Mechanical obstruction. Intestinal volvulus and twisting in animals Intestinal volvulus in pigs causes

Obstructive ileus: blockage of the rumen, stomach, intestines with stones, foreign bodies, phyto- and pylobezoars, potatoes, bones, rags, twine for wrapping hay bales, helminths, tumors. It is found in horses, large and small cattle, and dogs. Complications are gastric dilatation and intestinal flatulence.

Strangulating ileus(displacement): torsion, intussusception, hernia, prolapse, rupture. Found in horses, cattle, and pigs.

Volvulus found in pigs, horses and dogs. It is characterized by rotation of its loops around the longitudinal axis of the mesentery or the formation of intestinal nodes.

At the site of the volvulus, due to twisting of the mesentery and compression of the venous vessels, a congestive infarction of the strangulated part of the intestine develops. In this case, the intestinal wall is thickened 2-5 times, dark red in color, the mucous membrane is covered with a gray coating (necrosis). The contents of the intestines are red. Histo: the blood vessels are greatly dilated, overflowing with blood, the tissue is saturated with hemorrhagic transudate, the mucous, submucous and muscular membranes are in a state of necrosis.

Intussusception found in pigs, dogs, horses. Develops as a result of the entry of one part small intestine into the lumen of its other part. The invaded area consists of three cylinders pushed into one another: external, middle and internal. The outer and middle cylinders face each other with mucous membranes, and the middle and inner cylinders face each other with serous membranes. During invagination, the mesentery and veins between the internal and middle cylinders are infringed, so congestive infarction develops in these cylinders. Invaded areas are not straightened out.

The difference from agonal intussusception is that with it the intussusception is easily straightened, the intestinal wall is normal, elastic, without signs of congestive infarction.

Hernia and prolapse.

Hernia– exit from abdominal cavity intestinal loops through an anatomical or pathological opening, preserving the peritoneum. In a hernia, the contents of the hernia, the hernial opening, the neck, and the hernial sac (its bottom and body) are distinguished. Hernias are reducible and irreducible. In an irreducible hernia, the prolapsed intestine is strangulated, i.e. it develops successively acute venous hyperemia, hemostasis and congestive infarction. The intestinal wall is thickened, swollen, edematous, dark red in color. The intestinal contents are bloody. In the part of the intestine strangulated in the hernial opening, anemia is noted (strangulation line). Variants of hernia - in the inguinal ring, in the opening of the peritoneum, diaphragm, femoral canal, scrotum, umbilical ring.

Bowel prolapse– displacement of its loops through an anatomical or pathological opening with rupture of the peritoneum. A congestive infarction develops in the strangulated intestinal loop. For example, intestinal prolapse through a rupture of the peritoneum into the subcutaneous tissue of a cow.

Stomach rupture occurs in horses usually as a complication of its acute expansion. The gap is observed along the greater curvature, somewhat to the side. First, the serous membrane ruptures, then the muscular and mucous membranes. The length of the rupture reaches 30 cm or more, its edges are uneven, fringed, riddled with hemorrhages, the mucous membrane is turned outward at the edges of the rupture as a result of contraction of the muscle layer. There is red turbid liquid and food masses in the abdominal cavity; signs of peritonitis may be observed in the peritoneum. It should be distinguished from post-mortem rupture of the stomach, in which the edges of the rupture are smooth, without hemorrhages, and the mucous membrane is not turned outward.

A hemorrhagic infarction may develop in the intestine if there is simultaneously venous hyperemia and the outflow of blood from the intestine is obstructed. In this case, the intestine is dark red, thickened, and the intestinal contents are red. The mucous membrane is in a state of necrosis, gray or brown, folded, gelatinous. With necrosis of the entire intestinal wall, fibrinous or fibrinous-hemorrhagic peritonitis develops.

Dyspepsia in calves.

This is a digestive disorder in newborn calves and piglets with signs of diarrhea (diarrhea). The word "dyspepsia" means indigestion. It belongs to the group of neonatal diseases of young animals (in the first days after birth). Dyspepsia can be simple or toxic.

Etiology: Weak immune defense of the body as a result of morphofunctional immaturity of the immune and digestive systems; inadequate feeding of breeding stock, use of poor quality feed; improper and untimely feeding of newborns, poor quality of colostrum or giving cold colostrum, as a result of which dysbacteriosis develops and putrefactive microflora accumulates. Dyspepsia may be of autoimmune origin.

Pathogenesis. There is an inability of the body of newborns to absorb colostrum due to the morphofunctional immaturity of the digestive organs. In physiologically mature offspring, indigestion develops due to overfeeding and deterioration in the quality of colostrum (cold, dirty). Dysbiosis, toxicosis, diarrhea, dehydration, and loss of appetite develop.

Clinic. The disease is more common in winter and spring. Morbidity is up to 100%, mortality is 20-50-80%. With simple dyspepsia - frequent bowel movements (diarrhea), liquid feces, depression, abdominal pain. Body temperature is normal or decreasing. With toxic dyspepsia, dehydration, severe depression, lack of appetite increases, and exhaustion develops. The duration of the disease is 2-5 days, after recovery the young animals long time lags behind in development.

Pathanatomy. Exhaustion, sunken eyes, the stomach is tucked in, the hunger pits are sunken, the skin around the anus, hind limbs and tail are stained with liquid feces. Subcutaneous tissue, the serous membranes are dryish (exicosis), in the abomasum of calves (the stomach of piglets) and the small intestine there is acute catarrhal inflammation, while the mucous membrane is swollen, edematous, patchy red, with pinpoint and small-spotted hemorrhages. In the cavity of the abomasum (stomach) there is a dirty gray cloudy mass, dense lumps of casein.

Mesenteric lymph nodes - serous inflammation, they are enlarged in volume, dense, juicy when cut, gray-red in color, the pattern of the follicles is erased.

In the liver and kidneys there is granular degeneration and venous hyperemia, thickened blood, bladder empty, the spleen and thymus are atrophied.

Pathological diagnosis.

1. Acute catarrhal gastritis (abomasitis) and enteritis.

2. Hemorrhages in the mucous membrane of the abomasum (stomach) and small intestine.

3. Dense convolutions of casein in the cavity of the abomasum (stomach).

4. Serous inflammation of the mesenteric lymph nodes.

5. Atrophy of the thymus and spleen.

6. Dehydration (exicosis), general anemia, exhaustion.

7. Granular dystrophy and venous hyperemia of the liver and kidneys.

Diagnosis. Is established on the basis of anamnesis, clinical symptoms, the results of autopsies, as well as bacteriological and virological studies. The age of the sick person (neonatal period) is taken into account.

Differentiate dyspepsia is needed from:

Colibacillosis, with sepsis expressed;

Viral gastroenteritis (there is necrosis of the mucous membrane of the small intestine, necessary laboratory research);

Salmonellosis, in which sepsis and Salmonella nodules in the liver are noted.

Peritonitis and ascites.

Peritonitis– inflammation of the peritoneum can be focal and diffuse, the form of inflammation is exudative (serous, fibrinous, hemorrhagic, purulent). The visceral and parietal peritoneum is focally or diffusely hyperemic, dotted with hemorrhages, matte, without shine, exudate in the abdominal cavity is serous, fibrinous, hemorrhagic, purulent or mixed. With a long course of fibrinous peritonitis, adhesions form between the intestinal loops, parietal peritoneum and intestinal loops as a result of the organization of fibrin (adhesive disease).

Ascites- dropsy of the abdominal cavity. Develops as a result of cardiovascular failure, impaired portal circulation, exhaustion, cirrhosis and echinococosis of the liver. In this case, the peritoneum is not changed: smooth, shiny, gray in color. The abdominal cavity contains serous (gray) or hemorrhagic (red) transudate (edematous fluid).

Topic 2.3. Digestive diseases

Independent work

Diseases of the digestive organs and peritoneum can be primary of alimentary, toxic or infectious etiology or secondary in various specific non-infectious, infectious and invasive diseases of acquired, congenital, or hereditary origin. According to the mechanism of development, diseases of a non-inflammatory and inflammatory nature are distinguished, and according to their course - acute and chronic. These include diseases of the oral cavity, pharynx, esophagus, stomach and intestines, liver, pancreas, and peritoneum.

Diseases of the oral cavity,
pharynx, esophagus, stomach and
intestines

Damage, obstruction and blockage. They can be in the mouth, pharynx, esophagus, stomach and intestines. Obstruction and blockage can be complete or incomplete, primary or secondary.

Dynamic obstruction associated with morphofunctional disorders that cause a slowdown and cessation of the movement of food mass while maintaining a free lumen in the digestive tract. Depending on the nature of the changes, dynamic obstruction can be spastic (including enteralgia) or paralytic.

Mixed form of obstruction intestines, caused by its displacement, occurs due to hernias (abdominal wall, umbilical, inguinal, scrotal, femoral, diaphragmatic, peritoneal), prolapses (through the rectum, abdominal wall, Winslowi hole in the omentum, omentum, diaphragm, mesentery, true and false ligaments) and intussusception. Intestinal obstruction during intestinal rotation causes tension and strangulation of the intestinal loops and mesentery, the vessels and nerves embedded in them with the development of congestive hyperemia and hemorrhagic infarction of the wall of the strangulated intestinal loop. The most commonly observed intestinal rotation around the longitudinal axis, intestinal twisting around the longitudinal axis of the mesentery, intestinal nodulation and kinks.

Diverticula and ectasia. A diverticulum is a local expansion of a tubular organ with a unilateral protrusion of its wall. Most often found in the esophagus and intestines. Pulsating diverticula occur when there is an obstacle to the movement of feed mass caused by damage and blockage of the organ, stenosis (narrowing) of scar or compression origin. Traction diverticula occur as a result of adhesion or fusion digestive tract with any affected neighboring organ (inflamed lymph node, abscess or tumor). Ectasia is an enlargement of an organ.

Acute dilatation of the stomach or intestines(acute tympany, rumen flatulence in ruminants, acute flatulence of the stomach or intestines). Often found in cattle and horses, less commonly in other animals, including those with a chronic course. The disease is characterized by a delay in the evacuation of food masses, increased fermentation, distension of the stomach or intestines with gases and severe bloating.

During an external examination of the corpse, severe swelling of the abdominal region, stagnation of poorly coagulated dark red blood with a bluish tint, in places with signs of edema in the venous vessels of the head, neck, and organs of the chest cavity are noted. The abdominal organs (especially the stomach and liver) are anemic, pale gray or brown in color, with semi-empty or gaping blood vessels. The diaphragm dome is shifted to chest cavity. When cutting the tightly stretched, tense and pale-colored walls of the stomach, gases come out noisily. The contents of the stomach, and often the intestines, consist of a large amount of semi-liquid foamy fermenting feed masses mixed with gas.

Lungs in a state of acute congestive hyperemia and edema with the presence large quantity foamy fluid in the bronchi, trachea, and sometimes in the upper respiratory tract. The right heart is enlarged, there is liquid blood and a small amount of loose clots in the cavities, there are numerous hemorrhages along the coronary vessels, also found on the serous tissues and in the lungs. The brain and its membranes are hyperemic, and there is a large amount of fluid in the cerebral ventricles.

Gastric volvulus. Sometimes it occurs in dogs with sudden movements of the right half of the stomach to the left side, as well as as a result of compression of the duodenum and jejunum. The stomach is swollen, spherical, dark red in color, with hemorrhagic infiltration of the wall and contents, the spleen is curved and hyperemic, the lungs are full-blooded and swollen, and there is poorly coagulated blood in the dilated cavities of the heart.

Stomach rupture. It can be primary when the previously unchanged wall of the stomach is ruptured, and secondary when there are dystrophic-necrobiotic or inflammatory changes in it that contribute to the rupture. There is a complete rupture of all layers of the stomach wall and incomplete - only the serous or serous and muscular membranes are torn, while the mucous membrane remains intact and protrudes into the resulting hole in the form of a bag. The wall of the stomach tears mainly along the greater curvature - the right half of it, several centimeters above the center, which, apparently, is explained by the weak development of muscles and elastic fibers in this place. Moreover, the serous membrane ruptures first - its gap is the longest, then the muscle layers - the gaps are shorter and, finally, the mucous membrane, the edges of which are wrapped outward at the edges of the gap. The length of the gap can be up to 30-40cm. Its edges are uneven, fringed, contaminated with food masses and soaked in blood. The collapsed stomach contains a certain amount of food masses, on the surface of which blood clots are noted.

Intussusception They are observed mainly in the thin section. A distinction is made between descending intussusception (invasion of the overlying intestinal loop into the lumen of the underlying one) and ascending (invagination of the underlying intestinal segment into the lumen of the anterior loop). The invaginated area consists of three cylinders pushed into one another: the outer - vaginal, the middle - connective and the inner - aqueous.

Hernias and prolapses. Hernia is the passage of a part of the intestine or other organ from the abdominal cavity through an anatomical or pathological opening with preservation of the peritoneum, forming a hernial sac. In case of rupture of the peritoneum (without a hernial sac), they speak of prolapse. Hernias can be congenital and acquired, umbilical, abdominal, inguinal (scrotal in males) and diaphragmatic. Particularly dangerous strangulated hernias with the development of colic, venous stagnation, edema, and heart attack. In birds, prolapse of part of the intestine in the form of a tube from the cloaca occurs, as well as prolapse of the oviducts due to difficulty in laying eggs.

Inflammation of the digestive tract. Inflammation of the mucous membrane of the stomach and intestines is more common, especially in young animals.

Inflammation of the oral mucosa. More often caused by traumatic, thermal, chemical and infectious factors and manifested by hyperemia and swelling of the mucous membrane with the development of catarrhal, vesicular, aphthous, pustular, ulcerative, fibrinous or phlegmonous stomatitis. With simultaneous inflammation of the mucous membrane of the tongue, or glossitis, swelling of the tongue and ulceration of its mucous membrane with the presence of gray-white or gray-yellowish deposits on it are observed. Inflammation of the gums, or gingivitis, is characterized by swelling, redness, and sometimes bleeding.

Inflammation of the pharyngeal mucosa- pharyngitis, soft and tonsils - sore throat, inflammation of the tonsils - tonsillitis. These organs are often affected with the formation of primary or secondary lesions in many infectious diseases.

Inflammation of the esophagus(in birds and goiter) are more often observed as a result of traumatic, physicochemical (including medicinal) effects. Inflammation of the esophagus can occur as a continuation of the pharynx or stomach, as well as with the introduction of gadfly larvae. With hypovitaminosis A, hyperkeratinization occurs, and with hypovitaminosis C, hemorrhages and ulcerations occur. In this case, the mucous membrane of the esophagus is swollen, hyperemic, with hemorrhages, sometimes with erosions.

Traumatic reticulitis. This is damage to the mesh wall by a foreign body with the development of septic acute, subacute or chronic inflammation.

At autopsy, damage and inflammation of the anterior surface of the mesh are more often found within the protruding cells or in the deep layers of the wall, up to its perforation, and sometimes the diaphragm and the cardiac shirt are involved in the process. Along the canal, purulent, abscessing or purulent-fibrinous necrotizing inflammation occurs in the damaged tissues with the formation of a cavity in which a foreign body is located, sometimes penetrating into the lumen of the pericardium. Between damaged organs, adhesions of granulation tissue that undergo fibrous transformation and hyalinization are possible. This indicates a chronic process. Such animals are poorly nourished. Sometimes foreign objects surrounded by inflamed tissue can be found in pleural cavity and lungs. If it penetrates the abdominal cavity, it often damages the liver. In this case, an abscess and adhesive inflammation of the peritoneum can be detected. Upon penetration foreign body through the diaphragm and chest cavity and damage to the heart, traumatic purulent-fibrinous pericarditis and myocarditis occur. In such animals, cardiovascular failure and edema are observed during life.

Inflammation of the stomach and intestines. Inflammation can occur and spread to the stomach, duodenum, ileum, cecum, colon and rectum, or affect the entire gastrointestinal tract. It occurs in all animals, but is especially common in young animals.

Acute serous inflammation The stomach and intestines are characterized by swelling, hyperemia and infiltration of the mucous membrane (superficial inflammation), submucosal layer and other layers of the wall (deep inflammation) with serous exudate, the appearance of focal hemorrhages.

Rice. 193. Serous inflammation of the stomach wall.

Acute catarrhal inflammation stomach and intestines occurs most often and manifests itself, along with the above symptoms, as pronounced mucous degeneration of the epithelium with hypersecretion of mucus, which, mixed with serous exudate, covers the mucous membrane in the form of gray-whitish cloudy deposits and flakes. Depending on the composition of the exudate, the amount of thick, viscous translucent mucus in it, the nature and degree of damage to the mucous membrane, serous, mucous, purulent or desquamative catarrh is distinguished.

Rice. 194. Catarrhal inflammation of the pig's stomach.

At chronic course inflammation, vascular response weakened, mucous membrane due to proliferation connective tissue condensed, and the glandular tissue is atrophied (atrophic catarrh); simultaneous hyperplasia of the connective and glandular tissues, including the submucosal layer (hypertrophic catarrh), is less common. Animals suffering from chronic catarrhal gastroenteritis are emaciated, and young animals are stunted in growth and development.

Fibrinous inflammation The stomach or, more often, the intestines is characterized by the detection of fibrinous exudate on the surface of the mucous membrane (superficial, or lobar, inflammation). Sometimes dead tissues are saturated with this exudate (deep or diphtheritic inflammation). With lobar inflammation on the surface of the mucous membrane, you can find a pityriasis-like plaque or easily removable gray-yellowish or gray-brownish films, sometimes forming a kind of casts of the affected part of the intestine in the form of hollow bodies with intestinal contents (membranous enteritis).

At diphtheritic inflammation the mucous membrane, and often the submucosal layer, looks like a leathery, rough, compacted film of gray-brown or greenish-brown color, after removal of which a deeply ulcerated surface remains. With focal inflammation, Peyer's patches and solitary follicles are most often affected; a dense, bud-shaped scab with a layered pattern protruding above the surface is visible. Once it is rejected, it leaves an ulcer that can heal through scarring. This inflammation is predominantly chronic and is often observed in piglets with plague complicated by salmonellosis, with chicken plague, etc.

Rice. 195. Diphtheritic inflammation of the intestines of a pig.

Hemorrhagic inflammation stomach and intestines in a diffuse or focal form with acute course and an unfavorable outcome is observed in cases of poisoning, intoxication and many infectious diseases. In this case, the mucous membrane of the stomach and intestines, and often other layers of the wall, as well as their contents, are saturated with hemorrhagic non-coagulating exudate and colored dark red or red-brown (due to the formation of hydrochloric acid during the breakdown of red blood cells).

Purulent inflammation more often occurs in the form of purulent catarrh, abscess and phlegmonous inflammation in septic-pyemic diseases, helminthiases and traumatic injuries gastrointestinal tract. On the surface of the mucous membrane, less often in its thickness, a semi-liquid or thick mucopurulent exudate of gray-green color is found. The mucous membrane is swollen, dull, eroded, with hemorrhages. The outcome is determined by the nature of the underlying disease.

Liver diseases

Hepatoses This is a group of liver diseases of various etiologies caused by metabolic disorders. Based on the predominance of impaired metabolism, granular, amyloid, carbohydrate and fatty liver degenerations are distinguished.

Pathological changes are quite varied and depend on the type of hepatosis, but are always characterized by more or less pronounced dystrophic changes The process can begin from the periphery of the hepatic lobule (perilobular dystrophy), from the center (centrilobular dystrophy) or the entire hepatic lobule(diffuse dystrophy).

If the stroma of the organ is preserved, these changes are reversible; with severe lesions, hepatic coma can occur. If the disease lasts for a long time, reparative regeneration, fibrosis and cirrhosis of the organ are noted at autopsy.

Toxic liver dystrophy. This is a kind of hepatosis of toxic origin, characterized by general toxicosis, primary dystrophic processes in the liver cells and a very weak mesenchymal reaction. All animals get sick, and in piglets the disease sometimes becomes widespread.

Rice. 196. Toxic dichtrophy of the pig liver: the variegated color of the organ is pronounced.

If the disease is acute or subacute, then at autopsy it is noted that the liver is somewhat enlarged and flabby. In chronic cases, it is of normal size or even reduced, its pattern is variegated or mosaic: on a red-brown background, areas of irregular shape, gray and white-yellowish in color are visible due to granular, carbohydrate and fatty degeneration (fatty decomposition). The center of the lobules is necrotic.

Rice. 197. Toxic dystrophy. The central part of the lobules is filled with blood,
liver cells have disappeared. Histological section from a pig liver

Hepatitis. This is a group of liver diseases of an inflammatory nature, characterized by the development of a vascular-mesenchymal reaction to damage to the organ. In cattle, the most common are nonspecific reactive and purulent-necrotizing hepatitis.

Nonspecifically reactive, or immune (acute and chronic non-purulent parenchymal), hepatitis - inflammation of the liver, expressed by a complex of alterative, exudative and proliferative changes that occur in the organ secondary to various diseases.

There are active and persistent, periportal, portal and lobular hepatitis.

In acute hepatitis, the liver is enlarged in volume, has a flabby consistency, is unevenly full-blooded, the pattern of lobules is smoothed, the color of the organ is variegated: red-brown, red-brown, gray and reddish-yellow, spotted hemorrhages are also found. In chronic hepatitis, the liver is less enlarged in volume, dense, gray or brown-brown in color with dark red stripes and spots.

Purulent hepatitis- acute, subacute and chronic liver disease with the formation of purulent foci in the organ. It is more common in adult cattle, growing animals, especially during bard fattening, and sometimes in newborn calves.

The liver is noticeably enlarged in volume, with the presence of fibrinous deposits or connective tissue growths on the surface of the organ. Under the capsule or in the deep layers of the parenchyma, multiple lesions ranging in size from hazelnut to walnut, yellow-brown or gray-brown in color with a dryish crumbly or greasy, more late stages with granular-caseous contents. There are also numerous small, about the size of a millet grain, or individual large, about the size of a chicken egg, abscesses containing creamy pus, with a more or less pronounced fibrous capsule.

Liver cirrhosis. Cirrhosis is a group of chronic liver diseases of various etiologies, pathogenesis with common features: structural restructuring of the organ and diffuse proliferation of connective tissue. They are found in animals of all species and are currently considered as chronic proliferative (interstitial) inflammation of the liver, consequences of hepatosis and hepatitis.

Dystrophic, necrobiotic liver damage and vascular disorders are accompanied by interlobular and intralobular proliferation of reticular, granulation and fibrous tissue of different histogenesis.

At atrophic cirrhosis(Laennec) liver is gray-brown or, in the presence of fatty infiltration and jaundice, yellowish-brown in color, reduced in volume, hard in consistency, with an uneven coarse and finely tuberous or granular (shagreen) surface.

Histologically, a violation of the beam structure, tissue atrophy and diffuse growth of connective tissue around the lobules or their groups (ring-shaped or anular cirrhosis) are noted. Atrophic cirrhosis is usually accompanied by ascites due to stagnation of blood in the portal circulation, and sometimes by parenchymal jaundice.

At hypertrophic cirrhosis the liver is significantly, sometimes 2-3 times, increased in volume, dense or hard in consistency, its surface is smooth. The color of the organ is gray-brown or brown. Histologically, diffuse interlobular and intralobular proliferation of connective tissue, disruption of the lobular and lamellar structure with separation of liver cells and their dystrophic and, in some places, proliferative changes are noted. Ascites Not expressed, but parenchymal jaundice and splenic hyperplasia are natural.

Postnecrotic cirrhosis develops as a result of extensive necrosis of the liver parenchyma, leading to liver failure. It occurs after toxic hepatodystrophy, chronic congestive hyperemia of the organ (congestive cirrhosis) and other diseases that cause massive necrosis of hepatocytes. It proceeds like atrophic cirrhosis, but with predominant damage to the central areas of the lobules. In places where the liver parenchyma dies, fibrous tissue grows, giving the organ a denser consistency and a large or small nodular pattern. Protein dystrophy and necrosis of liver cells are characteristic.

Biliary cirrhosis liver diseases occur due to stagnation of bile (choleostasis), caused by blockage and inflammation of the bile ducts (cholangitis), blockage of the bile ducts by stones (cholelithiasis), helminths, tumors, abscesses, etc. The liver is slightly enlarged or more often reduced in volume, lumpy, yellow in color.

Congestive jaundice, catarrhal enteritis, and chyme and feces discolored due to the lack of bile are also noted. Histologically, along with the proliferation of connective tissue in the area of the Glissonian triad and bile ducts, atrophy of hepatocytes, a large amount of bile and blood clots in the bile capillaries are noted.

Infectious cirrhosis- secondary. They are found in tuberculosis, salmonellosis, brucellosis and other infectious diseases. They occur against the background of the underlying disease, mainly of the type of hypertrophic cirrhosis.

Pancreatic diseases
glands

Stone formation (pancreolithiasis). In the pancreatic ducts, this phenomenon is observed in fattening animals aged 5-10 years and older.

In the ducts, single, large or more often multiple (from several tens to hundreds) small, grains of sand to pea-sized, white concretions of irregular, spherical or polyhedral shape are found total mass up to 260 g. The affected ducts are dilated and thickened. In the pancreas, hyperplasia of glandular tissue, induration, or wrinkling is noted.

Gynoglycemic ketosis, diabetes (respectively hyperglycemic ketosis) and morbid obesity. In cattle and others, with these diseases, protein-fatty degeneration and atrophy of the pancreatic parenchyma, partial replacement of its parenchymal cells with fibrous and adipose tissue, which are visible in the form of large and small nests in the thickness of the organ, are noted. Histologically, protein (granular) hydropic and partially fatty degeneration, simple and numbering atrophy of the exocrine parenchyma, islets of Langerhans, and reduction of the insular apparatus, i.e., its beta cells, are noted. The process may end in cirrhosis of the organ.

Inflammation of the pancreas (pancreatitis). It can occur acutely, subacutely or chronically.

Macroscopically acute pancreatitis manifests itself as serous edema, hemorrhage, purulent inflammation with the formation of abscesses, and rarely - hemorrhagic-necrotic inflammation. Catarrhal enteritis is also usually observed. At chronic pancreatitis along with lymphoid-histioplasmacytic infiltration, atrophic fibrosis, cirrhosis of the organ, sclerosis and hyalinosis of its stroma develop with impaired patency of the ducts, the formation of stones and cysts. The organ acquires cartilaginous and, in some places, bone density.

Tumors. Rarely found in the pancreas of cattle. Leukotic neoplasms, sarcomas, adenomas and carcinomas have been described in him. Clinically the disease is difficult to determine. A decrease in the concentration of insulin, alpha-amylase and lipase in the blood serum is of diagnostic significance. The decisive role is played by pathomorphological diagnosis (including intravital necessary cases examination of organ biopsies).

Peritoneal diseases

Peritonitis. This is inflammation of the peritoneum. It occurs with limited or diffuse damage to the serous membrane, with accumulation of exudate in the abdominal cavity.

In acute peritonitis, they depend on the type of exudate (serous, fibrinous purulent, ichorous, etc.). The abdominal cavity contains a turbid gray-reddish liquid with increased amount protein, leukocytes and erythrocytes, with an admixture of fibrin, pus and feed mass or chyme. The peritoneum is swollen, reddened, with hemorrhages, with fibrinous or purulent deposits.

In chronic peritonitis (often found in cattle with traumatic reticulitis), fibrinous exudate undergoes organization and often with the formation of connective tissue adhesions of the visceral and parietal layers of the peritoneum with the serous membranes of the organs. Encapsulated abscesses are detected in the abdominal organs.

Ascites (abdominal dropsy). It occurs chronically and is caused by the accumulation of fluid in the abdominal cavity.

At autopsy, a clear yellowish or reddish liquid is found in the abdominal cavity (up to 150 liters in large animals). The peritoneum is somewhat thickened, and the abdominal organs are anemic.

Control questions

What are gastritis and enteritis? What are their types and causes?
What macro- and microscopic changes are observed in catarrhal, fibrinous and hemorrhagic gastritis and enteritis?
What is colic in horses, its classification, causes and autopsy picture when animals die?
What is rumen tympany and what changes occur in the body?
What is the mechanism of death in ruminal tympany in ruminants and various types of intestinal confusion in horses?
What are digestive tract diverticula? What are the mechanisms of their occurrence and their significance for the body?
What changes are observed in the liver during toxic dystrophy?
What is cirrhosis of the liver? What types of cirrhosis are known in animals and their differences from each other in macro- and micropicture?
What diseases of the pancreas occur in animals and their significance for the body?
What is peritonitis and how does it differ from ascites? How often are peritoneal diseases observed and what connection do they have with damage to the gastrointestinal tract?

Literature

pathological anatomy of farm animals. /ed. Shishkova V. P.; M.: Kolos, 1980
Pichugin L. M., Akulov A. B. Practical lessons on pathological anatomy of domestic animals, Selkhozizdat, 1980.
Zharov A. B. et al. Autopsy and pathological diagnosis of diseases of agricultural animals. M.: Kolos, 1982.
Kokurichev P. M. et al. Atlas of pathological anatomy of farm animals. 1973
Kokurichev P. M., Dobin M. A. Fundamentals of forensic veterinary examination. M.: Kolos, 1977.

Volvulus is a condition in which intestinal loops twist around their axis or around the mesenteric ligament. The intestinal lumen is blocked, normal bowel function becomes impossible. In this case, compression of large blood vessels, feeding the intestinal walls, as a result of which the blood supply and nutrition are disrupted or completely stopped.

As a result: complete intestinal obstruction and necrosis of bloodless tissue (death). If nothing is done at this moment, the process is complicated by developing sepsis, as well as peritonitis, after which it becomes almost impossible to save the life of a cat or dog. The segment of the small intestine most often suffers; torsion of the large intestine is much less common. The concept of intestinal volvulus also includes gastric torsion (volvulus).

What you need to know about volvulus, the main causes

The main (but not official) reason, according to many experts, is congenital anomaly development and formation of the mesentery, the very ligament that holds the intestines in the correct location, attaching it to back wall abdominal cavity. Everything else is already considered only provoking factors, due to which volvulus develops as a secondary pathology.

The main predisposing factors in both cats and dogs include:

prolonged inflammation in the peritoneum, accompanied by adhesions;
sudden changes in the level of intraperitoneal pressure due to excessive activity of animals immediately after eating food;
non-compliance with the diet, when prolonged hunger is replaced by excessive overfeeding, which provokes increased intestinal motility. It is observed when a dog/cat is fed once a day, but not enough;
entry of a foreign body into the stomach with its subsequent passage to the intestinal tract;
prolonged unregulated constipation;
very low quality feed;
intensive helminthic infestations leading to blockage of the stomach or intestines;
hormonal disruptions in the body, which lead to changes in the elasticity of the mesentery, causing its excessive stretching;
any neoplasms in the gastrointestinal tract;
heredity (the gene associated with this pathology has not been identified, but there is an opinion that bloat is inherited);
large size of animals and breed predisposition.

In cats, bloat is extremely rare, and the risk group mainly includes kittens and young animals under the age of 1 year. In dogs this pathology– is not uncommon, and affects mainly medium- and large-sized breeds (weighing 40 kg or more) and more often males than females.

The disease is most often registered in:

Great Danes;
St. Bernards;
German Shepherds;
Giant Schnauzers.

What are the signs to identify volvulus in dogs/cats?

Of course, it will not be possible to make a diagnosis on your own without auxiliary diagnostic methods (ultrasound, x-ray). True, animals usually fall into the hands of a veterinarian in such a condition that there is no time to additional examination simply no. Therefore, there are a number of symptoms that should alert cat and dog owners and prompt them to immediately contact a veterinarian. These signs are quite pronounced, and at their first manifestations, you should contact a specialist within the next 6-8 hours. The signs of bloat in both types of animals are approximately the same.

Signs of volvulus in dogs

the stomach increases, becomes swollen and hard, like a barrel;
body temperature is either excessively high or significantly below normal (more often - below);
signs of weakness, apathy, which are periodically replaced by fuss and anxiety;
signs of pain: the animal whines, looks for a comfortable, forced position in order to reduce painful sensations, sometimes it seems that the paws have lost their strength;
strong salivation, vomiting white foam. Sometimes there is the urge to vomit, but there is no vomiting - this is an important clinical sign;
pallor of the mucous membranes;
shortness of breath may occur;
absence of bowel movements;
septic shock due to oxygen starvation of intestinal tissues and the occurrence of necrosis (the body poisons itself), loss of consciousness.

Signs of volvulus in cats

because of severe pain in the abdominal cavity, the cat meows, fusses, becomes irritated, can hide from people, drag its paws behind it, as with paresis;
the belly swells, sometimes asymmetrically from different sides, the cat does not allow you to touch it, it is hard to the touch, like a drum (“sharp” belly - this distinguishes volvulus from flatulence);
the animal refuses water and food (sometimes even the most favorite treats) or eats/drinks a little, but immediately vomits (sometimes there may be blood or blood clots in the vomit);
on the eve of an exacerbation of the condition, there is no feces for more than 2 days;
increased body temperature;
literally in a couple of days the cat becomes thin, clearly exhausted and dehydrated (intestinal function is disrupted, the body does not absorb anything for itself);
shock from intoxication against the background of decomposing areas of the intestine, which are left without access to oxygen due to squeezing of blood vessels, loss of consciousness.

Attention: if more than 2 signs from the lists are detected at the same time, one of which is a painful enlargement of the abdomen, the count of the pet’s life can count for hours - you should take the pet to the veterinarian immediately!

Treatment of volvulus

Unfortunately, this situation requires only surgical intervention in a veterinary clinic. Only surgery can correct the condition. There is nothing you can do to help yourself at home! Most often, upon arrival to the veterinarian, the animal immediately goes to the operating table.

Before the operation, the animal is given emergency care

a puncture is made in the abdominal cavity (laparocentesis) in order to release stagnant gases and reduce intra-abdominal pressure;
painkillers, antiemetics, antispasmodics, and steroid hormones are administered.

The operation usually includes

mandatory complete audit of the entire intestinal tract;
the fastest possible restoration of blood circulation in those areas of the intestine that can still be rehabilitated by restoring the correct course of intestinal loops and removing dead areas affected by necrosis and not performing their digestive and absorption functions;
mandatory gastric lavage and suturing it to the abdominal wall.

After the operation, it is necessary to prescribe

infusion therapy (drip administration of solutions that relieve intoxication of the body, replenish blood loss, if any, performing the function of artificial carbohydrate nutrition);
antibiotic therapy.

The sooner the diagnosis is made, the higher the chances of saving the animal. If volvulus is suspected, the animal should be immediately taken to a veterinary clinic for an accurate diagnosis.

Postoperative complications cannot be excluded even after a successfully performed operation.

The main consequences of eliminated volvulus include

adhesions,
excessive stretching of the mesentery with subsequent relapses;
short bowel syndrome (when a large section of intestine is removed, the process of digestion and absorption is disrupted nutrients, diet and enzyme preparations are indicated for life);
long period for artificial nutrition liquid food through a tube or through a special tube passed directly into the rectum (artificial fistula).

Very often there are cases when dogs and cats cannot be saved, because... pet owners are late in seeking qualified help.

Prevention of volvulus in dogs and cats

After surgery to eliminate the disease, you must follow some rules to minimize the risk of relapse. Not a single animal is 100% insured against repeated bloat, no matter how successful the first surgical intervention ends.

What should you do to reduce the likelihood of recurrence of the disease:

strict diet: feeding high-quality feed or natural nutrition with highly digestible foods,
dry food is excluded;
feed the animal no more than 3 times a day, if necessary, give enzyme preparations, which are prescribed by a veterinarian individually in each specific case;
do not allow active games with pets immediately after feeding;
protect the dog/cat from stress factors as much as possible;
If a family adopts a purebred puppy or kitten, it is better to ask whether their parents had similar pathologies (if such information exists).

Simple measures to prevent volvulus in pigs should be taken this summer to avoid sudden deaths.

According to Duncan Berkshire, there has been an increase in such cases in England this summer. A large difference in summer temperatures, as a rule, causes an increase in morbidity, mainly in fattening. Heat may lead to a decrease in feed intake, but when it falls the pigs try to satisfy their hunger. As a result, the intestines suddenly become overcrowded, causing them to twist and die within two hours.

Symptoms are also difficult to detect. You can sometimes see symptoms of discomfort in pigs similar to colic in horses, which are signs of pain. But since this happens quickly, the first sign will most likely be a corpse that appears bloated.

Another factor that can influence access to feed and its passage through the intestines is social hierarchy. With absence free space feeder or deficiencies in the automatic feeding system, pigs may greedily swallow the feed when it arrives. In addition, pigs lower in the hierarchy may also be able to ingest food quickly to avoid collisions with pigs higher in the social hierarchy.

This is why it is important to ensure that pigs are in stable social groups, with adequate access to feed and water, and sufficient space in the pen. Frequent movement of pigs may also increase the risk of volvulus, so all environmental and social factors must be taken into account.

However, the prevalence of pig deaths from volvulus may be underestimated because not all pig carcasses are sent for autopsy. But, when sudden death occurs, then one should try to find the cause so that proper measures can be taken.

According to Derek Armstrong, BPEX VET Advisor, volvulus occurs randomly. With liquid feeding, if whey is used, gases are released as a result of fermentation of carbohydrates, which leads to instability in the intestines. The same thing happens with other feedings with a high carbohydrate content. Mr. Armstrong recommends the use of organic acids in feed and water if such cases occur.

Feeding large amounts of whey and dairy products can be particularly risky when it comes to volvulus, agrees Richard Pearson of George Vet Group. When whey makes up more than 20% of the diet, you are in the danger zone. And when producers have a lot of whey at their disposal, the mortality rate due to volvulus can be as high as 2%. To minimize the risk of pigs becoming gluttonous, producers should feed them ad libitum.

Rotation of the intestines in the abdominal cavity is one of the most common reasons sudden death when raising pigs, according to veterinarian Mark White, published in the latest health bulletin from Nadis (Health Bulletin NADIS).

Sudden death of growing pigs is not uncommon in modern production. One of the most common causes of such losses is the rotation of the intestines in the abdominal cavity around all or part of its attachments to the lower part. spinal column. This twist cuts off the blood supply to the intestines, causing necrosis and rapid death. Such conditions may occur sporadically or as an outbreak. Adult animals, although sometimes susceptible to intestinal torsion, more often suffer from distension and torsion of the stomach, which is also fatal.

Volvulus

Signs and diagnosis

Figure 1. Typical secondary infection of twisted bowel

Figure 2. In a rolled intestine, the cecum is located in the opposite direction from normal.

In most cases, pigs are found dead. This can happen at any age, but most often during the fattening stage between 25 and 100 kg. Typically, the abdomen of the corpse is greatly distended, often with protrusion of the rectum, accompanied by rapid discoloration and decomposition. The corpse looks pale.

At autopsy, the intestinal loops are distended with gases, dark purple in color and filled with bloody fluid. (Fig. 1) The intestinal walls are thinned, in contrast to acute porcine intestinal adenomatosis/hemorrhagic proliferative enteropathy (Lawsonia int.). As a rule, bloody fluid accumulates in the abdominal cavity. Depending on how twisted the intestine is, nodes can be felt in the tissues on which it is suspended and which maintain its normal position. Throughout the intestine, torsion can be as much as 360°, although typically less so that the most visible part of the intestine, the cecum, will not be directed towards the pelvis and anus, which is its normal orientation (Fig. 2) .

Sometimes, such pigs can be seen before death, they will look pale, depressed, inactive, and, if very early, with signs of acute pain. They usually lie on their chest in a hunched position and grind their teeth. Which is a sign of pain. As the intestinal tissue dies, the pain goes away and death occurs quietly.

Causes

The pig is particularly susceptible to volvulus and, in this regard, can be considered “deficient”, which applies equally to boars and gilts. The entire intestine is attached to the body by a suspensory mechanism called the mesentery, which loops about 20 m of intestine to the lower spine in the abdominal cavity, which is several centimeters long. Such a system is fundamentally unstable. The onset of a volvulus is likely to be when all or part of the intestine becomes too full of gas, which increases instability in the intestine as it hangs down in the abdomen. Sudden movements that allow the bowel loops to rotate can cause compression due to twisting.

Thus, the main causes of volvulus are conditions that stimulate the formation of gases in the intestines. These include the following:

1. Binge eating.

2. Winter feeding with fermenting wet food, such as whey - in summer, the higher summer storage temperature allows them to partially ferment before feeding, thereby reducing the possibility of gas formation in the intestines, which does not happen in winter.

3. Disorderly feeding , especially, but not exclusively, wet food. Where feeding is interrupted, such as on weekends due to broken or frozen pipes, resuming feeding can lead to a wave of volvulus.

4. High diet density including a diet that includes very high level specific raw materials, such as soybean, that promote rapid growth.

5. Colitis- If this condition exists, the proliferation of bacteria in the colon leads to greater production of gases from fermentation and increased curdling. The main conditions of intestinal volvulus (twisting is known as volvulus) become the main ones where there is any manifestation of diarrhea in growing pigs.

Control (prevention) of volvulus is obviously central to nutritional control, diet selection and control of intestinal diseases. However, in a population where feed intake and growth are high, the prevalence of volvulus can be considered an intensive management disease and is often a sign that the pigs are doing well. This will require careful assessment of the cost of mortality versus the potential increase in losses if feeding levels or ration density are reduced. This may also be influenced by certain breed characteristics.

Dilatation and torsion of the stomach

Figure 3. Infection Clostridium novyi (the liver looks like airy chocolate), may be considered due to gastric distension in sows.

Figure 4. Non-pregnant sows in restrained pens, where gastric torsional distension problems are particularly common.

Compared to intestinal volvulus, gastric distension—inflating the stomach with gases—and its ability to rotate to create similar intestines pathological processes, are more often observed in adult pigs.

Typically, strong fermentation is not characteristic of the stomach, and small volumes of gas may be regurgitated. If gas production becomes excessive, the junction of the esophagus and stomach closes like a valve. (The condition is similar to that seen in some dog breeds, such as the Basset Hound).

While there is no definitive data to estimate the prevalence of this condition, clinically it is much less common in non-pregnant sows, except where sows are kept in cramped pens and tethered. In such a situation, hand feeding sows once a day tended to result in some sows waiting a long time to receive feed after the start of the feeding cycle and becoming very anxious. This led to greedy absorption of feed, possibly with the ingestion of large volumes of air, which began the process of distension of the stomach. However, questionable hygiene may promote anaerobes, which are important in promoting gas formation. On some farms, Clostridium novyi infection (liver shaped like puffed chocolate) is reported as a separate cause of death.

With sows now free-range in the UK and predominantly fed straw, this condition is now more prominent post-farrowing/early lactation, probably due to reduced feed volume and changes in diet. In some cases, mycotoxicosis occurred.

Clinical signs

In a live pig, the abdomen, especially the front part, will be noticeably distended and the sow will show signs of pain similar to volvulus in growing pigs.

More often, a sow is found dead with an extremely swollen abdomen - fermentation continues and even increases after death, although pallor is not a necessary sign.

When opened, the extremely dilated stomach may be twisted (along with the spleen) and the lungs will be compressed as a result of pressure on the diaphragm.

Control

Availability of clean barley straw good quality Provides sows with a large amount of fiber, which is needed to reduce the risk of gastric fermentation. Giving bran (1 kg/day) during farrowing can help maintain fiber intake and avoid problems if they arise during farrowing. In the maternity ward, with good lactation, feeding at least two or even three times a day reduces the risk of gastric fermentation. As always, good food hygiene is also key. (The use of clostridia vaccine alone has been shown to have little effect on the problem.)

Expenses

If a farm has a problem with intestinal volvulus at the beginning of fattening, mortality due to this cause can reach two to three percent. If they occur at the final stage of fattening, the losses amount to over£ 100 from each case at current prices – a herd of 500 sows can lose£500 per week, and from £ 25000 per year. If growth retardation is a preventative option, it should be worth the cost.

There have been outbreaks of distension and volvulus (in pens) where 10 percent of the herd could die within three months. Death of 50 pregnant sows (at different stages pregnancy) can lead to a shortage of farrowings throughout the six-month cycle, leaving the herd without 500 piglets in addition to the mortality of the sows themselves. Most often, this condition is seen as a minor problem, accounting for up to two percent of deaths during the year. Such costs are very difficult to quantify.

January 2010