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Understanding intestinal vulnerability to perforation in the extremely low birth weight infant

Phillip V Gordon1

  • 1Department of Pediatrics, Ochsner Health System, New Orleans, Louisiana, 70121, USA. pvgordon@ochsner.org

Pediatric Research
|September 13, 2008
PubMed

Insights

Spontaneous intestinal perforation (SIP) in extremely low birth weight (ELBW) infants is linked to factors like early steroids and indomethacin. These risks converge on signaling pathways, potentially causing ileal damage and vulnerability during motility recovery.

Area of Science:

  • Neonatalogy
  • Gastroenterology
  • Pathology

Background:

  • Spontaneous intestinal perforation (SIP) is a significant concern in extremely low birth weight (ELBW) infants.
  • Recent advancements have improved understanding of SIP's multifactorial etiologies, including iatrogenic risks, microbiology, and histopathology.
  • Histopathology reveals focal perforations with muscularis externa necrosis, distinct from typical preterm bowel ischemic damage.

Purpose of the Study:

  • To elucidate the complex etiologies of spontaneous intestinal perforation (SIP) in extremely low birth weight (ELBW) infants.
  • To investigate the convergence of various risk factors on specific cellular signaling pathways.
  • To understand how these pathways contribute to ileal trophism and intestinal vulnerability.

Main Methods:

  • Review of existing literature on SIP etiologies, risk factors, microbiology, and histopathology.
  • Analysis of animal models to identify converging signaling pathways.
  • Examination of the role of nitric oxide synthases (NOS), insulin-like growth factors (IGFs), and epidermal growth factors (EGFs) in SIP pathogenesis.

Main Results:

  • Identified associations between SIP and extreme prematurity, early postnatal steroids (EPS), and early indomethacin use (EUI).
  • Common pathogens like Candida and Staphylococcus epidermis are frequently implicated.
  • Animal models suggest risk factors converge on NOS, IGFs, and EGFs signaling pathways, leading to ileal trophism (submucosal thinning, mucosal hyperplasia).
  • Global NOS depletion correlates with impaired intestinal motility and reduced transforming growth factor-alpha (TGF-alpha) in the muscularis externa.

Conclusions:

  • Multiple insults, including prematurity and medical interventions, converge on specific signaling pathways (NOS, IGFs, EGFs) in ELBW infants.
  • These pathways disrupt ileal trophism and diminish TGF-alpha, increasing susceptibility to perforation.
  • The findings suggest that altered intestinal motility during recovery phases, coupled with these molecular changes, renders the distal intestine vulnerable to SIP.

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