Intrauterine fetal infections presentation. Intrauterine infections of the fetus and newborn

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The presentation on the topic “Intrauterine infections” can be downloaded absolutely free on our website. Project subject: Medicine. Colorful slides and illustrations will help you engage your classmates or audience. To view the content, use the player, or if you want to download the report, click on the corresponding text under the player. The presentation contains 27 slide(s).

Presentation slides

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Intrauterine infections. Age-related features of the infectious process. Pathogenetic features of infections in young children

Completed by: Shavenkova M 223 OMF

State Medical University of Semey

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Introduction 1. Intrauterine infections 1.1 Epidemiology and Etiology 1.2 Source and routes of infection 1.3 Symptoms 1.4 Risk factors for the development of IUI 1.5 Diagnosis and clinical picture 2. Pathogenetic features of infection in young children Conclusion Literature

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Introduction

Intrauterine infections (IUI) are infectious diseases that are detected either prenatally or shortly after birth, but they arise as a result of intranatal or antenatal infection of the fetus. This is a group of diseases in which both infection and manifestation of the disease occurred in utero.

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1. Intrauterine infections

1.1 Epidemiology and Etiology The true frequency of congenital infections has not yet been established, but, according to a number of authors, the prevalence of this pathology in the human population can reach 10%. Intrauterine infections have the same patterns as infectious diseases in general. They have a leading place in the structure of infant mortality. The share of IUI in the structure of perinatal mortality in our country is almost 25%, however, transplacental infection of the fetus is considered one of the most likely causes of 80% of congenital malformations, which, in turn, account for about 30% of all deaths of children under 1 year of age

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It is noteworthy that infection with the same infections in the postneonatal period occurs in most cases asymptomatically or in the form of a mild infectious process. The causative agents of infectious diseases that the mother first encountered during pregnancy are especially dangerous for the fetus, since during this period the primary immune response is reduced, while the secondary one is normal. 1.2 Source and routes of infection The source of infection is the mother. But there are also iatrogenic causes of infection during medical procedures. Routes of infection * Transplacental (hematogenous) route - from mother to fetus through the placenta. Viral IUIs are more often transmitted, since the virus easily penetrates the blood-placental barrier and toxoplasmosis. * Ascending - when an infection from the genital tract enters the uterine cavity and can then infect the fetus. More often these are bacterial infections, STDs, chlamydia, fungi, mycoplasmas, enterococci. * Descending route - from the fallopian tubes into the uterine cavity * Contact (intranatal) route - infection during passage through the birth canal.

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1.3 Symptoms All IUIs have a number of common symptoms. The similarity of symptoms is associated with several points: the characteristics of the pathogens are often intracellular infections, the body cannot independently eliminate infections - as a result, a persistent course. In addition, newborns have age-related weakened immunity, which is why infections take a slow course. As a result of the effect of infection on the fetus, a complex of effects occurs, such as hyperthermia, the pathological effect of microorganisms and their toxins, resulting in a disruption of the placentation process and metabolic processes. 1. Manifestations of infection are determined by the timing of infection of the fetus in the first 2 weeks after conception - blastopathy, which often ends in spontaneous abortion in a very early period from 2 to 10 weeks of pregnancy - true malformations due to lesions at the cellular level.

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from 10 to 28 weeks of pregnancy - early fetopathies. The fetus can respond to the introduction of an infection with a generalized inflammatory reaction (the 1st and 3rd phases of inflammation, alteration and proliferation and fibrosis are clearly expressed, and the 2nd phase - exudation is not pronounced) as a result of which the child develops multiple malformations, for example fibroelastosis. from 28 to 40 weeks of pregnancy - late fetopathies. The fetus can already respond with a full-fledged inflammatory reaction, most often several organs are involved; infection during childbirth - inflammation more often than one organ - pneumonia, hepatitis. 2. Teratogenic effect 3. Generalization of the process 4. Persistent, long-term course 5. High frequency of mixed, concomitant pathology 6. Low clinical specificity

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General signs: * intrauterine growth retardation * hepatosplenomegaly * minor developmental anomalies (stigmas of disembryogenesis) early or prolonged or intense jaundice * rashes of various types * respiratory distress syndrome * cardiovascular failure * severe neurological disorders * febrile conditions in the first day of life

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1.4 Risk factors for the development of IUI * Complicated obstetric and gynecological history * Pathological course of pregnancy * Diseases of the genitourinary system in the mother * Infectious diseases of any other organs and systems in the mother that occur during pregnancy * Immunodeficiencies, including AIDS * Repeated blood transfusions * Condition after transplantation 1.5 Diagnosis and clinical picture Diagnosis of IUI is extremely difficult. First of all, they rely on anamnesis data, features of the course of pregnancy. Methods for laboratory diagnosis of IUI can be divided into direct and indirect. Direct ones include: * microscopy * cultural method, virus replication on tissues * Detection of antigens by RIF or ELISA * PCR

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The clinical picture of intrauterine infections significantly depends on the time and route of infection. In the first 8-10 weeks of intrauterine development, only an alterative phase of inflammation is possible; the process ends either in the death of the embryo or in the formation of congenital malformations. Later, the proliferative component of inflammation begins to appear. Infection at later stages (11-28 weeks) causes proliferation of connective tissue (for example, myocardial fibroelastosis), dysplasia and hypoplasia of internal organs, intrauterine growth retardation and generalized infectious processes. When the fetus becomes infected after 28 weeks, three components of inflammation are involved - alterative, proliferative and vascular. With localized forms of intrauterine infections, internal organs are damaged (fetal hepatitis, hepatolienal syndrome, cardiomyopathy, interstitial nephritis, intrauterine pneumonia, enterocolitis, etc.) and the central nervous system (encephalitis or meningoencephalitis).

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The process of formation of the fetal brain continues throughout pregnancy, therefore congenital malformations and lesions of the central nervous system are recorded much more often than pathologies of other organs. Since the clinical manifestations of intrauterine infections are mostly nonspecific, in most cases a diagnosis of “perinatal encephalopathy” or “cerebrovascular accident” is made. The clinical picture of a generalized intrauterine infection resembles sepsis (damage to internal organs, hemolytic anemia, thrombocytopenia, hemorrhagic syndrome, adrenal insufficiency, infectious toxicosis). Possible asymptomatic onset followed by development of the clinical picture (delayed pathology): hypertensive-hydrocephalic syndrome, progressive cataracts, diabetes mellitus, hepatitis, pathology of the urinary system, etc.

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It should be noted that vulvovaginitis in girls, young women and postmenopausal women are predominantly of bacterial origin and are often accompanied by an allergic component. It is important to note that these age periods are characterized, as a rule, by hypoestrogenism, which is the background for the occurrence of vulvovaginitis of bacterial etiology with the addition of an allergic component, which, unfortunately, is not always taken into account by doctors when treating patients. The need to include desensitizing therapy in the treatment of inflammatory diseases, including the lower genital tract, in this group of patients is pathogenetically justified.

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2. Pathogenetic features of infection in young children

An important distinctive feature of an infectious disease is its cyclical course with alternating periods: incubation, prodromal (initial), height (development) and convalescence (recovery). The incubation period is from the introduction of the pathogen into the body until the appearance of the first clinical symptoms of the disease. During this period, the pathogen multiplies, immunological changes and other processes are observed that disrupt the normal activity of tissues, organs and systems of the macroorganism. The duration of the incubation period varies - from several hours (influenza, foodborne illnesses) to several months (viral hepatitis B, infectious mononucleosis) and even years (leprosy, leishmaniasis).

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The prodromal period is manifested by a number of symptoms, usually nonspecific for this infection (fever, malaise, loss of appetite). Changes develop at the site of the entrance gate, i.e., a primary focus is formed (tonsillitis, catarrhal phenomena in the upper respiratory tract, etc.), with the subsequent spread of pathogens to various organs and tissues. In some diseases, pathognomonic symptoms, characteristic only of this nosological form, are observed (for measles - the Velsky-Filatov-Koplik symptom). The duration of the prodromal period varies - from several hours to several days; sometimes it is missing. The peak period - along with clinical manifestations common to many infections, symptoms and syndromes characteristic of this disease appear

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Changes in the site of the primary focus are pronounced; with a number of infections, rashes appear on the skin (scarlet fever, measles, chicken pox, rubella); with whooping cough - paroxysmal convulsive cough; hematological, biochemical and morphological changes become typical. The period of convalescence begins due to the development of specific immunity and is characterized by gradual normalization of functional and morphological parameters. With some infections, recovery of impaired functions occurs slowly. At this time, specific sensitization remains, the risk of developing allergic complications and superinfection

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Conclusion

Intrauterine infection is a disease of the fetus or newborn resulting from its antenatal or intrapartum infection with the causative agent of any infectious disease. Previously, the term TORCH syndrome was widely used. Currently, it is rarely used, since it includes only five diseases: toxoplasmosis, syphilis, rubella, cytomegalovirus infection and herpes.

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Infectious diseases are a large group of human diseases that arise as a result of exposure to viruses, bacteria and protozoa. They develop through the interaction of two independent biosystems - a macroorganism and a microorganism under the influence of the external environment, and each of them has its own specific biological activity. Infection is the interaction of a macroorganism with a microorganism under certain conditions of the external and social environment, as a result of which pathological, protective, adaptive, compensatory reactions develop, which are combined into an infectious process. The infectious process is the essence of an infectious disease and can manifest itself at all levels of organization of the biosystem - submolecular, subcellular, cellular, tissue, organ, organism.

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Bibliography

Degtyarev D.N., Degtyareva M.V., Kovtun I.Yu., Shalamova L.V. Principles of diagnosing intrauterine infections in newborns and tactics for managing children at risk. - M.: Perinatology today, 1997. - T. 3. - P. 18-24. Volodina N. N., Degtyareva D. N. Diagnosis and treatment of intrauterine infections. - M.: Method. rec. for neonatologists, 1999. Cheburkin A.V., Cheburkin A.A. Perinatal infection.. - M.: 1999. N. N. Volodin Current problems of neonatology.. - M.: GEOTAR-MED, 2004. - 448 pp. . A. Ya. Senchuk, Z. M. Dubossarskaya Perinatal infections: practical. allowance. - M.: MIA, 2004. - 448 p.

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Intrauterine infections are various infectious diseases of the embryo, fetus and newborn, infection of which occurs in utero and during childbirth. The causative agents of infection can be viruses, bacteria and (less commonly) parasites. The route of transmission is vertical, from mother to fetus. The result of infection can be a miscarriage, congenital malformations or an acute infectious process in a newborn. infectious diseases viruses bacteria parasites The true frequency of congenital infections has not yet been established, but, according to a number of authors, the prevalence of this pathology in the human population can reach 10%. IUIs are characterized by the same patterns as infectious diseases in general. Have a leading place in the structure of infant mortality.infant mortality

The share of IUI in the structure of perinatal mortality in our country is almost 25%, however, transplacental infection of the fetus is considered one of the most likely causes of 80% of congenital malformations, which, in turn, account for about 30% of all deaths of children under 1 year of age. In 1971, WHO identified the concept of TORCH syndrome. This is an abbreviation for the most common intrauterine infections (T - Toxoplasmosis, O - others, which include mycoplasma, syphilis, hepatitis, streptococci, candida and other viral and bacterial infections, R - rubella, C - cytomegalovirus, H - herpes) and if not clear etiological diagnosis, then they talk about TORCH syndromeTORCH syndrome Toxoplasmosis rubella cytomegalovirus herpes

Outcome of fetal infection 1) Infectious disease 2) Sanitation of the pathogen with the acquisition of immunity 3) Carriage of an infectious agent with the possibility of developing the disease in the future. Thus, the presence of an infection in the mother, an infectious lesion of the placenta and infection do not mean 100% development of IUI in the fetus and newborn. For all IUI there are a number of common symptoms, which is associated with several points: the characteristics of the pathogens are often intracellular infections, the body cannot independently eliminate infections as the consequence is a persistent course. In addition, newborns have age-related weakened immunity, which is why infections take a slow course. As a result of the effect of infection on the fetus, a complex of effects occurs, such as hyperthermia, the pathological effect of microorganisms and their toxins, resulting in a disruption of the placentation process and metabolic processes.

1. Manifestations of infection are determined by the timing of infection of the fetus - in the first 2 weeks after conception, blastopathy, most often ends in spontaneous abortion at a very early stage; blastopathy - from 2 to 10 weeks of pregnancy; true malformations due to lesions at the cellular level. malformations - from 10 to 28 weeks of pregnancy early fetopathy. The fetus can respond to the introduction of an infection with a generalized inflammatory reaction (the 1st and 3rd phases of inflammation, alteration and proliferation and fibrosis are clearly expressed, and the 2nd phase exudation is not pronounced) as a result of which the child develops multiple malformations, for example fibroelastosis. fetopathy alteration proliferation fibrosis exudation malformations fibroelastosis – from 28 to 40 weeks of pregnancy, late fetopathies. The fetus can already respond with a full-fledged inflammatory reaction, most often several organs of fetopathy are involved - infection during childbirth, inflammation more often than one organ, pneumonia, hepatitis, pneumonia, hepatitis 2. Teratogenic effect 3. Generalization of the process 4. Persistent, long-term course 5. High frequency of mixed, combined pathology 6. Low clinical specificity

The presence of intrauterine infection in a newborn may be suspected already during childbirth. Intrauterine infection may be indicated by the discharge of turbid amniotic fluid, contaminated with meconium and having an unpleasant odor, and the condition of the placenta (plethora, microthrombosis, micronecrosis). Children with intrauterine infection are often born in a state of asphyxia, with prenatal hypotrophy, enlarged liver, malformations or stigmas of dysembryogenesis, microcephaly, hydrocephalus. Asphyxia and hypotrophy microcephaly hydrocephalus From the first days of life they have jaundice, elements of pyoderma, roseolous or vesicular rashes on the skin, fever, convulsive syndrome, respiratory and cardiovascular disorders. jaundice, pyoderma or fever, convulsive syndrome

Risk factors for the development of IUI: Compounded obstetric and gynecological history. Pathological course of pregnancy. Diseases of the genitourinary system in the mother. Infectious diseases of any other organs and systems in the mother that occur during pregnancy. Immunodeficiencies, including AIDS. Immunodeficiencies AIDS Repeated blood transfusions, condition after transplantation

The early neonatal period with IUI is often aggravated by interstitial pneumonia, omphalitis, myocarditis or carditis, anemia, keratoconjunctivitis, chorioretinitis, hemorrhagic syndrome and others. coma, congenital heart defects, cysts and brain calcifications. cataracts glaucoma congenital heart defects In the perinatal period, the child experiences frequent and profuse regurgitation, muscle hypotension, central nervous system depression syndrome, and gray skin color. In the later stages, with a long incubation period of intrauterine infection, the development of late meningitis, encephalitis, osteomyelitis, osteomyelitis encephalitis is possible

Congenital rubella occurs when a pregnant woman contracts rubella. Moreover, the probability and consequences of fetal infection depend on the gestational age: in the first 8 weeks the risk reaches 80%; The consequences of intrauterine infection can include spontaneous abortion, embryo- and fetopathy. In the second trimester, the risk of intrauterine infection is 10-20%, in the third – 3-8%. Spontaneous termination of pregnancy Children are born premature or with low body weight. The neonatal period is characterized by a hemorrhagic rash and prolonged jaundice. The classic manifestations of congenital rubella are represented by Greg's triad: eye damage (microphthalmia, cataracts, glaucoma, chorioretinitis), congenital heart disease (patent ductus arteriosus, ASD, VSD, pulmonary stenosis), damage to the auditory nerve (sensorineural deafness). Patent ductus arteriosus ASD Pulmonary artery stenosis

If an intrauterine infection develops in the second half of pregnancy, the child usually has retinopathy and deafness. retinopathy In addition to the main manifestations of congenital rubella, the child may also have other anomalies: microcephaly, hydrocephalus, cleft palate, hepatitis, hepatosplenomegaly, malformations of the genitourinary system and skeleton. cleft palate In the future, intrauterine infection reminds itself of the child’s retardation in physical development, VMT or mental retardation.

Congenital cytomegaly Intrauterine infection with cytomegalovirus infection can lead to local or generalized damage to many organs, immunodeficiency, and purulent-septic complications. Congenital developmental defects usually include microcephaly, microgyria, microphthalmia, retinopathy, cataracts, congenital heart disease, etc. The neonatal period of congenital cytomegaly is complicated by jaundice, hemorrhagic syndrome, bilateral pneumonia, interstitial nephritis, and anemia. Long-term consequences of intrauterine infection include blindness, sensorineural deafness, encephalopathy, liver cirrhosis, pneumosclerosis. liver cirrhosis pneumosclerosis

Congenital herpetic infection can occur in a generalized (50%), neurological (20%), mucocutaneous form (20%). Generalized intrauterine herpetic infection occurs with severe toxicosis, respiratory distress syndrome, hepatomegaly, jaundice, pneumonia, thrombocytopenia, hemorrhagic syndrome. respiratory distress syndrome. The neurological form of congenital herpes is clinically manifested by encephalitis and meningoencephalitis. Intrauterine herpes infection with the development of skin syndrome is accompanied by the appearance of a vesicular rash on the skin and mucous membranes, including internal organs. Limb hypoplasia (cortical dwarfism) may also occur. Late complications include encephalopathy, deafness, blindness, delayed psychomotor development. When a bacterial infection develops, neonatal sepsis develops. Sepsis of newborns

Diagnosis of IUI includes two mandatory components: 1) clarification of the nature (etiology) of the infection and 2) proof of the intrauterine genesis of the disease. Diagnosing IUI is extremely difficult. Anamnesis data and features of the course of pregnancy can only suggest the possibility of intrauterine infection. Accurate diagnosis involves examining 1) the mother, 2) the placenta, and 3) the fetus (newborn, child). The study of the placenta (placenta, membranes and umbilical cord) must be of high quality, which involves studying at least 2 pieces of the umbilical cord, 2 rollers of the membranes (twisted from the site of rupture to the place of attachment to the placenta) and 10 pieces of the placenta. It is necessary to conduct bacteriological and immunohistochemical (IHC) studies of the placenta and membranes. The introduction of IHC studies into the practice of a pathologist is absolutely necessary. This is the only way to overcome the existing overdiagnosis of chlamydia, mycoplasmosis, toxoplasmosis, “deenkova” and other infections. The immunofluorescence method when examining the placenta gives a large number of false positive results.

Methods for laboratory diagnosis of IUI can be divided into direct and indirect. Direct methods include: microscopy, culture method, virus replication on tissues, replication Detection of antigens RIF, ELISA and IHCC. RIFIFIC HCC PCR Indirect diagnostic methods are serological studies using enzyme-linked immunosorbent assay (ELISA) qualitative and quantitative analysis of Ig M, Ig G, Ig A. A newborn is examined blood. The presence of Ig G may indicate transplacental transfer of maternal antibodies, so the newborn’s blood is tested again after 3-4 weeks. ELISA Ig MIg GIg A An increase in the Ig G titer by 4 times or more is diagnostically significant. The detection of Ig M in the blood of a newborn indicates the presence of an active infection in the child. Additional studies in a general blood test can detect leukocytosis with a shift to the left, leukocytosis with neutropenia, toxic granularity of neutrophils, and anemia. In addition, children with suspected IUI need to undergo an abdominal ultrasound to detect hepatosplenomegaly and neurosonography.

A serological examination should be carried out before the administration of blood products (plasma, immunoglobulins, etc.). - Serological examination of newborns and children in the first months of life should be carried out with simultaneous serological examination of mothers (to clarify the origin: “maternal” or “own”). - Serological examination should be carried out using the “paired sera” method with an interval of 2-3 weeks. In this case, the study must be performed using the same technique in the same laboratory. It should be especially noted that in cases where, after the initial serological examination, the child was administered blood products (immunoglobulin, plasma, etc.), the study of “paired sera” is not carried out. Evaluation of the results of serological studies should be carried out taking into account possible features of the nature and phase of the immune response. It should be especially emphasized that seroconversion (the appearance of specific antibodies in a previously seronegative patient or an increase in antibody titers over time) appears later than the onset of clinical manifestations of the infection.

Avidity (Latin - avidity) is a characteristic of the strength of the connection of specific antibodies with the corresponding antigens. During the body's immune response to the penetration of an infectious agent, a stimulated clone of lymphocytes begins to produce first specific IgM antibodies, and somewhat later specific IgG antibodies. IgG antibodies initially have low avidity, that is, they bind the antigen quite weakly. Then the development of the immune process gradually (this can be weeks or months) moves towards the synthesis by lymphocytes of high-avidity IgG antibodies, which bind more firmly to the corresponding antigens. High avidity of specific IgG antibodies allows one to exclude recent primary infection. Confirming or excluding the fact of recent primary infection with Toxoplasma gondii, Cytomegalovirus and Herpes simplex virus is especially important when examining pregnant women, since the risk of pathology of fetal development is significantly increased with acute primary infection during pregnancy, compared to chronic infection and reactivation of latent infection. Therefore, there is a constant search for new diagnostic approaches that allow the most reliable assessment of the stage and form of the infectious process.

The use of IgG antibody avidity as an indicator of the duration of primary infection, first proposed by Finnish researchers (Hedman K. M. et al., 1989), has now been introduced into the practice of serological studies for TORCH infections in a number of countries. Thus, in France, where, as in Ukraine, the problem of toxoplasmosis is still relevant, this test is included in the mandatory examination algorithm for suspected toxoplasmosis in pregnant women. The detection in serum of the presence of both IgG and IgM antibodies to an infectious agent can be interpreted as evidence of a recent primary infection, since, as is known, the disappearance of IgM antibodies is usually about 3 months from the onset of the infectious process. But the period of circulation of IgM antibodies can vary significantly depending on the infectious pathogen and the individual characteristics of the body’s immune response. When infected with Toxoplasma gondii, Cytomegalovirus and Herpes simplex virus, trace amounts of IgM antibodies to these infectious agents are detected in some cases for 1-2 years or more.

Thus, their presence in the blood of a pregnant woman does not always confirm primary infection during pregnancy. In addition, the specificity of even the best commercial test systems for detecting IgM antibodies is not absolute. In some situations, as a consequence of the very high sensitivity of the tests, nonspecific false-positive results are possible. Detection of high-avidity IgG antibodies in the blood in this situation allows one to exclude recent primary infection. Low-avidity IgG antibodies, on average, are detected within 3-5 months from the onset of infection (this may depend to some extent on the method of determination), but are sometimes produced over a longer period. In itself, the detection of low-avidity IgG antibodies is not an unconditional confirmation of the fact of fresh infection, but serves as additional confirmatory evidence among other serological tests. When the infection is reactivated, specific high-avidity IgG is detected.

Indications for the analysis: An avidity test is indicated in a set of serological tests for the diagnosis of toxoplasmosis, cytomegalovirus and herpesvirus infections - with positive results for determining IgG and IgM antibodies (in order to exclude or confirm the likelihood of a recent primary infection). Preparation for the study: not required. Material for research: serum. Units of measurement: results are given as % (avidity index).

Treatment of congenital CMV infection consists of etiotropic and syndromic therapy. The indication for etiotropic therapy for congenital CMV infection is the active period of the clinically manifest form of the disease. The criteria for the activity of the CMV infectious process are laboratory markers of active viral replication (viremia, DNAemia, AHemia). Serological markers of CMV activity (seroconversion, anti-CMV IgM and/or an increase in the dynamics of the concentration of low-avidity anti-CMV IgG) are less reliable. This is due to the fact that the results of a serological examination often turn out to be both false-positive (for example, anti-CMV IgG detected in a child may be maternal, transplacentally transmitted, etc.) and false negative (for example, the absence of specific antibodies to CMV due to immunological tolerance or due to a low concentration of antibodies to CMV (beyond the sensitivity limit of test systems) in the initial period of the immune response, etc.).

General principles for the treatment of intrauterine infections involve immunotherapy, antiviral, antibacterial and syndromic therapy. Immunotherapy includes the use of polyvalent and specific immunoglobulins, immunomodulators (interferons). Targeted antiviral therapy is carried out mainly with acyclovir. For antimicrobial therapy of bacterial intrauterine infections, broad-spectrum antibiotics (cephalosporins, aminoglycosides, carbapenems) are used; for mycoplasma and chlamydial infections, macrolides are used. Syndromic therapy of intrauterine infections is aimed at relieving individual manifestations of perinatal damage to the central nervous system, hemorrhagic syndrome, hepatitis, myocarditis, pneumonia, etc.

The drug of choice for the etiotropic treatment of congenital CMV infection is cytotect-specific hyperimmune anticytomegalovirus immunoglobulin for intravenous administration. The therapeutic effectiveness of Cytotect is due to the active neutralization of the cytomegaly virus by specific anti-CMV IgG antibodies contained in the drug, as well as the activation of antibody-dependent cytotoxicity processes. Cytotect is available in the form of a 10% solution, ready for use. To newborns, Cytotect is administered intravenously using a perfusion pump at a rate of no more than 5–7 ml/hour. For manifest forms of CMV infection, Cytotect is prescribed: 2 ml/kg/day with administration every 1 day, for a course of 3–5 administrations or 4 ml/kg/day administration every 3 days on the 1st day of therapy, on the 5th and 9th day of therapy. Subsequently, the daily dose is reduced to 2 ml/kg/day, and depending on the clinical symptoms and activity of the infectious process, Cytotect is administered another 1–3 times at the same interval.

Due to the high toxicity of anti-CMV drugs (ganciclovir, foscarnet sodium), they are not used for the treatment of neonatal CMV infection. The question of the need for etiotropic treatment of newborns with asymptomatic congenital CMV infection has not been completely resolved. The advisability of prescribing various immunomodulators is also not recognized by everyone. Recombinant interferon alpha-2b (Viferon, etc.) is used as antiviral and immunomodulatory therapy. Viferon is available in the form of rectal suppositories containing IU interferon alfa-2b (Viferon-1) or IU interferon alfa-2b (Viferon-2): 1 suppository 2 times a day - daily, for 7-10 days, followed by administration 1 suppository 2 times a day every other day for 2–3 weeks.

Forecast and prevention of intrauterine infections In generalized forms of IUI, mortality in the neonatal period reaches 80%. In local forms, serious damage to internal organs occurs (cardiomyopathies, COPD, interstitial nephritis, chronic hepatitis, cirrhosis, etc.). In almost all cases, intrauterine infections lead to damage to the central nervous system. Cardiomyopathy COPD Prevention of IUI consists of preconception preparation (i.e. preparation for pregnancy), treatment before pregnancy, exclusion of contacts of the pregnant woman with infectious patients, correction of the pregnancy management program in women at risk. Women who have not previously had rubella and have not received rubella vaccinations should be vaccinated no later than 3 months before the expected pregnancy. In some cases, IUI may be the basis for artificial termination of pregnancy. management of pregnancy, vaccination against rubella, and termination of pregnancy.

Components of pre-pregnancy preparation Preparation for pregnancy begins with planning what the future parents will have to do and in what time frame. Preconception preparation must be read not a month or two before conception, but at least six months or better, a year before the expected moment of conception. It includes: determining the health status of future parents; preparing the body of each parent for conception and the woman for pregnancy; determining the optimal days for conception.

For a man and a woman, it all starts with taking a blood test, both from a finger and a vein, giving urine and other biological materials. The tests, among other things, will determine the Rh factor of the blood. This is necessary in order to know whether a Rh conflict between the woman and the fetus is possible during pregnancy. Rh factor In general, the list of tests is quite large, but it allows us to clarify many questions regarding the hormonal status of a woman, her body’s resistance to viruses dangerous to the child, as well as the presence or absence of sexually transmitted diseases and infections in both future parents. It is quite important for the doctor to collect and analyze information from the woman’s outpatient record, which shows previous illnesses, injuries or operations. The doctor also determines whether either parent is employed in hazardous work or is exposed to environmental risks. Determining the health status of future parents.

The expectant mother also needs to visit a number of specialists, primarily a gynecologist. The woman and/or man may need to consult a geneticist. The reason for this may be genetic diseases of close relatives, as well as the age of the future parents, which is not very favorable for conception. Age of the future parents All of the above will take quite a bit of time, but will allow you to answer a number of important questions. For example: is it possible to conceive naturally? Is a woman capable of bearing a child and giving birth? Is it possible that the embryo will become infected with infections in utero and during childbirth?

Preparing the body for conception and pregnancy If the results of a health study are favorable, future parents can prepare for conception, and the woman can prepare for pregnancy. First of all, you need to give up bad habits, follow a daily routine, moderate physical activity, get enough sleep and rest, and avoid negative emotions and stress. It's no secret that our body is what we eat. Therefore, future parents should eat a balanced and high-quality diet, especially during the preconception period. During this period, a woman needs to take vitamin B 9 (folic acid). Conceiving is facilitated by the intake of vitamin E by both future parents. But, as often happens, vitamins must be taken in moderation. Therefore, they should be taken only after consultation with a doctor and as prescribed.

Determining the optimal days for conception When preparing for pregnancy, you need to establish the optimal days for conception. To do this, it is necessary to determine the moment of ovulation - the period when the egg is ready for fertilization by sperm. To determine the moment of ovulation, both not very accurate (calendar method) and more reliable methods (measuring basal temperature, using a test to determine ovulation) can be used. Such methods are available to every woman and she can do them on her own. Measuring basal temperature One hundred percent determination of ovulation is possible only in a medical institution using ultrasound and under the supervision of doctors. After determining the moment of ovulation and if they want to conceive a boy or a girl, future parents can plan the day of conception, since, for example, some methods of planning the sex of a child are based on choosing a certain day of the menstrual cycle or time of year. Conceive a boy or girl on a certain day of the menstrual cycle, time of year Preconception preparation - a necessary, and sometimes even mandatory, condition for successful conception, smooth pregnancy and childbirth without complications. A responsible approach and good preparation will allow a woman to enjoy her pregnancy, and the fetus to grow and develop properly.

Completed by: Shavenkova M 223 OMF Semey State Medical University

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Plan

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Introduction

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1. Intrauterine infections

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Routes of infection to the fetus

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Congenital cytomegalovirus infection

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2. Pathogenetic features of infection in young children

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Conclusion

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Bibliography

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Intrauterine infection indicates only the fact of infectious infection of the fetus during intrauterine development or during childbirth.

Infectious process (infection) - dynamic process developing in a macroorganism as a result of the introduction into it

microorganism

So the term “infection” is not equivalent to the term “infection”. These terms are not synonymous! Term “infection” carries mainly an epidemiological load, while the term “infection” has a broader interpretation - clinical and epidemiological.

Intrauterine infections - infectious diseases in which the fetus is infected during the ante- or intranatal period.

Congenital infection -

an infectious disease in which infection and clinical manifestation of the disease occur

in utero.

That is why it is advisable to classify congenital infectious and inflammatory diseases as those that manifest themselves in the first three days of life.

The term “TORCH syndrome” denote congenital infectious diseases, the etiology of which remains

undeciphered.

“TORCH syndrome” is a term coined from the first letters of the names of the most common intrauterine infections:

T (Toxoplasmosis), Q (other diseases), R (Rubella),

C (Cytomegalovirus),

N (Negrez simplex virus)

Routes of transmission of infection from mother to fetus:

1. Transplacentral - hematogenous. 2.Ascending.

3. Descending.

4. Contact – through contaminated amniotic fluid.

The outcome of fetal infection depends on:

Type of pathogen; -its virulence; -amount of infection;

Conditions of the immune system of the fetus and pregnant woman;

Routes of penetration; - gestational age of the fetus.

depending on timing

infection

1. Tubal infertility (lethal infectious blastopathies)

2. Fetal death - early and late miscarriages, stillbirth (lethal infectious embryo-fetopathies)

3. Recurrent miscarriage (infectious fetopathies)

4. Manifestations of IUI in live births can be observed in various ways

Manifestations of IUI in

live births:

a) by the time of birth, the inflammatory process is completed (residual form), the child is “virtually healthy,” however, morphological changes in organs and systems indicate a previous infection (high level of stigmatization) - embryopathy. Infection at 8-12 weeks;

b) the inflammatory process passed in the early fetal period, but left behind sclerotic complications (liver cirrhosis or biliary atresia, cardiac fibroelastosis, non-hereditary forms of polycystic kidney disease, hydrocephalus, congenital secondary immunodeficiency, etc.). The latter is also reflected in the postnatal state of the child (early infectious fetopathy). Infection from 4 to 6 months of intrauterine development (16-26 weeks);

c) generalized and local forms of intrauterine infections - sepsis, pneumonia, meningoencephalitis, carditis, pyelonephritis, etc. - late infectious fetopathies. From 27 weeks;

d) bacteriological and virological carriage without clinical and morphological manifestations of the disease - intrauterine infection without clinical manifestation. However, pathogens can be fixed in the tissues of the body for decades, causing a variety of reactions: polymorphic signs of immaturity, malnutrition, neurovegetative and mental disorders can also be caused by the infectious process.

e) transit of maternal antibodies in the newborn;

f) immunological tolerance - an organism infected with a pathogenic agent in utero loses the ability to actively produce antibodies when re-infected with the same pathogen. The inability to eliminate the microorganism is a consequence of immunological tolerance after contact of pathogen antigens with immature cells of the immune system during its embryogenesis.

g) intranatal infection – incubation period.

Intrauterine infections Pre-natal infections Purulent-septic diseases Purulent - septic diseases

Lecture structure Physiological infection Infection: – Prenatal – Intranatal – Postnatal Immune protection of the child

Lecture structure Infection physiological Infection: – prenatal – intranatal – post-natal Immune protection of the child

Intrauterine infection Characteristics of intrauterine infections: – Definition – Time of intrauterine damage and outcomes High-risk groups – Adverse obstetric history – Pathological course of this pregnancy – Diseases of the genitourinary system – Infectious diseases – Immunodeficiency conditions

Pre-natal infections Characteristic of pre-natal infections: Definition Time of pre-natal defeat and outcomes Groups of high risk Adverse obstetric anamnesis Pathological course of the real pregnancy Diseases of urinogenital system Infectious diseases Immunoscarce conditions

Etiology: The virus The bacterial The parasitic Transfer ways: Transplacentary, hematogenny Through the infected Para fetal waters When passing through patrimonial ways Signs of pre-natal infection: The main Additional clinical and laboratory Short characteristic of separate diseases Diagnostics and treatment

Purulent septic diseases 1. Skin and its pathology: Vesiculopustulosis Pemphigus of newborns Phlegmon of newborns

Purulent — septic diseases Skin, pathology: — Ve siculopustules — Puzyrchatka of newborns — Phlegmon of newborns

2. Umbilical wound and its pathology: – Physiology of the umbilical wound – Weeping navel – Fungus of the navel – Pyorrhea of the navel – Purulent omphalitis – Phlegmon of the navel – Thrombarteritis of the umbilical vessels

2. Umbilical wound, pathology: Physiology of an umbilical wound Soak (wet) of a navel Fungus of a navel Piorey of a navel Purulent omphalitis Navel phlegmon Tromboarter y of umbilical vessels

3. Gastrointestinal tract, pathology: Colonization Dominant and subdominant flora Dysbiocinosis Infection with the mammary gland and mother's milk Antibiotic therapy

3. Gastroenteric path of AFO and pathology: Colonization Dominating and subdominating flora Dysbiosynose Infection by a mammary gland milk of mother Antibiotics therapy

4. Organs of vision, pathology Congenital dacryocystitis Phlegmon of the lacrimal sac Abscess of retrobulbar tissue Ethmoiditis

4. T he eye pathology Congenital dacryocyst Phlegmon of the lacrimal sac Abscess of the retrobulbar fiber E thmoiditis

Physiological process of colonization 1. The process of bacterial colonization is the initial and necessary stage in the formation of a normal biocenosis. 2. The first contact with microorganisms occurs when the fetus passes through the birth canal 3. Stages of colonization: surface of the newborn’s body, nose, mouth and pharynx, gastrointestinal tract. 4. Value of nutrition: a) breast - bifidus factor (bifidobacteria up to 75%), b) artificial (enterococci, anaerobes, more putrefactive microflora, much less bifidobacteria).

Physiological process of colonization The process of bacterial colonization of the initial and necessary stage in the formation of normal biocenosis. The first contact with the microorganisms occurs when passing the fetus through the birth canal Stages of colonization: the surface of the body of the newborn, nose, the mouth and throat, gastro-intestinal tract. 4. The value of supply: (a) breast-feeding - bifidy-factor (bifidobacteria up to 75%), b) artificial (enterococci, anaerobes, and more putrefactive microflora, much less bifidobacteria).

Pathological colonization 1. Intensive therapy with the use of antibiotics for pathological conditions in the maternity hospital: Asphyxia Respiratory distress syndrome Intrauterine infections Birth injuries and subarachnoid hemorrhages

Pathological colonization Intensive therapy with the use of antibiotics in the treatment of pathological conditions in the hospital: Asphyxia Syndrome of respiratory disorders Intrauterine infections Birth injuries and subarachnoid hemorrhage

Characteristics of intrauterine infections Definition: intrauterine infection means infection of the fetus with an infectious agent before birth or during the passage of the birth canal (intrapartum infection) with the development of an inflammatory process in individual tissues or toxemia. A prerequisite is that the mother has a source of infection. The highest risk is observed with primary infection of the mother

Characteristics of fetal infections. Definition of terms. Definition: the intrauterine infection imply an infection of the fetus infectious agent before birth or during the ancestral ways (intranatal infections) with the development of the inflammatory process in certain tissues or toxemia. The compulsory condition is the presence of the mother of infection The highest risk is observed in the primary infection of the mother

Definition of terms. Intrauterine infection should be understood as an established or suspected fact of intrauterine penetration of viruses or microorganisms into the fetus, in which no signs of an infectious disease of the fetus are detected. By intrauterine infection, as stated above, we should understand the established fact of intrauterine penetration of viruses or microorganisms into the fetus, in which pathophysiological changes characteristic of an infectious disease occurred in the body of the fetus and newborn, detected prenatally or shortly after birth.

Definition of terms. Under the intrauterine infection should be understood installed or the alleged fact of intrauterine penetration to the fetus viruses or micro-organisms, at which is not detectable signs of infectious diseases of the fetus. Under the intrauterine infectious disease, as it was mentioned above, you should understand the fact of intrauterine penetration to the fruit of viruses and microorganisms, which in the body of the fetus and newborn occurred characteristic for infectious disease pathophysiological changes revealed in the prenatal period or soon after birth.

High-risk group for intrauterine infection. unfavorable obstetric history (spontaneous abortion, stillbirth, recurrent miscarriage, the birth of children with multiple malformations or those who died at an early age, infertility), pathological course of the present pregnancy and childbirth: (threatened miscarriage, miscarriage, incomplete or premature placental abruption, polyhydramnios, premature birth water)

The group of high risk of fetal infection. adverse obstetric anamnesis (spontaneous abortions, stillbirths, and the noncarrying of, the birth of children with multiple developmental defects or who had died at an early age, infertility), pathological during the present pregnancy and childbirth: (threat of interruption, noncarrying of, incomplete or premature detachment of the placenta, polyhydramnios, premature discharge of water)

diseases of the genitourinary system: (cervical erosion, endocervicitis, colpitis, vulvovaginitis, ovarian cyst, intrauterine adhesions, salpingitis, salpingophoritis, urinary tract infection), infectious diseases that manifested themselves during pregnancy as rash, jaundice, hepatosplenomegaly, lymphadenopathy, catarrhal phenomena, prolonged hyperthermia (including ARVI), immunodeficiency conditions (including AIDS), repeated blood transfusions, conditions after transplantation, the use of immunosuppressive therapy.

diseases of the genitourinary system: (cervical erosion, endocervicitis, vulvovaginitis, colpitis, cyst of the ovary, intrauterine adhesions, salpingitis, salpingo-oophoritis, urinary tract infection), infectious diseases, as demonstrated during pregnancy rash, jaundice, hepatosplenomegaly, catarrhal phenomena , lymphadenopathy, long hyperthermia (including ARVI), immunodeficiency s tates (including AIDS), repeated transfusion, condition after the transplantation, the use of immunosuppressive therapy

Etiology fetal infections. 1. Viral intraurerine infection s: rubella, cytomegalovirus, herpes infection, varicella, parotitis, ARVI, enterovirus infection Coxsackie and ECHO, viral hepatitis. 2. Bacterial: listeriosis, tuberculosis, syphilis, intraurerine bacterial infection (syndrome infected amnion). 3. Parasitic and others: toxoplasmosis, mycoplasmosis, chlamydia.

Pathogenesis of intrauterine infections Routes of transmission from the mother: 1. Transplacental - hematogenous (viruses and toxoplasma are transmitted this way), 2. Through infected amniotic fluid (bacteria). 3. When passing through the birth canal (any).

The pathogenesis of intrauterine infections Ways of infection transmission from mother: 1. Via placenta - hematogenous (thus transmitted viruses and toxoplasma), 2. Via infected amniotic fluid (bacteria). 3. When passing through the birth canal (if any).

Signs of intrauterine infection Intrauterine infection should be suspected if the newborn has the following clinical, laboratory or instrumental signs: 1. The appearance on the skin in the first 2 days of elements of pyoderma, herpetic or roseolous rashes. 2. The presence at birth of a dense, enlarged liver. 3. Jaundice from the first days of life in the absence of hemolytic disease. 4. Intrauterine malnutrition.

Signs of fetal infection Intrauterine infection should be suspected in the presence of the newborn following: clinical, laboratory or instrumental signs: 1. The appearance of the skin in the first 2 days of elements pyodermia, herpes or roseolous rash. 2. Available at birth dense, enlarged liver. 3. Jaundice from the first days of life in the absence of a hemolytic disease. 4. Intrauterine malnutrition.

TORCH syndrome T - toxoplasma O - other R - rubella C - cytomegaly H - herpes

TORCH sindrom T - Toxoplasma O - other (other) R - rubella C - cytomegalovirus H - herpes

Additional signs: malformations or stigmas of dysembryogenesis, non-immune fetal hydrops, micro- or hydrocephalus, fever in the first day of life, neurological disorders (including seizures) first registered a few days after birth, interstitial pneumonia, myocarditis or carditis, keratoconjunctivitis, cataract or glaucoma, changes in peripheral blood (thrombocytopenia, anemia, increased ESR, leukopenia, lymphocytosis, monocytosis, erythroblastosis) detected in the first days of life, characteristic changes in neurosonography (cysts, scattered and periventricular calcifications of the brain).

Additional features: malformation or dysembryogenesis, not immune fetal hydrops, micro-or hydrocephalus, fever in the first day of life, neurological disorders (including convulsions), for the first time registered a few days after birth, interstitial pneumonia, myocarditis or carditis, kerato c on j un gtivitis cataracts or glaucoma, changes in the peripheral blood (thrombocytopenia, anemia, increased erythrocyte sedimentation rate, l euc openia, l ymphocyt os, monocytosis, erythroblastose), identified in the first days of life, the characteristic changes in erythroblastosis (cysts, scattered and intracerebral calcification of the brain).

BASIC PRINCIPLES OF DIAGNOSTICS. 1. A set of anamnestic, clinical and routine laboratory parameters (not very specific, you can say “... yes, this is some kind of intrauterine infection”). 2. Enzyme immunoassay method (the most commonly used, but not always giving a reliable result). 3. Polymerase chain reaction (PCR) method. It was first developed in 1983 by Nobel Prize winner Carrie Mulis. The essence is the direct detection of the chain of a given virus or bacteria in any tissue. ELISA and a polymerase chain reaction method called immuno-PCR (100,000 times more sensitive).

BASIC PRINCIPLES OF DIAGNOSIS. 1. Collection of anamnesis, clinical and routine laboratory indicators (little specific, you can say “... Yes, this is some kind of intrauterine infection”). 2. Immunoenzyme method of the study, the most commonly used, but not always giving reliable results). 3. The method of polymerase chain reaction (PCR). It was first developed in 1983 by Nobel prize winner Kary Mullis. The essence lies in the direct detected t s e p I g e n a of this virus or bacteria in any tissue. EIA and method of polymerase chain reaction, called immuno-PCR (on 100, 000 times more sensitive).

BASIC PRINCIPLES OF TREATMENT. 1. When the process subsides at the time of birth, immunocorrection: a) immunoglobulins, b) leukenferron, c) thymolin, thymosin, T-activin. 2. In the generalized form: - a combination of antiviral drugs intravenously for 7-10 days (very toxic) and immunocorrection: a) acyclovir, virolex, virazol, etc. b) stimulants of immunogenesis and passive immunization. 3. Infections caused by chlamydia, bacteria and protozoa are treated with appropriate antibiotics and chemotherapy in combination with immunocorrection.

BASIC PRINCIPLES OF TREATMENT. 1. When subside process to the birth of immunocorrection: and immunoglobulins), b) leukenferron, in) timolin, Timosin, T-activin. 2. In generalized form: - a combination of antiviral drugs intravenously 7 -10 days (very toxic) and immunocorrection: a) acyclovir, virolex, virazol, etc. b) stimulants immunogenesis and passive immunization. 3. Infections caused by chlamydia, bacteria and protozoa, are treated with the appropriate antibiotics and chemotherapy in combination with immunocorrection.

EVENTRATION is an acutely developing defect of the abdominal cavity and muscles, the aponeurotic layer of the abdominal wall, as a result of which conditions are created for the intestines to exit the abdominal cavity.

Eventration developing a defect in the abdominal and muscle-aponeurosis layer of the abdominal wall, in results education which conditions are created for depressurization of the abdominal cavity and the exit of the interior for its limits.

PHOCOMELIA PHOCOMELIA (Greek phoke - seal, melos - part of the body, limbs). Hereditary diseases, the appearance of dysontogeny. Characteristic: underdevelopment or absence of forearms. The patient's hands resemble the flippers of a sea lion. The arms and legs seem to be attached directly to the body. Profound dementia. The same kind of manifestations were observed when taken by pregnant women.

Hereditary diseases, the appearance of dysontogeny. Characteristic of underdevelopment or absence of the forearm. The hands of the patient remind flippers sea lion. Hands and feet as if attached directly to the body. Deep dementia. The same kind of manifestations have been observed at the reception of pregnant.

Phocomelia (Greek phoke - seal, melos - part of the body, the limb).

Encephalocele A traumatic brain hernia, containing shell and the substance of the brain, but not including his the ventricles

PURIFIC-SEPTIC DISEASES. Predisposing factors are, first of all, the immaturity of the immune defense mechanisms in newborns: First factor: Phagocytic activity is significantly reduced, phagocytosis is incomplete, in children passive immunity is mainly associated with Ig. G, which are transferred to the child from the mother through the placental barrier (it is impenetrable for other immunoglobolins), the active response is quickly depleted.

PURULENT-SEPTIC DISEASES. Predisposing factors are the first of all the immaturity of the mechanisms of immune protection in newborns: The first factor: phagocytes activity is significantly reduced, phagocytosis is incomplete, children have passive immunity is mainly associated with Ig. G, which transferred to the child from the mother through the placental barrier (for other immunoglobulins it is impassable), active response rapidly depleted.

Second factor: all internal organs of excretion take part in the elimination of bacteria and toxins from the body (purulent foci easily arise). Third factor: the protective barriers of the skin and mucous membranes are imperfect: the thickness of the epidermis is reduced by almost 30% of adults; the basement membrane between the epidermis and the dermis is poorly developed, so the epidermis is easily separated from the dermis (blisters quickly appear during infection); poorly developed protective functions during sprain, injury, compression; a significant amount of toxins and metabolic products are released.

The second factor: the elimination of bacteria and toxins from the body take part of all of the internal organs of excretion (easily occur purulent foci). The third factor: the protective barriers of the skin and mucous imperfect: reduced thickness of the epidermis by almost 30% from adults; poorly developed basal membrane between the epidermis and the derma, so the epidermis is easily separated from the derma (quickly there are bubbles on infections); poorly developed protective functions in tension, injury, compressed; allocated a significant amount of toxins and metabolic products.

LOCAL PURULENT-SEPTIC DISEASES 1. Skin diseases: VESICULOPUSTULOSIS. PEMBIGUS OF NEWBORN. PHLEGMON OF NEWBORNS. PSEUDOFURUNCULOSIS. PURULAR MASTITIS OF NEWBORNS. Omphalitis is a bacterial inflammation of the bottom of the umbilical wound, umbilical ring, subcutaneous fatty tissue around the umbilical ring, and umbilical vessels.

LOCAL PURULENT-SEPTIC DISEASES 1. Diseases of the skin: VESICULOPUSTULES PEMPHIGUS NEWBORNS. P HLEGMON OF NEWBORNS. PSEUDOFURUNCULES. PURULENT MASTITIS NEWBORNS.

Omphalitis is a bacterial inflammation in the lower part of the umbilical wound, umbilical ring, subcutaneous fatty tissue around the navel ring, and umbilical cord vessels. Omphalitus bacterial - inflammation of the bottom of the umbilical wound, the umbilical ring, subcutaneous adipose tissue around the navel rings, umbilical vessels)

DISEASES OF THE UMBILICAL WOUND. Weeping navel Wetter navel Pyorrhea of the navel. Purulent omphalitis. Omphalitus bacterial inflammation of the bottom of the umbilical wound, the umbilical ring, subcutaneous adipose tissue around the navel rings, umbilical vessels. Phlegmon of the navel. Phlegmon navel of newborn Phlebitis of the umbilical vessels Flebit umbilical vesels

SEPSIS Main causes: unfavorable premorbid background (intrauterine infection); postnatal infection with particularly virulent microorganisms or a large number of them; morpho-functional immaturity; prematurity; long-term presence of local foci of infection failure of the immune system irrational antibacterial therapy in the early neonatal period

S epsis, septicaemia, septicemia The basic reasons: adverse premorbid background (intrauterine infection) postnatal infection particularly virulent micro-organisms or their great quantity; morpho-functional immaturity; prematurity; the prolonged presence of local foci of infection the failure of the immune system irrational antibiotic therapy early neonatal period

CLASSIFICATION OF SEPSIS 1. Depending on the entrance gate: - cutaneous, - pulmonary, - umbilical, - otogenic, - intestinal, - renal, - cryptogenic (with an unknown entrance gate) 2. According to etiology: - staphylococcal, - streptococcal, - pneumococcal, - caused by opportunistic flora, - meningococcal, etc. 3. According to the clinical picture: - septicopyemia (presence of purulent foci), - septicemia (toxemia), 4. According to the course: - acute, - sluggish (subacute, prolonged).

Depending on the input of the gate: - skin - pulmonary, - navel, - otogenous, gastrointestinal, - kidney, - cryptogenous (with unidentified entrance gate) On the etiology: - Staphylococcus, - streptococcus, pneumococcus - caused by conditionally pathogenic flora, - meningococcal, etc. By the clinical picture: - septicopyemia (the presence of purulent foci), - septicaemia (toxemia), 4. Downstream: - sharp, - slow (subacute, prolonged).

Criteria for a generalized process. Signs and symptoms of bacterial infection: 1. Clinical: respiratory distress syndrome of unknown etiology, feeding intolerance of unknown etiology (frequent regurgitation, vomiting, anorexia, flattening of the weight curve, malnutrition), temperature instability, drowsiness, irritability, change in skin color (pallor, subicterus , gray color), bloating, dyspeptic disorders, hepatosplenomegaly, depression of central nervous system functions.

Criteria for generalized process. Signs and symptoms of bacterial infection: Clinical: respiratory distress syndrome of unknown etiology, intolerance of the feeding of unknown etiology (frequent regurgitation, vomiting, anorexia, flattening the weight of the curve, malnutrition), the instability of temperature, drowsiness, irritability, change the color of the skin (pallor, yellowness, gray color), bloating, diarrhoea disorders, enlarged liver and spleen (hepatosplenomegaly), the oppression of the Central nervous

Laboratory signs of sepsis. 1. Peripheral blood: - leukocytosis or leukopenia, - neutrophilia, shift to the left, - early anemia, - thrombocytopenia, - accelerated ESR. 2. Hemorrhagic syndrome (vitamin K deficiency, disseminated intravascular coagulation syndrome, thrombocytopenia): - increased bleeding at the injection site, - petechiae, - hematuria, etc.

The laboratory signs of sepsis. 1. Peripheral blood: - leucocytosis or l eucopenia, - neutrophilia, the shift to the left, - early anemia, thrombocytopenia, - accelerated ESR. 2. Haemorrhagic syndrome (deficiency of vitamin K, disseminated intravascular coagulation syndrome, thrombocytopenia): - increased bleeding at the site of injection, - petechiaea, - hematuria, etc.

3. Biochemical blood test: - hypoproteinemia, - hypoalbuminemia, - dysproteinemia, - increased ALT, AST in hepatitis, - increased C-reactive protein. 4. Positive results of blood culture studies at the height of fever in different foci.

3. Biochemical blood test: - hypoproteinemia, - hy poalbuminemia, - d i sproteinemia, - increase of A LT, AST for hepatitis, - the increase of C-reactive protein. 4. Positive results of a study cultures at a height of fever in different places.

5. The presence of several foci of inflammation. 6. Edema syndrome: edema mainly in the area of the anterior abdominal wall, pubis and lower extremities. 7. Changes in parenchymal organs: - hepatomegaly - more often (toxic liver damage, or hepatitis with direct hyperbilirubinemia), - splenomegaly - less often. 8. Temperature reaction is not typical.

5. The presence of several foci of inflammation. 6. edema syndrome: swelling mainly in the field of a front abdominal wall, vulva and lower extremities. 7. Change of parenchymatous organs: - enlarged liver (hepatomegaly) - more often (toxic liver damage, or hepatitis with direct hyperbilirubinemia), - enlarged spleen (splenomegaly) - less. 8. Temperature reaction is not typical.

UMBILICAL SEPSIS Entrance gate: umbilical wound. Infection of the umbilical arteries (2) – venous blood. After the umbilical cord is separated, blood clots form. The umbilical vein is arterial blood. Infection - most often during manipulation (replacement blood transfusion for HDN) Thromboarteritis of the umbilical vessels develops, a local process, and then generalization.

UMBILICAL SEPSIS Entrance gates: umbilical wound. Infection of the umbilical arteries (2) - venous blood. After the separation of the umbilical cord blood clots are formed. Umbilical Vein - arterial blood. The infection is most often during manipulation (exchange transfusion of blood when hemolytic disease) Develops thromboarteritis of umbilical vessels, local process, and then the generalization.

Clinical picture 1. Symptoms of infectious toxicosis. 2. Local symptoms: - damage to the navel and blood vessels, - a symptom of a “secondary” opened navel, - abdominal distension (venous network, shiny surface of the anterior abdominal wall), - Krasnobaev’s symptom (tension of the rectus abdominis muscle on the side of the affected vessel), - palpation of the umbilical vessels, the appearance of pus in the umbilical wound (tube symptom).

Clinical picture 1. Symptoms of infectious toxicosis. 2. Local symptoms: the defeat of the navel and blood vessels, - a symptom of “secondary” (again revealed) the navel, - swelling of the abdomen (venous network, shiny surface of the abdominal wall), - a symptom of prof . Krasnobaev (voltage direct abdominal muscles on the affected side of the vessel), - palpation of umbilical vessels the emergence of pus in an umbilical small wound (a symptom of a tube).

Diagnosis is established on the basis of local symptoms, previously listed criteria septic process and laboratory performance.

Principles of treatment of sepsis 1. Breastfeeding if mother's milk is sterile. In all other cases, feeding with adapted, preferably fermented milk, formulas. a) number of feedings 8-10 times a day (50 ml each), every 2-2. 5 o'clock. Water load - up to 150 -200 ml in fractions between soakings with boiled water. b) after relief of dyspeptic syndrome, a rapid transition to a physiological rhythm of nutrition.

Principal treatment Breastfeeding mother, if the mother’s milk is sterile. In all other cases, breastfeeding adapted, better cultured milk, mixtures. (a) the number of feedings 8 -10 times a day (50 ml), every 2 -2. 5 hours. Water load - up to 150 -200 ml of fractional between boiling water. b) after the relief of dyspeptic syndrome rapid transition to the physiological rhythm of power.

Fighting infection: Antibiotics protected from the action of beta-lactamase pathogens: Initial therapy: cephalosporin drugs in combination with aminoglycosides until sensitivity is obtained, then monotherapy taking into account sensitivity

Infection control: Antibiotics, protected from the action of beta-lactam pathogens: Starting therapy: cephalosporin drugs in combination with aminoglucosides to receive sensitivity Further monotherapy with view of the sensitivity

Doses: Increased by 2 times compared to the nominal value, Route of administration in young children: intravenous, Frequency of administration is maximum, taking into account the pharmacodynamics of the drug, Condition: during the half-life of the drug, its concentration in the blood and other biological fluids must remain bactericidal

Doses Increased in 2 times in comparison with the nominal value, Way of administration in children of early age intravenous The frequency of the introduction of the maximum, with the account of pharmacodynamics of the product, Condition: in the half-life of the product, its concentration in the blood and other body fluids should be bactericidal

Pathogenetic therapy 1. Infusion therapy for the purpose of detoxification (pain with infectious-toxic shock), correction of metabolic disorders (combat metabolic tissue acidosis, electrolyte disturbances), improvement of hemodynamic parameters (elimination of symptoms of centralized circulation), relief of disseminated intravascular coagulation syndrome:

pathogenetic therapy 1. Infusion therapy with the purpose of detoxification (fight with infectious-toxic shock), correction of metabolic disorders (struggle with metabolic tissue acidosis, electrolyte disorders), improvement of gemodinamic indicators (elimination of the symptoms of centralization of the circulatory system), mild DIC-syndrome:

2. Passive immunization: - hyperimmune plasma intravenously every 3-4 days. - toxoids, - antitoxic serums. — immunoglobulins intravenously, drip. It is impossible to immunize with vaccines in this condition, since the child cannot synthesize antibodies in this situation. 3. Sanitation of foci of infection

2. Passive immunization: - hyperimmune plasma intravenous drip every 3 -4 days. — toxoids, — Antitoxic serum s. — immunoglobulins intravenously Immunized with vaccines in this state it is impossible, as the child may not synthesize antibodies in this situation. 3. Remediation of sites of infection

Prevention of purulent-septic diseases 1. Prenatal, it is better before predicting the birth of a child - sanitization of foci of infection. 2. Constant monitoring of the pregnant woman with correction of identified disorders (toxicosis, viral and bacterial diseases, etc.). 3. Prevention of infection in the maternity hospital. 4. Refusal of uncontrolled prescription of antibiotics. 5. Careful care of the child in the neonatal period.

Prophylaxis of purulent-septic diseases 1. Prenatal, better than before predicting the birth of a child - readjustment of infection foci. 2. Constant monitoring of the pregnant woman with the correction of the revealed violations (toxicosis, viral and bacterial diseases, etc.). 3. The prevention of infection in the hospital. 4. Refusal from without control prescribing antibiotics. 5. Thorough care for the child in the neonatal period.