1. Displaced
Abomasum
Barb Knust
Jenny Kohn

2. 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!

3. 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)

4. 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

5. 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.

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

7. 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

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

9. 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

10. 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.

11. 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)

12. 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 ( mg %)

13. 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 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

14. 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

15. 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

16. 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)

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

18. Treatment of Displaced Abomasum

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

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

21. How to Fix?

22. 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

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

24. 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

25. 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

26. 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
                             

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

28. 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

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

30. 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

31. 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!

32. 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

33. 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

34. 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

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

36. 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

37. 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

38. 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

39. 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

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

41. Questions???

42. References 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.