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whitlock
abomasal disorders and ulcers


a "ping" is a gas 
filled viscus, and not always an abomasal displacement.

ping: a variable 
pitched resonant sound detected by simultaneous auscultation and 
percussion. 

you hold your stethescope in one spot and flick the body 
wall of the cow very firmly with your finger - if there is gas under 
that, you should hear a high pitched "ping" sound. the pitch doesn't 
indicate the type of viscus that is gas filled. Then you keep doing this 
and make an outline of where the pinging sound is found. 

back of 
handout shows areas of the cow where you may hear pings. start 
auscultating for ping in area from tuber coxae to elbow. if you find a 
ping, stop at that area, hold your stethescope in place, and then flick 
all around the area to find the borders of the gas filled viscus. 


"ping" on left side:

ddx: Left abomasal displacement (LDA), gas in rumen 
(rumen tympany), gas in peritoneal cavity (pneumoperitoneum). You have to 
outline the size of the area to tell these apart. 

outline size of area

anatomic location
rectal exam
liptak test - needle placed in viscus to 
remove fluid and measure pH (6-7 = rumen, 2-3 = abomasum). not commonly 
done
common sense

The most common is LDA - usually centered under 12th 
or 13th rib, often extending a little bit caudal to 13th rib but almost 
never does it go back to the tuber coxae. if it does, it is probably 
rumen gas, or pneumoperitoneum. in the handout, dotted outline = large or 
chronic LDA.

slide: greater curvature of abomasum in LDA cow - is 
located caudal to the last rib, cranial to rumen. this abomasum is very 
large. 

expect abomasum to be within area between ribs 10 and 13. really 
doesn't generally extend back to tuber coxae. 

pneumoperitoneum - ping 
bilaterally
rumen gas - ping only on left

pneumoperitoneum also extends 
back to the sacrosciatic ligament area, more caudal to the rumen. 


remember for pings on left: LDA, rumen gas, pneumoperitoneum are your 
ddx.

slide: cow with two areas outlined on her side. you can have a cow 
with an LDA & a rumen ping. they can occur together. pneumoperitoneum can 
occur, too. here is where pitch is important. this isn't seen often.


Right sided pings:

Gas in the spiral colon:

most common cause of "ping" 
on the right
centered on upper 13th rib
size: usually small, but may be 
12-15 inches in diameter
associated with anorexia (due to metritis, 
mastitis, indigestion)
variable pitch to ping.
you expect to find this is 
any cow which has been off feed for some reason.

to hear: put head of 
stethescope just caudal to 13th rib, flick in intercostal space. 

RDA 
(right displaced abomasum) - this is going to involve the same area as 
gas in the spiral colon and cecum, but extend forward to the 8th rib. if 
there is a right abomasal volvulus, can be cranial to the 8th rib and 
almost back to tuber coxae.

cecal volvulus: from about the 10th rib to 
the mid-fossa. to detect this - rectal examination will help you figure 
out what's going on. cecums tend to extend further back toward tuber 
coxae or stifle.

slide: cow with RDA - bulge caudal to 13th rib. pings 
come about 3 inches caudal to last rib and go forward to about 10th rib.


Right abomasal volvulus always larger than RDA

spiral colon - most 
common source of ping on right side - centered under dorsal part of 13th 
rib. 

so these areas overlap. rectal exam is important to tell them 
apart.

cecal displacement again - more caudal.

pneumoperitoneum is easy 
to differentiate - will be bilateral, will go fairly dorsal and will 
extend into sacrosciatic ligament area.  extends into pelvic inlet. most 
common following abdominal surgery; also seen after parturition. causes: 
surgery, punctured vagina or uterus, peritonitis (septic), lung rupture 
at parturition/emphysema. this isn't a big deal, btw.

more unusual - gas 
in rectum and colon - most often in cows with diarrhea - on rectal, they 
can aspirate air into there.

chronic rumen distension
air in the uterus 
(physometra)

both are rare causes of right sided pings. with severe 
chronic rumen distension sometimes you hear the ping on the right. 
cows 
with twins and retained placenta and septic metritis may develop 
physometra.

questions about pings?

on right side - most common is air 
in spiral colon and cecum
second - RDA
third - abomasal volvulus
4th - 
cecal volvulus
9 or 10 things compared to 3 on the left.

Abomasal 
displacements:

history:

1. recent parturition - 50% within 2 weeks, 80% 
within 1 month, but can see unrelated to parturition also, in bulls, 
calves, etc.
2. anorexia (partial)
3. milk production - gradual disease

4. mimics ketosis

clinical signs - off feed, mimics ketosis, moderate 
decrease in milk production. 

LDA: clinical findings:
TPR normal
rumen 
motility decreased in intensity and rate
manure abnormal - scanty
ketones 
moderately positive
ping localized on left side
treading

functional 
obstruction with LDA:
usually these cows have metabolic alkalosis due to 
trapping of ions in abomasum and reflux into rumen. 
acid trap - relative 
excess HCO3
K+ shift into cells, H+ out of cells, decreased potassium 
intake, continued loss in urine via kidney, continued GI loss
expect to 
find hypochloremia, hypookalemia, and metabolic alkalosis
the key feature 
is the hypochloremia
the key factor in hypokalemia is decreased K+ intake 
b/c off feed.
you can almost predict that when cows are off feed, and 
maybe have a stomach, abomasal or small intestinal problem, they will 
develop metabolic alkalosis due to reflux etc.

liptak test: was on 
national boards
18 gauge needle 1 1/2 - 2 inches long. insert over the 
ping. aspirate fluid. measure pH: 1-2 = abomasum; 6-7 = rumen.Liptak came 
up with this idea as a student. he's retired and living in NJ now.


postulated causes of displacements - mechanical, nutritional, 
hypotonia/atony

under PE findings - rumen motility, number 3 - the rumen 
motility is almost always present, but decreased amplitude and rate of 
contraction. sometimes increased rate of contraction (common with 
ketosis). but the point is the contractions are less strong. (uh, they're 
weaker).

simultaneous auscultation and percussion are key to diagnosis 
of LDA.

a few other points - maybe you have this cow who calved 2 weeks 
ago has decreased feed intake, some ketosis, you suspect LDA...cows can 
have LDA and NOT have a pint. sometimes vets are so convinced the history 
is compatible with LDA and still can't find a ping and they go ahead and 
do surgery. other times they decide to wait an hour and check again. LDA 
can occur, go away, within an hour or two. so reexam is reasonable. cow 
could have LDA and then get RDA and then go back to LDA. if she lies 
down, it can swing over to the other side. 

hypoglycemic, hypocalcemic, 
aciduria
regarding the aciduria - cows that are off feed and anorectic 
often have aciduria. normal bovine urine is alkaline. but when off feed 
and using their own body muscle for protein, they get aciduria. this 
despite the metabolic alkalosis. it's related to urinary potassium 
excretion.

a few comments re: pathogenesis:
information in handout is 
for your info only except two or three main points:
mechanical, 
nutritional factors may contribute but main factors are decreased tone or 
relative atony of the abomasum, and increased gas production.

some 
people believe that cows are hypocalcemic and then get displaced abomasum 
- that hypocalcemia is a predisposing factor. a study found 26 cows with 
abnormal calcium - 7 had displaced abomasum. 64 cows had normal calcium 
and one of those had displaced abomasum.

why is there a tendency for 
hypocalcemia? onset of lactation, decreased food intake. early postpartum 
cows very prone to hypocalcemia which may cause decreased abomasal tone.


increased gas production: measured abomasal gas production - normally 
make 500 ml/hr on basal diet...with hay, up to 800; with increased 
concentrates, up to 2200 ml/hr! this causes abomasum to float up in 
abdomen.

other factors:
recent parturition
high milk production
ketosis, 
milk feever
retained placenta, metritis
basically - stuff that drains 
calcium or makes them reduce intake

gas: mostly methane esp with 
concentrate feeding; with chronic displacements, more CO2. some vets 
would drain off gas and burn it - and use intensity of flame to dx 
chronic vs acute. but some guy started a barn fire this way so most 
people do not do it :)

treatment of abomasal displacements:
nonsurgical 
- drugs, rolling
surgical - open, blind
supportive care

slides: rolling 
a cow - put rope around her b/w front shoulders and neck, then half 
hitch, then another hh in front of tuber coxae, pulling her down on her 
left. get her on her back, roll her back and forth. abomasum will float 
to top (ventral surface), let her back onto her left side....this can 
temporarily move the abomasum back into normal spot, but can recur. 


toggle approach is also done by flipping her over like this (?) but must 
be very careful b/c you must get the abomasum, not the rumen or 
something. 

drugs: motility enhancers:
calcium gluconate - SQ in a few 
locations, IV best
dextrose - for hypoglycemia and ketosis
cascara 
sagrada
neostigmine - parasympathomimetic
lentin - parasympathomimetic

coffee - thought to stimulate motility - 1 lb with warm water (??)


various surgical approaches - at NBC, ventral paramedian. 

prevention of 
displacements:
do not lead feed
feed concentrate several times a day
feed 
ample roughage > 8 lbs/day
maintain normocalcemia
minimize metabolic 
alkalosis
minimize concurrent dz: metritis, mastitis, other

RDA:


clinical signs very similar to LDA but ping is on the right and you have 
to tell apart from cecal displacment, spiral colon, abomasal volvulus.

can do litpak test
can see if is behind last rib 

abomasal volvulus:

history: as with displacements except sudden, marked decrease in milk 
production, nearly complete anorexia, and a "sicker cow."
size of viscus 
much larger - 16-20 inches in diameter, almost always extending behind 
last rib, sometimes palpable per rectum. 

pulse weak, > 100: HR is much 
higher than with displacement
marked depression
fetid, watery feces
more 
severe abdominal distension
more severe dehydration

RDA with volvulus is 
a surgical emergency requiring immediate treatment or else cow must be 
sent for salvage. Simple RDA you could come back tomorrow and operate.


reflux of chloride - abomasum is obstructed functionally at pylorus, so 
chloride is refluxed into rumen, which is a chloride trap - so you get 
hypochloremia. key feature of metabolic alkalosis in cows with abomasal 
disorders. the more severe it is, relates to severity/duration of the 
abomasal problem.

the more severe, the lower the serum chloride.
looking 
at about 60 cows, as the volvulus increased in severity, the outcome got 
much more grim. the longer the duration, the more intense the 
hypochloremia, the poorer the px. so operate immediately.

slide: 
thrombus of gastroepiploic vein - these occur during torsions, and these 
are why the cows can still die with surgery, and these are why it's an 
emergency.

abomasal volvulus: metabolic crisis - thrombosis, stretching, 
vagal nerve damage.
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Abomasal ulcers:

five syndromes:
I. 
ulcers - slight ulceration and erosion
II. ulcers - benign bleeding 
ulcers with anemia
III. lymphosarcoma associated bleeding ulcers
IV. 
ulceration-perforation with circumscribed peritonitis
V. ulceration - 
perforation with diffuse peritonitis

I. ulcers - slight ulceration and 
erosion

these are the most common, in adults and young calves. may be in 
up to 100% of calves. secondary to septic metritis, mastitis, 
salmonellosis, downer cattle, fatty liver, etc in adults. clinically 
manifested by dark, fetid, loose manure in animals with "endotoxic 
disease" states. these ulcers heal as primary disease improves. 
definitive dx only at necropsy. erosions are usually multiple - 10-100 
sites. primary goal is to tx initial dz. as that improves, ulcers 
improve. it's not easy to dx. you just expect them to be there. by 
definition, remember - erosions extend to basement membrane, ulcers go 
through it. usually these small multiple lesions do not perforate, don't 
cause serious clinical signs, do not require separate tx, will resolve 
with tx of primary dz.

the other classifications are more serious.

II. 
ulcers - benign bleeding ulcers with anemia
these ulcers cause clinical 
anemia
-most common in early postpartum period, seen secondary to 
mastitis, metritis, LDA, ketosis, RP. dark tarry manure is typical
anemia 
- pale mms, tachycardia > 80/min (>140/min = grave px)
singular ulcers 
often erode the gastroepiploic artery in the greater curvature - 
producing variable blood loss
generally one single large ulcer as opposed 
to many small ones. manure in these cattle is much darker, more black, 
tarry, than in cows above. ddx black tarry stool - gastric bleeding, 
haemonchosis, ostertagia, lung abscess (cough up blood, swallow it)

slide: unusual case - cow came in for LDA, which she did have. the next 
day at milking she collapsed and died. found huge 15 L blood clot in 
abomasum associated with one large abomasal ulcer. this is unusual, 
usually not peracute bleeding like that.

III. lymphosarcoma associated 
bleeding ulcers
same clinical scenario - bleeding ulcer - but 
pathogenesis is different - solid tumor in wall of abomasum interfering 
with normal blood supply. these cows have some different signs: gradual 
onset of anemia, hypophagia, decreased milk production. NOT closely 
associated with parturition. benign bleeding ulcers typically occur 
within 1 month of calving. LSA ulcers occur any time. cattle over 5 yrs 
old are predisposed to LSA as well - this is rare in 2-5 yr old cattle. 
may be accompanied by other signs of LSA like lymphadenopathy, heart 
failure, weight loss, uterine masses, etc. onset is more gradual - over 
2-3 weeks. cows with benign bleeding ulcers usually bleed fairly acutely 
and then show signs over a few days. duration here is slower. timing is 
different - any time. animals are older. those are key factors to keep in 
mind. 
slide showing rates of tumors associated vs benign ulcers. LSA 
ulcers all in cows 5 or older. *** age of animal is very clinically 
pertinent. may be on an exam!**
BLV AGID test - bovine leukemia virus is 
the cause of bovine lymphosarcoma. if BLV negative, not exposed to virus 
(45-60 days). if positive, exposed to virus. if test is positive, cow 
might or might not have lymphosarcoma. if test is negative, that rules 
out the adult gastric form lymphosarcoma, though. 
other forms of LSA not 
associated with BLV: skin form, thymic form (herefords), juvenile form. 
the form that is associated with BLV is called the "adult form". sites of 
predilection of adult form are abomasum, heart, and uterus.

when you 
look at abomasum you will see an ulcer with a tumor under it.
cutting 
into it reveals yellowish lymphosarcomatous tissue.

case:
7 yr old 
holstein cow
history: calved 2 mos ago, listless x 10 days, black tarry 
manure x 2 days.
dx: type III ulcer - based on onset (over a month since 
calving), age (over 5) and gradual onset (10 days instead of 2-3 days)


PE: T 102, P 160, bounding referred pulse, RR 24, emaciated, enlarged 
supramammary LNs, black tarry feces, pale MMs, PCV 14, TP 5.0 -> low 
protein with low PCV = blood loss. 

problem list: anemia, diarrhea, 
lymphadenopathy, hypomotility
leukocytosis, lymphocytosis, increased 
retics and nRBCs.

ddx: abomasal LSA, benign bleeding ulcer, duodenal 
ulcers, other upper GI bleeds
plan: LN biopsy, BLV test, transfusion

necropsy: LSA of abomasum

IV. ulceration-perforation with circumscribed 
peritonitis

signs resemble traumatic peritonitis. ulcers that perforate 
do not bleed; ulcers that bleed rarely perforate. why, he does not know.


sharp drop in milk production (50%)
low fever, mild tachycardia, 
decreased feed intake (esp grain), decreased rumen motility
minimal 
evidence of bleeding - almost none.  not anemic. syndrome is associated 
with local peritonitis.
most common in early postpartum period

V. 
ulceration - perforation with diffuse peritonitis
a fulminating syndrome 
- death often within 24-48 hrs
rapidly progressive shock - tachycardia, 
cold extremities, recumbency
hypoproteinemia, or normoproteinemia, with 
hemoconcentration, is strongly suggestive of massive peritonitis. this is 
very important and needs to be remembered. the hypoproteinemia especially 
in relation to high PCV is key.
early postpartum is typical time of 
occurence. surgical correction is possible, but rarely successful. 


normal PCV is 33, TP 7.6

cow with acute peritonitis came in last week - 
PCV 39, TP 4.6. cow is dehydrated so PCV is increased , while protein is 
going into the peritoneal cavity. perforating abomasal ulcers are the 
most common cause of diffuse peritonitis in the early bovine postpartum 
period.

hypoproteinemia + hemoconcentration = diffuse peritonitis

temperature could be normal, fibrinogen could be normal.

same syndrome 
occurs in young, dairy replacement heifers at 4-8 mos of age. growing 
well, bouncing around, doing fine, then next day dull, depressed, 
lethargic, then down, weak, can't move - diffuse peritonitis. occurs 
sporadically, almost impossible to prevent these. the rest of the 
abomasum looks normal. we see it 2-3 times/yr.

once you dx diffuse 
peritonitis, there is almost nothing you can do but recommend salvage if 
the cow is still able to stand and go to the slaughterhouse. damage is 
already done.

pathogenesis of ulcers:
balance of defensive factors vs 
aggressive factors:

defensive:
normal blood flow to mucosa - LSA 
disrupts
mucous barrier
mucosal cell resistance - protein in diet 
important (low protein reduces resistance)
duodenal break with excessive 
gastric acid in duodenum

aggressive:
hyperacidity promoted by 
hypercalcemia, stress
pepsin excess
trauma in milkfed calves, diet 
changes - as calves go from milk diet to roughage diet the belief is the 
diet change can cause erosions  and ulcers. 
hormonal factors esp 
steroids vs progesterone - progesterone may be protective, may be why we 
see so few ulcers during late gestation (also true of women)

you want 
balance b/w these things. 

diagnostic rule outs:

duodenal ulcers - rare 
in cattle - seen sometimes in foals
traumatic reticulitis - not related 
to parturition
abomasal displacements - may coexist with ulcers esp with 
chronic LDA
diffuse peritonitis - IP injections, ruptured uterus

salmonellosis - profuse diarrhea, several animals affected
coccidiosis - 
diarrhea and frank blood, in younger animals
severe advanced uremia - 
rare in cattle
intestinal hemorrhage - new syndrome that may be hard to 
differentiate from bleeding ulcers. 

diagnostic plan: history is the big 
thing to check first
occult blood in manure; feces are black with 
clinically significant bleeding ulcers
anemia - PCV is decreased, 15-20% 
is significant
with LSA anemia less severe than with benign bleeidng 
ulcers
WBC for LSA: lymphocytosis may be present. BLV AGID + if >3 yrs; - 
in juvenile, thymic, and skin forms
rectal exam - detect neoplastic 
masses or peripelvic adhesions, palpate LNs, consider abdominocentesis


therapeutic plan - type 1 - symptomatic tx
type II - cimetidine doesn't 
work well in cattle, antacids like a quart at a time, surgical resection 
possible rarely, transfusions for severe anemia, ranitidine is more 
potent than cimetidine, sucralfate not proven in cattle, bismuth 
subcitrate or subsalycate...none of this is really proven in cattle. 

main thing is to buy time, tx symptomatically w/fluids, blood as needed; 
buy time. >80% will survive.

no tx for LSA, diffuse peritonitis.
for 
local peritionitis treat as for traumatic reticuloperitonitis

ulcers 
that perforate do not bleed, ulcers that bleed do not perforate. a rule 
of thumb. usually one type or the other. 

slide: calf abomasum - ulcers 
secondary to aspirin - aspirin causes a mycotic ulcer. 

Cecal 
displacements/volvulus:
ping on right side 
patient profile - 
adult 
cattle, within two months of parturition, no sex/breed predilection
with 
only partial twist, like RDA, with full twist, like RDA-volvulus.

history: very similar to displacement cows
capricious appetite, decreased 
milk, more abdominal pain than the displacement cows - may tread with 
feet, shift weight, get up and lie down, kick at abdomen. displacement 
cows don't kick their abdomens.
PE similar to ketosis - TPR WNL, HR 
related to severity
ketonuria
rumen motility down, ping on right, 
**rectal exam is definitive** either you feel the end of the cecum within 
pelvic inlet, or it is flexed over like a knee.
HR can be normal; or all 
the way up to >100. high HR goes along with cecal volvulus and pain.

manure tends to be scant. 
some cows have no pain but most show signs of 
pain, most show signs of severe pain. kicking of abdomen.
lab data: 
metabolic alkalosis - related to severity of duration. chloride is 
refluxed again into the rumen. even though this is a lower obstruction, 
that happens. vascular compromise depends on degree of twisting. 

dx 
rule out:
abomasal displacements
traumatic reticulitis
as before


therapy: 
medical: Ca gluconate, stimulants, exercise
surgical: 
decompression
px excellent with surgical tx
can recur

slide: affected 
cecum - humongous.
slide: gangrenous one. it's blue. have to remove the 
whole cecum, anastomose ileum to colon. she recovered.

acute abdomen

ping on right
rectal exam 
surgery
good px.
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