The most common portal of entry for neonatal sepsis. Causes of sepsis in newborns

However, pediatric neonatologists are not inclined to be optimistic. According to statistics, 1-2 babies out of a thousand full-term babies born develop umbilical sepsis (and among premature babies the percentage is an order of magnitude higher), which, according to doctors, makes the situation quite serious.

Neonatal sepsis is an invasive infection, usually bacterial, that develops in the neonatal period. Symptoms of sepsis are varied and include decreased spontaneous activity, poor feeding, apnea, bradycardia, temperature fluctuations, respiratory distress, vomiting, diarrhea, abdominal bloating, irritability, seizures and jaundice. Treatment begins with a combination of ampicillin with gentamicin or cefotaxime, subsequently moving to drugs more sensitive to the identified pathogen.

Neonatal sepsis is detected with a frequency of 0.5-8.0 per 1000 newborns. The highest incidence of sepsis is typical for infants with low birth weight, with impaired respiratory function at birth.

Several maternal perinatal and obstetric factors increase the risk, especially of early-onset sepsis.

These factors include:

• premature rupture of membranes occurring >18 hours before birth;
• bleeding in the mother (for example, with placenta previa, placental abruption);
• preeclampsia;
• rapid labor;
• premature birth;
• infection in the mother (particularly of the urinary tract or endometrium, most often manifested as maternal fever shortly before or during labor);
• high colonization with group B streptococci.

Some bacterial pathogens (for example, L monocytogenes, Mycobacterium tuberculosis) can enter the fetus transplacentally, but most of them are transmitted via upward path in utero or during the passage of the fetus through a colonized birth canal.

Amniotic fluid contaminated with meconium or original caseous masses: promotes the growth of group B streptococci and E. coli. The organisms usually reach the fetal bloodstream through aspiration or ingestion of contaminated amniotic fluid.

late start. Most important factor risk for sepsis late start- premature birth.

Other factors include:

• long-term use of intravascular catheters;
• associated diseases (can be markers only when using invasive procedures);
• exposure to antibiotics (which selects for resistant strains of bacteria);
• long-term hospitalization;
• contaminated equipment or intravenously or enterally administered solutions.

Gram-positive microorganisms can come from the environment or the patient's skin. Gram-negative enteric bacteria typically come from the patient's endogenous flora, which may have been altered by previous antibiotic therapy or colonized by resistant microorganisms acquired by personnel (the main mode of spread) or contaminated equipment. Thus, situations that increase exposure to these bacteria increase the prevalence of hospital-acquired infections. Risk factors for sepsis due to Candida sp. include long-term (>10 days) use of central intravenous catheters, overfeeding, use of older antibiotics, necrotizing enterocolitis or other abdominal pathology, and previous surgery.

The initial foci of infection may be in the urinary tract or digestive tract and can subsequently disseminate into the meningeal membranes, kidneys, peritoneum, etc.

What are the causes of sepsis in newborns?

Group B streptococci and gram-negative intestinal microorganisms (mainly Escherichia coli). Culture testing of vaginal or rectal swabs from women in late pregnancy reveals group B streptococci in up to 30%. About 55% of children born to such mothers are contaminated. The higher the density of contamination, the higher the risk of early onset of the disease, however, sepsis caused by group B streptococci develops in only 1 out of 100 newborns, and during the first 6 hours of life - in more than 50% of cases. Haemophilus influenzae is a common cause of sepsis in premature newborns.

In other cases, gram-negative intestinal bacteria (eg, Klebsiella sp.), gram-positive organisms, enterococci, group D streptococci (eg, Streptococcus bovis), α-hemolytic streptococci, and staphylococci can also cause sepsis.

In late-onset sepsis, the pathogen usually comes from the environment. Staphylococci cause 30-60% of late-onset sepsis and are most often associated with the use of intravascular devices (particularly an umbilical artery catheter or a venous catheter). E. coli is also increasingly recognized as a major cause of late-onset sepsis, especially in very low birth weight infants. Isolation of Enterobacter cloacae or E. sakazakii from blood or cerebrospinal fluid suggests contamination by feeding. Although universal screening and intrapartum antibiotic prophylaxis for group B streptococcal infections have significantly reduced the incidence of early-onset disease caused by this organism, the incidence of late-onset sepsis has remained unchanged.

The role of anaerobes (especially Bacteroides fragilis) in the development of late-onset sepsis remains unclear. Anaerobes may cause some culture-negative cases in which sepsis has been identified at autopsy.

Early and late start. Some viral infections (eg, disseminated HSV, enterovirus, adenovirus, and respiratory syncytial virus) may present as early- or late-onset sepsis.

First of all, the infection develops because young children have reduced resistance to pathogenic microflora. Physiologically, the body has not yet matured: protective reactions are very weak, barrier functions are not fully developed. Therefore, the internal systems of the newborn do not eliminate, but support inflammatory processes.

It is also important that the baby’s body does not receive immune bodies against septic infections from the mother. It is septic immune deficiency that makes umbilical sepsis quite common.

The causative agents of neonatal sepsis are streptococci, staphylococci, pneumococci, infection of which can occur in utero, during childbirth and in the first days of life.

Any infectious disease expectant mother, accompanied by an increase in temperature, is dangerous for her child. The bacteria themselves do not cross the placental barrier, but their toxins enter the fetus and poison the body of the unborn baby. During childbirth, the infection enters the baby through ingestion of amniotic fluid; after childbirth, through the air, unclean linen, or even the milk of a sick mother.

Pathogenic pathogens can enter the baby through scratches on the skin, digestive tract, respiratory tract, in girls - through the mucous membranes of the genital organs, however, the most common route of infection is the umbilical wound, where very large blood vessels emerge.

In most cases, neonatal sepsis begins 8-10 days after birth, but identifying any characteristic symptoms is not easy. The child may be lethargic, gain weight poorly, have a grayish skin color, and an enlarged liver, however, such signs often go unnoticed because the body temperature remains normal. The presence of staphylococcus is detected only during laboratory tests, when the skin tone becomes yellowish color. This is the so-called hemolytic jaundice, which occurs due to a septic infection.

In premature babies, sepsis often occurs without any detectable symptoms at all: the child simply loses weight and that's it. The ambiguity of the signs often delays the start of treatment, and in such cases it should be immediate.

If the infection is introduced through the intestinal tract, then sepsis is caused by colibacilli (E. coli, etc.). In this case, the general symptoms are usually so blurred that the first a clear sign already developed meningitis serves. Coli meningitis in newborns is manifested by bulging of the fontanelle and convulsions.

Neonatal sepsis is treated with antibiotics according to an intensive scheme, taking into account the resistance of the pathogen to drugs.

Is it possible to avoid septic infection in newborns? Yes, you can.

Expectant mothers, especially in the last period of pregnancy, should in every possible way avoid infectious diseases, and if they appear, they should be actively treated, of course, subject to all the recommendations of an obstetrician-gynecologist.

Today, in maternity hospitals, all the rules of asepsis are observed, and the navel is processed competently. But the newfangled trends of home delivery are far from complying with sanitary standards, so it is possible for babies to become infected during childbirth.

Children of the first days of life should be wrapped in sterile diapers, the skin treatment oil should also be sterile. Mothers must be able to properly handle the baby’s mucous membranes so as not to accidentally cause damage, since any scratch or abrasion may have the potential for the introduction of pathogenic microflora.

Nursing mothers are usually taught to clean their nipples so as not to infect the baby, but, unfortunately, not all of these recommendations are followed.

Umbilical sepsis of newborns

Due to reduced levels of specific and nonspecific immunity, when bacterial flora gets into the umbilical wound, so-called umbilical sepsis can develop. More than half of all sepsis in newborns is caused by omphalitis, which is then complicated by inflammation of the anterior abdominal wall, which is fraught with adhesive fusion of the peritoneum with the intestines, and then peritonitis.

The infection spreads hematogenously, that is, through the circulatory system.

The causative agent is most often Staphylococcus aureus and fungi, in particular thrush, which, once in an insufficiently well-treated umbilical cord, cause blood poisoning within a period of 3 to 12 days. Inflammatory process can develop in both the umbilical vein and the umbilical artery. The result of inflammation is the formation of blood clots, where microbes nest, causing suppuration. Purulent foci during sepsis can develop in many internal organs.

Pyogenic microbes can enter vascular system not only with insufficient treatment of the umbilical fossa, but also with various medical manipulations, which are used when nursing premature babies, since it is the umbilical vein that is used to administer medicinal solutions to infants.

With umbilical sepsis, the child may vomit, refuse to eat, and in the area of ​​the umbilical fossa, serous discharge first appears, and then (after 2-3 days) purulent discharge. The area around the navel becomes swollen, the skin in this area turns red, and the navel protrudes. When similar signs urgent hospitalization is required in specialized neonatal pathology departments of children's hospitals or maternity hospitals.

The umbilical cord is treated in a comprehensive manner: antibiotics are applied to the pathogen, drugs are simultaneously prescribed to maintain the body’s defenses, the child’s metabolism is corrected, sometimes blood transfusions are prescribed, protection against dehydration is provided, etc.

Not all antibiotics are due to their toxic effect suitable for administration to newborns; in addition, after a few days it is necessary to change the drugs to avoid the microbial flora becoming accustomed to them. Only competently prescribed treatment can help the child recover.

Asepsis and antisepsis of the umbilical wound in newborns

Caring for a newborn after discharge from the hospital falls entirely on the baby’s parents. It is very important for all household members to know the hygiene rules that must be followed until the umbilical wound is completely overgrown.

In the first days it is covered with a bloody crust, but bloody discharge is still released from it. This period is quite dangerous with regard to the introduction of pathogenic pathogens into tissues, causing, in particular, umbilical sepsis. Therefore, the umbilical wound requires close attention and careful care.

Usually, in healthy full-term children, the wound heals by the 8-10th day, but in weakened infants this period can be much longer, and at this time the rules of asepsis and antiseptics must be strictly followed.

Symptoms and signs of sepsis in newborns

Early signs are often nonspecific and do not vary between microorganisms (including viruses).

Particularly common early signs include:

• decreased spontaneous activity;
• poor sucking;
• apnea;
• bradycardia;
• fluctuations in body temperature (hypothermia or hyperthermia).

Fever occurs in only 10-15% of cases, but persistent fever (eg, >1 hour) usually indicates infection. Other symptoms and signs: neurological symptoms (eg, seizures, irritability), jaundice (especially occurring within the first 24 hours in the absence of Rh or ABO blood group incompatibility and higher than expected direct bilirubin concentrations), vomiting , diarrhea and bloating.

If there are specific signs of the affected organ, one can suspect the causative agent of the infection or the cause (etiology) of their occurrence.

• Most early-onset neonates infected with group B streptococci (and many with L monocytogenes) have respiratory distress that is difficult to distinguish from respiratory distress syndrome.
• Periumbilical erythema, discharge, or bleeding without hemorrhagic diathesis suggests omphalitis. Coma, convulsions, opisthotonus, or a bulging fontanel may indicate the presence of meningitis, encephalitis, or a brain abscess.
• Decreased spontaneous movement of the limbs and swelling, fever, redness or tenderness of the joints indicate osteomyelitis or suppurative arthritis.
• Skin vesicles, mouth ulcers, and hepatosplenomegaly (particularly with disseminated intravascular coagulation) may indicate disseminated HSV infection.

Early-onset group B streptococcal infection may present as fulminant pneumonia. Obstetric complications are often detected. Signs of meningitis may be present, but with less frequency. When infected with late-onset group B streptococci, meningitis often develops.

Diagnosis of sepsis in newborns

If there is a high risk of developing sepsis, it is necessary to conduct a culture test of blood, urine and cerebrospinal fluid.

Early diagnosis is essential and requires knowledge of risk factors. In newborns with suspected sepsis, as well as in children whose mothers had chorioamnionitis, it is necessary to perform a blood test to determine leukocyte formula, conduct blood and urine cultures, and perform spinal tap. Patients with respiratory symptoms should have a chest x-ray.

For preterm infants born without complications but whose mother received inadequate amounts of intrapartum antibiotics against group B streptococci, the Academy of Pediatrics recommends a limited study.

Complete blood count, differential diagnosis and smear. The number of white blood cells in newborns varies normally, but the values<4000/мкл или >25,000/µL is abnormal. Subpopulation counts are not sensitive enough to indicate the presence of sepsis, but the ratio of immature forms to total polymorphonuclear leukocytes<0,2 имеет высокую отрицательную прогностическую ценность. Стремительное падение абсолютного числа эозинофилов и морфологические изменения в нейтрофилах (например, токсичная грануляция, тельца Князькова - Деле, интрацитоплазматическая вакуолизация в крови без цитрата или этилендиаминтетрауксусной кислоты [ЭДТА]) предполагают наличие сепсиса.

The platelet count may fall several hours or days before the onset of clinical manifestations of sepsis, but most often remains elevated until the onset of sepsis. clinical symptoms or within a few days after their appearance. This is sometimes accompanied by other symptoms of disseminated intravascular coagulation (eg, increased degradation of fibrin products, decreased fibrinogen levels, increased international normalized ratio).

Because of the large number of circulating bacteria, microorganisms can sometimes be detected directly or indirectly associated with polymorphonuclear leukocytes using Gram, methylene blue, or acridine orange stains to yellow.

Regardless of the results of a blood test or lumbar puncture, antibiotic therapy should be started in all neonates with suspected sepsis (eg, those who appear ill, or those with fever or hypothermia).

Lumbar puncture. There is a risk of increased hypoxia when performing a spinal tap in newborns. However, lumbar puncture should be performed in newborns with suspected sepsis as soon as they are able to tolerate this procedure (for neonatal bacterial meningitis). Before and during the puncture, it is necessary to carry out 02 inhalations to prevent hypoxia.

Bacteriological blood test. Umbilical cord vessels are often contaminated with microorganisms at the site of the umbilical cord, especially after a few hours, so culture of blood from the umbilical catheter is of little information. Thus, it is preferable to obtain blood for seeding from two peripheral veins, in compliance with all the rules for blood sampling, after treating the injection site with an iodine-containing liquid, then treating it with a 95% ethanol solution and allowing it to dry. Blood cultures should be performed on both aerobic and anaerobic media. If catheter-associated sepsis is suspected, a specimen for culture should be obtained from both the catheter and a peripheral vein. In more than 90% of culture-positive cases, growth is detected within 48 hours. Since bacteremia in newborns is associated with a high density of organisms and their delayed elimination, a small amount of blood (for example, > 1 ml) is often sufficient to detect microorganisms. The data obtained from capillary blood cultures are insufficient to recommend its implementation.

Candida sp. are grown in blood cultures and on blood agar plates, but if other fungi are suspected, a fungal culture medium should be used. Fungi other than Candida may produce positive result culture method only after 4-5 days, and the test result can be negative even with clearly disseminated disease. Confirmation of colonization (in the mouth, in stool, or on the skin) may be helpful until culture results are available.

Urine examination. Although culture alone is diagnostic, finding >5 leukocytes per visual field or any organisms in fresh Gram-stained urine is suggestive of urinary tract infection.

Other tests for infection and inflammation. Numerous tests, often inappropriate in sepsis, have been evaluated as possible early markers. In general, however, their sensitivity tends to decrease in the later stages of the disease, and their specificity is suboptimal.

The most significant acute phase protein produced in the liver under the influence of IL-1 is C-reactive protein. Its concentration of 1 mg/dL can be either a false positive or a false negative, with a frequency of about 10%. Levels rise within one day, peak on days 2–3, and return to normal within 5–10 days in neonates who recover.

ESR often increases in sepsis, but has an equally high percentage of false-negative results (especially in the early stages and in DIC) and returns to normal more slowly after clinical recovery.

Prognosis of sepsis in newborns

Premature babies born with a small body have a mortality rate 2-4 times higher than that of full-term newborns. The overall mortality rate for early onset sepsis is 3-40% and for late onset sepsis - 2-20%. More recent studies have shown a reduction in mortality.

Treatment of sepsis in newborns

Antibacterial therapy. Prompt initiation of empiric antibiotic therapy is recommended, with medications subsequently adjusted according to the sensitivity of the infection. If bacterial cultures show no growth after 48 hours (although some pathogens are detected after 72 hours) and the neonate's health improves, antibiotics are discontinued.

Maintenance therapy. Basic supportive measures, including respiratory and hemodynamic management, are combined with antibiotic therapy.

Antimicrobial therapy. Healthy newborns from communities in which late-onset sepsis is common should also receive ampicillin + gentamicin or ampicillin + cefotaxime therapy. If gram-negative meningitis is suspected, ampicillin, cefotaxime and aminoglycosides can be used. In late stages of nosocomial sepsis, initial therapy should include vancomycin (active against methicillin-resistant S. aureus) + aminoglycosides. If P. aeruginosa is prevalent in the ward, ceftazidime can be used instead of aminoglycosides.

If coagulase-negative staphylococci are suspected (for example, when using an indwelling catheter for >72 hours) or if they are isolated from the blood or others normally sterile liquids, and if these microorganisms are considered causative agents, initial therapy for late-onset sepsis should include vancomycin. However, if the pathogen is sensitive to nafcillin, vancomycin should be replaced with cefazolin or nafcillin. Removal of the suspected source of infection (usually the intravascular catheter) is necessary to treat the infection.

Other treatments. Exchange transfusion has previously been used for critically ill (particularly hypotensive and metabolic acidosis) neonates. Their putative implications are increased levels of circulating immunoglobulins, decreased amounts of circulating endotoxin, increased hemoglobin levels (with higher levels of 2,3-bisphosphoglycerol), and improved perfusion. However, no controlled prospective studies have been conducted.

Fresh frozen plasma can help restore heat-stable and heat-labile opsonin deficiencies that occur in low birth weight infants. However, data from controlled studies of this therapeutic technique are not available, and the risks of complications associated with transfusions must be taken into account.

Granulocyte transfusions have been used in neonates with sepsis and granulocytopenia, but this has not significantly improved outcome.

Prevention

Intravenous immune globulin given at birth can prevent sepsis in some high-risk, low-birth-weight infants, but does not help if infection has developed.

Invasive diseases caused by group B streptococci often appear within the first 6 hours of life. Women who have previously given birth to a child with illness caused by these pathogens should receive antibiotic therapy during labor. During pregnancy, women with severe or asymptomatic bacteriuria (group B streptococcal) should receive intrapartum antibiotics upon diagnosis.

Sepsis is an acyclic disease (i.e., leading to death without treatment), which is based on a systemic inflammatory response of an immunocompromised organism to a bacterial, usually conditionally pathogenic (usually hospital-acquired) infection, leading to generalized damage to the endothelium of the vascular bed, persistent microcirculation disorders , hemostasis disorders with obligatory disseminated intravascular coagulation and further multiple organ failure.

Etiology. The causative agents of sepsis, which begins in the first 4-5 days of life, are most often group B streptococci, enterococci and, less commonly, listeria, i.e., the bacterial flora of the mother’s birth canal. In case of neonatal sepsis, which began later, the dominant pathogens are those that reach the child as a result of cross-infection through the hands of personnel, equipment, and care items (Gram-negative bacteria - Klebsiella, Escherichia, blue-green pus bacillus, Akinetobacter, Proteus). Meanwhile, in recent years, staphylococci aureus and coa-gulase-negative epidermal staphylococci have increasingly begun to be identified in sepsis.

The most significant factors for a high risk of developing neonatal sepsis:

Death of previous children in the family due to systemic bacterial infections under the age of 3 months (suspicion of hereditary immunodeficiency).

History of numerous abortions. Maternal gestosis lasting more than 4 weeks.

Clinically detected bacterial vaginosis in the mother during pregnancy and childbirth.

Clinically pronounced bacterial infectious processes in the mother immediately before childbirth and during childbirth, including pyelonephritis, chorioamnionitis.

Detection of streptococcus B or its antigens in the mother's birth canal.

Anhydrous interval of more than 12 hours.

The birth of a child with very low and especially extremely low body weight.

Fetal tachycardia without maternal fever, hypotension, blood loss, or maternal drug administration causing tachycardia.

Asphyxia at birth or other pathology requiring resuscitation and prolonged abstinence from enteral nutrition.

Surgical operations, especially with extensive tissue trauma.

Congenital defects with damaged skin, burns.

SDR syndrome type I and pulmonary edema.

Multi-day catheterization of the umbilical and central veins.

Intrauterine infections.

Multiple malformations or stigmas of dysembryogenesis.

Clinical picture. There are no specific clinical symptoms of sepsis. The most common symptoms of sepsis include: loss of communication, lethargy or hyperexcitability, hypo- or hyperthermia, anorexia, lack of weight gain, bloating, regurgitation, diarrhea, respiratory disorders and apnea, tachycardia, peripheral circulatory disorders, hypotension, jaundice, skin rashes , lactic acidosis, unstable blood glucose levels (hyperglycemia or hypoglycemia).

Our experience has made it possible, based on an integrative assessment of the body’s reactions (organ function, blood system and connective tissue, immunity, metabolic processes), to identify two variants of sepsis in newborns: hypoergic and hyperergic.

What do we mean by the concepts of hypoergistic and hyperergic sepsis? When hypoergic, there is no hyperplastic reaction adequate to the infectious process on the part of the hematopoietic and immunogenesis organs, the local vascular-proliferative component of inflammation is absent or minimally expressed, an adequate reaction of the neuroendocrine system, and also there are severe violations metabolism, and above all energy. Characteristic is the predominance destructive changes at the site of inflammation, inhibition and degenerative changes in the hematopoietic organs and peripheral blood cells. Typical hypoergic sepsis develops in children with very low birth weight (it has been shown that with a body weight of less than 1.5 kg, sepsis occurs 10 times more often), IUGR of the hypoplastic and dysplastic types, or primary hereditary immunodeficiencies, deep neutropenia of various origins . In full-term infants, examples of a hypoergic variant of sepsis can be candida sepsis and pseudomonas sepsis.

In hyperergic sepsis, the proliferative reaction of connective tissue and blood is maximally expressed; reactions of excessive activation of the production of proinflammatory cytokines and a cascade of plasma proteases (“proteolytic explosion”), granulocytes, platelets, and endothelium dominate. This variant of sepsis most often develops in full-term infants and those weighing more than 1.5 kg. Hyperergic sepsis is often caused by streptococci B, listeria, and escherichia. Hyperergic sepsis usually occurs under the influence of supervirulent, special strains of microbes.

Transitions from one form of sepsis to another are possible, in particular, with inadequate antibacterial, hormonal and immune therapy. Possible hyperergic variant in low birth weight infants rarely.

Diagnosis. In newborns, it is necessary to distinguish between clinical and laboratory criteria for systemic inflammatory response (SIR).

Clinical criteria for SVR:

1. Temperature homeostatic disorder (hyperthermia or hypothermia).

Dyspnea or tachypnea more than 60 breaths per minute.

Tachycardia more than 160 per 1 minute or bradycardia less than PO per 1 minute.

Loss of communication skills, anorexia, depression and/or seizures.

5. Oliguria for 6 hours or more against the background of adequate infusion therapy (diuresis less than 1 ml/kg/h).

Laboratory signs of SVO in newborns:

Sudden onset of severe metabolic lactic acidosis with hypocapnia (the latter in the absence of lung damage).

Leukocytosis (the number of leukocytes in children of the first day of life is more than 30,000, in children aged 2-7 days of life - more than 15,000, in older ones - over 15,000 in 1 μl of capillary blood) or leukopenia (the number of leukocytes in 1 μl of blood is less than 5,000) with neutrophilosis (the number of neutrophils in 1 μl of capillary blood in children on the first day of life is more than 20,000, from 2 to 7 days of life - more than 7,000, from 8 days of life and older - more than 6,000) or neutropenia (respectively, on the above days the number of neutrophils is - less than 5000, 2000 and 1750 in 1 µl of capillary blood). Criteria for assessing the main changes in the hemogram are presented in Table 3.18.

Regenerative or regenerative-degenerative shift in the leukocyte formula when the number of band and younger forms is more than 2000 per μl (on the first day of life - more than 5000 per μl).

Toxic granularity of neutrophils.

Thrombocytopenia.

7. Sudden shortening or prolongation of activated partial thromboplastin time (aPTT) or prothrombin time (PTT).

Increased levels of CR protein or other acute phase proteins.

Increase in ESR more than 10 mm/h.

Bacteremia.

Hyperglycemia more than 6.5 mmol/l.

Diagnosis criteria. Sepsis should be diagnosed in children with high-risk factors who have 4 clinical and 4 laboratory signs of SVR. If a child has a clinically obvious focus of infection or bacteremia, then four clinical and three laboratory signs of SVO are sufficient to diagnose sepsis.

The most important in the diagnosis of sepsis is a rational and thorough bacteriological examination. The volume of bacteriological examination is very significant, including three blood cultures (the amount of blood for culture is at least 1 ml), urine cultures and all that substrate that needs to be obtained from the patient - the contents respiratory tract, cerebrospinal fluid, pus, etc. In different maternity hospitals and neonatal pathology departments, different pathogens of sepsis may dominate, but most typically, sepsis in the first days of life is often caused by group B streptococci, in later periods - by gram-negative microbes - Escherichia, Klebsiella , a stick of blue-green pus. In recent years, the frequency of isolation of staphylococci, especially coagulase-negative ones, as causative agents of neonatal sepsis, has increased again.

Premature infants with suspected sepsis must be examined for intrauterine infections (at least cytomegalovirus, herpes, mycoplasma, chlamydia and toxoplasma).

Treatment- rational choice of antibiotics, asepsis and natural feeding, specific passive immunotherapy. At early appearance signs of severe bacterial infection (in the first three days of life) begin with the appointment of ampicillin (active against streptococci B, enterococci - streptococci D). Next, the antibiotic is chosen depending on the identified pathogen, but more often “protected penicillins” (aminopenicillins + betalactamase inhibitors) are prescribed in combination with III-IV generation cephalosporins or aminoglycosides. Very rarely (for health reasons) carbopenems and ciprof-loxacin are used.

In the hypoergic variant with granulocytopenia, transfusion of granulocyte mass, the use of granulocyte hematopoietin and sometimes fresh blood transfusion are especially indicated, which is important not only in terms of correcting the defect of the phagocytic link (in newborns the granulocytic reserve is 4 times less than in children early age), but also replenishment of blood coagulation factors and antithrombin III, that is, therapy of DIC syndrome.

In hyperergic sepsis, extracorporeal detoxification methods are highly effective, in particular plasmapheresis and hemosorption, which apparently reduce the level of cytokines, circulating immune complexes and proteolysis products.

The effectiveness of glucocorticoids is unconditional when sepsis is complicated by adrenal insufficiency, i.e. as replacement therapy. Regarding use large doses hormones affecting many metabolic processes, membranes, lymphoid tissue, then at present this issue cannot be considered scientifically developed; rather, it is of an empirical nature.

Prevention of purulent-septic diseases in newborns starts from timely detection and sanitation of foci of chronic inflammation (especially in the genitourinary area) in a pregnant woman, preventing acute infections in her, with dynamic observations of her in the antenatal clinic, creating conditions for a favorable course of pregnancy and early correction of disorders, preventing miscarriage.

Compliance by staff in maternity hospitals and neonatal pathology departments of children's hospitals with developed standards for anti-epidemic measures - with The most important of them is hand washing (!!!) nurses and doctors use antiseptic soap every time before and after contact with a newborn baby. You can use soap with chlorhexidine or betadine. It is necessary to use disposable needles, syringes, pacifiers, care items, and gloves. Diagnostic equipment, equipment for assisting the newborn and for monitoring his condition must be carefully processed in accordance with established rules. All solutions for infusion therapy and bottles with food should be prepared and sterilized centrally and delivered to the ward in single-use packages for direct use in a particular child. Putting the baby to the mother's breast within half an hour after birth- a very important measure to reduce the incidence of purulent-inflammatory diseases in both the newborn and the postpartum mother. Personnel with ARVI or other acute infectious diseases (in particular, herpes simplex on the lips) should not be allowed to work, and if there are minimal signs of illness, they should wear a mask and wash their hands thoroughly. Careful, local recording and analysis of all purulent-inflammatory morbidity newborns.

Sepsis of newborns, the causes of which are the effects of microbes on the child’s body, often manifests itself during the first months of life. This is due to the lack of full function of the immune system. Most often, infants born prematurely or with immunodeficiency pathology are affected. Due to the immaturity of the mucous membranes, the infection enters the child’s body without obstacles.

Bacterial sepsis of a newborn is caused by pathogens of opportunistic microbes. These include Pseudomonas aeruginosa and Escherichia coli. The defeat of the crumbs occurs when the wrong labor activity(if hygiene standards are not observed), during pregnancy, if the mother has had this infection, at home or on the street, if the baby has had contact with patients with sepsis.

Note to mom! If the mother suffers from a number of chronic inflammatory diseases, the fetus is at risk. Also, the child can be infected due to a long anhydrous period at the time of birth, as well as oxygen deficiency. These factors increase the likelihood of bacterial diseases and infectious diseases.

In addition, the most common cause of sepsis in newborns that causes damage to the body is the following:

• (particularly intracranial);
• violation of the integrity of the skin due to obstetric activities;
• venous catheterization (incorrect placement of catheters for the administration of drugs);
• tracheal incubation (connection to an oxygen machine);
• infection in the placenta or other organ of the pregnant woman (this is how congenital sepsis manifests itself in a child).

Regardless of the influencing factors and reasons why sepsis in newborns appeared, it is almost impossible to determine at what point and how the infection occurred.

Diagnosis of purulent-inflammatory sepsis in newborns and symptoms

Diagnosis of sepsis in newborns occurs exclusively on an outpatient basis through the collection of appropriate tests, as well as based on the external symptoms of the disease and the general condition of the baby. As the infectious disease progresses in the body of a child under one year old, the following symptoms appear:

• refusal of the breast and, accordingly, lack of appetite;
• change in skin color (pallor or cyanosis);
• late healing of the umbilical wound;
• may be accompanied by sluggish breastfeeding, regular breastfeeding, and weight loss (very rare).

These signs are used to determine neonatal and acquired sepsis. In the photo you can see the symptoms of inflammation.

Important! When infected, unexplained irritability often occurs. The disease occurs in an acute form and is protracted (to be treated for more than 6 months). IN infancy skin sepsis, ear sepsis, umbilical sepsis in children, blood sepsis and intestinal sepsis occur. Individual treatment is selected for each of these types.

Doctors consider the prognosis of such a diagnosis to be poor, but with proper therapy it is not hopeless. If treatment for sepsis in infants is started late, the chances of recovery and full adaptation of the child to the environment are significantly reduced.

Etiology of sepsis in newborns

When a child is exposed to pathogens, an inflammatory reaction occurs (sepsis in newborns), during which cytokines are released in large quantities. The inflammatory process affects the elements that make up the blood (leukocytes, red blood cells, proteins). At negative impact necrosis and leukemia may occur on the body. Blood clotting is impaired.

The excess composition of cytokines promotes the development of pathogen cells in the baby’s body, as a result of which sepsis is formed. At this moment, cartisol increases significantly, due to which the activity of the thyroid gland decreases.

Children say! We are traveling on the bus with our daughter (4 years old). The driver announces stops:
- Gorky's next stop.
Alla frowned and closed her eyes. I ask her:
- What's the matter, what happened?
- Uncle, a bitter stop.

On last stage As the infection progresses, multiple organ failure develops and thrombocytosis occurs, provoking a disorder of homeostasis, which often leads to death.

If a pregnant woman has obvious uterine abnormalities accompanied by polyhydramnios, there is a risk that the baby will develop neonatal sepsis.

Watch a video about the development of sepsis in newborns.

Attention parents! High neonatal mortality is most often associated with the influence of negative factors that cause sepsis in newborns, so the disease must be diagnosed on time.

Treatment of sepsis in newborns: effective actions

Care for a sick child is required; he is hospitalized in the pathology department for infants. Doctors recommend that during this period the mother stays close to the child and practices breastfeeding.

In the treatment of neonatal sepsis, the use of antibiotics is recommended, the classification of which allows us to divide drugs into primary and secondary, depending on the form of neonatal sepsis. Use Tetracycline, Erythromycin, Tetraolene in an age-specific dosage. It is important that they are chosen correctly, since many children have intolerance to some medical supplies. The state of the microflora is monitored infant, for this purpose, accompaniment in the form of bifido and lactobacilli is prescribed.

For premature babies, sometimes the use of certain antibiotics is considered ineffective, so more adequate therapy. Children with a similar diagnosis are administered drugs intramuscularly, or, if the effect is weak, intravenously. If Tetracycline does not help, it is replaced with Imex within two days.

Attention! After completing the course of treatment with antibacterial drugs, it is necessary to prescribe preventive measures to avoid complications therapeutic therapy(disorders of the intestinal and stomach microflora).For this, the child is prescribed Bifiform or Linex.

If the body has severe forms of neonatal sepsis, corticosteroid hormones are prescribed. As medicines, children are prescribed: Reopoliglyukin, Plasma, Hemodez, Glucose solution 10%. Phytotherapy, physiotherapy exercises, massage and homeopathic medicines. The transferred infectious process by newborns is a signal to ban vaccination for 1 year.

Complications after sepsis in newborns

As a rule, the consequences of any disease in infants, including sepsis, appear only in case of inadequate treatment.

1. In neonatal sepsis, the liver is damaged by toxins, which is accompanied by a serious form of jaundice. Based on this, there constant vomiting and lack of appetite.
2. Hemorrhages occur in internal organs a child, which is considered an unfavorable sign and is rarely treatable, especially if severe forms of neonatal sepsis are diagnosed.
3. The skin becomes blue at the fingertips and the nasolabial triangle.
4. Such infection of a child at a newborn age turns into purulent meningitis, which also needs to be treated in a timely manner.
5. The lethal outcome occurs due to mass intoxication of the infant's body, accompanied by the release of blood under the skin and a violation of the functions of the immune system.

Children's humor! Grandmother is in her hearts at her granddaughter’s tricks:

My grief!
Vika (4 years old):
- Your grief, but mother’s happiness!

To avoid these complications and protect the baby’s life, doctors recommend adhering to measures to prevent the disease itself and caring for the child. The most common cause of sepsis in newborns is associated with an unfavorable course of pregnancy.

Prevention of neonatal sepsis

First of all, preventive measures are aimed at eliminating acute infectious diseases in women planning pregnancy. If an infection is found during pregnancy, treatment begins in the second trimester; with primary infection before 15 weeks, women are advised to terminate the pregnancy.

Physicians must comply sanitary standards and a special hygienic regime during childbirth. To prevent sepsis from catching you at home, you must:

• wash your hands regularly with soap;
• monitor the cleanliness of the newborn’s bedding and underwear;
• You should not wash your child’s clothes together with adults;
• do not allow the newborn child to come into contact with sick children and relatives (acute respiratory infections, influenza, infectious manifestations);
• keep all baby toys separately;
• regularly disinfect cabinets and drawers for storing children's supplies;
• Do wet cleaning in the house at least 2 times a day.

Carrying out prevention at home and in medical institutions reduces the risk of newborns being affected by infections of various types. If you have any questions, you can go to the medical forum and discuss the topic with experienced parents.

In conclusion, we suggest studying video material about the causes of sepsis in infants.

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What is Sepsis in a newborn -

A generalized form of purulent-inflammatory infection, which is caused by an opportunistic bacterial microflora when the immune system is disrupted and an inadequate systemic inflammatory response occurs.

Diagnostic criteria are vague, so there is no accurate information on the frequency of sepsis among infants. According to foreign statistics, the frequency is from 0.1 to 0.8%. Among the patients, the majority of children are premature and are in intensive care units. Blood infections have a mortality rate of 30 to 40%.

Classification of neonatal sepsis

There is no generally accepted division of neonatal sepsis into types. In ICD-10, the disease is designated under code P36. The disease can be divided into types according to the time of appearance of infection in the blood, according to symptoms, according to the location of the entrance gates of infection, etc.

Recently, fumigation has been used to treat the umbilical cord, ultraviolet irradiation, antiseptics. Correct placement of Rogovin's brackets and Kocher's clamp is important.

To prevent sepsis in newly born children, hygienic baths with the addition of various disinfectants are used.

Some researchers advise giving a bath with a solution of potassium permanganate in the first hours of a baby’s life. A 3% hexachlorophene bath is also available.

Fighting pustular diseases in newborns, it includes a protective ointment, which is put into the folds of the skin. It contains: Amyli tritici aa 25.0, Zinci oxydati, Worsulfa-soli 0.5, etc.

Women in labor should be provided with sterile caps and scarves that completely cover their hair. Staff must wear sterile hoods.

To prevent the spread of staphylococci, masks should be worn, changing them every three hours. Masks should cover the mouth and the front of the nose, through which pathogenic staphylococci can enter the newborn's body.

Children with different shapes staphylococcal infection must be handled with gloves that are disinfected or changed frequently.

Specific prevention is also proposed in the form of immunization of pregnant women, which was proposed at the beginning of the 20th century by V. Ya. Yankelevich. He used killed streptostaphylococcal vaccine for immunization. Further research has shown that staphylococcal antitoxin is effective.

To increase the immunity of newborns, researchers suggest using sodium nucleic acid.

In cases of the development of nosocomial epidemics in maternity hospitals, a commission should be created, which will include a bacteriologist, an epidemiologist, clinicians and a sanitary doctor. Their goal is to establish sources of infection and current transmission mechanisms, to develop and evaluate systems of preventive and anti-epidemic actions.

Which doctors should you contact if you have Sepsis in a newborn:

Infectious disease specialist

Immunologist

Hematologist

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Other diseases from the group Children's diseases (pediatrics):

Bacillus cereus in children

Adenovirus infection in children

Nutritional dyspepsia

Allergic diathesis in children

Allergic conjunctivitis in children

Allergic rhinitis in children

Sore throat in children

Aneurysm of the interatrial septum

Aneurysm in children

Anemia in children

Arrhythmia in children

Arterial hypertension in children

Ascariasis in children

Asphyxia of newborns

Atopic dermatitis in children

Autism in children

Rabies in children

Blepharitis in children

Heart blocks in children

Lateral neck cyst in children

Marfan disease (syndrome)

Hirschsprung's disease in children

Lyme disease (tick-borne borreliosis) in children

Legionnaires' disease in children

Meniere's disease in children

Botulism in children

Bronchial asthma in children

Bronchopulmonary dysplasia

Brucellosis in children

Typhoid fever in children

Spring catarrh in children

Chicken pox in children

Viral conjunctivitis in children

Temporal lobe epilepsy in children

Visceral leishmaniasis in children

HIV infection in children

Intracranial birth injury

Intestinal inflammation in a child

Congenital heart defects (CHD) in children

Hemorrhagic disease of the newborn

Hemorrhagic fever with renal syndrome (HFRS) in children

Hemorrhagic vasculitis in children

Hemophilia in children

Haemophilus influenzae infection in children

Generalized learning disabilities in children

Generalized anxiety disorder in children

Geographical language in a child

Hepatitis G in children

Hepatitis A in children

Hepatitis B in children

Hepatitis D in children

Hepatitis E in children

Hepatitis C in children

Herpes in children

Herpes in newborns

Hydrocephalic syndrome in children

Hyperactivity in children

Hypervitaminosis in children

Hyperexcitability in children

Hypovitaminosis in children

Fetal hypoxia

Hypotension in children

Hypotrophy in a child

Histiocytosis in children

Glaucoma in children

Deafness (deaf-mute)

Gonoblenorrhea in children

Flu in children

Dacryoadenitis in children

Dacryocystitis in children

Depression in children

Dysentery (shigellosis) in children

Dysbacteriosis in children

Dysmetabolic nephropathy in children

Diphtheria in children

Benign lymphoreticulosis in children

Iron deficiency anemia in a child

Yellow fever in children

Occipital epilepsy in children

Heartburn (GERD) in children

Immunodeficiency in children

Impetigo in children

Intussusception

Infectious mononucleosis in children

Deviated nasal septum in children

Ischemic neuropathy in children

Campylobacteriosis in children

Canaliculitis in children

Candidiasis (thrush) in children

Carotid-cavernous anastomosis in children

Keratitis in children

Klebsiella in children

Tick-borne typhus in children

Tick-borne encephalitis in children

Clostridia in children

Coarctation of the aorta in children

Cutaneous leishmaniasis in children

Whooping cough in children

Coxsackie and ECHO infection in children

Conjunctivitis in children

Coronavirus infection in children

Measles in children

Clubhanded

Craniosynostosis

Urticaria in children

Rubella in children

Cryptorchidism in children

Croup in a child

Croupous pneumonia in children

Crimean hemorrhagic fever (CHF) in children

Q fever in children

Labyrinthitis in children

Lactase deficiency in children

Laryngitis (acute)

Pulmonary hypertension of the newborn

Leukemia in children

Drug allergies in children

Leptospirosis in children

Lethargic encephalitis in children

Lymphogranulomatosis in children

Lymphoma in children

Listeriosis in children

Ebola fever in children

Frontal epilepsy in children

Malabsorption in children

Malaria in children

MARS in children

Mastoiditis in children

Meningitis in children

Meningococcal infection in children

Meningococcal meningitis in children

Metabolic syndrome in children and adolescents

Myasthenia gravis in children

Migraine in children

Mycoplasmosis in children

Myocardial dystrophy in children

Myocarditis in children

Myoclonic epilepsy in early childhood

mitral stenosis

Urolithiasis (ICD) in children

Cystic fibrosis in children

Otitis externa in children

Speech disorders in children

neuroses in children

Mitral valve insufficiency

Incomplete intestinal rotation

Sensorineural hearing loss in children

Neurofibromatosis in children

Diabetes insipidus in children

Nephrotic syndrome in children

Nosebleeds in children

Obsessive-compulsive disorder in children

Obstructive bronchitis in children

Obesity in children

Omsk hemorrhagic fever (OHF) in children

Opisthorchiasis in children

Herpes zoster in children

Brain tumors in children

Tumors of the spinal cord and spine in children

Ear tumor

Psittacosis in children

Smallpox rickettsiosis in children

Acute renal failure in children

Pinworms in children

Acute sinusitis

Acute herpetic stomatitis in children

Acute pancreatitis in children

Acute pyelonephritis in children

Quincke's edema in children

Otitis media in children (chronic)

Otomycosis in children

Otosclerosis in children

Focal pneumonia in children

SYNONYMS

Neonatal sepsis, bacterial sepsis of the newborn, congenital septicemia, generalized infection of bacterial etiology.

DEFINITION

Sepsis is a generalized acyclic purulent-inflammatory infection caused by opportunistic bacterial microflora, the development of which is based on dysfunction of the immune, predominantly phagocytic, system of the body with the development of an inadequate systemic inflammatory response.

In recent years there has been an increase chronic pathology and deterioration in women's health childbearing age. New methods of managing high-risk pregnant women with prenatal hormonal and immunoreplacement therapy have been developed and implemented. The birth rate of children with extremely low body weight is increasing. At the same time, diagnostic and treatment methods are being improved with the use of new powerful broad-spectrum antibiotics. All this leads to a change in the clinical picture of sepsis, especially in very premature newborns, and to a rethinking of the concept of “newborn sepsis” from the standpoint of practical neonatology. To streamline the formulation of this diagnosis in clinical practice, a working group of experts from the Russian Association of Perinatal Medicine Specialists, as a result of a multicenter analysis of medical histories of newborns for 2000-2003. proposed the following definition of neonatal sepsis: neonatal sepsis is a generalized infectious disease with an acyclic course, caused by opportunistic bacterial microflora, which is based on dysfunction of the body’s immune system with the development of a focus (foci) of purulent inflammation or bacteremia, a systemic inflammatory reaction and multiple organ failure in children in the first month of life.

ICD-R36 CODE Bacterial sepsis of the newborn, congenital septicemia.

P36.0 Sepsis of a newborn caused by group B streptococcus.

P36.1 Sepsis of the newborn due to other and unspecified streptococci.

P36.2 Sepsis of a newborn caused by Staphylococcus aureus.

P36.3 Sepsis of the newborn due to other and unspecified staphylococci.

P36.4 Sepsis of a newborn caused by Escherichia coli.

P36.5 Sepsis of a newborn caused by anaerobic microorganisms.

P36.8 Sepsis of the newborn caused by other bacterial agents.

P36.9 Bacterial sepsis of the newborn, unspecified.

Examples of diagnosis formulation: early neonatal sepsis caused by group B streptococci, septicemia, septic shock, or umbilical sepsis caused by staphylococci, septicopyemia, purulent meningitis.

Examples of diagnosis formulation: “early neonatal sepsis caused by group B streptococci, septicemia, septic shock” or “umbilical sepsis of staphylococcal etiology, septicopyemia (purulent meningitis, bilateral small-focal pneumonia, NEC stage 2), acute respiratory failure stage 3, circulatory failure 2B, oliguric acute renal failure, disseminated intravascular coagulation syndrome.”

EPIDEMIOLOGY

In the domestic literature there is no reliable information on the incidence of sepsis among newborns, which is due to the lack of generally accepted criteria for diagnosis. According to foreign authors, sepsis in newborns occurs in 0.1-0.8% of cases. A particular problem is presented by children in the NICU and premature infants, among whom sepsis occurs on average in 14% of cases (from 8.6% among full-term infants in the NICU to 25% among premature infants with a gestational age of 28-31 weeks).

In the structure of neonatal mortality in the Russian Federation, sepsis as a cause of death has been ranked IV-V for several decades. Mortality rates from sepsis are also quite stable at 30-40%.

CLASSIFICATION

Currently, we do not have a unified classification of newborn sepsis in our country.

There are early sepsis, in which clinical symptoms appear in the first three days of a child’s life, and late neonatal sepsis - sepsis that manifests clinically later than the 4th day of life.

Early sepsis is typically characterized by intrauterine, predominantly antenatal, infection through the ascending or hematogenous route. Less commonly, infection occurs during childbirth or in the early postnatal period. There is usually no obvious primary source of infection in the child. The source of infection is most often the microflora of the mother's birth canal. Risk factors for the development of early neonatal sepsis include prematurity, intrauterine hypotrophy and intrauterine growth retardation, premature rupture of the membranes, an anhydrous interval of more than 12 hours, increased body temperature and the presence of foci of infection in the mother during childbirth and in the early postpartum period, chorioamnionitis, complicated course perinatal period (perinatal hypoxia, birth trauma). The disease usually occurs in the form of septicemia, which refers to the presence of microbes or their toxins in the bloodstream. Characteristic is the fulminant development of clinical symptoms, systemic inflammatory response and multiple organ failure in the absence of metastatic purulent foci.

In late sepsis, infection of the newborn usually occurs postnatally. A primary site of infection is usually present. More often septicopyemia is recorded, i.e. sepsis occurs with the formation of one or more septicopyemic, metastatic purulent-inflammatory foci. A typical manifestation of septicopyemia and its criterion is the same type of pathogen isolated from foci of inflammation and from the patient’s blood. The source of infection can be both the mother's microflora and the environmental microflora. Risk factors for the development of late neonatal sepsis: prematurity, malnutrition, disruption of the natural protective barriers of the skin and mucous membranes during resuscitation, tracheal intubation, venous catheterization, unfavorable epidemiological situation. The disease can be characterized by both a hyperergic, fulminant course and a slowly progressive development of clinical symptoms, a hyporeactive nature.

Sepsis is also classified according to its etiology and the source of infection. The etiology of the disease is determined by the results of microbiological examination of blood, CSF, tracheal aspirate, urine, and the contents of purulent-inflammatory foci in a sick child. If the results of blood cultures are negative, the spectrum of the most likely pathogens of the disease should be predicted on the basis of anamnesis, the dynamics of the patient’s clinical condition against the background of a previous course of antibiotics, and the epidemiological situation in the department, knowledge of which is important for the rational choice of antibacterial therapy.

In case of sepsis, it is advisable to indicate in the clinical diagnosis the etiology and localization of the entrance gates of infection, since this characteristic of the disease has a certain epidemiological significance and is important for the development of anti-epidemic and preventive measures. There are umbilical, cutaneous, otogenic, urogenic, catheterization, pulmonary, abdominal and other less common types of late neonatal sepsis.

Organ failure syndromes determine the severity and often the outcome of the disease, require a specific therapy program, and therefore it is also advisable to highlight them in the clinical diagnosis. Among them, due to the severity of the prognosis special attention deserves the symptom complex of septic shock (infectious-toxic shock).

Septic shock is understood as the development in conditions of sepsis of progressive arterial hypotension, not associated with hypovolemia, not eliminated by the administration of sympathomimetics.

ETIOLOGY

The spectrum of the most likely pathogens is determined by the time of infection of the fetus or child (antenatal, intranatal or postnatal) and the location of the entrance gate. E. coli and, less commonly, other representatives of intestinal gram-negative microflora can cause intrauterine infection of the fetus. In all these cases, the clinical manifestation of the disease is noted in the first 48-72 hours of the child’s life.

In late-onset neonatal sepsis, group B streptococci play a role, but significantly larger number cases of the disease account for E. coli, St. aureus, Klebsiella pneumoniae, Pseudomonas spp. and Enterobacter spp.

Over the past decade, the frequency of occurrence of gram-positive and gram-negative conditional pathogenic microorganisms in the general etiological structure of neonatal sepsis has become approximately the same. In the structure of gram-negative pathogens of sepsis, the role of microorganisms such as Pseudomonas spp., Klebsiella spp. has increased. and Enterobacter spp. As a rule, these bacteria act as the causative agent of sepsis in NICU patients on mechanical ventilation and PN, and in surgical patients.

The etiological structure of the postnatally developed disease is significantly influenced by the localization of the primary septic focus: in the etiology of umbilical sepsis, the leading role is played by staphylococci and, to a lesser extent, Escherichia coli, and in the etiology of skin sepsis - staphylococci and f-hemolytic streptococci of group A. A certain selectivity of the spectrum of pathogens and nosocomial sepsis depending on the entrance gate of infection: in catheterization sepsis, the predominant role is played by methicillin-resistant staphylococci or mixed microflora caused by the association of staphylococci or gram-negative microflora with fungi of the genus Candida; in abdominal hospital sepsis, pathogens such as enterobacter and anaerobes are relevant.

PATHOGENESIS

The starting point in the pathogenesis of sepsis is the primary purulent focus, which, due to the initial failure of anti-infective protection and the massive microbial contamination, leads to the penetration of microorganisms into systemic blood flow patient and the development of bacteremia.

Bacteremia and associated antigenemia and toxemia are factors that trigger a number of cascades defensive reactions organism. The absorption (phagocytosis) of bacteria and their decay products by activated cells of a monocyte-macrophage nature, the processes of recognition and presentation of Ag by macrophages to lymphocytes are accompanied by an excessive release of pro-inflammatory cytokines into the systemic circulation, among which IL-1, tumor necrosis factor-a, IL-8, interferon-γ, granulocyte-macrophage colony-stimulating factor. By interacting with specific receptors for cytokines on the membranes of various cells of the body, high concentrations of pro-inflammatory cytokines lead to the development of a symptom complex of a systemic inflammatory response. In particular, they contribute to the activation of the thermoregulation center and the occurrence of fever, change the protein-synthesizing function of the liver, suppress albumin synthesis and induce the production of acute-phase inflammatory proteins by hepatocytes (C-reactive protein, haptoglobin, orosomucoid), contribute to increased catabolic metabolism and the development of cachexia. High concentrations of chemokines, the main one being IL-8, contribute to increased bone marrow hematopoiesis, granulocytopoiesis, the release of young forms of neutrophils from the bone marrow into the blood, and increased directional movement of neutrophils to the site of infection (chemotaxis). Neutrophils are able to quickly change their metabolism in response to any stimulating effect, up to the development of a “respiratory explosion” during phagocytosis and the generation of toxic oxygen radicals, as well as secretory degranulation, which releases enzymes with bactericidal activity. Moving to the foci of infection, neutrophils come into contact with adhesion molecules on the surface of vascular endothelial cells, fibroblasts, and cells of other tissues and organs. As a result of adhesion, the sensitivity of the receptors of neutrophils themselves to cytokines and other mediators changes, which allows granulocytes to adequately respond to changes in tissues.

The contents of neutrophil granules induce platelet aggregation, the release of histamine, serotonin, proteases, derivatives arachidonic acid, factors that activate blood coagulation, the complement system, the kinin-kallekrein system, etc.

Thus, the systemic inflammatory reaction is a general biological nonspecific reaction of the human body in response to the action of a damaging endogenous or exogenous factor. In sepsis, a systemic inflammatory reaction develops in the presence of a primary purulent-inflammatory focus. The development of a systemic inflammatory response contributes to induced apoptosis and, in some cases, cell necrosis, which determines its damaging effect on the body. The dominance of the destructive effects of litokines and other inflammatory mediators leads to disruption of the permeability and function of the capillary endothelium, disruption of microcirculation, and the triggering of disseminated intravascular coagulation syndrome.

An excessively pronounced systemic inflammatory response underlies excessive activation of the hypothalamic-pituitary-adrenal system, which normally ensures an adequate response of the body to stress. Excessive activation of the hypothalamic-pituitary-adrenal system during septic shock and fulminant sepsis contributes to the appearance of an inadequate response to the release of ACTH (a type of latent adrenal insufficiency). Along with this, a decrease in the functional activity of the thyroid gland is noted. With fulminant progression and septic shock, a number of patients experience a drop in the level of growth hormone.

Another manifestation of an inadequate systemic inflammatory response may be uncontrolled activation of the blood coagulation system, which, under conditions of increasing depression of fibrinolysis, inevitably leads to the development of thrombocytopenia and consumption coagulopathy (DIC syndrome).

The systemic inflammatory response is the basis for dysfunction of all organs and systems. It leads to the formation of multiple organ failure, which is manifested by severe homeostasis disorders, increasing the risk of death.

Currently, more attention is paid to the concept that there is an increased entry into the bloodstream of endotoxin or endotoxin lipopolysaccharide complex from gram-negative bacteria that colonize the upper parts of the small intestine in conditions of impaired circulation. Endotoxin increases the intensity of the systemic inflammatory response, leading to the development of arterial hypotension that is insensitive to therapy.

The continued entry of bacteria and their Ag into the bloodstream leads to disorganization of the systemic inflammatory response. Antigenic overload causes severe exhaustion defense mechanisms, immunosuppression, which, in conditions of bacteremia and impaired microcirculation, promotes the formation of secondary, metastatic purulent foci that support the systemic inflammatory response, bacteremia, toxemia and antigenemia.

CLINICAL PICTURE

The clinical picture of sepsis, regardless of its form (septicemia or septicopyemia), is characterized by the severity of the general condition of the newborn. It is manifested by pronounced disturbances in thermoregulation (in full-term, morphofunctionally mature newborns, fever is more often observed; in premature, low-birth-weight children and children with a burdened premorbid background, progressive hypothermia is more likely), a violation of the functional state of the central nervous system (progressive depression or quickly exhausted anxiety, subconsciousness). Characterized by a dirty-pale or dirty-gray shade of the skin, often with hemorrhages, areas of sclerema, pronounced marbling of the skin, and sometimes acrocyanosis can be observed. In the early neonatal period there may be rapidly increasing jaundice. The development of general edematous syndrome is often noted. There is a tendency to spontaneous bleeding.

Facial features are often pointed. Typical developments are respiratory failure in the absence of inflammatory changes on the radiograph and cardiac dysfunction such as toxic cardiopathy, which may be accompanied by the development of heart failure. Characterized by an increase in the size of the spleen and liver, bloating, a pronounced venous network in the abdomen, a tendency to regurgitation, vomiting and anorexia, gastrointestinal dysfunction, up to the development of intestinal paresis, and lack of weight gain.

All these syndromes and symptoms reflect various degrees severity of multiple organ failure in a newborn (Table 39-1).

Table 39-1. Clinical and laboratory criteria for organ failure in neonatal sepsis

Organ system dysfunctions	Clinical	Laboratory
Respiratory failure	Tachypnea or bradypnea	Ra02
	Perioral cyanosis, general Auscultatory weakened breathing, possible crepitus	Sp02
	Need for mechanical ventilation or PEEP	Respiratory or mixed acidosis
Cardiovascular failure	Tachycardia or bradycardia Expansion of the boundaries of the heart	Changes in central venous pressure, wedge pressure pulmonary artery
	Rhythm disorders	Reduced ejection fraction
	Arterial hypotension	Decreased cardiac output
	Liver enlargement, edemaNecessity of hemodynamic support	Changes according to ECG data of a metabolic nature
Kidney failure	OliguriaAnuriaEedema	Increased blood levels of creatinine and/or urea Decreased diuresis Decreased GFR and tubular reabsorption of water and sodium, hyperkalemia Proteinuria

Liver failure	Enlarged liver Jaundice	Increased levels of AST, ALT Impaired synthetic function of the liver Impaired bilirubin conjugation or cholestasis syndrome Prolongation of PT Prolongation of APTT
Insufficiency of the hemostasis system	Tendency to spontaneous bleeding, bleeding from injection sites, thrombosis	Increased PT or APTT Prolongation of thrombin time, increase in the content of soluble fibrin-fibrinogen monomer complexes, fibrin degradation products, prolongation of ACT, positive ethanol test Depression of fibrinolysis Decreased protein level STrombocytopeniaAnemia
Failure of the digestive system	Regurgitation, vomiting Congestion in the stomach, inability to absorb EPD Diarrhea Intestinal paresis Gastrointestinal bleeding Pathological impurities in the stool (mucus, greens, blood) Ischemia or infarction of the small intestine	Radiographic evidence of intestinal paresis or NEC. Dysbacteriosis

Violations of the functions of the nervous system	Syndrome of inhibition of unconditioned reflex activity Syndrome of increased neuro-reflex excitability Neonatal convulsions Coma	Ultrasound signs of ischemic damage to the central nervous system Signs of cerebral edema on NSG Signs of hypertensive-hydrocephalic syndrome on NSG Ultrasound signs of IVH Disturbances in the bioelectrical activity of the cerebral cortex Slight increase in protein levels with normal or increased CSF cytosis
Insufficiency of endocrine glands	Weight loss Signs of adrenal insufficiency Edema syndrome Transient thyroid hormone deficiency syndrome	Hypoglycemia (initially hyperglycemia) Transient decrease in cortisol levels (in the initial phase of shock there may be hypercortisolemia) Decreased levels of T3, T4, especially in shock Normal or increased TSH level, in shock - a decrease in the level of TSH; a decrease in the level of growth hormone, especially in shock

Primary septic focus

After implementation in clinical practice modern methods of primary treatment of the umbilical cord and caring for umbilical wound There was a decrease in the incidence of omphalitis and umbilical sepsis, which now occurs in less than a quarter of cases. Against this background, the frequency of pulmonary (up to 20-25%) and intestinal sepsis (at least 20%) has increased significantly. Other localizations of the primary focus are much less common and do not exceed 2-6%. In some cases, the entrance gate of infection cannot be established. This is especially true for children with small gestational age.

Septicemia

Septicemia is clinically manifested by the presence of the above-described symptom complexes of toxicosis, systemic inflammatory reaction and multiple organ failure, accompanying the development of the primary purulent-inflammatory focus.

Septicopyemia

Septicopyemia is characterized by the development of one or more septicopyemic foci, which determine the characteristics of the clinical picture and course of the disease. Among metastatic foci of sepsis in newborns, purulent meningitis ranks first in frequency; pneumonia, enterocolitis, and osteomyelitis often develop. Other localizations of pyemic foci: liver and kidney abscesses, septic arthritis, mediastinitis, carditis, panophthalmitis, purulent inflammation of the skin, soft tissues, walls of the stomach, intestines, pyelonephritis, peritonitis and others.

Septic shock

Septic shock is observed, according to various authors, in 10-15% of cases of neonatal sepsis, with the same frequency in septicemia and septicopyemia. In most cases, septic shock develops with sepsis caused by gram-negative microorganisms. Coccal gram-positive microflora is rarely the cause of shock. The exceptions are group B streptococci and enterococci: with this etiology of sepsis, shock develops with almost the same frequency as with the gram-negative etiology of the disease. Mortality in the development of septic shock is more than 40%.

The clinical picture of septic shock in newborns is characterized by a rapid, sometimes catastrophic increase in the severity of the condition, a progressive tendency towards hypothermia, pallor of the skin, progressive depression of unconditioned reflexes and reactions to stimuli, tachycardia can be replaced by bradycardia, increasing shortness of breath is characteristic (often in the absence of infiltrative changes on radiographs of the lungs ). Bleeding appears from the injection sites, sometimes a petechial rash or bleeding of the mucous membranes, pastiness, and then swelling of all tissues appear. Exicosis can be observed in combination with swelling of tissues and organs, especially parenchymal ones.

The most characteristic signs: gradually increasing arterial hypotension, insensitive to the administration of adrenergic agonists, sharp violation microcirculation (symptom of “pale spot” for more than 3 seconds), disseminated intravascular coagulation syndrome with the development of consumption thrombocytopenia, consumption coagulopathy and depression of fibrinolysis. In such cases, along with bleeding, multiple necrosis can rapidly develop, including the walls small intestine, cortical parts of the kidneys, myocardium, brain and other organs.

Shock is accompanied by severe hormonal dysfunction, severe disturbances of almost all mechanisms of regulation of homeostasis, including the systemic mediator response of the body.

The acute course of the disease is observed in 75-85% of cases.

With a favorable course of the process, the duration of the disease is on average 8-10 weeks. Period acute manifestations, the clinical picture of which is similar to that described above, lasts 3-14 days with modern treatment methods. Then comes the reparation period, which is characterized by the fading of symptoms of toxicosis, gradual restoration of functions individual organs and systems, sanitation of metastatic foci. Along with this in clinical picture the increase in the size of the liver and/or spleen, pallor of the skin, lability of the functions of the central and autonomic nervous systems, dysbacteriosis of almost all loci of the body in contact with external environment, absence or insufficient weight gain, leading to the formation of postnatal malnutrition.

During this period, cross-infection (bacterial, fungal or viral) easily occurs. There are frequent sources of superinfection such as child autoflora and hospital microflora.

The hematological picture in the acute period of sepsis is characterized by pronounced leukocytosis (less often - normal values ​​or leukopenia), a neutrophilic shift of the formula to the left to juvenile forms. Thrombocytopenia (or a tendency towards it), eosinophilopenia, lymphopenia, a tendency towards monocytosis, and anemia can be observed. During the reparation period, there may be moderate monocytosis. Neutrophilia in 1/3 of cases is replaced by neutropenia, in 2/3 of cases - by normal values. A tendency to eosinophilia is characteristic. Basophils and plasma cells appear in the peripheral blood.

DIAGNOSTICS

Diagnosis of sepsis consists of several stages.

The first stage is the identification of foci of infection. It is necessary to take into account such a feature of early neonatal sepsis as possible absence primary septic focus located in the mother's body or in the placenta. Based on the history, physical examination, relevant laboratory and instrumental diagnostics, speakers pathological symptoms it is necessary to exclude or confirm the development of meningitis, pneumonia, enterocolitis, pyelonephritis, arthritis, osteomyelitis, peritonitis, carditis, abscesses and phlegmon of soft tissues, etc. in a child.

The second stage of diagnosis is assessment of functional activity critical systems maintaining homeostasis and diagnosing organ failure. In table Table 39-1 shows the main clinical, laboratory and instrumental characteristics of multiple organ failure that accompany sepsis in a newborn and determine its outcome. Monitoring of these indicators is necessary to carry out adequate etiotropic and syndromic therapy.

The third stage of diagnosis is the assessment of the systemic inflammatory response of the newborn’s body. The criteria for a systemic inflammatory response in newborns include:

Axillary temperature > 37.5 °C or
changes in the general blood test (Table 39-2):

An increase in the level of C-reactive protein in the blood serum more than 6 mg/l;

An increase in the level of procalcitonin in the blood serum more than 2 ng/ml;

An increase in the level of IL-8 in the blood serum more than 100 pg/ml;

Index	Child's age	The value at which it is legal to use the corresponding indicator (x10\l)
Leukocytosis	1-2 days	> 30 LLC
	3-7 days	> 20 000
	>7 days	> 15 000
Leukopenia
	1-2 days	> 20 000
Neutrophilia	3-7 days	> 7000
	> 7 days	> 6000
	1-2 days
Neutropenia	3-7 days
	> 7 days
Increase in the number of young forms of neutrophils	1-2 days	>5000
	from day 3	>1500
Neutrophil index (ratio of the number of juvenile forms to the total number of neutrophils)		>0,2

If additional laboratory diagnostics are possible, such indicators are informative systemic inflammation, as an increase in serum levels of other pro-inflammatory cytokines (IL-1 in tumor necrosis factor-a, interferon-γ, IL-6), changes in the levels of acute phase proteins of inflammation as positive reactants (increase in the presence of systemic inflammation, for example, haptoglobin, orosomucoid, C3-component of complement and others), and negative reactants (decreased with inflammation, for example, C4-component of complement, prealbumin).

In the first three days of life, the presence of at least three of the above signs can serve as good reason to assume a diagnosis of sepsis and immediately prescribe empirical antibacterial therapy, as well as carry out the entire necessary amount of therapeutic measures.

In newborns over 4 days of age, the diagnosis of sepsis should be assumed in the presence of a primary infectious-inflammatory focus, dysfunction of two or more body systems, and at least three of the listed signs of a systemic inflammatory response. This is also an indication for the immediate initiation of antibacterial therapy and a set of therapeutic measures.

However, realizing that sepsis still remains clinical diagnosis, it is advisable to either confirm or reject it within 5-7 days. The disappearance of signs of a systemic inflammatory response in parallel with the sanitation of the source of infection, and especially the lack of connection between the clinical manifestations of a systemic inflammatory response and the infection, argues against the diagnosis of sepsis and requires further diagnostic search.

The diagnosis of sepsis can be immediately established in the presence of a primary septic focus and metastatic pyemic lesions with a single pathogen. A mandatory stage in the diagnosis of sepsis is a microbiological study, i.e. culture of blood, CSF (according to clinical indications), aspirate from the trachea, urine, separated from purulent foci.

The rules for collecting blood for sterility culture should be strictly followed. It is necessary to carry out collection under aseptic conditions during puncture of an intact peripheral vein or the first puncture central vein for placing a catheter. It is unacceptable to draw blood for culture from a long-functioning catheter (this is only advisable when studying the epidemic situation in the department). The optimal blood volume for culture is 1 ml or more. With technical difficulties and obtaining a smaller volume of blood, the risk of obtaining negative blood culture results in the presence of low concentrations of bacteria in the bloodstream increases, especially against the background of effective antibacterial therapy.

Bacteremia is not an absolute diagnostic sign of sepsis. False negative results Blood cultures can be obtained when collecting material after the start of antibacterial therapy. In addition, false-negative blood culture results may be due to a small blood volume with a small degree of bacteremia and imperfect laboratory diagnostics for present stage, because whole line pathogens require special, specific nutrient media and cannot be determined by standard testing. False-positive blood cultures are also possible, since bacteremia can be observed with any infectious disease bacterial nature.

Along with blood culture studies, etiological diagnosis sepsis includes microbiological examination of discharge from primary and metastatic pyemic foci. It should be noted that microbiological examination of body loci in contact with the environment (conjunctival mucosa, nose, oral cavity, skin, urine, feces), if this is not a primary purulent-inflammatory focus, cannot be used for etiological diagnosis sepsis. At the same time, microbiological examination of these media is indicated to assess the degree and nature of dysbiosis (one of the constant manifestations of sepsis); it reflects a general decrease in the immunity of the sick child.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis of sepsis must be carried out in severe purulent-inflammatory localized diseases ( purulent peritonitis, purulent mediastinitis, purulent-destructive pneumonia, purulent meningitis, purulent hematogenous osteomyelitis, necrotizing enterocolitis of the newborn). Unlike sepsis, they have the following dependence:

The presence of a purulent focus -> the presence of signs of a systemic inflammatory response,

Sanitation of a purulent focus -> relief of the systemic inflammatory response. It should be noted that sepsis, in contrast to severe localized purulent-infectious pathology, such as neonatal meningitis, destructive pneumonia, osteomyelitis, ulcerative necrotizing enterocolitis, phlegmon and others, is characterized by the presence in the clinical picture of the disease of at least three symptom complexes of organ failure.

Sepsis should also be differentiated from congenital generalized forms viral infections. Differential diagnosis is based on molecular biological or virological research blood, CSF, urine, tracheal aspirate or saliva by PCR or culture, serological studies of the levels of specific antiviral IgM and IgG in the blood serum, as well as their avidity.

Sepsis must be differentiated from generalized mycoses, primarily candidiasis and, much less frequently, aspergillosis. Differential diagnosis is based on the results of microscopic and mycological (culture on Sabouraud's medium) examination of blood, CSF, and discharge from pyaemic foci.

Finally, in newborns, sepsis must be differentiated from hereditary metabolic pathologies. Thus, hereditary defects in amino acid metabolism are characterized by a rapid deterioration in the condition of the newborn after birth, progressive shortness of breath, pulmonary heart failure, depression of central nervous system functions, hypothermia, leukopenia, thrombocytopenia, and anemia. A distinctive feature is persistent and pronounced metabolic acidosis, in some cases the appearance of a persistent odor. Due to the severity of the condition, bacteremia can be detected in a child, reflecting severe dysbiosis and a decrease in the body’s resistance. The main thing in differential diagnosis is biochemical research blood, urine, genetic diagnostics. Galactosemia can also occur under the guise of umbilical or late neonatal sepsis. The manifestation of this disease is characterized by a deterioration in the condition of the newborn, an increase in regurgitation and vomiting, an increase in body temperature, the development of hemolytic jaundice and hemolytic anemia, an increase in pathological neurological symptoms, impaired liver function with increased levels of transaminases, the development of cholestasis, hypoglycemia, and metabolic acidosis. In contrast to sepsis, inflammatory changes in the general blood test in uncomplicated forms of galactosemia are not pronounced; the results of microbiological and molecular biological studies are negative. The diagnosis of galactosemia can be confirmed by detecting high levels of galactose (more than 0.2 g/l) in the blood serum (Guthrie test), as well as changes in the levels of galactokinase and other enzymes involved in galactose metabolism, genetic studies.

A child with suspected sepsis or with an established diagnosis of neonatal sepsis must be hospitalized in the NICU or neonatal pathology department, depending on the severity of the condition (in acute phase diseases must be treated in the NICU).

An important role in the prevention of sepsis is played by hygiene measures (hygienic treatment of the skin and visible mucous membranes, bathing) and proper feeding newborns. For full-term babies in the neonatal pathology department, preference is given to feeding with native mother's milk (breastfeeding, feeding milk from a bottle, feeding it through a tube, depending on the condition of the newborn). In the absence of mother's milk, adapted formulas are used for feeding newborns, including those enriched with bifidobacteria (HAH 1, Frisolak, Nutrilon, Humana 1, fermented milk NAN, Lactofidus and others).

The use of a mixture of fermented milk NAN with bifidobacteria helps to inhibit the growth of pathogenic intestinal microflora and enhance the local immune response. However, it should be remembered that in children with transient lactase deficiency and severe acidosis, the use of fermented milk formulas often leads to regurgitation and diarrhea. In this case, it is advisable to use low-lactose and lactose-free adapted mixtures, including those enriched with prebiotics (lactose-free NAN, low-lactose Nutrilon, Nutrilon-omneo, etc.). For premature infants in the absence of breast milk, special adapted formulas (pre-NAN, Friso-pre, etc.) are used. With the development of enterocolitis and peritonitis, EN is canceled for 7-14 days, and with the subsequent resumption of nutrition in children with intestinal pathology and malabsorption, it is recommended to use mixtures containing protein hydrolyzate and medium-chain triglycerides (Alfare, Nutrilon-Pepti, Nutramigen, Pregistimil, etc.).

The Alfare mixture is distinguished by the presence of special LCPUFAs - gamma-linolenic and docosahexaenoic acid, which have pronounced anti-inflammatory properties. Highly hydrolyzed whey protein, enriched with alpha-lactalbumin, contains fat component Alfare mixtures of medium-chain triglycerides, as well as maltodextrin as a carbohydrate component, make the mixture easily digestible and allow it to be prescribed as enteral nutrition to children with severe malabsorption.

During the period of acute manifestations, it is advisable for the sick child to stay in the incubator at a temperature of at least 30 ° C and a humidity of at least 60%.

Correction of vital functions is carried out under control, including the following parameters:

Assessment of CBS, p02, hemoglobin oxygen saturation;

Hb, Ht level;

Levels of glucose, creatinine (urea), K, Na, Ca, Mg, according to indications - bilirubin, transaminases, total protein, albumin and other indicators;

Evaluation of blood pressure, ECG.

Sepsis therapy should include medical events, simultaneously carried out in two directions:

Etiotropic therapy is an effect on the infectious agent (causative agent of the disease), which includes, along with systemic antibiotic therapy local therapy, aimed at the rehabilitation of primary or metastatic foci, correction of disturbances in the biocenosis of the surfaces of the child’s body in contact with the environment.

Pathogenetic therapy aimed at restoring changes in homeostasis, including immune system disorders and organ disorders.

Etiotropic therapy

Antibacterial therapy is a fundamental and urgent direction that determines the etiological component of the treatment of sepsis.

The general principles for choosing antibacterial therapy are as follows:

The choice of drugs at the beginning of therapy (before the etiology of the disease is clarified) is carried out depending on the time of occurrence (early, late sepsis), conditions of occurrence (in a medical or surgical department, or NICU), localization of the primary septic focus, if any.

The drugs of choice for empirical therapy should be antibiotics or a combination of antibacterial drugs with a bactericidal type of action that are active against potential pathogens of sepsis, including associated pathogens (de-escalation principle of choosing antibiotic therapy). When clarifying the nature of the microflora and its sensitivity, antibacterial treatment is adjusted by changing the drug and switching to drugs with a narrower, targeted spectrum of action.

When choosing antibiotics, preference is given to drugs that penetrate the blood-brain barrier and other biological barriers of the body and create a sufficient therapeutic concentration in the CSF, in the brain and other tissues of the body (bone, lung, etc.).

When choosing drugs, in all cases, preference is given to antibiotics with the least toxicity, and the nature of organ disorders must be taken into account.

Preferred drugs with the possibility of intravenous administration.

CHOICE OF ANTIBIOTICS DEPENDING ON THE TYPE OF SEPSIS

For early neonatal sepsis, the drugs of choice are ampicillin in combination with aminoglycosides (gentamicin or amikacin).

For community-acquired umbilical sepsis, the first choice antibiotics should be a combination of oxacillin or 2nd generation cephalosporins (cefuroxime) with aminoglycosides (amikacin). If a disease caused by methicillin-resistant strains of staphylococci or enterococci is suspected, vancomycin is prescribed either as monotherapy or in combination with an aminoglycoside (amikacin).

For skin sepsis, the antibiotics of choice are penicillins (oxacillin and ampicillin) and 1st and 2nd generation cephalosporins (cefazolin or ceforuxime), used in combination with aminoglycosides (amikacin).

Ventilator-associated pulmonary sepsis in newborns is often caused by Ps. aeruginose, Acinetobacter spp., Klebsiella spp. Therefore, the antibiotics of choice are “protected” penicillins (ticarcillin/clavulanic acid), ureidopenicillins (piperacillin) or 3rd generation cephalosporins with activity against Ps. aeruginosae (ceftazidime) in combination with aminoglycosides (amikacin).

Alternative antibiotics are carbapenems (imipenem/cilastatin) as monotherapy or in combination with aminoglycosides. At high probability Given the etiological role of methicillin-resistant staphylococcal strains, it is advisable to use vancomycin or, if its ineffectiveness is suspected, linezolid.

For intestinal sepsis, the antibiotics of choice are 3rd generation cephalosporins, carboxypenicillins as monotherapy or in combination with aminoglycosides (amikacin).

Alternative antibiotics for intestinal and urogenic sepsis are imipenem (Tienam), and for abdominal sepsis - ticarcillin/clavulanic acid, ureidopenicillins (piperacillin), metronidazole, lincosamides, linezolin as monotherapy or in combination with aminoglycosides (amikacin).

Catheter-associated sepsis is one of the forms of nosocomial sepsis. Its main causative agent is considered to be S. aureus, and methicillin-resistant strains of the microorganism are often cultured. Therefore, the antibiotics of choice in this case are vancomycin and linezolid.

Antibacterial therapy is considered effective if, within 48 hours, the patient’s condition is stabilized or even some improvement is achieved.

Therapy is considered ineffective if the severity of the condition and organ failure increase within 48 hours. This is an indication for switching to alternative antibiotic therapy and intensifying detoxification infusion therapy.

With successful antibacterial therapy, its duration is on average four weeks, and with the exception of aminoglycosides, the course duration of which cannot exceed ten days, the course of the same drug, with its obvious effectiveness, can reach three weeks.

The basis for discontinuation of antibacterial drugs can be considered the sanitation of primary and pyemic foci, the absence of new metastatic foci, relief of signs of an acute systemic inflammatory reaction and multiple organ failure, persistent weight gain, normalization of the peripheral blood count and platelet count, negative results of microbiological examination of blood, CSF, aspirate from the trachea, urine.

Pathogenetic therapy

Pathogenetic therapy of sepsis includes the following main areas:

Immunocorrective therapy;

Infusion therapy;

Restoration of water and electrolyte balance, correction of blood acid-base balance;

Antishock therapy;

Restoration of the functions of the main organs and systems of the body.

Carrying out immunoreplacement therapy with immunoglobulin preparations for intravenous administration can reduce the mortality rate in sepsis, accelerate the normalization of the vital functions of the body, restore homeostasis, and help stop the systemic inflammatory reaction and multiple organ failure. Particularly effective for neonatal sepsis are immunoglobulin preparations for intravenous administration, enriched with IgM (Pentaglobin). Their use in the treatment of neonatal sepsis significantly reduces mortality from this disease.

Infusion therapy makes it possible to replenish the deficit of blood volume, correct electrolyte disorders and improve the hemorheological characteristics of circulating blood. In some cases (if it is impossible to feed) infusion therapy becomes a component of the PP of the newborn.

Intravenous administration of immunoglobulins (preferably enriched with IgM) allows to slightly reduce the concentration and synthesis of pro-inflammatory cytokines in the blood, facilitates phagocytosis and improves the elimination of the pathogen.

Antishock therapy includes two main areas:

Therapy with vasopressor and inotropic drugs (dopamine with dobutamine) in combination with low doses of glucocorticoids, which allows to stop hidden adrenal insufficiency and provide reserve capabilities of the hypothalamic-pituitary-adrenal system. If dopamine and dobutamine are ineffective, epinephrine (adrenaline) is used. The use of glucocorticoid therapy (hydrocortisone at a dose of 5-10 mg per kg of body weight) significantly increases the survival rate of patients with septic shock.

Correction of hemostasis, which includes transfusions of fresh frozen plasma in combination with the administration of heparin at a dose of 50-100 mg per kg of body weight per day. Fresh frozen plasma contains, as is known, AT, proteins, and also contains antithrombin III, the level of which drops significantly with the development of sepsis, which, in turn, causes depression of fibrinolysis and the development of DIC syndrome.

Rehabilitation therapy for neonatal sepsis

During the recovery period, strict adherence to a hygienic regime, correction of intestinal biocenosis, antifungal therapy (if necessary), and provision of breastfeeding are necessary. During the same period of time, it is advisable to carry out neurotrophic and metabolic therapy aimed at restoring oxidative intracellular processes and increasing the anabolic orientation of metabolism. For this purpose, the administration of complexes of vitamins and microelements, essential amino acids, enzymes, and carnitine is indicated.

In case of severe disturbances of immune homeostasis, confirmed by laboratory tests, immunotherapy is indicated. During this period, depending on the nature of the immune disorders, drugs such as glucosaminil muramyl dipeptide (Likopid), interferon-alpha 2 (Viferon) can be used.

The prognosis for neonatal sepsis is serious, mortality is various types sepsis now ranges from 25 to 55%.