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1PERINATAL COMPLICATIONS OF CHILDREN WITH EXTREMELY LOW BIRTH WEIGHT
Turdieva D.E.
Tashkent Pediatric Medical Institute https://doi.org/10.5281/zenodo.12501673
In the morbidity patterns of preterm infants in the neonatal period, combined pathologies are most common. Respiratory distress syndrome, asphyxia, and hypoxia are typically the top two ailments. Infectious diseases rank third in terms of prevalence. [1]. Respiratory distress syndrome is the primary cause of respiratory issues in extremely low birth weight infants, often resulting in fatality. Neonatal mortality rates from RDS vary from 20% to 95%. The severity of respiratory problems in this group of infants is influenced by factors such as gestational age, birth weight, infant gender, and maternal history. [17],[10]. [18,23].
RDS develops due to a lack of surfactant produced by type II alveolocytes in the lungs and the immature morphology of lung tissue. Surfactant production typically starts at 26 weeks of pregnancy, so the risk of RDS increases with lower gestational age and birth weight. Studies show that RDS occurs in 78-88% of cases at gestational ages up to 28 weeks, 70% at 29-30 weeks, and 50-55% at 31-32 weeks according to local researchers. [10, 12].
Recently, the main approach to treating respiratory disorders in RDS was through invasive methods like artificial ventilation (ALV). However, today there are various strategies for using surfactant treatments, with a focus on preventative therapy. Early administration of surfactant in the delivery room, as opposed to later in the neonatal intensive care unit, has been shown to reduce complications such as neurological issues, bronchopulmonary dysplasia, necrotizing enterocolitis, and mortality in preterm babies.
Research suggests that administering surfactant and CPAP soon after birth in ELBW infants with respiratory issues can also decrease their time in intensive care and early rehabilitation units. Despite advancements in resuscitation techniques, bronchopulmonary dysplasia remains a challenging complication to prevent in RDS, impacting the long-term health outcomes of ELBW infants, with severe cases posing a risk to their lives. [17].
According to the authors, BPD is formed as a result of impaired lung development under the influence of prenatal and postnatal factors against the background of incomplete alveolar and angiogenesis processes [2,28]. The leading perinatal risk factors for the development of BPD in extremely premature infants are aggravated somatic (bronchial asthma, alcohol and nicotine addiction) and obstetric history of the mother (chorioamnionitis during childbirth), prolonged mechanical ventilation with the need for high concentrations of oxygen, extensive intraventricular hemorrhages, a functioning patent ductus arteriosus, and the male sex of the child [20, 30, 31].
In accordance with a number of authors, there is a relationship between BPD and preeclampsia [30, 33], fetal growth restriction syndrome (FGR), and the role of genetic predisposition is also proven [3,17,34]. Modern authors state that the "new" or post-surfactant form of BPD in very premature infants is characterized by a more favorable course [3, 22, 31-33].
However, for children with an extreme degree of immaturity in the presence of concomitant risk factors, severe forms of the disease are more typical [18]. The classification as claimed by A.H. Jobe, E.H. Bancalari (2001), three degrees of severity of BPD are distinguished: mild - the need for oxygen support up to 28 days of life and older and its cessation up to 36 weeks of gestational age; moderate - the need for oxygen support up to 28 days of life and older with FiO2 0.3. The duration, severity and prognosis of BPD are determined by the development of
complications, which include chronic respiratory failure, acute respiratory failure against the background of chronic, pulmonary hypertension, systemic arterial hypertension, hypotrophy, osteoporosis, and anemia [13]. The incidence of BPD is inversely proportional to birth weight and gestational age. Thus, according to the results of various studies, in children with a birth weight of 501-750 g, BPD is observed in 35-67%, and in children with a birth weight of VLBW - in 1-3.6% of cases [2,11]. As stated by the Russian authors, in newborns born at less than 32 weeks, there is a certain tendency towards a decrease in the incidence of BPD (15-30%), which is probably due to the improvement of respiratory support methods and intensive care, as well as changes in diagnostic criteria. However, mortality in the first year of life remains quite high (11-36%) [20]. By the time of discharge from the hospital, the majority of children with severe BPD have concomitant diseases caused by perinatal damage to the central nervous system, vision, hearing and other organs and systems, and by the age of one year they have disturbances in psychomotor development and constitute a risk group for the development of obstructive pulmonary disease [3, 18, 26, 27]. Perinatal hypoxia, together with morphofunctional immaturity, anatomical, physiological and adaptive capabilities of the body, has a pronounced effect on the course of the neonatal period and long-term prognosis of a deeply premature newborn child [24]. Considering the profound immaturity of the brain and the compensatory mechanisms capable of ensuring its protection, perinatal damaging factors and failure of the child's adaptation to extrauterine life can disrupt the genetically determined normal development and differentiation of neurons and become a substrate for the implementation of the pathological process, especially in the periventricular zones [12,19]. The absence of mechanisms of autoregulation of the vascular network in the periventricular zones directly depends on the state of systemic hemodynamics [19, 24]. In this regard, the problem of preventing subependymal hemorrhages (SCH) is particularly relevant, given their frequency, high morbidity and thanatogenic role [19,24]. There is an extremely fine line between the process of increasing the severity of SCH and their transformation into intraventricular hemorrhages (IVH), so it is very important to prevent this process in the period of early neonatal adaptation of children with ELBW [22]. Due to the anatomical and physiological characteristics of the nervous system, IVH is characteristic mainly of premature infants; the frequency and severity of IVH is inversely proportional to gestational age. PVL develops in 1015% of premature infants with ELBW, causing the development of cerebral palsy and visual impairment [17]. The literature provides data on the relationship between the development of PVL and the severity of respiratory disorders; thus, extremely premature infants who retained spontaneous breathing from birth developed PVL in 6% of cases, while newborns who were unable to breathe independently developed PVL in 60% [19]. The incidence of PVL in children born in the early preterm period who died after the end of the early neonatal period was 75%, while in surviving children it was 4-10% [19]. According to the literature data of domestic authors, the most significant infections such as intrauterine pneumonia, sepsis, and necrotic enterocolitis occupy a leading place in the causes of mortality in very premature babies and are defined as the most important prognostic factor in relation to unfavorable delayed outcomes [4,24]. The predisposition of children with ELBW to a generalized infectious process is primarily due to the failure of the immune system, immaturity of the skin and epithelial barriers, and the high frequency of invasive manipulations [14]. The mortality rate of extremely premature infants with infectious pathology reaches 25-65%, significantly (5-10 times) exceeding the level in full-term newborns [9]. In recent years, the issue of the nosocomial nature of infectious pathology in children with ELBW who survived the early neonatal period and were kept in the NICU for a long time has been
actively discussed [8]. The most significant cause of infectious pathology in the perinatal period of deeply premature infants is intrauterine infection (IUI) [7], which is characterized by placentitis, leading to chronic placental insufficiency and the birth of premature infants [6, 24]. The difficulty in diagnosing the infectious process is associated with the complexity of interpretation or the absence of a number of clinical symptoms and laboratory parameters in newborns with ELBW due to the protracted course, which imitates RDS in the first days of life, damage to the central nervous system, especially with the aggravation of IUGR, IVH, developmental defects, and extreme immaturity [15, 24]. Modern treatment and preventive approaches aimed at reducing the incidence of infectious pathology in this category of children are not effective enough [24,29], and the clinical and diagnostic aspects of sepsis are constantly being revised [12,19,24]. To diagnose sepsis, it is necessary to identify the systemic inflammatory response syndrome (SIRS) with multiple organ failure [24]. Neonatal sepsis is a risk factor for delayed neurological complications and a leading cause of mortality, accounting, according to the authors, for 25 to 45% [21, 29, 32, 33]. At the same time, overdiagnosis of bacterial infection in extremely premature infants leads to unjustified prescription of antibacterial therapy and polypharmacy. The authors prove that long-term routine prophylactic antibacterial therapy and the administration of immunoglobulins in case of negative blood culture results does not reduce the risk of developing an infectious process (pneumonia and sepsis) in children with ELBW [34] and can cause serious complications, increasing the risk of developing necrotizing enterocolitis (NEC) and death [24]. One of the reasons that worsens the quality of life of extremely premature infants is anemia, which develops due to the high growth rate and volume of circulating blood, which is disproportionate to the level of erythropoiesis, and repeated blood transfusions are an integral component of traditional therapy [24,25]. The incidence of anemia is inversely proportional to gestational age and birth weight. Red blood cell destruction occurs more rapidly due to the shorter lifespan of fetal red blood cells, and erythropoietin production remains reduced compared to full-term infants, who respond to minor hypoxia with a rapid increase in erythropoietin levels [16]. One of the pressing problems of modern neonatology is retinopathy of prematurity (ROP) - a pathology of immature, not fully vascularized retina, consisting of abnormal growth of 24 capillaries, the main risk factor of which is hyperoxia, leading in severe cases to retinal detachment and blindness. Therefore, it is extremely important to carefully monitor the parameters of oxygen homeostasis in children with ELBW and, from 4-6 weeks of life, provide consultations with an ophthalmologist and surgical treatment if necessary [17].
Thus, by the time of transfer to the early rehabilitation stage, children with ELBW have severe combined pathology - severe ischemic or ischemic-hemorrhagic damage to the central nervous system, intrauterine infections, RDS, are in a high-risk group for the development of BPD, movement disorder syndrome, retinopathy of prematurity and hearing impairment, in connection with which it is necessary to search for and implement effective diagnostic and prognostic approaches that can influence the reduction of chronic pathology and disability rates.
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