14. fresh cow GI disease

on which side is the abomasum most commonly displaced?

left

when is peak occurrence of abomasal displacement?

during first 6 weeks of lactation

abomasal displacement risk factors

• excessive production of VFAs caused by highly acidic feed materials — high-moisture corn, corn silage, haylage

  • negatively impacts abomasal motility

• GI stasis caused by metabolic or infectious disease

  • decreased feed intake leads to smaller rumen → more room for abomasum to float

• twins / large calf — leaves void in abdomen

• genetics — deeper-bodied cows

clinical signs of left displaced abomasum

• initial complaint: off feed & decreased milk production

• dull, mild dehydration

• vitals WNL

• decreased strength and/or frequency of rumen contractions

• sprung 13th rib on left

• simultaneous auscultation & percussion — high-pitched tympanic resonance “ping” corresponding to location of LDA

• simultaneous auscultation & ballottement — “succussible fluid”

LDA clinical pathology

(characteristic for cattle without concurrent disease)

• hypochloremia

  • HCl transport to duodenum is impaired → backflow into abomasum & rumen

• hypokalemia

  • decreased intake & absorption

• metabolic alkalosis → worsens hypokalemia

medical treatment of LDA

• treat primary disease (i.e. ketosis, hypocalcemia, hypokalemia)

• oral laxatives — stimulate evacuation of GI tract

• “fresh cow” drench (low volume)

• trailer ride

• encourage hay consumption to fill rumen with roughage

clinical signs of right displaced abomasum

• primary complaint & general systemic state of cow with simple RDA is same as LDA

• “ping” confined to an area under the last 5 ribs in the upper half of the abdomen

• should extend to at least the 9th rib, often 8th

• succussible fluid more dramatic than LDA

clinical signs of abomasal volvulus after RDA

• acute, dramatic decrease in appetite and milk production; scant feces

• severely depressed or colicky

• systemic compromise: severe dehydration, poor peripheral perfusion, amotile rumen

• vitals: normal temp, typically tachycardic & tachypneic

  • may have cardiac arrhythmia, atrial fibrillation

• often palpable per rectum

RDA volvulus — clinical pathology

• hemoconcentration

• moderate to severe hypochloremia, hypokalemia, metabolic alkalosis

complications of abomasal volvulus

• damage to vagal nerve

• vascular thrombosis along the axis of the volvulus in the lesser curvature

cow will improve initially, then begin to show evidence of abomasal outflow obstruction 4-5d post-op

• abdominal distention

• dehydration

• bradycardia

• decreased appetite and fecal production

type 1 abomasal ulcer

non-perforated ulcer with superficial mucosal defects, minimal hemorrhage

type 2 abomasal ulcer

bleeding ulcer **most common in adult cattle**

type 3 abomasal ulcer

perforated ulcer with local peritonitis

• leakage of abomasal contents, walled off by omentum and fibrinous adhesions

type 4 abomasal ulcer

perorated ulcer with diffuse peritonitis

• massive leakage of abomasal contents prevents localization of infection

type 5 abomasal ulcer

perforated ulcer causing peritonitis limited to the omental bursa

abomasal ulcer risk factors

• highly acidic diets — concentrate feeds (i.e. grain, corn silage)

• early lactation (4-6 weeks) — stress, diet change, housing change, peak milk production

• NSAIDs

• lymphosarcoma

clinical signs of type 1 abomasal ulcer

• most difficult to diagnose; abnormalities are subtle

• intermittently pass small piles of tarry manure

• mild abdominal pain, teeth grinding

• may appear interested in feed initially, but stop after a few bites

diagnostics for type 1 abomasal ulcer

• abdominocentesis: normal peritoneal fluid

• fecal occult blood: positive

clinical signs of type 2 abomasal ulcer

• melena

• complete anorexia

• hemorrhagic shock

  • pale-pink to white mucous membranes

  • weak, elevated pulse

  • rapid shallow breathing

  • weakness

  • low temperature, cool extremities

laboratory aids for type 2 abomasal ulcer

• PCV / TP

• blood lactate

(consider duration of clinical signs)

clinical signs of type 3 abomasal ulcer

• degree of clinical signs depend on extent of perforation

• variably anorexic

• usually febrile* (can have focal peritonitis without fever)

• rumen hypomotility / stasis

• reluctant to move, resentful to abdominal palpation — right ventral

additional diagnostics for type 3 abomasal ulcers

• abdominal ultrasound

  • increased peritoneal effusion with fibrin, typically right cranioventral abdomen

• abdominocentesis

  • elevated total white cell count & protein

clinical signs of type 4 abomasal ulcers

• complete inappetence, dehydration

• rumen & distal GI stasis

• fever*

• generalized abdominal pain

• tachycardia

• reluctant to rise

• endotoxemia → sepsis → death

additional diagnostics for type 4 abomasal ulcer

• abdominal ultrasound

  • increased volume of peritoneal fluid and fibrin, found on left and right sides of abdomen

• abdominocentesis

  • elevated total white cell count & protein

• CBC

  • neutropenia with degenerative left shift in acute cases

clinical signs of type 5 abomasal ulcers

• similar to type 4

• calves (pre-weaned) >>> adult cattle

• abdominal ultrasound will aid in determining whether it is contained in bursa

type 1 ulcer treatment

• dietary change

  • judicious feeding of concentrates in diet

  • decrease feeding of fermented silages

  • increase fibrous feeds like dry hay

• gastric coating agents — kaopectate

  • unproven efficacy

type 2 ulcer treatment

• dietary change as previously described

• gastric coating agents

• ± whole blood transfusion

  • base need for transfusion on heart rate, mucous membrane color, PCV / TP

• aminocaproic acid, administered IV

  • anti-fibrinolytic (stop bleeding)

type 3 ulcer treatment

• dietary changes as previously described

• broad spectrum antibiotics — 7-14d

  • ampicillin trihydrate

  • procaine penicillin and ceftiofur

• NSAIDs are contraindicated!!

type 4 & 5 ulcer treatment

• consider humane euthanasia

  • few cattle survive; those that do are usually not productive

• abdominal adhesions, vagal indigestion are common sequelae

• if opting for treatment

  • broad-spectrum antibiotics

    • IV penicillin + ceftiofur SQ

  • IV fluids with supplemental electrolytes

  • in peracute cases, surgery to oversew perforation can be attempted with high volume peritoneal lavage

  • prognosis is still poor to guarded