Gastrointestinal perforation risk factors: Difference between revisions
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===== '''Instrumentation''' ===== | ===== '''Instrumentation''' ===== | ||
* Instrumentation of the [[gastrointestinal tract]] includes [[upper endoscopy]], [[sigmoidoscopy]], [[colonoscopy]], [[stent]] placement, [[Sclerotherapy|endoscopic sclerotherapy]], [[nasogastric intubation]], [[esophageal dilatation]], 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, the part of the [[pharynx]] formed by the [[Inferior pharyngeal constrictor muscle|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]]. | ||
* [[Immunosuppressed]] individuals may be at increased risk for dehiscence and deep organ space infection following surgery. | * [[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> | ||
===== Other causes ===== | ===== Other causes ===== | ||
* 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]]. | * 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. | * 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. | * 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 | * 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]], 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 hernia|Abdominal wall]], [[Groin hernia|groin]], [[Diaphragmatic hernia|diaphragmatic]], [[internal hernia]], paraesophageal hernia, and [[volvulus]] can all lead to perforation due to ischemia. | * [[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 surgery|laparoscopic procedures]] are often not recognized during the procedure. | * Injuries to the [[small intestine]] during [[Laparoscopic surgery|laparoscopic procedures]] are often not recognized during the procedure. | ||
* [[Crohn's disease]] has a propensity to perforate slowly, leading to formation of fistula. | * [[Crohn's disease]] has a propensity to perforate slowly, leading to formation of fistula. | ||
* Diseases such as [[Typhoid fever|typhoid]], [[tuberculosis]], or [[schistosomiasis]] can perforate the small intestine. | * 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]]. | * 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. | * A reperforation rate of 21.3 percent has been reported for typhoid perforation closure. | ||
===== Large intestine causes ===== | ===== Large intestine causes ===== | ||
* [[Diverticulosis|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. | * [[Mesenteric ischemia]] increases the risk for perforation. [[Embolism]], mesenteric occlusive disease, and [[heart failure]] lead to gastrointestinal ischemia. | ||
* [[Neoplasm|Neoplasms]] can perforate by direct penetration and [[necrosis]], or by producing obstruction. | * [[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 (NEC): === | === Risk factors for necrotizing enterocolitis (NEC): === | ||
* Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract | * Ninety percent of NEC cases occur in [[Premature birth|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 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.<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> | * 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. | ||
| Line 49: | Line 49: | ||
* 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> | * 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> | * 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:<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] | * [[perinatal asphyxia]] | ||
* Recurrent [[apnea]] | * Recurrent [[apnea]] | ||
* [[Acute respiratory distress syndrome|Respiratory distress syndrome]] | * [[Acute respiratory distress syndrome|Respiratory distress syndrome]] | ||
* [[Hypotension]] | * [[Hypotension]] | ||
* [[Congenital heart disease] | * [[Congenital heart disease]] | ||
* [[Patent ductus arteriosus]] | * [[Patent ductus arteriosus]] | ||
* Umbilical arterial catheterization | * Umbilical arterial catheterization | ||
* [[Anemia]] | * [[Anemia]] | ||
* [[Polycythemia]] [54,55][59] | * [[Polycythemia]] [54,55][59] | ||
* Medications such as [[theophylline]] or [[phenobarbital]] might irritate the intestinal mucosa. | * 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 === | ||
* Placental [[chorioamnionitis]] appears to be an antenatal risk factor for SIP. | * 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> | ||
* Antenatal administration of [[glucocorticoids]], [[nonsteroidal antiinflammatory drugs]], [[Indomethacin|indomethacin,]] and [[magnesium sulfate]] had been initially reported to increase the risk of SIP | * Antenatal administration of [[glucocorticoids]], [[nonsteroidal antiinflammatory drugs]], [[Indomethacin|indomethacin,]] and [[magnesium sulfate]] had been initially reported to increase the risk of SIP. | ||
* Delayed onset of feeding | * Delayed onset of feeding | ||
* [[Intraventricular hemorrhage]] of Grade III or higher | * [[Intraventricular hemorrhage]] of Grade III or higher. | ||
==References== | ==References== | ||
<references /> | |||
Revision as of 16:12, 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.[1]
- 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.[2]
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.[3]
- 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.[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
- 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.[6]
- 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.
- 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.
Large intestine causes
- Colonic diverticulosis is common in the developed world. These diverticula can become inflamed and perforate and may lead to abscess formation.[7]
- 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.
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
- Placental chorioamnionitis appears to be an antenatal risk factor for SIP.[13]
- Antenatal administration of glucocorticoids, nonsteroidal antiinflammatory drugs, indomethacin, and magnesium sulfate had been initially reported to increase the risk of SIP.
- Delayed onset of feeding
- Intraventricular hemorrhage of Grade III or higher.
References
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.