Gastrointestinal perforation risk factors: Difference between revisions
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===== 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. | ||
* 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. [59] | ||
* 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. [64-66 | ||
== 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 preterm infants due to immaturity of the gastrointestinal tract. [7,8][39,40]. | ||
* 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 [4]. | ||
* 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. [22,74-77]. | ||
* 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]. | * 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. [8,21-24]. | |||
* 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]. | |||
* Events that have been implicated in the development of NEC include: | |||
* [[perinatal asphyxia]] [51] | |||
* Recurrent [[apnea]] | |||
* [[Acute respiratory distress syndrome|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: === | === 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|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== | ==References== | ||
Revision as of 17:10, 2 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. [22,74-77].
- 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. [8,21-24].
- 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].
- 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]