Necrotizing enterocolitis (NEC) most commonly occurs in premature infants, with the incidence of the disease being inversely proportional to the gestational age. It http://ebooksmedicine.net occurs in approximately 1 of 10 very-low-birth-weight infants (<1500 gm). In addition to prematurity, most cases are associated with enteral feeding, suggesting that some postnatal insult (such as the introduction of bacteria) sets in motion the cascade culminating in tissue destruction. Although infectious agents are likely to play a role in NEC pathogenesis, no single bacterial pathogen has been linked to the disease. A large number of inflammatory mediators have been associated with pathogenesis of NEC. One particular mediator, platelet-activating factor, has been implicated in increasing mucosal permeability by promoting enterocyte apoptosis and compromising intercellular tight junctions, thereby “adding fuel to the fire.”
NEC typically involves the terminal ileum, cecum, and right colon, although any part of the small or large intestine may be involved. The involved segment typically is distended, friable, and congested (
Fig. 7.26 ), or it can be frankly gangrenous; intestinal perforation with accompanying peritonitis may be seen. On microscopic examination, mucosal or transmural coagulative necrosis, ulceration, bacterial colonization, and submucosal gas bubbles are all features associated with NEC. Evidence of reparative changes, such as granulation tissue and fibrosis, may be seen shortly after resolution of the acute episode.
The clinical course is fairly typical, with the onset of bloody stools, abdominal distention, and development of circulatory collapse. Abdominal radiographs often demonstrate gas within the intestinal wall (pneumatosis intestinalis). When detected early, NEC often can be managed conservatively, but many cases (20% to 60%) require operative intervention including resection of the necrotic segments of bowel. NEC is associated with high perinatal mortality; infants who survive often develop post-NEC strictures from fibrosis caused by the healing process.
According to the National Institute of Child Health and Human Development, SIDS is defined as “the sudden death of an infant under 1 year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history.” It is important to emphasize that many cases of sudden death in infancy are found to have an anatomic or biochemical basis at autopsy (
Table 7.7 ); these should not be labeled as SIDS, but rather as sudden unexpected infant death (SUID). The Centers for Disease Control and Prevention estimates that SIDS accounts for approximately half of the cases of SUID in the United States. An aspect of SIDS that is not stressed in the definition is that the infant usually dies while asleep—hence the lay terms crib death and cot death. SIDS is the leading cause of death between the ages of 1 month and 1 year in U.S. infants, and the third leading cause of death overall in this age group, after congenital anomalies and diseases of prematurity and low birth weight. In 90% of cases, the infant is younger than 6 months; most are between the ages of 2 and 4 months. SIDS in an earlier sibling is associated with a fivefold relative risk of recurrence; traumatic child abuse must be carefully excluded under these circumstances.
SIDS is multifactorial condition, with a mixture of contributing causes in a given case. Three interacting variables have been proposed: (1) a vulnerable infant, (2) a critical developmental period in homeostatic control, and (3) one or more exogenous stressors. According to this model, several factors make the infant vulnerable to sudden