Gastrointestinal perforation risk factors: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 17: | Line 17: | ||
* 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. [51] | ||
'''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. | ||
* 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 [121]. | ||
'''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 [53], or due to iatrogenic or noniatrogenic traumatic mechanisms. | ||
* 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, groin, diaphragmatic, internal hernia, paraesophageal hernia, and volvulus can all lead to perforation either related to bowel wall ischemia from strangulation, or pressure necrosis. | ||
| Line 29: | Line 31: | ||
* 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, 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. | * 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 | * Neoplasms can perforate by direct penetration and necrosis, or by producing obstruction. [64-66 | ||
== Neonatal intestinal perforation risk factors == | |||
=== Risk factors for necrotizing enterocolitis: === | |||
* 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]. 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]. | |||
* Hyperosmolar medications may result in NEC. Oral medications such as theophylline, multivitamins, or phenobarbital contain hypertonic additives that might irritate the intestinal mucosa. [70]. | |||
=== 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). | |||
* 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]. | |||
* 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. | |||
* 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]. | |||
* 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== | ||
Revision as of 20:43, 1 January 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]
|
Gastrointestinal perforation Microchapters |
|
Differentiating gastrointestinal perforation from other diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Gastrointestinal perforation risk factors On the Web |
|
American Roentgen Ray Society Images of Gastrointestinal perforation risk factors |
|
Risk calculators and risk factors for Gastrointestinal perforation risk factors |
Overview
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.
- 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.
- 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]
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
- 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 [53], or due to iatrogenic or noniatrogenic traumatic mechanisms.
- 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.
- Injuries to the small intestine during laparoscopic procedures are often not recognized during the procedure. [22]
- Croh'n disease has a propensity to perforate slowly, leading to formation of entero-enteric or enterocutaneous fistula formation. [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:
- 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]. 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].
- Hyperosmolar medications may result in NEC. Oral medications such as theophylline, multivitamins, or phenobarbital contain hypertonic additives that might irritate the intestinal mucosa. [70].
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).
- 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].
- 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.
- 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].
- 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.