This case summary describes a 3-year-old Holstein cow presenting with a history of decreased milk production, diarrhea, anorexia, abdominal distension, and depression over 3 weeks. Upon examination, the cow showed signs of dehydration and metabolic alkalosis. Diagnostic testing revealed findings consistent with a left displaced abomasum, including hypochloremic metabolic alkalosis. Radiographs and bloodwork ruled out other potential causes, confirming the diagnosis of a left displaced abomasum as the primary disease.

1. Case Summary
Case #4 – Holstein with Abomasal Displacement
Dylan Djani, Chloe Hancock, Vivian McWilliams, Victor Oppenheimer,
Yaritbel Torres-Mendoza, Miranda Stockman, and Matthew Willman
Dr. Barton- Group #1
Due: December 8th, 2014

2. HISTORY,PHYSICAL EXAM,AND EMERGENCY MANAGEMENT
A 3 year-old Holstein cow presented to UGA VTH clinicians in the field with a history of
deteriorating health over the past 3 weeks, beginning with a drop in milk production and
diarrhea. The owner treated with penicillin (40 cc) IM for 5 days without improvement, and the
cow progressively became anorexic and depressed. One week prior to presentation the owner
noted that the stool became hard and scant and that the cow had bloated. She was given a
magnet and Carmalax at home, again with no improvement. Three days prior to presentation, the
owner treated with one dose of LA200 and tried unsuccessfully to stimulate appetite with a
variety of different feeds. The cow freshened 3 months ago and was bred by AI 1 ½ months prior
to presentation; she is believed to be pregnant. The cow belongs to a herd that is Johne’s free and
vaccinated annually in June with Triangle-9 and J-5 vaccine (Endovac); however, the herd’s
bovine leukosis virus (BLV) status is unknown. Upon physical exam, her mentation was
depressed and she was tachycardic (120 bpm) and tachypneic (54 bpm) with a normal rectal
temperature (101.5°F)1. She scored a BCS of 3/5 and weighed 1200 lbs. Her mucous
membranes were pale pink and tacky, and she had a CRT of approximately 3s. Furthermore, her
jugular refill was abnormally slow and she had a prolonged skin tent. Moderate abdominal
distension was observed on the left dorsal and ventral quadrants and right ventral quadrants
(papple-shaped). An audible ping was heard on the left abdomen from the 9th
intercostal space to
the paralumbar fossa at a level midway between the stifle and tuber coxae. The rest of the
physical exam was within normal limits. Urine dipstick analysis revealed the presence of a large
amount of ketones. Rectal exam revealed scant firm feces, a distended rumen, and confirmed
pregnancy. The California mastitis test was negative in all four quarters of the udder.
Emergency decompression of the forestomach was performed via orogastric intubation, resulting
in the reflux of 75 L of rumen fluid with a pH of 7. After decompression, the heart and
respiratory rates lowered to 88 bpm and 24 bpm respectively, the right abdomen was no longer
distended, and the ping was only audible from the left 9th to 13th intercostal spaces.
PROBLEM LIST:
 Decreased milk production
DDX: anorexia, gastrointestinal obstruction/torsion (LDA/RDA, hardware disease),
bacterial infection (mastitis, rumenitis, peritonitis, traumatic reticulopericarditis), viral
infection (BLV), poor quality nutrition, intestinal malabsorptive diseases, primary organ
disease (heart, liver), toxins (molybdenum or gossypol poisoning), prion disease (bovine
spongioform encephalopathy)
 Ruminal alkalosis
DDX: abnormal ruminal microfloral population (antibiotic use, grain overload, toxins),
gastrointestinal obstruction/torsion (LDA/RDA, pyloric outflow obstruction)
 Bloat and Vagal Indigestion Abdominal Distension Pattern
DDX: gastrointestinal obstruction/torsion (LDA/RDA, hardware disease, food
impaction), decreased gastrointestinal motility (increased sympathetic activation,
compression of vagus nerve: pregnant uterus, abscess, neoplasia)
 Depressed, anorectic, mucus on the nose
DDX: pain, infection/inflammation, non-specific sign of disease

3.  Scant, hardened feces
DDX: dehydration, anorexia, decreased gastrointestinal motility, gastrointestinal
obstruction
 Tachycardia
DDX: pain, stress, hypovolemia, hypoxemia, primary heart disease
 Slow jugular refill, tacky oral mucous membranes, slightly prolonged CRT, prolonged
skin tent,
DDX: hypovolemia, anorexia
 Ping: left side between 9th-13th intercostal space on line from olecranon to tuber coxae
DDX: left displaced abomasum, gas-distended rumen, pneumoperitoneum,
pneumometrium
 Ketonuria
DDX: anorexia, gastrointestinal disease (obstruction, torsion, malabsorptive diseases),
metabolic disease (endocrine disorders, periparturient energy drains)
 Elevated hematocrit and red blood cell count
DDX: dehydration (relative polycythemia), splenic contraction, myeloproliferative
disorders (polycythemia vera)
 Mature neutrophilia with lymphopenia
DDX: stress, infection/inflammation, myeloproliferative disorders
 Azotemia
DDX: pre-renal (hypovolemia), primary renal disease, post-renal ureteral or urethral
obstruction (urolithiasis, tumor)
 Hypokalemia
DDX: anorexia, metabolic alkalosis, hypocalcemia
 Hypocalcemia
DDX: anorexia during lactation, metabolic alkalosis, vitamin D deficiency,
hypoparathyroidsim
 Hypochloremia + Metabolic Alkalosis
DDX: HCl sequestration in abomasum (pyloric outflow obstructions: displaced
abomasum, food or foreign body obstruction, pyloric stenosis, abscess, neoplasia)
This cow presented with clinical signs of gastrointestinal disease in conjunction with many non-
specific signs of disease. The initial diarrhea that progressed to scant, hardened feces along with
the anorexia, ruminal alkalosis, ketosis, and abdominal distention pattern consistent with vagal
indigestion pointed towards the gastrointestinal tract. The non-specific signs of disease
(including tachycardia, decreased milk production, depression, and presence of mucus on the
nose) indicate clinical illness. The cow’s pale and tacky mucus membranes, slow jugular refill
time, and slow CRT indicated that she was approximately 5% dehydrated2, which is of further
concern due to the removal of a significant volume of alkalotic ruminal fluid during the
orogastric intubation. While we were still concerned with possible infection, the lack of right
abdominal distension and location of the audible ping that persisted following decompression of
the rumen were most consistent with a left displaced abomasum. Other sources for the ping
included a gas-distended rumen, pneumoperitoneum, and pneumometrium; however, these are
less likely than a left displaced abomasum because the rumen was deflated during orogastric
intubation, no abdominal trauma was observed during the physical exam, and air in
compartments of the abdominal cavity would result in bilateral pinging. The ketonuria indicates

4. a negative energy balance, which is consistent with a dairy cow in lactation; however, ketonuria
in the face of anorexia and decreased milk production is indicative of a metabolic shift towards
fat catabolism for energy and is consistent with a left displaced abomasum, as such a
displacement prevents nutrients from reaching the primary sites of absorption in the small
intestine. Other causes of decreased milk production include infection or inflammation of the
udder (mastitis) or other systemic infections, but mastitis is less likely the cause because of the
negative California mastitis test result in all four quadrants of the udder.
DIAGNOSTIC PLAN:
Radiographs of the cranioventral abdomen were taken to rule out gastrointestinal obstruction,
abdominal masses, and free gas in the abdomen. A complete blood count was performed in
order rule out infection and serum chemistry analysis to gain an idea of organ function and
electrolyte status.
DIAGNOSTIC INTERPRETATION
The radiographs showed no abnormalities and confirmed the placement of the magnet by the
owner in the reticulum.
The complete blood count revealed an elevated hematocrit, red blood cell count, mature
neutrophilia, and lymphopenia. The hematocrit of 51% and RBC values are consistent with the
clinical findings of dehydration, making other differentials for an increased circulating red cell
mass less likely. The mature neutrophilia and lymphopenia likely represent a stress leukogram
in response to the primary disease and does not likely represent infection due to the absence of
band neutrophils in circulation3. Stress leukograms in cattle are more likely to show
lymphopenia on top of a mature neutrophilia because of the proportionately higher lymphocyte
count in bovine peripheral blood compared to other species4.
The serum chemistry analysis revealed azotemia in the form of an elevated creatinine,
hypokalemia, hypochloremia, hypocalcemia, and an elevated bicarbonate level. Furthermore,
the total protein and albumin levels were towards the upper limit of normal. The azotemia likely
has a significant prerenal component, as multiple clinical signs indicated dehydration, which is
also consistent with the total protein and albumin values being upper normal. Renal or post-renal
azotemia was not suspected, as there were no clinical signs of urinary obstruction or history or
laboratory evidence of primary renal disease. The hypochloremia without an associated
hyponatremia indicates an acid-base disturbance, which is supported by the elevated bicarbonate
level. The elevated bicarbonate level indicates metabolic alkalosis, as bicarbonate ions
accumulate when there is a lack of acidic hydrogen ions for neutralization in plasma in order to
yield a physiologic pH3. Hypochloremic metabolic alkalosis is consistent with a left displaced
abomasum because the abomasal displacement results in the obstruction of pyloric outflow,
which sequesters of hydrochloric acid in the abomasum. Such sequestering of hydrochloric acid
results in circulatory depletion of hydrogen and chloride ions, accounting for the hypochloremic
metabolic alkalosis. The hypokalemia is a finding consistent with anorexia, as dietary potassium
contributes significantly to plasma potassium levels, and is also consistent with a left displaced
abomasum because pyloric outflow obstruction may reduce the amount of dietary potassium
delivered to the small intestine for absorption. Lastly, the hypokalemia may contribute to the
metabolic alkalosis by causing an intracellular shift of hydrogen ions in exchange for potassium
ions to restore normokalemia. Hypocalcemia, as seen in this cow, may be expected with a dairy

5. cow in lactation; although, the hypocalcemia may be exacerbated by the metabolic alkalosis due
to a renal tubular response in an attempt to preferentially reabsorb hydrogen ions instead of
calcium. Furthermore, the cow is likely truly hypocalcemic, as the lack of plasma hydrogen ions
in metabolic alkalosis frees up albumin binding spots, to which ionized calcium in the plasma
may bind, resulting in an artificially high total calcium level and a physiologically reduced level
of free ionized calcium in the plasma3. The hypocalcemia may also contribute to the
hypokalemia due to urinary potassium wasting and preferential reabsorption of calcium over
potassium. Other causes of hypocalcemia, including vitamin D deficiency or
hypoparathyroidism, were less likely in light of the other clinical signs and due of the lack of
laboratory evidence of organ disease. The working diagnosis is left displaced abomasum.
DIAGNOSTIC DISCUSSION
The cow’s initial presentation of bloat prompted immediate intervention to decompress the
rumen via placement of an orogastric tube, which yielded 75 L of alkalotic ruminal fluid.
Although the cow was in metabolic alkalosis due to sequestration of hydrochloric acid in the
abomasum, the refluxed fluid was also alkalotic likely due to the dilution of the sequestered
hydrochloric acid by water that accumulated in the forestomach due to the inability to flow out of
the pylorus. The cow-side tests conducted during the physical examination ruled out mastitis as
a cause for decreased milk production and showed significant ketonuria, indicating a metabolic
shift towards fat metabolism because the cow is not receiving enough volatile fatty acids from
the rumen. The decrease in milk production in light of the ketonuria indicates the redirection of
energy to more vital processes to maintain life. Moreover, the dehydration noted on the physical
and confirmed by the laboratory data also explains the decrease in milk production, as a
sufficient quantity of water is required for lactation. The ruminal flora may have been initially
compromised by the owner’s antibiotic administration and further complicated by the
displacement of the abomasum and subsequent bloating, which explains the decreased delivery
of volatile fatty acids from the rumen into circulation and the subsequent mobilization of fat
stores. The radiographs showed no abnormalities and ruled out hardware disease, as well as
abscesses and neoplasia as causes for the vagal indigestion, which supports the diagnosis of left
displaced abomasum because the resultant pyloric outflow obstruction is the best explanation for
the vagal indigestion. Neoplasia was an important rule-out because of the unknown BLV status
of the herd. The stress leukogram is clinically consistent with the tachycardia and increased
sympathetic activation due to the displaced abomasum. The hypochloremic metabolic alkalosis
is also clinically consistent with the left displaced abomasum due to the pyloric outflow
obstruction and also helps explain the hypocalcemia. The hypokalemia is likely a consequence
of the diseases process from anorexia and hypocalcemia and may also help explain the
tachycardia. The physical examination findings, including the ping in the left abdomen from the
9th to 13th intercostal spaces, in conjunction with the laboratory data, point towards a left
displaced abomasum being the primary problem.
TREATMENT AND CASE PROGRESSION
The presenting clinical signs and diagnostics were suggestive of gastrointestinal disease, with the
working diagnosis being left displaced abomasum. Exploratory surgery was suggested to
confirm and repair the displacement. The owner consented to surgery, and we performed a right
paravertebral block using lidocaine followed by a standing right flank laparotomy to allow the
greatest access to the gastrointestinal tract. A diagnosis of left displaced abomasum was

6. confirmed and a pyloropexy performed to repair it. Because this procedure was performed in the
hospital with appropriate precautions, we elected to not use antibiotic prophylaxis. Pain and
inflammation was managed peri-operatively with flunixin meglumine (1.1 mg/kg IV q 24 hrs).
The patient presented with dehydration and metabolic alkalosis. Therefore, we intravenously
administered acidifying fluids with higher levels of chloride, 40 L 0.9% NaCl.
Following the laparotomy, the patient remained depressed, eating and drinking very little. The
ketonuria persisted, likely due to a lack of volatile fatty acid production in the rumen, and
abdominal distention recurred within 12 hours yielding a ping in the left paralumbar fossa. The
patient once again displayed tachypnea and tachycardia, and we passed an orogastric tube.
Following passage of the tube, 60 L of rumen fluid and a large amount of gas were released, and
the heart and respiration rates returned to normal. A PCV and TS revealed that the patient had
been sufficiently hydrated. However, the serum chemistry indicated that despite the bicarbonate
and chloride approaching normal levels, the calcium and potassium were still low. Due to the
low recurrence of left displaced abomasum following pyloropexy and the location of the ping in
the left paralumbar fossa, the source of the bloat was likely the rumen. The patient’s anorexia,
atonic rumen secondary to distension, and persisting electrolyte derangements causing
gastrointestinal hypomotility were all implicated in the recurrence of bloat. We elected to
transfaunate with 20 L of fresh bovine rumen contents once daily for three days in order to
restore healthy ruminal flora. Furthermore, we started the cow on maintenance fluids consisting
of acetated Ringer’s, as the most recent serum chemistry indicated that the bicarbonate level was
returning to normal following the repair of the displaced abomasum. The acetated Ringer’s
solution was prepared with 5% dextrose in order to provide an immediate energy source to the
body and reduce ketogenesis, 20 mEq/L potassium chloride to support normokalemia and
counteract the effects of insulin release due to dextrose administration, and 500 mL of 23%
calcium gluconate at 50 mL/kg/day to restore normocalcemia. Once the patient’s normal water
intake resumed, intravenous fluid therapy was discontinued, and 60 grams of potassium chloride
was added to the transfaunate and 500 mL 23% calcium carbonate was administered orally to
maintain electrolyte balance. Flunixin meglumine was continued throughout the course of
therapy for pain and inflammation. Three days post-surgery the patient was responding well
with improved mentation, appetite, and gastrointestinal motility. Her milk production remained
low during hospitalization, but bloat did not recur.
DISCHARGE
We informed the owner of the low likelihood of recurrence of abomasal displacement following
pylorlopexy, but that recurrence is still a possibility. We instructed the owner to watch for loss
of appetite, abdominal distension, abnormal feces production and other signs of gastrointestinal
disease, and to contact a veterinarian if any of these signs are seen. In addition, we told the
owner to ensure that the cow is eating and drinking normally to continue to reestablish normal
rumen fauna. The prognosis is good, as she is already showing signs of improvement; however,
milk production will not likely reach peak during this lactation cycle, though future cycles
should not be affected. Her status as a show cow may not be ideal as udder size and milk
production may be decreased. We also made recommendations for proper nutrition based on
daily dry matter intake for pregnant, lactating cows. We also informed the owner of the
withdrawal times of the medications that were administered prior to presentation.

7. References
1. Hart, K. Physical Diagnosis Laboratory Material. University of Georgia, College of
Veterinary Medicine. Athens, GA. February, 2014.
2. Kopcha, M. Oral Fluid Therapy for Adult Cattle. Michigan Dairy Review, April 2008.
3. J Robert, Duncan., Latimer, Kenneth S., and Kenneth S. Latimer. Duncan & Prasse's
Veterinary Laboratory Medicine: Clinical Pathology. Chichester, West Sussex, UK: Wiley-
Blackwell, 2011. Print.
4. Jarrett, C. Veterinary Histology Laboratory Material. University of Georgia, College of
Veterinary Medicine. Athens, GA. September, 2013.