ogilivie's syndrome: case report - webmedcentral.comparasympathetic colonic innervation [5, 6,...

Article ID: WMC004641 ISSN 2046-1690

Ogilivie's syndrome: Case reportPeer review status:No

Corresponding Author:Dr. Sahal Khojah,Obstetrician and Gynaecologist, King Abdullah Medical City, Maternity and Children Hospital, Madinah, SaudiArabia - Saudi Arabia

Submitting Author:Dr. Mohammad Othman,Consultant Obstetrician and Gynaecologist, King Abdullah Medical City, Maternity and Children Hospital,Madinah, Saudi Arabia, 84 Bradfield Road, M32 9LE - United Kingdom

Other Authors:Dr. Taghread Alkholy,Senior Registrar, King Abdullah Medical City, Maternity and Children Hospital, Madinah, Saudi Arabia - SaudiArabia

Dr. Laila Rafie,Consultant Obstetrics and Gynaecology, King Abdullah Medical City, Maternity and Children Hospital, Madinah,Saudi Arabia - Saudi Arabia

Article ID: WMC004641

Article Type: Case Report

Submitted on:19-May-2014, 02:56:51 PM GMT Published on: 20-May-2014, 05:25:40 AM GMT

Article URL: http://www.webmedcentral.com/article_view/4641

Subject Categories:OBSTETRICS AND GYNAECOLOGY

Keywords:Ogilivie\'s syndrome, bowel perforation, paralytic ileus, ultrasound, abdominal x-ray, ICU

How to cite the article:Othman M, Khojah S, Alkholy T, Rafie L. Ogilivie's syndrome: Case report.WebmedCentral OBSTETRICS AND GYNAECOLOGY 2014;5(5):WMC004641

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Ogilivie's syndrome: Case reportAuthor(s): Othman M, Khojah S, Alkholy T, Rafie L

Abstract

Bowel perforation has been described followingcaesarean section. Ogilvie’s syndrome and paralyticileus are the two most common causes of functionalbowel obstruction.

We report here a case of ogilivie’s syndrome.Unfortunately, surgical intervention was late andpatient died.

Introduction

Large-bowel obstruction is an emergency conditionthat requires early identification and intervention [1].Etiology is age dependent, and it can result from eithermechanical interruption of the flow of intestinalcontents or by the dilation of the colon in the absenceof an anatomic lesion (pseudo-obstruction) [2]. Causesinclude neoplasms, inflammatory processes(diverticulitis), strictures, fecal impaction or volvulus [1].

It is well known that women who undergo Caesareansection may develop an acute postoperative ileuscharacterized by transient, occasionally severe,colonic dilatation that resolves spontaneously [1, 3, 4].The common places of injury are the large bowel,small bowel, rectum and rarely the gastric region [1, 2,4]. The incidence of bowel injuries is 0.08% in CS [1,4]. One-third of bowel injuries may be diagnosedduring the operation [1, 2, 4].

A perforated GIT after a Caesarean section has beendescribed in 20 previous case reports, the first from1954 [3, 5, 6]. Bowel obstruction can be due to eithermechanical or functional causes [1, 3, 4]. The mostcommon mechanical etiologies are adhesions (58%),volvulus (24%), and intussusception (5%) [1, 2, 4].Although Ogilvie’s syndrome and paralytic ileus arerare, they are the two most common causes offunctional bowel obstruction [4, 6]. One of the mostsevere sequelae of these etiologies is a bowelperforation, with the cecum being the mostSusceptible (because it is the thinnest part of the GIT,and largest diameter), this allows it to expand 3 timesfaster than any other area of the colon [3-6]. Mortalityrates from post operative GIT perforation range from30% to 72% [1, 2, 5].

Symptoms normally occur between 2 to 12 days postcaesarean section [1, 2, 5]. Progressive abdominaldistension (90-100% of cases) and abdominal pain(80%) are the commonest symptoms [1, 2, 4-6]. bowelsounds may vary from normal to hyperactive or absentand patients can still pass small amounts of faecalfluid and flatus [1, 5, 6]. Average cecal diameter afterCS is 6.4 cm. In patients with a caecal dilatation ofless than 10 cm in diameter, the treatment isconservative and consists of keeping the patient nil bymouth, nasogastric tube suction and insertion of rectaltube [2-4, 7, 8]. Any medication that can affect thecolonic motility such as narcotic analgesia andanti-cholinergic should be stopped [2, 7, 8]. Patientsshould respond to conservative treatment within 24 to48 hours [1, 2, 8]. The response to the treatment ismeasured by serial abdominal x-rays andimprovements in patient symptoms. Colonicdecompression with medication or endoscopicintervention is used if patient fails to respond toconservative treatment [1, 2, 4, 8].

Obstruction of the large bowel causes bowel dilatationabove the obstruction, which in turn, causes mucosaledema and impaired venous and arterial blood flow tothe bowel [1, 2, 4, 5]. Bowel edema and ischemiaincrease the mucosal permeability of the bowel, whichcan lead to bacterial translocation, systemic toxicity,dehydration, and electrolyte abnormalities. Bowelischemia can lead to perforation and fecal spoilage ofthe peritoneal cavity [1, 2, 4, 5, 7].

Pseudo-obstruction or Ogilvie’s syndrome is definedas distension of the colon that is similar to thatoccurring as a consequence of bowel obstruction butin which no physical obstruction exists and that occursespecially in seriously ill individuals and as acomplication of abdominal surgery [3, 5, 6, 9, 10]. Itwas first reported in 1948 by the British surgeon SirWilliam Heneage Ogilvie (1887–1971) [3, 9, 10]. Thetrue incidence of Ogilvie’s syndrome is unknown asmany mild cases resolved spontaneously and noreliable national or international data exist on itsfrequency [9, 10]. The use of drugs such assyntocinon and opioid in cases of Ogilvie’s syndromehas also been reported to increase the risk but anycausal relationship is unclear [6, 9, 10]. Caesareansection seems to be the most common operativeprocedure associated with this syndrome [5, 6]. Thereare cases reported after vaginal delivery, forceps



delivery, caesarean hysterectomy, and duringpregnancy with preterm labor, pre-eclampsia andmultiple pregnancies [2, 5, 6]. There is no data onpredisposing factors or any association with respect toethnic group, parity and indication for caesareansection [6, 9, 10]. Ogilvie’s syndrome occurs due toimbalance between the sympathet ic andparasympathetic colonic innervation [5, 6, 9, 10].Ogilvie’s syndrome in obstetric patients has beenattributed to declining levels of serum oestrogenfollowing childbirth and resulting decreasedparasympathetic tone [5-7, 9, 10]. Retrospective datasuggest the cut off value of 12 cm in diameter isassociated with an increased risk of bowel perforation[7, 9, 10]. Ogilvie’s syndrome develops gradually over3-5 days and takes longer to resolve than paralyticileus. If there is any sign of imminent perforation suchas colonic dilatation that is substantially greater than 9cm, pt should undergo a laparotomy in order toprevent intra-abdominal sepsis from leakage of bowelcontent [1, 6, 8]. Usually the patient has; abdominaldistention, Pain, altered bowel movements, nauseaand vomiting. Ogilvie’s syndrome usually resolves withconservative therapy stopping oral ingestions and anaso-gastric tube [1, 2, 6]. It may require Colonoscopicdecompression which is successful in 70% of thecases. Neostigmin is a potent pharmacological way ofdecompressing the colon [1-3, 6]. It is a seriousmedical disorder and the mortality rate approximately15% with early intervention and rises to 30-50% whenthe bowel is perforated or ischemic [1-4, 6, 7, 9, 10].

Case report

31 years old Saudi lady P1+0 admitted to labour wardMadinah Maternity and Children Hospital, SaudiArabia in October 2013, complaining of early labourpains. She is previous 1 caesarean section (CS),gestational age 38 weeks with antenatal care inprivate hospital. Previous CS was done for breechpresentation before 3y 9m. After 2 hours artificialrupture of membranes (ARM) was done she was 4cmcephalic presentation at -2 station with clear liquor andadequate pelvis. At 7 cm patient was prepared for CSfor failure to progress (FTP) with frequent strongcontractions. Lower segment caesarean sectioncarried out under general anaesthesia without anycomplications and with minimal maternal blood loss.Outcome was healthy baby boy 3.17 Kg’s with APGARscore 8/1 10/5. Post operatively patient recovered welland received Keflex (500mg IV three times daily),Flagyl (500mg IV three times daily), Clexan (0.4mg SConce daily) and Pethidine (100mg IM two doses).

Post operative day one, bowel sounds were positive,abdomen soft but distended, otherwise patient wasstable. On day two patient starts to have vomiting withsluggish bowel sounds and passed small amount offlatus and stool. Ultrasound abdomen and abdominalX-ray were done (Figure 1)i. Abdominal US reported;No intra or extra peritoneal collection seen but thesmall intestine seen loaded and arranged in parallellines above the fundus at epigastric area and noperistalsis movement seen but, large intestinemovement seen, differential diagnosis constipation.Abdominal X-ray reported; Marked dilation of colonwhich is loaded with gases, cecum is the most dilatedpart = 10+ cm. Ascending colon and transverse colonshow the same dilated = 9+ cm which slightly lessthan cecum. The descending colon appear dilated alsobut much less than cecum =7+ cm. The visualisedosseous structures appeared normal (Figure 2).Patient was started on dysflatyl orally and glycerinesuppositories rectally.

In the third post operative day, patient still havingvomiting with distension and positive bowel sounds.Patient seen by surgeon and was diagnosed asPseudo- Obstruction. Patient was kept NPO,Naso-gastric tube was inserted and potassiumreplacement started.

Fourth post operative day, Patient had the sameabdominal destination, bowel sounds positive.Surgeon contacted to evaluate patient, he adviced tocontinue same treatment. Patient transferred in thenight to Intensive care unit for close observation. In thefifth day patient was drowsy, tachypnic, tachycardiacand hypotensive. Patient started on dopamine withdistended abdomen, 400ml aspirate from NGT tubeand absent bowel sounds. Patient diagnosed as postCS intestinal obstruction? Perforation. Secondabdominal US done and reported; moderate free fluidin pouch of Douglas and anterior to Ut and in bothflanks and subphrenic area. Us guided aspiration doneshowing ascetic fluid, no intestinal content, nobleeding, sample sent for gram stain, C&S. Within thehour patient general condition deteriorated andabdominal destination became worse with markeddyspnea. Patient was taken for laparotomy. Duringlaparotomy odourless free intraabdominal collection1.5 Litre found with Small bowel amalgamated, withfibrin flakes and Perforation of the cecum 5mm, whichwas sealed by small bowel loop, no free intestinalcontent or local ised abscess seen. RightHemicolectomy done with side to side anastamosis in2 layers and Mesentery defect closed. Two drains onesubhepat ic the other in pe lv is inser ted.Post-operatively patient kept in ICU. The next five



days were uneventful with the effort to maintain patientblood pressure but in the early morning hours of thefifth day patient was declared dead.

Histopathology report post right Hemicolectomyshowed; Right Hemicolectomy specimen 19cm longincluding cecum, appendix, part of ascending colonand small part of small intestine. Cecum show markeddilatation about 9cm with closed perforation at itslower part, surrounded by very thin area covered bydirty greenish rough pseudo- membrane. Next to thisarea, mucosal fold are markedly oedematous and theremaining part of colon shows mild oedema. Appendixand small intestine has no apparent lesions. At theperforation site; cecum is very thin showing markednecrotic changes of all layers with dense acuteinflammatory cellular infiltrate on the surface, replacingnecrotic mucosal covering. Infiltrate cells extend downto submucosa, musculosa, subserosa & Serosallayers with dense collection on the Serosal coveringindicating peritonitis. Intestinal wall showing markedoedema, inflammatory cellular infiltrate, markedcongestion and focal mucosal necrosis. Serosal layerand surrounding facia extensively infiltrated with acuteinflammatory cells. Appendicular wall showing Serosalinfiltration with acute inflammatory cells indicatingacute peritonitis (Figure 3, 4).

Discussion

The exact aetiology of Ogilvie's syndrome is unknown,but it has been associated with several diseaseprocesses such as trauma, abdominal and/or pelvicsurgery, and sepsis [11]. Bed rest and abnormalelectrolytes are also listed as factors associated withthe development of the syndrome [12]. It was reportedthat the association between Ogilvie's syndrome andvaginal delivery may be due to the declining serumoestrogen levels in the postpartum period [13]. Themechanism of the condition is thought to involve lossof tone in the parasympathetic nerves S2 to S4. This,in turn, results in an atonic distal colon andpseudoobstruction [14]. Various sources report acut-off sign relating to an area of dilated and collapsedbowel around the splenic flexure corresponding to thetransition zone between the vagal and sacralparasympathetic nerve supplies [13, 15]. The cut-offs ign is used to support the hypothesis ofparasympathetic inhibition causing Ogilvie's syndrome[13-15].

The diagnosis of Ogilvie's syndrome is widely reportedto be troublesome due to the non-specific clinicalfeatures [2, 9, 11, 12]. Abdominal distension is

considered to be the common symptom, and Jetmoreet al. report no known cases of Ogilvie's syndrome tohave presented without distension of the abdomen [2,7, 9, 11, 14]. As with any case of suspected ileus orobstruction, electrolyte levels are an essentialinvestigation and in most cases of Ogilvie's syndrome,83% demonstrated at least one electrolyte disturbancewith hypocalcaemia being the most common [10, 12,14]. Abdominal radiography is a standard first-lineinvestigation, and it was reported that a caecaldiameter of nine cm or more is the 'only definitive signof imminent perforation [12, 14]. Several sources havediscussed non-surgical management options withdecompression of the bowel with intravenous fluidsupport as the standard of treatment, on the otherhand, other sources advocate for Colonoscopicdecompression as a successful method of avoidingsurgical management, unless signs of peritonitis areevident [2, 3, 7, 9, 12, 15].

Conclusions

This case illustrates three important points. Firstly,cecal perforation is a rare postoperative complicationafter a Caesarean section. Its etiology is a bowelobstruction which may be due to either Ogilvie’ssyndrome or a paralytic ileus. Early identification iscritical for successful treatment of these patients. If apostoperative patient presents with features consistentwith a bowel obstruction, prompt imaging should beperformed in order to aid early diagnosis andintervention. Secondly, abdominal ultrasonography isof limited value in detecting intraluminal colonicneoplasms. Thirdly, large bowel obstruction should betreated with urgency to avoid cecal perforation.

Acknowledgment

Authors wish to thank Dr F Aldaffeer Radiologist, Dr OElbahrawy Consultant Radiology, Dr H MissawiConsultant Histopathologist and Professor SAlgawhary Consultant Histopathologist for their effortsand all the help they provided for this paper to comeout.

References

1. Hopkins, C., et al., Large-Bowel Obstruction.Medscape Reference, 2014.2. Laskin, M., K. Tessler, and S. Kives, CecalPerforation Due to Paralytic Ileus Following Primary



Caesarean Section. Journal Obstetrics andGynaecology Canadian, 2009. 31(2): p. 167–171.3. Cartlidge, D. and M. Seenath, pseudo-obstruction ofthe large bowel with caecal perforation followingnormal vaginal delivery: a case report. Journal ofMedical Case Reports, 2010. 4: p. 123.4. Kammen, B., et al., Adynamic ileus after Caesareansection mimicking intestinal obstruction: ®ndings onabdominal radiographs. The British Journal ofRadiology, 2000. 73: p. 951-5.5. Dua, A. and B. Onyeka, Ogilvie SyndromeCompl icated By Caecal Per forat ion In APost-Caesarean Section Patient: A Case Report. TheInternet Journal of Gynecology and Obstetrics, 2005.5(2).6. Saha, A., et al., Ogilvie’s syndrome with caecalperforation after Caesarean section: a case report.Journal of Medical Case Reports, 2009. 3: p. 6177.7. Cagir, B., et al., Intestinal Pseudo-ObstructionT r e a t m e n t & M a n a g e m e n t .emedicine.medscape.com/article/2162306-treatment,2013.8. Jastaniah, S., Malignant Colonic Stricture withCecal Perforation: A Case Report and A Review ofLiterature. Bahrain Medical Bulletin, 2001. 23(2): p.93-4.9. Remy, P. and K. Kumbum, Ogilvie Syndrome.Emedicine Journal, 2012.10. Willacy, H. and G. Rull, Ogilvie's Syndrome. EgtonMedical Information Systems Limited, 2011.11. Kakaria, A., et al., Acute pseudo-obstruction of thecolon (Ogilvie's syndrome) following instrumentalvaginal delivery. International Journal of ClinicalPractice, 2006. 60(10): p. 1303-5.12. Jetmore, A., et al., Ogilvie's syndrome:colonoscopic decompression and analysis ofpredisposing factors. Diseases of the Colon andRectum, 1992. 35(12): p. 1135-42.13. Strecker, J. and V. Jaluvka, Spontaneous caecumperforation following caesarean section. GeburtshilfeFrauenheilkd, 1988. 48(7): p. 489-93.14. Camilleri, M., Acute colonic pseudo-obstruction( O g i l v i e ' s s y n d r o m e ) . http://www.uptodate.com, 2000.15. Stephenson, B., et al., Ogilvie's syndrome: a newapproach to an old problem. Diseases of the Colonand Rectum, 1995. 38: p. 424-7.



Illustrations

Illustration 1

Figure 1: Abdominal X-ray



Illustration 2

Figure 2: Ultrasound pictures



Illustration 3

Figure 3: Macroscopic histopathology post right Hemicolectomy



Illustration 4

Figure 4: Microscopic histopathology post right Hemicolectomy


ogilivie's syndrome: case report - webmedcentral.comparasympathetic colonic innervation [5, 6,...

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