ETIOLOGY

The etiology of the most common occurrence of gastric ulcers in the horse is unknown but several risk factors have been identified, which are described under epidemiology. The disease is common in horses undertaking regular exercise and might be related to decreased stomach volume and subsequent exposure of the squamous mucosa of the proximal parts of the stomach to acid during exercise (see Pathogenesis, below).

Individual cases of gastric ulcers are associated with parasitic gastritis, such as in horses infested with Gasterophilus spp., and Habronema megastoma larvae. Tumors of the stomach, such as gastric squamous cell carcinoma or lymphosarcoma, may cause ulceration of the gastric mucosa. Gastric phytobezoars and persimmon seeds (D. virginiana) have been associated with gastric impaction, ulceration and perforation of the glandular portion of the stomach of a horse.¹ There is no evidence that infection by Helicobacter sp. or similar organisms is associated with gastric ulcer disease in horses.

EPIDEMIOLOGY

PATHOGENESIS

The equine stomach is comparatively small relative to the size of the gastrointestinal tract. The stomach mucosa is divided into two parts. The proventricular part is glistening white in color, is composed of thick stratified squamous epithelium and contains no glands. It covers approximately one-third of the mucosal area and ends abruptly at the margo plicatus, a slightly raised irregular serrated border with the glandular mucosa. Most gastric lesions in horses occur in squamous mucosa.

The glandular mucosa has a velvet-like structure and is usually covered by a thick layer of viscous mucus. The mucosa contains three main gland types: mucus-secreting cardiac glands; fundic glands, which contain mucus-secreting cells, hydrochloric-acid-producing parietal cells and pepsinogen-secreting chief cells; and pyloric glands, which consist largely of mucus-secreting cells. The stratified squamous epithelial mucosa has minimal resistance to gastric acid. The glandular epithelium has elaborate mechanisms, including the mucus–bicarbonate barrier, prostaglandins, mucosal blood flow and cellular restitution, to protect itself from peptic injury. Hydrochloric acid and pepsinogens, which are converted to the proteolytic enzyme pepsin in an acidic environment, are secreted in the glandular mucosa by parietal cells and chief cells, respectively. The horse is a continuous, variable hydrochloric acid secretor, and the pH of equine gastric contents in the pylorus and antrum is often less than 2.0. Gastric pH is lowest, and acidity highest, when horses have been deprived of feed or have voluntarily stopped eating, often for as little as 2 hours. Thus there are periods during the day when gastric acidity is high. Periods of prolonged high gastric acidity (pH < 2.0) can be induced in horses by intermittent deprivation of feed, which often results in severe ulceration in the gastric squamous epithelial mucosa. Concurrent administration of the H₂ antagonist ranitidine during feed deprivation substantially reduces the area of lesion in the gastric squamous epithelial mucosa.¹⁷

The pathogenesis of gastric ulcer is uncertain. Exposure of squamous mucosa to acid is probably involved in the development of ulcers in most horses. During exercise intragastric pressure increases from approximately 14 mmHg at rest to as high as 50 mmHg, stomach volume decreases and the acidity of fluid within the proximal part of the stomach declines from 5–7 to 2–4.¹⁴ The combination of reduced blood flow and exposure to low pH increases the likelihood of mucosal damage, loss of protective mechanisms and development of gastric mucosal lesions.

Other factors, including physical injury to gastric mucosa, reflux of bile acids from the duodenum¹⁸ and presence of volatile fatty acids in the stomach all may contribute to the development of gastric lesions,¹⁹ but the definitive roles, if any, of each of these factors have not been determined.

CLINICAL FINDINGS

The vast majority of horses with lesions of the gastric mucosa, including ulceration, do not have clinical signs. Among race horses, signs of poor performance, feed refusal, fussy eating (not consuming all of the meal at a constant rate) and poor body condition have been associated with presence of gastric ulcers. Of these signs only poor hair coat and poor body condition have been proved to be associated with gastric ulcers.^7,8 The high prevalence of both some of the clinical signs, for instance failure to perform to expectation, and gastric ulcers means that there is a high likelihood that horses with a given clinical sign will have an ulcer by chance. However, clinical experience indicates that horses with more extensive or severe lesions will have more severe clinical signs, including colic.

Colic is associated with presence of lesions of the gastric mucosa, including ulceration. Ulceration can result from lesions elsewhere in the gastrointestinal tract, probably because of feed withholding or feed refusal by horses with colic. Alternatively, gastric ulceration can cause colic. The four criteria to determine whether gastric ulceration is the primary cause of colic in horses are:

Most gastric ulcers in horses are not associated with hemorrhage and so signs of anemia or melena are unusual in horses. Horses with severe gastric ulceration and reflux esophagitis often have bruxism and retching. Rupture of gastric ulcers, perforation and subsequent peritonitis, and exsanguination from a bleeding ulcer are rare in adult horses.

Involvement of the spleen in the horse with a perforating gastric ulcer, a rare event, results in fever, anorexia, toxemia, pain on deep palpation over the left flank and leukocytosis with a left shift.

Gastroscopic examination is the only means of demonstrating gastric lesions and assessing their extent and severity. Gastroscopic examination of the adult horse requires an endoscope of at least 2.5 m in length, although 3 m is preferable. Presence of feed material within the stomach prevents complete examination of the gastric mucosa, and in particular of the pylorus and antrum. The horse should be prepared by having feed withheld for at least 12 hours and water withheld for 4 hours before examination. If the horse is stabled on edible material such as straw or shavings, it should be muzzled to prevent it eating this material. The horse may need to be sedated before examination (xylazine hydrochloride 0.1–0.3 mg/kg intravenously) and a twitch applied. The gastric mucosa is examined in a systematic fashion. As the end of the endoscope passes through the cardia. the greater curvature and margo plicatus are examined. The endoscope is then advanced and rotated so that the lesser curvature and cardia are examined. The stomach should be inflated with air during the procedure. Excess fluid in the pylorus and antrum can be aspirated to allow better visualization of these regions. Careful attention should be paid to the margo plicatus as this is the most common site for lesions. The gastric glandular mucosa should be examined carefully for lesions as they are easily missed in this region.²⁰ Material adherent to the mucosa should be washed away by flushing water through the endoscope. The endoscope can be passed into the duodenum to permit complete examination of the antrum. Endoscopic examination usually underestimates the number of gastric ulcers, compared to necropsy examination, and does not accurately predict the severity or depth of ulcers.²⁰

Grading systems for description of gastric lesions in horses are:²⁰

A simplified scoring system recommended for use in practice is:²¹

Most lesions in race horses are in the gastric squamous mucosa with less than 20% of lesions being in the glandular mucosa. The situation is different in hospitalized adult horses, in which lesions in the squamous and glandular mucosa occur with about the same frequency (58%).²² Most lesions in the glandular mucosa of hospitalized horses occur in the antrum or pylorus, as opposed to the glandular mucosa of the body of the stomach.²²

Idiopathic gastroesophageal reflux disease occurs sporadically and rarely in adult horses.²³ Affected horses have bruxism and ptyalism that can be severe. Endoscopic examination reveals ulceration and erosion of the esophagus that is more severe in the distal esophagus. Often there is no evidence of impaired gastric outflow, as is common in foals with this disease.

CLINICAL PATHOLOGY

There are no specific laboratory tests for gastric ulceration. Horses with gastric ulcers have higher concentrations of creatinine and activity of alkaline phosphatase in serum than do unaffected horses, but these differences are not sufficient to be clinically useful.⁸ Horses with gastric ulcer disease are typically not anemic. A test using concentrations of sucrose greater than 0.7 mg/dL in urine after intragastric administration of 10% sucrose (1 g/kg orally after feeding) solution has a sensitivity and specificity of 83% and 90%, respectively, for detection of gastric ulceration.²⁴ Sucrose is absorbed intact across the damaged gastric mucosa and excreted in urine, whereas that entering the small intestine is degraded to fructose and glucose.

NECROPSY FINDINGS

Ulcers may be singular or multiple and are most commonly located in the squamous epithelial mucosa adjacent to the margo plicatus along the lesser curvature of the stomach. They may be linear or irregular in shape; with the exception of those in the glandular mucosa, they are rarely circular in appearance. Ulcers in the squamous mucosa often have slightly raised brown-stained keratinized borders and contain small amounts of necrotic material at their base; frank blood is uncommon. Ulcers in the glandular zone are less common and are usually circular or oval depressions surrounded by an intense zone of inflammation.

When perforation has occurred, there is an area of local peritonitis, the stomach wall is adherent to the tip of the spleen and an extensive suppurative splenitis may be present. In some cases, especially when the stomach is full at the time of perforation, a long tear develops in the wall and large quantities of ingesta spill into the peritoneal cavity. Tumor masses may be present and accompanied by several glandular ulcers.

TREATMENT

The goals of treatment of horses with gastric ulcer disease are: healing of the ulcer, suppression of pain and prevention of ulcer recurrence. The principle underlying treatment of gastric ulcers in horses is suppression of gastric acidity (increase intragastric pH). This can be achieved by inhibiting acid production or increasing buffering of acid. Mucosal protectants are administered with the aim of preventing exposure of damaged mucosa to acid. Management changes may reduce the risk of horses developing disease.

CONTROL

Prevention of gastric ulcer disease in athletic horses centers upon minimizing the effect of factors that promote ulcer development. This may involve the chronic administration of omeprazole (1 mg/kg orally once daily),²⁹ but should include attention to dietary and feeding practices (discussed above) that minimize the time that horses have no feed in their stomach. Ideally, horses at risk would be kept at pasture, but this is not feasible under many management or husbandry systems. All horses in athletic training and confined to stalls should be considered at high risk of development of gastric ulcers and should be managed accordingly. Horses at pasture, such as brood mares, are at minimal risk of development of gastric ulcer disease and no specific control measures are indicated.

ETIOLOGY

A working classification is outlined below.

Obstruction with infarction

Obstruction without infarction

Functional obstruction

The classification used above should be used only as a guide, as the actual clinical presentation may vary. For instance, intussusceptions usually result in infarction of the intussuscepted segment but, because this segment is effectively isolated from the body, the clinical signs are often not characteristic of a horse with an infarctive lesion. Similarly, horses with small intestine entrapped in the epiploic foramen often have less severe clinical signs than anticipated for the severity of the lesion.

EPIDEMIOLOGY

The epidemiology of colic is covered in a previous section. There are no recognized risk factors for small-intestinal volvulus and for many small-intestinal accidents. Epidemiological information is available for some small-intestinal obstructive diseases and is presented below. Obstructive diseases of the small intestine compromise approximately 20% of colic cases referred for further evaluation and treatment.²⁵ For small-intestinal diseases requiring surgical correction, the case fatality rate is 100% if surgery is not performed. Short-term survival of horses undergoing surgical correction of small intestinal obstruction is 34–74%.^26,27 Mortality rate is greatest in the perioperative period.²⁷ Survival rates vary depending on the nature and severity of the lesion, with long-term survival rates being lower for horses that require resection of intestine, especially for resections of more than 2 m or more than one surgery.^28,29

PATHOGENESIS

The effects of intestinal obstruction and the particular influence of the related endotoxemia in horses have been detailed earlier. The type of lesion is important, depending on whether the blood supply to a large section of intestine is occluded or whether effective circulation is maintained. Obstructions that do not cause widespread intestinal ischemia, such those caused by focal external pressure, such as occurs with some forms of disease caused by pedunculated lipomas, or caused by internal foreign bodies such as phytobezoars, are less acutely lethal and do not cause as severe signs as do volvulus and forms of intussusception that result in ischemia of large sections of intestine. In the latter case, endotoxins from the gut lumen pass through the devitalized tissues of the gut wall into the circulation, resulting in signs of toxemia and cardiovascular collapse.

CLINICAL FINDINGS

CLINICAL PATHOLOGY

While laboratory examinations of animals with intestinal obstruction may not be used in the diagnosis of the obstruction, they are useful in assessing its severity. In general, the laboratory findings in acute intestinal obstruction include the following:

NECROPSY FINDINGS

The physical lesions are characteristic of the disease.

TREATMENT

The principles of treatment of horses with small intestinal obstructive lesions are similar to those of any colic and are set out in detail under Equine colic, above.

Every attempt should be made to relieve the horse’s pain using appro-priate doses of effective analgesics (see Table 5.7). Care should be taken when using flunixin meglumine that signs of a lesion requiring surgical correction are not masked until the severity of the disease makes successful treatment unlikely.

Almost all obstructive lesions of the small intestine require surgical correction. In addition to surgery, attention should be paid to maintaining the horse’s fluid, acid–base and electrolyte status, as discussed under Equine colic and in Chapter 2. Treatment of postoperative ileus should be aggressive and include correction of acid–base, fluid and electrolyte abnormalities, continued gastric decompression through a nasogastric tube and administration of promotility drugs such as cisapride, lidocaine, erythromycin and metoclopramide (Table 5.8).

Ileal impactions can be treated medically by the administration of intravenous fluids, gastric decompression and administration of mineral oil.⁴² Horses treated medically should be closely monitored as prompt surgical intervention may be necessary if the horse’s condition deteriorates.

ETIOLOGY

The etiology of anterior enteritis is unknown. C. difficile might be involved¹ Experimental intoxication with culture media of Fusarium moniliforme produces histological, but not clinical, signs consistent with the disease.²

EPIDEMIOLOGY

The disease is reported from the USA and Europe.^2,3 There is no apparent effect of age, with the exception that the disease is not reported in horses less than 1 year of age and is uncommon in horses less than 2 years of age.⁴ There is no breed or sex predilection for the disease. There are anecdotal reports of farms with a high incidence of the disease, especially among brood mares. Similarly, some consider feeding of large amounts of concentrated feeds to horses to be a risk factor for the disease. Anterior enteritis occurs more commonly in the warmer months.⁴ There are no reports of the incidence, morbidity/mortality of anterior enteritis. The case fatality rate varies from 6% to 75%.^4,5

PATHOGENESIS

The primary lesion is inflammation and edema of the duodenum and jejunum with sloughing of villus epithelium and villus atrophy.⁵ These lesions are probably associated with ileus and failure of small intestinal absorptive function. Fluid accumulation in the atonic small intestine causes distension and pain and reflux of alkaline small-intestinal contents into the stomach. Sequestration of fluid, electrolytes and bicarbonate in the stomach and small intestine causes a reduction in blood volume, shock and metabolic acidosis. Gastric and small intestinal distension and hypovolemia cause tachycardia. Disruption of the small intestinal mucosal barrier allows absorption of toxins, including endotoxins, that further compromise cardiovascular and metabolic function. Death in untreated cases results from acute, diffuse peritonitis secondary to gastric rupture, or shock and metabolic disturbances secondary to hypovolemia and endotoxemia.

CLINICAL FINDINGS

The onset of clinical signs is usually abrupt and characterized by mild to severe colic. Affected horses are depressed, dehydrated and have prolonged capillary refill time and heart rates between 50 and 80/min. The respiratory rate is variable. The horse may sweat profusely and there are muscle fasciculations in severely affected cases. Borborygmi are absent although there may be tinkling sounds of gas bubbling in fluid-filled atonic intestine. Rectal examination usually reveals the presence of multiple loops of moderately to severely distended small intestine. Reflux of fluid through a nasogastric tube is a consistent finding, and usually results in marked relief of pain and resolution of tachycardia. The fluid is often sanguineous, malodorous, alkaline and of large (10–12 L) volume.⁴

Gastric decompression and administration of intravenous fluids results in marked improvement of clinical signs, although affected horses may continue to have nasogastric reflux for 24 hours to 10 days. Most cases resolve within 5 days. If untreated, horses develop severe gastric distension with subsequent rupture and death from peracute, diffuse peritonitis, or die as a result of hypovolemia and toxemia. A common sequela is the development of laminitis. Approximately 10% of horses with anterior enteritis have cardiac arrhythmias, including ventricular depolarizations and atrio-ventricular conduction disturbances.⁶ Arrhythmia resolves with resolution of the anterior enteritis.

CLINICAL PATHOLOGY

There is hemoconcentration with hematocrits as high as 0.70 L/L (70%) and total serum protein as high as 96 g/L (9.6 g/dL) in severely affected horses. The leukogram is variable and not diagnostic – leukocytosis and left shift are common.⁵ Serum potassium concentration may be mildly low and blood bicarbonate concentration and pH are low in most cases. Horses with anterior enteritis have serum bilirubin concentrations and serum gamma-glutamyl transpeptidase, aspartate aminotransferase and alkaline phosphatase activities higher than horses with small intestinal infarctive lesions.⁷ However, the differences are not sufficiently large for these variables to be useful in the differentiation of horses with anterior enteritis from horses with small-intestinal infarctive lesions.

Peritoneal fluid has a normal nucleated cell count in 65% of cases; in the remaining cases it is increased.⁴ Peritoneal fluid protein concentration is often normal in cases sampled early in the disease but may be increased in more severe or prolonged disease and is a useful prognostic indicator.⁸

NECROPSY FINDINGS

Gross lesions are restricted to the stomach, duodenum and jejunum in most cases. The affected stomach and small intestine are distended and the serosal surface has numerous petechial and ecchymotic hemorrhages.⁵ The mucosa is deep red and contains petechial hemorrhages and occasional foci of necrosis and ulceration. Histological changes include neutrophilic inflammation, edema, hyperemia, epithelial sloughing and villus atrophy. There is necrosis of mucosa, fibrin-rich edema and heavy neutrophil infiltration of the submucosa, and extensive hemorrhage in the tunica muscularis and serosa.⁵ A proportion of horses with anterior enteritis have biochemical and histological evidence of liver disease, including hepatocellular vacuolization and neutrophilic inflammation.⁷ Some horses with anterior enteritis have myocarditis.⁶

DIAGNOSTIC CONFIRMATION

Horses with small-intestinal obstructive lesions require urgent surgical correction, while horses with anterior enteritis respond well to medical therapy. The differentiation of anterior enteritis and a small-intestinal obstructive lesion on clinical grounds is difficult and there is no one variable that allows the distinction to be made reliably. Horses with anterior enteritis have a lower heart rate, higher rectal temperature (fever), lower volume of gastric reflux and less turgid small intestine on rectal examination than do horses with obstructive lesions,⁴ although others report that horses with anterior enteritis have a higher volume of reflux at first examination and during the first 24 hours of disease.⁷ However, these differences are not sufficiently great to be conclusive. Horses with anterior enteritis more often have normal peritoneal fluid than do horses with small-intestinal obstructive lesions. The response to gastric decompression and intravenous fluid therapy is useful in discriminating between diseases as horses with anterior enteritis have marked resolution of abdominal pain and tachycardia within minutes of gastric decompression, whereas horses with small-intestinal obstruction have minimal or no resolution of these signs. In general, horses with a heart rate below 60/min after gastric decompression, mildly to moderately distended loops of small intestine, resolution of abdominal pain after gastric decompression and normal peritoneal fluid probably have anterior enteritis. However, horses should be examined frequently for changes in clinical condition. Worsening pain and cardiovascular status in the face of adequate fluid therapy warrant reconsideration of a diagnosis of anterior enteritis.

TREATMENT

The principles of treatment of anterior enteritis are gastric decompression, correction of fluid, acid–base and electrolyte abnormalities and provision of maintenance fluid and electrolytes, relief of pain, and prophylaxis of laminitis.

Gastric decompression is an urgent need in affected horses and can be accomplished by nasogastric intubation. The nasogastric tube should be left in place, or replaced frequently, for as long as there is reflux of clinically significant quantities of fluid (more than 2–4 L/4 h in a 425 kg horse). Discontinuation of gastric siphonage should be approached cautiously and the should be patient monitored for any increase in heart rate or development of abdominal pain that may indicate recurrence of gastric distension. After the nasogastric tube is removed, the horse should be reintroduced cautiously to oral fluids and food. Small amounts (1–2 L) of water should be offered frequently (every 1–2 h) during the first 12–24 hours. Horses should not be given immediate access to ad libitum water as some horses in the early convalescent period from anterior enteritis will consume a large quantity of water and develop gastric dilatation and colic. Feed should be reintroduced gradually over 24–48 hours.

Complications of prolonged or repeated gastric siphonage through a nasogastric tube are pharyngitis, esophagitis, esophageal stricture and esophageal perforation with subsequent cellulitis.

Fluid, electrolyte and acid–base abnormalities should be corrected by the administration of intravenous fluid. Isotonic, polyionic fluids such as lactated Ringer’s solution are suitable. Affected horses may loss considerable chloride and potassium in reflux fluid necessitating supplementation of fluids with potassium (up to 20 mEq/L).

Analgesia can be provided by administration of any of a number of drugs, including flunixin meglumine or ketoprofen (Table 5.7). If the diagnosis of anterior enteritis is uncertain, potent analgesics such as flunixin meglumine should not be used until there is no possibility that a lesion requiring surgical correction exists.

Promotility agents such as lidocaine and cisapride (Table 5.8) and antacids such as cimetidine (Table 5.11) are sometimes administered, although their efficacy has not been determined.⁹

Antibiotics, such as penicillin and an aminoglycoside, are often administered to affected horses because of the presumed bacteremia associated with the disease.

Surgical treatment of the disease is described^3,5 but most cases resolve without surgical intervention.⁴

ETIOLOGY

There is strong support for a role of Anoplocephala perfoliata infestation in cecal disease of horses.^1-3 Infestation with A. perfoliata results in edema, hyperemia and hemorrhagic foci in the ileocecal valve mucosa with light parasitism through regional necrotizing enteritis, with extension of lesions to the muscularis mucosa and eosinophilic inflammation around arterioles and submucosal neural plexus with heavy parasitism.³

Larval cyathostomiasis is also associated with cecocolic and cecocecal intussusception in young horses.⁴ Other causes include intramural and extramural masses, including cecal abscesses, and alterations in cecal and colonic motility.

Disturbed cecal motility or dehydration of cecal contents secondary to dietary changes are thought to be the cause of most cases of cecal impaction and rupture.⁵ Horses with recurrent cecal impaction have lower neurone densities in muscle layers of the base of the cecum and cecal body than do normal horses, supporting the hypothesis that disturbed motility secondary to neuronal abnormalities is a cause of the disease.⁶ Administration of drugs that interfere with cecal motility or secretory function has the potential to increase the risk of cecal disease.

EPIDEMIOLOGY

Cecal disease accounts for approximately 4–10% of colic in horses examined for abdominal pain at referral centers.^7,8

PATHOGENESIS

Cecal impaction is probably a result of impaired or altered cecal motility, with resultant reduced cecal emptying into the right ventral colon.⁵ Accumulation of feed material causes cecal distension and excessive tension in the wall of the cecum with ischemia, necrosis and rupture. Infestation by tapeworms, including A. perfoliata, cause disruption of the cecal mucosa and submucosa, necrosis and inflammation, changes that could contribute to cecal dysfunction.³ Death results from peracute diffuse peritonitis.

Cecal rupture at parturition is probably the result of high intra-abdominal pressures associated with expulsion of the fetus. The pathogenesis of cecal rupture without cecal impaction is unknown.

CLINICAL FINDINGS

CLINICAL PATHOLOGY

Cecal impaction with feed material is usually associated with mild hemoconcentration. Cecal perforation results in severe leukopenia and left shift, hemoconcentration (hematocrit > 50%, 0.50 L/L) and azotemia.

Peritoneal fluid from horses with cecal impaction is usually normal. However, if the cecum becomes ischemic, then the fluid is sanguineous with an elevated white blood cell count (> 8000 cells/μL, 8 × 10⁹ cells/L) and protein concentration (> 2.5 g/dL, 25 g/L).¹⁰ Cecal perforation is evident as a high proportion of degenerate neutrophils, intra- and extracellular bacteria and plant material.

NECROPSY FINDINGS

The distended cecum and diffuse peritonitis are readily apparent. Cases of cecal perforation without distension will have diffuse peritonitis but the cause is only apparent on close examination of the intestinal tract. There is usually no underlying disease apparent on histologic examination.

TREATMENT

Treatment of cecal impaction involves control of pain (Table 5.7), restoration of normal fluid, acid–base and electrolyte status (see Ch. 2), and administration of fecal softeners such as sodium sulfate (Table 5.8). Mineral oil, although frequently used, may not be sufficient alone to facilitate passage of the impaction because it does not cause fecal softening.

Intravenous administration of fluid at 2–3 times maintenance needs is often used in an attempt to hasten fecal softening by increasing secretion of water into the impaction. Oral administration of large quantities of water (4 L every 2 h for 24 h) may soften the impaction.

Horses with cecal impaction should be closely monitored for signs of deterioration, and especially of cecal ischemia, by frequent physical examinations and repeated abdominocentesis. Lack of resolution within 24 hours or signs of deterioration should prompt surgical exploration with typhlotomy and evacuation of the cecum and possible partial cecal bypass.^12,21

Horses with cecal perforation always die and should be euthanized without delay.

Cecocecal and cecocolic intussusceptions must be corrected surgically.

ETIOLOGY

The etiology of these conditions is unknown but presumably involves some disturbance to normal colonic motility. Other causes of obstruction of the large colon include congenital abnormalities of the right ventral colon,¹ cystic duplication of the ascending colon,² defects in the mesocolon³ and incarceration in epiploic foramen or gastrosplenic ligament.^4,5 Intussusception of the large colon causes infarction and severe colic.⁵

The term volvulus refers to rotation of the segment of bowel about the long axis of its mesentery, while torsion refers to rotation about the long axis of the bowel. Because of the anatomical arrangement of the mesocolon, either term may be correctly used to describe displacements of the large intestine.⁵

EPIDEMIOLOGY

Left dorsal displacement of the large colon (Fig. 5.1) is the cause of 2–10% of colic cases referred for specialist treatment.⁶ There is no breed, age or sex predisposition, although some authors suggest that males and large horses are more likely to be affected. The case fatality rate is approximately 5% for horses treated correctly.^7-10

Fig. 5.1 A Left lateral view of abdomen of a normal horse. B Left dorsal displacement of the left colon, left lateral view. The left ventral and dorsal colon is displaced lateral and dorsal to the spleen and occupies the renosplenic space. 1 = liver, 2 = stomach, 3 = left dorsal colon, 4 = left ventral colon, 5 = spleen, 6 = left kidney and renosplenic ligament, 7 = pelvic flexure.

(With permission from Johnston JK, Freeman DE. Vet Clin North Am Equine Pract 1997; 13:317.)

Right dorsal displacement of the large colon (Fig. 5.2) occurs sporadically and without recognized risk factors. The case fatality rate is reported to be as high as 43%.¹⁰

Fig. 5.2 Right dorsal displacement of the colon, right lateral view. The colon has passed lateral to the cecum, the pelvic flexure is displaced cranially and the sternal and diaphragmatic flexures are displaced caudally. 1 = right dorsal colon, 2 = base of cecum, 3 = right ventral colon, 4 = liver, 5 = cecum, 6 = left ventral colon, 7 = pelvic flexure.

(With permission from Johnston JK, Freeman DE. Vet Clin North Am Equine Pract 1997; 13:317.)

Risk factors for noninfarctive displacement of the large colon include cribbing or wind sucking (odds ratio (OR) = 90), number of hours stabled per day (OR for 24 h stabling = 35), lack of regular exercise (OR = 3.3), change in exercise program (OR = 9), lack of anthelmintic administration (OR = 13) and history of transport in the previous 24 hours (OR = 17).¹¹

Volvulus of the large colon is the cause of colic in 11–17% of colic cases in which abdominal surgery is performed.¹² The disease occurs commonly in mares, especially those late in gestation or having recently foaled.^13,14 The disease has a recurrence rate of up to 15% in brood mares.¹⁵ The disease occurs in horses from 2 days of age and there does not appear to be an effect of breed on occurrence of the disease.¹⁶ The case fatality rate varies depending on the extent of the volvulus, with lesser degrees of volvulus (< 270°) having a 30% fatality rate and volvulus of 360° or more having a 65% fatality rate.¹³

Ingestion of large quantities of grain, such as might be fed to horses in heavy work, is associated with changes in plasma electrolyte concentrations, presence of dehydrated, foamy and homogeneous right dorsal colon contents, and fetid, less formed feces.¹⁷ These effects of a high-grain diet may be associated with colonic disease in horses.¹⁷

PATHOGENESIS

Proximate factors leading to volvulus or displacement are unknown, although risk factors have been identified (see above). A plausible scenario is that altered colonic motility and subsequent distension with gas or ingesta predisposes the colon to displacement, either spontaneously or as a result of the horse rolling or lying down in response to abdominal pain.

Left dorsal and right dorsal displacements of the colon rarely compromise colon blood flow and represent nonstrangulating obstructive lesions. Pathogenesis in equine colic section). The displacement of the large colon (Figs 5.1 & 5.2) impedes aboral movement of ingesta and gas and may result in colonic distension. Should the distension become sufficiently severe, colon blood flow will be impaired and cause ischemia and necrosis of the colon. The obstruction to blood flow is predominantly in venous drainage, resulting in hemorrhagic strangulating obstruction with progressive development of intramural edema, extravasation of red blood cells, microvascular thrombosis, mesothelial cell loss from the serosal surface, and mucosal necrosis with loss of colonic epithelium.¹⁸

Volvulus of the large colon of less than 270° does not compromise blood supply but does impede aboral movement of ingesta and gas.¹³ Volvulus of 360° or more causes ischemia through occlusion of both arterial and venous circulation of the involved large colon with rapid loss of colonic mucosal integrity and colon viability. Irreversible mucosal damage occurs after 3–4 hours of ischemia. Loss of mucosal integrity impairs normal barrier function and permits toxins and substances normally confined to the colonic lumen to enter the systemic circulation. Additionally, loss of barrier function allows leakage of vascular proteins and in severe cases red blood cells into the colonic lumen. Subsequent signs are typical of strangulating obstruction (see Equine colic) with development of toxemia, cardiovascular collapse and death within 12–18 hours.

The most common displacement is medial and dorsal movement of the ventral colon to complete a 360° volvulus of the large intestine (Fig. 5.3).¹⁶ Lateral and dorsal displacement of the ventral colon is much less common. The volvulus is usually at the level of the cecocolic fold, although volvulus involving the cecum or at the diaphragmatic and sternal flexures does occur.

Fig. 5.3 A 360° clockwise volvulus of the colon viewed from the right side. The volvulus has occurred in the direction of the arrow. 1 = cecum, 2 = right dorsal colon, 3 = right ventral colon.

(With permission from Johnston JK, Freeman DE. Vet Clin North Am Equine Pract 1997; 13:317.)

CLINICAL FINDINGS

CLINICAL PATHOLOGY

Changes in the hemogram, serum biochemical profile and peritoneal fluid are non-existent to mild in horses with uncomplicated left dorsal displacement, right dorsal displacement and volvulus of less than 270°. Horses with ischemic colon as a result of strangulation usually have a leukopenia with left shift, hemoconcentration and increased anion gap.¹⁶

Serum gamma glutamyl transferase (GGT) activity is elevated in approximately 50% of horses with right dorsal displacement of the colon, whereas such elevations are rare in horses with left dorsal displacement.²¹ The elevated GGT, and less commonly serum bilirubin concentration, in horses with right dorsal displacement is attributable to compression of the common bile duct in the hepatoduodenal ligament by the displaced colon.²¹

Horses with large-colon volvulus have a high prevalence of abnormalities in hemostatic variables, including thrombin– antithrombin concentration, d-dimer concentration, antithrombin activity, prothrombin time and platelet count. Nonsurviving horses have lower platelet counts, increased prothrombin time and reduced antithrombin activity.²²

Peritoneal fluid often has an increased total protein concentration (> 25 g/L, 2.5 g/dL) and white blood cell count (> 8000 cells/μL, 8 × 10⁹ cells/L) in horses with compromised bowel. Examination of peritoneal fluid is often not necessary to achieve a diagnosis in horses with colon torsion, although it does have prognostic value in that horses with blood-tinged peritoneal fluid have a poor prognosis. The risk of inadvertent enterocentesis is increased in horses with severe distension of the colon and abdominocentesis should be attempted with caution in such cases. Use of a bovine teat cannula or similar blunt instrument is preferred to the use of a needle.

NECROPSY FINDINGS

The colon is displaced as described above for each of the diseases. Death usually results from ischemic necrosis of the colon and the associated peritonitis, endotoxemia and shock. Histological lesions in horses dying of colon volvulus are more severe than of those that survive and are characterized by hemorrhage into the lamina propria, edema and loss of the mucosal cells and crypt architecture.¹³

TREATMENT

Treatment should consist of pain control, correction of fluid, acid–base and electrolyte abnormalities, support of cardiovascular function and correction of the underlying disease (Equine colic). Decompression by trocarization of gas-distended colon or cecum may be beneficial. Correction of colon volvulus or right dorsal displacement of the colon requires surgical exploration of the abdomen and manual correction of the displacement.

Left displacement

Correction of left dorsal displacement can be achieved by either nonsurgical or surgical means. Nonsurgical correction is achieved by rolling the anesthetized horse in a particular sequence that causes the displaced colon to return to its normal position in the abdomen. Nonsurgical correction is successful in approximately 80% of cases,^7,27 although complications are reported,²⁸ and is recommended as the initial definitive treatment for horses with uncomplicated left dorsal displacement.²⁷ The sequence of events following diagnosis of the condition is depicted in Figure 5.4.²⁹ Phenylephrine (0.02–0.04 mg/kg, intravenously as a 10 min infusion) causes splenic contraction and is thought to increase the chances of the colon returning to its normal position. The horse is anesthetized within 10 minutes of phenylephrine administration and placed in right lateral recumbency. The horse is then slowly rolled into dorsal recumbency and the abdomen is vigorously massaged in an attempt to cause the colon to move ventrally and medially. If a hoist is available the horse can be lifted into dorsal recumbency. The sequence ends with the horse being rolled into left lateral recumbency and a rectal or ultrasound examination being performed to determine the position of the colon.

Fig. 5.4 Steps in correction of left dorsal displacement of the colon (renosplenic entrapment). A Caudal view of abdomen of horse with left dorsal displacement of the colon. Entrapped colon is shown in black; K = left kidney, S = spleen. B Injection of phenylephrine and contraction of spleen. C Horse anesthetized and placed in right lateral recumbency. D–H Horse rolled through dorsal recumbency to left lateral recumbency. Entrapped colon moves ventrally and then medially to the contracted spleen.

(Modified with permission from Kalsbeek HC. Equine Vet J 1989; 21:442.)

An alternative means of nonsurgical correction involves administration of phenylephrine (0.01 mg/kg, intravenously, slowly) and then jogging the horse.^30,31 This technique was successful in correcting the displacement in 11 of 12 horses.³¹ It may be advantageous to relieve large-colon distension by percutaneous trocarization before jogging.⁹

Cases that are refractory to nonsurgical treatment require laparotomy (ventral midline or left flank) and manual correction of the displacement. Recurrence of the displacement occurs in 3–7% of cases.⁷ Horses with recurrent disease may benefit from surgical ablation of the nephrosplenic space.³²

ETIOLOGY

The cause of most impactions of the large colon is unknown. Known or speculated causes include:

EPIDEMIOLOGY

The disease occurs in horses of any age and is more common in females.⁶ There does not appear to be a breed predisposition. The disease represented 13% of colics treated at a referral facility.^6,7 An important risk factor is a change in management, especially one that involves a reduction in exercise and change in diet.⁶ Risk factors for nonstrangulating disease of the large colon, including pelvic flexure impaction, include cribbing or wind sucking, stabling with the risk increasing with the number of hours stabled per day, change in regular exercise program, travel within the previous 24 hours and lack of anthelmintic administration.⁸ The case fatality rate is approximately 1–20%.^6,7

PATHOGENESIS

Development of impaction of the large colon is frequently attributed to abnormal colonic motility.⁹ Other factors, including mild dehydration as a result of limited water intake or ingestion of poorly digestible material, cause impaction in many instances. Ingestion of large quantities of grain, such as might be fed to horses in heavy work, is associated with changes in plasma electrolyte concentrations, presence of dehydrated, foamy and homogenous right dorsal colon contents, and fetid, less formed feces.¹⁰ These effects of a high grain diet may be associated with colonic disease in horses.¹⁰ The end result is accumulation of a large mass of inspissated feed material in the large colon. Material usually accumulates first at the pelvic flexure or right dorsal colon, presumably because of the reduction in lumen diameter at those points. Accumulation of inspissated material causes distension of the colon and prevents aboral passage of ingesta. Distension causes pain and changes in colonic motility that exacerbate or perpetuate the impaction. If the distension is sufficiently severe or prolonged the colon may become ischemic and necrotic with subsequent rupture, peracute diffuse peritonitis and death.

CLINICAL FINDINGS

Moderate abdominal pain is the typical sign in affected horses and pulse rate and respiration are relatively normal. This often continues for 3–4 days and sometimes for as long as 2 weeks. The horse is not violent, the principal manifestation of pain being stretching out and lying down and the bouts of pain are of moderate severity occurring at intervals of up to a half-hour. There is anorexia and the feces are passed in small amounts and are hard and covered with thick, sticky mucus. Intestinal sounds are absent or much decreased in intensity. The pulse rate is usually less than 50/min.

On rectal examination impaction of the pelvic flexure of the large colon is the commonest site and the distended, solid loop of the intestine often extends to the pelvic brim or even to the right of the midline. Lying on the floor of the abdomen, it is easily palpated, the fecal mass can be indented with the fingers and the curvature and groove between the dorsal and ventral loops of the left colon can be easily discerned. Impaction of the right dorsal colon cannot usually be palpated per rectum and the only abnormality may be distension of the colon with soft ingesta that has accumulated behind the obstruction.

CLINICAL PATHOLOGY

Hemogram, blood chemistry and peritoneal fluid are normal until the colon becomes ischemic at which time there is a leukopenia with left shift, and an increase in the white blood cell count and protein concentration in peritoneal fluid.

NECROPSY FINDINGS

The large intestine is packed full of firm, dry fecal material and rupture may have occurred.

TREATMENT

The principles of treatment are pain control, correction of fluid and electrolyte abnormalities and softening of ingesta to facilitate its passage. Pain control is discussed in Table 5.7. Fluid therapy is discussed in Chapter 2.

Softening of ingesta is achieved by rehydrating the inspissated material and providing lubrication to hasten its passage. Fecal softeners (Table 5.8) such as magnesium sulfate or sodium sulfate can be given to increase the fecal water content and soften the impacted, inspissated ingesta. Magnesium sulfate is associated with a small risk of hypermagnesemia and neurologic signs¹² whereas sodium sulfate causes a mild hypernatremia and hypokalemia.¹³ Oral administration of a balanced, polyionic electrolyte solution is associated with the greatest increase in colonic water content and no change in serum electrolyte concentrations.¹³ Enteral administration of 10 L/h (to a 500 kg horse) of a balanced, isotonic, polyionic electrolyte solution is more effective than intravenous administration of the same quantity of fluid in combination with oral administration of MgO₄ in hydrating colonic contents in normal horses.¹⁴ Mineral oil (Table 5.8) is a lubricant and may not penetrate the impacted ingesta sufficiently to soften the material although it is frequently given to horses with colon impaction.

Overhydration by oral administration of polyionic, isotonic fluids at 3–5 times maintenance needs (approximately 10 L/h) is the treatment of choice for colon impaction.^6,13 Water can be given by nasogastric tube at a rate of 4–10 L for a 450 kg horse every 1–2 hours until the impaction softens. However, some horses develop decreased small intestinal motility or ileus with the disease, have delayed gastric emptying and have reflux of fluid through the nasogastric tube. Such horses should not be administered any medication or water through the nasogastric tube until reflux has resolved. Alternatively, isotonic fluids can be given intravenously at 10 mL/kg/h until the impaction is passed.

Promotility agents such as neostigmine are usually contraindicated because of the risk of rupture of the distended colon when vigorous contractions are induced pharmacologically.

Horses may need to be treated for 1–6 days until the impaction resolves and should not be fed during this time. When feed is again provided it should be easily digestible and initially be of limited volume. Horses recovered from impaction of the large intestine have a higher than expected rate of recurrence of colic (30%).⁶

Surgical treatment may be needed for refractory cases (about 15%) but is associated with a poor prognosis because of the risk of iatrogenic rupture of the colon during attempts to exteriorize it from the abdomen during surgery.⁶ Impaction of the right dorsal colon is more likely to require surgical treatment.¹⁵

ETIOLOGY

Enteroliths are rock-like concretions, which are either spherical or tetrahedral, that form in the large colon of horses, usually around a foreign body.¹ Most enteroliths in the large colon of horses are of two major types: magnesium phosphates/struvite and magnesium vivianite.^1,2 There is wide variability in macrotexture and ionic concentrations between and within enteroliths of ammonium magnesium phosphate (struvite).¹ Affected horses often have more than one enterolith and the enteroliths can weigh up to 12 kg.

Fecaliths are aggregations of indigestible material, such as fencing, plastic or rope, that often have an irregular shape.

EPIDEMIOLOGY

Enteroliths occur sporadically in horses in most regions of the world but there is a greater than expected incidence in certain areas, such as California.³ Equids with enterolithiasis represented 15.1% of patients admitted for treatment colic, and 27.5% of patients undergoing celiotomy for treatment of colic in a study from California but less than 2% of horses with colic examined at a referral center in Texas.^4,5 Arabians and Arabian crosses, Morgans, American Saddlebreds and donkeys are over-represented, and Thoroughbreds, Standardbreds, warmbloods and stallions are under-represented in some studies, suggesting a predilection of these breeds for the disease.^3-5 Enteroliths rarely occur in horses less than 4 years of age and are more common in older horses (> 11 years).^4,6 The disease is reported in American Miniature Horses.⁷ Feeding alfalfa hay and stabling for more than 12 hours a day are associated with increased risk of enterolithiasis.^5,8 The mean pH of colonic contents from horses with enterolithiasis is significantly higher than for control horses and horses with enterolithiasis have a significantly lower percentage of dry matter in colonic fecal samples and higher mean mineral concentrations than controls.⁸ About 15% of cases examined at referral institutions that see large numbers of cases develop a ruptured viscus caused by the enterolith and die. The long-term survival rate of horses treated surgically is approximately 90%.⁴

Fecaliths occur sporadically and appear to be more common in younger horses, perhaps because of their propensity to dietary exploration and ingestion of foreign materials.

PATHOGENESIS

The mechanism underlying enterolith formation is not known. Enteroliths are formed in the large colon and, rarely, the cecum. They are clinically inapparent, even if quite large, until they cause obstruction of aboral passage of ingesta, usually by occluding the right dorsal or transverse colon. Occasional enteroliths pass into the small colon. Obstruction of the colon causes mild to moderate, often intermittent, colic, presumably when the enterolith or fecalith obstructs the colon, with the pain resolving when the enterolith moves and the obstruction clears. Complete obstruction results in obstruction of aboral movement of ingesta, accumulation of gas and ingesta proximal to the obstruction and distension of the large colon. There is no loss of integrity of the colon early in the disease but with time and distension there is ischemia and necrosis of the colon, with subsequent perforation, development of acute peritonitis, and death.

CLINICAL FINDINGS

The most common historic manifestation of enterolithiasis in horses is recurrent, intermittent colic (about one-third of cases), often with passage of enteroliths in feces (about 10% of cases).^4,9 Horses with acute obstruction have signs typical of obstructive, nonstrangulating disease of the large colon, including mild to moderate colic with failure to pass feces. The heart rate is 50–70/min, borborygmi are decreased but not absent, and there is mild abdominal distension. Rectal examination may reveal mildly distended large colon but the offending enterolith is never palpable, except on the rare occasion that the enterolith or fecalith is lodged in the small colon. Over a period of 6–12 hours the severity of pain increases and there is readily apparent distension of the large colon. There is usually no reflux through a nasogastric tube. The terminal phase, which may take 72 hours to occur and is due to rupture of a viscus, is marked by moderate to severe pain, abdominal distension, tachycardia (> 80/min), decreased capillary refill time and discolored mucous membranes, sweating, muscle fasciculations and death. Rupture of a viscus and acute peritonitis occurs in approximately 15% of cases.⁴

Radiography of the abdomen is useful in identifying enteroliths in horses with colic.^10,11 The accuracy of the diagnosis is approximately 80% for enteroliths in the large colon and 40% for those in the small colon.¹¹ The most common reason for not detecting an enterolith is poor imaging of the abdomen because of inadequate penetration by the X-ray beam,¹¹ emphasizing the need for appropriate radiographic equipment.

CLINICAL PATHOLOGY

There are no diagnostic changes in the hemogram, serum biochemical profile or examination of peritoneal fluid. Horses with enteroliths have higher serum bilirubin concentrations on examination at referral centers, but this change is not sufficiently large to be useful as a diagnostic aid.⁵ Similarly, horses with enteroliths have higher protein and white cell counts in peritoneal fluid than do horses with other forms of colic but again these differences are too small to be of diagnostic significance.⁵ Changes in hematological and biochemical variables during the terminal phases of the disease are characteristic of acute, diffuse peritonitis and include leukopenia with left shift, hemoconcentration and azotemia.

NECROPSY FINDINGS

Enteroliths are frequent incidental findings at necropsy examination of mature horses and their presence should not be overinterpreted. Obstructive disease caused by an enterolith is characterized by colon distension, presence of an enterolith in the right dorsal, transverse or small colon and, in cases dying of the disease, acute diffuse peritonitis resulting from colon rupture or perforation at the site of the enterolith. Tetrahedral enteroliths with sharp points are believed to be more dangerous than are spherical enteroliths.⁶

TREATMENT

The definitive treatment is surgical removal of the enterolith. Supportive care including analgesia and fluid therapy should be provided as described under Equine colic.

CONTROL

Prevention of ingestion of foreign bodies, such as small pieces of metal, may decrease the incidence of the disease.³ Strategies that decrease fecal pH and mineral content of feces might also decrease the incidence of the disease.⁸

ETIOLOGY

EPIDEMIOLOGY

Small colon disease is present in approximately 2.5–5% of horses treated for colic at referral institutions and small colon impaction represents approximately 2% of horses with colic.^1,2,10 Aged female horses are most commonly affected although the conditions can occur in horses of any age.³ Arabians, ponies and Miniature horses are reported to be at increased risk of small colon disease although others have not detected this apparent predilection.^3,10. Rupture of the mesocolon occurs during parturition.⁴ The case fatality rate depends on the condition and is 30–40% for impaction of the small colon.^2,10 Small colon impaction can occur as limited outbreaks in a number of horses on a single farm over a period of days to weeks, without obvious predisposing causes or inciting events.

PATHOGENESIS

Obstruction of the small colon causes accumulation of ingesta and gas in the small colon aboral to the obstruction and in the large colon, with subsequent distension, pain and reduced motility. Distension of the small colon may impair blood flow with subsequent ischemia, necrosis and rupture or perforation of the small colon. Incarceration of the small colon results in ischemia of the entrapped segment and restriction of flow of ingesta. Subsequent signs are characteristic of toxemia and intestinal obstruction. The high proportion of affected horses from which Salmonella spp. are isolated suggests a role for colitis in the pathogenesis of small colon impaction.^2,10

CLINICAL FINDINGS

CLINICAL PATHOLOGY

There are no characteristic changes in the hemogram or serum biochemical profile. Peritoneal fluid is normal until the viability of the small colon is compromised, at which time the protein concentration and white blood cell count increase. Salmonella spp. are isolated from approximately 20% of cases of small colon impaction, suggesting a role for colitis in the pathogenesis of the disease.¹⁰

NECROPSY FINDINGS

Small colon impaction is evident as a tubular column of firm ingesta in the small colon with large colon distension. Small colon accidents, such as rupture of the mesocolon at parturition and intussusception, are readily apparent.^4,8

TREATMENT

ETIOLOGY

Spasmodic colic occurs sporadically and causative factors are not usually identified. Suggested causes include excitement, such as occurs during thunderstorms, preparations for showing or racing, and drinks of cold water when hot and sweating after work, although epidemiologic evidence of these associations is lacking. Presence of a heavy burden of tapeworms is associated with a high incidence of spasmodic (undiagnosed) colic.¹ Mucosal penetration and submucosal migration of Strongylus vulgaris larvae are known to cause changes in ileal myoelectrical activity that could lead to the development of colic in horses.² Psychogenic colic occurs rarely in horses.³

EPIDEMIOLOGY

The condition is sporadic. It affects horses of all ages but is not recognized in young foals. No apparent breed or sex predisposition is noted.

PATHOGENESIS

The hypermotility of spasmodic colic in horses is thought to arise by an increase in parasympathetic tone under the influence of the causative factors mentioned above.

CLINICAL FINDINGS

Spasmodic colic of horses is characterized by brief attacks of abdominal pain. The pain is intermittent, the horse rolling, pawing and kicking for a few minutes, then shaking itself and standing normally for a few minutes until the next bout of pain occurs. Intestinal sounds are often audible some distance from the horse and loud, rumbling borborygmi are heard on auscultation. The pulse is elevated moderately to about 60/min and there may be some patchy sweating, but rectal findings are negative and there is no diarrhea. Rectal examination is usually unremarkable. The signs usually disappear spontaneously within a few hours.

CLINICAL PATHOLOGY AND NECROPSY FINDINGS

Laboratory examinations are not used in diagnosis and the disease is not fatal.

TREATMENT

Acute hypermotility as manifested by spasmodic colic is usually transient and the use of specific spasmolytics is not necessary. Detomidine, xylazine or butorphanol are effective analgesics. Administration of hyoscine is effective. Affected horses are often administered mineral oil (1 mL/kg) by nasogastric intubation.

ETIOLOGY

The cause of most cases of idiopathic intestinal tympany is unknown, although the ingestion of highly fermentable green feed is considered to be a risk factor. Feeding of rations rich in grains is associated with changes in colonic contents that might predispose to tympany.¹ Intestinal tympany occurs secondary to obstructive diseases that prevent aboral passage of ingesta and gas.

PATHOGENESIS

The excessive production of gas or its retention in a segment of bowel causes distension and acute abdominal pain. Intestinal distension reduces intestinal motility and may contribute to the course of the disease. Severe tympany may interfere with normal respiration and cardiovascular function (see Pathogenesis of equine colic).

CLINICAL FINDINGS

Abdominal distension is evident and pain is acute and severe. Peristaltic sounds are reduced but fluid may be heard moving in gas-filled intestinal loops, producing a tinkling, metallic sound. Pinging sounds consistent with tightly distended viscus may be heard on simultaneous flicking and auscultation of the abdomen. On rectal examination, gas-filled loops of intestine fill the abdominal cavity and make proper examination of its contents impossible. In primary tympany much flatus is passed. It is important to differentiate primary tympany from that occurring secondary to obstructive diseases such as enterolithiasis and displacement of the colon.

CLINICAL PATHOLOGY

Laboratory examinations are of no value in diagnosis.

NECROPSY FINDINGS

In cases of secondary tympany, the causative obstruction is evident. In primary cases, the intestines are filled with gas and the feces are usually pasty and loose.

TREATMENT

The principles of treatment are the relief of pain and distension, maintenance of hydration and reduction of gas production. In secondary tympany the primary disease should be identified and treated.

Pain should be relieved by administration of xylazine, detomidine or butorphanol, or similar agents (Table 5.7). Distension of the bowel should be relieved by trocarization but trocarization should only be performed if there is no or minimal response to analgesic medication and no return of normal peristaltic activity. Normal hydration should be restored by intravenous administration of polyionic fluids. Intestinal gas production should be minimized by the administration of mineral oil or a similar laxative (Table 5.8).

ETIOLOGY

Unknown, although it is presumed to result from thromboemboli originating at sites of verminous arteritis in the cranial mesenteric artery.

EPIDEMIOLOGY

The disease is assumed to be more prevalent among horses on poor parasite control programs; however, except in extreme cases that die and have a necropsy examination or exploratory laparotomy, the diagnosis is not confirmed. Therefore accurate measures of its incidence are not available. Cases may occur in foals as young as 3–6 months.¹ The incidence of the disease has decreased remarkably with the advent of effective broad-spectrum anthelmintics and almost complete prevention of Strongylus spp. infection in horses in developed countries.

PATHOGENESIS

Migration of the larvae of Strongylus vulgaris into the wall of the cranial mesenteric artery and its branches occurs commonly in horses and may cause thromboemboli that restrict blood supply to the intestines, with subsequent ischemia and dysfunction.² The recurrent colic of verminous arteritis is possibly due to impairment of the vascular and nerve supply to the intestine. The disease is basically an infarction of bowel wall without displacement of the bowel. The small intestine, colon and cecum can be affected. The disease has been associated with larval cyathostomiasis.³

CLINICAL FINDINGS

Signs vary depending on the severity of the disease. It is assumed that mild, intermittent colics that respond to analgesics in the short term and anthelmintics in the long term are due to verminous arteritis. Affected horses are often depressed and spend long periods recumbent. Weight loss and inappetence are features of the disease in some horses. The disease can have a course of weeks to months.

Acute, severe cases of the disease are due to infarction of parts or all of the small intestine, cecum or colon. Affected horses have an acute onset of severe abdominal pain, tachycardia (> 100/min) and sweating. Auscultation reveals decreased borborygmi. There is mild distension of small intestine or large colon, depending on the segment of bowel affected, on rectal examination. There are rarely signs of intestinal obstruction. Palpation of the cranial mesenteric artery may reveal thickening and pain but is not a useful diagnostic sign for the acute disease. Death is due to peritonitis secondary to devitalization of the intestine, usually within 24 hours of the onset of signs.

CLINICAL PATHOLOGY

There are no diagnostic changes in the hemogram or serum biochemical profile. Peritoneal fluid in mild cases may have mild elevations in protein concentration and white blood cell count. In severe cases, peritoneal fluid protein concentration is increased (> 25 g/L, 2.5 g/dL) as is white blood cell count (9000–100000 cells/μL, 9–100 × 10⁹ cells/L).⁴

NECROPSY FINDINGS

Infarction of the colon and cecum is most common and evident as either gangrene of large sections of the organ or multifocal mottled lesions that are red and edematous. Histological examination rarely reveals the presence of thrombi. There may be verminous arteritis of the cranial mesenteric artery, evident as thickening of the intima and narrowing of the lumen.

TREATMENT

Mild, recurrent cases are treated with analgesics such as flunixin meglumine (Table 5.7), laxatives such as mineral oil (Table 5.8), and anthelmintics (ivermectin 200 μg/kg orally once; or fenbendazole 50 mg/kg orally every 24 h for 3 d).

Severe cases are treated with analgesics (Table 5.7), intravenous fluids (Ch. 2) and supportive care. Usually the severity of the colic prompts surgical exploration of the abdomen with resection of small lesions. Most severe cases do not survive.