Successful use of the "patch, drain, and wait" laparotomy approach to perforated necrotizing enterocolitis: is hypoxia-triggered "good angiogenesis" involved?

The traditional and most frequently employed surgical approach to perforated necrotizing enterocolitis (NEC), laparotomy and bowel resection with enterostomy creation, has been associated with an unacceptably high mortality and major morbidity (sepsis, short-gut syndrome, strictures, long-term total parenteral nutrition (TPN), prolonged and costly hospitalizations with multiple operations, the inevitable open-and-close procedure for "hopeless" extensive gut ischemia in approximately 10% of laparotomy cases, etc.). The use of the laparotomy "patch, drain, and wait" (PD&W) approach to this serious of NEC complication has provided a simple, direct, and effective means of dealing with this problem. The basic principle is to resect no gut and do no enterostomies. The details are presented here as well as the multiple types of "patching" and the importance of use of extensive direct-vision draining with bilateral small Penrose drains from the undersurfaces of both diaphragms into the pelvis with exit sites in both lower quadrants. Proper and effective patching and draining cannot be done blindly,but requires direct vision (laparotomy or laparoscopy). The critical components and timing of the "waiting" are emphasized, including the vital importance of strict avoidance of early post-drainage laparotomy in the 7- to 14-day post-drainage period (whether the drainage is percutaneous, laparotomy PD&W, or laparoscopy PD&W) due to the early, life-threatening-ending hypervascularity that occurs at this time and if left unmolested will function beneficially as life- and gut-saving "good angiogenesis". The bilateral Penrose drains capture fecal fistulas and function quite well as de-facto enterostomies as the peritoneal cavity is rapidly obliterated by adhesions and massive, florid hypervascularity/gut hypoxia triggered "good angiogenesis" (no peritoneal cavity, no peritonitis). Broad-spectrum triple antibiotics and the routine use of TPN contribute to favorable results. The lessons/experiments of nature encountered in newborns with midgut atresia(s) and remarkable levels of gut survival, in the occasional case with only meconium peritonitis and no obstruction ("auto-anastomosis") are pertinent here as the TPN of PD&W is provided in atresia(s) by the maternal-placental circulation and the sterile peritoneal cavity of atresia(s) is simulated by the combination of antibiotics and peritoneal-cavity obliteration. Life- and gut-saving "good angiogenesis" is common to both situations. A 15-year personal experience with the PD&W laparotomy approach to perforated NEC in 23 cases is reported here with no mortality in the initial 60 postoperative days, no major morbidity, and no second operation required in 70% (spontaneous "auto-anastomosis") of cases. All infants with extensive gut ischemia/necrosis (NEC totalis) who would otherwise be classified as "hopeless" and managed by open-and-close only were managed in this experience successfully by PD&W with preservation of both life and an adequate amount of gut, although a second operation was required in these cases to re-establish intestinal continuity. A particularly striking observation was the rapid transition of these infants from profound illness to near-normalcy in a matter of hours after the initiation of PD&W--much like the rapid clinical changes accompanying the lancing of a boil or an abscess. An involvement of hypoxia-induced "good angiogenesis" with marked hypervascularity and involving molecules, genes, and receptors of the vascular endothelial growth factor family of hypoxia-induced angiogenesis molecules is speculated upon, and clinical studies to document these speculations are suggested as well as studies evaluating the potential of laparoscopic PD&W. The usefulness of Argyle chest-tube "venting" and "stenting" by trans-anal passage above colonic "patched" areas as seen in 2 cases is worthy of further study and use.