Fig. 31.1
Clinical photograph of a premature infant who is typically susceptible to NEC
Incidence
The incidence of NEC is variable but generally affects 1–3 per 2000–4000 live births or between 1 and 5 % of neonatal intensive care unit admissions.
The condition is typically seen in premature infants with an incidence of 30 per 1000 live births for extremely low-birth-weight neonates and 7–10 % of infants who weigh < 1500 g.
Currently, NEC is occurring in more neonates, possibly because of the higher incidence and survival of premature and low-birth-weight neonates.
NEC sometimes seems to occur in “epidemics,” affecting several infants in the same nursery .
Etiology
The exact etiology of NEC is unknown.
NEC usually occurs within the first 2–3 weeks of life.
Term infants, however develop NEC much earlier, with the average age of onset within the first week of life or, sometimes, within the first 1–2 days of life.
The etiology is multifactorial.
An ischemic or toxic event that causes damage to the immature gastrointestinal mucosa and loss of mucosal integrity has been proposed to precede NEC development.
Conditions that compromise the intestinal circulation include:
Polycythemia/hyperviscosity
Birth asphyxia
Exchange blood transfusion
Severe congenital heart disease
An infectious agent has been suspected, as cluster outbreaks in neonatal intensive care units have been seen.
Gram-positive and gram-negative bacteria, fungi, and viruses have all been isolated from affected infants; however, many infants have negative cultures.
Infectious organisms are thought to play a key role in the development of NEC.
Positive blood cultures are found in 30 % of patients; the most commonly identified organisms are Escherichia coli and Klebsiella pneumoniae. Other organisms include Proteus mirabilis, Staphylococcus aureus, S. epidermidis, Enterococcus species, Clostridium perfringens, and Pseudomonas aeruginosa.
There are several risk factors for developing NEC. These include:
1.
Premature neonates (less than 34 weeks’ gestation)
2.
Those of low birth weight (< 5 lb; 2.3 kg)
3.
Enteral formula feeding
4.
A difficult delivery and lowered oxygen levels during labor
5.
Mechanical ventilation
6.
Umbilical artery catheterization
7.
Patent ductus arteriosus
8.
Premature rupture of membranes
9.
Patients treated with indomethacin to close PDA
10.
Polycythemia/hyperviscosity and exchange blood transfusion
Clinical Features
NEC most commonly affects the terminal ileum and the proximal ascending colon.
However, varying degrees of NEC can affect any segment of the small intestine or colon.
The near entire bowel may be also involved (NEC totalis) and may be irreversibly damaged.
NEC represents a significant clinical problem and the clinical features are variable depending on the severity and extent of bowel involvement. Symptoms may come on slowly or suddenly.
The classic clinical triad consists of:
Abdominal distension
Bloody stools
Pneumatosis intestinalis
The clinical presentation of NEC however includes nonspecific symptoms such as vomiting, diarrhea, feeding intolerance, and high gastric residuals following feedings.
With disease progression, abdominal tenderness, abdominal wall edema, erythema, or palpable bowel loops indicating a fixed and dilated loop of bowel may develop.
Systemic signs, such as apnea, bradycardia, lethargy, labile body temperature, hypoglycemia, and shock, are indicators of physiologic instability.
The Bell system is the staging system most commonly used to describe NEC.
Bell stage I suspected NEC:
Stage IA characterized by the following:
Mild, nonspecific systemic signs such as apnea, bradycardia, and temperature instability.
Mild intestinal signs such as increased gastric residuals and mild abdominal distention.
Radiographic findings can be normal or can show some mild nonspecific distention.
Stage IB diagnosis is the same as stage IA, with the addition of grossly bloody stool.
Bell stage II definite disease:
Stage IIA characterized by the following:
Patient is mildly ill.
Diagnostic signs include the mild systemic signs present in stage IA.
Intestinal signs include all of the signs present in stage I, with the addition of absent bowel sounds and abdominal tenderness.
Radiographic findings show ileus and/or pneumatosis intestinalis.
This diagnosis is sometimes referred to as “medical” NEC as surgical intervention is not needed to successfully treat the patient.
Stage IIB characterized by the following:
Patient is moderately ill.
Diagnosis requires all of stage I signs plus the systemic signs of moderate illness, such as mild metabolic acidosis and mild thrombocytopenia.
Abdominal examination reveals definite tenderness, erythema, and/or right lower quadrant mass.
Radiographs show portal venous gas with or without ascites.
Bell stage III advanced disease:
This stage represents advanced, severe NEC that has a high likelihood of surgical intervention.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
