Exam 3: Diseases of the Bovine Forestomach and Abomasum

what is the cause of traumatic reticuloperitonitis

• perforation of the reticulum by a metallic foreign body

• disease of confined cattle

• rarely affects other ruminant species

what are the sequela to foreign body penetratiion

• attachment to magment if present

• acute inflammaton and mild clinical disease (acute localized perionitis)

• chronic localized peritonitis and abscess formation

• abscess formation in the thoracic or peritoneal cavity, vagal indigestion, pericarditis, and myocarditis

• diffuse peritonitis

what are the clinical signs of acute localized peritonitis

• partial or complete anorexia

• acute drop in milk production

• cranial abdominal pain

• pyrexia

• tachycardia

• tachypnea and decreased depth of respiration

• reumen hypomotility

• free gas bloat

what are clinical signs of chronic localized peritonitis

• subtle signs of abdominal pain

• partial anorexia and decreased milk production

• decreased fecal ouput

  poorly digested feed material

what are the clinical signs of reticulopericarditis

• cranial abdominal or caudal thoracic pain

• abnormal thoracic auscultation

• exercise intolerance

• distendied peripheral veins and jugular pulsation

• peripheral edema

• portal hypertension, ascites, diarrhea

what are the clinical signs of diffuse peritonitis

• severe signs that are often fatal

• tachy

• pyrexia

• severe dehydration

• diarrhea

• profound depression

how does TRP present on CBC

• neutrophilia with left shift

• nyperfibrinogenemia

• elevated plasma protein

how will peritoneal fluid evaluation present with TRP

• nucleated cells >6000

• total protein >3

• >40% neu, <10% eos

what are your ancillary diagnostics for TRP

• reticular rads and ultrasound

what findings of TRP are seen on ultrasound

• reticular reticular motility

• abnormal position or contour

• perireticular fibrin or abscessation

• localized or generalized abdominal effusion

what defines ruminal tympany aka bloat

• not excessive gas production!

• failure to reructate via mechanical or functional disturbances

what is free gas bloadt

• type 1 vagal indigestion

• not a disease itself but a manifestation of an underlying disease

• sporadic

• usually a single animal

what is frothy bloat

• primary disease

• ruminal gas trapped as small bubbles within abnormally viscous ingestioa

• diet related, seen with legumes, heat or rye grass, high carbs

what are the clinical signs of bloat

• asymmetrical abdominal distention in the left paralumbar fossa

• abdominal discomfort

• respiratory and cardiovascular compromise

• severe distention compresses diaphragm and venous return

• open mouth breething

• death in 30min to 4hrs

what structure can you NOT palpate when it is displaced? when does this change

reticulum
if RAD progresses to volvulus, can be felt again

what is vagal indigestion

• a functional or mechanical disruption of forestomach or abomasal outflo
  -damage to the vagal nerve
  -physical or functional obstruction of forestomach or abomasal outflow

• decreased milk production, progressive abdominal distention, altered motility, decreased appetite and fecal output, weight loss

• site of distubrance classifes into 1-4

describe the 4 types of vagal indigestionn

• type 1- failure to eructate

• type 2- omasal transport failure

• type 3- abomasal outflow failre

• type 4- indigestion associated with pregnancy

describe type 1 vagal indigestion

• failure to eructate due to esophageal obstruction or physiological disruption

• may be accompanied by signs involving other body systems

• distention of the left paralumbar fossa easily relieved by tube

• abdominal discomfort

• rumen hypomobility

• rumen fistula until function returns

what is type 2 vagal indigestion

• most common

• omasal transport failure

• common sequela to TRP

• disturbed motility due to neurapraxia or neuritis

• may be the result of mechanical obstruction of reticulomasal orifice

what are the signs of type II vagal indigestion

• abdominal distention with characteristic papple shape

• rumen hypermotility intially

• frothy ingesta

• bradycardia

• L shaped rumen on rectal

• anorexia, weight loss, decreased fecal production

• gradual decline in milk production

what is type III vagal indigestion

• aomasal outflow failure

• primary impaction, lymphosarcoma, mechanical obstruction, sequela to abomasal volvulus

what are the signs of type III vagal indigestion

• difficult to differentiate from type II

• rumen hypermotility, frothy ingesta, and bradycardia inconsistently present

• ballottement of impacted abomasum through right body wall

what is type IV vagal indigestion

• usually occurs in 3rd trimester of gestation

• can present as type II or III

• only consistent finding is late gestation

what is the use of clin path for vagal indigestion

• most important for differentiating between II and III

• CBC and fibrinogen

• biochem

• rumen fluid analysis

how might CBC present for vagal indigestion

• elevated PCV and TP due to hemoconcentration

• neutrophilia and hyperfibrinogenemia if associated with TRP

• persistent lymphocytosis

how might vagal indigestion present on biochem

• metabolic alkalosis

• hypokalemia and hypocalcemia

• azotemia

• hypochloremia consistent with type III

what is the use of rumen fluid analysis for vagal indigestion

• rumen chloride >30

• MOST important factor for abomasal outflow failure

what ancillary diagnostics can be used for vagal indigestion

• reticular rads

• reticular and abomasal ultrasound

• exploratory laparotomy and rumenotomy

what is rumen lactic acidosis

• ingestion of larger than normal quantities of highly fermentable carbohydrates causing increased VFA production and decreased rumen pH

• alterations in normal rumen microflora

• rumen lactate production decreases pH and increases osmolality of rumen fluid

• increased absoprtion of fluid from ECF and endotoxin release into systemic circulation

what are the chemical concequences of rumen lactic acidosis

• histamine levels increase

• ethanol, methanol, tyramine, tryptamine production contribute to CNS depression

• thiaminase production may result in development of polioencephalomylasia

what are the lesions of rumen lactic acidosis

• acidic rumen pH damages mucosal surfaces in the forestomach and intestine

• blood vessels thrombose and sections of rumen mucosa and submucosa slough allowing bacteria to invade

• bacteria travel to liver via portal circulation and cause liver abscesses

• mycotic ruminits may develop

what are the clinical signs of rumen lactic acidosis

• rumen distention

• dehydration

• diarrhea

• signs of endotoxic shock

• anorexia, rumen stasis, abdominal pain

• neurologic signs

• recumbency and death

how might a rumen fluid analysis present with rumen lactic acidosis

• milky grey to yellow, sour smelling fluid

• pH <5

• no normal protozoa

• proliferation of gram + rods

ho does rumen lactic acidosis present on bloodwork

• consistent with hemoconcentration

• elevated liver enzymes

• acidemia

generally describe abomasal ulcers

• benetrate the basement membrane of the abomasal mucosa, erosions do not penetrate

• clinical presentation based on depth and structures

• 4 types, though individual animals may have multiple

where are abomasal ulcers most commonly seen

• cattle under intensive management such as high producing dairy, feedyard cattle, veal and beef calves

• stress

describe type 1 abomasal ulcers

• local infmallation with serosal thickening and serositis

• often subclinical

• up to 50% may not have clinical signs → poor performance, abdominal pain, melena

• concurrent disease is common

describe type 2 abomasal ulcers

• ulceration over sub-mucosal vessels resulting in significant hemorrhage

• hallmark sign is melena

• positive fecal occult blood

  • lymphosarcoma or no lymphosarcoma

what are the clinical signs of non-lymphosarcoma type 2 abomasal ulcers

• acute drop in milk production

• melena and loose feces

• pale mucuos membranes

• anemia

describe type 3 abomasal ulcers

• perforating areas covered by omentum or those associated with LDA → localized peritonitis, omental bursitis

• often identified during investigation of concurrent disease

what is type 4 abomasal ulcers

• rapidly occuring

• areas not covered by omentum

• acute generalized peritonitis

• surviors often exhibit chronic clinical signs associated with adhesions

what are the clinical signs of type 3 abomasal ulcers

• lack signs specific to perforation

• intermittent anorexia

• melena

• abdominal pain

• right cranial abdominal pain

• abdominal distention

• ± fecal occult blood

• lab data suggestive of peritonitis

what are the clinical signs of type 4 abomasal ulcers

• anorexia

• agalactia

• depression

• signs of shock

• pyrexia

• abdominal pain

• low serum protein in the face of hemoconcentration

how are abomasal ulcers diagnosed

• hematology for decreased PCV, TP, erythrocyte count and MCHC

• serum pepsinogen , though limited value with unknown parasite status

• decal occult blood helpful if melena is not obvious
  -low for type 1 ulcers

what factors contribute to abomasal displacement

• abnormally high VFA accumulation

• hypicalcemia

• intra luminal gas accumulation

• high producing dairy cows in early lactation

• often accompanied by other medical conditions such as metritis, mastitis, and ketosis

describe the hallmark clinical sign of abomasal displacement

• the ping

• right or left depending on direction of displacement

• cranial extent 8-10 ICS

• caudal extent cranial paralumbar fossa

• ventral extent ½ distalce of abdominal wall

what are other clinical signs of abomasal displacement

• fluid splash

• depression

• complete or partial anorexia

• decreased milk production

• rumen hypermotility

• sunken paralumbar fossa

• sprung rib

• medial displacement of the kidney and rumen on rectal

• signs of accompanying disease such as urine ketones, abnormal uterine fluid, CMT

how does abomasal displacement present on ultrasound

• fluid filled viscus between left body wall and rumen

• rugal folds

  

what is important to note abut right displaced abomasum vs left

• far less common

• signs are similar

• SURGICAL EMERGENCY due to likelyhood to develop into volvulus

what is abomasal volvulus

• rotation of the abomasum around an axis through the lesser omentum

• generally considered a sequela to RDA

• not a torsion

• rotation most often counterclockwise

• obstruction of abomasal outflow

• neurovascular compromise

describe the process of an abomasal volvulus

• gas accumulates in the abomasum and the pyloric antrum moves dorsally

• abomasal body floats dorsally along the right body wall

• abomasum and attached structures rotate counterclockwise around an axis through the center of the lesser omentum

• any degree of rotation results in neurovascular compromise

what are the clinical signs of abomasal volvulus

• right sided ping in 8th ICS to PLF and as far ventrally as the fold of the flank

• fluid splash

• complete anorexia and scant feces

• acute drop in milk production

• abdominal pain

• absent rumen motility

• severe dehydration

• abdominal distention

• greater curvature palpable per rectum

how does abomasal volulus present on CBC

• initially elevated PCV and TP due to dehydration

• PCV and TP decrease with compromised abomasal wall intraluminal emorrhage and transudate

how does abomasal volvulus present on chemistry

• azotemia

• hypochloremia

• initial hypokalemia that normalizes

• elevated TCO2

• evelated anion gap with progression

• blood gas will show elevated HCO3, BE and pH