Forestomachs to rectum Flashcards
What do you look at when doing a visual exam on a PE
Abdominal contours, stance of the animal
What can you appreciate during asculation on a PE
Frequency of ruminal contractions
strength, duration, frequency, mixing verses eructation
(1)what is noted on the palpation of the left paralumbar fossa and (2) deep palpation of the left abdominal wall
(1)Presence and strength of ruminal contractions
(2) Degree of rumen fill; consistency of ruminal contents
(normal = doughy; dehydration = hard, fist indent stays)
How it the pain response test performed?
Withers depression test (“scootch test”; done where
scapulae come together); roll skin under your hand;
normal response is cow moving away from stimulus -
negative response means they are very painful
because they have pain deep in there abdomen that is
worse than you pulling on skin; negative scootch is
positive for pain in abdomen; they will also have
expiratory grunt
Deep palpation at the xiphoid process of the ventral
abdomen w/knee; can also use bar or board under that spot - if painful, makes an expiratory grunt = positive pain response
- Negative for pain = will kick you in the face
[“cast withers” = uterine prolapsed…not the same !]!
What is noted during percussion and auscultation on a PE?
Pings, gas-distended viscera (LDA and RDA). Stethoscope on 10th-11th rib and percuss in the paralumbar fossa and down and forward to where the abomasum is. Gas in rumen=Hallow sound (pong), gas in abomasum is high pitched “ping”!
What is noted when doing ballottement and auscultation on PE?
“Tinkling” of organs with a fluid-gas interface - checking rumen contents or fluid; can check for pregnancy advanced stages on R side, push fist into lower flank and see what material comes back and hits hand (fluid, fetus, rumen contents)
Rectal examination can appreciate … on PE
Dimensions of abdominal organs; presence of abnormal gas or fluid within or outside viscera; position of palpable organs (aorta, left kidney, sublumbar lymph nodes, iliac artery bifurcation)
What is examined when looking at the feces?
Quantity, consistency, color (indicative of what they have been eating), odor (pungent if in there for a long period of time), fiber length (large pieces = quick transit time, small pieces = slow transit time or not getting enough fiber)
What is the reason behind these abnormalities of the feces?
- blood (red/black)
- Mucus
- Fibrin
- sand/stones
- Undigested feedstuffs
Blood (red = bleed in rectum, black = upper GI bleed)
Mucus = obstruction
Fibrin = inflammation/infection (salmonella, BVD)
Sand/Stones=dietary deficiency (fiber)
Undigested feedstuffs?
How different is the PE of the right abdomen than the left?
It is not. Ballottement, auscultation, percussion, and palpation are used to assess the viscera on the right side as well.
What are the two most common clinical signs associated with cattle diseases in general. How do they direct the diagnosis?
anorexia and rumenal stasis. diagnosis of digestive diseases must be based on negative findings in other systems.
Primary vs. Secondary Indigestion (what causes each)???????
Primary: Bloat is the primary condition - Reticulum - Rumen – mixes, grinds to reduce fiber size - Omasum Secondary: Bloat is secondary to another condition - Abomasum - Liver - Pharynx - Severe systemic disease - High fever – mastitis, foot rot
The normal physiology of forestomachs (in order)
Contraction starts in reticulum (dorsal sac
then ventral sac) –>Takes 1 min for contraction to go all
the way around –>Rumen is like a big fermentation vat
that works best w/small amount of food often –>Mixing of fluid and solid ingesta –>Maceration of fibrous feedstuffs –> Circulation of ruminal fluid – increased
surface contact, increased absorption of VFAs –> Filtering material for the reticulo-omasal orifice and lower GIT –> Removal of gas through eructation –> Regurgitation of fiber for chewing.
What are the two cycles in rumination?
Primary cycle – mixing
Secondary cycle – eructation
Definition and mechanism of bloat
Distention of the rumen with gas – esp. upper part of left flank
- *Failure of eructation**
- Normal bovine does not produce gas during fermentation more quickly than it can be eructated
Microbial fermentation produces these two types of gas:
methane and carbon dioxide
What 3 factors does the gas production (in bloat) depend on
- Ruminal microbial population
- Ruminal pH
- Substrate that cow eats –cow that eats grain vs. grass (clover/alfalfa produce more gas than
timothy/Bermuda)
The role of eructation in bloat
Normally gas can be expelled quicker than it can be produced
Bloat is NOT due to excess gas production, bloat is due to failure of the eructation process
What are the three causes of bloat?
- Failure of cardia to relax
- Obstruction of the esophagus or cardia
- Failure of reticulo-rumenal muscular contraction
The normal function of the cardia.
When the animal gets ready to burb, the cardia relaxes and lets the gas out.
Three ways the cardia can fail to relax
- reflex closure when the cardia isn’t cleared of ingesta
- Anatomic distortion – abscess, tumor (commonly lymphosarcoma), lymph node, mass or space
occupying lesion next to cardia changing position - Frothy bloat – gas trapped in foamy bubbles (not enough surfactant in rumen), not in free form,
can’t be eructated (froth physically blocks the cardia)
• Legume pasture bloat – clover, alfalfa, soybean
• Legume hay bloat - try to feed hay before putting out to pasture
• High concentrate bloat – grain and not enough fiber in diet
What can cause failure of reticulo-rumenal muscular contractions and what are the symptoms?
hypocalcemia (milk fever)
Complete stasis
Abomasal distention*
What are the 2 ways to help diagnose bloat?
- History – what has the animal been eating
- Physical examination
- General - auscult abdomen - from point of shoulder up to 13th rib and area of rumen
- Passage of stomach tube – determine if obstruction, free gas, frothy bloat
True or False: Bloat is never life-threatening
False: During diagnosis we need to rule out acute life-threatening forms – cows can bloat quickly and severely
Treatment of bloat in an emergency situation
Trocharization
• Risk of peritonitis
• Before removing trochar – install some potassium penicillin, procaine penicillin
• Has to be emergency because you are creating a hole in the rumen and that will cause
some leakage upon removal, which can lead to peritonitis
• Can use trochars on horses - ie cecal trochar
o Can also inject Penicillin into cecum to try and kill off organism producing the gas
Treatment of acute bloat (non-emergency) – 4 therapies
Remove esophageal obstruction
Administer foam destabilizers (for frothy bloat)
• Turpentine
• Gasoline
• Detergent (Tide)
• Therabloat (Poloxalene - DOC) – a surfactant
specifically designed for bloat – number one tx for
acute/frothy bloat!
Release gas via stomach tube
Administer calcium in cases of hypocalcemia
Treatment of chronic, free gas bloat
Release gas through stomach tube
Surgical fistulation
Where is chronic free gas bloat usually seen?
common in feedlot cattle d/t pain from respiratory disease
To eructate the animal needs to inspire against a closed thorax…painful respiratory infections can prevent
animals from taking deep inspirations therefore causing them to bloat
What is the medullary center’s neuronal control of rumen and reticulum contractions?
Motor impulses to the reticulum and rumen are generated when excitatory input exceeds inhibitory input
o Ratio of excitatory to inhibitory input determines:
- Rate / Magnitude / Duration of primary cycle of
contractions
What is the splanchnic nerve’s imput to the rumen and reticulum contractions? Inhibit or excite?
Inhibitory
The Vagus nerve’s imput to rumen and reticulum contrations? Inhibit or excite?
Excitatory
What nervous issues can cause rumen hypomotility or stasis?
Absence of vagal input from gastric centers,
Ineffective motor response
4 things that can result in decreased motor response (in reference to rumen hypomotility or stasis)
Decreased excitatory input to gastric centers
Increased inhibitory input
Depression of gastric centers
Defective vagal innervation
What 2 things can cause depression of gastric centers?
Drugs that depress the CNS
Endotoxemia
Describe the anatomy of the vagus nerves. What are the branches and what do those innervate?
Right and left vagus nerves
• Dorsal and ventral branches of vagus nerves
o Dorsal – to rumen, other stomachs
o Ventral – to reticulum, omasum, lesser curvature
of abomasum
Defective vagal innervation can cause what secondary forestomach disease?
Bloat
What 3 factors can increase ruminal motility?
Mild distention, tension generated during contraction
Eating, chewing
Increased acidity as abomasum empties
What 4 factors can decreased ruminal motility?
Severe ruminal distension
Pain (anywhere in body), but esp. abdominal pain
Abomasal distention (severe)
Increased concentration of undissociated VFAs
associated w/ ruminal acidosis, probably certain toxins
These receptors are stimulated by “Mild distension and tension generated during contraction” and are located at the Reticulum, reticuloruminal fold, and cranial ruminal wall
Low threshold tension receptors
Buccal receptors in the mouth are stimulated by what?
Eating and chewing
These “acid receptors” in the abomasum respond to what stimulus?
Increased acidity as abomasum empties
These receptors located in the Reticulum and cranial rumen and respond to severe ruminal distension
High threshold tension receptors
These chemical receptors respond to Increased concentration of undissociated VFAs associated w/
ruminal acidosis, probably certain toxins. Where are they located?
The mucosae of the reticulum and rumen
receptors in the abomasum that respond to abomasal distension are called…
Tension receptors
Two other names for traumatic reticuloperitonitis
traumatic gastritis and hardware disease
Etiology of hardware disease
foreign object penetration of the reticulum resulting in localized or generalized peritonitis
- Animal has eating nail/wire, fell into reticulum
- As reticulum contracts, nail/wire is pushed through peritoneal cavity leading to peritonitis - can also push into heart - if penetrates heart, animal will drop dead;
if just penetrates pericardium it inoculates that with bacteria –> pericarditis
The severity of hardware disease depends on these factors:
- Size, shape and nature of FB
- Location and degree of damage at the puncture site
- Degree of contamination at the time of puncture and subsequent to puncture
What are the common sequelae to traumatic reticuloperitonitis?
Perforation
Acute local peritonitis
• Recovery
• Chronic local peritonitis
o Vagus indigestion
o Diaphragmatic hernia
• Acute diffuse peritonitis
• Acute pericarditisWhat are some uncommon sequelae to traumatic reticuloperitonitis?
Rupture of left gastroepiploic artery – death
due to internal hemorrhage.
Splenic, hepatic, diaphragmatic, pleural abscesses
Pneumonia
Endocarditis
Arthritis
Nephritis
Rupture of coronary artery or ventricular wall – cardiac tamponade
Fibrinous adhesions are an acute process in hardware disease. What do they turn into and how quickly does this occur?
They turn fibrous and this can happen in 10-14 days
What are some clinical signs in the acute phase of Hardware disease?
Acute phase – fever, anorexia, depressed, decreased or absent rumen contractions
What are some signs seen later in hardware disease?
Cranial abdominal pain (anterior part of abdomen) reluctance to move or lie down, trembling of triceps muscle
Expiratory grunt, arched back stance – stand w/neck stretched out
Often stand with front limbs higher than hind limbs to take weight off chest - elbows abducted from body – stand uphill
Vomiting sometimes observed
Other signs referable to penetration
• Muffled heart sounds
• Distended jugular veins associated with heart
failure
Neutrophilic leukocytosis with a left shift - above 12,000; btw 12,000and 20,000
• Immature WBCs seen in peripheral blood b/c mature WBCs are being used up quickly due to infection – can’t keep up with demands.
Other differentials for hardware disease:
- Other causes of peritonitis
- Other causes of heart failure – if distended jugular veins
- Systemic diseases accompanied by pain and/or sepsis
What are the conservative treatments suggested for cattle with hardware disease?
- Earliest method of treatment – put cow on inclined plane w/ front limbs higher to take weight off diaphragm, object may fall back into reticulum and heal.
- Conservative medical treatment
- Magnet – FB attracted to magnet, can give
prophylactically to heifers 1.5-2 years - heavy
magnet, drops into reticulum, attracts metal
objects and holds them in place until they erode
away- Can use compass, stud finder, another magnet or
ULS to see if cow already has a magnet. - Abx (Can also place cow on incline place to relieve pressure and give Abx to help recovery)
- Can use compass, stud finder, another magnet or
True or false: surgery is a treatment for hardware disease.
True
How can hardware disease be prevented?
Give magnet to heifers around 16 mo. of age - will attract any metals that animal eats
Vagal indigestion is characterized by what?
gross distention of the rumen and sometimes bloat – food doesn’t pass through the rumen into other stomachs
T/F: Vagal indigestion is presented acutely
False it is more of a chronic condition
What is an old term for vagus indigestion
“Hoflund’s syndrome”
By experimentally cutting the vagus nerve what 4 experimental conditions can occur?
- Functional stenosis between the reticulum and the omasum with atony of the rumen and reticulum
- Functional stenosis between the reticulum and omasum with normal or hyperactive ruminal and reticular motility
- Permanent functional stenosis of the pylorus with atony or normal activity of the reticulum
- Incomplete pyloric stenosis
What are the two natural conditions that occur with vagal indigestion?
- Anterior functional stenosis – omasal transport failure
2. Posterior functional stenosis – failure of abomasum to empty into pylorus
Which is more common; anterior or posterior functional stenosis?
Anterior functional stenosis
Describe the pathophysiology of an Anterior functional stenosis? Where would associated pathology be found?
Ingesta fails to flow through into the abomasums – distention leads to lack of motility.
(Ruminal hypermotility is more common than hypomotility)
o Reticulo-omasal orifice is wide but food won’t flow through due to lack of motility.
**Associated with pathology of the posterior thorax or anterior abdomen.
Which two stomachs does posterior functional stenosis distend with ingesta?
The rumen and abomasum
What causes a posterior functional stenosis?
Caused by tumor, fat necrosis – something that obstructs pyloric outflow.
May also be sequel to disease which affects the blood supply to the muscular wall of the abomasum
Sequestration of what element is common with posterior functional stenosis? How can this be identified and why does it happen?
Sequestration of chloride is a common problem and can be identified by serum determination
o Cow regurges fluid from abomasum back into rumen
What are the clinical signs of vagal indigestion?
- Gradual onset, gradual abdominal distention, decreased fecal output
- Typical abdominal appearance – rumen greatly distended in ventral sac (so that rumen takes
entire left side and lower half of right - can feel this upon palpation) - LN get enlarged due to inflammation of this part of abdomen
- Hypochloremia – differentiate anterior from posterior - nothing wrong on CBC; normal Cl in a cow 99-110; if Cl is sequestered in stomach/digestive tract, end up with failure of Cl absorption and a drop in Cl in blood, can get as low as 55-60 - lower it gets, the worse the prognosis
- <99 = alkalotic
o if can’t differ - will have to do surgery on L side to differ from rumen or reticulum
o Auscultation reveals bradycardia and A fib.
Which clinical signs are a good indications that a case of vagal indigestion might need surgery?
Enlarged ventral abdomen and enlarged LN are a good indication that surgery is needed
Differential diagnoses for Vagal indigestion
- True intraluminal intestinal obstruction: Plant material (Phyto-bezoar), Blood clot – BVD or clostridial disease, Twine
- Diaphragmatic herniation
- Advanced pregnancy or hydrops of the uterus – uterus fills up whole abdominal cavity and
blocks flow of ingesta out of the abomasum into the rest of the GIT
Therapy for vagal indigestion
Surgery –L side approach usually exploratory laparo-rumenotomy or other specific corrective procedure
o Overall recovery rate is about 30% for vagal indigestion type problems
T/F: Motor dysfunction can cause fermentation issue, but fermentation issues cannot cause motor dysfunction.
False: Fermentation disorders can cause motor dysfunction
What can motility disturbances be attributed to?
Motility disturbances may result in decreased microbial activity but are primarily attributable to
changes in ruminal fluid or from feed changes; they result from lesions that disrupt neuromuscular
impulses
How do primary fermentation issues occur?
Arise from food abnormalities – change of food in any kind of way
o Ration adjustments are part of the solution
What are the properties of normal rumen fluid?
Properties:
- Olive, brownish-green - varies slightly based on what animal is eating
- Slightly viscous – due to saliva
- Aromatic, strong odor
- pH - remember that it is usually slightly acidic (normal pH = 5.5-7)
- Roughage diet – 6.0 to 7.0
- Grain diet – 5.5 to 6.5 (more acidic)
- Multiple forms of protozoa, all of which are active
- Chloride concentration < 30 mEq/liter – tells you about obstruction
The animal control factors that influence normal rumen fluid
Salivation
Mixing and rumination
Ingesta outflow - blocked makes more alkaline (?)
Eructation
