2Outline: Displaced Abomasum History and SignalmentPathophysiologyDiagnosisClinical signs, clin path, R/O’sTreatmentNon-surgicalSurgical (4 approaches)Ancillary care (Fluids, Abx, …)Risk Factors for LDAThe dairy cow has been selectively bred to produce much more than a calf requires.This means a greater intake of nutrients than the high fiber diet of cattle, especially at the beginning of lactation.There is a fine balance between increasing a cow’s nutrient intake while maintaining a stable metabolism.Due to our rapidly improving management and feeding practices,the incidence of DA’s has increased tremendously over the past 2 decades.Currently, DA’s occur in about 2-6% of dairy cows worldwide.In Michigan, the incidence of DA’s can be as low as 0% in some herds, but also as high as 25% in one herd!
3Displaced Abomasums DA’s, LDA’s, RDA’s, RTA’s Adult lactating dairy Production problemHerd problem [related to nutrition]Majority of DA’s have concurrent diseasesI’m here today to dispell all misconceptions that this is the real reason why abomasums displace.During the “critical six weeks” = 3 wks b/f and a/f calving = aka the “transition period”,there is a dramatic change in nutrient requirements.The cow’s metabolism has to adapt (sometimes it doesn’t)
4History and Signalment of DA Age: older lactating dairy cattleTiming: 80% occur during first month after parturitionNutrition:Dry cow rations: +DCAD / inadeq efv fiberFresh cow: excess NSC’s / inadeq efv fiberAge: DA occur primarily in older adult dairy females, often those on 3+ lactation.Heavy yielding cows are more often affected.Timing: (range: 2 weeks prepartum to 2 months postpartum)RDA’s more spread out throughout 3 months post calving.Seasonal peaks in January (RAV) or March (LDA).Nutrition: Dry cow rations with positive dietary cation-anion difference (DCAD). DCAD = cations(Na + K) – anions(Cl + S) in mEq/100 gWant DCAD to be –10 to –15 mEq/100g to minimize incidence of milk fever.Fresh cow rations with inadeq effective fiber and/or excess non-structural carbohydrates (NSC’s).Carbohydrates are primary E source for ruminants – divided into structural and nonstructural fractions. The structural portion of the plant is the cell wall material = NDF = neutral detergent fiber (cellulose, hemicellulose, lignin). NSC=nonstructural carbohydrates = cell contents (sugars, starches, pectins, etc) estimated by the formula [100-(CP+NDF +ether extract +ash)] = NSC = easily digestible and rapidly fermented.Concurrent disease: 40% of DA’s have concurrent retained placenta/metritis/mastitis.Can also see ketosis, diarrhea, calving complications, and abomasalperforating ulcers.Concurrent disease:40% of DA’s have retained placenta, mastitis, or metritis
5Normal location of abomasum Right view of bovine stomach.Abomasum normally lies in down on the abdominal floor, on the right front quadrant of the abdomen, just inside the 7th thru 11th ribs.
6Left view bovine stomach On the left side of the NORMAL abdomen, you primarily see rumen.
7Why does the abomasum displace? (1) Abomasal atony(2) Increased abomasal gas production(1) + (2) => abomasum moves (LDA,RDA)Atony = absence/ lack of normal tone+ filled (2) => abomasum moves:to left (about 90% of time) => Left Displaced Abomasumto right (about 10% of time) => Right Displaced Abomasum(and if the RDA twists => Right Torsed Abomasum, a sx emergency)This displacement interferes with normal digestion and normal flow of ingesta.In addition, uterus void can also contribute of predisposition of DA’s.Lots of room in there makes it easier for things to move around.Normal position of abomasumLeft displacement
8Displacing Abomasum In Action Superficial wall of greater omentumDeep wall of greater omentumDescending duodenum
9LDAIn an LDA, the abomasum comes to lie to left of rumen, just back of the omasumPoint out greater curvature in left lower flankPoint out greater omentum
10Why does abomasal atony occur? Hypocalcaemia due to+DCAD, [Ca]blood, mastitis, - E balance7 times more likely to develop DA’sInadequate effective fiberVFA’s reach abomasum => abomasal hypomotility => HCl refluxes back into rumen => systemic metabolic alkalosisEndotoxemiaReleased during Gm – sepsis (mastitis/metritis)HYPOCALCEMIADry cow rations with + DCAD predispose dairy cows to hypocalcemia.Decr [Ca] from 2 wks prepartum thru early lactationConcomitant mastitis/metritis may lower serum Ca further due to anorexiaNeg E balance also decreases Ca (b/c lipolysis and depo of FA-Ca soaps in extravascular spaces.)Cows with hypocalcemia are 7 times more likely to develop DA’s.Inadequate effective fiberRemember, The primary end products of carbohydrate digestion in the rumen by microbes are volatile fatty acids (VFA),Lots of VFA’s reach the abomasum directly => abomasal atony / hypomotilityHCl refluxes back into rumen instead of going into sm. Intestine =>so HCl is sequestered in the rumen and abomasumand pancreas continues to secrete bicarb (not counteracted)=> relative excess of bicarb systemically =>systemic alkalosis (mild in LDA)So high concentrate rations increase the likelihood of abomasal atony => DA’sEndotoxemiaEndotoxins released during Gm – sepsis (mastitis/metritis) contribute to abomasal stasis.Essentially, any time a cow goes off feed => can get atony => risk for DA.
11Why increased gas productn? NSC : effective fiber ratioDiet TypeGas volume(methane,O2,N2)Hay800 ml/hrConcentrate 3 lb1100 ml/hrConcentrate 15 lb2200 ml/hrToo much NSC (nonstructural carbs) in relation to the amount of effective fiberExamples of feeds high in NSC’s are: high moisture corn, high E concentrates (such as ground corn, hominy, barley, wheat, or oats)
12Clinical Pathology Normal CBC Metabolic alkalosis(slight) Hypo Ketosis (mild)DehydrationHypoglycemia (maybe)Hyperbilirubinemia*** TAKE HOME POINT *** Clin path is not remarkable in LDA casesNormal CBC in uncomplicated casesSlight metabolic alkalosis in most cases. HCl refluxes into rumen. Rumen = “acid trap”Slight hypochloremia (90-95 mEq/L). B/c HCl is refluxed into rumenNormal to slight hypokalemiaMild ketonuriaMild hypoCa ( mg %)
13Clinical Signs of DA’s Normal TPR (most cases) Partial anorexia (“off feed”)Hypogalactia (“down in milk” ~ 5-10 lb/day)Depression (ADR)Secondary ketosismild to moderateScant stoolfirm/looseundigested particlesNormal TPR (in uncomplicated cases I.e. not torsed)Off feed: selectively eat hay and grass (don’t eat grain, silage, hi moisture corn)Down in milk: drop between 3-5 lbs each milking (5-10 lb / day)(Untreated cows may be culled for poor milk production)Chronic ketosis:Recall ketosis is when the intake of nutrients (esp E) are inadeq to meet production demands. They are in Negative Energy Balance => mobilizing body stores of fat and protein. In the liver, fat is changed to ketones, causing an increase in ketones in the blood. Ketosis usually occurs 3 wks after calving (range weeks).Most high producing cows go thru subclinical ketosis in early lactation (unable to consume enuf E to meet E output of milk). This is called primary ketosis.Secondary ketosis results from other problems such as retained placenta, DA, hardware dz, anything else which decreases appetite.(Since ketosis is secondary, does not respond well to antiketotic therapy alone)Scant stool: firm and putty-like or loose and brown(cows with loose stool have worse prognosis)occasionally the feces may have large undigested particles in them
14Clinical Signs (continued) Paralumbar fossa:“slab-sided” abdomenVisualize / Palpate PLFRectal palpation (can’t)Mild colicMild hypocalcemiaHypotonic rumenCold ears, widely dilated pupilsSlab-sided abdomen IN LDA:Look at her from the back. Instead of normal barrel conformation, the left paralumbar fossa flattens where the abomasum is between the rumen and the left body wall (ribs 10-13)You canVisualize/palpate gas: if the greater curvature of the abomasum extends beyond the 13th ribRectal palpation : usually can’t (except in ¼ of RDA’s in which you can palpate the greater curvature of abomasum)Mild colic: abdomen tucked up, tailswitching, treading (shifting wt on rear legs)Signs of hypocalcemia (MILD b/c cow still standing)hypotonic/atonic rumencold ears and widely dilated pupils slowly respond to light
15Clinical Signs (continued) LDA: Ping & SplashAscult and percussPing high pitchedBallottment for splash of fluidAll pings are not created equal – rumen pingFIRST THE PING: Draw an imaginary line on the cow from tuber coxae to elbow,Ascult and percuss ( flicking your finger ) around esp between 9th and 13th ribThe ping occurs over the gas pocket.LDA pings are high pitched (except one that has been going on for weeks)and the tone changes as you percuss along this imaginary line.NOW THE SPLASH: Remember “ballottment” from first year animal handling class?Ballott behind the ribs--- take your fist and move it in and out quickly and ascult.You are trying to make the fluid move and “Splash”.Now rumen fluid with all the bugs and hay and such is a thick fluid.But the fluid below the gas cap in the abomasum will be more watery and make a splashing sound.Many things, besides LDA’s, can create a “ping”, soIt is important to classify pings wrt size location characterThis will help you decide what the ping is due to.DIAGNOSITC DILEMMA: ~15% of LDA’s do NOT ping or ping intermittentlyNote: ~15% of LDA’sDO NOT PING or ping sporatically
16Differential Diagnosis LDA R/O’s1° ketosis (non-pinging LDA)Rumen pingRDA R/O’s1° ketosis (non-pinging RDA)Other Right-sided pings:Uterus, cecum, peritoneum, colon, rectum“off feed” pingPing does not imply DA !we said LDA ping was high-pitched and located betw 9th and 13th ribsCompared toRumen Pinglargerlower pitchedpalpable gas cap via rectummay not be bloated in L paralumbar fossa (e.g. chronic anorexia)
22Non-Surgical Technique: Rolling Cast cow with ropes into right lateral recumbencyRoll onto back & extend the rear legsRoll in a 90-degree arc for 3 minutes, ending in left lateral recumbencyBring the cow to sternal position & allow to standAscult the left thorax to ensure LDA is relieved
23Rolling Technique Advantages DISADVANTAGES Quick & easy technique No invasive surgeryDISADVANTAGES>50% redisplaceIf RDA or RTA are present, can exacerbate problems
24Surgical Techniques- Roll & Toggle +/- Tranquilization or SedationCast cow onto right side & roll onto backClip & scrub operational site:Area of loudest “ping”4-7 inches behind Xiphoid
25Roll &Toggle Assistant places pressure on lower abdominal quadrant Trocharize the abdomen 4-7 inches behind xiphoid & 3 inches right of midlineRemove handle & push rod from trochar
26Roll & TogglePlace toggle suture and push through cannula, then remove trocharTrocharize 2nd site 2-3 inches proximallyTie two toggle suture ends together, leaving space between skin & the knots
27Roll & Toggle Advantages: Disadvantages: Simple, quick, inexpensive Minimally invasiveHigh success rate (60-80%)Disadvantages:Blind technique- cannot see abomasumDorsal recumbent position
28Surgical Techniques: Right Flank Omentopexy Paravertebral/Invert-ed L/ Line Block20 cm vertical incision in right paralumbar fossaLeft arm moves over top of rumen to left side of abdomen, locates abomasum
29Right Flank Omentopexy Feel abomasum for adhesionsDeflate gasBring arm under rumen, grab top of abomasum & scoop back to ventral position
30Right Flank Omentopexy Pull out omentum through incision until pylorus can be seenMattress sutures through peritoneum, omentum, & muscleContinuous sutures on inner layers of muscle incorporating omentum
31Right Flank Omentopexy Advantages:High success rate in experienced surgeonsStanding procedureCan perform exploratoryDisadvantages:Omentum can tear & redisplacementCannot see abomasum to evaluateNeed long arms to reach across abdomen!
32Surgical Techniques: Left Flank Abomasopexy Anesthetize Left Flank20 cm incision of left paralumbar fossaLocate abomasumPlace sutures in greater curvature– simple continuous or interlocking & tabDeflate abomasum
33Left Flank Abomasopexy Attach a cutting needle to sutures & bring to ventral surface of abdominal wallStab needle through abdominal wall & reposition abomasum by traction on sutureAnchor sutures in skin
34Left Flank Abomasopexy AdvantagesDirect fixation of abomasum to body wallStanding surgeryCan see abomasumDisadvantagesNot as secure of anchorage as ventral paramedian approach
35Surgical Techniques: Ventral Paramedian Abomasopexy Sedated & blocked cow in dorsal recumbancyIncision between midline & milk vein 8 cm behind Xiphoid
36Ventral Paramedian Abomasopexy Bring abomasum back to normal position directly below incisionTrochar to remove gasSuture lateral aspect of greater curvature to peritoneum & internal rectus sheathClose
37Ventral Paramedian Abomasopexy AdvantagesVery secure fixation with good adhesionCan visualize abomasumCasting usually repositions abomasumDisadvantagesStressful to cast the cow, danger of regurgitation in dorsal recumbencyRest of abdomen cannot be explored
38Replacement FluidsIsotonic Saline, Lactated Ringer’s IV to replace deficitK, Ca salts as needed to correct electrolyte imbalancesFree-choice oral fluids with NaCl, KCl
39Antibiotics??? The Three T’s: Time- how long was the procedure? Trash- how clean was the surgical site?Trauma- are tissues damaged?Also evaluate for other concurrent problems, cost, withdrawal times, route, and ability of agent to reach the tissue
40Risk Factors for LDA High-production Dairy Cows Post-partum High concentrate, low roughage dietLarge body sizeLimited exercisePost-partumAbomasal Atony
42References Dr. Kent Ames Web references: Books: Books:Noordsy, John, L. Food Animal Surgery, 3rd ed.Oehme, Frederick W. Textbook of Large Animal Surgery, 2nd ed.Smith, Bradford P. Large Animal Internal Medicine.Turner, McIlwraith. Techniques in Large Animal Surgery, 2nd ed.