Vagus Indigestion in Dairy and Beef Cattle
Cattle affected with vagus indigestion develop progressive
intermittent, then chronic abdominal distention. Improper
forestomach emptying, due to a functional outflow problem,
can be caused by damage to the ventral vagal trunk. Mechanical
inhibition of motility from adhesions or abscesses can also
decrease forestomach emptying.
The vagus nerve runs along both sides of the esophagus
and terminates in branches that innervate the forestomachs
and abomasum. Inflammation or traumatic damage to the nerve
can result from pharyngeal trauma or abscesses,
mediastinitis,thoracic inflammation, ischemia from a torsion
and traumatic reticuloperitonitis. "Hardware disease"
is the most common cause of vagal nerve damage.
Not all animals affected with the "vagus indigestion
syndrome" have detectable nerve damage. Forestomach
and abomasal motility can be mechanically inhibited by adhesions.
Hardware disease or perforating abomasal ulcers with a diffuse
peritonitis can also cause outflow obstructions with no
evidence of vagal nerve damage.
Four types of vagus indigestion have been described. Type
I vagus indigestion is failure of eructation, and results
in free gas bloat and ruminal distention. Inflammatory lesions,
chronic pneumonia or a localized peritonitis following hardware
disease of the vagus nerve cranial to the cardia have been
implicated. Mechanical factors not related to vagus nerve
damage that cause esophageal obstruction may also cause
failure of eructation.
Type II vagus indigestion is a failure ofomasaltransport
preventing aboral movement of ingestafrom the reticulum
to the abomasum. The rumen becomes distended with feed (instead
of free gas). Omasal transport failure can be the result
of functional or mechanical outflow disturbances. Functional
disturbances in omasal motility are the result of vagus
nerve damage from inflammation due to conditions such as
mycoticomasitis, reticular abscesses and localized adhesions.
The reticulo-omasal orifice can be mechanically obstructed
by an ingested placenta,papillomas or lymphosarcoma.
Type III vagus indigestion is primary or secondary abomasal
impaction. Primary impactions occur when animals are
fed dry, course feed with limited water. Secondary impactions
are the result of disturbances in abomasal motility or pyloric
outflow failure. Altered motility following an episode of
traumatic reticuloperitonitis is common. Ischemia of the
vagus nerve as asequelae to right abomasal torsion also
may occur. Mechanical obstruction or neurogenic dysfunction
at the level of the pylorus can both occur with lymphosarcoma.
Type IV vagus indigestion is partial forestomach obstruction,
more common in late pregnancy. During advanced pregnancy,
the enlarged uterus displaces the abomasumcranially which
physically interferes with normal motility.
Diagnosis of vagus indigestion is based on history,
physical examination findings, ancillary diagnostic tests
and exploratory surgery. Clinical signs of all types of
vagus indigestion are chronic, progressive weight loss and
abdominal distention. Affected animals gradually become
inappetant, have a reduced fecal output and drop off in
milk production. Rumen motility can be static, hypomotile
or hypermotile.Bradycardia may occur due to increased parasympathetic
tone from the injured vagus nerve. Affected animals may
be dehydrated due to fluid sequestration and osmotic draw
within the forestomachs.
Physical exam includes rectal palpation of an L shaped
rumen with the ventral rumen sac to the right of the midline.
The left paralumbarfossa and right ventral abdominal quadrant
will be distended, resulting in the characteristic "papple"
shaped abdominal contour. (The left side looks "apple"
shaped and the right side looks "pear" shaped.)
Palpation of the pharynx and esophagus can help to locate
inflammation, cellulitis or a foreign body. Hydration status
can be assessed by tenting the skin above the eye and observation
of the eye's location in the orbit. Passage of a Kinginan
tube will determine if rumen distention is due to free gas
Ancillary data can help determine the primary cause ofvagal
nerve damage and the type of vagus indigestion present.
An elevated rumen chloride content following reflux of abomasalingesta
and chloride into the rumen is seen with type III vagus
indigestion. A complete blood count can indicate acute or
chronic inflammation, lymphosarcoma or diffuse peritonitis.
Abdominal paracentesis aids in the diagnosis of peritonitis
or lymphosarcoma. Serology can provide a more definitive
diagnosis of bovine lymphosarcoma.
Surgical exploration of the abdomen can help determine
the primary cause of vagal nerve damage, the animal's prognosis
and may aid in therapy.
Treatment of Type I vagus indigestion focuses on relieving
free gas accumulation via a rumen fistula or stomach tube.
An open-ended plastic syringe sutured into the rumen allows
gas to escape. (Diagnosis and removal of any possible esophageal
foreign bodies should precede surgery.)
Therapy for early cases of Type II vagus indigestion
is mostly supportive. Fluids, electrolytes, rumen
cathartics, access to water and exercise are important.
Subcutaneous administration of calcium borogluconate may
be indicated. Advanced cases of Type II vagus indigestion
usually require surgery. A left paralumbarfossaceliotomy
and rumenotomy allows the clinician to palpate the reticulo-omasalorifice
for foreign bodies, placenta,papillomas or impactions.Biopies
can be obtained and abscesses can be drained using this
Type III vagus indigestion causes hypokalemia,
hypochloremia and metabolic alkalosis. Intravenous fluid
administration can be used to correct these abnormalities.
A left paralumbarfossaceliotomy and rumenotomy allows the
clinician to administer mineral oil directly into the abomasum
via the omasal-abomasal orifice, or removal of impacted
abomasalingesta. Severe cases of abomasalimpaction may require
an abomasotomy via a right paracostalapproach, but affected
animals have a poor prognosis.
Type IV vagus indigestion is treated with fluids, electrolytes,
calcium and possibly therapeutic abortion. A rumenotomy
using a left paralumbarfossa approach can be utilized to
detect and treat underlying disease processes.
- by Joel Russo, Diagnostic Pathology Clerk
- edited by Lydia