Numerous mechanisms have been considered in the pathogenesis of MU which can be divided into surgical and non-surgical factors.

It has now become a routine by surgeons to prescribe PPI routinely following RYGB. The same was also shown by an international survey where 88 % of surgeons routinely preferred prophylactic PPI usage [37]. But whether this usage really impacts the outcome of MU and when used, the exact duration of usage has not been outlined.

In literature, the duration of postoperative PPI usage has been reported to be between 30 days to 2 years, a few have suggested lifelong usage too. But with the understanding that the gastric acidity has a big role in the pathophysiology of MU, PPIs continue to be widely used. Gumbs et al. had the rate of MU falling to zero with prophylactic PPI therapy compared to no PPI therapy, but the sample size was small [46]. A recent report also showed that prophylactic PPI usage had an impact in preventing MU [47]. D’Hondt et al. found no statistical difference in the incidence of MU with/without PPI prophylaxis in patients without H.pylori infection [42]. But what was interesting to note was that in pre-operatively H.pylori positive patients with eradication, PPI had a beneficial effect in protecting against MU. They hypothesised that pre-operative H.pylori infection could lead to gastritis leading to increased ulcer risk, which was reduced by PPI usage. Currently no Level 1 evidence exist on the actual impact of this usage.

Also based on the understanding of pathophysiology, it is also now clear that the first 12 months is when most MU’s are seen. Hence it is more logical to continue PPI therapy for atleast for 1 year. The risks of continuing PPI for longer periods needs special consideration. Carr RJ has recently analyzed the existing literature to propose a management algorithm for MU [48]. For prophylaxis PPIs were recommended for 6–12 months along with risk factor modification for low risk patients with longer duration to be considered for higher risk patients e.g. patients with NSAID usage, smoking etc. Long term PPI therapy can cause calcium malabsorption with increasing risk of osteoporosis and hip fracture, iron and B12 deficiency and hence is to be used with caution [49–51].

Diagnosis of MU requires a high index of suspicion and a low threshold for endoscopic evaluation. For patients with MUs, the treatment involves modification of patient risk factors and inhibition of gastric acid secretion which is successful in treating 68 to 100 % of MU s with relapse rates of 8 % [48]. Medical treatment consists of PPIs, H2 antagonists, Sucralfate, or a combination of these. The International survey by Steinemann et al. had shown that 68 % surgeons preferred PPI alone and 32 % preferred in combination with Sucralfate [37]. H2 blockers alone or in combination with sucralfate was less frequently used. High dose PPI monotherapy is highly successful in the treatment of MU’s with healing rates varying between 2 and 7 months as documented by endoscopy [46, 52]. Dallal and Bailey had used a combination regimen of PPI and sucralfate with a step down management regime involving a month of high dose PPI and sucralfate which were weaned on a monthly basis [53]. They also claimed that sucralfate offers better treatment than PPI monotherapy. Hence we believe that sucralfate could be used for patients who develop MU during PPI prophylaxis. However, Azagury et al. [10],noted no difference in healing rates comparing PPI monotherapy to PPI and sucralfate.

The duration of PPI that needs to be continued after ulcer healing has also not been studied by any clinical trial. The international survey showed that more than 50 % of surgeons would continue medical therapy for a median of 6 months to prevent recurrence, most of them preferring PPI monotherapy [37]. Carr et al. in his review had suggested a lifelong PPI in patients with MU s after the healing of the ulcer [48]. But for this to be validated we need more long term and level 1 data.

Refractory MU is defined as persistence of an ulcer after initial conservative treatment. Evaluation is important at this juncture to find out anatomic abnormalities which could be the potential contributing factor for the refractory nature. This should include identification of a dilated gastric pouch, gastro-gastric fistulae and foreign body in the ulcer. If any of the above factors are identified, the treatment should be directed at appropriate correction of the same. This can be done using a combination of endoscopic and surgical techniques [10, 19, 22, 42, 54]. Although the majority of data has been for the open approach which is known to have greater complication rates and mortality, the recent data on laparoscopic revisions have proven safer and also effective [19, 36, 55–60].

The controversy is in patients without any identifiable abnormalities. The international survey showed that 56 % of surgeons preferred to continue with conservative treatment and would consider surgery only when complications arise. Forty one percent of surgeons preferred to revise the gastrojejunostomy with 18 % of those preferring to add a vagotomy. What was interesting to note in this survey was that the choice of approach was related to experience, with more than 50 % of surgeons with more than 200 surgeries experience, preferring a surgical approach compared to less experienced surgeons [37]. Although data on the right approach is lacking, surgical revision of the GJ can be considered in the event of failure of medical management, but the exact duration for failure needs further research. Some authors also advocate a vagotomy in an attempt to reduce the secretion of gastric acid [7, 10, 22, 61]. Even thoracoscopic vagotomy has been reported in one series, but with very high complication rates [62]. El-Hayek et al. suggested smoking as a major risk factor for development of MU and recommended urinary nicotine testing, reserving surgical intervention only for patients with negative tests [15]. Similar principles would hold good for recurrent MU’s too, with importance being given to identification of the risk factor and lifelong PPI therapy.

The incidence of perforated MU after LRYGB is around 1–2 % of the general population, which means about 20 % of the patients with MU present with a perforation [5]. It is important to note that 70 % of the patients with perforation after MU have some identifiable risk factor like smoking, use of NSAIDS, steroids etc. Twenty percent of patients may not have any warning signs prior to perforation [9]. Based on the understanding of the treatment of perforated duodenal ulcer, laparoscopic approaches can reduce morbidity, post-operative pain, hospital stay and early return to work [63–65]. The same principle could be applied to perforated MU as well, where majority of the ulcers occur on the jejunal side of the GJ anastomosis on the anti-mesenteric border suitable for laparoscopic repair and patch closure. Laparoscopic patch repair has been shown to be an optimum solution [59, 66–68]. Although surgical revision with refashioning of the GJ is also possible, it is better avoided in an emergency which has higher blood loss, operating time and length of stay [35].