Ogilvie syndrome pathophysiology: Difference between revisions
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*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==== | |||
*The majority of [[Ileus|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:<ref name="pmid14699497">{{cite journal |vauthors=Schwarz NT, Kalff JC, Türler A, Speidel N, Grandis JR, Billiar TR, Bauer AJ |title=Selective jejunal manipulation causes postoperative pan-enteric inflammation and dysmotility |journal=Gastroenterology |volume=126 |issue=1 |pages=159–69 |year=2004 |pmid=14699497 |doi= |url=}}</ref> | |||
***Intestinal manipulation leads to intestinal [[ischemia]], and shifting of endogenous cellular danger molecules and [[Cytokine|cytokines]] away from the site of trauma. | |||
***[[White blood cells|Leukocytic]] infiltration, [[macrophage]] and [[mast cell]] stimulation commences and causes muscular dysfunction, and therefore inflammation in the manipulated segment. | |||
**Neural reflexes:<ref name="pmid14699497">{{cite journal |vauthors=Schwarz NT, Kalff JC, Türler A, Speidel N, Grandis JR, Billiar TR, Bauer AJ |title=Selective jejunal manipulation causes postoperative pan-enteric inflammation and dysmotility |journal=Gastroenterology |volume=126 |issue=1 |pages=159–69 |year=2004 |pmid=14699497 |doi= |url=}}</ref> | |||
***Inhibitory sympathetic neural reflexes increase due to noxious spinal afferent signals, therefore, the use of [[epidural]] local anesthetics or topical [[capsaicin]] is encouraged to prevent paralytic ileus.<ref name="pmid11034732">{{cite journal |vauthors=Jørgensen H, Wetterslev J, Møiniche S, Dahl JB |title=Epidural local anaesthetics versus opioid-based analgesic regimens on postoperative gastrointestinal paralysis, PONV and pain after abdominal surgery |journal=Cochrane Database Syst Rev |volume= |issue=4 |pages=CD001893 |year=2000 |pmid=11034732 |doi=10.1002/14651858.CD001893 |url=}}</ref> | |||
**Neurohormonal peptides:<ref name="pmid10648460">{{cite journal |vauthors=Kalff JC, Schraut WH, Billiar TR, Simmons RL, Bauer AJ |title=Role of inducible nitric oxide synthase in postoperative intestinal smooth muscle dysfunction in rodents |journal=Gastroenterology |volume=118 |issue=2 |pages=316–27 |year=2000 |pmid=10648460 |doi= |url=}}</ref><ref name="pmid7515341">{{cite journal |vauthors=Cullen JJ, Eagon JC, Kelly KA |title=Gastrointestinal peptide hormones during postoperative ileus. Effect of octreotide |journal=Dig. Dis. Sci. |volume=39 |issue=6 |pages=1179–84 |year=1994 |pmid=7515341 |doi= |url=}}</ref> | |||
***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]]. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
[[Category:Needs content]] | [[Category:Needs content]] | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Pathogenesis
The precise mechanism by which colonic dilation occurs in patients with acute colonic pseudo-obstruction is unknown. The association with trauma, spinal anesthesia, and pharmacologic agents suggests an impairment of the autonomic nervous system. Interruption of the parasympathetic fibers from S2 to S4 leaves an atonic distal colon and a functional proximal obstruction . However, there is no proposed mechanism to explain colonic dilation in those patients without obvious involvement of the parasympathetic nerves.
In patients with acute colonic pseudo-obstruction, increasing colonic diameter accelerates the rise in tension on the colonic wall, increasing the risk of colonic ischemia and perforation. The risk of colonic perforation increases when cecal diameter exceeds 10 to 12 cm and when the distention has been present for greater than six days [12]. The duration of dilation is probably more important than the absolute diameter of the colon.
Rare cases have been reported in association with atrophic visceral myopathy with an extremely thin colonic wall, atrophic circular, and longitudinal muscularis propria without inflammation or fibrosis, and unaffected ganglion cells and myenteric plexus. The cause of the smooth muscle atrophy was unclear and the only potential association was with prior hypothyroidism.
Ogilvie's syndrome
- The association of spinal anaesthesias, drugs and nervous trauma has lead to the understanding that Ogilvie syndrome (colonic dilatation without pseudo-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]
References
- ↑ 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.