Laparoscopic short floppy Nissen fundoplication for gastroesophageal reflux disease

The original fundoplication technique as described by Rudolf Nissen in 1955 consisted in wrapping the fundus of the stomach around the esophagus, while leaving the gastrosplenic vessels and the diaphragmatic hiatus intact. Additionally, the vagus nerves were little or not preserved. The basic principles of a fundoplication are: - tension-free repositioning of the gastroesophageal junction (along with 2 cm of lower esophagus in a subphrenic position); - use the gastric fundus to create the fundoplication; - make sure that the resistance generated by the anti-reflux mechanism matches the preoperative assessment of esophageal peristalsis.

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Laparoscopic   short   floppy   Nissen   fundoplication   for   gastroesophageal   reflux   disease

Authors
B Dallemagne
Abstract
The original fundoplication technique as described by Rudolf Nissen in 1955 consisted in wrapping the fundus of the stomach around the esophagus, while leaving the gastrosplenic vessels and the diaphragmatic hiatus intact. Additionally, the vagus nerves were little or not preserved.
The basic principles of a fundoplication are:
- tension-free repositioning of the gastroesophageal junction (along with 2 cm of lower esophagus in a subphrenic position);
- use the gastric fundus to create the fundoplication;
- make sure that the resistance generated by the anti-reflux mechanism matches the preoperative assessment of esophageal peristalsis.
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2006-11
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WeBSurg.com, Nov 2006;6(11).
URL: http://www.websurg.com/doi-ot02en331.htm

Laparoscopic   short   floppy   Nissen   fundoplication   for   gastroesophageal   reflux   disease

1. Introduction
The original fundoplication technique as described by Rudolf Nissen in 19551 consisted in wrapping the fundus of the stomach around the esophagus, while leaving the gastrosplenic vessels and the diaphragmatic hiatus intact. Additionally, the vagus nerves were little or not preserved.
The modern tools of study when analyzing the physiology of the proximal digestive tract and the review of clinical results have led to numerous changes to the original concept.
The complete 360-degree wrap (“Nissen” fundoplications) is currently more used than the partial fundoplications (Toupet 270-degree fundoplication, 240-degree Guarner wrap, Dor or partial 180° and anterior fundoplication2,7, etc.).

The basic principles of a fundoplication are:
- tension-free repositioning of the gastroesophageal junction (along with 2 cm of lower esophagus in a subphrenic position);
- use the gastric fundus to create the fundoplication;
- make sure that the resistance generated by the anti-reflux mechanism matches the preoperative assessment of esophageal peristalsis.
2. Types of total fundoplications
There are two different types of total fundoplication.

1. Nissen-Rossetti fundoplication:
The technique was described by Mario Rossetti, one of Nissen’s pupils8.
Technical features:
- mobilization of the cardioesophageal junction by division of the phrenoesophageal membrane;
- mobilization of the fundus by division of the gastrophrenic ligament;
- creation of a 360° fundoplication fashioned with the anterior wall of the fundus which is brought to the anterior aspect of the esophagus, without systematic division of the short gastric vessels.

2. Laparoscopic short floppy Nissen fundoplication:
The full concept of this fundoplication was introduced by Donahue and Bombeck in 19779, and accredited by DeMeester in 198610.
Technical features:
- mobilization of the cardioesophageal junction by division of the phrenoesophageal membrane;
- mobilization of the gastric fundus by division of gastrosplenic ligament, short gastric vessels and gastrophrenic ligament;
- short (<2 cm) 360-degree fundoplication fashioned with the posterior and anterior walls of the fundus which are brought to the anterior aspect of the esophagus.

One same denomination is used for two slightly different techniques, even though they obey to the same original concept.
The technique described in this chapter is the “short floppy Nissen”. It respects the basic principles of the Nissen fundoplication whilst insisting particularly on the necessity of both restoring a segment of intra-abdominal esophagus in a tension-free manner and carrying out an efficient and systematic repair of the crura11,12.
3. Anatomy
• Anatomy
1. Lesser omentum
2. Left liver lobe
3. Esophageal hiatus
• Lower esophagus
The lower esophagus may be divided into 3 portions from cephalad to caudal:
1. a sub-diaphragmatic portion often referred to as “ampullar region”, without there being a real ampulla anatomically speaking. It corresponds to a zone often exposed to negative intrathoracic pressure, anterior to a high pressure zone.
2. a high pressure zone: it corresponds to the diaphragmatic zone and to the lower esophageal sphincter (LES).
3. an intra-abdominal segment or “vestibule”. Its linking with the stomach creates the angle of His (esophagogastric angle).
The squamoglandular junction, Z line, can be found in 60% of cases 1 cm above the gastroesophageal junction.
• Attachments lower esophagus/stomach
The phrenoesophageal membrane is composed by the transversalis fascia on the inferior surface of the diaphragm and by elements of the endothoracic fascia. This important structure links the lower esophagus to the diaphragm allowing vertical movements during breathing. It inserts itself circumferentially on the muscle structure of the esophagus and around the junction of esophageal and gastric mucosa.
• Short gastric vessels
The short gastric vessels originate from the splenic artery. They run along the posterior surface of the stomach, in the gastrosplenic ligament and end on the fundus of the stomach.
1. Gastrosplenic ligament
2. Splenic artery
3. Left kidney
4. Toldt’s fascia
5. Diaphragmatic crura
• Diaphragm and diaphragmatic crura
The esophageal hiatus is the opening through which the esophagus and the vagus nerves enter the abdominal cavity. It is usually formed by the right diaphragmatic crus with a small contribution of the left crus. The right crus originates from the anterior (longitudinal) vertebral ligament that covers the lumbar vertebras. It then constitutes two muscular strips that cross each other, build the edges of the hiatus and merge anterior to the esophagus.
4. Classification of hiatal hernias
• Normal anatomy
1. Thoracic esophagus
2. Thoracic cavity
3. Right crus
4. Left crus
5. Abdominal esophagus
6. Gastric fundus
A hiatal hernia is a defect in the anatomy of the gastroesophageal junction: structures normally confined within the abdomen move through the hiatal orifice.

A hiatal hernia is often associated with gastroesophageal reflux disease (GERD). However, it can be present without GERD. Certain voluminous hernias can lead to specific symptoms (see chapter about Technique for laparoscopic treatment of giant hiatal hernias).
• Types of hiatal hernias
• Type I
In type I, or sliding HHs, the hiatal opening is enlarged and the phrenoesophageal membrane is circumferentially mobile, allowing part of the cardia to herniate itself above the diaphragm.
The phrenoesophageal membrane remains intact.

Most of type I hiatal hernias are symptom-free. The usual clinical consequence is the occurrence of GERD whose probability increases according to the size of the hernia.

The migration of the abdominal esophagus results in:
- the disappearance of the esophagogastric valve (EGV) due to the widening of the esophagogastric angle (angle of His);
- a weakening in the lower esophageal sphincter effect (LESE) due to the loss of normal anatomical relationships and lowered extrinsic (intra-abdominal) pressures
• Type II
Type II, or paraesophageal hernias, represent 5 to 15% of hiatal hernias.
Some of those may be associated with GERD, but above all they can lead to mechanical and ischemic complications.
They occur through a defect in the phrenoesophageal ligament. The gastroesophageal junction nevertheless remains in the abdominal cavity. The gastric fundus migrates towards the mediastinum.
• Type III
Type III hiatal hernias combine elements of type I sliding hernias with elements of type II hiatal hernias (i.e. defect of the phrenoesophageal membrane).
In some cases, the whole stomach lies in a supradiaphragmatic position and can rotate, turning into what is usually called the “upside-down stomach”.
• Type IV
Type IV hiatal hernias are characterized by a very large defect in the gastroesophageal membrane through which the stomach, but also other viscera may migrate to the mediastinum.
5. Antireflux barrier
• Antireflux barrier
The anti-reflux barrier corresponds to a high pressure zone that protects the esophagus against reflux of gastric substances that are highly corrosive and likely to cause damage.
The tone of the anti-reflux barrier results from of three elements: the lower esophageal sphincter, the diaphragm and its crura, and the muscular architecture of the gastric cardia (its most distal element). In addition, the tangential joining of the esophagus to the stomach constitutes an anatomical intragastric flap13,14.
• Lower esophageal sphincter
• Description
The lower esophageal sphincter corresponds to a muscular zone of the lower esophagus that extends 1 to 1.5 cm above and 2 cm below the junction between the gastric and esophageal mucosa (Z line). At that level, the architectural disposition of the muscular fibers of the cardia contributes in huge part to its basal tone.
1. Z line
• Sphincteric mechanism
The lower esophageal sphincter (LES) presents a basal tone that is determined by complex mechanisms: a neurologic control in which both the central nervous system and the peripheral and enteric nervous system intervene.
The LES tone is reinforced by contact with the right diaphragmatic crus (extrinsic component of the high pressure zone).
The simultaneous contraction of the cardia’s semi-circular muscle fibers and of the stomach’s oblique muscle fibers will determine the sphincteric mechanism (Korn O, Stein HJ, Richter TH, Liebermann-Meffert D. Gastroesophageal sphincter: a model. Dis Esophagus 1997;10:105-9).
Accentuation of the angle of His will also amplify the intragastric valve.
6. Operating room set-up
• Patient
- general anesthesia;
- endotracheal intubation;
- 30° reverse Trendelenburg;
- supine position, arms at a 90° angle and legs apart;
- dual lumen gastric tube;
- urinary catheter (not mandatory).
The reverse Trendelenburg position results in spontaneous lowering of the abdominal organs.
Anesthetic paralysis of the patient must be adequate to increase the space within the abdominal cavity and limit diaphragmatic movements.
The maximum operating pressure of the pneumoperitoneum will be 12 mm Hg.
Gastric clearance:
A dual lumen gastric tube is placed to decompress the stomach.
It is moved up to the middle third of the esophagus once the stomach has been decompressed before starting the esophageal dissection.
• Steep table position
To enable a steep reverse Trendelenburg position (30°), which is sometimes compulsory, especially for obese patients, the patient is strapped to the table with thick adhesive strips.
• Team
1. The surgeon stands between the legs of the patient.
2. The assistant stands on the patient’s left.
3. The scrub nurse stands on the patient’s right.
• Equipment
The monitor is used by the surgeon and the assistant.
1. The laparoscopic and video units are placed on the patient’s right, behind his shoulder.
2. Operating table
3. Anesthetic unit
7. Trocar placement
• Anatomical landmarks
1. Xiphoid process
2. Costal margin
3. Midline
4. Midclavicular line
5. Anterior axillary line
• Pneumoperitoneum
The pneumoperitoneum is established in normal fashion, with the usual precautions, at a maximal intraperitoneal pressure of 15 mm Hg.
• Trocars
Trocar A, size 10 mm (laparoscope), on the midline, 2/3 from the xiphoid to the umbilicus
Trocar B, size 5 mm (grasping forceps), on the epigastrium just below the xiphoid
Trocar C, size 5 mm (liver retractor), on the anterior axillary line just below the right costal margin
Trocar D, size 5 mm (atraumatic grasper), on the anterior axillary line just below the left costal margin
Trocar E, size 5 mm (dissecting and suturing devices), on the midclavicular line in the left upper quadrant
8. Instrumentation
• Placement
Trocar A: 0° laparoscope
Trocar B: Grasping forceps
Trocar C: Liver retractor
Trocar D: Atraumatic grasper, scissors, suction-irrigation device
Trocar E: Ultrasonic scissors, scissors, clip applier, suction-irrigation device, needle holder
• Optical device
A: Most procedures are completed using a 0° laparoscope.
A 30-degree laparoscope may be recommended, especially in stout patients as it will provide an easier access to the cardioesophageal junction.
• Operating devices
B: Grasping forceps
E: 5 mm ultrasonic scissors, 5 mm scissors, suction-irrigation device, needle holder
• Retracting devices
C: Liver retractor (atraumatic; it will be fixed onto an articulated arm, on the right of the operating table), expandable liver retractor
D: Atraumatic grasper
9. Exposure
• Hiatus approach
The liver retractor, held by a mechanical arm fixed to the right of the operating table, is used to lift the left liver lobe. The mechanical arm is then locked into position to maintain the retractor in the chosen position.
The assistant holds the laparoscope and retracts the cardia with an atraumatic grasper (through trocar D) using caudal and leftwards traction.
• Reducing the hiatal hernia
If present, the contents of the hiatal hernia is reduced and maintained in the abdomen with the assistant’s atraumatic grasper (through trocar D) placed on the fat pad anterior to the gastroesophageal junction.
10. Dissection/cardioesophageal junction
• Principles
The intervention begins with the mobilization of the gastroesophageal junction.
The successive dissection steps allow to identify the essential anatomical structures: the diaphragmatic crura, the esophagus, the vagus nerves, the mediastinal pleura and the aorta.
• Incision of pars condensa
The pars condensa (superior part) of the lesser omentum is opened whilst making sure to preserve the hepatic branch of the vagus nerve and the left hepatic artery. This phase helps to identify the right diaphragmatic crus, the essential anatomic landmark that needs to be identified before beginning the dissection of the esophagus.
• Dissection of right crus
Incision of the phrenoesophageal membrane is continued on the medial relief of the right crus.
Non-traumatic dissection of the cleavage plane that is found internal to the right crus allows to identify the position of the esophagus. Finding that area is facilitated by lifting the distal portion of the esophagus and the cardia anteriorly and to the left. That step allows access to the crura, the posterior edge of the esophagus and the posterior vagus nerve.
• Dissection of esophageal hiatus
Incision of the phrenoesophageal membrane and dissection of the left crus:
Once the position of the esophagus is identified, the phrenoesophageal membrane is opened transversally along the anterior border of the hiatal orifice and towards the left crus. At that level, a blunt dissection of the internal aspect of the crus is recommended to avoid damage to the anterior vagus nerve that may be found proximal to it.
The dissection is then continued towards the most posterior part of the crus to prepare the retroesophageal dissection.
• Dissection/posterior aspect of esophagus
• Retroesophageal window
Dissection of the posterior aspect of the esophagus allows to create the retroesophageal window. It is carried out from right to left posterior to the esophagus and in contact with the external border of the left crus.
The posterior vagus nerve is identified and retracted against the wall of the esophagus.
The window is created when the fat pad of the gastrosplenic ligament and/or the upper aspect of the spleen are visible.
Identification of such landmarks is essential during this dissection: the right crus and the left crus help to guide the dissection. A dissection performed above the left crus could lead to a pleural injury.
The adjacent anatomical structures must be clearly identified.
• Identifying the gastroesophageal junction
A Penrose drain or a loop, held with a grasper by the assistant (through trocar D), is passed through the enlarged retroesophageal window, and then placed around the esophagus. It permits to avoid any traumatic grasping of the organs and helps to mobilize the gastroesophageal junction in different directions during the next surgical steps.
11. Mobilization of esophagus
• Objectives
- to free the lower esophagus and cardia on their anterior and posterior aspects;
- to create a retroesophageal window of sufficient size to allow passage of the fundus;
- to sufficiently mobilize the esophagus in the abdominal cavity (and obtain a segment of esophagus more than 2 cm long inside the abdominal cavity in a tension-free manner).
• Dissection into mediastinum
Dissection of the esophagus into the mediastinum lengthens the abdominal portion of the esophagus. This portion should be at least 2 cm long without tension.
This dissection can be extended up to the pulmonary veins, if not to a greater length in some circumstances. The vagus nerves must systematically be identified and protected.
If the cardia cannot be lowered despite this dissection, further dissection of the esophagus into the mediastinum should be performed. A Collis gastroplasty procedure (i.e. elongation/lengthening of the esophagus) is advisable in the case of a short esophagus.
• Posterior dissection
Division of the posterior attachments of the cardia on the diaphragm allows to enlarge the retroesophageal window. The possibility of a left diaphragmatic artery crossing through that space must be kept in mind.
12. Mobilization of gastric fundus
• Operative protocol
The surgical technique described includes mobilization of the gastric fundus, which is used to create the antireflux valve.
Division of the gastrosplenic ligament, of two or three short gastric vessels, and in certain cases, of the posterior fundic artery makes up the essentials of this operative time.
• Gastrosplenic ligament
The gastrosplenic ligament is exposed using traction on the fundus of the stomach towards the patient’s right (trocar B) and lateral traction on the gastrosplenic ligament towards the patient’s left (trocar D).
The ligament is first divided to its cephalad origin where some fat folds may be found. Monopolar or bipolar cautery, ultrasonic scissors or a vessel sealing device may be used through trocar E.
• Division of short gastric vessels
Incision of the gastrosplenic ligament gives access to the omental sac.
Cephalad traction on the fundus (trocar B) exerts tension on the short gastric vessels and posterior attachments of the stomach. Retraction of the body of the stomach caudally and to the patient’s right helps to expose these structures (trocar D).
Two to three short gastric vessels are divided. Division of the posterior layer of the gastrosplenic ligament is continued cephalad. It is then followed by division of the gastrophrenic ligament. At the end of dissection, the left crus is entirely visible.
13. Cruroplasty
Plasty of the diaphragmatic opening should be performed routinely as it not only contributes to restoring one of the elements of the antireflux barrier but also stabilizes the antireflux wrap into the abdominal cavity.
The esophagus is retracted distally from the crura using the loop that is passed around the gastroesophageal junction (trocar D). Grasper and needle holder are used through trocars B and E.
Interrupted non-absorbable sutures are placed on the crura to repair the hiatal defect posterior to the esophagus.
At the beginning of the experience, it is recommended to place a 55 French bougie into the esophagus to accurately size the esophagus and avoid any strangulation.
Sutures may be placed anterior to the esophagus in cases of very large hiatal defects.
If the crura are fragile, Teflon pledgets might be useful to apply sutures.
Prosthetic reinforcement may be used when needed.
14. Creation of the fundoplication
• Principle
For Nissen fundoplications, the anterior and posterior walls of the gastric fundus are mobilized contrarily to Nissen-Rossetti fundoplications where the anterior wall only is mobilized.
• Retroesophageal passage
The esophagus is pulled up using the loop.
The posterior wall of the gastric fundus is brought to the right of the esophagus through the posterior esophageal window. The anterior fundic wall slides towards the posterior aspect of the esophagus.
Once tailored, the valve should be sufficiently stable without tension towards the spleen. When tension is still encountered, a wider mobilization of the stomach is to be performed to avoid any tension on the valve and prevent any twisting of the lower esophagus postoperatively.
• Adjusting the fundoplication
The valve should be positioned at the level of the Z line, 1 to 1.5 cm above the anatomical junction. It must always be positioned way above the omental folds.
The valve should be tailored using the gastric fundus. Caution must be taken not to fashion the valve with the body of the stomach as there is a risk of partitioning the stomach into two parts.
In case of doubt about the positioning of the fundoplication (especially in the case of short esophagus), it is recommended to perform an intraoperative esophagoscopy.
• Suturing/fixing the fundoplication
The two parts of the valve are joined together using three non-absorbable sutures.
The first most cephalad suture does not attach the valve to the esophagus. It helps to check the fundoplication, the absence of plications of gastric walls, and controls correct positioning of the valve on the esophagus.
The next two sutures complete the fundoplication and fix it to the anterior aspect of the esophagus and to the right of the anterior vagus nerve. The 360-degree Nissen fundoplication is 1.5 to 2 cm in length and height. It is maintained in position by three interrupted, non-absorbable, U-shaped sutures (0.0). An additional stitch may be used to fix the left part of the valve to the left border of the esophagus at the insertion of the phrenoesophageal membrane.
15. Intraoperative complications
Perforations
Frequency:
- rare (approximately 1%),
- dangerous if not immediately recognized intraoperatively as they carry a mortality of 20% to 50%15,17.
Mechanisms:
- placement of a bougie or nasogastric tube;
- traumatic manipulations of the esophagus sometimes attenuated by an inflammation;
- blind dissection in the absence of fixed anatomic landmarks.
What to do:
- primary closure of the perforation covered with the fundoplication.

Hemorrhage
Frequency:
- rare, often mild, not requiring transfusions.
Mechanism:
Bleeding could originate from:
a. the abdominal wall, at a trocar insertion site;
b. a short gastric vessel;
c. a diaphragmatic artery, especially at the level of the left crus;
d. hepatic trauma with a retractor or instrument;
e. a splenic laceration.
What to do:
a. suture ligation,
b. and c. hemostatic control using bipolar coagulation,
d. compression with a retractor or use of argon beam coagulator,
e. use of argon beam coagulator or fibrin glue.

Pneumothorax
Frequency:
- CO2 pneumothorax is a specific but benign complication of the laparoscopic approach,
- its incidence is approximately 3%, but is likely to be underestimated.
Mechanism:
It is caused by rupture of the pleura, more often on the left than on the right one, during a prolonged mediastinal dissection.
What to do:
- the treatment of the pneumothorax involves modification of the ventilation parameters with the addition of PEEP (positive end expiratory pressure),
- thoracic drainage is not necessary: the postoperative chest radiograph is often normal as the CO2 is rapidly absorbed when insufflation is discontinued.

Emphysema
Frequency:
- rare
Mechanism:
- mediastinal and/or subcutaneous emphysema can present occasionally during or after an operation when the hiatal dissection is too deep or prolonged.
What to do:
- the first therapeutic measure is to adjust the ventilation rate with or without a reduction of the insufflated pressure.

Vagus nerve trauma
Frequency:
- rarely reported, as it is often unrecognized.
Mechanism:
- the nerve can inadvertently be divided using electrocautery or damaged by diffusion of electrocautery current:
A: during the dissection of the posterior aspect of the esophagus for the posterior vagus nerve.
B: during the dissection of the phrenoesophageal membrane for the anterior vagus nerve.
What to do:
- prevention: careful dissection and identification of the 2 nerves.
16. Closure
The peritoneal cavity is rinsed with warm normal saline.
No drains are placed.
The trocars are removed and the skin openings are closed with staples.
Fluid intake begins on the same day.
Solid intake begins on the first postoperative day.
The patient is usually discharged on the second postoperative day.
17. Bibliographic references
1.Nissen R. [A simple operation for control of reflux esophagitis.]. Schweiz Med Wochenschr 1956; 86(Suppl 20):590-2.

2.Fein M, Bueter M, Thalheimer A, et al. Ten-year Outcome of Laparoscopic Antireflux Surgery. Journal of Gastrointestinal Surgery 2008; 12(11):1893-1899.

3.Mardani J, Lundell L, Lonroth H, et al. Ten-year results of a randomized clinical trial of laparoscopic total fundoplication with or without division of the short gastric vessels. Br J Surg 2009; 96(1):61-5.

4.Dallemagne B, Weerts J, Markiewicz S, et al. Clinical results of laparoscopic fundoplication at ten years after surgery. Surg Endosc 2006; 20(1):159-65.

5.Broeders JA, Rijnhart-de Jong HG, Draaisma WA, et al. Ten-year outcome of laparoscopic and conventional nissen fundoplication: randomized clinical trial. Ann Surg 2009; 250(5):698-706.

6.Cai W, Watson DI, Lally CJ, et al. Ten-year clinical outcome of a prospective randomized clinical trial of laparoscopic Nissen versus anterior 180( degrees ) partial fundoplication. Br J Surg 2008; 95(12):1501-5.

7.Booth MI, Stratford J, Jones L, Dehn TC. Randomized clinical trial of laparoscopic total (Nissen) versus posterior partial (Toupet) fundoplication for gastro-oesophageal reflux disease based on preoperative oesophageal manometry. Br J Surg 2008; 95(1):57-63.

8.Rossetti M, Hell K. Fundoplication for the treatment of gastroesophageal reflux in hiatal hernia. World J Surg 1977; 1(4):439-43.

9.Donahue PE, Larson GM, Stewardson RH, Bombeck CT. Floppy Nissen fundoplication. Rev Surg 1977; 34(4):223-4.

10.DeMeester TR, Bonavina L, Albertucci M. Nissen fundoplication for gastroesophageal reflux disease. Evaluation of primary repair in 100 consecutive patients. Ann Surg 1986; 204(1):9-20.

11.Dallemagne B, Weerts JM, Jehaes C, et al. Laparoscopic Nissen fundoplication: preliminary report. Surg Laparosc Endosc 1991; 1(3):138-43.

12.Dallemagne B. Laparoscopic Nissen Fundoplication. in Grandertath,Kamolz and Pointner (eds) Gastroesophageal Reflux Disease. Springer Wien NewYork. 2005.

13.Liebermann-Meffert D. [Surgical anatomy of the esophagogastric junction]. Helv Chir Acta 1981; 47(6):667-77.

14.Korn O, Stein HJ, Richter TH, Liebermann-Meffert D. Gastroesophageal sphincter: a model. Dis Esophagus 1997; 10(2):105-9.

15.Schauer PR, Meyers WC, Eubanks S, et al. Mechanisms of gastric and esophageal perforations during laparoscopic Nissen fundoplication. Ann Surg 1996; 223(1):43-52.

16.Catarci M, Gentileschi P, Papi C, et al. Evidence-based appraisal of antireflux fundoplication. Ann Surg 2004; 239(3):325-37.

17.Carlson MA, Frantzides CT. Complications and results of primary minimally invasive antireflux procedures: a review of 10,735 reported cases. Journal of the American College of Surgeons 2001; 193(4):428-439.