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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. | * 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. | * 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. | * 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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Overview
Instrumentation
- Instrumentation of the gastrointestinal tract includes upper endoscopy, sigmoidoscopy, colonoscopy, stent placement, endoscopic sclerotherapy, nasogastric intubation, esophageal dilatation, and surgery. [10,11, 12, 13]
- The area of the esophagus at most risk for instrumental perforation is Killian's triangle, the part of the pharynx formed by the inferior pharyngeal constrictor and cricopharyngeus muscle.
- Immunosuppressed individuals may be at increased risk for dehiscence and deep organ space infection following surgery. [32]
Other causes
- Medications: Aspirin, potassium supplements, disease-modifying antirheumatic drugs (DMARDs), and nonsteroidal anti-inflammatory drug (NSAID) use has been associated with perforation of colonic diverticula. 43 48, 44
- Foreign bodies such as sharp objects, food with sharp surfaces, or gastric bezoar. 34-37
- 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
- Perforation of the small intestine can be related to bowel obstruction, acute mesenteric ischemia, inflammatory bowel disease, or due to iatrogenic or noniatrogenic traumatic mechanisms. [53]
- Abdominal wall, groin, diaphragmatic, internal hernia, paraesophageal hernia, and volvulus can all lead to perforation due to ischemia.
- Injuries to the small intestine during laparoscopic procedures are often not recognized during the procedure. [22]
- Crohn's disease has a propensity to perforate slowly, leading to formation of fistula. [52,53]
- Diseases such as typhoid, tuberculosis, or schistosomiasis can perforate the small intestine.
- The perforations usually occur in the ileum at necrotic Peyer's patches.
- A reperforation rate of 21.3 percent has been reported for typhoid perforation closure. [136] [61]
Large intestine causes
- Colonic diverticulosis is common in the developed world. These diverticula can become inflamed and perforate and may lead to abscess formation.
- Mesenteric ischemia increases the risk for perforation. Embolism, mesenteric occlusive disease, and heart failure lead to gastrointestinal ischemia. [59]
- Neoplasms can perforate by direct penetration and necrosis, or by producing obstruction. [64-66
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:
- Placental chorioamnionitis appears to be an antenatal risk factor for SIP. [11].
- Antenatal administration of glucocorticoids, nonsteroidal antiinflammatory drugs, indomethacin, and magnesium sulfate had been initially reported to increase the risk of SIP. [13,15,16].
- Delayed onset of feeding
- Intraventricular hemorrhage of Grade III or higher [24,25]
References
- ↑ Lin PW, Stoll BJ (2006). "Necrotising enterocolitis". Lancet. 368 (9543): 1271–83. doi:10.1016/S0140-6736(06)69525-1. PMID 17027734.
- ↑ 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.
- ↑ 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.