Ileus pathophysiology: Difference between revisions

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===Normal physiology===
===Normal physiology===
*The [[gastrointestinal tract]] is regulated by the [[enteric nervous system]], [[autonomic nervous system]] and interactions with [[central nervous system]].
*The [[gastrointestinal tract]] is 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 and consists of neurons located in the walls of [[GI tract]].  
*The [[enteric nervous system]] (ENS) is also known as intrinsic neural network and consists of [[neurons]] located in the walls of [[GI tract]].  
**ENS includes [[myenteric plexus]] ([[Auerbach's plexus|Auerbach's]]) and [[Meissner's plexus|submucosal (Meissner's]]) plexuses.  
**ENS includes [[myenteric plexus]] ([[Auerbach's plexus|Auerbach's]]) and [[Meissner's plexus|submucosal (Meissner's]]) plexuses.  
**The [[myenteric plexus]] is located in the [[muscular]] layer and is also known as [[Auerbach's plexus]].  
**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 [[submucosal plexus]] is located in the [[submucosal]] layer and is also known as [[Meissner's plexus]].
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**The [[sympathetic nervous system]] is [[inhibitory]] to [[visceral]] [[smooth muscle]] activity and decreases [[peristalsis]] and [[GI]] motility.
**The [[sympathetic nervous system]] is [[inhibitory]] to [[visceral]] [[smooth muscle]] activity and decreases [[peristalsis]] and [[GI]] motility.
**The [[parasympathetic nervous system]] is stimulatory 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 [[visceral]] sensory [[afferents]] of [[GI tract]] are located in the [[Parasympathetic nervous system|parasympathetic ANS]] while the [[visceral]] motor efferents are located in both [[Sympathetic nervous system|sympathetic]] and [[Parasympathetic nervous system|parasympathetic]] ANS.  
**The [[visceral]] sensory [[afferents]] of [[GI tract]] are located in the [[Parasympathetic nervous system|parasympathetic ANS]], while the [[visceral]] motor efferents are located in both [[Sympathetic nervous system|sympathetic]] and [[Parasympathetic nervous system|parasympathetic]] [[Autonomic nervous system|ANS]].  
**In addition, the extrinsic nervous system synapse with [[enteric nervous system]] and relay information to the [[central nervous system]].
**In addition, the extrinsic nervous system synapse with [[enteric nervous system]] and relay information to the [[central nervous system]].


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**The highest risk for postoperative ileus has been observed with [[colorectal]] [[surgery]].
**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]].  
**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 or adynamic ileus.
**Postoperative ileus that lasts longer than 3 days is termed as paralytic ileus or adynamic ileus.
**When a patient undergoes a [[surgical procedure]], it often puts the body under significant [[stress]].  
**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 inhibition of intestinal motility and development of ileus.<ref name="pmid19580945">{{cite journal |vauthors=Doherty TJ |title=Postoperative ileus: pathogenesis and treatment |journal=Vet. Clin. North Am. Equine Pract. |volume=25 |issue=2 |pages=351–62 |year=2009 |pmid=19580945 |doi=10.1016/j.cveq.2009.04.011 |url=}}</ref>
***This [[Surgery|surgical]] [[stress]] may lead to release of [[inflammatory]] and [[neuroendocrine]] mediators (such as [[nitric oxide]], [[VIP]] and [[substance P]]) that may result in inhibition of [[intestinal]] motility and development of ileus.<ref name="pmid19580945">{{cite journal |vauthors=Doherty TJ |title=Postoperative ileus: pathogenesis and treatment |journal=Vet. Clin. North Am. Equine Pract. |volume=25 |issue=2 |pages=351–62 |year=2009 |pmid=19580945 |doi=10.1016/j.cveq.2009.04.011 |url=}}</ref>
***[[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.
***[[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 (biology)|cells]] leading to the initiation and maintenance of the [[inflammatory]] process and release of chemical mediators.
***Recent research has shown that '''inhibition''' of [[inflammatory]] mediators (such as [[nitric oxide]] & [[Vasoactive intestinal peptide|VIP]]) may lead to improved [[gastrointestinal]] [[peristalsis]] and function.  
***Recent research has shown that inhibition of [[inflammatory]] mediators (such as [[nitric oxide]] & [[Vasoactive intestinal peptide|VIP]]) may lead to improved [[gastrointestinal]] [[peristalsis]] and function.  
***The site of the [[surgery]] is the most commonly affected part of the [[Gastrointestinal tract|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]].<ref name="pmid11740765">{{cite journal |vauthors=Bederman SS, Betsy M, Winiarsky R, Seldes RM, Sharrock NE, Sculco TP |title=Postoperative ileus in the lower extremity arthroplasty patient |journal=J Arthroplasty |volume=16 |issue=8 |pages=1066–70 |year=2001 |pmid=11740765 |doi=10.1054/arth.2001.27675 |url=}}</ref>
***The site of the [[surgery]] is the most commonly affected part of the [[Gastrointestinal tract|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]].<ref name="pmid11740765">{{cite journal |vauthors=Bederman SS, Betsy M, Winiarsky R, Seldes RM, Sharrock NE, Sculco TP |title=Postoperative ileus in the lower extremity arthroplasty patient |journal=J Arthroplasty |volume=16 |issue=8 |pages=1066–70 |year=2001 |pmid=11740765 |doi=10.1054/arth.2001.27675 |url=}}</ref>
***Moreover, [[intestinal]] distention as seen in ileus also contributes to [[Serosa|serosal]] injury and may aggravate [[intestinal]] [[ischemia]].  
***Moreover, [[intestinal]] distention as seen in ileus also contributes to [[Serosa|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 the severity of ileus. <ref>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</ref><ref>Vachon AM, Fisher AT. Small intestinal herniation through the epiploic foramen: 53 cases (1987-1993). ''Equine Vet J'' 27: 373, 1995</ref>
***Prolonged ileus leads to increased contact between various segments of [[intestine]] which predispose to [[fibrous]] [[adhesion]] formation, thereby further contributing to the severity of ileus. <ref>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</ref><ref>Vachon AM, Fisher AT. Small intestinal herniation through the epiploic foramen: 53 cases (1987-1993). ''Equine Vet J'' 27: 373, 1995</ref>
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**Abdominal [[incision]] leads to activation of [[inhibitory]] [[spinal reflex]] which results in decreased movements of [[intestine]], as a regulatory mechanism.<ref name="pmid8967419">{{cite journal |vauthors=Barquist E, Bonaz B, Martinez V, Rivier J, Zinner MJ, Taché Y |title=Neuronal pathways involved in abdominal surgery-induced gastric ileus in rats |journal=Am. J. Physiol. |volume=270 |issue=4 Pt 2 |pages=R888–94 |year=1996 |pmid=8967419 |doi=10.1152/ajpregu.1996.270.4.R888 |url=}}</ref>
**Abdominal [[incision]] leads to activation of [[inhibitory]] [[spinal reflex]] which results in decreased movements of [[intestine]], as a regulatory mechanism.<ref name="pmid8967419">{{cite journal |vauthors=Barquist E, Bonaz B, Martinez V, Rivier J, Zinner MJ, Taché Y |title=Neuronal pathways involved in abdominal surgery-induced gastric ileus in rats |journal=Am. J. Physiol. |volume=270 |issue=4 Pt 2 |pages=R888–94 |year=1996 |pmid=8967419 |doi=10.1152/ajpregu.1996.270.4.R888 |url=}}</ref>
***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 nervous system|(sympathetic ANS]]).
***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 nervous system|(sympathetic ANS]]).
***Additionally, manipulation of [[intestine]] leads to activation of [[afferent]] pathways that travel to the [[Brain stem|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]].
***Additionally, manipulation of [[intestine]] leads to activation of [[afferent]] pathways that travel to the [[Brain stem|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).<ref name="Di NardoDi Lorenzo2017">{{cite journal|last1=Di Nardo|first1=G.|last2=Di Lorenzo|first2=C.|last3=Lauro|first3=A.|last4=Stanghellini|first4=V.|last5=Thapar|first5=N.|last6=Karunaratne|first6=T. B.|last7=Volta|first7=U.|last8=De Giorgio|first8=R.|title=Chronic intestinal pseudo-obstruction in children and adults: diagnosis and therapeutic options|journal=Neurogastroenterology & Motility|volume=29|issue=1|year=2017|pages=e12945|issn=13501925|doi=10.1111/nmo.12945}}</ref><ref name="pmid23831693">{{cite journal |vauthors=Iida H, Ohkubo H, Inamori M, Nakajima A, Sato H |title=Epidemiology and clinical experience of chronic intestinal pseudo-obstruction in Japan: a nationwide epidemiologic survey |journal=J Epidemiol |volume=23 |issue=4 |pages=288–94 |year=2013 |pmid=23831693 |pmc=3709546 |doi= |url=}}</ref><ref name="pmid23108319">{{cite journal |vauthors=Yeung AK, Di Lorenzo C |title=Primary gastrointestinal motility disorders in childhood |journal=Minerva Pediatr. |volume=64 |issue=6 |pages=567–84 |year=2012 |pmid=23108319 |doi= |url=}}</ref>
*Another [[chronic]] and a more severe form of [[ileus]] is known as chronic intestinal pseudo-obstruction (CIPO).<ref name="Di NardoDi Lorenzo2017">{{cite journal|last1=Di Nardo|first1=G.|last2=Di Lorenzo|first2=C.|last3=Lauro|first3=A.|last4=Stanghellini|first4=V.|last5=Thapar|first5=N.|last6=Karunaratne|first6=T. B.|last7=Volta|first7=U.|last8=De Giorgio|first8=R.|title=Chronic intestinal pseudo-obstruction in children and adults: diagnosis and therapeutic options|journal=Neurogastroenterology & Motility|volume=29|issue=1|year=2017|pages=e12945|issn=13501925|doi=10.1111/nmo.12945}}</ref><ref name="pmid23831693">{{cite journal |vauthors=Iida H, Ohkubo H, Inamori M, Nakajima A, Sato H |title=Epidemiology and clinical experience of chronic intestinal pseudo-obstruction in Japan: a nationwide epidemiologic survey |journal=J Epidemiol |volume=23 |issue=4 |pages=288–94 |year=2013 |pmid=23831693 |pmc=3709546 |doi= |url=}}</ref><ref name="pmid23108319">{{cite journal |vauthors=Yeung AK, Di Lorenzo C |title=Primary gastrointestinal motility disorders in childhood |journal=Minerva Pediatr. |volume=64 |issue=6 |pages=567–84 |year=2012 |pmid=23108319 |doi= |url=}}</ref>
**CIPO is a more severe form of [[ileus]] resulting from disturbances in [[enteric nervous system]], [[autonomic nervous system]] and [[Smooth muscle|smooth muscle cell]] function.   
**CIPO is a more severe form of [[ileus]] resulting from disturbances in [[enteric nervous system]], [[autonomic nervous system]] and [[Smooth muscle|smooth muscle cell]] function.   
**The cause of CIPO can be [[idiopathic]], sporadic, or secondary to [[metabolic]], [[connective tissue]], endocrinological, neurological, and [[Paraneoplastic syndrome|paraneoplastic disorders]].<ref name="pmid15880314">{{cite journal |vauthors=Stanghellini V, Cogliandro RF, De Giorgio R, Barbara G, Morselli-Labate AM, Cogliandro L, Corinaldesi R |title=Natural history of chronic idiopathic intestinal pseudo-obstruction in adults: a single center study |journal=Clin. Gastroenterol. Hepatol. |volume=3 |issue=5 |pages=449–58 |year=2005 |pmid=15880314 |doi= |url=}}</ref>
**The cause of CIPO can be [[idiopathic]], sporadic, or secondary to [[metabolic]], [[connective tissue]], [[Endocrinology|endocrinological]], [[Neurology|neurological]], and [[Paraneoplastic syndrome|paraneoplastic disorders]].<ref name="pmid15880314">{{cite journal |vauthors=Stanghellini V, Cogliandro RF, De Giorgio R, Barbara G, Morselli-Labate AM, Cogliandro L, Corinaldesi R |title=Natural history of chronic idiopathic intestinal pseudo-obstruction in adults: a single center study |journal=Clin. Gastroenterol. Hepatol. |volume=3 |issue=5 |pages=449–58 |year=2005 |pmid=15880314 |doi= |url=}}</ref>
**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.
**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 lack of propulsive [[intestinal]] 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 [[sepsis]].
**The enhanced intra-[[bowel]] pressure leads to [[malabsorption]] and [[bacterial]] [[translocation]]. Over time, it can progress to present with [[malnutrition]] and [[sepsis]].


*The other common cause of [[ileus]] are the [[drugs]] that affect [[intestinal]] [[motility]] and [[Electrolyte disturbance|alteration in electrolyte levels]].
*The other common cause of [[ileus]] are the [[drugs]] that affect [[intestinal]] [[motility]] and [[Electrolyte disturbance|alteration in electrolyte levels]].
**Drugs affecting [[intestinal]] [[motility]] primarily includes antimotility agents and [[anesthetics]].
**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]].
***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.
***[[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 (mu) 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]], [[hypocalcemia]], [[hypomagnesemia]], and [[metabolic acidosis]].
**[[Electrolyte abnormalities]] such as [[hypokalemia]], [[hyponatremia]], [[hypocalcemia]], [[hypomagnesemia]], and [[metabolic acidosis]] may also lead to the development of intestinal ileus.


==Associated Conditions==
==Associated Conditions==

Revision as of 16:54, 27 February 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Overview

Ileus is defined as a temporary cessation of intestinal peristalsis in the absence of mechanical obstruction. The pathogenesis of ileus is based on its multifactorial etiology. Ileus is most commonly seen during the postoperative period (ileus present for > 3 days after surgery). When a patient undergoes a surgical procedure, it often puts the body under significant stress. It is thought that ileus is the result of surgical stress induced inflammatory process, that leads to release of inflammatory and neuroendocrine mediators (such as nitric oxide, VIP and substance P). Additionally, manipulation of the intestine leads to activation of afferent pathways that travel to the brainstem. In turn, the brainstem sends increased autonomic output to the sympathetic neurons resulting in increased secretion of adrenergic neurotransmitters and decreased intestinal motility. Commonly used pain medications such as opiates and intraoperative anesthesia may also aggravate the development of ileus. Conditions commonly associated with ileus include diabetes mellitus, hypothyroidism, and hypoparathyroidism. On gross pathology findings of ileus include bowel contortion with distended small and large intestine. On microscopic histopathological analysis, findings of ileus include inflammatory cells predominantly macrophages and mast cells.

Pathophysiology

Ileus is defined as temporary cessation of intestinal peristalsis in the absence of mechanical obstruction. The pathogenesis of ileus is based on its multifactorial etiology. Intestinal peristalsis is primarily regulated by enteric nervous system, autonomic nervous system and their interactions with central nervous system (CNS). However, certain medications and metabolic 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

Neural control of gut.(By Boumphreyfr (Own work) [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], via Wikimedia Commons)

Pathophysiology

Associated Conditions

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

  1. ↑ 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.
  2. ↑ 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.
  3. ↑ 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.
  4. ↑ 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.
  5. ↑ 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.
  6. ↑ 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
  7. ↑ Vachon AM, Fisher AT. Small intestinal herniation through the epiploic foramen: 53 cases (1987-1993). Equine Vet J 27: 373, 1995
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ Yeung AK, Di Lorenzo C (2012). "Primary gastrointestinal motility disorders in childhood". Minerva Pediatr. 64 (6): 567–84. PMID 23108319.
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.

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