Presentation on the topic of intrauterine infections. Intrauterine infections of the fetus and newborn

Completed by: Shavenkova M 223 OMF Semey State Medical University

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Plan

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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Routes of infection to the fetus

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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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Congenital cytomegalovirus infection

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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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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 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.

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 “practically 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.

Slide 3

The range of pathogens that can lead to intrauterine infection of the fetus is very wide. A group of infections has been identified that are common in the population and have similar clinical manifestations and cause persistent structural defects in various systems and organs in the fetus. This group was united and designated by the abbreviation "TORCH", where T - toxoplasmosis (toxoplasmosis), O - other (other infections, including absolute - syphilis, chlamydia, enteroviruses, hepatitis A, B, gonorrhea, listeriosis; probable - measles, mumps and hypothetical - influenza A, human papillomavirus infection), R - rubeola (rubella), C - cytomegalia (CMV), H - herpes (herpes viral infection).

Slide 4

routes of intrauterine infection

Ascending Hematogenous Descending Contact intrapartum transmural).

Slide 5

In 89% of cases, the infection occurs through the ascending spread of external urogenital infection (bacterial and viral), which can occur with any type of initiating agent. The dependence of this process on the state of local immunity and the anatomical and physiological properties of the cervix is shown. Predisposing factors for the development of intrauterine infection through the ascending route in the presence of external urogenital infection are: - gestational age (gravid stage), - changes in the barrier properties of the fetal membranes, violation of the anatomical and physiological properties of the cervix, partial rupture of the membranes, a long anhydrous interval, instrumental diagnostic methods . The hematogenous route of infection is characteristic mainly of viral diseases, and is also often observed with latent carriage of Toxoplasma. The descending route is possible in women with foci of chronic inflammation in the ovaries and fallopian tubes. Contact infection of the fetus often develops during childbirth through direct contact with infected tissues of the birth canal or transdecidually, with existing infectious pathology of the uterus.

Slide 6

In the antenatal period, the infection can be transmitted transplacentally: 1) as a result of penetration of the pathogen from maternal blood into the blood of the fetus in the absence of inflammatory foci in the placenta; 2) when the pathogen enters the maternal part of the placenta and forms an inflammatory focus in it, followed by penetration of the infectious agent into the blood of the fetus; 3) with damage to the chorion and the development of an inflammatory process in the fetal part of the placenta, membranes and infection of the amniotic fluid (Fig. 1). The second route of infection of the fetus is an ascending infection from the vagina and cervix through a damaged or intact amniotic sac. Rice. 1. Ways of spread of intrauterine infection (diagram)

Slide 7

Features of fetal infection depending on developmental stages

Slide 8

The stages of pregnancy development are distinguished: -embryonic, -fetal and -antenatal. In the embryonic stage of pregnancy (first trimester), the occurrence of any infectious process in the mother’s body is a serious threat. Due to the incomplete formation of the uteroplacental barrier, this threat can be realized through ascending or hematogenous infection of the fetal bladder, which leads to severe inflammatory complications and early miscarriage, or underlies further pathology of pregnancy caused by various embryopathies and fetal malformations. In the first case, the etiological factor is usually a various bacterial infection, and in the second - viral agents. The existence in the early stages of pregnancy in the developing placenta of a pronounced layer of cytotrophoblast prevents the penetration of certain pathogens, in particular spirochetes, to the fetus.

Slide 9

In the second (fetal) trimester of pregnancy, the main manifestations of intrauterine infection include, on the part of the placenta, signs of inflammatory pathology in the membranes and placental tissues; on the part of the fetus, signs of aspiration bronchopneumonia or a generalized infectious process, various types of fetopathies, as well as intrauterine growth retardation. The noted pathology can result in late spontaneous miscarriage or cause the development of isthmic-cervical or placental insufficiency. In the third trimester of pregnancy, there remains a high risk of transplacental spread of many bacterial and especially viral agents, which is due to involutional changes and increased permeability of the fetoplacental barrier. The noted danger increases many times if the infectious pathology of the placenta begins in earlier stages of pregnancy. Thus, timely detection and targeted treatment of infectious pathology of the genital tract can serve as one of the ways to reduce the incidence of adverse perinatal outcomes as a result of intrauterine infection.

Slide 10

risk factors for the development of intrauterine infection

●Exacerbation of a chronic infection present in a pregnant woman (chronic diseases of the respiratory system, digestion, caries, tonsillitis). ●Urogenital infections (pyelonephritis, bacteriuria, colpitis, endocervicitis, STIs). Intestinal dysbiosis and bacterial vaginosis. ●Complications of pregnancy: anemia, gestosis, isthmic-cervical insufficiency, exacerbation of chronic diseases and acute respiratory viral infections suffered in the second half of pregnancy. ●ARVI during childbirth, prenatal rupture of amniotic fluid, pathology of labor, use of obstetric aids.

Slide 11

pathogenesis of intrauterine infection

In the pathogenesis of intrauterine infection, the “maternal”, “successional” and “fetal” stages of development are distinguished. The staging is determined not only by the stages of spread of the pathological process from the mother’s urogenital system to the fetal tissues, but also by the order of inclusion of protective-adaptive systems in the process. The “maternal” stage reflects the initial stage of infectious aggression, formally limited to the external parts of the urogenital system of a pregnant woman. A characteristic feature of the “maternal” stage is the often latent course of urogenital infections, which to a certain extent depends on the effectiveness of local immunocellular reactions in the reproductive system of pregnant women, primarily in the cervix.

Slide 12

The “secondary” stage serves as a continuation of the progressive inflammatory process in the genitourinary system of a pregnant woman or occurs in common infectious diseases accompanied by viremia or bacteremia. The placenta has high antibacterial resistance due to the accumulation of lysozyme, transferrin, β-lysine, opsonins, peroxidase, IgG in the amniotic fluid and fetal membranes and the presence of cellular protective factors such as leukocytes and macrophages. In case of ascending infection, the state of the filtration properties of the fetal membranes is important, as well as those leukotropic substances that, as bacteria multiply, accumulate in the amniotic fluid and act as primary mediators of the inflammatory reaction. The amnion epithelium is capable of adsorbing bacteria, including chlamydia, on its surface.

Slide 13

In the tissues of the amniotic membrane there are motile Kashchenko-Hoffbauer cells that have the functions of macrophages. These cells appear for the first time at the end of the 4th week of gestation and by the 9-10th week they acquire pronounced macrophage activity. The antimicrobial activity of amniotic fluid against many types of opportunistic microorganisms is weak and can retard their growth for several hours (from 3 to 12 hours), but not suppress. The fetal membranes, especially when they are stretched to their maximum at the end of pregnancy, are permeable to many opportunistic microorganisms, so infection of the fetus can occur even with the entire amniotic sac.