Necrotizing enterocolitis: symptoms, diagnosis, treatment, and prognosis in newborns

Necrotizing enterocolitis is a severe inflammatory necrotic disease of the intestines of newborns, which damages the mucosa and, in severe cases, affects deeper layers of the intestinal wall. The disease most often develops in premature and seriously ill newborns, especially in very low birth weight infants, and is considered the most common gastrointestinal emergency in neonatology. [1]

The essence of the disease is that an immature intestinal wall, disrupted microbiota, inflammatory response, ischemia, and bacterial invasion combine to trigger intestinal damage. As a result, gas may appear in the intestinal wall, pneumatosis intestinalis develops, and necrosis, perforation, peritonitis, sepsis, and death of the child are possible. [2]

The disease is particularly dangerous because the initial signs are often nonspecific: the child tolerates feeding poorly, becomes lethargic, the abdomen swells, vomiting, blood in the stool, unstable temperature, respiratory arrest, or signs of sepsis appear. Therefore, in neonatal intensive care units, necrotizing enterocolitis is always considered a diagnosis requiring rapid assessment and team decision-making. [3]

It's important to understand that necrotizing enterocolitis is not a "common bowel disorder" in infants. It is a potentially life-threatening condition, and treatment is only performed in a hospital, usually in a neonatal intensive care unit (NICU), with the participation of a neonatologist, pediatric surgeon, radiologist, infectious disease specialist, dietitian, and respiratory support specialists. [4]

Modern medicine has made significant progress in caring for extremely premature infants, but necrotizing enterocolitis remains one of the major unsolved problems in neonatology. The US National Institute of Child Health and Human Development, in a 2024 working report, emphasizes that the lack of a single, standardized definition of the disease complicates estimating the true incidence, comparing studies, and developing preventative measures. [5]

Key point	Meaning
Main risk group	Premature infants, especially very low birth weight infants
Main affected area	The intestine, most often the terminal ileum and large intestine
Early signs	Feeding intolerance, bloating, blood in stool, lethargy
The main radiographic sign	Gas in the intestinal wall, that is, pneumatosis intestinalis
Severe complications	Perforation, peritonitis, sepsis, short bowel syndrome
Basic therapy	Enteral feeding withdrawal, gastric decompression, intravenous fluids, antibiotics, intravenous feeding
Surgery	Required in case of perforation, necrosis, deterioration of the condition or ineffectiveness of conservative therapy

Code according to ICD 10 and ICD 11

In the International Classification of Diseases, 10th revision, necrotizing enterocolitis of the fetus and newborn is classified under category P77. This category is used for perinatal necrotizing enterocolitis, that is, the disease associated with the neonatal period, and not for all inflammatory bowel diseases in older children. [6]

In the International Classification of Diseases, 11th revision, the disease is classified in block KB88 Necrotizing enterocolitis of newborn. Within this section, codes are provided for stages: KB88.0 for stages 1A and 1B, KB88.1 for stages 2A and 2B, KB88.2 for stage 3A, KB88.3 for stage 3B, as well as specified and unspecified variants. [7]

In clinical documentation, the code alone does not replace the diagnosis. The physician additionally specifies the stage, presence of perforation, sepsis, shock, surgery, stoma, affected bowel segment, nutritional complications, and sequelae, as these details determine treatment, prognosis, and follow-up. [8]

For parents, something else is important: the code in the discharge report does not always fully reflect the severity of the condition. Two children may have the same International Classification of Diseases category, but different clinical scenarios: in one, the disease was limited to suspicion and conservative treatment, while in the other, surgery was required to remove a section of the intestine. [9]

Classification	Code	What does it mean?
ICD 10	P77	Necrotizing enterocolitis of the fetus and newborn
ICD 10	KB88	Necrotizing enterocolitis of the newborn
ICD 11	KB88.0	Stages 1A and 1B
ICD 11	KB88.1	Stages 2A and 2B
ICD 11	KB88.2	Stage 3A
ICD 11	KB88.3	Stage 3B
ICD 11	KB88.Y	Another refined version
ICD 11	KB88.Z	Unspecified version

Epidemiology

Necrotizing enterocolitis occurs predominantly in premature infants. According to the MSD Manual, the vast majority of cases occur in premature infants, with approximately 85% of these infants weighing less than 1.5 kilograms at birth or having a gestational age of less than 32 weeks. [10]

The incidence of the disease depends on the definition used in a particular study and which infants are included in the calculation. Different sources provide different ranges, but for very low birth weight infants, rates of around a few percent are often cited, and in certain groups of extremely premature infants, the risk is higher. [11]

Globally, the disease remains rare among all neonates, but is highly significant in intensive care units. StatPearls indicates that necrotizing enterocolitis occurs in approximately 2-5% of premature infants, and overall mortality varies widely across series and can be very high in cases of perforation, peritonitis, and sepsis. [12]

A working group from the US National Institute of Child Health and Human Development notes that in 2022, 356 deaths associated with necrotizing enterocolitis were recorded in the US Centers for Disease Control and Prevention's mortality database, or 9.7 deaths per 100,000 infants. However, the total number of cases per year remains unknown due to the lack of a reliable recording system and a uniform definition of the disease. [13]

Epidemiology is changing along with advances in neonatology. As more very-early gestational age and very-low-birth-weight infants survive, the group of children at risk for developing this disease grows; therefore, preventing necrotizing enterocolitis remains a critical goal of modern perinatal care. [14]

Indicator	Approximate value and commentary
Main group	Premature newborns
The most vulnerable body mass	Less than 1500 grams
The most vulnerable period of gestation	Less than 32 weeks
Frequency in premature infants	In different sources, several percent, higher in extremely premature babies
Mortality	Depends significantly on the stage, body weight and perforation
The main problem with statistics	There is no single definition and no single accounting system.
The greatest risk of severe outcome	Perforation, peritonitis, sepsis, extremely low body weight

Reasons

There is no single, simple cause for necrotizing enterocolitis. It is a multifactorial disease that combines intestinal immaturity, impaired blood supply, microbial imbalance, excessive inflammatory response, bacterial invasion, nutritional factors, and the severity of the newborn's overall condition. [15]

In a premature infant, the intestinal barrier is not yet fully mature. The mucosa, immune cells, mucus, antimicrobial peptides, blood supply, motility, and intestinal microbiota function differently than in a full-term infant, making the intestine less able to withstand stress, hypoxia, feeding, and bacterial load. [16]

Dysbiosis, a disruption of the intestinal microbiota, is considered one of the early stages. A report from the US National Institute of Child Health and Human Development indicates that dysbiosis can be detected 48-72 hours before clinical diagnosis, and then triggers an excessive inflammatory response with damage to the epithelial barrier. [17]

Nutrition plays a dual role. On the one hand, enteral nutrition is essential for intestinal growth and maturation; on the other hand, in immature intestines, the presence of intraluminal nutrient substrate can become a component of the pathological chain. The MSD Manual describes three typical intestinal conditions: prior ischemic injury, bacterial colonization, and the presence of intraluminal substrate, i.e., feeding. [18]

In full-term infants, necrotizing enterocolitis is less common, but still possible. In this group, it is more often associated with severe hypoxia, congenital heart defects, impaired blood flow, sepsis, perinatal stress, or other conditions that impair intestinal oxygen supply. [19]

Causal mechanism	How does he participate?
Intestinal immaturity	Weaker barrier and inflammation regulation
Dysbiosis	Increases bacterial invasion and inflammation
Ischemia	Damages the mucous membrane and increases the risk of necrosis
Enteral nutrition	May become a substrate in immature and damaged intestines
Inflammatory response	Damages the epithelium and blood vessels
Bacterial invasion	Increases necrosis and the risk of sepsis
Severe general condition	Reduces the child's reserves

Risk factors

The main risk factor is prematurity. The shorter the gestational age and birth weight, the greater the vulnerability of the intestines, and the more frequently the child requires respiratory support, catheters, antibiotics, long-term parenteral nutrition, and other interventions that indirectly change the risk of intestinal complications. [20]

Risk factors include low birth weight, early gestational age, small for gestational age, birth asphyxia, congenital heart defects, anemia, exchange transfusion, microbiota disruption, artificial nutrition, and severe ischemic conditions. These factors are listed in the MSD Manual as clinically important conditions that increase the likelihood of the disease. [21]

Maternal and perinatal factors also play a role. A working report from the US National Institute of Child Health and Human Development lists preeclampsia, intrauterine infection, premature rupture of membranes, placental abruption, intrauterine growth restriction, low Apgar scores, and low oxygen levels at birth as risk factors. [22]

After birth, the risk increases with the need for mechanical ventilation, the use of vasopressors, low hemoglobin, elevated lactate, patent ductus arteriosus, and severe general condition. These signs are important not only as risk factors for the development of the disease, but also as markers of a more severe course and an increased risk of death. [23]

Nutrition deserves special attention. Non-human milk, especially formula in very premature infants, is associated with a higher risk, while the mother's own milk is considered the most protective factor; when the mother's milk supply is insufficient, donor human milk is considered an important preventative alternative. [24] [25]

Risk factor	Practical significance
Prematurity	The main common factor
Weight less than 1500 grams	High intestinal vulnerability
Less than 32 weeks	Immaturity of the barrier and immunity
Asphyxia and hypoxia	Risk of ischemic bowel injury
Congenital heart defect	Possible intestinal perfusion disorder
Artificial nutrition	Higher risk compared to human milk
Dysbiosis	Early link in pathogenesis
Intensive care and ventilation	Marker of severity and additional risk

Pathogenesis

Pathogenesis can be conceptualized as a "perfect storm" in the intestines of premature infants. The immature mucosa provides poorer protection from bacteria, the immature immune system can overreact, and intestinal blood flow and motility are easily disrupted by hypoxia, sepsis, shock, or severe respiratory failure. [26]

When dysbiosis and inflammation damage the epithelial barrier, bacteria and their components more easily penetrate the intestinal wall. This intensifies the inflammatory response, damages cells, disrupts microcirculation, and can lead to ischemia and necrosis. [27]

Pneumatosis intestinalis occurs when gas accumulates within the intestinal wall. On radiography or ultrasound, it is one of the key signs of confirmed necrotizing enterocolitis, but it reflects a more advanced process rather than the very first stage of the disease. [28]

If inflammation and necrosis progress, the intestinal wall may weaken and perforate. This causes intestinal contents to leak into the abdominal cavity, leading to peritonitis, increased sepsis, impaired circulation, and the child may require emergency surgery. [29]

Current research is actively searching for early biomarkers that could predict the disease before irreversible damage occurs. A 2025 systematic review describes promising markers, including calprotectin, urine protein panels, and human milk components, but emphasizes that the evidence is still mixed and does not replace clinical assessment. [30]

Pathogenesis link	What's happening
Immature intestinal barrier	Bacteria penetrate tissues more easily
Dysbiosis	The balance of microbiota is disturbed
Hypoxia and ischemia	The intestines receive less oxygen
Inflammation	Damages the epithelium and blood vessels
Pneumatosis	Gas appears in the intestinal wall
Necrosis	Sections of the intestine die
Perforation	The contents of the intestine enter the abdominal cavity
Sepsis	Inflammation becomes systemic

Symptoms

Early symptoms often include decreased feeding tolerance. The baby may experience abdominal distension, residual milk in the stomach, vomiting, especially with bile, constipation, diarrhea, blood in the stool, or a positive occult blood test. [31]

Systemic manifestations can be no less significant than intestinal ones. The child becomes lethargic, reacts less well, develops an unstable temperature, episodes of respiratory arrest, a slow heart rate, impaired peripheral blood flow, respiratory failure, or signs of sepsis. [32]

When examining the abdomen, the doctor looks for increased abdominal circumference, tenderness, tension, visible intestinal loops, changes in abdominal skin color, decreased peristalsis, and signs of peritonitis. These signs are especially alarming if they appear in a premature baby in the 2nd to 3rd week of life. [33]

Severe symptoms include marked respiratory depression, a drop in blood pressure, acidosis, impaired clotting, decreased platelet count, shock, lack of urine output, and free gas in the abdominal cavity if perforation occurs. In this situation, treatment becomes urgent, and the decision to surgical intervention is made quickly. [34]

The challenge for parents and doctors is that some of the early signs can also be seen in other conditions: sepsis, feeding intolerance, intestinal obstruction, spontaneous intestinal perforation, or bloating associated with respiratory support. Therefore, diagnosis is always based on a combination of symptoms, tests, dynamics, and imaging. [35]

Symptom	What could it mean?
Feeding intolerance	Early non-specific sign
Bloating	Intestinal inflammation, paresis or obstruction
Vomiting bile	Possible severe intestinal disorder
Blood in the stool	Damage to the mucous membrane
Lethargy	Systemic deterioration
Respiratory arrest	Sepsis or severe condition
Pressure drop	Shock
Free gas in the abdominal cavity	Possible perforation

Classification, forms and stages

Modified Bell criteria are widely used in clinical practice. They categorize the disease as suspected, confirmed, and severe, and help link symptoms, radiographic findings, and treatment strategies. A 2025 systematic review indicates that the Bell criteria remain the basis for staging, although they have limitations due to the nonspecificity of early signs. [36]

Stage 1 is suspected. The child may have non-specific signs: feeding intolerance, mild abdominal distension, lethargy, temperature instability, blood in the stool, but the radiographic image may be normal or show only moderate intestinal paresis. [37]

Stage 2 is considered confirmed disease. More convincing clinical features and characteristic imaging findings typically appear: pneumatosis intestinalis, portal vein gas, or more pronounced changes in intestinal loops. At this stage, full treatment with discontinuation of enteral feeding, antibiotics, and close monitoring is required. [38]

Stage 3 is the severe form. It is accompanied by severe systemic instability, metabolic acidosis, respiratory failure, shock, coagulation disorders, peritonitis, necrosis, or perforation. Stage 3B in the International Classification of Diseases, 11th revision, actually corresponds to perforated necrotizing enterocolitis. [39]

Based on its form, the disease can be divided into medically treatable, surgical, perforating, fulminant, recurrent, and postnecrotic with complications. This classification does not replace Bell's stage, but it helps explain to the family why one child's treatment is limited to intensive care without surgery, while another requires removal of part of the intestine. [40]

Stage	Clinical meaning	Typical signs
1A and 1B	Suspicion	Non-specific symptoms, possibly blood in the stool
2A and 2B	Confirmed disease	Pneumatosis, more pronounced intestinal signs
3A	Severe form without obvious perforation	Shock, acidosis, severe systemic condition
3B	Heavy form with perforation	Free gas, peritonitis, need for surgery
Medical uniform	Non-surgical therapy is possible	No perforation or uncontrolled deterioration
Surgical form	Intervention is required	Necrosis, perforation, or deterioration despite treatment

Complications and consequences

The most feared acute complication is intestinal perforation. This occurs when the damaged intestinal wall ruptures, allowing gas, bacteria, and intestinal contents to enter the abdominal cavity, leading to peritonitis and a sharply increased risk of sepsis and death. [41]

Sepsis and shock are common companions of severe necrotizing enterocolitis. The child may require mechanical ventilation, vasopressors, correction of acidosis, blood transfusions, and prolonged intensive monitoring. [42]

Complications associated with the loss of a section of intestine are possible after surgery. If a significant portion is removed, short bowel syndrome develops, making it difficult for the child to absorb nutrients, fluids, and electrolytes, and may require long-term parenteral nutrition. [43]

Late sequelae include intestinal strictures, adhesions, impaired intestinal motility, growth retardation, rehospitalizations, and an increased risk of neurodevelopmental disabilities. A 2025 systematic review emphasizes that the sequelae of necrotizing enterocolitis create a long-term medical burden for the child, family, and the healthcare system. [44]

The psychological impact on the family is also significant. Parents of a premature baby already endure intensive care, and a diagnosis of necrotizing enterocolitis adds fear of surgery, sepsis, stoma, long-term intravenous feeding, and an uncertain prognosis. [45]

Complication	Possible consequences
Perforation	Peritonitis, emergency surgery
Sepsis	Shock, respiratory and organ failure
Intestinal stricture	Late obstruction
Short bowel syndrome	Long-term nutrition and absorption problems
stoma	The need for care and subsequent restoration of intestinal continuity
Adhesions	Risk of obstruction
Growth retardation	Long-term malnutrition
Neurodevelopmental disorders	Increased risk in severe cases and prematurity

When to see a doctor

If the baby is at home after discharge from the neonatal unit, urgent medical attention is needed if there is abdominal distension, green or yellow vomit, blood in the stool, sudden lethargy, refusal to feed, unstable temperature, bruising, respiratory arrest, or a sudden deterioration in condition. These signs do not prove necrotizing enterocolitis but require immediate evaluation. [46]

In hospital, parents should immediately notify the staff if they notice their baby's belly has become larger, the skin on the belly has changed color, the baby has become unusually lethargic, spitting up more frequently, not tolerating feedings well, or blood has appeared in the stool. In a premature baby, even small changes can be significant, as the disease can sometimes progress rapidly. [47]

Immediate assistance is needed if signs of shock appear: cold extremities, grayish or mottled skin, poor reaction, decreased breathing, falling blood pressure, or infrequent urination. This is no longer a situation for observation, but a reason for urgent intensive care. [48]

In children with a history of necrotizing enterocolitis, it is important to consult a doctor after discharge if they experience poor weight gain, repeated vomiting, bloating, constipation, blood in the stool, signs of dehydration, poor appetite, or suspected intestinal obstruction. Late strictures and motility disorders may appear after the acute phase. [49]

If a child has a stoma, parents should seek immediate help if there is a sudden change in the volume of discharge, signs of dehydration, darkening or swelling of the stoma, bleeding, severe skin irritation, or a deterioration in general condition. These situations require evaluation by a surgical and neonatal team. [50]

Sign	Why is it dangerous?
Green vomit	Possible severe intestinal disorder
Blood in the stool	Damage to the mucous membrane or inflammation
Rapid bloating	Paresis, inflammation or perforation is possible.
Lethargy	Systemic deterioration
Respiratory arrest	Sepsis or instability
Cold extremities	Circulatory disorders
Poor weight gain after discharge	Possible consequences of the disease
Vomiting and bloating after discharge	Possible stricture or obstruction

Diagnostics

The first step is a clinical assessment. The physician evaluates the gestational age, body weight, age in days, type of feeding, feeding tolerance, abdominal circumference, presence of vomiting, blood in the stool, respiratory episodes, temperature, blood pressure, perfusion, and the general condition of the baby. [51]

The second step is immediate abdominal imaging. Classically, abdominal radiography is performed, sometimes in multiple projections, to detect dilated loops, pneumatosis intestinalis, portal venous gas, or free gas in the presence of perforation. StatPearls emphasizes that abdominal radiography remains a key test for diagnosis and follow-up. [52]

The third step is a laboratory assessment of severity. A complete blood count, platelets, acid-base balance, lactate, electrolytes, glucose, renal function tests, inflammatory markers, blood cultures, and coagulation assessment are used. These tests are nonspecific but help to understand the presence of sepsis, acidosis, thrombocytopenia, dehydration, and organ instability. [53]

The fourth step is a dynamic reassessment. If necrotizing enterocolitis is suspected, the child's condition can change within hours, so the examination, radiography, tests, abdominal circumference monitoring, and assessment of breathing, circulation, urine, and response to treatment are repeated. [54]

Ultrasound is increasingly being used as a complement to radiography. It can help assess intestinal wall blood flow, free fluid, portal vein gas, wall thickness, and signs of necrosis, but the results depend on the specialist's experience and do not replace clinical judgment. [55]

In the most severe cases, definitive confirmation sometimes occurs only during surgery or postmortem examination. The US National Institute of Child Health and Human Development emphasizes that a definitive diagnosis is made by identifying intestinal inflammation, infarction, and necrosis during surgery or autopsy. [56]

Diagnostic stage	What is being assessed?
Clinical examination	Abdomen, feeding, respiration, perfusion, general condition
X-ray	Pneumatosis, portal vein gas, free gas
Blood tests	Inflammation, acidosis, platelets, electrolytes
Blood culture	Possible sepsis
Ultrasound examination	Blood flow, fluid, intestinal wall
Dynamic observation	Change of state by hour
Surgical evaluation	Perforation, necrosis, peritonitis

Differential diagnosis

Necrotizing enterocolitis must be distinguished from spontaneous intestinal perforation. Spontaneous perforation may present with free gas in the abdominal cavity, but classic pneumatosis and widespread intestinal inflammation are not always present; this is especially important in extremely premature infants. [57]

Neonatal sepsis can mimic early necrotizing enterocolitis. Lethargy, unstable temperature, respiratory arrest, poor perfusion, and feeding intolerance may be manifestations of generalized infection without primary intestinal necrosis, so the clinician evaluates cultures, inflammatory markers, abdominal examination, and imaging together. [58]

Intestinal obstruction, malrotation with volvulus, congenital intestinal anomalies, and meconium ileus are also included in the differential diagnosis. Bilious vomiting and rapid abdominal distension in a newborn always require the exclusion of surgical pathology, as intestinal volvulus can very quickly lead to ischemia. [59]

Feeding intolerance in preterm infants can be functional and does not always indicate necrotizing enterocolitis. Gastric residuals, moderate distension, and irregular stools may be due to immature motility, respiratory support, medications, or general conditions, but the presence of blood, pneumatosis, or systemic deterioration greatly increases concern. [60]

Infectious enterocolitis, allergic proctocolitis, Hirschsprung's disease, ischemic bowel disease secondary to heart disease, and drug-induced complications can also resemble necrotizing enterocolitis. Therefore, a diagnosis cannot be made based on a single symptom: a consistent assessment of risk, clinical features, tests, radiography, and progression is required. [61]

State	What is similar?	How to distinguish
Spontaneous intestinal perforation	Free gas, serious condition	Fewer signs of disseminated enterocolitis
Sepsis	Lethargy, apnea, unstable temperature	Crops, abdominal dynamics, visualization
Volvulus	Bilious vomiting, ischemia	Urgent surgical evaluation
Functional food intolerance	Residues, bloating	No pneumatosis or systemic deterioration
Hirschsprung's disease	Bloating, constipation	Anamnesis, contrast studies, biopsy
Allergic proctocolitis	Blood in the stool	Usually there is no pneumatosis or severe sepsis
Congenital obstruction	Vomiting and bloating	Visualization and surgical diagnostics

Treatment

Treatment begins immediately if there is serious suspicion, as waiting for full confirmation is dangerous. The first principle is "bowel rest": enteral feeding is stopped, a gastric tube is inserted for decompression, air and contents are removed from the stomach, pressure on the intestines is reduced, and the risk of further distension is reduced. [62]

The baby is prescribed intravenous fluids, electrolyte, glucose, and acid-base balance adjustments. If feeding is withheld for a long time, parenteral nutrition is required, as premature babies have very limited reserves and quickly develop energy, protein, and micronutrient deficiencies. [63]

Broad-spectrum antibiotics are standard treatment because the damaged bowel allows bacteria to penetrate the wall and cause sepsis. The specific regimen depends on local protocols, severity, risk of anaerobic infection, cultures, and the child's condition; one clinical guideline recommends a duration of 7-14 days, depending on the clinical presentation. [64]

Respiratory and circulatory support are provided simultaneously. If abdominal distension impairs breathing, or if there is apnea, acidosis, shock, or sepsis, the child may require oxygen, noninvasive support, mechanical ventilation, vasopressors, blood transfusions, platelets, or plasma. [65]

Consultation with a pediatric surgeon is necessary not only when perforation has already occurred. Many protocols recommend early involvement of a surgical team in all suspected or confirmed cases, because the decision to operate sometimes needs to be made before catastrophic signs appear. [66]

Surgery is indicated for free abdominal gas, obvious perforation, peritonitis, bowel necrosis, deterioration despite intensive care, persistent shock, increasing acidosis, or clinical signs of nonviable bowel. The surgeon may excise the necrotic area, create a stoma, or perform abdominal drainage in extremely unstable infants. [67]

The choice between laparotomy and primary peritoneal drainage depends on the baby's weight, gestational age, stability, severity of peritonitis, and the center's experience. In extremely low birth weight and unstable babies, drainage is sometimes used as a temporary or life-saving option, but the final approach is always individualized. [68]

Resumption of feeding is a separate stage of treatment. It is initiated only after clinical improvement, normalization or improvement of test results, abdominal stabilization, and reduction of radiographic signs; in severe or recurrent cases, a contrast study may be considered before feeding to exclude strictures. [69]

Current new approaches focus on early diagnosis, biomarkers, standardized staging, safer nutritional strategies, donor milk, and cautious evaluation of probiotics. A 2025 systematic review suggests that biomarkers show promise but remain an adjunct to clinical judgment, not a definitive test. [70]

Probiotics remain a controversial topic. Meta-analyses have shown a reduced risk of necrotizing enterocolitis in some groups of preterm infants, but the US Food and Drug Administration has warned of the risk of invasive infections and death in preterm infants and emphasized that no probiotic products are approved in the US as drugs or biological products for infants. [71]

Treatment direction	What does it include?
Bowel rest	Cancellation of enteral nutrition
Decompression	Gastric tube with removal of contents
Intravenous support	Fluids, electrolytes, glucose
Parenteral nutrition	Intravenous feeding during long feeding breaks
Antibiotics	Coverage of intestinal flora and sepsis
Respiratory support	Oxygen, ventilation if necessary
Surgery	Removal of necrosis, stoma or drainage
Monitoring	Follow-up examinations, x-rays, tests
New approaches	Biomarkers, standardization, cautious prevention

Prevention

The most compelling preventative measure is the use of breast milk whenever possible. A working report from the US National Institute of Child Health and Human Development emphasizes that mother's own milk is the most protective factor against necrotizing enterocolitis in preterm infants. [72]

If a mother's own milk is insufficient, donor human milk is considered an important alternative to formula for very preterm infants. An updated 2024 Cochrane review found that donor human milk reduces the risk of necrotizing enterocolitis by approximately half in very preterm or very low birth weight infants. [73]

Prevention also includes careful management of enteral feeding. The neonatal team assesses bowel readiness, volume and rate of feed increase, gastric residuals, stool, abdominal circumference, and general condition, especially in the most immature infants. [74]

Antibiotics should be used judiciously. While they are necessary in cases of suspected infection and in the treatment of necrotizing enterocolitis, prolonged or unnecessary use can disrupt the intestinal microbiota, which is theoretically associated with increased vulnerability. [75]

Probiotic prophylaxis should not be considered a simple home measure. Even if individual countries or units have protocols for the use of specific strains, in extremely preterm infants this decision is at the level of specialized neonatology, product quality control, safety monitoring, and assessment of the risk of invasive infection. [76]

Preventive measure	Level of evidence and practical significance
Mother's own milk	The most protective factor
Donor human milk	Reduces risk compared to formula in very preterm infants
Careful increase in nutrition	Reduces stress on the immature intestines
Infection control	Reduces systemic inflammation and septic risks
Rational antibiotics	Protection against infection without unnecessary damage to the microbiota
Command observation	Early detection of deterioration
Probiotics	Potential benefits, but safety and quality concerns

Forecast

The prognosis depends on gestational age, body weight, stage, presence of perforation, sepsis, volume of affected intestine, and the speed of treatment. In the suspected or moderate form without perforation, the child may fully recover, but in the surgical form, the risk of death and long-term consequences is significantly higher. [77]

Mortality increases significantly with extremely low body weight, peritonitis, sepsis, shock, and the need for surgery. According to StatPearls, overall mortality can range from 10% to 50%, and in the most severe scenarios with perforation, peritonitis, and sepsis, the risk becomes especially high. [78]

Even after survival, the child may require long-term monitoring. The physician evaluates growth, nutrition, stool quality, signs of strictures, nutrient absorption, liver function during long-term parenteral nutrition, neurodevelopmental status, and the need for surgical restoration of intestinal continuity after the stoma. [79]

The best prognosis is associated with early recognition, use of human milk, prompt weaning if suspected, timely antibiotics, good monitoring, early surgical involvement, and treatment in a center with experience in caring for extremely preterm infants.[80]

It's important to be honest: even ideal prevention does not eliminate the risk completely. A working group from the US National Institute of Child Health and Human Development emphasizes that the causes of the disease are not fully understood, and existing definitions and diagnostic criteria are still imperfect; therefore, scientific research is ongoing. [81]

Scenario	Forecast
Suspected but not confirmed necrosis	Often favorable with observation and treatment
Confirmed form without perforation	Depends on the response to therapy
Perforation	High risk of surgery and complications
Extremely low body weight	The forecast is more cautious
Sepsis and shock	The risk of death is higher
Major bowel resection	Risk of short bowel syndrome
Early diagnosis	Improves chances
Long-term observation	It is necessary even after discharge.

FAQ

What is necrotizing enterocolitis in simple terms?
It's a severe intestinal disease in newborns, in which the intestinal wall becomes inflamed, damaged, and, in severe cases, partially destroyed. The disease most often develops in premature babies and requires urgent hospital treatment. [82]

Why is the disease more common in premature infants?
In premature infants, the intestinal barrier, immune system, blood supply, motility, and microbiota are still immature. Therefore, the intestines are less able to cope with feeding, bacterial colonization, hypoxia, and inflammation. [83]

Is it possible to completely prevent necrotizing enterocolitis?
Complete prevention of the disease is currently impossible because its causes are multifactorial and not fully understood. However, the risk can be reduced by using breast milk, donor human milk if your own milk is insufficient, careful nutrition, infection control, and close monitoring. [84]

What is the most alarming symptom?
Particularly dangerous are rapid abdominal distension, green vomit, blood in the stool, lethargy, respiratory arrest, cold extremities, a drop in blood pressure, and a sharp deterioration in condition. These signs require immediate medical attention. [85]

How is the diagnosis confirmed?
The diagnosis is made based on a combination of clinical signs, tests, and abdominal imaging. The most important imaging features are gas in the intestinal wall, gas in the portal vein, and free gas in the abdominal cavity in the case of perforation. [86]

Is surgery always necessary?
No. Many children are treated conservatively: weaning, gastric decompression, intravenous fluids, parenteral nutrition, and antibiotics. Surgery is needed in cases of perforation, necrosis, peritonitis, or deterioration despite intensive care. [87]

Why is the baby stopped feeding?
The intestines need rest, because continuing to feed during inflammation and the threat of necrosis can increase distension, stress, and the risk of deterioration. Nutrition is temporarily provided through a vein. [88]

Why is breast milk so important?
Human milk contains protective immune, anti-inflammatory, and nutritional components that support the intestinal barrier and microbiota. A mother's own milk is considered the most protective factor, and donor milk reduces the risk compared to formula in very preterm infants. [89] [90]

Is it safe to give probiotics to a premature baby on your own?
No. Premature babies should not be given probiotics on their own. The U.S. Food and Drug Administration has warned of the risk of invasive infection and death in premature infants given probiotic products and has stated that such products are not approved for use in infants. [91]

Can the disease recur?
Yes, relapse is possible, especially in very premature babies and after a severe course. Therefore, after the first episode, feeding is resumed cautiously, and in complex cases, additional tests may be performed before feeding to rule out strictures. [92]

Key points from experts

Jaime Belkind-Gerson, MD, MS, University of Colorado, emphasizes in the MSD Manual that necrotizing enterocolitis is an acquired disease, primarily in premature or sick neonates, characterized by necrosis of the mucosa or deeper layers of the intestine, and treatment includes decompression, intravenous support, antibiotics, parenteral nutrition, and sometimes surgery. [93]

Alicia R. Pekarsky, MD, State University of New York Upstate Medical University, Upstate Golisano Children's Hospital. As a reviewer of the updated MSD Manual, she supports the current clinical emphasis: diagnosis is confirmed by imaging, and the risk is particularly high in premature infants weighing less than 1.5 kilograms (3.3 pounds) or with a gestational age of less than 32 weeks. [94]

Jacob G. Ginglen, MD, Mercyhealth Hospital and Midwestern University Chicago College of Osteopathic Medicine, and Nikolai Butki, MD, McLaren Oakland and Michigan State University College of Osteopathic Medicine, emphasize in a StatPearls review that the disease can rapidly progress from nonspecific signs to perforation, peritonitis, sepsis, and death, so a high clinical index of suspicion is necessary. [95]

Mary Quigley and co-authors of the 2024 Cochrane Review. Their key finding for prevention: donor human milk approximately halved the risk of necrotizing enterocolitis in very preterm or very low birth weight infants compared with formula.[96]

Experts from the US National Institute of Child Health and Human Development, 2024 Working Group. Their main scientific thesis: necrotizing enterocolitis remains a disease with incompletely understood causes, no uniform definition, and a great need for standardized diagnosis, prevention, and early biomarker research. [97]

Peter Marks, MD, PhD, director of the U.S. Food and Drug Administration's Center for Biologics Evaluation and Research, issued a practice warning regarding probiotics: Products containing live microorganisms may pose a serious risk to hospitalized premature infants if used prophylactically or therapeutically without a full evaluation of safety, effectiveness, and quality. [98]