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Diseases of the liver and gall bladder
With the development of possibilities for diagnosing diseases of internal organs, it was found that liver disease (hepatopathy) is much more common than previously thought, and that many vague signs of disease are based on hepatosis. Due to the importance and variety of functions, the liver is endowed with a natural ability for high regeneration. Therefore, pathological processes arising under the influence of various factors in it become noticeable and manifest clinically only in the progressive stages of the disease. So, jaundice associated with hepatopathy, unmistakably indicates the worst condition of the liver.
The main symptoms that characterize hepatopathy:
dyspeptic syndrome: lethargy, depression, anarexia, vomiting, defecation disorders;
jaundice: bradycardia, brown staining of urine, light gray clay feces, icteric staining of mucous membranes, skin itching;
hemorrhagic syndrome: hemorrhages in the skin and mucous membranes, anemia, an increase in bleeding time;
portal hypertension syndrome: an increase in the abdomen in the epigastrium, ascites, expansion of the saphenous veins of the abdomen;
hepatolienal syndrome: enlarged liver, simultaneous enlargement of the spleen.
X-ray enlargement of the liver is not always evidence of impaired organ function. Equally, one cannot immediately conclude that there is no pathology only by the favorable results of studies of urine and blood samples. Crucial are the bromosulfalein test, the determination of alkaline phosphatase activity or the assessment of transaminase samples in dynamics.
Hepatopathy is a toxic and inflammatory degenerative damage to the cells of the liver parenchyma that occurs under the influence of a number of factors. According to the degree of significance in the etiology of liver disease, they are distributed as follows:
1) toxins supplied with food (when fed with spices and smoked meats - the action of phenols!), And toxins formed during incomplete digestion of food with intestinal disease;
2) toxic substances arising from renal failure;
3) toxic products of protein breakdown in large malignant tumors, hemolytic processes and leukemia;
4) poisoning with hepatotoxic substances;
5) disorders of protein, carbohydrate, fat metabolism, diabetes;
6) heart failure and circulatory failure;
7) infections (leptospirosis, adenovirus hepatitis);
8) infestations (toxocariasis, hookworm, coccidiosis, dipylidiosis, opisthorchiasis);
9) alimentary protein deficiency (with poor feeding of dogs).
Depending on the intensity and duration of the action of these factors, fatty degeneration, liver cell necrosis, inflammation of the liver tissue, lymphoid leukemic infiltration, tumor destruction or diffuse growth of the connective tissue develop. However, under practical conditions it is impossible to make such a distinction between morphological lesions, because in the arsenal of veterinarians there are still not enough special research methods. Therefore, it is proposed to distinguish acute and chronic hepatopathies, chronic hepatopathy with cholestasis and cirrhosis, which covers the whole complex of painful manifestations and at the same time is a sufficient distinction for a differentiated therapeutic approach.
Acute hepatopathy. Acute liver failure. Hepatic coma. Massive damage to the liver parenchyma in severe poisoning by hepatotoxic poisons, infections, and sepsis, despite the significant compensatory capabilities of this organ, are accompanied by deep violations of its numerous and extremely important functions for organs, which is distinguished by practical doctors as acute liver failure syndrome. The syndrome develops within a few hours or days immediately after the onset of the action of the pathological factor. The development of acute liver failure is based on diffuse fatty degeneration and total necrosis of hepatocytes, which is manifested by a significant decrease in all liver functions, the formation of numerous vascular collaterals between the portal and vena cava, due to which toxic products bypass the liver. Severe self-poisoning of the body due to the almost complete cessation of liver activity leads to the development of hepatic coma. The most toxic are the unreacted products of bacterial intra-intestinal breakdown of the protein - especially ammonia. Phenols, normally inactivated by the liver, also have a toxic effect. In acute liver failure, electrolyte metabolism is disturbed, hypokalemia, hyponatremia, metabolic acidosis occur.
Symptoms The clinical manifestations of acute liver failure quickly develop into a coma. Progression of consciousness up to its complete loss. The animal is in a state of prostration and constant indomitable vomiting. A sweet, fetid, fetid odor emanates from the jaws of the animal, due to the release of methyl mercaptan resulting from metabolic disturbances in methionine. In the terminal phase, vascular insufficiency and shock develop.
As a rule, hepatic coma ends in the death of the animal. However, in some cases, recovery is possible. In acute liver failure, the patient dies not so much from an excess of toxic products, for example, in acute renal failure, but from a catastrophic lack of necessary and irreplaceable substances.
Diagnosis. They put it taking into account the data of a biochemical study of blood serum (table. 6).
6. Differentiation of hepatopathies based on radiological and serological data (Nimand 1980)
Designations: - decrease in values; 0 is the norm; + increase in values
Treatment. The main objective of the treatment of acute liver failure is the drug maintenance of the body's life until the onset of liver regeneration. If the causes that caused hepatonecrosis are eliminated, then hepatocytes regenerate within 10 days.
Therapy of acute liver failure is divided into the following components: stopping hepatonecrosis, improving the preserved liver functions, biochemical correction and elimination of concomitant syndromes. For this, animals are prescribed prednisone at least 30 mg per day and diuresis is stimulated with mannitol in order to decompress swollen liver tissues. A solution of glucose with hemodesis (20: 1), choline chloride and glutamic acid, which binds ammonia, is dripped into the vein. Alvezin is infused, oxygen therapy is carried out. To prevent the formation of ammonia, they cleanse the intestines and prescribe antibiotics. You should strive for the longest possible application of medications for several hours, calculating the total allowable amount of injected fluid 30-50 ml / kg. The longer and more continuous therapy, the more pronounced and fuller the expected effect.
Chronic hepatopathy. Chronic liver failure. Jaundice. The definition of hepatopathy in relation to liver diseases was not chosen by chance, since the distinction between the concepts of hepatitis and hepatosis in itself is very relative from the modern point of view. Severe acute and chronic liver diseases (fatty degeneration, infectious hepatitis, leptospirosis, tuberculosis, cirrhosis, tumors, lymphoid infiltration of the liver) due to the gradual progressive degeneration and death of hepatocytes lead to the development of chronic liver failure, which, in contrast to acute, worsens for weeks, months and is complicated sometimes jaundice. Jaundice and hyperbilirubinemia result from a disorganization of the structures of the liver and cholestasis in the blood, when the kidneys cease to cope with the removal of excess bile pigments. Unrealized bile pigments are poison for the body, and their accumulation in the blood of an animal almost always predicts a poor outcome. Due to impaired synthesis in the liver of albumin and severe hypoalbuminemia, hypoproteinemic edema in the chest and ascites can appear. The development of ascites in liver disease is also associated with portal hypertension due to impaired blood flow in the portal vein system. An important consequence of disturbed protein metabolism is a decrease in the production of blood coagulation factors, leading to hemorrhagic diathesis, which is partly due to a violation of the absorption of vitamin K from the intestine.
The clinical manifestations of chronic liver failure are usually combined with symptoms of liver disease, which led to the failure of its function. In the initial stage, the development of liver failure is mainly indicated by dyspeptic symptoms (anarexia, vomiting, diarrhea). There may be symptoms of a fever. An X-ray examination showed an increase in the size of the liver and spleen (hepatolienal syndrome) (Fig. 40). In the blood serum, an increase in bilirubin is detected, transaminases see table. 6). An increase in creatinine in some cases indicates a secondary involvement of the kidneys in the pathological process (hepatorenal syndrome). Rarely, only in some diseases of the liver (leptospirosis, infectious hepatitis, tumors in the area of the portal of the liver), ictericity of the mucous membranes and skin integuments appears.
Fig. 40 Pathological liver hypertrophy, splenomegaly: 1 - costal arch, 2 - diaphragm border, 3 - liver contours outside the costal arch, caudal angle of the liver edge more than 30 °, 4 - enlarged spleen contours
In the final stage of the disease, precursors of coma develop depression, lowering body temperature below normal. Against this background, jaundice intensifies, hemorrhages occur under the epithelial integument, often there is an admixture of blood in the feces. Radiologically, a decrease in the liver is sometimes noted. Laboratory studies show mild anemia, leukocytosis, increased ESR, low platelet count, prolonged bleeding time and blood clotting time.
Diagnosis. The final set according to biochemical blood tests, in particular aminotransferases (see table. 6), and in case of infections - according to serological studies.
Differential diagnosis. First of all, it is extremely important to determine the degree of impaired liver function, and then to distinguish parenchymal jaundice from obstructive and hemolytic. Parenchymal jaundice is directly associated with hepatopathy and destruction of the liver parenchyma; obstructive due to the closure of the lumen of the biliary tract, hemolytic - hemolytic processes occurring in the body.
Differential signs of hepatopathy and types of jaundice are shown in tables 6 and 7. Additional differentiation of parenchymal jaundice from mechanical jaundice is possible using a prednisolone test: 30 mg of prednisolone per day is prescribed. In the case of parenchymal jaundice, the icterity of the integument will greatly decrease after a few days.
Forecast. Mild forms of chronic compensated hepatopathy are asymptomatic and not of great importance for the life of the animal. But with long-existing liver failure, the kidneys, heart, spleen, pancreas, intestines are involved in the dystrophic process. Then the forecast worsens. The progression of liver failure with the addition of jaundice, ascites, coma and shock is always a very unfavorable sign.
Treatment. Chronic hepatopathies, depending on the severity of the condition and taking into account the need to eliminate the causes of the disease, provide a package of measures:
peace. It is recommended to stop sporting activities, to exclude loads;
diet. They compose a diet containing little protein (not higher than 17% crude protein), easily digestible fats (sunflower oil - 60% linoleic acid), easily digestible carbohydrates (increase gluconeogenous reactivity of the liver). Obese animals reduce the total calorie intake. For better bowel movement, it is recommended to give flaxseed decoction or glycerin. To reduce putrefactive processes in the intestine, reduce ammonia production and eliminate flatulence, bifidumbacterin is prescribed;
antibiotics. Prescribe with suspected leptospirosis and other bacterial infections, putrefactive decomposition of chyme in the intestine;
glucocorticoids. Always appointed! It is preferable to use prednisone. An initial dose of 30 mg per day daily (regardless of the size of the animal). The dose is maintained until the transaminase activity indicators are normalized, then halved and then every five days - by 5 mg. After a daily dose of 5 mg for a long time, for 1-2 months, a dose of 2.5 mg is maintained;
vitamins. Shown are B1, B6, B12 and E;
choleretic drugs. Silibinin;
glucose, electrolytes. Drip intravenously infusion of drugs with progression of signs of liver failure. Drugs are used after 1-2 days until the condition stabilizes.
Cirrhosis of the liver. This is a chronic progressive hepatopathy characterized by dystrophy and necrosis of the hepatic parenchyma, accompanying its nodal regeneration of the parenchyma and diffuse proliferation of connective tissue with a deep restructuring of the architectonics of the liver. Cirrhosis of the liver is very rare in dogs, since animals usually do not live to see this condition. It develops as a resolving phase of acute and chronic hepatopathy, but sometimes due to alimentary protein deficiency, with congestive liver events associated with heart disease.
Symptoms They are generally the same as in chronic hepatopathies, but there may be deeper loss of organ function. The idea of cirrhosis may be prompted by a combination of symptoms of liver failure with gynecomastia in males and genital dysfunction in females due to the delayed breakdown of steroid hormones (estrogens) in the liver.
The course is usually progressive. The total duration of the disease usually does not exceed 1 year.
Diagnosis. Intravital diagnosis is difficult.
Treatment. With the active process, glucocorticoid hormones, sirepar, silibinin, vitamins are prescribed. Periodic diuretics are recommended. With ascites, which is not amenable to treatment with diuretics, a fluid is released using laparocentesis.
Gall bladder stones. Gall bladder stones in dogs are very rare, and they are discovered by chance during revision of the abdominal cavity during surgery. Whether dogs have cholelithiasis (cholelithiasis) is still not clear. With non-specific phenomena: the presence of vomiting, mucous stools, increased activity of alkaline phosphatase and normal values of transaminases - the formation of stones in the gall bladder can be assumed.
The diagnosis is proved by cholecystography. In the evening, it is recommended that the dog intestines be cleaned with vaseline oil or flaxseed decoction. In the morning on an empty stomach, bilivestan in a dose of 0.3-0.5 mg / kg is slowly injected into a vein for 5 minutes and after 90 minutes a picture is taken. The gall bladder is projected in the 5-6th intercostal space. In case of violation of the concentration ability of the gallbladder or obstruction of the cystic duct, the shadow of the gallbladder in the picture is absent. In the presence of stones, the shadow of the gallbladder looks heterogeneous, in it the areas of enlightenment are determined according to the number and size of the stones. A contraindication to this diagnostic procedure is a severe condition of the liver and kidneys, severe cardiovascular failure.
The course of the disease is long asymptomatic.
Treatment. It is carried out in case of a painful condition or the appearance of jaundice associated with obstruction of the bile duct. Perform cholecystotomy with stone extraction or cholecystectomy.
Technique of operations. General anesthesia, dorsal position of the animal, laparotomy in the supra umbilical region.
Open the wound of the abdominal wall and make an audit of the organs. In the presence of stones, the gallbladder has an glaze cartilage-like appearance. The gall bladder is isolated, its walls are opened in the apex region, stones are removed and the cavity is washed with an isotonic sodium chloride solution. The wall is sewn with a hermetic one-story continuous seam with silk No. 0.
In cases of severe inflammatory changes in the wall of the gallbladder, when it ruptures and outflow of bile into the abdominal cavity, obstruction of the bile duct causes cholecystectomy with a stone (Fig. 41). The neck of the bubble is closed with clamps and intersected between them. A stone localized in the bile duct is pushed through. The stump of the neck is tightened with two silk ligatures No. 0. The wound of the abdominal wall is closed in the usual way.
Figure 41. Cholecystectomy 1 - the place of clamping and intersection of the neck of the gallbladder, 2 - the place of application of the ligature
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