The main risk factors for SIP are prematurity, VLBW, ELBW, stress, hypoxia, shock, premature rupture of membranes, umbilical catheterization, and indomethacin therapy. Congenital defects of the intestinal musculature is also a well-known risk factor for SIP [3,4,5]. Many of these factors are present in this reported case. The tools for differentiation between SIP and NEC are clinical, radiological examination, exploratory laparotomy and confirmation by histology [1, 2]. In this odd case (which we believe to be the youngest in the literature), the sequence of SIP followed by perforated NEC was present. SIP occurred in the first week while NEC perforation occurred in the second. Both conditions were identical clinically and radiologically and both showed the same picture of pneumoperitonium without the specific radiological signs of NEC. Upon exploration, SIP showed evidence of sealed perforation and completely normal stomach, small and large bowel (no histopathology specimens). Perforated NEC showed a 7 centimeters NEC affected segment with a 7-mm-wide perforation 40 cm proximal to the ileocecal junction. NEC perforation occurs due to coagulative necrosis which is unlikely to seal within few hours. It is possible for a tiny or small perforation to seal in a case of SIP. In contrast to NEC, histopathologic picture of SIP may show focal hemorrhagic necrosis, candida invasion, congenital defects with hypoplasia of the muscularis layer and thinning of the vessels in the submucosa [6, 7]. The histology in SIP shows normal mucosa and muscularis mucosa with high villi. Around the perforation, the mucosa and submucosa are congested, edematous with bloody infiltration. In the perforated area, the muscularis propria may be absent and no fibrosis nor thrombotic phenomena [3,4,5]. In our case, there was a mixed histopathological picture of coagulative necrosis and hemorrhagic necrosis co-existing together. Clinical and radiological pictures were not enough to differentiate between the two conditions. Hence, laparotomy and histopathologic examination were the tools to confirm the diagnosis . One case was reported in 1992 to have the two events of SIP at 2 days of age followed by NEC several weeks later when the case developed a typical clinical, radiological, and histological picture of NEC .
PPD can be used as a definitive treatment in stable patients of SIP without need for laparotomy [8,9,10,11]. The disadvantages of this conception is that it is successful at best in only 50% of patients , definitive diagnosis is never confirmed, proper management is not achieved and the golden hours for laparotomy may be missed. We believe that PPD is indicated only in unstable patients as a step for stabilization for laparotomy, proper surgical procedure and histological sampling.
In a case of perforated NEC, the authors believe that resection and stoma formation is the best option since the level of NEC extension into the bowel can be difficult to assign during surgery and the possibility of a delayed distal stricture to develop is always present. A water soluble distal loopogram is mandatory before stoma closure 2–3 months later. After SIP, the prognosis is usually better than perforated NEC. Primary closure of the perforation or resection and primary anastomosis is a well-accepted option. Postoperative feeding can be started earlier than NEC perforation, the stoma can be closed earlier, and distal stricture is unlikely .