Fig. 17.1
The Roux-en-Y gastric bypass. The stomach is staple divided creating a very small gastric pouch and the remnant fundus. The small intestine is divided at a short distance beyond the ligament of Treitz. The distal cut end (Roux limb) is then brought up to the small gastric pouch and attached to it. The proximal cut end (biliopancreatic limb) is anastomosed back on to the Roux limb at a measured distance
Fig. 17.2
The Roux-en-O. The biliopancreatic limb is mistaken for the Roux limb and anastomosed to the gastric pouch. The Roux limb is then anastomosed at a measured distance onto the biliopancreatic limb. In this situation, the bile and pancreatic juices can more easily reflux into the gastric pouch and esophagus (Used with permission from Springer. Sherman V, Dan AG, Lord JM, Chand B, Schauer PR. Complications of gastric bypass: avoiding the Roux-en-O configuration. Obes Surg. 2009 Aug;19(8):1190–4)
If this atypical complication goes unnoticed at the time of surgery, patients may present clinically with intermittent upper abdominal pain, nausea, and bilious vomiting [7–9]. Patients report difficulty with oral intake as the food bolus must travel against the reverse peristalsis of the biliopancreatic limb, and possibly through a kinked enteroenterostomy before progressing distally in an isoperistaltic fashion [7–9]. Bilious vomiting in a gastric bypass patient is usually secondary to an obstruction of the common channel such as an adhesive band, internal hernia, or kinked jejunojejunostomy. In the absence of a distal obstruction, the differential diagnosis should include misconstruction of the gastric bypass into a Roux-en-O configuration.
The diagnosis can be difficult to make even using multiple radiological modalities. CT is usually nonspecific and images may only be indicative of a proximal bowel obstruction [7, 10, 11]. UGI series with fluoroscopy may show diminished peristalsis or even reverse peristalsis of the “Roux” limb [7, 10, 11]. HIDA scanning may demonstrate reflux of radioactive tracer from the duodenum into the esophagus [7]. However, without a high index of suspicion, many radiological tests can be read as normal. With this in mind, surgical exploration may be the only sure way to diagnose and fix the problem. Whether the Roux-en-O misconstruction is diagnosed early or late, patients may have a prolonged hospital course and experience multiple complications such as deep vein thrombosis, pulmonary embolus, aspiration pneumonia, intraabdominal abscess, and wound infection [7].
Multiple factors may be responsible for creation of a Roux-en-O. Surgical experience may be one of the most important factors. Surgeons with limited bariatric experience may inadvertently lose control of the biliopancreatic and Roux limbs after dividing the small bowel, thereby misconstructing the anastomoses. Long biliopancreatic limbs, greater than 75 cm, can be confused for the Roux limb as it has the potential to reach the gastric pouch, albeit on occasion, under tension [7]. Confusion may also happen with revisional surgery [7]. To avoid confusion of the limbs, many surgeons will label the Roux limb with a silk stitch or a penrose drain, as is the practice of the authors. In addition, keeping the bilio-pancreatic limb short may help eliminate the chance of a Roux-en-O misconstruction as it will more easily be identified by locating the ligament of Treitz and less likely to comfortably reach the gastric pouch. If there is still confusion as to the identity of the limbs, the biliopancreatic limb can always be traced back to the ligament of Treitz.
Incidental diagnosis of congenital intestinal malrotation at the time of gastric bypass may also lead to confusion for the surgeon. Here, the ligament of Treitz cannot be identified in its usual location at the base of the transverse mesocolon. Moreover, it may be easy to mistake the identity of the distal ileum for the ligament of Treitz. Should this be overlooked at the time of surgery, patients are very likely to develop significant diarrhea and protein deficiency. As a result, some surgeons advocate running the entire length of the small bowel in order to distinguish proximal from distal small bowel prior to any small bowel transection if there is any question as to the location of the ligament of Treitz [12, 13]. For malrotation, the cecum and appendix will be on the patient’s left side, while the pylorus and duodenum will be visualized in the right upper quadrant after dividing Ladd’s bands. The biliopancreatic and Roux limbs can be created in the usual fashion with a few minor alterations. The length of the biliopancreatic limb is measured from the pylorus rather than the ligament of Treitz. In addition, the Roux limb may need to be placed in a paracolic, antegastric position in order to avoid twisting the small bowel along its narrow base [12, 14]. In this manner, even for patients with malrotation, the creation of a RYGB can be made safe and feasible.
Generally speaking, surgeons should take extra care in locating the ligament of Treitz. In addition, proper orientation of the biliopancreatic and Roux limbs is critical, thereby ensuring a proper Roux-en-Y configuration and avoiding potentially devastating complications.
Superior Mesenteric Artery Syndrome
Superior mesenteric artery syndrome is a rare condition caused by the compression of the third part of the duodenum by the superior mesenteric artery leading to a proximal bowel obstruction. One of the main risk factors includes rapid weight loss [15]. In fact, there have been a few case reports of superior mesenteric artery syndrome after gastric bypass [16–18]. These patients often complain of recurrent episodes of abdominal pain, back pain, and nausea. Symptoms most commonly occur at night while in the supine position with relief of pain when sitting up and leaning forward. A careful weight loss history reveals an excess weight loss approaching 85–95% [16–18]. Fatty tissue is lost throughout the whole body including the retroperitoneal fat behind the superior mesenteric artery [17, 18]. This produces a decrease in the aorto-mesenteric angle, which causes the superior mesenteric artery to compress the third part of the duodenum [19].
Radiological imaging may aid in the diagnosis. A CT scan usually reveals a distended gastric remnant and duodenum while the remainder of the biliopancreatic limb is decompressed. This suggests a transition point in the third part of the duodenum. A gastrostomy tube contrast study will also show an obstruction in the duodenum that is relieved when the patient leans forward [16–18].
Treatment options for superior mesenteric artery syndrome include conservative management with enteral or parenteral nutrition as well as operative interventions. The goal of conservative therapy is to restore positive nitrogen balance and retroperitoneal fat, thereby increasing the aorto-mesenteric angle and relieving the duodenal obstruction. Goitein et al. reported successful weight gain and resolution of symptoms of one patient after several weeks of oral and parenteral nutrition [17]. Alternatively, surgical intervention does not aim to change the aorto-mesenteric angle, rather it creates an intestinal bypass to circumvent the obstruction. The operation of choice is a duodenojejunostomy. For gastric bypass patients, the anastomosis is completed using a part of the proximal common channel to bypass the obstruction [16–18]. This often affords patients suffering from superior mesenteric artery syndrome a chance of complete resolution of symptoms more quickly than waiting for the return of a normal aorto-mesenteric angle by oral or parenteral nutrition alone.
Nesidioblastosis
Some gastric bypass patients report episodes of postprandial sweating, flushing, cramps, diarrhea, and dizziness. The constellation of these symptoms describes dumping syndrome. The early phase occurs approximately 15 min after a meal and is attributed to the rapid entrance of hyperosmotic foods (especially sugars) to the jejunum. In response, isotonic fluid passes from the plasma into the jejunal lumen. This leads to a fall in blood volume resulting in complaints of lightheadedness and dizziness. Patients are instructed to have small frequent meals that are high in protein and low in carbohydrates. In addition, they are to avoid simultaneous drinking and eating. The late phase of dumping starts 1.5–3 h after a meal that is high in sugars. The food is rapidly absorbed resulting in hyperglycemia. This evokes hyperinsulinemia and a resulting hypoglycemia. Some patients report profound neuroglycopenia. Gastric bypass patients, more than 1 year after surgery, who exhibit hypoglycemia and neuroglycopenia after a meal despite normal fasting glucose and insulin levels are diagnosed with hyperinsulinemic hypoglycemia [20] (Table 17.1). Kellogg et al. evaluated dietary modifications for 12 patients who fit such a diagnosis [20]. Those patients who had meals low in carbohydrates and high in protein reported improvement and/or resolution of their symptoms as opposed to those who had meals high in carbohydrates and low in protein. In addition, he noted the hyperinsulinemic response usually seen after a mixed meal was abolished after a low-carbohydrate meal [20]. Alpha-glucosidase inhibitors blunt the peaks and nadirs of plasma glucose levels as well as plasma insulin levels in response to a meal [21]. As a result, patients whose symptoms are refractory to dietary modifications alone may benefit from this class of medications [20].
Table 17.1
Definition of post-gastric bypass hyperinsulinemic hypoglycemia
Postprandial hypoglycemia with neuroglycopenia occurring >1 year after gastric bypass |
Spontaneous correction of hypoglycemia |
Normal fasting plasma glucose and serum insulin levels |
Hyperinsulinemia just before hypoglycemia, or after a mixed meal, a plasma glucose level of <50 mg/dL and serum insulin level >50 mU/L |
Lack of such a response after a low-carbohydrate mixed meal |
However, when neuroglycopenia continues despite implementing lifestyle modifications, bariatric surgeons should avoid simply labeling the symptoms as part of the dumping syndrome and instead search for an organic cause of hyperinsulinemic hypoglycemia. Two such causes are insulinoma and nesidioblastosis. The investigation may include multiple radiological modalities including a CT scan and transabdominal ultrasound. If these are negative, selective arterial calcium stimulation had been recommended as the next step to potentially localize hyperfunctioning β-cells [22, 23]. The doubling of the basal insulin level in the right hepatic vein in response to injection on 0.025 mEq of calcium per kilogram body weight into the splenic, superior mesenteric and gastroduodenal arteries is considered positive for hyperfunctioning β-cells in the vascular distribution of the artery studied. In the case of nesidioblastosis, an abnormal insulin response would be evident from the entire pancreas and not one specific region as would be the case for an insulinoma.
For those patients whose symptoms fail to improve with lifestyle changes and testing suggests an organic cause for the hyperinsulinemia, surgeons have argued that surgical intervention in the form of pancreatectomy is the only cure. However, nesidioblastosis is a diffuse process of the pancreas and not due to a discrete mass. Consequently, the extent of the pancreatectomy is not known. Some recommend resecting as much as 75–80% of the pancreas as recurrences of symptoms have been noted in patients who have had more conservative resections [22–25]. Recently, a more analytical approach to guide the extent of pancreatectomy has gained acceptance. Here, the results of the selective arterial calcium stimulation test are used in what has been coined the gradient-guided pancreatectomy [22, 23]. The decision of where to resect is fraught with knowing that removing insufficient amounts of pancreatic tissue may lead to recurrences and too much tissue will lead to pancreatic insufficiency and insulin-dependent diabetes.
Although approximately 40% of nesidioblastosis cases occur in gastric bypass patients, the exact mechanism is not clearly understood [22]. There are a number of hypotheses currently being investigated. One such mechanism postulates that β-cells of the pancreas hyperfunction in response to obesity-related insulin resistance [20, 26]. Postoperatively, after gastric bypass, there is a decrease in the fat mass and an improvement in insulin resistance. However, the β-cells may not “reset” and continue to secrete large amounts of insulin in response to a meal, thereby producing neuroglycopenia. Meier et al. examined pancreas specimens after resection for nesidioblastosis and noted large β-cell nuclei whose diameter appeared to correlate to preoperative body mass index [26]. This finding together with the notion that the nucleus of an endocrine cell provides an index of secretory activity supports the hypothesis of hyperfunctioning β-cells that do not “reset” as weight is lost [27, 28].
Another likely mechanism includes hypertrophy of β-cells in the pancreas secondary to an elevation of β-cell trophic factors after gastric bypass [22]. Glucagon-like peptide (GLP-1) is one such trophic factor that is elevated after gastric bypass [29]. GLP-1 has multiple functions including inhibiting β-cell apoptosis, thereby increasing β-cell mass [30]. In animal models, GLP-1 also increases β-cell mass via proliferation and neogenesis [30]. In this hypothesis, the elevation of GLP-1 leads to the hypertrophy and hyperfunctioning of the β-cells, resulting in hyperinsulinemic hypoglycemia. In support of this notion, pancreatic specimens obtained after resection for nesidioblastosis noted a variable pattern of islet cell hypertrophy and hyperplasia. In addition, large islet cells staining positive for insulin were visualized budding off the pancreatic duct [22]. Others have also reported hypertrophic β-cells and increased periductular islet cells [31, 32]. Overexpression of other growth factors such as insulin-like growth factor 2 (IGF2), insulin-like growth factor 1 receptor-α (IGF1Rα), and transforming growth factor receptor β3 (TGFRβ3) has been reported in gastric bypass patients with nesidioblastosis [25]. This supports the hypothesis that islet cell growth factors and growth factor receptors may play an integral role in the development of nesidioblastosis in gastric bypass patients.
Intussusception
Bowel obstructions in gastric bypass patients can be due to numerous causes such as adhesions, ventral hernias, internal hernias, anastomotic strictures, and rarely intussusception. The incidence of intussusception in post-gastric bypass patients is approximately 0.07–0.15% [33, 34]. These patients present with the usual signs and symptoms of a small bowel obstruction: periumbilical pain, nausea, and bilious vomiting. The abdomen may be distended with diffuse tenderness on exam. CT is the diagnostic modality of choice as plain abdominal X-rays seldom show any degree of bowel obstruction. CT images reveal proximal bowel dilatation and distal bowel decompression. Images may also show the pathognomonic “target” sign to suggest intussusception as the cause for obstruction (Fig. 17.3). The treatment of choice is prompt surgical intervention.
Fig. 17.3
CT demonstration of an intussusception. The target sign is obvious on the right side of the abdomen (see red arrow) (Images provided courtesy of Scott A. Shikora, MD)
In adults, intussusception is usually due to a lead point, such as a polyp, diverticulum, or mass. The direction of telescoping is anterograde; the proximal bowel (intussusceptum) invaginates into the distal bowel (intussuscipiens). Although anterograde variants have been reported in gastric bypass patients, the majority of cases are retrograde in nature [33, 35–39]. Here, the proximal common channel telescopes into the jejunojejunostomy progressing proximally and may cause obstruction of both the biliopancreatic and Roux limbs (Fig. 17.3). The exact mechanism of retrograde intussusception in gastric bypass patients is not quite understood. Some have postulated that suture and staple lines as well as postoperative adhesions may act as a lead point [35, 40, 41]. Others have postulated ectopic myoelectric pacemakers in the Roux limb produce retrograde migratory motor complexes that lead to intestinal dysmotility and may be the main culprit in retrograde intussusceptions [42–44].
The surgical principles of bowel resection for an obstruction hold true even for gastric bypass patients. Intussusception in adults usually has an identifiable lead point. As a result, the tenet is to perform an en bloc resection to be sure of removal of the instigating factor. However, in gastric bypass patients, many have noted no identifiable lead point. This raises the question of the optimal surgical therapy. Some have argued for gentle reduction of the bowel, assessment for viability, and resection of any necrotic bowel [38, 40]. Others propose en bloc excision with reconstruction of a new jejunojejunostomy without an attempt at reduction to avoid any risk of perforation and subsequent sepsis [35] (Fig. 17.4). It does appear that manual reduction of the intussusception in conjunction with observation is not enough treatment as recurrences and subsequent resection were noted in one series [34]. Without knowing the exact mechanism behind retrograde intussusception in gastric bypass patients, the extent of surgical resection, whether to only resect clearly necrotic tissue or to include viable jejunojejunostomy and a presumed lead point, remains to be determined.
Fig. 17.4
Intussusception specimen. A resected jejunojejunostomy demonstrating the intussuscepted common channel into the jejunojejunostomy (Images provided courtesy of Hector de la Cruz, MD)
Unusual Ulcer Presentations: Perforation and Duodenal Ulcers
Marginal ulceration is a well-known complication of gastric bypass. The incidence of marginal ulcers after gastric bypass is 3–5% [45–50]. The formation of ulcers is multifactorial. The most common risk factors include smoking, alcohol, aspirin and nonsteroidal anti-inflammatory use, steroids, and ischemia [51, 52]. Recently, Helicobacter pylori (H. pylori) has also been identified as a possible risk factor for marginal ulcers [53]. These ulcers commonly produce epigastric pain, burning sensation, nausea, and vomiting. Persistent ulcers that are not identified and treated may progress to hemorrhage and perforation.
Perforated marginal ulcers may present in a number of ways: abdominal pain with peritonitis, fever, pneumoperitoneum visualized on abdominal films, or even a subphrenic abscess on a CT scan [51]. Surgical therapy includes repairing the defect with or without an omental patch and wide drainage. As patients will remain NPO until the ulcer heals, feeding access (gastrostomy placed in the fundus) should be considered at the time of surgery. Medical therapy consists of proton pump inhibitors, broad spectrum antibiotics, treatment of H. pylori if seropositive, and cessation of all risk factors for ulceration [51].
Ulcer healing is dependent on eliminating all risk factors. Felix et al. reported three patients with perforated marginal ulcers who continued to smoke and subsequently reperforated [51]. This suggests smoking also plays an important role in whether the ulcer heals. It is unclear if H. pylori has a role in marginal ulcer formation or perforation. Schirmer et al. noted a significant decrease in marginal ulcer rate after screening and treating for H. pylori preoperatively [54]. Interestingly, Rasmussen noted that marginal ulceration was significantly more common among patients infected with H. pylori preoperatively, even when adequately treated prior to surgery [53]. He postulates prior infection and treatment may predispose to ulcer formation after gastric bypass [53]. Consequently, many bariatric centers will screen for H. pylori and initiate therapy if the results are positive.
Duodenal ulcers, in contrast to marginal ulcers, are rare after gastric bypass. The pathophysiology is not well understood. The gastric remnant is able to maintain its acid secreting capabilities [55, 56]. In addition, the normal stimulus for bicarbonate secretion from the pancreas is absent after gastric bypass [57]. Some have hypothesized that the unneutralized acid in the duodenum is thought to play a role in the formation of duodenal ulcers [57]. Patients often will present with peptic ulcer-like pain or with evidence of gastrointestinal bleeding. This bleeding may be acute and episodic or more indolent in nature. The acute bleeds can cause hematochezia or melena and may require transfusions. Patients may even present as hemodynamically unstable. Instability or intractability may result in surgical exploration. The more indolent bleeding may present as an iron deficiency anemia.
It can be extremely challenging to assess the duodenum and gastric remnant for these ulcers by standard endoscopy and other radiological modalities resulting in delayed diagnoses. On occasion, endoscopists are successful in reaching the excluded fundus by piloting the endoscope down the Roux limb and up into the biliopancreatic limb. However, if the Roux limb is particularly long, this may not be successful. In these instances, a laparoscopic-assisted endoscopy can be considered. Here, the excluded fundus is surgically identified. A gastrostomy is made to allow a trocar to be inserted into its lumen. The endoscope can then be passed into the lumen of the fundus and directed into the duodenum.
There are isolated case reports of perforated duodenal ulcers, and one center reported an incidence of 0.25% [58–60]. Patients who suffer a perforated duodenal ulcer may present with right upper quadrant pain and fevers. These symptoms together with the lack of a pneumoperitoneum on imaging may lead to an incorrect diagnosis of acute cholecystitis as opposed to a perforated duodenal ulcer. After a gastric bypass, the gastric remnant is usually decompressed and without air. It stands to reason that a perforation in the duodenum will not exhibit free air. Instead, biliary and gastric secretions will be present in the area of the duodenum, represented as free fluid on CT scanning.
The management of perforated duodenal ulcers is similar to that of perforated marginal ulcers: closure of the defect, wide drainage, broad spectrum antibiotics, proton pump inhibitors, and treatment of H. pylori. Some surgeons even propose resection of the remnant stomach as definitive treatment to eliminate the acidic environment in the duodenum [57, 58, 60]. However, the ideal time for resection remains unclear: resection at the time of perforation may lead to a duodenal stump leak secondary to the inflammation and edema in the area of the perforation; on the other hand, resection at a later time requires a return to the operating room and scar tissue may preclude a safe operation. Clearly, perforated duodenal ulcers can be a both diagnostic and therapeutic dilemma. The inability to access and evaluate the remnant stomach and duodenum may delay treatment. When deciding to go to the operating room for suspicion of acute cholecystitis or persistent abdominal pain, there should always be a high index of suspicion that the patient may in fact have a perforated duodenal ulcer.
Vitamin Deficiencies
Vitamin deficiencies after gastric bypass are well known, and are covered in more detail in Chap. 14. In this chapter, we will review two deficiencies that have serious consequences if left undetected: thiamine and cobalamin. It is routine for bariatric centers to initiate vitamin supplementation after surgery with scheduled assessments of vitamin levels starting 6 months after surgery and continuing every 6–12 months thereafter [61]. It is the practice of the authors to routinely check a complete blood count (CBC), calcium, albumin, folate, RBC folate, iron, iron binding capacity, ferritin, 25-hydroxlyated vitamin D, vitamin B12, vitamin B1, and parathyroid hormone. Compliance with long-term follow-up and vitamin supplementation is vital as deficiencies are easily treated and serious problems can be avoided. Here, we would like to review the signs and symptoms of a few vitamin deficiencies as devastating outcomes can happen if they are overlooked.
Thiamine is a water-soluble vitamin involved in carbohydrate metabolism and is absorbed in the small intestine. Thiamine deficiency, also known as beriberi, can present in a variety of ways: dry beriberi usually entails neurological symptoms, while wet beriberi usually presents with congestive heart failure or even fulminant cardiac failure [62]. Neurological symptoms may include confusion and opthalmoplegia. Without therapy, symptoms can progress to include nystagmus and ataxia. Together these characterize Wernicke’s encephalopathy. In addition, anterograde and retrograde amnesia may ensue, along with confabulation and hallucinations – better known as Korsakoff’s psychosis. Wernicke–Korsakoff syndrome is the end stage of a severe thiamine (vitamin B1) deficiency.
In terms of gastric bypass and thiamine deficiency, there are no reported cases of patients presenting with cardiac failure. However, gastric bypass patients will present with neurological complaints that may vary along a spectrum. A typical history entails a patient who is a few weeks status post-gastric bypass and develops persistent nausea, vomiting, and dehydration. Neurological exam may reveal a wide range of cognitive impairment, paresthesias and hyperesthesias, dysarthria, nystagmus and other opthalmoplegias, weakness, or even ataxia [62–67]. The neuropathy associated with this deficiency is symmetrical, sensory motor and is most prominent distally [62]. The pathophysiology is thought to be due to abnormal carbohydrate metabolism in the central nervous system leading to axonal degeneration involving the thalamus, ocular motor nuclei, vestibular nuclei, cerebellum, and around the third and forth ventricles [66, 68]. Interestingly, there are conflicting MRI findings in patients with thiamine deficiency. Some centers report a normal MRI, while others report gadolinium enhancement and increased T2 signal in affected areas of the brain [64, 65, 67].
In gastric bypass patients, thiamine deficiency is usually due to inadequate oral intake (vitamin supplementation or food) secondary to protracted vomiting. Patients may vomit for a number of reasons: stenotic gastrojejunostomy, intestinal obstruction, influenza or upper respiratory tract infection, gastroenteritis, and hyperemesis associated with pregnancy. Treatment consists of intravenous thiamine supplementation, which may produce variable degrees of symptomatic improvement. However, some patients may continue to have chronic neurological impairment after therapy [66]. Care should be taken to initiate thiamine supplementation prior to administration of any intravenous fluids containing dextrose. As thiamine is required for glucose metabolism, the administration of dextrose prior to thiamine will deplete already deficient thiamine stores in the body and may worsen any symptoms.