Duodenal stricture treatment

Duodenal stricture treatment DEFAULT

ISPUB.com

 

Introduction

In the modern era of proton pump inhibitors (PPI), benign duodenal strictures are a rare cause of gastric outlet obstruction in adults, whilst malignancy is the main culprit. The causes of duodenal stenosis and obstruction may be classified as congenital and acquired, and the latter may be subdivided into benign and malignant causes (Table 1).

Figure 1
Table 1: Aetiology of duodenal stenosis and obstruction

We report our experience with the laparoscopic management (duodenal resection and bypass) of five patients who developed gastric outlet obstruction secondary to benign duodenal strictures. The applications of laparoscopic surgery in patients with benign duodenal pathology are discussed.

Material and Methods

Patients

Between February 2001 and March 2003, we have treated six patients (4 men, 2 women) with a median age of 46.5 years (range 31-74 years) who presented with symptoms of gastric outlet obstruction secondary to duodenal strictures/stenoses. The patient details are summarised in Table 2. The median duration of preoperative symptoms was 4 months (range 1-42 months).

Figure 2
Table 2: Details of the patients

Preoperative assessment of the duodenal pathology

All patients underwent thorough investigations to assess the nature of the duodenal strictures including endoscopy, endoscopic biopsies, computed tomography (CT), and barium meal (Table 3). These demonstrated a diaphragm-like stricture at the junction between the first and second parts of the duodenum in one patient, a long post-bulbar proximal duodenal stricture in one patient, duodenal stenosis (second part) in two patients (Figure 1), and long distal duodenal strictures (third & fourth parts) in two patients (Figure 2).

Figure 3
Figure 4
Figure 5
Figure 1: Barium study via a percutaneous gastrostomy in Patient No. 3 with severe necrotising pancreatitis showing a tight stricture/stenosis (arrow) in the second part of duodenum (passage of contrast into the distal duodenum was delayed)
Figure 6
Figure 2: Endoscopic contrast study in Patient No. 5 showing a long stricture in the third/fourth parts of the duodenum with marked proximal duodenal dilatation

One of the patients (Patient No. 2) developed a further proximal diaphragm-like stricture at the junction between the first and second parts of duodenum two months after resection of a benign distal duodenal stricture. No tumour mass was shown on CT imaging of any of the patients In addition to the investigations above, hormonal assessment in one of the patients with recurrent duodenal and gastro-enteric anastomotic stricture (Patient No. 2) ruled out a gastrinoma. The data available from these investigations, as well as from post-resection pathological evaluation (Patient No. 2), and from clinical, radiological and endoscopic follow up (Table 5) confirmed or supported their benign nature (Table 3).

Figure 7
Table 5 : Results and follow up
Figure 8

Options for non-operative management of these strictures including prolonged intravenous feeding (in the patient with acute necrotising pancreatitis), high-dose PPI therapy, discontinuation of NSAID, and balloon dilatation as appropriate were explored and exhausted before embarking on surgery (Table 3).

Operative procedures

The six patients underwent seven laparoscopic operative procedures to treat their duodenal disease (Table 4). These included a gastroenterostomy that was fashioned as a loop (=5) or in a Roux-en-Y configuration (=1), and a pancreas-preserving distal duodenectomy [3] with a duodeno-jejunal anastomosis (=1). In one of the patients (No. 4) who suffered with alcohol-related chronic pancreatitis, the laparoscopic loop gastroenterostomy was combined with a Roux-en-Y hepaticojejunostomy for a symptomatic benign distal bile duct stricture and a concomitant bilateral thoracoscopic splanchnotomy for an opiate-dependent intractable abdominal pain [2].

Figure 9
Table 4: Details of surgery

Operative technique

All the laparoscopic gastroenterostomies were fashioned in an antecolic anterior arrangement. Every effort was made to ensure that the gastroenteric anastomosis was placed distally on the gastric/antral wall. The anastomoses were fashioned in a side-to-side manner using two or three firings of an endo-stapler (ATB45 45mm-articulating, Ethicon Endo-Surgery, Cincinnati, Ohio, USA), and the common gastro-enteric side opening was closed with a continuous Vicryl 2-0 suture (Ethicon Inc., Somerville, New Jersey, USA). The Roux-en-Y entero-enteric anastomoses were fashioned in a similar manner.

The Roux-en-Y hepaticojejunostomy was constructed in a retrocolic side-to-side manner (previous open cholecystectomy) to the common hepatic duct, and the anastomosis was fashioned with a single firing of an endo-stapler (TSW35 35mm, Ethicon Endo-Surgery, Cincinnati, Ohio, USA), and completed with interrupted absorbable sutures (Vicryl 3-0).

The operative technique for the laparoscopic distal duodenectomy has been described previously [3].

Results

Operation-related outcomes

The intraoperative course was uneventful in all cases and all procedures were completed laparoscopically. The operating time (median 160 minutes) ranged between 30 minutes for a loop gastroenterostomy to 355 minutes for the combined laparoscopic gastric and biliary bypass and bilateral thoracoscopic splanchnotomy (Table 4).

The recovery from surgery was uneventful in five of the seven procedures (Table 5). Intraperitoneal bleeding developed on the first postoperative day following the duodenectomy, and was managed by re-laparoscopy and peritoneal lavage successfully (no source of bleeding was identified). Central line sepsis presented on the second postoperative day in a patient who had a prolonged preoperative course and was fed parenterally.

The median duration of postoperative hospital stay (Table 5) was 4 days (range 3-19 days), and appeared to relate to the duration of preoperative hospital stay (Table 2). All patients were discharged on long-term PPI therapy.

Aetiology of duodenal disease

Determination of the aetiology of the duodenal strictures was based on the preoperative data as well as the histological findings of operative specimens (Patients No. 2 and No. 6) and was supported by follow up information. The aetiology is shown in Table 3.

Follow up

The median duration of follow up was 9 months (range 2-32 months). One of the patients (Patient No. 2) developed a further NSAID-related diaphragm-like duodenal stricture at the junction of the first and second parts of duodenum 2 months after a distal duodenectomy and duodeno-jejunal anastomosis [4] that was initially managed by endoscopic balloon dilatation with only a short-lived response. A month later she underwent a laparoscopic Roux-en-Y gastroenterostomy, which subsequently occluded (stricture) and was managed by laparoscopic revision gastroenterostomy with a successful outcome. At the time of writing, all patients remain symptom-free, but for occasional vomiting in one of the patients (Patient No. 5).

Discussion

Patients presenting with benign duodenal strictures that fail to respond to medical or endoscopic therapy may be managed successfully with minimally invasive surgery without the need to resort to a laparotomy. Relief of the obstruction may be simply accomplished in the majority of patients with a laparoscopic gastroenterostomy. This procedure was employed by Nagy et al [30] in a patient with duodenal obstruction secondary to peptic ulcer disease and by Reissman et al [35] in three patients with duodenal Crohn's disease, and we have applied it successfully in five patients. However, laparoscopic resection of the diseased distal duodenum (with preservation of the pancreas) was necessary in one of our patients who also had clinical evidence of recurrent bleeding from the stricture [3]. In addition, uncertainty about the diagnosis of a ‘benign' pathology in this good-risk ‘young' patient supported a duodenal resection.

The role of laparoscopic surgery in the palliation of malignant duodenal and biliary obstruction is now well recognised, and is associated with significant reduction in hospital stay compared with open surgery [7,36,38]. In addition, laparoscopic surgery has its applications in the management of benign duodenal conditions in adults and children.

In adults, the laparoscopic approach to closure of perforated duodenal ulcers is well established [4]. In addition, laparoscopic transgastric or transduodenal resection of large duodenal villous adenomas [40], Brunner's gland hamartoma (Brunneroma) [5] or duodenal stromal tumour [48], resection of bleeding distal duodenal diverticulum [45] or a carcinoid tumour of the duodenal bulb [47], transgastric removal of an obstructing gallstone impacted in the duodenum (Bouveret's syndrome) [26], duodenotomy and under-running of actively bleeding duodenal ulcers [27], and duodenojejunostomy for the superior mesenteric artery syndrome [19] have all been described. In paediatric patients, laparoscopic duodenoduodenostomy for duodenal atresia [6] as well as laparoscopic division of congenital Ladd's bands that cause intermittent duodenal obstruction in neonates with malrotation of the gut [13] have been practiced.

It is essential to establish the diagnosis of a ‘benign' disease and to explore non-surgical management options before embarking on a laparoscopic gastric bypass as a definitive treatment. Although the benign nature of the stricture may be readily evident as the case was in one of our patients who developed the stricture a month into an acute attack of severe necrotising pancreatitis, the establishment of a benign aetiology often poses a diagnostic dilemma. Endoscopic evaluation with repeated biopsies, a barium study to examine the length, morphology and location of the stricture, and cross-sectional imaging to exclude a tumour mass are essential investigations. The detection of hsitologically benign, diaphragm-like duodenal strictures in patients with a history of NSAID intake and absent tumour mass on computed tomography may suggest a NSAID-related disease [23,41]. Absence of a tumour mass on imaging in patients with an established history of chronic pancreatitis attests to the benign nature of the duodenal stenosis, although caution should be exercised in order to avoid missing a progression of disease to pancreatic cancer [25,49]. Other causes shown in Table 1 ought to be considered when a long distal duodenal stricture is detected.

In patients with benign duodenal strictures, it is worthwhile exploring the non-surgical treatment options in the first instance. Either medical treatment (PPI therapy) alone [17] or in combination with endoscopic balloon dilatation [44] may provide a long-lasting relief of gastric outlet obstruction secondary to peptic ulcer disease in some patients, though some 50 per cent of patients way still require further endoscopic or surgical intervention [29]. We employed the techniques of endoscopic balloon dilatation in four of the five patients and found its results disappointing. Duodenal obstruction secondary to Crohn's disease may respond to medical therapy [14]. Duodenal tuberculosis causing obstruction is a rare condition that is usually seen in the tropics; it is rarely diagnosed preoperatively by endoscopic biopsy and may then respond to drug therapy [33].

Surgery for benign duodenal obstruction should therefore be reserved to patients in whom non-operative management options fail, and when the diagnosis remains in doubt. In the former scenario, relief of the obstruction may be accomplished by a laparoscopic gastroenterostomy; whilst in the latter a duodenal or pancreaticoduodenal resection is warranted in the good surgical-risk patient and may be safely accomplished laparoscopically.

Correspondence to

Mr. Basil J. Ammori, FRCS, MD Consultant Hepato-Pancreato-Biliary and Laparoscopic Surgeon Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK Tel: 0044-161-2763510 Fax: 0044-161-2764530 E-mail: [email protected]

References

1. Akel S, Halabi J, Shawis R (1998) Abdominal situs inversus with congenital duodenal stenosis: rare association. Eur J Pediatr Surg 8:55-57.
2. Ali ASM, Ammori BJ (in press) Concomitant laparoscopic gastric and biliary bypass and bilateral thoracoscopic splanchnotomy: the full package of minimally invasive palliation of pancreatic cancer. Surg Endosc. Epub 2003 Oct 28.
3. Ammori BJ (2002) Laparoscopic pancreas-preserving distal duodenectomy for duodenal stricture related to nonsteroidal antiinflammatory drugs (NSAIDs). Surg Endosc 16:1362-1363. Epub 2002 Jun 20.
4. Arnaud JP, Tuech JJ, Bergamaschi R, Pessaux P, Regenet N (2002) Laparoscopic suture closure of perforated duodenal peptic ulcer. Surg Laparosc Endosc Percutan Tech 12:145-147.
5. Baladas HG, Borody TJ, Smith GS, Dempsey MB, Richardson MA, Falk GL (2002) Laparoscopic excision of a Brunner's gland hamartoma of the duodenum. Surg Endosc 16:1636. Epub 2002 Aug 29.
6. Bax NM, Ure BM, van der Zee DC, van Tuijl I (2001) Laparoscopic duodenoduodenostomy for duodenal atresia. Surg Endosc 15:217. Epub 2000 Dec 21.
7. Bergamaschi R, Marvik R, Thoresen JE, Ystgaard B, Johnsen G, Myrvold HE (1998) Open versus laparoscopic gastrojejunostomy for palliation in advanced pancreatic cancer. Surg Laparosc Endosc 8:92-96.
8. Blinder GH, Hautekeete ML, Holvoet JP, Kockx MM, Hubens HK (1994) Duodenal diaphragmlike stricture induced by acetylsalicylic acid. Dig Dis Sci 39:1365-1369.
9. Bradley EL 3rd, Clements JL Jr (1981) Idiopathic duodenal obstruction: an unappreciated complication of pancreatitis. Ann Surg 193:638-648.
10. Chapoy P, Guidon MJ, Louchet E (1984) Duodenal complications of rheumatoid purpura. Endoscopic aspects. Gastroenterol Clin Biol 8:604-608.
11. Chattopadhyay A, Kumar V, Maruliah M, Rao PL (2002) Duodenojejunal obstruction by a hemangioma. Pediatr Surg Int 18:501-502.
12. Douie WJ, Krige JE, Bornman PC (2002) Annular pancreas in adults. A report of two cases and a review of the literature. Hepatogastroenterology. 49:1716-1718.
13. Fernandez MS, Vila JJ, Ibanez V, Lluna J, Barrios JE, Gutierrez C, Roca A, Garcia-Sala C (1999) [Laparoscopic transsection of Ladd's bands: a new indication for therapeutic laparoscopy in neonates]. Cir Pediatr 12:41-43.
14. Fitzgibbons TJ, Green G, Silberman H, Eliasoph J, Halls JM, Yellin AE (1980) Management of Crohn's disease involving the duodenum, including duodenal cutaneous fistula. Arch Surg 115:1022-1028.
15. Frey CF, Suzuki M, Isaji S (1990) Treatment of chronic pancreatitis complicated by obstruction of the common bile duct or duodenum. World J Surg 14:59-69.
16. Hashim S, Abdullah BJ, Rajasingam V, Moosa F (1999) Duodenal obstruction secondary to metastatic synovial sarcoma--a case report. Med J Malaysia 54:267-269.
17. Khandekar S, Chandler ST, Trewby PN (1998) Successful medical treatment of peptic pyloric stenosis: Dr Sippy revisited. J R Coll Physicians Lond 32:354-357.
18. Kikuchi M, Endo S, Kuwata Y, Kasai T (1997) Useful treatment modality for postoperative duodenal fistula with somatostatin analogue. Nippon Geka Gakkai Zasshi 98:466-469.
19. Kim IY, Cho NC, Kim DS, Rhoe BS (2003) Laparoscopic duodenojejunostomy for management of superior mesenteric artery syndrome: two cases report and a review of the literature. Yonsei Med J 44:526-529.
20. Komuro H, Makino S, Tahara K (2000) Choledochal cyst associated with duodenal obstruction. J Pediatr Surg 35:1259-1262.
21. Kullendorff CM (1983) Atresia of the small bowel. Ann Chir Gynaecol 72:192-195.
22. Landen S, Delugeau V, Lhonneux C, Michel P (2001) Annular duodenal stricture due to Brunner's gland hyperplasia. Acta Gastroenterol Belg 64:35-37.
23. Levi S, de Lacey G, Price AB, Gumpel MJ, Levi AJ, Bjarnason I (1990) "Diaphragm-like" strictures of the small bowel in patients treated with non-steroidal anti-inflammatory drugs. Br J Radiol 63:186-189.
24. Lottini M, Neri A, Vuolo G, Testa M, Pergola L, Cintorino M, Guarnieri A (2002) Duodenal obstruction from isolated breast cancer metastasis: a case report. Tumori 88:427-429.
25. Malka D, Hammel P, Maire F, Rufat P, Madeira I, Pessione F, Levy P, Ruszniewski P (2002) Risk of pancreatic adenocarcinoma in chronic pancreatitis. Gut 51:849-852.
26. Malvaux P, Degolla R, De Saint-Hubert M, Farchakh E, Hauters P (2002) Laparoscopic treatment of a gastric outlet obstruction caused by a gallstone (Bouveret's syndrome). Surg Endosc 16:1108-1109.
27. Martin I, O'Rourke N, Bailey I, Branicki F, Nathanson L, Fielding G (1998) Laparoscopic underrunning of bleeding duodenal ulceration: a minimalist approach to therapy. Aust N Z J Surg 68:213-215.
28. Mentes AS (1990). Parietal cell vagotomy and dilatation for peptic duodenal stricture. Ann Surg 212:597-601.
29. Misra SP, Dwivedi M (1996) Long-term follow-up of patients undergoing ballon dilation for benign pyloric stenoses. Endoscopy 28:552-554.
30. Nagy A, Brosseuk D, Hemming A, Scudamore C, Mamazza J (1995) Laparoscopic gastroenterostomy for duodenal obstruction. Am J Surg 169:539-542.
31. Ngan H (1970) Involvement of the duodenum by metastases from tumours of the genital tract. Br J Radiol 43:701-705.
32. Phelan MS, Fine DR, Zentler-Munro PL, Hodson ME, Batten JC, Kerr IH (1983) Radiographic abnormalities of the duodenum in cystic fibrosis. Clin Radiol 34:573-577.
33. Ray JD, Sriram PV, Kumar S, Kochhar R, Vaiphei K, Singh K (1997) Primary duodenal tuberculosis diagnosed by endoscopic biopsy. Trop Gastroenterol 18:74-75.
34. Razzaq R, Laasch HU, England R, Marriott A, Martin D (2001) Expandable metal stents for the palliation of malignant gastroduodenal obstruction. Cardiovasc Intervent Radiol 24:313-318.
35. Reissman P, Salky BA, Edye M, Wexner SD (1996) Laparoscopic surgery in Crohn's disease. Indications and results. Surg Endosc 10:1201-1204.
36. Rhodes M, Nathanson L, Fielding G (1995) Laparoscopic biliary and gastric bypass: a useful adjunct in the treatment of carcinoma of the pancreas. Gut 36:778-780.
37. Rothenberg SS (2002). Laparoscopic duodenoduodenostomy for duodenal obstruction in infants and children. J Pediatr Surg 37:1088-1089.
38. Rothlin MA, Schob O, Weber M (1999) Laparoscopic gastro- and hepaticojejunostomy for palliation of pancreatic cancer: a case controlled study. Surg Endosc 13:1065-1069.
39. Roy PK, Venzon DJ, Shojamanesh H, Abou-Saif A, Peghini P, Doppman JL, Gibril F, Jensen RT (2000) Zollinger-Ellison syndrome. Clinical presentation in 261 patients. Medicine (Baltimore) 79:379-411.
40. Sample CB, Dutta S, Anvari M (2003) Transgastric endoluminal laparoscopic resection of a villous adenoma of the duodenum. Surg Endosc 17:352. Epub 2002 Oct 31.
41. Schmutz GR, Chapuis F, Morel E, N'Guyen D, Dion C, Regent D (1997) Drug-induced stenosis of the small bowel. Value of enteroclysis J Radiol 78:33-39.
42. Shah P, Applegate KE, Buonomo C (1997) Stricture of the duodenum and jejunum in an abused child. Pediatr Radiol 27:281-283.
43. Sidorenko VD, Izosimov VV (1988) [Post-traumatic cicatricial stricture of the descending part of the duodenum.] Vestn Khir Im I I Grek 141:73.
44. Solt J, Bajot J, Szabo M, Horvath OP (2000) Balloon dilatation in the management of gastric outlet stenoses: long-term results. Orv Hetil 141:1975-1980.
45. Tagaya N, Shimoda M, Hamada K, Ishikawa K, Kogure H (2000) Laparoscopic duodenal diverticulectomy. Surg Endosc 14:592. Epub 2000 May 15.
46. Tamisani AM, Di Noto C, Di Rovasenda E (1992) A rare complication due to sulfuric acid ingestion. Eur J Pediatr Surg 2:162-164.
47. Toyonaga T, Nakamura K, Araki Y, Shimura H, Tanaka M (1998) Laparoscopic treatment of duodenal carcinoid tumor. Wedge resection of the duodenal bulb under endoscopic control. Surg Endosc 12:1085-1087.
48. van de Walle P, Dillemans B, Vandelanotte M, Proot L (1997) The laparoscopic resection of a benign stromal tumour of the duodenum. Acta Chir Belg 97:127-129.
49. van Gulik TM, Moojen TM, van Geenen R, Rauws EA, Obertop H, Gouma DJ (1999) Differential diagnosis of focal pancreatitis and pancreatic cancer. Ann Oncol 10:85-88.
50. Williams AJ, Palmer KR (1991) Endoscopic balloon dilatation as a therapeutic option in the management of intestinal strictures resulting from Crohn's disease. Br J Surg 78:453-454.
51. Zalev AH, Sacks JS, Warren RE (1997) Pancreaticoduodenal tuberculosis simulating metastatic ovarian carcinoma. Can J Gastroenterol 111:41-43.
Sours: https://ispub.com/IJS/7/1/4997

Symptomatic duodenal Crohn's disease: Is strictureplasty the right choice?

Abstract

Primary duodenal localization of Crohn's disease (CD) is rare. Medical therapy can control symptoms, but surgery is required when progressive obstructive symptoms occur. Surgical options include bypass, resection, or strictureplasty, but it is still not clear which should be the treatment of choice. Reviewing the medical records of 1253 patients undergoing surgery for CD between January 1986 and December 2011 at the Digestive Surgery Unit of the Department of Clinical Physiopathology of the University of Florence, 10 patients (6 males and 4 females) underwent operations for duodenal CD. Four patients had only a duodenal localization, 6 patients had synchronous involvement of other intestinal tracts. Strictures were distributed in all the duodenal portions: in 7 patients there were single lesions, in 3 patients there were multiple lesions. Eight patients were treated with strictureplasty: 5 with the Heineke–Mikulicz technique, 2 with Jaboulay, and 1 with a pedunculated jejunal patch. Two patients were treated with resection: one with a B2 gastro-duodenal resection, and 1 with a duodenal–jejunal resection and an end to side duodeno-jejunal anastomosis. Follow up of the patients was from 2 to 18 years. No recurrence of duodenal CD was observed in the 2 patients treated with resection, while 2 of the 8 patients treated with strictureplasty had a recurrence. In our experience, strictureplasty is indicated when less than 2 strictures are present in the 2nd or 3rd duodenal portion. In cases with multiple strictures localized in the 1st or the distal duodenal portion, resection is preferable.

Crohn's disease;, Duodenal Crohn's disease;, Strictureplasty;, Resection;, Intestinal derotation

Abbreviations

    Abbreviations

  • CD

  • TPN

    Total parenteral nutrition

  • H–M

  • SSIS

    side-to-side isoperistaltic strictureplasty

  • UGI

  • PPI

1 Introduction

Primary duodenal localization of Crohn's disease (CD) is rare if compared with small bowel or large bowel localization.1 The incidence of duodenal involvement of CD varies from 0.5 to 4.0% of all the patients affected by CD, but most duodenal lesions are asymptomatic and incidentally discovered during gastroduodenoscopy.2,3 Symptoms of duodenal CD, such as epigastric pain, nausea, vomiting, and progressive weight loss, happen only when there are severe strictures of the duodenal wall. In the majority of the patients, other intestinal sites affected by CD are evident at the time of diagnosis, or will occur some years later. Medical therapy can control symptoms, but surgery is required in more than one-third of the affected patients. The most frequent indications for surgery are progressive obstructive symptoms.2 Surgical options include bypass, resection, or strictureplasty.4,5 It is not clear which of these should be the treatment of choice: bypass is a relatively simple method, but there are concerns for peptic ulcer or persistence of the disease in the excluded duodenum; resection may be difficult, with a risk of complications such as pancreatitis or lesions of the papilla of Vater; strictureplasty can preserve the activity or promote recurrence of stricture or gastric inertia. We have revised our experience with duodenal CD over the past 25 years: patients were prevalently treated with strictureplasty. This study presents the immediate and long-term results.

2 Methods

A retrospective review was conducted on the medical records of 1253 patients undergoing surgery for Crohn's disease between January 1986 and December 2011 at the Surgery Unit of the Department of Clinical Physiopathology of the University of Florence. The data were collected from chart records and operating room registers. In the chart records we observed: gender, age, familiarity, smokers/non-smokers, duodenal location as initial or metacronous, symptoms, extra-intestinal manifestations of CD, anemia, weight loss, malnutrition, pre/post-operative medical therapy, pre/post-operative artificial nutrition, indications for surgery, postoperative mortality, morbidity rates, and long-term recurrence. In the operating room registers we observed: localization and morphology of the disease, and type of surgery, especially the number and types of strictureplasties performed. The patients were followed up periodically, by means of laboratory and/or instrumental exams, when necessary.

2.1 Patients

Ten patients (6 males and 4 females, with an age at surgery ranging from 18 to 49 years, 35 years as mean) underwent operations for duodenal CD. No familiarity of CD was recorded. Five patients were smokers. All the patients complained of epigastric pain, vomiting, and progressive obstruction. Six patients showed signs of severe malnutrition, such as hypoalbuminemia, hypo-pre-albuminemia, and lymphocitemia (< 1000). Four patients were affected by hyposideremic anemia. The symptoms were refractory to several attempts of medical therapy: 1 patient was treated with 5-ASA only, 3 patients were treated with steroids, 3 with steroids plus 5-ASA, 2 with steroids plus Azathioprine, and 1 with steroids, Azathioprine, and Thalidomide. When signs of malnutrition were found, 6 of the patients were treated before the operation with a TPN for a period of time ranging from 5 to 8 days.

Seven patients had a duodenal localization as the first manifestation of CD. One of them had been treated in another center, 17 years before, for a diffused duodenal–jejunal and ileal CD with a Heineke–Mikulicz (H–M) strictureplasty on the 2nd portion of the duodenum, a duodeno jejunal bypass for multiple stenoses in jejunum, and an ileo-cecal resection. This patient was hospitalized for recurrent strictures of the 3rd and 4th duodenal portion. Three patients had duodenal CD after prior operations for colonic (2) or ileal (1) CD.

2.2 Surgical technique

At surgery, a complete kocherization of the duodenum was employed in order to assess the strictures by visual inspection and palpation. A section of the Treitz's ligament and intestinal derotation were utilized for better exposure of the lesions, especially when the 3rd or 4th portion was affected. At initial intestinal opening, a 16 mm diameter marble was introduced in the intestinal lumen and pushed through the bowel to test any possible further stricture. When lesions appeared near the pylorus, or in case of multiple strictures of the distal part of the duodenum and the first jejunal loop, a resection was the treatment of choice. Strictureplasty was preferred when the local situation enabled its implementation. The type of strictureplasty was selected according to the length of the stricture. In case of short strictures, an H–M was performed (Fig. 1); in case of long strictures, a Finney, Jaboulay, or Roux en-Y technique was preferred.

A nasogastric tube was introduced through the strictureplasty of the duodenum and placed in the jejunum for duodenal decompression during the first 24/48 h, and for enteral nutrition, subsequently.

2.3 Type and site of the lesions

At surgery, 4 patients had only duodenal disease, whereas 6 patients had synchronous involvement of other portions of the intestinal tract: jejunum in 4 patients, ileum in 1 patient, and jejunum–ileum in 1 patient.

The strictures were distributed in all of the duodenal portions: in 7 patients there was a single lesion (1st portion: 2 patients, 2nd portion: 2 patients, 3rd portion: 2 patients, 4th portion: 1 patient), in 3 patients there were multiple lesions (3rd and 4th in 2 patients, 1st, 2nd and 3rd in 1 patient). The length of the single duodenal strictures ranged from 3 to 6 cm (mean 3.7 cm), whereas the length of the multiple duodenal strictures ranged from 1 to 10 cm (mean 5.6 cm).

No signs of fistula or abscess were recorded at the duodenal site. Surgery was indicated in 1 patient for a suspected biliary fistula. During the operative evaluation, the fistula was not detected, but a patulous Vater papilla, simulating a fistulous tract, was found.

3 Results

3.1 Type of surgery

Eight patients were treated with one or more strictureplasties, and 2 patients with resection. The patients prevalently affected by a stricture in the 2nd or 3rd duodenal portion were treated with strictureplasty: 5 with H–M technique, 2 with Jaboulay technique, and one with a pedunculated jejunal patch because of the multiple strictures (1st, 2nd and 3rd portion of duodenum) whose total length was 6 cm (Fig. 2). One patient who had the stricture in the 1st portion (length 4 cm) was treated with a B2 gastro-duodenal resection, 1 patient who had the stricture in the 3rd–4th portion of duodenum (10 cm) and proximal tract of jejunum (20 cm) was treated with a duodenal–jejunal resection and an end to side duodeno-jejunal anastomosis.

Five patients had synchronous CD lesions, four in the jejunum and one in the terminal ileum. All these lesions required surgery: jejunal strictures were treated with strictureplasties, the ileal strictures with resection.

3.2 Post-operative outcome

Following surgery, 6 patients were treated with TPN, 2 with enteral nutrition, and 2 with both enteral and TPN. Neither post-operative mortality nor surgical complications were found in any of the patients. Post-operative hospital stay was 7 days on average (range 6–11).

3.3 Follow-up

Patients were followed up for a period ranging from 2 to 18 years (mean 11 years). All patients reported improvement of their symptoms. Seven out of 10 patients were submitted to medical treatment for prevention of CD recurrence (cycles of budesonide in 4 and 5-ASA in 3 patients). Five patients had no recurrence of CD, 3 had recurrence of CD elsewhere (one patient in the ileum, treated with Finney's strictureplasty; one patient with a left colon recurrence was treated with left hemicolectomy; one patient with recurrence in the jejunum was treated with an H–M strictureplasty). No recurrence of CD was observed in the 2 patients treated with resection, whereas 2 out of the 8 patients treated with strictureplasty had a recurrence.

One of the 2 patients had a recurrence at the site of the prior Heineke–Mikulicz strictureplasty two years later. He was treated with a new strictureplasty, utilizing a pedunculated jejunal loop. The intra-operative biopsy of the stricture, which was found to be negative at frozen examination, resulted to be a cancer at the final pathological examination. Therefore, after 2 months, he was treated with a duodenopancreatectomy. The clinical condition progressively deteriorated and the patient died after 15 months. This case was previously referred.6

The other patient was treated at first with an H–M strictureplasty for a 3 cm stenosis of the 2nd portion of duodenum and then with a Michelassi strictureplasty for multiple 36-cm jejunal stenoses. After 9 months, this patient had obstructive symptoms of the upper digestive tract. A UGI endoscopy was performed, which showed recurrent ulcers at the pylorus, 1st and 2nd duodenal portions, and at the beginning of the prior SSIS. At reoperation, a critical stricture at the beginning of the prior SSIS was discovered and treated with an H–M strictureplasty. After 2 years, due to persistent ulcerations, intestinal transit disorder caused by thickening of the third duodenal portion, and anemia which did not respond to medical therapy including infliximab, we performed a duodenal–jejunal resection including the previous strictureplasties. Histological examination confirmed the presence of chronic active inflammation of the mucosa, focally ulcerative, with occasional architectural alterations of the epithelium. Currently, the patient has neither more obstructive symptoms nor anemia. The patient's post-operative symptoms were due both to the persistence of inflammation activity and to gastro-duodenal inertia.

None of the 7 patients with less than 2 duodenal–jejunal strictures had recurrences; 2 of the 3 patients with more than 2 duodenal jejunal strictures had a recurrence.

4 Discussion

The duodenal CD strictures are usually short and surrounded by granular, nodular and ulcerated mucosa. More than one stricture may be found in the duodenum: in 12% of the patients observed at the Cleveland Clinic,7 and in 30% of our cases. All duodenal sites may be involved: 1) the proximal duodenum, usually as continuity with pyloric and antrum lesions; 2) the 2nd or 3rd duodenal portions, usually as a single stricture; and 3) the distal duodenum, usually in association with several strictures of the proximal jejunal loops. According to our experience, the 3rd duodenal portion was more affected than the others, as it was seen in half of the patients observed. A duodenal fistula or perforation arising from primary intrinsic duodenal CD seems to be missing in literature.8 Conversely, a duodenal fistula may be the consequence of CD in other sites (colonic or ileal) when the phlogosis involves the duodenal wall. The presence of aerobilia or filling of the biliary or pancreatic ducts with contrast medium at imaging examinations can be due to an incontinence of Oddi's sphincter, and not to a sign of fistulization, as we have observed in one of the our patients.

A combined medical treatment with proton-pump inhibitors (PPI) and anti-inflammatory/immunosuppressive drugs is useful at initial symptoms, and anecdotal successful treatment with antiTNFα drugs has been reported. The main indication for surgery is the persistence of obstructive symptoms together with progressive weight loss and signs of malnutrition. Less frequently, severe gastrointestinal bleeding or acute pancreatitis can indicate surgery.9 Endoscopic dilatation of the duodenal stricture may be considered an alternative to surgery. Matsui et al. reported 5 patients with successful endoscopic balloon dilatation.10 In several of these patients, recurrent obstructive symptoms required repetition of the balloon treatment. Like in other CD strictures, strictures suitable for dilatation are single, short, and moderately thick.11

There are several surgical options, i.e. duodenal or gastro-duodenal resection, gastro-enteric or duodenal enteric bypass, or strictureplasty3,7,1215 (Table 1). The choice between these types of surgery is related to the site, number, length, type of inflammatory pattern, and the concomitant Crohnian gastric or jejunal lesions. In literature, resections were associated to a high rate of severe morbidity: duodenal fistula, common duct transection, bleeding, or abscess.4 We observed a satisfactory outcome for resection in a few selected patients with strictures of the proximal duodenal portion, associated to antral gastric CD, or for strictures of the distal duodenal portion associated to jejunal strictures. Therefore the procedure which has been most frequently employed for duodenal CD, especially if localized in the middle portion of duodenum, is the gastro-jejunal bypass. An alternative type of bypass can be a duodenal–jejunal bypass or a gastro-duodenal bypass. Complete relief of upper gastrointestinal symptoms after surgery is observed; most patients remain symptom-free for a long period of time. Nevertheless, the procedure involves major complications during the immediate follow up in a considerable percentage of cases.12,13 Almost 20% of the patients have difficulties in regaining intestinal function, and need a prolonged period of TPN.7

In recent years, relatively few experiences with strictureplasty were reported for the treatment of CD duodenal strictures. Theoretical advantages of strictureplasty versus bypass are: preservation of duodenal transit and, consequently, less likelihood of having dumping syndrome, and less risk of peptic ulcer and biliary reflux gastritis, especially if the pylorus is preserved. Furthermore, vagotomy has not been commonly used, or was used less frequently, than in bypass procedure.7 Usually, selective criteria have been adopted for indicating strictureplasty: according to the experience of Birmingham University, only 50% of duodenal CDs were treated with strictureplasty,12 whereas according to the Cleveland Clinic only 35% were.7 The type of strictureplasty most frequently employed is the H–M, given that the stricture is seldom longer than 5 cm. Failure of this procedure was frequently observed in the Birmingham experience, due to postoperative complications or re-strictures.12 These authors exclusively adopted an H–M technique. However, other authors7,13,16 consider strictureplasty a safe and effective operation for duodenal CD. The latter authors frequently or exclusively employed a Finney type of strictureplasty. A metanalysis of 506 patients who underwent 1825 strictureplasties for small bowel CD showed that Finney strictureplasty involves significantly less recurrences and lower reoperation rates compared to H–M strictureplasty.17 Our experience showed that strictureplasty is a safe procedure without post-operative complications. We noticed that an accurate complete mobilization of the duodenum is an important step of the procedure, as it allows sutures without tension. In this context, intestinal derotation can be useful either for avoiding tension of the suture, or for a better exposure of the duodenum. Moreover, maintaining a nose-duodenal tube for several days can decompress the duodenum and prevent leakage. Although we prevalently adopted the H–M technique, re-strictures were reported in only two patients, both affected by multiple strictures. Treatment of multiple strictures by strictureplasty can expose the patient to anemia, gastro-duodenal inertia, and major risk of re-stricture. Conversely, the two patients operated with a duodenal–jejunal resection had an uneventful postoperative outcome, and complete resolution of the symptoms. Therefore, in case of more than 2 duodenal strictures, a resection should be preferred.

Patients with CD also have an increased risk of developing carcinoma, because prolonged inflammation of the small bowel may predispose the development of dysplasia and, subsequently, cancer. Diagnosis of malignant transformation of inflammatory lesions can be difficult, even though the site of the stricture can easily be reached endoscopically. For these reasons, it is challenging to macroscopically define whether a stricture is inflammatory or neoplastic. Few cases are reported about this; biopsies in the strictureplasty site must be performed every time a masked thickening of the involved wall is found.6

In conclusion, our experience points out that strictureplasty may preferably be used in the presence of less than 2 strictures preferentially localized in the 2nd and 3rd portion of the duodenum. In cases with multiple strictures, especially if localized in the distal portion of duodenum, patients treated with strictureplasty have a higher risk of persistence of symptoms or recurrence of stricture, and may respond better to resection. Complete kocherization and intestinal derotation facilitate sutures without tension and prevent postoperative complications. Recurrence in other portions of the intestinal tract is frequent.

Conflict of Interest

Authors certify that there is no actual or potential conflict of interest in relation to this article and they state that there are no financial interests or connections, direct or indirect, or other situations that might raise the question of bias in the work reported or the conclusions, implications, or opinions stated – including pertinent commercial or other sources of funding for the individual author(s) or for the associated department(s) or organization(s), personal relationships, or direct academic competition.

Authors' contribution

All authors contributed equally to this work: G.A. and A.F. collected the data, G.A., F.B. and A.S. analyzed data, G.A., F.B., A.S. and F.T. wrote the manuscript and F.T. supervised all the manuscript, F.G. revised the manuscript.

References

Figure 1

Intraoperative view of the duodenum stricture sited in the middle duodenal portion before (a) and after a longitudinal duodenal opening (b). A strictureplasty according to H–M technique was performed (c, d).

Figure 1

Intraoperative view of the duodenum stricture sited in the middle duodenal portion before (a) and after a longitudinal duodenal opening (b). A strictureplasty according to H–M technique was performed (c, d).

Figure 2

Multiple duodenal strictures in the 1st, 2nd and 3rd portion of duodenum are visible at gastro-duodenal follow-through contrast X-ray (a). After longitudinally opening of the duodenum for 6 cm, a pedunculated jejunal patch strictureplasty was performed (b).

Figure 2

Multiple duodenal strictures in the 1st, 2nd and 3rd portion of duodenum are visible at gastro-duodenal follow-through contrast X-ray (a). After longitudinally opening of the duodenum for 6 cm, a pedunculated jejunal patch strictureplasty was performed (b).

Table 1

Summary of duodenal Crohn's disease surgical treatment studies.

Study (year) Period of study No. of patients Type of surgery Post-operative complications (no. of patients) Recurrence (no. of patients) Mean follow-up (mo) 
Alexander-Williams and Haynes (1985)151985 Strictureplasty N/A 
Poggioli et al. (1997)31978–93 3 2 Strictureplasty Roux-en-Y 2 0 N/A N/A N/A 30 
Eisenberger et al. (1998)141997–98 Strictureplasty 
Yamamoto et al. (1999)121974–97 13 13 Strictureplasty By-pass 6 4 6 6 143 192 
Worsey et al. (1999)71980–97 13 21 Strictureplasty By-pass 2 2 1 1 42 96 
Takesue et al. (2000)161999 Strictureplasty N/A 32 
Shapiro et al. (2008)131995–06 2 24 Strictureplasty By-pass 1 6 0 2 85 56 
Tonelli et al. 1986–11 8 2 Strictureplasty Resection 0 0 2 0 132 
Study (year) Period of study No. of patients Type of surgery Post-operative complications (no. of patients) Recurrence (no. of patients) Mean follow-up (mo) 
Alexander-Williams and Haynes (1985)151985 Strictureplasty N/A 
Poggioli et al. (1997)31978–93 3 2 Strictureplasty Roux-en-Y 2 0 N/A N/A N/A 30 
Eisenberger et al. (1998)141997–98 Strictureplasty 
Yamamoto et al. (1999)121974–97 13 13 Strictureplasty By-pass 6 4 6 6 143 192 
Worsey et al. (1999)71980–97 13 21 Strictureplasty By-pass 2 2 1 1 42 96 
Takesue et al. (2000)161999 Strictureplasty N/A 32 
Shapiro et al. (2008)131995–06 2 24 Strictureplasty By-pass 1 6 0 2 85 56 
Tonelli et al. 1986–11 8 2 Strictureplasty Resection 0 0 2 0 132 

Open in new tab

Table 1

Summary of duodenal Crohn's disease surgical treatment studies.

Study (year) Period of study No. of patients Type of surgery Post-operative complications (no. of patients) Recurrence (no. of patients) Mean follow-up (mo) 
Alexander-Williams and Haynes (1985)151985 Strictureplasty N/A 
Poggioli et al. (1997)31978–93 3 2 Strictureplasty Roux-en-Y 2 0 N/A N/A N/A 30 
Eisenberger et al. (1998)141997–98 Strictureplasty 
Yamamoto et al. (1999)121974–97 13 13 Strictureplasty By-pass 6 4 6 6 143 192 
Worsey et al. (1999)71980–97 13 21 Strictureplasty By-pass 2 2 1 1 42 96 
Takesue et al. (2000)161999 Strictureplasty N/A 32 
Shapiro et al. (2008)131995–06 2 24 Strictureplasty By-pass 1 6 0 2 85 56 
Tonelli et al. 1986–11 8 2 Strictureplasty Resection 0 0 2 0 132 
Study (year) Period of study No. of patients Type of surgery Post-operative complications (no. of patients) Recurrence (no. of patients) Mean follow-up (mo) 
Alexander-Williams and Haynes (1985)151985 Strictureplasty N/A 
Poggioli et al. (1997)31978–93 3 2 Strictureplasty Roux-en-Y 2 0 N/A N/A N/A 30 
Eisenberger et al. (1998)141997–98 Strictureplasty 
Yamamoto et al. (1999)121974–97 13 13 Strictureplasty By-pass 6 4 6 6 143 192 
Worsey et al. (1999)71980–97 13 21 Strictureplasty By-pass 2 2 1 1 42 96 
Takesue et al. (2000)161999 Strictureplasty N/A 32 
Shapiro et al. (2008)131995–06 2 24 Strictureplasty By-pass 1 6 0 2 85 56 
Tonelli et al. 1986–11 8 2 Strictureplasty Resection 0 0 2 0 132 

Open in new tab

© 2013 European Crohn's and Colitis Organisation

Sours: https://academic.oup.com/ecco-jcc/article/7/10/791/378833
  1. Green bay carpet cleaners
  2. Lazy dog loveland
  3. Xps docking
  4. Imo whatsapp

Copyright©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.

World J Gastrointest Endosc. Mar 16, 2019; 11(3): 256-261
Published online Mar 16, 2019. doi: 10.4253/wjge.v11.i3.256

Choledochoscope with stent placement for treatment of benign duodenal strictures: A case report

Ryan Sung-Eun Cho, John Magulick, Department of Gastroenterology and Hepatology, San Antonio Uniformed Services Health Education Consortium, San Antonio, TX 78253, United States

Shelby Madden, Department of Internal Medicine, San Antonio Uniformed Services Health Education Consortium, Dallas, TX 78253, United States

James Steven Burdick, Depart of Gastroenterology and Hepatology, Baylor University Medical Center, San Antonio, TX 78253, United States

Author contributions: Cho RS, Magulick JM, Madden S and Burdick JS contributed equally to this work. Cho RS wrote the paper.

Informed consent statement: All study participants, or their legal guardian, provided informed written consent prior to study enrollment.

Conflict-of-interest statement: The authors declare that they have no conflicts of interest.

CARE Checklist (2016) statement: The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).

Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:

Corresponding author: Ryan Sung-Eun Cho, BSc, MD, Assistant Professor, Department of Gastroenterology and Hepatology, San Antonio Uniformed Services Health Education Consortium, 3551 Roger Brooke Drive, JBSA Ft Sam Houston, San Antonio, TX 78253, United States.

Telephone: +1-210-9169737

Received: February 9, 2019
Peer-review started: February 10, 2019
First decision: February19, 2019
Revised: March 7, 2019
Accepted: March 11, 2019
Article in press: March 11, 2019
Published online: March 16, 2019


Sours: https://www.wjgnet.com/1948-5190/full/v11/i3/256.htm
Duodenal Atresia

Surgical and Endoscopic Options for Benign and Malignant Gastric Outlet Obstruction

Abstract

Gastric outlet obstruction (GOO) can be due to a variety of causes of both benign and malignant sources. As the etiology of GOO shifts from mostly benign to mostly malignant, treatment options have also evolved. Traditional options have only included surgery, but an increase in technology has seen the emergence of endoscopic alternatives. For benign disease, such as peptic ulcer disease, endoscopic balloon dilation has reduced the number of patients needing to undergo larger and more invasive surgical procedures. It has also proven successful in treating obstruction from stricture following bariatric surgery, but surgical revision or reversal remains the gold standard. Numerous surgical procedures have shown effectiveness when treating GOO, with new procedures constantly emerging. When malignancy is the cause, the procedural focus shifts from curative to palliative with the main focus being resumption of oral intake. Endoscopic stenting provides a viable alternative to gastro-jejunostomy, but due to problems with re-obstruction and stent migration, it should be reserved for patients with shorter life expectancies.

Introduction

Gastric outlet obstruction (GOO) is defined as a spectrum of diseases that produces mechanical impedance to gastric emptying. The most common pathophysiology is intrinsic or extrinsic obstruction of the duodenum or pyloric channel, but the mechanism of obstruction depends on the underlying etiology [1]. Etiologies of GOO are often divided into two categories, mechanical and non-mechanical. Once non-mechanical causes, such as diabetic gastroparesis, have been ruled out, benign and malignant mechanical causes must be differentiated. Through the 1970s, benign disease was the most common, with studies reporting up to 91 % of cases were from benign rather than malignant causes [2]. With the discovery of H2 blockers and PPIs, there has been a change in ratio between benign and malignant causes of GOO. Recent studies have shown malignancy may account for as many as 60 % of cases [3], with peripancreatic malignancy the most common etiology and reported in 15–20 % [1]. The most common causes of benign obstruction are peptic ulcer disease (PUD) and corrosive ingestion, but NSAIDs, gastric polyps, pyloric stenosis and pancreatic pseudocysts have all been implicated (Table 1). While obstruction used to be the most common complication of PUD, it is now the least common at less than 5 %. On the other hand, in cases of ingestion of strong caustics, as many as 36–44 % of patients will develop GOO [4, 5].

Full size table

Benign Gastric Outlet Obstruction

While surgery used to be the gold standard treatment for benign GOO, recent advancements in endoscopy have provided other treatment options. Prior to the 1980s, conservative medical treatments and surgery were the only treatment options. While some patients initially responded to medications, most eventually required some sort of surgical intervention. In 1982, Weiland et al. [6] conducted a retrospective review of 87 patients with GOO. All were treated initially with medications, but 56 % required operative intervention during the same hospital stay. On late follow-up, 98 % of patients with chronic PUD and 64 % with acute PUD ultimately required an operation. Additionally, Jaffin et al. [7] reviewed 69 patients who were admitted with GOO from 1970–1979; 81 % of cases were due to PUD. All were initially managed conservatively, but 62 % required surgical decompression during that hospital stay. An additional 20 % underwent an operation after a subsequent obstructive episode. Of the ten patients who did not have surgery, six died in the next 3 years, and three continued to have recurrent symptoms. Overall, 92 % of patients who lived for more than 3 years required surgery. With the invention of PPIs in 1989, treatment of PUD trended toward being non-surgical in nature. Shabbir et al. [8] using data from the turn of the century showed 83 % of patients placed on PPIs had complete resolution of pyloric peptic stenosis, with patients responding on average 9 days after initiation of treatment. While in the 1970s and early 1980s surgical intervention for benign GOO was very common, it is now infrequently needed, and the invention of PPIs has drastically increased the number of patients who can be treated with medical therapy alone.

In the mid 1980s, Benjamin et al. first described technical and clinical success using endoscopic balloon dilation (ED) [9]. Of the seven patients they reported who underwent balloon dilation, only one ended up requiring surgical intervention. Since then, numerous reports have surfaced documenting the efficacy and safety of the procedure, but with mixed results. Initial success rates are reported from 16–100 %, with most being >80 % [10–16]. Follow-up ranged from 3 months to 10 years with symptoms eventually returning in 0–84 % [10–18]. If surgical intervention was required, it was usually for restenosis, continuation of symptoms, or perforation following dilation. Surgical intervention rates are reported to be 0–51 % [10–13, 17, 19]. Factors that increased the likelihood of eventual surgical intervention included more than two courses of dilation, younger age, longer duration of the treatment course, continued use of NSAIDs, pancreatitis-related GOO and corrosive strictures [10, 12, 14, 17]. While ED generally has good initial success rates, its high rate of restenosis is concerning.

Helicobacterpylori has also been implicated in the effectiveness of ED therapy. Lam et al. [20] prospectively treated 33 patients with benign GOO by ED. Antral biopsies showed 14 had H. pylori and 11 were H. pylori negative. All patients who were positive for H. pylori were treated for eradication after ED was performed. After a median follow-up of 24 months, there was a significant difference between the number of patients with H. pylori who developed further ulcer complications as opposed to those who were H. pylori negative (21.4 vs. 54.54 %, respectively). In a French study of 16 patients, all whom were H. pylori positive, 93.75 % underwent successful ED treatment after a follow-up of 13 months [21]. For those patients who are H. pylori positive, eradication of H. pylori may increase the success rate of endoscopic therapy and decrease the need for surgical intervention. However, if patients are found to be H. pylori negative, they should be counseled that a higher failure rate is expected.

Special Circumstances

An infrequent cause of benign GOO is obstruction from bariatric surgical procedures (Fig. 1), which include vertical banded gastroplasty (VBG), transected banded vertical gastric bypass (TBVBGP) and Roux-en-Y gastric bypass (RYGB). VBG used to be a common weight loss procedure, but due to its high complication and re-operative rates, it has fallen out of favor. GOO has been reported in as many as 8 % of patients undergoing VBG, with staple line leaks, inadequate weight loss and gastroesophageal reflux as additional complications [22]. Two different surgical procedures have been described to relieve the obstruction from a failed VBG, RYGB and VBG reversal via a gastro-gastrostomy. A retrospective review of 34 patients who underwent a VBG that ultimately required revision compared laparoscopic VBG reversal with open and laparoscopic RYGB [23]. While there was no difference in complication rates, patients who had the RYGB procedure had a significant decrease in BMI 1–2 years postoperatively, while VBG reversal patients had a significant increase. For those VBG reversal patients, this meant going from an average BMI in the moderately obese range (31.9 ± 4.8) to one in the morbidly obese range (48.6 ± 12.2). If weight loss is still the goal, RYGB appears to be the better option.

Bariatric surgical procedures

Full size image

VBG is not the only bariatric procedure to have problems. In a review of 2,949 patients undergoing TBVBGP, band erosion was documented in 48 patients (1.63 %), and 17 (36.42 %) of them presented with GOO [24]; 54.17 % of those with band erosion then required subsequent surgical intervention to relieve the obstruction and remove the eroded band. Multiple studies have reported success in removing the eroded band laparoscopically through a gastrostomy in the body of the stomach [25, 26]. In our experience, after accessing the stomach laparoscopically, the band may be simply cut to allow expansion of the stenotic channel. Figure 2 shows stenosis from an eroded Lap-Band.

Stenosis from an eroded Lap-Band

Full size image

While RYGB seems to be an effective procedure to relieve obstruction from other failed bariatric surgeries, it too can cause obstruction. Go et al. [27] reviewed 562 patients who underwent RYGB during their 2-year study period. Thirty-eight patients (6.8 %) developed stomal stenosis, an average of 7.7 weeks postoperatively. All underwent ED as treatment, requiring on average 2.1 dilations. All but two of the dilations were successful and relieved the obstruction (95 %). One patient failed dilation and another sustained complications, both requiring surgical intervention. Another series examined 28 patients with GOO after VBG (n = 9) and RYGB (n = 19) [28]; 30 % of the patients with previous VBG had relief after one dilation, while 42 % of patients with previous RYGB experienced relief. However, 28.5 % still required eventual surgical intervention. While more research is needed, endoscopic dilation may be a feasible alternative to surgical intervention for bariatric surgery stenosis.

Surgical Techniques

Numerous surgical techniques over the years have been described to treat GOO. Finey, Jaboulay or Heineke-Mikulicz pyloroplasty, antrectomy without or without vagotomy, or gastro-jejunostomy techniques have all been routinely described. In a prospective study of 90 patients with GOO secondary to duodenal ulcer, subjects were randomly assigned to three surgical groups: highly selective vagotomy (HSV) + gastro-jejunostomy (GJ), HSV + Jaboulay gastro-duodenostomy or selective vagotomy (SV) + antrectomy. No differences were found in the postoperative courses, but one patient in the HSV + Jaboulay gastro-duodenostomy group died from acute pancreatitis. After a mean follow-up time of 90 months, the clinical state of the patients was graded using the Visick scale. The Visick scale subjectively classifies the severity of GERD by the patients’ reported symptoms, on a scale of 1–4, with 1 (no complaints) being the least severe and 4 (complaints not decreased by surgery) the most severe. In the study by Csendes et al. [29], there were significantly better results after HSV + GJ (80 % Visick I) than after HSV + Jaboulay gastro-duodenostomy (70 % Visick I), but not after SV + antrectomy (75 % Visick I). They concluded that HSV + GJ was the treatment of choice. Tsai et al. [30] examined the same surgical procedures, focusing on the outcomes of elderly patients with benign obstructing GOO. Forty-seven patients were studied over the time period of 2000–2008. Fifteen of the patients were considered elderly, 32 young, and they underwent Finney or Jaboulay pyloroplasty (n = 26), antrectomy (n = 13) or GJ (n = 8). The mean hospital stay was 14.9 days with a modest correlation between age and length of stay (p = 0.04, r = 0.294). There was no increase in morbidity or mortality in the elderly population. While elderly patients did appear to have an increased length of stay, morbidity was not different no matter which surgical procedure they underwent. While multiple surgical procedures appear to be effective, no single procedure has been proven to be the treatment of choice.

Malignant Gastric Outlet Obstruction

When malignancy is of concern, or verified, surgical options can be curative or palliative. Traditionally, an open GJ was the treatment of choice, but with the advent of laparoscopic surgery, laparoscopic GJ has become the gold standard (Fig. 3). Multiple studies have shown an advantage of laparoscopic GJ over open. In one series, there was no difference in the operating time or number of patients receiving blood transfusions, but laparoscopic GJ was statistically better for decreased need for opiate analgesia, hospital stay, IV hydration requirement and morbidity [31]. A separate study also found a significant reduction in length of hospital stay with laparoscopic GJ as well as decreased intraoperative blood loss [32]. Choi found that open GJ caused more immune suppression than laparoscopic GJ, with increased levels of serum ESR, TNF-α and IL-6 [33]. It is now widely accepted that laparoscopic GJ has clear advantages over open GJ when it is technically feasible.

Malignant gastric outlet obstruction from gastric adenocarcinoma

Full size image

Recently, new surgical procedures have emerged in the treatment of malignant GOO (Fig. 4). Two separate series have described success with using a partial stomach-partitioning gastro-jejunostomy (PSPG). Arrangoiz et al. [34] performed PSPG in 55 patients with metastatic tumors causing GOO. They noted good success, with 0 % mortality and 16.4 % complication rates. The median survival of patients was 9 months, with 95 % still tolerating an enteral diet 8 months postoperatively. Eguchi et al. [35] reported PSPG in 18 patients with a similar complication rate, 17 %. Their patients had a mean time to oral intake of 4.5 days with a mean duration of 133 days. A Japanese group developed a new technique called the modified Devine exclusion with vertical stomach reconstruction (MDVSR) [36]. The procedure involves laparoscopically transecting the stomach, vertically stretching the proximal portion and then re-resecting horizontally with a stapler (Fig. 5). A loop of jejunum was then brought up to the pouch and anastomosed in a horizontal side-to-side fashion. They have reported great success with this technique when comparing it to conventional gastrojejunostomy, and none of the patients who underwent MDVSR had reoccurrence of GOO. Additionally, hospital stay, time to oral intake, and need for NG decompression were all reduced in the MDVSR group, while survival was increased. While both techniques shows promise, more data is needed.

Conventional GJ versus modified devine exclusion and partial stomach partitioning gastrojejunostomy

Full size image

MDVSR showing shaded resection portion

Full size image

Emerging Technologies

Expandable metal stents have been approved for use in treating malignant disease causing obstruction throughout the GI tract. They are made of different metal alloys, come in a variety of sizes and shapes, and may be covered or uncovered. Gastro-duodenal stents have emerged as a safe and effective alternative to surgical therapy. Technical and clinical success rates have proven to be high at 89–98 % and 85.5–89 %, respectively [37–40]. However, the procedure is not without complications. A large review study by Dormann et al. [38] identified 606 patients who underwent endoscopic stent placement. While there were no mortalities, severe complications such as bleeding and perforation occurred in 1.2 %, stent migration in 5 % and re-obstruction in 18 %. Mansoor et al. [39] described similar rates of stent-related complications, 14 %, including blockage and migration. Another study by Cho et al. [40] found much higher re-obstruction rates at 31 %, with covered stents and chemotherapy after stent placement significant prognostic factors for stent patency.

Covered stents were designed with a membrane within the mesh wall to prevent ingrowth of tumor and thus obstruction of the stent [41]. Autopsies of human corpses that have had previous uncovered stents placed have shown incorporation of the stent into the tumor itself, causing pressure necrosis. Theoretically, covered stents are designed not to embed into the surrounding tissue, and while they may have lower rates of re-obstruction, it may result in higher migration rates. Woo et al. showed evidence of this after analyzing 70 patients with covered (n = 24) and uncovered (n = 46) stents [42]. While technical and clinical success rates were similar, the covered group had a statistically higher complication rate (62.5 vs. 34.8 %, respectively) and was primarily attributed to a higher migration rate (20.8 vs. 0 %). While not statistically significant, the patency rate tended to be lower for covered stents (13.7 + 8.6 weeks) than for uncovered stents (not reached). Maetani et al. [43] produced contrary evidence in a randomized trial of covered versus uncovered self-expandable stents. Both groups had a technical success rate of 100 % and similar clinical success rates. While there was no statistical difference between patency rates, covered stents had less frequent rates of dysfunction, and reoccurrence of obstructive symptoms was higher in the uncovered group. Patient survival did not differ between the two groups. Larger prospective studies would be useful in determining the benefits of covered versus uncovered stents.

Given the reported success of endoscopic stent placement, numerous studies have been published comparing it to traditional surgical intervention. Most studies agree that stenting provides the following advantages over laparoscopic or open gastro-jejunostomy: shorter operative time, shorter hospital stay and decreased time to oral intake [44–52]. However, they almost universally report decreased patency of stents with higher rates of recurrent obstruction and need for re-intervention [46••, 49, 50, 53]. There have been mixed reports on the technical and clinical success rates, cost of procedure and complication rates. More commonly, studies found no difference between technical and clinical success rates [49–51, 53], but in a meta-analysis of 307 procedures by Hosono et al. [45], clinical success was higher in the stenting group. A recent 10-year retrospective study of stenting versus GJ by Khashab et al. [46••] found statistically higher rates of technical success in the GJ group (96 vs. 99 %). The same group also found a statistical increase in the cost of stenting procedures compared to GJ when stent reintervention procedures were included ($34,250 vs. $27,599). A retrospective study using the Medicare database by Roy et al. [47] previously reported stenting to be a cheaper procedure than GJ ($15,366 vs. $27,391). However, re-intervention stenting procedures were not included when calculating costs. Complication rates are also widely debated. Both impact, major vs. minor, and timing, early versus late, have been studied. Mixed data have shown both no difference in early minor and major complications [49, 50, 53] and a decrease in time to late major complications in the stenting group [49, 53]. Perhaps the most important statistic for patients is the length of post-procedure survival. Thirty-day survival has been reported as both no difference [45, 48] and decreased for the stenting group [44]. However, mean survival seems to favor the GJ group over the stenting group (90–293 vs. 65–189 days) [50, 52, 53]. Given the higher rates of re-intervention for recurrent obstruction, palliative stenting may best be reserved for patients with shorter expected survival times.

Conclusions

Gastric outlet obstruction is a phenomenon caused by a variety of factors. For benign causes, such as PUD or post-bariatric surgery stenosis, ED may be a viable alternative to traditional surgical treatment. However, for patients that are H. pylori negative or have required multiple dilations, surgical GJ appears to be the treatment of choice. Multiple surgical procedures have been used to treat GOO successfully, and new procedures continue to emerge. When malignancy is the cause of GOO, the procedural goal becomes palliation and resumption of oral intake. Endoscopic stenting is a reasonable alternative to laparoscopic or open GJ, but is better reserved for patients who are very poor surgical candidates or have short expected survival times.

References

Recently published papers of particular interest have been highlighted as: •• Of major importance

  1. 1.

    Appasani S, Kochhar S, Nagi B, Gupta V, Kochhar R. Benign gastric outlet obstruction–spectrum and management. Trop Neurogastroenterol. 2001;32(4):259–66.

    Google Scholar

  2. 2.

    Goldstein H, Boyle JD. The saline load test—a bedside evaluation of gastric retention. Gastroenterology. 1965;49:375–80.

    PubMedCAS Google Scholar

  3. 3.

    Shone DN, Nikoomanesh P, Smith-Meek MM, Bender JS. Malignancy is the most common cause of gastric outlet obstruction in the era of H2 blockers. Am J Gastroenterol. 1995;90:1769–70.

    PubMedCAS Google Scholar

  4. 4.

    Zarger SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of corrosive acids. Spectrum of injury to upper gastrointestinal tract and natural history. Gastroenterology. 1989;97:702–7.

    Google Scholar

  5. 5.

    Zarger SA, Kochhar R, Nagi B, Mehta S, Mehta SK. Ingestion of strong corrosive alkalis: spectrum of injury to upper gastrointestinal tract and natural history. Am J Gastroenterol. 1992;87:337–41.

    Google Scholar

  6. 6.

    Weiland D, Dunn DH, Humphrey EW, Schwartz ML. Gastric outlet obstruction in peptic ulcer disease: an indication for surgery. Am J Surg. 1982;143:90–3.

    PubMedArticleCAS Google Scholar

  7. 7.

    Jaffin BW, Kaye MD. The prognosis of gastric outlet obstruction. Ann Surg. 1985;201(2):176–9.

    PubMed CentralPubMedArticleCAS Google Scholar

  8. 8.

    Shabbir J, Durrani S, Ridgway PF, Mealy K. Proton pump inhibition is a feasible primary alternative to surgery and balloon dilatation in adult peptic pyloric stenosis (APS): report of six consecutive cases. Ann R Coll Surg Engl. 2006;88(2):174–5.

    PubMed CentralPubMedArticleCAS Google Scholar

  9. 9.

    Kochhar R, Kochhar S. Endoscopic balloon dilation for benign gastric outlet obstruction in adults. World J Gastrointest Endosc. 2010;2(1):29–35.

    PubMed CentralPubMedArticle Google Scholar

  10. 10.

    Boylan JJ, Gradzka MI. Long-term results of endoscopic balloon dilatation for gastric outlet obstruction. Dig Dis Sci. 1999;44(9):1883–6.

    PubMedArticleCAS Google Scholar

  11. 11.

    Cherian PT, Cherian S, Singh P. Long-term follow-up of patients with gastric outlet obstruction related to peptic ulcer disease treated with endoscopic balloon dilatation and drug therapy. Gastrointest Endosc. 2007;66(3):491–7.

    PubMedArticle Google Scholar

  12. 12.

    Rana SS, Bhasin DK, Chandail VS, Gupta R, Nada R, Kang M, Nagi B, Singh R, Singh K. Endoscopic balloon dilatation without fluoroscopy for treating gastric outlet obstruction because of benign etiologies. Surg Endosc. 2011;25(5):1579–84.

    PubMedArticle Google Scholar

  13. 13.

    Lau JY, Chung SC, Sung JJ, Chan AC, Ng EK, Suen RC, Li AK. Through-the-scope balloon dilation for pyloric stenosis: long term results. Gastrointest Endosc. 1996;43:98–101.

    PubMedArticleCAS Google Scholar

  14. 14.

    Solt J, Bajor J, Szabó M, Horváth OP. Long-term results of balloon catheter dilation for benign gastric outlet stenosis. Endoscopy. 2003;35:490–5.

    PubMedArticleCAS Google Scholar

  15. 15.

    Misra SP, Dwivedi M. Long-term follow-up of patients undergoing balloon dilation for benign pyloric stenoses. Endoscopy. 1996;28:552–4.

    PubMedArticleCAS Google Scholar

  16. 16.

    Kuwada SK, Alexander GL. Long-term outcome of endoscopic dilation of nonmalignant pyloric stenosis. Gastrointest Endosc. 1995;41:15–7.

    PubMedArticleCAS Google Scholar

  17. 17.

    Perng CL, Lin HJ, Lo WC, Lai CR, Guo WS, Lee SD. Characteristics of patients with benign gastric outlet obstruction requiring surgery after endoscopic balloon dilation. Am J Gastroenterol. 1996;91:987–90.

    PubMedCAS Google Scholar

  18. 18.

    Kozarek RA, Botoman VA, Patterson DJ. Long-term follow-up in patients who have undergone balloon dilation for gastric outlet obstruction. Gastrointest Endosc. 1990;36:558–61.

    PubMedArticleCAS Google Scholar

  19. 19.

    DiSario JA, Fennerty MB, Tietze CC, Hutson WR, Burt RW. Endoscopic balloon dilation for ulcer-induced gastric outlet obstruction. Am J Gastroenterol. 1994;89:868–71.

    PubMedCAS Google Scholar

  20. 20.

    Lam YH, Lau JY, Fung TM, Ng EK, Wong SK, Sung JJ. Endoscopic balloon dilation for benign gastric outlet obstruction with or without Helicobacter pylori infection. Gastrointest Endosc. 2004;60:229–33.

    PubMedArticle Google Scholar

  21. 21.

    Cheikh I, Younes R, Said Y, Chaabouni H, Chebbi F, Ben Ammar A. Peptic pyloroduodenal strictures treated by endoscopic balloon dilation and eradication of helicobacter pylori. Results of a prospective study. Tunis Med. 2003;81(4):258–63.

    PubMed Google Scholar

  22. 22.

    Nocca D, Aggarwal R, Blanc P, Gallix B, Di Mauro GL, Millat B, des De Seguin Hons C, Deneve E, Rodier JG, Tincani G, Pierredon MA, Fabre JM. Laparoscopic vertical banded gastroplasty. A multicenter prospective study of 200 procedures. Surg Endosc. 2007;21(6):870–4.

    PubMedArticleCAS Google Scholar

  23. 23.

    Tevis S, Garren M, Gould J. Revisional surgery for failed vertical-banded gastroplasty. Obes Surg. 2011;21:1220–4.

    PubMedArticle Google Scholar

  24. 24.

    Fobi M, Lee H, Igwe D, Felahy B, James E, Stanczyk M, Fobi N. Band erosion: incidence, etiology, management and outcome after banded vertical gastric bypass. Obes Surg. 2011;11:1–9.

    Google Scholar

  25. 25.

    Abu-abeid S, Szold A. Laparoscopic management of lap-band erosion. Obes Surg. 2001;11(1):87–9.

    PubMedArticleCAS Google Scholar

  26. 26.

    Basa N, Dutson E, Lewis C, Derezin M, Han S, Mehran A. Laparoscopic transgastric removal of eroded adjustable band: a novel approach. Surg Obes Relat Dis. 2008;4:194–7.

    PubMedArticle Google Scholar

  27. 27.

    Go MR, Muscarella P, Needleman BJ, Cook CH, Melvin WS. Endoscopic management of stomal stenosis after Roux-en-Y gastric bypass. Surg Endosc. 2004;18(1):56–9.

    PubMedArticleCAS Google Scholar

  28. 28.

    Vance PL, delange EE, Shaffer HA, Schirmer B. Gastric outlet obstruction following surgery for morbid obesity of fluoroscopically guided balloon dilation. Radiology. 2002;222(1):70–2.

    PubMedArticle Google Scholar

  29. 29.

    Csendes A, Maluenda F, Braghetto I, Schutte H, Burdiles P, Diaz JC. Prospective randomized study comparing three surgical techniques for the treatment of gastric outlet obstruction secondary to duodenal ulcer. Am J Surg. 1993;166(1):45.

    PubMedArticleCAS Google Scholar

  30. 30.

    Tsai CH, Liou GJ, Liu CL, Pan JS, Lee JJ, Cheng SP, Liu TP. Surgical management of benign gastric outlet obstruction in the elderly. Hepatogastroenterology. 2012;59(117):1643–6.

    Google Scholar

  31. 31.

    Al-Rashedy M, Dadibhai M, Shareif A, Khandelwal MI, Ballester P, Abid G, McCloy RF, Ammori BJ. Laparoscopic gastric bypass for gastric outlet obstruction is associated with smoother, faster recovery and shorter hospital stay compared with open surgery. J Hepatobiliary Pancreat Surg. 2005;12(6):474–8.

    PubMedArticle Google Scholar

  32. 32.

    Bergamaschi R, Marvik R, Thoresen JE, Ystgaard B, Johnsen G, Myrvold HE. Open versus laparoscopic gastrojejunostomy for palliation in advanced pancreatic cancer. Surg Laparosc Endosc. 1998;8(2):92–6.

    PubMedArticleCAS Google Scholar

  33. 33.

    Choi YB. Laparoscopic gastrojejunostomy for palliation of gastric outlet obstruction in unresectable gastric cancer. Surg Endosc. 2002;169(11):1620–6.

    Article Google Scholar

  34. 34.

    Arrangoiz R, Papavasiliou P, Singla S, Siripurapu V, Watson JC, Hoffman JP, Farma JM. Partial stomach-partitioning gastrojejunostomy and the success of this procedure in terms of palliation. Am J Surg. 2013;206(3):333–9.

    PubMedArticle Google Scholar

  35. 35.

    Eguchi H, Yada K, Shibata K, Matsumoto T, Etoh T, Yasuda K, Inomata M, Shiraishi N, Ohta M, Kitano S. Laparoscopic stomach-partitioning gastrojejunostomy is an effective palliative procedure to improve quality of life in patients with malignant gastroduodenal outlet obstruction. Asian J Endosc Surg. 2012;5(4):153–6.

    PubMedArticle Google Scholar

  36. 36.

    Oida T, Mimatsu K, Kawasaki A, Kano H, Kuboi Y, Amano S. Modified devine exclusion with vertical stomach reconstruction for gastric outlet obstruction: a novel technique. J Gastrointest Surg. 2009;13(7):1226–32.

    PubMedArticle Google Scholar

  37. 37.

    Van den Berg MW, Haijtink S, Fockens P, Vleggaar FP, Dijkgraff MGW, Siersma PD. First data on the evolution duodenal stent for palliative outlet obstruction (DUOLUTION study): a prospective trial. Endoscopy. 2013;45(3):174–81.

    PubMedArticle Google Scholar

  38. 38.

    Dormann A, Meisner S, Verin N, Wenk Lang A. Self-expanding metal stents for gastroduodenal malignancies; systematic review of their clinical effectiveness. Endoscopy. 2004;36(6):543–50.

    PubMedArticleCAS Google Scholar

  39. 39.

    Mansoor H, Yusuf M. Outcomes of endoscopic pyloric stenting in malignant gastric outlet obstruction: a retrospective study. BMC Res Notes. 2013;6:280.

    PubMed CentralPubMedArticle Google Scholar

  40. 40.

    Cho YK. Clinical outcome of self-expandable metal stent and prognostic factors for stent patency in gastric outlet obstruction caused by gastric cancer. Dig Dis Sci. 2010;55(3):668–74.

    PubMedArticleCAS Google Scholar

  41. 41.

    Baron T. Expandable metal stents for the treatment of cancerous obstruction of the gastrointestinal tract. New Engl J Med. 2001;344(22):1681–7.

    PubMedArticleCAS Google Scholar

  42. 42.

    Woo SM, Kim DH, Lee WJ, Park KW, Park SJ, Han SS, Kim TH, Koh YH, Kim HB, Hong EK. Comparison of uncovered and covered stents for the treatment of malignant duodenal obstruction caused by pancreaticobiliary cancer. Surg Endosc. 2013;27(6):2031–9.

    PubMedArticle Google Scholar

  43. 43.

    Maetani I, Mizumoto Y, Shigoka H, Omuta S, Saito M, Tokuhisa J, Morizane T. Placement of a triple-layered covered versus uncovered metallic stent for palliation of malignant gastric outlet obstruction: a multicenter randomized trial. Dig Endosc. 2013. doi:10.1111/den.12117.

  44. 44.

    Del Piano M, Ballare M, Montino F, Todesco A, Orsello M, Magnani C, Garello E. Endoscopy or surgery for malignant GI outlet obstruction? Gastrointest Endosc. 2005;61(3):421–6.

    PubMedArticle Google Scholar

  45. 45.

    Hosono S, Ohtani H, Arimoto Y, Kanamiya Y. Endoscopic stenting versus surgical gastroenterostomy for palliation of malignant gastroduodenal obstruction: a meta-analysis. J Gastroenterol. 2007;42(4):283–90.

    PubMedArticle Google Scholar

  46. 46.

    •• Khashab M, Alawad AS, Shin EJ, Kim K, Bourdel N, Singh VK, Lennon AM, Hutfless S, Sharaiha RZ, Amateau S, Okolo PI, Makary MA, Wolfgang C, Canto MI, Kalloo AN. Enteral stenting versus gastrojejunostomy for palliation of malignant gastric outlet obstruction. Surg Endosc. 2013;27(6):2068–75. Very recent large, 10year retrospective study of gastrojejunostomy versus endoscopic stenting for malignant gastric outlet obstruction.

  47. 47.

    Roy A, Kim M, Christein J, Varadarajulu S. Stenting versus gastrojejunostomy for management of malignant gastric outlet obstruction: comparison of clinical outcomes and costs. Surg Endosc. 2012;26(11):3114–9.

    PubMed CentralPubMedArticle Google Scholar

  48. 48.

    Ly J, O’Grady G, Mittal A, Plank L, Windsor JA. A systematic review of methods to palliate malignant gastric outlet obstruction. Surg Endosc. 2010;24(2):290–7.

    PubMedArticle Google Scholar

  49. 49.

    Jeurnink SM, Steyerberg EW, Hof GV, Van Eijck CH, Kuipers EJ, Siersema PD. Gastrojejunostomy versus stent placement in patients with malignant gastric outlet obstruction: a comparison in 95 patients. J Surg Oncol. 2007;96(5):389–96.

    PubMedArticleCAS Google Scholar

  50. 50.

    Jerunink SM, Van Eijk CH, Steyerberg EW, Kuipers EJ, Siersema PD. Stent versus gastrojejunostomy for the palliation of gastric outlet obstruction: a systematic review. BMC Gastroenterol. 2007;8(7):18.

    Article Google Scholar

  51. 51.

    Zheng B, Wang X, Ma B, Tian J, Jiang L, Yang K. Endoscopic stenting versus gastrojejunostomy for palliation of malignant gastric outlet obstruction. Dig Endosc. 2012;24(2):71–8.

    PubMedArticle Google Scholar

  52. 52.

    Maetani I, Akatsuka S, Ikeda M, Tada T, Ukita T, Nakamura Y, Nagao J, Sakai Y. Self-expandable metallic stent placement for palliation in gastric outlet obstructions caused by gastric cancer: a comparison with surgical gastrojejunostomy. J Gastroenterol. 2005;40(10):932–7.

    PubMedArticleCAS Google Scholar

  53. 53.

    No JH, Kim SW, Lim CH, Kim JS, Cho YK, Park JM, Lee IS, Choi MG, Choi KY. Long-term outcome of palliative therapy for gastric outlet obstruction caused by unresectable gastric cancer in patients with good performance status: endoscopic stenting versus surgery. Gastrointest Endosc. 2013;78(1):55–62.

    PubMedArticle Google Scholar

Download references

Author information

Affiliations

  1. Department of Surgery, Cambridge Health Alliance-Harvard Medical School, 1493 Cambridge St, Cambridge, MA, 02139, USA

    Amie Miller & Steven Schwaitzberg

Corresponding author

Correspondence to Amie Miller.

Additional information

This article is part of the Topical Collection on Acute Care Surgery.

About this article

Cite this article

Miller, A., Schwaitzberg, S. Surgical and Endoscopic Options for Benign and Malignant Gastric Outlet Obstruction. Curr Surg Rep2, 48 (2014). https://doi.org/10.1007/s40137-014-0048-z

Download citation

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

Keywords

  • Gastric outlet obstruction
  • Pyloroplasty
  • Gastro-jejunostomy
Sours: https://link.springer.com/article/10.1007/s40137-014-0048-z

Treatment duodenal stricture

Management of a postbulbar duodenal ulcer and stricture causing gastric outlet obstruction: A case report

1. Yuan Y., Padol I.T., Hunt R.H. Peptic ulcer disease today. Nat. Rev. Gastroenterol. Hepatol. 2006;3:80–89. [PubMed] [Google Scholar]

2. Wang Y.R., Richter J.E., Dempsey D.T. Trends and outcomes of hospitalizations for peptic ulcer disease in the United States, 1993 to 2006. Ann. Surg. 2010;251:51–58. [PubMed] [Google Scholar]

3. Walsh J.H., Peterson W.L. The treatment of Helicobacter pylori infection in the management of peptic ulcer disease. N. Engl. J. Med. 1995;333:984–991. [PubMed] [Google Scholar]

4. Kim J.H., Shin J.H., Di Z.H., Ko G.Y., Yoon H.K., Sung K.B., Song H.Y. Benign duodenal strictures: treatment by means of fluoroscopically guided balloon dilation. J. Vasc. Intervent. Radiol. 2005;16:543–548. [PubMed] [Google Scholar]

5. Kochhar R., Kochhar S. Endoscopic balloon dilation for benign gastric outlet obstruction in adults. World J. Gastrointest. Endosc. 2010;2:29–35.[PMC free article] [PubMed] [Google Scholar]

6. Profili S., Meloni G.B., Bifulco V., Conti M., Feo C.F., Canalis G.C. Self-expandable metal stents in the treatment of antro-pyloric and/or duodenal strictures. Acta Radiol. (CPH) 2001;42:176–180. [PubMed] [Google Scholar]

7. Agha R.A., Fowler A.J., Saeta A., Barai I., Rajmohan S., Orgill D.P., SCARE Group The SCARE statement: consensus-based surgical case report guidelines. Int. J. Surg. 2016;34:180–186. [PubMed] [Google Scholar]

8. Appasani S., Kochhar S., Nagi B., Gupta V., Kochhar R. Benign gastric outlet obstruction–spectrum and management. Trop. Gastroenterol. 2012;32:259–266. [PubMed] [Google Scholar]

9. Borody T.J., George L.L., Brandl S., Andrews P., Ostapowicz N., Hyland L., Devine M. Helicobacter pylori-negative duodenal ulcer. Am. J. Gastroenterol. 1991;86:1154–1157. [PubMed] [Google Scholar]

10. Ferzoco S.J., Soybel D.I. Gastric outlet obstruction, perforation and other complications of gastroduodenal ulcer. In: Wolfe H.M., editor. Therapy of Digestive Disorders. second ed. Elsevier Inc;; New Delhi: 2007. pp. 357–375. [Google Scholar]

11. Cherian P.T., Cherian S., Singh P. Long-term follow-up of patients with gastric outlet obstruction related to peptic ulcer disease treated with endoscopic balloon dilatation and drug therapy. Gastrointest. Endosc. Gastrointest. Endosc. 2007;66:491–497. [PubMed] [Google Scholar]

12. Hamzaoui L., Bouassida M., Mansour I.B., Medhioub M., Ezzine H., Touinsi H., Azouz M.M. Balloon dilatation in patients with gastric outlet obstruction related to peptic ulcer disease. Arab. J. Gastroenterol. 2015;16:121–124. [PubMed] [Google Scholar]

13. Perng C.L., Lin H.J., Lo W.C., Lai C.R., Guo W.S., Lee S.D. Characteristics of patients with benign gastric outlet obstruction requiring surgery after endoscopic balloon dilation. Am. J. Gastroenterol. 1996;91:987–990. [PubMed] [Google Scholar]

14. Gibson J.B., Behrman S.W., Fabian T.C., Britt L.G. Gastric outlet obstruction resulting from peptic ulcer disease requiring surgical intervention is infrequently associated with Helicobacter pylori infection. J. Am. Coll. Surg. 2000;19:32–37. [PubMed] [Google Scholar]

15. Shah S.K., Walker P.A. Springer International Publishing; 2017. Gastric Outlet Obstruction. In Common Problems in Acute Care Surgery; pp. 221–232. [Google Scholar]

Sours: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5911670/
Laparoscopic Management of Duodenal Obstruction

Abstract

Duodenal strictures in Crohn’s disease (CD) are rare, and surgical management is challenging. Although short segment duodenal strictures may be managed by strictureplasty, longer strictures historically were managed with gastroduodenal bypass, and rarely with Whipple’s procedure. However, both those operations are associated with significant short- and long-term complications. For long strictures of the third portion of the duodenum, a duodenojejunal (DJ) bypass procedure, which has rarely been reported in the CD surgical literature, may be a more physiologic option in select cases. We present a case of a patient with diffuse jejunoileitis with 26 strictures, including a 7-cm stricture of the third portion of the duodenum, who was managed successfully with a DJ bypass, multiple strictureplasty procedures, and a limited small bowel resection with a focus on intra-operative technique. DJ bypass is an alternative for successfully managing such strictures.

Lay Summary

Crohn’s disease is an inflammatory condition of the intestine with an unknown cause and can result in inflammation, narrowing (stricuture) or penetrating disease (fistula that inflammation goes through the wall of the bowel and into another structure). Unfortunately Crohn’s disease can affect anywhere in the gastrointestinal tract, all the way from the mouth to the anus. Sometimes Crohn’s disease can affect the duodenum, the portion of the small intestine just after the stomach. When Crohn’s disease is in the duodenum and causes narrowing, it is difficult to treat medically, and often needs a surgical intervention. When the narrowing is short, less than a few centimeters, the surgeon can do a strictureplasty which means opening the intestine across the stricture and sewing it back shut in the horitzontal direction to make the opening larger. When the narrowing, or stricture, is longer, then the surgeon may have to connect the stomach to another part of the small intestine (gastrojejunostomy) to avoid or bypass the duodenum, or may have to perform a large reconstructive operation to remove that portion of the small intestine. the challenge is that those operations have significant potential complications associated with them. Therefore, sometimes a bypass operation can be done instead to connect the duodenum to the next part of the small intestine, the jejunum. In this manuscript the authors describe this surgical technique is a 38 year old male with Crohn’s disease who was referred with multiple areas of narrowing in his intestine.

Crohn’s disease, enteritis, duodenal strictures, obstruction, strictureplasty, bypass

CLINICAL CASE

A 38-year-old male with Crohn’s disease (CD) was referred to our colorectal surgery clinic with concerns of multiple duodenal and small bowel strictures based on endoscopic and radiologic findings. He was initially diagnosed with CD 10 years prior with clinically quiescent disease, without any perianal involvement, and was managed expectantly off medications. However, 3 months before presentation, he was admitted as an outpatient for an episode of acute exacerbation of CD with obstructive symptoms and was treated with a corticosteroid taper and anti-TNF antibody therapy with infliximab. At that time, esophagogastroduodenoscopy (EGD) revealed a long segment stricture (7 cm in length) in the third part of duodenum (D3); in addition, he had multiple strictures throughout the jejunum and ileum on a small bowel follow-through study (Fig. 1).

FIGURE 1.

Small bowel follow-through demonstrating long stricture of the third/fourth portion of duodenum. ©Cleveland Clinic Foundation 2019.

FIGURE 1.

Small bowel follow-through demonstrating long stricture of the third/fourth portion of duodenum. ©Cleveland Clinic Foundation 2019.

Upon evaluation he endorsed a 9-month history of post-prandial abdominal pain associating with poor appetite, was only tolerating a liquid diet, and had lost 7 kg in weight over 2 months. He had no previous abdominal surgery and had already tapered off steroids. Clinical examination revealed a thin young male with a body mass index of 23 kg/m2; his abdominal examination revealed a scaphoid nontender but diffusely tympanic abdomen. Laboratory evaluation revealed a mild microcytic anemia (hemoglobin 9.9 g/dL, mean corpuscular volume of 77.6 fL); and mildly elevated C-reactive protein of 9 mg/dL. Prealbumin was within normal range (36 g/dL) but albumin was low (3.0 g/dL). The patient subsequently had a repeat EGD for further evaluation at our institution which demonstrated one long stricture with variable luminal diameters in the third part of duodenum (Fig. 2). Biopsy taken from this area confirmed chronic active duodenitis with detached fragments of fibrinopurulent debris consistent with ulcers and no evidence of malignancy. The strictures were not amendable to balloon dilatation due to their length.

The decision was made to perform an elective exploratory laparotomy to manage his duodenal and jejunoileal strictures 4 weeks after his last dose of anti-TNF therapy.

Preoperatively, his nutritional status was optimized by using exclusive enteral nutrition with a commercially available clear high-protein diet supplementation (6 cans of Ensure per day), which was well tolerated and resulted in weight gain of several pounds.

OPERATIVE FINDINGS

The entire length of small bowel was measured at 575 cm. A total of 26 small bowel strictures were identified intraoperatively, including a long stricture of the third and fourth portion of the duodenum, extending to the proximal jejunum (Fig. 3).

FIGURE 3.

Gross intra-operative photo, diffuse jejunoileitis with creeping fat, pseudo- sacculation between strictures. ©Cleveland Clinic Foundation 2019.

FIGURE 3.

Gross intra-operative photo, diffuse jejunoileitis with creeping fat, pseudo- sacculation between strictures. ©Cleveland Clinic Foundation 2019.

The first and second part of duodenum remained pliable without any evidence of disease, and the stomach was not excessively dilated. To expose the second and third parts of the duodenum, we mobilized the right colon and proximal transverse colon medially and Kocherized the duodenal c-sweep and head of the pancreas. We proceeded to perform a hand-sewn 2-layered duodenojejunal (DJ) bypass (Fig. 4) by bringing a loop of proximal jejunum, within 10 cm distal to the ligament of Treitz in a segment without any strictures, through a retrocolic mesenteric window. The intervening bowel between the proximal and distal ends of the stricture was left in situ. Step-by-step photographs of the anastomotic technique are shown in Supplementary File A. Interrupted seromuscular 3-0 slowly absorbable sutures were used for the back and front walls, while a single running full-thickness 3-0 slowly absorbable suture was used for the inner wall. An omental flap was constructed to close the mesenteric defect to prevent internal herniation, and a Stamm gastrostomy tube placed for gastric decompression given the chronic nature of the duodenal obstruction. The remaining small bowel strictures were managed using a combination of surgical techniques depending of the length of strictures, including 12 Heineke–Mikulicz (H–M) strictureplasty procedures for short (5–10 cm) strictures and 1 Finney strictureplasty for a 15-cm stricture (Fig. 5). Step-by-step photographs demonstrating the H-M technique are shown in Supplementary File B. There were clusters of mid-distal ileal strictures that were not amenable to strictureplasty and were managed by resecting 75 cm of ileum and a stapled anastomosis. A total of 500 cm of small bowel remained in situ at the end of the case.

FIGURE 4.

Gross intra-operative photo, handsewn duodenojejunal bypass (left, marked by long suture) and a Heineke–Mikulicz strictureplasty (right). ©Cleveland Clinic Foundation 2019.

FIGURE 4.

Gross intra-operative photo, handsewn duodenojejunal bypass (left, marked by long suture) and a Heineke–Mikulicz strictureplasty (right). ©Cleveland Clinic Foundation 2019.

FIGURE 5.

Gross intra-operative photo, 12 handsewn Heineke–Mikulicz and a single Finney strictureplasty. ©Cleveland Clinic Foundation 2019.

FIGURE 5.

Gross intra-operative photo, 12 handsewn Heineke–Mikulicz and a single Finney strictureplasty. ©Cleveland Clinic Foundation 2019.

The patient was recovered on an enhanced recovery pathway. A nasogastric tube was not used postoperatively, and the gastrostomy was left to gravity drainage for the first 48 hours. He then resumed a clear liquid diet with nutritional supplements (Ensure Clear) 2 days after surgery. An upper gastrointestinal series with water soluble contrast was performed day 5 which showed no anastomotic leak. He was discharged 6 days after surgery. He was tolerating soft diet and remained well. At the 6 weeks visit, he had gained weight and experienced no post-operative complications and resumed on anti-TNF therapy.

DISCUSSION

Duodenal strictures remain a rare clinical entity in patients with CD with reported incidence ranges from 0.5 to 4.0%.1 The duodenal bulb tends to be the most commonly affected site.2 Optimal management of these complex patients requires a multi-disciplinary team approach. Fixed fibrostenotic disease requires mechanical intervention.

Endoscopic balloon dilatation (EBD) is a safe and feasible option in managing short segment upper GI strictures secondary to CD. In a pooled analysis evaluating technical efficacy of EBD in CD-related ileal strictures, technical and clinical success rates were 89.1% and 80.8%, respectively.3 Unlike ileal disease, there is paucity of data in regard to the use of EBD for CD-related upper tract strictures. Recent published case series from the Cleveland Clinic reported high technical success rate (93%) and clinical efficacy (88%) of EBD for short segment strictures (<5 cm). Although 47% of duodenal strictures required re-dilatation within the follow-up period of 23 months, none in this series required surgical intervention.4

Importantly, EBD can be used to a “bridge to surgery” to facilitate enteral feeding as nutrition optimization in perioperative period in patients with CD-related duodenal stricture is crucial. On the basis of the most recent European Society for Parental and Enteral Nutrition (ESPEN) guidelines, enteric feeding is recommended with modified texture and exclusive enteral nutrition in our case was well tolerated even without EBD.5 Another option to consider for nutritional optimization in these cases is poststenotic enteric feeding via endoscopic or radiographically placed feeding tubes, with total parental nutrition reserved for those with severe malnutrition or who cannot tolerate enteric feeding.5

Long segment strictures in third part of duodenum (D3) pose a significant challenge owing to its strategic location in relation to major vasculature of the small bowel and the pancreas. Surgical options for duodenal strictures CD range from least to most morbid. Least invasive is H-M strictureplasty which is interesting as the original indication for this procedure was peptic ulcer disease-related duodenal strictures. When performing H-M strictureplasty on the duodenum, care must be taken to avoid the ampulla and pancreaticoduodenal structures, and the rate limiting step is the stricture length and location, with this choice being obviated for long (>10 cm) strictures or those involving the third/fourth portion of the duodenum. Historically, the next option includes gastroduodenal bypass with a gastro-jejunostomy, although other variations exist such as duodeno-duodenal bypass and DJ bypass as in this case. Antecolic or retrocolic gastrojejunal bypass has historically been the work-hose bypass in these cases, but patients are at risk of developing marginal ulcers and dumping syndrome, and given widespread antacids, vagotomy has become a lost art. Finally, resection in this area may be accomplished, including pancreas-sparing duodenectomy and pancreaticoduodenectomy (Whipple’s procedure); however, these approaches carry significant morbidity and, given a normal pancreas, Whipple procedure for CD has been abandoned and relegated to the history books. Jejunal resection in this region is the less favorable option as mobilization of D3 can be technically difficult and carries risk of pancreatic leak and superior mesenteric vessels injuries.

To date, literature in surgical management in CD-related duodenal stricture is limited due to their low frequency. In 1999, Worsey et al. published their experience from the Cleveland Clinic describing the surgical outcome of 34 patients with predominantly proximal duodenal strictures. Although symptomatic improvement was observed in both groups with similar recurrence rate, the author advocated the use of strictureplasty in order to avoid dumping syndrome and marginal ulcers seen after gastrojejunal bypass.6 In the same year, conflicting results were reported in a retrospective series originating from Birmingham, the United Kingdom. Yamamoto et al. reported high anastomotic leak rate in the strictureplasty group (2 out of 13 patients, 15%); in addition, nearly half (6 out of 13 patients, 46%) required reoperation due to stricture recurrence.7 Nonetheless, results based on more contemporary series suggest that each surgical technique such as strictureplasty, bypass and resection each has a unique role and these options need to be tailored to strictures characteristics (number, length, and location) and patient’s co-morbidities.8,9 An update of the Cleveland Clinic experience with both stricturing and fistulizing upper track CD is forthcoming.10 Nonetheless, the report herein represents one of the few, if not only, reports of the successful use of DJ bypass in CD. It is more physiologic as it minimizes dumping syndrome and marginal ulcer which occur in 10% of patients who had gastro-jejunostomy for duodenal CD.6 DJ bypass is a safe alternative and is easy to perform without the need of excessive mobilization.11,12

Of note, the construction of our bypass was facilitated by several factors. First, the most proximal segment of jejunum was free from strictures for a length of about 10 cm, which gave a soft pliable segment to work with, and also allowing the diverticularized segment of strictured duodenum to drain both proximally and distally. Second, the patient had a favorable anthropoid body habitus, specifically he was tall and thin with minimal visceral adiposity with a thin mesocolon and obvious bare area between the ascending and middle colic vasculature, all of which facilitated swinging the jejunal loop through the mesenteric defect. Finally, the mesentery of this loop was soft and pliable, and not foreshortened.

CONCLUSIONS

CD resulting in duodenal strictures is rare, and a multidisciplinary approach and optimizing preoperative nutrition are paramount to ensure superior outcomes. Perioperative management of biologics requires close liaison between gastroenterologists and IBD surgeon. Surgical management of duodenal strictures can be managed by endoscopic balloon dilation or strictureplasty in most cases. Bypass is the alterative option with minimal morbidity. DJ bypass is a feasible option, particularly for long strictures of the third portion of the duodenum, and should be in armamentarium of an IBD surgeon.

Conflict of interest: FR is consultant to Allergan, AbbVie, Boehringer-Ingelheim, Celgene, Cowen, Gilead, Gossamer, Helmsley, Jannsen, Koutif, Metacrine, Pliant, Pfizer, Receptos, RedX, Roche, Samsung, Takeda, Thetis, UCB and receives funding by NIH, Cleveland Clinic, UCB, Celgene and Pliant.

REFERENCES

3.

Bettenworth

D

,

Gustavsson

A

,

Atreja

A

, et al. 

A pooled analysis of efficacy, safety, and long-term outcome of endoscopic balloon dilation therapy for patients with stricturing Crohn’s disease

.

Inflamm Bowel Dis.

2017

;

23

:

133

142

.
4.

Singh

A

,

Agrawal

N

,

Kurada

S

, et al. 

Efficacy, safety, and long-term outcome of serial endoscopic balloon dilation for upper gastrointestinal Crohn’s disease-associated strictures—a cohort study

.

J Crohns Colitis.

2017

;

11

:

1044

1051

.
10.

Schwartzberg

D. JA

,

Holubar

SD

,

Steele

SR

,

Shen

B

,

Stocchi

L

,

Hull

T

,

Shawki

S

.

Duodenal strictures in Crohn’s disease

.

Diseases of the Colon and Rectum

.

2018

;

61

:

P140

.
11.

Zilberstein

B

,

Sorbello

MP

,

Orso

IR

,

Cecconello

I

.

Laparoscopic duodenal-jejunal bypass for the treatment of duodenal obstruction caused by annular pancreas: description of a surgical technique

.

Surg Laparosc Endosc Percutan Tech.

2011

;

21

:

e60

e64

.

© 2019 Crohn’s & Colitis Foundation. Published by Oxford University Press on behalf of Crohn’s & Colitis Foundation.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact [email protected]

Download all slides

Sours: https://academic.oup.com/crohnscolitis360/article/1/1/otz002/5486289

You will also like:

At the first opportunity, as soon as he was alone, he pulled his hand to his fly and began to wrinkle himself through his. Jeans. It was getting harder and harder to hold back. His cock was like wood and whined sweetly.



556 557 558 559 560