
lead to exacerbation of pyhwic slcm~sis ,rod a single
layer ¢)1"simple apl)ositional sutt,rcs shtmld hc nsed.
T h e d i s a d v a n t a g e is that in s o m e cases pyloric
mucosal hypertr.l)hy is s¢~ extensive the teclmi(lt,e
is ineffective even with mucosal stril)ping (,~lalllOll
el al., 1987).
3. ( ; a s t r . d u o d e m ~ s t o m y with p y l o r e c t . m y (Bill-
roth 1) involves resection of the diseased sections of
pyloric canal a n d a n t r m n with end-to-end a n a s l o -
,nosis of the d u o d e n a l and antral stumps. The short
hepatogastric ligament and m e s o d u o d e n u n l make
apposition of the stunaps awkward. Partial resection
of the hepatogastric ligament will reduce tension at
the anastomosis site. This techniqne has been asso-
ciated with increased enterogastric rellux causing
alkaline reflux gastritis (Mason et aL, 1988).
4. Gastrojejunostomy with pylorectomy (Bilh'otla
II) is used w h e n large sections of d u o d e n u m or
antrum are removed and a simple end-to-end anas-
tomosis is n o t possible. T h e antral a n d d u o d e n a l
stumps are closed with inverting suture patterns or
linear stapler. A mobile loop of j e j u n u m is anasto-
m o s e d to the gastric b o d y u s i n g a side-to-side
apposition. Although this technique enables sutur-
i n g u n d e r m i n i m a l t e n s i o n c o m p a r e d to t h e
Billroth I, bilious e n t e r o g a s t r i c reflux can still
Occur.
In conclusion, pyloroplasty techniques cause min-
imal e n t e r o g a s t r i c reflux b u t may allow clinical
signs to recur. The more complex procedures are
associated with enterogastric reflux (Kilby, 1970).
Anorexia, vomiting and weight loss have been asso-
ciated with the g a s t r o j e j u n o s t o m y t e c h n i q u e s
although the pathogenesis is unclear. The simpler
techniques such as the Y-U antral advancement
flap have the advantage of maintaining normal
 GASTRIC DISEASE IN THE DOG AND CAT
a n a t o m y a n d s h o u l d be c o n s i d e r e d b e f o r e m o r e
c o n t p l e x p r o c e d u r e s are u n d e r t a k e n .
Foreig~ bodies
Gastric f o r e i g n b o d i e s are m o r e c o l n m o n in clogs
than cats a n d t e n d to be seen in y o u n g e r animals. If"
the f o r e i g n b o d y b e c o m e s l o d g e d in t h e p y l o r u s ,
the a n i m a l will p r e s e n t acutely. In m a n y cases, how-
e v e r , t h e o b j e c t will r e m a i n in t h e b o d y o f t h e
stomach moving into the pylorus internlittently.
This can lead to delayecl gastric e m p t y i n g a n d vom-
iting s o m e time after f e e d i n g as well as the o t h e r
s i g n s a s s o c i a t e d with g a s t r i c o u t l e t o b s t r u c t i o n .
Col~firlnation can often be a t t a i n e d by r a d i o g r a p h y
w h e r e the t o , e i g n b o d y may I)e d e t e c t e d on plain o r
c o n t r a s t filnts. E n d o s c o p y is yenT useful for confirnt-
i n g t h e p r e s e n c e o f a f o r e i g n b o d y a n d in s o m e
cases allow retrieval. In ntany cases, g a s t r o t o n t y will
be necessa D, to r e m o v e the foreign body.
REFERENCES
Ai~Am, R. K. & Wl,~me~, (i. (1968). hmic changes in Parley
pouches after iusttlin hypoglycaemia, gastrin and
pen tagastri n. A rchive~ 0f.S'uI{g+'Py9 7 , 4 2 3 - 3 9 .
AI.I.EN, A. & (,.\rxI-R, A. (1980). MIIClIS and bicarbonate
secrelioil ill tile stonlach alld their possil)le l-oie in
Illtlcosal p r o t e c t i o n , (;lit' 21, 24{)-62.
Bi.:xst.t.:v, R. R. (1899). The slructure of mammalian gas-
tric glands. Quarterlr flmr, al el Microscopical Science 41,
3(51-89.
BII.[.ER, D. S., P.\RTIN(;I()N, B. P., MP,'\BA','.\SlII, T. cox:LFVEII.I.I.:,
R. (1994). Uhrasonographic appearance oF chronic
hypertrophic pyloric gast,'opathy in the dog. Veteri.arv
ICadiolg©' and Ulll'gl.StHlHd35, 30-33.
Born;, 1. (1959). Bile achnixturc in gastric juice in heahh
and in peptic ulcer befine and after operation accord-
ing to Bilholh I and Bilholh 11. ,-1eta Chir,~]ffira
Sca,di,avica (Suppl 251 ), 97-112.
Br~clrs(:i iw~:rm, E. B. (1992). Immunoproliferative enter-
opathy of Basel!jis. Semi,ars in l:elerina O, Medici,e a,d
Sm]t¢e~y (Small A,imal) 7, 153-6 I.
(](m~-, C. F. (1981). Defence mechanisms of the gastric
mtlCOS;.l. Scandinavian Journal r!f Ga.stmenlerolotO, 16
(Suppl 67), 201-4.
D.\\'l.:xptmr, H. W. (1968). Destruction of the gastric
nlucosal barrier by detergents and urea. Ga.slroenlerolgt,q'
54, 175-81.
Dl.:Xxts, R., Hl.:rrr.xt;l.:, M. E.,JH:l.-rll.:S, A. R., l¥[.VllC, S. E. &
WlirNq R. A. S. (1987). A case of gastric hype,trophy in
a cat../ourna/oJSmall Animal Prattle* 28, 491-504.
E[.Hsox, (i. W. (1993). Gastric dilatation volvuh,s--surgi-
cal prevention, l'eleri,aly Clinics of Norlh America 23.
513-30.
Ex(;l.is~l, R. E., BrI.:HS(:~iWI.:RI)T, E. B., (;riXlil.:Xl, C. B.,
Tlm.xH., D. E. & (;Mxsmr~., L. A. (1988). Zollinger-
Ellinson syndrollle and m velofil)rosis ill a dog. Journal
rf/lhe Ame~4can l'etedna O' Medical Assodalion 192, 1430-4.
105
FH.:xlstr(-).xl, (;. & (;ArXEr, A. (1982). Gastroduodenal
H(:O:¢ transport: characteristics anti proposed role in
acidity regulation and mucosal pr(/tection. American
.]ournal ~?/l"l~sioh)D, 242, G 183-G 193.
Fox, S. M. (1987). Crisis management: dealing with gas-
tric dilatation-volvulus syndrome. Vete~na o, Medicine
82, 36-50.
F()x, S. IVl., M(:('lx)v, C. P., ('o(wl-r, R. C. & BMxv, J. C.
(1988). Circumcostal gastropexy versus tube gastros-
tomy: Histological comparison of gastropexy
adhesions../ournal ~?/the America, Animal Hospital Ass0d-
alien 24, 273-9.
(;.u), A. (1986). Erosion: A correlative endoscopic histo-
pathologic muhicenter study. E,dosco/o, 18, 76-9.
(h.t(:Kxt.~x, L. T., (;LU:KXJ.XX,N. W., PI::RrZ, (:. M., S(:lU.:l.l.l-x-
m.:m;, D. B. & L.~xrz, (;. C. (1994). Analysis of risk factors
ti)r gastric titillation and gastric dilatatio,l-volvuhls in
dogs..]our, al of tile America, Veterinmy Medical Associa-
lion 204, 1465-71.
(htsl.:, H. (1990). Epidemiolo~' in peptic ulcer disease:
(:re'rent status and future prospects. Scandinavian/ou~:
,a l of Gaslroe, terolo.©' 25 (Suppl 175), 13-18.
l-l.Xl.l.,.J.A., TWEDr, D. C. & Bt'rm)ws, C. F. (1990). Gastric
,notilitv in clogs. Part II. Disorders of gastric motility.
Compe,dium o, Conli,uin,¢ l".ducation for the Practising
Vetel4narian 12, 137.'),-89.
i l.u'l't::, R. P., V.xx D~:x Br()xv, W. E. & VAX DI-r (;..vu;, I.
(1982). Duodenogastric reflux in the dog, a clinico-
pathoh)gical study, leesearth i, I.),terinaU Sdence 33, 280-
96.
HAPPI::, R. P., \:Ax Dl-r (;.vu;, I., W()t.\'l-K.xxu,, W. Tll. C. &
VAX Tcl()rl.;xmr(., J. (1977). Multiple polyps of the gas-
Iric mucosa of two dogs. flmrnal elSmall A,imal Practice
18, 179-89.
11 \~alt.:y, D. W. & Fl.~:lst:lIM,XX,R. W. (1977). Scirrhous eosi-
nophilic gastritis in dogs with gastric arteritis. Veterinan.'
Palholot,9, 14, 441-8.
H..xZl.:t.I, S. L. & [A.:e,A. (1986). Campyh, bacterpylo14dis, ure-
ase, hydrogen ion back ditl'usion and gastric ulcers.
La,cel ii, 15-17.
Hexl)wu:~, M. (1981). A spectrum of hypereosinophilic
syndrome exemplified by six cats with eosinophilic
eute,'itis, l'elerinmy Patholo~' 18, 188-200.
Hn.LS, B. A., Bt'TH-r, B. D. & Lu:lrr:-:xm.:m;Er,L. M. (198"~).
(iastric mucosal ba,rier: hyd,ophobic lining to the
lumen of lhe stomach. Ame~4can .]ournal of Physioh~,
244, (1561-(1568.
Hosc;(nm, G. (1994). Gastric dilalation-volvuhls in clogs.
.]ournal r~fthe Amedcan Vt,te14naU Medical A.~sociation 204,
1742-7.
.l.x(:ol~s, G., (]()I.I.INS-KEI.I.Y, L., I,.\I'PIN, M. & T',l.l-r, D.
(1990). Lymphocytic-plasmacytic enteritis ill 24 clogs.
.]ournal of Vetelinal), l , ternal Aledicine 4, 45-53.
.Jer(.t-xs, A. E., MoorE, F. M., H..xx.xes,J. S. &. MII.ES, K. (i.
(1992). Idiopathic inflammato D, bowel disease in clogs
and cats: 84 cases ( 1987-199[))..lou rnalo/ tile A merican
15"le~,a ~y Medical Association 201, 1603-8.
.JOIINS()N, S. E. (1992). Canine eosinophilic gastroenteri-
tis. Seminars in 1~5'teri,aO, Medicine and .S'ulgeU (Small
Animal) 7, 145-52.
.J(IllNSl)N, A. (;. (1972). Pyloric fimction ancl gallstone dys-
pepsia. BHtish ]ournal of Su~igeU 59,449-54.
 106 THE VETERINARY.IOURNAL, 156. 2
KAUFFMAN,G. L., REFvv,J.J. & GROSSMAN,M. 1. (1980). Gas-
tric bicarbonate secretion: effect of topical and
intravenous 16,16-dimethyl prostaglandin E 2. American
Journal of Physiolo©, 239, G44-G48.
KnJn', J. (1970). Duodenogastric reflux and pylo,'ic su,--
gery. Gastmenterolo~, 58, 593-5.
L,\NTZ, G. C. (1992). T r e a t m e n t of reperfitsion inju D, in
dogs with experimentally indt,ced gastric dilata-
tion-volvulus. AmeHcan flntrnal of l:etednaly Research 53.
1594-8.
LHB, M. S. & M..\Rrm, R. A. (1987). The,'apy ofgast,ic dila-
tation-vol~aflus it+ dogs. Compendium on Conlinuin£r
Education fin the Practising l'elerinafian 9, 155-63.
MA.-\ROOS, H. I., IL:u;o, T., S[I'I'()NEN, P. & SIt'P~\l..\, M.
(1991). Heliolmct:r pylori and gastritis in children with
abdominal complaints. Scandinavian Journal r)/Gastroen-
temlolo' 26 (Suppl 1861, 96-99.
M.-\C;NI.:,M. L. (Iq92). l~atlu)pl-~ysiolog3 ' ot +inflammato,'v
bowel disease. Seminar~ in l'eh,rina~l, Medicine and Suvg'r'U
(Small Animal) 7, 112-6.
M.\sox, R. C., Tau.¢m, R. R., FnJp,.:, M. I. & M¢:(]ot..., I.
(1988). Pancreaticoduodenal secretions alld the gene-
sis of gastric stump carcinoma in the rat. (;ut 29, 8311-4.
M.-\TIItl-Sl-:N,D. T. (1983). The gastric dilatation complex:
medical and surgical considerations, flmrnal o/the A mer-
iran Animal Hospital A.vwdation 19,925-32.
MI.:','I~R-LINIH.:NBt'RG,A., R-\III.FS, 1., HARI~I:R, A. & Fv~tR, M.
(1995). A long term st\trey of n m n a g e m e n t of gastric
dilatation/volvulus in the dog with a moditied gas-
tropexy technique. European .Journal r~[" Companion
Animal 15at\ice V, 65-71.
Moore.:, R. P. (1983). Feline eosinophilic enteritis, lu ('uw
n,nt li,terinan, Therapy 1711 led R. W. Kirk). p.791.
Philadelphia: W.B. Saunders.
Mum, W. W. (1982a). Gastric dilatation-volvuhts in the
dog, with emphasis on cardiac a,-rhytlmfias..]ournal 0/
the American VeteHna+y Medical Association 180, 739-42.
MUtR, W. W. (1982b). Acid-base and electrolyte distu,'-
bances in clogs with gastric dilalation-volvulus..Journal
of the A,n,,rican l'eterinar), AIMical Association 181, 229-
231.
MtRp,..\v. M. M., Romxsox, F'. B., M{:K}:.vwx<;,F.J., B.xm-I~.,(;.
J. & k.\t,I)e~, I. M. (1977). Peptic ulceration in the dog:
A clin ico-pathological study. Veterinary' RecoM 91,441-7.
OsrRO, M.J. (1987). Phamnacodynamics and pharmacok-
inefics of parenteral histamine (H2)-receptor
antagonists. Amerirrm./ournal of Medicine 83 (Suppl 6A),
15-22.
PntAX, G., M:~lZOt'Bt, D., H..\t:m.:xsc~Ht.D,C., TRIER, J. S. &
SZ..\B(), S. (1986). Ea,ly microcirculato D' stasis in acute
gastric rnucosal inju D, in the rat and prevention bv
16,16-dimethyl prostaglandin E,2 or sodium thiosui-
phate. Gastroenterololo, 91, 1415-26.
Ru:lrrF:~, K. (1992). Lympllocytic-i~lasnlacytic enterocoli-
tis ill dogs. Seminars in Velerinal), Medicim, and 3'ulgmO'
(Small AnimaO 7, 134-44.
R(,m.:RT, A. (1976). AntisecreloD,, anti-ulcer, cytoprotec-
tire and diar,'hoegenic properties of p,'ostaglmldins. In
Advances in Pmstagrlandin and 7'hromhoxane l&search. Vol
2, eds B. A,nuelso,l & R. Paolette, p.507. New York:
Raven Press.
SI.()MIANY, A., Y.-\N(~, S., NI.t)MIANY, B. & (;L.kSS, (;. B . J .
(1978). Lipid COml)ositio,1 of gastric mt,cous barrier in
fll e ral. tim rn al of Bioloffical ('hemist~v 253, 3 7 8 5 - 9 I.
S()NNI-NBI-R(;, A., ~¢|(!I+I.H~-[,ISSNI(I~.,S. A., S(:I IA'I'I'I~NMANN,(;.,
SIVW}:RT,J. R. & BI.I'M, A. L. (1982). Duodenogastric
rellux in the dog. American .]ournal oJ Physiolog9, 242,
(;603-G607.
Spmo, I I. M. (1982). Pharmacology, clinical efficacy, and
adverse effects of sucralfate, a nonsvstemic agent for
peptic ulce,. Pharmacotherapy 2, 6 7 - 7 i .
SrAxroy, M. E. & BRIcart, R. M., Tc~.\t., R. (1989). Gas-
Iroduodenal ulceration in dogs..]ournal +~/ l'eterinrw3,
Internal Medicine 3, 238-44.
Sr.\xTox, M. E., BRU.ln, R. M., DI-Nov~), R. C., M~:CR.u:m<x,
M. & M d , u m : x , . ] . B. (1987). Effects if flw Y-U pylo,'o-
l)lasty on gastric emptying and cluodenogastric rellux
in the dog. 1"elerinaO, SulLrr"O' 16, 392-7.
S OR<~Xmt.:t:K, D. R. & (;t+H.v<roD, W. (;. ( 1991 a). (;astric Dila-
tation, Gastric l)ilatation-Volvuhts and (3u'onic (;as\rio
Dilatation. Clmpter 14. In Small Animal (;astroenlerolog7.
2rid ed, p. 228. l+<mdon: Wolfe Pul)lishing l+td.
S rm>Mm-CK, D. R. 8,: (;t'HJ:t>p,l+, W. G. (lt)91b). Chronic
(;astritis, Gastric Relention, (;astric Neoplasma, anti
Gastric Surgery (:hapter 13. In Small Animal (;aslroenler-
olot,% 2rid ed, I).208. I.¢mdon: Wolfe l:'ul)lishi,lg l.td.
St'L[JVAX, M., I+H-, R., FISlIEI~,E. W., N xml, A. S. & M(:(:.\x-
mJsll, I. est. P. (1987). (;astric carcinoma in the dog: A
review of 31 cases, t"eterina~T Ib,coM 120, 79-83.
W.\t.l_\c}:,J. I.. & WItlrctJ.:, B . J . R . (1986). Role of ,nttcus
in tim repair of gastric epithelia damage in the rat.
Inhibition of cl+ithelial recovm~, by mvcolvlic agents.
(;astroenteroh)k,3' 91, 6113-1 I.
W.UJLXrXRK, B. (19861. Mechanism of action of omepra-
zole. Scandinavian./ournal o/ (,astroentemloKq, 21 (Suppl
118), I 1-16.
~'VY,I.I+I.:R,~'1. (:. /2~ M.\rllll(Sl.:X, 1). T. (1993). Acquired a n l r a l
I)yloric hyl)ertropl W in the clog. 17,lerinarv (:linic~ o/
North A merica 23, 547-54.
I,~r()l.[:, A. PVI. (1992). Feline lymphocytic-plasmacytic
e,Herocolilis. Seminam in l~,h,rina,y Medicine and 5hw:wO,
(Small Animal) 7, 128-33.
YI.:<>MAXS,N. D., ST..]otlx, D..J.B. & Dt.: Bcn.:R, W. (;. R. M.
(1973). Regeneration of gastric mucosa afler aspi-
rin-induced injunT in Ihe rat. American ./ournal r!/
Digestive Disease+ 21,533-41.
(Aca'ph,d fi,r publi,alion 23 Seph,mber1997)