Failed anti-reflux surgery: Causes and management

Failed anti-reflux surgery: Causes and management

Hany Rafik1, MD; Amr Kamel1, MD; Ahmed Nafei1, MD; M. Magdy1, MD; Ibrahim N. Elwardany2, MD

1) Department of General Surgery, Ain Shams University, Cairo, Egypt.

2) Department of General Surgery, Misr University for Science and Technology, Cairo, Egypt.

Background: Failure of anti-reflux surgery means persistence of the previous symptoms of gastro-oesophageal reflux disease (GERD) or appearance of new symptoms of over correction after surgery. This needs a careful evaluation & management. The aim of this study is the diagnosis of the causes of failed anti-reflux surgery and to select patients who are in need for re-do surgery.

Patients and methods: Over a 31-month period (April 2009 to October 2011), 31 patients (mean age 39.44 ± 7.5) presented with symptoms of failed anti-reflux surgery starting shortly after the primary surgery. 18 patients (58.1%) were complaining of symptoms of recurrence and 13 patients (41.9%) were complaining of symptoms of overcorrection. Conservative management was tried first and the integrity of the previous fundoplication was evaluated by upper endoscopy, barium oesophago-gastrogram, manometric studies and 24-hours ambulatory pH monitoring.

Results: 11 patients (35.4%) were managed conservatively, 4 patients (12.9%) required oesophageal dilatation and 16 patients (51.6%) were in need for revision of the primary surgery. Improvement was noted in all patients with redo surgery, only 3 patients developed postoperative dysphagia that was managed conservatively.

Conclusion: The rate of redo surgery may be further reduced by a meticulous surgical technique; redo surgery should be offered for only selected patients with failed anti-reflux surgery and should be done by an experienced surgeon to ensure the best results.

Key words: Gastroesophageal reflux disease, fundoplication, re-do.

Introduction:

Laparoscopic     fundoplication     became the gold standard in the surgical therapy of GERD. In comparison with open procedures, laparoscopic antireflux surgery has a lower morbidity rate, a better early and late postoperative outcome and is more cost- effective. Laparoscopic 360 degrees Nissen- fundoplication with crurorrhaphy is the standard procedure, whereas the 270 degrees Toupet technique is the technique of choice for oesophageal motility disorders.1

Despite the variety of surgical operations and strategies employed, the overall failure rate is constant at approximately 11%–14% and almost 4%–7% of dissatisfied patients require a re-operation.2

Failure of anti-reflux surgery means persistence    of    the    previous    symptoms or   appearance   of   new   symptoms   after surgery and this needs a careful evaluation. Investigations should be directed at both the original preoperative evaluation and current situation. Esophageal manometry might show borderline function predisposing to persistent symptoms postoperatively. The operative report  should  be  obtained  and  reviewed, with attention to such details as esophageal length, use of a dilator to size a wrap, closure of the hiatus, and division of the short gastric vessels.3

Unsuccessful results of surgery for GERD whether associated with hiatal hernia (HH) or not, is a frustrating event for the surgeon,

Ain-Shams J Surg 2014; 7(2): 231-240                                                                                                                                                                                                          231

but far more so for the patient because of the well-known poor quality of life.4

The aim of this study is the diagnosis  of the  causes  of failed  anti-reflux  surgery  and to select patients who are in need for re-do surgery.

Patients and methods:

This prospective, randomized study was conducted in Ain Shams university hospitals from  April  2009  to  October  2011.  A total of 31 adult patients with failed anti-reflux surgery   shortly  after  the  primary   surgery within the first 1-3 months were included in the study. Eleven patients (35.5%) were with previous laparoscopic fundoplication and twenty patients (64.5%) were with previous open fundiolication.

These     patients      were      assessed      for

either   recurrence   of  symptoms   of   reflux or   appearance   of   new   symptoms   which were symptoms of overcorrection such as dysphagia and gas-bloat syndrome, and then the need for repeated surgery was assessed. Any patient with preoperative dysphagia was excluded from the study.

These  patients  were  classified  into  two

groups.  The  1st group  who  complained  of recurrence of symptoms and the 2nd group who complained  of symptoms  of  overcorrection like dysphagia and gas bloating syndrome.

The  diagnosis   of  recurrence   was  made

in  out   patient  clinic   on  basis  of  typical history including recurrent heart bum and regurgitation or appearance of new symptoms like laryngitis, asthma or atypical chest pain.

In another group, the main complaint was

dysphagia and gas bloating. Assessment of dysphagia was done using the dysphagia scoring scale and the average score was between 1-3 Table (1).

The preoperative workup in all patients included upper gastrointestinal endoscopy (UGE)  and a barium study for visualization of the anatomical-morphological reason for failure.  In  addition,  esophageal  manometry and 24-hour ph monitoring were performed routinely in every patient preoperatively.

Diagnostic     24-h    pH    monitoring     was

performed    according    to    a   standardized

procedure   after  manometric   determination of the LES position. The pH electrode then was positioned 5 em above the upper border of the LES for evaluation of esophageal acid exposure. Patients were instructed to stop potential intake ofH2 blockers or proton pump inhibitors at least 1 week before monitoring. The existence of pathological acid reflux was defined as a DeMeester score13 >14.72.

The type of refundoplication  was tailored to the results of esophageal manometry. 360° Nissen fundoplication was performed in all patients with normal esophageal motility, whereas  patients  with  poor  esophageal motility  (a  pressure  of  <30  mm  Hg  in the lower esophageal segments in response to wet swallows) or disordered peristalsis (>40% simultaneous contractions in wet swallows) underwent 270° Toupet fundoplication or floppy Nissen fundoplication.

Operative  technique:  Revision  antireflux

surgery was more difficult than primary surgery for reflux, particularly if the previous procedure was performed using an open technique.  Open procedure was our protocol in recurrent surgery.

Anathesia: The operation was done under

general endotracheal anesthesia with muscle relaxant.

Positioning  and  instrumentation:  The patient was placed on the operating table in the supine position. The operating table was placed in a reverse Trendelenburg position. Excellent exposure  of the esophageal hiatus was paramount in performing an open procedure. This was achieved by utilizing an upper hand retractor  fit with two  blades for the right and left costal margins. Extra-long surgical   instruments   were  usually   needed for the operative procedure, especially when operating on men and obese patients.

Surgical steps: An uppermidline abdominal

incision was used for access. Proximally, this extended  between the  xiphisternum  and the left costal margin, and distally it finished just above or just below the umbilicus.

a)  Hiatal  Dissection:   Upper  abdominal

adhesions were dividedto exposethe operative field. The left lobe of the liver was usually adherent  to  the  anterior  wall  of  the  upper

_  :       --4

stomach   and  the  previous   fundoplication. This was first separated from the stomach to expose the hiatal region.

The left lobe of the liver was displaced forward  and to the right to expose the upper stomach and the region of the esophageal diaphragmatic  hiatus.  It was not  necessary to divide  the triangular  ligament  of the  left lobe of the liver to displace the lobe medially, except when the liver was enlarged.

The  tissue   planes  in  the   hiatal  region

were often difficult to find, and the hiatal rim and esophagus  were  dissected  with  caution to avoid perforation of the esophagus or stomach.  A nasogastric  tube  was  passed to aid  in the  identification  of  the  esophagus. It was important to mobilize  the  esophagus till  the  gastro-esophageal  junction  and  the upper  stomach.   This  was  done  anteriorly by dividing the adhesions from the stomach to the liver and diaphragm using sharp dissection. Posteriorly the lesser sac was entered and the stomach was dissected free from the pancreas and retroperitoneal tissues. The  vagal  nerve  trunks   were  difficult  to identify during revision and there was high incidence of division of at least one of them.

b)      Identification      of      the      previous

fundoplication: It was  only  when  the gastroesophagel junction and the proximal stomach were completely free that any assessment was made to know the cause of failure. In 6 patients, recurrence of symptoms was due to intrathoracic wrap migration and this required reduction of the herniated part. Restoration of the normal anatomy by fully reversing and breaking down the previous fundoplication.

c) Formation  of a new fundoplication  in

cases  of  recurrent  reflux: After  breakdown of the  wrap,  the  esophagus  was  mobilized and a retroesophageal  window was created. The right and left crura and the crural commissure   were  dissected  exactly.  After exact identification of the hiatal crura, crural closure   was   performed   using   interrupted

2-0   non-absorbable    polyprolene    sutures.

After closing the crura posteriorly, the esophagus   was  lying  loose  in  the  hiatus. An oval sheet was cut out of a 10 x 15-cm

polypropylene  mesh which we normally use for hernial repair. For the esophageal body, a

3- to 4-cm keyhole in the center of the oval mesh was cut out. After bringing the mesh intra-abdominally, it was placed around the esophagus  at the  gastroesophageal  junction, so that the esophageal body was lying through the keyhole of the mesh. The circular mesh was fixed onto the diaphragm by interrupted

2-0 non-absorbable  polypropylene sutures.

It was  usually  necessary  to  make  sure that all short gastric vessels were ligated and divided in order to have enough stomach to carry out a good fundoplication Figure (1).

The stomach  was then grasped  with two

pairs of long non traumatic Babcock forceps, and manipulated to ensure that it came around the back of the esophagus loosely. If the stomach was tight, and did not sit comfortably without undue tension, the Babcock forceps was progressively adjusted and a looser piece of  stomach   grasped.   This  was  continued until a satisfactorily  loose piece of stomach was identified. Three interrupted 2-0 non­ absorbable  polyprolene  sutures  were placed to  form  the  fundoplication   (either   Nissen or Toupet). The sutures were passed deeply through the serosa and muscle of the stomach wall on both sides, and also more superficially through the muscle ofthe esophageal wall.

d)  Formation  of a new fundoplication  in

cases of dysphagia: The hiatus was routinely repaired without mesh (except in one patient who was having para-oesophageal herniation) using posteriorly placed sutures. These should narrow  the  hiatus  to  approximately  2.5 em in  diameter.  To  do  this,  the  reconstructed hiatal rim sat loosely (not tightly) around the esophagus  with  a 52 Fr bougie sited across the  gastroesophageal  junction.  At the  time of Nissen fundoplication  a 56 Fr bougie was advanced orally through the hiatus by the anesthesiologist.

Follow-up :Arrangements were made for

clinical follow-up review in the out patient clinic  at  3,  6  and   12  months.  Objective follow-up investigations through 24-hour pH monitoring and esophageal manometry were performed 6 & 12 months later.

Statistical methodology: Data analysis was

Am-ShamsJSurg2014; 7(2):231-240

performed with SPSS version 12.0 (SPSS, Chicago,IL).  Frequencies  were  used  to describe statistics for qualitative categorical variables. Nonparametric variables are expressed as median (range), and normally distributed variables are expressed as mean (±standard deviation), Paired t-test was used to compare quantitative  variable in the same group, P value >0.05 insignificant P<0.05 significant P<O.01 highly significant.

Results:

31 patients entered the study, 14 (45.1%) of them were males and 17 (54.9) were females Table (2), ranging from 27 to 52 years (mean age  39.44  ±7.5).  Eleven  patients  (35.5%) with   previous   laparoscopic   fundoplication and  twenty  patients  (64.5%)  with  previous open fundoplication.

These  patients  were  classified  into  two

groups.   The   1st  group   who   complained of   recurrence   of  symptoms   and  the   2nd group who complained of symptoms of overcorrection  like  dysphagia  and  gas bloating syndrome Table (3).

Redo surgery was performed to 12 out of

18 patients from the recurrence  group and 4 patients out of  13 from the dysphagia group. The operating  time varied between 120 and

230 min depending on the extent of intra­ abdominal adhesions; there were no intra­ operative complications.

As regard the recurrence group they were

18 from 31 (58.1%), 8 males and 10 females.

2  patients  from  the  recurrence  group  were also complaining of dysphagia. 12 pattients underwent intially Nissen fundoplication (66.7%) and 6 patients underwnt initially Toupet fundoplication (33.3%).

Medical treatment started first which consisted  mainly of proton  pump inhibitors and life style modification for 3-5 months and this was very effective only in 6 patients and all were having Nissen fundoplication.

Investigations  were done for the other 12

patients of the recurrence group who failed to have complete relief of symptoms on medical treatment  and included  UGE, barium  study,

24-hours   pH   monitoring   and   esophageal

manometry.

Barium    study    revealed     intrathoracic wrap  migration   in  6  patients   Figure (2), UGE  revealed  oesophagitis  in  all of  them; pH monitoring revealed DeMeester score between 52 and 56 (mean 54.0 ± 8.3). Esophageal manometry revealed lower oesophageal   sphincter   (LES)  pressure between 5 and 9 mm Hg (mean 6.9± 0.6).

Intra-operative findings in the 12 patients revealed intrathoracic wrap migration in 6 patients  (50%), fundoplication  disruption  in

4 patients (33.3%) due to poor ligation and division  of  the  short   gastric  vessels,   and slipped fundoplication in 2 patients (16.7%) Table (4), Figures (3,4).

Nissen       or      Toupet      refundoplication

was done according to the pre-operative manometric findings as mentioned before.

As regard the dysphagia group they were

13 from 31 (41.9%),  5 males and 8 females.

12 pattients  (92.3%)  underwent  intially Nissen fundoplication  and  1 patient  (7.7%) underwnt initially Toupet fundoplication.

The 13 patients were treated  with dietary

modification and reassurance, the dysphagia resolved  spontaneously   within  2-3  months in 5 patients out of 13. However 8 patients experienced  dysphagia that persisted beyond

3 months.

Investigations  were  done  in these  8 patients  and  included  UGE,  barium  study,

24-hours pH monitoring and esophageal manometry.  UGE  and barium  revealed  that the   previous   fundoplication   had   resulted in a mechanical obstruction of the lower esophagus   in  5  patients;  barium   revealed para-oesophageal  herniation  in 1 patient. Esophageal manometry revealed resting LES between 20 and 35 mm Hg. (mean 29± 0.6) in the 8 patients. 24-hours pH monitoring was normal in all.

7 out of the  above mentioned  8 patients

(apart from the patient with para-oesophageal herniation) required a single session of dilatation with polyvinyl bougies to a mean diameter of 18 mm (54 Fr gauge). This was very effective in 3 out of 7 patients. 2 months later, the remaining 4 patients underwent another    session   of   pneumatic    dilatation

using 30 mm to 40 mm diameter  balloons;

_  :       --4

Figure (1): Ligation and division of short gastric vessels.

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Figure (3): Causes of failure of anti-reflux surgery in our study.

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Figure (5): shows the type of treatment in relation to the Jsl fundoplication.

this was vety effective in 1 out of 4 patients. The remaining 3 patients were scheduled for redo surgery adding to them the patient with

Figure      (2):     Barium     study     showing intrathoracic wrap migration.

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Figure (4): Cause of failure in relation to the first }undoplication.

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Figure (6): Types offundoplicationfailures. A: Disrupted wrap. B & C: Slipped fundoplication. D: Intrathoracic migration of the fundoplication.

para-oesophageal hemiation.

Intra-operative, a para-oesophageal  hiatus hernia wasa cause of post-operative dysphagia

Table (1): Scoring  system for dysphasia.

Table 2: Sex distribution.

Table 3 : Type of failure.

Table 4: Showing causes of failure of anti-reflux failure in our study.

Table 5: Showing summary of treatment after failure.

as mentioned before  in one patient,  too tight fundoplication was  found   in  2 patients   and too  long fundoplication (4 em)  in 1 patient.

Floppy  Nissen  was done for these  4 patients Tables (4) Figures (3,4). Table  (5)  shows  that  16  patients   out  of

_  :       --4

Table 6 : Showing  treatment after failure in relation to the type of first surgery.

Table (7): Lists the causes of persistent postfundoplication dysphagiaJ 3

31  (51.6%)  with  failed   anti-reflux surgery were in need for revision of fundoplication through  a redo  surgery,  11 patients  (35.5%) were managed conservatively, and 4 patients (12.9%)  required  endoscopic dilatation.

Table (6) shows the type of treatment after failed  anti-reflux surgery  in relation to the 1st fundoplication and  reveals   that  concerning the redo surgery there is no significance difference whether the patient had underwent Nissen  or Toupet (P>0.05), however oesophageal  dilatation  was   more   common with Nissen fundoplication Figure (5).

As     regard     the     recurrence     group Significant improvement in heart bum and regurgitation was  noted  in this  group,  with no difference between those who underwent Nissen refundoplication and those who underwent Toupet. However  3 patients experienced mild dysphagia to solids in those who   underwent  Nissen  fundoplication that was managed  conservatively and disappeared after 3 months.

One patient had a gastric perforation which was diagnosed on the 3rd postoperative day, the  patient  was  re-explored with  closure  of the  perforation over  a gastrostomy tube  and insertion  of a feeding jejunostomy tube.

Objective     follow     up:     24-hour     pH monitoring:    Esophageal    acid     exposure improved    significantly  after   surgery.   The preoperative mean DeMeester score of 54.0 ± 8.3 decreased significantly to 14.7 ± 3.8 at 6 months  (p=O.OOl) and to 13.8 ± 5.4 at 1 year.

Esophageal manometry : The pre-operative mean  resting  LES  pressure  of  6.9±  0.6  mm Hg increased to 13.6± 0.6 after 6 months  and to 13.1± 0.4 after  1 year.

As regard the dysphagia group : Significant

improvements in dysphagia was noted in this group.

Esophageal      manometry          The     pre-operative  mean resting LES pressure  of mean 29 ±0.6  mm  Hg has  decreased to 16.6  ±0.4 after 6 months  and to 15.5 ±0.8 after 1 year.

Discussion:

Fundoplication  either   Nissen   or  Toupet is  the  most  popular   of  the  anti-reflux procedures in patients with GERD. Failure of fundoplication occurs  when the patient,  after the repair, experiences persistent or recurrent reflux symptoms, or develops new symptoms as inability to  swallow   normally,  or  suffers from  upper abdominal discomfort or other gastrointestinal  symptoms.  The  assessment of   these   symptoms  and   the   selection   of patients  who  need further surgery  remains  a challenging problem.4

Persistent or recurrent postoperative reflux symptoms    are   usually    due   intrathoracic wrap migration, wrap disruption, slipped fundoplication, twisting of the fundoplication and   improper   construction    of   the   wrap using the body rather than the fundus of the stomachS Figure (6).

Intrathoracic  wrap  migration  can  occur due to  inadequate  crural closure,  disruption of the crural repair, insufficient esophageal mobilization,  shortened  esophagus or severe retching soon after surgery. Recent studies recommend prosthetic hiatal closure in cases of recurrence.6

Gamderath  et aF showed  that in a study that included 33 patients who underwent laparoscopic refundoplication for recurrent symptoms of GERD after primary failed laparoscopic or open antireflux surgery, the underlying      morphological      complication for symptom recurrence in all patients was intrathoracic migration ofthe fundoplication.

In our study 6 patients out of 12 patients who underwent redo for recurrent symptoms were having a migrated fundoplication.

Wrap disruption is one ofthe most common causes  of failure. It frequently  occurs early during the postoperative course. This reflects the widespread use of absorbable suture material when creating the wrap, inadequate suture   technique    (i.e.,   taking   inadequate bites of tissue)  and insufficient mobilization of the fundus may also contribute to wrap disruption.8

In our study 4 patients out of 12 patients who underwent redo for recurrent symptoms were having a wrap disruption.

A  slipped  fundoplication   "the  so-called telescope   phenomenon"  can  occur  in  two ways:  (1)  The  fundoplication   is  fashioned in the correct location, but a portion of the stomach    later   herniates    "slips"    through the  fundoplication;  or (2)  The surgeon mistakes the proximal stomach for the distal oesophagus, and inadvertently fashions the fundoplication  around the stomach. Although the  later situation represents a technical surgical error rather than a true slippage, the condition is called a slipped fundoplication despite the misnomer.

Type  (1)  slippage  usually  occurs  if the sutures are not passed through the esophageal wall. Type (2) slippage occurs due to unrecognized esophageal shortening and inadequate mobilization of the esophagus leading to a wrapping of stomach around stomach,   rather  than  stomach   around  the lower esophagus. Patients with slipped fundoplication usually complain of both heartburn and dysphagia occurring after a symptom free postoperative interval.9

In our study 2 patients were having a slipped fundoplication  and they were complaining of both heart bum and dysphagia but the most annoying complaint was recurrence of heart bum and that's why they were categorized in the recurrence group.

For patients with persistent or recurrent symptoms   after  fundoplication,   endoscopy can answer  several important  questions. (1) Is  there  reflux  oesophagitis?  The  presence of reflux oesophagitis provides objective evidence that the operation has not controlled GERD. (2) Is there any another lesion that can explain the symptom as gastric or duodenal ulcer.  (3)  Does  the  fundoplication   appear to be anatomically correct? Fundoplication creates characteristic folds in the proximal stomach  that usually  can be seen  best with the  endoscope   in  the  retroflexed  position. If the folds  are  seen  above the  diaphragm, it   indicates   wrap   migration.   If   there   is a  pouch  of  the  stomach   proximal  to  the folds of fundoplication, it indicates slipped fundoplication. Finally, the absence of fundoplication folds suggests total disruption ofthe wrap. 10

In our study, all patients  who underwent redo for recurrent symptoms were having oesophagitis,  and  were  negative  for  peptic ulcer   but   unfortunately    the    endoscopist did not aid us to identify the anatomical or morphological problem of the failed wrap.

Ambulatory   monitoring    of   esophageal pH  is also  an important  diagnostic tool  for patients with persistent or recurrent symptoms after  fundoplication,  the  demonstration   of abnormal  acid reflux  and the  correlation  of symptoms with reflux episodes establish that the operation  has failed at its primary  goal.

However   para-oesophageal   herniation   and

_  :       --4

anatomical  relationships  among  organs may be better appreciated by barium studies.ll

Approximately 50% of patients experience dysphagia immediately after fundoplication, presumably  as a consequence  of the  edema and inflammation caused by surgery. The patients  are treated  by dietary modifications and reassurance, and the dysphagia usually resolves spontaneously within 2-3 months.l2

In cases of postfundoplication  mechanical dysphagia as a result of too long or too tight wrap or if the diaphragmatic  crural repair constricts the  oesophagus,  dilatation  can relive  the  dysphagia  in  50-70%  of  cases. For  patients  who  have  dysphagia   due  to slipped fundoplication or para-oesophageal herniation, dilatation therapy usually will fail and  re-operation  will  be necessary  in most cases. 10

The creation of a too tight or too long wrap is manifested by persistent dysphagia starting shortly after the anti-reflux procedure. Postoperative manometry in these patients shows a high-pressure  sphincter which  does not relax on swallowing.l2

In our study, dilation was effective in 4 out of 7 patients (57.2%) who showed failure to conservative management of postoperative fundoplication   dysphagia,   this   percentage is relatively  low when compared  with other studies.

In a similar study, dilation was successful to  relieve  dysphagia   in   12  of  18  (67%) patients.l3

Summing up all available data and studies, failure rates of primary fundoplication  range as high as 30%.14 However, there is a lack of clarity concerning how failure is defined and what  the  therapeutic   consequences   should be. For example, what ifthe symptom is still present but only improved to the point that it is more tolerable  or more readily controlled with medication?  Is that a failure or an incomplete success?l5

In our own clinical practice, the usual definition of failure is a combination of recurrent or persistent gastroesophageal reflux disease  (GERD)  symptoms  or  appearance of   new   symptoms   developing    from   an anatomical   or  morphological   complication that usually needs a redo surgery.

Conclusion :

This analysis of the reasons for failure fundoplication  indicates  that  several factors are   essential   for   a   successful    outcome after  fundoplication.   These  are:  1)  a meticulous surgical technique: careful fundic mobilization, secure diaphragmatic closure, esophageal   lengthening   construction   of  a wrap of optimum length (not too long and not too short) better around a large bougie. 2) The identification and careful selection of patients who might  benefit from  anti-reflux surgery; and 3) a sound interpretation of the data taken from oesophageal manometry and 24-hours ambulatory pH monitoring. Attention to these factors will avoid failures in most instances.

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2-   :Migliore M, Jeyasingham K: Re-operations for failed anti-reflux surgery. Lessons from the past and prospects for the future. Ann ]tal Chir 2009; 80: 267-274.

3-   Siewert   JR,   Isolauri   J,   Feussner   H: Reoperation following failed fundoplication. World J Surg 1989; 13: 791.

4-   Horgan S, Pohl D, Bogetti D, Eubanks T, Pellegrini C: Failed antireflux surgery. What have we learned from reoperations? Arch Surg 1999; 134: 809-817.

5-   Warting        JP:          Management        of postfundoplication   complications.  Semin Gastrointest Dis 1999; 10: 121-129.

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