NORMAL APPEARANCE

The peritoneal lining can be seen as a very thin, smooth hyperechoic line adjacent to the body wall. Minimal free abdominal fluid is seen within the peritoneal cavity. Retroperitoneal adipose tissue appears as a hypoechoic layer of varying thickness between the body wall and abdominal viscera and should not be misinterpreted as cellular peritoneal effusion. Adipose tissue may also be seen within the omentum and mesentery, demonstrating a similar appearance between or among the gastrointestinal viscera. This omental and mesenteric adipose tissue can often demonstrate an organized appearance with visible fine vasculature that can be mistaken for liver, especially in small ruminants.

ABNORMAL FINDINGS

Peritoneal fluid is readily identified on ultrasound as anechoic to echogenic fluid between the body wall and abdominal organs (Fig. 32-89). In cases of severe effusion, the abdominal organs and viscera appear to float within the free fluid. Fibrin deposits are commonly seen in ruminants with inflammatory peritoneal effusion and appear as linear strands extending between organs or between peritoneal surfaces and serosal surfaces of abdominal organs (Fig. 32-90).^329,367 Fibrin can also demonstrate a “shag carpet” appearance along the peritoneal and/or serosal surface. Localized peritonitis may also be seen and has been reported in cows secondary to left flank laparotomy.³⁶⁷ Hemoabdomen appears as hypoechoic cellular-appearing fluid that swirls with ballottement, peristalsis, or respiration. (Fig. 32-91)

Fig. 32-89 Sonogram of mild peritoneal effusion (arrows) seen between several loops of normal small intestine and the ventral body wall viewed from the right ventral abdomen in a 2-year-old Hampton cross ram. This image was obtained with an 8.5-MHz curvilinear transducer at a depth of 7 cm.

Fig. 32-90 Sonogram of severe fibrinous peritonitis thought to be secondary to an intestinal rent viewed from the right paralumbar fossa region in a 3-year-old Holstein dairy cow. Note the hyperechoic fibrin strands creating a weblike appearance within the peritoneal cavity. This image was obtained with a 5-MHz curvilinear transducer at a depth of 27 cm.

Fig. 32-91 Sonogram of severe hemoabdomen viewed from the right cranioventral abdomen in a 2-year-old Shorthorn heifer with metastatic granulosa cell tumor. Note the very cellular appearance to the fluid within the peritoneal cavity. The liver is displaced from the body wall and appears to float in the effusion. This image was obtained with a 2.5-MHz curvilinear transducer at a depth of 27 cm.

Other abnormalities of the peritoneal cavity include mesenteric abscessation, mesenteric lymphadenopathy, and neoplasia. Intraabdominal abscessation may be identified within the mesentery or associated with abdominal incisions. Abscesses are generally well encapsulated with anechoic to echogenic contents. Enlarged mesenteric lymph nodes can be seen within the small intestinal mesentery and are a nonspecific finding that has been seen by the author in cases of abdominal disease from numerous causes (Fig. 32-92). Ruminants with neoplasia may demonstrate severe peritoneal effusion, most notably in cases of mesothelioma.^384,385 In cases of mesothelioma, multiple echogenic nodules are seen overlying the serosal surfaces of the peritoneum and abdominal organs (Fig. 32-93). Nodules can also be seen in the omentum.^384,385

Fig. 32-92 Sonogram of an enlarged mesenteric lymph node viewed from the left ventral abdomen in an 8-month-old Angora kid with disseminated Rhodococcus equi infection. This image was obtained with a 7.5-MHz curvilinear transducer at a depth of 5 cm.

Fig. 32-93 Sonogram of multiple peritoneal masses (arrows) between the rumen and body wall viewed from the left paralumbar fossa region in a 10-year-old pygmy doe with mesothelioma. This image was obtained with an 8.5-MHz curvilinear transducer at a depth of 6 cm. Dorsal is to the right and ventral is to the left.

Definition and Etiology

Indigestion is a general term for a group of diseases characterized by dysfunction of the reticulorumen. Some texts have limited the use of the term to a single, poorly defined entity that includes inappetence, decreased reticuloruminal motility, and abnormal feces, with a nonspecific cause that involves intake of abnormal feed.

The more generalized term applied here incorporates a pathophysiologic classification scheme of forestomach disturbances that has been devised by workers in Germany.³⁸⁶ An absolute division of the pathologic processes is impossible because the various forestomach functions are interdependent; that is, abnormal motor function affects microbial fermentation by altered mixing or passage of ruminal fluid out of the forestomach chambers, whereas abnormal fermentation products secondarily alter motor function. Nevertheless, this classification provides a clinically useful diagnostic framework by emphasizing the underlying pathophysiologic mechanisms of different forestomach disturbances.

The primary indigestions include those diseases in which the reticulorumen is directly affected and responsible for the major disease signs (Box 32-5). These problems can be divided into two categories:

Secondary indigestions are the sequelae of systemic problems or disease in other organ systems. For example, problems such as endotoxemia, fever, or depression can produce anorexia, secondary ruminal hypomotility, and decreased microbial fermentative function. Primary abomasal disease can depress ruminal function, inhibit ruminal outflow, and reflux abomasal contents back into the rumen.

With the exception of penetrating foreign bodies and sporadic infections of the forestomach wall (e.g., actinomycosis, mucormycosis), indigestions are physiologic abnormalities. In the adult ruminant one or more of the homeostatic processes of the fermentative environment are disturbed (e.g., an excessive carbohydrate intake generates an excessive amount of acid product; abnormal neural regulation of the ruminal motility pattern disturbs the mixing or aboral passage of ingesta). In the young ruminant the forestomachs are actively developing, and indigestions can result from disturbances of the developmental mechanisms. The forestomach diseases of young ruminants generally have received little attention, but they can be recognized and appropriately treated within a classification scheme similar to that for adult ruminants.³⁸⁷

Pathophysiology

Digestion of feedstuffs in the reticulorumen is accomplished by microbial fermentation. The mucosal epithelium absorbs and exchanges products of fermentation but performs essentially no secretory function. Appropriate forestomach fermentation depends on the coordination of processes that provide a fairly constant reticuloruminal environment. The requirements include addition of appropriate amounts and types of feed substrate and water by ingestion; buffering of substances from the saliva to counteract the acid nature of fermentation products; eructation of the gaseous products of fermentation; coordination of reticuloruminal motility to provide mixing; rumination and remastication; aborad passage of ingesta; temperature maintenance; and exchanges of electrolytes and VFAs across the ruminal wall. Because these functions are intimately interrelated, abnormalities of any one of them can lead to digestive disturbances.

Normal Motor Activity

The two reticuloruminal contraction sequences function independently. The primary cycle of contraction occurs approximately once a minute but more often during feeding and rumination. It consists of a biphasic contraction of the reticulum followed by a contraction that runs caudally across first the dorsal and then the ventral ruminal sacs. At the height of the second reticular contraction the omasal orifice relaxes, and fluid, mostly composed of reticular ingesta, passes into the omasum. This reticuloruminal motility pattern directly influences ruminal fermentation by mechanically mixing the ingesta to provide contact with the microbes and to macerate the particulate matter. The mixing function prevents local accumulations of substrate or end products of fermentation, distributes the buffering saliva for neutralization of acids, and provides increased contact of the fluid with the ruminal wall to promote VFA absorption. The coordinated sequence of contraction of various parts of the ruminal wall maintains a stratification of fluid and particulate matter that selectively sorts the ingesta by particle size. The sorting function serves to retain large particles for further digestive breakdown while promoting passage of small particles (smaller than 6 mm) into the omasum and lower gastrointestinal tract.^388-391

The secondary contraction cycle does not involve the reticulum. It begins in the caudal blind sacs, and a wave of contraction runs cranially across the dorsal rumen, pushing the gas cap into the cardia region. Eructation ensues, eliminating the gases generated by fermentation. Typically one secondary cycle contraction follows two primary cycles, so that three contractions occur every 2 minutes.^389-391 Two additional special contractions have been identified in sheep: primary-secondary contractions and prosecondary contractions.^392,393 These contractions appear when intraruminal pressure becomes elevated and function as secondary contractions by expelling ruminal gas. The primary-secondary and prosecondary contractions appear to help minimize free gas bloat when gas production is high.

Maintenance of the motility patterns requires well-coordinated neural control. The pathophysiologic mechanism of the first group of primary indigestions (i.e., diseases of the reticuloruminal motor function) involves disturbance of the mechanisms of normal ruminal motility, which secondarily affects ruminal fermentation.

The ruminal contraction sequences described rely almost completely on motor nerve activation arising from the medulla oblongata, in contrast to the intrinsic segmental and peristaltic movements of the intestine. Gastric centers in the medulla integrate sensory input and generate motor impulses, both of which are carried in the vagus nerves. The gastric centers have neither spontaneous activity nor an inherent rhythm. Generation of motor impulses relies on a greater excitatory than inhibitory input from the sensory nerves to determine the rate, magnitude, and duration of primary cycle contractions. During the quiescent period between the primary contractions, while the medulla collects the sensory information, there are no tonic vagal motor impulses.^394-400

The splanchnic nerves also affect reticuloruminal motility by direct innervation and by neurohumoral effects of adrenal secretion. These nerves are not required for generation of normal contractions. The effect of splanchnic stimulation is inhibition of reticuloruminal motility. Splanchnic sensory nerves innervate sensory receptors in other areas of the gastrointestinal system, and some abnormalities such as intestinal distention or surgical manipulation produce reticuloruminal inhibition by means of reflex from splanchnic afferent activity.^390,398,401

Primary Cycle Activity

A decrease or absence of normal primary cycle activity (i.e., ruminal hypomotility or stasis) implies either a decrease of vagal motor discharges originating from the gastric centers or an ineffective motor response after motor impulse, as in cases of hypocalcemia. Causes of decreased motor discharges can include the following:

Secondary Cycle Activity

The secondary cycle activity responsible for eructation is elicited independently of the primary cycles. An increase in ruminal gas pressure excites tension receptors in the medial wall of the cranial ruminal sac. This triggers relaxation of the cardia and eructation of the gas accumulated in the cardia region by the secondary contraction cycle. Receptors that apparently distinguish gas from fluid or solid matter inhibit opening of the cardia if it is covered by material other than gas.⁴²⁰ This reflex inhibition of cardia opening is responsible for bloat in cases in which abnormal ingesta cover the area, such as in recumbent animals, in frothy bloat, and when abnormal motility or overfilling of the rumen precludes clearing of the cardia. Under such circumstances and when ruminal distention is not yet extreme, both primary and secondary cycle contractions may increase in frequency. In other forms of bloat, hypomotility is a prominent feature, and the gas accumulates as a result of the poor motility function.³⁹¹ This is the most probable cause of bloat in some of the disturbances of fermentative function.

Gross overdistention of the ruminal wall may inhibit motility by stretching the musculature beyond its ability to contract forcefully. If the process leading to the distention develops slowly, the high-tension receptor inhibition of motility appears to adapt, and complete inhibition of motor impulses does not seem to occur. Rather, in these cases motility is present but weak and relatively ineffective. This motility disturbance is likely when poorly digestible roughage accumulates in the forestomach. Patients with this condition often have mild to moderate chronic free gas bloat, which may result from poor ability of the weakened rumen to clear the cardia and dispel the gas.³⁸⁶

Free Gas Bloat

Accumulation of free gas in the dorsal rumen should not be considered a primary disease entity but rather a sign of disease (Table 32-12). However, because free gas bloat often is the most prominent sign and because it accompanies several different forms of indigestion, its pathogenesis is reviewed briefly here.

Table 32-12 Causes of Ruminal Tympany (Bloat)

Ruminal microbial fermentation and neutralization of salivary bicarbonate continually produce gas as an end product (primarily methane and carbon dioxide) in proportion to the rate of fermentation. Normally the ruminant can eructate volumes of gas that exceed the amount produced even at maximum rates of fermentation.^392,393 Therefore an excessive production of gas is not the cause of bloat. Bloat develops either because the evacuation of gas is hindered by a physical obstruction or because the mechanisms that expel the gas are inhibited.^421-424

As in choke, physical obstruction of the esophagus by a foreign body can produce dramatic and peracute bloat. Other forms of esophageal occlusion (which may additionally involve inflammation of nerves or ruminal muscle malfunction) include muscular spasm (e.g., tetanus), swollen mediastinal lymph nodes (e.g., chronic pneumonia, thymic lymphosarcoma), and tumorous or inflammatory swellings of the cardia region (e.g., papilloma, actinomycosis). These problems tend to show bloat of a slowly progressive or chronic nature, although the degree of bloat may be marked.

Bloat is a common feature of indigestions caused by microbial fermentative disorders. When ruminal hypomotility occurs, the fermentative rate may decline, but weak ruminal contractions may be inadequate to move the gas layer and to clear the cardia preparatory to eructation. Thus dietary, microbial, or metabolic factors that affect the excitability of the gastric centers or the reticulorumen can result in bloat. Ruminal stasis can result in bloat because eructation occurs only with ruminal contraction. Bloat also accompanies indigestions that produce gross distention of the reticulorumen with fluid or solid ingesta (e.g., vagal indigestion, ruminal acidosis, and microfloral inactivity caused by indigestible roughage). The cause of bloat in these cases may be a combination of ruminal stasis, weakening of the ruminal wall caused by the gross distention, and failure to clear the cardia.

Some authors have attributed chronic bloat in calves to a form of vagal nerve damage resulting from mediastinal inflammation.^425,426 However, it has not been demonstrated that vagal nerve involvement is the source of the failure to eructate in these cases. It appears that free gas bloat in calves has numerous causes, as is true in adult cattle, including fermentative indigestions, ruminal wall disturbances, and esophageal involvement in an intrathoracic inflammatory process.⁴²⁷ Distinguishing between vagal nerve impairment and esophageal compression or inflammation as the cause of free gas bloat requires a thorough assessment of ruminal motor function, as described under the section on clinical signs (p. 832).

Reticulitis and Rumenitis

The most important inflammatory problem is reticuloperitonitis caused by sharp foreign body punctures (TRP, hardware disease). This disease is discussed elsewhere in the text (p. 848). The localized infection established by reticuloruminal perforation causes inflammation of the forestomach wall and adjacent peritoneal cavity and pain in the anterior abdomen, inhibiting forestomach motility, appetite, and aborad flow of ingesta. Other causes of ruminal wall inflammation can cause acute or chronic forestomach dysfunction.

Most infections of the ruminal wall follow primary mechanical or chemical damage to the mucosa. The secondary invaders colonize the damaged areas and may gain access to the circulation and invade other tissues as well. The ruminal wall may be the niche for some of these microorganisms, and isolates from the ruminal wall have been matched with those isolated from liver abscesses.⁴²⁸ Probably the most common cause of the initial mucosal injury is acute ruminal acidosis produced by grain engorgement. Chemical damage resulting in ruminal ulcers also occurs in oak or acorn toxicosis and with ingestion of caustic chemicals. Common secondary ulcer invaders include Arcanobacterium (Actinomyces) pyogenes, Fusobacterium necrophorum, and several mycotic species.^428,429 Mycotic rumenitis can follow ruminal acidosis and septic diseases, especially after the use of oral antibiotics; it also can occur after feeding spoiled and moldy feeds and without apparent predisposing causes.^430-434 Diseases that cause anorexia plus abomasal reflux of gastric acids may predispose an animal to mycotic rumenitis and omasitis. Mycotic rumenitis can be severe, with vascular thrombosis and infarction and mural necrosis and gangrene sufficient to cause death. Less frequently occurring specific infections of the ruminal wall include actinobacillosis, actinomycosis, and tuberculosis. These infectious inflammatory diseases of the ruminal wall may be distributed widely throughout the forestomach, depending on the initial site of mucosal injury, but they tend to localize in the ventral regions of the reticulorumen. The granulomatous inflammatory lesions of actinobacillosis and actinomycosis are most commonly found in the cranial forestomach in the area of the esophageal groove.

Neoplastic growths in the rumen have also been identified. These uncommon lesions include papillomas, myxomas, fibromas, carcinomas, and lymphosarcoma.^386,435,436 These lesions are most commonly localized in the reticulum and cranial rumen near the cardia and esophageal groove.

The importance of these inflammatory reticuloruminal lesions depends on their extent and location. Acute and extensive lesions have been associated with signs similar to those of reticuloperitonitis caused by foreign body puncture, including pain, inappetence, impaired forestomach function, and in some cases death. The more chronic cases may cause forestomach motility disturbances and signs of vagal indigestion. Pedunculated masses especially, but not exclusively, may obstruct the cardia or reticuloomasal orifice, leading to bloat or reticuloruminal outflow disturbance.

Reticuloruminal inflammation can also result from certain generalized infections. These include BVD, FMD, MCF, and RP. In these cases the forestomach problems are unlikely to be the most important clinical manifestation.

Ruminal Parakeratosis

In parakeratosis the papillae are darkly colored, enlarged, thickened, and clumped together. Histologic changes of the epithelial cells include a thickened, cornified layer with abnormal retention of nuclei in the cornified cells. These morphologic changes appear to represent a reaction to persistently high concentrations of VFAs. The changes occur predominantly in animals on pelleted or very finely ground rations, especially when the ration contains a high amount of energy. These rations tend to increase the proportions of propionate and butyrate, reduce the proportion of acetate generated by microbial fermentation, and produce a lowered ruminal fluid pH. The growth of the ruminal papillae is promoted by contact with the VFAs, especially butyrate, and secondarily propionate.^388,423 It appears that a disproportion of the concentrations of these VFAs may be the cause of an excessive change in the epithelium of the papillae.^437,438 Initial changes in the epithelium under these conditions appear to increase the absorption of the VFAs, but in severe cases the absorption decreases. This disease of the ruminal wall is not usually diagnosed as a primary problem. Although it may lead to impaired performance of the animal, the disease signs that lead to its discovery are usually those of chronic acidosis, a disease with which it often coexists. Parakeratosis can predispose to other injuries of the ruminal wall, however, because the abnormal papillae are more easily traumatized, leading to chronic inflammatory disease of the wall as discussed previously. In calves the problem is also associated with the development of hairballs (trichobezoars) because of the propensity of calves on the rations associated with parakeratosis to lick their hair coat.^{386,422,439,440}

Vagal Indigestion

Vagal indigestion syndrome (vagus indigestion, Hoflund’s syndrome) is composed of a group of motor disturbances that hinder passage of ingesta from the reticulorumen or abomasum or both. The pathogenesis of the disease has been debated for years and has yet to be completely clarified because many investigations have yielded conflicting information.*

The name vagus indigestion was introduced by Hoflund, who experimentally produced motor defects and disease signs similar to those seen in clinical cases by transecting various branches of the abdominal vagal nerve.⁴⁴² On the basis of his experimental results, he defined four types of functional disturbance, with obstruction of ingesta flow at two sites:

Hoflund’s description of the syndrome is convenient for explaining the observed functional defects, but its presumed pathogenesis is not supported by the findings of several later investigators.^{400,441,444,449} The use of the term stenosis has also led to some confusion, although it was appropriate in its original context. Functional stenosis suggested that the defect was a functional one that mimicked a stenosis at the site of outflow. However, vagal denervation does not produce a true stenosis, but rather a paralysis and relaxation of either the reticuloomasal orifice or the pylorus. The paralysis can be appreciated in both experimental and clinical cases.

FAILURE OF OMASAL TRANSPORT

Failure of omasal transport with hypermotility of the rumen is the most common naturally occurring form of the disease. Accumulation of ingesta in the reticulorumen leads to gradually progressive distention of the forestomachs, whereas the omasum and abomasum remain relatively empty. The animal’s appetite diminishes as the rumen becomes overfilled, producing one of the most characteristic signs of the disease: inappetence with gross distention of the rumen in the left flank. Continued dilation of the rumen eventually leads to a marked and almost pathognomonic overfilling of the ventral ruminal sac. The rumen assumes an L shape because the ventral sac occupies both the right and left ventral quadrants of the abdomen. The resultant characteristic abdominal contour often is called a “papple” shape (Fig. 32-94, E) because the left side of the abdomen is distended and assumes the appearance of an apple, whereas the right side assumes the contour of a pear. The diminished passage of ingesta results in reduced fecal volume. The normal ruminal process of selective retention of fibrous material is disturbed, leading to large particle passage and feces with increased fiber length and a greasy or pasty consistency. Some cases show firm feces with large particle size.^447,450 Affected animals often continue to drink water, but absorption from the rumen is poor, and the water accumulates in the forestomach while the animal becomes mildly dehydrated. Vigorous contractions of the rumen can be palpated in the left paralumbar fossa in most affected animals, although some display almost complete atony. The contraction pattern does not produce the typical stratification of material in the forestomach, but rather it churns the ruminal contents into a uniform frothy fluid.^450,453

Fig. 32-94 Abdominal contours (viewed from the rear) and abdominal palpation findings characteristic of cattle with various types of indigestion and other abdominal diseases. A thin line for the abdominal contour indicates the normal configuration. Bold lines indicate areas of the abdominal contour that typically deviate from normal in affected animals. A, Normal. B, Acute onset of ruminal stasis with simple indigestion, traumatic reticuloperitonitis (findings: mild ruminal distention with normal layering of ruminal content). C, Prolonged ruminal stasis, anorexia. The most common result of subacute or chronic disorders such as microbial or fermentative indigestions, traumatic reticuloperitonitis, and secondary indigestions (findings: reduced ruminal fill, “tucked-up abdomen,” firm, doughy contents that gravitate ventrally). D, Ruminal inactivity with indigestible roughage (findings: rumen distended with firm, doughy contents that accumulate ventrally; recurrent free gas bloat often present). E, Omasal transport failure (findings: L-shaped rumen with gross accumulation of frothy ingesta; ruminal hypermotility often present; free gas accumulation varies). F, Pyloric outflow failure (findings: fluid accumulation in abomasum; abomasal reflux to rumen common; doughy ruminal content that usually accumulates dorsally until ruminal stasis or anorexia is prolonged; abdominal contour similar to that for omasal transport failure). G, Acute ruminal acidosis (findings: rumen distended with fluid; some free gas bloat common). H, Frothy bloat. I, Free gas bloat or chronic free gas bloat (findings: accumulation of gas in dorsal sac; layering or ruminal contents usually normal; with chronicity, ruminal fill often decreased; associated with some microbial or fermentative disorders and with esophageal and cardiac disorders). J, Left displaced abomasum (findings: gas-filled abomasum that often causes slight bulge of paralumbar fossa; ruminal fill usually reduced). K, Right displaced abomasum, abomasal volvulus, cecal torsion (findings: distention of right flank with gas-filled viscus; ruminal fill and consistency usually normal). L, Hydrops (findings: ventral abdomen distended with fluid-filled uterus: ruminal fill usually decreased). M, Abomasal impaction (findings: abdominal contour similar to E and F; abomasum filled with firm ingesta).

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The signs just described, with abnormal flow of ingesta and normal or increased forestomach contractions, can be experimentally reproduced by sectioning the ventral vagal trunk at the cardia and the dorsal trunk just distal to the branching of the ruminal nerves.^397,442 The forestomach distention, empty omasum and abomasum, and stasis of the forestomach with resultant free gas bloat can be reproduced by sectioning both abdominal vagal trunks along the esophagus. The paralysis produced by vagal denervation can explain the failure of ingesta flow into the omasum by two mechanisms. First, the lower end of the esophageal groove is formed by two muscular lips. These overlap in a manner that allows a passive valve effect that blocks flow into the omasum when they are relaxed or paralyzed. Second, it appears that the flow into the omasum is accomplished by an active pumping motion of the omasum that reduces pressure and draws fluid through the reticuloomasal orifice. Paralysis of the omasal musculature after denervation would eliminate this effect. Decreased reticular motility caused by adhesion or paralysis may contribute to the changes in ruminal content and the alteration in particle passage.^450,453

The most common predisposing cause of naturally occurring omasal transport failure (anterior functional stenosis) is TRP. Other causes of anterior functional stenosis include abscesses, adhesions, and peritonitis at the reticulum (especially the right side of the reticulum) or reticuloomasal area without identification of an offending foreign body; hepatic abscesses; diffuse peritonitis; neoplasia of the ruminoreticular fold and esophageal groove; inflammatory disease of the reticular and ruminal walls; papilloma or other mass at the reticuloomasal orifice; and herniation of the reticulum through a diaphragmatic defect. Foreign bodies that obstruct the reticuloomasal orifice cause a syndrome indistinguishable from vagal indigestion except by exploratory rumenotomy.⁴³⁶ To reconcile the experimental findings with those from clinical cases, the development of omasal transport failure has been explained as involvement of the vagal trunks in the inflammatory process at the reticulum. Several findings make this an unlikely explanation in most clinical cases^{396,397,443,449,451}:

1 Although sectioning the vagus nerves as described reproduces the syndrome, disturbing only one of the two trunks still allows normal cyclic contractions in most cases. For a clinical lesion to produce disease development, massive involvement of the vagal nerves would be required. By contrast, less than a third of examined cases reported show actual lesions in the nerve branches.

2 The ratio of sensory to motor nerve fibers in the abdominal vagi is approximately 9:1, suggesting the important sensory role of the nerve.

3 Inflammatory lesions of the reticuloruminal wall reported in cases of vagal indigestion are predominantly in the same areas as the important tension receptors that send afferent excitatory impulses to the gastric centers. Induration of the right (medial) wall of the reticulum and in the esophageal groove region may affect intramural nerves and ganglia and reduce the tension receptor activity and therefore the drive for primary cycle activity.

These considerations allow an explanation of some of the inconsistencies found in various cases. Anterior functional stenosis may occur with insufficient vagal sensory excitation, which in turn reduces excitatory input to the gastric centers, diminishes primary cycle motor drive, and results in paralysis of the omasum and reticuloomasal orifice. Alternatively, substantial reticular adhesions that develop after TRP could prevent normal delivery of small particle ingest, with fluid consistency, to the reticuloomasal orifice.⁴⁵³ Because this reduces or abolishes flow into the omasum, both the omasum and abomasum would remain relatively empty, a common finding in these cases. The hypermotility observed in these cases may be the result of secondary rather than primary cycle contractions. Distention of the cranial ruminal sac would still be able to induce the secondary contractions if this region is not involved in the induration. Without normal primary cycle activity, the typical stratification of the ingesta would be disturbed, as is usually observed. The existence of hypermotile secondary contractions with absence or severe reduction of primary contractions can be detected clinically. Damage to the thoracic or abdominal vagi by inflammatory or neoplastic lesions may lead to the occasional cases that show both anterior functional stenosis and atony of the forestomachs, with resultant free gas bloat. This would be similar to the experimental sectioning of both vagal trunks.

Pyloric Outflow Failure

Failure of pyloric outflow (posterior functional stenosis) causes accumulation of ingesta in the abomasum and omasum. Advanced stages of this form of the syndrome also display gross distention of the reticulorumen. Generally the motility of the forestomach is not markedly affected in the early stages, and normal stratification of ingesta is maintained. Overfilling of the forestomach as a result of reflux of ingesta from the abomasum (internal vomiting) may occur, causing the chloride content of the ruminal fluid to increase (normal is less than 30 mEq/L). In contrast, the ruminal fluid of animals with anterior functional stenosis has a normal chloride content.^{444,446,447,453} With severe distention forestomach motility is reduced, and the ruminal contents become more fluid. Failure of ingesta to flow into the intestinal tract, combined with sequestration of chloride-rich fluid in the stomach chambers, can cause both marked dehydration and hypochloremic metabolic alkalosis. In cases with a gradual, prolonged development, however, as in anterior stenosis, any dehydration tends to be mild, and body fluid electrolyte concentrations do not show remarkable abnormalities. Fecal production in these cases tends to be even less than with the anterior stenosis form of the syndrome.^441,453

Failure of pyloric outflow can be experimentally reproduced by sectioning the ventral vagus trunk at the cardia and the continuation of the dorsal trunk as it crosses the omasum.^397,442 This mimics the usual clinical form of the disease, which is characterized by complete inhibition of flow from the abomasum. Combinations of more distal resections of the nerves produce the syndrome of recurrent atony of the abomasum as it occurs in natural clinical cases. Again, the term stenosis is a misnomer, because a true stenosis or spasm of the pylorus is not identified. Rather, the experimental vagal nerve resection and the naturally occurring cases show a flaccid paralysis, and ingesta accumulate as a result of failure of propulsive activity. The dilation of the abomasum is in the fundus and body and not in the pyloric part.^399,441,442

A common predisposing cause of pyloric outflow failure syndrome is volvulus of the abomasum. Other abomasal disturbances, including right and left displacements of the abomasum and abomasal ulceration, can cause the disease as well. After surgical correction of a volvulus, the abomasum remains atonic, and the disease may develop within several days. Clinical signs compatible with vagal indigestion may arise from gross distention and twisting of the abomasum and lesser omentum, resulting in potentially coexisting but distinct injury to the vagal nerves or structural damage to the gastric wall, with or without peritonitis. Although focally extensive vagal nerve lesions have been associated with concomitant vascular damage, indicating that even with nerve regeneration there may not be a return to normal function, the damage appears reparable in some cases, because a return to normal function has been observed.⁴⁵²

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Inflammation and adhesions involving the abomasal fundus and reticulum have been associated with posterior functional stenosis in some studies.^441,453 Inflammation of the reticular wall may account for the reticular atony reported in some cases. This form of vagal indigestion may be more frequently associated with true vagal nerve impairment than appears to be the case in anterior functional stenosis. Alternatively, reticular adhesions may prevent normal motility, alter the flow of ingesta to the omasum and abomasum, and lead to abnormal filling of the abomasum because of decreased fluidity of abomasal contents.⁴⁵³

Another predisposing cause of pyloric outflow failure is advanced pregnancy with a large fetus. An exact pathogenesis has not been clearly defined. Presumably the large, gravid uterus distorts the positioning of the abomasum or physically compresses and obstructs the anterior small bowel, preventing outflow of ingesta from the abomasum. In these patients the gravid horn typically occupies most of the space in the omental sling. In support of these conclusions, the problem can be resolved by inducing delivery of the calf or performing a cesarean section. Supportive care may be required for severely affected cows, but the gastrointestinal system returns to normal function, suggesting that it was secondarily affected by the pregnancy. This problem is referred to as a form of vagal indigestion because it appears as a pyloric outflow failure. Some patients have such severe obstruction of ingesta passage that they may be diagnosed as having an anterior bowel obstruction. This disease has been called indigestion of late pregnancy.

Animals affected with any form of vagal indigestion for a prolonged time lose body condition because the failure to pass ingesta into the intestinal tract produces a state of starvation. The weight loss may be overlooked because of the impression of full body size produced by the abdominal distention.

Obstruction of the Cardia or Reticuloomasal Orifice

True mechanical obstruction of the forestomach is an uncommon occurrence. The obstruction can be either full or partial and can occur at either the cardia or the reticuloomasal orifice. The inflammatory and neoplastic conditions described previously can appear to be obstructive disease when the tissues are sufficiently distorted and lesions involve one of these orifices. Papillomas are most prone to causing an obstruction when they become pedunculated. A variety of foreign bodies create obstruction. In calves, trichobezoars are most commonly the cause, occurring predominantly in animals on a low roughage diet that consequently lick their hair coats vigorously. In adult cows, ingestion of the placenta occasionally results in an obstruction. Curious ruminants, especially goats, sometimes consume plastic bags or discarded rectal palpation sleeves. These and other nondegradable materials can lead to obstruction even after considerable time has passed.

Cardia obstruction leads to the signs typical of esophageal obstruction, with free gas bloat as a prominent, perhaps life-threatening development. Obstruction of the reticuloomasal orifice produces the same consequences as some forms of vagal indigestion. Failure of ingesta flow beyond the rumen results in accumulation of fluid material in the forestomach and diminished or no passage of ingesta through the intestines. The degree and duration of obstruction determine the severity of associated problems such as dehydration, depression, elevated heart rate, forestomach stasis, colic, and muscular weakness. Only rumenotomy can effectively differentiate these obstructive diseases from other problems with similar signs.

Diaphragmatic Hernia

Defects in the diaphragms of cattle are uncommon. Most cases involve a tear through which the reticulum can herniate. Other abdominal organs may also be involved if the rent is large. The diaphragmatic defect may be congenital or an acquired lesion caused by a local inflammatory process (TRP), sudden external trauma (fighting, hanging up on a fence), or internal pressure (parturition, acute tympany). Entrapment of the reticulum may lead to acute changes in intrathoracic pressure and cause sudden dyspnea, tachycardia, and poor venous return to the heart. Generally, however, this reticular problem causes signs identical to those of vagal indigestion with anterior functional stenosis.^386,445 Failure of flow through the reticuloomasal orifice may result from vagal nerve damage, or the anatomic distortion alone may explain the motility defect. Entrapment of the reticulum hinders normal reticular movements and distorts the esophageal groove and reticuloomasal orifice. Reticular ingesta can be heard moving inside the thorax; therefore complete reticular paralysis is unlikely. Motility disturbance is reflected by hypermotility of the rumen, generation of frothy ingesta, persistent or recurrent moderate tympany, and overfilling of the rumen. Signs of pain may also be present, as in cases of TRP. Rumination usually is impaired, and large volumes of ingesta may be vomited, especially after eating.

Forestomach Microbial Population

The continuous culture system of the rumen involves an ongoing selection of microorganisms best adapted to grow in a variety of ecologic niches that are in a dynamic state. Numerous control mechanisms govern the environment and the resultant microbial population. Some of these mechanisms are related to the animal itself, such as salivation, mixing and rumination, removal of substances by absorption or diffusion, outflow through the reticuloomasal orifice, and eructation. Others are related to the diet, including nutrient quality of the substrate (feed), balance of required elements, solubility, particle size, presence of inhibitory substances, nutrient quantity, and rate of delivery to the rumen. Control of fermentation also results from microbial interactions such as competition and symbiosis: cross-feeding between species, removal of inhibitory end products, and maintenance of the oxidation-reduction potential. The complexity of the system tends to promote an overall stability. Changes in the controlling factors create selective pressures that lead to population changes in the rumen.^424,455-456

The ruminal bacteria are predominantly anaerobes, with some coexisting facultative anaerobes. Although the facultative organisms are not important in normal ruminal function, they may be in some forms of ruminal dysfunction. Some microbes ferment the primary nutrients in the feed such as cellulose, hemicellulose, pectin, starch, and simple sugars. Other species ferment the products of the primary group, such as pentoses, glucose, lactate, succinate, and formate. Many species are very specialized and have numerous growth requirements that may be supplied by the general fermentation. The last group is important for its role in removing end products and cycling essential factors back to the other organisms.^424,455-457

Effects of Feed Characteristics

The concentrations and proportions of the microbial species vary with the composition of the diet (Table 32-13). An abundant supply of a certain substrate tends to favor a microbial population with a predilection or high capacity for using that material. The most important factors in the rate of digestion are the properties of the carbohydrates and protein in the feed. High-protein diets favor proteolytic organisms, whereas high-starch, low-fiber diets favor starch users. Cellulolytic bacteria are prominent in a high-fiber diet, but their numbers also depend on the fiber size, as this factor determines the rate of passage or retention in the forestomach; therefore cellulolytic species can be abundant with a high-concentrate diet if some long-stemmed roughage is included because the retention time of the fiber is prolonged. Diets with readily fermentable carbohydrates and low fiber favor species capable of rapid metabolism and tolerant of low pH. Acid production is rapid and high, and populations of microbes less tolerant of such changes decline.^455,457,458

Table 32-13 Effects of Feed Characteristics on Ruminal Digestion and Health

NPN, Nonprotein nitrogen; VFA, volatile fatty acid.

The microbial population is also influenced by the limits of supply of certain feed substrates.⁴⁵⁵ High rates of fermentation and microbial growth on the abundant substrates depend on sufficient amounts of the more limited nutrients. Optimum carbohydrate use requires adequate sources of nitrogen, sulfur, and essential mineral nutrients.⁴⁵⁹ When any essential nutrient is deficient, the rate of digestion and therefore the digestibility of the feedstuff decrease. Whether the affected animal shows signs of nutrient deficiency or forestomach dysfunction with microbial and forestomach inactivity depends on the limiting nutrient and relative requirement of the host and bacteria for the nutrient. Substances and conditions that inhibit fermentation further reduce digestibility.

The feed material also affects ruminal fermentation by influencing the rate of passage from the reticulorumen. Fine grinding and pelleting of feed increase the rate of passage of the particulate matter from the rumen. Very finely ground rations also reduce the stratification of fibrous material in the rumen. This affects the ability to sort material in the rumen selectively by particle size and density, so that larger particles less thoroughly fermented pass more readily into the lower bowel. Microbes associated with the feed particles are passed out of the rumen with the feed. Thus a faster rate of passage influences the bacterial population because it competes with the generation time of the organisms. Populations of slower-growing microbes tend to be most influenced by changes in the retention or passage times. Slow-growing cellulolytic bacteria decline in numbers as the passage rate increases (transit time decreases). High passage rates usually produce faster digestion rates. Although these factors are primarily important to the feed efficiency of the animal, they also affect ruminal function and the adaptation of microbes to feeding changes.³⁸⁸

Adaptation of the microbial flora to dietary changes requires a week or longer. The abruptness of a dietary change determines the degree of alteration of the ruminal microbial population and fermentation pattern and the potential for digestive disturbances. With abrupt and dramatic shifts to higher-carbohydrate diets, the facultative species may overwhelm the more normal flora by producing excessive acid and lowering the pH. The importance of microbial adaptation to a particular diet is evidenced by the reduction in forestomach disturbances seen when the rumen is inoculated, before a feeding change, with fluid from animals already adapted to the new ration.^424,456

The end products of microbial fermentation influence not only the microbial population but also ruminal function. High concentrations of nondissociated VFAs excite sensory epithelial receptors that reflexively inhibit ruminal motility.^424,460,461 If a sudden increase in concentrate feeding induces lactic acid fermentation, the ruminal pH suddenly declines and a greater proportion of the VFAs shift to the nondissociated state, inducing ruminal stasis. A consistently high level of concentrate feeding produces rapid fermentation, a high concentration of VFAs, and low pH, and the nondissociated VFA level may reach the threshold for stimulation of the inhibitory epithelial receptors. The ruminal stasis reduces the fermentation rate. Mild cases of ruminal acidosis may show spontaneous recovery of ruminal functions as the absorption of VFAs reduces the concentrations to a noninhibitory level. With more severe ruminal acidosis the generation of acid continues despite the ruminal stasis, giving rise to more severe complications of the disease.

In some instances the effects of ruminal microbial metabolism and microbial end products extend beyond impacts on nutritional status and digestive system function. Several ruminant diseases represent rumen-generated toxicities. These have extremely variable manifestations and include toxicoses from ammonia, nitrate and nitrite, 3-methylindole, dimethylsulfide (Brassica species, onion toxicity), and sulfur-associated polioencephalomalacia.^462-465

In summary, excesses, deficiencies, or rapid changes of feed substrate can cause imbalance in the microbial population and the fluid milieu. The result can be bacterial overgrowth and overproduction of microbial end products or insufficient microbial growth and fermentation. The effects of these abnormalities on the animal range from ruminal motility dysfunction to poor growth and performance to outright toxicity and organic damage.

Inactivity of Ruminal Microbial Flora (Caused by Poor-Quality Roughage, Haybelly, or Ruminal Impaction)

In ruminal microbial flora inactivity, the microbial populations and their metabolic and fermentative processes are diminished as a result of deficiencies of one or more nutrients. This occurs most commonly with poor-quality roughage deficient in protein and readily digestible carbohydrates (late-cut, highly lignified hay or straw). Microfloral inactivity can also occur when specific mineral nutrients are deficient, or it can be caused by inhibitory substances such as antibiotics or some plant products.^388,424,459 Microfloral inactivity also occurs with prolonged anorexia, which abolishes the intake of all nutrients and is the primary pathogenesis of many cases of secondary indigestion.

When microbial digestive processes decline, the breakdown of ingested feedstuffs is prolonged. Failure to reduce the particle size of the ingesta leads to a prolonged retention in the forestomach and gradual accumulation of the undigested feedstuff. Gradual distention of the reticulorumen is commonly observed (haybelly). In extreme cases this can mimic the signs of vagal indigestion. Forestomach distention can result in weak contractions and moderate recurrent tympany. Ruminal hypomotility alters the normal stratification of the ruminal contents, and the fibrous components are found mixed in the fluid or compacted ventrally on the ruminal floor. Abnormal passage of ingesta from the forestomach results in decreased fecal passage, and the feces usually are dried and contain undigested plant fibers. Other effects on the animal are those of generalized or specific nutrient deficiencies (e.g., decreased growth or production, ketosis, emaciation, and a poor hair coat). When anorexia is the cause of the microbial inactivity, the ruminal fill decreases and the lack of normal distention also induces ruminal stasis.^386,466

Simple Indigestion

Simple indigestion is the most common sequela of an abrupt change in the ration. Such feed changes present the ruminal microflora with nutrient substrates (1) to which they are not metabolically adapted, (2) to which they are adapted but in lesser quantities, or (3) that contain inhibitory substances or produce inhibitory substances on fermentation. The result is an imbalance in the microflora and its fermentation products. The difference between this problem and some of the other fermentation disorders is mostly a matter of degree. Generally the disease is relatively mild and self-limiting. Most affected animals show anorexia for 1 to 2 days, break with diarrhea in about 24 hours, and return to feed without treatment when the ruminal fermentation has stabilized and inhibitory substances have been eliminated. Ruminal motility is reduced but usually not absent, the filling of the rumen is not remarkably altered, and if bloat occurs, it is mild. In some cases the ruminal fluid pH may change, but usually not dramatically. Mild acidosis or alkalosis of the ruminal fluid may develop, depending on the nature of the causative feedstuff and its resultant fermentative degradation. Signs of ruminal microfloral inactivity are common. Simple indigestion is an acute problem, in contrast to the microfloral inactivity discussed in the previous paragraphs, in which deficiencies produce microfloral inactivity over time.

Feeds commonly implicated as causes of simple indigestion include moldy or overheated feeds, frosted forages, and partly fermented, spoiled, or sour silages. This form of indigestion also occurs in animals fed high-quality feed, usually after an increase in the rate of feeding or after a change of one of the feed constituents. Thus these mild forms of indigestion can range from a mild acidosis to an excess of VFAs to the generation of some bacterial inhibitory products. Because the rumen and its fermentative bacteria are very adaptable, the ways, if any, in which animals given a certain feed experience the problem vary considerably. Often only one or a few animals from a group on the ration may have signs.

Acute Ruminal Lactic Acidosis (Grain Overload, Toxic Indigestion)

Acute ruminal acidosis is the most dramatic of the forms of ruminal microbial fermentative disorders and in some cases is lethal in less than 24 hours. It has also received the most research attention; therefore the events in its pathogenesis are more clearly defined than those of the other forestomach disorders. The condition has been named lactic acidosis, acute ruminal impaction, ruminal overload, acid indigestion, toxic indigestion, grain engorgement, grain overload, and D–lactic acidosis.

This problem is the result of excessive consumption of readily fermentable carbohydrates, which causes a rapid fermentation with production of lactic acid and a decrease in ruminal pH to physiologically inappropriate levels. This occurs when animals consume an excess of concentrate feeds (e.g., if animals are suddenly exposed to the feeds without prior adaptation; if animals already on such feeds suddenly consume an excessive quantity because of accidental access; or if animals that have been off feed return to feed and are offered unrestricted access to concentrates). The problem is more common when animals are grouped than when they are separate, probably because the psychology of competition induces them to overconsume. In general the feeds involved include the cereal grains commonly used in high-production rations and fruit and root crops (e.g., feed beets, sugar beets, potatoes) where they are available. Starch and soluble sugars promote an overgrowth of bacteria that produce glucose and organic acids. The acid end products increase ruminal acidity and osmolality, inhibit or destroy other ruminal microbes, and cause forestomach dysfunction and metabolic disturbances.^467-469

Specific characteristics of the feedstuffs contribute to acidification of the ruminal fluid. Cereal grains inherently possess less buffering capacity than the fibrous forages. Low structured fiber content and decreased forage particle size induce less salivation at the time of ingestion and less rumination subsequently; therefore salivary buffering declines when concentrate feeds are consumed. Some silages contain both high carbohydrate and lactic acid and thus introduce more acid at both ingestion and fermentation.^{437,468,470,471}

Feeding regimens that include significant fibrous roughage limit carbohydrate availability and rates of microbial fermentation and growth. Carbohydrate fermentation efficiency relative to the amount of ATP derived from each sugar provides competitive survival value. Slower-growing cellulolytic bacteria use substrate most efficiently. When starch or sugar is available in excess, the faster growing species such as Streptococcus bovis metabolize carbohydrate faster and produce more ATP per unit time, even though they are less efficient in ATP production per carbohydrate molecule. Under these conditions they can overgrow, producing lactic acid as their end product.^458,472

The severity of ruminal acidosis and disease signs varies considerably, depending on the amount and type of carbohydrate-rich feed consumed and the degree of prior ruminal microbial adaptation to the carbohydrate substrate. The disease can range from a mild form of indigestion to an overwhelming toxemia that may be difficult to distinguish from other acute toxicities or various diseases with endotoxemia.

If consumption of fermentable carbohydrate is only mildly excessive, S. bovis proliferation decreases when the carbohydrate has been fermented, pH rises toward normal, and the efficient fermenters reestablish dominance. If the carbohydrate source is abundant and its supply is not exhausted, the acidosis becomes more severe. Continued production of lactate by S. bovis reduces the fluid pH to the range of 5 to 5.5, and the ruminal fluid osmolality rises concurrently. Both of these factors inhibit or kill the ruminal protozoa, which normally use starch and small sugars and help to limit increasing lactic acid levels. There are also numerous species of lactate-using bacteria, of which Megasphaera elsdenii and Selenomonas ruminantium are the primary examples. These bacteria, which increase in numbers when animals slowly adapt to a high-concentrate diet, are eliminated by abrupt changes and generation of excessive acid; therefore lactate use decreases when the acid is generated too quickly.⁴⁵⁸

The lactobacilli are the major group of lactic acid producers in the rumen. The increasing acidity of the fluid enhances the growth of these organisms. Because the lactate-using bacteria are killed off before the lactobacilli overgrow, their diverse end products are unavailable as substrate for other bacteria. The lactobacilli are left as the predominant organisms to use the available carbohydrates. Even the S. bovis organisms that began the lactic acid production are inhibited below pH 4.5, leaving the lactobacilli, the most acid-resistant species, to generate more lactic acid.⁴⁷⁰

The acidification of the fluid milieu enhances lactic acid production by altering microbial metabolism. The loss of the fluid bicarbonate buffer and the increase in available hydrogen ions block the conversion of lactate to propionate even before the lactate users die off. Also, when the pH is above 5, as pH declines, ruminal fluid amylase activity increases, liberating more free glucose from starch. However, glucose use is reduced, and ruminal glucose accumulates. Apparently the lactate-using bacteria such as S. ruminantium degrade less lactate to acetate in the presence of increased glucose concentrations. Therefore not only does the microbial population change, but the characteristics of the fluid accelerate the lactic acid production when the available carbohydrate is excessive.

The effects on the animal from the ruminal fluid changes are numerous and detrimental. In the early stages of the acidic fermentation, the VFAs are produced in abundance. Although VFA production decreases as the microbes are increasingly inhibited, VFA concentrations remain elevated in advanced acidosis. The VFAs are much weaker acids than lactic acid; thus, as pH drops they accept hydrogen from lactic acid and serve as buffers in the fluid, so that a greater proportion of the VFAs exist in the nondissociated state. This form is more readily absorbable than free ions through the ruminal wall. During absorption some VFAs undergo metabolism by the ruminal wall epithelium, resulting in the release of lactate and ketone bodies into the circulation. Excessive absorption of the VFAs leads to systemic acidosis, and circulating lactate and VFAs may also directly damage the liver.⁴⁷³ In addition, the high concentration of nondissociated VFAs at the ruminal epithelium provides a strong inhibitory effect on reticuloruminal motility and leads to ruminal stasis. This effect tends to protect the animal because it reduces the absorption of detrimental fermentation products from the rumen.^{460-466,468-470}

The osmotic pressure of the ruminal fluid increases as lactic acidosis develops.^{437,468-470,474} In a normal animal, ruminal osmolality remains relatively constant at approximately 280 mOsm/L, but osmolality may double in some cases of acute acidosis. Lactic acid accounts for a major fraction of the increase, but some of the components of this change remain unidentified. The increased osmolality inhibits and kills some of the microflora and draws fluid into the rumen, mostly from the extracellular compartment. This accounts for the increased ruminal fluid volume, ruminal distention, and severe dehydration observed clinically. The loss of circulating fluid volume leads to circulatory impairment, decreased renal blood flow and glomerular filtration, and in some cases eventual anuria. Poor peripheral circulation results in hypoxic metabolism and contributes to systemic acidosis.

Although it has been assumed that the systemic acidosis that develops with this disease is attributable to ruminal lactic acid absorption, such absorption does not appear to occur readily.^470,475,476 Lactate is absorbed from the rumen at a much slower rate than are the VFAs because it is highly ionized at a pH near physiologic normal, which tends to inhibit absorption. At lower pH the rumen becomes static, thereby also inhibiting absorption. The hypertonicity of the ruminal fluid further limits absorption of lactate and other substances. It appears that the peak entry of lactate into the circulation occurs in the early phases of the disease. Some lactate may be absorbed from the intestinal tract from fluid passed before the onset of complete stasis. Many experimental trials do not show the development of severe systemic acidosis in the early phase of the disease. It may be that a large component of the later severe systemic acidosis is attributable to circulatory insufficiency rather than to absorption of lactic acid.

Some absorption of the lactic acid does occur, however, as evidenced by the appearance of D–lactic acid in the circulation.^422,470,475 Microbes produce both the L and D forms of lactic acid, whereas animal tissues produce only L–lactic acid. The animals’ pathways for metabolism of D–lactic acid are not as efficient as those for L–lactic acid; therefore absorption of both forms leads to an accumulation of predominantly D-lactate in the animal’s system. The lactate is eliminated by oxidation, gluconeogenesis, and renal excretion. The animal’s hydration status, liver and muscle metabolism, and renal function determine how readily it can eliminate excess lactate. Animals that survive ruminal acidosis often have metabolic alkalosis after the acidotic phase, as a result of lactate metabolism and production of bicarbonate.

Lactic acid is a strong corrosive agent that can destroy the ruminal epithelium, giving rise to the name toxic rumenitis. The increased ruminal fluid osmolality also damages the epithelium as extracellular water influx across the epithelium occurs in response to osmotic pressure imbalance and disturbed Na transport.⁴⁶⁷ The effects of epithelial destruction can be far-reaching because the damage persists after resolution of the acute acidosis.^437,477 Some yeast and fungi that are resistant to the high acidity readily colonize the damaged sites, invade the vasculature, and cause thrombosis or spread to the liver and other organs.^430,431 Ruminal acidosis is considered one of the primary causes of mycotic rumenitis (discussed earlier under Reticulitis and Rumenitis) and mycotic omasitis, although other predisposing causes have been identified.^430-434 Bacterial rumenitis can also result from the chemical damage and may lead to abscess formation, diffuse cellulitis, or perforation and peritonitis. If the animal survives the acute acidosis, it may succumb to secondary ruminal damage.^431,433 Alternatively, the rumen may heal uneventfully, leaving scars in the ruminal wall, but access of bacteria to the circulation through these chemical lesions can result in hepatic abscessation, a common problem of animals fed high-concentrate rations.^429,478,479

In addition to lactic acid, several toxic factors have been implicated in acute ruminal acidosis.^422,458,470 The altered metabolism of the ruminal microflora has been shown to generate increased quantities of histamine, ethanol, methanol, tyramine, and tryptamine. These may play a role in the pathogenesis of the disease, but conclusive evidence is lacking. Histamine has been implicated as an agent in the development of laminitis that sometimes accompanies ruminal acidosis. However, histamine is poorly absorbed from the rumen, especially at diminished pH levels. The destruction of ruminal gram-negative bacteria has been suggested to release large quantities of endotoxin for absorption through damaged mucosal surfaces. Endotoxin would contribute to most of the signs of the disease such as ruminal stasis, poor tissue perfusion with cardiovascular deterioration, weakness, and depression. Increased ruminal and blood concentrations of endotoxin and increased blood arachidonic acid metabolites have been found in cattle with experimentally induced ruminal acidosis, but their importance in naturally occurring disease is not clear.^480-483 With liver impairment or ruminal wall damage, toxin absorption and clearance are likely to be altered. Premature delivery and retained placenta may occur in pregnant animals after acute ruminal acidosis, possibly resulting from the effects of these circulatory toxins and metabolites.⁴⁸⁴

Subacute Ruminal Acidosis

Like acute ruminal acidosis, subacute ruminal acidosis (SARA) is caused by feeding of excessive quantities of concentrate with low levels of well-structured fibrous roughage; however, SARA results from continued ingestion of these feeds over a prolonged period rather than sudden exposure without adequate adaptation. Beef feedlot cattle may be chronically exposed to a ruminal pH of 5 to 5.5 from the start of the feeding period until slaughter. Dairy cattle are more likely limited to short periods of low ruminal pH typically between calving and approximately 5 months postpartum, with the risk for SARA very low outside these time periods.^485,486 The ruminal microbial population adapts to the high grain ration, and large numbers of lactate-using and lactate-producing organisms are found. The proportion of cellulolytic bacteria decreases, whereas the starch- and glucose-fermenting species proliferate. The overall effect of the adaptation is development of a microbial population that rapidly ferments the ingested feedstuffs. Lactic acid does not accumulate because it is further metabolized by the bacteria. The high rate of fermentation instead produces high concentrations of VFAs, resulting in moderately acidic ruminal fluid with pH values usually ranging from 5 to 5.5.⁴⁸⁷ Ruminal buffering of the increased acid load is impaired because the fine particle size of the high-energy rations induces less chewing and less saliva production. As the name implies, the effects on the animal are chronic and insidious.

Along with the high concentration of VFAs and the low pH, a shift occurs in the proportions of the VFAs in the ruminal fluid. The proportions of butyric and propionic acids increase, and acetate decreases. Butyric and propionic acids stimulate proliferation of the ruminal papillae epithelium. When this process is exaggerated, it can progress to parakeratosis. The ruminal papillae develop an excessively keratinized epithelium and clump together. The parakeratotic changes are associated with decreased absorption of the VFAs and increased susceptibility to trauma and inflammation. Epithelial damage and the acidic nature of the ingesta appear to be responsible for inflammation of the deeper tissues of the ruminal wall in some cases. The ruminal wall lesions allow penetration by bacteria with dissemination to the liver. This commonly results in liver abscessation in a high proportion of affected animals. Liver abscesses usually have no pathognomonic signs. Affected animals tend to show reduced productivity and may have signs of a chronic inflammatory response.*

The diagnosis of SARA is made on a herd level rather than on an individual cow basis. Cattle afflicted with SARA may demonstrate numerous clinical signs including reduced appetite and ruminal hypomotility.⁴⁸⁶ High ruminal VFA concentrations can inhibit ruminal motility by stimulating the inhibitory receptors in the epithelium. The finely ground ingesta also induce less active ruminal motility because it lacks the physical bulk of high-roughage diets that stimulate strong and sustained contractions. Although the bacterial population is metabolically very active, the number of species of bacteria is reduced. Likewise the protozoal population is inhibited when the pH remains in the lower end of this range. The microfloral environment is less stable when fewer species are present and is therefore more susceptible to sudden changes in the diet.

A continual high acid load may also reduce metabolic efficiency and overall animal performance. High-concentrate diets have been associated with poor use of dietary protein.^457,489 Other pathologic conditions have been attributed to SARA, including chronic laminitis⁴⁹⁰ and cerebrocortical necrosis. These conditions may be induced by some of the toxic by-products of acidic ruminal fermentation, such as endotoxins and hydrogen sulfide.^{464,465,470,480-483,488}

Ruminal Alkalosis

An alkaline ruminal fluid pH occurs most commonly when microbial fermentation is reduced while the animal continues to ingest saliva. A ruminal fluid pH between 7 and 7.5 is found with prolonged anorexia, microfloral inactivity caused by poorly digestible roughage, and some cases of simple indigestion. The low rate of fermentation does not generate enough acid to neutralize the alkaline pH of the saliva. In addition, the absorption of VFAs through the ruminal epithelium proceeds with the generation of bicarbonate in the ruminal fluid.⁴⁹¹ Acetate absorption is associated with greater generation of bicarbonate than is absorption of the other VFAs, and acetate is the predominant VFA produced during fermentation of roughage. Although the fermentation rate is low, the VFA absorption contributes to the ruminal alkalinity. Ruminal alkalosis occurring with these diseases is not the primary problem; therefore these entities are discussed separately.

Ruminal alkalosis can occur with the generation of excessive ammonia. Ammonia concentrations rise when high-protein diets are fermented. The pH usually does not increase above neutral because these diets also contain sufficient readily fermentable carbohydrate to maintain a slightly acidic pH.

More dramatic elevations in the ammonia concentration, with a ruminal fluid pH above 7.5, occur with overfeeding of nonprotein nitrogen sources such as urea, biuret, and ammonium phosphate (see Chapter 54). Accidental ingestion of some common fertilizers that contain ammonium salts can produce the same results. For the purpose of this discussion, it is important to realize that some of the signs of urea poisoning involve ruminal dysfunction. Severe cases of urea poisoning result in generalized signs such as muscle tremors, incoordination, weakness, tachypnea, and CNS excitation, and affected animals die quickly. Signs of forestomach dysfunction such as ruminal hypomotility, bloat, vomiting, and abdominal pain are also present. In milder cases, diminished appetite, ruminal hypomotility, recurrent tympany, and diarrhea may be the most prominent signs, along with muscular weakness and incoordination. Thus the disease may appear as a form of forestomach disease. The ruminal fluid shows an alkaline pH between 7.5 and 8.5 and has a strong odor of ammonia.^462,492,493

Putrefaction of Ruminal Ingesta

Putrefaction of ruminal ingesta infrequently results from overgrowth of a microflora that decomposes feed material in a putrefactive manner. The existence of a high ruminal fluid pH, such as occurs with high-protein feeds, and repeated inoculation with abnormal bacteria allow the development of the putrefactive decomposition. Fermented feeds undergoing spoilage, feed and water contaminated with feces, and spoiling, contaminated concentrates supply the offending microflora, which includes the coliform group and Proteus species.³⁸⁶ This type of abnormal decomposition is normally inhibited by the existence of an active physiologic microflora. Therefore most cattle are remarkably resistant to aberrant digestive patterns even when spoiled feeds are ingested. Cattle affected with this form of indigestion typically follow a chronic course of disease. Ruminal motility declines, appetite is poor, and recurrent tympany develops, sometimes with the generation of frothy ruminal contents. The ruminal fluid characteristically has a blackish-green color, a foul, putrefactive odor, poor protozoal and bacterial activity, and a pH in the neutral to alkaline range of 7 to 8.5. The cause of the forestomach hypomotility may be inhibitory products generated by the abnormal fermentation. In cases of prolonged duration, animals lose weight and display a poor hair coat, probably as a result of dietary deficiencies in the abnormal fermentation products.

Esophageal (Reticular) Groove Function

Liquid feed bypasses the reticulorumen in the young ruminant, flowing directly into the abomasum through the esophageal groove. The groove consists of two lips that extend from the cardia to the reticuloomasal orifice. These lips close together, forming a tube to shunt liquid material to the abomasum when the soluble proteins and salts of milk stimulate a reflex through the glossopharyngeal nerve. Other salt solutions and even water can stimulate the reflex in very young animals, but the reflex weakens with age, especially after weaning. The response to stimuli varies among individuals, but generally milk produces the strongest response and plain water the weakest. Both nipple and bucket feeding stimulate closure in very young calves, but beyond 12 weeks of age closure is weak unless stimulated by nipple feeding. In older, weaned animals the reflex can be stimulated weakly for short durations by orally administered strong solutions such as copper sulfate or sodium salts. Intravenous vasopressin can induce more profound closure of the groove and has been advocated to aid ruminal bypass of orally administered treatment.^497,498

Milk replacers that contain nonmilk protein appear to stimulate a weaker closure of the esophageal groove than do whole milk or milk replacers containing real milk protein. Likewise unpalatable fluids and spoiled milk do not seem to induce normal closure of the groove. Even in healthy calves that consume unspoiled whole milk, some overflow into the forestomach may occur.⁴⁹⁹ Failure of esophageal groove closure allows these fluids to pass into the rumen rather than bypassing it. Milk or other fluid administered through a stomach tube or esophageal feeder does not contact the pharynx; therefore the reflex closure is not stimulated and the fluid deposits in the forestomachs. Under normal conditions fluid in the forestomach of neonatal calves less than 2 weeks old overflows into the abomasum when an amount more than 400 mL has accumulated.⁵⁰⁰

Reticuloruminal Milk Accumulation (Ruminal Drinking)

Milk can gain access to the reticulorumen by several means. Failure of esophageal groove closure, just discussed, is one possibility. In addition, if calves are maintained as preruminants for longer than 3 to 4 months, groove closure weakens and may allow greater escape of fluid to the reticulorumen. Fluid can also accumulate in the forestomach from abomasal reflux (Fig. 32-95). Overfeeding fluids beyond the capacity of the abomasum (approximately 2 L in the newborn, 35-kg calf) promotes backflow into the reticulorumen. Certain fluids affect abomasal motility and emptying times, prolonging their retention in the organ. These include acidic and hypertonic fluids and severely heat-treated skim milk powder. Nonmilk protein does not curd in the abomasum, as does casein, when it contacts the abomasal enzyme renin. Prolonged fluid retention and failure of curd formation in the abomasum may promote backflow into the rumen, especially when more fluid feed is consumed. Abomasal inflammation or ulceration may also inhibit normal emptying and promote abomasal reflux.

Fig. 32-95 Abomasal reflux in calves.

Some amount of milk reflux from the abomasum appears to be a physiologically normal occurrence. In fact, this route supplies some of the inoculum for ruminal microfloral development and strongly influences the species distribution of the microbial population. But prolonged, repeated, or excessive retention of milk in the forestomach can lead to the development of abnormal fermentation patterns. Although amounts of fluid greater than 400 mL do not normally accumulate in the forestomach of the neonate, more fluid can accumulate when the abomasum is already filled and when ruminal size has increased during the development process. In some cases milk flow into the rumen accumulates significantly over prolonged periods.⁴⁹⁹

The predominant organisms comprising the forestomach microflora of the 1- to 4-week-old ruminant are the coliforms and lactobacilli. These lactose-fermenting, facultative anaerobes tend to maintain the ruminal pH in the acidic range before the adult-type, anaerobic, cellulolytic flora becomes established. The high fat and protein content of milk in the rumen can predispose to a flora that decomposes these constituents and produces spoiled and rancid ruminal ingesta. Problems associated with ruminal milk accumulation are compounded when the milk or other fluid ingested is already contaminated or spoiled. The abnormal microflora established under these circumstances does not supply the young animal with the necessary digestive end products, and signs of dietary insufficiency develop. Affected animals fail to grow normally, show a poor hair coat potentially with widespread alopecia, and may have a depraved appetite. The stimuli for normal forestomach development are also deficient; affected animals have a potbellied appearance, and the rumen is distended with fluid and clots of milk. Ruminal motility is poor, and recurrent bloat is a common sequela. The ruminal fluid pH may be alkaline as a result of the proteolytic formation of ammonia, but in most cases the ruminal pH is acidic (below 6) because of an accumulation of VFAs and lactic acid from bacterial fermentation, and the fluid has a putrid, foul odor.⁵⁰¹ An enteric imbalance also seems to occur, and the feces are commonly pasty or fluid in consistency. Ruminal “drinking” appears to compound problems in calves with infectious enteritis and diarrhea, and affected calves frequently develop systemic acid-base and fluid balance disturbances.^502-504

Problems in Ruminal Development

The age at which the calf has reticuloruminal digestion depends largely on its diet. A plentiful supply of milk delays the time until the calf consumes significant quantities of dry feed. Veal calves maintained without access to solid feed do not have forestomach development. The nervous reflexes that drive ruminal motility, eructation, and regurgitation are already functional before birth, awaiting only the drive of normal stimuli to begin operating. Dry feeds pass into the rumen, and bacterial inoculation from the environment or from abomasal reflux stimulates fermentation to begin. This process can be initiated as early as 1 week of age when calves are encouraged to consume dry feeds.^495,505

The increase in the size of the forestomach results from the bulk effect of ingestion of bulky, fibrous feeds.⁵⁰⁶ Mild distention stimulates ruminal motility and the development of the muscular wall. Mucosal development is stimulated by the presence of VFAs in the ruminal fluid, resulting from microbial fermentation. Butyrate and propionate are most effective in this regard, whereas acetate is less stimulatory. The thickness of the mucosa increases with proliferation of the ruminal epithelium and elongation of the papillae.⁴³⁸ These changes serve to increase the ability of the mucosa to absorb the VFAs. Dietary excesses or deficiencies affect the developing rumen by altering the balance of these stimuli.

Calves fed concentrate diets to the exclusion of forages or mixed diets with the hay pelleted or finely ground may experience ruminal parakeratosis as a result of a lack of feed abrasion⁵⁰⁷ and the excessive production of the stimulatory VFAs: butyrate and propionate.⁴³⁸ These calves can have a form of chronic ruminal acidosis that results in a reduced growth rate and poor body condition. Ruminal contents are typically fluid with an acidic pH, ruminal hypomotility occurs, and recurrent free gas bloat is common. Affected calves often display a craving for fibrous materials. Hair coat licking is common in these individuals, and hairball formation in the reticulorumen is a common sequela. The hairballs may not be deleterious, but occasionally they cause obstructive disease or abrade the parakeratotic papillae or the abomasal mucosa, predisposing to ulcers and inflammatory lesions. Acute ruminal acidosis is not typically recognized in the young, developing ruminant, probably because feed consumption is limited and because the predisposing adult-type ruminal microflora has not yet developed.

An opposite extreme can occur when the young calf is fed dry forage to the exclusion of more readily digestible carbohydrates. Concentrates and grass contain soluble carbohydrates and are well digested by the developing ruminant. Hays contain much less soluble carbohydrate and an abundance of the structured, slowly digestible forms. These substances are not as well digested by calves because the appropriate cellulolytic microflora is not fully developed. With moderate hay intake and the supply of other sources of nutrition, problems are rarely encountered. When dry roughage is the only available feed, especially when the hay is of poor quality, adequate breakdown of the fiber is prolonged. The low availability of nutrient substrate that results from delayed digestion of the structured carbohydrates decreases microbial proliferation and fermentation. Inadequate fermentation of the feedstuff deprives the animal of required nutrients as well and results in poor performance and growth. When the only available feed source is the hay ration, the calf continues to consume while the long undigested fiber accumulates in the rumen. The rumen continues to expand as a result of the increased filling, eventually becoming grossly distended. Recurrent bloat is common in these animals because of the overfilling and poor ruminal contractility. This phenomenon is a frequent occurrence under some management conditions and has commonly been called “haybelly.” Affected animals display a typical abdominal contour, with gross distention of the abdominal wall that is more prominent on the left side. The ruminal contents are very firm, the fluid has a pH around neutral and shows little microbial activity or odor, ruminal motility is poor, and despite the full abdomen the animal is thin. This form of microfloral inactivity is more common in calves than in adults because the young ruminant is less able to ferment fibrous roughage.^386,387

Recurrent Bloat (Ruminal Tympany)

Moderate gas distention of the rumen is a common sign of disease in calves, usually as a result of free gas accumulation, whereas frothy fermentation is very uncommon in the young ruminant. The pathogenesis of free gas bloat has been discussed, and the same principles hold for the young ruminant. The differences between free gas bloat in the adult and in the young calf are more a matter of chronicity and frequency of occurrence than cause. Digestive disturbances of the adult rumen tend to develop more rapidly and are more readily identified than those of the calf. Because of the involvement of ruminal developmental processes in the pathogenesis of calf indigestion, in young ruminants the diseases are more chronic than acute in nature. In most cases the calf continues to consume feed, and the abnormal ruminal function and development may be easily overlooked.

Ruminal tympany seems to accompany indigestion in calves more often than in adult cattle and also assumes a more prominent appearance in calves than adults. These factors may be reflections of the juvenile anatomy and the incomplete development of adult function. It is worth noting, for instance, that although left-sided abomasal displacement is an uncommon occurrence in young calves, it almost invariably is accompanied by marked ruminal tympany.⁵⁰⁸ In contrast, the disease is common in adult cattle, but ruminal tympany is an infrequent sign of the disease.

Purulent lung infections appear to be a common cause of bloat in calves, probably as a result of intrathoracic compression or irritation of the esophagus or possibly the vagal nerves. However, other causes of bloat that are associated with abnormal ruminal function are also common in calves with indigestion. They include overdistention of the rumen, insufficient clearing of the cardia, and inhibition of motility by abnormal fermentation products. A thorough examination is required to determine the underlying cause of the individual case.

One presumed cause of bloat in calves that is not a cause of adult bloat is sudden filling of the abomasum by milk feeding during weaning. Calves not yet completely converted to a diet of solid feed still consume milk eagerly. In some cases acute free gas bloat occurs immediately after the milk feeding. Because the esophageal groove directs the milk into the abomasum but the abomasum is already partly filled by ingesta from the developing rumen, acute overdistention of the organ can occur and reflexively inhibit forestomach motility. Feeding smaller milk meals or discontinuing the milk feeding resolves the problem in these cases, lending support to the presumed cause.

Clinical Signs and Differential Diagnosis of Indigestion (Table 32-14)

Clinical Pathology

Treatment and Prognosis

Fermentative Disorders

With the exception of severe acute ruminal acidosis, the disturbances of reticuloruminal fermentation generally are not fatal unless the disease is undiagnosed for a prolonged period, leading to extreme debility. Treatment of fermentation disorders centers around restoring a normal ruminal fluid environment that allows normal microbial metabolism. Identification of ruminal fluid parameters (see Table 32-16) and the nature of the forestomach ingesta directs the appropriate treatment (Box 32-7).

Prevention

Some of the sporadically occurring diseases of the forestomach wall such as granulomatous infections, neoplastic invasions, and diaphragmatic herniation cannot be foreseen or prevented. The most common cause of vagal indigestion syndrome is inflammation of the reticular area caused by TRP. Prevention of this disease by keeping metallic foreign bodies out of the feed or by prophylactic administration of a ruminal magnet is the best prevention of vagal indigestion as well.

The microbial-fermentative forestomach disorders are best prevented by proper feeding management. A well-balanced diet of palatable feeds with an adequate amount of well-structured roughage (not finely ground or pelleted) prevents most problems. Dietary changes should be introduced slowly (over 2 to 3 weeks) to allow adaptation of the microbial flora to the new substrate. Calves undergoing ruminal development and cattle fed high-production diets or changing between production groups are at risk of oversights in proper feeding management. Some feed additives have proved effective in preventing the overgrowth of the high-acid—producing ruminal microflora. Feed-grade buffers are widely used in both dairy and beef cattle production, in which high-concentrate diets are fed to maximize production. These buffers stabilize the ruminal pH and alter the mechanics of ruminal fluid outflow, thus decreasing the chances of overgrowth of the lactate-producing organisms. Commonly used buffers include sodium bicarbonate, sodium sesquicarbonate, sodium bentonite, magnesium oxide, and calcium-magnesium carbonate, of which only the sodium carbonates are truly buffering agents in the chemical sense. The other agents do tend to stabilize ruminal pH, however, and all of these have shown some benefit in reducing the disease problems associated with heavy grain feeding and diets that are low or marginal in effective fiber.⁵³¹ The ionophore antibiotics (e.g., lasalocid, monensin) and some other antibiotics (e.g., the sulfur-containing peptide antibiotic thiopeptin) have also proved effective in reducing lactate production in animals fed high-grain diets. The effect of these agents is to suppress the lactate-producing organisms while not appreciably affecting the lactate users. The ionophores are in common use in feedlot cattle and dairy heifer rations because the selective effects of these antibiotics on the ruminal microbes alter the ruminal metabolism in a manner that promotes increased animal weight gain.^532,533 In 2004 the FDA approved the use of the ionophore monensin for lactating cattle in the United States. Although approval was based on increases in milk production efficiency, ionophore use may also reduce the risk of ruminal acidosis and ketosis.⁵³⁴

History

Complete Physical Examination

A thorough and complete physical examination is the most important step when approaching an acute abdomen.

Ancillary Tests

Diagnostic Imaging

Medical or Surgical Decision

A differential diagnosis list and a decision for surgical or medical treatment should be established based on clinical signs and ancillary tests results (Fig. 32-96). If a precise diagnosis is made, adequate treatment can be instituted. When a precise diagnosis cannot be established, attempts should be made to differentiate surgical and medical cases (Fig. 32-97). Among surgical cases, intestinal obstructions are those requiring immediate surgery. A mechanical obstruction may be suspected when there is a suspicion of intestinal or cecal torsion on rectal examination, pings indicating a right abomasal displacement or volvulus, peritoneal fluid indicating bowel devitalization, or severe signs of active colic or rapid deterioration.^557,577 If an intestinal mechanical obstruction is not suspected during the first examination, exploratory surgery may be delayed for up to 36 hours.⁵⁵⁷ However, frequent monitoring should be performed and appropriate medical treatment provided to the animal.

MEDICAL AND SUPPORTIVE TREATMENT

The goal of therapy in an animal with acute abdomen is to initially correct the hemodynamic and metabolic imbalances associated with hypovolemic or septic shock, to control pain, and to correct or treat the primary cause of the disease, when identified. Consequently, medical treatment is based on fluid therapy, NSAIDs, and antimicrobial drugs.

Fluid Therapy

Crystalloid solutions (0.9% NaCl, Ringer’s solution) are indicated initially to replenish fluid loss and improve the circulating blood volume.^560,581 To resuscitate critically ill neonatal patients, recommended intravenous fluid administration rates of isoosmotic crystalloid solution are 80 to 90 mL/kg of body weight per hour.⁵⁸¹ However, such rates are difficult to achieve through a catheter in adult ruminants. Studies demonstrated that perfusion rates of 40 and 80 mL of an isoosmotic crystalloid solution per kilogram of body weight per hour can be used safely in adult ruminants and dehydrated calves, respectively.^582-584 If the animal is not critically ill, fluid and electrolyte deficits should be corrected over 2 to 8 hours. The maximal flow rate usually achieved through a catheter in an adult is 15 to 20 mL/kg/hr.

Hypertonic solutions (7.2% or 7.5% NaCl) are also an alternative. Intravenous administration of hypertonic saline provides rapid resuscitation in dehydrated or endotoxemic ruminants.⁵⁸⁵ A rate of 4 to 5 mL of hypertonic solution per kilogram should be administered IV through the jugular vein over 4 to 5 minutes. Animals should be provided with a supply of fresh water immediately after the treatment, or an intravenous infusion of an isotonic crystalloid solution should be instituted. Cattle not observed to drink within 5 minutes should have 20 L of water pumped into the rumen.⁵⁸⁵ An administration rate for a hypertonic solution of over 1 mL/kg/min should be avoided because it induces a potentially fatal hypotension coupled with a decrease in cardiac contractility.⁵⁸⁵

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Correction of Acid-Base and Electrolyte Imbalances

Correction of electrolyte imbalances should be based on laboratory results when available. Previous treatments should be considered (e.g., intravenous calcium, orally administered magnesium hydroxide) to initiate the most appropriate fluid therapy if no laboratory results are available.⁵⁶⁰ Most animals with acute abdominal diseases suffer from metabolic alkalosis, hypochloremia, and hypokalemia.

Calcium homeostasis is in a precarious balance in postpartum dairy cattle. Hypocalcemia is common in anorectic ruminants or in ruminants with gastrointestinal diseases.^560,581 Moreover, metabolic alkalosis, frequently observed in cases of acute abdomen, is strongly associated with subclinical hypocalcemia.^540,586 Calcium ions are of particular importance in gastrointestinal motility. First, in the gastrointestinal smooth muscles, the channels responsible for generating action potentials are calcium-sodium channels.⁵⁵¹ Second, gastrointestinal smooth muscle contraction occurs in response to the entry of calcium into the muscle fiber.⁵⁵¹

Based on these considerations, the intravenous solutions used for the medical treatment of acute abdomen, secondary to a suspected digestive disorder, should contain Na, Cl, K, and Ca.

The Ringer’s solution containing 8.6 g of NaCl per liter, 0.3 g of KCl per liter, and 0.3 g of CaCl₂ per liter, yielding 147 mEq/L Na, 155 mEq/L Cl, 4 mEq/L K, and 4 mEq/L Ca, is the commercially available solution of choice. In our clinics in Quebec, we use a beneficial homemade solution composed of 7.5 g of NaCl per liter, 1.5 g of KCl per liter, and 5.75 g of Ca²⁺ per liter (25 mL of 23 % calcium borogluconate per liter), yielding 128 mEq/L Na, 148 mEq/L Cl, 20 mEq/L K, and 26 mEq/L Ca, for adult cattle. We usually begin our fluid therapy with rapid administration of a 0.9% NaCl solution (15 to 20 mL/kg/h, which is the highest rate possible through a catheter) for rapid correction of dehydration and then administer this homemade solution with an infusion rate of approximately 4 to 5 mL/kg/hr.

Control of Pain and Inflammation

Pain and inflammation are important causes of gastrointestinal hypomotility (Fig. 32-98). Gastrointestinal pain increases sympathetic tone, causing general inhibition of the gastrointestinal tract.^551,587,588 Numerous inflammatory mediators are released during disease of the gastrointestinal tract, leading to alteration of intestinal motility.^587,589 Peritoneal inflammation or irritation and associated pain are well-recognized initiating factors of ileus in multiple species.^587,589 Release of proteinases, vasoactive substances, free oxygen radicals, and endorphins secondary to ischemia and reperfusion injury, or to endotoxemia, impairs cardiovascular function and decreases gastrointestinal motility.⁵⁸⁹ Inflammatory mediators lead to a pain response and modulate the intensity of noxious stimuli.^588,587 Consequently, analgesic and antiinflammatory drugs appear essential in the management of acute abdomen. These drugs must be used with caution. NSAIDs may induce abomasal ulcers, particularly in an anorectic patient. Analgesics may mask clinical signs (pain, fever) and compromise adequate case management by delaying surgery.

Fig. 32-98 Causes of abdominal pain in ruminants.

NSAIDs are the most commonly used drugs for gastrointestinal pain management in cattle. There is no information comparing the efficacy of the different NSAIDs available in food animal medicine related to their use in the management of acute abdomen. Some authors report that, based on clinical observations, flunixin provides an excellent visceral analgesia.⁵⁹⁰ Ketoprofen and flunixin appear to have similar activities in endotoxic calves.⁵⁹¹ Consequently, no single NSAID can be recommended based on scientific evidence for the management of abdominal emergencies in cattle. The choice of NSAID becomes a matter of previous experience, comparative medicine, legislation, and cost. In our experience, flunixin and ketoprofen are both adequate for the management of acute abdomen in cattle. In equine gastrointestinal pain, a poor or short duration response to NSAIDs indicates a need for surgery.⁵⁸⁸ This principle can be applied to cattle with caution because of their unpredictable behavior in response to pain.

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α₂-Agonists that function as sedatives and analgesics, such as xylazine, detomidine, and medetomidine, could also be used to relieve pain in cases of acute abdomen. All are considered to be strong analgesics that can alleviate most visceral pain, at least temporarily, in equine medicine.⁵⁸⁸ There are few data on the use of α₂-agonists for the management of acute abdomen in cattle. In a cow with a large intestinal obstruction, signs of abdominal discomfort disappear immediately after the administration of a single dose of xylazine (0.05 mg/kg IV) for at least 1 hour.⁵⁹² Different side effects must be considered before the administration of alpha-2 agonists. Xylazine is reported to have significant effects on the gastrointestinal tract in cattle, decreasing reticuloruminal and intestinal motility.⁵⁹³ Because of the hemodynamic changes associated with the administration of α₂-agonists, these drugs must be used with caution in patients with arterial hypotension and/or shock.⁵⁹⁴ α₂-agonists can mask surgical pain and delay the decision for surgery. This is particularly critical with the use of detomidine.⁵⁸⁸ Finally, dose and administration of α₂-agonists should be used with care if standing surgery is planned.

Antimicrobial Drugs

Bacterial translocation from the intestines can occur in cases of mechanical or functional ileus secondary to bacterial overgrowth, inflammation, and impairment of barrier function of the intestinal wall.^555,595 A systemic broad-spectrum antibiotic treatment should be instituted when a septic process is suspected, until bacterial culture results become available. This initial antibiotic therapy should be effective against gram-negative, gram-positive, aerobic, and anaerobic pathogens. The choice of antibiotic should also take into consideration legal aspects and the cost of the treatment. β-Lactams, tetracyclines, and trimethoprim-sulfadoxine appear to be good choices. In cattle there is no accepted recommendation for the duration of treatment. In human medicine, prolonged broad-spectrum antibiotic therapy in case of surgical acute abdomen does not appear beneficial.⁵⁹⁶ Prevention of infective complications was not affected by prolonging the course of antibiotic treatment.⁵⁹⁶ In human medicine the current recommended dose is a single prophylactic antibiotic administration when there is no or minimal evidence of contamination, and 5 to 7 days when pus or contamination, either localized or diffuse, is present.⁵⁹⁶

Other Treatments

The use of purgatives (magnesium hydroxide, mineral oil, liquid paraffin) in cases of suspected gastrointestinal obstruction or ileus in cattle has no therapeutic basis.⁵⁵⁷ Moreover, these treatments may exacerbate the condition. Because the intestines are already filled with gas and fluid, purgatives only impose additional distention. In human medicine, laxatives are frequently used for the treatment of postoperative ileus (POI); however, no study could demonstrate their actual benefit.⁵⁹⁷ Braun and colleagues reported that the use of purgatives for the treatment of cecal disorders delayed the time to first defecation.⁵⁵⁵ Moreover, magnesium hydroxide may be responsible for detrimental effects such as metabolic alkalosis,⁵⁹⁸ sedation caused by hypermagnesemia,⁵⁹⁸ increased ruminal pH,⁵⁹⁹ and decreased ruminal microbial activity.⁵⁹⁹

Motility-modifying agents may be used in the management of gastrointestinal disorders. In most cases intestinal motility is restored when pain is relieved and electrolytic imbalances are corrected. Steiner reviewed the different prokinetics that can be used in ruminant medicine and their clinical implication.⁵⁹³ For cattle, he recommends the use of bethanechol (0.07 mg/kg SC tid for 2 days; not approved for food animal use in the United States) alone or in combination with metoclopramide (0.1 mg/kg SC or IM tid for 2 days; not approved for food animal use in the United States), or erythromycin in polyethylene glycol (10 mg/kg IM bid for 2 days, Erythro-200) for the postoperative treatment of right abomasal displacement or torsion.⁵⁹³ Bethanechol (0.07 mg/kg SC tid for 2 days; not approved in the United States) can be used for conservative or postoperative treatment of cecal disorders and treatment of paralytic ileus.⁵⁹³ Contrary to cattle and sheep, in goats metoclopramide (0.5 mg/kg IM or IV; not approved in the United States) has been reported to significantly increase myoelectric activity of the duodenum.⁵⁹³ Continuous infusion of neostigmine (87.5 mg in 10 L of sodium chloride-glucose infusion at 2 drops/sec per cow) was successfully used for the conservative and postoperative treatment of cecal disorders.⁵⁵⁵ In this clinical report, this protocol was preferred to those previously reported (neostigmine SC every hour over 2 to 3 days in doses that gradually decreased from 12.5 mg to 2.5 mg).⁵⁵⁵ Drug administration was easier and involved fewer disturbances for the animal.⁵⁵⁵ However, no control group was included in this study. Also, neostigmine has been reported to have a pronounced effect on intestinal contractility, causing uncoordinated spikes to become more frequent, thereby compromising the potential beneficial effect.⁶⁰⁰

No prokinetic drug is reported to directly increase ruminal motility. In cases of prolonged anorexia or acute indigestion, ruminal flora can be disturbed and reduced. Transfaunation may help to rapidly reconstitute the ruminal flora and hasten return to normal function of the rumen and the digestive tract. The technique for and beneficial effects of transfaunation (reduction of ketonuria, increased feed intake, and higher milk yield) have been reported in the postsurgical treatment of left abomasal displacement.⁶⁰¹

Follow-Up

When a definitive diagnosis cannot be made, a close monitoring of the animal may be indicated. Follow-up must also be performed secondary to surgery to ensure adequate response to surgical treatment and to allow possible adjustment of treatment. In a referral hospital the animal should be reevaluated every 4 to 6 hours. In field practice, vital parameters, rectal examination, presence and consistency of feces, and pain may be reevaluated every 6 to 12 hours. A significant reduction of heart rate was observed 4 and 6 hours after the initiation of treatment in cases of cecal dilatation.⁵⁵⁵ Feces are passed within 4 to 6 hours after surgery in cases of intestinal volvulus⁵⁴⁶ or cecal disorders.⁵⁵⁵ Failure to defecate for 24 hours or more is abnormal in cattle and therefore indicates persistence of intestinal obstruction and may adversely affect the prognosis.⁵⁵⁷ Deterioration or persistence of clinical signs despite the initiation of supportive treatment is also an indication for surgery. Surgical exploration is indicated if the following clinical signs are observed: persistence of colic, development of abdominal distention, heart rate over 100 beats/min, scant feces, typical abomasal or cecal pings, or paracentesis indicating bowel devitalization.

The decision for surgery or medical treatment remains challenging in cases of acute abdomen in ruminants. Optimal management of acute abdomen prevents any unnecessary delay in cases requiring surgery and avoids unnecessary surgery. Knowledge of diseases associated with signs of acute abdominal pain is important, but no clinical signs are specific for a particular problem, and a specific diagnosis cannot be established postoperatively in many cases. Based on a systematic approach to clinical examination and a judicious use of ancillary tests, the clinician may be able to identify cases that require immediate or delayed surgery, avoid unnecessary surgery, and establish a cost-effective management plan.

Definition and Etiology

TRP or hardware disease is a common disease of cattle but is rarely seen in small ruminants. It is the most common cause of anterior abdominal pain in cattle. The ingestive behavior of cattle predisposes them to the accidental swallowing of metal foreign objects that settle in the reticulum. Ingestion of a foreign body may also be associated with diseases that cause pica, such as phosphorus deficiency. Subsequently, the foreign object may enter the reticulum and (1) attach to a magnet without clinical diseases; (2) penetrate the reticulum wall only with intramural inflammation; (3) perforate the reticulum wall, penetrate into the peritoneal cavity, and create localized peritonitis; or (4) migrate into the peritoneal and thoracic cavities.⁶⁰² The diaphragm, pericardium, and heart muscle are located just cranial to the reticulum, with the liver positioned medially and dorsally and the spleen laterally and dorsally. These organs may sometimes be penetrated by foreign bodies and become involved in the inflammatory process.

Clinical Signs and Differential Diagnosis

TRP in the most severe, acute form is characterized by fever, anorexia, decreased or absent ruminal contractions, and evidence of cranial abdominal pain. Pinching of the withers or upward pressure on the xiphoid region may elicit a grunt on expiration. Affected cattle may stand with an arched back and resist ventral flexion of the back when pinched over the withers (normal cattle flex ventrally). Some cattle grunt spontaneously when forced to move or when defecating or urinating. Lactating cows show a sudden decrease in milk production.^603,604 Some cows regurgitate ruminal fluid, especially if the oropharynx is mechanically stimulated. Tachycardia, reluctance to move or lie down, mild bloat, constipation, or abducted elbows may also be seen. These typical signs often abate within the first day or two, making diagnosis more difficult. Auscultation may reveal a pounding heart or muffled heart sounds bilaterally if pericarditis with effusion has developed by the time of examination. Sudden death has occurred as a result of the laceration of a coronary blood vessel or puncture of the heart by the foreign body.

Less severe or more long-standing cases may have signs that are more subtle and confusing. Cows in early lactation may have ketosis; however, a distinguishing feature of hardware disease is the abrupt onset of anorexia and hypogalactia. Fever may be absent. Weight loss, rough hair coat, diarrhea, or generalized lameness, along with cranial abdominal pain that is difficult to localize, may be the only signs.

If the pericardial sac has been seeded with bacteria, pericarditis usually develops. There is no initial change in heart sounds, but over a period of several weeks as septic fluid accumulates, the heart may become muffled. When there are both fluid and gas in the pericardium, sloshing sounds like a washing machine may be auscultated. Distended jugular and superficial abdominal veins and other signs of congestive right-sided heart failure are most common after pericardial effusion. Dyspnea may occur if left-sided failure is also present.

The foreign body may penetrate the liver or spleen, leading to abscess formation. These abscesses as well as reticular adhesions may be responsible for ruminoreticular outflow problems and may lead to vagal indigestion.⁶⁰⁵ These are further discussed with vagal indigestion.

TRP must be differentiated from other causes of cranial abdominal pain. They mainly include abomasal ulcers, hepatic abscesses from other causes, and pleuritis. More informations about the differential diagnosis of abdominal pain is presented in the section on acute abdomen in cattle. When thoracic structures are involved, TRP must be differentiated from primary pneumonia or pleuritis, diaphragmatic hernia, and heart diseases such as endocarditis, lymphosarcoma of the heart, and cor pulmonale. Finally, TRP must be differentiated from others causes of ruminal distention and vagal indigestion.

Clinical Pathology

The WBC count and differential, as well as the determination of plasma proteins and fibrinogen, may indicate an acute or chronic inflammatory process depending on the stage of the TRP. Neutrophilia and a left shift are expected in acute cases. However, in more chronic cases changes are less pronounced, and WBC count as well as differential may be normal.^602,606 High fibrinogen concentration may be observed in acute cases (2 to 3 days after the beginning of the disease) and chronic active cases. Studies in referral centers^607,608 have demonstrated highest plasma fibrinogen concentration with TRP compared with other abdominal disorders. High total plasma proteins, primarily reflecting high globulin levels, were expected in chronic cases of TRP. Higher concentrations of total plasma proteins have been observed in cases of TRP compared with other abdominal disorders.^607-609 Plasma protein concentration cutoff points of 87 to 100 g/L have been proposed in these studies. All the results of the studies demonstrated that high values of plasma fibrinogen and plasma protein concentrations are highly suggestive of TPR. However, other disorders can induce the same modifications, and absence of these abnormalities does not rule out TRP. Consequently, other diagnostic tests (diagnostic imaging) must be performed to confirm the diagnosis. Biochemical profile and blood gas analysis are usually within normal range but may reflect hypochloremic metabolic alkalosis associated with ileus and dysfunction of the abomasum.

Radiography and ultrasonography of the reticulum are very useful for the diagnosis of TRP. Radiographs of the reticulum are limited to referral centers. They are performed on standing animals and allow the detection of a metallic foreign body and the determination of its location in or outside the reticulum. Different parameters may be observed on radiographs for the diagnosis of TPR. They include presence or absence of a foreign body, position of the foreign body, presence of focal gas shadows or gas-fluid interface near the reticulum, and the shape, size, and location of the reticulum.^610-612 Of these parameters, location of the foreign body is the most reliable indicator for the diagnosis of TPR.^610,612 Ultrasonography of the reticulum is presented elsewhere in this chapter. Ultrasonography and radiography are two complementary methods that provide different useful information for the diagnosis and the management of TPR.⁶¹³ Ultrasonography is also the most useful complementary examination for the diagnosis of pericardial effusion.

Abdominocentesis and pericardiocentesis may be performed blind or with ultrasound guidance. Abdominal fluid analysis and its limitations in cattle are discussed in the section on peritonitis. Pericardiocentesis may be performed at the level of the point of the elbow in the fifth left intercostal space. Aseptic preparation of the skin and local anesthesia of the region to be punctured are required; pulling the left forelimb forward may be helpful. A 5- to 10-cm spinal needle or intravenous catheter can be used; the length required depends on the size of the animal and the amount of subcutaneous fat. Previous ultrasonographic examination is helpful for the choice of the needle. Caution is advised when advancing the needle to prevent laceration of the myocardium. Ultrasound-guided centesis prevents trauma to the myocardium. Visual inspection of the fluid obtained is usually adequate to confirm the diagnosis of pericarditis; it is cloudy and foul smelling. The fluid may be examined bacteriologically and cytologically.

If ileus occurs or vagal indigestion develops, analysis of the ruminal fluid may reveal elevated chloride ion concentration as a result of reflux from the abomasum and omasum.

Pathophysiology

The indiscriminant eating habits of cattle lead to accidental consumption of foreign bodies. Those that are of high specific gravity initially settle to the bottom of the ventral sac of the rumen. Subsequent contraction cycles of the forestomach move those objects from the rumen into the reticulum. If the object is large enough and sharp enough, it can be pushed, most often through the cranial wall of the reticulum, by the forceful, normal reticular contractions. Normal forestomach bacteria leak through the hole thus created and may establish infection locally along the foreign body. Infection also may spread as in the pericardium or locally during abscess formation. The pain and inflammation associated with the trauma and infection lead to decreased appetite and ruminal hypomotility or stasis. Agalactia is abrupt because of the acute anorexia and subsequent failure to absorb precursors for milk synthesis.

Rehage and colleagues⁶⁰⁵ demonstrated that the disturbances of digesta through the forestomachs and the abomasum in cows affected with TRP develop in three phases. The first one, characterized by poorly comminuted feces, occurs secondary to virtual immobilization of the reticulum caused by pain and inflammatory adhesions. With extension of the adhesions, additional impairment of reticulum motility develops. At this time, stratification of the food particles in the reticulorumen is lost, volume of these two forestomachs is increased, and ruminal outflow is inhibited. Finally, the consistency of ruminal contents is changed to a pasty mass with high viscosity. Increase in viscosity of ruminal outflow leads to inhibition of the transpyloric outflow. At this time, abomasumal volume increases and internal vomiting occurs.

Epidemiology

The ingestive techniques of cattle allow sharp nonfood items to be prehended and swallowed. Ingestion of such items by sheep or goats is extremely rare. The disease affects confined cattle where mechanical processing of forages or construction activities increase the chances that wire or nails will be included in the feed. Most cases are sporadic, but outbreaks have occurred when such things as multistranded cable have been chopped up by a forage harvester and ensiled.

Necropsy Findings

Cattle that die peracutely may have a lacerated myocardium with resulting hemorrhage or cardiac tamponade. Diffuse peritonitis characterized by copious, foul-smelling peritoneal fluid with an obvious reticular defect may be seen in acute cases. More chronically affected animals may have extensive pericardial effusion with a thick epicardial layer of fibrin. The penetrating foreign body generally is still present in the wall of the reticulum or pericardium.

Treatment and Prognosis

Conservative treatment generally is attempted first and includes the administration of a forestomach magnet, parenteral antibiotic therapy, and confinement. Often the animal is confined to a stanchion or box stall. Many cattle recover after such a course of therapy with resumption of forestomach motility and appetite within 1 to 3 days. Different drugs have been used to enhance the chance of the magnet to enter the reticulum cavity. The effects of premedication with atropine, scopolamine, or xylazine and of standing the cow with its forelimbs 30 cm lower than the hindlimbs on successful administration of a magnet (i.e., adequately located in the reticulum cavity) have been evaluated in healthy cows.⁶¹⁴ Adequate location of the magnet was evaluated radiographically 1½ hours after the administration of the magnet. None of the procedures increased the chance of the magnet being successfully placed in the reticulum. Moreover, in all groups (treatment groups and control groups) only 57% of the magnets were adequately located in the reticulum.⁶¹⁴ Braun and co-workers demonstrated that foreign bodies that have penetrated the reticulum wall or that have clearly perforated the reticulum had about 54% and 32% chance, respectively, to become attached to the magnet.⁶¹⁵ Animals that have not significantly improved by the third day may require a rumenotomy to remove the foreign object. Ideally, radiography combined with ultrasonography is recommended at this time to verify the diagnosis and objectively assess the response to treatment, but ultrasonography alone is most feasible in most practices.⁶¹⁵

During rumenotomy, abscesses that are tightly adhered to the reticulum may be drained into the lumen of the reticulum.⁶¹⁶ In some instances reticular abscesses may also be drained through an ultrasound-guided transcutaneous incision,⁶¹⁷ ultrasound-guided insertion of a chest trocar, or insertion of a trocar during ventral laparotomy.⁶⁰² Treatment of peritonitis requires systemic antibiotic therapy and possibly drainage of the affected area; surgical correction of the inciting cause is discussed in the section on peritonitis.

Prognosis

The prognosis of TRP depends mainly on the location of the foreign body and the other organs affected. The prognosis is fair to good when TRP is associated with localized peritonitis and when only the spleen or the liver is also affected. In most cases as inflammation diminishes, the reticular function can return to normal.⁶¹⁸ The prognosis is poor to guarded in TRP associated with pericarditis, pleuritis, or diffuse inflammatory adhesions in the abdomen.^602,618

Prevention and Control

Eliminating sources of sharp foreign objects in the feed supply prevents TRP. Installation of large magnets on feed handling equipment and prophylactic administration of forestomach magnets to all animals at 6 to 8 months of age prevent almost all cases caused by magnetizable objects.

REVIEW OF PERITONEAL CAVITY

Normal Peritoneal Fluid

The peritoneum is a highly permeable membrane. Most of it acts as a bidirectional semipermeable barrier to the diffusion of water and low—molecular-weight solutes between the blood and the peritoneal fluid.^620-624 Peritoneal dialysis uses this principle to treat renal failure. Normal peritoneal fluid provides lubrication for the movement of abdominal organs and apposed peritoneal surfaces.⁶²⁵ It is formed and resorbed constantly. Normal fluid movement is achieved by normal movement of the viscera and contraction of the diaphragm during respiration. A normal animal has no more than 1 mL of peritoneal fluid per kilogram of body weight.⁶²⁴ In acute severe peritonitis, the inflammatory process may induce a net flow of liters of proteinaceous fluid (80 mL/kg/day in humans), leading to hypoproteinemia and/or hypovolemic shock.⁶²⁰

Normal peritoneal fluid has a wide range of values.^622,626-629 It should be clear, with a specific density less than 1.016 (Table 32-17). Protein content should be less than 3 g/dL, although some authors have reported normal values up to 6.3 g/dL for cattle.⁶²⁹ Normal bovine peritoneal fluid may contain some fibrinogen and may clot when exposed to air.⁶³⁰ Normal fluid contains fewer than 10,000 cells with a majority of macrophages. Lymphocytes, eosinophils, and desquamated mesothelial cells may also be present, but there are normally very few neutrophils. Normal periparturient cattle have significantly more abdominal fluid with a lower protein concentration.⁶³⁰ With peritonitis there may be a complete absence of collectable peritoneal fluid because of dehydration or fibrous adhesions.

Table 32-17 Normal Range for Classification of Bovine Peritoneal Fluid According to Different Authors