This issue of the Minimal Access Surgery Center Fall Update focuses on adult gastrointestinal surgery. Strictly speaking, obesity may not be a GI disease, but the only effective treatment for morbid obesity is surgery on the GI tract. Clearly, obesity is a major health problem in the United States, and nearly all clinicians, regardless of specialty, see patients who are severely obese. Dr. Marc Bessler reviews the indications for the surgical treatment of the severely obese, and discusses the surgical options currently in use. In the second article I review other laparoscopic surgical procedures on the foregut. The surgical treatment of these less common conditions can be quite complex, but in many cases the surgery can be safely and effectively completed laparoscopically.

A little more than a year ago, Dr. Jeff Milsom joined our faculty as Chief of the Colorectal Surgery Service at Weill Cornell. He has a large experience in the treatment of inflammatory bowel disease, and also has been very active in the evaluation of laparoscopic surgery for diseases of the colon and rectum. He writes a review of the role of laparoscopic surgery in the treatment of inflammatory bowel disease.

We hope you enjoy these discussions. Please feel free to write or call or e-mail any of us in the Minimal Access Surgery Center if you have questions or suggestions for future issues of this newsletter.

-Dennis L. Fowler, M.D.

Marc Bessler, M.D.
Assistant Professor of Surgery, Columbia University
Director of Laparoscopic Surgery, Columbia University
Director, New York Presbyterian Center for Obesity Surgery

Obesity is currently second only to smoking as the leading cause of preventable death in the United States. Despite an estimated 30 billion dollars spent each year in an effort to combat obesity in the U.S., the incidence has risen in the past 20 years to the point where presently 30% of the population is obese. Obesity related diseases include type II diabetes, hypertension, sleep apnea, GERD, osteoarthritis, coronary artery disease, congestive heart failure and lower extremity venous disease among others. The estimated cost of treating these obesity related co-morbidities in the U.S. alone is 70 billion dollars per year. Though many medical therapies have come and gone in the effort to treat severe obesity, the disappointing fact is that current medical therapies are only minimally effective.

Obesity is defined medically as being 30% over one's ideal body weight or over a body mass index (BMI) of 30. BMI is defined as weight in kg divided by the square of height in meters (kg/m2). Normal BMI is 20-25. The most severe form of obesity is known as morbid obesity and is defined as being 100 pounds or more overweight or BMI=40. With significant co-morbidity, the definition shifts to 80 pounds over ideal weight or BMI=35. Treatment of morbid obesity with diet and medication results in modest weight loss of 5-10% of starting weight, which is then regained in its entirety by 95% of patients within only 2 years. This dismal prognosis with medical therapy is in large part responsible for the recent explosion in the number of patients seeking surgical treatment for weight loss and a doubling number of procedures performed over the past 2-3 years. Other factors that have contributed to the rapid growth of this field include the availability of long term data supporting the safety and durability of weight loss with gastric bypass, the application of laparoscopy to bariatric surgery and newer less risky procedures. This article will review the physiology of obesity and its co-morbidities, the available surgical options including minimally invasive surgical approaches and the long-term outcomes of these procedures.

There is a growing body of evidence indicating that hormonal feedback and CNS control of weight are out of balance in obesity.

Perhaps the last bastion of politically acceptable discrimination, obesity is seen by many as not a disease but a physical sign of a personality defect or lack of self-control. That this is not the case is supported by the fact that a greater percent of ones weight is genetically determined (80%) than is height (70%) as evidenced by studies of twins reared apart. In fact most morbidly obese adults have been obese since childhood and report struggling to lose weight and keep it off without success their entire lives. If not a lack of willpower than what causes obesity? The simple answer is we do not yet know, but there is increasingly more that we do know.

The recent rise in the incidence of obesity is certainly not representative of a change in the genetic makeup of our population; therefore the environment must play a significant role. The ubiquitous presence of readily available, high fat, tasty fast foods as well as processed grains and simple carbohydrates in the American diet may be partly to blame. However, many people stay thin despite eating these foods so individual differences in the intake and storage of these calories must be present. Even though exercise plays an important role in any weight loss and maintenance plan (including after surgery), 70% of one's energy is actually expended at rest and therefore differences in amount of exercise are not likely the major factor separating normal weight and morbidly obese individuals. Certainly an imbalance in energy intake and expenditure is at the heart of the problem of obesity. Increased caloric intake accompanied by decreased physical activity are likely the major issues that have caused the recent epidemic rise in the incidence of obesity. Yet there is now increasing evidence of physiologic and hormonal factors that are associated with and point to a physiologic origin of the problem of obesity.

Basal metabolic rate (BMR) is the energy expended by an individual at rest as a function of the normal physiologic processes of life and is expressed as calories burned/unit time. It is logical to expect that obese patients would have a slower metabolic rate as part of the cause of their obesity yet this does not seem to be the case. Studies have shown that BMR does not correlate well with obesity. What has been shown is that when patients gain weight in an experimental setting their BMR rises in proportion to the weight gain and that when patients lose weight in an experimental setting their BMR falls in similar proportion. This has led to a "set point" theory that suggests a person's weight is tightly controlled by physiologic processes that tend to keep it stable over time. However, if this is the case, then the fact that many obese patients gain weight over time points to a problem in this tightly controlled system. Obese patients may in fact have a higher set point but it now seems increasingly likely that many have an abnormality in the feedback loop that controls one's weight. There is a growing body of evidence indicating that hormonal feedback and CNS control of weight are out of balance in obesity.


Figure 1: division of stomach pouch and small bowel in preparation for Roux-limb

Leptin, a hormone produced in fat cells, has been shown to be deficient in some rodent models of obesity. Though it was initially thought that a leptin deficiency might be the cause of obesity in humans there have only been a dozen or so leptin deficient individuals found. In fact, most obese patients turn out to have significantly higher than normal levels of leptin circulating in their blood, with these levels correlating strongly with degree of obesity. It is believed but not yet demonstrated that a defect in leptin receptor function or downstream signaling may explain the high leptin levels associated with human obesity. When obese individuals lose weight, leptin levels fall and it was hoped that leptin replacement would aid in weight loss and maintenance. Clinical trials have shown minimal success with this strategy and the search for5 the role of leptin in the treatment of human obesity continues.

Ghrelin, a peptide hormone produced by the distal stomach, has been shown to be associated with hunger. In normal individuals, ghrelin levels fall after a meal and then rise steadily until the next meal. Recent studies have shown that obese individuals have higher average ghrelin levels but maintain the cycling with meals. The higher levels of ghrelin may explain the increased hunger and food intake in obese individuals. It is hoped that if ghrelin activity can be blocked, significant weight loss will result. Interestingly, 5 gastric bypass patients studied post-operatively have been shown to have a 70% lower ghrelin level and no cycling with meals. The explanation for this finding is unclear, as it is believed that food in the distal stomach causes the decrease in ghrelin production with meals and gastric bypass prevents food from entering the distal stomach. Clearly more work in this area is needed to help elucidate this piece of the complex control of energy intake and balance. However, the leptin and ghrelin findings clearly point to a physiologic rather than psychological cause for obesity.



...the leptin and ghrelin findings clearly point to a physiological rather than psychological cause for obesity.

Surgical treatment of obesity has had a long and checkered history. The first operation for obesity, jejuno-ileal bypass (JIB), was performed in 1954. This procedure had unacceptably high rates of serious complications and death and was replaced with safer ones, including horizontal gastroplasty and loop gastric bypass. However, these procedures proved to be ineffective over time. Modern surgical treatment relies on Roux-en-Y gastric bypass (GBP) and Vertical Gastric Banding (VBG) or Adjustable Silastic Gastric Banding (ASGB). Based on the long-term safety and efficacy of GBP, bariatric surgery has come out of the shadows and is now poised to become on the of more common abdominal surgical procedures and a mainstay of treatment for morbid obesity. VBG, a purely restrictive operation, is declining in usage because of questions about long-term efficacy and a safer, minimally invasive alternative restrictive procedure, ASGB.


Figure 2: Anatomy of gastric bypass and retrogastric Roux-limb

Roux-en-Y gastric bypass with a more or less vertical lesser curve pouch is the most common surgical procedure performed for obesity in the U.S. today. The operation is performed via laparotomy or laparoscopy and involves partitioning or division of the stomach to create a small gastric pouch of less than 30cc volume from the cardia of the stomach. The lack of an adequate length endoscopic TA stapler and possible advantages of a divided rather than partitioned pouch have led Laparoscopic surgeons to divide the stomach with serial applications of a GIA stapler. The roux limb is created by division of the proximal jejunum with re-anastomosis of the afferent limb 45-150cm distal to the point of initial division. This anastomosis is usually formed by intraluminal firing of a GIA stapler through an enterotomy in both the afferent and distal limbs. The enterotomies are either closed with sutures or an additional staple line.



Greatly improved quality of life is reported by nearly every patient...many patients count their surgical date as a new birthday.

The Roux-limb is brought up to the proximal gastric pouch following one of 3 paths; ante-colic and ante-gastric which is the longest path and requires division of the omentum, retro-colic and ante-gastric which obviates the need to divide the omentum and retro-colic retro-gastric which is the shortest path but technically most challenging. The gastro-jejunostomy is then fashioned with one of 3 basic techniques; EEA anastomosis with a 21mm or 25mm stapler, which seems to have a high rate of stricture, GIA with suture closure of the enterotomy-gastrotomy, and entirely sutured. Testing for leakage from this anastomosis prior to completion of the case is standard practice and can be performed with instillation of dye into the gastric pouch via an NG tube or air insufflation via an endoscope or NG tube with the anastomosis under saline and occlusion of the jejunum distally.

Mesenteric defects should be closed to prevent internal hernias that can result in potentially fatal bowel obstructions. With the ante-colic ante-gastric approach there is no transverse mesocolon defect and reports of obstruction even without closure of the mesenteric defects appear to be less frequent. This may be secondary to tension holding the defects in a closed position.

The incidence of serious complications including anastomotic leaks (1-2%) possibly higher with laparoscopy (2-4%), pulmonary emboli (0.2-1%) and other respiratory complications as well as mortality (0.5-1%) are in general outweighed by the excellent weight loss results of 50-80% excess weight loss and maintenance for 15 years documented in long term studies. Vitamin and mineral deficiencies can develop in over 30% of patients and therefore supplementation with iron, calcium, B-12 and a multivitamin is recommended as is long term regular follow up with evaluation of serum levels and for biochemical signs of deficiencies. Vitamin D absorption or metabolism may also be altered and supplementation as well as long-term regular evaluation seems prudent. Complications such as anastomotic stricture and ulcer can usually be well controlled with endoscopic treatment and medication respectively.

Side effects of gastric bypass including dumping syndrome which often leads to intolerance of sweets and fat malabsorption are generally considered positive effects of the operation for weight loss and can usually be well controlled with patient education and dietary restriction or modification. Clearly the need for extensive patient education and follow up means that a significant commitment of resources is needed for patient support and this is not an area to be entered into without careful consideration.


Figure 3

Adjustable silastic gastric banding with the Lap-Band has been FDA approved in the US since June 2001. This is a purely restrictive operation that does not alter digestion or absorption of nutrients. The Lap-Band is placed around the proximal stomach usually via laparoscopy and the diameter of the stoma or outlet of the proximal gastric pouch is adjusted via saline infusion into a subcutaneous port, which is attached to a bladder on the internal surface of the band by a thin silastic tube. The Lap-Band is placed through a retro-gastric tunnel preferable superior to the lesser sac and is closed around the proximal stomach with a self-locking buckle. The anterior stomach is sutured over the band to provide for fixation to prevent pouch enlargement or band slippage both of which can be the cause of outlet obstruction requiring re-operation. The tubing is then brought through the abdominal wall where it is attached to a port that is sutured to the anterior rectus fascia.

Weight loss is slower, more variable and less predictable with Lap-Band than after gastric bypass. On average in the rest of the world 50% excess weight loss at about 2 years with maintenance at 5 years and beyond is reported. In the US trials 40% excess weight loss with a revision and removal rate of 25-30% and beyond have been reported but similar early experience in the rest of the world improved and long term results beyond the learning curve are not yet available in the U.S. In general the band is left deflated for 6 weeks post-operatively and then slowly adjusted to provide adequate resistance to solid food intake and early, sustained satiety. Monthly visits in the first year aid the patient in learning to eat slowly and chew thoroughly and allow for gradual adjustment in band diameter as the patient learns to adapt. Erosion and infection of the band or port as well as the above-mentioned slippage or pouch enlargement are reported in fewer than 10% of patients in recent series worldwide and can usually be dealt with via laparoscopy.

Clearly with Lap-Band the risks of serious complications as well as mortality (0.1%) are significantly lower than with gastric bypass and this as well as the absence of significant vitamin and mineral malabsorption have made it an increasingly attractive option. The need for frequent (3-4) adjustments in the first year as well as the need to voluntarily abstain from sweets, liquid calories and simultaneous eating and drinking makes Lap-Band a more demanding option on patients as well as surgeons in some regards. Fear of inadequate weight loss and "cheating" leads many patients who are otherwise good candidates for Lap-Band to choose gastric bypass.

Overall the effects of significant weight loss on patients' co-morbidities and quality of life are incredible. 80% of patients with NIDDM, 75% of those with sleep apnea, 50% of hypertensives, over 90% of GERD symptoms and almost every other co-morbid condition is completely controlled without medication or greatly improved with less treatment than before surgery. Greatly improved quality of life is reported by nearly every patient and has been well documented in the literature; many patients count their surgical date as a new birthday. It is clear that bariatric surgery more than almost any other surgical intervention provides multiple and dramatic benefits for patients' lives.

Dennis L. Fowler, M.D.
Leon C. Hirsch Professor of Clinical Surgery, Weill Cornell Medical Center
Professor of Clinical Surgery, Columbia College of Physicians and Surgeons
Director, Minimal Access Surgery Program, New York-Presbyterian Hospital

The use of laparoscopy as a method of access for foregut surgery started with laparoscopic cholecystectomy. Surgeons now routinely use laparoscopy as the method of choice not only for cholecystectomy, but also for anti-reflux surgery. Along with bariatric surgery, these procedures account for the most commonly performed upper GI surgical procedures. However, there are definite indications for other laparoscopic surgical procedures on the foregut, but the disease processes that require these surgical treatments occur less frequently. Examples of these include neoplasms of the esophagus, stomach and pancreas, as well as achalasia. Effective laparoscopic techniques are now available to treat these less common foregut conditions. The following discussion includes brief reviews of laparoscopic/thoracoscopic esophagectomy, laparoscopic myotomy for achalasia, laparoscopic gastrectomy, and laparoscopic distal pancreatectomy.

The incidence of esophageal cancer increased during the second half of the 20th century, and this increase was at least in part due to the increased incidence of gastroesophageal reflux disease (GERD).

Patients with GERD have an increased incidence of esophageal carcinoma compared with the rest of the population.

This increase in esophageal carcinoma is due to an increase in adenocarcinoma of the esophagus, not squamous cell carcinoma of the esophagus and the most common etiology for adenocarcinoma is reflux. In most cases, the neoplasia is preceded by metaplasia that is called Barrett's esophagus.

Barrett's esophagus is defined by the presence of intestinal metaplasia of the mucosa of the esophagus, and this is histologically apparent when there are goblet cells in the columnar mucosa. Biopsies of this mucosa can demonstrate the progression of mucosal change from simple metaplasia, to metaplasia with low-grade dysplasia, to metaplasia with high-grade dysplasia, to adenocarcinoma. Esophagectomy is indicated for high-grade dysplasia or carcinoma.

Esophagectomy is a procedure usually completed with major, open surgery through the abdomen (transhiatal esophagectomy), through the chest (transthoracic esophagectomy), or using both incisions (Ivor-Lewis technique). Reconstruction of the GI tract usually involves replacement of the esophagus with either a stomach tube or a segment of colon. In the past few years, surgeons have begun to use a minimal access surgical approach for the treatment of selected patients with high-grade dysplasia or cancer 1-2. This minimal access approach can occasionally be completed with laparoscopic dissection, but will frequently also require thoracoscopy to complete the mobilization and resection of the middle portion of the esophagus. The esophagus is replaced with a gastric tube prepared laparoscopically and pulled through the esophageal hiatus and mediastinum up to the neck. The resected esophagus is removed through a supraclavicular incision and the esophagogastric anastomosis is also completed through this neck incision.

Several small series have reported significant recovery benefits using this technique and the preliminary oncologic data with sort-term follow-up is consistent with results after open surgery 3-4. Long-term follow-up in larger studies will be required to define the role of this approach for all cancers of the esophagus. For patients with benign disease or high-grade dysplasia, laparoscopic/thoracoscopic resection is a valid consideration.

The primary symptom of achalasia is dysphagia. This is usually progressive over time, and begins with dysphagia to solid food and eventually may cause problems with drinking liquids. The pathophysiology of the condition is related to a failure of the nerves within the esophagus to function normally. The result is a severe dysmotility that manifests in two ways. First, the body of the esophagus becomes aperistaltic. Although there may be contractions of the esophagus, sometimes even with nearly normal pressures, the contractions are simultaneous throughout the body of the esophagus. In the most advances condition, there are no contractions. The second manifestation of achalasia is a failure of the lower esophageal segment (LES) to relax after a swallow. This compounds the failure of normal peristalsis and results in retention of food in the esophagus. Secondary symptoms included regurgitation, particularly at night after a late meal. Some patients think this is due to reflux, but the real mechanism with achalasia is that the food retained in the esophagus then rolls back up into the pharynx, particularly when the patient is supine.

The diagnosis of achalasia may be suggested by history, and is often further suggested by a Barium esophagram or an endoscopy. In patients with achalasia, each study demonstrates some dilatation of the esophagus and narrowing of the LES. The definitive test for achalasia is an esophageal manometry. This will document the function of the body of the esophagus as well as document whether the LES relaxes. Additionally, the study provides excellent baseline information against which future determinations can be made, regardless of the type of treatment that the patient chooses.




Figure 1: The arrow demonstrates the exposed esophageal mucosa. The edge of the cut muscularis is sutured to the fundus on each side to create a partial posterior Fundoplication.

Treatment of achalasia focuses on making the LES incompetent. In most patients with achalasia, this will result in a reduction or elimination of dysphagia. There are three clinically available treatments that render the LES incompetent. The first is injection of Botulinum toxin into the LES. Although this is often very effective, it only lasts for a few months until the dysphagia recurs. The second option is pneumatic dilatation. This technique provides patients with relief of the dysphagia, but is long lasting (effective more than 5 years) in only about half of patients. The third option is surgical myotomy of the LES. Traditionally, this was performed through a left thoracotomy. In the past decade laparoscopic myotomy has become the surgical procedure of choice with excellent relief of dysphagia. Patti, et al.5, report that 94% of patients have relief of their dysphagia after laparoscopic cardiomyotomy. (Figure 1) The long-term results after laparoscopic cardiomyotomy are better than the results after nonsurgical treatment of achalasia. Additionally, these data suggest that the laparoscopic approach to surgical myotomy does confer recovery benefits with a shorter length of stay and a quicker overall recovery.

...the laparoscopic approach to surgical myotomy does confer recovery benefits with a shorter length of stay and a quicker overall recovery.


Figure 2: For an antrectomy, the stomach is mobilized and then divided with a laparoscopic linear cutting stapler


Figure 3: After antrectomy, a gastrojejunostomy is created with the laparoscopic linear cutting stapler

Because of a better understanding of the pathophysiology of peptic ulcer disease (PUD), medical treatment for PUD is now quite successful in healing and preventing recurrence of peptic ulcers. For that reason, gastric resection for PUD is rarely necessary. Currently, gastric bypass for severe obesity is the most commonly performed gastric surgery. However, most benign and malignant neoplasms of the stomach are still best treated with surgical resection. Most surgeons would recommend an open gastrectomy for an invasive adenocarcinoma of the stomach, although there are now reports of laparoscopic gastrectomy tailored to the location in the stomach (distal gastrectomy or antrectomy for lesions in the antrum and proximal gastrectomy for lesions in the body or fundus) is indicated. (Figures 2,3) This is technically possible laparoscopically, but large series with long-term follow-up have not been reported.

Benign neoplasms of the stomach, most commonly submucosal lesions such as a gastrointestinal stromal tumor (GIST), are particularly amenable to laparoscopic resection. In published reports, these patients experience the anticipated benefits of a shorter recovery and quicker return to normal activities6-7. For these lesions, a wedge resection or partial gastrectomy is usually sufficient treatment. Patients undergoing this partial gastrectomy usually require a 3-day stay in the hospital and can complete their recovery in two to three weeks. Most patients will require a nasogastric tube for one day or less.

Pancreatic surgery can be one of the most challenging procedures for an abdominal surgeon. Experience with laparoscopic pancreaticoduodenectomy has been small, and has not demonstrated any benefit when compared to open pancreaticoduodenectomy. However, a growing experience with laparoscopic distal pancreatectomy has demonstrated both technical feasibility and benefit for the patient8. Typical indications for laparoscopic distal pancreatectomy have included mucinous cystadenomas or cystadenocarcinomas, islet cell tumors, and pseudocysts requiring resection. Adenocarcinoma of the tail of the pancreas is still treated with open distal pancreatectomy.


Figure 4: The splenic artery and vein lay side by side after the body and tail of the pancreas have been laparoscopically removed.

Laparoscopic distal pancreatectomy was initially performed to include splenectomy. Typical surgical technique for distal pancreatectomy includes dividing the splenic artery and vein at the line of resection in the pancreas. This is usually thought to devascularize the spleen such that it should be removed. There are also oncologic reasons to take the spleen en block when the resection is for cancer. But if the disease is benign, it is desirable to leave the spleen. This requires a more difficult dissection to try to preserve the splenic artery and vein. However, there are now numerous reports of spleen sparing laparoscopic distal pancreatectomy9. (Figure 4) Preliminary results suggest that it is possible to preserve the function of the spleen while still providing an adequate resection with a quicker recovery.

Laparoscopic surgery to treat diseases of the foregut offers patients the anticipated benefits associated with laparoscopic surgery (quicker recovery, better cosmesis). At the same time it appears to offer satisfactory treatment of the disease process (achalasia, high-grade dysplasia in Barrett's esophagus, benign gastric and pancreatic neoplasms).

1. Luketich JD, Nguyen NT, Shauer PR. Laparoscopic transhiatal esophagectomy for Barrett's esophagus with high grade dysplasia. JLSL 1998;2 75-77
2. Nguyen NT, Follette DM, Lemoine PH, et al. Minimally invasive Ivor Lewis esophagectomy. Ann Thorac Surg 2001;72: 593-596
3. Swanstrom LL, Hansen P. Laparoscopic total esophagectomy. Arch Surg 1997;132: 943-949
4. Luketich JD, Schauer PR, Christie NA, et al. Minimally invasive esophagectomy. Ann Thorac Surg 2000;70: 906-912.
5. Patti MG, Molena D, Fisichella PM, et al. Laparoscopic Heller myotomy and Dor Fundoplication for achalasia: analysis of successes and failures. Arch Surg 2001;136: 870-877.
6. Otani Y, Ohgami M, Igarashi N, et al. Laparoscopic wedge resection of gastric submucosal tumors. Surg Laparosc Endosc Percutan Tech 2000;10: 19-23.
7. Matthews BD, Walsh RM, Kercher KW, et al. Laparoscopic vs open resection of gastric stromal tumors. Surg Endosc 2002;16: 803-807.
8. Patterson EJ, Gagner M, Salky B, et al. Laparoscopic pancreatic resection: single-institution experience of 19 patients. J Am Coll Surg 2001;193: 281-287.
9. Tagaya N, Ishikawa K, Kubota K. Spleen-preserving laparoscopic distal pancreatectomy with conservation of the splenic artery and vein for a large insulinoma. Surg Endosc 2002;16: 271-218.