Digestive System 2 PDF

Horses may be reluctant to take the bit, shake their head when being ridden, or resist training techniques due to irregularly worn cheek teeth and sharp edges on the maxillary cheek teeth and accompanying buccal mucosa laceration. The presence of “wolf” teeth in horses may or may not be associa...

Horses may be reluctant to take the bit, shake their head when being ridden, or resist training techniques due to irregularly worn cheek teeth and sharp edges on the maxillary cheek teeth and accompanying buccal mucosa laceration. The presence of “wolf” teeth in horses may or may not be associated with resistance to the bit. Irregular Wear Except for pigs, most large animals have an intermandibular space that is narrower than the intermaxillary space; that is, they are anisognathic. Periodontal Disease In all animals, a degree of inflammatory change occurs during the eruption of both the deciduous and permanent teeth. However, if malocclusion occurs, severe periodontal disease is inevitable. In horses, this is a common sequela of oral trauma, dental fractures, impactions, and most importantly irregular wear. Dental Decay Infection may be introduced into the pulp chamber of the teeth by various routes, eg, after amputation of teeth (in pigs or in new world camelids). In horses, hypoplasia of the enamel of the upper cheek teeth may predispose to caries of cementum and subsequent pulpitis and apical osteitis. Depending on the site of the tooth that is decayed, there may be accompanying signs of maxillary sinusitis, local cellulitis, periostitis, alveolar periodontitis, and fistula formation. When dental decay is advanced, extraction of the affected tooth is recommended. Small animal Dentistry Periodontal Disease This bacterial infection of the tissue surrounding the teeth causes inflammation of the gingivae, periodontal ligament, cementum, and alveolar bone. Ultimately, teeth are lost due to the loss of their supporting tissues. This is the major reason for tooth loss in dogs. Etiology and Pathogenesis: Periodontal disease is caused by gross accumulation of many different bacteria at the gingival margin due in part to a lack of proper oral hygiene. Over a period of weeks, the flora changes from nonmotile, gram-positive, coccoid, aerobic bacteria to more motile, gram-negative, rod-shaped, anaerobic bacteria. As the local bacterial flora increases in mass to 10-20 times normal, gingivitis occurs. The accumulation of bacterial metabolic products increases epithelial permeability in crevicular epithelial desmosomes and allows antigens to contact connective tissue. Metabolic products of bacterial metabolism include hydrogen sulfide, ammonia, endotoxin, hyaluronidase, chondroitin sulfatase, mucopeptides, lipoteichoic acids, acetate, butyrate, isovalerate, and propionate. These bacterial products and host defense mechanisms cause tissue necrosis. Polymorphonuclear leukocytes (PMN) migrate through the sulcular epithelium and form a barrier between the subgingival bacteria and the gingiva. With overwhelming bacterial challenge, PMN die in increasing numbers and release breakdown products. The immune system produces lymphokines that participate in tissue destruction, which follows the path of the local vascular supply. Accelerated tissue destruction and inappropriate repair cause loss of periodontal support. Two forms of disease are recognized: gingivitis and periodontitis. In gingivitis, the inflammation of the marginal gingival tissues is induced by bacterial plaque and does not affect the periodontal ligament or alveolar bone. There is a change from coral-pink to red or purple, swelling of the gingival margin, and a serous or purulent exudate in the sulcus. The gingivae tend to bleed on contact. Fetid breath is common. Gingivitis is reversible with proper tooth cleaning but, if untreated, may lead to periodontitis. In periodontitis, the destructive inflammatory process of the periodontium is induced and driven by bacterial plaque that contains specific bacteria that destroy the gingiva, periodontal ligament, alveolar bone, and root cementum. It usually occurs after years of plaque, calculus, and gingivitis. It is irreversible and results in permanent loss of tooth support. There is apical migration of the epithelial attachment and resorption of supporting alveolar bone. Affected teeth may show increased mobility, concurrent gingivitis, and subgingival calculus. Dogs on a hard diet develop fewer problems due to the mechanical cleaning effect of the food. Caudal teeth have more problems than rostral teeth. The maxilla is affected more severely than the mandible, and buccal surfaces have more disease than lingual surfaces. Gingivitis often becomes severe at ~2 yr of age but resolves if treated. Periodontitis usually begins at 4-6 yr of age and, if untreated, progresses to tooth loss. Treatment: The basic principle is that active periodontal disease will not develop around a clean tooth. Gingivitis usually can be treated by thorough cleaning of the teeth, including below the gingival margin. Merck Veterinary Manual - Summary 28  Periodontitis needs to be treated with thorough cleaning above and below the gum line. In areas of increased subgingival depth (>4 mm), surgical means (usually gingivectomy) should be used to gain access to the root surface for cleaning. Teeth can generally be salvaged until they have lost 75% of their bone support from one or more roots. This can be evaluated by radiography of the jaws, which should be performed if periodontal disease is advanced. Infrabony defects (defects below the crest of the alveolar bone) require flap surgery. Defects on the palatal surface of maxillary canine teeth, which are infrabony in character and invade or approximate the nasal cavity, should be treated with infrabony grafting procedures before a decision is made to extract the tooth. Extraction of such teeth frequently leaves oronasal fistulas, which require surgical repair. Gingival Hyperplasia (Fibromatosis gingivae, Fibromatous epulis, Epulis) This benign overgrowth of the epithelial and connective tissue of the gums usually originates near the gingival margin. The tissue is relatively insensitive and tough and has the density of fibrous connective tissue. The growths usually have a broad base of attachment, are the color of the normal gum or more pale, and may grow large enough to completely cover the surfaces of several teeth. Predisposition may exist among brachycephalic breeds, in which the condition is termed familial gingival hypertrophy. Epulis sometimes refers to giant-cell epulis or tumor of the gum of dogs. This tumor usually is localized to a single tooth. Biopsy is encouraged to assure proper diagnosis, treatment, and prognosis. Gingival hyperplasia is most common in older dogs and is usually asymptomatic. Hair, food, and debris may collect between the growth and the teeth and cause irritation and halitosis. Gingivectomy by electrosurgical techniques is the most satisfactory treatment. Endodontic Disease Pulpal Hyperemia: The pulp may become acutely inflamed due to trauma or extension of lesions adjacent to the pulp (eg, caries and resorption). Because the pulp is totally confined in dentin, inflammatory swelling may result in pressure necrosis if the insult is prolonged. Severity of the reaction appears to be directly proportional to the extent of injury. Therefore, small injuries that produce transient hyperemia of the pulp may resolve, and a healthy pulp may be reestablished. Steroid therapy is indicated immediately after trauma. Cleaning out carious lesions and placing zinc oxide eugenol into resorptions and former carious areas may allow local anesthesia and resolution of hyperemia. Pulpitis: Inflammation of the pulp with pressure necrosis and abscessation is irreversible. In general, the abscess cavity is initially sterile unless the tooth has been opened to the oral environment by trauma, resorption, or caries. Teeth with pulpitis often are acutely painful, and the animal resents manipulation or percussion of the tooth. As the pulp dies and gas pressure increases in the pulp cavity, blood is forced into the dentinal tubules and the teeth often change to a reddish brown or dark gray color. Periapical Lesions: A periapical abscess is a cavitational lesion at the end of the root due to pulpal disease. These areas generally can be seen on radiographs as radiolucent circular areas around the end of the root. Such abscesses can sometimes be palpated over the bony prominence of root ends. Abscesses may extend by pressure drainage into adjacent bone and soft-tissue areas and exit extraorally into the soft-tissue space between the jaws, beneath the eye, or into the buccal vestibule. Treatment is endodontic therapy (root canal) on the associated tooth, and the abscess and associated fistula usually resolve within a few weeks. When endodontic therapy cannot be done, the tooth should be extracted. Dental Caries Dental decay is uncommon in dogs and cats, possibly because of differences in oral flora, diets largely free of readily fermentable carbohydrates, and the slightly alkaline pH of canine saliva. In dogs, decay usually is seen as pits on the flat surfaces or on the necks of the molar teeth. “Neck” Lesions in Cats In domestic cats, a destructive disease involving tooth crown and roots is commonly called “neck” lesions. Three variations of this disease have been recognized: cervical line erosions, external odontoclastic resorption, and internal odontoclastic resorption. Merck Veterinary Manual - Summary 29  Cervical line erosions are characterized by a superficial loss of enamel from the crown of the tooth with clean dentin margins. The cause of cervical line erosions is unknown but may have dietary implications. This group represents ~10% of the neck lesions in the feline population. External odontoclastic resorption represents ~70% of the neck lesions in cats. It is characterized by the presence of osteoclasts, odontoclasts, and osteoblasts in the lesion. While restorative techniques are moderately successful in early lesions, most restoration attempts are futile, and extraction is the treatment of choice. Internal odontoclastic resorption starts as a destructive process in the odontoblast layer inside the tooth and extends into the dentin. Vasodentin, found in the dentinal layer of feline teeth, may also act as a site for resorption to start. Ultimately, tooth perforation occurs. Treatment in the early stage includes root canal treatment when feasible. In all three forms of “neck” lesions, dental radiography is essential to determine whether treatment is feasible. Feline Stomatitis Complex The oral cavity of the domestic cat may react intensely to disease and result in painful, severe inflammation of the oral cavity. Soft-tissue biopsy includes heavy infiltration of plasma cells and lymphocytes. “Plasmacytic- lymphocytic stomatitis” is a sign of one or more severe diseases in the cat and must be diagnosed accurately to ensure successful treatment. Causes of plasmacytic-lymphocytic stomatitis include retrovirus infection (feline leukemia, feline immunodeficiency virus), calicivirus infection (especially in cats with chronic faucitis), concurrent odontoclastic resorption (“neck” lesions), polyclonal gammopathy (hypergammaglobulinemia), concurrent diabetes mellitus, chronic interstitial nephritis, or other debilitating diseases and malnutrition. Initial treatment includes controlling or eliminating the cause and aggressive dental prophylaxis with mandatory home care. Unfortunately, many cats have advanced disease and are far too painful to allow home care. The treatment of choice is full mouth extractions, although fortunately, the canine teeth can usually be salvaged. Steroid therapy is only palliative and is best used only on a short-term basis after surgical intervention. Surgical pain is controlled with mandibular and maxillary nerve blocks followed by butorphenol PO for 3 days. Antibiotic therapy controls any chance of septicemia. Developmental Abnormalities Malocclusion: Malposition of the teeth within the jaw can result in a poor bite. Frequently, it occurs when deciduous teeth are retained and the permanent teeth erupt adjacent to, rather than directly under, them; the roots of the deciduous teeth are not resorbed, and they tilt the erupting permanent teeth into an abnormal position. Other types of dental malocclusion relate to improper relationships between the size of the teeth and that of the jaws. For example, a jaw may be too small for the size of the teeth developing within it, which causes crowding and subsequent malocclusion. Malocclusion may be treated to obtain a functional bite by early extraction of retained deciduous teeth, selective extraction of permanent teeth, or orthodontics. Skeletal malocclusions result from an abnormal relationship of the upper and lower jaws to each other, although the teeth may be properly aligned within the jaw. Treatment is much more difficult and should attempt to achieve a functional bite rather than perfect occlusion. Selective extractions, orthodontics, and in severe cases, orthognathic surgery may be necessary. Enamel Hypoplasia and Dysplasia: During the development of enamel (both deciduous and permanent teeth), fevers and deposition of chemicals within the tooth may cause permanent damage. The canine distemper virus is especially damaging in that it attacks the ameleoblasts (enamel-producing cells) and causes a systemic fever. This results in generalized full-thickness loss of enamel, or enamel hypoplasia. Treatment of enamel hypoplasia includes composite bonding and frequent dental prophylaxis. Treatment of enamel dysplasia includes aggressive polishing of the remaining enamel and possible composite bonding. Maxillofacial Trauma Fractured teeth should be inspected for damage to the pulp. If fractures extend into the pulp, endodontic therapy is required, or extraction must be performed. Lengthwise fractures that extend below the gingival margin can be difficult to repair; if substantial tooth has been lost, what remains should probably be extracted. Fragmented teeth, especially those with multiple roots, often are left to “see what happens”; extraction is usually better due to poor general healing. within a few hours. Thick tissue that has become avascular due to trauma should be removed. Bone fractures require stabilization. Acrylic splints, arch bars, interdental wiring, and cerclage wires can be used. Coccidiosis: Introduction Coccidiosis is a usually acute invasion and destruction of intestinal mucosa by protozoa of the genera Eimeria or Isospora. Infection is characterized by diarrhea, fever, inappetence, weight loss, emaciation, and sometimes death. Coccidiosis is a serious disease in cattle, sheep, goats, pigs, poultry, and also rabbits, in which the liver as well as the Merck Veterinary Manual - Summary 30 intestine can be affected. In dogs, cats, and horses, it is less often diagnosed but can result in clinical illness. Other species, of both hosts and protozoa, can be involved, sarcocystosis, and toxoplasmosis. In coccidiasis, animals are infected with coccidia but do not have clinical signs. Coccidiasis is much more prevalent than coccidiosis and is thought to result in poor feed efficiency under intensive rearing conditions. Etiology and Epidemiology: Eimeria and Isospora typically require only one host in which to complete their life cycles. Oocysts enter the environment in the feces of an infected host, but oocysts of Eimeria and Isospora are unsporulated and therefore not infective. Under favorable conditions of oxygen, humidity, and temperature, oocysts sporulate and become infective in several days. During sporulation, the amorphous protoplasm develops into small bodies (sporozoites) within secondary cysts (sporocysts) in the oocyst. In Eimeria spp , the sporulated oocyst has four sporocysts, each containing two sporozoites; in Isospora spp , the sporulated oocyst has two sporocysts, each containing four sporozoites. When the sporulated oocyst is ingested by a susceptible animal, the sporozoites escape from the oocyst, invade the intestinal mucosa or epithelial cells in other locations, and develop intracellularly into multinucleate schizonts (also called meronts). Each nucleus develops into an infective body called a merozoite; merozoites enter new cells and repeat the process. After a variable number of asexual generations, merozoites develop into either macrogametocytes (females) or microgametocytes (males). These produce a single macrogamete or a number of microgametes in a host cell. After being fertilized by a microgamete, the macrogamete develops into an oocyst. The oocysts have resistant walls and are discharged unsporulated in the feces. Oocysts do not survive well at temperatures below -30°C or above 40°C; within this range, they may survive up to 1 yr or more. Coccidia are opportunistic pathogens. If pathogenic, their virulence may be influenced by various stressors. Therefore, clinical coccidiosis is most prevalent under conditions of poor nutrition, poor sanitation, or overcrowding, or after the stresses of weaning, shipping, sudden changes of feed, or severe weather. Of the numerous species of Eimeria or Isospora that can infect a particular host, not all are pathogenic. Most animals acquire Eimeria or Isospora infections of varying degrees when between 1 mo and 1 yr old. Older animals usually are resistant to clinical disease but may have sporadic inapparent infections. Such clinically healthy, mature animals usually can be sources of infection to young, susceptible animals. Clinical Findings: Clinical signs of coccidiosis are due to destruction of the intestinal epithelium and, frequently, the underlying connective tissue of the mucosa. This may be accompanied by hemorrhage into the lumen of the intestine, catarrhal inflammation, and diarrhea. Signs may include discharge of blood or tissue, tenesmus, and dehydration. Diagnosis: Oocysts can be identified in feces by salt or sugar flotation methods. Finding appreciable numbers of oocysts of pathogenic species in the feces is diagnostic, but because diarrhea may precede the heavy output of oocysts by 1-2 days and may continue after the oocyst discharge has returned to low levels, it is not always possible to find oocysts in a single fecal sample; multiple examinations may be required. Treatment: The life cycles of Eimeria and Isospora are considered self-limiting and end spontaneously within a few weeks unless reinfection occurs. Sick animals should be isolated and treated individually whenever possible to ensure delivery of therapeutic levels of the drug and to prevent exposure of other animals. Sulfonamides may be used. Sulfaquinoxaline has been reported to give excellent clinical results. Amprolium has been reported to be effective during outbreaks in calves, sheep, and goats. Prevention: Continuous low-level feeding of amprolium, decoquinate, lasalocid, or monensin during the first month of feedlot confinement has been reported to have preventive value. Coccidiosis of Cats and Dogs Many species of coccidia infect the intestinal tract of cats and dogs. All species appear to be host-specific. Cats have species of Isospora , Besnoitia , Toxoplasma , Hammondia , and Sarcocystis. Dogs have species of Isospora , Hammondia , and Sarcocystis. Neither dogs nor cats have Eimeria. Hammondia has an obligatory two-host life cycle with cats or dogs as final hosts and rodents or ruminants as intermediate hosts, respectively. Hammondia oocysts are indistinguishable from those of Toxoplasma and Besnoitia but are nonpathogenic in either host. See also besnoitiosis, sarcocystosis, and toxoplasmosis. The most common coccidia of cats and dogs are Isospora. Almost every cat eventually becomes infected with I felis. The most common clinical signs in severe cases are diarrhea (sometimes bloody), weight loss, and dehydration. Usually, coccidiosis is associated with other infectious agents, immunosuppression, or stress. In kennel conditions when the need for prophylaxis might be predicted, amprolium is said to be effective, although it is not approved for use in dogs. In severe cases, in addition to supportive fluid therapy, sulfonamides such as sulfadimethoxine. Merck Veterinary Manual - Summary 31  Coccidiosis of Cattle Of the species of Eimeria that infect cattle, E zuernii , E bovis , and E auburnensis are most often associated with clinical disease. Experimentally, other species have been shown to be mildly or moderately pathogenic. Coccidiosis is commonly a disease of young cattle (1-2 mo to 1 yr) and usually is sporadic during the wet seasons of the year. The incubation period is 17-21 days. The most characteristic sign of clinical coccidiosis is watery feces, with little or no blood, and the animal shows only slight discomfort for a few days. Severe infections are rare. Severely affected cattle develop diarrhea, which consists of thin bloody fluid, that may continue for > 1 wk, or thin feces with streaks or clots of blood, shreds of epithelium, and mucus. Calves with concurrent infections (eg, coronavirus) may be more severely affected than calves with coccidia infections alone. In addition, management factors, such as weather, housing, feeding practices, and how animals are grouped, are important in determining the expression of clinical coccidiosis in cattle. The pathogenic coccidia of cattle can damage the mucosa of the lower small intestine, cecum, and colon. The first- generation schizonts of E bovis appear as white macroscopic bodies in the villi of the small intestine. Differential diagnoses include salmonellosis, bovine virus diarrhea, malnutrition, toxins, or other intestinal parasites. Coccidiosis of Goats The Eimeria spp are host-specific and are not transmitted from sheep to goats. Eimeria arloingi , E christenseni , and E ninakohlyakimovae are highly pathogenic in kids. Clinical signs include diarrhea with or without mucus or blood, dehydration, emaciation, weakness, anorexia, and death. Some goats are actually constipated and die acutely without diarrhea. Usually, stages and lesions are confined to the small intestine, which may appear congested, hemorrhagic, or ulcerated, and have scattered pale, yellow to white macroscopic plaques in the mucosa. Histologically, villous epithelium is sloughed, and inflammatory cells are seen in the lamina propria and submucosa. In addition, there have been several reports of hepatobiliary coccidiosis with liver failure in dairy goats. Coccidiosis of Pigs Eight species of Eimeria and one of Isospora infect pigs in the USA. Isospora suis is prevalent in neonatal pigs. Infection is characterized by a watery or greasy diarrhea, usually yellowish to white and foul smelling. Piglets may appear weak, dehydrated, and undersized; weight gains are depressed, and sometimes piglets die. A contributing factor to mortality is that piglets become covered with diarrheic feces and stay damp. Piglets that recover from infection are highly resistant to reinfection. Coccidiosis of Sheep Infections with some species of Eimeria are one of the most economically important diseases of sheep. The parasites are now considered host-specific. Cryptosporidiosis Cryptosporidiosis is an enterocolitis of cosmopolitan distribution caused by the coccidian parasite Cryptosporidium parvum. It is not host-specific and is common in young ruminants. The disease in calves, characterized by weight loss and watery diarrhea, is clinically indistinguishable from many other causes of calf diarrhea. Unless the immune system is compromised, it is self-limiting. Cryptosporidium parvum infections from animals and other people pose a significant risk to immunocompromised people, who can develop protracted diarrhea and die. Etiology and Transmission: Cryptosporidium parvum is a minute protozoan that is transmitted by the fecal-oral route. Clinical Findings and Lesions: Although C parvum can infect virtually the entire intestinal tract, the distal small intestine usually is affected most severely. Infection in horses is limited to the small intestine. Gross lesions may consist of hyperemic intestinal mucosa and yellowish intestinal contents. Microscopically, mild to severe villous atrophy with spherical organisms in the brush border is evident. Unlike Eimeria and Isospora spp , which are intracellular parasites, C parvum is intramembranous and resides within the brush border of the intestinal epithelial cells. Treatment and Control: There is no effective specific treatment; however, because the disease is self-limiting, supportive therapy, such as rehydration, correction of acidosis, and maintenance of energy requirements, is usually sufficient. Giardiasis: Introduction Giardiasis is a chronic, intestinal protozoal infection that occurs worldwide in most domestic and wild mammals, many birds, and people. There is circumstantial evidence that the Giardia spp that infect domestic animals can infect people. Merck Veterinary Manual - Summary 32  Etiology and Transmission: Flagellate protozoa (trophozoites) of the genus Giardia inhabit the mucosal surfaces of the small intestine, where they multiply by binary fission. Transmission occurs in the cyst stage by the fecal-oral route. Incubation and prepatent periods are generally 5-14 days. Cysts can survive in the environment but trophozoites cannot. Clinical Findings and Lesions: Giardia infections in dogs and cats may be inapparent or produce weight loss and chronic diarrhea or steatorrhea, which can be continuous or intermittent, particularly in puppies and kittens. Clinical giardiasis has been reported in calves. Giardiasis must be differentiated from other causes of nutrient malassimilation (eg, exocrine pancreatic insufficiency, intestinal malabsorption. Diagnosis: Because Giardia are excreted intermittently, several fecal examinations should be performed if giardiasis is suspected. Treatment: No drugs are approved for treating giardiasis in animals. Albendazole and fenbendazole have effectively cleared Giardia cysts from the feces of infected dogs and cats. No side effects are reported; however, albendazole is not approved for use in cats and dogs, and because it is suspected of being teratogenic, should not be administered to pregnant animals. Fenbendazole at 50 mg/kg/day, PO, for 3 days, effectively removes Giardia cysts from the feces of dogs; no side effects are reported, and it is safe for pregnant and lactating animals. Anal Sac Disease Anal sac disease is the most common disease entity of the anal region in dogs. Small breeds are predisposed; large or giant breeds are rarely affected. In cats, the most common form of anal sac disease is impaction. Etiology and Pathogenesis: Anal sacs may become impacted, infected, abscessed, or neoplastic. Failure of the sacs to express during defecation, poor muscle tone in obese dogs, and generalized seborrhea (which produces glandular hypersecretion) lead to retention of sac contents. Such retention may predispose to fermentation, inflammation, and secondary bacterial infection. Clinical Findings, Lesions, and Diagnosis: Signs are related to pain and discomfort associated with sitting. Scooting, licking, biting at the anal area, and painful defecation with tenesmus are also common. Induration, abscesses, and fistulous tracts are common. In impaction, hard masses are palpable in the area of the sacs; the sacs are packed with a thick, pasty, brown secretion, which can be expressed as a thin ribbon only with a large amount of pressure. When the sacs are infected or abscessed, severe pain and often discoloration of the area are present. Fistulous tracts lead from abscessed sacs and rupture through the skin; these must be differentiated from perianal fistulas. Anal sac neoplasms are usually nonpainful and are associated with perineal edema, erythema, induration, or fistula formation. Apocrine gland adenocarcinomas of the anal sac occur typically in older female dogs. These dogs are presented for signs secondary to hypercalcemia, such as polyuria and polydipsia, or for problems related to the perineal mass. Diagnosis of impaction, infection, or abscessation is confirmed by digital rectal examination, at which time the sacs can be expressed. Microscopical examination of the contents from infected sacs reveals large numbers of polymorphonuclear leukocytes and bacteria. A tumor should be suspected (anal sac apocrine adenocarcinoma) in anal sacs that are firm, enlarged, and nonexpressible even with irrigation. In these cases, the diagnosis should be confirmed by biopsy. Regional and systemic metastasis should be evaluated and serum calcium assessed. Treatment: Impacted anal sacs should be gently manually expressed. A softening or ceruminolytic agent can be infused into the sac if the contents are too dry to express effectively. Infected sacs should be cleaned with antiseptic, followed by local and systemic antibiotic therapy. Repeated weekly flushings combined with infusion of a steroid-antibiotic ointment may be needed. If medical treatment is ineffective, or if neoplasia is present, surgical excision of the sac is indicated. However, fecal incontinence, which is a common complication of anal sac surgery, may result from damage to the caudal rectal branch of the pudendal nerve and may be complete if damage is bilateral. Scar formation in the external anal sphincter may result from surgical trauma and may produce tenesmus. Perineal Hernia Perineal hernia is a lateral protrusion of a peritoneally lined hernial sac between the levator ani and either the external anal sphincter muscle or the coccygeus muscle. Incidence in intact 6- to 8-yr old male dogs. Etiology and Pathogenesis: Many factors are involved, including breed predisposition, hormonal imbalance, prostatic disease, chronic constipation, and weakness of the pelvic diaphragm due to chronic straining. The higher incidence among sexually intact males is evidence that hormonal influences probably play a primary role. Prostatic hypertrophy attributed to sex-hormone imbalance has been strongly implicated. Both estrogens and androgens have been cited as causative agents. Merck Veterinary Manual - Summary 33  Clinical Findings and Diagnosis: Common signs include constipation and obstipation, tenesmus, and dyschezia. Stranguria may occur secondary to retroflexion of the bladder and prostate. A perineal swelling ventrolateral to the anus is evident. Herniation may be bilateral, but two-thirds are unilateral and >80% of these are on the right side. The mass is soft and fluctuant and may be reduced digitally. A firm, painful swelling may be compatible with retropulsion of the bladder and prostate. Determination of contents is often made by rectal examination. Over 90% of perineal hernias contain a rectal deviation, which is a sacculation of the rectum into the hernial sac, where the layers of the rectal wall remain intact. Treatment: Perineal hernia is rarely an emergency, except when the bladder has strangulated and the animal is unable to urinate. Rectal Prolapse In rectal prolapse, one or more layers of the rectum protrude through the anus due to persistent tenesmus associated with intestinal, anorectal, or urogenital disease. Prolapse may be classified as incomplete, in which only the rectal mucosa is everted, or complete, in which all rectal layers are protruded. Etiology: Rectal prolapse is common in young animals in association with severe diarrhea and tenesmus. Causal factors include severe enteritis, disorders of the rectum (eg, foreign bodies, lacerations, diverticula, or sacculation), neoplasia of the rectum or distal colon, urolithiasis, urethral obstruction, cystitis, dystocia, colitis, and prostatic disease. Rectal prolapse is probably the most common GI problem in pigs due to diarrhea or weakness of the rectal support tissue within the pelvis. In cattle, it may be associated with coccidiosis, rabies, or vaginal or uterine prolapse; occasionally, excessive “riding” and associated traumatic injury may be causative in young bulls. It is common in sheep with short tail docking or especially in feedlot lambs, in which high-concentrate rations may be causative. Clinical Findings, Lesions, and Diagnosis: An elongated, cylindrical mass protruding through the anal orifice is usually diagnostic. However, it must be differentiated from prolapsed ileocolic intussusception by passing a probe, blunt instrument, or finger between the prolapsed mass and the inner rectal wall. In rectal prolapse, the instrument cannot be inserted due to the presence of a fornix. Ulceration, inflammation, and congestion of the rectal mucosa is common. Early, there is a short, nonulcerated, inflamed segment; later, the mucosal surface darkens and may become congested and necrotic. Treatment: In all animals, identifying and eliminating the cause is of primary importance. In small animals, treatment includes prompt replacement of viable prolapsed tissue to its proper anatomic location, or amputation if the segment is necrotic. Small or incomplete prolapses can be manually reduced under anesthesia by using a finger or bougie. Hypertonic sugar solution (50% dextrose or 70% mannitol) applied directly to the mucosa relieves edema and eases reduction. The placement of a loose, anal purse-string suture for 5-7 days is indicated. Postoperatively, a moistened diet and a fecal softener (eg, dioctyl sodium sulfosuccinate) are recommended. In large animals, caudal epidural anesthesia is suggested to reduce straining, facilitate repositioning of the prolapse, and permit surgical manipulations. Reduction and retention with a purse-string suture is recommended. The suture should be loose enough to leave a one-finger opening into the rectum in pigs and sheep, and slightly larger in cattle and horses. Rectal Tears A separation, rent, or tear in the rectal or anal mucosa occurs as a result of a laceration inflicted within the lumen. Foreign bodies (eg, sharp bones, needles, and other rough material) have been implicated. Clinical Findings and Diagnosis: Constipation and reluctance to defecate are usually attributed to pain. Diagnosis is based on tenesmus and hemorrhage, perineal discoloration, and inspection of the rectum and anus; fresh blood found on a glove or on feces after rectal examination is good evidence of a rectal tear. Treatment: In all species, treatment should be initiated immediately. In cattle and horses, accidental perforation during rectal examination necessitates immediate treatment to reduce the risk of peritonitis and death. Rectal tears in horses have been classified according to the tissue layers penetrated. Grade I tears involve the mucosa or submucosa. Grade II tears involve rupture of the muscular layers only. Grade III tears involve mucosa, submucosa, and muscular layers, including tears that extend into the mesorectum. Grade IV tears involve perforation of all layers of the rectum and extension into the peritoneal cavity. Grade I tears may be treated conservatively with broad-spectrum antibiotics and IV fluids. Flunixin meglumine may be given to prevent or treat endotoxic shock. Mineral oil is given via stomach tube to soften feces, and the diet should consist of pasture grasses or alfalfa. Grade II and III tears require immediate and more extensive surgery. Grade IV tears carry a Merck Veterinary Manual - Summary 34