JAUNDICE

From Big Medical Encyclopedia

JAUNDICE (icterus) — a symptom of coloring in yellow color of mucous membranes, scleras and skin. is a symptom of a number of diseases and it is, as a rule, connected with hyperbilirubinemia (see).

Being external manifestation of disease state of the person. drew attention of doctors since the most ancient times. Its description is available in Hippocrates's book «About internal sufferings». By the end 19 and to the beginning of 20 centuries were numerous theories trying to explain pathogenetic essence. at damages of a liver [Libermeyster (To. Liebermeister), 1864; F. Pick, 1894; O. Minkowski, 1904; H. Eppinger, etc.]. All these mechanistic theories reduced essence. to changes of the direction of current of bile in the affected liver. In 1949. A. L. Myasnikov explained development. at diffusion damages of a liver preferential functional frustration of a hepatic parenchyma — hepatocytes.

On problem Zh. big theoretical and practical material on the basis of achievements a wedge, biochemistry, a submicroscopy is saved up. medical cybernetics thanks to all-round development a wedge, disciplines. Big contribution to studying of a pathogeny. brought A. A. Vishnevsky, 3. A. Bondar, X. X. Mansurov, I. D. Mansurova, A. L. Myasnikov., A. D. Ochkip. E. V. Smirnov, E. M. Tareev, S. P. Fedorov, A. F. Blyuger, G. Albot, I. Arias, I. Pavel, S. Sherlock, etc.

Classification and a pathogeny

at the heart of the existing classifications. various principles lie: pathophysiological, anatomic, pathomorphologic, biochemical, clinical. S. Sherlock (1968) divides. on the following types: 1) hemolitic (at the raised bilirubinovy load of a liver); 2) connected with disturbance of transport of bilirubin (through a sinusoidal membrane of a hepatocyte); 3) connected with disturbance of conjugation of bilirubin in a hepatocyte; 4) connected with disturbance of excretion of the conjugated bilirubin (an intra hepatic, extrahepatic, subhepatic cholestasia). According to classification Pavel and Kympyana (I. Pavel, J. Campeanu, 1970). it can be connected: 1) with a mechanical obstacle to current of bile; 2) with a functional obstacle to current of bile; 3) with dysfunction of a hepatic cell — and) disturbance of biliary secretion, b) disturbance of a water retroresorption at the level of Disse's spaces, c) hepatocellular damages; 4) with pigmental hyperproduction — and) inborn hyper hemolysis, b) the acquired hyper hemolysis; c) hyperreactivity of reticuloendothelial system; 5) with the raised threshold of filtering of bilious pigments; 6) with fermentopatiya; 7) mixed Zh.

A. F. Blyuger (1968) offered the following classification.: 1) suprahepatic; 2) hepatic; 3) subhepatic. On 3. A. Bondar (1970) Zh. shares on: 1) hemolitic (suprahepatic); 2) hepatocellular (hepatic); 3) mechanical (subhepatic).

All listed classifications characterize a problem from the different parties. However traditional division. by the pathogenetic principle on hemolitic, obturatsionny (mechanical) and hepatic (parenchymatous) remains to the main though idea of each look. went deep and extended. A concept about these three types. conditionally and shall be considered as a concept about the syndromes observed at many diseases with various etiology and clinic.

Understanding pathogeny . it is connected with idea of a pathway of bilirubin in an organism which looks as follows. An erythrocytolysis and transformation gem in a bilirubinovo-albuminous complex — so-called free bilirubin (see), Wang giving indirect reaction with Ehrlich's diazoreactant - den - Berg (see. Wang - den - Berg reaction ), occurs preferential in reticuloendothelial system. Besides, formation of bilirubin happens directly in marrow in the course of an inefficient hemopoiesis and in the fabrics rich with gemsoderzhashchy enzymes — so-called shuntovy the bilirubin making 5 — 20% of the general bilirubin. The following stage of exchange of bilirubin is penetration of a bilirubinovo-albuminous complex through a sinusoidal membrane of hepatocytes. In hepatic cells bilirubin connects to one or two remains glucuronic to - you with the participation of enzyme of a glyukuroniltransferaza, forming water-soluble mono - and diglucuronides of bilirubin. Then bilirubin-glyukuronidny a complex gets through a biliary membrane of a hepatocyte and as a part of bile is removed on intra hepatic and extrahepatic zhelchevydelitelny system (see. Zhelchevydeleniye ) in a cavity of a duodenum. Disturbances in each of the specified links and furthermore the combined disturbances can lead to Zh. Chislo's emergence of the diseases which are followed., it is big, and it is logical to group them according to disturbances in this or that link of exchange of bilirubin. So, at disturbances of formation of free bilirubin in reticuloendothelial system arises., observed at hemolitic anemia (see), and in the presence of an inefficient hemogenesis develops., accompanying dizeritropoetichesky anemia (see), different from hemolitic states normal term of life of erythrocytes. Disturbance of penetration of a bilirubinovo-albuminous complex through a sinusoidal membrane of a hepatocyte, its transport through a hepatic cell and process of formation of glucuronides of bilirubin leads to development. newborns (see. Hemolitic disease of newborns ) and some hereditary pigmental hepatoses (see). Some medicinal hepatoses (e.g., aminazine), a recurrent high-quality cholestasia of pregnant women are followed., being a consequence of disturbance of transport a bilirubin-glucuronide-nogo of a complex through a biliary membrane of hepatocytes. Disturbance of advance of bile on intra hepatic bile-excreting system is the cornerstone. at cholestatic damages of a liver (Cholestatic hepatitises) — a viral hepatitis (see. viral hepatitis ), medicinal and patoimmunny hepatitis (see). The combination of disturbances in the listed links is the reason. at acute hepatitises and hepatoses, acute toxic dystrophy liver (see), hron, active hepatitis, a so-called congestive liver at heart failure (see), and also at metabolic reticuloses of a liver: hemochromatosis (see). to Gosha of a disease (see) etc., caused by disturbance of advance of bile on extrahepatic bilious ways, etiologically it is diverse and caused by the diseases leading to obturation of bilious ways with emergence of secondary biliary cirrhosis (see). Treat them cholelithiasis (see), cholecystitis (see), cholangitis (see), pancreatitis (see), strictures, benign and malignant tumors, and also any other reasons of a mechanical prelum in the field of extrahepatic bilious channels (see).

Diagnostic and clinical value

Various extent of icteric coloring depends hl. obr. from extent of accumulation of bilirubin in blood. Distinguish latent, or initial, a form Zh., when icteric coloring of skin and mucous membranes is absent, but there is insignificant (to 2 mg of %) an increase in content of bilirubin in blood serum;. explicit, at a cut there is strengthening of bilirubin in blood, an icteric prokrashivaniye of skin and mucous membranes, but bilirubin is not found in urine yet; sharply expressed., at a cut there is an intensive icteric coloring of skin and mucous membranes, considerable hyperbilirubinemia (see), in urine bilirubin is found (see. Bilirubinurea ) and (or) other bilious pigments.

Distribution of bilirubin in fabrics happens unevenly. Earlier all paints scleras, a lower surface of language, the sky, then skin folds on a face, skin around a nose and a mouth, a palm and a sole. In mild cases icteric coloring is limited only to coloring of scleras (subicterus). Almost all body tissues are painted: before everything serous covers, then connecting and fibrous fabric, later epithelial, further a bone tissue; cartilages are not painted. Secrets of an organism (sweat, saliva, tears, milk) even at intensive. contain not enough bilirubin. The exception is made by urine. Bilirubin is found in transudate and exudate of serous cavities. Bilirubin does not get into cerebrospinal liquid.

Intensity of seen. can be various: people with the developed muscles and poorly expressed hypodermic cellulose look usually more icteric since bilirubin at them is taken fabrics to a lesser extent, content in blood is higher than it and it is more intensively postponed in skin. Stout persons less zheltushna since at them the considerable mass of bilirubin is absorbed by a fatty tissue. At anemia. it seems less expressed. Depending on a shade of coloring of skin clinically distinguish the following types.: with a reddish shade of skin (rubin icterus), with a citreous or straw shade (flavin icterus), with a greenish shade (verdin icterus) and with the dark gray-greenish shade turning into black color (icterus melas). . well it is found in the afternoon at natural light and difficult comes to light in the evening at artificial lighting

., caused by a prokrashivaniye of fabrics bilirubin, it is easy to distinguish from yellow coloring of the skin arising at long reception of quinacrine picric to - you, carotene; in the latter case scleras are not painted over, urine light, is painted by kcal, amount of bilirubin in blood normal, and reaction to bilirubin in urine negative

., caused by an obstacle to outflow of bile in intestines, and also in cases of the liver, quite often is followed by an itch. On skin of such patients raschesa and bruises because of hemorrhages can be found. Quite often. is followed by disturbance of cholesteric exchange, the shown adjournment of cholesterol in skin in the form of yellow-white spots in the field of a century (ksantelazma) or in other areas of a body (xanthoma).

In certain cases (at cirrhoses of a liver). is followed by emergence on face skin, a trunk and other parts of a body of focal teleangiectasias — so-called asterisks; which development is connected with disturbance of metabolism of estrogen in a liver. At the same patients it is possible to observe a thickening of final phalanxes of fingers of hands and legs in the form of drum sticks.

The described symptoms in diverse combinations meet at the diseases of various etiology which are followed.

Hemolitic jaundice (suprahepatic, pleyokholichesky) meets at the inborn and acquired hemolitic anemias, is a symptom of some diseases (Addison's disease — Birmera, sepsis, a radial illness, malaria, a long septic endocarditis, some forms of cirrhosis, malignant tumors, etc.), and also at intoxications the poisons or substances capable to cause hemolysis (see) — hydrogen arsenide, trinitrophenol, phosphorus, sulfanamide drugs at incompatible blood transfusions, etc.

At the heart of hemolitic. extrahepatic hyperproduction of bilirubin (the strengthened erythrocytolysis) in combination with the lowered excretory function of a liver lies.

Fig. 3. Face of the patient with hemolitic jaundice. Under drawings color of urine (1), a calla (2), blood serum (3) and contents of a duodenum are specified (4).

Coloring of skin at hemolitic. (tsvetn. fig. 3) of a citreous shade, does not reach big intensity, is not followed by a skin itch. The liver can be not increased, the spleen is more often increased. At this form Zh. in some cases pigmental stones are formed, develops hron. calculous cholecystitis (see). The cholemic phenomena and dystrophy of a liver are not observed. appears or amplifies in connection with hemolitic crisis, cooling, nervous or physical. tension, infection, reception of some drugs etc. In blood the amount of free bilirubin increases to 3 — 6 mg of %. In urine bilirubin is absent, urobilin (see) contains much, in Calais there is a lot of stercobilin (see). Hemolitic. it is, as a rule, combined with anemia of regenerator character. In some cases decrease in osmotic resistance of erythrocytes, or positive test of Koombs takes place (see. Koombs reaction ). Functional hepatic trials are changed slightly.

Obturatsionny jaundice (mechanical, podpechenochpy, congestive, regurgitatsionny). The mechanical obstacle to outflow of the bile which came from a liver to system of bilious ways is the cornerstone of it: impassability of the general bilious channel in connection with its stricture, a prelum or obstruction. The prelum can be caused by a tumor of a head of a pancreas, gall bladder, and also increased limf, nodes of portal fissures. Sharp increase in a right kidney, aneurysm of a ventral aorta, a hepatic artery, the cicatricial tyazh caused by a perigastritis, a pericholecystitis, syphilis can also cause a prelum of the general bilious channel.

Obstruction of the general bilious channel is caused most often by a stone that is followed by inflammatory swelling of a mucous membrane and the joining spasm of smooth muscles. Less than stones, the general bilious channel close worms, echinococcal bubbles, foreign bodys, etc.

Origins of obturatsionny. consists in disturbance of excretion of the connected bilirubin in a duodenum. The obstacle to current of bile leads to build-up of pressure in the bilious ways lying above. The bilious pigment at the same time diffuses through walls of expanded bilious capillaries, they are quite often broken off. Hepatocytes are filled with bile, it arrives in limf, cracks and blood.

Fig. 1. Person sick obturatsionny jaundice (cancer of a head of a pancreas).

Obturatsionny jaundice is characterized by gradual increase of yellowness of integuments, in rare instances — the alternating its current (a valve stone, growth and disintegration of a tumor). With strengthening. integuments get greenish or gray-green coloring (tsvetn. fig. 1), appears a skin itch, hemorrhagic diathesis sometimes joins. At obstruction of the general bilious channel a stone. kolikoobrazny pains precede. At cancer of a head of a pancreas to the period. the aching dorsodynias and an anticardium accompany. Temperature increase is sometimes observed. Increase in a liver is caused first of all by stagnation of bile in it. At this form. in blood all components of bile — bilirubin, cholesterol, bilious to - you collect. In blood serum the amount of bilirubin reaches '15 — 20 mg of %. Urine gains color of beer with bright yellow foam because of emergence of bilirubin in it. At full closing of the general bilious channel urobilin in urine is not found. Kal becomes colourless, has clay white-gray color, contains a large number fat to - t and soaps, stercobilin is not found. In blood increase in amount of cholesterol is observed, collect bilious to - you and activity of an alkaline phosphatase increases. The expressed disturbance of functional hepatic trials, as a rule, is absent in the beginning.

Hepatic jaundice (parenchymatous). Origin of this look. it is connected with infectious (viral hepatitis) and toxic damage of a liver (poisoning with chemical substances, intolerance of drugs etc.). Hepatic. it is observed also at cirrhoses of a liver, some parasitic diseases, acute and hron, infections, etc. To hepatic. carry also some special forms of damage of a liver, napr, holangiolitichesky (Cholestatic) hepatitises.

Various disorders of education and release of bilirubin are caused by emergence of messages between bilious ways, circulatory and limf, vessels, damage of a wall of the small bilious courses and formation of the blood clots creating intra hepatic obstacles to passing of bile that is promoted by also inflammatory hypostasis of periportal spaces.

Fig. 2. Person sick hepatic jaundice.

At hepatic. (tsvetn. fig. 2) yellowness of a lemon or reddish shade; in blood serum the content of the connected bilirubin to 20 mg of % and increases above. In urine there is a bilirubin and bilious to - you still to seen., and then their quantity increases. Full decolouration a calla is observed seldom. From the very beginning of a disease, in addition to pigmental, also other functions of a liver are broken.

The most typical wedge, manifestation of hepatic. is. at an infectious disease (see. viral hepatitis ).

The differential diagnosis

the Differential diagnosis at. any gepatobiliarny pathology presents considerable difficulties and it consists of the following main stages: 1) establishment of a symptom. with an exception of a pseudoicterus; 2) definition of pathogenetic option Zh. (hemolitic, hepatic, subhepatic) on the basis of a data set a wedge, and laboratory and tool inspection of the patient; 3) establishment nozol, the diagnosis with its justification and the solution of a question of conservative or surgical treatment. It is almost important to differentiate the main pathogenetic options Zh. The major differential diagnostic characters are given in table 1.

Treatment

With expansion of knowledge of a pathogeny of various types Zh. became possible in many cases to carry out them etiol, the therapy supplementing to lay down. the actions directed to elimination of a disease a symptom to-rogo is.

Patients with. it is necessary to hospitalize perhaps quicker for the purpose of final clarification of the diagnosis, creation of the corresponding mode and performing treatment. Appoint a bed rest and, as a rule, fractional dietary food with restriction of fats and enough carbohydrates and vitamins. Considering tendency to the bleedings sick appoint phthiocol, Vikasolum, ascorbic to - that, vitamins of group B, intravenous administration of calcium chloride. At severe forms. intravenous administration of glucose, sometimes in combination with subcutaneous injections of insulin is recommended. Plentiful drink, especially mineral waters is useful (borzhy, Yessentuki No. 4, No. 17, etc.). Widely apply cholagogue means (Cholosasum, dekholin, etc.), and in the presence of an infection in bilious ways — antibiotics. In certain cases make duodenal sounding (see) that promotes department of bile and drainage of bilious ways. For the purpose of simplification of an itch (is more often at mechanical.) appoint heat baths with addition of vinegar, soda, carbolic to - you, rubdowns by weak solution carbolic to - you, camphoric alcohol; inside — drugs of bromine, atropine, Pilocarpinum.

Jaundice at children

At children. happens more often than at adults, it is noted often at newborns.

Due to the features of bilirubinovy exchange at children, features of development of the diseases which are followed., the last divide into four types: 1) pairing; 2) hemolitic; 3) hepatic; 4) mechanical.

Pairing jaundice it is caused by disturbance of processes of binding of bilirubin. At this form insufficient activity of enzyme of a glyukuroniltransferaza is noted, with the help the cut is carried out transformation of indirect (free) bilirubin in a straight line therefore in blood of the child there is an accumulation of an indirect bilirubin in the absence of the strengthened hemolysis. This. it is characterized by lack of increase in a liver and spleen, normal content in blood of erythrocytes, hemoglobin, reticulocytes. Treat this form: fiziol., jaundice premature, a tranzitorny not hemolitic hyperbilirubinemia of newborns, an inborn not hemolitic hyperbilirubinemia of newborns from nuclear. (prokrashivaniye of kernels of a brain), constitutional hepatic dysfunction youthful and adults (Gilbert-Meylengrakhta's syndrome).

Physiological jaundice (fiziol, a hyperbilirubinemia) develops at most of babies not earlier than 36 hours of life, a thicket for the 3rd day, at first comes to light on a face, then on a trunk, extremities, a conjunctiva and mucous membranes. On 4 — the 6th day the amount of bilirubin in blood reaches 8 — 14 mg of % then contents it begins to decrease gradually. Yellowness loses intensity and disappears at the end of the first — the beginning of the second week. The general condition of the child at fiziol. it is not broken, treatment is not required. Only at expressed. intravenous injection of 5 — 10% of solution of glucose, in rare instances — plasmas is recommended.

Jaundice occurs at premature children more often than at full-term, it is expressed more sharply and keeps is long. Level of bilirubin in blood reaches a maximum on 5 — the 6th day. Duration of jaundice is up to 4 — 5 weeks. There are data that at concentration in blood of bilirubin of 9,5 — 12 mg of % damage of a brain is possible though at the concentration exceeding 15 mg of % it can not be. It depends on the nature of distribution of free bilirubin in an organism and on its activity at penetration through a vascular wall. Expressiveness of a hyperbilirubinemia at premature does not depend on weight at the birth, but is in direct dependence on degree of a maturity of a fruit and existence of pathology at mother during pregnancy. Toxicity of bilirubin depends on bilirubin binding ability of blood (the it is lower, the at more low concentration of bilirubin it is shown), edges is defined by the level of protein of a blood plasma at premature newborns. Sharply expressed. demands active treatment using phenobarbital from premature (0,005 g on 1 kg of weight a day), phototherapy (fluorescent lamp), and at a speed of accumulation of an indirect bilirubin of more than 0,05 mg of % an hour and exchange hemotransfusion is shown to low bilirubin binding ability of plasma.

Tranzitorny negemoliticheskaya the hyperbilirubinemia of newborns is a consequence of the fact that blood serum of mothers of such children possesses inhibitory action on system of a glyukuroniltransferaza in connection with the high content of estrogen. In hard cases the tranzitorny not hemolitic hyperbilirubinemia can begin in 1 — the 2nd days after the birth that causes suspicion of a hemolitic disease of newborns. Treatment: maternal milk is replaced donor, intravenously pour in 5 — 10% solution of glucose; 5% solution of glucose with ascorbic to - that is appointed also enterally. At sharply expressed hyperbilirubinemia which is followed by accumulation of an indirect bilirubin of more than 0,3 mg of % for an hour zamenny hemotransfusion for the prevention of development of cerebral complications (bilirubinovy encephalopathy) is shown.

The inborn not hemolitic hyperbilirubinemia with a kernicterus (Krigler's syndrome — Nayara) is for the first time described in 1952 by Kriglerom and Nayar (J. F. Crigler, V. A. Najjar) under the name of inborn family not hemolitic. (see. Hepatoses ). At these hereditary, rather rare enzymopathies there is a deficit of enzyme of a glyukuroniltransferaza. appears in 1 — 3 days of life in connection with increase in content in blood of an indirect bilirubin to 12 — 45 mg of %; its increased level remains all life. There is no increased hemolysis of erythrocytes. Bile is deprived of the conjugated (direct) bilirubin, functional trials of a liver are normal. At a biopsy of a liver of changes does not come to light. At parents of such patients. it was not observed, however at inspection their reduced ability to conjugation is noted glucuronides (see) in comparison with control. Due to the intensive accumulation of an indirect bilirubin at most of children nuclear develops. They often perish at chest age; in certain cases nevrol, disturbances develop in 3 — 5-year age.

Constitutional hepatic dysfunction youthful and adults (N.A.Gilbert's syndrome — Meylengrakhta) it is for the first time described by N.A.Gilbert in 1901 under the name «cholemia simple family». Reason., according to one authors, disturbance of capture of bilirubin a hepatic cell is; according to others — disturbance of conjugation of an indirect bilirubin with glucuronic acid that is caused by hereditary inferiority of glyukuroniltransferazny system.

The disease on autosomal dominantly type is inherited.

Clinically the disease is characterized., changing on intensity, times of completely disappearing. it is connected with accumulation in blood of an indirect bilirubin, level to-rogo in blood fluctuates from 5 to 8 mg of %.

The beginning of emergence of jaundice considerably varies, beginning from the period of a neonatality to 10-year age. is followed by disturbances from outside went. - kish. path: nausea, morbidity in the right upper half of a stomach, feeling of completeness in a stomach. Emergence and strengthening. at children of advanced age it is quite often noted after physical. overloads, emotional pressure, reception of some drugs (Prednisolonum, tetracycline, streptocides), at accession of intercurrent diseases — quinsies, an acute respiratory infection, etc. Signs of the strengthened hemolysis at Gilbert's syndrome — Meylengrakhta are noted.

The sizes of a liver and spleen within norm. Coloring calla and urine normal.

Treatment: in a phase of strengthening. appoint a sparing diet with restriction of fats. Reduction physical is recommended. loadings.

Forecast of a disease favorable.

Hemolitic jaundice it is connected with the strengthened hemolysis of erythrocytes coming under the influence of maternal antibodies at isoimmunization, at deficit or inborn insufficient activity of glyukozo-6-fosfatdegidrogenazy erythrocytes and also at disturbance of structure of an erythrocyte or structure of hemoglobin. Accumulation in blood of free bilirubin, normokhromny anemia a hyper regenerator-nogo of character, increase in a liver and spleen is noted. To this type Zh. belong:. at a hemolitic disease of newborns, connected with incompatibility of blood of mother and a fruit;. at deficit of fermental systems of an erythrocyte; hemoglobinoses. Treatment is carried out taking into account etiol, the factor which caused strengthening of hemolysis and is directed to the prevention of sharp accumulation of an indirect bilirubin which at high concentration can cause damage to c. N of page with the subsequent lag of the child in physical. and mental development.

Hepatic jaundice, caused by defeat of a parenchyma of a liver. Various diseases caused by bacteria, viruses, the elementary, etc. are the reason of defeat. In cases., connected with hepatitis of newborns, in blood both indirect, and direct bilirubin can raise. If at the same time the level of the general bilirubin exceeds 3 — 5 mg of %, then irrespective of etiol, the factor which was the reason of hepatitis approximately constant ratio between both forms of bilirubin is established, and the level of an indirect bilirubin sometimes can even prevail a little. Defeat of a parenchyma of a liver is especially adverse for newborns in connection with lability of exchange of bilirubin. Hepatic. it is characterized by accumulation in blood of indirect and direct bilirubin, coloring of skin and mucous membranes in yellow color with a greenish shade, increase in a liver. At increase in blood of level of direct bilirubin the chair becomes slabookrashenny, light, urine intensively paints diapers in yellow color. In blood increase in activity of enzymes — zymohexases, transaminases, urokinases is noted. On 1 — the hemorrhagic syndrome comes to light 2nd week of life. The damage of a liver at newborns which is followed., it is observed at a viral hepatitis of newborns (see. Hepatitis, fetalis ), it is purulent - septic diseases, a toxoplasmosis, listeriosis, syphilis. Occasionally. appears in connection with genetically caused defect of the enzymatic systems of a liver responsible for exchange of carbohydrates (a glikogenovy disease, a galactosemia). Besides, damage of a liver with development. at newborns it can be observed at disturbance of activity of hemadens (e.g., at an inborn hypothyroidism), and also at the children who were born from mothers suffering from a diabetes mellitus. At newborns the considerable metabolic disturbances which are followed by hypostasis, a hypoglycemia, acidosis are noted; level of bilirubin reaches 10 — 20 mg of %. Treatment of hepatogenous. there are of actions for elimination of the main reason which caused a disease and uses of the complex therapy directed to recovery of the broken functions of a liver.

Mechanical jaundice it is caused by a mechanical scholia. It is characterized by increase in a liver and spleen, accumulation in the blood of direct bilirubin, existence of the decoloured chair which is intensively painted in yellow color of urine. Develops at an atresia of bilious ways, a ring-shaped pancreas, a syndrome of a pachycholia at a hemolitic disease of newborns. In all these cases treatment is directed to elimination of the reason which caused.: at an inborn atresia of bilious ways operational treatment in the first 1,5 months of life is shown; at a syndrome of a pachycholia appoint massage of area of a gall bladder, 15% solution of magnesium sulfate enterally on 1 chayn. l. 3 times a day, the hormonal drugs (Prednisolonum) improving zhelchevydelitelny function of a liver.

Differential diagnosis of different types. at children of the period of a neonatality and chest age it is presented in tab. 2.


Table 1. The differential and diagnostic characteristic of different types of jaundice at adults

Table 2. The differential and diagnostic characteristic of different types of jaundice at newborns and babies

  • Different types of jaundice are given in an order of frequency

of development.




Bibliography Blyuger A. F. and Krupnikova E. 3. Hereditary pigmental geiatoza, L., 1975, bibliogr.; Cooper 3. A. Klinicheskaya of hepathology, page 19, M., 1970, bibliogr.; Dunayevsky O. A. Differential diagnosis of jaundices, L., 1977; Magyar I. Diseases of a liver and bilious ways, the lane with Wenger., t. 1, page 16, Budapest, 1962; A. L. Butchers. Diseases of a liver, M., 1949; Fundamentals of hepathology, under the editorship of A. F. Blyuger, Riga, 1975; Tabolin V. A. Biliru-binovy exchange and jaundices of newborns, M., 1967; Round A. F. Fiziologiya and pathology of children of the period of a neonatality, page 18, 257, M., 1947; D u s about 1 M. and. S with h i f f E. R. Clinical approach to jaundice, Postgrad. Med., v. 57, p. 118, 1975; Jaundice, ed. by C. A. Goresky and. M of M. Fisher, N. Y., 1975; K n i 1 1-Jones R. P. a.o. Use of sequential bayesian model in diagnosis of jaundice by computer, Brit. med. J., v. 1, p. 530, 1973; Pavel I. et GampeanuS. Physiopathologie des icteres, Bucarest, 1970; Sherlock S h. Diseases of the liver and biliary system, Oxford, 1975.

A. V. Suchkov; V. A. Tabolin (ped., author of tab. 2).

Яндекс.Метрика