Laparoscopic reversal of Roux-en-Y gastric bypass: Technique and utility for treatment of endocrine...

Post on 30-Dec-2016

212 views 0 download

transcript

1550-7289/14/$http://dx.doi.org

This study waAdvancing Tranthe official view

*CorrespondAv., K4/730 CS

E-mail: cam

Surgery for Obesity and Related Diseases 10 (2014) 36–43

Original article

Laparoscopic reversal of Roux-en-Y gastric bypass: Technique and utilityfor treatment of endocrine complications

Guilherme M. Campos, M.D.a,*, Martynas Ziemelis, B.S.a, Rodis Paparodis, M.D.b,Muhammed Ahmed, M.D.b, Dawn Belt Davis, M.D., Ph.D.b,c

aDepartment of Surgery, Division of General Surgery, Section of Foregut and Bariatric Surgery, University of Wisconsin School of Medicine and PublicHealth, Madison, Wisconsin

bDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Wisconsin School of Medicine and Public Health, Madison,Wisconsin

cWilliam S. Middleton Memorial Veterans Hospital, Madison, Wisconsin

Received February 11, 2013; accepted May 25, 2013

Abstract Background: The anatomic and physiologic changes with Roux-en-Y gastric bypass (RYGB) may lead

– see/10.10

s supslatios of tence:C. Mpos@

to uncommon but occasionally difficult to treat complications such as hyperinsulinemic hypoglycemiawith neuroglycopenia and recalcitrant hypocalcemia associated to hypoparathyroidism. Medical man-agement of these complications is challenging. Laparoscopic reversal of RYGB anatomy with restorationof pyloric function and duodenal continuity is a potential treatment. The objective of this study was topresent the indications, surgical technique, and clinical outcomes of laparoscopic reversal of RYGB.Methods: Prospective study of consecutive patients offered laparoscopic reversal of RYGB.Results: Five patients with remote laparoscopic RYGB underwent laparoscopic reversal of RYGBto normal anatomy (n ¼ 2) or modified sleeve gastrectomy (n ¼ 3). Indications were medicallyrefractory hyperinsulinemic hypoglycemia with neuroglycopenia (n ¼ 3), recalcitrant hypocalcemiawith hypoparathyroidism (n ¼ 1), and both conditions simultaneously (n ¼ 1). Before reversal, allpatients had a gastrostomy tube placed in the excluded stomach to document improvement ofsymptoms. Laparoscopic reversal was accomplished successfully in all patients. Three postoperativecomplications occurred: bleeding that required transfusion, gallstone pancreatitis, and a superficialtrocar site infection. Average length of stay was 3 days. At a mean follow-up of 12 months (range 3to 22), no additional episodes of neuroglycopenia occurred, average number of hypoglycemicepisodes per week decreased from 18.5 � 12.4 to 1.5 � 1.9 (P ¼ .05), and hypocalcemia becameresponsive to oral replacement therapy in both patients.Conclusions: Laparoscopic reversal of RYGB to normal anatomy or modified sleeve gastrectomyis feasible and may be a therapeutic option for selected patients with medically refractory hyper-insulinemic hypoglycemia and/or recalcitrant hypocalcemia associated with hypoparathyroidism.(Surg Obes Relat Dis 2014;10:36–43.) r 2014 American Society for Metabolic and BariatricSurgery. All rights reserved.

Keywords: Hypoglycemia; Hyperinsulinemic hypoglycemia; Hypocalcemia; Gastric bypass; Reversal; Sleeve gastrectomy;

GLP-1; Hypoparathyroidism; Nesidioblastosis; Laparoscopic reversal; Bariatric surgery

front matter r 2014 American Society for Metabolic and Bariatric Surgery. All rights reserved.16/j.soard.2013.05.012

ported by the Clinical and Translational Science Award (CTSA) program, through the National Institutes of Health National Center fornal Sciences (NCATS), grant UL1TR000427. The content is solely the responsibility of the authors and does not necessarily representhe NIH or the federal government.Guilherme M. Campos, M.D., Department of Surgery, University of Wisconsin, School of Medicine and Public Health, 600 Highlandadison, WI 53792-7375.surgery.wisc.edu

Laparoscopic Reversal of Gastric Bypass / Surgery for Obesity and Related Diseases 10 (2014) 36–43 37

The anatomic changes with Roux-en-Y gastric bypass(RYGB) allow the food bolus to promptly reach the smallbowel after passing through the gastrojejunostomy, and theexcluded stomach and duodenum have no contact with thefood bolus. These changes lead to alterations in glucosekinetics [1], absorption of micronutrients and minerals [2],and postprandial levels of a variety of gastrointestinal (GI)and pancreatic hormones [3]. With dietary modificationsand supplementation of standard micronutrients and miner-als, most patients adapt and benefit from these changes afterRYGB; as exemplified by the low rates of nutritionalcomplications [4] and the outstanding remission and aswell as prevention rates of type 2 diabetes that are observedafter RYGB [5,6]. However, these anatomic changes maylead to uncommon and challenging treatment complica-tions, such as hyperinsulinemic hypoglycemia with orwithout hypoglycemia unawareness [7,8] and recalcitranthypocalcemia related to hypoparathyroidism and inadver-tent parathyroidectomy [9,10]. The etiology of hyperinsu-linemic hypoglycemia remains controversial, and besttreatment recommendations for these conditions areunknown. In patients with recalcitrant postRYGB hyper-insulinemic hypoglycemia, surgical treatment with subtotalor total pancreatectomy has been offered in selected cases[11,12], because the condition has been linked to de novopostRYGB nesidioblastosis or pancreatic islet overgrowthas its potential cause [12]. However, this pathologic findinghas been challenged by other groups, and clinical resultswith pancreatectomy are suboptimal [13–15]. Recalcitranthypocalcemia with associated hypoparathyroidism has beendescribed recently in patients with RYGB [10,16], and nostandard treatment is available.Laparoscopic reversal of RYGB anatomy with restoration

of pyloric function and duodenal continuity may be a lastresort therapeutic option in these rare cases. In this report,examples of these unique medical indications, guidelinesfor preoperative clinical evaluation, details of surgicaltechnique, and clinical outcomes of laparoscopic reversalof RYGB are presented. This represents a novel approach torare but challenging endocrine complications after RYGBsurgery.

Material and methods

A prospective study was conducted, including patientswho had prior remote RYGB and presented with medicallyrefractory and well-documented episodes of hyperinsuline-mic hypoglycemia with hypoglycemia unawareness andpatients with recalcitrant hypocalcemia related to hypopar-athyroidism due to previous inadvertent parathyroidectomy.Patients were jointly evaluated by the Section of Foregutand Bariatric Surgery and Endocrinology Service. Patient’sdemographic characteristics before RYGB, RYGB techni-que, and other pertinent history were obtained by review ofmedical records. Patients’ demographic characteristics,

preoperative and postoperative symptom evaluation, diag-nostic and therapeutic strategy, and clinical outcomes wereprospectively collected.The diagnosis of hyperinsulinemic hypoglycemia with

neuroglycopenia was based on medical history and doc-umentation of multiple episodes of hypoglycemia, normalfasting c-peptide and insulin levels, review of data fromglucometer, and/or continuous glucose monitoring studyand testing as indicated below. Preoperative clinical datawere obtained while patients were on maximally toleratedmedical therapy. Postoperative clinical data were obtainedat last follow-up visit. Before medical treatment, patientshad an upper GI endoscopy to document the RYGBanatomy and an abdominal and pelvic computed tomo-graphic (CT) scan to exclude other possible causes for thesymptoms. In addition, a 2-hour 75 g oral glucose tolerancetest was obtained to document postprandial hyperinsuline-mia and hypoglycemia.Patients with hyperinsulinemic hypoglycemia were ini-

tially treated with standard dietary modifications, consistingof minimizing intake of simple carbohydrates and increas-ing intake of fiber and protein. In addition, pharmacologictreatment was attempted with escalating doses and combi-nations of acarbose, diazoxide, and/or verapamil. Glucagonwas used as needed for neuroglycopenia.The diagnosis of recalcitrant hypocalcemia related to

hypoparathyroidism due to previous inadvertent parathyr-oidectomy was based on medical history, documentation ofmultiple episodes of hypocalcemia, and a low intact para-thyroid hormone (PTH) level. Patients were initially treatedwith escalating doses of calcium citrate tablets, calciumcarbonate (CaCO3) suspension, calcitriol, ergocalciferol,and/or subcutaneous recombinant parathyroid hormone(rPTH). Both patients required frequent hospital admissionsfor intravenous calcium infusions as well.After failed attempts of medical management, a laparo-

scopic gastrostomy tube (G-tube) was inserted in theexcluded stomach. The tube was used to deliver nutrientsand/or calcium supplementation to the excluded stomachand the duodenum. Patients had the gastrostomy tube inplace for 8-12 weeks before reversal surgery. If nutritionaland medication administration through the G-tube resultedin symptom improvement, patients were then consideredcandidates for reversal. After G-tube insertion, 3 times dailyadministration of a standardized nutritional supplementationthrough the G-tube was recommended, consisting of 450kcal in 150 mL liquid containing 9.9 g of simple sugars in atotal of 38 g carbohydrate, 10 g of fat, and 15 g of protein.Patients were monitored clinically for 2 weeks for symp-toms of hypoglycemia. At 4 weeks after G-tube insertion,all patients underwent a Meal Tolerance Test by adminis-tering, through the G-tube, a standardized 300 kcal in 100mL liquid meal containing 9.9 g of simple sugars in a totalof 38 g carbohydrate, 10 g of fat, and 15 g of protein. Bloodsamples, obtained through an intravenous catheter inserted

G. M. Campos et al. / Surgery for Obesity and Related Diseases 10 (2014) 36–4338

in the forearm, were drawn at 0, 5, 15, 30, 60, 120, andþ180 minutes relative to the end of the meal administration.After collection, the samples were processed on site andstored at �701C for subsequent batch analysis of glucoselevels.The surgical treatment was offered under the guidelines

for innovative medical therapy [17], and a clinical researchproject to study symptom improvement after laparoscopicreversal was approved by the Institutional Review Boardand Clinical Research Center (CRC) Advisory Committee.Written consent was obtained from each participant.

Fig. 1. Division of the gastrojejunostomy and alimentary limb just abovethe jejuno-jejunostomy using linear staplers.

Technique for Laparoscopic reversal of RYGB: circularstapled gastrogastrostomy with the transoral anvil

Under general anesthesia and in a modified lithotomyposition, pneumoperitoneum was obtained at 15 mm Hgusing a direct trocar insertion or Hasson technique. Twoadditional 5-mm trocars (subxiphoid for liver retraction andleft flank for retraction) and 3 additional 12-mm trocars (leftupper quadrant for dissection and insertion of circularstapler, right flank, and left to the umbilicus for dissectionand linear stapling) were inserted. Dissection of adhesionsfrom the undersurface of the left lobe of the liver was doneusing a combination of sharp and ultrasonic dissection, anda liver retractor was placed. After taking down the gastro-stomy site, the gastrojejunostomy was identified; thealimentary limb was measured to the jejuno-jejunostomyand from the jejuno-jejunostomy to the ileo-cecal valve.The gastrojejunostomy was dissected free circumferentiallyto allow space for a 4.8-mm linear stapler to divide thegastric pouch at a location immediately above the gastro-jejunostomy (Fig. 1). After ascertaining presence of aminimum of 3.0 meters from the jejuno-jejunostomy tothe ileo-cecal valve, the alimentary limb was excised usingultrasonic coagulation and 2.5 mm linear staplers; preserv-ing the jejuno-jejunostomy (Fig. 1). The greater curvatureof the stomach was opened to accommodate the circularstapler. The gastrogastric anastomosis was performed usinga 25-mm anvil (OrVil, Autosuture, Norwalk, CT) passedtransorally through a small opening in the stapled gastricpouch (Fig. 2), using a technique similar to the one used tocreate a standard gastrojejunostomy, but with a 4.8-mmstaple height stapler. The OrVil 25-mm combines the anvilhead, secured in the tilted position, mounted on a 90-cmlong polyvinyl chloride delivery tube, and secured to thetube with a suture. The polyvinyl chloride delivery tube isinserted through the patient’s mouth, delivered through asmall opening in the stapled gastric pouch, and pulled fromone of the abdominal port sites to assist bringing the anvilshaft into the gastric pouch. Once the anvil shaft has beenexteriorized through the gastric pouch, the suture that holdsit to the delivery tube is cut and the tube is disconnectedfrom the anvil while holding the anvil in place. Theanastomosis was completed by joining the anvil to an

end-to-end circular stapler (EEA XL 25 mm with 4.8-mmstaples, Autosuture, Norwalk, CT) inserted into an openingof the greater curvature of the stomach (Fig. 2). Then, theEEA stapler and anvil were removed, and the anastomosiswas inspected and reinforced at the corners with 2-0 braidedpolyester sutures. If reversal without a sleeve gastrectomywas chosen, the greater curvature of the stomach openingwas closed using an additional firing of a 3.5-mm linearstapler (Fig. 3). If reversal with a sleeve gastrectomy waschosen, the gastroepiploic arcade was divided about 4 cmfrom the pylorus and the gastric fundus completely mobi-lized. A 12-mm (36 FR) gastroscope was inserted underdirect endoscopic visualization through the gastrogastricanastomosis into the duodenum and the sleeve created bysequential firings of linear staplers (4.8 mm height in thegastric antrum and 3.5 mm height in the gastric body andfundus) while taking care not to encroach on the newlycreated gastrogastric anastomosis (Figs. 4 and 5). Sutureline reinforcement was routinely used while creating themodified sleeve, and a leak test was performed.

Postoperative care

On postoperative day 1, all patients underwent an upperGI radiologic examination under fluoroscopic guidance withgastrografin initially, followed by thin diluted barium. After

Fig. 2. Gastrogastric anastomosis: 25 mm transoral anvil in the gastricpouch being connected to the 4.8 mm, 25 mm circular stapler inserted inthe excluded stomach.

Laparoscopic Reversal of Gastric Bypass / Surgery for Obesity and Related Diseases 10 (2014) 36–43 39

imaging was reviewed, a liquid diet was started, andpatients were discharged when tolerating a pureed diet.

Statistical analysis

Data are summarized as mean and standard deviationunless otherwise stated. Changes in continuous variableswere compared among patients using two-tailed paired ttests. Statistical significance was considered to be P r .05.SPSS, version 13.0.1 (SPSS Inc., Chicago, IL) was used forall statistical analyses.

Fig. 3. Final aspect—laparoscopic reversal to normal anatomy.

Results

From March 2011 to October 2012, 5 patients (4 femaleand 1 male) underwent laparoscopic reversal of RYGB tonormal anatomy (n = 2) or modified sleeve gastrectomy(n = 3). Mean age was 43 (range, 38-49), mean body massindex (BMI, weight in kilograms divided by the square ofheight in meters) before index RYGB was 43 (range 38-49),and on average, index RYGB was done 4.6 years (range 3to 8 years) before reversal. Average BMI immediatelybefore reversal was 28 (range 25-33).The indications for reversal were medically refractory

hyperinsulinemic hypoglycemia (n = 3), recalcitrant hypo-calcemia with hypoparathyroidism (n = 1), and

hyperinsulinemic hypoglycemia combined with recalcitranthypocalcemia with hypoparathyroidism (n = 1).All patients with hyperinsulinemic hypoglycemia had

multiple documented episodes of hypoglycemia unaware-ness/neuroglycopenia and/or seizures. The average docu-mented number of hypoglycemic events per week were 18.5(range 8 to 35). Before reversal, the oral glucose tolerancetest documented normal fasting levels of insulin (6.1 � 2.9mU/mL) and glucose (82.6 � 10.9 mg/dL), followed byhyperinsulinemia at 30 minutes (227.3 � 113.3 mU/mL)and hypoglycemia at 60–120 minutes (50 � 11.3 mg/dL).Both patients with recalcitrant hypoparathyroidism had

multiple hospital admissions and/or emergency room visitsfor severe, symptomatic hypocalcemia despite maximumoral replacement.Before reversal, all patients had a laparoscopic G-tube

placed in the excluded stomach. During the 2 weeks thatthey received nutritional supplementation through the G-tube, the patients with medically refractory hyperinsuline-mic hypoglycemia reported no hypoglycemia symptoms.No patient developed hypoglycemia during the mealtolerance test administered through the G-tube.Laparoscopic reversal was offered 8–12 weeks after the

laparoscopic G-tube was placed. Laparoscopic reversal wassuccessfully accomplished in all patients. The average

Fig. 4. Initial gastric stapling to create a modified sleeve gastrectomy.

Fig. 5. Final aspect – laparoscopic reversal to modified sleeve gastrectomy(excised stomach is then removed from the abdominal cavity).

G. M. Campos et al. / Surgery for Obesity and Related Diseases 10 (2014) 36–4340

laparoscopic reversal surgery duration was 175 minutes(range 125–230 min), and estimated blood loss was 50 mL(range 30–100 mL). Three 30-day postoperative complica-tions occurred: a limited postoperative bleed (without GImanifestations, most likely from intraabdominal staplerlines or dissection sites) that required transfusion of 3 unitsof red blood cell, a superficial trocar site infection, and areadmission for gallstone pancreatitis that was treated bylaparoscopic cholecystectomy. Average length of stay was 3days (range 2 to 5). One patient developed a symptomatictrocar site hernia at 9 months follow-up that was treatedwith surgery.At a mean follow-up of 12 months (range 3 to 22 months),

no additional episodes of neuroglycopenia occurred. Theaverage number of documented hypoglycemic events perweek decreased to 1.5 � 1.9, range 0 to 4 (P = .05). Patientshad no or minimal symptoms with the documented episodes.Hypoparathyroidism became amenable to oral replacementtherapy. Both patients are maintaining serum calcium at agoal of around 8 mg/dL; one receives calcium citrate 600mg/d, calcitriol 2 mcg/d, and vitamin D2, and the otherreceives calcium citrate 1,200 mg/d, calcitriol 1 mcg/d, andvitamin D2.The average BMI at last follow-up after reversal was 28.4

(range, 21–41); thus, BMI did not change significantly afterreversal (P = .9). Two patients gained weight: one patient

with reversal to normal anatomy (pre-reversal BMI of 25 toBMI of 31 at 22 months follow-up) and one patient after amodified sleeve gastrectomy (pre-reversal BMI of 33 toBMI of 41 at 10 month follow-up), and the other 3 patientslost weight (BMI 26 to 21, 33 to 26, and 29 to 23).

Discussion

In this study, the technique for laparoscopic reversal ofRYGB to normal anatomy or modified sleeve gastrectomyusing a circular stapler for the gastrogastrostomy isdescribed. We also show that laparoscopic reversal maybe a therapeutic option for selected patients with medicallyrefractory hyperinsulinemic hypoglycemia with hypoglyce-mia unawareness and/or recalcitrant hypocalcemia secon-dary to hypoparathyroidism.Laparoscopic reversal of RYGB to normal anatomy for

reasons other than hypoglycemia [18] and sleeve gastrec-tomy for weight regain after RYGB [19] were originallyreported by Dapri G et al., and laparoscopic reversal ofRYGB to sleeve gastrectomy was recently described byAnderwald et al. [20] as an option for intractable dumpingsyndrome and excessive weight loss. To our knowledge,this is the first case series of laparoscopic reversal of RYGBused to treat hyperinsulinemic hypoglycemia with hypo-glycemia unawareness and/or recalcitrant hypocalcemia dueto hypoparathyroidism. In addition, our technique for

Laparoscopic Reversal of Gastric Bypass / Surgery for Obesity and Related Diseases 10 (2014) 36–43 41

reconstruction, using a circular stapler for the gastrogas-trostomy is, in our opinion, simpler, safer, and more easilyreproduced. The resection of the alimentary limb may notbe necessary or desired; thus, a possible technical alter-native could be to divide the jejuno-jejunostomy andreconnect the bilio-pancreatic limb to the proximal end ofthe alimentary limb. There were some postsurgical compli-cations, but all were resolved in a short time frame withappropriate intervention. Overall, the treatment required forall postoperative complications was relatively minimal incomparison with that needed for preoperative endocrineconditions. In view of the symptomatic improvement in allpatients, we propose that laparoscopic reversal of RYGBshould be considered a well-tolerated and effective treatmentoption for hyperinsulinemic hypoglycemia with hypoglyce-mic unawareness and for recurrent severe hypocalcemia dueto hypoparathyroidism.The etiology, prevalence, diagnostic algorithm, and treat-

ment recommendations for hyperinsulinemic hypoglycemiaafter RYGB are still controversial [21]. The prevalence ofsymptomatic hyperinsulinemic hypoglycemia after RYGBis estimated to be from .3%–1% [22], and asymptomaticpostprandial hypoglycemia may have a prevalence of up to72% after ingestion of large amounts of carbohydrate[23,24]. Symptomatic hyperinsulinemic hypoglycemia hasbeen described many years ago and is known to mostgastrointestinal and general surgeons and the generalmedical community as part of the commonly describeddumping syndrome after gastric resection [25,26]. For mostRYGB patients. dumping symptoms may be beneficial,because patients learn to avoid dense foods with simplecarbohydrates, and even when persistent, these symptomscan be managed with additional dietetic counseling andmedications, without revisional surgery in most patients[27]. It has been shown that the anatomic changes withRYGB, i.e., the small gastric pouch connected without asphincter to the jejunum, lead to changes in postprandialglucose kinetics [1] and in gastrointestinal and pancreatichormones that are known to regulate blood glucose andaffect other glucose regulatory mechanisms [28]. Thoughthese changes are beneficial to most patients with type 2diabetes and also to nondiabetic patients with underlyinginsulin resistance [28], the changes may lead to recurrentsymptoms of hyperinsulinemic hypoglycemia in a fewpatients. In the small subset of patients who developpostprandial hypoglycemia after RYGB that is recalcitrantto dietary and medical therapy, recurrent hypoglycemia canlead to hypoglycemic unawareness, seizures, and significantdisability.Hypoglycemia is important because it is associated with

deprivation of the sole source of fuel to the brain, whichshows detectable malfunction at plasma glucose of around54 mg/dL. With persistence of hypoglycemia, this canevolve to confusion, reduced conscious level, coma, seiz-ures, and even death. The standard regulatory mechanisms

activated to respond to hypoglycemia involve reduction inendogenous insulin secretion, increased release of pancre-atic glucagon, increase in hepatic and glucose production byglycolysis and gluconeogenesis, and activation of thesympathetic nervous system with adrenaline release, growthhormone, and cortisol [29]. After RYGB, these regulatorymechanisms are affected by the changes related to RYGBanatomy. The postprandial changes in glucose kinetics andGI and pancreatic hormones likely affect some of thedynamics involved in the body response to hypoglycemia,and thus adds to the difficulty in the management of thesepatients.Earlier reports suggested that increased pancreatic beta

cell mass or nesidioblastosis was causative in patients withhyperinsulinemic hypoglycemia [12], and some centershave offered subtotal or total pancreatectomy as a surgicalsolution for medically refractory hyperinsulinemic hypo-glycemia [12,27,30]. However, the data from the originalpublication that supported the existence of novo nesidio-blastosis after RYGB [12] has been disputed using adifferent control group from autopsy specimens [13], so itremains unclear whether pancreatectomy actually addressesthe underlying pathophysiology leading to hypoglycemia.Subtotal or total pancreatectomy has elevated perioperativemorbidity and may lead to brittle diabetes and otherdysfunctions related to extensive or complete pancreaticresection [31,32]. Additionally, partial pancreatectomy doesnot lead to resolution of symptoms in some patients [30].Therefore, we propose that laparoscopic reversal of RYGBprovides a safer and potentially more effective treatmentoption for recalcitrant hypoglycemia.After RYGB, calcium and vitamin D absorption is

impaired, and patients with combined hypoparathyroidismand RYGB are at greater risk for persistent and recurrentsevere hypocalcemia [16,33], as exemplified in our patients.Hypoparathyroidism is a known complication of totalthyroidectomy, and with high-volume endocrine surgeons,the risk of definitive hypoparathyroidism is low (approx-imately .7%). However, higher rates are reported whenthyroidectomy is done by lower volume surgeons [34]. Therisk of hypoparathyroidism is acceptable in a normalpopulation, because the traditional treatment of hypopar-athyroidism after total thyroidectomy is successful in mostpatients with ingestion and absorption of high doses ofcalcium and vitamin D. However, in patients with RYGB,total thyroidectomy needs to be carefully considered. Forexample, one of our patients had a total thyroidectomy afterRYGB for a benign goiter, which may not be a necessarysurgery given the potential risks. If necessary, total thyroi-dectomy in patients with a history of RYGB should beperformed only by experienced surgeons, after obtaininginformed consent regarding the increased morbidity ofpotential of hypoparathyroidism. In addition, patients con-sidering RYGB should be carefully screened for history oftotal thyroidectomy and/or hypoparathyroidism. Our 2

G. M. Campos et al. / Surgery for Obesity and Related Diseases 10 (2014) 36–4342

patients had severe recurrent hypocalcemia, requiring fre-quent intravenous calcium infusions, hospitalizations, anddisability. Postoperatively, they were controlled with tradi-tional oral calcium and vitamin D replacement. We proposethat laparoscopic reversal of RYGB is a safe, effectivetreatment for life-threatening hypocalcemia due to hypopar-athyroidism in individuals with RYGB.A common concern of all patients was weight regain, but

all opted for revisional surgery in view of their debilitatingsymptoms. Laparoscopic reversal to a modified sleevegastrectomy may offer the better chance to decrease thepossibility for weight regain. However, sleeve gastrectomyalso is associated with changes in glucose kinetics and gutand pancreatic hormones; although to a lesser degree than isseen after RYGB, the changes may possibly leave thesepatients still at some risk for hypoglycemic events [35]. Forthese reasons, 2 patients in our series opted for reversal tonormal anatomy as opposed to reversal to sleeve gastrec-tomy. In addition, the insertion of a G-tube may not be anessential step in all these patients, but further research isneeded to define best practices. Limitations of our studyinclude a small sample size, relatively short follow-up, andlack of detailed metabolic data to document the changes inglucose kinetics, calcium, and hormone levels.

Conclusions

In view of these limitations, we have shown thatlaparoscopic reversal of RYGB to normal anatomy ormodified sleeve gastrectomy is feasible and may success-fully reduce hypoglycemic events and significantly improvesymptoms in selected patients with medically refractoryhyperinsulinemic hypoglycemia and/or recalcitrant hypo-calcemia with hypoparathyroidism.

Disclosures

The authors have no commercial associations that mightbe a conflict of interest in relation to this article.

References

[1] Rodieux F, Giusti V, D'Alessio DA, Suter M, Tappy L. Effects ofgastric bypass and gastric banding on glucose kinetics and guthormone release. Obesity (Silver Spring) 2008;16:298–305.

[2] Salameh BS, Khoukaz MT, Bell RL. Metabolic and nutritionalchanges after bariatric surgery. Expert Rev Gastroenterol Hepatol2010;4:217–23.

[3] Mingrone G, Castagneto-Gissey L. Mechanisms of early improve-ment/resolution of type 2 diabetes after bariatric surgery. DiabetesMetab 2009;35:518–23.

[4] Bal BS, Finelli FC, Shope TR, Koch TR. Nutritional deficiencies afterbariatric surgery. Nat Rev Endocrinol 2012;8:544–56.

[5] Arterburn DE, Bogart A, Sherwood NE, et al. A multisite study oflong-term remission and relapse of type 2 diabetes mellitus followinggastric bypass. Obes Surg 2013;23:93–102.

[6] Carlsson LM, Peltonen M, Ahlin S, et al. Bariatric surgery andprevention of type 2 diabetes in Swedish obese subjects. N Engl JMed 2012;367:695–704.

[7] Kellogg TA, Bantle JP, Leslie DB, et al. Postgastric bypass hyper-insulinemic hypoglycemia syndrome: characterization and response toa modified diet. Surg Obes Relat Dis 2008;4:492–9.

[8] Kapoor RR, James C, Hussain K. Advances in the diagnosis andmanagement of hyperinsulinemic hypoglycemia. Nat Clin PractEndocrinol Metab 2009;5:101–12.

[9] Salinger EM, Moore JT. Profound hypocalcemia after near-totalthyroidectomy in a Roux-en-Y gastric bypass patient. Am Surg2010;76:E7–8.

[10] Durr ML, Saunders JR, Califano JA, Tufano RP, Koch WM, Ha PK.Severe hypocalcemia complicating thyroid surgery after Roux-en-Ygastric bypass procedure. Arch Otolaryngol Head Neck Surg2009;135:507–10.

[11] Clancy TE, Moore FD Jr, Zinner MJ. Post-gastric bypass hyper-insulinism with nesidioblastosis: subtotal or total pancreatectomy maybe needed to prevent recurrent hypoglycemia. J Gastrointest Surg2006;10:1116–9.

[12] Service GJ, Thompson GB, Service FJ, Andrews JC, Collazo-ClavellML, Lloyd RV. Hyperinsulinemic hypoglycemia with nesidioblasto-sis after gastric-bypass surgery. N Engl J Med 2005;353:249–54.

[13] Meier JJ, Butler AE, Galasso R, Butler PC. Hyperinsulinemichypoglycemia after gastric bypass surgery is not accompanied byislet hyperplasia or increased beta-cell turnover. Diabetes Care2006;29:1554–9.

[14] Butler AE, Galasso R, Matveyenko A, Rizza RA, Dry S, Butler PC.Pancreatic duct replication is increased with obesity and type 2diabetes in humans. Diabetologia 2010;53:21–6.

[15] Butler PC, Meier JJ, Butler AE, Bhushan A. The replication of betacells in normal physiology, in disease and for therapy. Nat Clin PractEndocrinol Metab 2007;3:758–68.

[16] Miñambres I, Chico A, Pérez A. Severe hypocalcemia due to vitaminD deficiency after extended Roux-en-Y gastric bypass. J Obes Epub2011 May 18.

[17] Agich GJ. Ethics and innovation in medicine. J Med Ethics 2001;27:295–6.

[18] Dapri G, Cadiere GB, Himpens J. Laparoscopic reconversion ofRoux-en-Y gastric bypass to original anatomy: technique andpreliminary outcomes. Obes Surg 2011;21:1289–95.

[19] Dapri G, Cadiere GB, Himpens J. Laparoscopic conversion of Roux-en-Y gastric bypass to sleeve gastrectomy as first step of duodenalswitch: technique and preliminary outcomes. Obes Surg 2011;21:517–23.

[20] Anderwald CH, Tura A, Promintzer-Schifferl M, et al. Alterationsin gastrointestinal, endocrine, and metabolic processes after bari-atric Roux-en-Y gastric bypass surgery. Diabetes Care 2012;35:2580–7.

[21] Ceppa EP, Ceppa DP, Omotosho PA, Dickerson JA, 2 nd, Park CW,Portenier DD. Algorithm to diagnose etiology of hypoglycemia afterRoux-en-Y gastric bypass for morbid obesity: case series and reviewof the literature. Surg Obes Relat Dis 2012;8:641–7.

[22] Marsk R, Jonas E, Rasmussen F, Naslund E. Nationwide cohort studyof post-gastric bypass hypoglycaemia including 5,040 patients under-going surgery for obesity in 1986–2006 in Sweden. Diabetologia2010;53:2307–11.

[23] Goldfine AB, Mun EC, Devine E, et al. Patients with neuroglycopeniaafter gastric bypass surgery have exaggerated incretin and insulin secretoryresponses to a mixed meal. J Clin Endocrinol Metab 2007;92:4678–85.

[24] Roslin M, Damani T, Oren J, Andrews R, Yatco E, Shah P. Abnormalglucose tolerance testing following gastric bypass demonstratesreactive hypoglycemia. Surg Endosc 2011;25:1926–32.

Laparoscopic Reversal of Gastric Bypass / Surgery for Obesity and Related Diseases 10 (2014) 36–43 43

[25] Banerjee A, Ding Y, Mikami DJ, Needleman BJ. The role of dumpingsyndrome in weight loss after gastric bypass surgery. Surg Endosc2012;27:1573–8.

[26] Hammer HF. Medical complications of bariatric surgery: focus onmalabsorption and dumping syndrome. Dig Dis 2012;30:182–6.

[27] Mathavan VK, Arregui M, Davis C, Singh K, Patel A, Meacham J.Management of postgastric bypass noninsulinoma pancreatogenoushypoglycemia. Surg Endosc 2010;24:2547–55.

[28] Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypass forobesity: mechanisms of weight loss and diabetes resolution. J ClinEndocrinol Metab 2004;89:2608–15.

[29] Mitrakou A, Mokan M, Ryan C, Veneman T, Cryer P, Gerich J.Influence of plasma glucose rate of decrease on hierarchy of responsesto hypoglycemia. J Clin Endocrinol Metab 1993;76:462–5.

[30] Patti ME, McMahon G, Mun EC, et al. Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inap-propriate insulin secretion and pancreatic islet hyperplasia. Diabeto-logia 2005;48:2236–40.

[31] Slezak LA, Andersen DK. Pancreatic resection: effects on glucosemetabolism. World J Surg 2001;25:452–60.

[32] Mezhir JJ. Management of complications following pancreaticresection: an evidence-based approach. J Surg Oncol 2013;107:58–66.

[33] Palal B, Sinsakul M, Reutrakul S. Life-threatening hypocalcemiafollowing subtotal parathyroidectomy in a patient with renal failureand previous Roux-en-Y gastric bypass surgery. Case Report Endo-crinol. Epub 2011 July 5.

[34] Zambudio AR, Rodriguez J, Riquelme J, Soria T, Canteras M, ParrillaP. Prospective study of postoperative complications after totalthyroidectomy for multinodular goiters by surgeons with experiencein endocrine surgery. Ann Surg 2004;240:18–25.

[35] Dimitriadis E, Daskalakis M, Kampa M, Peppe A, Papadakis JA,Melissas J. Alterations in gut hormones after laparoscopic sleevegastrectomy: prospective clinical and laboratory investigational study.Ann Surg 2012;257:647–54.