NEONATAL SURGERY - 1976
2. SPECIAL SECTIONS
9. Purulent-Inflammatory Diseases
Purulent-Inflammatory Diseases continue to be one of the leading causes of neonatal mortality. The number of such patients shows no tendency to decrease and, According to the Department of Neonatal Surgery of our clinic, accounts for 40 to 60% of the total number of children treated in the department. The clinical manifestations and disease course of purulent-inflammatory conditions in newborns differ significantly from those in older children and adults. The Nature of the newborn's systemic response to purulent-inflammatory processes is determined by anatomical and functional characteristics.
Selection/11.html">General features of the Course of Purulent-Inflammatory Diseases in Newborns
Newborn infants are more susceptible to purulent-inflammatory diseases than children of other age groups. This fact is explained by the specific relationship between pyogenic microflora and the newborn's Organism. Having been a homobiont during intrauterine development, the newborn encounters microflora (including pathogenic ones) for the first time at the moment of birth, while passing through the mother's birth canal. When a pathological process develops in a newborn, its essence boils down to the interaction of two factors (the pathogenic microorganism and the newborn's organism) rather than three (the microorganism, the symbiont, and the macroorganism), as observed in older children and adults (S. Ya. Donetsky, 1965). This largely determines the specific course of the purulent-inflammatory process in newborns (Fig. 113). Long-term use of Treatment Methods aimed at eliminating pathogenic microorganisms is impractical in such cases, as it disrupts the establishment of relationships between the symbiotic microflora and the sick child's organism.
Class="center">Fig. 113. Diagram of the onset of purulent-inflammatory diseases.
In newborn infants (a), such diseases arise differently than in older children (b1, b2) and adults. In the first case, two factors are present: the body's defense mechanisms and the microorganisms that colonize the newborn's body and simultaneously serve as the source of the purulent-inflammatory process. In older children and adults, three factors are always present: defense mechanisms, symbionts, and pyogenic microbes. In exogenous infection (b1), pyogenic microbes appear from the outside; in endogenous infection (b2), "rebellious" symbionts become the source.
The relatively high frequency of purulent-inflammatory diseases in newborns is also explained by the undeveloped barrier Functions of Organs and Tissues. The epithelial barrier of the Skin and mucous membranes is more permeable to microflora in newborns than in adults. For instance, the ciliated epithelium of the respiratory tract is easily deformed, epithelial Cells are weakly connected to each other and to underlying tissues, and they easily desquamate into the tracheal lumen (M. A. Skvortsov, 1960; Essbach, 1961).
The thinness and extreme fragility of the integuments, frequent macerations and diaper rash facilitate the penetration of microflora (A. Andronescu, 1970). The structural and Blood supply characteristics of subcutaneous adipose tissue, the epiphyses of long tubular bones, and other structures are of great importance in the onset and specific course of purulent-inflammatory diseases. In particular, the predominance of a terminal blood supply pattern contributes to the rapid progression of necrotic processes in subcutaneous tissue (neonatal Phlegmon) and the epiphyseal ends of long tubular bones (Osteomyelitis).
The specific clinical manifestations of purulent-inflammatory diseases in children, and the predominance of general symptoms over local ones in the clinical picture, are caused by the insufficient Differentiation of the newborn's central and Peripheral Nervous system.
Of great importance are the specific and nonspecific reactivity CHARACTERISTICS OF THE newborn organism. It is known that the response of a developing organism to various stimuli, including infectious agents, is in direct proportion to its degree of maturity.
Newborns and infants in the first months of life exhibit pronounced resistance to A number of infectious diseases, predominantly of viral origin. They practically do not fall ill with measles, scarlet fever, mumps, etc. It is generally accepted that young children are protected from these diseases by Antibodies received from the mother via the transplacental route (Danois et al., 1961). It has now been proven that the Placenta is capable not only of passing antibodies but also of synthesizing them. The placental barrier is relatively easily crossed by virus antibodies; The transfer of toxin antibodies is less pronounced.
Studies by N. E. Ryazantseva, E. V. Smirnova, L. A. Kozlovskaya (1959) and others have shown that passive Immunity is transmitted from the mother only to those infections that the mother has had or against which she has been vaccinated. Antibodies transferred via the transplacental route provide passive immunity characterized by high duration and potency. Antibodies with which a child is born persist in the body for up to 3–6 months.
Recent studies have shown that newborn infants are themselves capable of producing antibodies, particularly in infectious diseases (L. S. Lozovskaya, 1969; Eichenwald et al., 1960). In this process, mainly the A- and M-fractions of IMMUNOGLOBULINS are produced. The Synthesis of the G-fraction, which helps protect the body against pyogenic flora, particularly staphylococcal flora, is minimal in the newborn. The G-fraction begins to be synthesized no earlier than 3 months of life. This largely explains The high frequency of purulent-inflammatory diseases in newborns and the severity of their course.
The level of nonspecific immunity factors in the blood of a newborn infant differs little from that of older children.
Premature infants are characterized by the rapid depletion of the body's reserve capacities and a significant decrease in nonspecific immunity factors during diseases of infectious origin. The latter occurs much earlier compared to full-term newborns.
The aforementioned main anatomical and PHYSIOLOGICAL CHARACTERISTICS OF the newborn organism, the absence of symbiotic microflora, insufficient maturity of the central and peripheral nervous system, inadequate barrier capabilities of the skin and mucous membrane, the terminal type of Blood supply to individual organs and tissues, Relative immaturity of the reticuloendothelial system, etc., are the main Prerequisites for the greater susceptibility of newborns to purulent-inflammatory diseases and the specific clinical manifestations of such conditions in newborns. Therapy for such patients can be effective only when therapeutic measures are carried out taking these features into account.
Neonatal Sepsis. General Principles of Treatment of Purulent-Inflammatory Diseases in Newborns
Sepsis is a specific infectious disease in which microbes, their metabolic products, toxins, and Cell decay products enter the patient's body from a primary or metastatic focus. Sepsis is a clinical concept (M. S. Maslov, 1959). G. N. Speransky (1937) pointed out that sepsis is not so much an independent nosological disease entity as a phase of the infectious process.
The Nature of the clinical course of sepsis in newborns, its severity, and unsatisfactory treatment outcomes are caused by Anatomical and physiological characteristics, the peculiar reactivity of the newborn organism, and the pronounced virulence and resistance of pyogenic microflora to widely used Antibiotics (Z. N. Vikhireva, 1965; A. D. Ostrovsky, 1970).
Staphylococcus occupies a leading place in the Etiology of neonatal sepsis (G. I. Chistovich, 1961; L. G. Kvasnaya, 1972; A. R. Shurinok, 1965; A. D. Ostrovsky, E. A. Suslennikova; Z. D. Khozova, 1967; V. N. Geraskina et al., 1970). Sepsis can also be caused by Streptococcus, Proteus, Pseudomonas aeruginosa, Escherichia coli, etc.
Infection of the newborn can occur during delivery and subsequently in the maternity hospital. The microflora of the mother's birth canal and staff carriage are of great importance (E. G. Isaeva, 1965; E. I. Glotkina, 1970; Parker, 1966). Sources of infection can also include items used for infant care, instruments, equipment, etc.
The portals of entry for neonatal sepsis are the umbilical wound, damaged skin, and mucous membranes. In the majority of newborns who develop sepsis, it is possible to detect a primary focus—Omphalitis, Pyoderma, neonatal phlegmon, etc. In some cases, the primary focus cannot be identified.
Depending on the portal of entry of the infection, umbilical, cutaneous, pulmonary, intestinal, mixed, and focus-free (cryptogenic) sepsis are distinguished (E. G. Isaeva, 1965; L. G. Kvasnaya, 1972).
In The Development of the septic process, L. G. Kvasnaya (1972) distinguishes three periods: the Introduction of the infection, the latent period of the disease, and the development of overt symptoms. The latter period occurs 5 to 10 days after infection.
The premorbid Background is of great importance in the Development of the septic process. In The history of sick children, one typically finds maternal illness during Pregnancy, birth trauma and other labor complications, prolonged umbilical weeping, bloody-purulent discharge from the umbilical wound, inflammatory skin changes, respiratory tract diseases, dyspeptic disorders, etc. Sepsis in premature infants is more common and follows a severe course (E. Ch. Novikova, 1967, 1967; V. G. Andreeva et al., 1969).
Clinical picture. In most cases, neonatal sepsis lacks pathognomonic clinical symptoms and often proceeds under various "masks". Premonitory signs (prodrome), early symptoms, and overt manifestations of the disease are distinguished.
Premonitory signs of sepsis include delayed shedding of the umbilical cord remnant, weight gain delay, pustular skin diseases that are difficult to treat, prolonged skin maceration, etc.
Early symptoms include lethargy, regurgitation, poor appetite, pallor of the skin, inflammatory Changes in the area of the umbilical vessels, a network of engorged Veins on the anterior abdominal wall, and edema in the umbilical region.
During the stage of overt disease, all organs and systems are affected. Two forms of the disease are distinguished: septicaemia and septicopyaemia. According to its clinical course, sepsis is classified as mild, moderate, or severe (E. I. Glotkina, 1970). Neurotoxicosis, pulmonary syndrome, intestinal syndrome, and others come to the forefront in the clinical picture.
Septicaemia predominates in newborns (N. V. Orlova, Z. D. Hozova, 1969). The latter is characterized by a slowly progressive deterioration of the patient's condition and increasing signs of toxicosis. Temperature response is not characteristic. Septicaemia has a wave-like course, with periods of improvement alternating with deterioration. Pallor, grayish skin tone, decreased appetite, and weight stabilization or loss are typical. The dynamics of the child's weight is of great DIAGNOSTIC AND PROGNOSTIC significance. Progression of the disease is accompanied by increasing signs of Central Nervous System involvement—the child becomes lethargic, adynamic; in some cases, convulsions, nystagmus, and meningeal signs are observed. Respiratory rhythm disturbances may occur. The pulse is rapid, and muffled or even distant Heart sounds are detected. Gastrointestinal disorders causing regurgitation, vomiting, and intestinal dysfunction are frequent.
The Liver is enlarged in the majority of patients. A decrease in cholinesterase activity and an increase in transaminase levels are noted. In some cases, bilirubin METABOLISM is impaired, resulting in icterus of the sclera and skin. Splenomegaly is characteristic of the terminal Stages of the disease (E. Ch. Novikova, 1965). Protein, leukocytes, erythrocytes, and renal epithelium appear in the urine of such patients, indicating renal irritation. Pyuria is frequently observed.
Anemia is the most constant symptom of sepsis. The younger the infant, the less pronounced the changes in THE RED BLOOD cell count; as the child grows, the manifestations of anemia progress. Changes in the WHITE BLOOD CELL count are less characteristic: some patients exhibit moderate leukocytosis, while others show leukopenia. A left shift in the leukocyte differential is more distinct. The platelet count is generally reduced, and the ERYTHROCYTE SEDIMENTATION RATE is accelerated.
In severe forms of sepsis, total protein levels decrease. The content of α1- and α2-globulins is elevated, indicating the progression of the process. The amount of γ-globulins decreases at the peak of the disease. Septicaemia is accompanied by distinct Water-Mineral Metabolism disorders. In the terminal stages of the disease, sclerema and hemorrhagic manifestations frequently join the picture. Recent studies (V. N. Geraskina, 1970) have revealed exhaustion of adrenal cortex function in sepsis, which is significant for justifying Pathogenetic Therapy.
Newborns with manifestations of septicaemia are generally observed and treated by pediatricians. They are referred to surgical departments in most cases when septicopyaemia develops. The appearance of metastatic purulent foci is accompanied by fever and a sharp deterioration in the condition (V. K. Mazurova, 1969; N. I. Margulis, 1971). Abscesses can occur in various organs, but the Lungs are most frequently affected, initially manifesting clinically as Pneumonia. In polysegmental, large-focal, and confluent pneumonia, destruction of lung tissue is observed with subsequent abscess formation, rupture into the Pleura, and the development of pyopneumothorax. Purulent foci also develop in the Middle ear and subcutaneous adipose tissue. Osteomyelitis is one of the frequent manifestations of septicopyaemia. The development of septic ulcerative-necrotic enterocolitis with subsequent intestinal perforation and Peritonitis is characteristic of premature infants (E. Ch. Novikova et al., 1966, 1967, 1971; L. M. Kondratyeva et al., 1968; B. B. Gavryushov et al., 1971). The onset of septicopyaemia sharply worsens the prognosis.
The reactivity of the newborn's organism is of decisive importance in the development, Clinical Features, and outcome of the septic process. The studies of Z. I. Vikhireva (1965), A. D. Ostrovsky (1966, 1970), T. A. Bogomaz (1965, 1967), F. Ts. Gokhberg (1968), and others are dedicated to studying the state of specific and nonspecific immunity in purulent-septic diseases. Conducted studies have shown that phagocytosis is enhanced in the majority of patients with sepsis. In severe cases with an unfavorable prognosis, phagocytosis indices are reduced. A specific dependence of the dynamics of the completed phagocytosis index on the localization and character of the septic process is revealed. The more severe the process, the higher the completed phagocytosis index.
The antitoxin content in staphylococcal sepsis is reduced in most patients. A decrease in Lysozyme and Complement levels is also noted (V. A. Snonkova, G. L. Bilich, 1966; L. B. Balayan, 1969).
General principles of treatment. Complex therapy for purulent-inflammatory diseases and neonatal sepsis provides for targeting the pathogen (microorganism), influencing the host organism (enhancing the latter's defense capabilities), and performing Procedures to sanitize purulent foci (S. Ya. Doletsky, A. I. Leshoshkin, 1965; L. G. Bilich et al., 1969; Bechamps e. a., 1970; Fardito e. a., 1970, et al.).
The administration of antibiotics remains the main method of targeting the pathogen in purulent-inflammatory diseases in newborns. When carrying out antibiotic therapy, the physiological characteristics of the newborn's organs and tissues are taken into account. In particular, the morphological and functional immaturity of the Kidneys leads to delayed excretion of penicillin. Enzymatic immaturity and the resulting hepatic insufficiency can cause serious complications when chloramphenicol (levomycetin) is used in newborns. The Toxic Effect of chloramphenicol manifests as the so-called gray baby syndrome: refusal to suck, abdominal distension, respiratory disorders, lethargy, and a gray skin color. Due to the spread of staphylococcal diseases, The Use of novobiocin in newborns has led to an increased incidence of neonatal jaundice, which is associated with a reduced capacity of the liver to excrete bilirubin when this drug is administered (L. E. Goldberg, V. I. Batsmshtein, 1964). When prescribing antibiotics to newborns, one must keep in mind the children's special sensitivity to the direct pharmacological toxicity of the drugs, as well as the risk of dysbiosis and superinfection development.
The route of antibiotic administration is of particular importance. The enteral route is often impossible due to the vomiting that typically accompanies the toxic state. Intramuscular administration is difficult in cases of general emaciation, sclerema, and certain skin lesions. Thus, in most cases, the intravenous route is the method of choice.
Antibiotics are divided into several groups.
Penicillin group. This includes various benzylpenicillin preparations—sodium and potassium penicillin salts, long-acting Penicillins (bicillin-3 and bicillin-5), the iodine ester of penicillin (eficillin), oral penicillin (phenoxymethylpenicillin), low-allergen penicillin (almecillin), and broad-spectrum penicillins (ampicillin, carbenicillin, cenorin, cephalothin).
Biosynthetic Penicillins are effective against Gram-positive microorganisms. Semisynthetic penicillins—methicillin, oxacillin, dicloxacillin—are resistant to penicillinase, the enzyme that destroys penicillin. Penicillins are widely used to treat purulent-inflammatory diseases in newborns. Combinations of biosynthetic penicillins with semisynthetic ones, and of penicillinase-resistant penicillins with broad-spectrum penicillins, are effective.
Among the Adverse effects of penicillin group drugs, allergic reactions are the most dangerous. Neurotoxic reactions are possible at high doses.
"Reserve" antibiotic group. This group includes drugs that act predominantly on Gram-positive Bacteria (erythromycin, oleandomycin, lincomycin, ristomycin, novobiocin).
Lincomycin has a good ability to penetrate Bone tissue and be retained there. It is recommended for the treatment of osteomyelitis, septic pneumonia, and for the Prevention of complications after heart and vascular surgeries. Novobiocin is indicated for the treatment of staphylococcal sepsis, especially staphylococcal pneumonia. Ristomycin is retained in Internal Organs for a prolonged period, which distinguishes it favorably from Other Antibiotics. In combination with monomycin, ristomycin is advisable to prescribe in cases of peritonitis.
Streptomycins and the aminoglycoside group—streptomycin, dihydrostreptomycin, monomycin, neomycin, kanamycin, garamycin (gentamicin). These antibiotics exert a bactericidal effect and penetrate well into the exudate of the abdominal and thoracic cavities. Antibiotics of the streptomycin group are toxic. Prolonged uncontrolled use of them can lead to Impairment of the cochlear and vestibular apparatus; furthermore, they affect neuromuscular junctions. Drugs of the aminoglycoside group irritate the renal parenchyma, which manifests as Hematuria, albuminuria, cylindruria, and they negatively affect the nitrogen balance.
The aforementioned complications necessitate strict adherence to treatment schedules (5–7 days) and dosages.
Dihydrostreptomycin is not recommended for use in newborns due to its pronounced ototoxic effects.
Streptomycin and Aminoglycosides are prescribed in combination with antibiotics from other groups, such as penicillins, Tetracyclines, and reserve antibiotics.
Tetracycline-group antibiotics include tetracycline, chlortetracycline, oxytetracycline, dibioamycin, rolitetracycline, reverin, geomycin, vibramycin, morphocycline, and glycocycline. Tetracyclines exhibit predominantly bacteriostatic properties. Notably, they accumulate in bone tissue, lungs, and liver. These drugs are characterized by cross-resistance. Tetracyclines irritate the mucous membrane of the gastrointestinal tract and impair the Glycogen-synthesizing function of the liver. Prolonged administration disrupts the normal intestinal microflora, creating favorable conditions for fungal superinfections or staphylococcal enterocolitis. Therefore, when prescribing tetracyclines, nystatin and Vitamins are co-administered.
Due to significant adverse effects, the enteral route of administration for tetracyclines is not clinically indicated in newborns.
Nitrofuran derivatives. Derivatives of 5-nitrofuran—such as furacilin (furatsizin), furadonin (nitrofurantoin), furazolidone, furagin, and furagin K—have found widespread clinical application in treating various purulent, inflammatory, and septic Infections caused by staphylococci and enteric bacteria. A primary prerequisite for prescribing nitrofuran drugs is the Antibiotic Resistance of the pathogen.
Nitrofurans are frequently combined with antibiotics from other groups, including penicillins, tetracyclines, reserve antibiotics, and sulfonamides. Among adverse effects, nitrofurans most commonly cause gastrointestinal symptoms, such as vomiting, loss of appetite, epigastric pain, and mild diarrhea.
Antifungal antibiotics include nystatin, levorin, and amphotericin B. Antibiotics of this class exert exclusively antifungal activity and do not affect pathogenic bacteria. Antifungal agents are prescribed for prophylactic purposes during prolonged antibiotic therapy.
The formulation of a rational antibiotic regimen involves: 1) selecting the most effective drug; 2) initiating treatment early; 3) making a well-founded choice of drug combinations; 4) determining optimal dosages, administration schedules, and duration of therapy. The use of low (sub-bacteriostatic) doses is discouraged, as they facilitate The Emergence of resistant microbial strains. The duration of antibiotic therapy is determined by strict clinical indications, given that prolonged use contributes to the development of dysbiosis.
Antibiotic therapy is tailored to the individual characteristics of the patient, the clinical course of the disease, and concurrent pathological processes.
Of paramount importance is the response of the newborn's macroorganism. In most cases, the reactivity and defense mechanisms of the body are decisive factors that determine the outcome of the acute stage of the disease, the likelihood of chronicity, and the ultimate prognosis. Interventions targeting the patient's organism are planned taking into account the aforementioned characteristics of neonatal reactivity. Primary emphasis is placed on stimulating therapy and enhancing both specific and nonspecific immune factors in the newborn's blood. Given the relative immaturity of the neonatal reticuloendothelial system—specifically its reduced capacity to produce specific antibodies—therapy aimed at supplying preformed immune factors directly into the patient's blood is considered appropriate. Blood transfusion is an effective method for treating neonates with purulent-inflammatory conditions. It is successfully employed both in the acute phase and during the chronic and subsequent reparative stages. The most widespread technique involves transfusing small volumes (10–15 ml per kg of body weight) of fresh stored blood once every 2–3 days. Blood transfusions are alternated with plasma infusions and the administration of gamma globulin. Direct blood transfusion offers distinct advantages, as it delivers unmodified, fully functional blood to the recipient.
The optimal donor for an infant is a parent or close relative (sibling, grandmother, grandfather) belonging to the same blood group. This approach significantly minimizes the risk of allergic reactions by reducing antigenic differences between the donor and the recipient.
Direct transfusions are performed with strict adherence to established blood transfusion protocols. Donors undergo comprehensive screening at a blood transfusion center. Direct transfusions are performed using a syringe or a domestic direct transfusion device (Model 210) designed by the Research Institute of Experimental Surgical Apparatus and Instruments (RIIESAI). For stimulating blood transfusions, a volume of 10–15 ml per kg of body weight is sufficient. The number of transfusions ranges from 1–2 to 10 or more, with intervals of 3–4 days between procedures.
To enhance the therapeutic efficacy of direct blood transfusions in patients with staphylococcal purulent-inflammatory diseases and impaired reparative processes, donors—either parents or relatives—are immunized with staphylococcal toxoid according to the following schedule: three injections of 0.5 ml of staphylococcal toxoid at 5-day intervals. Concurrently, the donor is administered 50 mcg of prodigiosan. Prodigiosan is a polysaccharide of microbial origin that stimulates the body's defense and adaptive reactions by acting on the reticuloendothelial and hypothalamo-pituitary-adrenal systems. Its administration leads to an increased release of leukocytes into the peripheral blood, enhanced phagocytic activity of leukocytes, and elevated lysosomal activity of macrophages (G. E. Weisberg, 1964).
As studies have shown, the concentration of alpha-antitoxin in the blood of donor parents gradually increases during the immunization process. In the majority of immunized individuals, accumulation of alpha-antitoxins was observed as early as the 4th to 5th day following the first toxoid injection. By the 14th to 15th day from THE START OF immunization, it averaged 1.8 ± 0.3 IU/ml, increasing to 10 ± 2.6 IU/ml by the 20th to 25th day, and remained elevated over the subsequent 10–12 days. Only from the 30th to 40th day was a gradual decline in specific antibody levels noted. Following the third injection of staphylococcal toxoid combined with prodigiosan, alpha-antitoxin levels in individual donors reached as high as 18–24 IU/ml. A sharp increase in specific alpha-antitoxic antibodies was also observed in the breast milk of immunized mothers. While the level of alpha-antitoxic antibodies was 7 ± 0.8 IU/ml by the 15th day of immunization, it rose to 20 ± 4 IU/ml by the 20th to 25th day. Concurrently, the concentration of staphylococcal agglutinins in the milk also increased.
Targeted immunization induces a statistically significant increase in antibodies not only against staphylococci but also against other microorganisms, presumably due to nonspecific stimulation of the reticuloendothelial system.
The immunization process induces immunological restructuring in the donor's body, which also affects nonspecific immune factors such as serum lysozyme and complement levels. By the end of immunization, both the lysozyme and complement activity of blood serum significantly exceeded baseline levels. Thus, immunization substantially enhances the defense capabilities of the parent-donor's organism, making each subsequent blood transfusion from that donor more therapeutically effective than the preceding one.
Direct blood transfusions from pre-immunized donors lead to elevated levels of alpha-antitoxins in the recipient's (infant's) blood. The concentration of these antibodies reached 1 ± 1.5 IU/ml as early as the 10th to 11th day post-infusion and subsequently increased to 6 ± 0.7 IU/ml. Concurrently, the recipient's blood demonstrated elevated lysozyme and complement activity. Notably, infants exclusively breastfed by their immunized mother exhibited significantly higher serum lysozyme activity compared to older children or those who received direct blood transfusions from an immunized father. This suggests that milk from an immunized mother serves as a potent factor in boosting the infant's resistance.
Direct blood transfusion has been widely utilized in the neonatal surgery department of the Department of Pediatric Surgery at the Central Institute for Advanced Medical Training (CIAMT) since 1970. Initially, indications for direct blood transfusion were established in cases where prolonged conventional therapy, including stored blood transfusions, failed to yield a clear therapeutic response. As clinical experience accumulated and the efficacy of direct hemotransfusions—particularly using blood from pre-immunized donors—became evident, the indications for direct transfusion were expanded. Direct transfusions were typically performed in combination with comprehensive antibacterial, detoxifying, and physical therapy, alongside the sanitation of local infectious foci. In most cases, significant clinical improvement was observed after just 1 to 3 direct hemotransfusions: the infant's appetite improved, weight loss ceased, and the condition of the purulent focus ameliorated.
Substantial therapeutic efficacy can be achieved through the use of anti-staphylococcal plasma (V. A. Tabolin et al., 1970; S. V. Skurkovich et al., 1971) and anti-staphylococcal gamma globulin (T. V. Golosova et al., 1969; N. S. Zakharyevskaya et al., 1972). Hyperimmune anti-staphylococcal plasma is obtained from donors immunized with staphylococcal toxoid. It differs from standard plasma by possessing a high titer of specific anti-staphylococcal antibodies. The plasma is administered intravenously at a dose of 6–10 ml per kg of the infant's body weight. The course of transfusions consists of 3 to 6 procedures at intervals of 2 to 3 days. Alternating transfusions of blood, plasma, and gamma globulin proves highly effective.
A crucial objective of complex therapy in purulent-inflammatory Diseases of Newborns is the correction of Homeostasis parameters in the broad sense of the term: combating respiratory, circulatory, and tissue Hypoxia; eliminating hypovolemia and Circulatory Disorders; maintaining normal cardiac function; managing hyperthermia; reducing proteolysis and the pathological impact of its end products; normalizing water-electrolyte balance and renal function; and correcting metabolic shifts.
Management of hypoxia begins with Oxygen therapy. A humidified oxygen-air mixture (2:3) is administered continuously around the clock via a nasal or nasopharyngeal catheter. Respiratory failure is exacerbated by the accumulation of mucus in the respiratory tract, a frequent occurrence in newborns. In such cases, airway hygiene facilitated by direct laryngoscopy and bronchoscopy AIDS in improving Respiration. Patient age and severity of condition do not constitute contraindications to these procedures (I. G. Klimkovich, 1963; S. Ya. Donetsky, V. M. Balagan, L. A. Geldt, 1972). To improve tissue respiration and oxidative processes, B-complex vitamins and cocarboxylase are prescribed. Circulatory disorders are corrected through infusions of blood, plasma, and colloidal solutions (polyglucukin, polyvinylol, gelatinol, albumin, protein) at 10–15 ml per kg of body weight daily. Aside from mitigating hypovolemia, the administration of protein solutions exerts a direct detoxifying effect, as their molecules adsorb microbial toxins. Low-molecular-weight polyvinylpyrrolidone and its preparations—such as hemodez, neocompensan, and periston—exhibit pronounced detoxification properties. Their molecules form complexes with toxins that are subsequently excreted in the urine.
Water and Electrolyte deficits, as well as the organism's Energy Expenditure—which increases sharply under conditions of inflammation and hyperthermia—are replenished through the intravenous administration of glucose-electrolyte solutions. To alleviate tachycardia, intestinalparesis, and muscular hypotonia resulting from potassium deficiency, potassium is administered as a 7.5% potassium chloride solution in a glucose solution.
Potassium salt loads are tolerated quite satisfactorily by newborns and even premature infants. Conversely, sodium ions are excreted slowly, and their excess can precipitate hypervolemia, edema, and exacerbate Heart Failure (Yu. E. Veltishchev, 1967). Given these circumstances, extreme caution must be exercised when prescribing sodium chloride-containing solutions to neonates. Rehydration in young infants should be performed under the monitoring of hematocrit values, central venous pressure, and circulating blood volume.
In the presence of cardiovascular failure, therapeutic measures are aimed at unloading the lesser (pulmonary) Circulation (using aminophylline, lasix, or uregyd) and enhancing myocardial contractility (strophanthin, corglycon, and subsequently digoxin).
The proteolytic activity of microbial toxins and endogenous Enzymes activated by the infectious process, along with the pathological effects of proteolytic products, are neutralized by administering protease inhibitors—such as trasylol and kontrical—as well as antihistamines.
To combat hyperthermia, the child's skin is intensively rubbed with alcohol. Against the background of the ganglion-blocking action of antihistamines, this manipulation helps dilate the cutaneous capillary network and enhance heat dissipation. Physical cooling methods and antipyretics (such as pyramidone) are employed.
The escalation of metabolic shifts in the blood's acid-base balance toward acidosis necessitates the use of Buffer solutions (sodium bicarbonate, trisamin). These agents are administered under the control of acid-base balance parameters in cases where fluid infusion, oxygen therapy, and measures aimed at lowering body temperature fail to normalize blood pH (in newborns, the normal blood pH ranges from 7.28 to 7.31).
Addressing the infection focus in newborns, as in older children, involves timely and maximally complete debridement of the lesion. The nature of surgical intervention depends on the localization and character of the process. In all cases, it is fundamentally important to strive for optimal conditions for pus outflow with minimal damage to surrounding tissues (e.g., joint puncture in osteomyelitis with metaepiphyseal localization, multiple small incisions for neonatal phlegmon, etc.).
Wide incisions and wound packing with gauze turundas should be avoided. Small incisions followed by the insertion of thin rubber-glove drains are preferred.
In the acute stage of the process, the time factor is of decisive importance. Opening the lesion is an urgent intervention. Delaying the incision by even a few hours can significantly worsen the course of the disease as well as immediate and long-term treatment outcomes.
Purulent-inflammatory Diseases of the skin and subcutaneous tissue
Neonatal phlegmon is a specific purulent-inflammatory disease of infants in their first weeks of life, characterized by the primary involvement of the subcutaneous tissue. It features an acute onset, rapid progression of the local process, followed by extensive Necrosis of the skin and underlying tissues. Neonatal phlegmon was first classified as an independent nosological entity by S. A. Vasilyev in 1939.
In most cases, the skin serves as the portal of entry for the infection; the possibility of pathogen penetration through the umbilical wound, mucous membranes, etc., cannot be excluded.
In neonatal phlegmon, the primary inflammatory process is localized in the subcutaneous tissue. Focal leukocytic infiltrates develop around the Sweat Glands, accompanied by hemorrhages in the dermis. Macroscopically, a dense infiltrate is present; the skin is hyperemic, bleeds profusely upon incision, and there is no pus. As the process progresses, the skin becomes purplish-cyanotic, and areas of fluctuation with skin detachment appear. On cross-section, the subcutaneous tissue looks dull gray, yellowish in places due to The breakdown of adipose tissue, and does not bleed; it is initially sloughed off in small pieces and subsequently in whole sheets.
The local process in neonatal phlegmon can be localized in various areas, rarely confined to a single anatomical region. The chest, lumbosacral, and gluteal regions are most frequently affected (61.8% of observations). The neck ranks third in frequency of involvement. The palmar surface of the hands and the plantar surface of the feet are not affected by neonatal phlegmon.
Clinical presentation. The disease begins acutely with a rise in temperature to 38 — 39° C, restlessness, Sleep disturbances, and refusal to feed. Within the first few hours upon examining the infant, a dense red area is discovered, which is sharply painful upon Palpation. Its borders are clear, the skin is hyperemic, hot to the Touch, and cannot be gathered into folds. The redness and induration rapidly spread in all directions. The initial skin changes resemble erysipelas. As the inflammatory process spreads, the patient's condition worsens, toxemia joins in, and sometimes dyspeptic disorders occur. After 36 — 48 hours, the skin over the infiltrate acquires a cyanotic tint in places, and palpation is painful. Gradually, areas of softening form at the site of the infiltration focus, and the disease transitions into the second period—the period of subcutaneous tissue necrosis. From this time on, the General condition of the infant improves slightly; they suck more actively, are less restless, and the temperature drops critically or lysis occurs. Bluish areas of skin appear over the lesion at the sites of its detachment. On the 2nd to 3rd day of the disease, liquid pus with pieces of necrotic tissue is discharged through incisions or resulting fistulas. During this period, the spread of the process stops in the majority of patients, and the disease may end in recovery.
In other children (17%, according to our observations), the disease takes a subacute course and transitions into the next period—the period of skin necrosis and The formation of wound defects. Areas of skin necrosis are located at the site of the initial localization of the process, where subcutaneous tissue death occurs first. The skin in this area becomes cyanotic, cold, painless, and is gradually sloughed off. The wound takes on a characteristic appearance: the bottom is covered with fragments of gray necrotic tissue, the edges are undermined and uneven; underlying tissues—fascia, Muscles, and bones—are exposed. A tendency toward granulation and epithelialization is generally absent, and the local changes resemble postoperative gangrene. The general condition of the patient during this period progressively worsens, the temperature remains normal or subfebrile, and intoxication increases. Clinical manifestations indicate the development of sepsis. The child becomes lethargic, nurses poorly, the skin loses its characteristic elasticity and freshness, becomes pale with a dirty-gray tint, and tissue turgor decreases. The weight curve flattens and often drops; multiple petechial rashes are characteristic. In some cases, septic complications join in, wound exhaustion increases, and the patient dies. The larger the affected area, the higher the likelihood of a fatal outcome. Mortality increases sharply when 10 — 12%
of the body surface is affected.
An infant with neonatal phlegmon. Inflammatory changes have spread beyond the performed incisions within 6 hours (left). A newborn with congenital sepsis. Gangrene of the right lower extremity resulting from Thrombosis of the right umbilical and iliac Arteries (right).
A newborn with congenital sepsis. Amputation of the right arm As a result of previous congenital osteomyelitis (left). Direct blood transfusion to a newborn performed using a special roller-pump device (right).
A newborn female with an ulcerating cavernous hemangioma of the right shoulder and shoulder girdle (left). The same patient one year after a course of short-focus radiotherapy (right).
A newborn with a lymphangioma of the neck (left). The same patient 6 months after Surgical treatment (right).
In some children, skin necrosis does not reach threatening proportions; after the sloughing of the dead skin, wounds 2 — 5 cm in diameter are formed. The disease enters the repair period. Small wounds gradually fill with granulations, epithelialization begins at the edges, leading to the closure of the wound, and the child recovers.
Extensive wound defects left to heal on their own epithelialize over a long period (up to 5 months) and leave cosmetically unfavorable and even disfiguring scars.
Complications are divided into: a) general (pneumonia, parenteral dyspepsia, otitis, etc.); b) hematogenous purulent metastases (abscessing pneumonia, meningitis, multiple abscesses, etc.); c) local ones developing per continuitatem (osteomyelitis, purulent Pleurisy, purulent pericarditis, etc.).
Complications of the first two groups occur in neonatal phlegmon, as in any purulent-inflammatory disease, and do not depend on the localization of the local process. Local complications are a consequence of the progression of the local process and depend on the localization and spread of the lesion. The most severe complications of this group occur when the process is localized in the chest area. With further progression of the process, purulent pleurisy, pneumonia, and, as a final stage, purulent pericarditis develop. These complications lead to a fatal outcome.
Differential Diagnosis. Phlegmon of the newborn must be differentiated from several conditions with similar clinical manifestations. These include lymphadenitis, erysipelas, mastitis of the newborn, acute Hematogenous osteomyelitis, peritonitis, and subcutaneous fat necrosis of the newborn. The greatest diagnostic challenges arise with erysipelas (S. D. Ternovsky, 1959), rib osteomyelitis, and subcutaneous fat necrosis.
Erysipelas begins acutely with a temperature rise to 38 — 39°. The area of skin hyperemia rapidly expands, the lesion borders are well-defined, and palpation is painful. Erysipelas most commonly affects infants older than one month, with the process localizing around the portals of entry, which may include abrasions, the umbilical wound, broken skin, or the genitalia, especially with inadequate infant care. In erysipelas, skin hyperemia is brighter, shiny, and lacquered; the hyperemic area presents in Tongue-like shapes (the so-called geographic delineation of borders). Small vesicles sometimes appear against the background of the hyperemia. Edema, redness, and tenderness resolve from the center toward the periphery (G. Fanconi, A. Wallgren, 1960). The edema creates a slight elevation of the lesion above healthy skin, which can be detected by running a finger from healthy skin onto the lesion.
Unlike erysipelas, newborn phlegmon typically occurs in infants during their first month of life. The infectious focus is characterized by dense infiltration. Regression of the lesion begins at the periphery.
Major diagnostic difficulties arise in cases of osteomyelitis of the rib. The clinical picture resembles newborn phlegmon. Even in a hospital Setting, the correct diagnosis is not made immediately, and is sometimes established only during the course of observation.
Subcutaneous fat necrosis — a condition affecting infants in their first days and weeks of life. It is observed primarily in large-birth-weight infants (S. G. Zvyagintseva et al., 1963). Many authors consider the etiological factor to be mechanical birth trauma, asphyxia, or resuscitation procedures for newborns (Anbari, 1961; Marks, Beasch, 1962, etc.). The local process is characterized by the appearance of firm nodules in the skin and subcutaneous adipose tissue during the infant's first days of life. Just as in newborn phlegmon, the palms and soles are not affected. Small indurations (ranging from 0.2 to 3 — 5 cm in diameter) gradually merge into larger lesions that sometimes involve the entire back or buttocks. The skin is hyperemic, warm to the touch, and tender upon palpation. In rare cases, areas of fluctuation appear (Bernard, 1957). During this period, the lesion resembles newborn phlegmon. Subcutaneous fat necrosis resolves spontaneously within 3 — 5 months and requires no special treatment. The prognosis is favorable. The patient's general condition, as a rule, is not compromised. Taking the history into account helps establish the correct diagnosis. In unclear cases, observation aids in proper diagnosis.
Treatment. Patients with newborn phlegmon require emergency surgical care.
In the acute stage of the disease, the inflammatory infiltrate is infiltrated with a 0.25% novocaine solution from multiple points, following the technique of A. V. Vishnevsky's short novocaine block. It is not recommended to inject novocaine beneath the affected area, as this increases skin Separation. Immediately after the novocaine block, multiple staggered skin incisions are made across the entire lesion and into healthy skin, 0.5 — 1 cm away from the affected zone. The incision length is 1.5 cm. The incisions must penetrate into the subcutaneous tissue (Fig. 114). Small incisions relieve tissue tension and create conditions for the outflow of pus and necrotic tissue. Incisions in the adjacent healthy skin prevent the spread of the process. A dressing with a hypertonic solution (25% magnesium sulfate solution, 10% sodium chloride solution) is applied over the entire surface of the phlegmon. To detect the spread of the lesion in a timely manner and make additional incisions, dressings are changed every 4 — 6 hours for the first 2 — 3 days.
Fig. 114. Principle of skin incisions in newborn phlegmon (after S. Ya. Doletsky).
Since the inflammatory process extends beyond the visually apparent skin zone, incisions (b) should be made not only within the visible lesion area (a), but also at a distance from it. Active perifocal drainage prevents the spread of inflammation (c).
To improve the drainage of pus during dressing changes, wound edges are separated and washed through a microirrigator with a furacilin solution or isotonic sodium chloride solution containing antibiotics. From the 2nd–3rd day, general baths are used to facilitate the removal of necrotic tissues. Physiotherapy is applied on the 1st–2nd day after the patient's admission. It begins with ultraviolet irradiation in an erythema dose. Simultaneously, a UHF electric field is applied to the affected area to promote the resorption of the infiltrate (K. E. Dikaya et al., 1972).
Treatment of the local lesion in the subacute stage involves its sanitation and plastic closure of wound defects. Necrotomy is performed as soon as demarcation forms. After removing the dead skin and tissue, the edges of the resulting wound are approximated with adhesive tape or managed under ointment dressings, which leads to granulation and wound healing. Achieving the closure of extensive wounds is extremely difficult. Granulation can be successfully induced by applying biological stimulating dressings (fibrin film, preserved placenta Applications, preserved fetal homograft). Temporary wound closure with biological material accelerates the patient's recovery from a critical state and helps prepare the wound surface for subsequent autoplasty. Various skin grafting techniques are used for complete wound closure. Autograft fixation can be performed using fibrin film or homograft (F. I. Kainov, G. A. Ostromoukhova, 1972).
Antibacterial therapy, detoxifying and stimulating treatment, as well as rational feeding are essential prerequisites for treating these patients.
The weight curve serves as an indicator of effective treatment. Criteria for recovery include a sustained improvement in the child's general condition, weight gain, absence of inflammatory signs in the affected area, and normal temperature.
The prognosis for newborn phlegmon is serious. The outcome depends on timely diagnosis and hospitalization, along with early, rational, and comprehensive therapy.
Prior to the introduction of antibiotics, mortality from newborn phlegmon reached 70% (O. S. Bokastova, 1939); the use of antibiotics reduced mortality to 16.6% (F. I. Zheleznyakova, 1950). In recent years, with the introduction of comprehensive therapy for this neonatal condition, mortality has decreased to 6 — 7% (F. I. Kainov, G. A. Ostromoukhova, 1972).
The majority of children who have undergone newborn phlegmon grow and develop in accordance with their age. Some children experience recurrent purulent-inflammatory diseases. In rare cases, long-term follow-up reveals delayed physical development. Cosmetic Outcomes of surgical intervention are good in 89% of cases, though gross deforming scars are possible in cases of extensive skin necrosis (N. P. Karpenko, 1960).
Purulent-inflammatory diseases of the thoracic organs
Abscessing pneumonias in newborns are primarily caused by pathogenic staphylococci or their associations with diverse microflora. The most dangerous combination is staphylococcus with *E. coli*, *Proteus*, and especially *Bacillus pyocyaneus*. Among purulent-inflammatory diseases in newborns, pneumonias rank among the highest in terms of clinical severity and mortality rates, which reach 46 — 64% (N. L. Kushch et al., 1970; Bechamps et al., 1970). Lung involvement may be primary in nature. Bacterial infection in these cases is usually superimposed on a viral one, which explains the high frequency of abscessing pneumonias during outbreaks of respiratory VIRAL INFECTIONS AND Influenza pandemics. At the same time, secondary pulmonary lesions occur more frequently in newborns than in older age groups, when pneumonia is a manifestation of septicopyemia caused by umbilical sepsis, pyoderma, purulent otitis, newborn phlegmon, or acute hematogenous osteomyelitis. Prematurity, birth trauma, hypotrophy, neonatal Atelectasis, and diathesis contribute to the development of staphylococcal pneumonias by creating an unfavorable premorbid background.
Based on the clinical course, intrapulmonary and pleuropulmonary forms of abscessing pneumonia are distinguished (V. F. Baklanova, 1973). The former is characterized by the formation of inflammatory infiltrates and abscesses in the lung parenchyma, while the latter involves the development of pleural complications.
Lung abscesses
In newborns, small, subpleurally located microabscesses occur more frequently, which can merge into a single giant cortical abscess. Along with this, patients may present with large, clearly visible on radiographs "macroabscesses" within the thickness of the lung parenchyma.
The clinical picture of abscessing pneumonia in newborns is characterized by pronounced symptoms of toxicosis and respiratory failure. Dry skin, cyanosis of the nasolabial triangle and mucous membranes, acrocyanosis, and severe dyspnea with nasal flaring are observed. A wet cough and nasal congestion appear early. Heart failure develops rapidly, manifested by muffled heart sounds, tachycardia, enlargement of cardiac borders, and hepatomegaly. Pneumonia is typically accompanied by Digestive System dysfunction, intestinal paresis, abdominal distension, and vomiting. Some patients develop seizures resulting from central nervous system hypoxia.
In certain cases, severe hyperthermic syndrome develops. Hyperthermia increases fluid loss, accelerates the body's energy expenditure, and exacerbates hypoxia and Metabolic Disorders. Hyperthermic syndrome is particularly dangerous due to adrenal exhaustion and acute adrenal insufficiency. The onset of the latter frequently leads to sudden fatal outcomes. Along with fever, a number of newborns present with cases of severe pneumonia accompanied by normal or subfebrile temperatures. The absence of a febrile response is characteristic of premature infants and is a manifestation of organism areactivity.
Identifying physical symptoms in the Cytology/cytology/16.html">Early stages of pneumonia in newborns requires clinical expertise. Auscultation reveals weakened breath sounds in the affected lung, which may become harsh or occasionally bronchial in character. Rales, predominantly dry, are heard across the entire lung surface, reaching peak intensity in the ROOT zones. The Percussion note acquires a tympanitic or box-like quality. When one lung is affected, a lag of the corresponding hemithorax is observed. After 1 to 2 days, the clinical picture changes. An area of dullness to percussion appears, over which breath sounds take on a bronchial quality accompanied by moist, sometimes crepitant rales. Later, signs of a cavity emerge: localized tympany or an area of dullness surrounded by a zone of tympanitic Resonance. Breath sounds in this area are bronchial or amphoric, accompanied by moist rales of varying caliber.
Laboratory Diagnostics. Peripheral blood analysis in the majority of infants shows moderate leukocytosis and relative lymphopenia. Marked shifts in the leukocyte formula are generally uncharacteristic of newborns. Nevertheless, some infants exhibit hyperleukocytosis and a sharp shift of the hemogram toward immature forms, up to myelocytes, along with plasma cells and pronounced toxic granularity of leukocytes. In protracted cases, anemia progressively worsens.
Changes in total serum protein levels and protein fractions are highly characteristic. In the vast majority of patients, against a background of relatively stable total protein levels, a significant decrease in the albumin fraction is detected—on average by 33% compared to normal values. Alongside marked hypoalbuminemia, the levels of $\alpha_1$- and $\alpha_2$-globulins are elevated, indicating an acute inflammatory process. The content of $\beta$- and $\gamma$-globulins changes very little relative to normal values for newborns. As a result of the reduction in albumin, which possesses the highest hydrophilicity, the colloid-Osmotic Pressure of the blood drops significantly (by an average of 22%). This facilitates the leakage of plasma fluid beyond the vascular bed and contributes to the development of hypovolemia.
Analysis of partial oxygen pressure (pO2), blood oxygen saturation (HbO2), and arterial blood oxygen content (CaO2) reveals marked hypoxemia in most patients. Partial oxygen pressure and arterial blood oxygen saturation are most severely affected (averaging 62.5 ± 4.3 mm Hg and 82.46 ± 5.4%, respectively). The oxygen-carrying capacity of the blood remains high in a number of patients, which is regarded as a compensatory mechanism of the body in response to hypoxia.
Analysis of acid-base balance reveals that the majority of children exhibit pronounced metabolic or mixed acidosis. In the latter case, alongside a depleted alkaline reserve, There is a substantial increase in the partial pressure of carbon dioxide, indicating impaired pulmonary respiratory function and significant metabolic disturbances. In milder cases, a shift in acid-base balance toward alkalosis is observed. This alkalosis is respiratory in nature and associated with carbon dioxide loss resulting from severe tachypnea.
Laboratory diagnostics is of paramount importance in newborns, as it provides objective data on internal environment disorders and enables targeted correction.
Radiological findings. The diagnosis of staphylococcal necrotizing (abscessing) pneumonia is based primarily on radiological findings. Early signs of the disease include areas of pulmonary tissue compaction and infiltration that span 1 to 2 segments and have fairly well-defined borders. Infiltrative foci may appear in various PARTS OF THE lung and tend to coalesce within a lobe. Subsequently, against the background of lung tissue consolidation, a rounded radiolucent area may appear with clear contours and a moderately pronounced perifocal reaction (Fig. 115, a). Most radiologists interpret these formations as emphysematous bullae resulting from check-valve inflation of microabscesses or areas of alveolar
tissue. Stretching due to the elastic recoil of the surrounding lung tissue is also a possibility (S. I. Borisov, 1934; V. F. Baklanova, 1967, 1973; Potts, Biker, 1950; Caffey, 1956). Bullous cavities can be multiple. They usually appear during the resolution phase of infiltrates. Frequently, they remain dry throughout the entire course of the disease and have almost no impact on the patients' general condition.
Fig. 115. Chest radiograph.
a — a 2-month-old infant, diagnosis: bilateral abscessing pneumonia. Emphysematous bullae are visible in the right lung at the site of a resolving infiltrate; inflammatory infiltration of the lung tissue is seen in the left lung; b — the same infant 3 days later. A cavity with a fluid level (“macroabscess”) has formed at the site of the infiltrate in the left lung, and the bullae on the right have merged.
Along with bullous cavities, abscessing pneumonia in newborns can give rise to necrotic cavities, which radiologically show coarser and wider contours, are surrounded by a zone of perifocal inflammation, and contain fluid (Fig. 115, b). Their Pathogenesis remains controversial. According to V. F. Baklanova (1961) and S. Ya. Doletsky et al. (1969), these cavities are infected bullae filled with purulent exudate. G. A. Bairov (1969), E. A. Stepanov, and V. I. Geraskin (1971, 1972) consider them to be “macroabscesses” resulting from necrosis and breakdown of lung tissue. The appearance of necrotic cavities/abscesses significantly worsens the course of pneumonia and necessitates intensive, targeted treatment.
Treatment. Comprehensive management of abscessing pneumonia includes antibiotic therapy, correction of homeostasis disorders, immunotherapy, and sanitization of the infection focus.
Semisynthetic penicillins (oxacillin, methicillin, cloxacillin) combined with broad-spectrum agents—ampicillin (pentrixyl), ceporin—occupy a leading place in the treatment of staphylococcal pneumonia in newborns. The advantage of these antibiotics is their relatively low toxicity and the resulting ability to achieve high concentrations in the blood and the lesion site. Tetracycline antibiotics (glycyclin, morphocycline, reverin) combined with oleandomycin or erythromycin, as well as ready-made combination drugs (sigmamycin, tetraolean, oleandomycin-tetracycline, oleomorphocycline), are also effective. Most of these antibiotics can be administered intravenously, which is critical for establishing high blood concentrations. For continuous intermittent infusions in newborns, percutaneous catheterization of the subclavian vein is advisable (O. A. Timoshchenko, V. M. Balagan, 1969). Penicillin retains its significance, though its dosages have changed. Recently, for the treatment of severe pneumonia, it has been prescribed at a dose of at least 200,000 to 400,000 IU per kg of body weight per day. When staphylococci are combined with *Pseudomonas aeruginosa*, garamycin (gentamicin) proves effective; however, like other aminoglycosides, it must be used with extreme caution and in strict accordance with age-appropriate dosages.
Sulfonamides are used concurrently with antibiotics. Prolonged-action agents have proven effective: madribon, sulfapyridazine, sulfadimethoxine, poteseptil. Massive antibiotic therapy requires protection against dysbiosis. To this end, infants are prescribed levorin, nystatin, and the intestinal eubiotic mexase (mexaform). The use of acidic milk formulas, kefir, lactobacillus, and bifidumbacterin is recommended. B-group vitamins and ascorbic acid are administered parenterally.
Staphylococcal cavities—bullae—generally do not require special treatment. Their appearance does not complicate the course of pneumonia, and they disappear spontaneously within a few weeks or months. Rare exceptions include cases of check-valve enlargement of bullous cavities. The resulting picture of intrapulmonary tension requires immediate surgical intervention.
Necrotic cavities and lung abscesses require drainage. The simplest method—puncture—can lead to severe complications, such as rupture of the cavity wall and the development of pyopneumothorax. These circumstances dictate that treatment should begin with attempts at bronchial drainage of the cavity. Antibiotic and enzyme inhalations, postural drainage, and bronchoscopy with intrabronchial drug administration are employed. If ineffective, puncture treatment is initiated. After aspirating the Contents of the purulent cavity, it is rinsed with antiseptic solutions and enzymes, followed by antibiotic administration.
When conservative treatment fails, Yu. F. Isakov, E. A. Stepanov, and V. I. Geraskin (1969) recommend that newborns more frequently undergo radical surgery—thoracotomy and resection of the affected lung segments.
Purulent Pleurisy
Involvement of the pleural cavity in the purulent process marks the transition of the disease into a qualitatively different phase—purulent pleurisy, or Pleural Empyema.
Clinical picture. In newborns, total involvement of the pleural cavity is more common; a tendency toward encapsulation is uncharacteristic. Pleural complications develop early: in almost half of the patients, within the first 5 days of disease onset. An early sign of pleurisy is clinical deterioration, increased toxicosis, and worsening respiratory failure. The infant becomes restless and stops nursing. Abdominal distension and intestinal paresis progress. The latter can cause diagnostic errors, wherein severe abscessing pneumonia is mistaken for intestinal obstruction.
Percussion reveals dullness, which is more pronounced along the posterior surface of the lung. As fluid accumulates in the pleural space, mediastinal shift increases. In newborns, the Mediastinum is weakly fixed and shifts even with the accumulation of the first 50 to 75 cm3 of fluid. Breath sounds over the affected lung are weakened. Rales may be absent. Classical symptoms of pleurisy (Damoiseau's line, Ellis-Damoiseau sign, Grocco's triangle, etc.) are virtually undetectable in newborns. The diagnosis is confirmed following pleural puncture.
Radiological findings. In the early stages of purulent pleurisy, the effusion forms a mantle-like layer enveloping the lung. Radiography in these cases reveals decreased pneumatization of the lung field on the affected side and the appearance of a pericostal shadow band (V. F. Baklanova, 1973). Sometimes the lung appears veiled. As pleurisy progresses, the density of the opacity increases, merging with the shadow of the chest wall and Diaphragm (the liver, in right-sided localization). Widening of the intercostal spaces and a low-standing diaphragmatic dome are observed on the affected side. In some patients, conversely, the affected hemithorax appears smaller due to early-onset spinal curvature toward the diseased side.
Fig. 116. Chest radiograph of a 22-day-old infant. Diagnosis: right-sided purulent pleurisy.
Treatment. Diagnostic puncture of the pleural cavity also serves as a therapeutic measure. In serous effusion, puncture treatment is continued: the contents are aspirated each time, the pleural cavity is washed with antiseptics, and antibiotics are administered.
If pleurisy progresses and the effusion is purulent, pleural drainage is performed. The best outcomes in purulent pleurisy in newborns have been achieved with active aspiration combined with continuous pleural irrigation.
Pyopneumothorax
Pyopneumothorax—the most frequent and formidable complication of necrotizing pneumonia—occurs when an abscess or necrotic bulla ruptures into the pleural cavity, forming a bronchopleural fistula.
Clinical presentation. The development of pyopneumothorax is typically marked by a sudden and sharp deterioration in the patient's condition. Cyanosis increases, accompanied by severe dyspnea and a grunting, moaning respiration. A particularly critical picture emerges in valve (tension) pyopneumothorax. Respiratory failure is compounded by cardiovascular failure resulting from marked mediastinal shift and kinking of the large vessels. More severe symptoms accompany the Displacement of the heart to the right due to compression of the venae cavae and impaired blood inflow to the right Chambers of the heart (Swan, Aragon, 1954).
Physical examination reveals a combination of tympanitic percussion note and dullness in the lower parts of the chest cage. The Heart borders are shifted to the opposite side. Breath sounds are barely audible on the affected side. Heart sounds are muffled and rapid. The pulse is shallow and thready.
Radiological findings. A sudden deterioration in the child's condition necessitates an urgent chest X-ray. In pyopneumothorax, radiolucency of one hemithorax is observed, along with a fluid level that may reach the II — III rib. In most cases, the shadow of the collapsed lung, compressed against the mediastinum, can be clearly identified. The mediastinal shadow is shifted toward the contralateral lung. The intercostal spaces on the affected side are widened, and the diaphragmatic dome is positioned lower than usual (Fig. 117).
Fig. 117. Chest radiograph of a 15-day-old infant. Diagnosis: left-sided tension pneumothorax.
Treatment. Treating pyopneumothorax in newborns is a complex challenge. The presence of a bronchopleural fistula requires emergency drainage of the pleural cavity. When the area of destruction is small and negative pressure can be established in the pleural space, lung re-expansion and fistula closure can be expected. With a wide fistula or multiple lung defects, drainage rarely leads to recovery. The delicacy of neonatal tissues causes rapid necrosis around the drainage site, leading to chest wall phlegmon, rib osteomyelitis, and progression of the septic process. Consequently, radical surgery must be resorted to more frequently in newborns. Pleuroscopy, performed prior to pleural cavity drainage, helps determine the extent of the lesion and the volume of destruction.
Radical surgery for pyopneumothorax in neonates carries a high degree of risk, requiring excellent anesthesia and meticulous surgical technique. It consists of three stages: thoracotomy and pneumolysis, lung decortication, and resection of the destruction zone. The Specific features of surgical intervention in newborns are dictated by the fragility of their tissues and reduced resistance to infection, which necessitate gentle handling; limitation of segmental and atypical resections due to the risk of bronchopleural fistula recurrence; high sensitivity to blood loss; and the difficulty of manipulating the lungs through a narrow access and a limited operating field.
The most challenging phase of treatment for newborns who have undergone pulmonary surgery is the postoperative period. Patients in this age group experience rapid respiratory depression, with a high propensity for developing atelectasis, areas of hypoventilation, and pneumonia. Therefore, During the first 6 — 8 days post-surgery, the infant requires intensive monitoring in a postoperative ward or intensive care unit.
Long-term outcomes. The Study of long-term outcomes of necrotizing pneumonia treatment in newborns over a period ranging from 6 months to 11 years confirms the high reparative capacity of lung tissue (V. F. Baklanova, 1970). According to clinical data, good treatment results were obtained in 89.4% of patients. The children develop well and have no Complaints. Physical and radiological examinations reveal no pulmonary pathology. Satisfactory results were noted in 7.1% of patients. These patients complain of periodic recurrences of respiratory infections and recurrent pneumonia. During exacerbations, they develop a wet cough, rales, and fever. Bronchography reveals moderate bronchial deformation in the form of localized deforming Bronchitis. Such patients require ongoing dispensary observation and periodic courses of tracheobronchial hygiene.
Treatment results were considered unsatisfactory in one child who suffered from the intrapulmonary form of necrotizing pneumonia. Bronchography revealed saccular Bronchiectasis and focal pneumosclerosis, which necessitated a lower lobectomy of the lung at the age of 2 1/2 years.
The results of surgical treatment for purulent pulmonary lesions in newborns are favorable. A major role in increasing the volume and restoring the normal Structure of lung tissue after partial lung resections in children of this age is played by postnatal lung development during the first years of life (V. I. Puzik, 1953; Engel, 1947). The remaining lung tissue increases in size due to the generation of new Bronchi and alveoli, acquiring a normal structure and becoming fully functional.
Purulent-inflammatory diseases of the Abdominal cavity organs
Purulent-inflammatory diseases of the abdominal organs in newborns generally follow a very severe course, resulting in a high rate of complications and unfavorable outcomes.
Purulent peritonitis
In the majority of patients, purulent peritonitis develops secondarily as a complication of sepsis, resulting from the spread of the inflammatory process from the anterior abdominal wall or adjacent organs, or from perforation of abdominal organs. INTRAUTERINE DEVELOPMENT OF peritonitis is also possible when the infection spreads via the placenta.
ETIOLOGY AND PATHOGENESIS. The multi-etiological nature of neonatal peritonitis accounts for The Diversity of microflora cultured from the abdominal cavity of such patients. According to our data, the most frequent causative agents of peritonitis are staphylococcus and Escherichia coli.
The causes of intestinal perforation in newborns are diverse and can be congenital or acquired. Most frequently, perforation of the intestinal wall is caused by a developmental defect of its muscular layer (I. A. Bobrik, 1965), impaired trophic supply to the bowel wall due to mechanical compression in patients with meconium ileus or intestinal atresia (M. D. Grashchenko, 1963; Birtsch et al., 1967), ulcerative-necrotic processes in the bowel wall during septic enterocolitis (I. I. Mironchik, 1964; Erick, 1966), or trophic impairment of the intestinal wall in sepsis, generalized forms of Toxoplasmosis, cytomegalia, organic central nervous system lesions, etc. Rare causes of neonatal bowel perforation include exchange blood transfusion (Caralps-Riera, Colin, 1970). The first two groups of causes are classified as congenital, while the subsequent ones are acquired.
Intestinal perforations of congenital origin most often occur intrauterinely or within the first days and weeks of the child's life. The pathogenesis of perforation depends on the nature of the underlying cause. When the muscular layer of the intestine is underdeveloped, even a slight increase in intra-abdominal pressure (trunk compression during delivery, crying, straining) is sufficient. Perforation of the intestinal wall in patients with ulcerative-necrotic enterocolitis is mainly due to the predominance of the necrotic process over the inflammatory one, which is one of the main Features of purulent-inflammatory diseases in newborns and infants. As a result, the muscular and serous layers are rapidly destroyed at the site of a small erosion, leading to bowel perforation.
Clinical presentation. In the Initial Stages of the disease, clinical manifestations of the underlying condition that caused the peritonitis come to the fore (umbilical sepsis, perforation of an atretic bowel, etc.). The infant's condition is severe; the child is lethargic, pale, and dehydrated. Most patients have an elevated temperature. Vomiting appears early. Stool may be delayed at the onset of the disease and subsequently becomes loose and frequent. Respiratory disorders are also noted.
Among local symptoms, marked abdominal distension due to intestinal paresis is characteristic. In cases of obstruction, dilated, sluggishly peristalsing intestinal loops are often visible. Subcutaneous VEINS OF THE anterior abdominal wall are dilated. Pastiness and edema of the abdominal wall are a constant and most reliable sign of peritonitis. In pronounced peritonitis, the edema extends to the genitalia. As the process progresses, hyperemia of the skin of the anterior abdominal wall develops. Peristalsis is sluggish or entirely absent. Percussion often reveals free fluid in the lateral recesses or lower parts of the abdominal cavity. Palpation detects tension in the abdominal wall muscles. Palpation is generally painful, and the infant becomes restless.
The clinical picture of intestinal perforation of congenital origin has several characteristic features. Within a few hours after birth, the infant exhibits vomiting, abdominal distension, and delayed stool. The initial portions of vomitus typically consist of gastric contents and swallowed Amniotic Fluid. This is followed by an admixture of Bile and, finally, intestinal contents. The sign of absent liver dullness cannot be considered entirely reliable. The newborn's liver is relatively large, and with a small amount of gas in the abdominal cavity, liver dullness persists. Stool in these patients is either absent or very scant, consisting of grayish mucus-meconium plugs that fill the distal parts of the intestine.
Acquired perforations resulting from ulcerative-necrotic enterocolitis typically develop in premature infants at the end of the first or the beginning of the second month of life. The case history and clinical course in such patients are usually quite characteristic. Typically, during the first 3 to 4 weeks of life, a premature infant begins to gain weight and their condition improves. Later on, due to concurrent pneumonia, purulent-inflammatory conditions, or sepsis, the infant's condition deteriorates and weight gain ceases. This period coincides with the development of sepsis and the formation of ulcerations in the intestinal mucosa. At the moment of intestinal wall perforation, the infant's condition sharply worsens, and a peculiar state of Shock develops. The infant becomes lethargic and cyanotic. Breathing is rapid and shallow. Abdominal distension progresses. The abdominal wall is stretched and pasty, with a prominent superficial venous network. Vomiting occurs. Temperature changes are atypical: some patients present with fever, others remain normothermic, or even hypothermic. In most cases, there is a tendency toward leukopenia (due to the generalized areactivity of a premature, weakened infant) and a left shift in the leukocyte differential count.
If a localized perforation is present, the clinical manifestations unfold more slowly and are less pronounced. When there is a large amount of gas in the abdominal cavity, liver dullness may be absent. Gram-positive cocci are frequently cultured from the stool of such patients (Dietel, Hartmann, 1967).
Radiological findings. The diagnosis of intestinal perforation is confirmed by a plain abdominal radiograph in the upright position, which reveals free gas in the peritoneal cavity (Fig. 118). However, as our observations have shown, this sign is not present in all patients admitted with Clinical symptoms of intestinal perforation. Frequently, in areas most affected by the ulcerative-necrotic process (the ileocecal angle, and the hepatic and splenic flexures of the colon), radiographs reveal a characteristic "honeycomb" pattern caused by small amounts of air trapped between the intestinal loops, the greater omentum, and adhesions (Fig. 119). The "honeycomb" sign is pathognomonic for walled-off, covered intestinal perforations. No free gas is detected in the abdominal cavity in such patients.
Fig. 118. Plain abdominal radiograph of a newborn. Free gas in the peritoneal cavity. Diagnosis: septic ulcerative-necrotic enterocolitis.
Fig. 119. Plain abdominal radiograph of a newborn. In the upper left quadrant of the abdomen, small air bubbles (pneumatosis) are visible against a background of soft, homogeneous shadowing—the "honeycomb sign"—an indicator of a covered intestinal perforation.
Treatment. The diagnosis of perforated peritonitis or suspected perforation is an absolute indication for transferring the infant to a surgical hospital and initiating intensive care. When choosing among various treatment modalities, the authors unanimously favor surgery and consider intestinal perforation an absolute indication for operative intervention.
Surgical technique. Following appropriate preparation, the infant undergoes laparotomy. To prevent intestinal Evisceration, we believe that laparotomy in such patients should be performed exclusively through a supraumbilical cruciate incision with transverse division of the skin and subcutaneous tissue (see the section "Specifics of Surgical Technique"). Upon opening the abdominal cavity, a thorough exploration of the intestines is carried out. Special attention is paid to the most common sites of perforation (the terminal ileum, ileocecal angle, cecum, ascending, transverse, descending, and sigmoid colon). Perforated ulcers, which may number a dozen or more, are closed with a double-layer intestinal suture using atraumatic needles. Pre-perforational ulcers appear as white dots shining through the serosa and must also be meticulously sutured.
If the perforation is caused by a developmental anomaly in specific areas of the muscular layer of the Large Intestine, the abnormal segments are closed with sero-serous sutures. In cases of necrosis involving large sections of the intestinal wall that cannot be sutured, the operation concludes with resection of the affected segment, followed by Mikulicz enterostomy or the creation of a Y-shaped anastomosis. Patients with intestinal atresia or meconium ileus are operated on according to standard general principles. After eliminating the perforation sites, the abdominal cavity is thoroughly lavaged with antibiotic solutions. The abdominal wall is closed tightly in layers, leaving a micro-irrigator in place for subsequent antibiotic administration. Utilizing a transverse approach without cutting the rectus abdominis muscles has minimized the risk of postoperative intestinal evisceration.
The management of perforated peritonitis is one of the most challenging areas in neonatal surgery. Outcomes to this day remain unsatisfactory. Most authors (G. A. Bairov, 1963; V. M. Derzhavin, 1963; Dietel, Hartmann, 1967, et al.) report only isolated cases of recovery. It is only in recent years that treatment results for patients with perforated peritonitis have improved somewhat (Stevenson et al., 1971). We have successfully treated 9 out of 55 children operated on for perforated peritonitis. Due to the high mortality rate, in recent years we have reconsidered the management principles for patients with covered intestinal perforations in favor of conservative treatment.
Once a covered perforation is diagnosed, the infant is placed in an incubator and closely monitored. Intravenous drip infusions of glucose, electrolytes, blood, and plasma are prescribed in doses determined by the infant's weight and condition. Broad-spectrum intravenous antibiotics are preferred. According to our data, the administration of sigmamycin (25 mg per kg of body weight per day) is effective. Oxygen is prescribed, along with cardiac medications and analeptics as indicated. With this strategy, the subsequent course of the disease may follow one of two paths. In cases where other ulcers perforate or a covered perforation transforms into an open one, the infant's condition sharply deteriorates, and free gas appears on control abdominal radiographs, serving as an absolute indication for surgery. Under these circumstances, the preceding conservative therapy is regarded as preoperative preparation.
In other patients, repeat perforation does not occur, and their condition gradually improves under conservative management. In 6 of the 14 patients treated conservatively, an infiltrate formed at the site of the covered perforation, which subsequently underwent central abscess formation. Upon the appearance of a fluctuation center, a skin incision is made to drain the abscess, from whose cavity feces and pus typically discharge. The intestinal fistula at this site closed spontaneously in all our observed patients within 3 weeks to 6 months. In one patient, recovery occurred without the formation of a fistula.
Late complications of ulcerative-necrotic enterocolitis may include intestinal strictures, the formation of cystic cavities within the intestinal wall, and internal entero-enteric fistulas (Lloyd, Cywes, 1973).
Appendicitis
Appendicitis in newborns is rare. Prior to 1970, Fornara found descriptions of only 20 cases of neonatal appendicitis in the world literature. Most authors describe isolated observations (A. G. Bogina, 1958; A. A. Pershava, 1960; I. Yu. Ibadov, V. P. Ilyinov, 1969; Calvani, 1961; Pilotti et al., 1972). We have observed and successfully operated on 2 newborns with acute appendicitis.
The local process is characterized by a rapid clinical course and swift necrosis of the Appendix. The necrotic process quickly spreads through all its layers, leading to perforation and the development of peritonitis.
The clinical picture is indistinct. The deterioration of the infant's general condition comes to the forefront. The baby refuses to feed, becomes restless, and draws up their legs. Vomiting and dyspeptic symptoms quickly join the picture. Elevated temperature and leukocytosis are characteristic. Among local signs, in most patients, symptoms of peritonitis demand immediate attention. The abdomen is distended, and there is frequently edema and hyperemia of the anterior abdominal wall. Palpation reveals marked tenderness, predominantly in the right half of the abdomen, along with guarding of the anterior abdominal wall muscles. As the process progresses, signs of generalized peritonitis dominate the clinical picture, which in most such patients serves as the indication for surgical intervention.
Differential diagnosis is performed with other inflammatory abdominal conditions. The absence of distinct local signs creates significant diagnostic difficulties, making a preoperative diagnosis of acute appendicitis in a newborn practically impossible in many cases.
Treatment is surgical. When the clinical picture is distinct, the abdominal cavity is opened via an incision along the skin crease in the right iliac fossa. In doubtful cases, laparotomy via a pararectal or transverse approach is indicated. Exploration of the abdominal organs is performed. Appendectomy is carried out using the ligation technique without prior crushing of the Base of the appendix.
Purulent-inflammatory diseases of the Urogenital System
Purulent-inflammatory diseases of the urogenital organs are frequent in newborns and can cause severe renal damage. The inflammatory process may be localized to the external genitalia and spread to the Urinary Tract and kidneys.
Balanoposthitis
Balanoposthitis refers to the combined inflammation of the prepuce ( foreskin) and the glans Penis.
Etiology and pathogenesis. Predisposing factors for the development of balanoposthitis in newborns include: physiological phimosis, a long foreskin, attempts at prepuce retraction, and inadequate hygiene, which predisposes the perineal skin to dermatitis. The accumulation of urine and smegma residues in the preputial sac, followed by secondary infection, leads to acute inflammation of the foreskin. Compromised perineal skin easily becomes infected with pyogenic agents, and the inflammatory process spreads to the penis. Alongside bacterial infection, causative agents may also include Fungi, such as Candida albicans. Viral infections lead to the development of balanoposthitis in cases of herpes simplex localized to the glans penis. In rare cases, recurrent balanoposthitis in newborns leads to thickening and cicatricial narrowing of the foreskin (acquired phimosis).
Clinical presentation. Edema is observed around the preputial ring, making it impossible to retract the foreskin over the glans. During urination, the infant is restless, and in cases of phimosis, the prepuce balloons out. Pus discharges from the narrowed foreskin.
Treatment. For mild cases, local warm baths with potassium permanganate solution and compresses applied to the external surface of the penis are recommended. The newborn should be bathed more frequently, as urine accumulation in the preputial sac sustains the inflammation. In severe cases of the disease, the pre
puce is washed with an antibiotic solution and treated with antibiotic ointments. The procedures are performed 2 to 3 times a day until the inflammatory process subsides.
Vulvovaginitis
This condition occurs predominantly in infants, but may also manifest during the neonatal period.
Etiology and pathogenesis. The infantile vulva is covered with delicate, easily traumatized skin that is highly susceptible to infection. A high concentration of minor vestibular glands and crypts contributes to the development of the inflammatory process. In young children, the Vagina is rich in folds and recesses, lined with a delicate and thin mucous membrane (only 2 to 4 layers thick) whose cells are poor in glycogen. Döderlein bacilli are absent. The vaginal secretion reaction is alkaline or amphoteric, and its immune properties are insufficient. Maternal Sex Hormones passed to the infant protect the vaginal mucosa from infection during the first weeks of life. Nevertheless, lapses in newborn care or maternal infections (Trichomoniasis, Gonorrhea) can lead to the development of vulvovaginitis. The causative agents of primary vulvovaginitis include staphylococci, streptococci, Escherichia coli, gram-positive and gram-negative bacteria, diplococci, Friedländer's bacillus, and others.
Genital thrush is caused by the Yeast-like fungus Monilia albicans. The condition is frequently observed in pregnant women (I. I. Bogorov, 1966). Female infants become infected from infected mothers during childbirth. Additionally, fungal infections of the vulva and vagina occur in debilitated, dystrophic children following prolonged antibiotic therapy.
Occasionally, trichomonads are found in smears from the infant vagina, having been transmitted from the mother during delivery. However, the physiological characteristics and biochemical environment of the infant vagina, along with the absence of prolonged estrogenization, do not favor the proliferation of trichomonads within it.
Vulvovaginitis gonorrhoica has become rare in recent years. Gonococcal infection can occur immediately after birth, but is more commonly noted at the end of the first to the beginning of the second week due to a failure of Sanitary and hygienic rules by maternity hospital personnel or by a mother with gonorrhea. Vulvovaginitis may arise on The basis of mechanical, chemical, and thermal injuries. Starch granules from dusting powder entering the newborn's vagina, or excessively hot water (38°C), can trigger an inflammatory reaction.
Clinical presentation. The primary symptom of the disease, regardless of the etiological factor, is mucopurulent or bloody vaginal discharge. Hyperemia of the vulva and edema of the labia complete the clinical picture. Itching and pain cause infant restlessness. Involvement of the distal Urethra is accompanied by dysuric phenomena. The pathogen is identified through vaginal discharge culture and microscopic smear examination. Given the potential for ascending infection of the urinary tract, urine analyses must be monitored.
Differential diagnosis. Neonatal desquamative vulvovaginitis is distinguished as a physiological process that, under unfavorable conditions, facilitates the development of true inflammation. A consequence of the latter can be labial synechiae (adhesions) in newborn girls. In some girls, the normal epithelial replacement of the inner surface of the Labia minora by cutaneous epithelium fails to occur at the usual time (by 3 to 4 years of age). An accompanying superficial adhesive inflammatory process promotes the fusion of the inner labial surfaces.
Treatment. For bacterial infections, antibiotic therapy is indicated, administered either topically as genital wash solutions, orally, or parenterally, depending on the severity of the process. Thrush is treated by swabbing or instilling a 3–4% aqueous solution of methylene chloride (methylene blue) into the vagina via a catheter. Alternatively, gauze strips soaked in a 5–10% solution of borax in glycerin may be inserted into the vagina for 8–12 hours daily or every other day. If trichomonads are detected in smears, no specific treatment is administered; general hygienic measures suffice. In gonorrheal vulvovaginitis, good efficacy is achieved with parenteral penicillin. Regardless of the pathogen, genital hygiene is maintained: daily washings with boiled water and soap, and sitz baths with chamomile decoction and potassium permanganate solution. For vulvar and vaginal care, 2–5% soda solution, 2–4% boric acid solution, and 2% silver nitrate solution are used. The treatment course lasts 8–15 days. In stubborn cases, short-term administration of estrogens may be prescribed to enhance the local resistance of the vaginal mucosa. Recurrent vulvovaginitis requires prolonged treatment even after the inflammatory process subsides.
Recent studies have established that every urinary tract infection in childhood should be regarded and treated as pyelonephritis. Nonspecific bacterial inflammation rapidly spreads from the renal pelvis to the parenchyma, resulting in focal interstitial nephritis. The tubules, Blood Vessels, and glomeruli are secondarily involved in the process. Urinary tract infections most commonly arise during the neonatal period and in infants during their first year of life. The incidence of neonatal pyelonephritis is driven by the prevalence of purulent-septic diseases among this age group, the increased virulence of staphylococci, and the specific features of neonatal immunity. Infected urine is found in 1–2% of all infants (O’Doherty, 1968). A comparative evaluation of age groups indicates a higher morbidity rate among girls. During the neonatal period, the sex difference is negligible, pointing to a uniform pathway of infection spread.
Etiology and pathogenesis. Maternal illnesses during pregnancy exert a significant influence on the development of pyelonephritis. Prematurity, intracranial birth trauma, asphyxia, and Congenital Malformations reduce the newborn's resistance to infection and predispose them to the disease. Urogenital disorders (balanoposthitis, vulvovaginitis, phimosis, synechiae) facilitate the spread and development of infection. The primary causative agents are Escherichia coli, staphylococci, streptococci, and Proteus. Urine cultures frequently reveal two or more pathogens. The hematogenous route of infection spread is predominant in newborns, particularly regarding coccal flora. Enteric bacteria more frequently invade the renal pelvis from the lower urinary tract via an ascending pathway. These infection pathways may also occur in combination. Malformations of the urinary tract and focal Dysplasia of the renal parenchyma play a crucial role in the disease pathogenesis. Impaired normal urine flow drives the further progression of the infection.
Pyelonephritis in which infection affects a previously intact urinary apparatus is termed primary, non-obstructive pyelonephritis. Conversely, in secondary, obstructive pyelonephritis, the clinical picture consists of symptoms from the underlying urological disorder combined with pyelonephritis itself. Pyelonephritis in Children occurs in 45% of cases with anatomically normal kidneys, in 25% in the presence of vesicoureteral reflux, and in 30% of cases due to obstruction of various origins (Stansfeld, 1966).
Clinical presentation. Pyelonephritis in newborns presents as a severe systemic infectious process characterized by a diverse range of clinical manifestations: urinary syndrome, profound intoxication, disturbances in acid-base balance, electrolyte and Protein metabolism, and acute impairments of renal, hepatic, and urinary tract functions.
In ⅔ of children, the disease begins with a high fever. In debilitated, hypotrophic infants, it may run its course without a temperature elevation. Refusal to feed, vomiting, and sometimes diarrhea accompanied by severe exicosis lead to the initial suspicion of a gastrointestinal disorder. Newborns are often restless and cry continuously. They become sensitive to touch, and meningeal signs may appear. Against the backdrop of a high fever, a generalized convulsive seizure is possible. Local symptoms of urinary tract involvement are atypical for this age group. The diagnostic challenges of pyelonephritis are compounded when it coexists with other conditions such as pneumonia or otitis media.
The acute phase of pyelonephritis in newborns can take various courses. With adequate treatment, all symptoms resolve within 3 to 4 weeks, while pyuria and bacteriuria disappear by the 5th to 6th week. Another form is characterized by a protracted and undulating course, where the acute phase drags on for 8 to 12 weeks, and in some cases for 5 to 6 months. When conservative treatment proves ineffective, underlying urinary tract malformations can frequently be identified.
Laboratory diagnostics. A febrile state in a newborn, behavioral changes, loss of appetite, pallor, and anemia should serve as indications for urinalysis. The decisive criteria for establishing a diagnosis of pyelonephritis are leukocyturia and bacteriuria.
Collecting urine from a newborn presents well-known difficulties. The infant's genitalia are meticulously prepared, and in boys, the foreskin is retracted whenever possible. A test-tube is positioned mid-stream during urination. For girls, a plastic collection bag adhered to the perineal region is used, whereas boys are fitted with a rubber tubing over the penis. In certain cases, suprapubic puncture is employed; this is indicated when there is a need for an urgent pyelonephritis diagnosis, when difficulties arise in obtaining uncontaminated urine samples due to inflammatory perineal skin lesions, vulvovaginitis, or balanoposthitis.
Puncture technique: the needle is inserted 1.25 to 2.5 cm above the Pubic Symphysis, regardless of the timing of the previous urination. For bacteriological and microscopic examination, 1 to 2 ml of urine is sufficient. Catheterization in newborns carries the risk of introducing infection.
In clinical practice, leukocyturia is assessed by examining urine sediment, determining The Cell count per 1 mm3 of urine (A. Z. Nechiporenko, 1965; Stansfeld, Webb, 1953). A count of no more than 10 cells per 1 mm3 is considered normal. Finding 10 to 20 leukocytes is evaluated as a borderline state, while more than 20 cells is considered pathological. According to A. Z. Nechiporenko, 1 ml of normal urine contains up to 2,000 leukocytes and up to 1,000 erythrocytes. Bacteriological urine analysis is performed to identify the pathogen in order to guide targeted treatment. Quantitative bacterial enumeration is useful, with up to 1,000 cells per 1 ml of urine taken as the norm. The presence of 1,000 to 10,000 cells is viewed as a borderline finding requiring verification, whereas more than 10,000 bacteria per 1 ml is considered pathological. Blood test results and measurements of residual nitrogen and plasma creatinine levels Supplement the diagnosis of pyelonephritis and help assess renal parenchymal damage in the newborn. Renal Dysfunction significantly exacerbates the baseline mild metabolic acidosis, shifting blood pH down to 7.15. Tubular disorders and acidosis cause a drop in calcium levels; a level below 9 mg% during the first few days of life may likewise indicate renal impairment. Performing clearance tests in newborns presents significant difficulties and is unreliable.
Radiological findings. There are no pathognomonic radiological signs of acute pyelonephritis. Radiological studies help identify congenital anomalies, obstructive processes, calculi, and other abnormalities. Indications for excretory urography include relapsing pyelonephritis and persistent bacteriuria after 3 weeks of antibiotic therapy. When interpreting the radiographs, the size and contour of the Kidney within the pyelonephritic focus are evaluated, alongside any anomalies and tone disturbances of the pelvicalyceal system. In rare cases, the affected side shows poor contrast on the radiogram, and individual caliceal systems appear disconnected. Cystourethrography provides information regarding infravesical stenosis, anomalies, bladder tone abnormalities, and vesicoureteral reflux. Radioisotope imaging methods are indicated in cases of non-functioning kidneys (Winter, 1963; Sack, Mitrab, 1966).
Treatment. The primary objective is the elimination of bacterial infection. In acute cases, the duration of treatment spans several weeks, requiring close communication between inpatient and outpatient physicians. Detoxification therapy and portion-controlled Nutrition complement antibacterial therapy. The best outcomes in newborns have been achieved with ampicillin; other antibiotics are prescribed once pathogen resistance is established. Antibiotic therapy is administered for 2 to 3 weeks until urinalysis normalizes, after which patients can be transitioned to nitrofurans (5 mg/kg daily for 2 to 3 weeks), dividing the total daily dose into 3 administrations. Subsequent medical management involves 10-day courses of alternating drugs (antibiotics, nitrofurans, sulfonamides) over a period of 3 to 4 months. Urine is examined weekly. Following treatment completion, urine analyses are monitored once every 2 weeks for several months (up to a year). The average duration of treatment for the acute phase of pyelonephritis is 3 months. The prognosis is favorable with timely and correct management.
Purulent-Inflammatory diseases of Bones and joints
Hematogenous osteomyelitis — inflammation of the Bone Marrow — in newborns most frequently presents as panostitis (involving all elements of the bone in the inflammatory process). Osteomyelitis is one of the most common purulent-inflammatory conditions in neonates. It predominantly affects the long tubular bones with a meta-epiphyseal localization (G. A. Bairov, 1963; S. Ya. Doletsky, A. I. Lenyushkin, 1965; V. M. Derzhavin, 1965; Urmalis, 1967). This is facilitated by the Anatomical Features of the newborn's bones, which are characterized by a coarse-fibered reticular structure. The ground substance consists of bundles interwoven in various directions, with large bone cells situated between them. The spongy substance is loose, with wide vascular spaces. Abundant bone vascularization is a characteristic feature. Arteries are numerous and have a wide diameter. The epiphyseal ends of the bones consist primarily of cartilaginous tissue and are nourished by an independent Vascular System of an end-artery type, which creates conditions for slowed blood flow, potential fixation of pathogenic microflora, and the subsequent development of a purulent-inflammatory process.
Etiology and pathogenesis. Hematogenous osteomyelitis is in most cases the consequence of bacteremia. From purulent foci in pyoderma and furunculosis, the pathogen enters the bloodstream through the umbilical wound, damaged skin, and mucous membranes. The CAUSATIVE AGENT OF hematogenous osteomyelitis in newborns is predominantly Staphylococcus, which is cultured from pus or blood in 80 — 90% of osteomyelitis patients. In recent years, the proportion of mixed, Gram-negative flora has increased.
Widely accepted theories of pathogenesis — embolic, infectious-allergic, and reflex — explain The Mechanism of disease development to a certain extent. The specific Features of the newborn infant's organism reactivity are of great importance.
Clinical presentation. The clinical manifestations of acute hematogenous osteomyelitis consist of general and local symptoms. T. P. Krasnobaev distinguishes three forms of the disease.
Toxic, or adynamic, form of osteomyelitis. Characterized by rapid (within hours) progression of the disease. Phenomena of toxicosis and sepsis predominate. The patient's condition is extremely severe, and the temperature is high. The disease can result in the child's death on the 2nd — 3rd day. Bone changes in such patients are often discovered only upon autopsy.
Septicopyemic form. The disease runs a severe course with a significant rise in temperature. Dyspeptic symptoms are frequent. General and local signs are pronounced. In A large number of patients, metastatic purulent foci form in the bones, internal organs, and elsewhere.
Local-focal form. Local inflammatory phenomena predominate in the clinical picture. Metastasis is rarely observed. The child's general condition is significantly less affected.
Hematogenous osteomyelitis in newborns, as a rule, begins acutely and progresses rapidly. In the toxic form, the disease often starts with loss of consciousness, convulsions, and adynamia. The septicopyemic form is characterized by the parallel progression of general symptoms and local changes. The disease begins with a deterioration in the child's condition (lethe, loss of appetite), body temperature rises rapidly, and signs of toxicosis appear. Vomiting and diarrhea are frequently joined. The child presents as a severely septic patient. Facial features become sharp, the skin dries out, and the child is pale. Petechial rashes of a septic nature are common. Exicosis progresses. Toxic tachypnea and tachycardia develop. Heart sounds become muffled.
Concurrently, local manifestations increase — pain at the site of the focus, restricted mobility of the affected limb, and progression of inflammatory signs. A constant local symptom of osteomyelitis is pain, which worsens with movement. Edema rapidly increases and spreads to adjacent areas. The skin of the affected limb acquires a vitreous appearance. In the first days of the disease, most patients experience a temperature rise to 38 — 40° C, after which the fever becomes remittent. In individual patients, the temperature may be elevated only slightly or remain normal. Such cases are diagnostically challenging. Blood changes in most newborns are identical to those in other purulent-inflammatory processes — an increase in leukocytosis and a shift of the formula to the left are noted. A progressive increase in anemia is characteristic.
In the local-focal form, the patient's condition is relatively less compromised. Local tenderness, limited mobility, and Swelling of the affected area prevail.
The localization of the process in acute hematogenous osteomyelitis of newborns is characteristic. The meta-epiphyseal regions of long tubular bones — the Femur and humerus — are primarily affected (up to 85%). Lesions of other bones, particularly flat bones, are possible but rarer. Diaphyseal localization of the process in newborns is uncommon.
Osteomyelitis of the proximal femur and pelvic bones has the most severe course. The general condition of these patients is extremely grave. The limb on the affected side is motionless, flexed at the knee and hip joints. Passive movements are limited, accompanied by severe pain and distress in the infant. Edema appears late; often upon examination, it is difficult to determine the localization of the process. In some cases, there is a marked dilation of the vascular network in the upper third of the thigh and inguinal region, which can be a cause of misdiagnosis.
Metastasis of the process and the emergence of multiple foci of osteomyelitis are characteristic of newborns. Multiple osteomyelitis occurred in every third patient under our observation. In most cases, the foci appear sequentially, though simultaneous involvement of several bones is possible. The most characteristic feature of osteomyelitis in newborn infants is the rapid spread of the process to the joint with the development of Purulent Arthritis.
Radiographic presentation. X-ray Examination helps establish the diagnosis of osteomyelitis in a newborn as early as the 3rd — 4th day of the disease. The earliest radiographic sign of neonatal osteomyelitis, detectable by the 3rd — 4th day, is widening of the joint space. Identification of this symptom is possible only through radiographs of symmetrical joints under identical positioning conditions. Foci of bone destruction and periosteal reaction appear on the 6th — 10th day of the disease, depending on the localization of the process (Fig. 120). These signs are defined more clearly with electro-roentgenography.
Fig. 120. Radiographs of a newborn's joints. Symptom of joint space widening in the right hip joint (a). Lesion of the right femoral HEAD (b). Destruction focus in the area of the proximal meta-epiphysis of the right humerus (c). Diagnosis: acute osteomyelitis.
Differential diagnosis is carried out with diseases that present similar local manifestations and general symptomatology. The former include neonatal phlegmon, intermuscular phlegmon, lymphadenitis, bone fractures, paresis, and birth paralysis of the limbs; the latter include sepsis and pneumonia.
In neonatal phlegmon, there is a sharp inflammatory reaction with secondary painful contracture and restricted limb mobility. Phlegmon is characterized by the rapid spread of the inflammatory process around the periphery of the focus. Passive Movements of the limb in the affected area are possible. The joint space widening sign is absent. Intermuscular phlegmon is accompanied by severe pain, painful contracture, and limb edema. However, in these cases as well, passive movements in the limb are possible, foci of softening are detected faster than in osteomyelitis, and the joint space widening sign is absent. In doubtful cases, puncture of the lesion focus is indicated. In bone fractures, the general reaction is significantly less pronounced, and limb deformity is frequently observed. The diagnosis is clarified by radiography. Paresis and paralysis are characterized by the absence of an inflammatory process.
The treatment of hematogenous osteomyelitis is conducted according to the general rules for treating purulent-inflammatory diseases in newborns.
Surgical methods of intervention on the focus in neonatal osteomyelitis have their own specifics. The predominant involvement of the meta-epiphyseal regions of long tubular bones, with rapid breakthrough of the abscess into the cavity of the adjacent joint, makes puncture treatment the method of choice. In this approach, it is not the lesion site that is punctured, but the joint. During the puncture, pus is aspirated, and the joint cavity is washed with antibiotic solutions. The inner diameter of the needle must be at least 1 mm to prevent the needle from clogging with thick pus. Puncture and sanitation of the joint cavity are performed daily until the inflammatory process subsides.
The shoulder joint is punctured along the posterior surface directly below the acromion process. THE POSITION OF the needle is controlled by periodically pulling back the plunger. When the needle enters the joint, pus appears in the syringe. The elbow joint is punctured in a flexed position between the lateral epicondyle and the olecranon above the head of the radius. When puncturing the hip joint, the needle is inserted above the apex of the greater trochanter and advanced strictly in the frontal plane. Puncture of the joint from the anterior approach is also possible. The knee joint is punctured according to general rules.
Arthrotomy is resorted to extremely rarely — in cases of extensive lesions of the bones constituting the joint and when puncture treatment proves ineffective. If a subperiosteal phlegmon forms, it is opened and drained with strips of surgical rubber. Osteoperforation is generally not used in the treatment of neonatal osteomyelitis. Wide Haversian canals facilitate the free outflow of pus.
Simultaneous immobilization of the affected limb is mandatory. It ensures complete rest for the extremity and prevents the development of subsequent deformities, dislocations, and subluxations. The upper limb is immobilized using Desault-type bandages. For lower limb fixation in the acute stage of hematogenous osteomyelitis in newborns, Schede traction is the method of choice. Traction applied to both legs is advisable, as it provides better rest and facilitates infant care. When the lesion is localized in the BONES OF THE lower leg, the limb is immobilized with a removable plaster splint. Fixation is continued even after the acute process subsides. This is particularly important in lesions of the proximal femur, where there is a high risk of pathological hip dislocation. Following the resolution of the inflammatory process, such patients are prescribed a Vylensky splint or a CITO splint for a period of at least 6 to 10 months.
Immediate treatment outcomes for osteomyelitis have improved significantly in recent years. However, long-term outcomes do not always satisfy surgeons. Significant epiphyseal involvement frequently leads to limb length discrepancies. Pathological dislocation or Varus deformity of the hip may occur. When the distal femoral epiphysis is affected, valgus deformity of the lower leg is more common, and limb growth retardation ensues. Joint ankylosis in newborns typically does not develop. Timely and proper limb immobilization, followed by regular orthopedic follow-up, in most cases helps prevent or promptly correct potential deformities.
Last update: 10/08/2026
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