Cirrhosis

Cirrhosis - proliferation of connective tissue in the parenchymal organs (liver, lungs, kidneys, etc.), accompanied by a rearrangement of their structure, compaction and deformation.

There is a gradual replacement of normal tissue of the body with scar tissue: sclerosis goes to fibrosis, and then to cirrhosis and is the outcome of hepatitis, proliferative inflammation, microcirculation disorders in tissues, necroses of various origin, intoxications and other adverse effects.

[1], [2], [3], [4], [5]

Cirrhosis of the liver

With cirrhosis of the liver, there is no system that would not be involved in the process, so the clinical picture is polymorphic, but there are general manifestations that depend on the severity of liver damage and the form of cirrhosis in etiology. The disease develops gradually, slowly but steadily progresses, with an alternation of improvement and worsening of the patients. In a third of cases, cirrhosis is clinically manifested only in the stage of decompensation.

Compensated liver cirrhosis (latent form) is more often detected during preventive examinations, since the clinical manifestations are weak and of little specificity. The most important symptom is the enlargement of the liver, its edge is rounded, compacted, weak or painless. Splenomegaly in this stage is rarely detected and is a sign of starting portal hypertension, but most likely with a superhepatic block. More worried about dyspeptic disorders: flatulence, constipation, alternating with diarrhea. Asthenic vegetative syndrome is characteristic: sweating, skin hyperemia, tachycardia attacks, sleep disturbance, skin itching, paresthesia, tremor of fingers, cramps of calf muscles. There are no abnormalities in laboratory tests of blood, but there is a tendency to disproteinemia, decrease of sediment samples, especially sulemic, coagulation samples, increased activity of aminotransferases, bound bilirubin, hepatic enzymes.

Subcompensated cirrhosis has already clear clinical manifestations. Disturbed weakness and fatigue, irritability, decreased appetite, nausea, vomiting, flatulence, bitterness in the mouth, intolerance to fatty foods, baking, alcohol. Pain blunt, aching in the right hypochondrium and epigastrium. Characteristic persistent manifestations: hepatomegaly (the liver is enlarged, dense, painful on palpation, its surface is uneven, the edge is rounded); splenomegaly. Often there is a subfebrile condition, the skin is dry, yellowish-gray in color. On the upper half of the trunk and neck, telangiectasias are formed, the skin of the palms of the erythema ("liver palms"). Often there are nosebleeds. There may be the first signs of portal hypertension caused by the intrahepatic block: varicose veins of the trunk and esophagus, usually without bleeding, ascites is not yet expressed, but with ultrasound is detected. Asthenic-vegetative syndrome is aggravated, sleep disturbance acquires a characteristic feature: sleeplessness at night and drowsiness during the day. Skin itching and paresthesia become pronounced, especially at night. Gradually, the phenomenon of psycho-organic syndrome in the form of memory decline, inertia of thinking, propensity to detail, resentment and suspicion, inclination to conflicts and hysteria are gradually growing.

Laboratory changes are expressed clearly: disproteinemia due to hypoalbuminemia and hypergammaglobulinemia, reduction of sediment samples, especially sulemic, coagulation samples with a decrease in fibrinogen, prothrombin, etc. The indicators of bound bilirubin, aminotransferases, hepatic enzymes grow.

Decompensated hepatic cirrhosis is accompanied by an aggravation of all the above symptoms and laboratory changes. Developing severe weakness, vomiting, diarrhea, weight loss, muscle atrophy. Characteristic manifestations of portal hypertension: parenchymal jaundice, ascites, varicose veins of the trunk, esophagus and stomach, often with bleeding. Gradually evolve adynamy, constant drowsiness, frustration of consciousness, right up to the coma. Develops a hepatorenal syndrome. Often an infection is associated with the development of pneumonia, peritonitis, sepsis, tuberculosis.

Depending on the etiological form of liver cirrhosis, other specific manifestations that allow them to differentiate are revealed.

Alcoholic cirrhosis of the liver - often develops in men, but it is more difficult for women. For the development of cirrhosis there is no need for massive alcohol intoxication and the nature of drinks, cirrhosis can develop even with regular use of only beer. With regular use by an alcoholic (do not confuse with household drunkenness, in which there is no alcohol dependence) a man of 50 ml of alcohol, and a woman - 20 ml of alcohol per day, cirrhosis is guaranteed within the next 10 years.

Specific manifestations of it: earlier hair loss on the head, down to alopecia, lack of hairiness in the armpits and pubic, men often have gynecomastia and testicular atrophy; can develop polyneuritis, atrophy of the muscles of the shoulder girdle, Dupuytren's contracture. The face is puffy, the skin color is uneven, with bluish spots and a nose, often the skin is tuberous. Teleangiectasia and erythema of the palms are not expressed, but the nails are often white in color. Portal hypertension develops in 100% of cases in the early periods.

Active forms of cirrhosis of the liver are a polyethyl group that combines the presence of chronic hepatitis, against which cirrhosis develops. The most common is active cirrhosis against hepatitis B and C, as well as long-term use of hepatotoxic drugs, including drugs (chlorinated hydrocarbons, diphenyls, phosphorus, methotrexate, plant poisons, fluorothane, isoniazid, inhibitors, MAO, methyldofa, nitrofurans and etc.);

Active liver cirrhosis caused by viral hepatitis is more common in men. Markers of this form of hepatitis are: surface-active antigen to hepatitis B virus - HBsAg and core antigen HBcAg. They are manifested by an increase in body temperature, wounds caused by the appearance of numerous telangiectasias, jaundice, the growth of aminotransferases is 5-10 times higher than normal.

Active cirrhosis of the liver of autoimmune genesis develops more often in women, it can also be caused by viral hepatitis, but is characterized by a combination with other autoimmune systemic diseases. The course is very active, decompensation and portal hypertension develop very quickly. In the study of blood, autoimmune disorders, high gamma globulinemia, hyperproteinemia are revealed.

Primary biliary cirrhosis develops mainly in women in menopause. It begins gradually with skin itching, worse at night, development is very slow, jaundice and compensation appear late, portal hypertension is practically not noted. Cirrhosis often combines with the diseases of Shergen and the Rhine Often, osteoporosis is formed, up to spontaneous fractures of the bones, mainly the neck of the hip and spine.

Secondary biliary cirrhosis is formed on the background of cholangitis, cholestasis, cholangiolitis: chills, fever, leukocytosis, jaundice, pain syndrome.

Characteristic increase in activity of alkaline phosphatase, 5-nucleotiaz, hyperlipidemia. Decompensation develops late.

Tactics: observation and treatment by a gastroenterologist; in surgical care the patient needs only if there is esophageal or gastric bleeding. With portal hypertension, the question of examination and surgical treatment is decided individually in the center of hepatology.

[6], [7], [8], [9], [10]

Cirrhosis of the lungs

Pneumosclerosis (fibrosis, cirrhosis) - development of scar tissue in the lungs with a violation of their function, which is the consequence (outcome) of chronic inflammation and adverse effects (dust, coal, allergens, etc.). Pneumosclerosis is considered a reversible form of cicatricial changes in the lungs, for example, with: bronchitis, bronchiectasis and most pulmonologists, especially in English literature, is considered a symptom of regenerative proliferative inflammation. In the formation of irreversible degeneration, the terms pneumofibrosis or pneumocirrhosis are used.

These disagreements have made it difficult to classify sclerotic processes in the lungs:

1. For etiology, cirrhosis is divided into: infectious specific (metatuberculous, syphilitic, mycotic, parasitic); nonspecific (pyogenic and viral); post-traumatic, including after aspiration, foreign bodies, burns; toxic; pneumoconiotic; dystrophic (with radiation pneumonitis, amyloidosis, ossification); allergic exogenes (medicinal, fungal, etc.) and endogenous (fibrosing alveolitis Hashin-Rich, Goodpasture, Kartagener, with collagen diseases, hemosiderosis or with eosinophilic pneumonia, Wegener's granulomatosis, Beck's sarcoidosis, etc.); cardiovascular (with heart diseases accompanied by pulmonary hypertension, vascular disorders of the small circle of blood circulation).
2. According to the pathogenesis there are: inflammatory sclerotic processes (bronchogenic, bronchoectatic, bronchiolar, post-pneumonic, pleurogenic); atelectaceous (for foreign bodies, long atelectasis of the lung, bronchogenic carcinoma); lymphogenous (mainly cardiovascular etiology); Immune (with limited or diffuse alveolitis).
3. According to the morphological feature diffuse processes (mesh, lymphogenous, alveolar, myofibrosis, bronchioles and small bronchi) and local (inflammatory, fibro-telecatal, dysplastic, allergic granulomatous) are distinguished.
4. According to the state of lung function, lung cirrhosis can occur without disrupting lung function and with obstructive ventilation according to obstructive, restrictive and mixed types; with pulmonary hypertension and without it.
5. With the course of cirrhosis can be progressive and non-progressive.

Given that sclerotic changes in the lungs are the outcome or manifestation of many diseases of the pulmonary and cardiovascular system, there are no specific manifestations of this pathology, but it should be identified, since it is a formidable complication that can give complications during surgical pathology, anesthesia and in the postoperative period. The leading manifestation of sclerotic processes is a violation of ventilation. In the obstructive type, the development of emphysema, lungs is noted, with restrictive and mixed type, gas exchange with the formation of hypoxic syndrome and respiratory failure is disrupted.

Confirm diagnosis of chest radiography and tomography, spirography or spiroanalysis (examination of the function of external respiration with the help of special spiroanalyzatrrov instruments, whose work is based on the method of pneumotachography), examination of KHS, bronchoscopy. Less commonly used scintigraphy with iodine-131, bronchography, angiopulmonography.

Tactics: depends on the underlying disease - either a referral to an anti-tuberculosis dispensary, or to a pulmonology department, or to a thoracic surgical department. At hospitalization in surgical or traumatological departments use active tactics of conducting such patients, anesthesia is carried out with increased caution in the amount of ventilation to prevent rupture of rigid or emphysema lung.

[11], [12],

Cirrhosis of the kidneys

Nephrosclerosis (fibrosis, cirrhosis) - replacement of the renal parenchyma with a connective tissue, leading to their densification, wrinkling and impaired function, which develops in various diseases of the kidneys and their vessels.

According to the pathogenesis, there are 2 forms of sclerotic changes: a primary-wrinkled kidney and a second-wrinkled kidney. Depending on the prevalence of the process and the features of the clinical course, a benign form is distinguished with a slow development of the process and a malignant form with rapid development of renal failure.

Primarily shriveled kidney develops with blood flow disorders in the kidneys due to hypertensive disease of severe degree, atherosclerosis of renal vessels, arteriolosclerosis with the development of multiple infarcts of the kidney.

Cirrhosis of the kidneys is clinically manifested by polyuria with a predominance of nocturnal diuresis (nocturia), low and variable proteinuria, low specific gravity and decreased osmolarity of urine, microhematuria, and sometimes macrohematuria, arterial hypertension, which is set on high figures, with a particularly high diastolic pressure level 120-130 mm Hg), which can not be medicated. Renal failure develops slowly. Heart failure, encephalopathy, edema of the optic nerve papilla and retinal detachment are often detected.

Secondary-wrinkled kidney develops as an outcome of infectious diseases of the kidneys (chronic glomerulonephritis, pyelonephritis, urolithiasis, tuberculosis, syphilis, etc.) or degenerative processes in it after injuries, repeated operations on the kidney, irradiation, in systemic diseases accompanied by development of amyloidosis in the kidneys Rheumatism, lupus erythematosus, diabetes mellitus, sepsis, etc.). Manifestations are the same as in the primary wrinkled kidney, can range from minor to severe renal failure.

The diagnosis of cirrhosis of the kidneys is confirmed by ultrasound (volume reduction and deformation of the kidneys), radioisotope renography using mercury hypurate (slowing the accumulation and excretion of the drug), urography (reduction of the kidney volume, deformation of the renal tubules, a decrease in the cortical layer). Other methods of investigation (angiography of the kidneys, scintigraphy, chromoscystoscopy) are used according to indications determined by the nephrologist.

Tactics: when a patient is treated with a surgical pathology, cirrhosis in the kidneys should be identified (characteristic blood pressure, changes in urinalysis), as these conditions are threatened during operations, anesthesia, in the postoperative period and with drug treatment. The patient should be consulted by a nephrologist or urologist. It is advisable to spend the postoperative period in the intensive care unit.

[13], [14], [15], [16], [17], [18], [19],