Академический Документы
Профессиональный Документы
Культура Документы
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
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
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.
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.
References
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.