nose ring application. diseases of the forestomachs m. s. gill, d.v.m., m.s
TRANSCRIPT
Ruminant Carbohydrate Engorgement
• Grain overload
• Lactic acidosis
• Carbohydrate intoxication
• Grain engorgement
• Founder
History• Access to highly fermentable feedstuffs
– by unaccustomed animals, or– in larger than normal amounts
• May involve several animals in herd
• Rapid clinical course
Clinical findings• Abdominal pain
• Dehydration (6-12 %)
• Diarrhea – fluid, fetid
• Splashy rumen, bloat
• Depression
• Lameness
• Scleral injection
Clinical findings• Elevated temp initially, may be
subnormal when presented
• HR = 80-140 bpm
• RR elevated (blow off CO2)
• Rumen fluid analysis– pH < 5– sour odor– protozoa dead, predominance of gram +
Clinical findings• Metabolic acidosis
• PCV
• protein
• Elevated BUN, creatinine, phosphorous
• Increased anion gap
• Decreased calcium
Pathogenesis
• Excess CHO ingestion, VFAs, rumen pH, rumen motility, Strep bovis proliferates producing lactic acid, further pH (4-5)
• Acid resistant Lactobacillus spp. proliferate producing lactic acid
Pathogenesis
• Lactic acid accumulation in the rumen osmolarity of the rumen fluid drawing more body water into the rumen (creates the “splashy rumen”)
• Loss of body water causes dehydration contributing to acidosis
• Lactic acid is absorbed from rumen as well as from small intestine & profound lactic acidosis develops
Pathogenesis
• Acidic rumen pH damages mucosal surfaces in the forestomachs & intestine
• Blood vessels thrombose & sections of rumen mucosa & submucosa slough allowing bacteria to invade
• Bacteria travel to liver via portal circulation & cause liver abscesses
• Mycotic ruminitis may develop
Pathogenesis
• Histamine levels increase
• Ethanol, methanol, tyramine, tryptamine production contribute to CNS depression
• Thiaminase production may result in development of polio
• Death of Gram – bacteria can cause endotoxin release
What feeds can cause carbohydrate engorgement?
• Cereal grains
• Industrial byproducts (brewers grains, sugars)
• Fruits
• Tubers (potatoes, sugar beets)
What feeds can cause carbohydrate engorgement?
• Finely ground feeds with large surface area promote rapid fermentation
• Hay and grass are are not highly fermentable due to cellulose and large particle size
• Corn silage usually not a problem because much of CHO already reduced to VFAs in ensiling process and also due to large particle size
Diagnosis
• History
• Clinical signs and clinical findings
• Rumen fluid analysis
• CBC, chem panel, blood gas
Therapy
• Remove rumen contents– Kingman tube– Rumenotomy– Ice water
administration– Procaine pen G
(10 million IU, P.O.)
Therapy
• Fluid and electrolyte replacement IV• Anti-inflammatory agents –flunixin
meglumine (Banamine)• Antibiotics• Antimycotic therapy• Rumen transfaunation• Thiamine• B-complex vitamins
Client education
• Make dietary changes very gradually– Addition of antibiotics, HCO3-, and
ionophore antibiotics to the feed have been beneficial but do not replace good management
• Rumen adaptation may take 6 weeks
Rumen tympany (bloat)
• Gas production is a normal occurrence during rumen fermentation
• Bloat occurs if eructation is prevented for any reason
Clinical findings
• Distended left paralumbar fossa• Discomfort (grunting, colic)• Open-mouth breathing• Anorexia• Salivation• Anxious• Depressed terminally• Sudden death
Types of bloat
• Primary– Eructation normal but gas cannot be expelled
• frothy bloat – legumes or grain (Strep bovis)
• Secondary– Failure of eructation
• esophageal FB’s• vagus indigestion• positional• hypocalcemia• pharyngitis
THERAPY
• Free gas bloat– Pass a stomach tube (carefully) either
nasogastric or orogastric– If positional, roll cow into sternal recumbency– Force exercise– If hypocalcemia, administer calcium – Rumen stimulents– Rumen trocharization for emergencies only
THERAPY
• Frothy bloat– Reduce surface tension
• Poloxalene – 2 oz.• Household detergent (Tide 2-3 oz.)• Mineral oil• Dioctyl sodium sulfosuccinate (DSS)
*All of the above reduce surface tension allowing consolidation of tiny bubbles into a free gas bloat which can be eructated or relieved via tube
THERAPY
• Chronic bloat – typically free gas bloat associated with high grain diets that may cause a permanent shift in microflora– Increase fiber in diet & reduce grain– Rumen transfaunation– Temporary rumenostomy in severe cases
• May be 2° to another problem such as vagus indigestion
Client education
• Slow adaptation to grain
• Limit legume grazing
• Poloxalene in feed, molasses, salt or block
• Maintain sufficient long stem hay (fiber) in ration to stimulate good rumen motility
Rumenitis, rumen parakeratosis, chronic rumen acidosis
• Long-term ingestion of high grain, low roughage diet
• Poor appetite
• Poor weight gain
• Chronic laminitis
Rumenitis, rumen parakeratosis, chronic rumen acidosis
• Clinical findings– Hypomotile rumen– Elevated liver enzymes– Rumen protozoa, gram + bacteria
Rumenitis, rumen parakeratosis, chronic rumen acidosis
• Chronic exposure to high grain diet• Low rumen pH (5.0-5.5)• Increased propionic & butyric acid which
stimulates proliferation of rumen papillae epithelium and even parakeratosis
• Fine particle size, less cud chewing, less saliva buffering rumen contents
• Damage to rumen leads to liver abscesses
Rumenitis, rumen parakeratosis, chronic rumen acidosis
• Treatment includes increasing proportion of long stem hay in the diet
Vagus indigestion syndrome
• Motor disturbances which impair passage of ingesta from the reticulorumen and/or abomasum into the lower GI tract
Vagus indigestion syndrome
• “Vague” signs• Slow loss of production• Slow weight loss• Poor appetite• Scant, pasty feces• Abdominal enlargement - “papple”
shape• Rumen hyper motility, bradycardia
Vagus indigestion syndrome
• Classification:– Lesions anterior to cardia– Lesions at the cardia– Lesions at the reticulum– Lesions distal to the reticulum
Vagus indigestion syndrome
• Treatment involves correction of underlying problem
• Lymphosarcoma hopeless
• Rumen lavage
• Rumenotomy to remove contents & ‘shrink’ rumen or to treat reticular abscesses
Traumatic reticuloperitonitis (TRP, hardware disease)
• Sudden decrease in appetite & milk production
• Anterior abdominal pain
• Kyphosis
• Low grade fever (103°)
• Mild leukocytosis with neutrophilia
• Hyperfibrinogenemia
Traumatic reticuloperitonitis (TRP, hardware disease)
• Diagnostics– History– Clinical findings– Paracentesis– Reticular radiography– ultrasound
Traumatic reticuloperitonitis (TRP, hardware disease)
• Medical treatment– Antibiotics– Magnet
• Surgical treatment– Rumenotomy to approach reticulum
Abomasal ulcers
• Occur in all ages of cattle• Associated with stress & high concentrate
diets and lymphosarcoma in older animals• Four categories
– Non-perforating– Non-perforating with severe blood loss*– Perforating with localized peritonitis– Perforating with diffuse peritonitis*
*life threatening
Abomasal ulcers
• Diagnostics– Fecal occult blood– Abdominocentesis– WBC – leukocytosis with neutrophilia, high
fibrinogen– Serology for BLV
Abomasal ulcers
• Calves– Usually see perforation with peritonitis– May be associated with copper deficiency
• Adults– 1/3 significant hemorrhage– 1/3 perforating with localized peritonitis– 1/3 perforating with diffuse peritonitis
Abomasal ulcers
• Treatment– Dietary changes– Decrease stress– Avoid steroid & NSAID use– Treat concurrent problems– Blood transfusions– Antibiotics– GI protectants– H2 antagonists
Clinical case
• History:– Yearling BFM show heifer– History of mild abdominal pain– Mild bloat– Off feed– Change in feed in last week
• Clinical findings:– T – 103°– Leukocytosis, neutrophilia– Increased fibrinogen– Abdominocentesis
• Protein > 3.5• WBC > 10,000• Neutrophilic inflammation
• Treatment:– Antibiotics– Decrease stress– Dietary change – hay, ryegrass, no grain– Rumen transfaunation– Avoid NSAIDS & steroids
Abomasal impaction
• Causes:– Poor quality roughage for overwintering beef
cows– Calves fed poor quality milk replacers– Animals on low fiber diets– Abomasal volvulus– Lymphosarcoma
Abomasal impaction
• Clinical signs:– Takes weeks to develop– Decreased appetite– Firm, dry feces– Rumen enlargement, stasis– Poor BCS– Abomasal rupture may occur
Abomasal impaction
• Differentials– Hydrops– Chronic peritonitis– Vagus indigestion– Omasal impaction
Abomasal impaction
• Poor quality roughage is poorly digested so fibrous material passes to the abomasum creating accumulation of fibrous material in the abomasum which can not pass through
• May develop post abomasal volvulus due to vagus nerve dysfunction
Abomasal impaction
• Prognosis poor if advanced (slaughter)• Fluid therapy*, laxatives, metaclopramide to early cases• Terminate pregnancy• Rumenotomy, backflush abomasal contents into rumen • Place NG tube directly into abomasum for post-op
medication
*usually don’t develop metabolic alkalosis & hypochloremia
Abomasal emptying defect (AED)
• Suffolk sheep• Anorexia, weight loss, abdominal enlargement• Abomasum is enlarged and palpable• DDx:
– Malnutrition– Parasitism– Dental attrition– Johne’s– Caseous lymphadenitis– Neoplasia– Chronic pneumonia
Abomasal emptying defect (AED)
• Diagnostics– Increased rumen chloride (normal = 8-15
mEq/L)– Ultrasound abomasum – normal diameter is
2-3”, with AED may see abomasal diameter of 6-10”
• Pathophysiology remains unknown