What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Print
0 Find synonyms

Find synonyms Find exact match

Laparoscopic sleeve gastrectomy
UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
Laparoscopic sleeve gastrectomy
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Sep 25, 2017.

INTRODUCTION — Bariatric surgery has been recognized as the most effective long-term treatment modality for severe obesity. Among various bariatric procedures, laparoscopic sleeve gastrectomy (LSG) has rapidly gained popularity to become most frequently performed worldwide [1,2]. In the United States alone, over 100,000 LSGs were performed in 2015, which accounted for 54 percent of all bariatric procedures performed that year [3].

LSG entails resecting the greater curvature and fundus of the stomach; the partial gastrectomy is oriented vertically, parallel to the lesser curvature of the stomach. Originally described in the 1990s as the "Magenstrasse and Mill procedure," the principle of LSG derives from the physiologic "Magenstrasse" (German for "street of the stomach"), which conveys food from the esophagus to the antral "Mill" to be ground and propelled into the duodenum (figure 1). Although LSG was initially regarded as a purely restrictive procedure, we now know that it also promotes weight loss by inducing anorexia through removal of the majority of ghrelin-producing cells located in the gastric fundus [4].

Overall, LSG results in excellent weight loss and remission of most obesity-related comorbidities. LSG is also less morbid than some of the other bariatric operations, such as laparoscopic Roux-en-Y gastric bypass, because of its technical simplicity and its limited alteration of the normal anatomy [5].

The mechanisms of action, indications, techniques, and outcomes of LSG will be discussed here. Other bariatric operations are described elsewhere. (See "Bariatric procedures for the management of severe obesity: Descriptions".)

MECHANISMS OF ACTION — LSG promotes weight loss through two principal mechanisms of action, mechanical (creation of restriction) and endocrine (creation of anorexia):

Mechanical — Following LSG, the sleeved stomach is reduced in volume and distensibility, both of which contribute to the restrictive mechanism of weight loss.

LSG results in a gastric volume reduction of 70 to 80 percent. In a study that quantified the volume and pressure of the stomach immediately before and after LSG, the mean volumes of the original and the sleeved stomach were 1553 mL (600 to 2000 mL) and 129 mL (90 to 220 mL), respectively [6].

In the sleeved stomach, a reduction in volume results in an increase in intraluminal pressure. In the same study cited above, a sleeved stomach filled with saline had a pressure of 43 mmHg (32 to 58 mmHg), compared with 34 mmHg (21 to 45 mmHg) of the original stomach filled with saline [6]. The high intraluminal pressure is a significant contributing factor to a higher leak rate associated with LSG. (See 'Leak' below.)

Endocrine — It has been well established that the centrally regulated weight homeostasis is profoundly influenced by a complex interaction of diet, gut, and brain hormones [7,8]. These hormones are mainly secreted by the gastrointestinal tract and adipose tissue. LSG alters the levels of such hormones to the advantages of weight loss (table 1):

Ghrelin is a 28-amino-acid peptide secreted mainly by the oxyntic glands in the fundus of the stomach [4]. The main function of ghrelin is to stimulate appetite. LSG removes the gastric fundus and, therefore, significantly decreases the postprandial levels of ghrelin and promotes weight loss by inducing satiety. (See "Ghrelin".)

Glucagon-like peptide-1 (GLP-1) is a 30-amino-acid peptide mainly secreted by the small intestine L cells after contact of food. This hormone increases insulin secretion (incretin effect) on one end and slows gastric emptying and intestinal motility on the other (ileal brake) (figure 2). GLP-1 is increased after LSG, and it is postulated that increased levels of GLP-1 contribute to weight loss by improving glucose metabolism, reducing hunger, and increasing satiety [7]. In a study of 18 obese type 2 diabetic patients, glucose-induced early insulin secretion increased after LSG, whereas late insulin secretion decreased. The latter is thought to be due to increased insulin peripheral sensitivity [9].

Although GLP-1 has been shown to slow gastric emptying, the gastric emptying time accelerated after LSG (47.6±23.2 versus 94.3±15.4 minutes) in one study [10]. It is likely that more than one mechanism is in play when determining the gastric transit time after LSG. GLP-1 is further discussed in another topic. (See "Glucagon-like peptide-1 receptor agonists for the treatment of type 2 diabetes mellitus", section on 'Glucagon-like peptide-1'.)

LSG has also been shown to alter the levels of glucose-dependent insulinotropic peptide (GIP) [7], bile acids [11-13], and leptin [14], the clinical significance of which is still under investigation.

INDICATIONS — Similar to other bariatric operations, LSG is indicated in all patients meeting the 1991 National Institutes of Health (NIH) consensus conference criteria [15]. These criteria include (see "Bariatric operations for management of obesity: Indications and preoperative preparation", section on 'Indications'):

Body mass index (BMI) ≥40 kg/m2 with or without any associated comorbidities.

BMI between 35 and 40 kg/m2 with at least one serious weight-related comorbidity, including but not limited to diabetes, obstructive sleep apnea, hypertension, and coronary artery disease.

BMI between 30 and 35 kg/m2 with uncontrollable type 2 diabetes or metabolic syndrome.

Besides being a primary bariatric operation, LSG has also been used as a bridging procedure in super morbid obese patients (BMI of 50 kg/m2 and above) before biliopancreatic diversion with duodenal switch. Additionally, LSG is also a good revisional procedure for patients who fail laparoscopic adjustable gastric banding [16].

According to a consensus statement released by an expert panel representing 24 centers in 11 countries, LSG is safe for patients with diabetes, metabolic syndrome, and inflammatory bowel disease [5]. Although some bariatric surgeons disagree, the majority of the experts consider LSG an effective treatment for type 2 diabetes [16]. LSG can also be offered to high-risk patients such as those with Child's A or B liver cirrhosis and those awaiting kidney or liver transplant (with the goal of improving future graft function) [17]. Finally, LSG has been safely performed in both adolescents and older adult patients.

Absolute contraindications to LSG include prohibitive anesthesia risks, severe uncontrolled psychiatric illnesses (including certain eating disorders such as malignant hyperphagia), and coagulopathy. Barrett's esophagus and uncontrolled severe gastroesophageal reflux disease (GERD) are relative contraindications to LSG.

Some surgeons do not perform LSG in the presence of Barrett's esophagus, for fear that a sleeve gastrectomy would preclude a future gastric pull-up procedure, which may be required if Barrett's esophagus progresses to esophageal cancer [16]. Others do not consider Barrett's esophagus a contraindication to LSG [18]. Hiatal hernia without esophagitis is not a contraindication to LSG.

Performing LSG in patients with known GERD is controversial, with evidence existing for both exacerbation and improvement of GERD symptoms after surgery [19]. Roux-en-Y gastric bypass (RYGB) is a better surgical option of weight loss than LSG in patients with severe GERD. Patients who develop debilitating symptoms of GERD after LSG may require conversion to RYGB. (See 'GERD' below.)

PREOPERATIVE WORKUP — Prior to any bariatric surgery, patients need to undergo psychologic, medical, and anesthetic risk assessment, the details of which are discussed in another topic. (See "Bariatric operations for management of obesity: Indications and preoperative preparation", section on 'Preoperative assessment'.)

Prior to LSG, patients with upper gastrointestinal tract symptoms (eg, acid reflux, dysphagia) can be evaluated, at the surgeon's discretion, with an upper gastrointestinal contrast series (UGI) and/or an esophagogastroduodenoscopy (EGD) to exclude ulcers, polyps, masses, or dysplastic changes and to identify any anatomical abnormalities such as a hiatal hernia.

Such patients may also undergo esophageal pH testing and manometry to assess the severity of any existing gastroesophageal reflux disease (GERD) and exclude esophageal motility disorders [20]. Although esophageal motility disorders such as achalasia are not considered contraindications to LSG, they could potentially be addressed before or at the same time of LSG. (See "Clinical manifestations and diagnosis of gastroesophageal reflux in adults", section on 'Additional evaluation' and 'GERD' below.)

Although a baseline gallbladder ultrasound is usually performed prior to LSG, the incidence of symptomatic gallstone disease developing after LSG is lower than that after gastric bypass. Additionally, biliary diseases such as choledocholithiasis are also easier to treat after LSG than after gastric bypass because LSG maintains normal duodenal anatomy, which permits per oral endoscopic retrograde cholangiopancreatography (ERCP) [21]. (See "ERCP in patients with Roux-en-Y anatomy".)

TECHNIQUE — LSG is a vertically oriented gastrectomy that removes approximately 70 to 80 percent of the greater curvature of the stomach, resulting in the creation of a narrow gastric tube with a volume of approximately 150 to 200 mL based on the less distensible lesser curvature (figure 1) [6]. The remnant stomach after LSG is referred to as a sleeved stomach or simply "sleeve."

Patient position — The patient is positioned supine on and appropriately secured to the operating table. All pressure points are padded, and a mechanical deep vein thrombosis prophylaxis device is applied. The surgeon and the camera holder stand on the patient's right side; the first assistant and surgical technician stand on the patient's left side.

Trocar placement — Although variability exists, the authors' preference is to access the abdomen via a supraumbilical gasless optical trocar. Once pneumoperitoneum has been established, additional trocars are inserted under direct vision:

A 5-mm trocar is inserted in the subxiphoid area for the liver retractor.

A 5-mm trocar is placed in the left upper quadrant at the anterior axillary line just below the 12th rib for the assistant.

Additional 12-mm trocars are placed in the right upper quadrant, epigastrium, left upper quadrant, and right paramedian regions for inserting staplers.

Identify pylorus — The first step is to identify the pylorus by visualizing the prepyloric vein of Mayo and palpating with laparoscopic instruments. The pylorus is a crucial landmark because gastric transection typically begins 2 to 6 cm from the pylorus [16]. Some surgeons transect the stomach close to the pylorus (eg, 2 cm), while others begin the gastric transection further away from the pylorus (eg, 6 cm) to preserve the entire gastric antrum to ensure proper gastric emptying postoperatively [22].

Mobilize greater curvature — Once the site of future gastric transection is identified, the greater curvature of the stomach is devascularized using an advanced vessel-sealing device. This process is continued proximally onto the posterior fundus until the left crus of the diaphragmatic hiatus is clearly identified. All the short gastric vessels should be divided along the way. A complete mobilization of the greater curvature ensures that a sizable portion of the posterior fundus is not left behind during gastric transection. Although the merit of such mobilization was once debated, it has been accepted by the majority of experts [16].

Assess hiatus — At this point, most surgeons would assess the hiatus for hernias. Any large hiatal hernia should be repaired using standard laparoscopic techniques [23]. The blood supply to the lesser curvature (ie, left gastric artery) must be preserved since it will become the sole blood supply to the sleeve after gastric transection. The technique of hiatal hernia repair is discussed in another topic. (See "Surgical management of paraesophageal hernia", section on 'Transabdominal repair'.)

Insert bougie — A bougie is then inserted transorally by the anesthesiologist, advanced under direct vision to the pylorus, and positioned against the lesser curvature. Although experts agree on the need for calibrating the sleeved stomach with a bougie, the optimal size of such a bougie is still debated. The majority of experts, however, agree that the optimal bougie size lies between 32 and 36 French [16]. Using a bougie smaller than 32 French could make the sleeve too tight, which increases the risks of leak and stenosis [5] (see 'Morbidity and mortality' below), whereas using a bougie larger than 36 French could result in loss of restriction and weight regain over time.

Transect stomach — The gastric transection is then performed using sequential applications of 60-mm linear staplers beginning at a point 2 to 6 cm proximal to the pylorus. As the gastric transection proceeds, the height of the staples may need to be adjusted according to the thickness of the tissue. In general, most experts would not use staples with closed height <2.0 mm to transect the antrum (the thicker part of the stomach) or staples with closed height <1.5 mm to transect the rest of the stomach (thinner parts) [5].

While transecting the stomach, the surgeon must avoid twisting the staple line along the longitudinal axis and avoid narrowing the sleeve, particularly at the level of the incisura angularis. A twisted or narrowed sleeve can cause distal obstruction, which is responsible for the majority of the occurrences and persistence of staple line leaks in the proximal sleeve (see 'Leak' below). Constant symmetric lateral traction during the transection provided by the assistant is paramount to avoiding corkscrewing, twisting, or narrowing of the sleeve. When performing the last stapler firing, it is important to avoid stapling too close to the gastroesophageal junction, which may result in ischemia and postoperative leak.

Most experts recommend reinforcing the staple line to reduce the risk of bleeding and leak [5]. This can be accomplished by using a buttressing material at the time of stapler firing or by oversewing the staple line. A combination of buttressing and oversewing, however, increased staple line leak rate compared with either method alone in one study [24]. Oversewing should be done with the bougie still in place to avoid excessive imbrication and narrowing of the sleeve lumen.

After the stomach is transected and the staple line oversewn, an intraoperative leak test can be performed. However, most surgeons do not perform such a test.

Extract specimen — The resected portion of the stomach is extracted through the periumbilical trocar site. The enlarged trocar site is then closed, completing the procedure.

POSTOPERATIVE CARE — Despite considerable national variation in clinical pathways used by bariatric centers [25,26], most patients are admitted for overnight observation after LSG, especially if they have a history of obstructive sleep apnea. Postoperative nausea is the most common complaint and should be treated with scheduled doses of intravenous antiemetics such as ondansetron, with other antiemetics, such as prochlorperazine and scopolamine patch, provided as needed for breakthrough symptoms. Minimizing narcotic use by liberal use of local anesthetic infiltration, transverse abdominis plane (TAP) blocks, and intravenous acetaminophen also contributes to the reduction of postoperative nausea and early discharge.

A clear liquid diet is usually started in the morning after the procedure. If the patient tolerates that, he/she can be advanced to a full liquid diet within 24 hours. Once the patient tolerates a liquid diet and his/her pain is controlled with oral pain medications, he/she can be discharged home with instructions to only take crushed or liquid medications and a full liquid diet for two weeks.

A postoperative contrast study is performed after LSG to detect leak by some surgeons but not others. Because most leaks from LSG occur late after patient discharge, routine contrast studies on postoperative day 1 have a very low yield of detecting leaks [27].

Other routine aspects of postoperative care after all bariatric operations, such as pain control and venous thromboembolic (VTE) prophylaxis, are described in detail by another topic. (See "Bariatric surgery: Postoperative and long-term management of the uncomplicated patient", section on 'In-hospital postoperative care'.)

OUTCOMES — Compared with other commonly performed bariatric operations, LSG is more effective but more morbid than laparoscopic adjustable gastric banding (LAGB) and less effective but less morbid than Roux-en-Y gastric bypass (RYGB) [28-30].

Weight loss — At five years after LSG, the average patient loses 60.5 percent (standard deviation 10.6 percent) of excess body weight and achieves a body mass index (BMI) of 30.2 kg/m2 (standard deviation 5.5 kg/m2) [16]. To put this into perspective, LAGB and RYGB result in typical excess weight loss (EWL) of 50 and 70 percent, respectively, at two years. (See "Bariatric procedures for the management of severe obesity: Descriptions", section on 'Contemporary procedures'.)

Based on our series of 1020 patients, the mean percent EWL at one, three, five, and eight years after LSG were 86, 63, 61, and 52 percent, respectively. This translated into an overall success rate (defined as percent EWL >50 percent) of 92 percent after one year, 89 percent after three years, 75 percent after five years, and 73 percent after eight years [31].

In another long-term study of 168 patients after LSG, the mean EWL was 76 percent at five years and 67 percent at eight years. Of the 116 patients who were followed for eight years, 71 percent had >50 percent EWL at eight years. Twenty-three patients required revisional surgery after a mean period of 50 months, 14 patients for weight regain, and 9 for severe reflux [32].

Correction of comorbidities — Besides weight loss, LSG has also been shown to result in improvement or resolution of a number of comorbid medical conditions [33].

Diabetes mellitus — In a systematic review of 27 studies, type 2 diabetes mellitus resolved in 66.2 percent, improved in 26.9 percent, and remained stable in 13.1 percent of patients after a mean follow-up of 13 months after LSG [34].

In a randomized trial of obese patients with type 2 diabetes, over 88 percent of patients were able to maintain healthy blood glucose levels without the use of insulin at five years after LSG. Twenty-three percent achieved and maintained normal blood glucose levels, compared with just 5 percent of patients treated medically [35,36].

In North America, RYGB and sleeve gastrectomy (SG) account for over 95 percent of bariatric procedures in patients with type 2 diabetes [37], both of which achieve remission in 50 to 70 percent of patients after short- to medium-term follow-up [36,38]. One retrospective study separated patients into categories of mild, moderate, and severe diabetes based on four independent variables: preoperative number of diabetes medications, insulin use, preoperative duration of diabetes, and hemoglobin A1c [39]. After a median follow-up of seven years (range 5 to 12), remission was observed in 49 percent of all patients after RYGB and 28 percent after SG. For patients with mild diabetes, the remission rates were 92 percent (RYGB) versus 74 percent (SG). For those with moderate diabetes, the remission rates were 60 percent (RYGB) versus 25 percent (SG). For those with severe diabetes, the remission rate was 12 percent after both procedures.

It is important to note that this tool was constructed for the sole purpose of maximizing glycemic control. In everyday practice, other anatomic or clinical factors must also be considered when choosing between RYGB and SG. As examples, patients with severe acid reflux, Crohn disease, or organ transplantation are better suited for SG than RYGB. Additionally, one must also be aware that RYGB has been associated with higher short- and long-term morbidity rates than SG in multiple studies [28,29]. (See "Laparoscopic Roux-en-Y gastric bypass", section on 'Indications' and "Laparoscopic Roux-en-Y gastric bypass", section on 'Preoperative workup'.)

The management of type 2 diabetes with bariatric surgery is further discussed in another topic. (See "Management of persistent hyperglycemia in type 2 diabetes mellitus", section on 'Surgical treatment of obesity'.)

GERD — The effect of LSG on gastroesophageal reflux disease (GERD) is debated [40], with low-quality evidence suggesting both improvement [19,41] and worsening [42-44] of the condition after surgery.

Nevertheless, new-onset GERD or worsening of preexisting GERD is a potential complication of LSG. After LSG, between 5 and 22 percent of patients suffered from GERD, with a small subset of those patients (2.9 percent) converting to another bariatric procedure (typically RYGB) because of debilitating symptoms [16]. Our own series of over 1000 patients showed a GERD prevalence of 5.6 percent after LSG and conversion rate of 0.37 percent [31].

NASH — Nonalcoholic steatohepatitis (NASH) is a stage of nonalcoholic fatty liver disease (NAFLD). Obesity and metabolic syndrome are two major risk factors for NASH and NAFLD. The prevalences of NAFLD and NASH in severely obese (BMI ≥35 kg/m2) patients are approximately 70 and 30 percent, respectively. Weight reduction via lifestyle modifications, medical therapy, and bariatric surgery is currently the most effective treatment for NAFLD and NASH. (See "Natural history and management of nonalcoholic fatty liver disease in adults", section on 'Management'.)

In a study of 70 patients who underwent laparoscopic RYGB (58.6 percent), LSG (32.9 percent), or LAGB (8.6 percent), scores for liver steatosis, inflammation, and fibrosis all improved on liver biopsies performed at 15±9 months after LSG, and no progression of grade or stage of liver disease was observed [45]. In subgroup analysis, although patients who underwent laparoscopic RYGB had greater improvement in liver grade and stage, they also had greater weight loss. After adjusting for percent EWL, LSG and RYGB were equally effective in improving liver morphology.

Although obesity has also been associated with hypertension, dyslipidemia, obstructive sleep apnea, arthritis, polycystic ovary syndrome, infertility, urinary incontinence, depression, eating disorder, and cancer, such conditions will not be discussed here because conclusive evidence that LSG can reverse or improve them does not exist. The medical outcomes following other bariatric procedures (eg, RYGB) are discussed in another topic. (See "Medical outcomes following bariatric surgery".)

MORBIDITY AND MORTALITY — In modern series, the overall mortality rate of LSG is approximately 0.3 percent [46]; the overall morbidity rates range from 2.9 to 15.3 percent [47,48].

Based on a large database review, the overall 30-day mortality rate after LSG is 0.11 percent, which compared favorably to that of laparoscopic (0.14 percent) and open Roux-en-Y gastric bypass (RYGB, 0.71 percent) but less favorably to that of laparoscopic adjustable gastric banding (LAGB, 0.05 percent) [29].

Similarly, the 30-day complication, readmission, and reintervention rates of LSG (5.6, 5.4, and 2.97 percent) are also positioned between those of laparoscopic (5.9, 6.4, and 5 percent)/open RYGB (15, 9.4, and 5.6 percent) and LAGB (1.4, 1.7, and 0.9 percent) [29].

In our own series of over 1000 LSG patients, early postoperative complications included leak in 0.1 percent, stricture in 0.1 percent, and bleeding not requiring reintervention in 3 percent of patients. Long-term complications included stricture in 0.49 percent and gastroesophageal reflux disease (GERD) in 6 percent of patients [31].

The main surgical complications of LSG and their management are as follows:

Bleeding — Postoperative bleeding after LSG has been described in up to 15 percent of cases. It can occur within the lumen of the stomach, intra-abdominally, or at the trocar/incision sites.

The source of intra-abdominal bleeding can usually be found along the greater curvature of the stomach, most commonly originating from the short gastric vessels or the spleen. Because the fundus of the stomach is in close proximity to the spleen, it is not uncommon to injure the spleen during LSG by either traction or burn to the splenic capsule. Small capsular tears can be managed with persistent and prolonged pressure and topical hemostatic agents, whereas larger tears and uncontrolled bleeding from the spleen might necessitate a splenectomy. Good exposure to the left upper quadrant during LSG is paramount to preventing this complication.

LSG creates likely the longest staple line in surgery. A long staple line in a well-vascularized organ is a perfect setup for both intraluminal and intra-abdominal bleeding. While intra-abdominal bleeding can be readily visualized and treated with clips, sutures, or fibrin glue, it is more difficult to diagnose intraluminal bleeding. After LSG, the combination of hematemesis or melena with a dropping hematocrit is suggestive of intraluminal bleeding. Evidence exists that staple line reinforcement reduces the risk of staple line bleeding [49]. While most episodes of intraluminal bleeding are self-limited, some may require endoscopic or surgical intervention. In addition to incurring blood loss, a bleeding staple line may also be weak and susceptible to leak. (See 'Leak' below.)

Bleeding at laparoscopic trocar/incision sites is rare but can be both insidious and significant. Immediate bleeding can be detected and treated by directly observing the trocar site after removal of the trocar. Delayed bleeding usually starts after the pneumoperitoneum is evacuated and the systemic blood pressure increases and can cause hematoma formation at the trocar site. Laparoscopic trocar/incision site bleeding and hematoma are discussed in another topic. (See "Abdominal access techniques used in laparoscopic surgery", section on 'Bleeding port' and "Complications of laparoscopic surgery", section on 'Minor vessels'.)

Leak — The staple line leak rate after LSG varies between 0 and 5.5 percent [46].

Although LSG does not involve an anastomosis, it is more susceptible to a leak than RYGB is (2.4 versus 0.7 percent) because of a long staple line and high intraluminal pressure [27]. As explained above, the high luminal pressure is generated by a narrow sleeved stomach sealed between an intact pylorus and lower esophageal sphincter. Leaks that occur after LSG are also less likely to close spontaneously because of the high luminal pressure. (See 'Mechanical' above.)

Other etiologies, besides a high intraluminal pressure, that also contribute to staple line leaks include ischemia, hematoma formation, and staple misfiring. Besides (rare) manufacturing issues, staple misfiring can be due to improper use of the stapler or improper selection of the staple height. When choosing staple cartridges, surgeons must be aware of the progressive decrease in the thickness of the gastric wall from the antrum to the fundus and adjust the staple height accordingly. (See 'Transect stomach' above.)

Based on the timing of onset, leaks can be classified as acute (within seven days), early (within one to six weeks), late (after six weeks), and chronic (after 12 weeks). The preferred treatment of leaks varies according to the timing of the leak. The following recommendations were suggested by an expert panel during a 2011 consensus conference [5] and were subsequently endorsed by the American Society for Metabolic and Bariatric Surgery as best practices [50]:

An unstable patient with a contained or uncontained symptomatic leak requires immediate reoperation.

A patient with fever and tachycardia but normal imaging studies requires surgical exploration to exclude a leak.

In stable patients, endoluminal stenting is a valid treatment option for an acute proximal leak that has failed conservative therapy.

Stenting has limited efficacy for chronic leaks. After 30 days, the likelihood of a leak to seal by means of exclusion via stent is very low.

In stable patients with a proximal leak, the surgeon should wait at least 12 weeks before reoperating to allow the body to heal and avoid thick adhesions.

Surgical options include revising the sleeve and converting to RYGB.

When revising the sleeve, the surgeon should oversew the leak with a bougie in place to avoid a stricture.

Converting to RYGB is a valid treatment option that is usually reserved as the last resort for patients with chronic proximal leaks. It converts a high-pressure system (LSG with distal obstruction) to a lower-pressure system (RYGB), which promotes healing of the leak/fistula [28].

Stricture — Although sleeve strictures have been reported in 0.26 to 4 percent of LSG operations [51-58], <1 percent result in symptoms that require endoscopic or surgical intervention [59]. A stricture can manifest acutely, early after surgery, or more chronically. Although strictures can occur anywhere along the long staple line, they are most often located at the level of the incisura angularis for anatomic reasons.

The etiologies of post-LSG strictures are either mechanical or functional. Mechanical strictures usually derive from the use of small bougies, stapling too close to the bougie (especially at the incisura angularis), twisting of the staple line creating a "spiral" sleeve, or aggressive imbrication of the staple line [5]. Functional stenoses derive from edema or hematomas at the staple line. As a result, functional stenoses are transient, which present immediately following LSG and resolve spontaneously with expectant treatment.

Patients who present with obstructive symptoms during the early postoperative period should be resuscitated with hydration and antiemetic medications and studied with an upper gastrointestinal (UGI) series. Stable patients with a stricture can be observed to allow postsurgical mucosal edema to resolve, typically in 24 to 48 hours. Patients who cannot handle their own secretions require nasogastric tube decompression, preferably placed under fluoroscopic guidance.

Patients with an acute stricture who do not respond to conservative management require early surgical reintervention. Laparoscopy could demonstrate kinking of the gastric tube, a tight suture, or a compressing hematoma [60]. Sutures used to oversew the staple line should be removed, after which an intraoperative endoscopy should be performed to confirm the resolution of the stricture. If no suture was used to oversew the staple line or if the stricture persists after all sutures have been removed, a seromyotomy of the greater curvature side of the sleeve can be performed to relieve the stricture [61]. The seromyotomy should be carried out from the antrum to the proximal sleeve using ultrasonic or monopolar energy, with the denuded mucosa covered with omentum.

By contrast, patients with chronic strictures often present with mild symptoms that mimic acid reflux. Such patients can be initially managed with proton pump inhibitors. Those who fail medical management or develop severe symptoms are candidates for further endoscopic or surgical interventions:

Endoscopy is a good initial treatment for short-segment strictures, most of which can be dilated with balloons. Multiple treatments in four- to six-week intervals are sometimes needed to treat the stricture and improve patient symptoms [62]. Stents have also been tried but are not effective for post-LSG strictures [62-65]. Long-segment strictures are not amenable to endoscopic dilation. Long strictures and strictures that have failed endoscopic treatment require surgical intervention.

Laparoscopic seromyotomy is a treatment option for long-segment strictures [16]. In a small retrospective study, patients treated with laparoscopic seromyotomy had good symptomatic relief [61]. However, further studies with longer follow-ups are required to validate this procedure.

Conversion to an RYGB is the last option for patients with a refractory stricture who have failed all other treatments [5,47,51,55,66].

Portal vein thrombosis — Portomesenteric vein thrombosis is a rare complication of laparoscopic bariatric surgery, most commonly after LSG. In a study of 5706 patients who underwent laparoscopic bariatric surgery, 17 had portomesenteric vein thrombosis, of which 16 did so after a sleeve gastrectomy [67].

Portomesenteric vein thrombosis has been reported in up to 1 percent of patients undergoing LSG, presenting at a median of 10 to 20 days after surgery [68,69]. Epigastric pain is the most common presenting symptom. Stable patients with nonocclusive disease can be treated with anticoagulation alone. Patients with occlusive disease require thrombolysis and/or operative thrombectomy and subsequent anticoagulation [70]. (See "Acute portal vein thrombosis in adults: Clinical manifestations, diagnosis, and management".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bariatric surgery".)

SUMMARY AND RECOMMENDATIONS

Laparoscopic sleeve gastrectomy (LSG) is one of the most commonly performed bariatric procedures. LSG promotes weight loss by mechanical restriction of the gastric volume/distensibility and by hormonal induction of satiety and anorexia. (See 'Introduction' above and 'Mechanisms of action' above.)

The indications for LSG are the same as for other bariatric procedures, namely body mass index (BMI) ≥40 kg/m2, BMI between 35 and 40 kg/m2 with one or more comorbid conditions, or BMI between 30 and 35 kg/m2 with uncontrolled type 2 diabetes or metabolic syndrome. LSG is safe for select high-risk patients as well as for both adolescent and older adult patients. (See 'Indications' above.)

Absolute contraindications to LSG include prohibitive anesthesia risks, severe uncontrolled psychiatric illnesses (including certain eating disorders such as malignant hyperphagia), and coagulopathy. Barrett's esophagus and uncontrolled severe gastroesophageal reflux disease (GERD) are relative contraindications to LSG. Roux-en-Y gastric bypass (RYGB) is a better surgical option of weight loss than LSG in patients with severe GERD. Patients who develop debilitating symptoms of GERD after LSG may require conversion to RYGB. (See 'Preoperative workup' above and 'GERD' above.)

LSG is a vertically oriented gastrectomy that removes approximately 70 to 80 percent of the greater curvature of the stomach, resulting in the creation of a narrow gastric tube with a volume of approximately 150 to 200 mL based on the less distensible lesser curvature. (See 'Technique' above.)

The greater curvature of the stomach is transected with sequential firing of staplers beginning at 2 to 6 cm from the pylorus. The sleeve should be calibrated with a 32- to 36-French bougie placed against the lesser curvature of the stomach. The greater curvature should be completely mobilized and retracted laterally to avoid narrowing (especially at incisura angularis), twisting, or spiraling of the sleeve during transection. Staple height should be constantly adjusted according to the thickness of the gastric wall. After gastric transection, the long staple line should be reinforced by buttressing or oversewing. (See 'Technique' above.)

Most patients are admitted for overnight observation after LSG and treated for nausea. Clear liquid diet is allowed on the first postoperative day, and patients are discharged home with instructions to only take crushed or liquid medications and a full liquid diet for two weeks. (See 'Postoperative care' above.)

At five years after LSG, the average patient loses 60.5 percent of excess body weight and achieves a BMI of 30.2 kg/m2. LSG has also been associated with improvement or resolution of type 2 diabetes and nonalcoholic fatty liver disease. (See 'Outcomes' above.)

In modern series, the overall mortality rate of LSG is approximately 0.3 percent; the overall morbidity rates range from 2.9 to 15.3 percent. Major surgical complications include bleeding, leak, stricture, and portal vein thrombosis. These complications can be treated nonoperatively, endoscopically, or surgically (eg, converting to Roux-en-Y gastric bypass) depending on severity and chronicity. (See 'Morbidity and mortality' above.)

Use of UpToDate is subject to the  Subscription and License Agreement.

REFERENCES

  1. Ponce J, DeMaria EJ, Nguyen NT, et al. American Society for Metabolic and Bariatric Surgery estimation of bariatric surgery procedures in 2015 and surgeon workforce in the United States. Surg Obes Relat Dis 2016; 12:1637.
  2. Buchwald H, Oien DM. Metabolic/bariatric surgery worldwide 2011. Obes Surg 2013; 23:427.
  3. ASMBS. ASMBS Estimate of Bariatric Surgery Numbers, 2011-2015 https://asmbs.org/resources/estimate-of-bariatric-surgery-numbers (Accessed on December 30, 2016).
  4. Abdemur A, Slone J, Berho M, et al. Morphology, localization, and patterns of ghrelin-producing cells in stomachs of a morbidly obese population. Surg Laparosc Endosc Percutan Tech 2014; 24:122.
  5. Rosenthal RJ, International Sleeve Gastrectomy Expert Panel, Diaz AA, et al. International Sleeve Gastrectomy Expert Panel Consensus Statement: best practice guidelines based on experience of >12,000 cases. Surg Obes Relat Dis 2012; 8:8.
  6. Yehoshua RT, Eidelman LA, Stein M, et al. Laparoscopic sleeve gastrectomy--volume and pressure assessment. Obes Surg 2008; 18:1083.
  7. Ionut V, Burch M, Youdim A, Bergman RN. Gastrointestinal hormones and bariatric surgery-induced weight loss. Obesity (Silver Spring) 2013; 21:1093.
  8. Korner J, Leibel RL. To eat or not to eat - how the gut talks to the brain. N Engl J Med 2003; 349:926.
  9. Basso N, Capoccia D, Rizzello M, et al. First-phase insulin secretion, insulin sensitivity, ghrelin, GLP-1, and PYY changes 72 h after sleeve gastrectomy in obese diabetic patients: the gastric hypothesis. Surg Endosc 2011; 25:3540.
  10. Melissas J, Koukouraki S, Askoxylakis J, et al. Sleeve gastrectomy: a restrictive procedure? Obes Surg 2007; 17:57.
  11. Lefebvre P, Cariou B, Lien F, et al. Role of bile acids and bile acid receptors in metabolic regulation. Physiol Rev 2009; 89:147.
  12. Nakatani H, Kasama K, Oshiro T, et al. Serum bile acid along with plasma incretins and serum high-molecular weight adiponectin levels are increased after bariatric surgery. Metabolism 2009; 58:1400.
  13. Aron-Wisnewsky J, Clement K. The effects of gastrointestinal surgery on gut microbiota: potential contribution to improved insulin sensitivity. Curr Atheroscler Rep 2014; 16:454.
  14. Korner J, Inabnet W, Conwell IM, et al. Differential effects of gastric bypass and banding on circulating gut hormone and leptin levels. Obesity (Silver Spring) 2006; 14:1553.
  15. Berrington de Gonzalez A, Hartge P, Cerhan JR, et al. Body-mass index and mortality among 1.46 million white adults. N Engl J Med 2010; 363:2211.
  16. Gagner M, Hutchinson C, Rosenthal R. Fifth International Consensus Conference: current status of sleeve gastrectomy. Surg Obes Relat Dis 2016; 12:750.
  17. Borbély Y, Juilland O, Altmeier J, et al. Perioperative outcome of laparoscopic sleeve gastrectomy for high-risk patients. Surg Obes Relat Dis 2017; 13:155.
  18. Gagner M. Is Sleeve Gastrectomy Always an Absolute Contraindication in Patients with Barrett's? Obes Surg 2016; 26:715.
  19. Rebecchi F, Allaix ME, Giaccone C, et al. Gastroesophageal reflux disease and laparoscopic sleeve gastrectomy: a physiopathologic evaluation. Ann Surg 2014; 260:909.
  20. Koppman JS, Poggi L, Szomstein S, et al. Esophageal motility disorders in the morbidly obese population. Surg Endosc 2007; 21:761.
  21. Li VK, Pulido N, Fajnwaks P, et al. Predictors of gallstone formation after bariatric surgery: a multivariate analysis of risk factors comparing gastric bypass, gastric banding, and sleeve gastrectomy. Surg Endosc 2009; 23:1640.
  22. Bernstine H, Tzioni-Yehoshua R, Groshar D, et al. Gastric emptying is not affected by sleeve gastrectomy--scintigraphic evaluation of gastric emptying after sleeve gastrectomy without removal of the gastric antrum. Obes Surg 2009; 19:293.
  23. Dakour Aridi HN, Tamim H, Mailhac A, Safadi BY. Concomitant hiatal hernia repair with laparoscopic sleeve gastrectomy is safe: analysis of the ACS-NSQIP database. Surg Obes Relat Dis 2017; 13:379.
  24. Stroh C, Köckerling F, Volker L, et al. Results of More Than 11,800 Sleeve Gastrectomies: Data Analysis of the German Bariatric Surgery Registry. Ann Surg 2016; 263:949.
  25. Telem DA, Majid SF, Powers K, et al. Assessing national provision of care: variability in bariatric clinical care pathways. Surg Obes Relat Dis 2017; 13:281.
  26. Telem DA, Gould J, Pesta C, et al. American Society for Metabolic and Bariatric Surgery: care pathway for laparoscopic sleeve gastrectomy. Surg Obes Relat Dis 2017; 13:742.
  27. Aurora AR, Khaitan L, Saber AA. Sleeve gastrectomy and the risk of leak: a systematic analysis of 4,888 patients. Surg Endosc 2012; 26:1509.
  28. Fridman A, Moon R, Cozacov Y, et al. Procedure-related morbidity in bariatric surgery: a retrospective short- and mid-term follow-up of a single institution of the American College of Surgeons Bariatric Surgery Centers of Excellence. J Am Coll Surg 2013; 217:614.
  29. Hutter MM, Schirmer BD, Jones DB, et al. First report from the American College of Surgeons Bariatric Surgery Center Network: laparoscopic sleeve gastrectomy has morbidity and effectiveness positioned between the band and the bypass. Ann Surg 2011; 254:410.
  30. Juodeikis Ž, Brimas G. Long-term results after sleeve gastrectomy: A systematic review. Surg Obes Relat Dis 2016.
  31. Alvarenga ES, Lo Menzo E, Szomstein S, Rosenthal RJ. Safety and efficacy of 1020 consecutive laparoscopic sleeve gastrectomies performed as a primary treatment modality for morbid obesity. A single-center experience from the metabolic and bariatric surgical accreditation quality and improvement program. Surg Endosc 2016; 30:2673.
  32. Noel P, Nedelcu M, Eddbali I, et al. What are the long-term results 8 years after sleeve gastrectomy? Surg Obes Relat Dis 2017; 13:1110.
  33. Boza C, Daroch D, Barros D, et al. Long-term outcomes of laparoscopic sleeve gastrectomy as a primary bariatric procedure. Surg Obes Relat Dis 2014; 10:1129.
  34. Gill RS, Birch DW, Shi X, et al. Sleeve gastrectomy and type 2 diabetes mellitus: a systematic review. Surg Obes Relat Dis 2010; 6:707.
  35. Schauer PR, Kashyap SR, Wolski K, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 2012; 366:1567.
  36. Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric Surgery versus Intensive Medical Therapy for Diabetes - 5-Year Outcomes. N Engl J Med 2017; 376:641.
  37. Khorgami Z, Shoar S, Andalib A, et al. Trends in utilization of bariatric surgery, 2010-2014: sleeve gastrectomy dominates. Surg Obes Relat Dis 2017; 13:774.
  38. Peterli R, Wölnerhanssen BK, Vetter D, et al. Laparoscopic Sleeve Gastrectomy Versus Roux-Y-Gastric Bypass for Morbid Obesity-3-Year Outcomes of the Prospective Randomized Swiss Multicenter Bypass Or Sleeve Study (SM-BOSS). Ann Surg 2017; 265:466.
  39. Aminian A, Brethauer SA, Andalib A, et al. Individualized Metabolic Surgery Score: Procedure Selection Based on Diabetes Severity. Ann Surg 2017; 266:650.
  40. Chiu S, Birch DW, Shi X, et al. Effect of sleeve gastrectomy on gastroesophageal reflux disease: a systematic review. Surg Obes Relat Dis 2011; 7:510.
  41. Petersen WV, Meile T, Küper MA, et al. Functional importance of laparoscopic sleeve gastrectomy for the lower esophageal sphincter in patients with morbid obesity. Obes Surg 2012; 22:360.
  42. Toro JP, Lin E, Patel AD, et al. Association of radiographic morphology with early gastroesophageal reflux disease and satiety control after sleeve gastrectomy. J Am Coll Surg 2014; 219:430.
  43. Del Genio G, Tolone S, Limongelli P, et al. Sleeve gastrectomy and development of "de novo" gastroesophageal reflux. Obes Surg 2014; 24:71.
  44. Burgerhart JS, Schotborgh CA, Schoon EJ, et al. Effect of sleeve gastrectomy on gastroesophageal reflux. Obes Surg 2014; 24:1436.
  45. Mattar SG, Velcu LM, Rabinovitz M, et al. Surgically-induced weight loss significantly improves nonalcoholic fatty liver disease and the metabolic syndrome. Ann Surg 2005; 242:610.
  46. Gagner M, Buchwald JN. Comparison of laparoscopic sleeve gastrectomy leak rates in four staple-line reinforcement options: a systematic review. Surg Obes Relat Dis 2014; 10:713.
  47. Burgos AM, Csendes A, Braghetto I. Gastric stenosis after laparoscopic sleeve gastrectomy in morbidly obese patients. Obes Surg 2013; 23:1481.
  48. Bellorin O, Lieb J, Szomstein S, Rosenthal RJ. Laparoscopic conversion of sleeve gastrectomy to Roux-en-Y gastric bypass for acute gastric outlet obstruction after laparoscopic sleeve gastrectomy for morbid obesity. Surg Obes Relat Dis 2010; 6:566.
  49. Shah SS, Todkar JS, Shah PS. Buttressing the staple line: a randomized comparison between staple-line reinforcement versus no reinforcement during sleeve gastrectomy. Obes Surg 2014; 24:2014.
  50. https://asmbs.org/resources/prevention-and-detection-of-gastrointestinal-leak (Accessed on February 21, 2017).
  51. Parikh A, Alley JB, Peterson RM, et al. Management options for symptomatic stenosis after laparoscopic vertical sleeve gastrectomy in the morbidly obese. Surg Endosc 2012; 26:738.
  52. Tucker ON, Szomstein S, Rosenthal RJ. Indications for sleeve gastrectomy as a primary procedure for weight loss in the morbidly obese. J Gastrointest Surg 2008; 12:662.
  53. Frezza EE, Reddy S, Gee LL, Wachtel MS. Complications after sleeve gastrectomy for morbid obesity. Obes Surg 2009; 19:684.
  54. Brethauer SA, Hammel JP, Schauer PR. Systematic review of sleeve gastrectomy as staging and primary bariatric procedure. Surg Obes Relat Dis 2009; 5:469.
  55. Zundel N, Hernandez JD, Galvao Neto M, Campos J. Strictures after laparoscopic sleeve gastrectomy. Surg Laparosc Endosc Percutan Tech 2010; 20:154.
  56. Cottam D, Qureshi FG, Mattar SG, et al. Laparoscopic sleeve gastrectomy as an initial weight-loss procedure for high-risk patients with morbid obesity. Surg Endosc 2006; 20:859.
  57. Lacy A, Ibarzabal A, Pando E, et al. Revisional surgery after sleeve gastrectomy. Surg Laparosc Endosc Percutan Tech 2010; 20:351.
  58. Dapri G, Cadière GB, Himpens J. Reinforcing the staple line during laparoscopic sleeve gastrectomy: prospective randomized clinical study comparing three different techniques. Obes Surg 2010; 20:462.
  59. Braghetto I, Korn O, Valladares H, et al. Laparoscopic sleeve gastrectomy: surgical technique, indications and clinical results. Obes Surg 2007; 17:1442.
  60. Sánchez-Santos R, Masdevall C, Baltasar A, et al. Short- and mid-term outcomes of sleeve gastrectomy for morbid obesity: the experience of the Spanish National Registry. Obes Surg 2009; 19:1203.
  61. Dapri G, Cadière GB, Himpens J. Laparoscopic seromyotomy for long stenosis after sleeve gastrectomy with or without duodenal switch. Obes Surg 2009; 19:495.
  62. Eubanks S, Edwards CA, Fearing NM, et al. Use of endoscopic stents to treat anastomotic complications after bariatric surgery. J Am Coll Surg 2008; 206:935.
  63. Moszkowicz D, Arienzo R, Khettab I, et al. Sleeve gastrectomy severe complications: is it always a reasonable surgical option? Obes Surg 2013; 23:676.
  64. Scheffel O, Weiner RA. Therapy of stenosis after sleeve gastrectomy: stent and surgery as alternatives--case reports. Obes Facts 2011; 4 Suppl 1:47.
  65. Jones M, Healey AJ, Efthimiou E. Early use of self-expanding metallic stents to relieve sleeve gastrectomy stenosis after intragastric balloon removal. Surg Obes Relat Dis 2011; 7:e16.
  66. Lalor PF, Tucker ON, Szomstein S, Rosenthal RJ. Complications after laparoscopic sleeve gastrectomy. Surg Obes Relat Dis 2008; 4:33.
  67. Goitein D, Matter I, Raziel A, et al. Portomesenteric thrombosis following laparoscopic bariatric surgery: incidence, patterns of clinical presentation, and etiology in a bariatric patient population. JAMA Surg 2013; 148:340.
  68. Salinas J, Barros D, Salgado N, et al. Portomesenteric vein thrombosis after laparoscopic sleeve gastrectomy. Surg Endosc 2014; 28:1083.
  69. Shaheen O, Siejka J, Thatigotla B, Pham DT. A systematic review of portomesenteric vein thrombosis after sleeve gastrectomy. Surg Obes Relat Dis 2017; 13:1422.
  70. Belnap L, Rodgers GM, Cottam D, et al. Portal vein thrombosis after laparoscopic sleeve gastrectomy: presentation and management. Surg Obes Relat Dis 2016; 12:1787.
Topic 109435 Version 7.0

Topic Outline

GRAPHICS

RELATED TOPICS

All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.