Cirrhosis

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

There is a gradual replacement of normal organ tissue with scar tissue: sclerosis turns into fibrosis, and then into cirrhosis and is the outcome of hepatitis, proliferative inflammation, tissue microcirculation disorders, necrosis of various origins, intoxication and other adverse effects.

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Cirrhosis

In liver cirrhosis, there is not a single system that is not involved in the process, so the clinical picture is polymorphic, but there are also general manifestations that depend on the severity of liver damage and the form of cirrhosis by etiology. The disease develops gradually, slowly, but steadily progresses, with alternating improvement and deterioration of the patient's condition. In a third of cases, cirrhosis is clinically manifested only in the decompensation stage.

Compensated liver cirrhosis (latent form) is more often detected during preventive examinations, since clinical manifestations are weakly expressed and of low specificity. The most important symptom is an enlarged liver, its edge is rounded, compacted, slightly or painless. Splenomegaly at this stage is rarely detected and serves as a sign of incipient portal hypertension, but most likely with a suprahepatic block. Dyspeptic disorders are more disturbing: flatulence, constipation alternating with diarrhea. Asthenovegetative syndrome is characteristic: sweating, hyperemia of the skin, attacks of tachycardia, sleep disturbance, itching of the skin, paresthesia, tremor of the fingers, cramps of the calf muscles. There are no deviations from the norm in laboratory blood tests yet, but there is a tendency towards dysproteinemia, a decrease in sedimentation tests, especially sublimate, coagulation tests, an increase in the activity of aminotransferases, conjugated bilirubin, and liver enzymes.

Subcompensated cirrhosis already has clear clinical manifestations. Weakness and rapid fatigue, irritability, decreased appetite, nausea, vomiting, flatulence, bitterness in the mouth, intolerance to fatty foods, baked goods, alcohol are disturbing. Dull, aching pains in the right hypochondrium and epigastrium. Characteristic persistent manifestations: hepatomegaly (the liver is enlarged, dense, painful to palpation, its surface is uneven, the edge is rounded); splenomegaly. Subfebrile temperature is often noted, the skin is dry, yellowish-gray. Telangiectasias form on the upper half of the body and neck, the skin of the palms is erythema ("liver palms"). Nosebleeds are often noted. The first signs of portal hypertension caused by intrahepatic block may appear: varicose veins of the trunk and esophagus, usually without bleeding, ascites is not yet expressed, but is detected by ultrasound. Asthenovegetative syndrome worsens, sleep disturbance acquires a characteristic feature: insomnia at night and drowsiness during the day. Skin itching and paresthesia become pronounced, especially at night. Gradually, the phenomena of psychoorganic syndrome increase in the form of memory loss, inertia of thinking, a tendency to detail, resentment and suspicion, a tendency to conflicts and hysteria.

Laboratory changes are clearly expressed: they are manifested by dysproteinemia due to hypoalbuminemia and hypergammaglobulinemia, a decrease in sedimentation tests, especially sublimate, coagulation tests with a decrease in fibrinogen, prothrombin, etc. The indicators of conjugated bilirubin, aminotransferases, and liver enzymes increase.

Decompensated liver cirrhosis is accompanied by aggravation of all the above symptoms and laboratory changes. Sharp weakness, vomiting, diarrhea, weight loss, muscle atrophy develop. Portal hypertension manifestations are characteristic: parenchymatous jaundice, ascites, varicose veins of the trunk, esophagus and stomach, often with bleeding. Adynamia, constant drowsiness, disorders of consciousness, up to coma gradually develop. Hepatorenal syndrome develops. Infection often joins with the development of pneumonia, peritonitis, sepsis, tuberculosis.

Depending on the etiological form of liver cirrhosis, other specific manifestations are identified, allowing them to be differentiated.

Alcoholic liver cirrhosis - develops more often in men, but is more severe in women. For the development of cirrhosis, there is no need for massive alcohol intoxication and the nature of the drinks, cirrhosis can develop even with regular consumption of only beer. With regular consumption by an alcoholic (not to be confused with everyday 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.

Its specific manifestations: early hair loss on the head, up to alopecia, sparse hair in the armpits and pubis, in men often gynecomastia and testicular atrophy; polyneuritis, atrophy of the muscles of the shoulder girdle, Dupuytren's contracture may develop. The face is puffy, the skin color is uneven, with glaucous spots and nose, the skin is often bumpy. Telangiectasias and erythema of the palms are not expressed, but the nails are often white. Portal hypertension develops in 100% of cases in the early stages.

Active forms of liver cirrhosis are a polyetiological group, which are united by the presence of chronic hepatitis, against which cirrhosis develops. Most often, active cirrhosis occurs against the background of hepatitis B and C, as well as with long-term use of hepatotoxic drugs, including medicinal ones (chlorinated hydrocarbons, diphenyls, phosphorus, methotrexate, plant poisons, fluorothane, isoniazid, inhibitors, MAO, methyldopa, nitrofurans, etc.);

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

Active liver cirrhosis of autoimmune genesis develops more often in women, can be caused by viral hepatitis, but a combination with other autoimmune systemic diseases is typical. The course is very active, decompensation and portal hypertension develop very quickly. Blood tests reveal autoimmune disorders, high gammaglobulinemia, hyperproteinemia.

Primary biliary cirrhosis of the liver develops mainly in women in the climacteric period. It begins gradually with skin itching, which intensifies at night, the development is very slow, jaundice and compensation appear late, portal hypertension is practically not observed. Cirrhosis is often combined with Schergen's and Reine's diseases. Osteoporosis often develops, up to spontaneous bone fractures, mainly of the femoral neck and spine.

Secondary biliary cirrhosis of the liver develops against the background of cholangitis, cholestasis, cholangiolitis: chills, fever, leukocytosis, jaundice, pain syndrome.

Characteristic is an increase in the activity of alkaline phosphatase, 5-nucleotidase, hyperlipidemia. Decompensation develops late.

Tactics: observation and treatment by a gastroenterologist; the patient requires surgical assistance only if esophageal or gastric bleeding occurs. In case of portal hypertension, the question of examination and surgical treatment is decided individually at the hepatology center.

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Cirrhosis of the lungs

Pneumosclerosis (fibrosis, cirrhosis) is the development of scar tissue in the lungs with dysfunction, which is a 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, in: bronchitis, bronchiectasis and most pulmonologists, especially in English-language literature, consider it a symptom of regenerative proliferative inflammation. When irreversible degeneration develops, the terms pneumofibrosis or pneumocirrhosis are used.

These differences have complicated the classification of sclerotic processes in the lungs:

1. By etiology, pulmonary cirrhosis is divided into: infectious specific (metuberculosis, syphilitic, mycotic, parasitic); nonspecific (pyogenic and viral); post-traumatic, including after aspiration, foreign bodies, burns; toxic; pneumoconiotic; dystrophic (with radiation pneumonitis, amyloidosis, ossification); allergic exogenous (medicinal, fungal, etc.) and endogenous (fibrosing alveolitis of Haschen-Rich, Goodpasture, Kartagener, with collagen diseases, hemosiderosis or eosinophilic pneumonia, Wegener's granulomatosis, Beck's sarcoidosis, etc.); cardiovascular (with heart defects accompanied by pulmonary hypertension, vascular disorders of the pulmonary circulation).
2. According to pathogenesis, the following are distinguished: inflammatory sclerotic processes (bronchogenic, bronchiectatic, bronchiolar, postpneumonic, pleurogenic); atelectatic (with foreign bodies, long-term atelectasis of the lung, bronchiogenic cancer); lymphogenous (mainly of cardiovascular etiology); immune (with limited or diffuse alveolitis).
3. According to morphological features, diffuse processes (reticular, lymphogenous, alveolar, myofibrosis, bronchioles and small bronchi) and local (inflammatory, fibroatelectatic, dysplastic, allergic granulomatous) are distinguished.
4. Depending on the state of lung function, pulmonary cirrhosis can occur without impairment of lung function and with ventilation impairment of obstructive, restrictive and mixed types; with pulmonary hypertension and without it.
5. Depending on the course of the disease, pulmonary cirrhosis can be progressive or non-progressive.

Considering that sclerotic changes in the lungs are the outcome or manifestation of many diseases of the pulmonary and cardiovascular systems, there are no specific manifestations of this pathology, but it should be identified, as 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 ventilation disorder. With the obstructive type, the development of emphysema, lungs is noted, with the restrictive and mixed type, gas exchange is disrupted with the formation of hypoxic syndrome and respiratory failure.

The diagnosis is confirmed by radiography and tomography of the lungs, spirography or spiroanalysis (study of the function of external respiration using special devices, spiroanalyzers, the operation of which is based on the pneumotachography method), acid-base balance study, bronchoscopy. Less commonly used are scintigraphy using iodine-131, bronchography, angiopulmonography.

Tactics: depends on the underlying disease - either referral to a tuberculosis dispensary, or to a pulmonology department, or to a thoracic surgery department. When hospitalized in surgical or traumatology departments, active tactics are used to manage such patients, anesthesia is administered with increased caution according to ventilation volumes to prevent ruptures of a rigid or emphysematous lung.

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Cirrhosis of the kidneys

Nephrosclerosis (fibrosis, cirrhosis) is the replacement of the renal parenchyma with connective tissue, leading to their compaction, wrinkling and dysfunction, developing with various diseases of the kidneys and their vessels.

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

Primary shrunken kidney develops due to impaired blood flow in the kidneys due to severe hypertension, atherosclerosis of the renal vessels, arteriolosclerosis with the development of multiple renal infarctions.

Renal cirrhosis 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 established at high numbers, and especially high diastolic pressure (at the level of 120-130 mm Hg), which does not respond to drug treatment. Renal failure develops slowly. Heart failure, encephalopathy, edema of the optic nerve papilla and retinal detachment are often detected.

Secondary shrunken kidney develops as a result of infectious kidney diseases (chronic glomerulonephritis, pyelonephritis, urolithiasis, tuberculosis, syphilis, etc.) or degenerative processes in it after injuries, repeated kidney surgeries, radiation, with systemic diseases accompanied by the development of amyloidosis in the kidneys (rheumatism, lupus erythematosus, diabetes mellitus, sepsis, etc.). The manifestations are the same as in the primary shrunken kidney, can vary from minor to the development of severe renal failure.

The diagnosis of renal cirrhosis is confirmed by ultrasound (reduction in volume and deformation of the kidneys), radioisotope renography using mercury hypurat (slowing down the accumulation and excretion of the drug), urography (reduction in kidney volume, deformation of the renal tubules, reduction of the cortex). Other research methods (renal angiography, scintigraphy, chromocystoscopy) are used according to indications determined by a nephrologist.

Tactics: when a patient with surgical pathology comes to us, cirrhosis in the kidneys should be identified (characteristic blood pressure, changes in urine tests), since these conditions are threatening during operations, anesthesia, in the postoperative period and during 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.

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