Gastrointestinal perforation pathophysiology
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
Perforation is full-thickness injury of the bowel wall. Perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction. Spontaneous perforation can be caused by inflammation, connective tissue disorders, and medications. Terminal ileum is the commonest site for spontaneous perforation and may be the jejunum and colon. In neonatal perforation, the terminal ileum and colon are the commonest sites for perforation. The pathogenesis of NEC remains unknown but there are many factors for infection such as: 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. Regarding anatomy of GIT, the esophagus travels 3 regions of the body: the neck, thorax, and abdomen. Accordingly, it is divided into 3 parts: cervical, thoracic, and abdominal. The gastrointestinal tract has a form of general histology with some differences that reflect the specialization in functional anatomy. The GI tract can be divided into four concentric layers in the following order: Mucosa, Submucosa, muscular layer, and Adventitia or serosa. Perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction. Spontaneous perforation can be caused by inflammation, connective tissue disorders, and medications. With bowel obstruction, perforation occurs proximal to the obstruction as pressure builds up within the bowel, exceeding intestinal perfusion pressure, and leading to ischemia and subsequently necrosis. Acute colonic pseudo-obstruction is an acute dilatation of the colon without mechanical obstruction of the flow of intestinal contents. The mechanism of perforation in patients with acute colonic pseudo-obstruction is unknown. Spinal anesthesia and pharmacologic agents are suggested to be the causes due to impairment of autonomic system.
Anatomy of gastrointestinal tract
Esophagus
- The esophagus is a 25-cm-long vertical muscular tube that normally remains collapsed and that runs from the laryngopharynx in the neck through the thorax to the stomach in the abdomen.
- The esophagus travels 3 regions of the body: the neck, thorax, and abdomen. Accordingly, it is divided into 3 parts: cervical, thoracic, and abdominal.
- The cervical esophagus begins at the level of C6; it is only 5 cm long. In the neck, the esophagus is enclosed in a sheath of deep cervical fascia.
Stomach
- The cardiac notch is the acute angle between the left border of the intra-abdominal esophagus and the gastric fundus.
- The body of the stomach leads to the pyloric antrum, which joins the duodenum at the pylorus, lying at the L1-L2 level to the right of the midline.
- The stomach has a shorter lesser curvature and a longer greater curvature. The lesser curvature is attached to the undersurface of the liver by lesser omentum and the greater curvature is attached to the transverse colon by greater omentum.
Intestine
- The lower gastrointestinal tract includes most of the small intestine and all of the large intestine.
- The small bowel is anatomically divided into three portions: the duodenum, jejunum, and ileum.
- Duodenum: It is about 20–25 cm long which receives chymefrom the stomach, together with pancreatic juice containing digestive enzymes and bile from the gall bladder.
- The duodenum contains Brunner's glands, which produce a mucus-rich alkaline secretion containing bicarbonate. These secretions, in combination with bicarbonate from the pancreas, neutralizes the stomach acids contained in the chyme.
- Jejunum: This is the midsection of the small intestine, connecting the duodenum to the ileum. It is about 2.5 m long, and contains the circular folds, and villi that increase its surface area. Products of digestion are absorbed into the bloodstream here.
- Ileum: The final section of the small intestine. It is about 3 m long, and contains villi similar to the jejunum. It absorbs mainly vitamin B12 and bile acids, as well as any other remaining nutrients.
- The large intestine is further divided into:
Histology of gastrointestinal tract
The gastrointestinal tract has a form of general histology with some differences that reflect the specialization in functional anatomy.
The GI tract can be divided into four concentric layers in the following order:
Mucosa
- The mucosa is the innermost layer of the gastrointestinal tract. that is surrounding the lumen.
- This layer comes in direct contact with chyme. The mucosa is made up of:
- Epithelium: innermost layer. Responsible for most digestive, absorptive and secretory processes.
- Lamina propria: a layer of connective tissue. Unusually cellular compared to most connective tissue
- Muscularis mucosae: a thin layer of smooth muscle that aids the passing of material and enhances the interaction between the epithelial layer and the contents of the lumen by agitation and peristalsis.
The mucosae are highly specialized in each organ of the gastrointestinal tract to deal with the different conditions. The most variation is seen in the epithelium.
Submucosa
The submucosa consists of a dense irregular layer of connective tissue with large blood vessels, lymphatics, and nerves branching into the mucosa and muscularis externa. It contains the submucosal plexus, an enteric nervous plexus, situated on the inner surface of the muscularis externa.
Muscular layer
- The muscular layer consists of an inner circular layer and a longitudinal outer layer.
- The layers are not truly longitudinal or circular, rather the layers of muscle are helical with different pitches. The inner circular is helical with a steep pitch and the outer longitudinal is helical with a much shallower pitch.
- Between the two muscle layers is the myenteric plexus.
- The gut has intrinsic peristaltic activity due to its self-contained enteric nervous system. The rate can be modulated by the rest of the autonomic nervous system.
Adventitia and serosa
- The outermost layer of the gastrointestinal tract consists of several layers of connective tissue.
- Intraperitoneal parts of the GI tract are covered with serosa. These include most of the stomach, first part of the duodenum, all of the small intestine, caecum and appendix, transverse colon, sigmoid colon and rectum.
- In these sections of the gut there is clear boundary between the gut and the surrounding tissue. These parts of the tract have a mesentery.
- Retroperitoneal parts are covered with adventitia. They blend into the surrounding tissue and are fixed in position.
- These include the esophagus, pylorus of the stomach, distal duodenum, ascending colon, descending colon and anal canal.
Pathophysiology of gastrointestinal perforation
- Perforation is full-thickness injury of the bowel wall.
- Perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction.[1]
- Spontaneous perforation can be caused by inflammation, connective tissue disorders, and medications.
- With bowel obstruction, perforation occurs proximal to the obstruction as pressure builds up within the bowel, exceeding intestinal perfusion pressure, and leading to ischemia and subsequently necrosis.[2]
Acute colonic pseudo-obstruction (Ogilvie's syndrome)
- Acute colonic pseudo-obstruction is an acute dilatation of the colon without mechanical obstruction of the flow of intestinal contents.
- The mechanism of perforation in patients with acute colonic pseudo-obstruction is unknown.
- Spinal anesthesia and pharmacologic agents are suggested to be the causes due to impairment of autonomic system.[3]
- Interruption of the parasympathetic fibers from S2 to S4 leaves an atonic distal colon and a functional proximal obstruction.
- The risk of colonic perforation are the absolute diameter of the colon (10 to 12 cm) and the duration of cecal dilation.[4]
Spontaneous perforation in neonates
- Terminal ileum is the commonest site for spontaneous perforation and may be the jejunum and colon.[5]
- Focal hemorrhagic necrosis with well-defined margins is observed in contrast to the ischemic and coagulative necrosis seen in necrotizing enterocolitis.[6]
- The bowel appears normal proximal and distal to the perforation.
- The mechanism is not clear yet but may be due to absence of the muscularis propria at the perforation site.[7]
Necrotizing enterocolitis (NEC)
- The terminal ileum and colon are the commonest sites for perforation.[8]
- The pathogenesis of NEC remains unknown but there are many factors for infection such as:
- Ninety percent of NEC cases occur in preterm infants due to immaturity of the gastrointestinal tract.[9]
- 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.
- 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.
- Ischemic insult to the GI tract has been proposed as a major contributor to NEC.
- Inflammatory mediators induced by ischemia, infectious agents, or mucosal irritants may cause mucosal injury.
- Circulatory events that have been attrubuted in the development of NEC include perinatal asphyxia, recurrent apnea, hypoxia from severe respiratory distress syndrome, hypotension, congenital heart disease, patent ductus arteriosus, heart failure, umbilical arterial catheterization, anemia, polycythemia, and red blood cell and exchange transfusions.
- Hyperosmolar medications may result in NEC. Oral medications such as theophylline, multivitamins, or phenobarbital contain hypertonic additives that might irritate the intestinal mucosa.[10]
References
- ↑ Bona D, Incarbone R, Chella B, Vecchi M, Bonavina L (2005). "Heartburn and multiple-site foregut perforations as primary manifestation of Crohn's disease". Dis Esophagus. 18 (3): 199–201. doi:10.1111/j.1442-2050.2005.00468.x. PMID 16045583.
- ↑ Browning LE, Taylor JD, Clark SK, Karanjia ND (2007). "Jejunal perforation in gallstone ileus - a case series". J Med Case Rep. 1: 157. doi:10.1186/1752-1947-1-157. PMC 2222670. PMID 18045463.
- ↑ 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.
- ↑ Sloyer AF, Panella VS, Demas BE, Shike M, Lightdale CJ, Winawer SJ; et al. (1988). "Ogilvie's syndrome. Successful management without colonoscopy". Dig Dis Sci. 33 (11): 1391–6. PMID 3180976.
- ↑ Drewett MS, Burge DM (2007). "Recurrent neonatal gastro-intestinal problems after spontaneous intestinal perforation". Pediatr Surg Int. 23 (11): 1081–4. doi:10.1007/s00383-007-1999-2. PMID 17828407.
- ↑ Holland AJ (2008). "Comment on Kubota et al.: focal intestinal perforation in extremely-low-birth-weight neonates: etiological consideration from histological findings". Pediatr Surg Int. 24 (3): 387. doi:10.1007/s00383-007-2076-6. PMID 18060416.
- ↑ Gordon PV, Herman AC, Marcinkiewicz M, Gaston BM, Laubach VE, Aschner JL (2007). "A neonatal mouse model of intestinal perforation: investigating the harmful synergism between glucocorticoids and indomethacin". J Pediatr Gastroenterol Nutr. 45 (5): 509–19. doi:10.1097/MPG.0b013e3181558591. PMID 18030227.
- ↑ Lee SK, McMillan DD, Ohlsson A, Pendray M, Synnes A, Whyte R; et al. (2000). "Variations in practice and outcomes in the Canadian NICU network: 1996-1997". Pediatrics. 106 (5): 1070–9. PMID 11061777.
- ↑ Book LS, Herbst JJ, Jung AL (1976). "Carbohydrate malabsorption in necrotizing enterocolitis". Pediatrics. 57 (2): 201–4. PMID 1250656.
- ↑ Farrugia MK, Morgan AS, McHugh K, Kiely EM (2003). "Neonatal gastrointestinal perforation". Arch Dis Child Fetal Neonatal Ed. 88 (1): F75. PMC 1756016. PMID 12496235.