The etiology of gastrointestinal perforations in the newborn

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Abstract

Perforations of the gastrointestinal tract occur in the newborn period as an apparently spontaneous event unrelated to such well-documented causes as peptic ulcerations, trauma due to intubation, perforations proximal to an obstruction, and brain damage. In spite of numerous theories proposed during the past century which attempt to demonstrate a cause and effect relationship, the majority of these lesions continue to be reported as spontaneous perforations of unknown etiology.

One is impressed with the consistent clinical picture presented by these infants with perforations of the gastrointestinal tract and it is only logical to assume that any lesion so consistent in symptoms and findings would have an equally consistent underlying cause. That gastrointestinal perforations in the newborn continue to be shrouded in mystery is not surprising in view of the following factors: (1) Individual series of cases so far reported are too small to permit recognition of a common etiologic factor. (2) In many instances, case reports are so poorly documented that it is useless to attempt to derive a common etiology from a study of cases collected from the literature. (3) There has been an artificial division of perforations based on their anatomic location (i.e., stomach, small bowel, or colon) and a concomitant failure to recognize that the histopathologic picture is essentially the same regardless of the location of the lesion. (4) There has been an interjection of misleading observations such as the theory of congenital muscular defects proposed by Herbut,1 in 1943. (5) The majority of authors have failed to recognize the similarity of so-called spontaneous perforations of the gastrointestinal tract regardless of the patient's age.

It is the purpose of this communication to dispel the myth of spontaneous perforation as well as to present evidence that perforations of the gastrointestinal tract are the result of ischemic necrosis related to an asphyxial defense mechanism characterized by selective circulatory ischemia which begins to function in the presence of stress, hypoxia, or shock.

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    Citation Excerpt :

    Although this study has limited power to determine the significance of risk factors for perforation, we observed that a higher proportion of babies with IIP had received antenatal NSAIDs and steroids, postnatal steroids and vasopressors, and initiation of enteral feeds and CPAP, when compared to controls. Previous studies, including a large data set from the Pediatrix Medical Group and several case series, have suggested possible antenatal risk factors including anatomic abnormalities (low birth weight, congenital diverticula, omphalomesenteric remnants, intussusceptions, compression from intraluminal meconium), physiologic deficiencies (hypoxia, ischemia), infections (chorioamnionitis), and medications (NSAIDs, steroids) [10,11,16,18,25,28–34]. Antenatal NSAIDs are commonly used as first-line agents in tocolysis (indomethacin), as well as for analgesia (ketorolac, ibuprofen), while steroids are used to accelerate fetal lung maturity and reduce mortality from respiratory distress syndrome [35,36].

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1

Attending Surgeon, The Children's Hospital of Michigan; Associate Surgeon, Harper Hospital; Instructor in Surgery, Wayne State University School of Medicine.

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