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 or ingesta.

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 approach.

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 Andrews-Jones, DVM