Chapter 5 Noninfectious Diseases of the Gastrointestinal Tract
The term indigestion is used to describe a wide spectrum of clinical syndromes in cattle that range from simple intestinal inflammation to more severe disease forms and finally to lactic acidosis. The rumen is most commonly affected, followed by the small intestine. These two gastrointestinal site disturbances can occur together or independently. Cecal indigestion may be part of the cecal tympany syndrome; this is discussed later. Individual animals, or a few animals (if it is ruminal indigestion), can be affected at any one time. They may be at any stage of lactation, although indigestion seems to be more common in cows in the first weeks following parturition. The diagnosis of ruminal or small intestinal indigestion is made by using a combination of history, clinical signs, abdominal ultrasound (for small intestinal indigestion), rumen fluid analysis (activity and concentration of large and small protozoa are reduced, and new methylene blue reduction is increased), and ruling out other diseases through a complete physical examination.
Simple ruminal indigestion results in signs of anorexia, decreased milk production, cold extremities, and rumen dysfunction. Colic is common if there is small intestinal indigestion (Figure 5-1). Although rumen stasis or hypoactivity is typical, some cattle have increased rumen contraction rates but decreased strength of contractions. The cow’s temperature, pulse rate, and respiratory rates are often normal with ruminal digestion, but tachycardia and tachypnea may develop in cows especially with small intestinal indigestion associated with colic. Abdominal distention may be present because of mild rumen distention, or gas and fluid distention may be present in the right lower quadrant, representing small intestinal distention. In small intestinal indigestion, enough fluid and gas can accumulate in the small bowel to put severe tension on the mesentery, resulting in signs of colic such as kicking at the belly, bellowing, violent behavior, getting up and down repeatedly, and treading with the hind feet. In fact, this form of indigestion may be the most common cause of true colic in the dairy cow. Colic resulting from small intestinal indigestion can be difficult to differentiate from a mechanical small bowel obstruction. Extremely distended loops of small intestine, fibrin or crepitus on rectal examination, blood in the stool, or deterioration in cardiovascular signs all suggest a physical obstruction rather than simple indigestion. On abdominal ultrasound examination, fluid-filled and dilated loops of small intestine are typical of indigestion and obstruction, with hypomotility being most severe with prolonged physical obstruction and/or strangulation (Figure 5-2). The fluid responsible for small bowel distention results from stasis associated with indigestion and quickly appears as diarrhea as the cow responds to therapy or self-initiates gastrointestinal activity. Potential lameness sequelae including laminitis, sole ulcers, and toe abscesses may be observed in some cases 2 to 6 weeks after a rumen indigestion episode.
Laboratory data are seldom helpful in establishing an absolute diagnosis of simple indigestion. Hypocalcemia is the only biochemical abnormality anticipated with mild ruminal indigestion. Hypocalcemia and hypochloremia are common with small intestinal indigestion.
These two goals are accomplished by administration of oral laxative-ruminotoric mixtures and calcium solutions parenterally. Many laxative-antacid-ruminotoric mixtures are available, and each practitioner has a favorite. If the rumen has some activity, boluses of these mixtures may be acceptable, but the powdered form of these products should be mixed with warm water and administered through a stomach tube to ensure distribution of the product if rumen activity is severely depressed. In cases with ruminal tympany, a stomach tube should be passed routinely to relieve gas distention before administering treatment. Excessive treatment with alkalinizing products should be avoided because these can result in hypermagnesemia and metabolic alkalosis, which will further decrease ionized calcium. Calcium solutions are administered for all cases of simple indigestion because inappetence and gastrointestinal stasis coupled with calcium loss resulting from continued, albeit reduced, milk production often leads to hypocalcemia. This hypocalcemia results in the clinical signs of cool peripheral parts and contributes to the already existing gastrointestinal stasis. For simple indigestion cases, 500 ml of calcium borogluconate intravenously (IV) or divided into four subcutaneous (SQ) locations is administered. Magnesium products (sulfate, oxide, or hydroxide) are commonly used as cathartics and/or alkalinizing products; in dehydrated cattle with low urine production, these may cause hypermagnesemia and clinical weakness when used excessively or repeatedly. Cows that demonstrate severe colic associated with small intestinal indigestion may require treatment with flunixin meglumine. Following treatment, a cow with small intestine indigestion should regain normal appetite and pass large amounts of loose manure within 12 to 24 hours. The patient’s feces tend to remain watery or looser than normal for 2 to 3 days. Laxative therapy should be continued on a reducing dose basis for 2 to 3 days to ensure complete evacuation of causative feed material from the rumen. Although the diagnosis of simple indigestion often seems like an “excuse diagnosis” in a cow that is off feed and down on milk, the entity does exist, and the veterinarian should not hesitate to make this diagnosis if other diseases have been eliminated through careful examination. An important differential diagnosis is primary ketosis, and this should be ruled out by testing for urinary ketones. The two disorders also may coexist in some recently fresh cattle.
More severe forms of ruminal indigestion may closely approximate lactic acidosis (lactic acid indigestion, toxic indigestion) and are difficult to categorize. There is a range of clinical signs possible, depending on the quantity and type of feed material ingested by the cow. A history of overingestion of grain or grain silage may exist. Although uncommon in modern dairy management feeding, bolus concentrate has historically been a common prelude to ruminal acidosis in cows (especially first calf heifers). A less common history would be that the cow had access to an apple orchard where large numbers of apples dropped from trees after a storm. Thus in cases of severe indigestion, the ingested material often is known as opposed to the usual case of simple indigestion, in which the causative feed material may not be known.
Signs of moderate to severe indigestion include a dramatic decrease in appetite and milk production, complete gastrointestinal stasis, cool peripheral parts, normal or subnormal rectal temperature, and normal or elevated heart and respiratory rates. Some affected cows are hypocalcemic enough to be recumbent and unable to rise. It should be emphasized that these cows have more severe signs than simple indigestion cases, including splashy rumen, dehydration, and tachycardia. As with any form of indigestion, clinical signs of lameness (laminitis) may occur 2 to 6 weeks later.
Treatment is similar to that described for simple indigestion, but slow IV or SQ administration of calcium solutions may be needed for recumbent cattle. Because rumen stasis is more severe, powdered ruminotoric-laxative-antacid products dissolved in water and 1 lb of activated charcoal administered through a stomach tube are recommended. If rumen fluid is readily regurgitated via the tube, rumen lavage would be indicated. If signs of severe indigestion occur within hours of known overingestion of rapidly fermentable feed material, a rumenotomy may be elected if, in the veterinarian’s judgment, potential for lactic acidosis exists. This is a very difficult decision to make because medical therapy often will suffice and no clear-cut rules exist as to how much of any feed material constitutes a potentially lethal dose. Response to therapy should be gradual over 24 to 48 hours, and treatment may need to be repeated at 24-hour intervals. As gastrointestinal motility returns, loose manure usually is observed. Milk production may be slow to return to previous levels because of the precipitous decrease that occurs with this form of indigestion.
Lactic acidosis (also called toxic indigestion, grain overload, rumen overload, and acute carbohydrate engorgement of ruminants) represents the most severe form of indigestion and is associated with overingestion of rapidly fermentable concentrate feed or the sudden change to a diet containing higher levels of finely ground rapidly fermentable feeds such as corn or wheat. Clinical examples of this may occur in feedlots where feeder steers are introduced to total concentrate diets rather than being gradually changed from high roughage to high concentrate feeds. Fortunately this is less often a herd problem in dairy cattle, but it has occurred when owners who have run out of one type of feed quickly change to another. For example, owners have switched cattle from pelleted grains containing some fiber to finely ground corn or wheat grains and thus induced lactic acidosis. Sudden introduction of highly fermentable small grain silage into the herd can also result in lactic acidosis. Another problem that can lead to lactic acidosis in modern dairy management systems is improper mixing of total mixed rations (TMRs). In these cases, equipment failure or human error can lead to stratification of feedstuffs used in the TMR, and cows at one end of the feed line receive mostly roughage, whereas those at the other end receive mostly concentrate. Cattle that accidentally overeat grain by gaining access to the grain room or by getting loose and eating from a grain bin also may develop lactic acidosis. Both volume and type of concentrate are important, but even a few pounds of a finely ground concentrate such as barley may constitute a dangerous quantity if the cow’s rumen flora is unfamiliar with the material. Because management factors often are involved, multiple animals in the herd tend to show signs. A basic understanding of the pathophysiology of lactic acidosis is essential for one to understand the signs that occur and be able to institute rational therapy. Within 6 hours of ingestion, the easily fermentable concentrate is broken down to lactic acid of both the D and L forms. Most of this occurs in the rumen, although substantial production of lactic acid may also occur in the lower gastrointestinal tract. The L isomer can be utilized rapidly, whereas the D isomer persists and results in D-lactic acidosis. Streptococcus bovis is the primary organism responsible for this conversion. As more and more lactic acid and volatile fatty acids are produced, the pH of the rumen contents decreases into the acid range. If sufficient substrate is available, the rumen pH may decrease to 4.5 to 5.0, at which time microbes other than S. bovis have been destroyed. Rumen stasis results. S. bovis continues to exist at this low pH and produces more lactic acid. Rapid accumulation of lactic acid in the rumen osmotically draws water into the rumen, causing the cow to dehydrate. In addition, the chemical or acid rumenitis damages the rumen mucosa, allowing plasma transudation into the rumen and endotoxin and escape of bacteria into the portal circulation.
Affected cattle are completely off feed, exhibit drastically decreased milk production, are dehydrated, and have elevated heart (90 to 120 beats/min) and respiratory rates (50 to 80 breaths/min). They typically have a splashy, totally static rumen, cool skin surface, subnormal temperature, and diarrhea or loose manure. Affected animals are weak and can be recumbent (Figure 5-3). Because of dehydration, titration of bicarbonate, hypotension, and high levels of lactic acid in the rumen and the blood, severely affected cattle have metabolic acidosis.
Figure 5-3 A Holstein steer with severe ruminal acidosis after eating recently ensiled oat silage. This steer, one of three affected, was unable to stand, severely dehydrated, obtunded, acidotic, and blind. This steer recovered after being treated with hypertonic saline and thiamine IV, draining rumen fluid via oral-rumen tube and administering 1 lb of activated charcoal intraruminally.
Diagnosis of lactic acidosis is made by combining clinical signs with a detailed history of feeding in the herd. In acute cases, obtaining a rumen fluid sample through a stomach tube, percutaneous left flank puncture, or at necropsy examination of acute fatalities will reveal a rumen pH of 4.5 to 5.0. It must be emphasized that cattle with lactic acidosis that survive for 24 hours or more often have rumen pH values that increase to 6.5 to 7.0 because of the buffering effects of swallowed saliva and plasma dilution of the rumen contents. Other laboratory aids include acid-base and electrolyte values that tend to reflect a metabolic acidosis, a neutropenia with left shift in the hemogram, and marked azotemia. This is true even for fatal cases that survive 24 hours or more after ingestion of toxic quantities of grain. The systemic acidosis and acidemia are the result of increases in both D and L lactic acid. In some cases, the diarrhea or loose manure that is passed contains whole particles of the causative concentrate and may represent a clinical diagnostic clue.
Treatment is difficult, and the veterinarian must decide whether medical therapy will suffice or a rumenotomy will be required. In addition, if signs have been present for 24 hours or more, the amount of rumen mucosal damage has already been determined and may not be affected by any treatment. When more than one cow is affected, the therapeutic difficulties multiply because the professional time commitment and expense of treatment are enormous.
Treatment must correct the rumen acidosis and attempt to discourage further lactic acid production. In an animal with a rumen pH of 5.0 or less, a heart rate greater than 100 beats/min, dehydration greater than 8%, and rumen distention and recumbency indicating a severe grain overload, a rumenotomy should be performed and the rumen contents evacuated. The rumen is then washed with water and emptied several times to remove as much lactic acid as possible. The cow is treated with laxatives, fresh hay in the rumen, rumen transfaunates if available, parenteral calcium, and IV fluid therapy. IV fluids should initially be hypertonic saline followed by balanced electrolyte solutions such as lactated Ringer’s solution, and supplemental sodium bicarbonate is added if acidemia is severe (pH, 7.15). Flunixin meglumine should be given (0.3 mg/kg every 8 hours) to combat excessive prostanoid production and shock. B vitamins should be administered for several reasons, one of which is that some cattle with ruminal acidosis develop polioencephalomalacia. The prognosis for severely affected cattle is poor. When such severe rumen acidosis affects a group of cattle or an individual animal of lesser economic value, the expense of treatment and the poor to grave prognosis that the condition carries for survival, let alone future production, should prompt at least consideration of salvage for slaughter.
Other treatments may be attempted for animals showing less severe signs and higher rumen pH values or when the number of animals affected precludes rumenotomies. One method involves passing a large-diameter stomach tube or Kingman tube and lavaging the rumen with warm water several times with the aid of a bilge pump. Several flushes with 10 to 20 gallons of water are necessary, and return flow of fluid must be effective for this treatment to be successful. Following lavage, antacid solutions such as 2 to 4 quarts of milk of magnesia, activated charcoal, and ruminotorics are administered, as well as supportive calcium solutions and IV fluids as indicated. Affected cattle should not be allowed to engorge on water because their atonic rumens will only distend again. Once rumen activity returns, free choice water may be made available. Another option that has been used successfully is to simply drain as much rumen fluid (Figure 5-4) as possible and administer 1 to 2 lb of activated charcoal into the rumen. This appears to be effective in binding rumen toxins (e.g., endotoxin). Additionally, affected cattle should receive SQ administered calcium solutions and IV administered isotonic fluids. Cows with moderate to severe rumenitis are generally treated with penicillin (10,000 to 20,000 IU/kg administered intramuscularly [IM] or SQ) in an effort to prevent bacteremia and liver abscess formation. Broad-spectrum antibiotics should not be used because these may predispose to fungal overgrowth.
Other treatments are empiric. They include antihistamines, penicillin solutions administered via a stomach tube in an effort to reduce the numbers of S. bovis organisms in the rumen, and roughage-only diets until the animals recover.
Cattle affected with lactic acidosis that survive the acute phase and have their rumen pH return to normal still are at risk for sequelae to the chemical rumenitis that has occurred. During the next several days, bacterial opportunists such as Fusobacterium necrophorum may invade the areas of chemical damage, attach to the rumen wall, and cause a bacterial rumenitis (Figure 5-5). If the animal lives 4 to 7 days or has been treated heavily with antibiotics or steroids, a mycotic rumenitis may occur in these previously damaged areas (Figure 5-6). Bacterial and mycotic opportunists invade the damaged rumen mucosa, ascend the portal circulation, and cause embolic infection of the liver, lungs, and other organs, resulting in fever and, in severe cases, death (Figures 5-7 and 5-8). Fever resulting from mycotic infection generally is unresponsive to antibiotic therapy. Embolic infections of the brain may cause bizarre neurologic signs 7 to 14 days following the original clinical signs of lactic acidosis.
Figure 5-6 Mycotic rumenitis 7 days following acute lactic acidosis in a cow. The dark areas represent necrotic rumen mucosa that has sloughed in several focal areas to expose punched-out ulcerative lesions with red peripheries typical of mycotic rumenitis
(Courtesy John M. King, DVM.)
Figure 5-7 Embolic hepatitis and pneumonia secondary to lactic acidosis in a cow. The acute lactic acidosis occurred 7 days before these postmortem findings. The focal lesions in the liver and red areas in the lung represent bacterial and mycotic embolic lesions.
This syndrome, also called subclinical ruminal acidosis (SARA), occurs more commonly in lactating cows than the previously discussed acute clinical syndromes of indigestion and/or ruminal acidosis and derives from modern feeding practices. In brief, feeding rapidly fermentable concentrates and highly acid feeds allows a degree of rumen acidosis for a transient period after ingestion. During this period of acidosis, small areas of rumen mucosa are damaged by the same chemical mechanism that causes more widespread lesions in lactic acid indigestion. These small areas of rumenitis may act as entry points for opportunistic bacteria that subsequently ascend the portal circulation and result in liver abscesses. These may be single or multiple and, when located near the hilus of the liver, predispose the cow to caudal vena caval thrombosis syndrome. Dairy cattle seldom develop the “sawdust liver” or miliary liver abscesses of feeder beef animals despite the similar pathophysiology.
Subclinical rumen or relative acidosis also may be present on a continual rather than a transient basis in some feeding programs. In addition to liver abscesses and caudal vena caval thrombosis syndrome, these herds often have a high incidence of abomasal disease, indigestion, decreased or fluctuating dry matter intakes, diarrhea, decreased milk production, milk fat depression, and laminitis with subsequent lameness. Laminitis may result from release of various mediators, including endotoxins, from rumen microbes destroyed by pH decreases associated with subclinical rumen acidosis. Mediator absorption is enhanced by chemical damage to the rumen mucosa. When this syndrome is suspected, the veterinarian should collect rumen samples from several cows in the herd to analyze pH and rumen microflora. A pH less than 6.0 would be suspicious, although a normal pH does not rule out the disease because the pH will increase to normal following a period of anorexia! The other problem is in the collection of the sample because oral-ruminal collection is difficult and is often contaminated with saliva; rumenocentesis requires puncture of the rumen through the left flank. Additionally, commonly used pH paper is not accurate because the green color of rumen fluid influences the interpretation. When sampling ruminal pH, practitioners should aim for the nadir in luminal pH; for component-fed herds, this is about 2 to 4 hours postfeeding, whereas in TMR-fed herds this point is reached about 6 to 8 hours postfeeding. In general, pH meters, appropriately maintained and calibrated before use, should be used whenever possible rather than pH paper for this purpose. Dr. Ken Nordlund at the University of Wisconsin has suggested that that a pH of less than 5.5 in 5 or more cows of a sample size of 12 should be used as an arbitrary cutoff point to define a herd problem with subacute rumen acidosis.
Correction or prevention requires natural or supplemental buffering of the diet, and a nutritional analysis should be performed to aid the dairy farmer, veterinarian, and any nutritional consultants in restructuring the diet to avoid relative acidosis. Sometimes this can be easily accomplished by feeding roughage before the concentrate to force natural buffering by saliva (i.e., that induced by roughage) that would precede the concentrate’s entrance to the rumen. In other situations (e.g., where component feeding is still being practiced), a switch to a TMR may be indicated. However, the feeding of a TMR does not preclude the opportunity for subacute rumen acidosis. Each herd needs to be assessed and corrected on an individual basis, however, and generalities are not acceptable because feedstuffs, production levels, and management practices vary widely. Chronic indigestion of milk-fed calves is well described but will be discussed in the following section on bloat.
Bloat can be defined as obvious ruminal enlargement resulting in left-sided abdominal distention in both dorsal and ventral quadrants (Figure 5-9, A and B). When severe, bloat may cause generalized distention resulting from ventral sac enlargement into the right lower quadrant and crowding of the remaining abdominal viscera into the right dorsal quadrant. Causes of bloat may be divided into acute and chronic etiologies.
Figure 5-9 A, Ruminal tympany or bloat in a heifer. The left-sided distention is uniform and extends to the dorsal midline. B, Severe ruminal distention with ingesta in a cow with vagal indigestion caused by a perireticular abscess. A lack of respiratory distress, despite marked ruminal distention, is typical of ruminal distention caused by gas or nonfrothy ingesta.
Acute ruminal distention may be caused by either free gas or frothy ingesta. Acute free-gas bloats may occur in association with hypocalcemia and resulting ileus, esophageal obstructions or injuries, pharyngeal injuries that damage the vagal nerve roots controlling eructation, indigestion with tympany, and acute localized peritonitis with resultant ileus. Acute frothy bloat in dairy cattle almost always is associated with indigestion of unknown causes or sudden availability and overingestion of green forage such as succulent alfalfa.
Clinical signs of acute bloat include a combination of acute onset, typical left-sided distention extending dorsally to the midline with a full paralumbar fossa, and rectal findings of ruminal distention extending into the right abdomen dorsally and ventrally. Dyspnea caused by increased abdominal pressure exerted on the diaphragm and thorax may be moderate to severe with acute frothy bloat.
Free-gas bloat causes a large gas ping on the left upper abdomen extending to the dorsal midline (Figure 5-10). In some cattle with free-gas bloat, an obvious ping may not be present. If a stomach tube can be passed easily and relieves the bloat, free-gas bloat is confirmed. Other physical signs and signalment data may allow a specific diagnosis of the cause of the bloat. For example, hypocalcemia may be considered if the cow is periparturient and shows signs of normal or subnormal temperature, cool peripheral parts, slow pupillary responses to direct light, recumbency, or weakness. Indigestion with tympany may cause few signs other than free-gas bloat, and signs other than free-gas bloat or signs referable to hypocalcemia mean other diseases must be ruled out. Animals with esophageal obstruction (choke), esophageal injury, or pharyngeal injury with perforation usually present with excessive salivation, an anxious expression, extended head and neck, bloat, and fever. Passage of a stomach tube would be impeded by a choke and be resisted by a cow with pharyngeal or esophageal injury. Frothy bloat is diagnosed based on the typical left-sided distention, less obvious pinging when simultaneous percussion and auscultation are performed, and failure to relieve the distention on passage of a stomach tube. The bloat may progress rapidly if it is frothy bloat, eventually distending both sides of the abdomen to its maximal limits (Figure 5-11) and causing respiratory distress, hypoxemia, poor venous return of blood to the heart, hypotension, and death.
Treatment requires relief of the ruminal distention and correction of the primary cause. In instances of free-gas bloat caused by hypocalcemia, parenteral calcium therapy and passage of a stomach tube are required. Indigestion with tympany requires relief of the gas accumulation with a stomach tube and treatment with a parenteral calcium solution, as well as laxatives, antacids, and ruminotoric mixtures as necessary. In esophageal obstructions or choke, the obstruction must be relieved by gentle manual or mechanical manipulation. Localized peritonitis with secondary ruminal tympany must be treated with antibiotics, stall rest, and either a magnet, rumenotomy (for hardware), or dietary changes (perforating abomasal ulcers). If pharyngeal trauma is suspected, broad-spectrum antibiotics, gentle passage of a stomach tube, and analgesics may be indicated (see the section on Pharyngeal Trauma).
In cases of acute frothy bloat, passage of a stomach tube seldom produces dramatic relief of the rumen distention but does aid in diagnosis and allows treatment with surfactant agents such as Therabloat (poloxalene drench concentrate; SmithKline Beecham Animal Health, West Chester, PA) or vegetable oil to break down the froth. In some frothy bloats, a Kingman stomach tube may permit decompression, but this is not the rule, and in severe cases with thoracic compression, passage of the tube may, on rare occasion, cause acute death. Oral ruminotorics-laxative-antacid powders in warm water and parenteral calcium solutions also should be administered to encourage rumen emptying. Emergency rumenotomy (Figure 5-12) is the treatment of choice for progressive and severe frothy bloat. In a hospital environment, hypertonic saline administration, intranasal oxygen, and analgesics (flunixin) are helpful in stabilizing the cow during standing surgery.
Percutaneous rumen trocharization as a treatment for acute bloat of any cause is contraindicated in the dairy cow except in extreme cases when emergency decompression is necessary. Trocharization in the dairy cow ensures peritonitis, which may be fatal or may confuse the primary diagnosis by causing fever and signs referable to peritonitis—including bloat—over the following days.
Prevention of acute bloat is possible only when managerial changes have allowed ingestion of causative feedstuffs, including sudden availability to lush alfalfa pastures. Fortunately most dairy farmers are aware of these dangers, and it seldom is necessary to educate owners concerning such hazards and appropriate preventative measures such as gradual introduction to succulent pasture, prefeeding with long-stem hay, pasture surfactant sprays, poloxalene salt blocks, or simple avoidance.
In calves, most cases of chronic bloat have a dietary or developmental etiology. Low fiber diets are the usual cause in calves fed only milk or milk replacers (Figure 5-13, A and B). Otherwise, these affected calves are healthy except for the free-gas bloat that develops shortly after eating. Calves that have been overtreated with oral antibiotics for systemic infections or diarrhea also may develop bloat associated with abnormal rumen flora. Calves affected with diarrhea and treated with methscopolamine or other parasympatholytic drugs may develop a paralytic ileus and subsequent bloat that persists for 24 to 72 hours after the administration of the drug. Although overdosage may have occurred, some calves develop bloat even after using the manufacturer’s recommended dosages of methscopolamine.
Calves that have suffered severe bronchopneumonia occasionally develop free-gas bloat from damage to the thoracic portion of the vagal nerve or enlarged thoracic lymph nodes that cause failure of eructation. Left displacement of the abomasum (LDA) in calves may cause chronic or intermittent free-gas bloat, thereby confounding a diagnosis of LDA. Intermittent or chronic bloat associated with unthriftiness, inappetence, claylike feces, and abdominal distention occasionally occurs in 3- to 8-week-old dairy calves fed milk (mostly by bucket rather than bottle) (Figure 5-14, A). These calves are called “ruminal drinkers” because they have failure of the reticular groove reflex, thus causing milk to flow directly into the rumen rather than the abomasum. Ruminal parakeratosis and hyperkeratosis result in addition to metabolic and endocrine abnormalities. The calves may have excessive intestinal production of both D and L lactic acid and become severely acidotic from the D-lactic acid. The bloat may occur acutely within 1 hour after feeding but may also become chronic, and in some cases there may be enough milk putrefaction to cause the calf to become quite ill. Passage of a stomach tube may cause reflux of a gray fetid fluid (Figure 5-14, B).
Figure 5-14 A, Acute ruminal bloat that occurred 1 hour after drinking milk replacer in a bucket. There had been several episodes of bloat in this calf, and its general condition and hair coat are adversely affected. B, Rumen ingesta collected from the calf.
Older calves that have been weaned off milk or milk replacers also may develop chronic free-gas bloat of dietary origin if fed a low fiber diet. Although this can occur on silage and grain diets, it is much more common in calves fed all-pelleted rations. Up to 10% or more of calves fed all-pelleted rations with no hay supplementation will develop chronic bloat that worsens shortly after they ingest pellets and then drink large quantities of water. Many other causes of chronic bloat also exist in postweaning calves but are more difficult to diagnose and treat. These include inherent tendencies of bloat as seen in dwarf animals and inherent defects in forestomach innervation or smooth muscle function. Other lesions such as abdominal abscess, umbilical or urachal adhesion, intestinal obstruction, LDA, focal peritonitis, and rarely abomasal impaction (Figure 5-15) may lead to chronic bloat as well.
Esophageal lesions also must be considered in the differential diagnosis of chronic bloat in the calf. These include pharyngeal and esophageal trauma induced by balling guns, stomach tubes, or esophageal feeders. These lesions may damage the intricate vagal nerve branches responsible for eructation, swallowing, and forestomach motility. Esophageal motility disorders, although rare, should be considered as a cause of bloat in calves with a dilated esophagus. Thymic lymphosarcoma and enlarged mediastinal or pharyngeal lymph nodes resulting from the juvenile form of lymphosarcoma are the most common neoplastic causes of chronic bloat in calves. Diaphragmatic hernias are rare in dairy cattle but can result in acute or chronic rumen distention and bloat (Figure 5-16). Generally the reticulum is entrapped in the chest through the diaphragmatic rent. Signs include decreased cardiac and lung sounds and dullness during percussion in the ventral thorax (unilateral or bilateral), abdominal distention, bloat, vomiting, and dyspnea. Diaphragmatic hernias may be congenital or acquired as a result of trauma, parturition, or progressive weakening of the diaphragm adjacent to a hardware perforation and reticuloperitonitis.
Chronic bloat in adult cattle most often involves lesions of the vagal nerve. These lesions may occur anywhere from the brainstem to the pharynx to the abomasum. Causes similar to those described in calves may be involved, as can adult diseases such as listeriosis, hardware, reticular abscesses, liver abscesses, volvulus of the abomasum, abomasal impaction, advanced pregnancy, and lymphosarcoma. These are discussed further in the section on Vagal Indigestion.
Forestomach neoplasms primarily include fibropapillomas of the distal esophagus or cardia and lymphosarcoma masses in the forestomach or abomasum. With fibropapillomas, a failure of eructation occurs because the tumor acts like a plug or one-way valve in the distal esophagus, thereby interfering with effective eructation. In lymphosarcoma and abomasal atony following correction of abomasal volvulus (AV), outflow disturbances with reflux of abomasal contents into the rumen, failure of eructation, or failure of motility all contribute to chronic rumen tympany. Rumen chloride content would be elevated (.51 mEq/dl) with abomasal reflux, and affected cows typically demonstrate moderate to severe hypochloremic, metabolic alkalosis on routine blood work.
Granulomatous lesions caused by Actinobacillus lignieresii and Actinomyces bovis may cause distal esophageal or reticular lesions that result in chronic bloat or indigestion. This is quite unusual, however.
Cattle with tetanus may have chronic (i.e., several days duration) bloat. In this instance, inability of the laryngeal, pharyngeal, and esophageal striated musculature to coordinate the intricate neuromuscular act of eructation because of tetany results in free-gas bloat. Bloat may also be observed in cows with listeriosis, botulism, or other neurological diseases.
In all cases of bloat, the veterinarian must confirm that the abdominal distention is caused by ruminal distention rather than pneumoperitoneum or LDA. In calves, simultaneous percussion and auscultation, ballottement, and abdominal palpation should differentiate abomasal, small intestinal, and cecal distention from that involving only the rumen. Observation, physical examination, and sometimes ultrasonography are extremely important in the calf because rectal examination is not possible. In adult cattle, rectal palpation coupled with other physical findings should easily confirm rumen distention.
The diagnosis of chronic bloat is confirmed by a combination of history and physical examination findings. Other causes of chronic abdominal distention such as ascites, displacement of the abomasum, cecal distention, and hydrops should be ruled out. In addition to abdominal auscultation and ballottement and rectal examination in cows, a stomach tube should be passed to determine whether the bloat is free gas or ingesta. Specific causes of chronic bloat should be sought through physical examination, ancillary data, and surgical exploration of the abdomen, if the value of the affected animal warrants this procedure.
Specific treatment depends on the specific cause of the chronic bloat. Because a portion of these cases involve lesions affecting the vagal nerve branches, treatment is discussed under Vagal Indigestion. Calves with unexplained chronic and/or intermittent free-gas bloat are best treated by making a temporary rumen fistula (Figure 5-17). Calves with chronic or intermittent bloat and ill thrift because of ruminal drinking of milk can be weaned or fed via a bottle rather than a bucket. If they become acutely ill in association with feeding milk and bloat, an oral-rumen tube should be passed to drain as much fluid as possible from the rumen, and the calf should be treated with systemic antibiotics and fluids.
Chronic free-gas bloat in tetanus patients may be relieved by gentle passage of a stomach tube or preferably with a surgically prepared rumen fistula that provides continuous escape of gas and a portal through which to provide feed and water to the patient. The creation of a therapeutic fistula is an important aid to the successful treatment of tetanus cases because affected animals are typically unable to eructate or swallow, and repeated passage of a stomach tube significantly increases their anxiety and stress level.
Patients with free-gas bloat and ileus secondary to the administration of atropine or methscopolamine require passage of a stomach tube as frequently as necessary. These patients usually improve spontaneously 48 to 72 hours after the last administration of the offending drug.
Traumatic reticuloperitonitis after ingestion of metallic foreign bodies is one of the oldest diseases recognized in cattle but still occurs with alarming frequency under modern management. Unlike sheep and goats, cattle do not use their lips to discriminate between very fibrous feed and metallic objects in feedstuffs. Cattle also are given a great deal of chopped feed that may contain wire remnants, machinery parts, or other metallic debris.
Metallic foreign bodies, such as wire and nails, are the most common agents of hardware disease. In most cases, the wires range in length from 5.0 to 15.0 cm and tend to be slightly bent or have a crook at one end. Nails of all sizes also have been recovered from cattle with hardware disease as have, on occasion, hypodermic or blood collection needles. Many clinically normal cows will have metallic objects, sand, stones, fence staples, and some gravel in their reticulum. Such objects are ingested, drop into the rumen, and within 24 to 48 hours are propelled into the reticulum where they remain because of gravity or entanglement with the reticular mucosa. Nonperforating objects found frequently include nuts, bolts, washers, and short wire fragments (less than 2.5 cm). These objects may be found routinely on radiographic surveys or slaughterhouse specimens. Therefore exposure to metallic foreign bodies should be anticipated in dairy cattle. Although perforation may occur randomly at any time in a cow harboring a sharp metallic foreign body, physical factors may contribute to perforation and subsequent clinical signs. The prime example of such a physical factor contributing to perforation is advanced gestation and a heavily gravid uterus. During the last trimester, the combined weight and size of the gravid uterus may allow the organ to act like a pendulum as a cow gets up and down; this can apply physical pressure to the rumen and reticulum, contributing to perforation by an existing sharp metallic object. Clinical incidence of hardware disease in cattle in the last trimester of pregnancy is high enough to warrant inclusion of this disease in a differential diagnosis for any acute illness in heavily pregnant or dry cows. Diseases or conditions causing tenesmus or straining, such as parturition, also may cause increased abdominal pressure, possibly contributing to perforation.
Hardware disease usually occurs in heifers or cows older than 1 year of age. It is not known whether discrimination during prehension or absence of exposure to certain high-risk feedstuffs protects the animal during the first year of life.
In light of the likely exposure of most dairy cattle to metallic foreign bodies in feedstuffs, perhaps the greatest single factor in the causative development of hardware disease is failure to have administered a prophylactic magnet to the animal at 12 to 18 months of age. This should be considered a mandatory component of preventative herd health.
Once a metallic foreign body perforates the reticular wall, clinical signs develop. These signs are extremely variable and influenced by the anatomic region of perforation within the reticulum, depth of perforation, associated abdominal or thoracic viscera injury by the perforating object, physical features of the causative object, and the affected cow’s stage of gestation or lactation.
Classic hardware disease causing acute localized reticuloperitonitis results in a sudden, dramatic, and often complete anorexia and cessation of milk production. Milk production may decrease to near zero within 12 hours and prompt the owner to seek veterinary attention for the cow. Affected cattle may have fever (103.0 to 105.0° F/39.44 to 40.56° C), normal to mildly elevated heart and respiratory rates, abducted elbows, an anxious expression, an arched stance (Figure 5-18), hypomotile rumen with or without mild tympany, scant dry feces, and abdominal pain localized in the cranial ventral abdomen near the xiphoid. When examined within 24 hours of onset, classic cases as described are relatively easy to diagnose. Many clinical cases show more variable signs (e.g., some cows stand up more than normal, whereas others lie down more than normal) and represent more difficult diagnostic challenges. In some cases, vague signs of partial anorexia, decreased milk production, and changing fecal consistency may be observed by the owner and may have been present for some time before veterinary attention is sought. Physical examination may reveal little beyond ruminal hypomotility or mild tympany suggestive of localized peritonitis, and cranial abdominal pain. In some mild cases, careful auscultation and observation may reveal treading with the hind feet because of the pain associated with localized peritonitis during ruminoreticular contraction. Affected cattle with less obvious signs may “grunt” or grind their teeth while being “poked” by a metallic foreign body embedded in the reticular mucosa or submucosa, or one that has penetrated full thickness and continues to cause pain intermittently. Occasionally cattle affected with hardware disease will “vomit” or regurgitate more material than they can retain as a cud. This represents a neurogenic or pressure-related triggering of the regurgitation reflex from reticular irritation. In these less obvious cases, careful physical examination and attention to detail when assessing abdominal pain are important keys to thediagnosis.
An important point concerning patients with hardware disease is that the body temperature may be normal. This statement is in direct conflict with textbook descriptions of the disease and seems difficult to explain in light of the obvious peritonitis that exists in these patients. In a review of the case records from more than 200 cattle confirmed by surgery or necropsy to be affected with hardware disease, the body temperature was normal in more than half of these patients. This may relate to the subacute or chronic nature of the disease in these referral patients, or they may have had an initial fever spike after the acute perforation that was not recorded. The fact remains that the veterinarian may not be called to attend a hardware disease case during the acute phase, and hardware disease should not be ruled out by finding a normal rectal temperature.
Cattle affected with chronic localized peritonitis have signs of weight loss, poor hair coat, intermittent anorexia, decreased milk production, change in manure consistency, and rumen dysfunction with or without mild tympany. Such cows may have an arched stance and detectable abdominal pain as well.
Cattle affected with traumatic reticuloperitonitis that results in a diffuse peritonitis have much more severe signs than those affected with localized peritonitis. Cattle developing diffuse peritonitis resulting from hardware disease have fever, elevated heart rates (90 to 140 beats/min), elevated respiratory rates (40 to 80 breaths/min), total rumen and gastrointestinal stasis, a total cessation of milk flow and appetite, generalized skin coolness, reduced mucous membrane capillary refill time, scant loose manure, and often have an audible grunt or groan associated with expiration. The grunt or groan is most apparent when the animal arises, lies down, or is made to move about. Abdominal pain can be difficult to detect in these patients because the diffuse severe pain overwhelms any localized attempt to elicit pain by deep abdominal pressure. The animal will be reluctant to rise or move about and in most instances will progress to a shocklike state within 12 to 48 hours. As the animal’s condition deteriorates, the body temperature also may plummet from the early fever to normal or subnormal. Risk of diffuse peritonitis is enhanced when a cow develops traumatic reticuloperitonitis in advanced gestation because the weight and movement of the gravid uterus tend to disseminate the peritonitis and make natural attempts at walling off the peritonitis difficult. Diffuse peritonitis caused by abomasal perforation is the principle differential diagnosis for cows with this presentation and signalment.
Laboratory tests may be helpful in diagnosing confusing cases. Peritoneal fluid containing elevated total solids and white blood cell numbers supports a diagnosis of peritonitis. A complete blood count (CBC) may or may not be helpful because many patients with hardware disease have normal CBCs, although almost all have elevated plasma fibrinogen levels. Some patients with hardware disease with acute localized peritonitis and most patients with acute diffuse peritonitis will show a degenerative left shift in the leukogram. In chronic (longer than 10 days) hardware disease, serum globulin is often elevated (.5.7 mg/dl), and the leukogram may be normal or confirm mature neutrophilia. Cows with peracute, diffuse septic peritonitis caused by hardware disease may have hypoproteinemia as a result of fluid and protein loss into the peritoneal cavity, but this does not occur as commonly as with abomasal perforation. Because of forestomach and abomasal hypomotility or stasis, patients with hardware disease have a hypochloremic, hypokalemic, metabolic alkalosis that varies in severity in direct proportion to the degree of stasis. Cattle affected with subacute or chronic hardware disease that has caused complete rumen stasis may have a profound metabolic alkalosis with serum chloride values in the 40 to 50 mEq/L range. It is debatable whether alkalosis of this magnitude totally results from the disease present or is accentuated by oral administration of ruminotoric laxative medications before blood collection. Regardless of pathophysiology for alkalosis of this magnitude, the prognosis is not hopeless. The most helpful ancillary tests are abdominal ultrasonography and reticular radiography. Abdominal ultrasound should reveal an abnormal pocket of fluid and fibrin in the anterior abdomen (Figure 5-19). Radiography is the best test for confirming metallic penetration of the reticulum (or rarely rumen), the current location of the metal object, and the presence and size of perireticular abscesses (Figure 5-20, A to D). Unfortunately, this is the least available test for the practicing veterinarian because extremely powerful radiographic equipment is necessary to penetrate the reticular region in adult cattle.
Figure 5-20 A, Radiograph of cow with traumatic reticuloperitonitis. Note fluid and gas interfaces around metallic foreign body suggestive of reticular abscess formation. B, Radiograph of cow with ventrally located draining fistula associated with traumatic reticuloperitonitis. The foreign body was a piece of bailing wire. C, Abdominal radiograph of a cow with hardware showing an abscess (gas) ventral to the reticulum floor. D, Radiograph of the anterior abdomen showing a fluid line of a large perireticular abscess.
Radiography of the reticulum has been a useful ancillary procedure in teaching hospitals and referral centers to aid in detecting reticular foreign bodies and abscesses of the reticulum or liver. The procedure is very helpful in confusing cases of abdominal disease or in confirmation of suspected hardware disease. Powerful radiographic units of 300 mA and 125 kVp using a 400 ISO speed film-screen combination are necessary for such studies. Experience with such radiographic studies and the subsequent surgical findings allow clinicians to diagnose, determine the need or approach for surgery, and prognosticate more specifically than possible without this ancillary aid. A portable unit has reportedly been used to take radiographs of the reticulum in cattle restrained in dorsal recumbency. However, it is difficult to keep cows in that position and the forced positioning of the cow could worsen the peritonitis.
The diagnosis of traumatic reticuloperitonitis is based primarily on physical examination and is aided by laboratory work in less obvious cases. In cattle with obvious signs of peritonitis, perforating abomasal ulcers are the chief differential consideration. Perforating abomasal ulcers tend to cause pain in the midventral abdomen on the right side of midline, are usually associated with fever, and are most common 2 weeks before freshening and up to 100 days postpartum. Acute pyelonephritis or necrotic lesions of the cervix or vagina may present similar to hardware. With pyelonephritis, the urine may be discolored and rectal examination reveals an enlarged ureter. Cows with necrotic cervicitis or vaginitis are often febrile, depressed, stand either hunched up or stretched out, and have rumen atony, but unlike hardware cases, they strain and frequently aspirate air in the rectum. If an active magnet is already present in a cow having signs of peritonitis, abomasal ulceration is more likely than hardware disease. A compass can be used during physical examination to detect an active magnet in the reticulum. The compass is moved slowly into position behind the elbow on the left thoracic wall. A 60- to 90-degree deflection indicates the presence of a strong magnet in the reticulum. In cows with normal rectal temperatures, hardware disease must be differentiated from indigestion and ketosis. This can be done based on the absence of abdominal pain in patients with ketosis, while cows with hardware have evidence of abdominal pain in addition to ruminal hypomotility and negative to trace urinary ketones. A cow affected with musculoskeletal diseases such as polyarthritis, laminitis, back pain, or trauma could be confused with one having hardware disease because of an arched stance, weight loss, anorexia, and decreased production. Physical examination should differentiate these diagnoses, however.
Except for valuable cows, conservative treatment is indicated in most acute cases of traumatic reticuloperitonitis. This treatment consists of a magnet administered orally, systemic antibiotics to control existing peritonitis, and stall rest to aid in the formation of adhesions; other symptomatic therapy such as oral fluids, ruminotorics, calcium solutions, and oral electrolytes also may be helpful. If dehydration is present and metabolic alkalosis is suspected or confirmed, fluid therapy and supplementation with potassium chloride orally (1 to 2 oz orally, twice daily) or IV are indicated. In severely alkalotic patients, alkalinizing ruminotorics should be avoided. Conservative therapy results should be evaluated within 48 to 72 hours. If the affected cow is beginning to eat and ruminate and production begins to increase, recovery can be anticipated. If the cow is not improving or if appetite and rumen activity wax and wane, rumenotomy may be indicated. Following oral administration of a magnet, the magnet first drops into the rumen. The magnet only moves to the desired location in the reticulum through effectual ruminoreticular contractions. Therefore if the rumen remains static, it is unlikely the magnet will move into the reticulum to grasp and hold the foreign body. It is revealing to note the number of cattle that are referred to teaching hospitals that possess a magnet or magnets within the rumen rather than the reticulum when the magnet has been administered as a therapeutic rather than prophylactic aid. If the affected cow already has a magnet at the time signs develop, exploratory laparotomy and rumenotomy may be indicated initially rather than conservative therapy. This situation may occur when the foreign body is extremely long (.15 cm) and extends off the magnet to a dangerous level or is not attached to a magnet, as in the case of an aluminum needle. Rumenotomy and object removal should be performed immediately in valuable cows to limit further movement of the object and worsening peritonitis. When laparotomy and rumenotomy are elected, it is best not to explore the serosal surface of the rumen and reticulum if adhesions are obvious. This will avoid dissemination of the peritonitis. During rumenotomy, a careful palpation of the entire reticulum is indicated to find the offending foreign body, which may remain only partially in the reticular wall. Left-sided laparotomy and rumenotomy allow for confirmation of the diagnosis, removal of the foreign body/bodies, and drainage of reticular abscesses into the lumen (Figure 5-21, A to C). Even with radiographic and/or ultrasonographic guidance, it can be challenging to identify and remove some foreign bodies that are embedded within mature, chronic, fibrous adhesions, and reaching a comfort level with abscess drainage by sharp scalpel incision into the reticular wall at the site of the adhesions takes some practice and experience. If there is a large reticular abscess, it could be drained via a ventral percutaneous approach, although cellulitis, reticular fistula, and dissemination of the peritonitis may occur.
Figure 5-21 A, A drawing depicting rumenotomy and lancing a perireticular abscess into the reticulum. B, Left paralumbar fossa laparotomy with rumen wall attached to a “rumen board.” C, Same cow as B with rumen open.
Antibiotic therapy should be continued a minimum of 3 to 7 days to control existing localized peritonitis completely and to discourage secondary reticular abscesses at the perforation site. Penicillin, ceftiofur, ampicillin, and tetracycline all have been used successfully for this purpose.
In subacute or chronic cases in which chronic anorexia, dehydration, and severe alkalosis exist, IV therapy, antibiotics, and rumenotomy are indicated at the time of diagnosis. Conservative therapy is unlikely to be successful in these patients, and further supportive care with rumen transfaunates, calcium solutions, and long-term antibiotic treatment often are necessary.
Cattle suffering from hardware disease may have myriad complications secondary to perforation and peritonitis. Septic pericarditis is perhaps the best-known complication and occurs when the metallic foreign body perforates in a cranial direction, perforating the diaphragm and pericardium (Figure 5-22, A and B). Reticular abscesses also are fairly common sequelae and often occur on the cranial or right wall of the reticulum where they directly, or indirectly, cause dysfunction of the ventral vagus nerve branches and result in signs of vagus indigestion. Signs of vagus indigestion vary from mild ruminoreticular disturbances to omasal transport difficulties or abomasal dysfunction/impaction. Septic pleuritis, pneumonia, thoracic abscesses, diaphragmatic hernias, and traumatic endocarditis are less frequent complications of a perforation of the diaphragm. Occasionally a metallic foreign body—usually a wire—associated with a ventral perforation migrates through the sternum or cranial ventral abdomen, resulting in a reticular fistula (Figure 5-23). Any perforation of the right wall of the reticulum may directly or indirectly, through associated inflammation and adhesions, injure, inflame, or irritate the ventral vagus nerve branches and result in signs of vagus indigestion. Therefore when hardware disease is suspected as the cause of vagus indigestion, a meticulous search of the right wall of the reticular mucosa is indicated during rumenotomy.
Figure 5-22 A, A cow with ventral edema, brisket edema, and intermandibular edema caused by pericarditis secondary to traumatic reticuloperitonitis. B, Radiograph of the anterior abdomen and ventral thorax of a 96-point cow with acute traumatic reticulitis. The wire has moved into the right thorax and was successfully removed via a standing thoracotomy.
All breeding age heifers or heifers 1 year of age, as well as young bulls, should receive strong prophylactic magnets. Not to recommend this for valuable cattle represents negligence, and the loss of a single valuable dairy cow because of traumatic reticuloperitonitis is inexcusable. Unfortunately hardware disease is still extremely common, and many cows die each year because the owner “forgot” to administer a magnet. Although occasional cows pass magnets through the gastrointestinal tract and some magnets do lose strength, the magnet remains the major means of preventing this disease. The effectiveness of magnets is apparent at slaughterhouses, where an impressive array of metallic foreign bodies are found trapped tightly to magnets. When purchasing magnets, the owner or veterinarian should assess the strength of the magnet by testing it against metallic objects. Inferior magnets should not be purchased.
Large electromagnetic plates to trap metal can be incorporated into automatic feeding lines or silo unloaders and are available commercially; they are very helpful on large farms with automated feeding assemblies. Use of these plates should be encouraged because they tend to trap many pounds of dangerous sharp metallic objects each year.
The vagus nerve may be damaged anywhere along its anatomic course to the forestomach and abomasum. Lesions capable of injuring, inflaming, or destroying the vagus nerve and its branches are discussed based on a regional basis, starting with the brainstem and progressing distally along the vagus nerve. All of these diseases lead to forestomach or abomasal dysfunction to some degree and have been included under the category Vagus Indigestion. Depending on the anatomic area involved and degree of damage to the vagus nerve or its branches, these diseases may cause a wide spectrum of forestomach or abomasal signs. In all cases, ruminal distention is present intermittently or constantly. This distention may be the result of functional or physical outflow obstruction from the forestomach, or failure of eructation causing free-gas distention. Physical or functional obstruction of the abomasum or pylorus may prevent outflow in more distal lesions.
The conditions discussed in this section are those that result in the syndrome called vagus indigestion. This syndrome must be thought of as a complex or set of signs secondary to a primary lesion along the course of the vagus nerve.
General signs suggesting vagus nerve damage include decreased appetite for several days or more, decreased milk production, abdominal distention that may be constant or intermittent but tends to be progressive, pasty manure that often varies in quantity in direct proportion to appetite and inversely with the degree of abdominal distention, and loss of body condition. Many cases develop bradycardia (heart rate 60 beats/min); however, not all cases develop this sign, and its absence should not rule out vagus indigestion. Bradycardia appears to be caused by reflex retrograde irritation of the vagus nerve, causing parasympathetic slowing of the heart rate. Bradycardia has also been associated with simple anorexia. Rumen contractions may be hypermotile, hypotonic, or atonic, and vagus indigestion has been categorized by some authors based on this sign. In some cases, rumen contractions occur more frequently than normal (3 to 6 contractions/min) but are ineffectual and fail to propel ruminoreticular ingesta into the omasum and abomasum, resulting in frothy ruminoreticular ingesta from constant churning activity.
The abdominal distention that develops is classical, with distention in the upper left, lower left, and lower right quadrants as the cow is viewed from the rear (Figure 5-24). In most cases, this distention results from progressive ruminal enlargement with the ventral sac enlarging toward the right. Therefore this typical distention results in an L-shaped rumen, as viewed from the rear or palpated per rectum. In severe cases, the rumen ventral sac not only fills the entire right lower quadrant of the abdomen but also may expand into the right upper quadrant so the rumen assumes a V shape. Extreme distention of the rumen into a V shape occasionally traps gas in the most dorsal region of the now expanded ventral sac, and this gas may result in an area of tympanitic resonance in the right upper quadrant. In very rare instances of true abomasal impaction or pyloric stenosis, the abomasum may be large enough to account for this right lower quadrant distention.
Depending on the primary lesions, signs of vagus nerve dysfunction may appear acutely or have a delayed onset. In most cases, onset of signs and typical abdominal distention occur several days to weeks after the affected cow initially developed signs of illness. Some primary lesions are relatively easy to diagnose, whereas others require extensive ancillary data or exploratory surgery. In all cases, primary lesions resulting in the syndrome of vagus indigestion should be sought because prognosis directly depends on the primary cause. Having discussed the general signs of vagus indigestion, specific primary causes will next be discussed, and individual signs referable to each will be included when pertinent. Table 5-1 summarizes the clinical results of long-term follow-up evaluation for 112 cases of vagus indigestion and illustrates relative occurrence of the various primary lesions.
Vagus nerve nucleus lesions are rare, but occasionally cattle affected with listeriosis will show vomiting and rumen inactivity as early signs, and this may reflect vagal nerve irritation. It also is possible that vomiting or normal regurgitation occurs but cannot be controlled when oral-pharyngeal neuromuscular function is impeded by specific cranial nerve deficits (V, VII, IX, X) at the brainstem level.
Pharyngeal trauma with typical signs of fever, dysphagia, salivation, extended head and neck, and soft tissue swelling in the pharyngeal area often results in vagal nerve dysfunction. This trauma invariably results from injudicious or unskilled use of balling guns, dose syringes, stomach tubes, specula, esophageal feeders, or magnet/foreign body retrieval apparatus when treating a cow. Vagal nerve dysfunction may be apparent as ruminal hypomotility, dysphagia, failure of eructation, and subsequent ruminal distention. Bradycardia is present in some cases. The complex neuromuscular act of eructation frequently is altered because vagus nerve branches controlling the pharynx, larynx, and cranial esophagus are subject to inflammatory or direct traumatic damage in these patients. Retropharyngeal abscess and pharyngeal foreign bodies may cause signs similar to those caused by pharyngeal trauma but are less common.
Esophageal lacerations from traumatic passage of stomach tubes, esophageal feeders, or magnet/foreign body retrieval apparatus may lead to severe cellulitis and associated vagus nerve dysfunction. Chemical or septic phlegmon with similar signs may follow perivascular injections of material intended for IV administration in the jugular vein. Fever, salivation, and severe inflammatory swelling in the cervical region usually accompany any signs of vagus nerve damage in these patients. Chronic choke may lead to esophageal necrosis and similar signs along with profuse salivation and reflux of ingested food or water.
Occasionally in calves and adult cattle, severe bronchopneumonia results in apparent inflammatory damage to the vagus nerve traversing the mediastinum. It is not known whether this syndrome involves direct inflammation of the nerve or indirect pressure from enlarged lymph nodes. In any event, the affected calf or cow develops signs of abdominal distention, ruminal tympany, and inappetence, despite apparent response of the pneumonia to broad-spectrum antibiotic therapy. Usually signs of ruminal tympany develop several days after the onset of the pneumonia. Passage of a stomach tube in these patients relieves and resolves a free-gas bloat, but the bloat recurs as a chronic problem and results in weight loss because the animal eats only during those times when the bloat is relieved. Failure of eructation seems to be the major cause of this recurrent free-gas bloat. Occasional cases of frothy-type bloat may occur in association with chronic bronchopneumonia in adult cattle, when pneumonic pathology involves thoracic branches of the vagus.
Neoplasms such as thymic, juvenile, or adult lymphosarcoma, neurofibromatosis, and pulmonary carcinomas sometimes may result in signs of vagus indigestion resulting from extraluminal compression of the esophagus or pressure on the vagus nerve and subsequent failure of eructation with chronic free-gas bloat.
Lesions at the cardia include fibropapillomas, other neoplastic processes, and granulomas caused by Arcanobacterium sp. or A. lignieresii. Generally lesions in this area mechanically occlude the distal esophagus during attempts at eructation or regurgitation and cause signs of vagal indigestion.
Most lesions involving the reticulum are located on the right or medial wall of the reticulum. These lesions damage the ventral vagal nerve branches with inflammation, pressure, or direct trauma. Traumatic reticuloperitonitis, reticular abscesses, liver abscesses, severe toxic rumenitis, and neoplasms such as lymphosarcoma would be included in this group. Some authors include adhesions of the cranial and medial reticulum in this category and imply that mechanical dysfunction results from these adhesions. Most authors, however, believe that neurogenic damage to the ventral vagal branches must occur even if adhesions are present. In this category, prognosis seems to vary depending on the cause. Traumatic reticuloperitonitis carries a variable prognosis based on the degree of peritonitis and involvement of the ventral vagal branches (13 of 32 cases had good outcomes), whereas reticular abscesses carry a more favorable prognosis (10 of 15 cases had good outcomes) (see Table 5-1) presumably because they tend to cause vagal nerve dysfunction by pressure on the nerve. This pressure dysfunction is alleviated by surgical drainage.
Lesions of the forestomach distal to the reticulum or involving the abomasum include a diverse group of problems such as lymphosarcoma (see video clip 10) and other neoplasms, diffuse peritonitis, peritonitis caused by perforating abomasal ulcers, abdominal abscesses, vagal nerve damage and possible vascular thrombosis secondary to right-sided AV, omasal impaction, and chronic or severe abomasal impaction. In general, prognosis is poor for cattle with signs of vagal indigestion secondary to these lesions (see Table 5-1) because of the extent of the pathology, the possibility of multiple sites being affected, and the likelihood of functional and mechanical outflow disturbances. In referral practice, a disproportionate number of cattle with right-sided AV are treated. Many of these cattle have been affected for 24 hours or more before referral, thereby being at high risk for subsequent signs of vagal nerve dysfunction. Usually these cattle appear to improve for 24 to 72 hours after surgical correction of their AV but then begin to show signs of an outflow disturbance. These cattle then develop bradycardia, typical ruminal distention, scant manure, poor appetite, and abdominal distention typical of an L-shaped rumen.
Most distention involves the forestomach compartments even though the abomasum was the primary problem. Recent work helps explain this syndrome. Because volvulus involves the abomasum, omasum, and reticulum, either neurogenic damage by stretching the ventral vagal branches or thrombosis of major vessels supplying the lesser curvature of the abomasum, omasum, and reticulum may result from prolonged volvulus. Most cattle that develop signs of vagal indigestion following right-sided DA and volvulus never recover despite attempts at therapy. Rumenotomy is seldom suggested for cows with vagus indigestion secondary to right-sided volvulus of the abomasum because the primary pathology is thought to be irreversible. Vagal nerve damage secondary to right-sided volvulus has an extremely poor prognosis with only 3 of 26 patients having a good outcome (see Table 5-1). Right-sided DAs and volvulus should be corrected on an emergency basis to minimize chances of vagal nerve damage or outflow disturbance. Valuable cattle that begin to develop symptoms of vagus indigestion following correction of right-sided volvulus of the abomasum by omentopexy may be considered for abomasopexy or abomasopexy following rumenotomy to ensure proper abomasal alignment that may improve outflow. The prognosis, however, remains guarded to poor.
Diagnosis of vagus indigestion is based on subacute to chronic history, typical abdominal distention, rectal findings of an L-shaped rumen (as viewed from the rear), and bradycardia (when present). The diagnosis is incomplete, however, until a primary cause of vagus nerve dysfunction is determined. The primary lesion is obvious in some instances, such as pharyngeal trauma, esophageal laceration, and vagus nerve dysfunction secondary to recent surgical correction of right-sided volvulus of the abomasum. In other instances, especially those with less common abdominal lesions or when associated with advanced pregnancy, the primary diagnosis may be difficult to determine unless exploratory laparotomy and rumenotomy are performed. Abomasal and sometimes ruminal impactions unrelated to any apparent vagal nerve injury sporadically occur. Abomasal impactions are a cause of decreased appetite and production in dairy cattle, and most have complete recovery following medical or surgical treatments and are likely unrelated to vagal dysfunction. Cows with abomasal impactions associated with vagal nerve dysfunction are much less amenable to treatment.