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==Pathophysiology== | ==Pathophysiology== | ||
Ileus is defined as temporary cessation of intestinal peristalsis in the absence of mechanical obstruction. The pathogenesis of ileus is multifactorial. Intestinal peristalsis is primarily regulated by enteric nervous system, autonomic nervous system and interactions with central nervous system. However, certain medications and metabolism products may also alter the normal intestinal equilibrium leading to temporary dysfunction in intestinal movements. With increasing time, intestinal aperistalsis results in accumulation of air and fluid in the bowel lumen. | Ileus is defined as temporary cessation of [[intestinal]] [[peristalsis]] in the absence of mechanical obstruction. The [[pathogenesis]] of ileus is multifactorial. Intestinal [[peristalsis]] is primarily regulated by [[enteric nervous system]], [[autonomic nervous system]] and interactions with [[central nervous system]]. However, certain [[medications]] and [[metabolism]] products may also alter the normal [[intestinal]] [[equilibrium]] leading to temporary [[dysfunction]] in [[intestinal]] movements. With increasing time, intestinal aperistalsis results in accumulation of air and fluid in the [[bowel]] [[lumen]]. | ||
===Normal physiology=== | ===Normal physiology=== | ||
*The gastrointestinal tract is are regulated by the enteric nervous system, autonomic nervous system and interactions with central nervous system. | *The gastrointestinal tract is are regulated by the enteric nervous system, autonomic nervous system and interactions with central nervous system. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Ileus is defined as temporary cessation of intestinal peristalsis in the absence of mechanical obstruction. The pathogenesis of ileus is multifactorial. Intestinal peristalsis is primarily regulated by enteric nervous system, autonomic nervous system and interactions with central nervous system. However, certain medications and metabolism products may also alter the normal intestinal equilibrium leading to temporary dysfunction in intestinal movements. With increasing time, intestinal aperistalsis results in accumulation of air and fluid in the bowel lumen.
Normal physiology
- The gastrointestinal tract is are regulated by the enteric nervous system, autonomic nervous system and interactions with central nervous system.
- The enteric nervous system (ENS) is also known as intrinsic neural network consists of neurons are located in the walls of GI tract.
- ENS includes myenteric plexus (Auerbach's) and submucosal (Meissner's) plexuses.
- The myenteric plexus is located in the muscular layer and is also known as Auerbach's plexus.
- The submucosal plexus is located in the submucosal layer and is also known as Meissner's plexus.
- The autonomic nervous system (ANS) is also known as extrinsic nervous system.
- The ANS consists of sympathetic and parasympathetic nervous system which control GI function.
- The sympathetic nervous system is inhibitory to visceral smooth muscle activity and increases peristalsis and GI motility.
- The parasympathetic nervous system is stimulatory to visceral smooth muscle activity and increases peristalsis and GI motility.
- The GI tract visceral sensory afferents located in the parasympathetic ANS while the visceral motor efferents are located in both sympathetic and parasympathetic ANS.
- In addition, the extrinsic nervous system synapse with enteric nervous system and relay information to central nervous system.
Pathophysiology
- The most common cause of ileus is abdominal surgery.[1][2][3]
- The risk of postoperative ileus depends upon the type of surgery; laparoscopic procedures have lower risk as compared to open laparotomy which have the highest risk.
- The highest risk for postoperative ileus has been observed with colorectal surgery.
- In fact, postoperative ileus (due to any surgery) is so common that it is sometimes regarded as a normal sequelae of surgery.
- Postoperative ileus lasting longer than 3 days is termed as paralytic ileus.
- When a patient undergoes a surgical procedure, it often puts the body under significant stress.
- This surgical stress may lead to release of inflammatory and neuroendocrine mediators (such as nitric oxide, VIP and substance P) that may result in the development of ileus.[4]
- Stress inducing conditions may lead to increased recruitment of dendritic cells, natural killer cells, monocytes, T cells, macrophages, and mast cells. The macrophages and mast cells are considered the key cells in initiating the inflammatory process and release of chemical mediators.
- Recent research has shown that inhibition of inflammatory mediators (such as nitric oxide & VIP) may lead to improved gastrointestinal peristalsis and function.
- The site of the surgery is the most commonly affected part of the GI tract. However, recent research has shown that inflammation of the intestinal muscle may extend from site of surgery to other parts of the intestinal tract.[5]
- Moreover, intestinal distention as seen in ileus also contributes to serosal injury and may aggravate intestinal ischemia.
- Prolonged ileus leads to increased contact between various segments of intestine which predispose to fibrous adhesion formation, thereby further contributing to severity of ileus. [6][7]
- Abdominal conditions such as gastroenteritis and peritonitis may also affect the intestinal motility leading to ileus.
- Abdominal incision leads to activation of inhibitory spinal reflex which results in decreased movements of intestine, as a regulatory mechanism.[8]
- The painful stimuli stimulates the spinal afferents that synapse in the spinal cord. In the spinal cord, the prevertebral adrenergic neurons are activated which leads to inhibition of intestinal motility via efferent nerves (sympathetic ANS).
- Additionally, manipulation of intestine leads to activation of afferent pathways that travel to the brainstem. In turn, the brainstem sends increased autonomic output to the sympathetic neurons located in the inter-medio-lateral column of the thoracic cord. An increased activity of sympathetic neurons results in increased secretion of adrenergic output and decreased intestinal motility.
- Another chronic and a more severe form of ileus is known as chronic intestinal pseudo-obstruction (CIPO).[9][10][11]
- CIPO is a more severe form of ileus resulting from disturbances in enteric nervous system, autonomic nervous system and smooth muscle cell function.
- The cause of CIPO can be idiopathic, sporadic, or secondary to metabolic, connective tissue, endocrinological, neurological, and paraneoplastic disorders.[12]
- CIPO is often due to dysfunction in the innervation of smooth muscle by the interstitial cells of Cajal resulting in partial or complete ineffective intestinal propulsion. However, any condition affecting the enteric nervous system, autonomic nervous system, smooth muscle cells and neuromuscular junction may lead to development of CIPO.
- The lack of intestinal propulsive movements may lead to increased intra-bowel pressure.
- The enhanced intra-bowel pressure leads to malabsorption and bacterial translocation. Over time, it can progress to present with malnutrition and bloodstream infection (sepsis).
- The other common cause of ileus are the drugs that affect intestinal motility and alteration in electrolyte levels.
- Drugs affecting intestinal motility primarily includes antimotility agents and anesthetics.
- Anesthetic drugs: Anesthetic agents have a direct inhibitory effect on the intestinal motility. Long acting anesthetic agents such as bupivacaine are more frequently associated with postopertaive ileus as compared to short acting agents such as propofol.
- Opiates: The use of opiates for pain alleviation is not without side effects. In fact opioid use has been associated with significant increase in the occurrence of postoperative ileus. Opioid medications that activate the µ receptors have been associated with decreased release of acetylcholine from cholinergic neurons, resulting in delayed intestinal motility. The most common opioid pain medication, morphine initially activates the migrating myoelectric complex and later on results in atony resulting in inhibition of propulsion and delay in intestinal transit.
- Electrolyte abnormalities such as hypokalemia, hyponatremia, hypercalcemia, hypomagnesemia, and metabolic acidosis.
- Drugs affecting intestinal motility primarily includes antimotility agents and anesthetics.
Associated Conditions
- Orthostatic hypotension
- Diabetes mellitus
- Hypothyroidism
- Hypoparathyroidism[13]
- Hirschsprung disease
- CNS neoplasms
- Leiomyosarcomas
- Radiation enteritis
- Chagas disease
Gross Pathology
On gross pathology, findings of ileus include:[14]
- Bowel contortion
- Distended small and large intestine
Microscopic Features
On microscopic histopathological analysis, findings of ileus include inflammatory cells predominantly macrophage and mast cells.
References
- ↑ Kalff JC, Schraut WH, Simmons RL, Bauer AJ (1998). "Surgical manipulation of the gut elicits an intestinal muscularis inflammatory response resulting in postsurgical ileus". Ann. Surg. 228 (5): 652–63. PMC 1191570. PMID 9833803.
- ↑ Espat NJ, Cheng G, Kelley MC, Vogel SB, Sninsky CA, Hocking MP (1995). "Vasoactive intestinal peptide and substance P receptor antagonists improve postoperative ileus". J. Surg. Res. 58 (6): 719–23. doi:10.1006/jsre.1995.1113. PMID 7540700.
- ↑ Kalff JC, Schraut WH, Billiar TR, Simmons RL, Bauer AJ (2000). "Role of inducible nitric oxide synthase in postoperative intestinal smooth muscle dysfunction in rodents". Gastroenterology. 118 (2): 316–27. PMID 10648460.
- ↑ Doherty TJ (2009). "Postoperative ileus: pathogenesis and treatment". Vet. Clin. North Am. Equine Pract. 25 (2): 351–62. doi:10.1016/j.cveq.2009.04.011. PMID 19580945.
- ↑ Bederman SS, Betsy M, Winiarsky R, Seldes RM, Sharrock NE, Sculco TP (2001). "Postoperative ileus in the lower extremity arthroplasty patient". J Arthroplasty. 16 (8): 1066–70. doi:10.1054/arth.2001.27675. PMID 11740765.
- ↑ Lundin C, Sullins KE, White NA and al. Induction of peritoneal adhesions with small intestinal ischaemia and distention in the foal. Equine Vet J 21: 451, 1989
- ↑ Vachon AM, Fisher AT. Small intestinal herniation through the epiploic foramen: 53 cases (1987-1993). Equine Vet J 27: 373, 1995
- ↑ Barquist E, Bonaz B, Martinez V, Rivier J, Zinner MJ, Taché Y (1996). "Neuronal pathways involved in abdominal surgery-induced gastric ileus in rats". Am. J. Physiol. 270 (4 Pt 2): R888–94. doi:10.1152/ajpregu.1996.270.4.R888. PMID 8967419.
- ↑ Di Nardo, G.; Di Lorenzo, C.; Lauro, A.; Stanghellini, V.; Thapar, N.; Karunaratne, T. B.; Volta, U.; De Giorgio, R. (2017). "Chronic intestinal pseudo-obstruction in children and adults: diagnosis and therapeutic options". Neurogastroenterology & Motility. 29 (1): e12945. doi:10.1111/nmo.12945. ISSN 1350-1925.
- ↑ Iida H, Ohkubo H, Inamori M, Nakajima A, Sato H (2013). "Epidemiology and clinical experience of chronic intestinal pseudo-obstruction in Japan: a nationwide epidemiologic survey". J Epidemiol. 23 (4): 288–94. PMC 3709546. PMID 23831693.
- ↑ Yeung AK, Di Lorenzo C (2012). "Primary gastrointestinal motility disorders in childhood". Minerva Pediatr. 64 (6): 567–84. PMID 23108319.
- ↑ Stanghellini V, Cogliandro RF, De Giorgio R, Barbara G, Morselli-Labate AM, Cogliandro L, Corinaldesi R (2005). "Natural history of chronic idiopathic intestinal pseudo-obstruction in adults: a single center study". Clin. Gastroenterol. Hepatol. 3 (5): 449–58. PMID 15880314.
- ↑ Lord, Reginald V. N.; Sillin, Lelan F. (2010). "Motility Disorders of the Small Bowel": 17–26. doi:10.1007/978-1-84996-372-5_2.
- ↑ Batke M, Cappell MS (2008). "Adynamic ileus and acute colonic pseudo-obstruction". Med. Clin. North Am. 92 (3): 649–70, ix. doi:10.1016/j.mcna.2008.01.002. PMID 18387380.