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Large Animal
Large Animal Medicine

Gastrointestinal
Diseases

Department of Veterinary Clinic


NUSDIANTO TRIAKOSO Faculty of Veterinary Medicine
AIRLANGGA UNIVERSITY
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• Principles of ruminant digestive system
• Principles of horse digestive system

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Gut Fermentor
Foregut fermentor Hindgut fermentor
• Cows • Horses
• Bufallos • Rabbits
• Goats
• Sheeps
• Deers
Function Ruminants Cecal Digestors
Ability to efficiently digest and extract energy from cellulose Yes Yes
Ability to utilize dietary hexose sources directly No Yes
Ability to utilize the protein from fermentative microbes Yes No

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Ruminal Fermentation
• Acetat acids, digunakan sedikit di dalam
hepar dan dioksidasi umumnya di dalam tubuh
untuk membentuk ATP. Selain itu asam asetat
merupakan bahan utama asetil KoA dalam
sintesis lemak.
• Propionate acids sebagian besar
dimetabolisme di hepar. Di dalam hepar
propionat merupakan substrat utama untuk
glukoneogenesis, yang ini sangat penting
dimana glukosa hampir tidak ada yang
mencapai usus dan diabsorbsi di intestinal.
• Butyric acids yang keluar dari rumen sebagai
benda keton β-hydroxy butyrate yang
dioksidasi di jaringan sebagai sumber energi.
• Ratio of acetic, propionate and butyric acids
roughly 70:20:10

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Reticuloruminal Motility
• A cycle of contractions occurs 1 to 3 times
per minute. The highest frequency is seen
during feeding, and the lowest when the
animal is resting
• Primary contractions originate in the
reticulum and pass caudally around the
rumen. This process involves a wave of
contraction followed by a wave of relaxation,
so as parts of the rumen are contracting,
other sacs are dilating.
• Secondary contractions occur in only parts of
the rumen and are usually associated with
eructation.
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PATHOPHYSIOLOGY
OF
GASTROINTESTINAL
SYSTEM

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PATHOPHYSIOLOGY
OF GASTROINTESTINAL SYSTEM

• Prehension and mastication


• Dysphagia
• Abdominal distension
• Acid-base and electrolyte change
• Abdominal pain
• Colic

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Prehension
• Prehention and mastication
– functions of the voluntary mucles of the lips, tongue and jaw.
• Problems :
– cranial nerve deficits
– local irritation
– ulceration
– foreign bodies
• Oral cavity, dental, tongue and pharyngeal should
carefully inspected for abnormalities
• Important to differentiate between lack of desire to eat
and inability unable to eat
– Animal showing interest in food pakan and “picking” at it,but
retaining it in the mouth (rabies, botulism, actinobacillosis, moldy
corn poisoning)

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Dysphagia
• Signs : sialosis, hypersalivation,swelling of the
pharyngeal tissue
• Causes :
– mechanics pharyngeal disturbance
• foreign bodies obstruction
• tumor
• enlarge mediastinal lymph node
• thoracic abcesses
– functional pharyngeal disturbance
• functional blockade of swallowing reflex occurs with
interference to the nervous supply of the smooth mucles
(rabies atau botulismus)

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Abdominal distension
• fat, fetus, flatus, feces and fluid (5F)
• Examination :
– rectal examination
– ballotement
– vital sign
– pH rumen
– others (eructation, ruminal contraction)

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normal Left flank filled free gas bloat
frothy bloat Ind. vagus

hydrops abm dialtation abormasal impaction


paralytic ileusl pneumoperitoneum

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abdominal distension

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Hematological Change
• PCV and TPP
• Inflammations :
– subacute or chronic inflammatory : low-normal PCV
(25-35%) and mild hyperproteinemia (TPP >7.5 g/dL)
– normal PCV with low TPP (<6.0 g/dL) has ominous
prognosis (protein-losing enteropathy, malabsorbsi
syndrome, diffus peritonitis or protein-losing
nephropathy (amiloidosis).
– Elevated PCV and TPP (acute massive dehydration
may occur with acute grain overload, salt poisoning,
severe profuse diarrhea)
• Leukocytosis : inflammation. Acute severe
inflammation : neutropenia
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Abdominal pain
• Restlessness
• Gelisah
• Meregang
• Arching back
• Abdominal kicking
• Sweating
• Tachycardia
• Narrow fast respiratory
• (Laboratory examination)

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Colic

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Colic
• Over 70 causes of colic in horse
• Causes of colic :
– impaction (large intestine); spasmodic
hypermotility (small intestine); intussusception
(ileocecal region); volvulus (smal intestine);
torsion (large colon); strangulation (may occur
with volvulus and torsion); tympany (cecum
and large colon); and colitis/enteritis and
tromboembolic

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Anatomic factors predisposing
• Horse cannot vomit
• Unfixed position of left colon
• Long mesentery of small intestine
• Cecum is a blind sac
• Upward movement of ingesta and
narrowing of lumen at the pelvic flexure
• Termination of right dorsal colon into much
narrow small colon
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History
• husbandry (diet and diet changes)
• habitat (box stall, pasture, sandy soil,
weather changes)
• routine (changes in training, exercise,
transport)
• vice (cribbing, windsucking, indiscriminant
appetite)
• medical history
• parasite control
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Historical aspects pertaining to
colic
• attitude (depressed, alert)
• signs (onset, duration)
• intensity and nature of pain
• possible causes
• therapy (type and response)
• defecation (frequency and composition)
• pregnancy, breeding history

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Physical examination
• Temperature, pulse rate, respiratory rate
– increased pulse : severe pain
– weak, thready, absent pulse : poor prognosis
• Presence abdominal distension (usually reflective of
cecal or large colon distension)
• Signs : pawing, rolling, lying down, kicking at the
abdomen, abrasions (eyes, head, tuber coxae, limbs),
looking at the flanks, sweating and attempts to urinate
• Spontaneous remission may accompany resolution of
this problem : danger/not??
– gastrointestinal decompression (dramatic reduction in the
manifestation of pain) may accompany rupture of a viscus
(rupture of the stomach)
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Medical management colic
• Pain control
– NSAID’s : phenylbutazone, dypirone, flunixin meglumin
– α-aderenoceptor agonist : Xylazine, detomidine
– Narcotics : morphin, oxymorphone, meperidine
• Laxatif/Lubricants :
– large volume intravenous fluids (100-120 ml/kg)
– mineral oils
– dioctyl sodium sulfosuccinate (DSS)
• Agents Affecting Gastrointestinal Motility
– Neostigmin
– Betanechol
– Metocloporamide
• Fluid therapy

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DIAGNOSTIC
APPROACH

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DIAGNOSTIC APPROACH
• History
• Physical examination
– Auscultation
– Rectal examination
• Laboratory tests
– Abdominocentesis
– Hematology
– Feces examination
• Liver examination
• Radiologies
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abdominocentesis

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Leukosit Total
Kondisi Visual (106/L atau per Protein Sitologi
µl) (g/dl)
Normal Kuning jernih <7.500 <2 Neutrofil 40-80%

Abses abdominal Kuning kecoklatan, 15.000-250.000 4-6,5 Neutrofil dengan sedikit


bercak darah perubahan denegerasi,
± cocci gram +
intraseluler

Impaksio kolon Kuning jernih 3000-15.000 <3 Neutrofil, kondisi


sederhana pada morfologi bagus
kuda

Enteritis anterior Kuning, kental, <10.000 3-4 Neutrofil, kondisi


serosanguineus morfologi normal

Strangulasi usus Merah kecoklatan, >5.000-50.000 2,5-6 Neutrofil, perubahan


halus bercak darah degeneratif
sedang/berat
Isi intestinal Hijau, kental, banyak <1.000 bervariasi Beberapa sel, banyak
(ruptura intestinal) partikulat bakteri bebas (gram -
dan gram +)

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Fecal examination
• Volume
– Normal 30-50 kg/d, interval 1-2 h
– Decrease/increase
• Color
– (diet, bilirubin, transit time)
– hemorrhage
• Odors
– Normal feces have no odors
• Consistency
– Cair/lembek(paste)/dry-firm
• Substante in feces
– Mucous, gelatinous, undigested material
– Blood stain, melena

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Liptank test

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DISEASE OF
PHARYNGEAL
AND
ESOPHAGUS

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Diseases of pharyngeal and
esophagus
• Pharyngeal and esophagus lesions is important
features of systemic diseases
• Primary lesions pharyngeal and esophagus less
common, but present serious medical problems
when they do occur
• Causes pharyngeal and esophagus lesions
– Infectious agent and physical trauma
– Chemical irritants, mycotoxic agent, parasitic larvae
– Neoplastic and developemental defect

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pathogenesis
• Pharyngeal paralysis
– suspect rabies
– Botulism also may cause pharyngeal paralysis
• Pharyngeal abcesses seringkali mengganggu refleks menelan.
• Faringitis sering berkaitan inflamasi saluran pernafasan atas.
• Esophageal erosion
– BVD, MCF
– Careless use of balling gun, syring, stomach tube
– Ingestion of large or sharp foreign bodies and some plants (sharp awns or barbs)
– The larvae of Hypoderma lineata cause severe tissue necrosis
– Some mycotoxin Trichothecene group, T-2 toxin produced by Fusarium tricinctum
and Stachyobotryo toxin produced by (Stachybortys arta) are epithelionecrotic
• Ingestion of certain type of foreign objects cause obstruction in PE
– Sites : cervical esophagus, thoracic inlet, over the base of heart, anterior to the
cardia of the stomach
– Lead to necrosis, esophageal stricture
• Limphomatosis lesion and peripharyngeal abcesses cause dysphagia or
obstruction in PE

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Clinical signs
• Acute inflammation in the region of pharynx:
– Local pain, dysphagia, depression and anorexia.
• Obstruction or paralysis of PE
– Inability to swallow, regurgitation of ingested food and water
through the nostrils, rumen tympany.
• Esophageal obstruction
– Acute : severe distress, anxiety and obvious violent at
swallowing
– Chronic : depression, dehydrated and hypersalivation
• Signs of local pain subside, the animals makes repeated
attempts to drink water and eat.
• PE obstruction maybe incomplete depending on the
specific cause and clinical signs will be modified
accordingly.
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diagnosis
• Diagnosis can be very difficult
– Differentiate primary obstructive with secondary lesions
• Pada kasus tanpa komplikasi, diagnosis dapat
ditegakkan base on anamnesis, oral and pharyngeal
inspection and esophageal exploration by stomach tube.
• Pada kasus yang mengalami komplikasi or chronical
lesions seperti pembesaran kelenjar limfe, esophageal
stricture, cacat perkembangan can more difficult.
• Radiography or esophagoscopy mungkin berguna tapi
diagnosis yang akurat sangat bergantung pada
pemeriksaan nekropsi.

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treatment
• Secondary FE lesion depend on treatment of the
primary condition.
• Foreign bodies obstruction can be relieved by
various mean (esophagotomy, esophagoscopy)
depending on location and the degree of
obstruction.
• Prognosis
– Persistent lesions : infausta
– bergantung kemampuan mengatasi nekrosis, striktura
atau perforasi yang terjadi.
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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 fore stomach
• 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
• Dairy cattle : unlimited silage
• Beef cattle :
– pakan yang masam (hasil fermentasi) atau feeder
– feed aditive : anoreksia memicu terjadi IS
– Variable signs depend volume and adaptation capability
– SI juga sering ditemukan berkaitan penyakit lain : pneumonia, retikulitis

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pathogenesis
• Rumen atony :
– Increase or decrease ruminal pH
– Intake bahan bahan yang sulit dicerna dalam
jumlah besar
– mengkonsumsi pakan yang masam/basi
– histamine (intrinsic or extrinsic)
• Sebab pasti mengapa terjadi atoni masih
belum diketahui dengan jelas.

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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 atau flock, decreased physical activity or alertness
– sulit dideteksi kecuali sapi yang sudah dikenal tingkah lakunya.
• Perubahan suhu tubuh tidak nyata
• Rumen stasis (reduction in the strength and frequency of
contraction) : palpation or auscultation
• Intestinal motility is 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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diagnosis
• Diagnosis base on clinical examination and on
rulling out other, more serious disease problems
• Careful evaluation of history. sangat berguna.
• Differential diagnosis
– Milk fever
– Early stage of lactation ketosis
– RPT
– LDA

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treatment
• Spontaneously resolve in 24-48 h
• Bila diperlukan dapat dilakukan
convensional treatment and supportif.
– If rumen is acidic : Magnesium hydroxide
(225-450 g) per adult animal
– If rumen is alakaline : 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
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Ruminal acidosis
• Sinonim : grain overload, rumen overload,
lactic acidosis, acute rumen engorgement
• Causes : highly fermentable feed or high
protein mudah cerna
• Sering terjadi pada pemeliharaan intensif

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Grain

rice barley hulled


corn

oat groat wheat berries


buck groat

rye berries spelt hulled


millet

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↑ KH yang mudah difermentasi

↑ laju pertumbuhan (semua bakteri)


↓ pH < 5

↑ VFA’s

↓ pH
↓ laju pertumbuhan ↓ S. bovis
(sebagian bakteri) ASIDOSIS ↑ Lactobacillus
RUMEN ↑ laju pertumbuhan S. bovis
↑ asam laktat

↓ pH

Stasis fermentasi

Absorbsi D/L asam laktat

Asidosis Metabolik
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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 and abdominal pain
– abdominal distension.
• Dehydration will done in 24-48 hours

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Clinical signs
• Diarrhea (tidak teramati bila hewan lebih dahulu
mati). Profus diarrhea akan terjadi pada hewan
yang tidak mengalami depresi yang parah.
• Ambruk (severe case) karena kelemahan and
toxemia in 24-48 hours.
– increased respiratory rate due to acidosis
– hypothermia
– weak pulse. Sapi ambruk diam tidak bergerak( seperti
signs hipokalsemia
– Daerah muzzle (mukus dan tampak kotor)
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Clinical signs
• Bila terjadi pada sekawanan sapi (herd)
– 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 24-48 hours, tapi banyak
kasus ditandai dengan signs membaik
namun suddent death due to secondary
complication. Jarang terjadi kasus
melanjut dalam 3-4 minggu.
• Resolve : bad conditition due to chronic
rumenitis and hepatic failure.

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diagnosis
• Diagnosis base on history and physical
examination
– Detail anamesis dan cermat sudah dapat menduga
– Mistake : pola pakan yang dikonsumsi tidak diketahui
dengan baik atau tidak dicurigai
• Laboratory tests
– rumen ingesta, plasma and urine pH
• Differential diagnosis
– Polioencephalomalacia
– Urolithiasis
– Peritonitis
– Parturient paresis (other diseases with depression)
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treatment
• Mild cases : spontaneous recovery
• Severe cases : treatment intensif (kerusakan
jaringan, perubahan fisiologis)
• Rumen emptying: oral lavage or rumenotomy
• Antasid peroral (magnesium carbonate or
magnesium hydrokside)
– Inisial dose 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 (isi rumen dapat dikurangi)
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treatment
• Rehydration and improve blood pH
– balance electrolyte solution and 5% sodium
bicarbonat IV
– Sapi 450 kg dengan tingkat dehidrasi 10% (cairan 50
liter dalam 2 jam) Sodium bicarbonat diberikan
dengan kecepatan 0,5 mEq/kg BB dan diulang dalam
24 jam bila perlu
– Memperbaiki pH darah merupakan hal vital meskipun
telah melakukan pengosongan rumen.

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treatment
• Antihistamine dapat dipertimbangkan
• Recently research
– thiabendazole with normal dose can control
secondary mikotic 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
• Vagal indigestion, chronic indigestion, vagus indigestion,
Hoflund’s syndrome
• 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)
• Distenended abdomen is a cardinal sign.
• Gangguan :
– Mechanical
– Functional

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pathophysiology
• Similarly with RPT atau tumor (lymphosarcoma
abomasum), abomasum torsion.
• Reticulum adhesion lesion (contraction,
eructation)
• Failure omasal transport (feces, undigeste, mild
dehydration) Physial obstruction (placenta,
plastic bag) or tumor
• Abomasal impaction (secondary)
• Kaitan dengan kebuntingan (compress digestion
organ, mempengaruhi aliran)

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Clinical signs
• Sebagian besar indigesti kronis progresif
– Anoreksia
– atoni rumen, pasase feses turun
– Distensi berat pada rumen bila penyakit telah melanjut.
– Hewan sangat haus akibat stasis rumen dan akumulasi cairan di
rumen.
• Jika obstruksi termasuk pilorus, abomasum will very
distense
– Abdomen tampak penuh tapi rumen atoni dan kosong
– Terjadi pengosongan isi abomasum masuk ke rumen dan terjadi
penumpukan klorida di dalam rumen.
• Gastric obstruction or cranial intestine intestinal akan
menyebabkan alkalosis dan dehidrasi berat dan
turunnya berat badan

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diagnosis
• Chronic indigestion suspected vagus indigestion
• Kasus LDA :
– abdominal distention sebesar indigesti vagus
– gases accumulation (percussion and auscultation)
• Other obstuctions (abomasal torsion, RDA) :
– acute
– dapat dibedakan melalui palpasi/eksplorasi rektal.
• Kasus ulserasi abomasum berat
– signs serupa
– kondisi obstruksi lebih parah
– feses penderita ulserasi abomasum tampak hitam/gelap,
menyerupai tar akibat perdarahan abomasum.

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treatment
• treatment biasanya tidak berhasil dengan
baik
– sangat sulit menghilangkan kausa primer
• conservative treatment
– mineral oil everyday (4 liter perday for adult
cow)
– systemic parasympatomimetic akan
memperbaiki sebagian dan bersifat temporer
(incomplete obstruction).
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treatment
• Emptying abomasum
– abomasotomy juga dapat menolong sesaat
– abomasum motility tidak pulih except bila
masih ada tersisa inervasi syaraf vagus
• Alternative : slaughter

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RPT
• Sinonim : hardware disease, traumatic
gastritis
• Most common in adult cows
• Goats and sheeps (lebih jarang karena
perilaku makan mengambil pakan yang
berbeda dengan sapi)

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pathophysiology
• Foreign bodies (dimakan, berkumpul di
retikulum, local peritonitis), pembentukan
fibrous tisuue (ikat)
• Akibat 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
• Headn and neck extension, arching back
• Berdiri dengan kaki depan abduksi
• Increase temperature (39.5-40.5 oC), and pulse
80-90 bpm
• Respirasi dangkal cepat
• Decrease rumen motility/atony
• Feses small, firm, dry and dilapisi mucus

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Clinical signs
• Peritonitis lokal kronik
– signs awal taa
– 24-48 jam
– Fungsi gastrointestinal menurun, tidak ada
signs spesifik.
– Vital sign normal

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diagnosis
• Rectal examination : small and hard rumen, bila
viscera didorong ke depan hewan kesakitan
• Wither pinch test
– Normal : ventrofleksi
– Abnormal : not ventrofleksi and feel pain
• Abdominal pain : tekan/tinju xiphoideus, angkat
bagian toraks, tekan dengan lutut bagian ventral
toraks
• DD
– IS, Asidosis rumen, LDA, Abomasal ulceration,
hepatic abcess, pyelonephritis

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treatment
• Rumenotomy or laparotomy
• Antibiotics
• Fluid therapy (isotonic polyioni)+ calcium
• Prevention :
– Perhatikan padang rumput agar bebas dari
benda asing (paku, kawat, dll)
– Pemberian magnet
– Indonesia (dirumputkan : aman)
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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
• Sinonim, tympani

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DISEASE OF
ABOMASUM
AND INTESTINE

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DISEASES OF
ABOMASUM DAN INTESTINE
• Left Displaced Abomasum
• Right Displaced Abomasum
• Abomasal impaction
• Intussusception

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LDA
• Left displaced abomasum (LDA) adalah kondisi
dimana terjadi abomasum yang seharusnya
terletak sedikit bagian kanan ventral abdomen,
berubah posisi ke sebelah kiri abdomen, antara
rumen dan dinding abdomen kiri.
• Sapi perah, khususnya paro umur (4-6 tahun)
dan baru laktasi
• Jarang terjadi pada pejantan, sapi dara, atau
sapi potong. Kadang terjadi pada sapi bunting
dengan tingkat insidensi rendah.

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Clinical signs
• Stadium awal signs tidak teramati
• Sebagian besar mengalami anoreksia, sapi
enggan makan biji-bijian (grain) namun masih
mau makan hijauan. Bila kondisi berlanjut,
terjadi penurunan berat badan dalam beberapa
minggu.
• Produksi susu turun bertahap (agalaktia)
• Sebagian besar akan mengalami ketosis
(sekunder)
• Feses bervariasi dari keras hingga normal

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Clinical signs
• Sebagian besar mengalami metabolik alkalosis.
(beberapa menderita metabolik asidosis atau
kondisi asam basa normal)
• Serum kalsium pada batas bawah, fosfor dan
magnesium normal atau sedikit meningkat.
Glukosa darah turun atau meningkat.
• Glukosuria terjadi bila kadar glukosa darah
meningkat. Ketonuria merupakan manifestasi
ketonemia karena peningkatan serum NEFA.

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diagnosis
• Auscultation and
percussion
• Liptak 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
• Medical treatment tidak memberikan hasil yang
diharapkan
• Rolling : abomasal reposition
– economic reason and client
• Surgery
– left flank abomasopexy
– right flank omentopexy
– right paramedian abomasopexy
– right paramedian percutaneous toggle pin (bar suture) fixation.
• Prevention
– feeding management
– beri pakan dalam jumlah kecil dan lebih sering (frekuen)
– kurangi resiko menderita penyakit peripartus
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RDA
• Right displaced abomasum (RDA) dikenal
juga dengan istilah 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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diagnosis
• diagnosis based on history and physical
examination. Liptank test sangat
membantu untuk 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
• treatment medis dapat diberikan smooth muscle
stimulant, namun pembedahan tetap merupakan
pilihan utama. Bila mungkin pembedahan tidak
ditunda, karena RDA dapat segera berkembang
menjadi abomasal torsion /volvulus.
• Rolling untuk mereposisi abomasum tidak boleh
dilakukan karena akan menyebabkan abomasal
torsion/volvulus.
• Pembedahan dapat dilakukan dengan teknik
right flank omentopexy or right paramedian
abomasopexy.
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Abomasal Impaction
• = impaksio abomasum
• Abnormal accumulation of solid ingesta in abomasum
• Causes : abomasal musculatory disorder sehingga tidak
dapat berkontraksi sebagaimana mestinya
– Unproper dietary
– Corpora aliena
• Signs tidak teramati dengan jelas hingga stadium
terminal karena penyakit berjalan secara bertahap
• Sering terjadi pada beef cattle, but can due to dairy
cattle.

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Bentuk spesifik
• Primary :
– Ingesti bahan pakan kasar dan tidak mudah cerna dalam jumlah
besar
– Benda asing yang terperangkap dalam abomasum, memicu
impaksio abomasum primer.
– Plasenta yang ditelan induk kadang tersangkut di abomasum,
membuntu pilorus sehingga terjadi impaksio
– Pedet kurang mendapat nutrisi, eat bedding or straw.
– Pedet senang menjilat rambut, kadang menelan rambut dalam
jumlah besar sehingga terbentuk trichobezoar (gumplan rambut)
yang memicu terjadi impaksio.
• Gangguan fungsi muskulatur abomasum sehingga tidak
dapat memompa makanan masuk ke dalam intestinal.
Kondisi ini dikenal sebagai bentuk sekunder impaksio
abomasum.
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signs klinis
• Di negara 4 musim, sapi potong pada musim
dingin (terbatas pemberian air dan kualitas
pakan yang buruk)
• Rambut tumbuh panjang kadang menutupi
kondisi tubuh yang kurus. Abdomen mengalami
distensi akibat ingesti sehingga sapi berbentuk
membulat, seakan-akan gemuk. Sapi tersebut
sering diduga gemuk dan sehat namun bila
diperiksa dari dekat sapi sangat kurus.

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signs klinis
• Cardinal signs :
– Abdominal distension pada sapi-sapi yang kurus dan dehidrasi
– Feces reduce in volume and hard and dry.
• Temperature, pulse and respiratory rate usually normal.
• Cow mengalami hipochloremia, metabolic alkalosis.
Dehidrasi akan meningkatkan gambaran PCV dan total
protein. Namun kondisi tersebut ditutupi akibat anemia
dan hipoproteinemia akibat kelaparan/kekurangan
nutrisi. Sehingga gambaran PCV dan total protein
seakan-akan normal.

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diagnosis
• Abdominal distention must differentiated with vagal
indigestion.
– vagal indigestion : isi rumen dan abomasum biasanya normal
(cair), yang dapat dibedakan melalui ballottement dibandingkan
dengan impaksio abomasum yang isinya keras. Ada signs-signs
yang bertahap (gradual) dan bahan pakan/nutrisi yang buruk
dapat mengarahkan pada penyakit ini. Pemeriksaan rektal
biasanya ditemukan rumen mengalami distensi dengan isi yang
padat dan berbentuk “L”. Abomasum biasanya tidak teraba.
• Malignant lymphoma abomasum juga dapat
menyebabkan pembesaran dinding abomasum dan
terjadinya akumulasi ingesta
– Hal ini dapat dibedakan dengan ditemukannya peripheal
limphadenopati and limphocytosis.

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treatment
• Individual treatment will effective on early stage.
– Magnesium hidroxide or magnesium sulphate
administration berguna untuk mengeluarkan isi
abomasum
– Pelunak feses seperti minyak mineral atau dioctyl
sodium sulfosuccinate (DSS) efektif untuk
melunakkan ingesta
• Rumenotomy : severe case and chronic
– isi rumen dikeluarkan
– abomasum ditreatment minyak mineral atau DSS
(stomach tube)
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treatment
• Abomasotomy : banyak complication dan hasil
tidak sesuai harapan
• treatment suportif, peroral or parenteral fluid
therapy dapat membantu memulihkan kondisi
dehidrasi. Selain itu juga dapat diberikan
glucose and amino acid secara parenteral as
supprotif treatment. Pada kasus yang lanjut
akibat kekurangan nutrisi, tidak ada respon yang
bagus terhadap treatment yang diberikan
• Agar berhasil maka treatment harus dilakukan
sedini mungkin, sebelum penyakit berlanjut dan
getting worse.
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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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Clinical signs
• Observation or inspection
– evidence of 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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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
• Elektrolytes deficits (hypokalemia,
hypochloremia) may occur due to pooling
of gastrics fluid
• Significant gastric reflux is common
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diagnosis
• Gastric rupture :
– immaediate reduction in pain, followed by progressive
deterioration of clinical signs (shock)
– abdominocentesis reveal evidence of ingesta and
bichemical 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)
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treatment
• Priority : gastric decompression
• Technique : nasogastric. Masukkan selang
dari hidung hingga ke dalam lambung.
Masukkan 500-1000 ml air hangat untuk
mempermudah melakukan flushing.
Selanjutnya segera ambil (hisap) isi
lambung. Lakukan berulang-ulang hingga
lambung tidak lagi mengalami distensi.

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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 or
Detomidine 10-20 µg/kg IV, Flunixin
meglumin 0,25 mg/kg IV.

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DIARRHEA AND
ENTERITIS

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DIARE DAN ENTERITIS
• Diare adalah terjadinya perubahan
frekuensi dan viskositas feses

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Patofisiologi
• Mekanisme diare terbagi dalam 5 macam
• Bahan hiperosmotik dalam
gastrointestinal, diare sekretoris, adanya
hambatan absorbsi, perubahan
permiabilitas mukosa dan perubahan
motilitas.

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Patofisiologi
• Diare osmotik dapat terjadi :
– bahan-bahan yang sulit diabsorbsi (magnesium sulfat
atau magnesium hindroksida), maldigesti karena
infsufisiensi pankreas dan cacat pada mukosa yang
mengakibatkan naiknya tingkat osmosis dalam
lumen. Pedet yang menderita cacat tidak mempunyai
enzim sukrase dalam mukosanya, bila diberi pakan
yang mengandung gula (sukrosa) akan mengalami
peningkatan osmosis dalam lumen sehingga terjadi
diare.

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• Diare sekretoris adalah meningkatnya sekresi elektrolit secara pasif
dari mukosa ke dalam lumen intestinal.
• Nutrisi, elektrolit dan air secara konstan akan diabsorbsi melalui vili
dan masuk ke dalam sirkulasi, kemudian air dan elektrolit akan
disekresi kembali ke dalam lumen sehingga terjadi bidirectional flux
melintas mukosa. Pada kasus inflamasi (Salmonellosis, BVD,
Johne’s disease dan invasi E. Coli) atau penyakit non inflamasi
(heart failure, limfosarkoma, obstruksi vena kava posterior, dan
amyloidosis) terjadi peningkatan sekresi ke dalam lumen intestinal,
sehingga mengganggu keseimbangan sekresi-absorbsi dan
menimbulkan diare. Pada kasus non inflamasi mungkin berkaitan
dengan meningkatnya tekanan hidrostatik akibat pengaruh venous
return atau menurunnya tekanan plasma onkotik pada kasus
amyloidosis.

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Patophysiology
• Absorbsi elektrolit dan air akan terganggu dengan adanya
kerusakan mukosa, toksin dan menurun transit time. Virus-virus
enteropatogenik (BVD, coronavirus, rotavirus), bakteri (E. Coli,
Salmonella sp.) mempengaruhi sel-sel epitel intestinal sehingga
menyebabkan bentuk malbasorbsi air dan elektrolit.
• Hambatan atau menurunnya absorbsi air dan elektrolit, merupakan
faktor penting pada perkembangan penyakit yang menimbulkan
diare. Pedet yang menderita coronavirus akan mengalami diare
secara parsial. Kondisi ini terjadi akibat sel-sel yang sudah pulih dan
berfungsi sementara yang lain masih rusak akibat replikasi virus,
menghasilkan akumulasi cairan digesti dan akan mencerna
sebagian susu dalam lumen. Infeksi selanjutnya merusak sel-sel
columnar yang berfungsi efektif mengabsorbsi dan menyisakan
epitel squamus atau cuboid yang tidak berfungsi efektif
mengabsorbsi. Sel-sel tersebut tidak mempunyai enzim-ensim
digesti dengan demikian menurunkan fungsi absorbsinya.

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Patofisiologi
• Permiabilitas mukosa dipengaruhi oleh adanya perubahan pada
area permukaan seperti terjadi pada coronavirus, sindroma
malabsorbsi, Johne’s disease dan limfosarkoma karena mukosa
terjadi infiltrasi sel-sel neoplatik. Faktor yang meningkatkan tekanan
jaringan seperti inflamasi, obstruksi limfatik dan menurunnya
tekanan koloid onkotik akan mengubah permiabilitas mukosa dan
menyebabkan diare.
• Borborigmus adalah suara yang dihasilkan dari bercampurnya gas
dan cairan dalam lumen yang dapat didengar saat auskultasi.
Borborigmus tidak sinonim dengan aktifitas peristaltik.
• Suara borborigmus didengar dari hewan dg pasase feses normal
• Kondisi diare tidak terdengar suara borborigmus
• Sebagian besar diare berkaitan dengan gangguan motilitas dan
kondisi ini akan meningkatkan volume intraluminal. Peningkatan
volume akan menurunkan transit time dan menimbulkan diare.
Meningkatnya aktifitas propulsif sangat jarang pada kasus diare.

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treatment
• Langkah utama treatment pada kasus diare akut :
REHIDRATION.
– treatment cairan untuk mengganti air dan elektrolit. Pemberian
larutan glukosa dan elektrolit peroral berhasil dalam mengobati
kondisi dehidrasi. Sebagian besar larutan elektrolit peroral
diformulasi untuk treatment diare.
• treatment antidiare nonspesifik seperti derivat opiate
(mempengaruhi motilitas intestinal) akan meningkatkan
kontraksi segmental sehingga lebih lama menahan laju
aliran ingesta dalam intestinal.
• Absorban (kaolin dan pektin) dapat mengabsorbsi toksin
dan bismuth salisilat dapat mengurangi hipersekresi
intestinal.

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treatment
• Broad spectrum antibiotics : primer diare karena
infeksi.
– resisten terhadap sebagian besar antibiotika (tidak
efektif
– diare pada pedet biasanya lebih kompleks ( interaksi
virus, bakteri dan defisiensi kekebalan). Antibiotika
tidak banyak memberikan respon positif pada kasus
virus dan defisiensi kekebalan, (cukup baik pada
kasus enterotoksemia kolibasilosis)
• Antibiotika dapat diberikan peroral dengan hasil
baik (dalam 36 jam)
– Penggunaan tak terkontrol dan jangka panjang
sebaiknya dihindari.
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treatment
• Indikasi pemberian antibiotika secara
parenteral bila terjadi septikemia (broad
spectrum antibiotics : chloramphenicol,
gentamycin atau nitrofuran)
• Penggunaan antibitotika tanpa kendali
menyebabkan terjadi resistensi kuman.

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DISEASES OF
COLON AND
RECTUM

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DISEASES OF
COLON AND RECTUM

• Proctitis
• Rectal strictura
• Prolapse rectum

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Proctitis
• Iatrogenik proctitis and tenesmus : cow
getting diarrhea due to use of plastic glove
in rectal exploration
• Prevention : epidural anesthesia and use
rubber glove (untuk bedah) after
menggunakan glove plastik with enough
lubrication. Xylazine or probanthine
bromide (30 mg/454 kg IV) administration
help rektum relaksasi.

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Proctitis
• Ruptura rektum dapat terjadi bila
perlakukan pemeriksaan rektal sangat
kasar dan tidak hati-hati, atau pada
parturisi (proses kelahiran).
• Peritonitis terjadi akibat dari perforasi
rektum. Namun kadang hanya terjadi
abses peripelvis akibat perlukaan
ekstraperitoneal rektum dan akan
menimbulkan sikatrik jaringan.

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Rectal strictura
• Rectum constriction karena jaringan parut akibat
perlukaan atau trauma pada mukosa, striktura
akibat lesi lokal, abses peripelvis atau nekrosis
dan cacat turunan yang berhubungan dengan
striktura vagina dan rektum.
• Rectal strictura syndrome pada babi merupakan
konstriksi rektum fibruous anular perolehan (2-5
cm anterior anus) yang menyebabkan konstipasi
kronis. Penyakit ini juga ditandai emasiasi yang
progresif dan timpani abdomen dengan feses
berbau.
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Rectal Prolapse
• Rectal prolapse usually due to tenesmus.
• Hereford have the highest rectal prolapse
incidence.
• Diagnosis mudah diketahui, namun agak sudah
ditreatment.
• Epidural anesthesia to reduce tenesmus
followed by jahitan purse-string untuk mencegah
rektum kembali keluar.
• Bila memungkinkan bagian belakang tubuh sapi
diposisikan lebih tinggi dari bagian anterior.

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Feed Impaction
• The most common form of colonic obstruction
• Frequent cause of colic
• Causes the impaction is not well established
• Motor dysfunction that disrupts bowel motility,
stress, diet (poor quality roughage) or dietary
change, poor dentition, parasites and possibly
decreased water intake.

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Clinical signs
• Mild to moderate abdominal pain is usual. Progress to
severe pain if left untreated (over several days, unlike
the more rapid succession of events with small bowel
obstruction)
• Heart rate maybe low initially. Progresive increase if
obstruction is not resolved (>50/65 beat/min).
• Abdominal distension maybe seen in association with
gas accumulation.
• Degree of dehydration is variable.
• Moderate to severe decrease in gastrointestinal sounds,
which progressively worsen over 1 to 2 days.

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diagnosis
• Rectal examination reveal a firm mass in the transverse
colon dan find gas filled large colon.
• Hematology and plasma biochemistry show few changes
(increase total protein). Acid-base status is usually
normal.
• Abdominocentesis is usually unremarkable (increase in
total nucelated cell count and mild increase in protein
concentration).
• Differential Diagnosis
– enterolith impaction, sand impaction, large colon displacement or
torsion, smal intestine obstruction or strangulation, acute colitis,
cholelithiasis, peritonitis, pluropneumonia.

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treatment
• Analgesics
• Fluid therapy is essential to correct dehydration and to soften the
impaction
• If gastric reflux is not present and there is evident of guts sounds,
fluid can be given by nasogastric or intravenous. (Isotonic polyionic
fluids 65-100 ml/kg/day IV).
• Laxatives : mineral oils or DSS (foreign bodies impaction are difficult
distinguish from food impaction).
• Medical therapy continued up to 5 to 7 days if :
– Pain is limited or easily controlled
– The horse voluntarily consumes fluids
– There is no deterioration in the animal metabolic status
– There is no significant increase in abdominal fluid total nucleated cell
cont or protein concentration.
• Deterioration in any of these signs constitues an indication for
surgery.

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Colonic volvulus
• Severe torsion (>270 degrees) of the large colon
and vascular compromise and tissue
devitalization are potent stimuli abdominal pain.
• Although less severe torsions do occurs,
corretion almost invariably requires surgical
intervention. Survival following surgery remains
low (30%).
• The etiology remains controversial. Some
speculate that brood mares are more commonly
affected related to parturition. However, this
association is not proven.
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Clinical signs
• Variable abdominal pain with severe
torsions, producing extreme, uncontrolled
pain.
• Physical examination : increase heart rate
(>75 beats per min).
• Progressive abdominal distension occurs
over several hours
• Dehydration is common, with signs of
cardiovascular compromised and shock.
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diagnosis
• Abdominal fluid analysis are variable
– increased in total nucleated cells, protein and
hemoglobins
– In the others, there are few change. Do not
reflect the extent of tissue devitalization that
has occured
• Rectal examination reveals a distensed
large colon. The colonic wall may feel
thickened (edema).
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diagnosis
• Diagnosis maybe confirm base on clinical
signs dan rectal examination. In others,
diagnosis is not confirm until an
exploratory celiotomy or necropsy is
perform.
• Differential diagnosis, other obstructive
disease of the large colon
– large colon displacement, small intestine
obstruction or strangulation, acute colitis,
peritonitis.
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treatment
• Initial therapy
– Pain control
– Reconstitution of the circulating volume with IV fluid
administration and therapy for endotoxemia (medical
managenet for colic).
• Surgery is required to correct the torsion, and
horse with suspected torsion should be reffered
to a surgical center
• Euthanasia constitutes a rational alternative in
cases where owners do not want surgical
intervention.
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Thank
You

khi 322 - triakoso

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