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{{Gastrointestinal perforation}}
{{Gastrointestinal perforation}}


==Overview==
==Overview==
'''Instrumentation/surgery''' 
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.  
 
Instrumentation of the gastrointestinal tract is the main cause of iatrogenic perforation and may include upper endoscopy, sigmoidoscopy, colonoscopy [10,11], stent placement [10,11], endoscopic sclerotherapy [12], nasogastric intubation [13], esophageal dilation, and surgery.
 
The incidence of perforation related to endoscopy increases with procedural complexity.
 
Perforation is less common with diagnostic compared with therapeutic procedures [14].
 
A perforation rate of 0.11 percent for rigid endoscopy contrasts with a 0.03 percent rate for flexible endoscopy [15,16]. When iatrogenic perforation occurs, there is often significant associated pathology. As an example, in the esophagus, there may be stricture, severe esophagitis [17], or a diverticulum, and the presence of cervical osteophytes also increases the risk [16]. 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. During endoscopy, perforations are frequently recognized at the time of the procedure. At other times, the perforation remains occult for several days.
 
Other procedures can also be complicated with perforation, such as chest tube insertion low in the chest [19], peritoneal dialysis catheter insertion, percutaneous gastrostomy [20], paracentesis, diagnostic peritoneal lavage, and percutaneous drainage of fluid collections or abscess.
 
With surgery, perforation can occur during initial laparoscopic access, during mobilization of the organs or during the takedown of adhesions, or as a result of thermal injury from electrocautery devices [21-23]. 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 [32]. Medical illnesses such as diabetes, cirrhosis, and HIV are associated with an increased risk of anastomotic leak after colon resection for trauma [33
 
'''Penetrating or blunt trauma''' 
 
Traumatic perforation of the gastrointestinal tract is most likely a result of penetrating injury, although blunt perforation can occur with severe abdominal trauma acutely related to pressure effects or as a portion of the gastrointestinal tract is compressed against a fixed bony structure, or more slowly as a contusion develops into a full-thickness injury. (See "Overview of esophageal perforation due to blunt or penetrating trauma" and "Traumatic gastrointestinal injury in the adult patient".)
 
'''Medications, other ingestions, foreign body''' 
 
Medications or other ingested substances (caustic injury) and foreign bodies (ingested or medical devices) can lead to gastrointestinal perforation. Foreign bodies, such as sharp objects (toothpicks), food with sharp surfaces (eg, chicken bones, fish), or gastric bezoar more commonly cause perforation, compared with dislodged medical implants [34-37]. Button batteries as an esophageal foreign body have a more pronounced perforation risk [38,39]. Surgically implanted foreign bodies such as hernia mesh [40] and artificial vascular grafts [41,42] can cause perforation with subsequent abscess and fistula formation or vasculoenteric fistulas. (See "Caustic esophageal injury in children" and "Caustic esophageal injury in adults" and "Foreign bodies of the esophagus and gastrointestinal tract in children" and "Ingested foreign bodies and food impactions in adults".)
 
Aspirin 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]. Some disease-modifying antirheumatic drugs (DMARDs) have been associated with lower intestinal perforations [44]. Rarely, NSAIDs have produced jejunal perforations [45]. Glucocorticoids, particularly in association with NSAIDs, are particularly problematic [46,47]. Further, because steroids suppress the inflammatory response, detection of a perforation can be delayed.
 
NSAIDs, antibiotics, and potassium supplements are also common causative medications for pill-induced esophageal ulcers [48]. Other medication-induced injury leading to perforation has been reported for immunosuppressive therapies, cancer chemotherapy in patients with metastases, and for iron supplementation causing esophageal injury [2,49,50].
 
'''Violent retching/vomiting''' 
 
Violent retching/vomiting can lead to spontaneous esophageal perforation, known as Boerhaave syndrome. This occurs because of failure of the cricopharyngeal muscle to relax during vomiting or retching causing an increased intraesophageal pressure in the lower esophagus [51]. (See "Boerhaave syndrome: Effort rupture of the esophagus".)
 
'''Hernia/intestinal volvulus/obstruction'''
 
Abdominal wall, groin, diaphragmatic, internal hernia, paraesophageal hernia, and volvulus (gastric, cecal, sigmoid) can all lead to perforation either related to bowel wall ischemia from strangulation, or pressure necrosis. Perforation can also occur with afferent loop obstruction after Roux-en-Y reconstruction. (See "Overview of abdominal wall hernias in adults" and "Epidemiology, clinical features, and diagnosis of mechanical small bowel obstruction in adults" and "Overview of treatment for inguinal and femoral hernia in adults" and "Surgical management of paraesophageal hernia" and "Gastric volvulus in adults" and "Postgastrectomy complications", section on 'Afferent and efferent loop syndrome'.)
 
'''Inflammatory bowel disease''' 
 
 Crohn disease has a propensity to perforate slowly, leading to formation of entero-enteric or enterocutaneous fistula formation [52,53]. (See "Operative management of Crohn disease of the small bowel, colon, and rectum"and "Surgical management of ulcerative colitis".)
 
'''Appendicitis''' 
 
Overall in the United States in 2010, approximately 30 percent of hospital stays for appendicitis involved a perforated appendix [54-56]. Rates for perforated appendix in children have not significantly changed from 2001 to 2010 (approximately 300/1000 appendicitis discharges), whereas the rate has declined 12 percent for adults (from 307/1000 to 270/1000appendicitis discharges). (See "Acute appendicitis in children: Clinical manifestations and diagnosis" and "Acute appendicitis in adults: Clinical manifestations and differential diagnosis".)
 
'''Peptic ulcer disease''' 
 
Peptic ulcer disease (PUD) is the most common cause of stomach and duodenal perforation but occurs in less than 10 percent of patients with PUD. In spite of the introduction of proton pump inhibitors, the incidence of perforation from PUD has not changed appreciably [57]. Marginal ulceration leading to perforation may also complicate surgeries that create a gastrojejunostomy (eg, partial gastric resection, bariatric surgery). (See "Overview of the complications of peptic ulcer disease".)
 
'''Diverticular disease''' 
 
 Colonic diverticulosis is common in the developed world. All clinical cases of diverticulitis represent some degree of perforation of the thinned diverticular wall, leading to inflammation of the adjacent parietal peritoneum [58]. (See "Acute colonic diverticulitis: Surgical management" and "Overview of colon resection", section on 'Primary closure versus ostomy'.)
 
Perforation can also occur with duodenal or small intestinal diverticula (jejunal, Meckel's). These diverticula can become inflamed, much as in colonic diverticulitis, and perforate, which may lead to abscess formation. (See "Meckel's diverticulum".)
 
'''Cardiovascular disease''' 
 
 Any process that reduces the blood flow to the intestines (occlusive or nonocclusive mesenteric ischemia) for an extended period of time increases the risk for perforation, including embolism, mesenteric occlusive disease, cardiopulmonary resuscitation, and heart failure that leads to gastrointestinal ischemia [59]. (See "Overview of intestinal ischemia in adults".)
 
'''Infectious disease''' 
 
 Typhoid, tuberculosis, and schistosomiasis can cause perforation of the small intestine [60,61]. With typhoid, the perforation is usually in a single location (ileum at necrotic Peyer's patches), but it can be multiple [62,63]. Typhoid perforation is more common in children, adolescents, or young adults. Cytomegalovirus, particularly in an immunosuppressed patient, can cause intestinal perforation.
 
'''Neoplasms''' 
 
 Neoplasms can perforate by direct penetration and necrosis, or by producing obstruction. Perforations related to tumor can also occur spontaneously, following chemotherapy, or as a result of radiation treatments when the tumor involves the wall of a hollow viscus organ [64-66]. Delayed perforations of the esophagus or duodenum in patients with malignancy can be related to stent placement for malignant obstruction.
 
'''Connective tissue disease'''
 
Spontaneous perforation of the small intestine or colon has been reported in patients with underlying connective tissue diseases (eg, Ehlers-Danlos syndrome), collagen vascular disease, and vasculitis [67-69]. (See "Clinical manifestations and diagnosis of Ehlers-Danlos syndromes" and "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)
 
'''''causes'''''
 
Perforation of the esophagus is more often iatrogenic (endoscopy or related to surgery), or due to noniatrogenic penetrating or blunt traumatic mechanisms [118].
 
Other causes include tumors, foreign body or caustic ingestion [34,35], pneumatic injury, peptic ulceration, intrinsic esophageal disease such as pill esophagitis [1,2], Crohn disease [3], eosinophilic esophagitis [4], foreign body ingestion, or, more rarely, it is spontaneous (Boerhaave's syndrome). During surgery, the esophagus can be injured during operations such as hiatal hernia repair, thyroidectomy, pulmonary procedures, and vagotomy.


'''''causes'''''
==Gastrointestinal perforation risk factors==
===== '''Instrumentation''' =====
* 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]]. 
* [[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>


Peptic ulcer disease is the most common cause of stomach and duodenal perforation.  
===== 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]].<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.  


Marginal ulcers may complicate procedures involving a gastrojejunostomy (eg, partial gastrectomy, bariatric surgery).  
* 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>


Although the frequency of elective surgery for peptic ulcer disease has declined, the incidence of peptic perforation has remained the same or is increasing [57].  
===== '''Gastric causes''' =====
* [[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]].
* Perforated gastric ulcer is associated with a higher mortality, possibly related to delays in diagnosis.  


Perforated duodenal ulcers are located on the anterior or superior portions of the duodenum and typically rupture freely, causing severe acute abdominal pain. 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.<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. 
* 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.  


Other causes include iatrogenic (endoscopy, surgery [open or laparoscopic]) or noniatrogenic trauma [14,19,59], ingested foreign bodies [36], neoplasm (particularly during chemotherapy) [64,65], tuberculosis [122], and perforated duodenal diverticulum. Gastric perforation during cardiopulmonary resuscitation can also occur [59].
* 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.


'''''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.<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>


Perforation of the small intestine can be related to bowel obstruction, acute mesenteric ischemia, inflammatory bowel disease [53], or due to iatrogenic (laparoscopic access, takedown of adhesions, endoscopy) or noniatrogenic traumatic mechanisms. Injuries to the small intestine during laparoscopic procedures are often not recognized during the procedure [22]. Severe pain or sepsis after a laparoscopic procedure should be investigated promptly [23]. Perforations caused by the tumor (eg, lymphoma [66]) can occur spontaneously or after chemotherapy. Further, because glucocorticoids suppress the inflammatory response, detection of a perforation can be delayed. Other causes of small intestinal perforation include foreign body ingestion, enteroliths/gallstones [5,6], or, more rarely, migrated stents (eg, esophageal, biliary).
* [[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.


Perforation of a diverticulum of the small intestine, such as in perforated Meckel's diverticulum, can occur and may lead to abscess formation. Occasionally, jejunal diverticula can become inflamed and perforate [135]. These rare diverticula are located along the mesenteric aspect of the proximal jejunum and decrease in number with increasing distance from the duodenal-jejunal junction. Rarely, nonsteroidal anti-inflammatory drugs (NSAIDs) have produced jejunal perforations [45].
== Neonatal intestinal perforation risk factors ==


Occasionally, particularly in developing countries, diseases such as typhoid, tuberculosis [136], or schistosomiasis [61] can perforate the small intestine. In typhoid, the perforation is usually single but can be multiple 28 to 37 percent of the time [62,63]. The perforations usually occur in the ileum at necrotic Peyer's patches. Typhoid perforation is more common in children, adolescents, or young adults and has a high mortality (3 to 72 percent) reflecting, in part, the severity of the illness these patients have in addition to the effects of the perforation. A reperforation rate of 21.3 percent has been reported for typhoid perforation closure. Cytomegalovirus, particularly in an immunosuppressed patient, can also cause intestinal perforation.
=== Risk factors for necrotizing enterocolitis (NEC): ===
* 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 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.  
* 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>


Colon and rectal perforation is more commonly due to diverticulitis, neoplasm, and iatrogenic and noniatrogenic traumatic mechanisms, including surgery (eg, anastomotic leak). Colonic diverticulosis is common in the developed world, affecting up to 50 percent of adults in Western countries. A younger age group is affected in left-sided diverticulitis, and it is more common in men. With increasing age, the number of diverticuli, which predominate in the sigmoid and left colon, increases with the disease moving more proximally. In Asian countries, the most common cause of right-sided colonic perforation is diverticulitis [138]. 
=== Risk factors for spontaneous intestinal perforation of the newborn ===
* 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.
* Delayed onset of feeding
* [[Intraventricular hemorrhage]] of Grade III or higher.


==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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