Rumen disorders Flashcards
Describe the pathophysiology of rumen acidosis
Consumption of easily digestible carbs -> bacterial population shifts to gram-positive in 2-6 hours -> fermentation is altered and there are increased volatile fatty acids, lactate, and glucose -> rumen pH is reduced -> protozoa decline and lactate accumulates more -> if pH drops below 5.0, gram-negative bacteria reduce greatly and endotoxin is released, if pH drops below 4.5, Lactobacillus dominates and produces lactate and histamine -> systemic lactic acidosis -> rumen epithelial damage, possible sepsis
How does rate of dietary adaptation affect rumen acidosis
Sudden introduction of fermentable carbs leads to increased risk of acidosis; dietary adaptation is necessary to build up populations of lactate-using bacteria
What types of feed predispose an animal to rumen acidosis
High sugar feeds, wheat and barley > corn > sorghum > oats
How does processing method affect likelihood of developing rumen acidosis
Small particle size, heat or pressure cooking, and high moisture of grain increase starch availability increasing risk of acidosis
How does forage availability affect likelihood of developing rumen acidosis
Feeding forage with grain increases chewing and salivation which increases the buffering of rumen pH and decreases chances of rumen acidosis. TMR have lower risk of acidosis and feeds that allow grain to be sorted preferentially over forage have higher risk of acidosis.
How does frequency of grain consumption affect rumen acidosis risk
Feeding small grain meals frequently decreases the risk of acidosis, feeding grain ad lib increases the risk
What life stages are predisposed to developing rumen acidosis
Feedlot animals, dairy cattle transitioning from dry to lactating or in early lactation, and show animals are predisposed to acidosis
What are clinical signs of acute rumen acidosis
Anorexia, depression, rumen distension, atony, and sloshy contents, dehydration, tachycardia, cold extremities, weakness or recumbency, watery diarrhea
How does the pathophysiology of rumen acidosis cause clinical signs
Rumen osmotic pressure is increased which causes fluid accumulation in the rumen leading to systemic dehydration and decreased peripheral perfusion. Increased rumen osmolality impairs VFA absorption and bicarb entry which worsens acidosis. Hyperosmotic diarrhea develops, worsening dehydration and hypovolemia. Low pH, high concentrations of undissociated butyric acid, and rumen distension can lead to rumen atony and bloat.
What are the clinical signs of chronic rumen acidosis
Clinical signs include decreased feed intake, decreased performance, increased culling rates, increased laminitis. Low milk fat concentration can also be seen.
What diagnostic findings are associated with acute rumen acidosis
History, rumen fluid that is watery, sour-smelling, contains a lot of grain, has a pH <5.5, lacks protozoa, and is dominated by gram-positive bacteria. Lab tests showing metabolic acidosis, increased anion gap, hemoconcentration and pre-renal azotemia.
How do you diagnose subacute rumen acidosis
Presumptive diagnosis can be made based on evaluation of ration and feeding practices and observing response to feeding changes. Rumenocentesis of several cattle performed post-feeding showing a pH <5.5 in more than 2 cows indicates subacute acidosis.
How do you decide which animals to treat for rumen acidosis in a herd outbreak
Treat animals that are likely to respond, euthanize animals that are already recumbent
How is rumen acidosis treated
Remove further grain. Evacuate rumen contents with rumenotomy or rumen lavage (rumenotomy generally has better results when possible). Correct dehydration and systemic acidosis by administering IV isotonic sodium bicarbonate and 500mL calcium gluconate IV (don’t mix with sodium bicarb solution). Neutralize rumen pH with oral administration of magnesium hydroxide or sodium bicarb. Reinoculate the rumen with rumen fluid from a healthy cow. Administer systemic antibiotics (procaine penicillin, 7-10 days) to target facultative anaerobic bacteria. People sometimes also treat with antihistamines, NSAIDs, and thiabendazole.
How is subacute/chronic rumen acidosis treated
Managed with dietary changes of the herd
What are possible sequela to acute rumen acidosis
Peritonitis, liver abscesses, caudal vena cava syndrome, rumen epithelial hyperkeratosis/parakeratosis, laminitis (chronic > acute)
How can rumen acidosis be prevented
Manage feed type and schedule, incorporate ionophores into feedlot and dairy cattle feed (inhibit gram-pos bacteria but not specifically approved for prevention of acidosis), add buffers to the ration (sodium bicarb, sodium sesquicarbonate, magnesium oxide), increased protein or NPN diet (increases ammonia and buffering), lactobacillus or yeast cultures in diet
What circumstances frequently lead to simple indigestion
Moldy or spoiled feed, heat or cold damaged feed, indigestible roughage, too much feed, new type of feed
What are clinical signs of simple indigestion
Decreased appetite, decreased milk production, rumen hypomobility, mild bloat, abnormal feces
How is simple indigestion diagnosed and treated
Rule out other causes, rumen fluid analysis may reveal changes. Signs recover spontaneously once feeding error is corrected.
What are clinical signs of vagal indigestion
Rumen hypo- or hyper-motility, decreased appetite, abdominal distension, weight loss, reduced milk production and fecal volume, abnormal rumen shape, sometimes bradycardia, may see long pieces of hay in the feces
What causes an left sided “apple shaped” cow
Gas accumulating at the top of the rumen causing mid-abdominal dorsal distension
What causes a right sided “pear shaped” cow
Disturbances in abomasal flow causing progressive distension of lower right abdomen
Describe a “papple” shaped cow and how this occurs
Distension of upper left abdomen and lower right abdomen, caused by gas and fluid distension of the rumen on the left and the ventral sac of the rumen pushing towards the right as it distends +/- abomasal distension on the ventral right side
What might be felt on a rectal of a cow with chronic vagal indigestion
The ventral sac of the rumen distended compared to the dorsal sac creating an “L” shape with the ventral sac eventually occupying up to 75% of the abdomen
What is type 1 vagal indigestion
Failure of eructation (free-gas)
What is type 2 vagal indigestion
Failure of omasal transport
What is type 3 vagal indigestion
Abomasal impaction
What is type 4 vagal indigestion
Partial obstruction of the forestomach compartments
What are causes of type 1 vagal indigestion
Esophageal obstruction (tumor, abscess, foreign body), inflammation adjacent to the vagus nerve. Can occur repeatedly in young calves (3-10 months) related to respiratory disease or idiopathically- usually improves over time
What are causes of type 2 vagal indigestion
Traumatic reticuloperitonitis, reticular adhesions, space occupying lesions that inhibit omasal transport or occlude the orifice
What are causes of type 3 vagal indigestion
Primary abomasal impaction (restricted water and dry coarse roughage) or secondary abomasal impaction (decreased abomasal emptying , can be related to hardware disease, perforated abomasal ulcers, lymphosarcoma, etc.). Can also be caused by foreign bodies obstructing the pylorus, but these are more commonly found in the omasal orifice.
What are the causes of type 4 vagal indigestion
Abomasum forced cranially by the uterus
What diagnostic findings are consistent with vagal indigestion
Hardware disease (elevated fibrinogen, total protein, and leukocytes), dehydration, metabolic alkalosis, hypochloremia (except in type 3), hypokalemia. Diagnosis requires exploratory rumenotomy/laparotomy.
How would you surgically approach a type 2 vagal indigestion
Left rumenotomy
How would you surgically approach a type 3 or 4 vagal indigestion
Abdominal exploratory from the right
How is type 1 vagal indigestion treated
Resolving esophageal obstruction, symptomatic treatment, prognosis poor for chronic cases
How is type 2 vagal indigestion treated
Left sided exploratory and rumenotomy to look for adhesions, abscesses, tumors, or foreign bodies. Abscesses can be drained and foreign bodies removed. If no cause is found, prognosis is poor.
How is type 3 vagal indigestion treated
DSS can be injected into the pylorus and the abomasum can be massaged to break down an impaction. Oral mineral oil is recommended for several days after.
Describe primary ruminal tympany (bloat)
Dietary factors lead to frothy or foamy rumen contents. Gas bubbles are trapped by the froth and foam and eructation of gas is prevented.
Describe secondary ruminal tympany
Physical obstruction of the cardia or impairment of rumenoreticular function with free gas accumulation in the rumen
What are clinical signs of ruminal tympany/type 1 vagal indigestion
Dyspnea, abdominal pain, staggering, death
Which animals are usually affected by primary ruminal tympany
Ruminants on pasture or on feedlots
How can a stomach tube help diagnose primary ruminal tympany
The tube will pass easily but will not significantly relieve bloat, frothy contents will usually be seen
How does pasture bloat occur
Soluble proteins in plants are readily degradable and produce gas at a rapid rate
How does feedlot bloat occur
High grain, low roughage diets result in mucopolysaccharide production by bacteria in the rumen. This produces slime which traps gas and slows rumen motility.
What is the preferred treatment of pasture bloat (ruminal tympany)
EMERGENCY- Oral administration of an ionic surfactant such as Poloxalene (Therabloat) in water. Once foam is destabilized, gas is eructated. Mineral or vegetable oil can be used but is not as effective. Rag in the mouth is recommended to increase salivation.
What is the treatment for feedlot bloat (ruminal tympany)
EMERGENCY- Intraruminal administration of mineral oil to destabilize froth, followed by walking. Antacids can be used if pH is acidic. Rag in the mouth is recommended to increase salivation.
How can primary ruminal tympany be avoided
Avoid high-risk pasture, limit time spent grazing, feed hay prior to grazing, drench with oil, use of sentinel animals, increased fiber and food particle size, decreased concentrate intake, add ionophores to food.
Describe secondary ruminal tympany (free gas bloat)
CO2 and methane is produced by the rumen and rises to form a “gas cap” on top of the rumen, impairing eructation.
How is secondary ruminal tympany diagnosed
Physical exam, lab testing, endoscopy, imaging, exploratory laparotomy, or at necropsy
What are causes of secondary ruminal tympany (free gas bloat)
Hypocalcemia, tetanus, rumen acidosis, anything causes impaired motility, outflow obstruction in upper GI tract, animal being in lateral or dorsal recumbency, masses (reticular papillomas, granulomas, abscesses)
How does a stomach tube help diagnose secondary ruminal tympany (free gas bloat)
Tube should pass (easily or with difficult) and will release free gas. If it doesn’t pass, esophageal obstruction or dysfunction is suspected.
What is the treatment for secondary ruminal tympany (free gas bloat)
Passing stomach tube to relieve gas and then treating the underlying cause. If stomach tube can’t be pass, an indwelling rumen trochar can be placed via rumen fistula- this is preferred in valuable animals because it reduces the risk of local or diffuse peritonitis.
Describe the pathophysiology of traumatic reticuloperitonitis
Foreign body penetrates reticulum, results in leakage of reticular contents into cranial abdomen. Localized peritonitis causes mild to severe impairment of rumenoreticular motility leading to vagal indigestion. Foreign body can sometimes penetrate the diaphragm or pericardial sac or pleural cavity, leading to pleuritis.
What clinical signs are consistent with traumatic reticuloperitonitis
Sudden anorexia, decrease in milk production, reluctance to move or lie down, low-grade fever, abnormal posture, cranial abdominal pain, sensitivity to pressure applied on xiphoid region, pain when withers are squeezed
How is traumatic reticuloperitonitis diagnosed
History and physical exam findings, increased fibrinogen and globulin, increased WBCs and protein in peritoneal fluid, reticular radiograph if available, ultrasound, exploratory laparotomy
How is traumatic reticuloperitonitis treated surgically
Left-flank laparotomy if strongly suspected, right flank laparotomy if unsure to rule out other differentials. Drainage of abscess through rumenotomy.
How is traumatic reticuloperitonitis treated medically
Indicated if the foreign body ruptures the reticular rumen- administer a magnet, procaine penicillin G, NSAIDs, IV fluids and electrolytes, stall rest. Prognosis fair-poor based on severity
How is traumatic reticuloperitonitis prevented
Administration of magnets, inspection of environment for foreign bodies
What are indications for rumen fluid collection and analysis
Animals off-feed, rumen atony, abdominal or rumen distension of unknown origin, history consistent with indigestion or rumen acidosis, or to assist in the diagnosis of feed quality or feed mixing problems
What are the advantages and disadvantages of collecting rumen fluid via aspiration by stomach tube or probe
Advantages- easy to perform, little risk to animal, can obtain a large sample easily
Disadvantages- tube must penetrate fibrous mat layer of rumen, sample will be contaminated with saliva which can elevate the pH, can’t determine the control or position of the tube in the rumen
How do you properly aspirate rumen fluid via stomach tube or probe
Use a weighted or “guarded” stomach tube, pass tube and collect sample as quickly as possible, get a large sample to minimize saliva contamination
What are the advantages and disadvantages of rumenocentesis
Advantages- fluid can be collected from a consistent location, no saliva contamination
Disadvantages- can only obtain a small sample, risk of peritonitis or local abscess, more dangerous to vet, may require sedation of animal
How is rumenocentesis performed
Hobble hind legs together and sedate with xylazine, clip and prep site 15-20cm caudoventral to costochondral junction of the last rib, have assistant tail the cow, insert 16 to 18 gauge 5” needle to hub, aspirate fluid with 20mL syringe
What are the normal colors for rumen fluid
Diet dependent- usually green for pasture or hay, yellow-brown for silage or grain, green-brown for mixed
Abnormal colors are dark brown to black, gray, milky gray
What is the normal viscosity of rumen fluid
Slightly viscous- can be watery with acidosis, anorexia, or microbial inactivity
What is the normal pH for rumen fluid
6.0-7.2 for high roughage diets, 5.5 to 6.5 for high concentrate diets
What does normal protozoal activity look like in rumen fluid
Numerous (>40 per field) highly active protozoa of various sizes
Which protozoa are more susceptible to environmental changes?
Large and medium sized (Entodiniomorphs)
What can you add to a slide to help visualize protozoa from rumen fluid
1 drop Giemsa solution or 1 drop Lugol’s iodine
What is methylene blue reduction time
Qualitative measure of the redox potential of rumen fluid
What is a normal vs. abnormal methylene blue reduction time
Normal is <3-4 minutes (high concentrate) or 3-6 minutes (mixed) up to 10 minutes (high roughage)
Abnormal is >8-10 minutes which indicates inactivity or death
How is methylene blue reduction time calculated
Mix 10mL rumen fluid with 0.5mL 0.003% methylene blue and invert. Record length of time for blue color to disappear and sample to return to original color.
What is sedimentation/flotation time of rumen fluid
Qualitative estimate of microbial activity and dietary particle size. Involves observation of the rate of sedimentation and flotation of rumen contents. Normal is 4-8 minutes.
What can chloride concentrate be used to detect
Abomasal reflux
What are normal and abnormal results of rumen fluid chloride concentration
Normal is 15-25mEq/L (cow) or 8-15mEq/L (sheep)
Higher concentration indicates reflux of chloride from the abomasum into the rumen, usually from abomasal outflow obstruction or generalized ileus
What type of bacteria should predominate in rumen fluid
Gram negative bacteria
Describe an abomasal ulcer
Penetrates mucosa and may extend through serosa, central crater has fibrinonecrotic covering. Heal by wound contraction and granulation tissue, leaving a permanent scar.
What is the epidemiology of abomasal ulcers
Common in 2-8 week old calves, occurs very commonly in many weanlings, rare in fattened cattle, somewhat rare in normal cows
Describe the pathophysiology of abomasal ulcers
pH of calves rapidly decreases, adult cows with left displaced abomasum have lower pH.
What is a type 1 abomasal ulcer
Non-perforating, minimal intra-luminal hemorrhage
What is a type 2 abomasal ulcer
Non-perforating ulcer with severe blood loss, ulcer erodes major submucosal blood vessel, leading to severe intraluminal hemorrhage. Can be fatal.
What is a type 3 abomasal ulcer
Perforating ulcer with local peritonitis
What is a type 4 abomasal ulcer
Perforating ulcer with diffuse peritonitis, ulcer perforates, massive abdominal contamination, 100% fatal
Where are abomasal ulcers located in beef calves
Mid-part of fundus or greater curvature of abomasum
Where are abomasal ulcers located in milk fed calves
Pyloric antrum
Where are abomasal ulcers located in feedlot cattle
Pyloric region, usually from increased grain
Where are abomasal ulcers located in dairy cows
Usually in the fundic region, associated with abomasal displacement
What are clinical signs of abomasal ulcers
Ulcer only- no clinical signs, possibly anorexia, bruxism, salivation, reduced milk production, mild melena
Ulcer with severe blood loss- above plus anemia and tachycardia, weakness, melena, death
Ulcer with peritonitis- above plus abdominal pain, increased WBC in peritoneal fluid, recumbency
How are abomasal ulcers treated
Mild ulcers- dietary change, avoid NSAID use
Major bleeding ulcer- blood transfusion, broad spectrum antibiotics, surgical correction of LDA if necessary, oral antacids, change diet
Calves can be given ranitidine
Perforating ulcer- broad-spectrum antibiotics, prognosis poor
