Displaced Abomasum Barb Knust Jenny Kohn

Outline: Displaced Abomasum History and Signalment Pathophysiology Diagnosis Clinical signs, clin path, R/O’s Treatment Non-surgical Surgical (4 approaches) Ancillary care (Fluids, Abx, …) Risk Factors for LDA The 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!

Displaced Abomasums DA’s, LDA’s, RDA’s, RTA’s Adult lactating dairy Production problem Herd problem [related to nutrition] Majority of DA’s have concurrent diseases I’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)

History and Signalment of DA Age: older lactating dairy cattle Timing: 80% occur during first month after parturition Nutrition: Dry cow rations: +DCAD / inadeq efv fiber Fresh cow: excess NSC’s / inadeq efv fiber Age: 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 g Want 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 abomasal perforating ulcers. Concurrent disease: 40% of DA’s have retained placenta, mastitis, or metritis

Normal 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.

Left view bovine stomach On the left side of the NORMAL abdomen, you primarily see rumen.

Why 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 Abomasum to 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 abomasum Left displacement

Displacing Abomasum In Action Superficial wall of greater omentum Deep wall of greater omentum Descending duodenum

LDA In an LDA, the abomasum comes to lie to left of rumen, just back of the omasum Point out greater curvature in left lower flank Point out greater omentum

Why does abomasal atony occur? Hypocalcaemia due to +DCAD, [Ca]blood, mastitis, - E balance 7 times more likely to develop DA’s Inadequate effective fiber VFA’s reach abomasum => abomasal hypomotility => HCl refluxes back into rumen => systemic metabolic alkalosis Endotoxemia Released during Gm – sepsis (mastitis/metritis) HYPOCALCEMIA Dry cow rations with + DCAD predispose dairy cows to hypocalcemia. Decr [Ca] from 2 wks prepartum thru early lactation Concomitant mastitis/metritis may lower serum Ca further due to anorexia Neg 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 fiber Remember, 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 / hypomotility HCl refluxes back into rumen instead of going into sm. Intestine => so HCl is sequestered in the rumen and abomasum and 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’s Endotoxemia Endotoxins released during Gm – sepsis (mastitis/metritis) contribute to abomasal stasis. Essentially, any time a cow goes off feed => can get atony => risk for DA.

Why increased gas productn? NSC : effective fiber ratio Diet Type Gas volume (methane,O2,N2) Hay 800 ml/hr Concentrate 3 lb 1100 ml/hr Concentrate 15 lb 2200 ml/hr Too much NSC (nonstructural carbs) in relation to the amount of effective fiber Examples of feeds high in NSC’s are: high moisture corn, high E concentrates (such as ground corn, hominy, barley, wheat, or oats)

Clinical Pathology Normal CBC Metabolic alkalosis(slight) Hypo Ketosis (mild) Dehydration Hypoglycemia (maybe) Hyperbilirubinemia *** TAKE HOME POINT *** Clin path is not remarkable in LDA cases Normal CBC in uncomplicated cases Slight metabolic alkalosis in most cases. HCl refluxes into rumen. Rumen = “acid trap” Slight hypochloremia (90-95 mEq/L). B/c HCl is refluxed into rumen Normal to slight hypokalemia Mild ketonuria Mild hypoCa (6.8-8.0 mg %)

Clinical Signs of DA’s Normal TPR (most cases) Partial anorexia (“off feed”) Hypogalactia (“down in milk” ~ 5-10 lb/day) Depression (ADR) Secondary ketosis mild to moderate Scant stool firm/loose undigested particles Normal 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 0.5-6 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

Clinical Signs (continued) Paralumbar fossa: “slab-sided” abdomen Visualize / Palpate PLF Rectal palpation (can’t) Mild colic Mild hypocalcemia Hypotonic rumen Cold ears, widely dilated pupils Slab-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 can Visualize/palpate gas: if the greater curvature of the abomasum extends beyond the 13th rib Rectal 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 rumen cold ears and widely dilated pupils slowly respond to light

Clinical Signs (continued) LDA: Ping & Splash Ascult and percuss Ping high pitched Ballottment for splash of fluid All pings are not created equal – rumen ping FIRST 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 rib The 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”, so It is important to classify pings wrt size location character This will help you decide what the ping is due to. DIAGNOSITC DILEMMA: ~15% of LDA’s do NOT ping or ping intermittently Note: ~15% of LDA’s DO NOT PING or ping sporatically

Differential Diagnosis LDA R/O’s 1° ketosis (non-pinging LDA) Rumen ping RDA R/O’s 1° ketosis (non-pinging RDA) Other Right-sided pings: Uterus, cecum, peritoneum, colon, rectum “off feed” ping Ping does not imply DA ! we said LDA ping was high-pitched and located betw 9th and 13th ribs Compared to Rumen Ping larger lower pitched palpable gas cap via rectum may not be bloated in L paralumbar fossa (e.g. chronic anorexia)

Right-sided pings Off-feed ping = intermittent; duodenal / spiral colon ping

Treatment of Displaced Abomasum

Therapeutic Goals Return Abomasum to proper position Create a permanent attachment Correct electrolyte, acid-base, & hydration deficits Treat other concurrent diseases

Therapeutic Choices Upper 25% of herd: “cut ‘em” Middle 50%: “tack ‘em” Lower 25%: “cull ‘em”

How to Fix?

Non-Surgical Technique: Rolling Cast cow with ropes into right lateral recumbency Roll onto back & extend the rear legs Roll in a 90-degree arc for 3 minutes, ending in left lateral recumbency Bring the cow to sternal position & allow to stand Ascult the left thorax to ensure LDA is relieved

Rolling Technique Advantages DISADVANTAGES Quick & easy technique No invasive surgery DISADVANTAGES >50% redisplace If RDA or RTA are present, can exacerbate problems

Surgical Techniques- Roll & Toggle +/- Tranquilization or Sedation Cast cow onto right side & roll onto back Clip & scrub operational site: Area of loudest “ping” 4-7 inches behind Xiphoid

Roll &Toggle Assistant places pressure on lower abdominal quadrant Trocharize the abdomen 4-7 inches behind xiphoid & 3 inches right of midline Remove handle & push rod from trochar

Roll & Toggle Place toggle suture and push through cannula, then remove trochar Trocharize 2nd site 2-3 inches proximally Tie two toggle suture ends together, leaving space between skin & the knots                              

Roll & Toggle Advantages: Disadvantages: Simple, quick, inexpensive Minimally invasive High success rate (60-80%) Disadvantages: Blind technique- cannot see abomasum Dorsal recumbent position

Surgical Techniques: Right Flank Omentopexy Paravertebral/Invert-ed L/ Line Block 20 cm vertical incision in right paralumbar fossa Left arm moves over top of rumen to left side of abdomen, locates abomasum

Right Flank Omentopexy Feel abomasum for adhesions Deflate gas Bring arm under rumen, grab top of abomasum & scoop back to ventral position

Right Flank Omentopexy Pull out omentum through incision until pylorus can be seen Mattress sutures through peritoneum, omentum, & muscle Continuous sutures on inner layers of muscle incorporating omentum

Right Flank Omentopexy Advantages: High success rate in experienced surgeons Standing procedure Can perform exploratory Disadvantages: Omentum can tear & redisplacement Cannot see abomasum to evaluate Need long arms to reach across abdomen!

Surgical Techniques: Left Flank Abomasopexy Anesthetize Left Flank 20 cm incision of left paralumbar fossa Locate abomasum Place sutures in greater curvature– simple continuous or interlocking & tab Deflate abomasum

Left Flank Abomasopexy Attach a cutting needle to sutures & bring to ventral surface of abdominal wall Stab needle through abdominal wall & reposition abomasum by traction on suture Anchor sutures in skin

Left Flank Abomasopexy Advantages Direct fixation of abomasum to body wall Standing surgery Can see abomasum Disadvantages Not as secure of anchorage as ventral paramedian approach

Surgical Techniques: Ventral Paramedian Abomasopexy Sedated & blocked cow in dorsal recumbancy Incision between midline & milk vein 8 cm behind Xiphoid

Ventral Paramedian Abomasopexy Bring abomasum back to normal position directly below incision Trochar to remove gas Suture lateral aspect of greater curvature to peritoneum & internal rectus sheath Close

Ventral Paramedian Abomasopexy Advantages Very secure fixation with good adhesion Can visualize abomasum Casting usually repositions abomasum Disadvantages Stressful to cast the cow, danger of regurgitation in dorsal recumbency Rest of abdomen cannot be explored

Replacement Fluids Isotonic Saline, Lactated Ringer’s IV to replace deficit K, Ca salts as needed to correct electrolyte imbalances Free-choice oral fluids with NaCl, KCl

Antibiotics??? 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

Risk Factors for LDA High-production Dairy Cows Post-partum High concentrate, low roughage diet Large body size Limited exercise Post-partum Abomasal Atony

Questions???

References Dr. Kent Ames Web references: Books: http://www.ldatogglesuture.com/ http://www.vet.ohio-state.edu/docs/ClinSci/bovine/prevmed/abomasum.htm http://www.ianr.unl.edu/pubs/dairy/g1201.htm http://muextension.missouri.edu/xplor/agguides/pests/g07701.htm 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.