Gastrointestinal perforation pathophysiology: Difference between revisions
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* 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]. | * 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]. | * Hyperosmolar medications may result in NEC. Oral medications such as theophylline, multivitamins, or phenobarbital contain hypertonic additives that might irritate the intestinal mucosa. [70]. | ||
==References== | |||
Revision as of 23:53, 24 December 2017
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
Anatomy
The esophagus begins in the neck and descends adjacent to the aorta through the esophageal hiatus to the gastroesophageal junction (figure 1). Perforations of the esophagus due to foreign body ingestion usually occur at the narrow areas of the esophagus such as the cricopharyngeus muscle, aortic arch, left main stem bronchus, and lower esophageal sphincter. The stomach is located in the left upper quadrant of the abdomen but can occupy other areas of the abdomen, depending upon its degree of distention, phase of diaphragmatic excursion, and the position of the individual. Anteriorly, the stomach is adjacent to the left lobe of the liver, diaphragm, colon, and anterior abdominal wall. Posteriorly, the stomach is in close proximity to the pancreas, spleen, left kidney and adrenal gland, splenic artery, left diaphragm, transverse mesocolon, and colon (figure 2 and figure 3). When the normal anatomy of the esophagus or stomach has been disturbed, such as after Roux-en-Y gastric bypass, great care should be taken with nasogastric intubation [9]. The small bowel is anatomically divided into three portions: the duodenum, jejunum, and ileum. The duodenum is retroperitoneal in its second and third portion and forms a loop around the pancreas. The jejunum is in continuity with the fourth portion of the duodenum beginning at the ligament of Treitz; there are no true lines of demarcation that separate the jejunum from ileum. The ileocecal valve marks the beginning of the colon in the right lower quadrant. The appendix hangs freely from the cecum, which is the first portion of the colon (figure 3). Foreign bodies that perforate the small intestines most commonly occur at sites of gastrointestinal immobility (eg, duodenum). The ascending and descending colon are retroperitoneal, while the transverse colon, which extends from the hepatic flexure to the splenic flexure, is intraperitoneal. The sigmoid colon continues from the descending colon, ending where the teniae converge to form the rectum. The anterior upper two-thirds of the rectum are located intraperitoneally and the remainder is extraperitoneal. The rectum lies anterior to the three inferior sacral vertebrae, the coccyx, and sacral vessels and is posterior to the bladder in men and the vagina in women. Foreign bodies that perforate the colon tend to occur at transition zones from an intraperitoneal location to fixed, retroperitoneal locations such as the cecum.
Pathophysiology of gastrointestinal perforation
- Perforation is full-thickness injury of the bowel wall.
- Full-thickness injury and subsequent perforation of the gastrointestinal tract can be due to many causes but main causes are instrumentation during surgery or bowel obstruction. [1-4]
- Spontaneous perforation can be related to inflammatory changes or tissues weakened by medications or connective tissue disorders.
- 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. 5,6
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. [1,11]
- 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. [12] 13,14].
Spontaneous perforation in neonates
- Terminal ileum is the commonest site for spontaneous perforation and may be the jejunum and colon. [1-5]
- Focal hemorrhagic necrosis with well-defined margins is observed in contrast to the ischemic and coagulative necrosis seen in necrotizing enterocolitis [4,26].
- The bowel appears normal proximal and distal to the perforation. [2,26-29]
- The mechanism is not clear yet but may be due to absence of the muscularis propria at the perforation site. [30]
Necrotizing enterocolitis (NEC)
- The terminal ileum and colon are the commonest sites for perforation. [5]
- 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. [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].