16. large animal med- bovine gastric disorders

what is indigestion related to in the bovine stomach?

rumenoreticular disease

what does good forestomach function require in ruminants?

requires joint coordination of motor function and microbial fermentation

what are primary and secondary bovine gastric disorders?

primary: dysfunction of motor function/microbial fermentation

secondary: arise out of a problem elsewhere that affects one or both of the primary functions

how do the 2 main primary functions of the bovine stomach affect each other?

good motor function is necessary for good microbial digestion, and the products of digestion have a large impact on motor activity

how can endotoxemia, fever, or depression have secondary effects on forestomach motor function?

may induce anorexia and rumen hypomotility

how can abomasal/intestinal disease have secondary effects on forestomach motor function?

may inhibit ruminal emptying and create a backflow of abomasal or intestinal contents

how can thoracic/cervical diseases have secondary effects on forestomach motor function?

may affect the esophagus or vagal nerve

how can hypocalcemia and/or dehydration have secondary effects on forestomach motor function?

by affecting muscle function

what is bloat?

aka ruminal tympany, distention of the rumen by gas

what is the pathogenesis of bloat?

methane and carbon dioxide gases produced during fermentation are not eructated and collect in the rumen

bloat is more a sign than a disease- what is more important than overproduction of gas (bloat)?

1. physical obstruction of the esophagus (choke, tetanus, masses, etc)

2. physical obstruction of the cardia

3. motor dysfunction

4. chemical inhibition

what may cause physical obstructions of the cardia?

-masses around the cardia (papillomatosis, actinobacillosis)

-feed or fluid in contact with cardia (gas trapped in stable foam, poor ruminal outflow, animal in lateral recumbency)

-adhesions (traumatic reticulitis, ruptured abomasal ulcer, liver abscess)

what may cause motor dysfunction leading to bloat?

-hypocalcemia

-chronic overdistention (vagal indigestion, undigested roughage, outflow obstruction)

-abomasal distention

-vagus nerve damage

what are causes of chemical inhibition leading to bloat?

microbial fermentative disorders (pH and VFA too high or too low)

what are clinical signs/diagnosis of bloat?

-left dorsal abdominal distention, with filling of paralumbar fossa and tightening of the skin

-may have a ping

-signs of colic

-rapid, shallow breathing

-possible cyanosis, eventual death

what do treatment options for bloat depend on?

tx options depend on whether gas is 'free' or trapped in stable foam 'frothy'

what causes frothy bloat?

usually the consequence of proteinaceous foods, mainly legumes (alfalfa, clover)

the fresher, the frothier

how is bloat treated?

***treat primary disorder (choke, recumbency, froth, hypocalcemia):

1. pass stomach tube

2. trochar (in emergencies- left dorsal paralumbar fossa)

3. for frothy bloat, must destabilize foam

how is frothy bloat treated?

must destabilize foam:

-poloxalene (therabloat, bloatguard)

-docusate sodium (bloat release)

-mineral oil/hand soap

these tx's decrease surface tension

--> put in cow, let her move, then pass a tube to release gas

when is bloat only the primary problem?

when respiratory function is impaired

-ventilation is inhibited by decreased capacity of the lung to expand

what are causes of inflammatory motor lesions of the bovine stomach?

1. traumatic reticulitis

2. chemical infectious rumenitis

what is the pathogenesis of traumatic reticulitis causing inflammatory motor lesions?

due to penetrating foreign body (hardware disease)

local inflammation, peritoneal inflammation, and adhesions affect ruminal wall function

what is the pathogenesis of chemical-infectious rumenitis causing inflammatory motor lesions?

chemical injury occurs first, injuring mucosa--> the most common cause is rumen acidosis (grain overload)

viruses (IBR, BVD, MCF), abomasal reflux, rhododendron, oak/acorn and caustic medications may play a role

common secondary invaders include: t. pyogenes, f. necrophorum, actinobacillus, fungi

what are clinical signs of inflammatory motor lesions of the bovine stomach?

may range from invisible (very low grade infections) to high-grade with fever, depression, anorexia, weight loss, decreased production, signs of abomasal discomfort

the actual mechanical perforation seen in traumatic reticulitis is usually less important than what?

mechanical perforation is usually less important than the subsequent contamination of internal tissues with rumen microbes

what are potential, serious, sequelae to traumatic reticulitis?

peritonitis, pleuritis, pericarditis

how is traumatic reticulitis diagnosed?

-usually by clinical signs

-reticular rads can be used to visualize metallic FB

-U/S to see fibrin and fluid accumulation around reticulum and in chest

what are the clinical signs of the acute stage of traumatic reticulitis?

in the acute stages of perforation:

-febrile

-completely anorexic

-completely agalactic

-signs of abdominal pain (refusing to ventroflex- positive grunt test)

-absent ruminations

what are the clinical signs of chronic traumatic reticulitis?

-intermittent fever and anorexia

-weight loss

-digestive dysfunction

what are signs of pericarditis due to chronic traumatic reticulitis?

if the heart or pericardial sac is infected, purulent pericarditis frequently leads to signs of heart failure, will hear a 'washing machine' murmur

what can chronic/healed inflammation around the cranial reticulum result in?

results in adhesions between that structure and the surrounding abdominal structures

these adhesions may impair regurg sequence of gastric motility/emptying, resulting in abnormal regurg or fluid distension of rumen

what is the pathogenesis of vagal indigestion?

still debated as is the role of the vagus nerve

this generally a chronic, gradually progressive disease

what are the different types of vagal indigestion?

type 1= bloat

type 2= omasal transport failure

type 3= pyloric outflow failure

type 4= ping-related

what is omasal transport failure (type 2)?

anterior functional stenosis, with either ruminoreticular hypomotility or normal to increased motility

hypermotile failure of omasal transport is most common cause

what causes hypermotile failure of omasal transport?

the ruminoreticulum gradually fills with ingesta and increases in size, which eventually inhibits appetite

ruminal hypermotility is stimulated by distention or gas accumulation--> when distension becomes extreme, hypomotility ensues

what is pyloric outflow failure?

posterior functional stenosis

can be complete or incomplete

what are possible etiologies of pyloric outflow failure?

adhesions and temporary ischemia during abomasal volvulus

how is type 3 (pyloric outflow failure) vagal indigestion treated?

-relieve distension (tube or sx)

-remove adhesions (sx)

-reduce inflammation (abx, NSAIDs)

what is the prognosis of pyloric outflow failure after treatment?

guarded to poor

what causes forestomach acidosis?

increased rate of VFA production causing pH or rumen liquor to decrease

what are 5 ways the cow can protect the stomach from increased ruminal acids?

1. non-ionized VFA (like propionate-most common under acidic conditions, rapidly absorbed across rumen wall)

2. hypertrophy of ruminal epithelium (papillation)

3. contraction cycles mix ingesta in contact with epithelium to increase rate of absorption

4. ruminal outflow drains VFA into abomasum/intestines

5. salivary flow and bicarbonate contents increase

what occurs with rapid increases in the energy content of the diets in cows?

mechanisms to protect the stomach from increased acids cannot keep up and papillary burn-off may occur

when carbohydrate concentration in the rumen is abundant, what bacteria tend to proliferate quickly? what do these bacteria produce?

energy-limited bacteria, especially streptococcus bovis

these bacteria then produce D- and L-lactic acid as their end products

why is lactate production by energy-limited bacteria in face of high carbohydrate loads problematic?

lactate is absorbed less readily than VFA, and will accumulate in the rumen, causing a rapid drop in pH

--> lactate is a stronger acid than VFA, more likely to be ionized

why is protozoal death due to rumen acidosis problematic?

protozoa in the rumen have a dampening effect on the rate of fermentation

with decreased ruminal pH, the death of protozoa speeds the rate of acid production

why is death of acid-intolerant bacteria due to rumen acidosis problematic?

many of the lactate-using bacteria die, decreasing rumen metabolism of lactate to proprionate

in general, there is a shift away from gram-negative and toward gram-positive bacteria

how does rumen acidity impair motility?

rumen acidosis (low rumen pH) decreases absorption and outflow of acid, as well as eructation of gas (bloat)

what occurs when the pH of the rumen reaches 4.5?

most bacteria are inhibited at this pH, but lactobacillus spp. thrive

these bacteria produce lactic acid

what occurs to blood osmolality as unabsorbed acid accumulates in the rumen?

increases the osmolality of the rumen liquor, causing water to shift into the rumen from the blood, increasing blood osmolality

the rumen becomes fluid distended and splashy

what may the die-off of gram-negative organisms in the rumen lead to?

endotoxemia

what occurs to the ruminal epithelium as acidity of ruminal fluid becomes greater?

acidity of fluid causes chemical injury to the epithelium

can then lead to fungal or bacterial invasion of the rumen wall

what does subclinical rumen acidosis result in?

changes in health and performance (milk fat depression) without causing overt clinical abnormalities

rumen wall damage or metastatic abscesses (liver) may be important

is clinical rumen acidosis a medical emergency?

yes

what are clinical signs of rumen acidosis?

fluid and gas distension of a hypomotile (splashy) rumen

-depression

-anorexia

-tachypnea

-tachycardia

-dehydration signs

-CNS signs

what lab work abnormalities may be seen with rumen acidosis?

-acidic pH of rumen

-systemic metabolic acidosis

-hyperglycemia

-hyperchloremia

-evidence of dehydration

-degenerative left shift

how should rumen fluid be collected for suspicion of rumen acidosis?

transcutaneous paracentesis is superior for subclinical acidosis, where risk of salivary contamination is higher and more confounding

how is rumen acidosis treated?

1. decrease ongoing fermentation (remove feed, lavage with large volumes of cold water)

2. correct acidosis (oral alkalinizing agents)

3. correct dehydration

4. prevent secondary infections

5. prevent secondary polioencephalomalacia (thiamine)

6. treat bloat

7. transfaunate in convalescent state

do severe, acute grain overload cases of rumen acidosis respond to conservative treatment?

no, they are unlikely to respond --> for these animals, rumenotomy or large volumes of IV fluids are often necessary

without rumenotomy, animals may relapse over the next 1-3 days due to continued fermentation

what tumor types may be seen in the rumen?

squamous cell carcinoma

lymphoma

others

which neoplasms are more commonly seen in the abomasum?

lymphoma or adenocarcinoma

what is squamous cell carcinoma in the stomach associated with in cows?

toxic plants (bracken fern(

what is lymphoma of the stomach associated with in cows?

bovine leukemia virus

what are clinical signs of tumors of the stomach in cows?

progressive weight loss

anorexia

gastric hypomotility

where does the abomasum usually sit?

on the ventral body wall

the cranial end is firmly attached to the reticulum, and no other firm attachments--> has great capacity to move

what may cause movement/dorsal displacement of the abomasum?

-ileus

-poor abomasal or ruminal fill

-gastric hyperacidity

-large abdominal volume

-gas production in abomasum

how do left displaced abomasums (LDA) occur?

when the greater curvature slides under the rumen first, followed by pulling of the abomasum dorsally

how do right displacements (RDA), abomasal volvulus, or omasal-abomasal volvulus occur?

when the abomasum is first pulled dorsally

either of these occur depending on whether the abomasum rotates around its lesser omental attachment as it displaces

what occurs as a result of abomasal displacements occluding pyloric outflow?

results in abomasal fluid distension, dehydration, and metabolic abnormalities

what metabolic abnormalities are seen with abomasal displacements?

hypokalemia, hypochloremia, and metabolic alkalosis

what is the difference of milk production seen with LDA/RDA vs volvulus?

LDA/RDA: gradual decline in milk production (often with concurrent increased ketogenesis)

volvulus: rapid decline in condition and cessation of milk production

what is the most common abomasal displacement seen in postparturient dairy cattle?

LDA

what does treatment for abomasal displacements involve?

surgical correction and correction of metabolic abnormalities

cows with LDA/RDA should be treated for ketosis as well, and cows with volvulus often require IV fluids

does LDA or RDA require more urgent surgical intervention?

RDA- requires immediate surgical intervention

LDA: can delay surgery for a day or two

what fluids should be given to manage alkalosis vs acidosis?

alkalosis: acidifying fluids (0.9% saline w/ KCl)

acidosis: buffered solutions

what is the prognosis for LDA, RDA, and abomasal volvulus?

RDA/LDA: excellent prognosis

volvulus: 70% survival (simple volvulus may do better (90%) than those with omasal involvement (10%))

what differences may be seen in cattle/cows who survive after abomasal volvulus?

cows with volvulus are less likely to regain their previous level of production, and are prone to develop vagal indigestion from tissue trauma/ischemia

what 3 groups of cattle appear to be prone to developing abomasal ulcers?

1. adult dairy cows

2. young calves

3. feedlot beef cattle

where do most abomasal ulcers occur?

most ulcers occur along the greater curvature of the fundus (except in milk-fed veal calves)

veal calves: most ulcers found around pylorus

what are abomasal ulcers though to be a result of?

inhibited mucosal protection in face of aggressive factors as well as impaired gastric emptying

what are the risk factors for young calves developing abomasal ulcers?

clostridium perfringens type A

copper deficiency

hair

geosediment

first exposure to rough feeds

what are the risk factors for dairy cows developing abomasal ulcers?

-first month of lactation (high-energy diet, stress)

-concurrent disease (DA, ketosis, mastitis, metritis)

what are the risk factors for feedlot beef cattle developing abomasal ulcers?

corn diet

geosediment

-do not appear to correlate to transport or hanlding

what are the 4 classifications of abomasal ulcers?

type1

type 2

type 3

type 4

what is a type 1 abomasal ulcer?

local erosion or ulcer with mild to no clinical signs

usually incidental findings, rarely treated

what are clinical signs of type 1 abomasal ulcers?

if clinical signs are evident:

-cranial abdominal pain (refuse to ventroflex, teeth grinding)

-anorexia

how are abomasal ulcers in cattle treated medically?

medical tx of abomasal ulcers is difficult, as H2-antagonists do not appear to work in cattle, and many other oral antiulcer meds are broken down in the rumen

decreasing stress and energy level of the diet and increasing roughage intake may be beneficial

what are type 2 abomasal ulcers?

bleeding ulcers

represents erosion into a significant vascular structure

what are clinical signs of type 2 abomasal ulcers?

-rapid drop in production

-melena

-tachycardia

-anemia

-pale mm

-weakness

what does treatment of type 2 abomasal ulcers include?

IV fluids or whole fresh blood

-surgery can be done to resect ulcer/ligate vessels

some cases (esp. older cows) bleeding is due to abomasal lymphoma, in which tx is purely palliative

which 3 directions can abomasal ulcers perforate?

1. towards abdominal wall

2. into omental attachment or bursa (most common, 85%)

3. into the intestinal recess

what are type 3 abomasal ulcers?

perforated ulcer with local peritonitis

how do type 3 abomasal ulcers present?

these are most often found during ex-laps for another problem (LDA/RDA) and are not a major contributor to clinical disease

but, adhesions from these can inhibit normal replacement of a displaced abomasum

what are type 4 abomasal ulcers?

perforated ulcer with diffuse peritonitis

what are consequences of type 4 abomasal ulcers?

can cause acute disease due to septicemia and immediate damage to other sections of the GI

or

can cause more chronic disease related to abdominal abscesses or adhesions

what are the acute clinical signs of type 4 abomasal ulcers?

-cessation of milk production

-tachycardia

-fever or hypothermia

-weakness

what lab abnormalities are seen with acute type 4 abomasal ulcers?

-high PCV with low serum protein

-degenerative neutropenia or neutrophilia with abnormal abdominal fluid

-metabolic acidosis

what is the prognosis for chronic type 4 abomasal ulcers?

adhesions may be broken down and abscesses drained/sterilized, but the prognosis for recovery is grave

true or false: cattle with long-standing, severe abomasal ulcers are likely to experience both bleeding and perforating ulcers.

true

are impactions/emptying defects of the stomach a common problem in ruminants?

no, these are rare (except in suffolk sheep)

what causes gastric impactions in sheep?

sheep have non-inflammatory local neurologic lesions resembling those seen with dysautonomia

these neuro lesions lead to ventral distension of the abdomen and often metabolic abnormalities compatible with pyloric outflow obstruction