Abstract

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Bowel perforation has been described following caesarean section. Ogilvie’s syndrome and paralytic ileus are the two most common causes of functional bowel obstruction.

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

Introduction

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Large-bowel obstruction is an emergency condition that requires early identification and intervention [1]. Etiology is age dependent, and it can result from either mechanical interruption of the flow of intestinal contents or by the dilation of the colon in the absence of an anatomic lesion (pseudo-obstruction) [2]. Causes include neoplasms, inflammatory processes (diverticulitis), strictures, fecal impaction or volvulus [1].

It is well known that women who undergo Caesarean section may develop an acute postoperative ileus characterized 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 diagnosed during the operation [1, 2, 4].

A perforated GIT after a Caesarean section has been described in 20 previous case reports, the first from 1954 [3, 5, 6]. Bowel obstruction can be due to either mechanical or functional causes [1, 3, 4]. The most common mechanical etiologies are adhesions (58%), volvulus (24%), and intussusception (5%) [1, 2, 4]. Although Ogilvie’s syndrome and paralytic ileus are rare, they are the two most common causes of functional bowel obstruction [4, 6]. One of the most severe sequelae of these etiologies is a bowel perforation, with the cecum being the most Susceptible (because it is the thinnest part of the GIT, and largest diameter), this allows it to expand 3 times faster than any other area of the colon [3-6]. Mortality rates from post operative GIT perforation range from 30% to 72% [1, 2, 5].

Symptoms normally occur between 2 to 12 days post caesarean section [1, 2, 5]. Progressive abdominal distension (90-100% of cases) and abdominal pain (80%) are the commonest symptoms [1, 2, 4-6]. bowel sounds may vary from normal to hyperactive or absent and patients can still pass small amounts of faecal fluid and flatus [1, 5, 6]. Average cecal diameter after CS is 6.4 cm. In patients with a caecal dilatation of less than 10 cm in diameter, the treatment is conservative and consists of keeping the patient nil by mouth, nasogastric tube suction and insertion of rectal tube [2-4, 7, 8]. Any medication that can affect the colonic motility such as narcotic analgesia and anti-cholinergic should be stopped [2, 7, 8]. Patients should respond to conservative treatment within 24 to 48 hours [1, 2, 8]. The response to the treatment is measured by serial abdominal x-rays and improvements in patient symptoms. Colonic decompression with medication or endoscopic intervention is used if patient fails to respond to conservative treatment [1, 2, 4, 8].

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

Pseudo-obstruction or Ogilvie’s syndrome is defined as distension of the colon that is similar to that occurring as a consequence of bowel obstruction but in which no physical obstruction exists and that occurs especially in seriously ill individuals and as a complication of abdominal surgery [3, 5, 6, 9, 10]. It was first reported in 1948 by the British surgeon Sir William Heneage Ogilvie (1887–1971) [3, 9, 10]. The true incidence of Ogilvie’s syndrome is unknown as many mild cases resolved spontaneously and no reliable national or international data exist on its frequency [9, 10]. The use of drugs such as syntocinon and opioid in cases of Ogilvie’s syndrome has also been reported to increase the risk but any causal relationship is unclear [6, 9, 10]. Caesarean section seems to be the most common operative procedure associated with this syndrome [5, 6]. There are cases reported after vaginal delivery, forceps delivery, caesarean hysterectomy, and during pregnancy with preterm labor, pre-eclampsia and multiple pregnancies [2, 5, 6]. There is no data on predisposing factors or any association with respect to ethnic group, parity and indication for caesarean section [6, 9, 10]. Ogilvie’s syndrome occurs due to imbalance between the sympathetic and parasympathetic colonic innervation [5, 6, 9, 10]. Ogilvie’s syndrome in obstetric patients has been attributed to declining levels of serum oestrogen following childbirth and resulting decreased parasympathetic tone [5-7, 9, 10]. Retrospective data suggest the cut off value of 12 cm in diameter is associated with an increased risk of bowel perforation [7, 9, 10]. Ogilvie’s syndrome develops gradually over 3-5 days and takes longer to resolve than paralytic ileus. If there is any sign of imminent perforation such as colonic dilatation that is substantially greater than 9 cm, pt should undergo a laparotomy in order to prevent intra-abdominal sepsis from leakage of bowel content [1, 6, 8]. Usually the patient has; abdominal distention, Pain, altered bowel movements, nausea and vomiting. Ogilvie’s syndrome usually resolves with conservative therapy stopping oral ingestions and a naso-gastric tube [1, 2, 6]. It may require Colonoscopic decompression which is successful in 70% of the cases. Neostigmin is a potent pharmacological way of decompressing the colon [1-3, 6]. It is a serious medical disorder and the mortality rate approximately 15% with early intervention and rises to 30-50% when the bowel is perforated or ischemic [1-4, 6, 7, 9, 10].

Case report

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31 years old Saudi lady P1+0 admitted to labour ward Madinah Maternity and Children Hospital, Saudi Arabia in October 2013, complaining of early labour pains. She is previous 1 caesarean section (CS), gestational age 38 weeks with antenatal care in private hospital. Previous CS was done for breech presentation before 3y 9m. After 2 hours artificial rupture of membranes (ARM) was done she was 4cm cephalic presentation at -2 station with clear liquor and adequate pelvis. At 7 cm patient was prepared for CS for failure to progress (FTP) with frequent strong contractions. Lower segment caesarean section carried out under general anaesthesia without any complications and with minimal maternal blood loss. Outcome was healthy baby boy 3.17 Kg’s with APGAR score 8/1 10/5. Post operatively patient recovered well and received Keflex (500mg IV three times daily), Flagyl (500mg IV three times daily), Clexan (0.4mg SC once daily) and Pethidine (100mg IM two doses).

Post operative day one, bowel sounds were positive, abdomen soft but distended, otherwise patient was stable. On day two patient starts to have vomiting with sluggish bowel sounds and passed small amount of flatus and stool. Ultrasound abdomen and abdominal X-ray were done (Figure 1)i. Abdominal US reported; No intra or extra peritoneal collection seen but the small intestine seen loaded and arranged in parallel lines above the fundus at epigastric area and no peristalsis movement seen but, large intestine movement seen, differential diagnosis constipation. Abdominal X-ray reported; Marked dilation of colon which is loaded with gases, cecum is the most dilated part = 10+ cm. Ascending colon and transverse colon show the same dilated = 9+ cm which slightly less than cecum. The descending colon appear dilated also but much less than cecum =7+ cm. The visualised osseous structures appeared normal (Figure 2). Patient was started on dysflatyl orally and glycerine suppositories rectally.

In the third post operative day, patient still having vomiting with distension and positive bowel sounds. Patient seen by surgeon and was diagnosed as Pseudo- Obstruction. Patient was kept NPO, Naso-gastric tube was inserted and potassium replacement started.

Fourth post operative day, Patient had the same abdominal destination, bowel sounds positive. Surgeon contacted to evaluate patient, he adviced to continue same treatment. Patient transferred in the night to Intensive care unit for close observation. In the fifth day patient was drowsy, tachypnic, tachycardiac and hypotensive. Patient started on dopamine with distended abdomen, 400ml aspirate from NGT tube and absent bowel sounds. Patient diagnosed as post CS intestinal obstruction? Perforation. Second abdominal US done and reported; moderate free fluid in pouch of Douglas and anterior to Ut and in both flanks and subphrenic area. Us guided aspiration done showing ascetic fluid, no intestinal content, no bleeding, sample sent for gram stain, C&S. Within the hour patient general condition deteriorated and abdominal destination became worse with marked dyspnea. Patient was taken for laparotomy. During laparotomy odourless free intraabdominal collection 1.5 Litre found with Small bowel amalgamated, with fibrin flakes and Perforation of the cecum 5mm, which was sealed by small bowel loop, no free intestinal content or localised abscess seen. Right Hemicolectomy done with side to side anastamosis in 2 layers and Mesentery defect closed. Two drains one subhepatic the other in pelvis inserted. Post-operatively patient kept in ICU. The next five days were uneventful with the effort to maintain patient blood pressure but in the early morning hours of the fifth day patient was declared dead.

Histopathology report post right Hemicolectomy showed; Right Hemicolectomy specimen 19cm long including cecum, appendix, part of ascending colon and small part of small intestine. Cecum show marked dilatation about 9cm with closed perforation at its lower part, surrounded by very thin area covered by dirty greenish rough pseudo- membrane. Next to this area, mucosal fold are markedly oedematous and the remaining part of colon shows mild oedema. Appendix and small intestine has no apparent lesions. At the perforation site; cecum is very thin showing marked necrotic changes of all layers with dense acute inflammatory cellular infiltrate on the surface, replacing necrotic mucosal covering. Infiltrate cells extend down to submucosa, musculosa, subserosa & Serosal layers with dense collection on the Serosal covering indicating peritonitis. Intestinal wall showing marked oedema, inflammatory cellular infiltrate, marked congestion and focal mucosal necrosis. Serosal layer and surrounding facia extensively infiltrated with acute inflammatory cells. Appendicular wall showing Serosal infiltration with acute inflammatory cells indicating acute peritonitis (Figure 3, 4).

Discussion

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The exact aetiology of Ogilvie's syndrome is unknown, but it has been associated with several disease processes such as trauma, abdominal and/or pelvic surgery, and sepsis [11]. Bed rest and abnormal electrolytes are also listed as factors associated with the development of the syndrome [12]. It was reported that the association between Ogilvie's syndrome and vaginal delivery may be due to the declining serum oestrogen levels in the postpartum period [13]. The mechanism of the condition is thought to involve loss of tone in the parasympathetic nerves S2 to S4. This, in turn, results in an atonic distal colon and pseudoobstruction [14]. Various sources report a cut-off sign relating to an area of dilated and collapsed bowel around the splenic flexure corresponding to the transition zone between the vagal and sacral parasympathetic nerve supplies [13, 15]. The cut-off sign is used to support the hypothesis of parasympathetic inhibition causing Ogilvie's syndrome [13-15].

The diagnosis of Ogilvie's syndrome is widely reported to be troublesome due to the non-specific clinical features [2, 9, 11, 12]. Abdominal distension is considered to be the common symptom, and Jetmore et al. report no known cases of Ogilvie's syndrome to have presented without distension of the abdomen [2, 7, 9, 11, 14]. As with any case of suspected ileus or obstruction, electrolyte levels are an essential investigation and in most cases of Ogilvie's syndrome, 83% demonstrated at least one electrolyte disturbance with hypocalcaemia being the most common [10, 12, 14]. Abdominal radiography is a standard first-line investigation, and it was reported that a caecal diameter of nine cm or more is the 'only definitive sign of imminent perforation [12, 14]. Several sources have discussed non-surgical management options with decompression of the bowel with intravenous fluid support as the standard of treatment, on the other hand, other sources advocate for Colonoscopic decompression as a successful method of avoiding surgical management, unless signs of peritonitis are evident [2, 3, 7, 9, 12, 15].

Conclusions

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This case illustrates three important points. Firstly, cecal perforation is a rare postoperative complication after a Caesarean section. Its etiology is a bowel obstruction which may be due to either Ogilvie’s syndrome or a paralytic ileus. Early identification is critical for successful treatment of these patients. If a postoperative patient presents with features consistent with a bowel obstruction, prompt imaging should be performed in order to aid early diagnosis and intervention. Secondly, abdominal ultrasonography is of limited value in detecting intraluminal colonic neoplasms. Thirdly, large bowel obstruction should be treated with urgency to avoid cecal perforation.

Acknowledgment

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Authors wish to thank Dr F Aldaffeer Radiologist, Dr O Elbahrawy Consultant Radiology, Dr H Missawi Consultant Histopathologist and Professor S Algawhary Consultant Histopathologist for their efforts and all the help they provided for this paper to come out.

References

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Source(s) of Funding

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MMCH

Competing Interests

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None what so ever