The following discussion will analyse the care of a baby who I have recently looked after in the high dependency who developed necrotising entero colitis(NEC) and consequently had to be re admitted to the NICU. According to Sankaran (2004) NEC is an inflammatory disease of the bowel, predominantly affecting premature infants but it sometimes occurs in ‘cohorts’. Whilst caring for the baby he became ill with a profound bradycardia and on turning him over he looked pale, cyanosed with a mottled skin and distended abdomen.
He weighed only 1050g, and had previously been moved from ITU to high dependency because he was tolerating full feeds of expressed breast milk (EBM). According to Boxwell (2010) NEC is characterised by transmural intestinal inflammation, ischaemia, necrosis and sometimes perforation which affects one to eight per cent of infants admitted to NICU. As a result of his condition the baby was transferred back to intensive care unit for close observation and further investigation. He had been born at 24 weeks +5 days gestation with a birth weight of 590g but was now 42 days old.
He had also had a blood transfusion the previous day and his mother had prolonged rupture of membranes. She had also received two doses of steroids prior to delivery. The actual cause of NEC is unknown but there are factors that are thought to contribute to the development of NEC such as birth asphyxia, umbilical catheterisation, artificial milk feeding and early feeding (Thomas and Harvey 1997). Blood transfusion, polycythemia and patent ductus arteriosus are other factors (Pearse and Roberton,1998).
Lin &Stoll (2006) suggests that giving feeds with high osmolarity or increasing the volume or rate of increase, can harm the bowel mucosa causing intra-mural milk providing a substrate for bacteria. According to Rennie and Roberton (2002) the severity of the condition can vary ranging from a stage where NEC is suspected to very severe symptoms, and lesions can occur anywhere from the stomach to the rectum and in some cases multiple areas may be affected. Several of these predisposing factors were noticed in the baby discussed.
He was premature and had respiratory distress syndrome and a PDA, and also had undergone umbilical catheterisation. The feed were increased rapidly due to his poor weight gain. According to McCormick (2000) neonatal nurses may also observe some early signs noting that the baby ‘doesn’t seem right’, or is experiencing difficulty absorbing the feed. She suggests that these are important observations of the possible early signs and the medical team need to be made aware of these if concerned.
As a result of the experience of caring for this baby I have decided to focus on the role of feeding as a factor in the pathogenesis of NEC, for this discussion. I need to increase my knowledge on this issue because neonatal nurses can often detect the early signs of NEC based on their observation of the baby’s feeding tolerance. The predisposing factors that contribute to the development of NEC will also be discussed. In relation to the baby in this case his feeding was increased rapidly as he also had a blood transfusion the previous day and had started to have episodes of bradycardia.
As identified previously he had a number of other predisposing factors such as prematurity, maternal steroids, PDA, blood transfusion and an umbilical catheter (Osborn 2005). Lucas and Cole (1990) carried out a prospective multicentre study on 926 preterm infants finding that cases of confirmed NEC was 6-10 times more common in exclusively formula fed babies than those who had been fed on breast milk alone and 3 times more common than in those who received formula plus breast milk. They also found a lower frequency of NEC was associated with delayed enteral feeding in formula fed infants.
Morgan, Young Land McGuire (2011) in a Cochrane review abstract found that slowly increasing the volume of milk feed to very low birth weight infants did not have any effect on the risk of NEC. According to Chabra (2006) advanced practices and monitoring and the use of specialist milks have reduced the risk of NEC in the first phase but it can still present weeks later. Osborn (2005) found that even though premature infants will be exposed to common risk factors, NEC develops in only 2-4 percent of infants admitted to NICU and that 90 % of reported cases occur in the preterm infant.
Beeby and Jeffrey (1992) highlight that NEC appears to increase with decreasing gestation and can be found in 10% of infants born at 25 weeks gestation compared to 0. 03% in term infants. According to Shelley (2009) the specific cause of NEC remains unknown despite intensive study over past 30 years though there is an association with ischemia. The initial ischemic insult may result from vasospasm of the mesenteric arteries, low blood flow during exchange transfusion, sepsis or use of hyperosmolar formulas (Cochram 2007).
Rennie and Roberton(2002) found that compromised placental blood flow can also increase the incidence. In contrast Merenstein and Gardner (2011) found that post natal diminished blood flow has increased incidence of NEC. According to Boxwell (2010) an increased incidence in the post transfusion period also has been reported also that congenital heart disease or arterial oxygen desaturation can lead to intestinal ischemia and as a result of the hypoxia and hypotension the body will divert the available oxygen and blood to vital organs instead of GI tract and as a result NEC will develop.
Increased intestinal permeability caused by the ischemic insult of the intestinal lining leaves the intestine susceptible to infection and predisposes to NEC (Cochram 2007). Furthermore, McComark (2000) states that ”exchange transfusions can be implicated because it can cause fluctuating mesenteric blood flow”. The baby in this case had a blood transfusion. Boyd (2000) points out that NEC and bowel perforation are common if the UAC is positioned at T7 and T8 due to occlusion of the superior mesenteric orifice.
Visceral blood flow may be disturbed and cause bowel injury if high UACs are left in situ for more than one week. “Part of the management of NEC should include removal of UAC if in situ” (McCormick 2000). The baby in this case had a UAC in situ at some point and also had a small PDA. Boxwell (2010) states that blood flow to the gut are compromised by left to right shunting through a PDA. According to Kliegman and Walsh (1992) even if no single organism is consistently associated with NEC, the blood cultures may be positive in more than a quarter of cases.
Crawford and Hickson (2002) state that the gas producing bacteria which normally reside in the intestine enters through the damaged intestinal mucosa, and the formula milk if started acts as a food source for the bacteria enhancing the bacterial proliferation. Kleigman et al (1992) states that isolated bacteria are often members of the normal gut flora. Klebsiella, E. coli, pseudomonas, enterobacter, salmonella, clostridium difficle, staphylococcus epidermis and viruses including corona virus, entero virus, and rota virus and some fungi are also organisms found in infants presenting with NEC (McComrmick 2000).
Because infection is the most consistent of all the risk factors, the policy in practice is to commence triple antibiotic therapy using gentamycin, flucloxacillin and metronidazole. Morris et al (1986), Bisset et al (1988) and Berseth (1989) suggests that prior to 29 weeks gestation immature peristaltic patterns exist which can lead to a slower passage of nutrients through the intestine with the possibility of an increase in number of bacteria. Udall (1990) supports this by stating these immature mechanisms as the most important factor in predisposing the infant to NEC.
This baby in this case immediately commenced on triple antibiotics. Using high osmolarity feeds or increasing the volume too quickly, can harm the mucosa (Lin and Stoll 2006) with intra mural milk providing a substrate for bacteria. However it has been found that preterm infants fed with colostrum appear to have a lower incidence of NEC (Schantler R J, Lau C, Hurst N M, Smith E O 2005) and the use of breast milk is shown to have a protective effect (Chauhan et al 2008). According to Boxwell (2010), 90% of infants with NEC have received enteral feeds.
In utero, most nutrition is provided via the placenta and the fetus swallows a 150ml/kg/day amniotic fluid but after birth this has to change from placental to enteral nutrition (McComark 2000). Lin and Stoll (2006) found that rapid advancement of enteral feeding leads to a greater incidence of NEC. In a retrospective study Anderson and Kleigman (1991) found infants with NEC had their feedings increased by a mean of 28ml/kg/day whereas control infants had their feedings increased by only 17ml/kg/day.
A greater incidence of NEC was also found in formula fed infants whose increments exceeded 30ml/kg/day McKeownet al (1992). In contrast, a study by Rayyis et al (1999) found the incidence was not increased with feeding increments of 35 ml /kg /day compared to 15ml/kg /day. Osterag et al (1986) warned against deciding to withhold milk in an effort to prevent NEC and that this should be carefully judged. They demonstrated that with holding milk feeds did not prevent NEC but merely delayed the onset. Lucas and Cole (1990) reports breast milk in some way protects and reduces the incidence of NEC.
Heiman and Schanler (2006) found that the use of banked breast milk is not as beneficial as mothers’ own milk because pasteurization affects the stability of cytokines. It has been observed that NEC is less likely to occur in infants fed with breast milk and conversely even may occur in some infants also have never received enteral feeds. Infant survival relies on early detection of NEC. McComark (2000) suggests that the early signs may be very subtle and easily mistaken or missed altogether also that the neonatal nurse is the best person to observe any early signs of NEC and alert the medical staff.
The nurses’ role is not only to assess the condition of the infant but also to inform a relationship with family in particular to help the parents understand their baby’s condition and to answer any questions. The parents of the baby discussed in this case were very distraught and angry towards staff and doctors because when their baby appeared to be doing well before he became ill with NEC. However once explanations had been given by a consultant they seemed to settle but always requested a consultant to speak to them. The precise factors involved in the development of NEC still remain unclear and unresolved.
I suggest that careful attention to feeding tolerance is the joint responsibility of the nurse and doctor. It is also important to observe the physical characteristics of the infant with regards to changes in condition such as lethargy, increased gastric residuals and abdominal distension because early treatment is associated with a decreased mortality (McCormick 2000). Also those cases can also occur in clusters or out breaks as reported by Koloske (1990). On analysis of the literature I have learnt that NEC can be due to a number of factors and not due to any single event.
It is also crucial to remember that not all infant presentations are the same and that careful nursing and medical care can significantly reduce the severity of NEC as it is often the nurse who is the first person to notice and suspect a change in the infants’ condition. The baby in this case was treated conservatively with antibiotics and resumed his feeding slowly with EBM and eventually recovered without surgery and was eventually transferred back to the special care baby unit. He slowly gained weight and managed on demand breast feeding.
The parents were very happy about his progress and their trust and confidence was restored as they were prepared to take him home. Sometimes parents feel overwhelmed when speaking to a doctor but generally feel more comfortable to talk about their baby with a nurse. It is also a part of the neonatal nurses’ role to recognise the parents requiring emotional, financial or psychological support. From this experience of nursing a baby with NEC I have learnt about the importance of close observation of the babies, in order to recognise the signs and symptoms early.
The benefits of breast milk in treatment and the responsibility of nursing staff to ensure that parents are aware of these benefits were also highlighted to me. I feel confident caring in such cases, and have better understanding of NEC, its signs and symptoms, predisposing factors, preventive measures and treatment. I hope that this will enable me to improve my practice and be able to share information with the parents and with new staff who have less experience in nursing infants.