Neonatal sepsis presentation. Medicine lectures

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Staphylococcus lesion

Bullous impetigo-group of superficial skin infections caused primarily by Staphylococcus aureus The incubation period is 1-10 days 30% of people are carriers of the Staphylococcus aureus strain. , in the navel, skin folds

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Forms of bullous impetigo

Vesiculopustulosis - the disease is caused by inflammation in the area of ​​the mouths of the sweat glands and is manifested by the fact that on the skin of the thighs, buttocks, natural folds, the head there are small bubbles filled with transparent and then cloudy contents. The course is good.

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Forms of bullous impetigo

Pemphigus of newborns (pemphigus). Benign - blisters 0.5-1 cm at different stages of development, serous-purulent contents. Nikolsky's symptom is negative. After opening, erosion, an increase in body temperature to subfebrile numbers. Recovery in 2-3 weeks. Malignant - a significant number of large blisters - up to 2-3 cm in diameter. Nikolsky's symptom may be positive. The condition is serious, intoxication, febrile temperature, sepsis may develop. In the blood - leukocytosis, neutrophilia, shift of the leukocyte formula to the left, accelerated ESR.

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C) Ritter's exfoliative dermatitis is the most severe form (septic pemphigus). Called by pathogenic strains of Staphylococcus aureus, which produces exotoxin-exfoliatin. Stages of the disease: Erythematous Exfoliative Regenerative Manifestations: Redness, oozing of the skin and the formation of cracks in the navel, groin folds, around the mouth. Erythema spreads to the skin of the abdomen, trunk, extremities. Nikolsky's symptom is positive. The body resembles "scalded with boiling water." A serious condition, an increase in body temperature. Staphylococcal Burned Skin Syndrome

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Pseudofurunculosisfinger - the main manifestations are subcutaneous nodes up to 1-1.5 cm in diameter, purple-red in color, then purulent contents appear in the center. Localization: the skin of the temporal part of the head, the back of the neck, back, buttocks, limbs. It is accompanied by an increase in temperature, a reaction of regional lymph nodes, anemia, leukocytosis, accelerated ESR.

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The defeat of the subcutaneous fat (SFA)

Anatomical and physiological features: PZhK in newborns is well expressed, well-supplied with blood Insufficiently developed connective tissue bridges rapid spread of infection along the periphery Prevalence of solid fatty acids rapid formation of seals.

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Necrotizing phlegmon of newborns

One of the most severe NHS, which initially appears as a spot. There are 4 stages: Initial (acute inflammatory process). Rapid (within a few hours) spread of the lesion.Alternative necrotic stage occurs after 1-1.5 days, areas of the skin are purple-bluish, softening in the center Stage of rejection - necrosis of exfoliated skin - wound defects with undermined edges (purulent pockets) Stage reparations - the development of granulation tissue, epithelialization of the wound surface with the formation of scars The disease proceeds against a background of high temperature, vomiting, dyspeptic foci of infection - sepsis

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Mastitis in newborns

A serious illness that begins against the background of physiological engorgement of the mammary glands. Manifestations: enlargement of the gland, infiltration, hyperemia, fever, intoxication, purulent discharge, metastatic purulent-septic complications.

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Omphalitis

Inflammatory process in the umbilical wound and underlying tissues Common cause of neonatal sepsis Causative agent - Staphylococcus aureus Classification: Simple (catarrhal) omphalitis Phlegmonous form Necrotizing omphalitis Treatment - systemic broad-spectrum antibiotics, infusion therapy, passive immunization. Treatment of phlegmonous forms together with children's surgeons.

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NHS treatment

Anti-epidemic measures Immediate transfer of the child to the hospital All contacts - changing diapers, prescribing bifidumbacterin Sanitary treatment of the room Examination of the skin with each swaddling General therapy: antibacterial, infusion, symptomatic, vitamins, maintaining immunity Local therapy

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Classification of neonatal sepsis When drawing up a clinical classification of the disease, it is necessary to take into account the time and conditions for the onset of blood infection - developed before
the birth of a child, after birth; localization
entrance gate and / or primary septic focus,
clinical features of the disease. These parameters
characterize the etiological spectrum of the disease,
the volume and nature of therapeutic, preventive and
anti-epidemic measures. Exactly these
parameters are advisable to use in
classification of sepsis in newborns.

Pathogenesis. The entrance gates of infection are: the umbilical wound, injured skin and mucous membranes (at the injection site,

Clinic.

Diagnostics

Care, treatment, prevention.

1. Intrauterine infection 1) Hematogenous route 2) Through the natural openings of the fetus 2. During childbirth due to infection with amniotic fluid and discharge during their aspiration. More often at birth: 1. Sources - mother 2. Attendants 3. Staff clothing 4. Care items 5. Patients with a bacterial carrier

A number of anatomical and physiological factors Immaturity: 1) cerebral cortex; 2) the endocrine system; 3) skin and lymph. systems; 4) detoxifying function of the liver 5) excretory function of the kidneys Factors that reduce the reactivity of the body: 1) prematurity; 2) irrational feeding; 3) decrease in T environment; 4) birth injury

Clinical manifestations 1. Violation of the general condition (agitation, sleep disturbance, cry, lethargy); 2. Decreased sucking activity or complete rejection of the breast; 3. Significant loss of body weight with a sufficient amount of milk from the mother. 4. Decrease or loss of physiological reflexes. 5. Changes in skin color, a drop in turgor, skin rashes. 6. Temperature reaction of varying duration and character.

7. Regurgitation, vomiting, dyspeptic symptoms. 8. Enlargement of the liver and spleen. 9. Rapid breathing, shortness of breath, cyanosis without much change in the lungs. 10. Deafness of tones, noise, tachycardia, falling A / D. 11. Decreased urine output, the appearance of protein, leukocytes, casts. 12. Leukocytosis with neutrophilic shift. Acceleration of ESR, anemia. 13. Jaundice (conjugation, thickening of bile) due to hemolysis of erythrocytes to the death of hepatocytes under the influence of toxins. In severe cases, septic hepatitis. 14. Encephalopathy in some children.

The main organ and system disorders observed in sepsis Respiratory system: - respiratory alkalosis; - hyperventilation; - weakening of the respiratory muscles; - adult respiratory distress syndrome; - diffuse infiltrates in the lungs; - the need for respiratory support

Cardiovascular system: - an increase in cardiac output at the onset of the disease; - decrease in peripheral resistance, vasodilation (preshock); - damage to the endothelium, decreased vascular tone and blood pressure (early shock); - myocardial depression, decreased cardiac output; - vasoconstriction, organ hypoperfusion; - refractory hypotension (late shock)

Mental status: - brain hypoperfusion, increased production of endorphins; - disorientation; lethargy; confused consciousness; - excitement or lethargy; - stupor, coma. Urinary system: - renal hypoperfusion; - damage to the renal tubules (azotemia and oliguria).

Hematological parameters: - neutrophilic leukocytosis in the initial stage (not always!); - vacuolization and toxic granularity of neutrophils (always); - thrombocytopenia, disseminated intravascular coagulation syndrome; - eosinopenia; - a decrease in serum iron (the phenomenon of redistribution and binding to proteins) as a constant symptom

Directions of therapy 1. Influence on the pathogen 2. Substitutional immunotherapy 3. Rehabilitation of piemic foci 4. Treatment of syndromes) DIC, NPC) 5. Therapy aimed at stabilizing metabolic processes 6. Treatment of concomitant diseases 7. Treatment of side effects of drug therapy (dysbacteriosis, candidomycosis )

Antibiotic therapy 1. Correct choice of antibiotics 2. Adequacy of its dose 3. Two antibiotics (synergism) 4. Penicillin, as a debut antibiotic, should be used: 1) when sensitivity to it is identified; 2) in the absence of disseminated intravascular coagulation; 3) with moderate intoxication.

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The urgency of the problem is determined by:

Definition of sepsis

Etiology and pathogenesis

The most common causative agents of sepsis, depending on the time of infection of the fetus and newborn

The most likely pathogens, depending on the localization of the primary focus in postnatal infection

Ways of infection to the fetus

In the postnatal period

Sources of infection:

Pathogenesis of sepsis (according to G.N.Speransky)

Systemic inflammatory response (SVR)

Sepsis pathogenesis

Figurative comparison of sepsis with a domestic fire

Classification of sepsis

Examples of clinical diagnosis:

Clinical picture

Septicemia

Sepsis after birth

To the harbingers of sepsis

Further development of sepsis

Septicopyemia

The course of sepsis

Features of sepsis in premature infants

Diagnosis of sepsis

Factors contributing to the development of sepsis in newborns

Signs of SVR

Laboratory signs of sepsis in newborns

Etiology of the disease

Sepsis treatment

General principles for choosing antibiotic therapy

Antibiotic therapy program for sepsis in children

Impact on a macroorganism

Dispensary observation

Sepsis of newborns Is a syndrome that manifests itself with clinical signs of infection in the presence of positive bacterial cultures of blood, urine and / or cerebrospinal fluid in infants of the first month of life.

Sepsis is a generalized infectious disease of a polyetiological nature that develops against the background of altered body reactivity.

Sepsis of a newborn

Was first obtained by Yippo in 1919 when a positive blood culture was obtained from a deceased child.

However, until 1930, there were no more reports in the pediatric literature of such a diagnosis.

In 1933, Dunham describes 33 cases of neonatal sepsis

In 60% of cases, the disease begins in the first week of life, in 10% of the symptoms occur immediately after birth

In 1949, Silverman and Homan describe 25 children with sepsis who had a positive blood culture

The term Systemic inflammatory response

syndrome (SIRS) - a systemic inflammatory reaction, adopted at the suggestion of Roger Bonet (1991) to define sepsis as a documented infection +

at least 2 signs of SIRS:

Body temperature above 38 ° C or below 36 ° C

Tachycardia above 90 beats per minute

Tachypnea over 20 per minute

The number of leukocytes is above 12x10 / μl, below 4x10 / μl, and the number of young forms of polymorphonuclear neutrophils exceeds 10%.

A systemic inflammatory response is a general biological nonspecific immunocytological response of the human body in response to the action of a damaging endogenous or exogenous factor. If sepsis develops, SVR develops in response to primary purulent-inflammatory focus. CBR is characterized by an increase, mainly, in the production of pro-inflammatory and, to a lesser extent, anti-inflammatory cytokines by almost all cells of the human body, including immunocompetent ones.

It has been established that the direct cause of systemic generalized inflammation in sepsis is the uncontrolled release of endogenous inflammatory mediators in the infectious focus (“mediator chaos”) and the lack of mechanisms limiting their damaging effect.

A common factor uniting all pathogens is microbial toxins, both exotoxins and endotoxins. The action of exotoxins or endotoxins leaves some, but not fundamental, imprint on the clinic and the outcome of sepsis.

Only from these positions can one explain such an unusual, stereotyped, and not specific reactivity of the organism, since it is based not on microbial invasion as such, but on the response of the immune system to microbial toxins, which are weak antigens.

In sepsis, there are no pronounced specific antigenic determinants, since the body's response is caused by toxins that are weak in antigenic terms. When they appear in the blood, macrophages probably recognize a foreign protein, but cannot identify specific antigenic determinants and, accordingly, provide the immune system with information about a specific pathogen. Macrophages in the focus of inflammation are "blinded" and information from the immune system is disrupted. In this situation, there is a hyperfunction of macrophages that respond to foreign influences, but are not able to determine the antigen.

Macrophages begin to throw out all biologically active substances contained in them. There is an inexpedient and unlimited release of various cytokines by macrophages, both pro-inflammatory and anti-inflammatory - IL 4, 10, 13, soluble receptors to TNF, etc. The formation of tissue and plasma mediators of inflammation and simultaneously reactants of the acute phase is also chaotically stimulated. All this leads to the development of the so-called "mediator chaos".

The predominance of the destructive effects of cytokines and other mediators of inflammation leads to impaired permeability and function of the capillary endothelium, impaired microcirculation, induction DIC syndrome.

As a result of all these processes, a systemic inflammatory response develops, which is also uncontrollable. due to the discoordination of various regulatory systems of the body that do not have information about a specific aggressor, its localization and processes occurring in each specific organ and system.

Thus, if we assume that the peculiar reactivity in sepsis is the response of the immune system not to microbial invasion as such, but to microbial toxins, then the features of sepsis become clear. Only from these positions can one explain such an unusual, stereotypical, and not specific reactivity of the organism in septicemia, because it is based not on microbial invasion, as such, but on the reaction of the immune system to microbial toxins. Sepsis for the pathogen is polyetiological, however, the body's main reaction is not to a microbe, but to a toxin that does not have the specificity of pathogens - it can only be either endotoxin or exotoxin