session title: postgraduate course: foregut â€“ beyond gerd

Session Title: POSTGRADUATE COURSE: Foregut – Beyond GERD & Hiatal Hernia

Date/Time: 4/17/2013; 7:30am-12pm

Session Chair: C. Daniel Smith, MD

Session Co-Chair: Bernard Dallemagne, MD

SESSION DESCRIPTION

This session will cover complex topics in foregut surgery increasingly encountered by surgeons caring for

patient with foregut conditions. World experts will discuss presentation, diagnosis and management

strategies for these conditions that go well beyond basic GERD and hiatal hernia. This session’s objectives are

a classical application of educational principles to adult learning. The problem is the increasing complexity in

managing foregut disease as new therapies become available and the diseases themselves are increasingly

advanced presentations. Participants will learn the varied presentations of these more complex conditions

and management strategies that go beyond managing basic foregut conditions. On returning to their practice,

they will be equipped to change how they operate by applying this knowledge in caring for foregut patients.

This improved understanding will allow for better patient selection and use of advanced interventions.

SESSION OBJECTIVES:

At the conclusion of this session, participants will be able to:

1. Understand and describe complex conditions and circumstances effecting surgical foregut diseases

2. Recognize some of the innovations and new technologies used in managing foregut disease

3. Be aware of the impact that advanced presentations of foregut disease can have on selecting management

strategies for these patients

4. Approach complex foregut conditions with greater confidence

SESSION OUTLINE

Time Presentation Title Faculty Name

7:30am

Introduction C. Daniel Smith, MD

Bernard Dallemagne, MD

GERD & Hiatal Hernia

7:35am

Management strategies for complex GERD

(stricture and Barretts)

Jeffrey Peters, MD

7:55am

Redo Operations – When, How and Who? Bernard Dallemagne, MD

8:15am Hiatal Hernia C. Daniel Smith, MD

8:35am What to Do in the Obese Samer Mattar, MD

8:55am Emerging Technologies and Techniques Reginald Bell, MD

9:15am Panel Discussion – Audience Questions and Cases

10:00am Break

Gastric Neoplasms

10:15am GIST and Submucosal Tumors David Rattner, MD

10:30am Early Gastric Cancer Han-Kwang Yang, MD

Other Esophageal Conditions

10:45am Submucosal Tumors Sricharan Chalikonda, MD

11:00am Esophageal Diverticulae and Achalasia Christy Dunst, MD

11:15am

MIS in Esophageal Neoplasms Giovanni Dapri, MD/ Guy B.

Cadière, MD

11:35am Panel Discussion – Audience Questions and Cases

1

MANAGEMENT OF COMPLEX GERD; STRICUTRES AND BARRETT’S

Jeffrey H. Peters, MD

University of Rochester, Rochester NY

The complications of gastroesophageal reflux result from the damage inflicted by gastric

juice on the esophageal mucosa, laryngeal or respiratory epithelium. These can be conceptually

divided into 1) mucosal complications such as esophagitis and stricture, 2) extra-esophageal or

respiratory complications such as chronic cough, asthma and pulmonary fibrosis and 3)

metaplastic (Barrett’s esophagus) and neoplastic (adenocarcinoma). The prevalence and severity

of complications is related to the degree of loss of the gastroesophageal barrier, defects in

esophageal clearance and the content of refluxed gastric juice.

Stricture and Esophageal Shortening

Esophageal strictures are among the most challenging complications of esophageal

disease. An esophageal stricture can be associated with severe esophagitis or Barrett's esophagus.

In the latter situation, it occurs at the site of maximal inflammatory injury (i.e., the columnar-

squamous epithelial interface). As the columnar epithelium advances into the area of

inflammation, the inflammation extends higher into the proximal esophagus, and the site of the

stricture moves progressively up the esophagus. Patients who have a stricture in the absence of

Barrett's esophagus should have the presence of gastroesophageal reflux documented before the

presence of the stricture is ascribed to reflux esophagitis. In patients with normal acid exposure,

the stricture may be due to cancer or a drug-induced chemical injury, the latter resulting from the

lodgment of a capsule or tablet in the distal esophagus. In such patients, dilation usually corrects

the problem of dysphagia. It is also possible for drug-induced injuries to occur in patients who

have underlying esophagitis and a distal esophageal stricture secondary to gastroesophageal

reflux. In this situation, a long string-like stricture progressively develops as a result of repetitive

caustic injury from capsule or tablet lodgment on top of an initial reflux stricture. These

strictures are often resistant to dilation.

Esophageal shortening is a consequence of scarring and fibrosis associated with repetitive

esophageal injury. The presence of a stricture is among the most reliable indicators of the

possibility of a short esophagus. Anatomic shortening of the esophagus can compromise the

ability to perform an adequate tension-free fundoplication and may result in an increased

incidence of breakdown or thoracic displacement of the repair. Esophageal length is best

assessed preoperatively using video roentgenographic contrast studies and endoscopic findings.

Endoscopically, hernia size is measured as the difference between the diaphragmatic crura,

identified by having the patient sniff, and the GE junction, identified as the loss of gastric rugal

folds. We consider the possibility of a short esophagus in patients with strictures or those with

large hiatal hernias (greater than 5 cm), particularly when the latter fail to reduce in the upright

position on a video barium esophagram.

The definitive determination of esophageal shortening is made intraoperatively when,

after thorough mobilization of the esophagus, the GE junction cannot be reduced below the

diaphragmatic hiatus without undue tension on the esophageal body. Surgeons performing

fundoplication have reported varying incidences of esophageal shortening, attesting to the

2

judgment inherent in defining and recognizing “undue tension.” An advantage of transthoracic

fundoplication is the ability to mobilize the esophagus extensively from the diaphragmatic hiatus

to the aortic arch. With the GE junction marked with a suture, esophageal shortening is defined

by an inability to position the repair beneath the diaphragm without tension. In this situation, a

Collis gastroplasty coupled with either a partial or complete fundoplication may be performed.

Barrett’s Esophagus

The relief of symptoms remains the primary force driving antireflux surgery in patients

with Barrett’s esophagus. Healing of esophageal mucosal injury and the prevention of disease

progression are important secondary goals. In this regard, patients with Barrett’s esophagus are

no different than the broader population of patients with gastroesophageal reflux. Antireflux

surgery should be considered when patient factors suggest severe disease or predict the need for

long term medical management, both of which are almost always true in patients with Barrett’s

esophagus.

An important consideration is that patients with Barrett’s esophagus generally have

severe GERD, with its attendant sequelae such as large hiatal hernia, stricture, shortened

esophagus and poor motility. Compared to mild and nonerosive reflux disease, severe erosive

disease and Barrett’s esophagus are associated with significantly greater loss of the mechanical

antireflux barrier because of associated hiatal hernias and a hypotensive lower esophageal

sphincter. Surgical treatment with a laparoscopic Nissen fundoplication reduces the hiatal hernia,

improves the antireflux barrier and consequently provides similarly excellent symptom control.

Large studies in patients with typical acid reflux symptoms have been published from the U.S.

and Europe. In patients having laparoscopic Nissen at Emory University, relief of heartburn and

regurgitation occurred in 90%, and 70% were off all reflux medications at a mean follow-up of

11 years. These results emphasize the durability of the procedure as well as the persistent relief

of typical symptoms. Risk factors for persistent use of antacids post antireflux surgery include a

partial fundoplication, older age and female gender.

Studies focusing on the symptomatic outcome following antireflux surgery in patients

with Barrett’s esophagus document excellent to good results in 72-95% of patients at 5 years

following surgery. The outcome of laparoscopic Nissen fundoplication in patients with Barrett’s

esophagus has been assessed at 1-3 years after surgery. Hofstetter et al. reported the experience

at the University of Southern California (USC) in 85 patients with Barrett’s esophagus at a

median of 5 years after surgery. Fifty-nine had long and 26 short segment Barrett’s and fifty

underwent a laparoscopic antireflux procedure. Reflux symptoms were absent postoperatively in

79% of the patients. Postoperative 24-hour pH was normal in 17/21 (81%). Ninety-nine percent

of the patients considered themselves cured or improved and 97% were satisfied with the

surgery. In addition to symptomatic improvement in reflux after surgery, there is evidence that

mediators of esophageal inflammation implicated in carcinogenesis are decreased as well. Cox-2

gene expression is elevated in the distal esophagus of reflux patients, but the expression of Cox-2

and another inflammatory mediator Interleukin 8 can be decreased in the distal esophageal

mucosa after a fundoplication.

Dysplasia in Barrett’s Esophagus: The prevalence of dysplasia at diagnosis in patients

presenting with Barrett’s esophagus ranges from 15-25%, and approximately 5% of patients will

3

develop dysplasia each year. The identification of dysplasia in Barrett’s epithelium rests upon

histologic examination of biopsy specimens. The cytologic and tissue architectural changes are

similar to those described in ulcerative colitis. By convention, Barrett’s metaplasia is currently

classified into four broad categories:

1. No dysplasia

2. Indefinite for dysplasia

3. Low grade dysplasia

4. High grade dysplasia

There are few prospective studies documenting the progression of non-dysplastic

Barrett’s epithelium to low or high grade dysplasia. Those that are available suggest that 5-6%/yr

will progress to dysplasia and 0.5-1%/yr to adenocarcinoma. Once identified, Barrett’s

esophagus complicated by dysplasia should undergo aggressive therapy. Patients whose biopsies

are interpreted as indefinite for dysplasia should be treated with a medical regimen consisting of

60-80 mg of PPI therapy for 3 months and re-biopsied. Importantly, esophagitis should be

healed prior to interpretation of the presence or absence of dysplasia. The presence of severe

inflammation makes the microscopic interpretation of dysplasia difficult. The purpose of acid

suppression therapy is to resolve inflammation that may complicate the interpretation of the

biopsy specimen. If the diagnosis remains indefinite, the patient should be treated as if low grade

dysplasia were present with continued medical therapy or antireflux surgery and repeat biopsy

every 6 months.

High grade dysplasia (HGD) should be confirmed by two pathologists knowledgeable in

GI pathology. Once HGD is confirmed, observation is less than optimal as > 50% of patients will

progress to multifocal HGD or cancer. Until recently esophagectomy was considered the

standard of care for patients with high grade dysplasia. With the Western acceptance of an

Eastern modality, endoscopic mucosal resection (EMR) coupled with radiofrequency ablastin, is

now the most common treatment for patients with high grade dysplasia and intramucosal

cancers. The aim of EMR is to excise the area of interest including the mucosal and submucosal

layers down to the lamina muscularis propria allowing optimal histologic interpretation. Reports

from specialized centers combining EMR with mucosal ablation using either photodynamic or

radiofrequency energy, are encouraging with a high prevalence of eradication of

dysplasia/neoplasia. Ell and others initially showed that EMR is feasible and safe; however, in

one of their earlier reports, recurrent or metachronous carcinomas were found in 14% of 64

patients during one year follow-up.

Longer success rates with EMR for early Barrett’s cancer have been reported from the

experienced centers. The largest study comes from Wiesbaden, Germany, involving over 300

patients with high grade dysplasia or intramucosal cancers and a mean follow-up of over 5 years.

A complete response was achieved in 97% of patients, and surgery was necessary in 3.7% after

endoscopic therapy failed. Metachronous lesions developed during the follow-up in 21% of the

patients. The risk factors most frequently associated with recurrence were piecemeal resection,

long-segment Barrett's esophagus and multifocal lesions.

1

Redo Operations – When, How and Who?

Bernard Dallemagne, M.D

Department of Digestive & Endocrine Surgery NHC - Les Hôpitaux Universitaires de Strasbourg Scientific Co-Director Digestive Cancer Research Institute (IRCAD) European Institute of Telesurgery (EITS)

1 place de l'Hopital - Hopitaux Universitaires 67091 STRASBOURG Cedex FRANCE

[email protected]

2

Since its introduction in 1991, laparoscopic antireflux surgery (LARS) has rapidly been

incorporated into the management algorithm of gastroesophageal reflux disease (GERD)

by both physicians and surgeons[1]. Given the lower morbidity rate of the laparoscopic

approach versus conventional open procedures for antireflux surgery, patients and

physicians have become more willing to consider surgery as an alternative to lifelong

medical therapy of GERD.

The results of most of the published clinical series have been excellent, with good

symptomatic outcomes in 85% to 90% of patients up to 10 years after surgery[2-4].

However, fundoplication has a published failure rate ranging from 3 to 30%[5].

Revisional surgery is necessary in 3% to 6% of these patients[6, 7].

Reoperative procedures are more technically demanding than primary fundoplications.

Moreover, anatomic defects that precipitated the failure may add to the technical

difficulty. A recent review found the average success rate after laparoscopic redo

operations to range between 65 to 100%. The broad range of values within this review,

65 to 100%[5], is at least partially due to the lack of a standard method for defining

success. Most studies have been directed toward the feasibility of and the subjective

outcome, whereas objective data on postoperative results are rarely available. Follow up

is rather short, not over 50 months.

Furnée et al.[8] reported symptomatic and objective success rate of 70% after 144 re-

operation regardless of the surgical approach laparotomy (34.7%), laparoscopy (11%) or

thoracotomy(54.2%). Mean follow-up was 60.1 months (37.2). They use a selective

approach, abdomen versus thorax, depending on the location of the wrap.

The pattern of anatomical failure of the fundoplication is similar after open and

laparoscopic procedures. Recurrent herniation, which includes migration of the wrap,

paraesophageal hernia or recurrent hiatal hernia with wrap disruption, and mis-

placement or displacement of the wrap on the stomach (slippage) are the leading

indications for redo (70-75%). Dysphagia and recurrent GERD are the most common

symptoms[5, 8, 9].

3

In a recent study of long term results (mean follow-up of 75 months) we observed rather

disappointing, both on an anatomical and subjective point of view[10]. Anatomical failure

is demonstrated in 46% of patients after redo for herniation and in 27% after slippage.

Resolution of the symptoms that justified redo surgery was achieved in 72 % of patients

operated for recurrence, and 68.7 % of patients operated for dysphagia. The global score

of GIQLI is significantly lower when compared to healthy patients and patients with a

successful primary repair GIQLI is significantly lower in patients with anatomical failure

(p=0.04). The probability of being free of failure at 5 years after the operation is 83%

after redo for herniation, 93% after redo for slippage. After 10 years the probability is

37% and 50% respectively. A third operation was needed in 7 patients (7.3%) in these

groups of failures.

Our 5 years results compare favourably with the 75 to 81% objective success rate

reported in the literature at a mean follow-up of 34.2 months[8]. Longest follow-up is

more disappointing and this highlights the need for long-term study in the evaluation of a

surgical procedure for functional disease.

Hypotheses that might explain failure rate may be the surgeon’s experience, the surgical

approach or the surgical reoperative procedure.

Surgeons involved in our study had a large experience in open and laparoscopic

antireflux surgery. Long term results obtained after primary repair were comparable to

those reported in the literature.

In a recent review of the literature, success rate after laparoscopic reoperation seemed

higher than after conventional approach, respectively 85.8 ± 5.6% and 78±10.1%[8].

This review highlighted the paucity of consistent reports and only 17 studies reported

objective outcomes. In the largest series of open redo, Deschamps reported 60.2% good

to excellent functional results at a median follow-up of 31 months in 156 patients[11].

Ten percents of patients required an additional operation. Complications occurred in

25.4% of these patients and length of stay was 9 days. At this point, we can consider

that the laparoscopic approach for redo is safer than open surgery, and yields similar

results at short or median follow-up[8, 12].

4

Therefore, surgical strategy may be questionable.

Herniation, in its different forms of presentation, can be caused by an inadequate crural

repair or an excessive traction applied on the esophagus when the GE junction is

repositioned below the diaphragm. Slippage or mis-placement of the antireflux wrap, can

be caused by an inadequate anchoring of the valve on the GE junction or by an excessive

traction on the esophagus. Crural repair is a point of controversy, some advocating wide

use of prosthetic reinforcement[13]. Yet, Koch et al.[14] recently reported a 50%

recurrence rate after reoperation for herniation with a mesh reinforced crural repair.

Similarly, in our experience, mesh does not prevent recurrence and achieves similar

results as sutures reinforced with Teflon pledegts. The risks associated with the latter are

nil, compared to some disastrous complications of mesh[15].

The common denominator for herniation and slippage recurrence, which is excessive

traction on the esophagus, addresses the question of short esophagus, which existence is

recognized by experienced centres[16-18]. In our technique, we perform systematically

an extensive mediastinal dissection, up to the level of the pulmonary veins. It’s obviously

insufficient and we probably missed some shortened esophagus. We performed only 5

Collis Nissen, and 3 of these patients are still free of symptoms and anatomical

recurrence more than 6 years after the operation. More liberal use of lengthening

procedure is probably the condition of success. In the Mayo series of open reoperations

described above, a Collis gastroplasty was performed in 62.7% of patients[11]. The

Pittsburgh group performed laparoscopic gastroplasty in 52.5% of patients in whom less

than 3 cm of tension-free intraabdominal esophagus is present[17].

Our experience and review of literature suggest that typical failure patterns after primary

antireflux repair should be initially approached laparoscopically, with a liberal use of

esophageal lengthening procedure for suspected esophageal shortening. Thoracotomy

does not provide clear and substantial advantages[19]. Failure to re-establish the normal

anatomy, which is more likely in patients with multiple failed antireflux surgeries, should

lead to consideration of other options such as near esophagojejunostomy or

esophagectomy[20].

5

References

1. Dallemagne B, Weerts JM, Jehaes C, Markiewicz S, Lombard R: Laparoscopic

Nissen fundoplication: preliminary report. Surg Laparosc Endosc 1991, 1(3):138-

143.

2. Dallemagne B, Weerts J, Markiewicz S, Dewandre JM, Wahlen C, Monami B, Jehaes

C: Clinical results of laparoscopic fundoplication at ten years after surgery. Surg

Endosc 2006, 20(1):159-165.

3. Lundell L, Miettinen P, Myrvold HE, Hatlebakk JG, Wallin L, Malm A, Sutherland I,

Walan A: Seven-year follow-up of a randomized clinical trial comparing proton-

pump inhibition with surgical therapy for reflux oesophagitis. British Journal of

Surgery 2007, 94(2):198-203.

4. Lafullarde T, Watson DI, Jamieson GG, Myers JC, Game PA, Devitt PG:

Laparoscopic Nissen fundoplication: five-year results and beyond. Arch Surg

2001, 136(2):180-184.

5. van Beek D, Auyang E, Soper N: A comprehensive review of laparoscopic redo

fundoplication. In: Surgical Endoscopy. Springer New York; 2010: 1-7.

6. Catarci M, Gentileschi P, Papi C, Carrara A, Marrese R, Gaspari AL, Grassi GB:

Evidence-based appraisal of antireflux fundoplication. Ann Surg 2004, 239(3):325-

337.

7. 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.

8. Furnee EJ, Draaisma WA, Broeders IA, Gooszen HG: Surgical reintervention after

failed antireflux surgery: a systematic review of the literature. J Gastrointest Surg

2009, 13(8):1539-1549.

9. Siewert JR, Isolauri J, Feussner H: Reoperation following failed fundoplication.

World J Surg 1989, 13(6):791-796; discussion 796-797.

10. Dallemagne B, Sanchez MA, Francart D, Perretta S, Weerts J, Markiewicz S, Jehaes

C: Long-term results after laparoscopic reoperation for failed antireflux

procedures. Brit J Surg 2011, 98(11):1581-1587.

11. Deschamps C, Trastek VF, Allen MS, Pairolero PC, Johnson JO, Larson DR: Long-

term results after reoperation for failed antireflux procedures. J Thorac

Cardiovasc Surg 1997, 113(3):545-550; discussion 550-541.

12. Hunter JG, Smith CD, Branum GD, Waring JP, Trus TL, Cornwell M, Galloway K:

Laparoscopic fundoplication failures: patterns of failure and response to

fundoplication revision. Ann Surg 1999, 230(4):595-604; discussion 604-596.

13. Granderath FA, Kamolz T, Schweiger UM, Pointner R: Laparoscopic

refundoplication with prosthetic hiatal closure for recurrent hiatal hernia after primary failed antireflux surgery. Arch Surg 2003, 138(8):902-907.

14. Koch O, Asche K, Berger J, Weber E, Granderath F, Pointner R: Influence of the size

of the hiatus on the rate of reherniation after laparoscopic fundoplication and refundopilication with mesh hiatoplasty. In: Surgical Endoscopy. Springer New

York; 2010: 1-7.

15. Zugel N, Lang R, Kox M, Huttl T: Severe complication of laparoscopic mesh

hiatoplasty for paraesophageal hernia. Surgical Endoscopy 2009, 23(11):2563-

2567.

16. Horgan S, Pohl D, Bogetti D, Eubanks T, Pellegrini C: Failed antireflux surgery:

what have we learned from reoperations? Arch Surg 1999, 134(8):809-815;

discussion 815-807.

6

17. Luketich JD, Fernando HC, Christie NA, Buenaventura PO, Ikramuddin S, Schauer

PR: Outcomes after minimally invasive reoperation for gastroesophageal reflux

disease. The Annals of Thoracic Surgery 2002, 74(2):328-332.

18. Khajanchee YS, O'Rourke R, Cassera MA, Gatta P, Hansen PD, Swanstrom LL:

Laparoscopic reintervention for failed antireflux surgery: subjective and objective outcomes in 176 consecutive patients. Arch Surg 2007, 142(8):785-901;

discussion 791-782.

19. Furnee EJB, Draaisma WA, Broeders IAMJ, Smout AJPM, Gooszen HG: Surgical

Reintervention After Antireflux Surgery for Gastroesophageal Reflux Disease: A Prospective Cohort Study in 130 Patients Arch Surg 2008, 143(3):267-274.

20. Pennathur A, Awais O, Luketich JD: Minimally Invasive Redo Antireflux Surgery:

Lessons Learned. The Annals of Thoracic Surgery 2010, 89(6):S2174-S2179.

HIATAL HERNIA

C. Daniel Smith, M.D., F.A.C.S.

Professor and Chair

Department of Surgery

Mayo Clinic

Jacksonville, Florida

Phone: 904-953-1491

Fax: 904-953-7368

e-mail: [email protected]

Paraesophageal Hiatal Hernia, CD Smith, Page 2

INTRODUCTION

The terms paraesophageal hernia and hiatal hernia are often intermixed and used

synonymously to describe enlargement of the esophageal hiatus and the subsequent

transdiaphragmatic migration of intraabdominal content, most commonly the gastric cardia and

fundus. While this exchange of terms is reasonable for healthcare providers who primarily

diagnose the anatomically enlarged esophageal hiatus, the distinction between paraesophageal

and hiatal hernia becomes important when considering how patients with this defect should be

managed. Hiatal hernia describes all types of defects involving the esophageal hiatus, of which a

subset are known as paraesophageal hernias. The anatomic differences help predict the natural

history and guide decisions about management.

PATHOPHYSIOLOGY AND CLASSIFICATION

While the exact etiology of a hiatal hernia is unknown, what is clear is that attenuation of

the phrenoesophageal membrane allows the gastroesophageal junction (GEJ) to migrate through

a patulous hiatus into the chest or the gastric fundus to herniate along side the GEJ and into the

chest. While the nature of these defects remains unknown, all types of hiatal hernias are more

common in older individuals, and recent studies suggest hiatal hernia is more common among

the obese and those with delayed gastric emptying. All of this suggests an acquired weakness of

tissue as a result of aging or excess strain on the diaphragm.

There is a well-described familial occurrence of hiatal hernias believed to represent an

autosomal-dominant link with variable clinical expression. Younger siblings of children who

have a hiatal hernia are twenty times more likely to have a hiatal hernia themselves. Some have

suggested that any hiatal hernia in a young patient indicates an underlying congenital problem.

Clearly, confounding data is available from which to guess about etiology.


Hiatal hernias are classified according to the anatomic position of the GEJ and the extent

of stomach herniated (Table 1). Type I hiatal hernia, also known as a sliding hiatal hernia,

consists of a simple herniation of the gastroesophageal junction into the chest. The

phrenoesophageal ligament is attenuated and there is no true hernia sac. This is the most

common type of hiatal hernia, is more common in women and in the fifth and sixth decades of

life. Type II hiatal hernia, commonly referred to as a true paraesophageal hernia, denotes when

the GEJ remains at the esophageal hiatus while the gastric fundus herniates alongside the

esophagus into the chest. The type III hiatal hernia is a combination of type I and type II hernia,

with the GEJ being displaced into the chest along with the gastric fundus and body.

Paraesophageal hernias (types II and III) have a true hernia sac accompanying the herniated

stomach. This becomes important when surgical repair is undertaken as the sac must be excised.

Finally, some have characterized a type IV hernia as an advanced stage of hiatal hernia where the

entire stomach and other intraabdominal content (e.g., colon, spleen, etc.) are herniated into the

chest. Use of this fourth classification is not widely accepted.

INCIDENCE

While the exact prevalence of hiatal hernia remains unknown, it is clear that it is a

relatively common abnormality and is the most common finding reported on barium studies of

the upper gastrointestinal tract. The difficulty in establishing the incidence of hiatal hernia lies in

the fact that a large number of patients with hiatal hernia are asymptomatic, and the diagnosis is

often made incidentally during investigation of other gastrointestinal problems.

In contrast to all hiatal hernias, paraesophageal hernia is a very rare type of hiatal hernia.

In a series of 46,236 Mayo Clinic patients with hiatal hernias, only 147 (0.32%) were type II or


true paraesophageal hernias, with women twice as likely to have this type of hernia as men. The

frequency of paraesophageal hernia increases with advancing age.

SYMPTOMS AND PRESENTATION

Most Type I and III hiatal hernias are diagnosed incidentally during a contrast upper GI or

during upper endoscopy performed for other reasons. Type II hernias can be similarly diagnosed,

but are also frequently found on a radiograph of the chest showing an air-fluid-level in the

mediastinum or the left chest. Occasionally, the inability to pass a nasogastric tube followed by a

contrast study reveals a twisted intrathoracic stomach, or a contrast study of the colon reveals

colon in the chest leading to the diagnosis of a type IV hernia.

When symptoms are present, sliding hernias have a different presentation than

paraesophageal hernias. Type I hernias are frequently accompanied by symptoms of

gastroesophageal reflux (GERD), most commonly heartburn or regurgitation. Type II and III

hernias tend to produce symptoms that are more mechanical in nature due to the anatomic

consequence of the hiatal outflow restriction. Typical symptoms include epigastric pain,

postprandial fullness or discomfort in the chest, dysphagia, abdominal bloating, and respiratory

problems. Again, these symptoms are caused by hiatal outflow restriction, altered gastric

anatomy, and distension of the intrathoracic portion of the stomach with esophageal or

pulmonary compression. Interestingly, patients often report a remote history of GERD type

symptoms that abruptly abate and are replaced by obstructive symptoms; this thought to occur as

the hernia enlarges and the esophageal outlet becomes obstructed.

Acute symptoms may develop as a consequence of complete obstruction or strangulation

of the stomach within the chest mimicking myocardial infarction. Type II hernias are at

particular risk for incarceration with obstruction, strangulation and perforation of the herniated


stomach. Borchardt’s triad comprised of chest pain, retching with inability to vomit, and

inability to pass a nasogastric tube is indicative of an incarcerated hernia and is a surgical

emergency.

An often-overlooked presentation is anemia from chronic GI blood loss. This occurs in

1/3 of patients with type II hernias and prompts an often-exhaustive evaluation for cause. This

anemia is caused by linear ulcerations of the gastric cardia resulting from the proximal stomach’s

repetitive movement across the diaphragm. Ninety two percent of patients will have their anemia

resolve after surgical correction of the hernia.

MANAGEMENT

While most hiatal hernias are asymptomatic, the diagnosis is rarely in question when

patients present with symptoms as outlined above and a chest x-ray or contrast esophogram

confirming the defect. An EGD should be attempted in all patients to assess the distal esophagus

and stomach for concomitant pathology, with caution not to over inflate the stomach that may be

incarcerated in the chest. While motility studies may help identify the patient with esophageal

motor abnormality and direct the type of fundoplication used in repair, the distortion of the GEJ

and distal esophagus makes motility studies difficult to acquire and interpret. For this reason,

motility studies are not useful for most type II and III hernias. The same is true of 24-hour pH or

gastric emptying studies. These studies can be difficult to interpret and rarely change the

decisions regarding management. A CT scan of the chest and abdomen may help confirm the

extent of the hernia, but are not necessary for straightforward cases.

Since hiatal hernia is a purely mechanical abnormality, there is no non-operative

treatment. Currently there is controversy about which patients should undergo repair.

Traditionally it has been held that all patients with type II or III hernias should undergo surgical


repair regardless of symptoms. This has been based on a report in 1967 documenting a 30%

mortality in patients with paraesophageal hernia (6 of 21 patients died secondary to

complications of their hernia). More recently, a series of 23 patients with a paraesophageal

hernia were followed for a median of 78 months and no life threatening complications developed

in this group and symptoms remained unchanged in 83% of these patients. This has lead many to

recommend repair in only select asymptomatic patients. In contrast, those with symptoms,

esophageal mucosal damage (esophagitis or Barretts), or anemia should undergo elective repair.

Similarly, a significant number of patients with type I hiatal hernias are asymptomatic and

remain so throughout the remainder of their life. Therefore, the presence of a sliding hiatal

hernia alone does not mandate intervention. However, those patients with a Type I hernia and

gastroesophageal reflux, chest pain, dysphagia, regurgitation or other symptoms referable to their

hernia, should undergo symptom specific workup, and may be best served with an operative

repair.

OPERATIVE TECHNIQUE

Operative correction of esophageal hiatal hernia regardless of technique should 1) return

the herniated content to its anatomically correct position below the diaphragm, 2) resect the

hernia sac, 3) establish adequate esophageal length and return the GEJ to an intraabdominal

position, 4) repair the hernia defect, and 5) prevent recurrence while minimizing associated

morbidity. There are a number of proven operations that can be performed through the chest or

abdomen to accomplish these goals.

Currently, the most common approach to hiatal hernia repair is transabdominal using

laparoscopy, although many advocate the open transabdominal approach. Debate continues over

whether a laparoscopic approach compromises the long-term outcome of the repair (see


Controversies below). While most would agree that the laparoscopic approach is preferred due

to the enhanced recovery associated with laparoscopy, especially in this typically more elderly

patient population, it is clear that the laparoscopic approach is more technically challenging and

if performed by inexperienced surgeons may lead to a higher incidence of peri-operative

complications or long-term failure. On the other hand, when performed by an experienced

laparoscopist and foregut surgeon, the technique of the operation should not differ from that

performed open and thereby lead to no differential outcome.

Historically the thoracic approach has been preferred for larger hernias and those with

suspected esophageal shortening. The relative ease of dissecting the hernia sac and mobilizing

the esophagus makes this approach appealing in select settings. However, the morbidity

associated with a thoracotomy, both immediately postoperatively and long-term with chronic

incisional problems makes this approach appealing in only a small subset of patients.

OUTCOMES

The outcomes of hiatal hernia repair can be broken into symptomatic outcomes and

anatomic outcomes. When considering symptomatic response to operative repair, 88% of

patients after hiatal hernia repair report a significant improvement or resolution of their

preoperative symptoms. This response appears durable with sustained symptom improvement

for up to 4 years after surgery. Ninety-two percent of those with anemia have resolution after

hernia repair. On the other hand, anatomic failure after hernia repair remains very high, with up

to 41% of patients demonstrating recurrent hernia an average of 4 years after repair. Some have

suggested that this rate of anatomic failure is lower when the repair is performed open (see

Controversies below). Regardless, the significance of these anatomic failures remains debated.

A small transdiaphragmatic migration of the wrap or GEJ, essentially an asymptomatic type I


hernia, is clinically inconsequential. To aspire to a higher rate of anatomic success risks over

treatment and potentially profound complications, especially when mesh is used in the repair.

CONTROVERSIES

Should an antireflux procedure accompany all hiatal hernia repairs?

Whether or not to include an antireflux procedure with all hiatal hernia repairs remains

controversial, especially when dealing with a type II paraesophageal hernia. Since most sliding

type hernias are repaired based on symptoms, adding an antireflux procedure seems more

straightforward due to the prevalence of reflux symptoms in type I and III hernias. In contrast,

most patients who have type II hernias do not have reflux symptoms, and adding an antireflux

operation in these patients may add little to the outcome. However, with careful questioning,

many patients with type II hernias give a history of GERD symptoms that spontaneously abated,

suggesting an anatomic change (perhaps hernia development) leading to this resolution of

symptoms. Recent data from small series are suggesting that GERD may be more prevalent in

type II hernia than earlier recognized, and up to 30% of patients without GERD preoperatively

will have GERD unmasked after hiatal hernia repair.

The role of fundoplication in patients with type II paraesophageal hernia remains

controversial. Conventional thinking suggests that because the lower esophageal sphincter is

located within the abdomen, it is competent and fundoplication is unnecessary. On the other

hand, a key principle in repairing a hiatal hernia is to anchor the stomach within the abdomen to

help prevent recurrence, and some surgeons are now using a fundoplication to serve as this

anchor (the wrap buttresses against the hernia repair and holds the distal esophagus and stomach

intra-abdominally). In up to one third of patients, adding fundoplication may avert the

unmasking of GERD following repair. This rationale is leading many surgeons to use


fundoplication routinely for all hiatal hernia repairs. Early data suggests that this is a safe and

effective means of managing paraesophageal hernias. However, few studies have objectively

evaluated addition of an antireflux procedure to hiatal hernia repair, and there is limited data

available to definitively answer this question.

Should hiatal hernias be repaired laparoscopically?

The role of laparoscopy in repairing hiatal hernias has recently been challenged.

Anecdotal data suggests that the risk of esophageal or gastric perforation and hernia recurrence is

higher following laparoscopic repair than after traditional open hiatal hernia repair. The

proposed basis for this is increased technical demands with a laparoscopic approach, the

difficulty closing the attenuated esophageal hiatus laparoscopically, and the relative absence of

intraabdominal adhesions that accompanies laparoscopic hernia repair as compared to open

operations. The absence of these adhesions to anchor the stomach and distal esophagus allows

the stomach to more readily “slip” back through the esophageal hiatus and into the chest than

would be the case with the adhesions associated with open repairs. These anecdotal experiences

need further investigation before any conclusions regarding route of abdominal access for repair

of hiatal hernia can be made, and most would agree that a laparoscopic repair performed by a

skilled laparoscopic foregut surgeon should not have any higher rate of complications or failure.

Should mesh be used to repair all hiatal hernias?

The high rate of anatomic failure of hiatal hernia repairs has lead many to suggest that

some sort of prosthetic should be used to reduce these failures. Many argue that the principle of

“tension-free” repair embraced for abdominal wall hernias is generalizable to hiatal hernias as

well. Over the past several years many types of prosthetic material has been used empirically for

reinforcement of the crural repair or hiatal reconstruction for the crura which cannot be


approximated. A non-randomized prospective study suggested a lower recurrence rate without

any increase in dysphagia in a series of patients where permanent mesh (polypropylene) was used

in all patients undergoing laparoscopic Nissen fundoplication. A more recent collection of

experience from several experienced foregut surgeons identified over 20 patients in whom mesh

was used to reconstruct the esophageal hiatus and subsequently eroded into the esophagus

leading to significant complications including progression to esophagectomy is several patients.

These findings have led many to advocatebioprosthetic mesh that can be used to decrease

the hiatal hernia recurrence rate without such complications. A multicenter, prospective

randomized trial compared the use of a crural buttress using a mesh constructed from porcine

small intestinal submucosa compared to primary repair.51 This study utilized barium swallow X-

rays performed at 6 months postoperatively that demonstrated anatomic hiatal hernia recurrence

in 24% of patients undergoing primary repair compared to only 9% of patients receiving the

bioprosthetic buttress. However, in an update at 5 years postoperatively, the recurrence rate was

nearly identical between the two groups, and in excess of 50%.52 It should be noted that the

majority of recurrent hiatal hernias were small type I hernias resulting in few symptoms. Thus, at

the current time, although the rationale for the use of mesh at the esophageal hiatus to decrease

tension and thus minimize hernia recurrence is cogent, it is unclear if mesh should be used, and if

so, what type.

These findings have led many to look to a bio-mesh that can be used to decrease the hiatal

hernia recurrence rate without such complications. A multicenter, prospective randomized trial

compared the use of a crural buttress using a mesh constructed from porcine small intestinal

submucosa compared to primary repair. Barium swallow performed at 6 months postoperatively


revealed anatomic hiatal hernia recurrence in 24% of patients undergoing primary repair

compared to only 9% of patients receiving the bioprosthetic buttress. However, at 5 years

postoperatively, the recurrence rate was nearly identical between the two groups and in excess of

50%. As had already been demonstrated in other studies, the majority of recurrent hiatal hernias

were small type I hernias with few symptoms. Thus, at the current time, although the rationale for

the use of mesh at the esophageal hiatus to decrease tension and thus minimize hernia recurrence

is appealing, it is unclear if mesh use provides any real benefit and is it should be used at all, and

if so, what type.


SUGGESTED READINGS

Skinner DB, Belsey RH: Surgical management of esophageal reflux and hiatus hernia. Long-

term results with 1,030 patients. J Thorac Cardiovasc Surg 1967; 53: 33.

Terry M, Smith CD, Branum GD, Galloway K, Waring JP, Hunter JG. Outcomes of laparoscopic

fundoplication for gastroesophageal reflux disease and paraesophageal hernia. Surgical

Endoscopy 2001;15(7): 691-699.

Mattar SG, Bowers SP, Galloway KD, Hunter JG, Smith CD. Long-term outcome of

laparoscopic repair of paraesophageal hernia. Surgical Endoscopy 2002;16(5): 745-749.

Lin E, Swafford V, Chadalavada R, Ramshaw BJ, Smith CD. Disparity between symptomatic

and physiologic outcomes following esophageal lengthening procedures for antireflux surgery.

Journal of Gastrointestinal Surgery 2004;8(1): 31-39; discussion 38-39.

Smith CD, McClusky DA, Rajad MA, Lederman AB, Hunter JG. When fundoplication fails:

redo? Annals of Surgery 2005;241(6): 861-869; discussion 869-871.

El Sherif A. Yano F. Mittal S. Filipi CJ. Collagen metabolism and recurrent hiatal hernia:

cause and effect? Hernia 2006; 10:511-20.

Oelschlager BK. Pellegrini CA. Hunter J. Soper N. Brunt M. Sheppard B. Jobe B. Polissar N.

Mitsumori L. Nelson J. Swanstrom L. Biologic prosthesis reduces recurrence after laparoscopic


paraesophageal hernia repair: a multicenter, prospective, randomized trial. Annals of Surgery

2006; 244:481-90.

Oelschlager BK, Pellegrini CA, Hunter JG, et al. Biologic prosthesis to prevent recurrence after

laparoscopic paraesophageal hernia repair: long-term follow-up from a multicenter, prospective,

randomized trial. Journal of the american college of surgeons. 2011;213(4):461-8.


TABLE

Table 1. Classification of Hiatal Hernias.

Hernia Type Location of Gastroesophageal Junction Hernia Contents

I (Sliding) Intrathoracic Gastric Cardia ± Fundus

II (True Paraesophageal) Intraabdominal Gastric Fundus ± Body

III (Combination I & II) Intrathoracic Gastric Fundus and Body

IV Intrathoracic Gastric Fundus, Body and other

abdominal organs (e.g., colon)

Beyond GERD and Hiatal

Hernia:

What To Do in the Obese?

Samer G. Mattar, MD, FACS, FASMBS

Associate Professor of Surgery

Indiana University School of Medicine

Epidemiology

• The prevalence of obesity has increased dramatically from 13% to 34% in US population.

• The prevalence of GERD has increased • The prevalence of GERD has increased significantly over past 40 years (20%-30% of

population).

• There appears to be a dose-response relationship between BMI and GERD (gain

BMI 3.5 units = 3 fold increase in GERD symptoms.)Friedenberg et al; Am Coll Gastroenterol:2008Serag; Dig Dis Sci:2008

Epidemiology

• Nearly all epidemiological studies have found an association between obesity and GERD.

• There is a linear relationship between BMI • There is a linear relationship between BMI and GERD symptoms.

• Central adiposity may be the most important risk factor.

Epidemiology

• Waist circumference, rather than BMI, appears

to be has a stronger link (OR 4.3) with long-

segment BE.

• In another study, patients obese > 20 years had • In another study, patients obese > 20 years had

an OR 16.2 for developing esophageal

adenocarcinoma.

• The incidence of esophageal cancer has

increased >650% over past 35 years.

Edelstein et al; Gastroenterol: 2007

Lagergren J et al; Gut 2000

Brown et al. J Natl Cancer Inst 2008; 100:1184-87

Epidemiology

• In a pooled analysis of 12 epidemiological international

studies (BEACON), there were 1997 OA cases, 1990

OGJA cases, and 11,160 control subjects.

• By logistic regression and random-effects meta-analysis, • By logistic regression and random-effects meta-analysis,

BMI ≥40 was associated with both OA (OR 4.76, 95% CI

2.96-7.66) and OGJA (OR 3.07, 95% CI 1.89-4.99).

• There was synergistic interaction between BMI and

GERD symptoms in relation to OA/OGJA risk.

Hoyo C et al. Int. J. Epidemiol. 2012;ije.dys176

Restricted cubic spline models of the relationship between body mass index and adenocarcinomas of the oesophagus and oesophagogastric junction.

OA

MalesFemales

Hoyo C et al. Int. J. Epidemiol. 2012;ije.dys176

OGJA

Males Females

Epidemiology

• There was no evidence of effect modification when

stratified by GERD symptoms, suggesting an indirect

proinflammatory route of association between BMI and

OA/OGJA exists.

• The higher prevalence in men may be due to the typical

android fat patterning, with highly metabolic visceral

adipose.

• Obesity-related hormones may induce esophageal

inflammatory damage, promoting proliferation and

malignant transformation.Hoyo C et al. Int. J. Epidemiol. 2012;ije.dys176

Esophageal Acid Exposure in the

Obese (48h)

8

10

12

Normal Weight

157 patients

0

2

4

6

Total Upright Supine

Normal Weight

Overweight

Obese

Percent pH<4

Crowell et al; Am J Gastroenterol:2009

Causes of GERD

• Reduced LES sphincter pressure.

• Increased frequency of transient LES

relaxations.

• Increased prevalence of hiatal hernias.• Increased prevalence of hiatal hernias.

• Increased prevalence of esophageal motor

disorders.

• Increased prevalence of gastric motor disorders.

• Pro-inflammatory agents?

Causes of GERD

Do these factors apply in the morbidly obese?in the morbidly obese?

Unidentified cause of GERD in the

Morbidly Obese?

15

20

25

599 patientsMO was independently associated with GERD severity

0

5

10

15

Normal Wt MO

HTN LES

HTN DE Amp

%

Herbella et al; J of Gastrointest Surg: 2007

Nissen Fundoplication in the

Morbidly Obese

20

25

30

35

187 patients

0

5

10

15

20

NW OW OB

Recurrence (%)

Perez et al; Surg Endosc:2001

Surgical Options

• Gastric bypass

• Adjustable gastric band

• Sleeve gastrectomy

• Duodenal switch• Duodenal switch

• NOTES

Roux-en-Y Gastric Bypass

• Significant weight loss

• Reduced abdominal

pressure

• Diversion of acid and • Diversion of acid and

bile

• Small gastric pouch

• Few parietal cells

Roux-en-Y Gastric Bypass

8

10

12

20 patients

0

2

4

6

Preop Postop

pH<4 (%)

Mejia-Rivas et al; Obes Surg: 2008

Adjustable Gastric Band

• Controversial

• Conflicting outcome

reportsreports

• MUST repair crural

defect if hiatus hernia

present.


• Initial improvement of GERD in band patients.

• Gastric band may act to reinforce anti-reflux mechanism.reflux mechanism.

• However, there is an increased incidence of 20.5 % of developing late GERD

Dixon and O,Brien; Obes Surg; 1999Himpens et al; Obes Surg: 2006


• Retrospective study

• 1298 LAGB only vs. 520 LABG + HHR

• Mean FU = 25 months vs. 20 months

• Reoperation rate = 5.6% vs. 1.7%• Reoperation rate = 5.6% vs. 1.7%

• Reoperations were for HH, band slip, or pouch dilatation.

• Conclusion: Adding HHR to LAGB reduced the reoperation rate.

Gulkarov et al. Surg Endosc 2008;22(4):1035-45

Sleeve Gastrectomy

SG may exacerbate GERD due to:

- generation of high

intragastric pressuresintragastric pressures

- division of sling fibers

- disruption of angle of

His

- narrowing at incisura

Sleeve Gastrectomy

Prerequisites in GERD patients:

- repair hiatal hernia- repair hiatal hernia

- do not use a very

small bougie

• 176 patients with Sleeve Gastrectomy

• 34.6% Pre-op GERD

• Post-op(<30d) GERD = 49%.

• Persistent(>30d) GERD = 47.2%.

• Medication for GERD 33.8%

Prevalent Thinking

• Medication for GERD 33.8%

Carter PR, Leblanc KA et al. SOARD 7 2011(569-574)

*Anterior repair of Hiatus Hernias

Prevalent Thinking

Himpens 2006: Band vs Sleeve:

Pre-existing GERD: 75% resolution after SG

butbut

22% denovo GERD cases developed at 1 year

but

GERD improved from year 1(22%) to 3(3%)

Himpens J, Dapri G, Cadiere GB. Obes Surg 2006;16:1450-6

Systematic review:

• 15 reports

• 4 showed increase in GERD

• 7 found reduced GERD

Prevalent Thinking

• 7 found reduced GERD

• 3 reported on only postoperative GERD prevalence.

• Conclusion: No consensus

Chiu, Birch et al. SOARD 7 (2011) 510-515

• 706 patients underwent sleeve gastrectomy

• 8 (1.1%) developed severe reflux symptoms and

proximal sleeve dilation.

Technical Factors: Effect on GERD

Keidar A, Baltasar A. Obes Surg. 2010 Feb; 20(2): 140-7.

proximal sleeve dilation.

• 1 required reoperation, 7 managed medically.

�20 patients had manometry pre and post SG

�BMI decrease: 38kg/m2 to 28.2kg/m2 at 6

months

Motility Factors: Effect on GERD

�Mean LESP preop 14.2 mmHg

�6 months postop 11.2 mmHg

�Ten with <6 mmHg.

�Explanation: resection of the sling fibers?.

Braghetto, I Obes Surg(2010) 20:357-362

Reasons why sleeve may REDUCE GERD

• Reduces acid production

• Removes the fundus which

is the source of relaxation

waves to the LES

• Reduces tension on gastric • Reduces tension on gastric

wall below the cardia

• Accelerates gastric

emptying

• Correct repair of HH

• Weight loss

Reasons why sleeve may

WORSEN or CAUSE GERD�� Aggressive encroachment at angle of His Aggressive encroachment at angle of His

may may resectresect sling fibers and reduce LESsling fibers and reduce LES

�� Narrowing at Narrowing at angularisangularis may create may create obstructionobstruction

�� Initial architecture may not remain static: Initial architecture may not remain static: �� Initial architecture may not remain static: Initial architecture may not remain static: pouch malformations leading to pouch malformations leading to obstruction and reflux can occur over obstruction and reflux can occur over time. time. IntrathoracicIntrathoracic migration, retained migration, retained fundusfundus..

�� Patent HH > 3cmPatent HH > 3cm

�� It may be “pseudoIt may be “pseudo--reflux” due to reflux” due to improper alimentation.improper alimentation.

Pouch Deformities may occur over time

and lead to reflux symptoms

• Coiling or Spiraling

• Dilated upper sleeve

• Others: angulation, volvulus, gastric atony, fundic regeneration, diverticulum.

• Options for Prevention:

– Avoid excess cardia

– Omental fixation to the new greater curve

– Create a slightly larger pouch at the angularis

Fixation

HH repair: Effect on GERD

• 378 SG pts

• All had preop manometry and 24h pH

• Preop GERD in 41pts.

• HH > 3cm was considered abnormal

• 97pts had concomitant posterior crural repair• 97pts had concomitant posterior crural repair

• GERD remission in 80% and reduction in 20%

• Denovo GERD in 23% of pts who had SG alone

• No denovo GERD in any pt with SG + HHR

• Is HHR protective against denovo GERD?

Soricelli E, Basso N, et al. SOARD 2012 in press

HHR and LRYGB

Controversial

• LRYGB is a very effective anti-reflux operation.

Herniated Gastric Pouch

Flanagin BA et al. Obes Surg 2010; 20(3):386

Impact of HHR and LRYGB

• Retrospective review of UHC data

• 1589 patients with HH had LRYGB only

• 644 patients had LRYGB + HHR

• There was no difference in mortality, • There was no difference in mortality, morbidity, 30 day readmission, LOS, and cost.

• Conclusion: LRYGB + HHR is safe

Kuthari et al Obes Surg 2012;22(10):1607-10

Summary

• Hiatus hernias are common in patients

undergoing bariatric surgery.

• It is recommended to repair HH in patients

having gastric band surgery.having gastric band surgery.

• In Sleeve Gastrectomy patients, there is

conflicting data, but trend is to offer it to patients

with HH and/or GERD.

• It is recommended that HH be repaired in

patients undergoing SG.

Summary

• In patients undergoing LRYGB, there is no additional M&M for concomitant repair of HH.

• Concomitant HHR and LRYGB may • Concomitant HHR and LRYGB may prevent gastric pouch herniation if HH are very large.

Emerging Technologies and Techniques in GERD

Reginald C.W. Bell M.D.

SurgOne Foregut Institute

401 W Hampden Place Suite 230

Englewood CO 80110

[email protected]

303-788-8989

Emerging Diagnostic Technologies

ENRD:

Current ambulatory imp/pH testing lacks sensitivity in diagnosis of endoscopy-negative GERD

(ENRD, no longer NERD), ranging from 0%-71%, and does not delineate injury to esophagus. The

finding of dilated intercellular spaces is considered a fairly specific finding of NERD, but is currently

not a practical test (where to biopsy, need for EM of biopsies).

Evaluation of mucosal impedance using a catheter at time of endoscopy may have a role in the

diagnosis of ENRD. [1] (Figures 1 and 2).

LPR:

Finding more specific methods of diagnosis LPR remains problematic, especially for surgeons

referred patients for antireflux procedures. Pepsin has been a topic of interest; recent report of no

Difference in pepsin or bile acids in induced sputum between patients with chronic cough and

controls[2].

Therapeutic Innovations The potential role of therapies other than laparoscopic fundoplication is significant.

Probably 30 million patients in the US have GERD. Thirty to 50% of patients treated with daily

PPIs are dissatisfied with the results of their therapy. Doubling PPI dose provides relief in 25% of this

subgroup.[3] Surgical treatment is often omitted from articles reviewing treatment of medically

refractory GERD (MRG) – indicating a failure of the surgical community to provide adequate treatment

options.

Laparoscopic fundoplication is performed approximately 25,000 cases per year in the US [4], or in

less than 1% of the 5-10 million patients with medically refractory GERD.

Antireflux surgery is invasive, creates a permanent change in gastroesophageal anatomy and

long-term outcomes are variable and highly dependent on the skill of the surgeon. Furthermore, the

efficacy of antireflux surgery deteriorates over time with substantial number of patients requiring

treatment with acid suppression medication for control of symptoms and revisional (re-do) surgery.

Antireflux surgery is associated with side effects such as dysphagia, bloating, inability to vomit, and

diarrhea, which, though infrequent, are genuine. These side effects and the need for reoperation are the

main drawbacks of antireflux surgery.

What should be the therapeutic goal of surgical treatment of GERD? A minority of patients with

refractory GERD do require near complete control of reflux to facilitate healing of esophagitis,

eliminate potential for aspiration, and so forth. However the majority of patients with refractory GERD

are looking for improved symptom control. 25-50% of patients rendered asymptomatic on PPIs have

excess esophageal acid exposure.

Radiofrequency Energy Delivery to the Lower Esophageal Sphincter

RF energy can be delivered to the LES using the Stretta Device. The device is currently available

commercially (Mederi Therapeutics Inc.,Greenwich, CT 06830).

A recently published metaanalysis of a total of 1441 patients from 18 studies were included.

Radiofrequency treatment improved heartburn scores (P=0.001), and produced improvements in quality

of life as measured by GERD–health-related quality-of-life scale (P=0.001) and quality of life in reflux

and dyspepsia score (P=0.001). Esophageal acid exposure decreased from a preprocedure Johnson-

DeMeester score of 44.4 to 28.5 (P=0.007) (Figure 3)[5].


A sham-controlled study indicated that decreased GEJ compliance after the Stretta procedure was

reversed by sildenafil, questioning the theory that the Stretta device produces fibrosis of the GE

junction[6].

Transoral Fundoplication

Currently the only commercially available device enabling transoral reconstruction of the GE

junction is the EsophyX device (EndoGastric Solutions, Redmond, WA). The technique of transoral

incisionless fundoplication (TF or TIF) using this device has evolved from a gastro-gastric plication to

an esophago-gastric fundoplication (Figure 4)[7].

Most reports of transoral fundoplication with the EsophyX device have been limited by small

numbers, frequently representing the learning curve, and with short follow-up. Results have been, not

surprisingly, quite variable (Figure 5)

Prospective 6 month and 1 year follow-up reports of a cohort of 100 patients undergoing TIF have

demonstrated a small decrease in clinical success between the two time periods (Figure 6). 24-month

and 36-month clinical follow-up is underway (24-month to be reported at SAGES 2013). Muls et al

reported long-term (3+ year) data on patients treated with an early TIF technique (ELF, TIF 1). Of 79

patients followed at 1 year, 13 were lost to f/u. Of remaining 66, 12 had undergone revisional

procedures. Sustained discontinuation of daily PPI use at median of 3.1 years was 61% (mITT) and

74%(PerProtocol) [8].

An important finding across multiple studies of the TIF procedure has been that the side-effect

profile (dysphagia, bloating, increased flatus) has been minimal (< 1%) and when reported have not

been severe.

Patients requiring laparoscopic revision to traditional fundoplication after TIF have been reported

to have a higher risk of infection[9] or postoperative dysphagia[10].

One limitation of all transoral antireflux procedures is the inability to repair hiatal hernias of any

significant size (generally 2cm axial height). Some surgeons have performed laparoscopic hiatal hernia

repair in combination with transoral fundoplication (with the premise that transoral fundoplication will

have a lower side-effect profile than laparoscopic fundoplication). However, prospective data is lacking,

with one retrospective study suggesting at least that the procedure was safe [11].

Patients who have a failed 360-degree fundoplication without an obvious hernia may benefit from

transoral revision of the fundoplication [12].

Magnetic Augmentation of the Lower Esophageal Sphincter (LINX system)

This system consists of a series of interlinked titanium beads with magnetic cores that is implanted

laparoscopically around the lower esophagus. The beads for a non-compressive Roman arch gently

resting around the lower esophagus. The lower esophagus, at rest, is typically closed. The beads will

separate when the intraluminal pressure at the beads reaches 15-20mmHg, and so will allow swallowed

food and liquids to pass through (as long as reasonable motility is present). Most gastroesophageal

reflux occurs with a pressure gradient of 9-11mmHg, and so will not occur with the LINX device in

place. However higher G-E pressure gradients (such as occur with vomiting) will open up the

augmented LES and allow retrograde bolus movement (Figure 7).

The LINX system gained FDA approval in May 2012 on the basis of two clinical trials (a

feasibility study conducted primarily in Europe, [13] [14] and a pivotal study conducted primarily in the

U.S. [15]) Patients entered into the study were partially but incompletely responsive to PPI therapy,

possessed early stage disease (HH < 3cm axial, no LA C or D, stricture, LSBE), and good esophageal

body motility (DEA >35 or DCI >400) without troublesome dysphagia.

The primary endpoint of both studies was objective – esophageal acid exposure. Eighty percent of

20 patients followed to 3 years in the feasibility trial normalized total esophageal acid exposure time. In

the FDA pivotal trial, the mean total acid exposure time was reduced from 11.6% at baseline to 5.1% at

12 months. 90% of treated subjects (86/96) had some reduction in their total acid exposure time.

Normalization of total acid exposure occurred in 67% (64/96) of pivotal trial subjects who completed

pH testing at 12 months (Figure 8).


The secondary endpoint of both studies was QOL, which showed sustained improvements in both

studies (Figure 9). Daily PPI use was eliminated in 80% of patients at 3 years follow-up in the

feasibility study; no PPI use was seen in 87% of pivotal study patients at 2 years.

Side effects: Early dysphagia has been experienced by 2/3 of patients. Dysphagia requiring dilation

occurred in 18% of patients, 10% reported persistent dysphagia. Device removal due to dysphagia or

pain has been reported in a small percentage of patients.

Bloating, excess flatulence, inability to vomit or vent air have not been reported as significant side

effects. Erosion or migration have not been reported.

Currently the LINX procedure is being offered in a limited number of centers in the U.S.

LES Electrical Stimulation

A device that delivers programmable electrical stimulation to the LES is currently under European

investigation; US FDA trials may begin shortly (EndoStim, St Louis, MO). A set of bipolar electrodes

are implanted and secured to the LES muscle using laparoscopic surgical techniques. An implantable

pulse generator (IPG) is buried under the anterior abdominal wall and connected to the bipolar

electrodes. External, wireless programming can be performed according to patient needs (Figure 10).

Initial human trials demonstrated that LESP increased significantly (8.6mmHg to 16.6mmHg) with

short (200microsec), low amperage (5-10 milliamp) electrical pulses. LES relaxation and esophageal

body peristalsis were not effected. Furthermore, 2-3 sessions of 30 min daily may be sufficient to

sustain the increase in LESP seen [16]. Cardiac rhythm was not affected, nor did patients report

sensation of the stimulation (with exception of one patient at 15ma).

Small clinical trials have demonstrated improvement in esophageal pH (Figure 11) as well as

HRQL [17].

Conclusions A huge therapeutic gap exists in the treatment of GERD. Laparoscopic fundoplication as practiced

by most US and European surgeons (360 degree or >180 degree partial fundoplication) has been unable

to fill this gap due to multiple reasons; probably the most significant is the side effect profile that

includes difficulty belching, inability to vomit, uncomfortable bloating, diarrhea, excess flatulence.

(Watson and Jamieson and the Adelaide group have published very interesting studies on lesser degrees

of fundoplication). Currently no medication regimens have promise in filling “the gap”.

Currently three commercially available antireflux treatments have demonstrated significant

improvement in QOL, decrease in daily PPI use, and improved esophageal acid control; without the

side effects of laparoscopic fundoplication. Though results in terms of reflux control are not as good as

laparoscopic fundoplication, the near absence of side effects has made these treatments quite appealing

to many patients in “the gap”. Insurance coverage for these procedures is variable, but acceptance of

these procedures as viable, non-experimental treatment options is increasing.

References:

1. Saritas Yuksel E, Higginbotham T, Slaughter JC, Mabary J, Kavitt RT, Garrett CG, Vaezi MF (2012)

Use of direct, endoscopic-guided measurements of mucosal impedance in diagnosis of gastroesophageal

reflux disease. Clinical gastroenterology and hepatology : the official clinical practice journal of the

American Gastroenterological Association 10:1110-1116

2. Grabowski M, Kasran A, Seys S, Pauwels A, Medrala W, Dupont L, Panaszek B, Bullens D (2011)

Pepsin and bile acids in induced sputum of chronic cough patients. Respiratory medicine 105:1257-1261

3. Fass R (2007) Proton-pump inhibitor therapy in patients with gastro-oesophageal reflux disease: putative

mechanisms of failure. Drugs 67:1521-1530

4. Finks JF, Wei Y, Birkmeyer JD (2006) The rise and fall of antireflux surgery in the United States. Surg

Endosc 20:1698-1701


5. Perry KA, Banerjee A, Melvin WS (2012) Radiofrequency energy delivery to the lower esophageal

sphincter reduces esophageal acid exposure and improves GERD symptoms: a systematic review and

meta-analysis. Surg Laparosc Endosc Percutan Tech 22:283-288

6. Aziz AM, El-Khayat HR, Sadek A, Mattar SG, McNulty G, Kongkam P, Guda MF, Lehman GA (2010)

A prospective randomized trial of sham, single-dose Stretta, and double-dose Stretta for the treatment of

gastroesophageal reflux disease. Surg Endosc 24:818-825

7. Bell RC, Cadiere GB (2011) Transoral rotational esophagogastric fundoplication: technical, anatomical,

and safety considerations. Surg Endosc 25:2387-2399

8. Muls V, Eckardt AJ, Marchese M, Bastens B, Buset M, Deviere J, Louis H, Rajan A, Daniel MA,

Costamagna G (2012) Three-year Results of a Multicenter Prospective Study of Transoral Incisionless

Fundoplication. Surg Innov

9. Furnee EJ, Broeders JA, Draaisma WA, Schwartz MP, Hazebroek EJ, Smout AJ, van Rijn PJ, Broeders

IA (2010) Laparoscopic Nissen fundoplication after failed EsophyX fundoplication. Br J Surg 97:1051-

1055

10. Witteman BP, Kessing BF, Snijders G, Koek GH, Conchillo JM, Bouvy ND (2013) Revisional

laparoscopic antireflux surgery after unsuccessful endoscopic fundoplication. Surg Endosc

11. Ihde GM, Besancon K, Deljkich E (2011) Short-term safety and symptomatic outcomes of transoral

incisionless fundoplication with or without hiatal hernia repair in patients with chronic gastroesophageal

reflux disease. Am J Surg 202:740-746; discussion 746-747

12. Bell RC, Hufford RJ, Fearon J, Freeman KD (2012) Revision of failed traditional fundoplication using

EsophyX((R)) transoral fundoplication. Surg Endosc

13. Bonavina L, Saino GI, Bona D, Lipham J, Ganz RA, Dunn D, DeMeester T (2008) Magnetic

augmentation of the lower esophageal sphincter: results of a feasibility clinical trial. J Gastrointest Surg

12:2133-2140

14. Lipham JC, DeMeester TR, Ganz RA, Bonavina L, Saino G, Dunn DH, Fockens P, Bemelman W (2012)

The LINX(R) reflux management system: confirmed safety and efficacy now at 4 years. Surg Endosc

26:2944-2949

15. Bonavina L, DeMeester TR, Ganz RA (2012) LINX() Reflux Management System: magnetic sphincter

augmentation in the treatment of gastroesophageal reflux disease. Expert review of gastroenterology &

hepatology 6:667-674

16. Rodriguez L, Rodriguez P, Neto MG, Ayala JC, Saba J, Berel D, Conklin J, Soffer E (2012) Short-term

electrical stimulation of the lower esophageal sphincter increases sphincter pressure in patients with

gastroesophageal reflux disease. Neurogastroenterology and motility : the official journal of the

European Gastrointestinal Motility Society 24:446-450, e213

17. Rodriguez L, Rodriguez P, Gomez B, Ayala JC, Saba J, Perez-Castilla A, Galvao Neto M, Crowell MD

(2012) Electrical stimulation therapy of the lower esophageal sphincter is successful in treating GERD:

final results of open-label prospective trial. Surg Endosc

Gastrointestinal Stromal Tumors

David W. Rattner, M.D Chief, Division of General and Gastrointestinal Surgery

Massachusetts General Hospital

The Warshaw Family Professor of Surgery, Harvard Medical School

Gastrointestinal Stromal Tumors (GIST) are one of the most common submucosal

lesions identified in the foregut. These tumors arise from the interstitial cells of

Cajal. Approximately 85% of tumors have c-kit mutations and 5% of tumors

have PDFGRA mutations. Although many of these tumors have a bland behavior,

all must be considered as potentially malignant. Tumors that have the c-kit

mutation respond to tyrosine kinase inhibitors such as Gleevac. Over the past two

decades the incidence of GIST tumors has doubled. This is in part due to the

greater use of diagnostic studies that detect these tumors incidentally. It is also

possible that for unknown reasons there truly is an increased incidence of GISTs

in the general population. 45% of GIST tumors are found incidentally either on

routine endoscopy or CT scans, 25% present with bleeding, about 20% are found

in patients complaining of abdominal pain, and 10% are found in the course of

other investigations.

GISTs can occur at any location in the GI tract. The most common site is

in the stomach. Gastric GIST tumors account for 60% of all GIST tumors. As a

rule of thumb, the more proximal in the GI tract that the GIST tumor occurs, the

better the prognosis. Of the gastric GIST’s, 40% occur in the body of the

stomach, 30% in the antrum, 20% in the fundus and 10% at the GE junction.

Surgical management for tumors in the central portion of the stomach is quite

straightforward, but resection of tumors at the GE junction or near the pyloris can

be technically challenging.

The differential diagnosis of a gastric submucosal mass includes GIST,

leiomyoma, schwannoma, and carcinoid tumors. Carcinoids can generally be

distinguished by their gross appearance. Lesions that are larger than 2 cm or those

that are enlarging on sequential imaging studies should probably be resected. In

borderline situations or in high risk surgical patients a biopsy may be useful and

provide information as to the nature of the tumor. However, an FNA biopsy

cannot always distinguish a GIST from a benign tumor such as a leiomyoma or

Schwannoma. In large tumors or in the setting of potential metastatic disease a

biopsy is very useful because neoadjuvant therapy is likely to be needed. For

GISTs that can be easily resected , no staging workup is necessary prior to

surgery. Once the tumor is resected it is relatively easy to assess the risk for

mestatasis and appropriate staging can be performed at that point in time. GIST

tumors that are exophytic, pendunculated , or are smaller than 5-6 cm are best

handled by a laparoscopic resection. For larger tumors the benefit of laparoscopic

resection is less clear cut. Small GIST’s have been resected successfully

endoscopically but it is important to remember that these are not mucoscal lesions

as they arise in th emuscularis layer and are frequently attached to the serosa.

Therefore one must be prepared to close a full thickness defect in the stomach

when attempting to resect a lesion endoscopically.

Special considerations for GIST resections in difficult locations:

Whereas GISTS in the body and fundus of the stomach can be easily

removed by a wedge resection of the gastric wall, other locations can present

technical challenges. When resecting GISTS arising on the lesser curvature

attention should me paid to preserving the nerves of Laterjet. If both the anterior

and posterior nerves are transected, the pylorus will be denervated and patients

may develop delayed gastric emptying.

GIST’s at the GE junction can be particularly challenging. There are two

good ways to approach these laparoscopically. In both techniques it is important

to protect the anterior vagus nerve. The most straightforward approach is to

sharply dissect out the GIST and then hand sew the defect closed. It is important

to make sure that the closure is air tight and that the esophageal lumen is not

narrowed. Addition of an anterior fundoplication- either a Thal Patch or Dor

Fundoplication may provide additional security. Another good technique for GE

Junction GISTs is a transgastric endoluminal resection. Transgastric laparscopic

trocars allow one to use a stapler for resecting the tumor endoluminally while a

gastroscope can be used for both visualization and retraction of the tumor. With

this technique the tumor can be extracted trans-orally if the tumor is 2 cm or less.

If one encounters a GIST that is 5 cm in size at the GE junction, there is a good

chance that it is malignant and it will be difficult to get adequate margins with a

local resection. In this setting one should consider performing an

esophagogastrectomy. Tumors in the antrum of the stomach often need a bit of

planning before resection. Attempting a simple wedge resection with a stapler can

narrow the pylorus and obstruct the gastric outlet. Therefore for pre-pyloric

lesions and for those in the distal anterim I prefer to excise them sharply in a

longitudinal fashion and then repair the defect with a hand sewn transverse

closure. No matter what approach is chosen one should always respect oncologic

principles and obtain a tissue margin of 1 cm. Lymph node dissection is not

necessary for GIST tumors since these tend to spread hematogenously.

When treating a locally advanced GIST Gleevac therapy can be extremely

helpful. If one can appreciate the tumor as locally advanced prior to surgery

neoadjuvant therapy is indicated. The maximum response is usually obtained

after six to nine months of treatment at this point surgical resection should be

undertaken.

Postoperatively one can assess the risk of recurrence and determine the need for

close follow up using the Sloan Kettering nomogram found at:

http://nomograms.mskcc.org/GastroIntestinal/GastroIntestinalStromalTumor

SELECTED REFERENCES:

Joensuu H. Vehtari A. Riihimaki J. et al. Risk of recurrence of gastrointestinal

stromal tumour after surgery: an analysis of pooled population-based cohorts.

Lancet Oncology. 13(3):265-74, 2012

Frankel TL. Chang AE. Wong SL. Surgical options for localized and advanced

gastrointestinal stromal tumors. Journal of Surgical Oncology. 104(8):882-7, 2011

Pisters PW. Patel SR. Gaastrointestinal Stromal Tumors: Current Management.

Journal of Surgical Oncology. 102(5):530-8, 2010

Gervaz P. Huber O. Morel P. Surgical management of gastrointestinal stromal

tumours. British Journal of Surgery. 96(6):567-78, 2009

Laparoscopic Gastrectomy for Early Gastric Cancer

Han-Kwang Yang, MD, PhD, FACS

Department of Surgery and Cancer Research Institute,

Seoul National University College of Medicine, Seoul, Korea

Laparoscopic gastrectomy for gastric cancer (GC) is rapidly popularized, because of the technical

development and the accumulated data of laparoscopic surgery in GC patients. Laparoscopic distal

gastrectomy (LDG) provides better or comparable outcomes, compared to conventional open distal

gastrectomy (ODG) in terms of short-term results. The long-term survival of LDG is expected to be

comparable to that of ODG in early stage GC, and ongoing Korean muticenter RCT (KLASS-01) will

provide more clear evidence. Laparoscopic total gastrectomy is still selectively performed compared to

LDG, and there is still debate on safe laparoscopic esophago-jejunostomy technique. Laparoscopic

pylorus preserving gastrectomy seems to be preferred for EGC in the middle third of stomach, in terms

of functional advantages and comparable oncologic outcome.

Even greater caution is advised when considering the application of a laparoscopic approach for total

gastrectomy as the lymph node (LN) dissection and particularly the reconstruction for a laparoscopic

total gastrectomy (LTG) are technically more demanding compared to a LADG and an anastomotic

leakage more consequential. To address this issue, KLASS group has just commenced KLASS-03 study,

a phase II study, aimed at assessment of technical safety of various reconstructive techniques after total

gastrectomy.

A laparoscopic gastrectomy for cancer is a technically challenging procedure with a steep learning

curve reported to last around 50 cases. Gastrectomy requires a large extent of LN dissection, much of it

in the immediate vicinity of major blood vessels that need to be preserved. As such, many of intra-

operative pitfalls relate to injury to either major blood vessels or bleeding from their branches or

tributaries that impair vision and subsequently lead to other major complications. Other pitfalls relate to

thermal injury to adjacent organs, particularly to the transverse colon, pancreas, duodenum and

esophagus, and steps of reconstruction which is more difficult by the minimally invasive approach.

D2 dissection has long been the standard of care in Japan and Korea and survival advantage of D2

dissection over D1 dissection has only recently been shown using Western data for the first time. The

3rd English version of Japanese Gastric Cancer Treatment Guideline published in 2010 recommends a

D2 dissection for clinical T2-4b tumor or T1 tumor with suspicion of nodal involvement . Most gastric

surgeons in Japan and Korea accept modified D2 (or D1+) dissection as a safe alternative in cT1N0

disease. One should note that the extent of lymphadenectomy is now defined according to the type of

gastrectomy indicated and not the location of the lesion

Laparoscopic sentinel node navigation surgery is yet experimental, and surgical procedure is not

standardized until now. Robotic gastrectomy is feasible to EGC in terms of similar outcome and but

with much higher cost compared to laparoscopic surgery. Its benefit over the conventional laparoscopic

gastrectomy is not proven yet

Figure 1. Recommended treatment algorithm. (From Japanese Gastric Cancer Association.

Japanese gastric cancer treatment guidelines: 3rd

English edition, Gastric Cancer 14:113-123,

2011)

Distal gastrectomy D0 Lymphadenectomy less than D1

D1 Nos. 1, 3, 4sb, 4d, 5, 6, 7

D1+ D1+ Nos. 8a, 9

D2 D1 + Nos. 8a, 9, 11p, 12a.

Total gastrectomy D0 Lymphadenectomy less than D1

D1 Nos. 1-7

D1+ D1+ Nos. 8a, 9, 11p

D2 D1 + Nos. 8a, 9, 10, 11p, 11d, 12a

Figure 2. Extent of lymph node dissection in

distal and total gastrectomies. (From

Gastric Cancer Association. Japanese gastric

cancer treatment guidelines: 3

edition, Gastric Cancer 14:113-123, 2011

Lymphadenectomy less than D1

D1 + Nos. 8a, 9, 11p, 12a.

Lymphadenectomy less than D1

+ Nos. 8a, 9, 10, 11p, 11d, 12a

ymph node dissection in

(From Japanese

Japanese gastric

cancer treatment guidelines: 3rd

English

123, 2011)

Figure 3. Room set-up.

Figure 4. Port positions.

5mm 5mm 12mm 5cm mini- laparotomy 5mm 11mm camera port

References

Kitano S, Yang HK (eds): Laparoscopic gastrectomy for cancer - standard techniques and clinical

evidences. Tokyo, Springer, 2012.

Japanese Gastric Cancer Association: Japanese gastric cancer treatment guidelines 2010 (ver. 3).

Gastric Cancer 2011;14:113-123.

Japanese Gastric Cancer Association: Japanese classification of gastric carcinoma: 3rd English edition.

Gastric Cancer 2011;14:101-112.

Lee HJ, Shiraishi N, Kim HH, Hiki N, Uyama I, Choi SH, Yang HK, Kitano S: Standard of practice on

laparoscopic gastric cancer surgery in Korea and Japan: experts' survey. Asian J Endosc Surg 2012;5:5-

11.

Viñuela EF, Gonen M, Brennan MF, Coit DG, Strong VE: Laparoscopic versus open distal

gastrectomy for gastric cancer: a meta-analysis of randomized controlled trials and high-quality

nonrandomized studies. Ann Surg 2012;255:446-456.

Kim HH, Hyung WJ, Cho GS, Kim MC, Han SU, Kim W, Ryu SW, Lee HJ, Song KY: Morbidity and

mortality of laparoscopic gastrectomy versus open gastrectomy for gastric cancer: an interim report-a

phase III multicenter, prospective, randomized Trial (KLASS Trial). Ann Surg 2010;251:417-420.

Nakamura K, Katai H, Mizusawa J, Yoshikawa T, Ando M, Terashima M, Ito S, Takagi M, Takagane A,

Ninomiya M, Fukushima N, Sasako M: A Phase III Study of Laparoscopy-Assisted Versus Open Distal

Gastrectomy with Nodal Dissection for Clinical Stage IA/IB Gastric Cancer (JCOG0912). Jpn J Clin

Oncol DOI: 10.1093/jjco/hys220.

Kitano S, Shiraishi N, Uyama I, Sugihara K, Tanigawa N; Japanese Laparoscopic Surgery Study

Group: A multicenter study on oncologic outcome of laparoscopic gastrectomy for early cancer in

Japan. Ann Surg 2007;245:68-72.

Strong VE, Devaud N, Allen PJ, Gonen M, Brennan MF, Coit D: Laparoscopic versus open subtotal

gastrectomy for adenocarcinoma: a case-control study. Ann Surg Oncol 2009;16:1507-1513.

Kodera Y, Fujiwara M, Ohashi N, Nakayama G, Koike M, Morita S, Nakao A: Laparoscopic surgery

for gastric cancer: a collective review with meta-analysis of randomized trials. J Am Coll Surg

2010;211:677-686.

Park DJ, Lee HJ, Jung HC, Kim WH, Lee KU, Yang HK: Clinical outcome of pylorus-preserving

gastrectomy in gastric cancer in comparison with conventional distal gastrectomy with Billroth I

anastomosis. World J Surg 2008;32:1029-1036.

Jiang X, Hiki N, Nunobe S, Fukunaga T, Kumagai K, Nohara K, Sano T, Yamaguchi T: Postoperative

outcomes and complications after laparoscopy-assisted pylorus-preserving gastrectomy for early

gastric cancer. Ann Surg 2011;253:928-933.

Suh YS, Han DS, Kong SH, Kwon S, Shin CI, Kim WH, Kim HH, Lee HJ, Yang HK: Laparoscopy-

assisted pylorus-preserving gastrectomy is better than laparoscopy-assisted distal gastrectomy for

middle-third early gastric cancer. Ann Surg (in press)

Yang HK: Sentinel node biopsy in early gastric cancer: constant exertion for clinical application. Ann

Surg Oncol 2012;19:353-354.

Wall J, Marescaux J: Robotic gastrectomy is safe and feasible, but real benefits remain elusive. Arch

Surg 2011;146:1092.

Submucosal Tumors

Presenter: Sricharan Chalikonda, MD

Disclosures:

I have relationships to disclose 1/30/2013 10:44:12 AM intuitive surgical Honoraria Independent Potential Conflict of Interest Contractor

Conflict Management:Does Not Relate

Christy M. Dunst, MD

Esophageal Surgeon

The Oregon Clinic

4805 SE Glisan St #6N60

Portland, Oregon 97213

503-281-0561

503-281-0575 (fax)

[email protected]

POSTGRADUATE COURSE: Foregut-Beyond GERD & Hiatal Hernia

4/17/2013 7:30am-12pm

Esophageal Diverticulae and Achalasia

There has been a recent revival in the interest in esophageal motility disorders primarily

due to the popularization of high resolution manometry (HRM) and the emergence of

new endoscopic therapies for esophageal diseases. HRM has beautifully enabled

esophagologists to more easily recognize and precisely characterize a multitude of

esophageal motor disorders including achalasia. Tried and true therapies such as

esophageal myotomy and endoscopic balloon dilation provide successful relief of

dysphagia for ~90% of patients with achalasia.

Per-oral esophageal myotomy (POEM) has emerged as a potential alternative to

esophageal myotomy in the treatment of spastic disorders such as achalasia, diffuse

esophageal spasm and nutcracker esophagus with poorly relaxing lower esophageal

sphincters. In brief, the POEM technique consists of 5 steps: 1) Diagnostic endoscopy

and measurements of landmarks 2) Mucosotomy 3) Creation of sub-mucosal tunnel 4)

Myotomy of the circular muscle fibers 5) Mucosotomy closure. Early results are

encouraging with excellent relief of dysphagia and virtually no postoperative pain.

Although no randomized trials have been done, retrospective comparisons to Heller

myotomy show the two therapies have similar outcomes.

As esophageal motility disorders are becoming easier to characterize and excitement

continues to grow regarding the application of POEM, the diagnosis of associated

problems such as esophageal diverticulae may also increase. Understanding the current

management strategies in this field is imperative. Esophageal diverticulae are defined as

simply outpouchings of the esophageal wall. Epiphrenic diverticulum(ED) is a rare

condition defined as a mucosal outpouching in the mid or distal esophagus as a result of

a weakening in the esophageal wall against an esophageal outflow obstruction. Most

commonly, the obstruction results from an underlying esophageal motor disturbance

but can also be seen with problems such as aggressive hiatal hernioraphy and/or

fundoplication. Esophageal diverticulae can also be the result of external traction due to

adherence of the esophageal wall to other mediastinal structures such as can be seen in

tuberculosis. As the pathogenesis of these two types of esophageal diverticulae are

quite distinct, correct diagnosis is important proper treatment.

Epiphrenic diverticulae can be confused clinically, and even sometimes radiographically,

with paraesophageal hernias. Common symptoms may include dysphagia, chest pain,

regurgitation and aspiration among others. As with paraesophageal hernias, the

presence of attributable symptoms dictates the need for surgical intervention. However

the surgical therapy is, of course, quite different making precise preoperative diagnosis

imperative for appropriate operative planning. Comprehensive esophageal testing

includes esophageal manometry, esophageal contrast radiography and endoscopy with

biopsy. The importance of the contrast study cannot be overemphasized as diverticulae

are frequently missed with endoscopy alone and it will more precisely identify the

location of the diverticulum relative to other mediastinal structures.

Most epiphrenic diverticulae can be resected laparoscopically but a combined

laparoscopic thoracoscopic approach can be helpful for diverticulae located above the

pulmonary hilum. An exception might be those diverticulae associated with a hiatal

hernia in which case the diverticulum becomes approachable after reduction of the

hernia. Although some minor controversy over details exists, the technique can

generally be summarized into the following steps: 1) Mobilization of the esophagus and

dissection of the diverticulum 2) Stapled esophageal diverticulectomy 3) Esophageal

myotomy 4) Partial fundoplication.

Epiphrenic diverticulectomy is associated with a relatively high complication rate (~20%)

most commonly from esophageal leak at the suture line. The most important step to

mitigate suture line failure is correct identification of the mucosal neck of the

diverticulum. Liberal use of intraoperative endoscopy is encouraged as it greatly

enhances visibility of the diverticular borders and can assist stapler positioning to avoid

incomplete resection.

Generally, the presence of an esophageal diverticulum is a contraindication to POEM,

especially early in ones learning curve. It would be unusual to encounter a clinical

scenario in which only the myotomy was indicated. Therefore, since the

diverticulectomy necessitates laparoscopy +/- thoracoscopy, standard myotomy is the

preferred approach. However, we have performed a combination POEM and

laparoscopic diverticulectomy for a specific situation involving extensive diffuse

esophageal spasm. Endoscopic diverticulectomy may one day be a possible adjunct to

POEM.

REFERENCES:

1. Hungness ES, Teitelbaum EN, Santos BF, Arafat FO, Pandolfino JE, Kahrilas PJ, Soper NJ.

Comparison of Perioperative Outcomes Between Peroral Esophageal Myotomy (POEM) and

Laparoscopic Heller Myotomy. J Gastrointest Surg. 2013 Feb;17(2):228-35. Epub 2012 Sep 28.

2. Hirano Y, Takeuchi H, Oyama T, Saikawa Y, Niihara M, Sako H, Omagari K, Nishi T, Suzuki H, Hibi T,

Kitagawa Y Minimally invasive surgery for esophageal epiphrenic diverticulum: the results of 133

patients in 25 published series and our experience Surg Today. 2013 Jan;43(1):1-7. Epub 2012

Oct 21.

3. Zaninotto G, Parise P, Salvador R, Costantini M, Zanatta L, Rella A, Ancona E Laparoscopic repair

of epiphrenic diverticulum Semin Thorac Cardiovasc Surg. 2012 Autumn;24(3):218-22.

4. Swanstrom LL, Kurian A, Dunst CM, Sharata A, Bhayani N, Rieder E Long-term outcomes of an

endoscopic myotomy for achalasia: the POEM procedure. Ann Surg. 2012 Oct;256(4):659-67. doi:

10.1097/SLA.0b013e31826b5212.

5. Boeckxstaens GE, Annese V, des Varannes SB, Chaussade S, Costantini M, Cuttitta A, Elizalde JI,

Fumagalli U, Gaudric M, Rohof WO, Smout AJ, Tack J, Zwinderman AH, Zaninotto G, Busch OR;

European Achalasia Trial Investigators Pneumatic dilation versus laparoscopic Heller's myotomy

for idiopathic achalasia. N Engl J Med. 2011 May 12;364(19):1807-16.

6. Inoue H, Minami H, Kobayashi Y, Sato Y, Kaga M, Suzuki M, Satodate H, Odaka N, Itoh H, Kudo S.

Peroral endoscopic myotomy (POEM) for esophageal achalasia. Endoscopy. 2010 Apr;42(4):265-

71.

7. Zaninotto G, Portale G, Costantini M, Merigliano S, Guirroli E, Rizzetto C, Rampado S, Ancona E.

Long-term outcome of operated and unoperated epiphrenic diverticula. J Gastrointest Surg. 2008

Sep;12(9):1485-90

8. Zaninotto G, Costantini M, Rizzetto C, Zanatta L, Guirroli E, Portale G, Nicoletti L, Cavallin F,

Battaglia G, Ruol A, Ancona E Four hundred laparoscopic myotomies for esophageal achalasia: a

single centre experience. Ann Surg. 2008 Dec;248(6):986-93.

MIS IN ESOPHAGEAL NEOPLASMS

GUY-BERNARD CADIERE MD, PhD

PROFESSOR OF SURGERY

CHIEF OF DEPARTMENT OF GASTROINTESTINAL SURGERY

DIRECTOR OF EUROPEAN SCHOOL OF LAPAROSCOPIC SURGERY

DIRECTOR OF BRUSSELS WEIGHT LOSS CENTER

SAINT-PIERRE UNIVERSITY HOSPITAL, BRUSSELS, BELGIUM

[email protected]

GIOVANNI DAPRI MD, FACS

ASS. PROF. DEPARTMENT OF GASTROINTESTINAL SURGERY

EUROPEAN SCHOOL OF LAPAROSCOPIC SURGERY

SAINT-PIERRE UNIVERSITY HOSPITAL, BRUSSELS, BELGIUM

[email protected]

MIS IN ESOPHAGEAL NEOPLASMS Surgical resection is considered standard treatment for patient with resectable esophageal cancer. Surgery for esophageal cancer should be aimed at achieving on Ro resection. Extensive two-field lymphadenetomy should be standard during esophagectomy. Minimal invasive esophagectomy by thoracoscopy, laparoscopy and or without cervicotomy has better outcomes than by open surgery. 2 techniques are described: esophagectomy by laparoscopy, cervicotomy and thoracoscopy and esophagectomy by laparoscopy and thoracoscopy (Ivor Lewis technique).

1. Esophagectomy by thoracoscopy, laparoscopy and cervicotomy

Minimally invasive esophagectomy access for cancer includes three steps: thoracoscopy in prone position for the mobilisation of the thoracic esophagus and mediastinal lymphadenectomy, laparoscopy in supine position for the celiac trunk lymphadenectomy and gastric tube manufacturing and left cervicotomy for the esophago-gastric anastomosis.

1.1. Thoracoscopy in prone position

1.1.1. Position of the patient and disposition of the trocars

The patient is placed in prone position after induction of general anesthesia and insertion of double-lumen endotracheal tube. The surgeon stands at the right side of the patient. Three trocars are required for the procedure. A 10 mm trocar for the 30 degree angled optical system in the 7

th

intercostals space, a second 5 mm trocar in the 9th intercostals space for the grasping forceps, and a third 5 mm

trocar in the 5th intercostals space for the coagulating hook.

1.1.2. Mobilisation of the intrathoracic esophagus and mediastinal lymphadenectomy

Thanks to gravity, the cardio-pulmonary window drops back and the space of dissection is directly opened. The mediastinal pleura overlying the esophagus is incised and the esophagus is circumferentially mobilizes along the trachea, the descending aorta, reaching the right diaphragmatic pillar. All fatty tissue is separated from the pericardium and descending aorta. The arch of the azygos vein is isolated, ligated by 2/0 silk stitches with clips, and divides. Para esophageal, paratracheal, subcarinal, bilateral tracheobronchial, right pulmonary artery, and veins lymph nodes are dissected so as to remain in block with the surgical specimen. A 28 French chest tube is inserted in the 11

th intercostals space on the anterior axillary line at the end of this step.

1.2. Laparoscopy

1.2.1. Position of the patient and disposition of trocars

The patient is placed in supine position with legs separated. The surgeon stands between the patient’s legs.Five trocars are used: a 10 mm trocar 2 cm above the umbilicus, a 5 mm trocar on the midleft costal margin, a 12 mm trocar half-way between the first two trocars, a 12 mm trocar on the right midunder the xyphoid process.

1.2.2. Mobilisation of the greater curvature and celiac trunk lymphadenectomy

The dissection of the lesser omentum starts to the The dissection of the gastrocolic ligament and thus opening of the lesser sac is carried out just lateral to the right gastroepiploic artery and vein. All lymphoglandulartowards the right is sampled, while preserving the left gastric artery and the hepatic pedicule.Dissection of all lymphoglandular tissue is completed along the abdominal aorta until diaphragmatic reached.

1.2.3. Gastric tube and intramediastinal dissection

The initial firing of the stapler begins at the level of the crow’s foot, perpendicular to the lesser curvature. Other firings are placed parallel to the greater curvature. The limits of the mediastinal dissection are the following: anteriorly, the pericardium and the left inferior pulmonary vein; on the left side, the left pleura; on the right side, the right pleura; posteriorly, the aorta.

1.3. Left cervicotomy

1.3.1. Position of patient

An incision is performed lateral to the left sternoLifting the esophagus containing the tumoral mass (protected by a plastic bag) is achieved under laparoscopic control. A totally mechanical side-to-side esophagosame stapler used for the gastric tube.

patient is placed in supine position with legs separated. The surgeon stands between the patient’s legs.Five trocars are used: a 10 mm trocar 2 cm above the umbilicus, a 5 mm trocar on the mid-clavicular line under the

way between the first two trocars, a 12 mm trocar on the right mid

1.2.2. Mobilisation of the greater curvature and celiac trunk lymphadenectomy

The dissection of the lesser omentum starts to the left of the left gastric artery. The dissection of the gastrocolic ligament and thus opening of the lesser sac is carried out just lateral to the right

artery and vein. All lymphoglandular tissue around the celiac trunk is removed from this point is sampled, while preserving the left gastric artery and the hepatic pedicule.

Dissection of all lymphoglandular tissue is completed along the abdominal aorta until diaphragmatic

tube and intramediastinal dissection

The initial firing of the stapler begins at the level of the crow’s foot, perpendicular to the lesser curvature. Other firings are placed parallel to the greater curvature. The limits of the mediastinal dissection are the following:

dium and the left inferior pulmonary vein; on the left side, the left pleura; on the right side, the

An incision is performed lateral to the left sterno-cleido-mastoid muscle. Lifting the esophagus containing the tumoral mass (protected by a plastic bag) is achieved under laparoscopic

side esophago-gastric anastomosis is performed using three firings of the

patient is placed in supine position with legs separated. The surgeon stands between the patient’s legs. clavicular line under the

way between the first two trocars, a 12 mm trocar on the right mid-clavicular

The dissection of the gastrocolic ligament and thus opening of the lesser sac is carried out just lateral to the right tissue around the celiac trunk is removed from this point

Dissection of all lymphoglandular tissue is completed along the abdominal aorta until diaphragmatic pillars are

The initial firing of the stapler begins at the level of the crow’s foot, perpendicular to the lesser curvature. Other firings are placed parallel to the greater curvature. The limits of the mediastinal dissection are the following:

dium and the left inferior pulmonary vein; on the left side, the left pleura; on the right side, the

Lifting the esophagus containing the tumoral mass (protected by a plastic bag) is achieved under laparoscopic gastric anastomosis is performed using three firings of the

2. Esophagectomy by laparoscopy and thoracoscopy (Ivor Lewis technique)

2.1. Laparoscopy (Cf. 1.2.) Comparing the technique by 3 ways, the stomach is introduced in the chest.

2.2. Thoracoscopy in prone position

The esophagus was sectioned approximately 4 cm proximal to the tumor, approximately 1 cm cranial to the azygos. The specimen was placed in a plastic bag and was alldeployed in the pleural cavity until the tip is

2.2.1 Esogastric suture

The anterior side of the gastric tube was sutured manually in two layers siderunning sutures: Maxon 4/0 internally and PDS 2/0 externally. The apex of the gastric tube was sutured to the esophagus and to the parietal pleura by a couple of silk 2/0 A nasogastric tube was left in place across the anastomosis; A 28 French chest tube wacostodiaphragmatic sinus and placed under 20 cm water seal.

sophagectomy by laparoscopy and thoracoscopy (Ivor Lewis technique)

technique by 3 ways, the stomach is entirely sectioned and stapled and the gastric tube is partially

2.2. Thoracoscopy in prone position (Cf. 1.1.)

The esophagus was sectioned approximately 4 cm proximal to the tumor, approximately 1 cm cranial to the azygos. The specimen was placed in a plastic bag and was allowed to drop inside the abdomendeployed in the pleural cavity until the tip is facing the proximal esophagus.

The anterior side of the gastric tube was sutured manually in two layers side-to-end to the esophagus, by two ures: Maxon 4/0 internally and PDS 2/0 externally. The apex of the gastric tube was sutured to the

esophagus and to the parietal pleura by a couple of silk 2/0 stitches. A nasogastric tube was left in place across the anastomosis; A 28 French chest tube was left into the right costodiaphragmatic sinus and placed under 20 cm water seal.

sectioned and stapled and the gastric tube is partially

The esophagus was sectioned approximately 4 cm proximal to the tumor, approximately 1 cm cranial to the owed to drop inside the abdomen. The gastric tube is

end to the esophagus, by two ures: Maxon 4/0 internally and PDS 2/0 externally. The apex of the gastric tube was sutured to the

s left into the right

session title: postgraduate course: foregut â€“ beyond gerd

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