Gastrointestinal Disease

Large Animal Medicine

Nusdianto Triakoso
triakoso.wordpress.com

Department of Veterinary Clinic

Faculty of Veterinary Medicine
AIRLANGGA UNIVERSITY
 DISEASES OF
FORESTOMACH
• Simple indigestion
• Lactic acidosis
• Rumenitis
• Vagal indigestion
• Retikuloperitonitis traumatic
• Bloat

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 Simple indigestion
• Characterized by anorexia and atony of the
forestomach
• Common disease in dairy cattle and less
common in feedlot cattle and others ruminant
• Causes :
– frosted feed, too coarse or too finely ground,
excessive consentrate
– switching from dry concentrate to lush pasture or from
dry pasture to rich concentrate
– prolonged or heavy oral dosing of sulfonamide or
antibiotics

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 Simple indigestion
• Causes:
– Dairy cattle: unlimited acces to good quality silage
– Beef cattle:
• Feed that have been permitted to soil or sour in bunks or
feeders
• Prolonged or heavy oral dosing of feed aditive leads to
indigestion
• Varying degree of severity is observed in herds or flocks
when management errors lead to abrupt increases in ration
levels of this feed conserving additive or variable signs
depend volume and adaptation capability
• SI also ascociated with another disease: pneumonia,
reticulitis

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 Simple indigestion
• Pathogenesis
– Rumen atony
• dramatic increase or decrease ruminal pH
• large intake of indigestible materials
• consumption of feeds containing large quantities of
stale, sour, or putrefied materials
• histamine (intrinsic or extrinsic)
– In many instances the exact sequence is
difficult to ascertain or to explain.

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 Simple indigestion
• Clinical signs
– First clinical sign : reduction in feed intake
• anorexia (>50%) with other outward signs
• Lactation cow : decrease milk production paralleling change in feed intake.
– Depression or dullness
• in herd or flock, decreased physical activity or alertness
• difficult to detect, unless one is closely familiar with the behavior of that particular group
of animals
– Changes in body temperature are not likely to be record
– Rumen stasis (reduction in the strength and frequency of contraction) :
palpation or auscultation
– Intestinal motility decreased, but gaseous intestinal sounds may be
increased and diarrhea maybe observe.
– Mild tympany maybe observed
– Rumen pH is highly suggestive in the absence clinical evidence of other
disease processes
– Other laboratory tests are not likely to be helpfull.

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 Simple indigestion
• Diagnosis
– Based on clinical examination and on rulling out other,
more serious disease problems
– Careful evaluation of the history is important.
– Differential diagnosis (complete clinical examination
and evaluation of response treatment will be
necessary to rule out each of these as diagnostic
possibilities)
• Milk fever
• Early stage of lactation ketosis
• RPT
• Displaced abomasum

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 Simple indigestion
• Treatment
– Spontaneously resolve in 24-48h (process takes 3-4 d)
– If the exact nature of the disturbance can be
established, the recovery process can possibly be
speed up by symptomatic therapy
• Rumen acidic : Magnesium hydroxide (225-450 g)/adult animal
• Rumen alkaline : Oral dose of acetic acid or vinegar (2 ml/kg)
• Mineral oil (4 liter or more) not directly to pH but help to move
indigestible material along and slow the absorbtion of toxic
materials
– Transfaunation: if rumen remains atonic for more than a
day or so

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 Ruminal acidosis
• Sinonim : grain overload, rumen overload, lactic
acidosis, acute rumen engorgement
• Causes :
– highly fermentable carbohydrate feed leads lactic
acidosis (acute dehydration and depression)
– highly fermentable proteinaceous leads excess
ammonium ion production with excitement and
hyperesthesia
• Both of these syndrome are commonly
observed wherever intensive livestock
management is practiced
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 Ruminal acidosis
• Mild degree of lactic acidosis are extremely
common in grain-fed cattle, and the affected
animals will frequently be found to have other
associated disease processes as well.
– liver abcesses
– rumenitis or rumen parakeratosis
– mycotic rumenitis
– feedlot bloat
– laminitis

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 Grain

rice barley hulled

corn

oat groat wheat berries

buck groat

rye berries spelt hulled

millet

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 ↑ high digestable

↑ growth (all microbe)

↓ pH < 5

↑ VFA’s

↓ pH
↓ microbial growth ↓ S. bovis
(some bacterial) RUMINAL ↑ Lactobacillus
ACIDOSIS ↑ growth S. bovis
↑ lactic acid

↓ pH

Stasis fermentation

Absorbsion D/L lactic acid

Acidosis Metabolic
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Rumen adaptations due to pH

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 Clinical signs
• Onset of action: variable depend on the amount of feed
consumed, feed composition, feed particle size, and previous
adaptation to the ration
• Clinical signs appear 12-36 h after grain consumed or
similarly feed
• Clinical syndrome may vary from acute and severe to mild
and similar to simple indigestion
• Clinical signs :
– initially: ataxia, muscle tremors, depression, lethargy
– anorexia and blidness signs
– complete ruminal stasis and abdominal pain (grunting and
grinding of the teeth)
– abdominal distension
• Significant dehydration will become apparent within 24-48 h

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 Clinical signs
• Significant dehydration will become apparent within 24 to
4 h. Fetid diarrhea develops, but may not be observed if
animal die early from the disease. Profus diarrhea
maybe considered a sign of improvement if animals are
not seriously depressed.
• In severe cases the animal may become recumbent
(weakness and toxemia) in 24-48 h.
– Increased respiratory rate due to acidosis
– Hypothermia
– Weak pulse
– Recumbent animal will lie quietly, often with the head tucked to
the side as in milk fever
– Crusty mucus present in muzzle (failure to clean its nostril)

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 Clinical signs
• Herd problem of acute rumen
engorgement with grain is observed:
– Some animal depressed and acute lactic
acidosis.
– Moderate condition: mild depressed with
diarrhea
– Feces foamy and liquid with acid smell and a
yellow-brown or grey color
– Feces may contain undigested feed material
– Some animal show acute laminitis
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 Clinical signs
• Suddent death occur in 24-48 hours, but
many case are characterized by apperent
recovery with later deterioration and death
from secondary complications
• It is not unusual for losses to continue for
3-4 wk in severily affected herds.
• Some animals will partially recover but
perform poorly in the feedlot owing to
chronic rumenitis or liver damage.
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 Ruminal acidosis
• Diagnosis
– Based on history and physical examination
• The history alone is often sufficient to establish the diagnosis
• Misleading diagnosis: if the feed consumption pattern is not
known or not suspected
– Laboratory evaluation (rumen ingesta, plasma and
urine pH)
– Differential diagnosis
• Polioencephalomalacia
• Urolithiasis; Peritonitis
• Parturient paresis
• Other diseases that cause profound depression

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 Ruminal acidosis
• Treatment
– Mild cases: spontaneous recovery
– Severe cases: intensive treatment
– Rumen emptying: oral lavage or rumenotomy
– Antacid PO (Mg carbonate or Mg hydroxide)
• Inisial dose up to 1 gram/kg BW (454 gram for adult cow)
followed smaller dose, interval 6-12 hours
• Mix with 8-12 liter warm water (stomach tube to rumen)
• Doses < 225 gram (if rumen has been evacuated)

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 Ruminal acidosis
• Treatment
– Fluid therapy and acid base balance
• Balance electrolyte solution and 5% sodium
bicarbonat IV
• A 450 kg animal w 10% dehydration (50 liters of
fluid over 24 h). Sodium bicarbonat should be
given at the rate of 0.5 mEq/kg BW initially and
repeated in 24 h if necessary
– Correction of blood pH within the normal
range is vital for survival even if the offending
rumen ingesta is removed.
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 Ruminal acidosis
• Treatment
– Antihistamine is considered to be of value by some
– Recently research: thiabendazole PO in normal
anthelmintic dose can control the development of
secondary mycotic rumenitis.
– Prevention
• Avoid abrupt changes and gradually adapt the rumen to
concentrates
• Maintain a minimum crude fibre content of 14% TDN for
fattening cattle and 18-22% for dairy cattle

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 Vagal indigestion
• Sinonim: vagal indigestion, chronic indigestion, vagus
indigestion, Hoflund’s syndrome
• Digestive tract disorders caused by lesion that interfere
with the vagus nerve supply to the ruminant stomach
• Refers to a group of condition that cause forestomach
outflow problems
• Most common in adult dairy cattle (anorexia, weight loss,
decrease milk production, mild bloat, abdominal
distention, decreased amounts of manure)
• Distended abdomen is a cardinal sign.
• Disorders (Mechanical; Functional)

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 pathophysiology
• Similarly with RPT or tumor (lymphosarcoma
abomasum), abomasum torsion.
• Reticulum adhesion lesion (contraction, eructation)
• Failure omasal transport (feces, undigeste, mild
dehydration)
• Physical obstruction (placenta, plastic bag) or tumor
• Abomasal impaction (secondary)
• Correlated with pregnancy (compress digestive organ,
interfere of flow)

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 pathophysiology
• Type I = impaired eructation, caused by
adhesions and subsequent failure to clear
cardia
• Type II = failure omasal transport = rumen
overfilling = omasal obstruction, caused by
abcesses on right side reticulum
• Type III = abomasal hypomotility = pyloric
outflow obstruction, caused by damage to vagus
nerve (peritonitis)

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 clinical signs
• Clinically recognized forms of vagus indigestion can be catagorized
as follows :
– Ruminal distention with hypermotility (functional blockage between
omasum and abomasum, increase in rumen content (fluid), rumen
contraction not audible on auscultation, uncoordinated primary and
secondary contraction (4-6/m), bradycardia, heart rate (40 bpm).
‘symmetrically rounded shape”
– Ruminal distention with hypomotility or atony rumen (similarly with
the first type, except the waves of contraction of the rumen are not
visible and no contraction audible by auscultation, heart rate will usually
be normal or may be increased in some cases). “symmetrically rounded
shape”
– Functional pyloric stenosis (the abomasum fails to empty properly
into the duodenum, fluid or semisolid ingesta accumulates within the
abomasum, the rumen distends w fluids secondarily because of a failure
of transport of ingesta through the abomasum. “papple shape”.
• Clinical signs are similar in all three syndromes

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 clinical signs
• Most case give the appearance of progressive chronic indigestion
– Anorexia
– Rumen atony, reduced fecal passage
– Severe distention of rumen may develop as the disease advances
– The animals develop excessive thrist owing to rumen stasis with
squestering of fluid in the rumen.
– There is severe loss of condition
• If the obstruction involves the pylorus, abomasum may become
greatly distended.
– Appearance of the abomasum fullness, but rumen may be atonic and
relatively empty
– Reverse emptying of the abomasum into the rumen with sequestering of
chloride in the rumen
• Gastric obstruction or anterior intestinal tract cause alkalosis with
severe dehydration and weight loss

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 diagnosis
• Progressive chronic indigestion suspected vagus indigestion
• On rectal examination the rumen will greatly distended and have a fluid consisteny in
all three syndromes. Posterior ventral blind sac of the rumen is so distended that it
extends to the right side of the abdomen (”L shape”). The abomasum is usually not
palpable. The fluid consistency can be appreciated by ballotement of left and right
side of the abdomen.
• Accumulation fluid within abdominal cavity (abdominal paracentesis)
– Ascites
– Ruptured urinary bladder
• LDA :
– abdominal distention as big as vagal indigestion
– gases accumulation (percussion and auscultation)
• Other obstuctions (abomasal torsion, RDA) :
– acute
– distinc by palpation/rectal examination.
• Severe abomasal ulceration
– similarly signs
– obstraction more obvious
– animal’s feces dark/black color like tar because of abomasal hemorrhage.

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 treatment
• Supportive therapy is of major importance
– Balance electrolyte solution IV to correct dehydration
– More specific fluid therapy can be accomplished if
blood gas and electrolyte data are available
• Treatment is usually unrewarding because of the
impossible of removing the primary cause.
• Conservative treatment
– mineral oil everyday (4 liter perday for adult cow)
– systemic parasympatomimetic will improve and
temporerly (incomplete obstruction).

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 treatment
• Emptying abomasum
– abomasotomy is helpful in some instance
– abomasal motility is not likely to return unless
partial innervation remains.
– Alternative: slaughter

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 RPT
• Synonim : reticuloperitonitis traumatica,
hardware disease, traumatic gastritis
• Most common in adult cows
• Goats and sheeps (less common, because
of their more discriminate eating behavior)

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 pathophysiology
• Sharp, metallic objects lodge in the reticulum partly
because of the honeycomb-like structure and because of
the active contraction in that organ
• Foreign bodies (ingested, in reticulum, local peritonitis),
pembentukan fibrous tissue.
• May include vagus indigestion or the lesions may heals
spontaneously only recur later (estrus, increased
physical activity or during late gestation)
• Caused of penetration :
– Pericarditis, pneumonia, pleuritis, chronic peritonitis, acute
diffuss peritonitis, internal bleeding, hernia diafragmatica,
traumatic hepatitis or splenitis

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 Clinical signs
• Acute local peritonitis
– Abdominal pain
– Head and neck extension, arching back
– Stand with foreleg abduction
– Increase temperature (39.5-40.5 oC), and
pulse 80-90 bpm
– Shallow fast respiratory
– Decrease rumen motility/atony
– Feses small, firm, dry and covered mucus

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 clinical signs
• Chronic local peritonitis
– Early sign undetectable
– 24-48 h
– Reduced gastrointestinal function, no specific
signs.
– Vital signs are normal

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 diagnosis
• Base on clinical finding (anorexia, increase temperature,
abdominal pain, absence of evidence of the other
disease)
• Rectal examination: small and hard rumen, if viscera
push toward the animal become pain
• Wither pinch test
– Normal: ventroflexion
– Abnormal: not ventroflexion and feel pain
• Abdominal pain [push xiphoideus, lifted thorax area,
push by knee at ventral of thorax] and absence of the
evidence of other disease processes
• DD
– IS, Lactic acidosis, Ketosis, LDA, Abomasal ulceration, hepatic
abcess, pyelonephritis

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 treatment
• Treatment will vary, depending on the severity of the
condition, the existing complication, economic
consideration, facilities available
• Rumenotomy or laparotomy
• Conservative methods
– Antibiotics
– Administration of rumen magnet to immobilized the foreign objects
– Restricting physical activity
– Elevating front quarters by a platform or other device
– Fluid therapy (isotonic polyionic)+ calcium
• Prevention :
– Exposure to areas of construction where nails, string and similar objects
have neen scattered should be prevented.
– Administration of ruminal magnet
– Indonesia (low incidence)

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Cheetah white magnet Rum-5 Heavy duty Magnet balck max
cow magnet

Flat cow magnet

Magnet Alni Max

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 Bloat
• Ruminal tympany is the accumulation of free gas
in the dorsal rumen following abnormal
fermentation and indigestion.
• Ruminal tympany in young calves may result
from failure of the oesophageal groove to close,
with the result that milk enters the rumen and
subsequent fermentation causes acidosis and
ruminal atony.

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 Bloat
• Type
– Primary ruminal bloat (frothy bloat)
• Pasture
• Feedlot
– Secondary ruminal bloat (free gas bloat)
• Emergency case

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 Causes
• Primary
– Pasture: lush pastures (release chloroplast--stable foam),
succulent forage (anti-foaming), legume
– Feedlot: high carbohydrate/finely ground grains, pH low,
decrease salivation. Most common 1-2 bulan
• Secondary
– Foreign bodies/stenosis
– Esophageal groove: vagal indigestion, diafragmatic hernia,
tumor
– Lesion of wall of the reticulum
– Grain overload: atomy rumen
– Hipocalsemia: atony rumen

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 Clinical signs
Primary Secondary
• Increase TPR • Inceased TPR
• Rumen is suddenly obvious • Hipersalivation, mouth-
distended. Entire abdomen breathing
enlarged • Abdominal distention (flank)
• Dyspnea, neck extension, • Percussion: higher pinch
tongue protrusion, mouth- ping than with frothy bloat
breathing, hipersalivation, • Lateral recumbency
frequent urination
• Decrease ruminal motility
• Death, 3-4 h after
presentation of clinical signs
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 Diagnosis
• Anamnesis
• Clinical signs, physical examination
• Passage of an orogastric tube
– Tube cannot be passed: free gas due to obstruction
– Tube is passed: free gas bloat with/without
obstruction
– Tube is passed, gas not readily escape: frothy bloat
• pH <5.5 = feedlot bloat
• pH >5.5 = pasture bloat

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 Treatment
• Stomach tube
– Move back and forth to locate rumen gas
– Administer antifoaming agent for frothy bloat
• Trocar (emergency)
– Administer antifoaming agent for frothy bloat
– If unsuccesful, emergency rumenotomy
• Rumenotomi
– Life-threatening cases
• Rumen fistula
– Temporary relief for acute gas bloat due to an esophageal mass
– Removal mass manually

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 Treatment
• Antifoaming agent
– Vegetable oil/mineral oil 250-500 ml PO
– Dioctyl Sodium Sulfosuccinate
– Poloxalene 25-50g PO
• For legume bloat (not feedlot bloat)
• Prevention
– Oil 60-120ml/head/day
– Ionophores (Monensin, Lasaloc)
– Synthetic nonionic surfactan (Polaxalene)
10-20g/ekor/h

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DISEASE OF
ABOMASUM
(STOMACH)

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 DISEASES OF
STOMACH (ABOMASUM)
• Left Displaced Abomasum
• Right Displaced Abomasum
• Abomasal Impaction
• Intussusception
• Gastric Impaction
• Gastric Ulcers
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 LDA
• Left displaced abomasum (LDA) is a condition in
which the abomasum, which normally lies to the
right of the ventral midline, assumes an
abnormal position on the left side of the
abdomen between the rumen and the left body
wall.
• Incidence
– Highest in cows of the middle aged group (4-6 y) in
early lactation (80% in the first month of lactation)
– Rarely in dairy bulls, virgin heifers and beef cows.
– Low in pregnant cows.

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 clinical signs
• Early signs of LDA are often subtle
• Anorexia in most case
• Cow refuse grain but continue to eat some hay. If the
condition is prolonged, weight loss may be continue for
several weeks and the cow culled from the herd for poor
body condition.
• Milk production gradually decline and may result
agalactia
• Most cows will be ketotic at some time during the course
of the disease
• The feces vary from more firm than normal (typical
ketosis) to being more loose than normal. Cow with
diarrhea have much poorer prognosis than those with
normal or dry feces. Many cows will have normal feces
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 clinical signs
• Alkalosis metabolic is common. (A few will
develops to acidosis metabolic or acid base are
normal)
• Calcium serum is low, phosphor and magnesium
are normal or slighly increase. Increased or
decreased blood glucose.
• Glucosuria terjadi bila kadar glukosa darah
meningkat. Ketonuria is manifest of ketonemia
because of increased of NEFA serum.

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 diagnosis
• Auscultation and
percussion
• Liptank test
– Abomasal (pH<5, no
protozoa)
– Ruminal (pH>6)
• Prognosis of LDA of
cow with diarrhea is
worse than with
normal or dry feces.
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diagnosis

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 treatment
• The goal in treatment of LDA is to return the abomasum
to its normal position, so that normal digestive function
can be returned.
• Treatment should be accomplished as quickly,
permanently, inexpensively as possible.
• Medical treatment unrewarding
• Conservative approach
• Rolling: abomasal reposition [economic reason and
client]

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 treatment
• Surgery
– left flank abomasopexy
– right flank omentopexy
– right paramedian abomasopexy
– right paramedian percutaneous toggle pin (bar suture)
fixation.
• Prevention
– feeding management [avoiding rapid dietary change,
maintain adequate roughage, feeding small volume
and more frequen]
– avoid risk factor of periparturient disease. Concurrent
disease problem shoud be prevented
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 RDA
• Right displaced abomasum (RDA), also
known as abomasal dilatation or abomasal
dilation.
• Patient of RDA have history and
predisposition on LDA.

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 clinical signs
• Clinical signs similarly with LDA, except
the “ping” is on the right abdominal cow.

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Right Displace Abomasum

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Right Displace Abomasum Volvulus

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 diagnosis
• Diagnosis based on history and physical
examination.
• Liptank test is useful to determine causes
of abdominal distention.
• Differential diagnosis are colonic gas,
rectal gas, caecal dilatation, caecal torsio,
abomasal torsio, pneumoperitoneum,
physometra.

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 treatment
• Medical treatment smooth muscle stimulant, but surgical
intervention is the main choice. Don’t put off surgical
intervention, because RDA become abomasal torsion
/volvulus immediately.
• Rolling to replace the abomasum to its normal position is
contraindication, because it will leads to abomasal
torsion/volvulus.
• Once abomasal torsion/volvulus is diagnosed, immediate
surgery is indicate.
• Surgery: right flank omentopexy or right paramedian
abomasopexy.

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 Abomasal Impaction
• Abnormal accumulation of solid ingesta in abomasum
• Causes :
– failure of the abomasal musculature to contract properly,
– dietary inadequacies
– ingestion of foreign material
• The history usually indicates gradual onset of disease
• The disease frequently goes unnoticed until terminal
stage
• Most common in commercial beef cattle fed on marginal
rations, but also found in dairy calves.

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 Specific forms of abomasal
impaction
• Primary, ingestion of excessive amount of coarse, indigestible
roughages.
– This indigestible feedstuffs impact in the abomasum dan secondarily fill
reticulum and rumen. Fermentation and digestion impaired, cows will
remain hungry and consume the offending feedstuff until physical
capacity of the rumen limits futher intake (unthrifty and in a state of
starvation)
– Hand-fed calves that receiving inadequate nutrition from poor quality
milk replacers will ingest bedding or other rough forages.
• Foreign material become entrapped in the abomasum, leading to a
primary impaction.
– Cow frequently eat the placenta following parturition
– Cattle sometimes chew on baling twine. Twine may become entrapped
in abomasal
– Unthrifty young cattle in the process of licking may ingest large
quantities of hairs. Hairs entrapped in abomasum may become
trichobezoar.
• Secondary, failure to the abomasal ”pump” owing to a lack of motility

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 clinical signs
• In beef cows: usually occurs in the winter.
• The growth of long hair tends to mask the poor
body condition of affected cows.
• The abdomen becomes distended with ingesta
giving the cow around, fat appearance.
• Cows often though to be fat and healthy (upon
close examination they can be seen to be very
thin).
• Cows may get to advance stages of disease and
death may occurs before owners realize that
problems exist.

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 clinical signs
• Cardinal signs :
– Abdominal distension coupled with poor body condition and
dehydration
– The fecal output is reduced in volume and hard and dry.
– Temperature, pulse and respiratory rate usually normal.
• Hypochloremic metabolic alkalosis.
• Catabolic state tend to produce metabolic acidosis,
which modifies the overall acid-base status
• Dehydration causes a tendency toward an increase in
the PCV and total protein. But these changes may be
overridden by anemia and hypoproteinemia resulting
from starvation. As a result, total protein and PCV may
be in the normal range.

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 diagnosis
• Abdominal distention must differentiated with vagal
indigestion.
– In vagal indigestion the content of abomasum and rumen are
usualy fluids in nature, as determine by ballotement, as compare
with the firm content in abomasal impaction. The history of a
gradual onset and the feeding of poor quality roughages will help
confirm diagnosis. Rectal examination usually reveal a rumen
distended with firm ingesta and ”L” shape. The abomasum is
usually beyond reach.
• Malignant lymphoma of the abomasum may cause
enlargement of the organ wall and accumulation of
ingesta.
– It can differentiated in some cases by the presence of peripheral
lymphadenopathy and lymphocytosis.

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 treatment
• Individual treatment is effective only in the early stages
– Mg hidroxide or Mg sulphate administration effective in
evacuating the abomasum
– Fecal softener (mineral oil or dioctyl sodium sulfosuccinate
(DSS) effective in softening the mass of ingesta
• Rumenotomy: severe case and chronic
– Rumen physically evacuated and abomasum may be medicated
by passing a stomach tube through the reticulo-omasal orifice
and administering mineral oil or DSS directly into abomasum
– Physical removal of the abomasal contents by abomasotomy
may be accomplished but has been unrewarding

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 treatment
• Supportif treatment
– IV or PO fluids to reestablish hydration
– IV glucose and amino acids to provide nutritional
support
• Advanced cases suffering from starvation as
well as abomasal impaction have consistenly
responded poorly to therapy
• To be succesfull, therapy should be institued as
early as possible during the course of this
disease
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 Gastric Impaction, Rupture
• Gastric impaction most commonly results from poor
dentition or consumsion of low quality foodstuffs (straw)
• Primary: ingestion of excessive amounts of food, water
or air
• Secondary :
– bowel obstruction (physical or functional), particularly disease of
small intestine
– obstruction of the large bowel
• Horse are unable to vomit, rupture of the stomach is a
frequent sequele to dilatation
• Gastric rupture is avoided by rapid recognition of
dilatation dan repeated decompression

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 Gastric impaction
• Clinical signs
– Observation or inspection
• dental abnormalities
• rapid eating, a common characteristics of horses low in the
social order
• consumption of poor-quality feed or large volumes of feed or
water, especially grain
• vices, (crib biting, windsucking)
• colic
– Abdominal pain ranging from mild to severe with
dilatation. Some horses ”dog sitting” to decrease
pressure on the stomach

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 Gastric impaction
• Diagnosis
– Rectal examination may reveal distended
loops of small or large bowel in cases of
secondary gastric dilatation
– Increased cardinal signs, dehydration and
shock are common in severe cases
– Electrolytes deficits (hypokalemia,
hypochloremia) may occur due to pooling of
gastrics fluid
– Significant gastric reflux is common

khd 301 - triakoso

 diagnosis
• Gastric rupture :
– immediate reduction in pain, followed by progressive
deterioration of clinical signs (shock)
– abdominocentesis reveal evidence of ingesta and
biochemical and cytologic changes consistent with
peritonitis
– euthanasia is the only option
• Differential diagnosis
– Consumption of poor-quality feed; ingestion of large
volumes of grain, others feed, water or air; anterior
enteritis; bowel obstruction; other causes of colic
(peritonitis, enteritis/colitis)
khd 301 - triakoso
 Gastric impaction
• Treatment
– Dioctyl sodium succinate (DSS), 5% solution, 400 to
800 g, in 4 to 6 L of water.
– Priority: gastric decompression
– Technique: nasogastric. Lavage the stomach with
water repeatedly by pumping 2-4L via nasogastric
tube and recovering the infused water and ingesta by
gravity flow or aspiration through the nasogastric
tube.
– Bethanechol, 0.02 mg/kg SC every 6 to 8 hours to
promote gastric emptying
khd 301 - triakoso
khd 301 - triakoso
 Gastric impaction
• Treatment
– Correction of the inciting cause is the key to
therapy, and this may required refferal surgery
if indicated.
– Symptomatic therapy, IV fluid required in
dehydrated horse (isotonic, polyionic fluid).
– Pain control :
• Xylazine 0,3-0,7 mg/kg IV
• Detomidine 10-20 µg/kg IV,
• Flunixin meglumin 0,25 mg/kg IV.

khd 301 - triakoso

 Gastric ulcers
• Found at any production stages of swine
• Risk factors:
– Finely ground feed, wheat feeds
– Stressors (concurrent disease, competition)
– Defisiencies: selenium, vitamin E
• Clinical signs
– Suddent death (perforates, acute/diffuse peritonitis)
– Melena
– Anemia, poor growth

khi 322 - triakoso

 Gastric ulcers
• Diagnosis
– Often made on necropsy or clinical signs
– Lab test: confirm anemia, blood in feces
• Therapy
– Affected animal may be culled
– Herd treatment
– Similar courses with other monogastric
(antacids, mucosal protectant, H2 receptor
blocking agents
khi 322 - triakoso
 Merci…

Terima kasih…
Matur nuwun…
ありがとう Gracias…

khd 301 - triakoso