Spontaneous resolution of colonic strictures caused by necrotizing enterocolitis: therapeutic implications

Tonkin, Ina L.D.; Bjelland, JC; Hunter, Tina D.; Mp, Capp; Firor, Hugh V.; Ermocilla, R

doi:10.2214/ajr.130.6.1077

Cited by 35 publications

(9 citation statements)

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“…This might explain spontaneous resolution of colonic strictures in some patients where the contrast studies were performed as early as two to three weeks after acute NEC. On the other hand, a group of infants with early and normal contrast studies was presented later in a life-threatening condition due to stricture formation with sepsis or perforation several weeks after apparently successful treatment of NEC (6,(12)(13)(14). In our conservatively treated group, we performed contrast studies only in patients who became symptomatic for an intestinal obstruction.…”

Section: Discussionmentioning

confidence: 99%

Late intestinal strictures following successful treatment of necrotizing enterocolitis

et al. 1994

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Between 1975 and 1992, in 16 infants (14%) out of 113 neonates with previous necrotizing enterocolitis (NEC) a total of 25 intestinal strictures had to be treated. Four (16%) were found in the ileum and 21 (84%) in the colon, and in 50% multiple strictures were present. In these 16 patients initial treatment for acute NEC included conservative treatment in 5, primary resection and enterostomies in 6 and proximal diverting enterostomies in 5. Therefore, the incidence of late strictures was 1 I YO after conservative therapy, 1 1 Yo after primary resection and 55% after primary proximal diverting enterostomies. An average of 49 days elapses between the recovery from NEC and the diagnosis of late strictures in conservatively treated patients. After initial surgical treatment, late strictures were detected on contrast studies on an average of 80 days. In pathologic specimens, marked fibrosis in the submucosa was consistently present in all strictures, whereas inflammatory changes in the mucosa, disruption or hypertrophy of the muscle layers or absence of ganglion cells were seen less frequently. All strictures were resected and primary end-to-end anastomosis was performed. But despite the development of late intestinal strictures, bowel preservation was improved after initial restrictive surgical therapy and aggressive medical treatment. 0 Late intestinal strictures, necrotizing enterocolitis G Schimpl,

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Section: Discussionmentioning

confidence: 99%

Late intestinal strictures following successful treatment of necrotizing enterocolitis

et al. 1994

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“…Ischemic lesions are replaced by submucosal granulation tissue which is transformed into a fibrotic obliterative scar (16,22). However, fibrotic scaring may not represent the only mechanism of stricture formations: Reports of pseudo-strictures (1) and spontaneous resolution of strictures following NNEC (25) had been explained by the formation of strictures which, after sustaining only moderate ischemic damage, heal without much fibrosis but the bowel subsequently continues to function abnormally. When assessment of nervous tissue had been included from histological examination, strictures showed an absence of ganglion cells in approximately 12 % (21).…”

Section: De(iciency O( Nanc-inhibitory Innervationimplication (Or (Unmentioning

confidence: 99%

Morphologic Alterations of the Enteric Nervous System and Deficiency of Non-Adrenergic Non-Cholinergic Inhibitory Innervation in Neonatal Necrotizing Enterocolitis

et al. 1998

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Although damage to intramural nervous tissue should be expected in neonatal necrotizing enterocolitis (NNEC), as the pathology of NNEC is defined by substantial destruction of the bowel wall, only a few studies have considered its implication. Thus, the aim of the study has been to examine morphological alterations of the enteric nervous system (ENS) in intestinal segments affected by NNEC. Immunohistochemical methods allowed the demonstration of both neuronal and glial elements and the assessment of an altered localization of non-adrenergic non-cholinergic (NANC) inhibitory mediators within the intramural plexuses. Intestinal segments from patients with NNEC (n = 8) and control subjects (n = 3) were obtained and submitted to immunohistochemical examination incubating with antibodies against protein gene product (PGP) 9.5, protein S-100, vasoactive intestinal polypeptide (VIP) and nitric oxide synthase (NOS). The most severe damage of nervous tissue was found within the plexus mucosus and plexus submucosus internus. The ganglionated plexuses showed a loss ot both glial and nerve cells with various stages of cell deterioration and the formation of central lesions within the myenteric ganglia. The observed neuropathologic changes correspond to the group of acquired segmental hypoganglionosis. Specimens from patients with NNEC were also characterized by an absence of immunoreactive VIP and NOS in the plexus submucosus and within the circular muscle layer. The deficiency in NANC inhibitory innervation may contribute to the formation of functional obstructions following acute NNEC. Furthermore, it is likely that the neuropathological lesions induced in early stages of NNEC may result in dysfunctional intestinal motility facilitating intraluminal bacterial overgrowth and translocation, and therefore, possibly promote the self-perpetuating pathophysiologic cycle culminating in progressive NNEC. As an additional finding, two patients with NNEC showed typical features of intestinal neuronal dysplasia (IND). The association of NNEC and IND is reviewed in the literature and possible causalties are discussed.

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“…Until recently, the only satisfactory treatment was by resection. Minor strictures, however, may not require resection; spontaneous healing has been documented in a few cases [25,27]. Such strictures may be amenable to nonoperative treatment.…”

Section: Late Operationsmentioning

confidence: 99%

Surgery of necrotizing enterocolitis

Kosloske

1985

World j. surg.

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Necrotizing enterocolitis (NEC) has become a frequent neonatal surgical emergency. This disease, characterized by crepitant intestinal necrosis, occurs primarily in premature infants. Operation is necessary if intestinal perforation or gangrene occurs. Of the many proposed indications for operation in NEC, those of proven validity are: pneumoperitoneum, a fixed dilated loop on serial x‐rays, erythema of the abdominal wall, an abdominal mass, or a positive paracentesis (consisting of brown fluid and/or bacteria on Gram's stain). Paracentesis has aided the early identification of infants with intestinal gangrene prior to perforation. Early recognition of gangrene is important because the mortality rate following operation after perforation (64%) is double that of operation for gangrene (30%). The cardinal principles of operation for acute NEC are excision of all the gangrenous bowel, exteriorization of the marginally viable ends, and preservation of as much intestine as possible. Our preferred method of exteriorization is by the Mikulicz enterostomy, because its subsequent closure appears to be safer than closure of a double enterostomy with separated stomas. The survival of infants operated on for NEC at the University of New Mexico Hospital was 34 of 63 (54%). Six late deaths occurred, for an overall survival of 28 of 63 (44%). Nine survivors (32%) required treatment for late intestinal strictures. Recent follow‐up studies on infants surviving NEC show an encouraging prognosis for normal growth and development.

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Spontaneous resolution of colonic strictures caused by necrotizing enterocolitis: therapeutic implications

Cited by 35 publications

References 0 publications

Late intestinal strictures following successful treatment of necrotizing enterocolitis

Late intestinal strictures following successful treatment of necrotizing enterocolitis

Morphologic Alterations of the Enteric Nervous System and Deficiency of Non-Adrenergic Non-Cholinergic Inhibitory Innervation in Neonatal Necrotizing Enterocolitis

Surgery of necrotizing enterocolitis

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