Ruminant Indigestion Flashcards
describe the pathophysiology of ruminant indigestion-primary cycle motility disorders
- decreased excitatory input to gastric centers
- increased inhibitory input to the gastric centers
- depression of gastric centers: CNS depressant drugs, anesthetics, endotoxemia, fever, blood pH
- defective vagal innervation: role under question
- other: hypocalcemia can decrease motor response
describe the pathophysiology of secondary cycle motility disorders of ruminant indigestion
- decreased secondary cycle activity causes decreased eructation
-independent of primary cycle activity
includes:
1. ingesta covering gas pressure receptors in cranial ruminal sac
2. gas accumulation due to poor motility function
-likely large role in fermentative dysfunction
3. gross overdistension: leads to weak, ineffective motility if develops slowly
-likely with poorly digestible roughage accumulation
describe important aspects of signalment/history for ruminant indigestion
- age
- use
-dairy vs beef
-stage of production:
–feeding requirements: feedlot, freshening
–concurrent disease: hypocalcemia - feeding history:
-affects fermentation pattern
-frothy bloat: low fiber, high concentrate, legumes
-ruminal impaction: poor quality hay or straw
-ruminal acidosis: high carbohydrate +/- sudden access - acuteness of onset:
-most not ER
-exceptions: frothy bloat, acute ruminal acidosis
describe clinical signs of ruminant indigestion
- non-specific systemic
-hypo or anorexia
-dullness/depression
-decreased productivity!!! - ruminal contraction and rumination
-decreased, absent, abnormal
-increased: frothy bloat, some vagal indigestion - failure to ID underlying disease: backs you into diagnosing it as primary reticuloruminal disease
- calves that are malnourished: poor growth rate, long rough hair coat
describe physical exam for ruminant indigestion
- fever:
-uncommon
-exceptions: traumatic reticuloperitonitis, occasionally rumenitis - shock: generally uncommon! typically chronic progressive so in acute stage rare
-severe, acute bloat: respiratory and CV compromise with distension
-acute ruminal acidosis: fluid shifts, acidosis, CV compromise
describe abdominal contour-reticulorumen fill with ruminant indigestion
- decreased:
-most primary and secondary indigestion due to hypomotility and anorexia
-especially with prolonged duration - increased:
-flow of forward ingesta impeded: overfeeding, vagal indigestion
-fluid sequestration: acute ruminal acidosis - ventral distension:
-rumen: left +/- right
-hydrops - left dorsal distension:
-ruminal tympany
- +/- LDA - right side distension:
-abomasal and other intestinal diseases
-can cause reflux into reticulorumen - bilateral/diffuse distension:
-generalized peritonitis
-prolonged obstruction
describe cranial abdominal pain and stance
- traumatic reticulopericarditis (TRP) and abomasal ulcers
- painful expression
- reluctance to move; short, stilted gait
-ddx: laminitis with ruminal acidosis - kyphosis
- extended neck
describe abdominal palpation of the left flank
- ruminal contents:
-normal layers: fluid, firm/doughy fiber mat, gas
-bloat: taut dorsal distension, frothy loose fiber mat
-rumen impaction: more firm/fibrous material
-stasis: fiber layer sinks below fluid layer (ex. TRP)
-fluid accumulation:
–acidosis: splashy
–vagal indigestion, abomasal outflow obstruction
-decreased fill
- rumen contractions:
-frequency, duration, strength
-norm: 1-2x per min, should be strong enough to push your hand out
describe abdominal palpation of cranial ventral abdomen and per rectum
cranial ventral abdominal pain:
-check scootch/withers pinch and/or grunt test
per rectum:
-rumen contents: easy to detect moderate gas
-rumen shape: L shape rumen vs abomasal distension/impaction
-rumen LN enlargement: rumenitis
-other intestine, urogenital as for acute abdomen
describe fecal abnormalities
changes common but delayed relative to other clinical signs!
-normal transit time: 1.5-4 days
- decreased amount, dry: anorexia, acute indigestion before other changes, other obstructions (often melena, blood discolored mucus)
- decreased amount, dry, firm, increased fiber length: TRP, omasal transport failure, rumen impaction, dental disease, abomasitis
- increased whole grain: ruminal acidosis
- greasy fine particles: abomasal displacement, pyloric outflow failure
- foamy, fluid, yellowish acidic odor: acute ruminal acidosis
- pasty to fluid with foul odor: fermentative, indigestions, enteritis
describe rumen fluid sampling
- rumenocentesis with needle
-easy access to fluid from ventral sac
-reliable test results
-potential for abdominal contamination - naso or orogastric tube
-can get stuck on top of fiber mat
-can get plugged with fibrous ingesta
-contamination with saliva: increased pH (worse with struggle/stress)
-specially designed tubes with steel to minimize above issues
-passing regular tube nasally may also decrease saliva contamination issues
describe normal ruminal fluid
color: olive, brownish green
consistency: slightly viscous
odor: aromatic, strong
pH: 6-7 on roughage, 5.5-6.5 on grain diet
sedimentation/flotation: 4-8 min
redox potential/methylene blue reduction time: 3-6 min
protozoal activity: multiple forms, active motion
gram stain: predominant gram negative population
chloride concentration: <30mEq/L
describe abnormalities in rumen fluid and interpretation
- color
-milky grey: acidosis
-dark greenish, black: prolonged stasis/decomposition
-grey with milk clots: ruminal drinking - consistency:
-watery: inactive flora
-viscous: saliva contamination - odor:
-decreased: inactive flora
-acidic: ruminal acidosis
-putrid: milk, putrification
-ammonia: urea poisoning - pH: must be eval QUICKLY after taking sample
-increased: saliva, anorexia, indigestible roughage, putrefaction, urea
-decreased: ruminal acidosis, abomasal content reflux - sedimentation and redox potential:
-inactive to rapid fermentation
-decreased anaerobic fermentation decreases redox - microscopic eval:
-protoza: numbers, types, activity; largest guys are most sensitive to disturbance (pH <5 kills all)
-increased gram positive cocci and rods with ruminal acidosis - chloride:
-increase with internal vomiting/abomasal reflux
for all these, compare to a healthy herdmate if can!
describe CBC of ruminant indigestion
- inflammatory leukogram with increased fibrinogen
-TRP
-rumenitis
-vagal indigestion: secondary to inflammation from pneumonia or TRP
-complications of ruminal acidosis bacterial translocation - hemoconcentration with dehydration
- anemia of chronic disease
describe the chemistry panel of ruminant indigestion
- anorexia:
-hypocalcemia, hypokalemia
-ketonemia, ketonuria: esp lactating dairy - ruminal acidosis:
-acidemia
-azotemia
-increased liver and muscle enzymes - vagal indigestions:
-omasal transport failure: minimal abnormalities
-abomasal outflow failure: significant abnormalities
describe imaging for ruminant indigestion
- ultrasound:
-peritoneum: free fluid, fibrin, abscesses
-reticulum: in cranioventral abdomen
–a semicircular structure, contractions move AWAY from body wall, gas contents
–abnormalities: TRP abscesses, fibrin, change in contour
-rumen:
–left paralumbar fossa and caudoventral abdomen
–smooth, thin wall, contractions of craniodorsal blind sac after reticular contractions, gas content
–abnormalities: thickening with rumenitis, abscesses, peritonitis
- radiographs: TRP
describe pathophysiology of TRP
- wire/metallic FB penetrates reticulum, leading to reticular wall abscess, peritonitis, pleural space, pericarditis
- reticulum becomes inflamed and painful resulting in progressive reticulum motility dysfunction
-ruminal stratification disappears and outflow of rumen is impaired
-change in consistency of rumen contents that enter abomasum
-abomasal emptying impaired - possible role of vagal indigestions
describe diagnosis of TRP
- severe, acute form:
-fever, anorexia, ruminal hypomotility, cranial abdominal pain
-decreased milk production, ketosis in lactating cows
-regurgitation of reticuloruminal fluid
-tachycardia, reluctance to move or ay down, abducted elbows, mild bloat - over time: signs become more subtle: weight loss, diarrhea, rough hair coat
- signs related to other organ involvement
-heart: pericardial effusion (muffles or sloshy sounds, heart failure, distended jug vein), acute death with coronary artery laceration
-liver and/or spleen abscesses
describe treatment, prognosis, and prevention of TRP
treatment:
-medical: magnet, abx, confinement
-sx: rumenotomy to remove wire +/- drain abscess into rumen
prognosis:
-fair to good if localized peritonitis and with liver or spleen involvement; when inflammation recedes, reticular function returns gradually
-poor to guarded with epcarditis, pleuritis, adhesions
prevention:
-place magnets at 6-8 months!!
-remove sharp foreign objects from feed
describe pathophysiology of free gas bloat
- prominent clinical sign of several causes of indigestion (not a primary disease)
- failure of eructation:
-mechanical obstruction: esophageal, cardia (papilloma, actinomycosis)
-motility dysfunction:
–fermentation disorders: dietary, microbial and metabolic factors decrease excitability of gastric centers and reticulum, leading to decreased erucation
–reticulorumen wall distension and blockage of cardia with vagal indigestion, ruminal acidosis, indigestible roughage (rumen impaction)
–chronic/recurrent bloat: vagal indigestion
describe diagnosis, treatment, and prognosis of free gas bloat
diagnosis: left dorsal distension, ping, relieved when pass tube!
treatment:
-tx underlying disease!!
-acute/severe: will result in systemic compromise to remove gas emergently via oro or nasorumen tube or trochar
-less severe, chronic, and/or recurrent: may consider temporary fistula while treating underlying disease
prognosis: depends on underlying disease
describe pathophysiology of frothy bloat
- digestion of feed that results in stable froth in rumen, causing severe distension, froth near cardia preventing relaxation, froth/feed obstructing cardia
-legumes, lush winter wheat pasture, sometimes during finishing with grain diets
-some cattle seem predisposed
- key diagnostic findings:
-clin signs: potentially severe distension, colic, stretched stance
-resp compromise: open mouth, dyspnea, cyanosis
-pass tube: CANNOT relieve gas, froth on tube
describe treatment, prognosis, and prevention/control of frothy bloat
treatment:
-poloxalene for pasture, legume
-mineral oil or animal tallow for feedlot
prognosis:
-at pasture death losses 0.5-2.5% of at risk cattle
-feedlot incidence lower
prevention/control:
-pasture: try to keep off during high risk times (difficult), supplement with poloxalene, oils, tallow, rumensin
-grain: increase fiber, slowly reintroduce concentrate, lasolacid
describe classification of vagal indigestion
functional obstruction of ingesta at 2 sites
- omasal transport failure:
-atony of reticulorumen: chronic bloat
-normal to increased ruminal motility - pyloric outflow failure
-continuous
-intermittent, incomplete, recurrent
describe failure of omasal transport pathophys and key dx findings
pathophys:
1. hypermotility of rumen most common
2. causes:
-TRP #1!!
-other abscesses/adhesions of reticulum, hepatic abscesses, diffuse peritonitis, masses at reticuloomasal orifice, reticular or diaphragmatic hernia
key dx findings:
1. accumulation of ingesta in reticulorumen: left pear-apple shape
2. empty omasum and abomasum
3. reduced fecal output, large particles
4. vigorous rumen contractions: esp secondary so eructation still occurs and not a lot of free gas
5. inappetance, mild dehydration
6. electrolyte imbalance over time
describe treatment and prognosis of failure of omasal transport
treatment:
1. med and/or sx tx of underlying disease
2. supportive care with fluids, electrolyte replacement (IV)
3. empty ingesta to resolve distension, repeat as necessary, resolve bloat if present
4. limit feed and water, transfaunate
prognosis:
1. response tot x often slow
2. positive indicators: return of normal contraction patter, improved appetite, resolved distension, weight gain, increased fecal output
3. negative indicators: continue distension, scant feces, poor motility, recurrent bloat
describe simple indigestion
- pathophysiology:
-common sequela to abrupt change in feed, moldy or overheated feeds, and/or bad sileage causing an imbalance in microflora and fermentation products - key dx findings:
-anorexia in 1-2 days, diarrhea after 24 hours
-ruminal activity decreased but not absent, if bloat is present it is mild
-ruminal pH may mild change - tx/prog:
-generally self limiting as rumen microflora adapts to change
describe acute ruminal lactic acidosis
- carb rich feed causes rapid fermentation and lactic acid production that decreases pH
- overproduction of lactic acid producing and using bacteria (also thiaminase producing)
- osmolarity of rumen increases, pulling fluid into the rumen and causing hypovolemia
- chemical damage to mucosa causes leakage of toxins and bacteria into bloodstream and secondary infections
-rumen wall: mycotic and bacterial
-distant: thrombi, liver abscesses, feet (laminitis) - hypovolemic and distributive shock, plus some leakage of lactic acid from rumen causes acidosis
- key dx findings:
-shock: hypovolemic and distributive
-ruminal distension, splashy - treatment:
-aggressive supportive care
-rumenotomy
-therapy for bacterial translocation, rumenitis, and severity of complications - prognosis: depends on if can stabilize and complications
describe subacute ruminal lactic acidosis
pathophys:
1. similar to acute form but milder and prolonged
2. ruminal wall changes: parakeratosis, rumenitis
3. liver abscessation, laminitis
key dx findings:
1. herd problem
2. decreased appetite and ruminal hypomotility
3. foamy, fluid feces, acidic
describe ruminal impaction
pathophys:
1. ruminal microbial flora become inactive due to lack of nutrients
2. poor quality roughage deficient in protein and digestible carbohydrates
3. with decreased activity, feedstuffs not broken down resulting in large fibers and distension
key dx findings:
1. distension can become severe over time: papple
2. roughage mixes with fluid or sinks to floor of rumen
3. decreased feces, long stem particles
4. decreased growth, production, ketosis, emaciation, poor haircoat
describe ruminal drinking
- failure of esophageal groove function:
-type of liquid, method of feeding, age - abomasal reflux: small amount normal to develop microflora
-abnormal microflora lead to poor nutrition - poor doers, potbellied, altered rumen pH, predisposed to enteritis and diarrhea, acid-base and e’lyte disorders
describe problems with ruminal development
- timing of reticuloruminal digestion depends on diet
-can begin as early as 1 week of age if consuming dry feeds
-can be delayed (milk only, like veal calves) - dietary excess or deficiencies alter forestomach development: size, mucosa
- too much concentrate = form of ruminal acidosis
-fluidy contents, hypomotility, poor BCS, recurrent bloat, hair licking (crave fibrous material) - too much roughage = form of rumen impaction:
-haybelly: large firm rumen, little microbial activity in rumen fluid, recurrent blaod
describe recurrent bloat (ruminal tympany)
- usually gas
- occurs frequently with disease
-indigestion
-LDA
-lung disease
-sudden filling of abomasum when already filled with other feed during weaning
describe simple obstruciton of reticuloomasal opening
- ingestion of foreign material
- common in small ruminants esp goats
- clin signs: like other outflow obstructions of reticulorumen
- sx removal via rumenotomy
- prognosis likely good
