Adult Chest Surgery

Chapter 31. Nissen Fundoplication 


Gastroesophageal reflux disease (GERD) is caused by the chronic reflux of gastric acid from the stomach to the esophagus. This may be the result of an incompetent lower esophageal sphincter (LES) or poor gastric emptying. GERD is an anatomic and physiologic problem that may lead to surgical consultation for treatment of either the symptoms or sequelae of reflux. It was first recognized as a clinical entity in the 1930s. Today, it is the most prevalent upper gastrointestinal disorder in the Western world.1

GERD gives rise to a spectrum of symptoms that range in intensity from mild to severe. Up to 80% of patients present with so-called typical symptoms of GERD. These include heartburn, regurgitation, sour taste, and intermittent dysphagia but no evidence of esophageal inflammation or injury. Approximately 20% of patients present with atypical symptoms, namely, chest pain, hoarseness, nocturnal choking, chronic cough, asthma, shortness of breath, and pneumonia. For some, GERD causes severe medical disabilities, such as recurrent aspiration, ulceration, end-stage lung disease, or recurrent esophageal stricture. Left untreated, these complications may lead to disability and rarely mortality. For most, however, GERD is not a life-threatening condition, and patients suffering from this disease seek treatment mainly to improve their quality of life.

The treatment options for GERD range from lifestyle change and medical therapy to antireflux surgery based on the severity of the patient's symptoms or presence of complications. Long-term treatment with proton pump inhibitor (PPI) therapy is highly effective in terms of symptoms but may require indefinite duration because 82% of patients have recurrent symptoms within 6 months of discontinuation. When conservative treatment fails, several interventions are possible. Herein we describe both the open Nissen fundoplication and the laparoscopic adaptation, the current surgical standard for the treatment of GERD. These operations were designed to fix the anatomic and physiologic problems that give rise to GERD.


The Nissen fundoplication consists of hiatal closure and a 360-degree wrap of stomach around the distal esophagus to augment and restore the function of the LES. The laparoscopic adaptation is associated with reduced morbidity compared with the open approach; however, a history of previous abdominal operation with dense scar and adhesion still poses a significant challenge. Since its conception,the Nissen fundoplication has been a successful operation with excellent long-term outcome. The morbidity associated with the upper midline incision of the open approach, however, limited its application to patients with symptoms refractory to medical therapy and severe complications of GERD.

The laparoscopic adaptation, first reported in 1991,revitalized interest in the surgical treatment of GERD. Factors underlying this increased interest include the rising incidence of GERD in Western countries, the decreased morbidity and mortality of the minimally invasive approach, poor compliance or dissatisfaction with long-term medical treatment, recognition of an association between GERD and esophageal cancer, and curative potential of the surgery. Patient demand for a permanent treatment led many surgeons to acquire expertise in the minimally invasive approach. The learning curve for laparoscopic fundoplication is relatively short, reaching a plateau at 20 cases for the individual surgeon4,5 and 50 cases for an institution.A two-surgeon collaborative approach can further reduce the learning curve.The long-term results of open and laparoscopic fundoplication appear to be equivalent, with larger series showing a sustained benefit in 95% of patients at 5 years and approximately 90% at 10 years.1

General indications for antireflux surgery include esophageal ulceration, severe esophagitis, Barrett's esophagitis, severe pulmonary symptoms, recurrent stricture, dysplasia, and failure or inability to comply with medical therapy. To be considered for this surgery, the patient must have normal esophageal motility and a normal-length esophagus. Patients with foreshortened esophagus likely will require a Collis extension coupled with this procedure.

It is essential to conduct an adequate preoperative evaluation to confirm the diagnosis because the symptoms of GERD overlap substantially with the primary esophageal motility disorders, which require different therapies for treatment (see Part 3, Overview). Experience with the open technique is a prerequisite because rapid conversion to the open procedure may be required if the laparoscopic approach fails or in the event of a serious complication. Depending on specific anatomic considerations, other procedures described in this section also may be necessary (e.g., a Nissen-Collis procedure or partial fundoplication).


Patients referred for surgical treatment of GERD often have had long-standing symptoms and have pursued at least medical and often lifestyle changes without success or satisfaction. Lifestyle changes include reductions in fatty food, peppermint, and alcohol consumption; cessation of tobacco smoking; and weight loss.

The evaluation for antireflux procedures is best accomplished using four studies that are designed to exclude related disorders of the esophagus(Table 31-1). These are the barium or cine esophagram (upper gastrointestinal series), endoscopy (esophagoduodenogastroscopy (EGD)), esophageal manometry, and esophageal pH probe analysis. If the findings are inconclusive, esophageal and gastric-emptying studies and even provocative testing may be useful.

Table 31-1. Standard Studies for the Evaluation of Antireflux

pH studies

Positive for reflux if the composite reflux score is more than 14.7 (see Table 31-2)


To assess esophageal length, webs and strictures, mucosal anomalies, the coexistence of a hiatal hernia or other pathology


Detects structural changes and evaluates surgical anatomy; sensitive in the detection of achalasia and diffuse esophageal spasm, both of which contraindicate Nissen fundoplication


To rule out esophageal motility disorders, which would call for a different operative approach



Barium Esophagram

The barium swallow or esophagram is the diagnostic modality of choice for the evaluation of dysphagia and chest pain likely to be related to the esophagus. It is a sensitive diagnostic modality for achalasia and diffuse esophageal spasm but not for nutcracker esophagus or scleroderma, the latter representing secondary esophageal motility disorders. Only 40% of patients with classic GERD symptoms have a positive esophagogram. Spontaneous regurgitation or moderate to severe reflux of contrast material to the esophagus confirms GERD.

Cine Esophagram

The cine esophagram is a dynamic video contrast study that records the transfer of contrast material from the oral cavity to the pharynx, showing the coordinated motion of the tongue, palate, epiglottis, laryngeal and pharyngeal walls, inferior constrictors, and upper esophageal sphincter. This study is indicated for patients with atypical chest pain and normal findings on barium esophagram.



Fiberoptic EGD is the most important tool for the diagnosis and management of esophageal disease. It is usually performed with topical anesthesia and IV conscious sedation in an outpatient setting (see Chap. 12). We routinely perform EGD before surgery for GERD to assess esophageal length, define and treat any strictures, exclude other pathology such as cancer, evaluate Barrett's esophagitis, and determine the presence of a hiatal hernia (esophageal or paraesophageal).

Esophageal Manometry

Esophageal manometry provides information about the motor function of the esophagus and its sphincters (upper and lower) at rest and during swallowing. Patients who undergo Nissen fundoplication must have a relatively normally functioning esophagus. Impaired motility increases the risk for obstructive symptoms postoperatively. One exception is the entity known as esophageal stunning, which is caused by prolonged acid exposure and reflected in decreased motility of the distal esophagus. This entity occasionally may be confused with diffuse esophageal spasm. At rest, the normal LES is a 3- to 4-cm high-pressure zone in the distal esophagus. It relaxes with a food bolus, permitting food to pass into the stomach. The LES has three components: resting pressure at midrespiration, overall length, and abdominal length (the lower limits of normal are 6 mm Hg, 2 cm, and 1 cm, respectively). If just one of these values is low, the LES will not function properly. Esophageal manometry is most useful for identifying nonobstructive causes of dysphagia because it is sensitive to pressure changes and does not provide information about the passage of food. It provides a definitive diagnosis of achalasia, diffuse esophageal spasm, nutcracker esophagus, hypertensive LES, and scleroderma, all of which are contraindications to Nissen fundoplication.

Esophageal pH Probe Monitoring

Ambulatory esophageal pH monitoring was introduced in 1985 for the diagnosis of GERD. The patient must cease H2-blocker therapy 48 hours before monitoring and PPI therapy 2 weeks in advance of study. The basic instrument consists of a tube with a number of pH channels. This tube is placed in the esophagus for 24 hours. The tube is positioned such that the first probe is located 5 cm above the LES (determined by manometry). The second is connected to the skin, and both are connected to a portable data recorder. The pH is sampled and recorded every second. In general, the patient is asked to eat a regular diet and carry out normal daily activities. A diary is used to document meals, symptoms, and sleep time. A composite reflux score is calculated, and a value above 14.7 represents pathologic exposure to acid. Ninety-five percent of individuals score under 14.7. The composite reflux score has a sensitivity of 90% and specificity of 85% for GERD. It is especially useful in diagnosing reflux with atypical pulmonary symptoms such as chronic cough, wheezing, asthma, and recurrent pneumonia. It can be used to assess the efficacy of medical therapy or the success of surgical therapy. It should be used to confirm GERD in all patients before antireflux procedures. This test does not detect "alkaline reflux," that is, reflux owing to bile with a pH > 7. It is considered the single most useful objective test for evaluating GERD(Table 31-2).

Table 31-2. Composite Reflux (DeMeester) Score9


Percent of total time pH <4

Percent of upright time pH <4

Percent of supine time pH <4

Total number of episodes pH <4

Number of episodes pH <4 lasting >5 minutes

Number of minutes of longest episode pH <4


<14.7 indicates absence of reflux (95% confidence interval)


Newer devices have been developed that cause less discomfort to the patient. The wireless Bravo capsule (Bravo, pH Monitoring System, Medtronic, Inc., Minneapolis, MN), for example, is clipped to the esophageal wall during endoscopy and is capable of transmitting pH data to a small external recorder for up to 48 hours. A new generation of instruments has been developed that measure pH and impedance simultaneously at multiple sites in the esophagus via a single multichannel intraluminal device.


On occasion, findings on the aforementioned studies are inconclusive. Nuclear scintigraphy (esophageal and gastric emptying studies) uses food (e.g., cereal, eggs, or juice) labeled with radioactive technetium-99m or indium-111 to record the transit of food over time through the body. Abnormal studies demonstrate rapid or delayed emptying. Normal transit time is 10–17 seconds for the esophagus, and 50% of gastric emptying occurs in 15–90 minutes for liquids and 45–100 minutes for solids.

Provocative testing was developed because many patients, particularly those with atypical symptoms, may be asymptomatic at the time of testing. These studies reproduce the type of pain characteristic of GERD but do not provide insight into the underlying pathology. The Bernstein acid perfusion test, developed in 1958, distinguishes esophageal from other causes of chest pain. A tube is placed in the distal esophagus, and 0.1 N hydrochloric acid is infused continuously at a rate of 5–10 mL/min for 10–30 minutes. The test is positive if the patient experiences pain when acid is introduced, and the pain abates with saline.


Laparoscopic Nissen Fundoplication

The critical steps of this operation are (1) placing the ports, (2) dividing the short gastric arteries, (3) hiatal dissection, (4) mobilization of the fat pad and assessment of esophageal length, (4) hiatal closure, and (5) fashioning and securing the wrap. The procedure is performed under general anesthesia. EGD should be performed by the surgeon at the time of the operation to confirm the anatomic findings, in particular, esophageal length. The bladder is decompressed, antibiotics are given, and prophylactic measures to prevent pulmonary embolus are instituted. The procedure can be performed in the supine or lithotomy position, with both arms tucked in at the sides.


Our preference is to perform the operation with the patient in the lithotomy position. The surgeon stands between the patient's legs, and the first assistant is positioned to the left of the surgeon (Fig. 31-1).

Figure 31-1.


With the patient in the lithotomy position, the surgeon stands between the patient's legs, and the first assistant is positioned to the left of the surgeon.

Typically, we create an 11-mm incision in the periumbilical region for the camera port using a modified Hassan technique to minimize inadvertent injury to the abdominal viscera. We then create a pneumoperitoneum by insufflating the abdomen with carbon dioxide to maximal pressure of 15–19 mm Hg. At our institution, we use a CO2 insufflator (Lexion Medical, Inc., St. Paul, MN), which humidifies and heats the peritoneum, improves visualization, and decreases hypothermia during surgery. Thereafter, we insert a fully adjustable 10-mm laparoscope with a deflectable tip to permit multiple planes of visualization; others use a 30-degree laparoscope. The table is positioned in a steep reverse Trendelenburg position for the duration of the procedure. Laparoscopy is performed to assess for the presence of adhesions. The remaining ports are placed sequentially under direct visualization in areas devoid of adhesions and are used, if needed, to perform further adhesiolysis until all five standard ports have been placed (see Fig. 31-1). All ports should be placed such that the instruments point naturally in the direction of the dissection (i.e., toward the gastroesophageal junction (GEJ)).


The assistant raises the left lobe of the liver using a self-retaining liver retractor. A grasper is placed high on the greater curvature, retracting the greater curve caudally, anteriorly, and medially, whereas a second grasper elevates the gastrosplenic ligament laterally (Fig. 31-2). An avascular plane is identified along the greater curvature at the midlevel of the short gastric arteries. Using a 5-mm LigaSure™ (Valleylab, Boulder, CO) device, the gastrosplenic ligament is gradually divided all the way to the left crus. The two leaves should be divided separately. All lateral attachments to the upper portion of the greater curve of the stomach are completely divided to mobilize the stomach. It is important to completely mobilize the fundus to later enable a tension-free wrap of the esophagus.

Figure 31-2.


The first grasper is placed high on the greater curvature, retracting the greater curve caudally, anteriorly, and medially, and a second grasper elevates the gastrosplenic ligament laterally.


After reaching the left crus, the left gastrophrenic ligament is opened, exposing the left crus down to its confluence with the right crus. Care must be taken to avoid injury to the anterior vagus, which courses between 3 and 12 o'clock. If a hiatal hernia is identified, as is extremely common in patients with GERD, its contents are reduced into the abdomen, and the peritoneal sac is amputated. Most often the hernia is of the sliding type (see Chap. 29), and the sac is very small. If the hernia is larger than 4 cm, special attention should be given to ensuring adequate esophageal length.

With the stomach retracted laterally, the lesser curvature is opened in an avascular region near the liver, exposing the caudate lobe, until the right crus of the hiatus is seen. Care is required to avoid the left gastric artery, a possible replaced hepatic artery, and vagal branches. Occasionally, a small branch from the left gastric artery to the left hepatic artery is divided without consequence to improve the exposure. The right crus is identified, and the overlying peritoneum is opened, exposing its edge. Because of the risk of perforation, we do not attempt to directly identify the esophagus before opening the crus. The right crus is dissected from its confluence to the median arcuate ligament, where it joins the left crus (Fig. 31-3). This dissection is done meticulously taking only a thin layer of peritoneum, and the esophagus is revealed by its orientation, longitudinal muscle fibers, and position of the posterior vagus nerve, which courses between 9 and 6 o'clock. Using blunt dissection with traction and countertraction, the peritoneum and phrenoesophageal ligament are divided, proceeding in a plane perpendicular to the esophagus. We divide the esophagophrenic attachments and peritoneum in a semicircular fashion down to the median arcuate ligament, with all due caution to avoid injury to the anteroposterior branches of the vagus. Great care is taken to avoid perforating the esophagus or stomach when mobilizing the GEJ. The esophagus is retracted upward, and a window is bluntly opened and widened to reveal the left side of the abdomen.

Figure 31-3.


The right crus is dissected from its confluence to the median arcuate ligament, where it joins the left crus.


The fat pad is medialized proceeding from the patient's left side to center, thereby exposing the true GEJ. The GEJ is identified by recognizing the confluence of the longitudinal muscles of the esophagus merging with the sling muscles of the stomach. The GEJ is not perpendicular. In approximately 85% of patients, there is adequate length of the abdominal esophagus (2 cm), and a lengthening procedure is not required. If a foreshortened esophagus is encountered (i.e., if the esophagus retracts into the mediastinum and there is less than 1 cm of abdominal esophagus), we perform a Collis extension (see Chap. 34) before the hiatus is closed.


The esophagus is retracted using an endoscopic Kittner retractor (Ethicon Endo-Surgery, Cincinnati, OH). The hiatal confluence then is visualized and closed by sewing the left crus to the right crus beginning at the confluence. Using the Endostitch device (Auto Suture, Norwalk, CT) inserted through the epigastric port, the crura are sewn to each other (1 cm of crus) moving from the patient's left side to the right side using Tevdek 0 suture. A Ti-rite knot (Ti-rite Knot Device, Wilson-Cook Medical, Winston-Salem, NC) then is placed to secure the suture. We prefer tying the sutures extracorporeally using a Ti-rite knot because it provides a more consistent and secure set of knots than manual intracorporeal tying. Additional stitches are placed in the same way at half- to three-quarter-centimeter intervals. The hiatus is usually repaired with three to five such sutures. As the opening narrows, the prospective last suture is placed but not tied. The retraction is relaxed, the nasogastric tube is removed, and a 58 bougie (range 52–60, with size depending on patient factors) is slowly and carefully introduced into the esophagus to a depth of 50 cm (10 cm below the GEJ). The bougie helps the surgeon to properly gauge the hiatal closure (Fig. 31-4). The esophagus then is retracted in an upward direction, tension is placed on the suture, and a visual assessment is made to determine if the prospective suture should be tied or removed. When the caliber of the hiatus with the bougie in the esophagus is deemed snug but not constricted, the bougie is retracted to 25 cm. If the hiatus is still lax, the bougie is withdrawn, and an extra suture is placed.

Figure 31-4.


The bougie is introduced into the esophagus to a depth of 50 cm (10 cm beyond the GEJ).


The GEJ is elevated, and a reticulating grasper is brought under the esophagus to pull the apical tip of the greater curvature to the right of the right side. The inverted stomach is grabbed with an endoscopic grasper. The surgeon aids by pushing the gastric fundus behind the esophagus, enabling the surgeon to assess the configuration of the wrap. After bringing the gastric fundus behind the esophagus, we choose the most apical point along the line of the greater curvature (the line of the short gastric vessels). Choosing the correct region of the stomach to wrap is essential for the success of the fundoplication.

Babcock clamps are applied to both sides of the stomach that now encircles the esophagus, and the 58 bougie is carefully readvanced into the stomach. Using the Babcock clamps, the stomach is "shoeshined" at both ends around the distal esophagus to ensure correct alignment, correct tension, lack of excess redundancy, and correct placement of the wrap (Fig. 31-5). The fat pad is now pulled caudad from the greater curvature in the area of the GEJ to enable better adhesion of the stomach to the esophagus.

Figure 31-5.


The wrap is "shoeshined" at both ends around the distal esophagus to ensure proper placement.


Using the Endostitch device, sutures are passed from the left side of the wrap to the esophagus and then to the right side of the wrap, taking 1 cm of stomach on each side, and the sutures are tied with a Ti-rite knot (Fig. 31-6). Additional stitches are placed in the same way at 5-mm intervals. The length of the fundoplication is 2–2.5 cm and typically consists of four nonabsorbable Tevdek 2-0 stitches. The first three stitches are taken through all three layers: stomach-esophagus-stomach. The last stitch is made from stomach to stomach. It is important to take small bites of serosa and muscularis without mucosa because the latter can lead to necrosis and leak if tied too tightly. After removing the bougie, an 18F nasogastric tube is placed by the anesthesiologist, and its entrance into the stomach and positioning are confirmed visually. The repair then is examined visually to ensure that the wrap is configured correctly. Hemostasis is ensured, and the fasciae underneath the large ports are closed, as is the skin.

Figure 31-6.


A Ti-rite knot then is placed to secure the suture.

Open Nissen Fundoplication

At one time, the open Nissen fundoplication, developed by Rudolph Nissen in the 1950s,was the "gold standard" of antireflux surgery. It was simple, easy to learn, yielded excellent outcome with an overall 10-year success rate of better than 90%, and was technically less challenging than other operations for reflux. However, after Dallemagne and colleagues adapted the technique laparoscopically in 1991,high patient demand for the minimally invasive procedure quickly followed. As a consequence, the open approach is now indicated only in the diminishing circumstances where a laparoscopic approach is not possible. In experienced hands, these circumstances are rare. Frankly, the laparoscopic approach is easier to perform and safer because of its better visualization and access. In our practice, we try to accomplish the wrap first laparoscopically, even when we plan to open the abdomen subsequently for another reason. We recommend that the equipment required for conversion be readily available and a system set up for rapid conversion. It is important for the staff to periodically discuss and simulate the conversion sequence.

The open procedure is performed with the patient in the supine position with the right arm extended or tucked and the left arm tucked in at the side. The bed is placed in a shallow reverse Trendelenburg position. A nasogastric tube is inserted for drainage and decompression of the stomach.


The abdomen is explored through an upper midline incision (Fig. 31-7). (If needed, the incision can be extended below the umbilicus.) Lysis of adhesions can be carried out in the left upper quadrant as needed. The falciform suspensory ligament is divided, and the triangular ligament (hepatophrenic ligament) is excised. An upper-hand retractor is placed to elevate the costochondral portion of the chest. A moist laparotomy pad is placed behind the spleen, and a liver retractor is positioned to retract the left lobe, exposing the esophageal hiatus.

Figure 31-7.


Midline incision for open technique.


As with the laparoscopic approach, three or four short gastric arteries are ligated either with clamps or with the LigaSure device (Valleylab, Boulder, CO) to avoid splenic injury. The phrenoesophageal ligament is opened using Metzenbaum scissors to make a semicircular incision. The anterior vagus is identified on the left and the posterior vagus is identified on the right side of the esophagus (Fig. 31-8). The gastrohepatic ligament is opened close to the liver, with vigilance to avoid injury to the left gastric artery, a replaced hepatic artery, or branches of the vagus. A finger is placed behind the esophagus, and then a Penrose drain is passed behind the esophagus to enable caudal retraction.

Figure 31-8.


The anterior vagus is identified on the left and the posterior vagus is identified on the right side of the esophagus.

The right crus is identified and dissected from its confluence to the median arcuate ligament, where it joins the left crus. As with the laparoscopic approach, attention is given to ensuring adequate esophageal length, and hiatal hernia, if present, is reduced into the abdomen and the peritoneal sac amputated. Consideration also should be given to reconstruction and repair of the hiatus with mesh if warranted. The assistant pulls the Penrose drain in a caudal direction as the surgeon pushes the gastric fundus behind the esophagus, enabling assessment of the region where the wrap will lie.


The hiatus is repaired using Tevdek 0 sutures. The left crus is sewn to the right, taking 1.5 cm of the crus on each side. After placing the first two sutures, a bougie (58–60 depending on patient size) is introduced into the esophagus, and the hiatus is closed with a few additional sutures to correctly gauge the closure. Note that insertion of the bougie is a critical step. If performed incorrectly, this maneuver can lead to esophageal or gastric perforation. It must be done under direct vision in a controlled manner to minimize potential complications.


After the gastric fundus has been brought behind the esophagus, the apical-most point along the line of the greater curvature (the line of the short gastric vessels) is identified. The apex of the stomach is brought behind the esophagus. Babcock clamps are applied to both sides of the stomach, and the bougie is reintroduced. Using the Babcock clamps, the stomach is "shoeshined" at both ends around the distal esophagus to ensure correct alignment, contour, tension, and placement of the wrap. One should see a straight line between both upper edges of the wrap. The fat pad is removed well away from the greater curvature in the area of the GEJ to prevent vagal injury in a medial-to-lateral direction to enable better adhesion of the stomach to the esophagus. We routinely wrap the stomach around a bougie to ensure that the wrap is not too tight. The length of our fundoplication is 2–2.5 cm and typically consists of three or four nonabsorbable Tevdek 2-0 stitches (Fig. 31-9). The first three stitches to close the wrap traverse all three layers: stomach-esophagus-stomach. Full-thickness bites of esophagus that incorporate the underlying mucosal layer are avoided. Avoiding the mucosal layer when stitching is important because the latter, if tied too tightly, can necrose and leak. The last stitch is made from stomach to stomach. To gauge the tightness of the wrap after the bougie is removed, we place an 18F nasogastric tube through the reinforced esophagus. If the fit is proper, the surgeon should be able to pass the fifth digit under the wrap (Fig. 31-10). Proper esophageal length prevents the wrap from slipping into the chest. Proper patient selection (adequate esophageal length), good technique, and correct placement of stomach and esophageal sutures will prevent the wrap from slipping in the caudal direction. If caudal slippage occurs, the stomach will constrict and assume an "hourglass" appearance, producing a partial obstruction (Fig. 31-11). This can be avoided by adhering to the aforementioned principles.

Figure 31-9.


A 2- to 2.5-cm fundoplication is created.


Figure 31-10.


A finger is slipped under the wrap to test it.


Figure 31-11.


Caudal slippage produces an "hourglass" appearance to the stomach and partial obstruction.


After assuring hemostasis, the retractors are removed, and pads and instruments are counted. The abdominal fascia is closed with two 1-0 PDS loop sutures, with attention to the corners of the incision and 1 x 1 cm bites of fascia. The subcutaneous layer is not closed. The skin is closed with a stapler or a running 3-0 Vicryl intracuticular stitch. The patient is aroused, extubated, and taken to the postoperative recovery room.

With adequate knowledge of the operative pitfalls, many technical errors can be avoided. These are summarized in Table 31-3.

Table 31-3. Operative Pitfalls

·   Splenic laceration usually involving traction injuries (uncommon with laparoscopic approach).

·   Injury to the vagus nerve or to vagal branches near the stomach in the gastrohepatic ligament.

·   Vascular injury to the left gastric artery or injury to a replaced hepatic artery.

·   Unidentified perforation of the stomach or the esophagus during retraction or dissection.

·   Improper hiatal closure owing to incomplete hiatal dissection. Loose hiatal closure may lead to postoperative hiatal hernia, whereas tight hiatal closure may lead to esophageal obstruction and consequently achalasia.

·   Inadequate mobilization of gastric fundus and distal esophagus leading to suboptimal position of the fundoplication and, as a result, inadequate function.

·   A fundoplication that is too long or too tight will result in dysphagia, gas bloating, and a functional obstruction.

·   A fundoplication that is too short or too loose will not alleviate GERD.




The patient is maintained on IV fluids. Pain medication is administered through patient-controlled analgesia and later with an oral analgesic cocktail. The patient is kept nothing by mouth with a nasogastric tube in place on the first postoperative day, but the tube is removed the following morning to prevent postoperative emesis because this has been linked to early wrap failure. A swallow study to rule out leak can be ordered in selected patients on postoperative day 1 or 2. We advocate early ambulation and begin the patient on a clear liquid diet the morning after surgery. The patient is discharged on this diet on postoperative day 2 or 3 and seen in follow-up at 2 weeks (when the diet is advanced as tolerated), at 6 weeks, and thereafter as needed while avoiding certain foods, such as bread.


The main complications of the Nissen fundoplication are splenic injury, esophageal or gastric perforation, and postoperative dysphagia. Less common complications include wrap failure, pancreatitis, gastric emptying problems, gastric necrosis, and bleeding. Mortality is less than 1%. Generally speaking, the laparoscopic technique is less morbid.

Splenic Injury

Iatrogenic trauma to the spleen is reported in up to 10% of open Nissen procedures but less commonly with the laparoscopic approach. Injury to the spleen can be prevented if the splenic attachments to the stomach are taken early in the operation. Care must be exercised when placing retractors or instruments on the spleen. In the event of splenic injury, an early decision should be made as to appropriate management. If the injury is lateral or peripheral, 10 minutes of direct pressure with Surgicel (Ethicon, Inc., a Johnson and Johnson Company, Somerville, NJ) or other hemostatic aids usually will stop the bleeding. In some cases, a splenic repair with suture is needed. A splenectomy should be performed if the splenic laceration is extensive or located in the area of the hilum. In the event that splenic repair is attempted and the blood loss exceeds 2 units of packed red blood cells, a splenectomy probably should be pursued, and this often can be performed laparoscopically.

Esophageal or Gastric Perforation

In a retrospective review of gastroesophageal leaks from a series of over 1000 antireflux surgeries, Urschel determined the incidence of leak to be 1.2%.10 The most significant predisposing risk factor was previous hiatal operation. Careful identification and avoidance of the esophagus are critical to preventing esophageal perforation. Gastric perforation usually is caused by aggressive traction or as a consequence of pulling the stomach inadvertently into a port. Careful inspection of the stomach and esophagus before closure will reveal most of these injuries, affording the opportunity for immediate and definitive repair.


Transient mild dysphagia is commonly reported during the first few postoperative weeks. It is usually caused by postoperative edema localized to the area of the wrap. A number of other possible causes have been reported, including tight hiatal closure (avoided by calibration), long fundoplication wrap (avoided by measuring it), slipped wrap (owing to a foreshortened esophagus or trauma), and impaction of food (owing to improper diet). However, if the dysphagia existed preoperatively, the possibility of a misdiagnosed esophageal motility disorder also must be considered.11–15


The number of patients seeking surgical treatment for early-stage GERD has increased dramatically since the popularization of laparoscopy. Before the era of laparoscopic antireflux procedures, despite a 30-year experience and documented 10-year success rate of approximately 90%,only about 13,000 patients had open antireflux surgery annually.16 Because of the morbidity of the open approach, surgery was principally reserved for patients with severe anatomic comorbidities, such as a large hiatal hernia, a paraesophageal hernia, a short esophagus, and severe physiologic symptoms including erosive esophagitis and failure of medical therapy. After its introduction in 1991 by Dallemagne, laparoscopic antireflux surgery evolved rapidly, producing techniques that simulated and improved on the original open procedures. By 2004, an estimated 70,000 individuals were referred for minimally invasive curative surgery for GERD. Today, laparoscopic Nissen fundoplication is the "gold standard" and most commonly performed antireflux procedure for the treatment of GERD. Understanding the indications, pitfalls, surgical technique, and most important, the contraindications [e.g., short esophagus (see Chap. 34), complex hiatal hernia (see Chap. 29), and primary esophageal motility disorders (see Part 3)] is essential, and familiarity with the open technique and other fundoplication procedures [e.g., Belsey–Mark IV (see Chap. 30), Nissen-Collis, and Hill, Toupet, or Dor (see Chap. 32)] is prerequisite to achieving a satisfactory outcome.


A 45-year-old man in general good health presented with a long-standing history of GERD that was treated with proton pump inhibitors with good symptomatic response but ultimately was limited by poor compliance. He had a previous history of multiple abdominal operations, including appendectomy for perforated appendicitis, negative laparotomy after a motor vehicle accident, and mesh repair for postoperative ventral hernia. Physical examination was remarkable only for multiple laparotomy incisions. He underwent evaluation that included normal findings on esophagoduodenogastroscopy (i.e., normal esophageal length, absence of Barrett's esophagus, and no evidence of peptic disease or other pathology) and a pH study that documented multiple episodes of acid reflux with a DeMeester score of 120. Manometry showed normal esophageal contractions and motility. An upper gastrointestinal study was normal. The patient was referred for a laparoscopic Nissen fundoplication, which was uneventful. The patient had an uneventful postoperative course and is without recurrence of GERD for 2½; years. The patient does not take any medication for GERD.


Careful attention to all the details and precise anatomical delineation during surgery are critical for good outcome. Calibration with a bougie is important and should be balanced, in my opinion, towards looser wraps to avoid debilitating dysphagia. In that scenario, patients who fail repeated dilatation and have an adequate wrap will ultimately improve after conversion to a less than 360 degree wrap.


1. DeMeester TR, Bonavina L, Albertucci M: Nissen fundoplication for gastroesophageal reflux disease: Evaluation of primary repair in 100 consecutive patients. Ann Surg 204:9–20, 1986. [PubMed: 3729589]

2. Nissen R: Eine einfache operation zur beeinflussung der reflux oesophagitis. Schweiz Med Wochenschr 86:590–2, 1956. [PubMed: 13337262]

3. Dallemagne B, Weerts JM, Jehaes C, et al: Laparoscopic Nissen fundoplication: Preliminary report. Surg Laparosc Endosc 1:138–43, 1991. [PubMed: 1669393]

4. Voitk A, Joffe J, Alvarez C, Rosenthal G: Factors contributing to laparoscopic failure during the learning curve for laparoscopic Nissen fundoplication in a community hospital. J Laparoendosc Adv Surg Tech A 9:243–8, 1999. [PubMed: 10414540]

5. Endzinas Z, Maleckas A, Mickevicius A, Kiudelis M: [Follow-up results and learning curve in laparoscopic gastrofundoplications.] Zentralbl Chir 127:939–43, 2002. [PubMed: 12476365]

6. Watson DI, Baigrie RJ, Jamieson GG: A learning curve for laparoscopic fundoplication: Definable, avoidable, or a waste of time? Ann Surg 224:198–203, 1996. [PubMed: 8757384]

7. Hwang H, Turner LJ, Blair NP: Examining the learning curve of laparoscopic fundoplications at an urban community hospital. Am J Surg 189:522–6; discussion 526, 2005. 

8. Yang S: Esophageal Function Tests. St Louis, Mosby, 1998:1–8.

9. DeMeester FK: Preoperative evaluation of gastroesophageal reflux. Curr Ther Cardiothorac Surg 217–20, 1989. 

10. Urschel JD: Gastroesophageal leaks after antireflux operations. Ann Thorac Surg 57:1229–32, 1994. [PubMed: 8179390]

11. Bais JE, Wijnhoven BP, Masclee AA, et al: Analysis and surgical treatment of persistent dysphagia after Nissen fundoplication. Br J Surg 88:569–76, 2001. [PubMed: 11298627]

12. Herron DM, Swanstrom LL, Ramzi N, Hansen PD: Factors predictive of dysphagia after laparoscopic Nissen fundoplication. Surg Endosc 13:1180–3, 1999. [PubMed: 10594261]

13. Hunter JG, Swanstrom L, Waring JP: Dysphagia after laparoscopic antireflux surgery: The impact of operative technique. Ann Surg 224:51–7, 1996. [PubMed: 8678618]

14. Patterson EJ, Herron DM, Hansen PD, et al: Effect of an esophageal bougie on the incidence of dysphagia following nissen fundoplication: A prospective, blinded, randomized clinical trial. Arch Surg 135:1055–61; discussion 1061–2, 2000. 

15. Polk HC Jr: Fundoplication for reflux esophagitis: Misadventures with the operation of choice. Ann Surg 183:645–52, 1976. [PubMed: 9914]

16. Centers for Disease Control and Prevention: Detailed Diagnoses and Procedures, 2005, 

If you find an error or have any questions, please email us at Thank you!