|Classification according to ICD-10|
|P77||Necrotic enterocolitis in the fetus and newborns|
|ICD-10 online (WHO version 2019)|
The necrotizing enterocolitis (abbreviation NEC or NEK ) is a disease of the intestine , which as a complication in the treatment of very small premature infants is feared with a birth weight below 1500 grams, and in this group of patients, the most common acute diseases of the bowel gastrointestinal tract is at all. A clear cause is not known. Various risk factors have been identified, but none of them are of decisive importance. The conservative treatment consists of a break in food and the administration of antibiotics or, if complications arise, in the surgical removal of the affected intestinal sections. Thus, necrotizing enterocolitis is a common cause of short bowel syndrome in childhood. A study from the United States on hospital mortality in premature infants estimates that mortality decreases with increasing birth weight to 42% in the lightest and 16% in the heaviest birth weight groups.
Necrotizing enterocolitis is most commonly responsible for the appearance of an acute abdomen in premature babies. It mainly occurs in the second to fourth week of life in very immature babies. For example, of all premature babies with a birth weight of less than 1500 g, around every tenth to twentieth - with consistent prophylactic early therapy in the first 24 hours up to one hundred and sixty - is affected by necrotizing enterocolitis. In the 1990s, the frequency of occurrence did not change, despite various advances in the treatment of premature infants. About 10% of all cases occur in full-term children. In relation to all newborns, the frequency is 0.3–2.4 cases per 1000 live births, with fluctuations from year to year and from treatment center to treatment center.
The origin of necrotizing enterocolitis is still not clearly understood. Volume deficiency shock , patent ductus arteriosus , lowering of blood pressure , heart failure with narrowing of the left ventricular outflow tract, such as coarctation of the aorta , respiratory distress syndrome with lack of oxygen in the blood , hypothermia , hypoglycemia , increased red blood cell count , insertion of a catheter into the umbilical cord vessels, various infections , and the gift of highly concentrated (hyper osmolar ) nutrient solutions and drugs have been named as risk factors . However, none of these known risk factors is individually of particular importance. It is possible that they are only an expression of a general high risk group for complications. The question of whether early enteral (via the gastrointestinal tract) nutrition represents a risk factor for the development of an NEC due to the immaturity of the intestine has long been controversial. After older studies suggested this, it has been refuted in more recent studies.
In a complex interplay of damage to the intestinal wall due to reduced blood flow (reduced perfusion) and infection, tissue destruction ( necrosis ) occurs in the intestinal wall, mostly in the area of the terminal ileum and the ascending colon, with the accumulation of putrefactive gases in the intestinal wall ( pneumatosis intestinalis ) . If the damage progresses, the intestinal wall can also perforate and inflammation of the abdominal cavity, especially the peritoneum ( peritonitis ), occurs due to the leaking intestinal contents . Sepsis is the result.
The main signs of necrotizing enterocolitis are distended abdomen with dilated loops of intestine that stop moving and become visible under the abdominal wall (bowel stiffness). The food is no longer tolerated and the newborns vomit bilious, bloody gastric juice. As a rule, the children no longer have a bowel movement or, if they do, the stool contains small amounts of blood. If the infection spreads from the intestinal loops throughout the body, causing sepsis, the general symptoms of sepsis also appear in newborns . These include a dirty gray skin color, restricted blood flow in the skin, respiratory and circulatory disorders. If the disease progresses, the abdomen becomes painful on pressure and the muscles of the abdominal wall tighten to defend themselves ( defense tension ), which indicates an inflammation of the peritoneum, a peritonitis . A reddening of the flanks is a late sign of peritonitis and often indicates that a hole has formed in the damaged intestinal wall .
Diagnosis and differential diagnosis
In addition to the repeated physical examination, the blood tests and the taking of blood cultures, various apparatus-based examination methods are used. In the x-ray of the abdominal cavity, the intestinal loops are enlarged and the intestinal walls thickened and, in the case of pneumatosis intestinalis , the gas bubbles in the intestinal wall and the intestinal veins that extend into the porta hepatic (portal veins) can be seen as lightened points. If the perforation has already occurred, free air can also be seen in the abdominal cavity. The intestinal walls also appear thickened on ultrasound and air bubbles can be seen in the intestinal wall and in the portal veins. A possible co-causing infection can be detected by a blood culture and appropriate stool examinations.
Necrotizing enterocolitis must be differentiated from a meconium plug , congenital malformations of the gastrointestinal tract and intestinal perforations of other causes with microcolons , including those that have arisen through medical measures ( iatrogenic ), if the symptoms are appropriate .
If the diagnosis is certain, nutrition via the gastrointestinal tract must be stopped for up to ten days and fully guaranteed via infusions ( total parenteral nutrition ). Treatment with antibiotics is the same as in other cases of sepsis in newborns. The circulation is supposed to be supported to improve the blood flow to the intestinal wall by volume administration and possibly also the catecholamine dopamine in low doses. Artificial ventilation is usually necessary. The food can be built up very carefully when the abdomen is clinically normal again. In the case of perforation or inflammation of the peritoneum (peritonitis), surgical therapy by a pediatric surgeon is required. It is better to do this at an early stage so that as few affected intestinal parts as possible have to be removed. An artificial anus ( enterostomy ) is temporarily created. 8-10 days after the operation you can begin to rinse the leg of the anus praeter leading to the anus with glucose solution and later also milk food or, better still, stool from the supplying leg.
Researchers are working on new therapeutic options for the disease. For example, attempts are being made to use stem cells from the amniotic fluid to cure the disease better. At least in the experiment with rats it was possible to achieve success.
The prognosis depends on how quickly the presence of necrotizing enterocolitis and the resulting sepsis is recognized and treatment is started. If the sepsis can be well controlled with medication, the prognosis of the affected newborn is not bad. About five to ten percent of newborns affected by necrotizing enterocolitis die. If the necrosis has spread to a large section of the intestine that must be removed if it does not recover, the child will develop short bowel syndrome .
As a preventive measure, attempts have been made to administer antibodies from blood donors ( immunoglobulins ) to premature babies either via the vein or orally. However, the preventive effect is not sufficiently guaranteed. Preventive treatment with oral antibiotics reduces the risk of necrotizing enterocolitis, but is not used routinely because of the generation of resistance . The administration of erythropoietin should be able to prevent the NEC because of the improvement in the oxygen supply and protection against cell death ( apoptosis ). Breast milk contains several factors that can protect against NEC, although it should be noted that these factors are likely to be destroyed by pasteurization . Drugs that contain certain natural intestinal bacteria ( probiotics ) or substances that specifically promote the growth of these bacteria ( prebiotics ) by promoting natural colonization of the intestines in premature babies may be able to reduce the frequency of NEC. This is the subject of current studies.
- Friedrich Carl Sitzmann (Ed.): Pediatrics. 2nd, completely revised edition. Georg Thieme Verlag, Stuttgart 2002, ISBN 3-13-125332-0 , pp. 124-126.
- Monica Epelman et al. a .: Necrotizing Enterocolitis: Review of State-of-the-Art Imaging Findings with Pathologic Correlation. In: RadioGraphics. 2007, 27, p. 2, 285–305, Radiological and histological images (English) accessed on January 11, 2014, doi: 10.1148 / rg.272055098
- ↑ Mortality of necrotizing enterocolitis expressed by birth weight categories. In: Journal of Pediatric Surgery. Volume 44, Issue 6, June 2009, p. 1074. (Abstract)
- ^ Dietrich von Schweinitz, Benno Ure: Pediatric surgery: Visceral and general surgery of childhood . Springer-Verlag, 2013, ISBN 978-3-642-29779-3 ( google.de [accessed on November 9, 2016]).
- ↑ a b c W. A. Mihatsch u. a .: Early enteral feeding in very small premature infants is not associated with necrotizing enterocolitis. In: Monthly Pediatrics. 2002, 150, pp. 724-733.
- ↑ a b c d e f g h R. Roos u. a .: Checklist neonatology. The neo-ABC. Georg Thieme Verlag, Stuttgart 2001, ISBN 3-13-125051-8 .
- ↑ A. Zani, M. Cananzi, F. Fascetti-Leon, G. Lauriti, VV Smith, S. Bollini, M. Ghionzoli, A. D Arrigo, M. Pozzobon, M. Piccoli, A. Hicks, J. Wells , B. Siow, NJ Sebire, C. Bishop, A. Leon, A. Atala, MF Lythgoe, A. Pierro, S. Eaton, P. De Coppi: Amniotic fluid stem cells improve survival and enhance repair of damaged intestine in necrotising enterocolitis via a COX-2 dependent mechanism. In: Good. doi: 10.1136 / gutjnl-2012-303735 .