Perforated Marginal Ulcer After Gastric Bypass

The epidemic of overweight and obesity in the United States of America along with its comorbidities continues to expand. Bariatric surgery has demonstrated to be the most effective and sustained method to control severe obesity and its comorbidities. For instance, type 2 diabetes mellitus was completely resolved in 76.8%, systemic arterial hypertension was resolved in 61.7%, dyslipidemia improved in 70% and obstructive sleep apnea-hypopnea syndrome was resolved in 85.7%. Furthermore, bariatric surgery significantly increases life expectancy (89%) and decreases overall mortality (30-40%), particularly deaths from diabetes, heart disease, and cancer. Lastly, preliminary evidence about downstream savings associated with bariatric surgery offset the initial costs in 2 to 4 years.

Since 2000, there has been a substantially progressive increase in bariatric surgery. In 2007, the ASMBS reported that 205,000 people had bariatric surgery in the United States from which approximately 80% of these were Gastric Bypass. Moreover, there is a mismatch between eligibility and receipt of bariatric surgery with just less than 1% of the eligible population being treated for morbid obesity through bariatric surgery. Along with the increasing number of elective primary weight loss procedures, up to 20% of post RYGB patients cannot sustain their weight loss beyond 2 to 3 years after the primary bariatric procedure. Thus, revisional surgery for poor weight loss and re-operations for technical or mechanical complications will rise in a parallel manner.

A common late complication after gastric bypass surgery is marginal ulceration that is defined as ulcers at the margins of the gastrojejunostomy, mostly on the jejunal side. Its incidence after RYGB ranges from as low as 0.6 to as high as 16%. After 1,040 laparoscopic RYGB surgeries, the incidence rate, in our hands, is 1.4% and mainly related to NSAID´s use. In observational cohort studies, the presence of specific technical factors - staple-line dehiscence or gastro-gastric fistula, enlarged pouch, foreign material and local ischemia - and environmental factors - tobacco, NSAID´s, alcohol consumption, and H pylori infection among others - have been associated with marginal ulceration however the exact etiopathogenesis has not been completely elucidated.

Similar to peptic ulcer disease, most marginal ulcers respond to medical therapy and complicated or complex ulcer disease warrants operative intervention. Specifically, perforated, penetrated, obstructing, bleeding and intractable marginal ulcers require surgical intervention.

The intestinal mucosa is not typically exposed to gastric acid, which is neutralized by the alkaline biliopancreatic secretions. The jejunal mucosa has no natural barriers; when exposed to gastric acid, it ulcerates easily. Capella \& Capella demonstrated that transecting the gastric segments significantly reduce staple-line dehiscence; this is the so-called divided gastric bypass. The incidence for gastro-gastric fistula (GGF) formation after undivided gastric bypass (GBP) was 23%, after a partially divided GBP was 19%, after a completely divided GBP was 2% and after complete transection with interposition of the jejunal limb was 0% (p <0.001).

An unusually large gastric pouch (such as horizontal pouches, retained fundus, long lesser curvature based pouches or enlarged after initially being sized adequately) contain more acid-producing parietal cells. Increased acid production in the pouch carries the risk of developing marginal ulcers. Acid secretion in the small pouch after RYGB is virtually absent.

The anastomotic techniques influence the incidence of marginal ulcers. Capella \& Capella reported a consecutive series with significant decrement from 5.1% to 1.5% (p< 0.001) after switching from a stapled to a hand-sewn anastomosis. Likewise, after changing from an inner layer of absorbable suture and an outer layer of nonabsorbable material to a double-layer of absorbable suture the incidence rate improved from 1.6% to 0%.

Local ischemia, in the immediate postoperative period, is probably secondary to technical reasons. Fundamental aspects for decreasing tension and local ischemia at the gastrojejunostomy are dissection of the tissues around the pouch without devascularizing the lesser curvature and complete mobilization of a well-perfused Roux limb.

NSAID´s inhibit prostaglandin synthesis 1) decreasing blood flow to the mucosa (mainly by PG subgroups E and I, which promotes vasodilatation), 2) increased adherence of neutrophils, 3) topical irritant effect, 4) impair of the repair/healing process, and 5) gastric-acid-related effects. In a retrospective cohort study, Wilson et al found NSAID´s consumption to correlate with the marginal ulcer development after RYGB. Numerous studies have identified NSAID´s use as a main risk factor for PUD; however, the precise relevance of NSAID´s as a factor in marginal ulcer development after RYGB is largely unknown.

In epidemiological, clinical and experimental studies, Tobacco has been identified as a major risk factor for peptic ulcer disease (PUD). Smoking carries an overall relative risk of 2.2 for developing PUD. A synergistic relationship for developing PUD exists between H pylori infection and smoking (2.3 vs. 6.1). Biological evidence suggests that smoking compromises the gastric mucosa barrier, decreases gastric emptying and increases gastric secretion. For marginal ulcer after RYGB, there are three cohort studies that showed positive correlation between smoking with developing anastomotic ulcer.

Helicobacter pylori (H pylori) infection carries an overall relative risk of 3.3 (95%CI, 2.6-4.4) for developing PUD. A synergistic relationship exists between H pylori infection and NSAID´s consumption for developing PUD with an overall risk of 3.5 (95%CI, 1.26-9.96) compared to either H pylori or NSAID´s negative individuals. Furthermore, a 61.1 (95%CI, 9.98-373) overall risk exist when compared to H pylori negative individuals not taking NSAID´s. For marginal ulcers after RYGB, three cohort studies have showed that H. pylori infection is not associated with the development of marginal ulcers. In Papasavas et al study, preoperative H. pylori testing with prophylactic eradication did not decrease the incidence of MU or erosive pouch gastritis.

The pathophysiological mechanisms of damage to the gastric mucosa of Ethanol and alcoholic beverages are poorly understood. There are scant retrospective epidemiological studies that determine if a relationship between alcohol consumption and PUD exists. Although alcohol is not associated with an increased risk of PUD, patients with PUD are advised to avoid alcoholic drinks. Basic science studies have showed that instillation of pure ethanol at lower concentrations (4-40% v/v) causes hemorrhagic gastritis in a dose-dependant fashion. Also a synergistic relationship exists between ethanol and NSAID´s, since both cause mucosal injury. On the other hand, there are no studies available about the effect of alcohol on marginal ulcer development after RYGB.

Cocaine use is responsible for approximately 143,000 Emergency Department visits annually; 19% of American, between 18 to 25 years old, have used cocaine: more than 1% of the Americans use cocaine at least once a week; and approximately 50% of all drug-related deaths were secondary to Cocaine. The temporal association between smoking cocaine (crack) and GI tract manifestations include ulceration, perforation, visceral infarction, and retroperitoneal fibrosis. Most ulcer perforations are juxtapyloric or duodenal (D1) however jejunal location has been reported. The physiopathologic hypothesis includes the following mechanisms 1) cocaine blocks the re-uptake of norepinephrine leading to intense vasoconstriction (alpha-adrenergic receptors), mesenteric ischemia, focal tissue ischemia, coagulative necrosis and perforation; and 2) cocaine causes thrombus formation and platelet aggregation mediated by endogenous Thromboxane B2. A few retrospective cohort studies suggest that primary patch repair is the recommended therapeutic option for this type of ulcers. However, Shuster et al reported a high recurrence rate (42%) after omental patch repair compared to a definitive anti-ulcer procedure (0%). Little information exists about the association between crack and gastroduodenal ulcer perforations other than the temporal association reported in small retrospective cohort studies. In a communication, Dr Mason recalls two patients with perforated "stomach ulcers" associated with cocaine use.

The following Critically-Ill patients have a significant increased risk of stress-related mucosal disease (SRMD): 1) mechanical ventilation > 48hrs conveys a 16-fold risk (p < 0.001), 2) coagulopathy has a 4-fold risk (p < 0.001), 3) shock carries a 3.7-fold risk (p= 0.08), 4) drop of intramural pH (from 8 to 6, 5), 5) increase of the number of risk factors (from 0 to 4), 6) recent major surgery, 7) major trauma, 8) severe burns, 9) head trauma, 10) hepatic or renal disease at admission, and 11) sepsis. SRMD encompasses stress-related injury (SRI), which is primarily erosion in the GI tract, and stress ulcer, which is a focal deep mucosal damage. The pathogenesis of SRMD has not being unraveled completely but there is strong evidence that hypoperfusion and reperfusion of the upper GI tract is the major cause. There is no literature available about marginal ulcer after RYGB associated to ICU or critically ill patients.

Diverse operative strategies for addressing perforated marginal ulcers after gastric bypass have been described including I) Omental (Graham) patch repair, II) Revision of gastrojejunostomy, III) Irrigation and drainage, IV) any previous procedure with truncal vagotomy, V) Esophagojejunostomy, and VI) Reversal.

Summarizing, there is scant information about late complications after gastric bypass especially after the widespread adoption of the laparoscopic approach and the modern anatomical construct of Roux-en-Y Gastric Bypass surgery.