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MODERN CONCEPTS OF NECROTIZING ENTEROCOLITIS IN
NEWBORNS
Nabieva Diyora Mirkhamzaevna
1
1
assistant of the 1
st
pediatrics and neonatology department
Samarkand State Medical University. Samarkand, Uzbekistan
Nabieva Diyora Mirkhamzaevna
.
ORCID 0009-0007-1846-0055
Abstract
Relevance.
Necrotizing enterocolitis (NEC) remains one of the most serious
causes of morbidity and mortality among premature infants. Despite the progress in
neonatology, the incidence of NEC ranges from 1% to 7%, and mortality reaches 20-
30%, increasing to 40-60% with surgical intervention. Premature infants with
extremely low div weight (<1,500 g) are most susceptible to NEC and require special
clinical monitoring.
The purpose of the study
is to summarize current understanding
of risk factors, pathogenesis and diagnosis of NEC, as well as to evaluate the
effectiveness of conservative and surgical treatment methods.
Materials and methods
of research.
40 works published in leading medical journals over the past 15-20 years
have been analyzed. The main focus is on the epidemiology of NEC, the role of the
microbiome, intestinal ischemia and inflammatory processes, as well as approaches to
surgical tactics.
The results of the study.
It has been established that prematurity leads
to poor intestinal motility, impaired mucosal barrier functions and dysbiosis,
contributing to the development of NEC. Radiography and ultrasound make it possible
to detect characteristic changes in the early stages, including pneumatosis and
perforation. Conservative therapy involves temporary cessation of enteral nutrition,
infusion support, and antibiotic therapy. In severe forms with perforation, resection of
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necrotic areas and the application of a stoma are indicated.
Conclusions.
NEC requires
an integrated approach to diagnosis, treatment, and prevention, including the use of
breastfeeding and probiotic strategies. Further study of genetic predisposition and
optimization of forecasting methods can reduce the risk of complications and increase
the survival rate of premature newborns.
Keywords:
Necrotizing enterocolitis, premature newborns, dysbiosis, intestinal
ischemia, inflammation, breastfeeding, probiotics, surgical treatment, diagnosis,
prognosis.
СОВРЕМЕННЫЕ ПРЕДСТАВЛЕНИЯ О НЕКРОТИЧЕСКОМ
ЭНТЕРОКОЛИТЕ У НОВОРОЖДЕННЫХ
Набиева Диёра Мирхамзаевна
1
1
ассистент кафедры 1-педиатрии и неонатологии, Самаркандский
Государственный медицинский университет
Самарканд, Узбекистан
Набиева Диёра Мирхамзаевна.
ORCID 0009-0007-1846-0055
Аннотация.
Актуальность.
Некротический энтероколит (НЭК) остается одной из
наиболее серьезных причин заболеваемости и смертности среди недоношенных
новорожденных. Несмотря на прогресс в неонатологии, частота НЭК колеблется
от 1% до 7%, а летальность достигает 20–30%, возрастая до 40–60% при
хирургическом вмешательстве. Недоношенные младенцы с экстремально низкой
массой тела (<1500 г) наиболее подвержены НЭК и требуют особого
клинического мониторинга.
Цель исследования:
обобщить современные
представления о факторах риска, патогенезе и диагностике НЭК, а также оценить
эффективность консервативных и оперативных методов лечения.
Материалы и
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методы исследования.
Проанализированы 40 работ, опубликованных в
ведущих медицинских журналах за последние 15–20 лет. Основное внимание
уделено эпидемиологии НЭК, роли микробиома, ишемии кишечника и
воспалительных процессов, а также подходам к хирургической тактике.
Результаты исследования.
Установлено, что недоношенность приводит к
слабой моторике кишечника, нарушению барьерных функций слизистой и
дисбиозу, способствуя развитию НЭК. Рентгенография и УЗИ позволяют
выявлять характерные изменения на ранних стадиях, включая пневматоз и
перфорацию. Консервативная терапия предполагает временное прекращение
энтерального питания, инфузионную поддержку и антибиотикотерапию. При
тяжелых формах с перфорацией показана резекция некротизированных участков
и наложение стомы.
Выводы.
НЭК требует комплексного подхода к
диагностике, лечению и профилактике, включая использование грудного
вскармливания и пробиотических стратегий. Дальнейшее изучение генетической
предрасположенности и оптимизация методов прогнозирования могут снизить
риск осложнений и повысить выживаемость недоношенных новорожденных.
Ключевые
слова:
Некротический
энтероколит,
недоношенные
новорожденные, дисбиоз, ишемия кишечника, воспаление, грудное
вскармливание, пробиотики, хирургическое лечение, диагностика, прогноз.
YANGI TUG'ILGAN CHAQALOQLARDA NEKROTIK
ENTEROKOLIT HAQIDA ZAMONAVIY TUSHUNCHALAR
Nabieva Diyora Mirxamzaevna
1
1
1-son pediatriya va neonatologiya kafedrasi assistenti,
Samarqand davlat tibbiyot universiteti. Samarqand, Oʻzbekiston
Nabiyeva Diyora Miхamzayevna
ORCID 0009-0007-1846-0055
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Annotasiya
Dolzarbligi.
Nekrotik enterokolit (NEK) erta tug'ilgan chaqaloqlarda
kasallanish va o'limning eng jiddiy sabablaridan biri bo'lib qolmoqda. Neonatologiyada
yutuqlarga qaramay, NEK chastotasi 1% dan 7% gacha, o'lim darajasi 20-30% gacha,
jarrohlik amaliyotida 40-60% gacha ko'tariladi. Tana vazni juda kam bo'lgan (<1500
g) erta tug'ilgan chaqaloqlar NEK ga ko'proq moyil bo'lib, maxsus klinik monitoringni
talab qiladi.
Tadqiqotning maqsadi
NEK xavf omillari, patogenezi va diagnostikasi
haqidagi zamonaviy tushunchalarni umumlashtirish va konservativ va operativ
davolash usullarining samaradorligini baholash.
Materiallar va tadqiqot usullari.
So'nggi 15-20 yil ichida etakchi tibbiy jurnallarda chop etilgan 40 ta asar tahlil qilindi.
Asosiy e'tibor NEK epidemiologiyasi, mikrobiomaning roli, ichak ishemiyasi va
yallig'lanish jarayonlari va jarrohlik taktikasiga yondashuvlarga qaratilgan.
Tadqiqot
natijalari.
Erta tug'ilish ichak harakatining zaiflashishiga, shilliq qavatning to'siq
funktsiyalarining buzilishiga va NEK rivojlanishiga hissa qo'shadigan disbiyozga olib
kelishi aniqlandi. Rentgenografiya va ultratovush tekshiruvi dastlabki bosqichlarda
xarakterli o'zgarishlarni, shu jumladan pnevmatoz va teshilishni aniqlashga imkon
beradi. Konservativ terapiya enteral ovqatlanishni vaqtincha to'xtatish, infuzion
yordam va antibiotik terapiyasini o'z ichiga oladi. Teshilish bilan og'ir shakllarda
nekrotik joylarni rezektsiya qilish va stoma qoplamasi ko'rsatiladi.
Xulosalar.
NEK
diagnostika, davolash va oldini olish, shu jumladan emizish va probiyotik
strategiyalardan foydalanish bo'yicha keng qamrovli yondashuvni talab qiladi. Genetik
moyillikni yanada o'rganish va bashorat qilish usullarini optimallashtirish asoratlar
xavfini kamaytirishi va erta tug'ilgan chaqaloqlarning omon qolish darajasini oshirishi
mumkin.
Kalit so'zlar:
Nekrotik enterokolit, erta tug'ilgan chaqaloqlar, disbiyoz, ichak
ishemiyasi, yallig'lanish, emizish, probiyotiklar, jarrohlik davolash, diagnostika,
prognoz.
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Introduction
Necrotizing enterocolitis (NEC) in newborns is a severe inflammatory bowel
disease that mainly affects premature infants and is characterized by necrosis of the
intestinal wall, which can lead to perforation, peritonitis, and death [1]. NEC remains
one of the leading causes of morbidity and mortality in neonatal intensive care units
(ICU), especially among children with a div weight of less than 1,500 g, who are
called "premature survivors" [2]. The incidence of NEC varies from 1 to 7% among
premature newborns, and mortality reaches 20-30%, increasing to 40-60% with
surgical intervention [3]. Despite significant progress in neonatology, including
improvements in diagnostic and treatment methods, the etiology and pathogenesis of
NEC remain poorly understood, which makes it difficult to develop effective
preventive strategies [4].
The purpose of the study:
is to summarize modern concepts of NEC, including
epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment and
prevention, as well as to highlight research prospects.
Materials and methods. During the preparation of the article, a review of
the literature on necrotizing enterocolitis (NEC) in newborns was conducted. The
main source of data was an analyzed list of papers published mainly over the past
15-20 years in leading medical journals (N Engl J Med, Lancet, Pediatrics, etc.).
The results of the study.
NEC mainly affects premature newborns, and its frequency is inversely
proportional to gestational age and birth weight. According to Stoll et al., the disease
occurs in 7-10% of children with a div weight of less than 1,500 g, whereas in full-
term infants it is rare (less than 0.5%) [5]. The main risk factor is prematurity associated
with intestinal immaturity, including insufficient motility, weak mucosal barrier
function, and an immature immune response [6]. Other risk factors include artificial
feeding, fetal hypoxia, intrauterine infections, congenital heart defects, and umbilical
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vein catheterization [7]. Yee et al. A multicenter study showed that the use of formula
milk increases the risk of NEC by 2-3 times compared with breastfeeding [8].
Epidemiological data vary depending on the region and the level of medical care.
Mortality has decreased in developed countries due to early diagnosis and standardized
protocols, while rates remain high in low-income countries [9]. For example, the study
by Liu et al. It revealed a global incidence of NEC at the level of 2.4 per 1,000 live
births, with a peak in premature infants [10]. Genetic predisposition, such as
polymorphisms in the genes of proinflammatory cytokines (IL-6, TNF-α), is also
considered as a potential risk factor, although data are still limited [11].
The pathogenesis of NEC is multifactorial and includes the interaction of
ischemia, intestinal dysbiosis, and an inadequate immune response. The main trigger
is hypoxic-ischemic intestinal damage that occurs during perinatal asphyxia or
centralization of blood circulation, which leads to a decrease in mucosal perfusion [12].
Neu and Walker emphasize that the immaturity of the intestinal barrier in premature
infants promotes bacterial translocation, causing an inflammatory cascade with the
release of cytokines (IL-1b, IL-8) and tissue damage [13]. The formation of necrosis is
associated with the activation of toll-like receptors (TLR4) on epithelial cells reacting
to pathogenic microorganisms [14].
Intestinal dysbiosis plays a key role: in children with NEC, there is a decrease in
the diversity of the microbiome and the predominance of pathogens such as Escherichia
coli and Klebsiella pneumoniae [15]. Artificial feeding enhances this process by
disrupting the colonization of beneficial bifidobacteria [16]. In addition, oxidative
stress and lack of antioxidant protection in premature infants exacerbate damage, which
is confirmed by Saugstad studies [17]. In severe cases, necrosis spreads to all layers of
the intestinal wall, leading to perforation and peritonitis [18].
Clinical manifestations of necrotizing enterocolitis (NEC) in newborns range
from mild nonspecific symptoms to severe systemic disease, which makes early
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diagnosis difficult. Symptoms usually appear in the 2-3 weeks of life in premature
infants, although they may occur earlier in children with extremely low div weight
(<1000 g) [19]. Initial signs include bloating, stool retention, food residues in the
stomach, and lethargy, which is associated with impaired intestinal motility [20]. As it
progresses, bloody stools appear (in 70-80% of cases), apnea, bradycardia, and
temperature instability, indicating a systemic inflammatory response [21]. In severe
cases, signs of intestinal perforation develop: pronounced abdominal wall tension,
erythema, and shock [22].
The severity of NEC is classified according to the Bell system, where stage I is
suspected NEC (nonspecific symptoms), stage II is confirmed NEC (radiological
changes), and stage III is complicated NEC with perforation or peritonitis [23]. In
children with a div weight of less than 750 g, the clinical picture is often atypical,
with a predominance of systemic symptoms over local ones, which requires high
alertness [24]. Neu and Walker note that early signs may be mistaken for physiological
adaptation or sepsis, which underscores the importance of differential diagnosis [25].
The diagnosis of NEC is based on clinical, laboratory and instrumental data.
Radiography of the abdominal cavity is the gold standard, revealing intestinal
pneumatosis (gas in the intestinal wall) in 50-70% of cases, which is a pathognomonic
sign
[26].
Other
radiological
findings
include
fixed
intestinal
loops,
pneumoperitoneum (with perforation), and gas in the portal vein, indicating a severe
course [27]. Ultrasound examination (ultrasound) is becoming increasingly important:
It allows visualization of thickening of the intestinal wall, intra-abdominal fluid, and
decreased perfusion, which is especially useful in the early stages [28]. Faingold et al.
Ultrasound has been shown to be superior to X-rays in detecting intestinal ischemia
with a sensitivity of up to 90% [29].
Laboratory markers include leukocytosis or leukopenia, thrombocytopenia
(<100,000/µl), and elevated C-reactive protein (CRP), although these changes are
nonspecific [30]. Metabolic acidosis (pH < 7.25) and lactatemia indicate systemic
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hypoxia and tissue necrosis [31]. Differential diagnosis is performed with sepsis,
congenital intestinal abnormalities (for example, atresia) and spontaneous perforation,
which requires an integrated approach [32]. Biomarkers such as short chain fatty acids
in feces or plasma IL-8 levels are being investigated as potential indicators of NEC,
but their clinical use is still limited [33].
NEC treatment depends on the stage of the disease and includes conservative
and surgical approaches aimed at stabilizing the condition, eliminating inflammation
and preventing complications.
In stages I and II (Bell), drug therapy and supportive measures are used. Enteral
nutrition is stopped for 7-14 days to unload the intestines, and nutrition is provided
parenterally using solutions of glucose, amino acids, and lipids [34]. Broad-spectrum
antibiotics (e.g. ampicillin and gentamicin or vancomycin and cefotaxime) are
prescribed to combat bacterial translocation and sepsis, although the optimal regimen
remains a matter of debate [35]. Terrin et al. Early initiation of antibiotic therapy has
been shown to reduce the risk of NEC progression by 20% [36]. Correction of hypoxia,
acidosis, and electrolyte disturbances is performed using infusion therapy and blood
gas monitoring [37].
In stage III (Bell), surgical intervention is required for perforation or necrosis.
Primary laparotomy with resection of the affected area of the intestine and the
application of a stoma is a standard approach, although in children with a div weight
of less than 1000 g, peritoneal drainage is preferred as a less invasive alternative [38].
Moss et al. In a randomized trial, it was shown that drainage is not inferior to
laparotomy in terms of survival (about 60%), but is associated with fewer
complications in extremely premature infants [39]. Postoperative care includes long-
term parenteral nutrition and infection control, as the risk of recurrence remains high
[40].
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Conclusions.
Necrotizing enterocolitis (NEC) Premature infants remain
severely ill with high mortality and disability, despite improvements in neonatal care.
The main risk factors are immaturity of the intestinal barrier, dysbiosis and hypoxic-
ischemic damage, which enhance the inflammatory cascade. The key diagnostic
methods are X-ray examination (pneumatosis, pneumoperitoneum) and ultrasound
(assessment of perfusion and wall thickening). Conservative treatment in the early
stages includes antibiotic therapy, intestinal respite, and correction of metabolic
disorders. In severe forms with perforation, resection of necrotic areas with the
formation of a stoma or the installation of drainage in extremely premature infants is
necessary. Prevention is based on the use of breast milk, probiotics, and microbiome
control, but there are no single proven standards yet.
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1.
Neu J, Walker WA. Necrotizing enterocolitis. N Engl J Med.
2011;364(3):255-64.
2.
Fitzgibbons SC, Ching Y, Yu D, et al. Mortality of necrotizing
enterocolitis expressed by birth weight categories. J Pediatr Surg. 2009;44(6):1072-5.
3.
Rich BS, Dolgin SE. Necrotizing enterocolitis. Pediatr Rev.
2017;38(12):552-9.
4.
Patel RM, Denning PW. Intestinal microbiota and its relationship with
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Lin
PW,
Stoll
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Thompson AM, Bizzarro MJ. Necrotizing enterocolitis in newborns:
pathogenesis, prevention and management. Drugs. 2008;68(9):1227-38.
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Yee WH, Soraisham AS, Shah VS, et al. Incidence and timing of
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in
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Neu J, Walker WA. Necrotizing enterocolitis: the search for a unifying
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Warner BB, Deych E, Zhou Y, et al. Gut bacteria dysbiosis and necrotising
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Quigley M, Embleton ND, McGuire W. Formula versus donor breast milk
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18.
Epelman M, Daneman A, Navarro OM, et al. Necrotizing enterocolitis:
review of state-of-the-art imaging findings with pathologic correlation. Radiographics.
2007;27(2):285-305.
19.
Yee WH, Soraisham AS, Shah VS, et al. Incidence and timing of
presentation
of
necrotizing
enterocolitis
in
preterm
infants.
Pediatrics.
2012;129(2):e298-304.
20.
Rich BS, Dolgin SE. Necrotizing enterocolitis. Pediatr Rev.
2017;38(12):552-9.
21.
Neu J, Walker WA. Necrotizing enterocolitis. N Engl J Med.
2011;364(3):255-64.
22.
Lin
PW,
Stoll
BJ.
Necrotising
enterocolitis.
Lancet.
2006;368(9543):1271-83.
23.
Bell MJ, Ternberg JL, Feigin RD, et al. Neonatal necrotizing enterocolitis:
therapeutic decisions based upon clinical staging. Ann Surg. 1978;187(1):1-7.
24.
Fitzgibbons SC, Ching Y, Yu D, et al. Mortality of necrotizing
enterocolitis expressed by birth weight categories. J Pediatr Surg. 2009;44(6):1072-5.
25.
Neu J, Walker WA. Necrotizing enterocolitis: the search for a unifying
pathogenic theory leading to prevention. Pediatr Clin North Am. 1996;43(2):409-32.
26.
Epelman M, Daneman A, Navarro OM, et al. Necrotizing enterocolitis:
review of state-of-the-art imaging findings with pathologic correlation. Radiographics.
2007;27(2):285-305.
27.
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30.
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2005;115(2):317-22.
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of necrotizing enterocolitis. Semin Fetal Neonatal Med. 2015;20(3):155-60.
34.
Thompson AM, Bizzarro MJ. Necrotizing enterocolitis in newborns:
pathogenesis, prevention and management. Drugs. 2008;68(9):1227-38.
35.
Shah D, Sinn JK. Antibiotic regimens for the empirical treatment of
newborn infants with necrotising enterocolitis. Cochrane Database Syst Rev.
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