Abomasal and Gastric Disease Flashcards
describe abomasal disease
2 categories:
- outflow obstruction:
-mechanical
–cattle: displacement, volvulus, impaction, pyloric obstruction, other intestinal obstructions
–camelid: pyloric bezoar
-functional
–cattle: vagal indigestion
–sheep: abomasal emptying defect of Suffolk
- inflammation/ulceration: ruminants and camelids
describe signalment/history of outflow obstruction
- dairy cows during early lactation: abomasal displacement and volvulus
- beed and dairy calves 3wks - 4 months: abomasal displacement and volvulus
- Suffolk sheep: abomasal dilation and emptying defect
- wintering, pregnant beef cattle: abomasal imapction
- pregnancy: vagal indigestion pyloric outflow failure
describe PE for outflow obstruction
- shock: not super common
-exception: abomasal volvulus - abdominal contourL overtime progress toward papple/L shape
- pings: displacements and volvulus
- rumen fluid: increased chloride with internal vomiting (abomasal reflux into rumen)
- clin path:
-with obstruction and time: hypochloremic metabolic alkalosis
describe pathophysiology of abomasal displacement and volvulus
- decreased motility: distension with gas from microbial fermentation
- concurrent diseases and changes that occur postpartum increase!
-ketosis, hypocalcemia, milk fever, retained placenta, mastitis, fatty liver, hyperinsulinemia
-changes in diet, exercise, abdominal fill
-60% in 1st two weeks, 80% in 1st month, 90% in 1st 6 weeks - sporadic in calves, dairy bulls, and beef cattle:
-FB, and rocks/sand predispose for LDA
describe LDA, RDA, AV
clinical signs:
1. drop in milk production
2. decreased appetite (concentrate 1st)
3. decreased feces
PE:
1. AV tend to have more signs of systemic shock
2. ping: canNOT differentiate RDA and AV IN ANY WAY OTHER THAN SX!!!!! (but AV in an emergency, which means an RDA is also an emergency!!)
3. rectal: AV more common to feel than others
clin path:
1. urine ketones
-AV usually have more severe electrolyte and acid-base abnormalities
CMT: should do on every dairy cow!
treatment:
1. correct and maintain position
2. blind, open, laparoscopy
3. RDA or AV emergency sx
prognsis:
1. LDA, RDA good, AV fair to good
2. underlying disease important, can develop motility disorders (esp AV)
prevention: dietary management, slow intro of concentrate, DCAD to prevent hypocalcemia
describe pathogenesis of abomasal impaction
- accumulation of ingesta in abomasum
- mechanical:
-abnormal, dry contents: poor quality roughage with decreased water intake (severe winter weather range cattle), hair, placenta, sand, gravel
-mural lesion: lymphosarcoma (like uterus, retrobulbar, spinal, heart, abomasum), abscess
-extramural lesions: masses (fat necrosis), adhesions
- functional:
-vagal indigestion
-TRP
-late pregnancy
-perforating abomasal ulcers
-AV
describe clin signs, PE, and clin path of abomasal impactions
clinical signs:
1. progressive anorexia
2. decreased fecal output
3. loss of condition
PE:
1. right or bilateral ventral or papple/L shaped distension
2. ballotment of abomasum right cranial abdomen
clin path:
-dehydration and electrolyte abnorm over time
describe treatment and prognosis of abomasal imapction
treatment:
1. medical mgmt:
-digestible feeds
-fluids
-laxatives
- +/- prokinetics
- sx tx difficult
prognosis:
1. overall poorL often caught late in disease, sx rarely successful
2. dairy cows limited to pyloric antrum tx medically can have good prognosis
prevention: attention to feeding, shelter, water in severe winter conditions
describe pathophysiology of vagal indigestion
- pyloric outflow failure causes accumulation of ingesta in abomasum and omasum
- initially, reticulorumen function normal, but with time abomasal contents back up and distension develops, leading to changes in ruminal contents and motility
- predisposing conditions:
-AV (also L/RDA)
-inflammation and adhesions of abomasal fundus or reticulum
-advanced pregnancy with large fetus
describe clinical findings of vagal indigestion pyloric outflow failure
- weight loss, abdominal distension, decreased fecal production, decreased appetite
- dehydration, electrolyte, acid base generally mild due to slow development
describe abomasal dilation and emptying defect of Suffolk sheep
pathophys/epi
- mainly suffolk sheep (but not rly hereditary)
- mech unknown:
-possible acquired dysautonomia
-contents often similar to ventral rumen contents, pylorus patent, ingesta present in distal GI tract
describe clinical presentation and prognosis of abomasal dilation and emptying defect of Suffolk sheep
clin presentation:
1. anorexia, weight loss
2. other signs: water green diarrhea or normal feces, ruminal tympany, ventral abdominal distension (pear), +/- changes to ruminal motility, ballotment of mass right cranial ventral abdomen
- clin path; min changes (hypocalcemia), increased rumen chloride usually
prognosis: generally poor
1. some success with sx and prokinetics
2. most die of cachexia
describe abomasal ulcers
- lesion that penetrates basement membrane of abomasal mucosa
- 4 grades based on depth in cattle
I: non perforating
II: non perforating but bleeding
III: perforating, local peritonitis (subset omental burstitis)
IV: perforating, generalized peritonitis
describe incidence and predisposing factors of abomasal ulcers
all ages of cattle, rarely sheep and goats, camelids C3 glandular portion
type 1:
-veal calves, 2-8wk old calves, weanling calves, and fattening cattle, as well as high producing dairy cows
-stress, changes in housing or feed, straw ingestion, infectious agent
-high incidence but often subclinical so true incidence unknown
type II:
-lymphosarcoma related: >5 years, throughout lactation period
-non-LSA related: <4 yrs, early lactation, concurrent postpartum disease
type III/IV:
-sporadic in adult cattle, often related to metabolic stress with one or more concurrent dz, high concentrate and corn silage diets
calves:
-veal and beef calves, 4-12 wks, yearling feedlot
-most symptomatic are perforating
-predisposing factors: nutritional deficiencies, bacterial and fungal agents, abrasive agents, stress
describe clinical signs, diagnostics, bloodwork, and BLV testing for abomasal ulcers
SEE CHART progress from less to more systemically ill
other clin signs: in calves of perforating seem to be severe, rapidly progressive
other dx:
-abdominocentesis
-abd US
bloodwork:
-CBC: inflam with peritonitis, anemia, hemoconcentration
-chem: stasis with hypochloremic, metabolic alkalosis, shock with acidosis
BLV testing: >5 year old with type II
describe treatment and prognosis of abomasal ulcers
treatment:
1. correct dietary problems, reduce stress, tx concurrent dz
2. supportive care includes transfusion if indicated
3. treat peritonitis
4. medications to reduce acid in abomasum: some oral may work in calves, not so much in adult and IV often ocst prohibitive
prognosis:
1. good for type I
2. okay for type II and III if get under control, but often lose that cycle of lactation
3. poor for type IV or LSA related type II
describe gastric disease in horses
- outflow obstruction
-mechanical
-functional
-ddx: gastric impaction, pyloric obstructions (neoplasia, abscess, pyloric stenosis), secondary to SI disease - inflammation/ulceration
- rupture
describe gastric impaction
- becoming relatively common dx
- pathogen:
-mech: bolus of poorly digested feed, phytobezoar persimmon seeds
-functional: ocncurrent with other GI dysmotility - clin signs:
-inappetence MOST COMMON BUT VAGUE
-colic: acute and recurrent (relapse as refeeding)
–variable severity, signs may worsen with NG tubes and/or fluids
-more chronic forms with dysmotility may have displaced spleen on rectal (significantly enlarged)
describe treatment for gastric impaction
- supportive care: correct fluid, acid-base e-
- enteral fluids and lavage
-good for smaller boluses of food that may be present related to other colic causing dysmotility or poor dentition/large fiber size
-not successful in very large, motility related impactions - other laxatives/agent to break up impaction:
-DSS, meat tenderizer, diet sugar-free decaf cola (persimmon seed impactions) - +/- motility agents
surgical access to stomach is poor!
describe equine gastric ulcer syndrome (EGUS)
- incorporates ulceration of distal esophagus, nonglandular (squamous), and glandular stomach, and proximal duodenum
- equine squamous gastric disease (ESGD)
-exposure to irritants: gastric acids, pepsin - equine glandular gastric disease (EGGD)
-acid injury
-compromise of protective mechanisms likely play a role
describe adult EGUS risk factors and clinical signs
risk factors:
-age, environment, training, concurrent GI disease, AE, diet, and environment
-induce ESGD: exercise, high concentrate low roughage diet, fasting, transport, stall confinement
clinical signs:
1. vague systemic: inappetance, poor BCS, weight loss, diarrhea, changes in behavior, poor performance
- other nonspecific: pain with tightening girth, stereotypic or abnormal behavior
- colic is common
- clinical signs of ESGD do not always correlate with presence or severity of ulcers
describe foal EGUS
- 25-50% prevalence, 2-6 months
- 4 clinical syndroms:
-subclin
-clin
-perforating
-gastric outflow obstruction secondary to pyloric stricture
describe clinical signs of foal EGUS
- bruxism, ptyalism, frothing or drooling milk
2 diarrhea: current or previous
- colic: roll into dorsal recumbency/dead bug’
- lethargy, unthrifty, interrupted nursing, tongue lolling
describe diagnosis of EGUS
- endoscopy = definitive
-ESGD: grading system, description (location, appearance: hyperemic, hemorrhagic, fibrinosuppurative, ulcerated, contour: depressed, raised, flat) - history, clin signs, response to empritic tx when not available
describe treatment of EGUS
- management changes:
-modify exercise intensity and duration
-increase pasture turnout
-eliminate bolus feeding and increase forage/fiber
-decrease CHO intake
-consider preventative dose of meds during increased risk times - pharmacotherapy:
- 4-6% resolve without tx
- acid reduction: proton pump inhibitors and H2 blockers (short acting)
- coating ulcers: sucralfate
- antacids: calcium carbonate, alfalfa
- PGE2 analog: misoprostol
describe pyloric stenosis in foals
clinical signs:
1. colic, reflux, regurg possible as obstruction becomes more severe
2. often occur as weaning/eating solid food
3. unthrifty, pot bellied
diagnosis:
1. endoscopy
2. contrast radiography: gastric emptying time
3. ultrasound: duodenal motility
treatment:
1. nutritional, gastric decompression, supportive care
2. surgery: bypass; prognosis great
describe gastric rupture
- secondary to stomach of SI obstructions
- usually present as acute septic peritonitis
-often were colicky and then no longer painful
-acute sweating and rapid respiration
-systemic deterioration
diagnosis:
1. ultrasound
2. abdominocentesis
3. surgery is definitive
