World J Surg (2014) 38:3007–3014 DOI 10.1007/s00268-014-2711-z

ORIGINAL SCIENTIFIC REPORT

Early Postoperative Small Bowel Obstruction is an Independent Risk Factor for Subsequent Adhesive Small Bowel Obstruction in Patients Undergoing Open Colectomy Soo Young Lee • Kyu Joo Park • Seung-Bum Ryoo Heung-Kwon Oh • Eun Kyung Choe • Seung Chul Heo



Published online: 15 August 2014 Ó Socie´te´ Internationale de Chirurgie 2014

Abstract Background This prospective study was performed to investigate whether postoperative ileus (POI) or early postoperative small bowel obstruction (EPSBO) affects the development of adhesive small bowel obstruction (SBO) in patients undergoing colectomy. Methods We prospectively enrolled 1,002 patients who underwent open colectomy by a single surgeon. POI was defined as the absence of bowel function for more than 5 days or as a delay in oral intake beyond 7 days postoperatively. EPSBO was defined as the clinical and radiologic identification of SBO after resuming oral intake between postoperative days 7 and 30. Adhesive SBO was defined as SBO developing after 30 days because of intraperitoneal adhesion. The associations between POI, EPSBO, patient- and surgery-related variables, and the development of adhesive SBO were analyzed. Results A total of 85 (8.5 %) patients developed POI, and 42 patients (4.2 %) developed EPSBO, with seven patients experiencing both POI and EPSBO. During the follow-up period (median 51 months), 70 patients (7.0 %) developed adhesive SBO, six (8.6 %) of whom needed laparotomy. The occurrence of adhesive SBO was significantly higher in patients with EPSBO than in those without EPSBO (26.5 vs. 7.5 % at 5 years, P \ 0.001), but not in patients with POI (13.4 vs. 7.8 % at 5 years, P = 0.158). Multivariable analysis showed colostomy (hazard ratio [HR] 2.530, P = 0.006) and EPSBO (HR 4.063, P \ 0.001) as independent risk factors for adhesive SBO. Conclusions The development of adhesive SBO after colectomy is more frequent in patients with EPSBO and colostomy; however, POI does not increase the risk of adhesive SBO. Introduction The abstract of this article was presented at the 7th Scientific and Annual Meeting of the European Society of Coloproctology in Vienna, Austria on 27 September 2012. S. Y. Lee  H.-K. Oh Department of Surgery, Seoul National University Bundang Hospital, Seongnam, Korea K. J. Park  S.-B. Ryoo Department of Surgery, Seoul National University Hospital, Seoul, Korea

Regardless of the type of surgery, patients who undergo a laparotomy procedure have a 90 % risk of developing

S. C. Heo (&) Department of Surgery, Seoul National University College of Medicine, Seoul Metropolitan Government Boramae Hospital, 20 Boramae-ro 5-gil, Dongjak-gu, Seoul 156-707, Korea e-mail: [email protected]

E. K. Choe Department of Surgery, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Korea

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intraperitoneal adhesions [1]. Although most of these patients remain asymptomatic, up to 20 % have a high risk of re-admission related to adhesion formation [2, 3]. Adhesive small bowel obstruction (SBO) impacts not only healthcare costs but also quality of life; therefore, identifying those at high risk of developing adhesive SBO is important. A review by Schnuriger et al. [4] suggested that open colectomy, open gynecological surgery, and ileal pouch–anal anastomosis were risk factors for adhesive SBO following abdominal surgery. Surgery-related factors, such as the type of procedure, preoperative peritonitis, or a long operation time are major concerns for adhesive SBO development. Postoperative ileus (POI) and early postoperative SBO (EPSBO) are also important issues because of the requirement for extended hospitalization for impaired bowel function following surgery. We hypothesized that delayed recovery of bowel movement or SBO in the early postoperative period may affect the development of subsequent adhesive SBO. In this study, we investigated whether POI or EPSBO are risk factors for subsequent adhesive SBO.

Material and methods Because open colorectal surgery is a risk factor for adhesive SBO [4, 5], this study targeted patients who underwent open colectomy. Patients were selected from a prospectively collected cohort of 1,148 consecutive patients who underwent open colectomy by a single surgeon between 2005 and 2007 at a tertiary referral center. Exclusion criteria included the following: 1) Patients with a postoperative diagnosis of pseudomyxoma peritonei, peritoneal carcinomatosis, seeding ileus, or colonic metastasis from another primary cancer. 2) Patients undergoing surgery for adhesive SBO or radiation enteritis. 3) Patients with a history of previous colectomy. 4) Patients who died during admission to the center. 5) Patients transferred to another hospital before commencement of oral intake. 6) Patients with a follow-up period of less than 1 month. 7) Patients with a delayed oral intake caused by prolonged tracheal intubation or anastomotic leakage. Adhesive SBO was defined as SBO that developed after postoperative day 30 because of intraperitoneal adhesion and necessitated admission to the hospital. After reviewing the patient interview records, we also included patients who were admitted to a different hospital because of adhesive SBO. Cases of SBO with obstruction caused by malignant seeding nodules, as judged by clinical and radiological findings, were excluded. POI was defined as the absence of passage of flatus for more than 5 days [6, 7] based on the time

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of bowel recovery [8]. Patients with a delayed diet intake of 7 or more days postoperatively because of abdominal distension, nausea, and vomiting were also classified as POI [9]. EPSBO was defined as the clinical and radiologic identification of SBO after resuming oral intake between postoperative days 7 and 30 [9]. When symptoms such as abdominal distension or nausea arise in the early postoperative period, it is very difficult to distinguish between POI and EPSBO. Therefore, we defined the 7th postoperative day as a cut-off for dividing patients with POI (within the 6th postoperative day) and EPSBO (between postoperative days 7 and 30) [9]. Clinicopathological data were collected and analyzed to eliminate the possibility of confounding factors between POI or EPSBO and adhesive SBO. Operation history included major laparotomy, except for appendectomy or cesarean section. Obstruction and perforation were defined on the basis of preoperative colonoscopy and radiological findings as well as operative findings. Chronic steroid use was defined as the use of steroid medication on a daily basis for at least 30 days at the time of admission. The type of surgery was classified using the following three criteria: (1) abdominal or pelvic surgery; (2) total/subtotal or segmental surgery; and (3) ileal pouch surgery or the others. A pelvic operation was defined as surgery that included pelvic dissection. The total/ subtotal surgery group included surgery for subtotal colectomy, total colectomy, and total proctocolectomy. Preoperative albumin level was the latest value obtained before surgery, and postoperative laboratory findings were the values obtained on the second postoperative day. Postoperative opioid use was calculated in morphine equivalents according to a conversion rate proposed by Nissen et al. [10] and was divided by the patient’s body weight. All colectomies were performed by one experienced colorectal surgeon using an open method. Anastomosis was performed by either the hand-sewing method or the doublestapling technique for rectal anastomosis. One or two Jackson–Pratt drains were inserted around the anastomosis site for all types of surgery during the operation and were removed within 5 days following surgery if the anastomotic leakage was not definite. Adhesion barriers were not used during the operation. Routine postoperative care included commencement of oral intake within 3 days of surgery unless obstructive symptoms such as vomiting occurred. An opioid-based intravenous patient-controlled analgesia was used for pain control. The patients were discharged within 7 days if there were no complications requiring their continued admission. The relationship between the categorical variables was analyzed using the v2 test. Clinical and laboratory factors were assessed for the likelihood of developing POI and EPSBO using univariable and multivariable logistic regression models. Kaplan–Meier survival analysis and Cox regression analysis were used to analyze adhesive SBO.

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Variables with a P value \ 0.05 were considered statistically significant and used for further multivariable analysis, with the exception of EPSBO, where a P value \ 0.1 was used as the entry criterion for multivariable analysis. Statistical analyses were conducted using SPSS software version 19.0 (IBM Inc., Armonk, NY, USA).

Results A total of 1,002 patients were enrolled in this study: 598 male and 404 female patients, with a median age of Table 1 Patient characteristics Characteristics

Values

Age (years)

61 (19–91)

Sex Male Female

598 (59.7) 404 (40.3)

Disease entity Benign Advanced adenoma

122 (12.2)

Crohn’s disease

24 (2.4)

Ulcerative colitis

11 (1.1)

Intestinal tuberculosis

19 (1.9)

Diverticulitis

7 (0.7)

Appendicitis/benign appendiceal neoplasm

10 (1.0)

Others

18 (1.8)

Malignancy Adenocarcinoma of colon/rectum TNM stage, n (% of adenocarcinoma)

33 (3.3) 880 (87.8) 863 (86.1)

0

12 (1.4)

I II

137 (15.9) 270 (31.3)

III

352 (40.8)

IV

92 (10.7)

Other malignancy Operation time (min)

61 years. The median follow-up period was 51 months (interquartile range 26–60). The most common diagnosis was colorectal adenocarcinoma, which accounted for 86.1 % of all cases. The most common surgeries performed were anterior resection, followed by right hemicolectomy. The median time of surgery was 95 min. Patient characteristics are summarized in Table 1. A total of 85 (8.5 %) patients developed POI, and 42 (4.2 %) patients developed EPSBO (Fig. 1). Seven (0.7 %) patients developed both POI and EPSBO. After the median follow-up of 51 months, adhesive SBO occurred in 70 patients (7.0 %). Overall, the cumulative probability of developing adhesive SBO was 4.1 % at 1 year, 6.9 % at 3 years, and 8.3 % at 5 years (Fig. 2). Patients with POI or EPSBO developed adhesive SBO more often than other patients (10.6 and 21.4 vs. 6.2 %) (Fig. 1). However, the cumulative probability of developing adhesive SBO in patients with and without POI was not significantly different (13.4 vs. 7.8 % at 5 years, P = 0.158) (Fig. 3a). When examining the association between the clinicopathological variables and POI, preoperative bowel perforation (P = 0.023), total or subtotal colectomy (P \ 0.001), ileal pouch surgery (P = 0.018), longer operation time ([ 120 min) (P \ 0.001), high blood loss ([ 100 mL) (P = 0.003), stoma formation (ileostomy, P \ 0.001; colostomy, P = 0.012), and a low preoperative serum albumin (3.5 g/dL) (P = 0.008) were associated with the development of POI (data not shown). Because ileal pouch surgery (odds ratio [OR] 3.090, 95 % confidence interval [CI] 1.217–7.843) and total or subtotal colectomy (OR 5.812, 95 % CI 3.285–10.286) were found to be strongly correlated (correlation coefficient 0.619,

17 (1.7) 95 (35–500)

Operation type Ileocecectomy

32 (3.2)

Right hemicolectomy

236 (23.6)

Transverse colectomy

14 (1.4)

Left hemicolectomy

30 (3.0)

Anterior resection

539 (53.8)

Miles’ operation

34 (3.4)

Hartmann’s operation

47 (4.7)

Subtotal/total colectomy

70 (7.0)

Total proctocolectomy with ileal pouch operation

28 (2.8)

Data are presented as n (%) or median (range) unless otherwise indicated IQR interquartile range, TNM tumor-node-metastasis

Fig. 1 Development of postoperative ileus (POI), early postoperative small bowel obstruction (EPSBO), and adhesive small bowel obstruction (SBO)

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Fig. 2 Cumulative probability of adhesive small bowel obstruction in 1,002 patients. SBO small bowel obstruction

World J Surg (2014) 38:3007–3014

P \ 0.001), ileal pouch surgery was excluded from the multivariable logistic regression. On multivariable analysis, total or subtotal colectomy remained the only significant risk factor for POI (OR 2.548, 95 % CI 1.151–5.644, P = 0.021) (Table 2). In contrast, the cumulative incidence of adhesive SBO in patients with and without EPSBO was 26.5 and 7.5 % each at 5 years, which showed a statistically significant difference (P \ 0.001) (Fig. 3b). Previous operation history (P = 0.044) was associated with the occurrence of EPSBO on univariable analysis (data not shown). A longer operation time ([120 min) (P = 0.083) and colostomy formation (P = 0.066) were not statistically significant, but indicated a higher tendency of developing EPSBO. On multivariable analysis, previous operation history was the only significant risk factor for EPSBO (OR 2.142, 95 % CI 1.023–4.489, P = 0.043) (Table 3). Ileal pouch surgery, colostomy formation, and EPSBO were all associated with the occurrence of adhesive SBO (Table 4). Multivariable Cox regression analysis showed that colostomy formation (hazard ratio [HR] 2.530, P = 0.006) and EPSBO (HR 4.063, P \ 0.001) were independent risk factors for the development of adhesive SBO (Table 4). In addition, three of the seven patients

Fig. 3 Development of adhesive small bowel obstruction according to (a) postoperative ileus and (b) early postoperative small bowel obstruction. The patients who experienced early postoperative small bowel obstruction showed a much higher incidence of adhesive small bowel obstruction (P \ 0.001, log rank test). EPSBO early postoperative small bowel obstruction, POI postoperative ileus, SBO small bowel obstruction

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World J Surg (2014) 38:3007–3014 Table 2 Risk factors for postoperative ileus

3011 POI/totala

Variable

Perforation Total/subtotal Operation time (min) EBL (mL) Stoma CI confidence interval, EBL estimated blood loss, OR odds ratio, POI postoperative ileus a

Preoperative albumin (g/dL)

Data are presented as n (%)

Table 3 Risk factors for early postoperative small bowel obstruction

9/52 (17.3)

No

76/950 (8.0)

OR (95 % CI)

P value

1.270 (0.467–3.456)

0.639

2.548 (1.151–5.644)

0.021

1.479 (0.817–2.677)

0.196

1.493 (0.833–2.674)

0.178

Yes

21/70 (30.0)

No

64/932 (6.9)

[120

42/307 (13.7)

B120

43/695 (6.2)

[100

44/371 (11.9)

B100

23/406 (5.7)

Ileostomy

16/66 (24.2)

1.702 (0.737–3.929)

0.213

Colostomy

12/83 (14.5)

1.732 (0.777–3.861)

0.179

None B3.5

57/852 (6.7) 31/245 (12.7)

1.408 (0.799–2.482)

0.237

[3.5

54/757 (7.1)

Variable

EPSBO/total, n (%)

Operation history

Yes

10/133 (7.5)

No

32/869 (3.7)

Operation time (min)

[120

18/307 (5.9)

B120

24/695 (3.5)

Stoma CI confidence interval, EPSBO early postoperative small bowel obstruction, OR odds ratio

Yes

Multivariable analysis

Multivariable analysis OR (95 % CI)

P value

2.142 (1.023–4.489)

0.043

1.750 (0.896–3.418)

0.102

Ileostomy

1/66 (1.5)

0.288 (0.038–2.198)

0.230

Colostomy

7/83 (8.4)

1.779 (0.725–4.365)

0.208

None

34/852 (4.0)

(42.9 %) who had both POI and EPSBO developed adhesive SBO; this incidence was significantly higher than that in the other patients (OR 10.388, P = 0.002). Most of the patients with EPSBO fully recovered via conservative management, while one (1/42, 2.4 %) patient required surgical intervention for EPSBO and subsequently developed adhesive SBO. Six of 70 patients (8.6 %) with adhesive SBO initially required surgery (Fig. 1). Of the 64 patients who had been initially treated conservatively, five patients required further surgical intervention because of adhesive SBO recurrence. Three of the nine patients with EPSBO (33.3 %) required surgery because of adhesive SBO, whereas eight of the 61 patients without EPSBO (13.1 %) received further surgery for adhesive SBO (P = 0.136).

Discussion In this study, we identified risk factors for POI, EPSBO, and adhesive SBO. To the best of our knowledge, this is the first study that demonstrates an association between POI or EPSBO and adhesive SBO. Interestingly, EPSBO was

found to be an independent risk factor for the development of subsequent adhesive SBO, whereas POI was not. POI is common after surgery; it differs from mechanical bowel obstruction arising from the configurational disarrangement of the bowels and is considered as the prolonged inhibition of coordinated bowel activity [11]. POI may be caused by several biological pathways such as the enteric nervous system, inflammatory response, and neuropeptide and hormonal factors [12]. Snoek et al. [13] reported that the manipulation of the small bowel can trigger an intestinal barrier disturbance and a mast cell-dependent inflammatory response to the muscle of the intestine, leading to POI, as demonstrated in their mouse study. Our study identified total or subtotal colectomy as an independent risk factor for POI. A longer operation time, higher blood loss, and stoma formation were also associated with POI, although this was not significant on multivariable analysis. Subtotal or total colectomy, a longer operation time, and ileostomy formation after colectomy may all be indicators of extensive small bowel manipulation. The more extensive operations are inevitably associated with more bowel manipulation, leading to POI, and this was reflected in our results.

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Table 4 Risk factors for adhesive small bowel obstruction Variable

Age (year) Sex BMI (kg/m2) ASA Operation history Obstruction Perforation Chronic steroid use Disease entity

Adhesive SBO/total, n (%)

Univariable analysis HR (95 % CI)

P value

B70

60/807 (7.4)

1.288 (0.659–2.517)

0.459

[70

10/194 (5.2) 0.752 (0.470–1.203)

0.234

1.352 (0.752–2.430)

0.313

0.655 (0.238–1.799)

0.412

1.165 (0.612–2.219)

0.642

1.613 (0.909–2.861)

0.102

0.845 (0.265–2.691)

0.845

0.894 (0.218–3.666)

0.894

1.274 (0.668–2.433)

0.462

0.763 (0.477–1.220)

0.258

1.617 (0.774–3.380)

0.201

2.807 (1.209–6.520)

0.016

1.385 (0.855–2.245)

0.186

0.954 (0.561–1.623)

0.863

M

37/598 (6.2)

F

33/404 (8.2)

B25

56/753 (7.4)

[25

14/245 (5.7)

3,4

4/88 (4.5)

1,2

63/873 (7.2)

Yes

11/133 (8.3)

No

59/869 (6.8)

Yes

15/172 (8.7)

No

55/830 (6.6)

Yes

3/52 (5.8)

No

67/950 (7.1)

Yes

2/25 (8.0)

No

68/977 (7.0)

Benign

11/122 (9.0)

Malignancy

59/880 (6.7)

Multivariable analysis HR (95 % CI)

P value

2.942 (0.886–9.771)

0.078

Type of surgery Pelvic operation Total/subtotal Ileal pouch Operation time (min) EBL (mL) Stoma

Preoperative albumin (g/dL) Postoperative albumin (g/dL) Postoperative Ca (mg/dL) Postoperative K (mmol/L) Postoperative opioid use (mg/kg)a POI EPSBO

Abdominal

37/595 (6.2)

Pelvic

33/407 (8.1)

Yes

8/70 (11.4)

No

62/932 (6.7)

Yes

6/28 (21.4)

No

64/974 (6.8)

[120

27/307 (8.8)

B120

43/695 (6.2)

[100

25/371 (6.7)

B100

30/406 (7.4)

Ileostomy

8/66 (12.1)

1.953 (0.926–4.120)

0.079

1.224 (0.426–3.517)

0.708

Colostomy

11/83 (13.3)

2.745 (1.428–5.275)

0.002

2.530 (1.310–4.885)

0.006

None

51/852 (6.0)

4.063 (1.995–8.275)

\0.001

B3.5

17/245 (6.9)

[3.5

53/757 (7.0)

B3.5

59/847 (7.0)

[3.5

11/154 (7.1)

B8.0

30/397 (7.6)

[8.0

40/600 (6.7)

B3.5

18/192 (9.4)

[3.5

51/807 (6.3)

[3

44/625 (7.0)

B3

26/377 (6.9)

Yes

9/85 (10.6)

No

61/917 (6.7)

Yes

9/42 (21.4)

No

61/960 (6.4)

1.137 (0.658–1.967)

0.645

1.031 (0.542–1.963)

0.926

1.152 (0.717–1.849)

0.559

1.496 (0.874–2.561)

0.142

1.000 (0.616–1.625)

1.000

1.652 (0.820–3.327)

0.158

4.121 (2.044–8.307)

\0.001

ASA American Society of Anesthesiologists score, BMI body mass index, CI confidence interval, EBL estimated blood loss, EPSBO early postoperative small bowel obstruction, HR hazard ratio, POI postoperative ileus, SBO small bowel obstruction a

Calculated in morphine equivalents/body weight

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EPSBO should be differentiated from POI. Sajja and Schein [14] suggested that causes of persistent ileus should be excluded and treated when bowel movements are not restored within 5 days after surgery. EPSBO also differs from adhesive SBO in many aspects. Although adhesion is a possible cause of EPSBO, several other pathophysiological causes, such as internal herniation, inflammation, intussusception, and intramural intestinal hematoma can cause EPSBO [14]. Previous studies have suggested that clinicopathological factors such as the American Society of Anesthesiologists (ASA) score, local remnant tumor, rectal cancer, open surgery, and a history of a previous laparotomy could also be risk factors for EPSBO [15–17], although there is a lack of consensus. Our results indicated that a previous abdominal operation may be an independent risk factor for EPSBO, and this was in accordance with the findings of a previous study [17]. Conservative treatment can be attempted initially in patients with EPSBO [14, 15, 18]. However, according to our results, patients who experienced EPSBO may be at higher risk of developing adhesive SBO. Therefore, when determining use of conservative management, surgeons should bear in mind that patients with EPSBO should be carefully monitored to determine whether they are likely to develop adhesive SBO. This study also demonstrated that colostomy and EPSBO were associated with subsequent adhesive SBO. Ileal pouch surgery was associated with the development of adhesive SBO on univariable analysis, although this association was not significant on multivariable analysis. Previous studies have reported that patients who underwent total proctocolectomy with ileal pouch–anal anastomosis and a diverting ileostomy were at increased risk of developing SBO [4, 19, 20]. Rotation of the small bowel at the ileostomy site may be a reason for this finding. Colostomy formation has been identified as an independent risk factor for subsequent adhesive SBO. The mechanism by which colostomy induces adhesive SBO is unclear; however, it can be inferred that the colonic axis towards the abdominal wall is perpendicular to the small bowel mesentery, thus triggering adhesion as well as rotation and internal herniation. It is universally accepted that the balance between fibrin deposition and fibrinolysis plays a key role in the development of adhesions. Surgery-induced peritoneal injury initiates inflammation with fibrinous exudates and fibrin formation [21]. Normal peritoneal healing occurs when fibrin is degraded completely; however, incomplete fibrinolysis within 5–7 days of the peritoneal injury may induce organized fibroblasts and may lead to adhesion formation [4, 22]. Therefore, the inflammation caused by the procedure is believed to be the initial process of adhesion formation. EPSBO is related to peritoneal inflammation and to adhesion formation in the early postoperative period, which

3013

is presumably the cause of adhesive SBO. Although POI arises from the inflammation of the intestine induced by bowel manipulation, it is not directly related to subsequent adhesive SBO according to our data, probably because inflammation associated with POI is within the bowel itself rather than in the peritoneum. However, compared with other patients, seven patients who developed both POI and EPSBO had a higher incidence of subsequent adhesive SBO. This finding suggests that the inflammatory environment in both the intestine and the peritoneum during the early postoperative period is likely to promote the development of adhesive SBO. Our study has some limitations. The retrospective nature of the analysis is an important limitation. However, we used data from a prospectively collected cohort, ensuring the reliability of the results. Another limitation is that we included only patients who underwent open colorectal surgery by a single surgeon, which could be construed as a selection bias. Nevertheless, our study included patients treated by an experienced surgeon performing standardized procedures, which could effectively control the potentially confounding variable.

Conclusion POI is not associated with adhesive SBO; however, EPSBO is a risk factor for subsequent adhesive SBO in patients undergoing open colectomy. Patients diagnosed with EPSBO should be followed more carefully as to whether they would develop adhesive SBO. This clinical information will contribute to further studies to investigate mechanism and risk factors of adhesive SBO.

Conflicts of interest The authors received no commercial support for this study. The authors declare no conflicts of interest.

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World J Surg (2014) 38:3007–3014 14. Sajja SB, Schein M (2004) Early postoperative small bowel obstruction. Br J Surg 91:683–691 15. Shin JY, Hong KH (2008) Risk factors for early postoperative small-bowel obstruction after colectomy in colorectal cancer. World J Surg 32:2287–2292. doi:10.1007/s00268-008-9652-3 16. Nakajima J, Sasaki A, Otsuka K et al (2010) Risk factors for early postoperative small bowel obstruction after colectomy for colorectal cancer. World J Surg 34:1086–1090. doi:10.1007/s00268010-0462-z 17. Shin JY (2011) Risk factors of early postoperative small bowel obstruction following a proctectomy for rectal cancer. J Korean Soc Coloproctol 27:315–321 18. Schein M, Sajja SB, Yenumula PR (2002) Early postoperative intestinal obstruction. Curr Surg 59:289–295 19. MacLean AR, Cohen Z, MacRae HM et al (2002) Risk of small bowel obstruction after the ileal pouch-anal anastomosis. Ann Surg 235:200–206 20. Marcello PW, Roberts PL, Schoetz DJ Jr et al (1993) Obstruction after ileal pouch-anal anastomosis: a preventable complication? Dis Colon Rectum 36:1105–1111 21. Holmdahl L (1997) The role of fibrinolysis in adhesion formation. Eur J Surg Suppl 577:24–31 22. Arung W, Meurisse M, Detry O (2011) Pathophysiology and prevention of postoperative peritoneal adhesions. World J Gastroenterol 17:4545–4553

Early postoperative small bowel obstruction is an independent risk factor for subsequent adhesive small bowel obstruction in patients undergoing open colectomy.

This prospective study was performed to investigate whether postoperative ileus (POI) or early postoperative small bowel obstruction (EPSBO) affects t...
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