The Necrotizing Enterocolitis ( NEC ) is a form of fragilisation of the bowel walls of the child which in most cases occurs among premature and new-born babies taken into intensive care units. While this condition is most likely to be controlled in its early stages, its diagnosis at that point is often difficult. Ensuing mortality rates of up to 80%, as we have experienced for infants in our care, make this one of the most fearsome challenges to be faced in Neonatology.

The origin and meaning of the processes leading to necrosis of the intestin have not yet been totally elucidated. Opinions differ on this subject, but the most widely accepted view purports that a prolonged ischemia caused by a vasoconstriction of the mesenteric system and affecting the terminal ileum and the colon be responsible. Several antecedents have been proposed as a cause for this vasomotor turmoil such as prenatal distress, hypoxia, blood exchange, catheterism of the umbilical artery, venous stasis due to an occlusion or enteritis, bacterial proliferation,or precocious feeding with cow's milk. Alternatively it can result from administering Theophylin to prevent premature deliveries, or Indometacin to activate the shutting down of the arterial canal.
However, not all distressed premature or new-born babies experiencing the same morbidity parameters fatally develop NEC. Such a dramatic physiological outcome would result from the compounded effect of several of the factors cited above occuring in conjunction with others linked to pre-exiting states of immaturity and hypoxia.
Epidemiological studies have confirmed the role played by the digestive mucous lining of the premature baby. In a hypoxic environment this lining tends to be permeable to germs and their toxins, as well as to the inflammation catalysts stemming from the fermentation of the enteral environment.

2. In any case, the nature of the resulting anatomical lesions vary. These can remain limited or even scar and give way to stenosis or ileal atresia type restructurings. In some cases, though admitedly rare, a lone septum abscess, a mesenteritis, or a gangrenous appendice are found. Present in the new-born these conditions can more appropriately be considered minor aspects of NEC. At other times the right iliatic pit is occupied by a front organized around one or several ileal, coecal, or colic perforations.

But more often, the intensity and the extent to which the morbidity process have occured are such that the digestive tube is unrecognizable; the ileal loops are dilated, dull, fragile, and bleeding at the lesser touch; perforations are numerous and staggered; the abdominal cavity is filled with nauseating liquid.
In these extreme cases a necropsic exploration shows evidence of the dissemination of the centers of purulence to the liver, pericard, and the lungs, as well as massive embolisation of the portal system due to bacterial fermentation.

3. From a clinical viewpoint the evolution is usually described in terms of a tiered progression:
    * the ileus phase characterized by abdominal distention and vomiting in conjunction with nauseating and glairy stools, quickly followed by
    * the occurrence of a toxic syndrome (lethargy, hypotonia, hypothermia) and an aggravation of digestive symptoms (bilious vomiting, bloody stools and a edematous infiltration of the abdominal wall) signifying a septic shock state the issue of  which can be fatal even in the absence of perforation.
    * the ultimate stage is peritonitis by intestinal perforation, and is clinically the most evocative of an NEC. The infiltration of the abdominal wall by an indurate edema and scleroerythematous plates is a good indication that flooding of the abdominal cavity by the intestinal contents has occured.

This classification in three distinct stages presents, in our view, only a didactic interest. Indeed, the intricate nature of these clinical symptoms in a context of pre-existing stress conditions does not manifest itself in such a succession of individualized evolutional states. In practice, it is only at the stercoral peritonitis stage of the NEC that surgical symptoms become so pre-eminent as to warrant an intervention under the most dramatic conditions one can imagine. Therefore, diagnosing an NEC prior to the preagonic stage requires one's full anticipation of this eventuality in the new-born at risk or in a state of distress. The proper attitude would require looking for precursory signs of perforation several times a day. In this regard, the input of medical imagery is essential since the radiological signs precede those of clinical symptomatology.

Radiological imagery of the abdomen can be repeated as often as necessary and does not call for any special preparation; its interpretation requires close scrutiny of the right iliac pit which is the area of predilection for the morbidity process to set in. As of late, the use of echography has tended to supersede that of conventional radiography and its need for laborious manipulations of a baby in a critical condition, and moored to numerous apparatus and ducts.
    * If symptoms of intraperitoneal effusion are easily recognizable, such is not the case when it comes to detecting the dissemination of gases between membranes of the digestive wall. When present, this pneumatosis appears as bright areas which are both thin and linear, or it can be detected as a rosary-like pattern of minute bubbles spread parallel to the intestinal tract. Indeed these images are very evanescent and variable from one picture to
the next.
    * More delicate still is the detection of gases migrating through the portal system. They can be located whithin the opacity of the liver's right lobe where one needs to look for clear and fine arborizations fanning out from a hilar starting point.
    * The intrabdominal effusion caused by the perforation of the digestive tract is on the other hand visible on X-rays taken of the vertical position. The underdiaphragmic gaseous crescent can then be reduced to its classical aspect. When abundant, these gases tend to suppress downward any mesocolic organs which come to float atop the fluid effusion below. This pneumoperitoneum is not as clear on X-rays taken in dorsal decubitus where it appears as a central gazous area from which project omphalic structures ( falciform ligaments, urachus, umbilical artery ).

5. A standard biological statement is of lesser value unless one can muster up the elaborate means required for an adequate appreciation of the inflammatory state, and the point at which it would be advisable to intervene (increase in immature granulocyts leucopenia and inflammatory thrombopenia, increase in inflammation catalysts ) or to adapt the antibiotherapy to germs identified in the culture sample.

6. The therapeutic step is complex and not yet adequately codified. The numerous proposed strategies attest to the divergence of opinions between pediatricians and surgeons as to the appropriate time for surgical exploration. In any case, given that effective means of controlling NEC are not yet available, therapeutical measures should be guided by the concern to prevent further deterioration. This entails restoring mesenteric irrigation, controlling bacterial proliferation, and identifying the appropriate time in the evolutive stages for surgical intervention.

. The medical follow up should be constantly readapted according to the evolutive changes occuring and ensure:
    * a minimum of hemodynamic confort and equilibrium,
    * an efficient hematosis,
    * continued antibacterial treatment,
    * resting the digestive tube while feeding adequately.
This intensive care schedule can only be successfull and help the infant overcome his distress if the medical staff adheres to certain imperatives, namely: an economy of gestures, discipline when it comes asepsy, and special care in avoiding aggravating factors such as hypothermia, promiscuity, aggressive handling, routine hygiene... Undertaken as early as possible, and constantly readjusted, this treatment is often effective.
The litterature is rich in observations of NEC cases exhibiting notable perforations which have favorably evolved in the absence of any surgical intervention.

6-2. What then are we to make of surgery's contribution in the context of this therapeutic program?
We are of the opinion that a child with an intestinal perforation should be put in the care of a surgeon, the child's condition and the extent of the anatomical lesions are what will in last resort decide of the appropriateness of surgical intervention notwithstanding three imperatives, namely, preserving Bauhin's value, resting the damaged segment of intestinal tract by performing an upper laparoenterostomy, and finally, reestablishing the continuity of the digestive tract at a later time if resection has occured.
In other words one should strive to do for the best and the least possible.

    * In the case of the moribund infant, surgical intervention, under local anesthesia, will consist of a simple " irrigation-drainage " procedure to be followed if possible by an upper laparoenterostomy.
    * The child's physical condition permitting, a more elaborate intervention should take place, namely explorative laparotomy to assess the lesions' extent and to conduct a complete peritoneal cleaning. Next, one can either undertake the resection of the perforated segment and a double enterostomia, or its extoriarization according to Mickulicz's procedure.
    * Finally, indications that a surgical approach is appropriate is not as straightforward for a simple  intestinal pneumatosis showing no peritonal syndrome, and no portal embolism. Under such  circumstances the reasonnable approach might better be described as one of "armed expectation".