Gastrointestinal perforation risk factors
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.