Ruminant Exam #1

How do you diagnose rumenitis (acute rumen acidosis)?

history and PE findings

rumen fluid analysis

- watery, sour smelling fluid with grain

- ph

What should always be included in the ruminant physical exam?

evaluation of the rumen should always be an important part of any ruminant physical exam

should include visual observation, auscultation, palpation (rectal) and sometimes fluid collection

What are rumen disorders to be aware of?

acute rumen acidosis (grain overload)

simple indigestion (often the most common)

bloat

traumatic reticuloperitonitis (hardware)

vagal indigestion

impaction or obstruction

hyperkeratosis

hypomotility or "dead" flora

What is rumen acidosis?

occurs when readily digestible carbohydrates (starch, sugars) are rapidly fermented in an unadapted rumen

this results in increased VFAs and lactate concentrations and a reduction in pH

the resulting disease can be mild (subactue rumen acidosis) or severe (grain overload, rumenitis, carbohydrate engorgement)

What is the pathophysiology for rumenitis?

within 2-6 hours after ingestion - the rumen bacterial populations begins to shift with increasing numbers of gram + bacteria

fermentation is altered - VFA production changes and concentrations of lactate and glucose increase

rumen protozoa decline and lactate begins to accumulate in the rumen (pH 5.5)

lower pH's favor the proliferation of streptococcus bovis and other gram+ bacteria that produce lactate (ie lactobacillus)

once rumen pH is below 5.0 - gram negative bacteria die and release endotoxin

the ability of the rumen to buffer acid is overwhelmed at pHs

What are sequella of rumenitis?

bacterial rumenitis

liver abscesses

peritonitis (from thrombosis of rumen vessels)

rumen parakeratosis (chronic rumen damage)

laminitis

fungal rumenitis

caval syndrome

What are the 6 prediposing factors of the etiology of rumenitis?

1. rate of dietary adaptation

- sudden introduction of fermentable carbohydrates leads to increased risk

- dietary adaptation is necessary to build-up populations of "lactate-using" bacteria

- so the classic rumenitis occurs when an animal accidentally "engorges" on grain

2. type of carbohydrates

- risk of acidosis: wheat = barley > corn > sorghum > oats

3. processing method

- small particle sizes, heat, or pressure processing, and high moisture grain storage all increase starch availability

4. forage availability

- feeding forage before or with grain increases chewing and salivation to increase the buffering capacity of the rumen

- TMRs have a low incidence of acidosis as long as particle size and effective fiber is adequate

5. mixing frequency

- feeding small grain meals frequently decreases the risk

- avoid "ad libitum" feeding of grain if possible

6. feed mixing and delivery

- errors or fluctuations in ration mixing or in amount fed to animals can cause acidosis

- feedlot animals, dairy cattle in transition or early lactation, and show animals are generally predisposed to rumen acidosis

What are the clinical signs for rumenitis (acute rumen acidosis)?

anorexia, depression

rumen distension, atony, sloshy/watery rumen

dehydration, tachycardia, cold extremities

weakness or recumbency

watery diarrhea +/- grain

death from acidemia

What are the clinical signs for rumenitis (subacute - chronic - rumen acidosis)?

clinical signs usually vague, but you see decreased feed intake, decreased milk production and increased culling rates

may see more laminitis (sole ulcers)

low milk fat concentrations is typical of chronic rumen acidosis in a dairy herd (may pick up on DHI records)

How do you diagnose rumenitis (subacute rumen acidosis)?

evaluate ration and feeding practices

may need to do rumen fluid analysis

- select several cows in different stages of production and collect rumen fluid after feeding - pH's >5.8 are normal - if more than 2/6 cows have pH's

What are the 7 steps of rumenitis treatment?

this is an emergency - in a herd outbreak you must triage animals and treat those that are most likely to respond

if animals are already recumbent - move on to a different animal - treat those that are still standing first

1. remove further access to grain if this has not already been done

2. evacuate rumen contents

- rumenotomy most effective - rumen lavage can be done but it is very difficult and stressful to the animal

- if you have a valuable animal with severe acute rumen acidosis - there is no substitute for rumenotomy

3. correct dehydration and systemic acidosis - administer sodium bicarb

4. neutralize rumen pH - magnesium hydroxide or sodium bicarb

5. re-inoculate the rumen - transfaunate animal with rumen fluid from a healthy donor - this speed up the repopulaiton of the rumen with healthy organisms

6. administer systemic antibiotic - ppg indicated (G+ bacteria) to treat bacterial rumenitis and prevent liver abscesses

7. other treatments of questionable benefit include antihistamines, NSAIDs

How do you prevent rumenitis?

primarily management - must feed to avoid the risk factors mentioned earlier

increased dietary roughage

gradual adaptation to increased concentrates

increased particle size/reduce grain processing

ensure consistent mixing and delivery of feeds

ionophores can be used in feedlot animals (they inhibit lactate producing bacteria)

buffers can be added to the ration (sodium bicarbonate; sodium sesquicarbonate; magnesium oxide)

commonly used in dairy cattle - associated with increased milk and milk fat production

What is the pathophysiology for caval syndrome?

thrombus develops in the vena cava and shed emboli

emboli lodge in the pulmonary artery (lungs) causing embolism, pulmonary abscesses, and chronic pneumonia

pulmonary hypertension also develops leading to aneurysms (these can rupture leading to intrapulmonary or intrabronchial hemorrhage

What is simple indigestion in ruminants?

the most common cause of transient diarrhea in ruminants

occurs following an abrupt dietary change as a result of alteration in rumen flora

can occur following:

- moldy or spoiled feed

- damaged feed

- indigestible roughage

- too much feed

- new types of feed

- too much grain

What are the clinical signs of simple indigestion?

decrease in appetite

decrease in milk production

rumen hypomotility (rumen atony)

mild bloat

abnormal feces (from scant and dry to watery)

clinical signs generally involve MULTIPLE ANIMALS (herd problem)

they are usually transient and recovery is rapid after the feeding error is corrected or animals become accustomed to new feed

diagnose primarily by ruling out other causes of diarrhea

What is rumen tympany (bloat) and what are the two types?

occurs when eructation is impaired and the rumen fills with gas or froth

primary bloat - occurs when dietary factors lead to frothy or foamy rumen contents - gas is trapped in the foam and prevents eructation

secondary bloat - caused by a physical obstruction of the cardia or esophagus or due to rumenoreticular dysfunction

despite the cause, bloat results in severe abdominal distension which can result in dyspnea, abdominal pain, staggering, and/or death

How is the type of bloat generally determined?

"tube that shit" via the passing of a stomach tube

Describe primary bloat.

primarily affects ruminants on pasture (pasture bloat) or those fed high concentrate diets (feedlot bloat)

all types of ruminants are susceptible

stomach tube is easily passed by does not significantly relieve bloat - can visualize frothy contents in tube

Describe pasture bloat.

The foaming agents are soluble proteins contained in the plant - lush, rapidly growing legumes (alfalfa, clovers, wheat, etc) contain large amounts of readily degradable proteins and gas is rapidly produced

there is both breed and individual variation to pasture bloat - may be related to differences in saliva production or salivary protein composition

Describe feedlot bloat.

usually associated with ingestion of high grain, low roughage diets

this results in mucopolysaccharide (slime) production by bacteria in the rumen

this slime increases the viscosity of rumen fluid - trapping gas and forming stable foam

What is the treatment of pasture bloat?

EMERGENCY

the preferred treatment for pasture bloat is oral administration of an ionic surfactant to lower the surface tension of the foam (ie poloxalene/therabloat)

once the foam is destabilized, the gas is eructated

mineral or vegetable oil can be used but doesn't work as well

What is the treatment for feedlot bloat?

EMERGENCY

intraruminal administration of mineral oil is used to destabilize froth, followed by walking of the animals

also consider antacids to raise rumen pH (magnesium hydroxide)

How do you prevent primary bloat?

avoid grazing of high risk pastures (make hay from those pastures)

limit the amount of time spent grazing, feed hay prior to grazing, etc

can drench with oils or provide access to poloxalene (bloat blocks or licks, etc)

sometimes turn small numbers of animals out on a pasture to determine it's "bloat potential"

feedlot bloat requires management changes

increased dietary fiber and/or particle size and decrease the concentrates

consider feeding of ionophores to inhibit growth of slime producing bacteria in the rumen - usually this will significantly help control feedlot bloat

Describe secondary bloat.

gas (mostly CO2 and methane) is produced continuously in the rumen (about 2L/min) as a consequence of fermentation

anytime eructation of rumen gas is impaired - secondary bloat can occur

there are several possible causes of secondary bloat and a physical exam, lab testing, and/or exploratory laparotomy may need to be done to diagnose the etiology

What are the causes of secondary bloat?

hypocalcemia, tetanus, and rumen acidosis can all impair reticular motility

hardware disease can impair reticular function and cause bloat

outflow obstructions in the upper GI tract may lead to obstruction of the cardia

anytime a ruminant is in lateral or dorsal recumbency and the cardia is obstructed

xylazine can slow rumenoreticular motility

masses or abscesses in the rumen or reticulum can obstruct the cardia

with any of the above, a stomach tube should easily pass and the excess "free gas" is relieved

when a stomach tube does not easily pass - esophageal obstruction is suspected (choke) - often caused by apples, potatoes, turnips, sugar beets, or extraluminal masses

What is the treatment for secondary bloat?

must first pass a stomach tube and see if the gas can be relieved

if the gas is relieved - attempt to diagnose the underlying cause if possible

when a stomach tube cannot be passed or if the cause is not determined and the animal repeatedly bloats - and indwelling rumen trochar and temporary rumen fistula can be used

temporary rumen fistulas are preferred over rumen trochars in valuable animals (reduced the risk of local peritonitis)

these fistula sites will generally close by themselves when no longer needed

"stabbing the rumen" with a knife should only be done as a last resort - high risk of peritonitis

How do you perform a temporary rumen fistula?

make small hole high in paralumbar fossa

pull rumen mucosa through hole

suture a deep rumen layer to the muscles

second layer will be rumen mucosa to skin

Describe a rumen fluid analysis and what indications you would use if for.

inexpensive, relatively easy to perform, and generally can be done in the field

indications include:

- animals off feed

- rumen atony

- abdominal rumen distension of unknown origin

- history of indigestion or rumen acidosis

- to assist in the diagnosis of feeding problems

How would you collect rumen fluid?

1. aspiration by stomach tube or probe

- advantages: fairly easy to perform, little risk to animal, can obtain a large sample

- disadvantages: tube must penetrate mat layer of the rumen, sample can be contaminated with saliva, can't determine or control position of tube in rumen

- use weighted tube (glue bolt in the end of a regular stomach tube) - then can use suction pump to aspirate fluid from rumen (low volume)

2. rumenocentesis

- advantages: fluid can be collected from a consistent location, no saliva contamination

- disadvantages: can only get a small sample, risk of peritonitis or local abscesses, more dangerous to veterinarian, may need sedation

- most commonly used on a herd basis for diagnosis of subacute rumenitis

What are the 6 parts to a rumen fluid evaluation?

1. pH increases with saliva contamination and varies depending on time after eating (pH increases after eating)

2. normal pH is 6-7.2 with high roughage diets and 5.5-6.5 with high grain diets

3. abnormal pHs include anything below 5.5 (acidosis) or anything above 7.5 (anorexia, urea toxicity, etc)

4. protozoal activity

- must be determined while sample is still warm

- there are 3 different sizes of rumen protozoa (small, medium, large)

- should see numerous protozoa per field - mostly smalls

- provide information on "general health" of rumen

5. methylene blue reduction time

- a qualitative measur of the redox potential generated by microbial fermentation

- indicated degree of bacterial activity in the rumen

- add MB stain to rumen fluid - look at time it takes for fluid to return to original color

- should be

What is traumatic reticuloperitonitis?

"hardware disease" - occurs when a foreign body (wire/nail) penetrates the reticulum resulting in a leakage of reticular contents into the cranial abdomen

results in local peritonitis which impairs rumenoreticular motility

may also penetrate the diaphragm and the pericardial sac or pleural cavity causing reticulopericarditis or pleuritis rather than peritonitis

What are the clinical signs of traumatic reticuloperitonitis?

generally vague

anorexia

decrease in milk

abnormal posture (abducted elbows)

evidence of cranial abdominal pain

failure to ventroflex when withers pinched

reluctance to move low grade fever

How do you diagnose traumatic reticuloperitonitis?

PE findings

increased TP, globulins, fibrinogen

abdominocentesis (increased neutrophil)

reticular radiograph (difficult)

ultrasound (difficult)

exploratory laparotomy (definitive)

What are the two types of treatment for traumatic reticuloperitonitis?

1. conservative - oral magnet plus antibiotics (procaine penicillin)

2. aggressive - surgery (rumenotomy) to try and remove foreign body or drain perireticular abscess - may or may not be of benefit

- prognosis for long term survival general poor - ranges from 45% (uncomplicated cases) to 10% (severe cases)

How do you prevent traumatic reticuloperitonitis?

should administer magnets to all cattle before breeding - this is very effective in preventing hardware disease

may need to inspect environment and/or feed processing equipment if TRP is a big problem

consider also adding magnets to feed processing and/or delivery equipment

What is vagal indigestion?

a term coined in 1940 to describe a condition in ruminants associated with a functional disturbance of the stomachs

a clinician named hoflund sectioned selected branches of the vagus nerve and was able to induce several different types of functional disturbance

hoflund stated that the symptoms seen with experimental vagal sectioning were similar to those seen in spontaneous cases

therefore he concluded that the syndrome of "vagal indigestion" was caused by injury to the vagus nerve

he then demonstrated pathologic damage in a few spontaneous cases of "vagal indigestion"

today the term "vagal indigestion" is used in veterinary medicine to describe any functional disturbance of forestomach motility in cattle

more recent studies have shown that these are likely NOT due to direct vagal damage

the term "vagal indigestion" is probably incorrect however for lack of a better term it is still commonly used

What are the clinical signs of vagal indigestion?

this is a chronic process leading to abdominal distension, decreased appetite, weight loss, reduced fecal volume, and abnormal rumen shape

there can be varying types of abdominal distension seen

sometimes there is obstruction of rumen outflow only and gas accumulates in the rumen (bloat) - this gives an "apple" appearance

"apple" = dorsal abdominal distension on the left side of the cow (bloat)

with abomasal impaction or primary disturbances of abomasal flow you have progressive distension of the lower right abdomen (abomasum) which gives a "pear" shaped appearance

"pear" = ventral abdominal distension

the classic "vagal indigestion" cow has both ruminal distension (apple on the left) and abomasal distension (pear on the right) - this is termed papple abdomen

papple = dorsal distension on the left and ventral abdominal distension on the right

rumen motility rates are variable with "vagus indigestion" ranging from rumen atony to hypermotility

rumen atony can be caused by various conditions however with hypermotility vagus indigestion should be suspected

strength of rumen contractions is almost always decreased

may see long pieces of hay in the feces of cows (omasal dysfunction)

rectal palpation is often helpful in making this diagnosis

in chronic cases, the ventral sac of the rumen is distended ("L shaped rumen")

also the ventral sac will cross over the midline of the cow and may occupy up to 75% of the abdomen

What is the pathophysiology of vagal indigestion?

there are many things that can cause disturbances in forestomach motility and thus produce clinical signs of "vagal indigestion"

hardware disease is the most common

we used to think this resulted in direct damage to the vagus nerve but now it have been proven that adhesions between the reticulum and body wall actually inhibit rumenoreticular motility producing these clinical signs

What is type 1 classification of vagal indigestion?

failure of eructation or free-gas bloat

- can be caused by esophageal obstruction or esophageal compression

- inflammation adjacent to vagus nerve or left ventral wall of reticulum (inhibits functions of the cardia)

- young calves commonly have idiopathic bloat - often will improve with time

What is type 2 classification of vagal indigestion?

failure of omasal transport

- space occupying lesions that prevent omasal transport - ie lymphosarcoma, papillomas,, FB, large liver abscesses

- omasal function can also be inhibited by adhesions between the reticulum and diaphragm (cranial to the omasum)

What is type 3 classification of vagal indigestion?

abomasal impaction

- primary abomasal impaction is associated with restricted access to water when cattle are fed a dry, coarse roughage (straw)

- secondary impaction results from a decrease in abomasal emptying (occurs secondary to hardware or perforated abomasal ulcers)

- can also have foreign bodies that obstruct flow

What is type 4 classification of vagal indigestion?

partial obstruction of the forestomach

- rare

- difficult to define - occurs most commonly in late gestation when the abomasum is forced cranially by the uterus

How do you diagnose vagal indigestion?

suspected in any case of progressive weight loss and decrease in appetite that is accompanied by abdominal distension

usually try to diagnose hardware disease initially (bloodwork)

common electrolyte abnormalities include hypochloremia (chloride sequestered in rumen or abomasum) and hypokalemia (decreased feed intake)

may also see increased rumen chloride with disturbances of abomasal outflow

definitive diagnosis = exploratory laparotomy

How do you treat vagal indigestion?

relieve esophageal obstruction if present

can treat bloat symptomatically (rumen trochar or fistula)

with most other causes, the prognosis is poor and affected animals should be culled

reticular abscesses can be drained into the rumen surgically - this will improve clinical signs

sometimes large liver abscesses can also cause "failure of omasal transport" and can be drained (thru ventral body wall)

remove any foreign body you find during an exploratory surgery

unless you find one of the above conditions at surgery - the prognosis becomes extremely poor for recoveyr

What is the epidemiology of abomasal ulcer?

occur in about 24% of 2-8 week old calves

occur in >75% of weanling calves

3% of fattened cattle (feedlot)

6% of cows (active ulcers seen at slaughter)

may be more common in high producing dairy cows

What is the pathophysiology of abomasal ulcers?

stress (unclear what specific causes of stress are)

trauma to the abomasum (rough feed, sand, hairballs)

hyperacidity from environmental or physical stress

vitamin E/copper deficiency

feeding frequency/feed type

inconsistency in feed type

What were the results of a study looking into pathophysiology of ulcers in cattle?

a study in austria looked as the microbiome present in the abomasum of normal calves vs those with ulcers

used 16s RNA pyrosequnceing

primary genera presnt were helicobacter, acetobacter, lactobaccillus, and mycoplasma

minimal differences in microbial communities seen in healthy vs ulcer calves

to this point - no data suggests that ulcers are caused by bacterial infection in cattle

What are the classifications of abomasal ulcers?

1. type 1 - non perforating ulcer - minimal intraluminal hemorrhage

2. type 2 - non-perforating with severe blood loss; ulcer erodes a major submucosal blood vessel - severe intraluminal hemorrhage

3. type 3 - perforating ulcer with local peritonitis

4. type 4 - perforating ulcer with diffuse peritonitis - massive abdominal contamination (fatal)

What are the clinical signs of abomasal ulcers?

1. ulcer only - usually no clinical signs - maybe anorexia, bruxism, salivation, decreased milk production

2. ulcer with severe blood loss - as above plus anemia, tachycardia, weakness, melena, death

3. ulcer with peritonitis - abdominal pain, increased WBC in peritoneal fluid, recumbency

How do you treat abomasal ulcers?

1. mild bleeding ulcer - consider dietary change (no grain) - control concurrent disease, avoid NSAID use

2. major bleeding ulcer - broad spectrum abx, correct LDA (if necessary)

- change diet - don't feed silage, high moisture corn, or finely ground concentrates for at least 2 weeks (feed more fibrous foods)

- ranitidine has been shown to be the most effective H2 antagonist in cattle (primarily used in calves)

3. perforating ulcer - medical treatment with anitbiotics better than surgical treatment - grave prognosis unless infection can be localized

What is hemorrhagic bowel syndrome?

a fairly new and emerging disease of adult cattle - characterized by necrohemorrhagic enteritis that primarily affects the small intestine

usually affects dairy cattle in various stages of lactation

see depression, abdominal distension, acute drop in milk production, recumbency, blood diarrhea, anorexia, and colic

may see dilated loops of intestine via ultrasound

at surgery, cattle have frank blood or blood clots in their SI lumen - very high mortality rate

the pathogenesis of this syndrome is unknown

it has been hypothesized that clostridium perfirngens type A is responsible for this syndrome - the organism that has been isolated from the intestines of affected cattle, however a definitive association has not been proven

other reports suggest that systemic infection with aspergillus fumigatus involved

What is percussion of the cow?

"pinging the cow"

high pitched sound created by gas-gluid interfaces

- playground ball bouncing on cement

What are your differentials for a left sided ping?

LDA - #1 concern

free gas in rumen

free gas in the abdomen

- peritonitis

- surgery

What are the diagnostics for pings?

location, location, location

determine borders by pinging in each direction from your stethoscope

In what locations on the left side does a ping most likely indicate an LDA?

paralumbar fossa

low LDA below and slightly caudal of paralumbar fossa

In what locations on left side does a ping most likely indicate free gas in the rumen?

caudally in the paralumbar fossa

dorsally

What are pathological and non-pathological reasons for a ping on the right side of a cow?

pathologic:

- RDA

- abomasal volvulus

- cecal volvulus

- mesenteric volvulus

- intestinal volvulus

non-pathologic:

- free gas in the abdomen (peritonitis/surgery)

- uterus

- intestinal gas

- cecal dilatation

- gas in colon or rectum

What are the most likely differentials for a ping in an area including the paralumbar fossa and cranial to the 10th rib on the right side?

RDA

abomasal volvulus

What is the differential for a small ping just cranial to the paralumbar fossa on the right side?

spiral colon

What is the differential for a ping on the right side in the paralumbar fossa?

cecal ping

What is the differential for a ping in a large area extending from the ventral edge of the paralumbar fossa ventrally on the right side?

mesenteric volvulus

What is the differential for a ping in the ventrocaudal area of the abdomen in the cow on the right side?

uterus

What are the risk factors for an LDA?

1. hypomotility of the abomasum

- endotoxemia, hypocalcemia, metabolic alkalosis, body positioning?

2. anorexia

- cow dependent on full rumen to "sit" on abomasum and prevent displacement

- "sick" cows that go off feed are at high risk for abomasal displacement

- much more common in diary cows that beef

What is the typical history for a cow presenting with an LDA or RDA?

recent calving (particularly twins)

other transition diseases (mastitis, metritis, ketosis)

decreased feed intake (particularly grain)

decreased milk production

How do you diagnose an LDA/RDA?

LDA and/or RDA determined by an abdominal percussion ("pinging cow")

location of the ping is critical

liptak test (measure pH)

rectal examination

- rumen pushed to the right (LDA)

- may feel caudal border of RDA

How do you treat an LDA or RDA?

cows with left or right displacements of the abomasum almost always require surgery

if cattle aren't valuable - recommend culling

however in most dairy cows - they will return to normal milk production and surgery is economical

this is the "spay-neuter" of dairy practice

several different techniques to repair LDA possible

What are the methods of correction for displaced abomasum repair?

roll

roll and toggle

laparoscopic toggle

paramedian abomasopexy

right flank omentopexy

left flank abomasopexy

Describe the cast and roll method to fixing a dispaced abomasum.

method:

- roll cow into dorsal recumbency

- allow abomasum to float to ventrum and gas to escape

- allow cow to stand and fill rumen with water

advantages:

- no surgery, cheap, and quick

disadvantages:

- high recurrence rate

Describe the roll and toggle method of fixing a displace abomasum.

method:

- similar to roll

- abomasum trocarized and bar sutures places

advantages:

- quick, cheap, and no incision

- 80-90% success

disadvantages:

- blind procedure

- wrong diagnosis

- improper positioning of abomasum

- casting and rolling

- toggling rumen, duodenum

- late term pregnancies

Describe the laparscopic roll and toggle as a method of fixing a displaced abomasum.

method:

- similar to toggle

- laparoscopic placement of toggle

advantages:

- same as toggle

- not a blind procedure

- can be done prophylactically

disadvantages:

- equipment cost

- casting and rolling

not commonly done in US

Describe the omenopexy (right sided) "hannover method" as a treatment for a displaced abosmasum.

advantages:

- animal standing, you can do it by yourself

- can do a thorough abdominal exploratory

- can use the same approach for most abdominal procedures

disadvantages:

- takes more time than roll and toggle

- invasive surgery

- need a long arm in some cows

method:

- suturing the omentum attached to the pylorus to the right abdominal wall in order to fix the pylorus to the right side

Describe the abomasopexy "utrecht method" as a way of fixing a displaced abomasum.

advantages:

- direct visualization of the abomasum

- strong adhesion between abomasum and body wall (theoretically lower redisplacement rates)

- proper anatomic position of the abomasum

- good for cows in late gestation

disadvantages:

- requires an assistant generally

- limited exploration of the abdomen

- can't use for other types of abdominal surgery

- needs to be a "high" DA

- risk of mammary vein perforation

- possibility of trapping intestines if suture pulled too tight

- cows may come back into milk slower

method:

- left flank entrance into the abdomen, suture to the abomasum, and then push those sutures through to the bottom of the abdomen and place there

Describe the abomasopexy paramedian as a method of fixing a displaced abomasum.

advantages:

- direct visualization of abomasum

- strong adhesion between abomasum and body wall

- abomasum in correct anatomic position

- can be done fast with help

- incision site barely visible

disadvantages:

- must role cow on its back (hard on cow, requires help)

- physically demanding for the surgeon

- risk of bloat, aspiration of rumen fluid

- no exploration of the abdomen

- shouldn't be done in toxic cows or those with respiratory disease

- risk of wound dehiscence

method:

- paramedian incision (avoid the milk vein) and then pexy the abomasum to the ventral abdominal wall

If you have a RDA or abomasal volvulus, what are your best surgical approaches?

right flank laparatomy (omentopexy) with cow standing

right paramedian with cow in dorsal recumbency

What are the surgical outcomes for LDA surgery?

typically, LDA surgeries are thought to have a very high success rates (

Describe the surgical outcomes of abomasal volvulus.

good post operative signs:

- diarrhea (particularly if abomasum was very large at surgery)

- good appetite withing 3 days of surgery

- increasing milk production after surgery

- rumen motility returns

keys to improving survival (goal is 70%)

- early diagnosis

- good surgical technique

- intra and post-operative intravenous fluids

- abx to prevent peritonitis

What are some conclusion we can make about displaced abomasums?

there may be no single best method for repairing LDAs

depends on the surgeons experience and the individual case

future studies that look at long term re-displacement rates are warranted

overall goal should be focused on DA prevention

What flank anesthesia methods can you do for standing abdominal surgeries?

proximal paravertebral

distal paravertebral

inverted L

line block

Describe the proximal paravertebral anesthesia method.

block dorsal and ventral nerves of T13, L1, and L2 as they emerge from vertebrae

- complete anesthesia of flank from skin to peritoneum

advantages

- specific nerve block

- small volume of lidocaine

- no lidocaine in the incision

disadvantages

- technically difficult

- requires 3in needle

- laceration of the aorta or caudal vena cava

What is the process of the proximal paravertebral anesthesia?

insert 3 in needle at the cranial edge of transverse process of L1 just lateral to vertebral body

advance needle ventral to the process

- inject 10-15 mL of lidocaine

repeat off caudal edge of L1 for L1 nerve

repeat off caudal edge of L2 for L2 nerve

Describe the distal paravertebral anesthetic block.

individually block dorsal and ventral nerves of T13, L1, and L2

- complete anesthesia of flank from skin to peritoneum

advantages

- easier than proximal paravertebral

- no lidocaine in the incision

- uses routine size needles

disadvantages

- difficult in fat dairy cows and beef cow

- variability in location of L2 nerve

- more lidocaine needed than proximal PV

Describe the process for the distal paravertebral anesthetic block.

insert a 1.5", 18 G needle directly at the end of the transverse process of L1 (to block T13)

- L1 can be difficult to identify

slide the needle dorsally over the top and insert to the hub needle

- inject 5 cc lidocaine in this area, 5 cc cranial, and 5 cc caudal

back the needle back to the end of the process and slide ventral to the process

- inject lidocaine as before

repeat for L2 (L1 nerve), L3 and L4 (L2 nerve)

Decribe the inverted L anesthetic block.

provides regional anesthesia to most of the flank

advantages

- relatively simple

- large area anesthetized than line block

- no lidocaine in incision

disadvantages

- less effective for deeper tissues

- multiple injections

- large volume of lidocaine

Describe the line block anesthetic block.

provide anesthesia to the tissues to be cut

advantages

- simplest technique

disadvantages

- less effective for deeper tissues

- multiple injections

- anesthesia in a limited area

- swelling and potentially delayed heating due to lidocaine in the incision

Describe the process of a rumenotomy.

Standing or right lateral restraint

- based on animal size

clip, prep, and block the left paralumbar fossa

- drape the surgery area

- wear sterile gloves

flank incision

tack the rumen dorsally and ventrally with a large, non-absorbable suture

circumferentially suture the rumen to the skin using a cushing pattern with a large non-absorbable suture

ensure a water tight seal

incise the rumen wall

evacuate the rumen contents

- enough for exploration

- complete for grain overload

explore the rumen

- reticulum

- omasal orifice

clean the cut edges of the rumen

suture with #1-2 absorbable suture

- monofilament

- simple continuous with cushings

- utrecht pattern

clean all ingesta from the area

remove skin sutures

change gloves, drape, and gown

close the abdominal wall routinely

- simple interrupted at ventral aspect of incision

Compare the use of the suturing technique with the rumen board for a rumenotomy.

suturing technique

- more effective seal

- less likely to contaminate abdomen

- no special equipment

- time consuming

rumen board

- quicker and easier (ideal for dealing with a large number of cows with grain overload)

- more likely to contaminate the abdomen

When should you intervene with a C section in a cow?

stage 1 should be no longer than 8 hours

- typically less for mature cow, longer for heifers

stage 2 should last no more than 2 hours

- did you see her actually "start"

the delivery should progress every 15-30 minutes

- if cow not done in 2 hours, or not progression for more than 30 minutes, check the cow

- if you know what the problem is and know how to correct it, proceed

- if the calf isn't delivered in 30 min, call vet (you)

What are indications for a c section?

live (valuable) calf or value of dam

fetotomy is impossible due to a small birth canal or prolonged labor, ephasematous calf

incomplete cervical dilation

relatively or absolutely large fetus, fetal monsters

uterine torsion

When in the best outcome for a c section and when are most c sections done?

best outcome: c-section elected and pursued before stage 1 ends

most are done in stage 2

What should you consider when deciding the approach to a c section?

consider animal, facility, producer, and practitioner factors when selecting approach

What are the positives and negatives of a standing left-side flank incision for c section?

positives

- less restraint needed

- less stressful to cow

- minimal tension on the suture line

- rumen inhibits evisceration potential intraoperatively

negatives

- uterine contents more likely to spill intraperitoneally

- requires adequate facilities to restrain cow

- requires a lot of physical strength on part of practitioner

What are the positive and negatives of a recumbent, dorsal position, midline, or paramedian incision for c section?

positives

- excellent exteriorization of uterus and fetus

- minimizes contamination of peritoneal cavity

-excellent for heifers as they are very likely to lie down

negatives

- requires assistance to position and restrain cow

- requires full sedation, more likely to bloat or aspirate

- rumen can come through incision

- causes some animals to strain more

- incisional complications post operatively

Describe the c section process from a standing left sided approach.

regional anesthesia

incise skin

exteriorize foot (if possible)

incise uterus over the hoof

find both feet and place chains

remove or replace placenta

suture uterus: no. 2 or 3 absorbable suture

closer peritoneum and muscle layers: no. 2 aborbable suture, 1 or 2 layers

close skin: no. 3 nonabsorbable suture

What is clostridial bacteria?

gram positive, anaerobic spore forming rods

spores are resistant to disinfectants and environmental conditions

- commonly found in soil

produce potent exotoxins and exoenzymes

What are the clinical signs of clostridial disease?

depends on

- type of toxin

- dose of toxin

- route of exposure

rapidly progressing

- treatment often difficult

- commonly found dead

emphysematous, necrotic lesions are commonly found

What are the 4 categories of clostridial diseases?

neurologic disease

enterotoxemia/GI disease

gas gangrene and malignant edema

liver disease

What are the neurologic clostridial diseases and their associated pathogens?

tetanus

- clostridium tetani

botulism

- clostridium botulinum

enterotoxemia/pulpy kidney disease

- clostridium perfringens type D

Describe tetanus.

C. tetani is normally found in the soil and the GI tract and feces of herbivores

- resistant to environmental conditions

contamination of anaerobic sites or wounds with spores

- postpartum uterus

- castration site

- puncture wound of the foot

cattle are more resistant than small ruminants

- postpartum cows

- calves that are banded for castration

most common in lambs/kids after processing

- banding/castration

- tail docking

What is the pathophysiology of tetanus?

the organism cannot invade healthy tissue

spores innoculate a wound

- germinate in anaerobic conditions

- toxins produced during growth of organism

- released upon cell lysis

3 toxins

- tetanolysin (destroys phagocytes and causes tissue necrosis, maintains infection)

- tetanospasmin (spread hematogenously to inhibitory neurons, inhibits the inhibitory neurons, muscles contract and cannot relax)

- non-spasmogenic toxin (sympathetic stimulation)

What are the clinical signs of tetanus?

stiffness and hyperesthesia

prolapse of 3rd eyelid

- not in sheep

bloat with normal rumen contractions

rigid paralysis

- pump handle tail

- lockjaw

- saw horse stance

tetanic convulsion

death 5-10 days after onset

- due to respiratory paralysis

- 80% case fatality rate