Gastrointestinal perforation risk factors: Difference between revisions

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* Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract. [7,8][39,40].  
* Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract. [7,8][39,40].  
* Preterm infants have lower concentrations or more immature function of contributing mucosal defense factors than do term infants and adults [4].  
* Preterm infants have lower concentrations or more immature function of contributing mucosal defense factors than do term infants and adults [4].  
* Preterm infants have high levels of cytokines such as tumor necrosis factor, IL-1, IL-6, IL-8, IL-10, IL-12, and IL-18 that increase vascular permeability and attract inflammatory cells. [22,74-77].
* Preterm infants have high levels of cytokines such as tumor necrosis factor, IL-1, IL-6, IL-8, IL-10, IL-12, and IL-18 that increase vascular permeability and attract inflammatory cells.<ref name="pmid17027734">{{cite journal| author=Lin PW, Stoll BJ| title=Necrotising enterocolitis. | journal=Lancet | year= 2006 | volume= 368 | issue= 9543 | pages= 1271-83 | pmid=17027734 | doi=10.1016/S0140-6736(06)69525-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17027734  }}</ref>
* Human milk is more protective against NEC in preterm infants than formulas. The mucus coat of the intestine is less affected by human milk than formulas.  
* Human milk is more protective against NEC in preterm infants than formulas. The mucus coat of the intestine is less affected by human milk than formulas.  
* Growth factors within human milk repair disturbed layers in intestine.
* Growth factors within human milk repair disturbed layers in intestine.
* Bacterial colonization is believed to play a pivotal role in the development of NEC.  
* Bacterial colonization is believed to play a pivotal role in the development of NEC.  
* Rapid colonization of the intestinal tract by commensal bacteria from the maternal rectovaginal flora normally occurs. [8,21-24].
* Rapid colonization of the intestinal tract by commensal bacteria from the maternal rectovaginal flora normally occurs.<ref name="pmid11157169">{{cite journal| author=Hooper LV, Wong MH, Thelin A, Hansson L, Falk PG, Gordon JI| title=Molecular analysis of commensal host-microbial relationships in the intestine. | journal=Science | year= 2001 | volume= 291 | issue= 5505 | pages= 881-4 | pmid=11157169 | doi=10.1126/science.291.5505.881 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11157169  }}</ref>
* Ischemic insult to the GI tract has been proposed as a major contributor to NEC. [30,49,50]. Inflammatory mediators induced by ischemia, infectious agents, or mucosal irritants may cause mucosal injury. [22,73].  
* Ischemic insult to the GI tract has been proposed as a major contributor to NEC. [30,49,50]. Inflammatory mediators induced by ischemia, infectious agents, or mucosal irritants may cause mucosal injury.<ref name="pmid2194011">{{cite journal| author=Caplan MS, Hsueh W| title=Necrotizing enterocolitis: role of platelet activating factor, endotoxin, and tumor necrosis factor. | journal=J Pediatr | year= 1990 | volume= 117 | issue= 1 Pt 2 | pages= S47-51 | pmid=2194011 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2194011  }}</ref>
* Events that have been implicated in the development of NEC include:
* Events that have been implicated in the development of NEC include:
* [[perinatal asphyxia]] [51]
* [[perinatal asphyxia]] [51]

Revision as of 15:45, 8 January 2018


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]

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  • Violent retching can lead to spontaneous esophageal perforation, known as Boerhaave syndrome due to increased intraesophageal pressure in the lower esophagus. [51]
Gastric causes
  • Peptic ulcer disease is the most common cause of stomach and duodenal perforation.
  • Marginal ulcers may complicate procedures involving a gastrojejunostomy.
  • Perforated gastric ulcer is associated with a higher mortality, possibly related to delays in diagnosis. [121].
Small intestine causes
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Neonatal intestinal perforation risk factors

Risk factors for necrotizing enterocolitis (NEC):

  • Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract. [7,8][39,40].
  • Preterm infants have lower concentrations or more immature function of contributing mucosal defense factors than do term infants and adults [4].
  • Preterm infants have high levels of cytokines such as tumor necrosis factor, IL-1, IL-6, IL-8, IL-10, IL-12, and IL-18 that increase vascular permeability and attract inflammatory cells.[1]
  • Human milk is more protective against NEC in preterm infants than formulas. The mucus coat of the intestine is less affected by human milk than formulas.
  • Growth factors within human milk repair disturbed layers in intestine.
  • Bacterial colonization is believed to play a pivotal role in the development of NEC.
  • Rapid colonization of the intestinal tract by commensal bacteria from the maternal rectovaginal flora normally occurs.[2]
  • Ischemic insult to the GI tract has been proposed as a major contributor to NEC. [30,49,50]. Inflammatory mediators induced by ischemia, infectious agents, or mucosal irritants may cause mucosal injury.[3]
  • Events that have been implicated in the development of NEC include:
  • perinatal asphyxia [51]
  • Recurrent apnea
  • Respiratory distress syndrome
  • Hypotension
  • Congenital heart disease [52,53]
  • Patent ductus arteriosus
  • Umbilical arterial catheterization
  • Anemia
  • Polycythemia [54,55][59]
  • Medications such as theophylline or phenobarbital might irritate the intestinal mucosa. [70].

Risk factors for spontaneous intestinal perforation of the newborn:

References

  1. Lin PW, Stoll BJ (2006). "Necrotising enterocolitis". Lancet. 368 (9543): 1271–83. doi:10.1016/S0140-6736(06)69525-1. PMID 17027734.
  2. Hooper LV, Wong MH, Thelin A, Hansson L, Falk PG, Gordon JI (2001). "Molecular analysis of commensal host-microbial relationships in the intestine". Science. 291 (5505): 881–4. doi:10.1126/science.291.5505.881. PMID 11157169.
  3. Caplan MS, Hsueh W (1990). "Necrotizing enterocolitis: role of platelet activating factor, endotoxin, and tumor necrosis factor". J Pediatr. 117 (1 Pt 2): S47–51. PMID 2194011.