Cow Qs

1. LDA - Left displaced abomasum

2. Empty rumen with large gas cap - rumen pings

Sunken eyes & skin tent = cow is dehydrated

Smelly vaginal discharge, open cervix & difficulty performing rectal = indicates infection (metritid)/retained placenta

High heart rate & resp rate - animal is in pain

Pings - indicative of gas collection, could be rumen pings (unlikely given symptoms)

From clinical signs think cow is suffering from LDA

What does each of the clinical signs mean?

Give your diagnosis based on clinical signs

- Ultrasound

- Take a blood sample

- Ballottement and auscultation

What further clinical examination steps would be important to perform in order to

help with your diagnostic assessment? (2.5 marks)

- Liptack test to measure the pH of the aspirated fluid.

- Blood lactate

What further diagnostics, apart from the clinical examination, may help you in

reaching a diagnosis? (1.5 marks)

- Likely to have alkalosis

- High pH

- Base excess increased

What electrolyte and acid-base balance problems are likely in this case? (1 mark)

Vagal indigestion syndrome

Chronic

Acute or chronic condition?

Traumatic reticuloperitonitis, causes abscesses that interfere with motility

What is the most common cause of this syndrome in cows?

Peritoneal fluid analysis will support if peritonitis present, the total protein or nucleated cells will increase.

A lateral radiograph should be performed to identify if there is a foreign body present, or a reticular abscess.

An ultrasound of the abdomen (cranioventral) will indicate if focal

peritonitis is present and examine the reticular contraction rate.

For a definitive diagnosis, explorative surgery is required (left paralumbar fossa laparotomy and rumenotomy).

Describe how you would further investigate, using both clinical examination and

diagnostic techniques, whether this particular cause was a factor in this case? (4

marks):

I believe that the cow is suffering from Omasal transport failure due to traumatic reticuloperitonitis, which is type II vagal indigestion.

Left paralumbar fossa laparotomy and rumenotomy

will help to identify and remove any foreign materials present.

Antibiotic therapy and supportive therapy should be given after

the surgery.

Your investigations confirm that this syndrome was caused by the common factor

you suspected. What are the potential treatment options in such a case as this? (3

marks):

Ballottement

Rectal exam

Caecal dilation

Caecal torsion/volvulus

List two differential diagnoses for the abdominal problem with this cow. (2 marks)

Hypocalcemic: The chloride is being sequestered in the abomasum leading to a drop of

negative ions in the blood.

BE: Bicarbonate is being produced by the kidneys to compensate for the loss of anions.

However this leads to a metabolic alkalosis.

Hypokalaemic: The metabolic alkalosis causes an exchange of K+ ions into the intracellular

fluid to stabilize blood pH. This ionic transfer rapidly leads to hypokalaemia.

Describe the major electrolyte and acid-base changes that are apparent on the

blood gas analysis of this cow as outlined in the table above. (1 mark)

increases in plasma L-lactate are most commonly caused by

poor systemic tissue perfusion because of dehydration, shock, endotoxemia, or a

combination of these conditions, as well as local hypoperfusion such as splanchnic

ischemia and abomasal necrosis seen in cows with abomasal volvulus

Comment on the blood lactate concentration as outlined in the blood gas analysis

results. (2 marks)

Correct hypocalcemia

increase fibre length

Decrease concentrates

Describe your post-op medical management of this cow.

Changes

Grossly

Microscopically

How does it cause diarrhoea?

Type-2 ostertagiosis: Fecal sample or pepsinogen in serum

Johne's disease (paratuberculosis): Serology (ELISA but low sensitivity) or fecal culture

(Herrold's egg yolk medium)

For each of these diseases give one diagnostic test that might assist in their

diagnosis ante-mortem.

The parasite causes the abomasum to take on a "moroccan leather"/ "cobblestone"

appearance in heavy infections. This appearance is due to the worms feeding and the

individual lesions they create eventually coalesce and give the abomasum this rough texture.

These lesions may be accompanied by a rise in pH (6-7). This means pepsinogen will no

longer be converted to pepsin as it requires a much lower pH (2.5-5). This results in the

subsequent leaking of pepsinogen across the damaged epithelium that will lead to increased

plasma levels. Adult Ostertagia can also cause hypersecretion of pepsinogen compounding

the issue. The increased pH also stimulates the production of gastrin which will cause

inappetence.

In severe cases such as above oedema is usually marked and can extend over the

abomasum and into the small intestine and omentum causing the ascites and oedema.

Why an 18 month-old bullock/steer with chronic abomasitis due to ostertagiosis

develops dependent oedema, ascites and inappetence? (pathology)