Complications of Bariatric Surgery Dumping Syndrome Reflux and Vitamin Deficiencies 2014 Best...

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See discussions, stats, and author profiles for this publication at: http://www.researchgate.net/publication/263812561 Complications of bariatric surgery: Dumping syndrome, reflux and vitamin deficiencies ARTICLE in BAILLIÈRE&#X027 S BEST PRACTICE AND RESEARCH IN CLINICAL GASTROENTEROLOGY · AUGUST 2014 Impact Factor: 3.48 · DOI: 10.1016/j.bpg.2014.07.010 CITATIONS 3 READS 366 2 AUTHORS, INCLUDING: Eveline Deloose University of Leuven 16 PUBLICATIONS 27 CITATIONS SEE PROFILE Available from: Eveline Deloose Retrieved on: 08 October 2015

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Seediscussions,stats,andauthorprofilesforthispublicationat:http://www.researchgate.net/publication/263812561

Complicationsofbariatricsurgery:Dumpingsyndrome,refluxandvitamindeficiencies

ARTICLEinBAILLIÈRE&#X027SBESTPRACTICEANDRESEARCHINCLINICALGASTROENTEROLOGY·AUGUST2014

ImpactFactor:3.48·DOI:10.1016/j.bpg.2014.07.010

CITATIONS

3

READS

366

2AUTHORS,INCLUDING:

EvelineDeloose

UniversityofLeuven

16PUBLICATIONS27CITATIONS

SEEPROFILE

Availablefrom:EvelineDeloose

Retrievedon:08October2015

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Best Practice & Research Clinical Gastroenterology 28 (2014) 741e749

Contents lists available at ScienceDirect

Best Practice & Research ClinicalGastroenterology

15

Complications of bariatric surgery: Dumpingsyndrome, reflux and vitamin deficiencies

Jan Tack, M.D., Ph.D., Professor of Medicine *,Eveline Deloose, M.Sc., Ph.D. fellowTranslational Research Center for Gastrointestinal Disorders (TARGID), University of Leuven, Leuven, Belgium

Keywords:Bariatric surgeryGastro-esophageal reflux diseaseRoux-en-Y gastric bypassSleeve gastrectomyDumping syndromeVitamin deficienciesMalabsorptionWernicke encephalopathy

* Corresponding author. Department of PathopHerestraat 49, B-3000 Leuven, Belgium. Tel.: þ32

E-mail address: [email protected] (J. T

http://dx.doi.org/10.1016/j.bpg.2014.07.0101521-6918/© 2014 Published by Elsevier Ltd.

a b s t r a c t

Bariatric surgical procedure are increasingly and successfullyapplied in the treatment of morbid obesity. Nevertheless, theseprocedures are not devoid of potential long-term complications.Dumping syndrome may occur after procedures involving at leastpartial gastric resection or bypass, including Roux-en-Y gastricbypass (RYGB) and sleeve gastrectomy. Diagnosis is based onclinical alertness and glucose tolerance testing. Treatment mayinvolve dietary measures, acarbose and somatostatin analogues, orsurgical reintervention for refractory cases. Gastro-esophagealreflux disease (GERD) can be aggravated by vertical banded gas-troplasty and sleeve gastrectomy procedures, but pre-existingGERD may improve after RYGB and with adjustable gastric band-ing. Nutrient deficiencies constitute the most important long-termcomplications of bariatric interventions, as they may lead to hae-matological, metabolic and especially neurological disorders whichare not always reversible. Malabsorptive procedures, poor post-operative nutrient intake, recurrent vomiting and poor compliancewith vitamin supplement intake and regular follow-up areimportant risk factors. Preoperative nutritional assessment andrigourous postoperative follow-up plan with administration ofmulti-vitamin supplements and assessment of serum levels isrecommended in all patients.

© 2014 Published by Elsevier Ltd.

hysiology, Division of Gastroenterology, University Hospital Gasthuisberg,16 34 42 25; fax: þ32 16 34 44 19.ack).

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Introduction

Bariatric surgical procedure are currently the most effective treatment modality to induce weightloss and reduce complications of obesity. However, bariatric interventions also inducemajor changes inthe anatomy and function of the gastrointestinal tract [1].

Several main types of bariatric surgery have been used over the last decades, and these include thebiliopancreatic diversion, the Roux-en-Y gastric bypass, the vertical banded gastroplasty and thelaparoscopic adjustable gastric band and the sleeve gastrectomy. The vertical banded gastroplasty,laparoscopic adjustable gastric band and sleeve gastrectomy are considered restrictive procedures,deriving their efficacy from interference with the volume capacity of the proximal stomach. The bil-iopancreatic diversion and the Roux-en-Y gastric bypass are considered malabsorptive procedures, asthey interfere with normal digestive and absorptive processing of food, although the latter is consid-ered mainly restrictive [1].

In this paper, potential adverse consequences of bariatric surgical procedures such as dumpingsyndrome, gastro-esophageal reflux and nutritional deficiencies, are summarized, with a focus onclinical management aspects.

Dumping syndrome after bariatric surgery

Dumping syndrome is characterized by vasomotor and gastrointestinal symptoms which can beattributed to rapid gastric emptying or rapid exposure of the small intestine to nutrients [2]. Dumpingsyndrome occurs readily after partial or complete gastrectomy, and hence is a potential complication ofsome bariatric surgical procedures involving partial gastrectomy. Furthermore, dumping syndrome canoccur as a consequence of damage to the vagus nerve [2].

In dumping syndrome, symptoms are typically triggered by meal ingestion and are somewhatarbitrarily subdivided into ‘early’ and ‘late’ dumping symptoms (Table 1) [2,3]. Early dumping symp-toms occur in response to the rapid passage of hyperosmolar nutrients into the small bowel, and theyreflect the release of gastrointestinal hormones whichmay be accompanied by a shift of fluids from theintravascular compartment to the lumen. Several candidate peptides can be involved in this response,including enteroglucagon, Vasoactive Intestinal Peptide, Peptide YY, pancreatic polypeptide and neu-rotensin. Late dumping occurs between one and three hours after the meal and is characterized bysymptoms of hypoglycaemia. Rapid gastric emptying leads to a high glucose concentration in the in-testinal lumen, from which it is rapidly absorbed. This is a trigger for peak insulin secretion, butbecause of the long half-life of insulin and the transient character of the initial rise in glycaemia, hy-poglycemia may occurs when all available glucose has been absorbed [2]. A recent paper providedevidence for a key role of glucagon-like-peptide-1 in the pathogenesis of late hypoglycemia aftergastric bypass [4].

Most patients present with early dumping, or a combination of both early and late dumping. Iso-lated late dumping, i.e. patients in whom hypoglycemia is the only symptoms, is very rare. In severecases, dumping syndrome is associated with significant impairment of quality-of-life [3] and maycontribute to significant weight loss by avoidance of food intake.

After bariatric surgery, dumping syndrome has mainly been reported in patients who underwentRoux-en-Y gastric bypass and other interventions involving partial gastrectomy. After gastric bypass,

Table 1Symptoms in dumping syndrome.

Early dumping� Gastrointestinal symptomsAbdominal pain, diarrhoea, borborygmi. bloating, nausea� Vasomotor symptomsFlushing, palpitations. perspiration, tachycardia, hypotension, syncopeLate dumping� HypoglycemiaPerspiration, palpitations, hunger, weakness, confusion, tremor, syncope

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around 40% of patients have dumping syndrome symptoms [5]. It has been speculated that dumpingsyndrome symptoms might be an essential component of the weight reduction after bariatric surgery,due to adverse effects on food tolerance and intake. However, a prospective series showed that weightloss after Roux-en-Y gastric bypass was not determined by the presence of dumping syndrome [5].

So-called restrictive interventions like sleeve gastrectomy would be expected not to predispose todumping syndrome. However, in two prospective studies, it was reported that up to 40% of patients hadsymptoms suggestive of dumping syndrome 6e12 months after sleeve gastrectomy [6,7]. The mech-anisms underlying dumping syndrome after sleeve gastrectomy remain to be elucidated, but it is clearthat this bariatric intervention also carries a risk of inducing both early and late dumping symptoms.

Dumping syndrome should be suspected in case of suggestive symptoms after a predisposingsurgical intervention. Symptom-based questionnaires, like Sigstad's score (Table 2) or Arts' dumpingquestionnaire, have been used to help and detect clinically meaningful dumping symptoms [2,3,6].Objective confirmation of the diagnosis is obtained by a modified oral glucose challenge test: 50 g ofglucose are ingested with water and for 3 h at 30-min intervals glycaemia, haematocrit and pulse rateare noted. The test is considered positive if there is initial hyperglycemia and late hypoglycaemia(<60 mg/dl or 3.33 mmol/l) or an early rise in haematocrit of >3% or an early rise in pulse rate of>10 bpm [2].

Initial therapy for dumping syndrome consists of dietary measures: patients are instructed to takesmaller more frequent meals (up to 6 per day) and to avoid drinking with meals or the first2 h postprandially. The latter aims at decreasing the spread of triggering nutrients over a largersegment of small intestine. Importantly, patients are taught to avoid rapidly absorbed sugars andlactose [2]. As reported in the literature, viscous food additives like pectin, guar gum and glucomannancan be added to meals to slow gastric emptying and intestinal spread, but these are experienced asunpalatable by the patients andmay be less effective after partial gastrectomy. Easier to use is acarbose,an inhibitor of intestinal alpha-glucosidase, which slows carbohydrate digestion and thus bluntspostprandial hyperglycemia and rebound hypoglycemia [2]. Usage of acarbose is limited by its lack ofefficacy for early dumping symptoms and occurrence of side-effects of carbohydrate maldigestion suchas flatulence, bloating and diarrhoea [2].

If these first-line measures fail, somatostatin analogues can be considered. These agents are themost effective treatment options available for dumping syndrome, as they are effective for both earlyand late dumping symptoms [3]. Somatostatin analogues can be administered either subcutaneouslythree times daily, or intramuscularly once every two to four weeks as a slow release formulation, andthey slow gastric emptying and inhibit the release of several gastrointestinal peptides implicated indumping syndrome pathophysiology [2,3,8]. In the management of dumping syndrome, initial therapyis usually a short-acting agent administered subcutaneously, e.g. 50e100 mg octreotide s.c. In case ofgood efficacy and tolerance, a slow release preparation can be used, e.g. octreotide L.A.R. 20 mg or

Table 2Sigstad's scoring system for diagnosing dumping syndrome. A total score>7 is suggestive of dumping syndrome, whereas a score<4 suggests other diagnoses.

Shock þ5Fainting, syncope, unconsciousness þ4Desire to lie or sit down þ4Breathlessness, dyspnoea þ3Weakness, exhaustion þ3Sleepiness, drowsiness, apathy, falling asleep þ3Palpitation þ3Restlessness þ2Dizziness þ2Headaches þ1Feeling of warmth, sweating, pallor, clammy skin þ1Nausea þ1Abdominal fullness, meteorism þ1Borborygmus þ1Eructation �1Vomiting �4

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20 mg i.m [2,3]. Pasireotide, a novel and more broadly acting somatostatin analogue, is currentlyundergoing phase 2 testing for the treatment of postoperative dumping [8].

In exceptionally difficult-to-manage patients, re-do surgery can be considered to reconstruct agastric reservoir, to add a restrictive intervention (band around the pouch, revision of pouch, endo-scopic procedures), to undo the surgery if possible, or to insert a short anti-peristaltic loop [2,9].

Gastro-esophageal reflux after bariatric surgery

Obesity is amajor risk factor for gastro-esophageal reflux disease [10] and it is important to considerthis co-morbidity in many patients in whom bariatric surgery is planned. Weight loss alone, forinstance by dietary interventions, may decrease GERD, as has been shown in controlled trials [11,12],although conflicting data have also been found [13]. The effect of bariatric surgery on GERD seems todiffer according to the type of surgery.

All but one of the available studies show improvement of GERD after Roux-en-Y gastric bypasssurgery. Two comparative studies found that the gastric bypass was superior to gastric banding inimproving GERD symptoms [13,14]. Although there are only limited mechanistic data on GERD beforeand after gastric bypass surgery, it seems that a consistent beneficial effect can be found. In a pro-spective study incorporating esophageal manometry and ambulatory pH/impedance monitoring,Roux-en-Y gastric bypass was associated with decreased lower esophageal sphincter pressure,decreased esophageal body contractile amplitude and significantly lower esophageal acid exposure,especially in the upright position [15]. Disappearance of the acid pocket at the gastro-esophagealjunction after Roux-en-Y gastric bypass has also been implicated in its favourable effects on GERD [16].

Other types of bariatric surgery are associated with more variable effects on GERD. After verticalbanded gastroplasty, conflicting effects on GERD have been reported: five out of eight studies found noeffect, one found worsening of GERD and two found improvement. Taken together, these studiessuggest that the putative beneficial effect of weight loss on GERD was counteracted by other effects ofthe procedure. Accumulation of gastric acid in the pouch has been implicated as a mechanism thatpromotes GERD in these patients [17].

Even more diverse outcomes were reported after laparoscopic adjustable gastric banding pro-cedures. While only two studies found no effect, six studies showed a positive effect on GERDsymptoms, in two of them only when preoperative esophageal motility was effective and when nodilated pouch occurred. Two studies found worsening of GERD mainly based on objective GERDmeasurements, and four studies found conflicting outcomes on symptoms or objective measure ofGERD [13]. The mechanisms implicated in worsening of GERD after gastric banding include not onlyaccumulation of acid in the proximal stomach compartment, but also pre-existing poor esophagealmotility. It has been suggested that the presence of a hiatal hernia may increase the risk of worseningGERD after laparoscopic gastric banding [13], but two studies prospectively evaluating this were notable to find a worse prognosis in case of hernia [18,19].

After sleeve gastrectomy, half of the studies reported an increase in GERD symptoms, while theother half found no such effect [20,21]. On one hand, some patients see improvement of GERD aftersleeve gastrectomy, and this may be related to decreased gastric acid production and decreased bodyweight [20,21]. On the other hand, based on a large database, it was shown that the outcomes of sleevegastrectomy are less favourable in case of pre-existing GERD, and it has been suggested that pre-existing GERD could be considered a contra-indication [22]. A hiatal hernia is considered a contra-indication for sleeve gastrectomy, unless it can be repaired. There is also evidence that new-onsetGERD symptoms may occur after sleeve gastrectomy in a group of patients who were previouslyasymptomatic. The mechanisms implicated in increased GERD include decreased gastric compliance,which may increase intragastric pressure and thereby promote reflux, as well as reshaping of the angleof Hiss. However, these studies were mainly based on symptom reporting. A recent prospective studyused manometry and pH/impedance monitoring before and after a sleeve gastrectomy in 25 patients[23]. After sleeve gastrectomy, the incidence of ineffective peristalsis increased, resulting in anincreased occurrence of swallows with complete bolus transit. Acid, but especially non-acid refluxepisodes were significantly increased after sleeve gastrectomy. The latter was attributable to increasedintragastric pressure, probably reflecting decreased gastric compliance and leading to postprandial

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regurgitation events [23]. While this study found no significant effect on lower esophageal sphincterpressure, another prospective study reported that sleeve gastrectomy was associated with a significantincrease in sphincter pressure, which was already present in the early postoperative phase and henceindependent of weight loss [24].

Nutritional deficiencies after bariatric surgery

Bariatric surgical procedures have been associated with nutritional deficiencies, but their preva-lence and nature depend on the type of surgery. Laparoscopic gastric banding, conceptually arestrictive rather than amalabsorptive intervention, is less frequently associated with deficiencies. Oneexception is the occurrence of early postoperative thiamine deficiency. Sleeve gastrectomy was alsoconceived as a restrictive intervention. Similar to the laparoscopic gastric banding, it leads lessfrequently to nutritional deficiencies, especially if patients adhere to intake of prescribed supplements.

The Roux-en-Ygastric bypass is a malabsorptive intervention and, hence, is associated with a higherprevalence of nutritional deficiencies. After this intervention, the exposure of food to bile andpancreatic juices is delayed, thereby diminishing completeness of digestion and absorption. Bil-iopancreatic diversion is a procedure in which a large section of small intestine is bypassed, and henceit carries the highest risk for nutritional deficiencies [25,26]. The Roux-en-Y gastric bypass was shownto decrease fat and protein, but not carbohydrate absorption [26]. After Roux-en-Y gastric bypass, thelength of the biliopancreatic limb is correlated to the amount of fat malabsorption, probably becausethis is inversely correlated with the length of the common channel, and because it delays contact ofnutrients with digestive enzymes [26]. Furthermore, a longer biliopancreatic limb may promote bac-terial overgrowth and further impaired fat digestion [26].

Another variable is the presence of micronutrient deficiencies prior to the surgery. Indeed, obesityhas been associated with vitamin D and iron deficiency, amongst others. Moreover, dietary restrictionsaimed at obtaining weight loss prior to going to surgery may also affect nutritional status. In general,these aspects are poorly studied and their impact on the postoperative course remain to be elucidatedin detail [25e27].

A common factor to all bariatric surgery is reduced overall nutrient intake in the (early) post-operative phase. Reduced overall intake may be associated with poor intake of specific micro-nutrientsand contribute to occurrence of deficiencies. Dietary adjustments in the immediate postoperativeperiod aim at protein supplementations, to avoid major loss of body protein. In a U.S. consensus, intakeof more than 60 g of protein per day has been recommended after bariatric surgery [25,27]. Prospectivefollow-up of dietary intake of patients after bariatric surgery shows that many do not reach the60 g protein intake, and over time intake of fatty foods and snacks may progressively increase [25e29].

Postsurgical diet and supplementation recommendations as well as recommendations for pre-vention of Wernicke's encephalopathy have been published [30,31]. For patients with Roux-en-Ygastric bypass, adequate intake of protein, more than 1 g/kg ideal body weight/day, is recommendedto prevent protein deficiencies [27]. In case of deficiencies, oral or enteral protein supplements can beadministered, or parenteral nutrition during a few weeks may be necessary in case of extensivecombined deficiencies. In addition, it has been recommended to treat all patients who underwentmalabsorptive surgical interventions with multi-vitamin supplements that contain at least double thedaily recommended dose, as well as 18 mg of elemental iron and 400 ug of folic acid. Ideally thesepreparations should also contain vitamin A, copper and zinc. Furthermore, intake of 2 g of calcium,1000 ug of vitamin B12 and 1000e2000 IU of vitamin D orally [27].

Malabsorption should be considered if patients after bariatric surgery present with abdominal(diarrhoea, abdominal distension, flatulence, abdominal pain and ascites) or general symptoms (per-sisting or excessive weight loss, anaemia, amenorrhoea, impotence, infertility, night blindness,xeropthalmia, peripheral neuropathy, tiredness, fatigue and weakness) [26]. A panel of blood tests canbe assessed, which may include blood cell count, triglycerides, cholesterol, albumin, alkaline phos-phatase, calcium, phosphorus, magnesium, zinc, iron, ferritin, prothrombin time, serum vitamin A,immunoglobulins, parathyroid hormone, serum vitamin D, folic acid, vitamin B12 (or methylmalonicacid if available, which may be more reliable), etc. It has been suggested to perform these test pre-operatively and then at 3- to 6-month intervals in the first 2 years, and later annually, after

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malabsorptive procedures [26,27]. Furthermore, preoperative and annual postoperative dual-energyX-ray bone absorptiometry have been recommended to screen for bone mineral loss and osteopo-rosis occurrence after Roux-en-Y gastric bypass and biliopancreatic diversion [30]. Specific deficienciesmay require specific approaches and supplements, as outlined below.

Thiamine (vitamin B1) deficiency has been reported in 0e29% of patients presenting for bariatricsurgery [25e27]. As this condition may lead to potentially irreversible neurological manifestations,clinical alertness and prompt adequate treatment in case of deficiency are required. Case series reportthiamine deficiencies in 0e30% of the patients who underwent bariatric surgery. Vomiting after bar-iatric intervention is the principal risk factor for developing thiamine deficiency, together with poorfood intake and lack of supplement intake [31]. The presence of vomiting should specifically beaddressed in history taking after bariatric surgery, as some patients do not readily mention thisproblem and consider it a ‘normal’ consequence of the intervention. Intravenous glucose adminis-tration is a risk factor for triggering acute symptomatic vitamin B deficiency leading to interruption ofthe citric acid cycle and lactate acidosis. Clinical manifestations of thiamine deficiency include Wer-nicke's encephalopathy, peripheral neuropathies, nystagmus and ocular palsies, and these can beprecipitated by intravenous infusion of glucose solutions [25e27,31]. Hence, it is recommended toprophylactically administer thiamine 100 mg i.v. when starting intravenous fluids in patients at risk.Prophylactic daily intake of a multi-vitamin preparation containing at least 3 mg of thiamine has beenrecommended after malabsorptive procedures, to be increased to 50 mg in those at risk for Wernicke'sencephalopathy [27]. For therapeutic purposes in symptomatic deficiency, especially with neurologicalsigns, initial doses of 100e500 mg daily intravenously administered are recommended.

Vitamin B12 deficiency has been reported in 0e18% of patients presenting for bariatric surgery[25e27]. Case series report Vitamin B12 deficiencies in 4e62% of the patients who underwent bariatricsurgery, often as a late complications as body stores become only slowly depleted in case of insufficientdietary uptake. Measurement of melthylmalonic acid concentrations in the serum may be a moresensitive marker for vitamin B12 deficiency. A prophylactic oral dose of at least 500 ug daily afterbariatric surgery has been recommended [27]. Factors underlying this deficiency are probably reducedintake of meat, diminished contact of food with gastric acid and decreased secretion of intrinsic factor[25e27]. Symptomatic vitamin B12 deficiency leads to megaloblastic anaemia, myelopathy and neu-ropathy. Supplementation by multi-vitamin preparations seems insufficient in case of vitamin B12deficiency and this may require elevated oral doses of vitamin B12 or parenteral administration. In caseof deficiencies, weekly intramuscular administration of 1000 ug for 8weeks is recommended. In case ofneurological manifestations, daily intramuscular administrations with life-long monthly injections arerecommended.

Folate deficiency is another cause of megaloblastic anaemia after bariatric surgery, and is especiallyof consideration in women who become pregnant after bariatric interventions: maternal folate defi-ciency is associated with neural tube defects in newborns [27]. For prevention, oral intake of 1 mg offolate daily is recommended, and for treatment doses of 5 mg daily are used.

Vitamin D deficiency has been reported in 25e75% of patients presenting for bariatric surgery[25e27]. Reduced intake and absorption may occur after bariatric interventions, but on the other hand,weight loss may liberate Vitamin D from the decreasing mass of adipose tissue during weight loss,thereby rising circulating levels. Case series report Vitamin D deficiencies in 7e60% of the patients whounderwent bariatric surgery. Intake of supplements of 800e2000 IU of cholecalciferol (vitamin D3) hasbeen recommended postoperatively [27]. In case of deficiencies, administration of 50,000 IU ofergocalciferol (vitamin D2) per week, either orally or intramuscularly, for 8 weeks is recommended[27]. Some sources recommend up to 150,000 IU daily for up to 2 weeks; follow-up is done bymeasuring serum 25(OH) vitamin D levels [27].

Vitamin D deficiency may lead to decreased intestinal calcium absorption, but this is also reducedby reduced gastric acidity and by bypassing the duodenum [25,26]. In conditions of decreased gastricacid secretion, calcium citrate may be the best absorbed calcium supplementation salt, and doses up to2 g daily have been recommended for prophylactic reasons [27]. Clinical manifestations of vitamin Ddeficiency include bone loss and osteomalacia. The prevalence of osteomalacia after bariatric surgery isnot well-established. Bone loss after bariatric surgery may occur through a number of mechanisms,including overall weight loss, decreased mechanical load and changes in gastrointestinal and sex

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hormone levels [25,26]. Increased risk of fractures after bariatric surgeries has been suggested, butsolid epidemiological data are lacking. Measurements of calcium, vitamin D and parathyroid hormoneas well as preoperative and postoperative follow-up of bone mineral density measurements have beenrecommended after bariatric surgery [30]. Parathyroid hormone levels are a more sensitive indicator ofcalcium malabsorption and risk of bone demineralisation, compared to calcium blood levels.

Iron deficiency has been reported in 5e44% of patients presenting for bariatric surgery [25e27]. Caseseries report iron deficiencies up to 47% of the patients who underwent bariatric surgery. Factorsunderlying this deficiency are probably reduced intake of meat, diminished contact of food with gastricacid and decreased intestinal absorption, and the risk is increased in menstruating or pregnant females[25e27]. For prevention, oral doses of 35e100 ug of elementary iron are recommended. Oral sup-plementation of up to 300 ug elemental iron daily is effective in the majority of patients with irondeficiency anaemia, andmay be enhanced by addition of vitamin C, but non-adherence to supplementsis a major risk factor for ongoing iron deficiency. In those not responding to oral iron supplements,intravenous iron administration may be necessary.

Vitamin A deficiency has been reported in up to 11% of patients after bariatric interventions [27].Clinical manifestations include a sensation of dry eyes and reduced night vision. Most multi-vitaminpreparations also contain vitamin A, but there is no consensus on a recommended prophyllacticdose vitamin A intake after bariatric surgery. In case of deficiencies, doses of 10,000e25,000 IU ofvitamin A daily until clinical improvement, which may take up to 3 weeks. In women who want tobecome pregnant, supplements of vitamin A should be used cautiously as hypervitaminosis A hasteratogenic effects.

Zinc deficiency has been reported to increase with 6% per year after bariatric surgery. Moreover, upto 30% of patients have abnormally low serum zinc levels prior to bariatric surgery, and this wasattributed to sequestration in adipose tissues [27]. These numbers indicate a high risk for zinc defi-ciency after bariatric surgery, but there is no consensus on routine supplementations of zinc post-operatively although it has been reported that zinc content of multi-vitamin supplement preparationsis insufficient in patients after bariatric surgery. In case of deficiency, the recommended dose is 60 mgof elemental zinc taken orally twice daily. Administration of zinc may deplete copper stores, and hencethis should be considered and measured when administering zinc supplements.

Copper deficiency has been reported in up to 18% of patients after bariatric surgery, usually severalmonths after the intervention [27]. Copper deficiency manifests itself with haematological (anaemia,leucopenia) and neurological signs (neuropathy, myelopathy, ataxia) and can be treated by oneweek of6 mg of elemental copper orally daily, followed by a week of 4 mg daily and then 2 mg daily asmaintenance dose [27].

Nutritional deficiencies after bariatric surgery

� Dumping syndrome may occur after any type of bariatric surgery involving partial gastric

bypass or distal resection.

� Clinical alertness for typical symptoms, especially postprandial palpitations, faintness and

hypoglycemia symptoms.

� A modified glucose tolerance test can confirm the diagnosis.

� Treatment starts with dietary measures, followed by acarbose in those with symptomatic

hypoglycemia. Somatostatin analogues are the most effective medical treatment modality.

� GERD may worsen after gastric banding interventions.

� Pre-existing GERD may improve after RYGB, and the latter is most likely the procedure of

choice in patients eligible for bariatric surgery and co-existing GERD.

� Preventing nutritional deficiencies is of the highest importance in bariatric surgery patients.

Management involves preoperative assessment of nutritional state, rigorous life-long clinical

and biochemical follow-up after interventions and supplements, tailored to the results of

biochemistry results. Any deficiencies must be treated aggressively.

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Research agenda

� Prospective studies should investigate the occurrence of dumping syndrome after RYGB and

sleeve gastrectomy, and further assess the benefits or disadvantages of early detection and

early treatment in terms of weight loss and quality-of-life outcomes.

� The relevance of early versus late dumping symptoms should be assessed, both for weight

loss and quality-of-life outcomes.

� The impact of sleeve gastrectomy on pre-existing or new-onset GERD requires additional

mechanistic and follow-up studies.

� Prospective studies should assess the relevance of pre-existing impaired esophageal

contractility on GERD incidence and severity after bariatric surgery. This may determine

whether there is any need for tailored interventions based on esophageal function.

� Prospective studies are needed that incorporate detailed analysis of nutritional state and

deficiencies before surgery, their evolution after all types of bariatric interventions and the

preventive effects of early corrections and supplementations.

� Studies are needed which evaluate strategies to improve patients' adherence to nutritional

supplementations and follow-up after bariatric interventions.

J. Tack, E. Deloose / Best Practice & Research Clinical Gastroenterology 28 (2014) 741e749748

Conclusion

Bariatric surgical procedures provide effective weight loss but may have a number of consequencesthat physicians should be aware of and consider in a pre- and postoperative management plan. The riskof gastro-esophageal reflux is a factor that may drive the choice for type of bariatric intervention. Astrict follow-up plan with administration of multi-vitamin supplements and assessment of serumlevels must be implemented in all patients, and preoperative assessments of potential nutritionaldeficiencies is also highly recommended. Finally, clinicians should be aware of the symptoms ofdumping syndrome and its diagnosis and management options.

Conflict of interest

None declared.

References

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