Vagal Indigestion (Chronic indigestion)
A condition known as vagal indigestion leading to impaction and enlargement of the abomasum and rumino-reticulum has been seen in cattle and sheep. This is a chronic or subacute problem resulting in forestomach distention, abdominal distention, decreased appetite, weight loss, decreased milk production, decreased manure production, and in some cases bradycardia. Often there are no morphologic changes to account for the presumed vagal nerve problems but abomasal impaction has been associated with chronic reticuloperitonitis or perireticular or periomasal abscess and a tumor of the vagus nerve was associated with this disease.
Vagal indigestion is characterized by gradual development of rumenoreticular and abdominal distention thought to be the result of lesions affecting the vagus nerve. However, vagal nerve involvement is not present in all cases. The most common cause is traumatic reticuloperitonitis (see Traumatic Reticuloperitonitis). Vagal indigestion is seen in cattle and has been reported in sheep.
The clinical signs vary to some extent with the location of the obstruction. In all cases, there is a gradual development (over days to weeks) of ruminoreticular and abdominal distention. Distention of the dorsal and ventral sacs of the rumen result in an 'L-shaped' rumen on rectal examination.
Left dorsal and left and right ventral distention of the abdomen causes a 'papple' (pear plus apple) shape. Cattle with vagal indigestion have a diminished appetite, which typically improves temporarily if distention is relieved. Milk production gradually decreases, fecal output is reduced and often contains long hay particles, and the rumen develops a 'splashy' fluid consistency. The feces are characteristically very scant and sticky. The strength of rumen contractions is decreased; however, rumen motility is often increased (3-4 contractions/min). It is commonly possible to see movements of the left abdominal wall that mirror the movements of the hyperactive rumen. However, rumen contraction sounds are not audible because the contents have become frothy due to the prolonged contractions and failure of the rumen to empty. Temperature and respiratory rate are usually normal; however, these can be increased depending on the cause. Bradycardia is present in 25-40% of cases. Because bradycardia is uncommonly associated with other conditions, vagal indigestion should be considered in the differential diagnosis in any case in which bradycardia is present. Tachycardia develops as the disease progresses. Over time, the animal develops a rough hair coat, loses condition, and becomes weak (in some cases to the point of recumbency) and dehydrated. On rectal palpation, the rumen is distended with gas or froth that occupies the entire left abdomen, pushing the left kidney to the right of the midline. The ventral sac of the rumen is enlarged and palpable to the right of the midline (the characteristic 'L-shaped' rumen). Palpation of the lower half of the right side of the abdomen below the costochondral junction may detect an impacted abomasum that feels doughy. Hematologic findings vary. The PCV can be increased because of dehydration or decreased because of bone marrow depression (anemia of chronic disease). The WBC may be normal, increased, or decreased. If an inflammatory condition such as peritonitis is present, the neutrophil to lymphocyte ratio is typically reversed, and a neutrophilia may be present. Lymphocytosis can be seen with vagal indigestion due to lymphosarcoma. Leukopenia may be present with diffuse peritonitis. Increased serum globulin and total protein can be seen with abscesses. Metabolic status is normal, or metabolic alkalosis may be present. The chloride level varies with the site of the obstruction. Low chloride indicates reflux of chloride from the abomasum into the rumen and obstruction at the level of the abomasum. The chloride levels of the rumen fluid may be increased. Metabolic alkalosis is typically present if serum chloride is decreased. The chloride is usually normal if the lesion is cranial to the abomasum. Potassium is usually low due to decreased potassium intake in the feed. Calcium is often moderately decreased because of ongoing milk production; however, it can be low enough to cause recumbency. BUN and creatinine increase with dehydration due to prerenal azotemia.
Cattle with vagal indigestion have a diminished appetite, which typically improves temporarily if distention is relieved. Milk production gradually decreases, fecal output is reduced and often contains long hay particles, and the rumen develops a “splashy” fluid consistency. The feces are characteristically very scant and sticky. The strength of rumen contractions is decreased; however, rumen motility is often increased (3-4 contractions/min). It is commonly possible to see movements of the left abdominal wall that mirror the movements of the hyperactive rumen. However, rumen contraction sounds are not audible because the contents have become frothy due to the prolonged contractions and failure of the rumen to empty.
Various diseases can cause vagal indigestion due to injury, inflammation, or pressure on the vagal nerve. However, conditions resulting in mechanical obstruction of the cardia or reticulo
- omasal orifice (eg, papillomas or ingested placenta) also have been included in the syndrome if ruminoreticular distention is present and the condition is subacute to chronic. There are 4 types of vagal indigestion based on the site of the functional obstruction. Type I is failure of eructation or free
- gas bloat, Type II is a failure of omasal transport, type III is abomasal impaction, and type IV is partial obstruction of the forestomach.
Type I vagal indigestion, or failure of eructation,
results in free
- gas bloat. It is most commonly due to inflammatory lesions in the vicinity of the vagus nerve, such as localized peritonitis, adhesions (usually after an episode of traumatic reticuloperitonitis), or chronic pneumonia. Less common causes include pharyngeal trauma, which affects a more proximal part of the vagus nerve, and esophageal compression by abscesses or neoplasia, such as lymphosarcoma. Free
- gas bloat can also be seen with esophageal obstruction by intraluminal foreign bodies or masses. However, this typically is an acute condition, which does not fit the definition of vagal indigestion.
Type II vagal indigestion, or failure of omasal transport
, develops as a result of any condition that prevents ingesta from passing through the omasal canal into the abomasum. Adhesions and abscesses (reticular or single liver abscesses) are the most common causes. They are usually on the right or medial wall of the reticulum near the route of the vagus nerve. Reticular abscesses and adhesions are almost invariably the result of traumatic reticuloperitonitis. Mechanical obstruction of the omasal canal by ingested material (eg, placenta) or masses (eg, lymphosarcoma, squamous cell carcinoma, granulomas, or papillomas) can also cause chronic ruminoreticular distention due to failure of omasal transport.
Type III vagal indigestion is abomasal impaction
, which tends to develop due to feeding of dry, course roughage, such as straw, in a chopped or ground form with restricted access to water and usually during extremely cold temperatures (see dietary abomasal impaction , Dietary Abomasal Impaction). Secondary impactions are seen after an episode of traumatic reticuloperitonitis or as a sequela of right abomasal displacement or abomasal volvulus or, less commonly, of obstruction of the pylorus (eg, by placenta or trichobezoars). Vagal indigestion can develop in cattle after abomasal volvulus without abomasal impaction. These cases would presumably fall into the category of failure of omasal transport (type II) with damage to the vagal nerve found more cranial in its course.
Type IV vagal indigestion, or partial forestomach obstruction
, is poorly defined. It typically develops in cattle during gestation. It may be related to the enlarging uterus shifting the abomasum to a more cranial position, which inhibits normal motility.
Diagnosis is based on the presence of subacute to chronic ruminoreticular and abdominal distention. Because vagal indigestion is by definition a subacute to chronic disease, this diagnosis should not be made in cattle that have not been sick for at least several days, which rules out acute rumen tympanites and acute frothy bloat. Other causes of abdominal distention, such as ascites and uterine enlargement, are included in the differential diagnosis and can almost invariably be ruled out by rectal palpation due to the absence of ruminoreticular distention. Occasional cases of longstanding obstruction of the cecum or small intestine can cause severe ruminoreticular and abdominal distention; however, palpable cecal or small-intestinal distention is also palpable rectally. In addition, the rumen is distended but not L-shaped, and a characteristic ping is present in the case of cecocolic volvulus.
Diagnosing the specific cause of vagal indigestion is more difficult but is important because of differences in treatment and prognosis. Physical examination, rectal examination, CBC, blood acid-base determination, and serum chemistry values are often useful. Peritoneal fluid analysis can support the diagnosis of peritonitis if total protein or nucleated cells are increased. Radiographs of the reticulum should be taken to identify a radiopaque linear foreign body (eg, wire) or reticular abscess. Definitive diagnosis often requires exploratory surgery (left paralumbar fossa laparotomy and rumenotomy).
Cannulation of rumen, cow.
Illustration by Dr. Gheorghe Constantinescu
Metabolic status is normal, or metabolic alkalosis may be present. The chloride level varies with the site of the obstruction. Low chloride indicates reflux of chloride from the abomasum into the rumen and obstruction at the level of the abomasum. The chloride levels of the rumen fluid may be increased. Metabolic alkalosis is typically present if serum chloride is decreased. The chloride is usually normal if the lesion is cranial to the abomasum. Potassium is usually low due to decreased potassium intake in the feed. Calcium is often moderately decreased because of ongoing milk production; however, it can be low enough to cause recumbency. BUN and creatinine increase with dehydration due to prerenal azotemia.
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- Bradycardia, slow heart beat or pulse
- Tachycardia, rapid pulse, high heart rate
- Abdominal distention
- Anorexia, loss or decreased appetite, not nursing, off feed
- Ascites, fluid abdomen
- Bloat in ruminants, tympany
- Bloody stools, feces, hematochezia
- Decreased amount of stools, absent feces, constipation
- Increased rate or strength rumen motility, hypermotility
- Mucous, mucoid stools, feces
- Pica, depraved appetite
- Rumen hypomotility or atony, decreased rate, motility, strength
- Fever, pyrexia, hyperthermia
- Generalized weakness, paresis, paralysis
- Hypothermia, low temperature
- Inability to stand, downer, prostration
- Internal abdominal mass, swellings, adhesions abdomen
- Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift
- Weight loss
- Dullness, depression, lethargy, depressed, lethargic, listless
- Pain on external abdominal pressure
- Agalactia, decreased, absent milk production
- Decreased respiratory rate
- Dyspnea, difficult, open mouth breathing, grunt, gasping
- Increased respiratory rate, polypnea, tachypnea, hyperpnea
- Mucoid nasal discharge, serous, watery
If the value of the animal justifies treatment, surgery is almost always needed to identify the underlying cause. Medical management alone is ineffective. A left paralumbar fossa laparotomy and rumenotomy provides the opportunity for definitive treatment in some cases. Emptying the rumen at the time of surgery may help restore normal rumen motility. Stimulation of low-threshold tension receptors in the reticulum occurs under normal circumstances and causes reflex reticuloruminal contractions. However, severe distention causes stimulation of high-threshold receptors that have the opposite effect and inhibit contractions.
Supportive or symptomatic therapy should be provided in all cases, which typically involves correcting dehydration as well as calcium and electrolyte deficits, commonly with oral fluids and electrolytes. Severely dehydrated animals and those with longstanding disease require IV fluids. Fresh water and normal feed should be available. Transfaunation at surgery and/or via stomach tube may help reestablish normal rumen flora in cattle with chronic anorexia. Antibiotics should be given if the underlying cause is infectious or if a rumen fistula is created. Choice of antibiotic should be based on culture results if possible.
Treatment of type I vagal indigestion (failure of eructation) also typically involves creating a rumen fistula to allow free gas to escape. If surgery is not economically feasible and the underlying cause of vagal indigestion has been identified and treated, a rumen trocar can be placed temporarily. Such trocars are commercially available and must be secure and self-retaining to prevent potentially fatal leakage of rumen contents into the peritoneal cavity. The trocar should not be removed for at least 2 wk to allow firm adhesions to form between the rumen and body wall.
The prognosis for animals with
type I vagal indigestion
is usually favorable. After creation of a rumen fistula, the signs of vagal indigestion resolve in nearly all cases. However, animals with chronic respiratory disease or pharyngeal trauma may not recover from the underlying condition. Leakage of ingesta from fistulas can cause off-flavored milk. Peritonitis can develop from leakage around the fistula or as a sequela of rumenotomy; however, this should not happen with good surgical technique.
Type II vagal indigestion
(failure of omasal transport) rarely responds to supportive or symptomatic therapy without surgical intervention. Left paralumbar fossa laparotomy and rumenotomy can be used to identify adhesions in the vicinity of the reticulum, reticular or hepatic abscesses, or obstruction of the omasal canal. Removal of foreign bodies, wires, and some masses at surgery affords an excellent prognosis. A diagnosis of lymphosarcoma at surgery warrants a grave prognosis. Reticular abscesses identified at surgery should be cautiously drained into the reticulum, and antibiotics given for 10-14 days. Reportedly, 83% of cattle with reticular abscesses respond favorably to treatment. Identification of adhesions in the vicinity of the reticulum warrants a fair to good prognosis with surgery, antibiotic therapy, and appropriate supportive treatment. Hepatic abscesses must be drained by a second surgery. Large-bore cannulas placed through the body wall, through the adhesions, and into the abscess will drain the pus. However, recurrence is more of a problem with hepatic abscesses than with reticular abscesses.
type III vagal indigestion
(abomasal impaction) diagnosed without surgery usually do not receive further treatment because of the poor prognosis, particularly if there is a history of traumatic reticuloperitonitis or abomasal volvulus. If the diagnosis is made at surgery or if the abomasal impaction is thought to be dietary, dioctyl sodium sulfosuccinate or magnesium sulfate can be infused directly into the abomasum via the reticulo-omasal orifice after emptying the rumen. A nasogastric tube can be passed into the abomasum at surgery and left in place for continued treatment. If possible, impacted material should be removed manually through the reticulo-omasal orifice. Other lesions, such as abscesses, should be identified and drained. Abomasotomy and removal of abomasal contents, using a right paracostal approach with the cow in left lateral recumbency, can be performed as a last resort. However, recurrence of the impaction is common. Pyloric obstruction in cattle is rare and is most often due to a foreign body obstructing the lumen.
Pyloromyotomy is almost never effective in resolving abomasal impactions.
Type III vagal indigestion
has a poor prognosis regardless of the cause or the treatment. However, some cattle with primary abomasal impactions will respond to therapy, although severely affected animals will not (see dietary abomasal impaction, Dietary Abomasal Impaction ). Cattle with secondary impactions due to traumatic reticuloperitonitis or as a sequela of right abomasal displacement or abomasal volvulus seldom recover. Animals with foreign bodies (eg, trichobezoars) obstructing the pylorus have a good prognosis if the obstruction is removed.
Therapeutic abortion has been recommended for treatment of cattle with
type IV vagal indigestion
(partial forestomach obstruction), and some cows have improved with this treatment; however, because type IV vagal indigestion is a poorly defined condition, the prognosis is always guarded. A more specific prognosis is based on response to therapy and identification of a specific lesion at exploratory celiotomy and rumenotomy.
The most common cause of vagal indigestion is traumatic reticuloperitonitis, which causes adhesions and abscesses that interfere with vagal nerve function. Therefore, prevention of traumatic reticuloperitonitis is important. Good management practices will prevent some cases of vagal indigestion resulting from chronic pneumonia. Early diagnosis of right-sided abomasal displacements and abomasal volvulus, and surgical correction the day the diagnosis is made, may prevent some cases. Prompt removal of the placenta from the cows enclosure after parturition will keep it from obstructing the cardia, reticulo-omasal orifice, or pylorus.