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Gastric bypass. Principles, complications, and results
Journal of Visceral Surgery (2010) 147S, e31—e37
Gastric bypass. Principles, complications, and results J.-P. Marmuse ∗, L.R. Parenti Hôpital Bichat, 46, rue Henri-Huchard, 75018 Paris, France
Gastric bypass (GBP) is generally considered the ‘‘gold standard’’ of bariatric surgery techniques because it results in more rapid and more substantial weight loss than ‘‘restrictive’’ procedures with less risk of failure or complication than other ‘‘malabsorptive’’ procedures. On the other hand, it is a complicated and technically demanding procedure, especially when undertaken laparoscopically. GBP requires two gastrointestinal anastomoses and a stapled partition of the upper stomach at a level where accessibility is difficult in morbidly obese patients; it is not surprising that GBP has a substantial risk of morbidity and mortality. This article lays out the principles, the most common complications, and the results of this procedure.
Principles and pathophysiology The GBP is a hybrid procedure combining elements of restriction (reduction of gastric capacity) with modest malabsorption. The principle is to divide the upper stomach delineating a small proximal pouch which is then drained by a Roux-en-Y jejunal limb (Fig. 1). The procedure’s effectiveness depends first and foremost on the size of the gastric pouch; experience has shown that pouch capacity should be no more than 20 to 30 ml. For a long-lasting restrictive procedure, the staple line delineating the pouch should extend vertically from high on the lesser curvature toward the angle of His, excluding the gastric fundus. It has been found that pouches created by a transverse staple line which includes a portion of the gastric fundus have a tendency to dilate over time; this leads to loss of effectiveness of the bypass and renewed weight gain. The malabsorptive element of the procedure lies in the Roux-en-Y montage, which results in three intestinal components: • a 30 to 60 cm ‘‘bilio-digestive limb’’ which is excluded from the alimentary flow and carries only the biliary and pancreatic secretions; • a 100 to 150 cm ‘‘alimentary limb’’ which drains the gastric pouch; poorly-digested food deprived of biliary and pancreatic digestive juices traverses this limb until it joins downstream with; • the remainder of the distal jejunum, a so-called ‘‘common segment’’ where food and digestive juices can mix and be absorbed as they pass downstream.
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Corresponding author. E-mail address: [email protected] (J.-P. Marmuse).
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Figure 1. Basic principle of gastric bypass. 1. Gastrojejunal anastomosis. 2. Excluded stomach. 3. Roux-en-Y jejunal limb (alimentary limb); 4. Bilio-pancreatic limb. 5. Common limb.
This intestinal montage results in a modest amount of malabsorption, particularly for fats (which cannot be absorbed in the absence of biliary salts) and, to a lesser degree, for proteins. Carbohydrates, on the other hand, are absorbed promptly from the alimentary limb; patient consumption of large amounts of sweets is one of the principal causes of failure of GBP [1]. In addition to the small size of the gastric pouch, two other factors contribute to a decrease in calorie intake. A decrease in gastric secretion of ghrelin, a peptide hormone, results in a persistent loss of appetite; GBP results in a marked fall in plasma levels of grhelin [2]. Dumping syndrome also develops frequently after gastrojejunostomy and results in an adaptive aversion to dietary sweets. In recent years, this procedure has usually been performed laparoscopically [1,3] with all the advantages that may accrue from this approach, particularly a decrease in the risk of wound infection, dehiscence, and incisional hernia. But laparoscopic GBP has a steep learning curve of up to 100 cases before the risks of complication and operative duration become equal to or less than those seen after open GBP [4,5]. With regard to postoperative complications, we must emphasize that the systematic closure of all mesenteric defects is one of the most important stages in the procedure. Whether the Roux-en-Y limb is brought up to the gastric pouch by an antecolic or a transmesenteric route, the montage results in the creation of several mesenteric defects through which the small intestine may become incarcerated — the mesenteric window at the base of the Roux limb, the transverse mesocolic window when this route is used, and the space of Petersen behind the Roux-en-Y limb (Fig. 2).
Early postoperative complications Mortality for GBP in large series ranges from 0.5 to 1%; anastomotic leakage and pulmonary embolus as the main causes of death. Other than the surgeon’s experience, the principal risk factors for complication are: age greater than 55 years,
J.-P. Marmuse, L.R. Parenti
Figure 2. The three mesenteric defects. A. Transmesocolic window when the Roux-en-Y limb is passed by this route. B. The orifice of Petersen: this is the space lying behind the Roux-en-Y limb beneath the transverse mesocolon. C. The mesenteric defect at the level of the jejunojejunal anastomosis.
weight greater than 160 kg, truncal obesity, and masculine gender [6,7].
Intestinal leaks and fistulas Anastomotic leaks are among the gravest of postoperative complications and are associated with a 6 to 22% mortality rate. Leaks may occur early — within the first 48 hours — if there is an error in anastomotic technique. More commonly, however, leaks are due to intestinal ischemia and become manifest by the fifth postoperative day. In various series, the incidence of intestinal fistula ranges from 0.8 to 15%; in 60% of fistulas, the leak occurs at the gastrojejunal anastomosis [8,9]. Fistulas arise at the jejunojejunal anastomosis in 15% of cases, and more rarely from a disrupted staple line of the excluded stomach or of the proximal gastric tube [10]. Prompt diagnosis and drainage of a leak or fistula is the principal determinant of prognosis [10—13]; an unrecognized leak can progress to peritonitis and septic shock within a few hours. But early symptoms may be misleading: the abdomen may be soft without guarding, fever is present only half of the time, and often the only early signs are tachypnea or tachycardia greater than 120 per minute [10]. An aggressive diagnostic strategy is essential whenever the postoperative course does not run perfectly smoothly. An Upper Gastrointestinal Series (UGIS) with watersoluble contrast will often demonstrate a leak from the proximal gastric pouch or the gastrojejunal anastomosis, but it may be falsely negative in 20 to 50% of cases [12]; an UGIS cannot visualize the excluded stomach or the jejunojejunal anastomosis. CT scan with oral contrast is the most sensitive diagnostic study. It not only localizes the leak but it also defines the extent of spillage and the presence of a collection. Even so, a normal CT scan cannot categorically exclude the possibility of an intestinal fistula. Fluid collections loculated between
Gastric bypass. Principles, complications, and results intestinal loops can be missed and the false-negative rate is close to 30% [10]. In the setting of severe clinical symptoms with a negative contrast CT, only exploratory laparoscopy allows exclusion of an intestinal leak with certainty. One should not hesitate to re-explore if there is the least clinical doubt, or even to proceed directly to laparoscopy without any imaging studies if the patient’s condition is alarming.
Leaks from the proximal gastric pouch and/or gastrojejunal anastomosis These are usually low-output fistulas with limited initial bacterial contamination. Some are asymptomatic, particularly if the leakage has been led out to the skin by drains placed intraoperatively avoiding peritoneal contamination [13]; low-output fistulas will often heal spontaneously with nonsurgical treatment consisting of parenteral nutrition and appropriate antibiotic therapy [10,12]. In other cases, drains may be introducd percutaneously or by laparoscopy depending on the patient’s clinical condition and the accessibility of a collection to a radiology-guided approach. In all cases, the goal is to direct drainage to the skin and to obtain a peritoneal cavity free of residual collections. Once drainage has been achieved, a gastroscopically placed coated endoprosthesis may serve to obturate the fistula [14]; this permits better control of fistula leakage, allows a quicker return to oral feeding, and often results in more rapid fistula closure.
Fistulas at the jejunojejunal anastomosis These are usually high-output fistulas and result in peritonitis and more rapid clinical deterioration; the mortality rate may be as high as 40% [15]. They require prompt surgical re-intervention to lavage the peritoneal cavity, repair the anastomosis, and/or bring out a diverting enterostomy.
Fistulas from the excluded stomach These may occur from a simple leak along the staple line but are more likely to occur if there is downstream obstruction of the bilio-pancreatic jejunal loop. An obstructed jejunal limb results in a high-output fistula with sizeable spillage and particularly aggressive bacterial contamination; urgent surgical re-intervention is required to close the leak, to wash out the peritoneal cavity, and to relieve the distal jejunal obstruction. A simple staple line leak results in a low-output fistula and has a more benign prognosis; conservative nonsurgical treatment is possible if the fistula can be controlled with drain placement.
Thromboembolic complications Despite the almost universal use of antithrombotic prophylaxis, pulmonary embolus (PE) remains one of the two major causes of death after bariatric surgery. Although it often occurs within hours of surgery, it may also occur days or even weeks later [16,17]. Risk factors for PE include super-obesity (BMI > 60), truncal obesity, chronic venous stasis, hypercoagulability, and a history of previous DVT and/or PE [18]. There is unanimous agreement on the need for preventive measures, but there is no consensus on which measures to take: some surgeons rely only on intermittent compression stockings during and after surgery, other surgeons use low-molecular-weight heparin anticoagulation, while many surgeons employ both measures. The duration of antithrombotic prophylaxis is equally controversial. In some series,
e33 anticoagulation is discontinued 10 days after surgery, while, in others, it is maintained for at least a month [19]. The placement of an inferior vena cava filter is often proposed for patients at high-risk of PE, but filter placement is a difficult procedure in the obese patient and not without risk.
Pulmonary complications One of the principal benefits of the laparascopic approach is decreased impairment of ventilatory function due to decreased incisional pain; this has resulted in a lower risk of pulmonary complications for laparoscopic GBP compared with open GBP (mean incidence: 0.6% vs. 1.1%) [20]. Pleural effusion, acute respiratory distress, and bronchopneumonia are the most common complications. They may occur autonomously or they may be a sign of underlying peritoneal sepsis; this possibility must be considered, particularly when the initial postoperative course was relatively benign.
Postoperative hemorrhage Hemorrhage occurs in up to 2% of cases [21], most commonly due to bleeding from a staple line which may be intraluminal or intraperitoneal. In order to minimize this risk, staple size should be carefully selected to match intestinal wall thickness, and pressure should be applied for at least 15 seconds when the stapler is fired. Staple lines can also be reinforced with a suture line [22], but there is no general agreement on this measure. Intraperitoneal bleeding usually occurs from either the gastric staple line or from a trocar site. The use of noncutting trocars and rigorous hemostasis at the termination of the procedure could decrease the incidence of bleeding. Intraluminal hemorrhage may occur at any of the anastomotic sites but, most typically arises at the gastrojejunal anastomosis. Hematemesis points immediately to this diagnosis, but diagnosis is more difficult and delayed when melena or hematochezia is the primary manifestation. Whatever the presentation, an upper endoscopy should be performed to localize the site of bleeding; oftentimes, hemostasis can also be performed at the same procedure. If bleeding persists even after the discontinuation of heparin, laparoscopic exploration and oversewing of the staple lines may be required [23].
Rhabdomyolysis This complication may occur due to muscular pressure necrosis on the operating table; while rare, it is potentially lethal since it can compromise renal function. Risk factors are super-obesity (BMI > 60) and a prolonged operative time (> 4 hours) [24]. The diagnosis of rhabdomyolysis may be missed if it does not cause renal complications: signs and symptoms are brown urine, myoglobinuria, and back pain of varying severity. Measurement of the CPK level on day 1 will allow prompt diagnosis [25]. Preventive measures include good patient position on the operating table, padding of pressure points, and reduction of operative time as much as possible. But prompt diagnosis is essential to avoid renal complications [24,26].
Early postoperative bowel obstruction In more than 60% of cases, intestinal obstruction is due to stenosis of the jejunojejunal anastomosis or to torsion of the bilio-pancreatic limb above the anastomosis due to a
e34 technical error in its construction [27]. This can result in acute gastric dilatation with lethal complications (gastric rupture) if diagnosis and treatment are not immediate [28]. Since the occluded intestinal segment is excluded from the alimentary circuit by the very nature of the Roux-enmontage, diagnosis may be difficult unless there are classical signs of obsruction. Isolated tachycardia often precedes more typical symptoms of nausea with epigastric pain radiating to the scapula. CT scan demonstrating gastric dilatation will confirm the diagnosis, but urgent re-intervention should not be delayed simply to obtain a confirmatory study. A gastrostomy may be required to decompress the distended stomach or an enteroenterostomy to bypass an intestinal stenosis [29]. Strangulation of the Roux limb as it traverses the transverse mesocolic window may result in obstruction manifested by vomiting and inability to eat [16]; this diagnosis is evident on an UGIS with water-soluble contrast. The mesocolic stenosis can easily be divided through a laparoscopic approach. All abdominal wall defects including the trocar sites are potential sites for small intestinal incarceration; commonly, this may be an incomplete lateral incarceration (Richter’s hernia). This diagnosis is particularly difficult since intestinal transit is not clearly obstructed; delayed diagnosis may result in intestinal necrosis. Systematic closure of all orifices for trocars greater than 5 mm in size will minimize the risk of this complication [30].
Abdominal wall infection Abdominal wall abscesses are rare; infection most typically occurs at the orifice used for introduction of the circular stapler, due to contamination when the stapler is withdrawn. Infections are best prevented by barrier protection of the abdominal wall and appropriate antibiotic prophylaxis [11,16]. Infection at the other trocar sites is exceptional and should lead to the suspicion of an underlying intra-abdominal complication.
Late postoperative complications Gastrogastric fistulas These occur more frequently after re-operation and are often due to an occult perforation which was missed at re-exploration [31,32]. They may be asymptomatic or may present with signs of abdominal pain and intolerance of solid foods. If the excluded stomach is opacified on UGIS, the diagnosis is evident [31]. While immediate repair is rarely necessary, the ability of gastric acid to leak back into the proximal gastric pouch may cause marginal peptic ulceration and requires proton pump inhibitors (PPI) medication to protect the jejunal mucosa. Remedial surgery is ideally performed at a significant interval from the initial surgery and often requires resection of the gastric fundus; indications for surgery include a failure to maintain weight loss or persistence of abdominal pain despite medical treatment [32—34].
Anastomotic ulcer The incidence of anastomotic ulcer ranges from 0.5 to 5% in various series. It usually occurs within the first 2 months after GBP and presents with abdominal pain, vomiting, and occasionally with bleeding. Anastomotic ulcer rarely occurs
J.-P. Marmuse, L.R. Parenti after the third month and there is usually a predisposing cause: i.e., an overlarge proximal gastric pouch, an anastomosis made with nonabsorbable suture, a gastrogastric fistula, or the use of nonsteroidal anti-inflammatory drugs (NSAID) medications [35]. Except for ulcers caused by gastrogastric fistula, marginal ulcers usually heal with PPI treatment.
Anastomotic stricture The incidence of gastrojejunal stricture varies from 1.4 to 14% and is a relatively frequent complication of GBP [36]. Most arise within the first 2 months and present with vomiting and inability to eat [33,36]. UGIS does not reliably define the degree of stenosis; gastroscopy provides much more accurate diagnosis. Almost all strictures can be effectively relieved by endoscopic dilatation.
Cholelithiasis Rapid weight loss in the obese patient predisposes to the development of cholecystolithiasis [37]. The anatomic rearrangements of GBP prevent endoscopic access to the ampulla of Vater/common bile duct which complicates management of common duct stones. Most surgeons routinely perform cholecystectomy at the time of GBP in patients with known cholecystolithiasis, in order to prevent gallstone migration into the common duct. There is controversy about management when there is no evidence of cholecystolithiasis prior to GBP; some surgeons advocate routine cholecystectomy [38] while others recommend prophylactic treatment with ursodesoxycholic acid [39].
Internal hernias Late bowel obstruction occurs in 1 to 6% of cases and 60% of these are due to internal hernia [29,40]. Diagnosis of internal hernia is difficult; in over half the cases, the obstruction is intermittent [41], and symptoms consist of repeated episodes of abdominal pain without obvious cause [42]. CT may be helpful if it demonstrates dilated small bowel loops or evidence of mesenteric vascular engorgement, but a negative CT does not permit exclusion of the diagnosis of internal hernia, particularly in Petersen’s space [43]. A false negative CT scan is not uncommon and, when faced with a patient with persistent or recurrent crises of abdominal pain, exploratory laparoscopy is often the only way to make or exclude the diagnosis. To avoid this complication, all mesenteric defects should be meticulously closed at the time of the GBP [9,41,42]. Other causes of pain or obstruction include adhesive bands, intussusception, and abdominal wall hernias [44].
Metabolic complications GBP results in diminished alimentary intake and minor malabsorption; the resulting nutritional deficiency may be further aggravated by deficiencies in vitamins and trace elements from which many obese patients suffer prior to surgery because of dietary regimes and/or deplorable eating habits. Deficiencies can be prevented by intake of a balanced diet (rich in proteins, fruits, and vegetables) supplemented by vitamins and trace elements, and monitored by and adjusted to the results of serial blood tests. Protein deficiencies occur rarely (0—1.4%) as long as the patient eats regularly and has no vomiting [45]. Levels of
Gastric bypass. Principles, complications, and results albumin and prealbumin will suggest the diagnosis before it becomes symptomatic (fatigue, edema, anorexia, and even ascites in severe cases). Daily protein intake should be at least 100 g to prevent malnutrition, particularly in the rapid weight loss phase of the first 6 months. Iron deficiency occurs more frequently in females who have ongoing menstrual blood loss. Oral iron supplements of 300 g/d are recommended, and treatment should be monitored with ferritin levels. Vitamin B12 deficiency is common occurring in 12 to 33% of patients [45,46]. It should be prevented with daily oral supplements and with intramuscular B12 injection every 3 months. B12 deficiency occurs gradually in the absence of supplementation and it can result in severe hematologic and neurologic complications. Absorption of dietary calcium is often inadequate, especially in patients who are lactose-intolerant; oral calcium (1000 mg/d) should be prescribed to prevent the development of osteoporosis [45,46]. All other vitamin deficiencies (folate, thiamine) can be prevented by a once-daily oral multivitamin. However, in patients with prolonged severe vomiting, thiamine deficiency can develop within a few weeks with a significant risk of acute encephalopathy, Wernicke-Korsakoff psychosis, or irreversible polyneuropathy [47,48]. In pregnancy, any nutritional or vitamin deficiency can be deleterious, particularly folate deficiency which increases the risk of fetal neurologic malformations. It is important to insist on the importance of effective contraception during the acute weight loss phase.
Functional complications During the early postoperative period, vomiting may be a problem, particularly when the patient starts to eat solid food; this symptom usually disappears rapidly. Persistence of vomiting should lead to the suspicion of an anastomotic complication. Constipation is a frequent problem, particularly in the first year, due to the decreased volume of food consumed. Diarrhea may develop in some patients related to milk intolerance or blind loop syndrome. Dumping syndrome occurs frequently and is triggered by the intake of sweets; it presents as malaise, sweating and tachycardia occurring minutes after a meal. Dumping can be avoided by dietary modifications and it usually diminishes over time [49]. Although dumping may cause discomfort, it is considered beneficial by many surgeons because it contributes to weight loss. Several cases of severe hypoglycemia have been reported recently. Symptoms typically occur 1 to 2 hours after a meal and can be severe enough to result in coma. This reactive hypoglycemia is linked to postprandial hyperinsulinemia; it is typically a late complication occurring more than a year after GBP. In most cases, these episodes have a purely functional cause (rapid passage of food into the proximal jejunum), but they can occasionally be due to islet cell hyperplasia (nesidioblastosis) [50].
e35 the third year and then there is usually a mild weight gain over the following years [51,52]. The average loss of excess weight varies from 68 to 83% at 2 years; this corresponds to a 40 to 50 kg weight loss and a 20-point decrease in BMI. The rate of successful weight loss (> 50% of excess weight) depends on the degree of obesity at the time of surgery [53]; the success rate is 90% in patients with morbid obesity (BMI = 35—50), but is less than 60% for super-obese patients (BMI > 60). There are few studies which document the long-term maintenance of weight loss. The SOS study [54] showed that weight losss was maintained in 74% of patients at 10 years, as long as these patients observed their dietary regime. Pories’ et al. study [52] had similar results showing that patients regained about 15% of the maximal weight loss at 10 years after GBP.
Improvement in co-morbidities Many co-morbidities improve simply due to the decrease in abdominal pressure (gastroesophageal reflux, urinary stress incontinence, venous stasis) or to weight loss for as long as it is maintained (arterial hypertension, dyslipidemia, arthritis of weight-bearing joints, asthma, sleep apnea) [55]. The effects of GBP on type 2 diabetes are more dramatic. GBP cures type 2 diabetes in more than 80% of cases and this improvement is often evident within days and long before it can be explained by weight loss alone [56]. Experimental studies have shown that bypassing the duodenum and proximal jejunum is responsible through a hormonal mechanism that has not yet been completely elucidated [57]. The chances of cure are not as good when diabetes is of long-standing or insulin-dependent [55]. Finally, two recent studies have shown that weight loss increases life expectancy in obese patients who underwent GBP [54], due to decreased mortality from diabetes, cardiac disease, and cancer [58]. This improvement is particularly notable in patients older than 40 and in those with BMI greater than 40.
Improvement in the quality of life Several studies have evaluated the improvement in quality of life after GBP. No matter which questionnaire is used as an evaluation tool (36-item short-form health survey [SF-36], bariatric analysis and reporting outcome system [BAROS], Moorehead-andelt II) [59—61], patients show improvement in all domains except for mental health; scores measured at 6 months after GBP are comparable to and sometimes even better than those of the general population [4]. Two studies show that this improvement is maintained at 1 and 3 years [39,62]. Longer-term results vary with the patient’s weight. If the patient regains weight, his evaluation of quality of life diminishes. Quality of life is better for surgical patients than for those who underwent medical treatment alone [63].
Results of gastric bypass Weight loss Weight loss occurs rapidly over the first 12 months and is usually maximal at 2 years after GBP. Weight plateaus during
Conflicts of interest statement Nothing declared.
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Gastric bypass. Principles, complications, and results [43] Iannuccilli JD, Grand D, Murphy BL, Evangelista P, Roye GD, Mayo-Smith W. Sensitivity and specificity of eight CT signs in the preoperative diagnosis of internal mesenteric hernia following Roux-en-Y gastric bypass surgery. Clin Radiol 2009;64(4):373—80. [44] Hwang RF, Swartz DE, Felix EL. Causes of small bowel obstruction after laparoscopic gastric bypass. Surg Endosc 2004;18(11):1631—5. [45] Skroubis G, Sakellaropoulos G, Pouggouras K, Mead N, Nikiforidis G, Kalfarentzos F. Comparison of nutritional deficiencies after Roux-en-Y gastric bypass and after biliopancreatic diversion with Roux-en-Y gastric bypass. Obes Surg 2002;12(4):551—8. [46] Brolin RE, Leung M. Survey of vitamin and mineral supplementation after gastric bypass and bilio-pancreatic diversion for morbid obesity. Obes Surg 1999;9(2):150—4. [47] Loh Y, Watson WD, Verma A, et al. Acute Wernicke’s encephalopathy following bariatric surgery: clinical course and MRI correlation. Obes Surg 2004;14(1):129—32. [48] Davies DJ, Baxter JM, Baxter JN, Chang ST, Stocker DJ, Labutta RJ. Nutritional deficiencies after bariatric surgery. Obes Surg 2007;17(9):1150—8. [49] Balsiger BM, Kennedy FP, Abu-Lebdeh HS, et al. Prospective evaluation of Roux-en-Y gastric bypass as primary operation for medically complicated obesity. Mayo Clin Proc 2000;75(7):673—80. [50] Z’Graggen K, Guweidhi A, Steffen R, et al. Severe recurrent hypoglycemia after gastric bypass surgery. Obes Surg 2008;18(8):981—8. [51] Brolin RL, Robertson LB, Kenler HA, Cody RP. Weight loss and dietary intake after vertical banded gastroplasty and Roux-en-Y gastric bypass. Ann Surg 1994;220(6):782—90. [52] Pories WJ, Swanson MS, MacDonald KG, et al. Who would have thought it? An operation proves to be the most effec-
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Gastric bypass. Principles, complications, and results J.-P. Marmuse ∗, L.R. Parenti Hôpital Bichat, 46, rue Henri-Huchard, 75018 Paris, France
Gastric bypass (GBP) is generally considered the ‘‘gold standard’’ of bariatric surgery techniques because it results in more rapid and more substantial weight loss than ‘‘restrictive’’ procedures with less risk of failure or complication than other ‘‘malabsorptive’’ procedures. On the other hand, it is a complicated and technically demanding procedure, especially when undertaken laparoscopically. GBP requires two gastrointestinal anastomoses and a stapled partition of the upper stomach at a level where accessibility is difficult in morbidly obese patients; it is not surprising that GBP has a substantial risk of morbidity and mortality. This article lays out the principles, the most common complications, and the results of this procedure.
Principles and pathophysiology The GBP is a hybrid procedure combining elements of restriction (reduction of gastric capacity) with modest malabsorption. The principle is to divide the upper stomach delineating a small proximal pouch which is then drained by a Roux-en-Y jejunal limb (Fig. 1). The procedure’s effectiveness depends first and foremost on the size of the gastric pouch; experience has shown that pouch capacity should be no more than 20 to 30 ml. For a long-lasting restrictive procedure, the staple line delineating the pouch should extend vertically from high on the lesser curvature toward the angle of His, excluding the gastric fundus. It has been found that pouches created by a transverse staple line which includes a portion of the gastric fundus have a tendency to dilate over time; this leads to loss of effectiveness of the bypass and renewed weight gain. The malabsorptive element of the procedure lies in the Roux-en-Y montage, which results in three intestinal components: • a 30 to 60 cm ‘‘bilio-digestive limb’’ which is excluded from the alimentary flow and carries only the biliary and pancreatic secretions; • a 100 to 150 cm ‘‘alimentary limb’’ which drains the gastric pouch; poorly-digested food deprived of biliary and pancreatic digestive juices traverses this limb until it joins downstream with; • the remainder of the distal jejunum, a so-called ‘‘common segment’’ where food and digestive juices can mix and be absorbed as they pass downstream.
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Corresponding author. E-mail address: [email protected] (J.-P. Marmuse).
1878-7886/$ — see front matter © 2010 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.jviscsurg.2010.08.014
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Figure 1. Basic principle of gastric bypass. 1. Gastrojejunal anastomosis. 2. Excluded stomach. 3. Roux-en-Y jejunal limb (alimentary limb); 4. Bilio-pancreatic limb. 5. Common limb.
This intestinal montage results in a modest amount of malabsorption, particularly for fats (which cannot be absorbed in the absence of biliary salts) and, to a lesser degree, for proteins. Carbohydrates, on the other hand, are absorbed promptly from the alimentary limb; patient consumption of large amounts of sweets is one of the principal causes of failure of GBP [1]. In addition to the small size of the gastric pouch, two other factors contribute to a decrease in calorie intake. A decrease in gastric secretion of ghrelin, a peptide hormone, results in a persistent loss of appetite; GBP results in a marked fall in plasma levels of grhelin [2]. Dumping syndrome also develops frequently after gastrojejunostomy and results in an adaptive aversion to dietary sweets. In recent years, this procedure has usually been performed laparoscopically [1,3] with all the advantages that may accrue from this approach, particularly a decrease in the risk of wound infection, dehiscence, and incisional hernia. But laparoscopic GBP has a steep learning curve of up to 100 cases before the risks of complication and operative duration become equal to or less than those seen after open GBP [4,5]. With regard to postoperative complications, we must emphasize that the systematic closure of all mesenteric defects is one of the most important stages in the procedure. Whether the Roux-en-Y limb is brought up to the gastric pouch by an antecolic or a transmesenteric route, the montage results in the creation of several mesenteric defects through which the small intestine may become incarcerated — the mesenteric window at the base of the Roux limb, the transverse mesocolic window when this route is used, and the space of Petersen behind the Roux-en-Y limb (Fig. 2).
Early postoperative complications Mortality for GBP in large series ranges from 0.5 to 1%; anastomotic leakage and pulmonary embolus as the main causes of death. Other than the surgeon’s experience, the principal risk factors for complication are: age greater than 55 years,
J.-P. Marmuse, L.R. Parenti
Figure 2. The three mesenteric defects. A. Transmesocolic window when the Roux-en-Y limb is passed by this route. B. The orifice of Petersen: this is the space lying behind the Roux-en-Y limb beneath the transverse mesocolon. C. The mesenteric defect at the level of the jejunojejunal anastomosis.
weight greater than 160 kg, truncal obesity, and masculine gender [6,7].
Intestinal leaks and fistulas Anastomotic leaks are among the gravest of postoperative complications and are associated with a 6 to 22% mortality rate. Leaks may occur early — within the first 48 hours — if there is an error in anastomotic technique. More commonly, however, leaks are due to intestinal ischemia and become manifest by the fifth postoperative day. In various series, the incidence of intestinal fistula ranges from 0.8 to 15%; in 60% of fistulas, the leak occurs at the gastrojejunal anastomosis [8,9]. Fistulas arise at the jejunojejunal anastomosis in 15% of cases, and more rarely from a disrupted staple line of the excluded stomach or of the proximal gastric tube [10]. Prompt diagnosis and drainage of a leak or fistula is the principal determinant of prognosis [10—13]; an unrecognized leak can progress to peritonitis and septic shock within a few hours. But early symptoms may be misleading: the abdomen may be soft without guarding, fever is present only half of the time, and often the only early signs are tachypnea or tachycardia greater than 120 per minute [10]. An aggressive diagnostic strategy is essential whenever the postoperative course does not run perfectly smoothly. An Upper Gastrointestinal Series (UGIS) with watersoluble contrast will often demonstrate a leak from the proximal gastric pouch or the gastrojejunal anastomosis, but it may be falsely negative in 20 to 50% of cases [12]; an UGIS cannot visualize the excluded stomach or the jejunojejunal anastomosis. CT scan with oral contrast is the most sensitive diagnostic study. It not only localizes the leak but it also defines the extent of spillage and the presence of a collection. Even so, a normal CT scan cannot categorically exclude the possibility of an intestinal fistula. Fluid collections loculated between
Gastric bypass. Principles, complications, and results intestinal loops can be missed and the false-negative rate is close to 30% [10]. In the setting of severe clinical symptoms with a negative contrast CT, only exploratory laparoscopy allows exclusion of an intestinal leak with certainty. One should not hesitate to re-explore if there is the least clinical doubt, or even to proceed directly to laparoscopy without any imaging studies if the patient’s condition is alarming.
Leaks from the proximal gastric pouch and/or gastrojejunal anastomosis These are usually low-output fistulas with limited initial bacterial contamination. Some are asymptomatic, particularly if the leakage has been led out to the skin by drains placed intraoperatively avoiding peritoneal contamination [13]; low-output fistulas will often heal spontaneously with nonsurgical treatment consisting of parenteral nutrition and appropriate antibiotic therapy [10,12]. In other cases, drains may be introducd percutaneously or by laparoscopy depending on the patient’s clinical condition and the accessibility of a collection to a radiology-guided approach. In all cases, the goal is to direct drainage to the skin and to obtain a peritoneal cavity free of residual collections. Once drainage has been achieved, a gastroscopically placed coated endoprosthesis may serve to obturate the fistula [14]; this permits better control of fistula leakage, allows a quicker return to oral feeding, and often results in more rapid fistula closure.
Fistulas at the jejunojejunal anastomosis These are usually high-output fistulas and result in peritonitis and more rapid clinical deterioration; the mortality rate may be as high as 40% [15]. They require prompt surgical re-intervention to lavage the peritoneal cavity, repair the anastomosis, and/or bring out a diverting enterostomy.
Fistulas from the excluded stomach These may occur from a simple leak along the staple line but are more likely to occur if there is downstream obstruction of the bilio-pancreatic jejunal loop. An obstructed jejunal limb results in a high-output fistula with sizeable spillage and particularly aggressive bacterial contamination; urgent surgical re-intervention is required to close the leak, to wash out the peritoneal cavity, and to relieve the distal jejunal obstruction. A simple staple line leak results in a low-output fistula and has a more benign prognosis; conservative nonsurgical treatment is possible if the fistula can be controlled with drain placement.
Thromboembolic complications Despite the almost universal use of antithrombotic prophylaxis, pulmonary embolus (PE) remains one of the two major causes of death after bariatric surgery. Although it often occurs within hours of surgery, it may also occur days or even weeks later [16,17]. Risk factors for PE include super-obesity (BMI > 60), truncal obesity, chronic venous stasis, hypercoagulability, and a history of previous DVT and/or PE [18]. There is unanimous agreement on the need for preventive measures, but there is no consensus on which measures to take: some surgeons rely only on intermittent compression stockings during and after surgery, other surgeons use low-molecular-weight heparin anticoagulation, while many surgeons employ both measures. The duration of antithrombotic prophylaxis is equally controversial. In some series,
e33 anticoagulation is discontinued 10 days after surgery, while, in others, it is maintained for at least a month [19]. The placement of an inferior vena cava filter is often proposed for patients at high-risk of PE, but filter placement is a difficult procedure in the obese patient and not without risk.
Pulmonary complications One of the principal benefits of the laparascopic approach is decreased impairment of ventilatory function due to decreased incisional pain; this has resulted in a lower risk of pulmonary complications for laparoscopic GBP compared with open GBP (mean incidence: 0.6% vs. 1.1%) [20]. Pleural effusion, acute respiratory distress, and bronchopneumonia are the most common complications. They may occur autonomously or they may be a sign of underlying peritoneal sepsis; this possibility must be considered, particularly when the initial postoperative course was relatively benign.
Postoperative hemorrhage Hemorrhage occurs in up to 2% of cases [21], most commonly due to bleeding from a staple line which may be intraluminal or intraperitoneal. In order to minimize this risk, staple size should be carefully selected to match intestinal wall thickness, and pressure should be applied for at least 15 seconds when the stapler is fired. Staple lines can also be reinforced with a suture line [22], but there is no general agreement on this measure. Intraperitoneal bleeding usually occurs from either the gastric staple line or from a trocar site. The use of noncutting trocars and rigorous hemostasis at the termination of the procedure could decrease the incidence of bleeding. Intraluminal hemorrhage may occur at any of the anastomotic sites but, most typically arises at the gastrojejunal anastomosis. Hematemesis points immediately to this diagnosis, but diagnosis is more difficult and delayed when melena or hematochezia is the primary manifestation. Whatever the presentation, an upper endoscopy should be performed to localize the site of bleeding; oftentimes, hemostasis can also be performed at the same procedure. If bleeding persists even after the discontinuation of heparin, laparoscopic exploration and oversewing of the staple lines may be required [23].
Rhabdomyolysis This complication may occur due to muscular pressure necrosis on the operating table; while rare, it is potentially lethal since it can compromise renal function. Risk factors are super-obesity (BMI > 60) and a prolonged operative time (> 4 hours) [24]. The diagnosis of rhabdomyolysis may be missed if it does not cause renal complications: signs and symptoms are brown urine, myoglobinuria, and back pain of varying severity. Measurement of the CPK level on day 1 will allow prompt diagnosis [25]. Preventive measures include good patient position on the operating table, padding of pressure points, and reduction of operative time as much as possible. But prompt diagnosis is essential to avoid renal complications [24,26].
Early postoperative bowel obstruction In more than 60% of cases, intestinal obstruction is due to stenosis of the jejunojejunal anastomosis or to torsion of the bilio-pancreatic limb above the anastomosis due to a
e34 technical error in its construction [27]. This can result in acute gastric dilatation with lethal complications (gastric rupture) if diagnosis and treatment are not immediate [28]. Since the occluded intestinal segment is excluded from the alimentary circuit by the very nature of the Roux-enmontage, diagnosis may be difficult unless there are classical signs of obsruction. Isolated tachycardia often precedes more typical symptoms of nausea with epigastric pain radiating to the scapula. CT scan demonstrating gastric dilatation will confirm the diagnosis, but urgent re-intervention should not be delayed simply to obtain a confirmatory study. A gastrostomy may be required to decompress the distended stomach or an enteroenterostomy to bypass an intestinal stenosis [29]. Strangulation of the Roux limb as it traverses the transverse mesocolic window may result in obstruction manifested by vomiting and inability to eat [16]; this diagnosis is evident on an UGIS with water-soluble contrast. The mesocolic stenosis can easily be divided through a laparoscopic approach. All abdominal wall defects including the trocar sites are potential sites for small intestinal incarceration; commonly, this may be an incomplete lateral incarceration (Richter’s hernia). This diagnosis is particularly difficult since intestinal transit is not clearly obstructed; delayed diagnosis may result in intestinal necrosis. Systematic closure of all orifices for trocars greater than 5 mm in size will minimize the risk of this complication [30].
Abdominal wall infection Abdominal wall abscesses are rare; infection most typically occurs at the orifice used for introduction of the circular stapler, due to contamination when the stapler is withdrawn. Infections are best prevented by barrier protection of the abdominal wall and appropriate antibiotic prophylaxis [11,16]. Infection at the other trocar sites is exceptional and should lead to the suspicion of an underlying intra-abdominal complication.
Late postoperative complications Gastrogastric fistulas These occur more frequently after re-operation and are often due to an occult perforation which was missed at re-exploration [31,32]. They may be asymptomatic or may present with signs of abdominal pain and intolerance of solid foods. If the excluded stomach is opacified on UGIS, the diagnosis is evident [31]. While immediate repair is rarely necessary, the ability of gastric acid to leak back into the proximal gastric pouch may cause marginal peptic ulceration and requires proton pump inhibitors (PPI) medication to protect the jejunal mucosa. Remedial surgery is ideally performed at a significant interval from the initial surgery and often requires resection of the gastric fundus; indications for surgery include a failure to maintain weight loss or persistence of abdominal pain despite medical treatment [32—34].
Anastomotic ulcer The incidence of anastomotic ulcer ranges from 0.5 to 5% in various series. It usually occurs within the first 2 months after GBP and presents with abdominal pain, vomiting, and occasionally with bleeding. Anastomotic ulcer rarely occurs
J.-P. Marmuse, L.R. Parenti after the third month and there is usually a predisposing cause: i.e., an overlarge proximal gastric pouch, an anastomosis made with nonabsorbable suture, a gastrogastric fistula, or the use of nonsteroidal anti-inflammatory drugs (NSAID) medications [35]. Except for ulcers caused by gastrogastric fistula, marginal ulcers usually heal with PPI treatment.
Anastomotic stricture The incidence of gastrojejunal stricture varies from 1.4 to 14% and is a relatively frequent complication of GBP [36]. Most arise within the first 2 months and present with vomiting and inability to eat [33,36]. UGIS does not reliably define the degree of stenosis; gastroscopy provides much more accurate diagnosis. Almost all strictures can be effectively relieved by endoscopic dilatation.
Cholelithiasis Rapid weight loss in the obese patient predisposes to the development of cholecystolithiasis [37]. The anatomic rearrangements of GBP prevent endoscopic access to the ampulla of Vater/common bile duct which complicates management of common duct stones. Most surgeons routinely perform cholecystectomy at the time of GBP in patients with known cholecystolithiasis, in order to prevent gallstone migration into the common duct. There is controversy about management when there is no evidence of cholecystolithiasis prior to GBP; some surgeons advocate routine cholecystectomy [38] while others recommend prophylactic treatment with ursodesoxycholic acid [39].
Internal hernias Late bowel obstruction occurs in 1 to 6% of cases and 60% of these are due to internal hernia [29,40]. Diagnosis of internal hernia is difficult; in over half the cases, the obstruction is intermittent [41], and symptoms consist of repeated episodes of abdominal pain without obvious cause [42]. CT may be helpful if it demonstrates dilated small bowel loops or evidence of mesenteric vascular engorgement, but a negative CT does not permit exclusion of the diagnosis of internal hernia, particularly in Petersen’s space [43]. A false negative CT scan is not uncommon and, when faced with a patient with persistent or recurrent crises of abdominal pain, exploratory laparoscopy is often the only way to make or exclude the diagnosis. To avoid this complication, all mesenteric defects should be meticulously closed at the time of the GBP [9,41,42]. Other causes of pain or obstruction include adhesive bands, intussusception, and abdominal wall hernias [44].
Metabolic complications GBP results in diminished alimentary intake and minor malabsorption; the resulting nutritional deficiency may be further aggravated by deficiencies in vitamins and trace elements from which many obese patients suffer prior to surgery because of dietary regimes and/or deplorable eating habits. Deficiencies can be prevented by intake of a balanced diet (rich in proteins, fruits, and vegetables) supplemented by vitamins and trace elements, and monitored by and adjusted to the results of serial blood tests. Protein deficiencies occur rarely (0—1.4%) as long as the patient eats regularly and has no vomiting [45]. Levels of
Gastric bypass. Principles, complications, and results albumin and prealbumin will suggest the diagnosis before it becomes symptomatic (fatigue, edema, anorexia, and even ascites in severe cases). Daily protein intake should be at least 100 g to prevent malnutrition, particularly in the rapid weight loss phase of the first 6 months. Iron deficiency occurs more frequently in females who have ongoing menstrual blood loss. Oral iron supplements of 300 g/d are recommended, and treatment should be monitored with ferritin levels. Vitamin B12 deficiency is common occurring in 12 to 33% of patients [45,46]. It should be prevented with daily oral supplements and with intramuscular B12 injection every 3 months. B12 deficiency occurs gradually in the absence of supplementation and it can result in severe hematologic and neurologic complications. Absorption of dietary calcium is often inadequate, especially in patients who are lactose-intolerant; oral calcium (1000 mg/d) should be prescribed to prevent the development of osteoporosis [45,46]. All other vitamin deficiencies (folate, thiamine) can be prevented by a once-daily oral multivitamin. However, in patients with prolonged severe vomiting, thiamine deficiency can develop within a few weeks with a significant risk of acute encephalopathy, Wernicke-Korsakoff psychosis, or irreversible polyneuropathy [47,48]. In pregnancy, any nutritional or vitamin deficiency can be deleterious, particularly folate deficiency which increases the risk of fetal neurologic malformations. It is important to insist on the importance of effective contraception during the acute weight loss phase.
Functional complications During the early postoperative period, vomiting may be a problem, particularly when the patient starts to eat solid food; this symptom usually disappears rapidly. Persistence of vomiting should lead to the suspicion of an anastomotic complication. Constipation is a frequent problem, particularly in the first year, due to the decreased volume of food consumed. Diarrhea may develop in some patients related to milk intolerance or blind loop syndrome. Dumping syndrome occurs frequently and is triggered by the intake of sweets; it presents as malaise, sweating and tachycardia occurring minutes after a meal. Dumping can be avoided by dietary modifications and it usually diminishes over time [49]. Although dumping may cause discomfort, it is considered beneficial by many surgeons because it contributes to weight loss. Several cases of severe hypoglycemia have been reported recently. Symptoms typically occur 1 to 2 hours after a meal and can be severe enough to result in coma. This reactive hypoglycemia is linked to postprandial hyperinsulinemia; it is typically a late complication occurring more than a year after GBP. In most cases, these episodes have a purely functional cause (rapid passage of food into the proximal jejunum), but they can occasionally be due to islet cell hyperplasia (nesidioblastosis) [50].
e35 the third year and then there is usually a mild weight gain over the following years [51,52]. The average loss of excess weight varies from 68 to 83% at 2 years; this corresponds to a 40 to 50 kg weight loss and a 20-point decrease in BMI. The rate of successful weight loss (> 50% of excess weight) depends on the degree of obesity at the time of surgery [53]; the success rate is 90% in patients with morbid obesity (BMI = 35—50), but is less than 60% for super-obese patients (BMI > 60). There are few studies which document the long-term maintenance of weight loss. The SOS study [54] showed that weight losss was maintained in 74% of patients at 10 years, as long as these patients observed their dietary regime. Pories’ et al. study [52] had similar results showing that patients regained about 15% of the maximal weight loss at 10 years after GBP.
Improvement in co-morbidities Many co-morbidities improve simply due to the decrease in abdominal pressure (gastroesophageal reflux, urinary stress incontinence, venous stasis) or to weight loss for as long as it is maintained (arterial hypertension, dyslipidemia, arthritis of weight-bearing joints, asthma, sleep apnea) [55]. The effects of GBP on type 2 diabetes are more dramatic. GBP cures type 2 diabetes in more than 80% of cases and this improvement is often evident within days and long before it can be explained by weight loss alone [56]. Experimental studies have shown that bypassing the duodenum and proximal jejunum is responsible through a hormonal mechanism that has not yet been completely elucidated [57]. The chances of cure are not as good when diabetes is of long-standing or insulin-dependent [55]. Finally, two recent studies have shown that weight loss increases life expectancy in obese patients who underwent GBP [54], due to decreased mortality from diabetes, cardiac disease, and cancer [58]. This improvement is particularly notable in patients older than 40 and in those with BMI greater than 40.
Improvement in the quality of life Several studies have evaluated the improvement in quality of life after GBP. No matter which questionnaire is used as an evaluation tool (36-item short-form health survey [SF-36], bariatric analysis and reporting outcome system [BAROS], Moorehead-andelt II) [59—61], patients show improvement in all domains except for mental health; scores measured at 6 months after GBP are comparable to and sometimes even better than those of the general population [4]. Two studies show that this improvement is maintained at 1 and 3 years [39,62]. Longer-term results vary with the patient’s weight. If the patient regains weight, his evaluation of quality of life diminishes. Quality of life is better for surgical patients than for those who underwent medical treatment alone [63].
Results of gastric bypass Weight loss Weight loss occurs rapidly over the first 12 months and is usually maximal at 2 years after GBP. Weight plateaus during
Conflicts of interest statement Nothing declared.
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