Necrotizing enterocolitis: Nursing

Necrotizing enterocolitis or NEC for short, is an inflammatory condition of the gastrointestinal tract characterized by mucosal damage and necrosis of the gastrointestinal wall. This is an urgent condition primarily seen in preterm infants.

Now, let’s cover some basic physiology and histology of the 4 main gastrointestinal layers. The outermost layer is called the adventitia or serosa and it’s thin and fibrous. Next up is the muscularis externa which is made up of smooth muscle cells located in the outer longitudinal layer and in the inner circular layer. These layers work together to move food forward via peristalsis which is a series of coordinated wave-like contractions.

The next layer is the submucosa, which consists of dense connective tissue that contains blood vessels, lymphatics, and nerves. Finally, the innermost layer is called the mucosa, which secretes mucus and digestive enzymes but also absorbs nutrients from the gastrointestinal lumen.

The intestines also contain a variety of non-pathogenic bacteria that make up a healthy intestinal flora. These aid with food digestion as well as protect the intestine from pathogenic microorganisms by out competing them. However, the fetus develops in a sterile environment, so their gastrointestinal tract is also sterile. Beneficial bacteria can only start colonizing their gastrointestinal tract during delivery and will continue after birth.

Now, the exact cause of necrotizing enterocolitis remains unknown, but some theories suggest that it’s associated with bacterial invasion of the gastrointestinal wall. Several risk factors have been associated with necrotizing enterocolitis, including prematurity, and low birth weight.

Another risk factor for necrotizing enterocolitis is formula-feeding, possibly due to the loss of protective components of breastmilk, such as oligosaccharides, lactoferrin, and cytokines. Other important risk factors include genetic predisposition and the use of antibiotics.

Now, the pathology of necrotizing enterocolitis is still not fully understood, but it’s thought to be due to the disruption of the normal bacterial flora of the gastrointestinal tract. So, when a trigger, like antibiotics or intestinal inflammation, kills off the beneficial bacteria, it allows pathogenic bacteria to multiply without competition.

In preterm infants, the immune system is weaker so it’s more difficult to eliminate the bacteria. However, it will still cause inflammation and damage nearby tissue. This allows the bacteria to invade into the gastrointestinal walls, where they can eventually cause transmural ischemia and necrosis of the gastrointestinal wall.

Necrotizing enterocolitis can lead to serious complications, including intestinal perforation, which can, in turn, cause peritonitis, and sepsis. In addition, short bowel syndrome can occur when a big part of the small intestine is damaged, which causes impaired water and nutrient absorption.

Now, clinical manifestations of necrotizing enterocolitis are initially nonspecific and include lethargy and poor feeding. But as the condition progresses, the infant usually develops gastrointestinal manifestations, such as nausea, bilious vomiting, diarrhea, and bloody stools.

Upon physical assessment, there can be abdominal distension, erythema, and tenderness, along with decreased bowel sounds, visible intestinal loops, or a palpable abdominal mass. In some cases, distended abdominal structures can compress the diaphragm and indirectly exert pressure on the lungs, so shallow and rapid breathing might be also observed.

In severe cases, an infant can develop systemic manifestations, like respiratory failure and circulatory collapse, which are typically associated with apnea, cyanosis, bradycardia, hypotension, and even shock.