Monitor Faecal Calprotectin Concentration in Infants With Heart Defects

Background:

Congenital heart disease is the most common birth defect in the U.K., affecting between 0.3-1.5% (9 in every 1000 live births) of infants (Hoffman and Kaplan 2002), and requires immediate surgical intervention. Infants with heart defects are known to exhibit early and progressive falls in their growth trajectory compared to healthy infants, increasing risk of death post-surgery (Eskedal, Hagemo et al. 2008). Lifesaving cardiac surgery and feeding can increase the infant's risk of developing gut inflammation and necrotising enterocolitis (NEC). NEC is a severe gastrointestinal disorder associated with high morbidity and mortality (Kelleher, Laussen et al. 2006).

Infants with cyanotic heart defects are at particular high risk of developing NEC due to impaired cardiac output which reduces blood flow to the gut, resulting in poor tissue oxygen perfusion, leading to gut ischemia (Neu and Walker 2011). It has been proposed that enteral feeding and lifesaving cardiac surgery - in particular the length of cardio-pulmonary bypass can further compromise the integrity of the gut wall (Golbus, Wojcik et al. 2011); however, the extent to which these interventions cause gut damage is unclear.

The initial clinical manifestations of NEC are nonspecific and indistinguishable from other type of sepsis. As a precautionary measure feed is often stopped in infants with suspected gut inflammation until symptoms have resolved, further contributing to poor growth. A six stage classification system has been devised to identify differing severity of NEC (Bell's Classification), stage six being the most severe level (Bell, Ternberg et al. 1978). A definitive diagnosis (Gold standard) of NEC is confirmed radiographically from abdominal X-Ray - signs include intramural gas, pneumatosis, and portal venus gas. The disease often has a rapid onset and therefore early detection of gut inflammation could avert severe gut damage and prolonged periods of parenteral nutrition on the cardiac intensive care unit (Sharma and Hudak 2013).

The relationship between feeding and the development of NEC has been well described in preterm infants with few incidences of NEC developing before feeding commences. However, this distinction is less clear in infants with cyanotic heart defects as compromised blood flow to the gut and cardiopulmonary bypass can result in damage before feeding commences (Iannucci, Oster et al. 2013). In light of the link between feeding and NEC it is imperative that the gastrointestinal tract is not overloaded by over feeding infants. Overfeeding can cause stasis of milk substrate in the gastrointestinal tract due to dysmotility leading to intestinal dilatation with fluid and gas and possibly to the impairment of the intestinal mucosal barrier. Intestinal dilatation in the presence of abnormal microbial colonisation (dysbiosis) can distort normal signal transduction across the intestinal wall barrier resulting in excessive inflammation and intestinal wall death (necrosis) (Ravindranath, Yoshioka et al. 1997).