Ogilvie syndrome pathophysiology: Difference between revisions
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__NOTOC__ | __NOTOC__ | ||
{{Ogilvie syndrome}} | |||
{{CMG}}; {{AE}} {{AEL}} | |||
==Overview== | ==Overview== | ||
The colonic pseudo-obstruction pathogenesis is believed to be due to impairment of the [[autonomic nervous system]]. The autonomic impairment may involve the [[Parasympathetic|parasympathetic fibers]] of S2-S4 which is responsible for [[innervation]] of the [[Colon|distal colon]] and may lead to atonic colon and [[Obstruction|proximal obstruction]]. In few cases, Ogilvie's syndrome (colonic pseudo-obstruction) may show [[atrophic]] [[myopathy]] with thinned colonic wall and intact [[myenteric plexus]]. | |||
==Pathophysiology== | ==Pathophysiology== | ||
=== Pathogenesis === | === Pathogenesis === | ||
====Ogilvie's syndrome==== | ====Ogilvie's syndrome==== | ||
*The association of [[Spinal anaesthesia|spinal anaesthesias]], drugs and nervous trauma has lead to the understanding that Ogilvie syndrome (colonic dilatation without | *The association of [[Spinal anaesthesia|spinal anaesthesias]], drugs and nervous trauma has lead to the understanding that Ogilvie syndrome (colonic dilatation without true obstruction) may be caused by impairment of the [[autonomic nervous system]].<ref name="pmid3753674">{{cite journal |vauthors=Vanek VW, Al-Salti M |title=Acute pseudo-obstruction of the colon (Ogilvie's syndrome). An analysis of 400 cases |journal=Dis. Colon Rectum |volume=29 |issue=3 |pages=203–10 |year=1986 |pmid=3753674 |doi= |url=}}</ref><ref name="pmid3319452">{{cite journal |vauthors=Ogilvie WH |title=William Heneage Ogilvie 1887-1971. Large-intestine colic due to sympathetic deprivation. A new clinical syndrome |journal=Dis. Colon Rectum |volume=30 |issue=12 |pages=984–7 |year=1987 |pmid=3319452 |doi= |url=}}</ref><ref name="pmid17643908">{{cite journal |vauthors=Saunders MD |title=Acute colonic pseudo-obstruction |journal=Best Pract Res Clin Gastroenterol |volume=21 |issue=4 |pages=671–87 |year=2007 |pmid=17643908 |doi=10.1016/j.bpg.2007.03.001 |url=}}</ref> | ||
*Damage to the [[Parasympathetic nervous system|parasympathetic]] fibers of S2 - S4 causes the distal colon to become atonic and become obstructed proximally. | *Damage to the [[Parasympathetic nervous system|parasympathetic]] fibers of S2 - S4 causes the distal colon to become atonic and become obstructed proximally. | ||
*However, the exact mechanism is unknown, especially in patients who present with this syndrome without an obvious injury to the parasympathetic nerves. | *However, the exact mechanism is unknown, especially in patients who present with this syndrome without an obvious injury to the parasympathetic nerves. | ||
*Acute colonic pseudo-obstruction occurs when the colon's diameter rises quickly, which increases the tension in the colonic wall, leading to colonic [[ischemia]] and possibly, [[perforation]] with a diameter exceeding 10 - 12cm. | *Acute colonic pseudo-obstruction occurs when the colon's diameter rises quickly, which increases the tension in the colonic wall, leading to colonic [[ischemia]] and possibly, [[perforation]] with a diameter exceeding 10 - 12cm. | ||
*A rare case of Ogilvie syndrome showed atrophic myopathy with a thinned out colonic wall, despite a perfectly intact [[myenteric plexus]] and unaffected [[Ganglion cell|ganglion cells]], with no evidence of [[fibrosis]] or [[inflammation]]. | *A rare case of Ogilvie syndrome showed atrophic myopathy with a thinned out colonic wall, despite a perfectly intact [[myenteric plexus]] and unaffected [[Ganglion cell|ganglion cells]], with no evidence of [[fibrosis]] or [[inflammation]]. | ||
====Paralytic ileus==== | ====Paralytic ileus==== | ||
*The majority of [[Ileus|paralytic (adynamic) ileus]] cases occur after major abdominal surgery, such as [[hysterectomy]]. | *The majority of [[Ileus|paralytic (adynamic) ileus]] cases occur after major abdominal surgery, such as [[hysterectomy]]. | ||
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***Inhibitory [[Neurotransmitter|neurotransmitters]] are released and cause the gut motility to slow down. | ***Inhibitory [[Neurotransmitter|neurotransmitters]] are released and cause the gut motility to slow down. | ||
***Inhibitory [[Neurotransmitter|neurotransmitters]] include, [[nitric oxide]], [[Vasoactive intestinal peptide|vasoactive intestinal polypeptide]], and [[substance P]]. | ***Inhibitory [[Neurotransmitter|neurotransmitters]] include, [[nitric oxide]], [[Vasoactive intestinal peptide|vasoactive intestinal polypeptide]], and [[substance P]]. | ||
== Associated conditions == | |||
* Ogilvie's syndrome (acute colonic psuedo-obstruction) may be associated with the following conditions:<ref name="pmid3753674" /> | |||
** Major [[surgeries]] as [[hip replacement surgery]] | |||
** Acute [[cardiac]] diseases as [[myocardial infarction]] | |||
** Systemic [[infections]] | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
Latest revision as of 16:43, 8 February 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Elsaiey, MBBCH [2]
Overview
The colonic pseudo-obstruction pathogenesis is believed to be due to impairment of the autonomic nervous system. The autonomic impairment may involve the parasympathetic fibers of S2-S4 which is responsible for innervation of the distal colon and may lead to atonic colon and proximal obstruction. In few cases, Ogilvie's syndrome (colonic pseudo-obstruction) may show atrophic myopathy with thinned colonic wall and intact myenteric plexus.
Pathophysiology
Pathogenesis
Ogilvie's syndrome
- The association of spinal anaesthesias, drugs and nervous trauma has lead to the understanding that Ogilvie syndrome (colonic dilatation without true obstruction) may be caused by impairment of the autonomic nervous system.[1][2][3]
- Damage to the parasympathetic fibers of S2 - S4 causes the distal colon to become atonic and become obstructed proximally.
- However, the exact mechanism is unknown, especially in patients who present with this syndrome without an obvious injury to the parasympathetic nerves.
- Acute colonic pseudo-obstruction occurs when the colon's diameter rises quickly, which increases the tension in the colonic wall, leading to colonic ischemia and possibly, perforation with a diameter exceeding 10 - 12cm.
- A rare case of Ogilvie syndrome showed atrophic myopathy with a thinned out colonic wall, despite a perfectly intact myenteric plexus and unaffected ganglion cells, with no evidence of fibrosis or inflammation.
Paralytic ileus
- The majority of paralytic (adynamic) ileus cases occur after major abdominal surgery, such as hysterectomy.
- Paralytic ileus is thought to occur with manipulation and trauma of the intestinal tract.
- Post operative dysmotility is associated with inflammation, impaired neural reflexes and the release of neural hormone peptides.
- Inflammation:[4]
- Intestinal manipulation leads to intestinal ischemia, and shifting of endogenous cellular danger molecules and cytokines away from the site of trauma.
- Leukocytic infiltration, macrophage and mast cell stimulation commences and causes muscular dysfunction, and therefore inflammation in the manipulated segment.
- Neural reflexes:[4]
- Neurohormonal peptides:[6][7]
- Inhibitory neurotransmitters are released and cause the gut motility to slow down.
- Inhibitory neurotransmitters include, nitric oxide, vasoactive intestinal polypeptide, and substance P.
- Inflammation:[4]
Associated conditions
- Ogilvie's syndrome (acute colonic psuedo-obstruction) may be associated with the following conditions:[1]
- Major surgeries as hip replacement surgery
- Acute cardiac diseases as myocardial infarction
- Systemic infections
References
- ↑ 1.0 1.1 Vanek VW, Al-Salti M (1986). "Acute pseudo-obstruction of the colon (Ogilvie's syndrome). An analysis of 400 cases". Dis. Colon Rectum. 29 (3): 203–10. PMID 3753674.
- ↑ Ogilvie WH (1987). "William Heneage Ogilvie 1887-1971. Large-intestine colic due to sympathetic deprivation. A new clinical syndrome". Dis. Colon Rectum. 30 (12): 984–7. PMID 3319452.
- ↑ Saunders MD (2007). "Acute colonic pseudo-obstruction". Best Pract Res Clin Gastroenterol. 21 (4): 671–87. doi:10.1016/j.bpg.2007.03.001. PMID 17643908.
- ↑ 4.0 4.1 Schwarz NT, Kalff JC, Türler A, Speidel N, Grandis JR, Billiar TR, Bauer AJ (2004). "Selective jejunal manipulation causes postoperative pan-enteric inflammation and dysmotility". Gastroenterology. 126 (1): 159–69. PMID 14699497.
- ↑ Jørgensen H, Wetterslev J, Møiniche S, Dahl JB (2000). "Epidural local anaesthetics versus opioid-based analgesic regimens on postoperative gastrointestinal paralysis, PONV and pain after abdominal surgery". Cochrane Database Syst Rev (4): CD001893. doi:10.1002/14651858.CD001893. PMID 11034732.
- ↑ 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.
- ↑ Cullen JJ, Eagon JC, Kelly KA (1994). "Gastrointestinal peptide hormones during postoperative ileus. Effect of octreotide". Dig. Dis. Sci. 39 (6): 1179–84. PMID 7515341.