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== Ogilvie syndrome ==
{{Short description|Acute colonic pseudo-obstruction}}


[[File:Ogilvie ct coronal.jpg|Ogilvie ct coronal|thumb|300px]]
'''Ogilvie syndrome''', also known as '''acute colonic pseudo-obstruction''', is a condition characterized by the acute dilation of the colon in the absence of any mechanical obstruction. It is named after Sir William Heneage Ogilvie, who first described the syndrome in 1948.


'''Ogilvie syndrome''' is the acute dilatation of the colon in the absence of any [[Bowel obstruction|mechanical obstruction]] in severely ill patients.<ref name="NEJM">{{cite journal |vauthors=Ponec RJ, Saunders MD, Kimmey MB |title=Neostigmine for the treatment of acute colonic pseudo-obstruction |journal=N. Engl. J. Med. |volume=341 |issue=3 |pages=137–41 |year=1999 |pmid=10403850 |doi= 10.1056/NEJM199907153410301}}</ref>
==Pathophysiology==
Ogilvie syndrome is thought to result from an imbalance in the autonomic nervous system, which leads to a dysfunction in the colonic motility. The exact mechanism is not fully understood, but it is believed that there is an excessive sympathetic nervous system activity or a lack of parasympathetic activity, leading to colonic atony and dilation.


Acute colonic pseudo-obstruction is characterized by massive dilatation of the [[Cecum#Cecum|cecum]] (diameter > 10&nbsp;cm) and right colon on abdominal X-ray.<ref name="Sleisenger">{{cite book |last1=Feldman |first1=Mark |first2=Lawrence S. |last2=Friedman |first3=Marvin H. |last3=Sleisenger |title=Sleisenger & Fordtran's Gastrointestinal and Liver Disease |edition=7th |url=https://archive.org/details/sleisengerfordtr0001unse |publisher=Elsevier |date=July 2002 |isbn=978-0-7216-8973-9 |url-access=registration }}</ref><ref name="RCCM">{{cite journal |vauthors=Pratt DS, Epstein SK |title=Recent advances in critical care gastroenterology |journal=Am. J. Respir. Crit. Care Med. |volume=161 |issue=5 |pages=1417–20 |year=2000 |pmid=10806132 |url=http://ajrccm.atsjournals.org/cgi/content/full/161/5/1417 |doi=10.1164/ajrccm.161.5.16159}}</ref> It is a type of [[megacolon]], sometimes referred to as "acute megacolon," to distinguish it from [[toxic megacolon]].
==Causes==
Ogilvie syndrome can occur in a variety of clinical settings. It is often associated with:
* [[Trauma]]
* [[Infection]]
* [[Surgery]], particularly abdominal or pelvic surgery
* [[Neurological disorders]] such as [[Parkinson's disease]] or [[multiple sclerosis]]
* [[Electrolyte imbalances]], such as [[hypokalemia]] or [[hypercalcemia]]
* Use of certain medications, including [[opioids]] and [[anticholinergics]]


<youtube>
==Symptoms==
title='''{{PAGENAME}}'''
The symptoms of Ogilvie syndrome are similar to those of a mechanical bowel obstruction and may include:
movie_url=http://www.youtube.com/v/Dg8SF_zTgIE
* Abdominal distension
&rel=1
* Abdominal pain
embed_source_url=http://www.youtube.com/v/Dg8SF_zTgIE
* Nausea and vomiting
&rel=1
* Constipation or inability to pass gas
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The condition carries the name of the British surgeon Sir {{ill|William Heneage Ogilvie|pl}} (1887–1971), who first reported it in 1948.<ref>{{cite journal | author=Ogilvie H | title=Large-intestine Colic due to Sympathetic Deprivation | journal=Br Med J | year=1948 | volume=2 | pages=671–673 | doi=10.1136/bmj.2.4579.671 | pmid=18886657 | issue=4579 | pmc=2091708}} Reproduced in: {{cite journal |author=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 |date=December 1987 |pmid=3319452 |doi=10.1007/BF02554291}}</ref><ref>{{WhoNamedIt|doctor|2895|Sir William Heneage Ogilvie}}</ref><ref>{{cite journal | author=Haubrich WS | title=Ogilvie of the Ogilvie Syndrome | journal=Gastroenterology | year=2008 | volume=135 | issue=2 | pages=337 | doi=10.1053/j.gastro.2008.06.071}}</ref>
==Diagnosis==
The diagnosis of Ogilvie syndrome is primarily clinical, supported by imaging studies. A plain abdominal [[X-ray]] or [[CT scan]] can show colonic dilation without evidence of mechanical obstruction. It is important to rule out true mechanical obstruction, which may require surgical intervention.


==Signs and symptoms==
==Treatment==
Usually the patient has [[abdominal distention]], pain and altered [[bowel movements]].<ref name="Sleisenger"/><ref name="IrwinRippe"/> There may also be nausea and vomiting.<ref>{{cite journal |vauthors= Skeik N, Jabr FI |title= Ogilvie Syndrome |journal=Consultant |volume=49 |issue=2 |year=2009 |url=http://www.consultantlive.com/photoclinic/article/10162/1376818}}</ref>
The management of Ogilvie syndrome involves both conservative and pharmacological approaches:
 
==Cause==
Ogilvie syndrome may occur after surgery, especially following [[coronary artery bypass surgery]] and [[total joint replacement]].<ref name="AoS">{{cite journal |vauthors=Tenofsky PL, Beamer L, Smith RS |title=Ogilvie syndrome as a postoperative complication |journal=Arch Surg |volume=135 |issue=6 |pages=682–6; discussion 686–7 |year=2000 |pmid=10843364 |doi= 10.1001/archsurg.135.6.682|doi-access=free }}</ref> Drugs that disturb colonic motility (e.g., [[anticholinergic]]s or [[opioid]] [[analgesic]]s) contribute to the development of this condition.<ref name="Sleisenger"/><ref name="IrwinRippe">{{cite book |last= Irwin |first= Richard S. |author2= Rippe, James M. |title= Intensive Care Medicine |url= http://www.lww.com/product/?0-7817-3548-3 |publisher= Lippincott Williams & Wilkins, Philadelphia & London |date= January 2003 |isbn= 0-7817-3548-3 |url-status= dead |archiveurl= https://web.archive.org/web/20051107202505/http://www.lww.com/product/?0-7817-3548-3 |archivedate= 2005-11-07 }}</ref>
 
==Pathophysiology==
The exact mechanism is not known. The probable explanation is imbalance in the regulation of colonic motor activity by the [[autonomic nervous system]].<ref name="NEJM"/> It has been postulated that reactivation of [[varicella zoster virus]] (which causes [[chickenpox]] and [[herpes zoster|shingles]]) in the [[Enteric nervous system|enteric ganglia]] may be a cause of Ogilvie syndrome.<ref name=Gershon2013>{{Cite journal | last1 = Gershon | first1 = A. A. | title = Varicella zoster vaccines and their implications for development of HSV vaccines | doi = 10.1016/j.virol.2012.10.006 | journal = Virology | volume = 435 | issue = 1 | pages = 29–36 | year = 2013 | pmid =  23217613| pmc =3595154 }}</ref>
 
Acute megacolon develops because of abnormal [[intestinal motility]]. Normal colonic motility requires integration of myogenic, neural, and hormonal influences. The enteric nervous system is independent but is connected to the [[central nervous system]] by [[Sympathetic nervous system|sympathetic]] and [[parasympathetic nerve]]s. The targets of the [[enteric neuron]]s are [[muscle cell]]s, secretory cells, [[endocrine cell]]s, [[microvasculature]], and inflammatory cells. The neurons in the enteric plexuses are stimulated by a food [[Bolus (digestion)|bolus]], which both distends the gut and stimulates the mucosal surface, leading to the release of factors that stimulate [[interneuron]]s. The stimulated interneurons transmit excitatory signals proximally, which cause contraction and inhibitory signals distally, and these in turn cause relaxation. These signals are transmitted by the [[neurotransmitter]]s [[acetylcholine]] and [[serotonin]], among others.<ref name="NEJM_2">{{cite journal |vauthors=Alam HB, Fricchione GL, Guimaraes AS, Zukerberg LR |title=Case records of the Massachusetts General Hospital. Case 31-2009. A 26-year-old man with abdominal distention and shock |journal=N. Engl. J. Med. |volume=361 |issue=15 |pages=1487–96 |date=October 2009 |pmid=19812406 |doi=10.1056/NEJMcpc0900643 }}</ref>
 
Acute megacolon can also lead to [[ischemic]] [[necrosis]] in massively dilated intestinal segments. This is explained by [[Pascal's law]] and [[Young–Laplace equation|Laplaces's law]]. Pascal's principle states that a change in pressure at any point in an enclosed fluid at rest is transmitted undiminished to all points in the fluid; the pressure across all parts of the lumen is equal. Laplace's law states that:
 
<math>
T=\frac{P r}{2t}
</math>


where T=wall tension, p=pressure, r=radius, t=wall thickness. Since the wall tension is proportionate to the radius, a dilated intestinal segment has a greater wall tension than a nondilated segment; if the dilatation and tension are sufficiently great, blood flow may be obstructed and ischemia of the bowel will occur.<ref name="NEJM_2"/> Ogilivie syndrome may precipitate [[volvulus]].{{fact|date=December 2016}}
===Conservative Management===
* Bowel rest and [[nasogastric decompression]]
* Correction of any underlying electrolyte imbalances
* Discontinuation of medications that may contribute to colonic atony


==Diagnosis==
===Pharmacological Treatment===
Diagnosis starts with physical exam, observation, and interview of the patient. Imaging to diagnose dilation of the colon involves one view abdominal xray or obstruction series (PA chest, erect abdomen, and supine abdomen images). If further imaging is needed CT may be ordered.
* Administration of [[neostigmine]], a cholinesterase inhibitor, can stimulate colonic motility and is often effective in resolving the condition.


==Treatment==
===Surgical Intervention===
It usually resolves with conservative therapy stopping oral ingestions, i.e. [[nil per os]] and a [[Feeding tube|nasogastric tube]],<ref name="Sleisenger"/> but may require [[colonoscopy|colonoscopic]] decompression which is successful in 70% of the cases. A study published in the ''[[New England Journal of Medicine]]'' showed that [[neostigmine]] is a potent pharmacological way of decompressing the colon.<ref name="NEJM"/> According to the [[American Society for Gastrointestinal Endoscopy]] (ASGE), it should be considered prior to colonoscopic decompression. The use of neostigmine is not without risk since it can induce [[bradyarrhythmia]] and bronchospasms.<ref name="IrwinRippe"/> Therefore, atropine should be within immediate reach when this therapy is used.<ref name="NEJM"/><ref name="Sleisenger"/><ref name="RCCM"/>
In cases where conservative and pharmacological treatments fail, or if there is evidence of colonic ischemia or perforation, surgical intervention may be necessary. This can include [[colonoscopy]] for decompression or, in severe cases, surgical resection of the affected bowel segment.


==Prognosis==
==Prognosis==
It is a serious medical disorder and the mortality rate can be as high as 30%.<ref name="IrwinRippe"/> The high mortality rate is likely a measure that this syndrome is seen in critically ill patients, rather than this syndrome being in itself lethal, although it can also present in otherwise healthy individuals (especially if the disorder was induced by pharmacologic agents). Drug induced megacolon (i.e. from [[clozapine]]) has been associated with mortality as high as 27.5%.<ref name="NEJM_2"/>
The prognosis of Ogilvie syndrome is generally good with appropriate treatment. However, if left untreated, it can lead to serious complications such as colonic perforation, peritonitis, and sepsis.
 
==References==
{{reflist}}


== External links ==
==Related pages==
{{Medical resources
* [[Colonic pseudo-obstruction]]
|  DiseasesDB    = 10868
* [[Bowel obstruction]]
|  ICD10          = K56.6
* [[Autonomic nervous system]]
|  ICD9          = {{ICD9|560.89}}
|  MedlinePlus    = 000253
|  eMedicineSubj  = article
|  eMedicineTopic = 2162306
|  MeshID        = D003112
}}
{{Digestive system diseases}}


[[Category:Diseases of intestines]]
[[Category:Gastroenterology]]
[[Category:Varicella zoster virus-associated diseases]]
[[Category:Syndromes]]
[[Category:Rare syndromes]]
[[Category:Syndromes affecting the gastrointestinal tract]]
{{stub}}

Revision as of 19:13, 22 March 2025

Ogilvie syndrome, also known as acute colonic pseudo-obstruction, is a condition characterized by the acute dilation of the colon in the absence of any mechanical obstruction. It is named after Sir William Heneage Ogilvie, who first described the syndrome in 1948.

Pathophysiology

Ogilvie syndrome is thought to result from an imbalance in the autonomic nervous system, which leads to a dysfunction in the colonic motility. The exact mechanism is not fully understood, but it is believed that there is an excessive sympathetic nervous system activity or a lack of parasympathetic activity, leading to colonic atony and dilation.

Causes

Ogilvie syndrome can occur in a variety of clinical settings. It is often associated with:

Symptoms

The symptoms of Ogilvie syndrome are similar to those of a mechanical bowel obstruction and may include:

  • Abdominal distension
  • Abdominal pain
  • Nausea and vomiting
  • Constipation or inability to pass gas

Diagnosis

The diagnosis of Ogilvie syndrome is primarily clinical, supported by imaging studies. A plain abdominal X-ray or CT scan can show colonic dilation without evidence of mechanical obstruction. It is important to rule out true mechanical obstruction, which may require surgical intervention.

Treatment

The management of Ogilvie syndrome involves both conservative and pharmacological approaches:

Conservative Management

  • Bowel rest and nasogastric decompression
  • Correction of any underlying electrolyte imbalances
  • Discontinuation of medications that may contribute to colonic atony

Pharmacological Treatment

  • Administration of neostigmine, a cholinesterase inhibitor, can stimulate colonic motility and is often effective in resolving the condition.

Surgical Intervention

In cases where conservative and pharmacological treatments fail, or if there is evidence of colonic ischemia or perforation, surgical intervention may be necessary. This can include colonoscopy for decompression or, in severe cases, surgical resection of the affected bowel segment.

Prognosis

The prognosis of Ogilvie syndrome is generally good with appropriate treatment. However, if left untreated, it can lead to serious complications such as colonic perforation, peritonitis, and sepsis.

Related pages