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==Overview==
==Overview==
Risk factors for gastrointestinal perforation varies between instrumentation during [[upper endoscopy]], [[sigmoidoscopy]], [[colonoscopy]], [[stent]] placement, [[Sclerotherapy|endoscopic sclerotherapy]], [[nasogastric intubation]], [[esophageal dilatation]], and surgery. Other risks include medications especially [[Aspirin]], potassium supplements, [[Disease-modifying antirheumatic drug|disease-modifying antirheumatic drugs]] (DMARDs), and [[Non-steroidal anti-inflammatory drug|nonsteroidal anti-inflammatory drug]]. [[Peptic ulcer disease]] is the most common cause of stomach and duodenal perforation. [[Diverticulosis|Colonic diverticulosis]] is common risk for colonic perforation in the developed world. [[Mesenteric ischemia]] increases the risk for perforation. [[Embolism]], [[mesenteric]] occlusive disease, and [[heart failure]] lead to gastrointestinal [[ischemia]]. In neonatal perforation, [[prematurity]] is the commonest risk factor. Antenatal administration of [[glucocorticoids]], [[nonsteroidal antiinflammatory drugs]], [[Indomethacin|indomethacin,]] and [[magnesium sulfate]] had been initially reported to increase the risk of perforation.


==Gastrointestinal perforation risk factors==
===== '''Instrumentation''' =====
===== '''Instrumentation''' =====
* Instrumentation of the gastrointestinal tract includes upper endoscopy, sigmoidoscopy, colonoscopy [10,11], stent placement [10,11], endoscopic sclerotherapy [12], nasogastric intubation [13], esophageal dilation, and surgery.
* Instrumentation of the [[gastrointestinal tract]] includes [[upper endoscopy]], [[sigmoidoscopy]], [[colonoscopy]], [[stent]] placement, [[Sclerotherapy|endoscopic sclerotherapy]], [[nasogastric intubation]], [[esophageal dilatation]], and surgery.<ref name="pmid19496201">{{cite journal| author=Akbulut S, Cakabay B, Ozmen CA, Sezgin A, Sevinc MM| title=An unusual cause of ileal perforation: report of a case and literature review. | journal=World J Gastroenterol | year= 2009 | volume= 15 | issue= 21 | pages= 2672-4 | pmid=19496201 | doi= | pmc=2691502 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19496201  }}</ref>
* The area of the esophagus at most risk for instrumental perforation is Killian's triangle [18], which is the part of the pharynx formed by the inferior pharyngeal constrictor and cricopharyngeus muscle.  
* 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 muscle|inferior pharyngeal constrictor]] and [[cricopharyngeus muscle]].
* Gastrointestinal leakage can also occur postoperatively as a result of anastomotic breakdown. [24-31].
* [[Immunosuppressed]] individuals may be at increased risk for dehiscence and deep organ space infection following surgery.<ref name="pmid21367368">{{cite journal| author=Ismael H, Horst M, Farooq M, Jordon J, Patton JH, Rubinfeld IS| title=Adverse effects of preoperative steroid use on surgical outcomes. | journal=Am J Surg | year= 2011 | volume= 201 | issue= 3 | pages= 305-8; discussion 308-9 | pmid=21367368 | doi=10.1016/j.amjsurg.2010.09.018 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21367368  }}</ref>
* Immunosuppressed individuals may be at increased risk for dehiscence and deep organ space infection following surgery. [32]


===== Other causes =====
===== 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, with diclofenac and ibuprofen being the most commonly implicated drugs. 43 48, 44
* Medications: [[Aspirin]], potassium supplements, [[Disease-modifying antirheumatic drug|disease-modifying antirheumatic drugs]] (DMARDs), and [[Non-steroidal anti-inflammatory drug|nonsteroidal anti-inflammatory drug]] (NSAID) use has been associated with perforation of [[Colonic diverticulitis|colonic diverticula]].<ref name="pmid27405509">{{cite journal| author=Strangfeld A, Richter A, Siegmund B, Herzer P, Rockwitz K, Demary W et al.| title=Risk for lower intestinal perforations in patients with rheumatoid arthritis treated with tocilizumab in comparison to treatment with other biologic or conventional synthetic DMARDs. | journal=Ann Rheum Dis | year= 2017 | volume= 76 | issue= 3 | pages= 504-510 | pmid=27405509 | doi=10.1136/annrheumdis-2016-209773 | pmc=5445993 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27405509  }}</ref>
* Foreign bodies such as sharp objects, food with sharp surfaces, or gastric bezoar. 34-37
* Foreign bodies such as sharp objects, food with sharp surfaces, or gastric bezoar.  


* Violent retching can lead to spontaneous esophageal perforation, known as Boerhaave syndrome due to increased intraesophageal pressure in the lower esophagus. [51]
* Violent retching can lead to spontaneous esophageal perforation, known as [[Boerhaave syndrome]] due to increased intraesophageal pressure in the lower esophagus.<ref name="pmid17993968">{{cite journal| author=Wu JT, Mattox KL, Wall MJ| title=Esophageal perforations: new perspectives and treatment paradigms. | journal=J Trauma | year= 2007 | volume= 63 | issue= 5 | pages= 1173-84 | pmid=17993968 | doi=10.1097/TA.0b013e31805c0dd4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17993968  }}</ref>


===== '''Gastric causes''' =====
===== '''Gastric causes''' =====
* Peptic ulcer disease is the most common cause of stomach and duodenal perforation.  
* [[Peptic ulcer disease]] is the most common cause of stomach and duodenal perforation.<ref name="pmid2730181">{{cite journal| author=Horowitz J, Kukora JS, Ritchie WP| title=All perforated ulcers are not alike. | journal=Ann Surg | year= 1989 | volume= 209 | issue= 6 | pages= 693-6; discussion 696-7 | pmid=2730181 | doi= | pmc=1494136 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2730181  }}</ref>
* Marginal ulcers may complicate procedures involving a gastrojejunostomy.  
* Marginal ulcers may complicate procedures involving a [[gastrojejunostomy]].  
* Perforated gastric ulcer is associated with a higher mortality, possibly related to delays in diagnosis [121].  
* Perforated gastric ulcer is associated with a higher mortality, possibly related to delays in diagnosis.  


===== '''Small intestine causes''' =====
===== '''Small intestine causes''' =====
* Perforation of the small intestine can be related to bowel obstruction, acute mesenteric ischemia, inflammatory bowel disease [53], or due to iatrogenic or noniatrogenic traumatic mechanisms.   
* 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.<ref name="pmid19357730">{{cite journal| author=Eid HO, Hefny AF, Joshi S, Abu-Zidan FM| title=Non-traumatic perforation of the small bowel. | journal=Afr Health Sci | year= 2008 | volume= 8 | issue= 1 | pages= 36-9 | pmid=19357730 | doi= | pmc=2408541 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19357730  }}</ref>  
* Abdominal wall, groin, diaphragmatic, internal hernia, paraesophageal hernia, and volvulus can all lead to perforation either related to bowel wall ischemia from strangulation, or pressure necrosis.   
* [[Abdominal wall hernia|Abdominal wall]], [[Groin hernia|groin]], [[Diaphragmatic hernia|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]
* Injuries to the [[small intestine]] during [[Laparoscopic surgery|laparoscopic procedures]] are often not recognized during the procedure.  
* Croh'n disease has a propensity to perforate slowly, leading to formation of entero-enteric or enterocutaneous fistula formation. [52,53]
* [[Crohn's disease]] has a propensity to perforate slowly, leading to formation of fistula.  


* 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]
* Diseases such as [[Typhoid fever|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.


===== Large intestine causes =====
===== Large intestine causes =====
* Colonic diverticulosis is common in the developed world. These diverticula can become inflamed and perforate and may lead to abscess formation.
* [[Diverticulosis|Colonic diverticulosis]] is common in the developed world. These diverticula can become inflamed and perforate and may lead to [[abscess]] formation.<ref name="pmid20064683">{{cite journal| author=Spoormans I, Van Hoorenbeeck K, Balliu L, Jorens PG| title=Gastric perforation after cardiopulmonary resuscitation: review of the literature. | journal=Resuscitation | year= 2010 | volume= 81 | issue= 3 | pages= 272-80 | pmid=20064683 | doi=10.1016/j.resuscitation.2009.11.023 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20064683  }}</ref>


* Mesenteric ischemia increases the risk for perforation. Embolism, mesenteric occlusive disease, and heart failure lead to gastrointestinal ischemia. [59]
* [[Mesenteric ischemia]] increases the risk for perforation. [[Embolism]], mesenteric occlusive disease, and [[heart failure]] lead to gastrointestinal ischemia.
* Neoplasms can perforate by direct penetration and necrosis, or by producing obstruction. [64-66
* [[Neoplasm|Neoplasms]] can perforate by direct penetration and [[necrosis]], or by producing obstruction.


== Neonatal intestinal perforation risk factors ==
== Neonatal intestinal perforation risk factors ==


=== Risk factors for necrotizing enterocolitis: ===
=== 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. [22,74-77].
* Ninety percent of NEC cases occur in [[Premature birth|preterm infants]] due to immaturity of the [[gastrointestinal tract]].  
* 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.
* Preterm infants have lower concentrations or more immature function of contributing mucosal defense factors than do term infants and adults.  
* 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].
* 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>
* 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]. Circulatory events that have been implicated in the development of NEC include perinatal asphyxia [51], recurrent apnea, hypoxia from severe respiratory distress syndrome, hypotension, congenital heart disease [52,53], patent ductus arteriosus, heart failure, umbilical arterial catheterization, anemia, polycythemia [54,55], and red blood cell [56-58] and exchange transfusions [59].
* 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.  
* Hyperosmolar medications may result in NEC. Oral medications such as theophylline, multivitamins, or phenobarbital contain hypertonic additives that might irritate the intestinal mucosa. [70].
* 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.<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.<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:<ref name="pmid25868405">{{cite journal| author=Fisher JG, Bairdain S, Sparks EA, Khan FA, Archer JM, Kenny M et al.| title=Serious congenital heart disease and necrotizing enterocolitis in very low birth weight neonates. | journal=J Am Coll Surg | year= 2015 | volume= 220 | issue= 6 | pages= 1018-1026.e14 | pmid=25868405 | doi=10.1016/j.jamcollsurg.2014.11.026 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25868405  }}</ref>
* [[perinatal asphyxia]]
* Recurrent [[apnea]]
* [[Acute respiratory distress syndrome|Respiratory distress syndrome]]
* [[Hypotension]]
* [[Congenital heart disease]]
* [[Patent ductus arteriosus]]
* Umbilical arterial catheterization
* [[Anemia]]
* [[Polycythemia]] [54,55][59]
* Medications such as [[theophylline]] or [[phenobarbital]] might irritate the intestinal mucosa.<ref name="pmid1174138">{{cite journal| author=Book LS, Herbst JJ, Atherton SO, Jung AL| title=Necrotizing enterocolitis in low-birth-weight infants fed an elemental formula. | journal=J Pediatr | year= 1975 | volume= 87 | issue= 4 | pages= 602-5 | pmid=1174138 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1174138  }}</ref>


=== Risk factors for spontaneous intestinal perforation of the newborn: ===
=== Risk factors for spontaneous intestinal perforation of the newborn ===
* Severe placental chorioamnionitis appears to be an antenatal risk factor for SIP. In one case-control study of 16 preterm infants with SIP, infants with SIP versus matched controls were more likely to have severe placental chorioamnionitis with evidence of fetal vascular response based upon a blinded retrospective histologic examination of the placenta and umbilical vessels (40 versus 12 percent) [11]. In this study, mothers of infants with SIP were more likely to have received antibiotics before or at delivery (93 versus 57 percent).
* Placental [[chorioamnionitis]] appears to be an antenatal risk factor for SIP.<ref name="pmid2348301">{{cite journal| author=Caplan MS, Sun XM, Hseuh W, Hageman JR| title=Role of platelet activating factor and tumor necrosis factor-alpha in neonatal necrotizing enterocolitis. | journal=J Pediatr | year= 1990 | volume= 116 | issue= 6 | pages= 960-4 | pmid=2348301 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2348301  }}</ref>
* Although antenatal administration of glucocorticoids, nonsteroidal antiinflammatory drugs (NSAIDs) and magnesium sulfate had been initially reported to increase the risk of SIP, subsequent data have not demonstrated a clear association of SIP with any of these factors [13,15,16].
* Antenatal administration of [[glucocorticoids]], [[nonsteroidal antiinflammatory drugs]], [[Indomethacin|indomethacin,]] and [[magnesium sulfate]] had been initially reported to increase the risk of SIP.
* In a small retrospective study, additional reported risk factors for SIP in VLBW infants in 8 cases versus 32 controls included oligohydramnios, velamentous cord insertion, lower one minute Apgar scores, and primigravidity [17]. However, these findings need to be confirmed in a larger cohort of cases.
* Delayed onset of feeding
* Exposure to glucocorticoids: Early administration of postnatal glucocorticoids increases the risk of SIP [18-20]. This was best illustrated in a meta-analysis of four trials of prophylactic dexamethasone for the prevention of bronchopulmonary dysplasia in which VLBW infants treated with dexamethasone before 48 hours of life had an increased risk of SIP compared with controls (odds ratio [OR] 1.91, 95% CI 1.21-3.07) [18].
* [[Intraventricular hemorrhage]] of Grade III or higher.
* Exposure to indomethacin: Although the postnatal use of indomethacin had been previously reported to increase the risk of SIP [15], subsequent publications have reported no association between indomethacin exposure and SIP [12,21,22].
* However, conflicting data from a Canadian retrospective cohort study of 4268 ELBW infants who were born at <30 weeks gestation found that the prophylactic administration of indomethacin, combined with early feeding, was associated with an increased odds of SIP, but early feeding alone was not associated with SIP. The study also noted marked variation in the use of prophylactic indomethacin across the 13 treatment centers [23].
* Other reported postnatal risk factors include the use of inotropic agents, delayed onset of feeding and intraventricular hemorrhage of Grade III or higher [24,25]. However, these risk factors might be surrogate markers for ill premature infants, rather than causative.


==References==
==References==
{{Reflist|2}}

Latest revision as of 02:26, 29 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

Risk factors for gastrointestinal perforation varies between instrumentation during upper endoscopy, sigmoidoscopy, colonoscopy, stent placement, endoscopic sclerotherapy, nasogastric intubation, esophageal dilatation, and surgery. Other risks include medications especially Aspirin, potassium supplements, disease-modifying antirheumatic drugs (DMARDs), and nonsteroidal anti-inflammatory drug. Peptic ulcer disease is the most common cause of stomach and duodenal perforation. Colonic diverticulosis is common risk for colonic perforation in the developed world. Mesenteric ischemia increases the risk for perforation. Embolism, mesenteric occlusive disease, and heart failure lead to gastrointestinal ischemia. In neonatal perforation, prematurity is the commonest risk factor. Antenatal administration of glucocorticoids, nonsteroidal antiinflammatory drugs, indomethacin, and magnesium sulfate had been initially reported to increase the risk of perforation.

Gastrointestinal perforation risk factors

Instrumentation
Other causes
  • Violent retching can lead to spontaneous esophageal perforation, known as Boerhaave syndrome due to increased intraesophageal pressure in the lower esophagus.[4]
Gastric causes
  • Peptic ulcer disease is the most common cause of stomach and duodenal perforation.[5]
  • Marginal ulcers may complicate procedures involving a gastrojejunostomy.
  • Perforated gastric ulcer is associated with a higher mortality, possibly related to delays in diagnosis.
Small intestine causes
Large intestine causes

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.
  • Preterm infants have lower concentrations or more immature function of contributing mucosal defense factors than do term infants and adults.
  • 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.[8]
  • 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.[9]
  • 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.[10]
  • Events that have been implicated in the development of NEC include:[11]
  • perinatal asphyxia
  • Recurrent apnea
  • Respiratory distress syndrome
  • Hypotension
  • Congenital heart disease
  • Patent ductus arteriosus
  • Umbilical arterial catheterization
  • Anemia
  • Polycythemia [54,55][59]
  • Medications such as theophylline or phenobarbital might irritate the intestinal mucosa.[12]

Risk factors for spontaneous intestinal perforation of the newborn

References

  1. ↑ Akbulut S, Cakabay B, Ozmen CA, Sezgin A, Sevinc MM (2009). "An unusual cause of ileal perforation: report of a case and literature review". World J Gastroenterol. 15 (21): 2672–4. PMC 2691502. PMID 19496201.
  2. ↑ Ismael H, Horst M, Farooq M, Jordon J, Patton JH, Rubinfeld IS (2011). "Adverse effects of preoperative steroid use on surgical outcomes". Am J Surg. 201 (3): 305–8, discussion 308-9. doi:10.1016/j.amjsurg.2010.09.018. PMID 21367368.
  3. ↑ Strangfeld A, Richter A, Siegmund B, Herzer P, Rockwitz K, Demary W; et al. (2017). "Risk for lower intestinal perforations in patients with rheumatoid arthritis treated with tocilizumab in comparison to treatment with other biologic or conventional synthetic DMARDs". Ann Rheum Dis. 76 (3): 504–510. doi:10.1136/annrheumdis-2016-209773. PMC 5445993. PMID 27405509.
  4. ↑ Wu JT, Mattox KL, Wall MJ (2007). "Esophageal perforations: new perspectives and treatment paradigms". J Trauma. 63 (5): 1173–84. doi:10.1097/TA.0b013e31805c0dd4. PMID 17993968.
  5. ↑ Horowitz J, Kukora JS, Ritchie WP (1989). "All perforated ulcers are not alike". Ann Surg. 209 (6): 693–6, discussion 696-7. PMC 1494136. PMID 2730181.
  6. ↑ Eid HO, Hefny AF, Joshi S, Abu-Zidan FM (2008). "Non-traumatic perforation of the small bowel". Afr Health Sci. 8 (1): 36–9. PMC 2408541. PMID 19357730.
  7. ↑ Spoormans I, Van Hoorenbeeck K, Balliu L, Jorens PG (2010). "Gastric perforation after cardiopulmonary resuscitation: review of the literature". Resuscitation. 81 (3): 272–80. doi:10.1016/j.resuscitation.2009.11.023. PMID 20064683.
  8. ↑ Lin PW, Stoll BJ (2006). "Necrotising enterocolitis". Lancet. 368 (9543): 1271–83. doi:10.1016/S0140-6736(06)69525-1. PMID 17027734.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ Fisher JG, Bairdain S, Sparks EA, Khan FA, Archer JM, Kenny M; et al. (2015). "Serious congenital heart disease and necrotizing enterocolitis in very low birth weight neonates". J Am Coll Surg. 220 (6): 1018–1026.e14. doi:10.1016/j.jamcollsurg.2014.11.026. PMID 25868405.
  12. ↑ Book LS, Herbst JJ, Atherton SO, Jung AL (1975). "Necrotizing enterocolitis in low-birth-weight infants fed an elemental formula". J Pediatr. 87 (4): 602–5. PMID 1174138.
  13. ↑ Caplan MS, Sun XM, Hseuh W, Hageman JR (1990). "Role of platelet activating factor and tumor necrosis factor-alpha in neonatal necrotizing enterocolitis". J Pediatr. 116 (6): 960–4. PMID 2348301.
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