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Complications of bariatric surgery:


Dumping syndrome, reflux and
vitamin deficiencies
ARTICLE in BAILLIRE&#X027 S BEST PRACTICE AND RESEARCH IN CLINICAL
GASTROENTEROLOGY AUGUST 2014
Impact Factor: 3.48 DOI: 10.1016/j.bpg.2014.07.010

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

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Best Practice & Research Clinical


Gastroenterology

15

Complications of bariatric surgery: Dumping


syndrome, reux and vitamin deciencies
Jan Tack, M.D., Ph.D., Professor of Medicine *,
Eveline Deloose, M.Sc., Ph.D. fellow
Translational Research Center for Gastrointestinal Disorders (TARGID), University of Leuven, Leuven, Belgium

a b s t r a c t
Keywords:
Bariatric surgery
Gastro-esophageal reux disease
Roux-en-Y gastric bypass
Sleeve gastrectomy
Dumping syndrome
Vitamin deciencies
Malabsorption
Wernicke encephalopathy

Bariatric surgical procedure are increasingly and successfully


applied in the treatment of morbid obesity. Nevertheless, these
procedures are not devoid of potential long-term complications.
Dumping syndrome may occur after procedures involving at least
partial gastric resection or bypass, including Roux-en-Y gastric
bypass (RYGB) and sleeve gastrectomy. Diagnosis is based on
clinical alertness and glucose tolerance testing. Treatment may
involve dietary measures, acarbose and somatostatin analogues, or
surgical reintervention for refractory cases. Gastro-esophageal
reux disease (GERD) can be aggravated by vertical banded gastroplasty and sleeve gastrectomy procedures, but pre-existing
GERD may improve after RYGB and with adjustable gastric banding. Nutrient deciencies constitute the most important long-term
complications of bariatric interventions, as they may lead to haematological, metabolic and especially neurological disorders which
are not always reversible. Malabsorptive procedures, poor postoperative nutrient intake, recurrent vomiting and poor compliance
with vitamin supplement intake and regular follow-up are
important risk factors. Preoperative nutritional assessment and
rigourous postoperative follow-up plan with administration of
multi-vitamin supplements and assessment of serum levels is
recommended in all patients.
2014 Published by Elsevier Ltd.

* Corresponding author. Department of Pathophysiology, Division of Gastroenterology, University Hospital Gasthuisberg,


Herestraat 49, B-3000 Leuven, Belgium. Tel.: 32 16 34 42 25; fax: 32 16 34 44 19.
E-mail address: jan.tack@med.kuleuven.be (J. Tack).

http://dx.doi.org/10.1016/j.bpg.2014.07.010
1521-6918/ 2014 Published by Elsevier Ltd.

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Introduction
Bariatric surgical procedure are currently the most effective treatment modality to induce weight
loss and reduce complications of obesity. However, bariatric interventions also induce major changes in
the anatomy and function of the gastrointestinal tract [1].
Several main types of bariatric surgery have been used over the last decades, and these include the
biliopancreatic diversion, the Roux-en-Y gastric bypass, the vertical banded gastroplasty and the
laparoscopic adjustable gastric band and the sleeve gastrectomy. The vertical banded gastroplasty,
laparoscopic adjustable gastric band and sleeve gastrectomy are considered restrictive procedures,
deriving their efcacy from interference with the volume capacity of the proximal stomach. The biliopancreatic diversion and the Roux-en-Y gastric bypass are considered malabsorptive procedures, as
they interfere with normal digestive and absorptive processing of food, although the latter is considered mainly restrictive [1].
In this paper, potential adverse consequences of bariatric surgical procedures such as dumping
syndrome, gastro-esophageal reux and nutritional deciencies, are summarized, with a focus on
clinical management aspects.
Dumping syndrome after bariatric surgery
Dumping syndrome is characterized by vasomotor and gastrointestinal symptoms which can be
attributed to rapid gastric emptying or rapid exposure of the small intestine to nutrients [2]. Dumping
syndrome occurs readily after partial or complete gastrectomy, and hence is a potential complication of
some bariatric surgical procedures involving partial gastrectomy. Furthermore, dumping syndrome can
occur as a consequence of damage to the vagus nerve [2].
In dumping syndrome, symptoms are typically triggered by meal ingestion and are somewhat
arbitrarily subdivided into early and late dumping symptoms (Table 1) [2,3]. Early dumping symptoms occur in response to the rapid passage of hyperosmolar nutrients into the small bowel, and they
reect the release of gastrointestinal hormones which may be accompanied by a shift of uids from the
intravascular compartment to the lumen. Several candidate peptides can be involved in this response,
including enteroglucagon, Vasoactive Intestinal Peptide, Peptide YY, pancreatic polypeptide and neurotensin. Late dumping occurs between one and three hours after the meal and is characterized by
symptoms of hypoglycaemia. Rapid gastric emptying leads to a high glucose concentration in the intestinal lumen, from which it is rapidly absorbed. This is a trigger for peak insulin secretion, but
because of the long half-life of insulin and the transient character of the initial rise in glycaemia, hypoglycemia may occurs when all available glucose has been absorbed [2]. A recent paper provided
evidence for a key role of glucagon-like-peptide-1 in the pathogenesis of late hypoglycemia after
gastric bypass [4].
Most patients present with early dumping, or a combination of both early and late dumping. Isolated late dumping, i.e. patients in whom hypoglycemia is the only symptoms, is very rare. In severe
cases, dumping syndrome is associated with signicant impairment of quality-of-life [3] and may
contribute to signicant weight loss by avoidance of food intake.
After bariatric surgery, dumping syndrome has mainly been reported in patients who underwent
Roux-en-Y gastric bypass and other interventions involving partial gastrectomy. After gastric bypass,

Table 1
Symptoms in dumping syndrome.
Early dumping
 Gastrointestinal symptoms
Abdominal pain, diarrhoea, borborygmi. bloating, nausea
 Vasomotor symptoms
Flushing, palpitations. perspiration, tachycardia, hypotension, syncope
Late dumping
 Hypoglycemia
Perspiration, palpitations, hunger, weakness, confusion, tremor, syncope

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around 40% of patients have dumping syndrome symptoms [5]. It has been speculated that dumping
syndrome 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 weight
loss 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 to
dumping syndrome. However, in two prospective studies, it was reported that up to 40% of patients had
symptoms suggestive of dumping syndrome 6e12 months after sleeve gastrectomy [6,7]. The mechanisms underlying dumping syndrome after sleeve gastrectomy remain to be elucidated, but it is clear
that 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 predisposing
surgical intervention. Symptom-based questionnaires, like Sigstad's score (Table 2) or Arts' dumping
questionnaire, have been used to help and detect clinically meaningful dumping symptoms [2,3,6].
Objective conrmation of the diagnosis is obtained by a modied oral glucose challenge test: 50 g of
glucose are ingested with water and for 3 h at 30-min intervals glycaemia, haematocrit and pulse rate
are 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 take
smaller more frequent meals (up to 6 per day) and to avoid drinking with meals or the rst
2 h postprandially. The latter aims at decreasing the spread of triggering nutrients over a larger
segment of small intestine. Importantly, patients are taught to avoid rapidly absorbed sugars and
lactose [2]. As reported in the literature, viscous food additives like pectin, guar gum and glucomannan
can be added to meals to slow gastric emptying and intestinal spread, but these are experienced as
unpalatable by the patients and may be less effective after partial gastrectomy. Easier to use is acarbose,
an inhibitor of intestinal alpha-glucosidase, which slows carbohydrate digestion and thus blunts
postprandial hyperglycemia and rebound hypoglycemia [2]. Usage of acarbose is limited by its lack of
efcacy for early dumping symptoms and occurrence of side-effects of carbohydrate maldigestion such
as atulence, bloating and diarrhoea [2].
If these rst-line measures fail, somatostatin analogues can be considered. These agents are the
most effective treatment options available for dumping syndrome, as they are effective for both early
and late dumping symptoms [3]. Somatostatin analogues can be administered either subcutaneously
three times daily, or intramuscularly once every two to four weeks as a slow release formulation, and
they slow gastric emptying and inhibit the release of several gastrointestinal peptides implicated in
dumping syndrome pathophysiology [2,3,8]. In the management of dumping syndrome, initial therapy
is usually a short-acting agent administered subcutaneously, e.g. 50e100 mg octreotide s.c. In case of
good efcacy and tolerance, a slow release preparation can be used, e.g. octreotide L.A.R. 20 mg or
Table 2
Sigstad's scoring system for diagnosing dumping syndrome. A total score >7 is suggestive of dumping syndrome, whereas a score
<4 suggests other diagnoses.
Shock 5
Fainting, syncope, unconsciousness 4
Desire to lie or sit down 4
Breathlessness, dyspnoea 3
Weakness, exhaustion 3
Sleepiness, drowsiness, apathy, falling asleep 3
Palpitation 3
Restlessness 2
Dizziness 2
Headaches 1
Feeling of warmth, sweating, pallor, clammy skin 1
Nausea 1
Abdominal fullness, meteorism 1
Borborygmus 1
Eructation 1
Vomiting 4

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20 mg i.m [2,3]. Pasireotide, a novel and more broadly acting somatostatin analogue, is currently
undergoing phase 2 testing for the treatment of postoperative dumping [8].
In exceptionally difcult-to-manage patients, re-do surgery can be considered to reconstruct a
gastric reservoir, to add a restrictive intervention (band around the pouch, revision of pouch, endoscopic procedures), to undo the surgery if possible, or to insert a short anti-peristaltic loop [2,9].
Gastro-esophageal reux after bariatric surgery
Obesity is a major risk factor for gastro-esophageal reux disease [10] and it is important to consider
this co-morbidity in many patients in whom bariatric surgery is planned. Weight loss alone, for
instance by dietary interventions, may decrease GERD, as has been shown in controlled trials [11,12],
although conicting data have also been found [13]. The effect of bariatric surgery on GERD seems to
differ according to the type of surgery.
All but one of the available studies show improvement of GERD after Roux-en-Y gastric bypass
surgery. Two comparative studies found that the gastric bypass was superior to gastric banding in
improving GERD symptoms [13,14]. Although there are only limited mechanistic data on GERD before
and after gastric bypass surgery, it seems that a consistent benecial effect can be found. In a prospective 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 signicantly lower esophageal acid exposure,
especially in the upright position [15]. Disappearance of the acid pocket at the gastro-esophageal
junction 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 vertical
banded gastroplasty, conicting effects on GERD have been reported: ve out of eight studies found no
effect, one found worsening of GERD and two found improvement. Taken together, these studies
suggest that the putative benecial effect of weight loss on GERD was counteracted by other effects of
the procedure. Accumulation of gastric acid in the pouch has been implicated as a mechanism that
promotes GERD in these patients [17].
Even more diverse outcomes were reported after laparoscopic adjustable gastric banding procedures. While only two studies found no effect, six studies showed a positive effect on GERD
symptoms, in two of them only when preoperative esophageal motility was effective and when no
dilated pouch occurred. Two studies found worsening of GERD mainly based on objective GERD
measurements, and four studies found conicting outcomes on symptoms or objective measure of
GERD [13]. The mechanisms implicated in worsening of GERD after gastric banding include not only
accumulation of acid in the proximal stomach compartment, but also pre-existing poor esophageal
motility. It has been suggested that the presence of a hiatal hernia may increase the risk of worsening
GERD after laparoscopic gastric banding [13], but two studies prospectively evaluating this were not
able to nd a worse prognosis in case of hernia [18,19].
After sleeve gastrectomy, half of the studies reported an increase in GERD symptoms, while the
other half found no such effect [20,21]. On one hand, some patients see improvement of GERD after
sleeve gastrectomy, and this may be related to decreased gastric acid production and decreased body
weight [20,21]. On the other hand, based on a large database, it was shown that the outcomes of sleeve
gastrectomy are less favourable in case of pre-existing GERD, and it has been suggested that preexisting GERD could be considered a contra-indication [22]. A hiatal hernia is considered a contraindication for sleeve gastrectomy, unless it can be repaired. There is also evidence that new-onset
GERD symptoms may occur after sleeve gastrectomy in a group of patients who were previously
asymptomatic. The mechanisms implicated in increased GERD include decreased gastric compliance,
which may increase intragastric pressure and thereby promote reux, as well as reshaping of the angle
of Hiss. However, these studies were mainly based on symptom reporting. A recent prospective study
used 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 an
increased occurrence of swallows with complete bolus transit. Acid, but especially non-acid reux
episodes were signicantly increased after sleeve gastrectomy. The latter was attributable to increased
intragastric pressure, probably reecting decreased gastric compliance and leading to postprandial

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regurgitation events [23]. While this study found no signicant effect on lower esophageal sphincter
pressure, another prospective study reported that sleeve gastrectomy was associated with a signicant
increase in sphincter pressure, which was already present in the early postoperative phase and hence
independent of weight loss [24].
Nutritional deciencies after bariatric surgery
Bariatric surgical procedures have been associated with nutritional deciencies, but their prevalence and nature depend on the type of surgery. Laparoscopic gastric banding, conceptually a
restrictive rather than a malabsorptive intervention, is less frequently associated with deciencies. One
exception is the occurrence of early postoperative thiamine deciency. Sleeve gastrectomy was also
conceived as a restrictive intervention. Similar to the laparoscopic gastric banding, it leads less
frequently to nutritional deciencies, especially if patients adhere to intake of prescribed supplements.
The Roux-en-Y gastric bypass is a malabsorptive intervention and, hence, is associated with a higher
prevalence of nutritional deciencies. After this intervention, the exposure of food to bile and
pancreatic juices is delayed, thereby diminishing completeness of digestion and absorption. Biliopancreatic diversion is a procedure in which a large section of small intestine is bypassed, and hence
it carries the highest risk for nutritional deciencies [25,26]. The Roux-en-Y gastric bypass was shown
to decrease fat and protein, but not carbohydrate absorption [26]. After Roux-en-Y gastric bypass, the
length of the biliopancreatic limb is correlated to the amount of fat malabsorption, probably because
this is inversely correlated with the length of the common channel, and because it delays contact of
nutrients with digestive enzymes [26]. Furthermore, a longer biliopancreatic limb may promote bacterial overgrowth and further impaired fat digestion [26].
Another variable is the presence of micronutrient deciencies prior to the surgery. Indeed, obesity
has been associated with vitamin D and iron deciency, amongst others. Moreover, dietary restrictions
aimed 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 elucidated
in detail [25e27].
A common factor to all bariatric surgery is reduced overall nutrient intake in the (early) postoperative phase. Reduced overall intake may be associated with poor intake of specic micro-nutrients
and contribute to occurrence of deciencies. Dietary adjustments in the immediate postoperative
period aim at protein supplementations, to avoid major loss of body protein. In a U.S. consensus, intake
of more than 60 g of protein per day has been recommended after bariatric surgery [25,27]. Prospective
follow-up of dietary intake of patients after bariatric surgery shows that many do not reach the
60 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 prevention of Wernicke's encephalopathy have been published [30,31]. For patients with Roux-en-Y
gastric bypass, adequate intake of protein, more than 1 g/kg ideal body weight/day, is recommended
to prevent protein deciencies [27]. In case of deciencies, oral or enteral protein supplements can be
administered, or parenteral nutrition during a few weeks may be necessary in case of extensive
combined deciencies. In addition, it has been recommended to treat all patients who underwent
malabsorptive surgical interventions with multi-vitamin supplements that contain at least double the
daily recommended dose, as well as 18 mg of elemental iron and 400 ug of folic acid. Ideally these
preparations 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, atulence, abdominal pain and ascites) or general symptoms (persisting or excessive weight loss, anaemia, amenorrhoea, impotence, infertility, night blindness,
xeropthalmia, peripheral neuropathy, tiredness, fatigue and weakness) [26]. A panel of blood tests can
be assessed, which may include blood cell count, triglycerides, cholesterol, albumin, alkaline phosphatase, calcium, phosphorus, magnesium, zinc, iron, ferritin, prothrombin time, serum vitamin A,
immunoglobulins, parathyroid hormone, serum vitamin D, folic acid, vitamin B12 (or methylmalonic
acid if available, which may be more reliable), etc. It has been suggested to perform these test preoperatively and then at 3- to 6-month intervals in the rst 2 years, and later annually, after

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malabsorptive procedures [26,27]. Furthermore, preoperative and annual postoperative dual-energy


X-ray bone absorptiometry have been recommended to screen for bone mineral loss and osteoporosis occurrence after Roux-en-Y gastric bypass and biliopancreatic diversion [30]. Specic deciencies
may require specic approaches and supplements, as outlined below.
Thiamine (vitamin B1) deciency has been reported in 0e29% of patients presenting for bariatric
surgery [25e27]. As this condition may lead to potentially irreversible neurological manifestations,
clinical alertness and prompt adequate treatment in case of deciency are required. Case series report
thiamine deciencies in 0e30% of the patients who underwent bariatric surgery. Vomiting after bariatric intervention is the principal risk factor for developing thiamine deciency, together with poor
food intake and lack of supplement intake [31]. The presence of vomiting should specically be
addressed in history taking after bariatric surgery, as some patients do not readily mention this
problem and consider it a normal consequence of the intervention. Intravenous glucose administration is a risk factor for triggering acute symptomatic vitamin B deciency leading to interruption of
the citric acid cycle and lactate acidosis. Clinical manifestations of thiamine deciency include Wernicke's encephalopathy, peripheral neuropathies, nystagmus and ocular palsies, and these can be
precipitated by intravenous infusion of glucose solutions [25e27,31]. Hence, it is recommended to
prophylactically administer thiamine 100 mg i.v. when starting intravenous uids in patients at risk.
Prophylactic daily intake of a multi-vitamin preparation containing at least 3 mg of thiamine has been
recommended after malabsorptive procedures, to be increased to 50 mg in those at risk for Wernicke's
encephalopathy [27]. For therapeutic purposes in symptomatic deciency, especially with neurological
signs, initial doses of 100e500 mg daily intravenously administered are recommended.
Vitamin B12 deciency has been reported in 0e18% of patients presenting for bariatric surgery
[25e27]. Case series report Vitamin B12 deciencies in 4e62% of the patients who underwent bariatric
surgery, often as a late complications as body stores become only slowly depleted in case of insufcient
dietary uptake. Measurement of melthylmalonic acid concentrations in the serum may be a more
sensitive marker for vitamin B12 deciency. A prophylactic oral dose of at least 500 ug daily after
bariatric surgery has been recommended [27]. Factors underlying this deciency are probably reduced
intake of meat, diminished contact of food with gastric acid and decreased secretion of intrinsic factor
[25e27]. Symptomatic vitamin B12 deciency leads to megaloblastic anaemia, myelopathy and neuropathy. Supplementation by multi-vitamin preparations seems insufcient in case of vitamin B12
deciency and this may require elevated oral doses of vitamin B12 or parenteral administration. In case
of deciencies, weekly intramuscular administration of 1000 ug for 8 weeks is recommended. In case of
neurological manifestations, daily intramuscular administrations with life-long monthly injections are
recommended.
Folate deciency is another cause of megaloblastic anaemia after bariatric surgery, and is especially
of consideration in women who become pregnant after bariatric interventions: maternal folate deciency is associated with neural tube defects in newborns [27]. For prevention, oral intake of 1 mg of
folate daily is recommended, and for treatment doses of 5 mg daily are used.
Vitamin D deciency 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 deciencies in 7e60% of the patients who
underwent bariatric surgery. Intake of supplements of 800e2000 IU of cholecalciferol (vitamin D3) has
been recommended postoperatively [27]. In case of deciencies, administration of 50,000 IU of
ergocalciferol (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 by
measuring serum 25(OH) vitamin D levels [27].
Vitamin D deciency may lead to decreased intestinal calcium absorption, but this is also reduced
by reduced gastric acidity and by bypassing the duodenum [25,26]. In conditions of decreased gastric
acid secretion, calcium citrate may be the best absorbed calcium supplementation salt, and doses up to
2 g daily have been recommended for prophylactic reasons [27]. Clinical manifestations of vitamin D
deciency include bone loss and osteomalacia. The prevalence of osteomalacia after bariatric surgery is
not 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, but
solid epidemiological data are lacking. Measurements of calcium, vitamin D and parathyroid hormone
as well as preoperative and postoperative follow-up of bone mineral density measurements have been
recommended after bariatric surgery [30]. Parathyroid hormone levels are a more sensitive indicator of
calcium malabsorption and risk of bone demineralisation, compared to calcium blood levels.
Iron deciency has been reported in 5e44% of patients presenting for bariatric surgery [25e27]. Case
series report iron deciencies up to 47% of the patients who underwent bariatric surgery. Factors
underlying this deciency are probably reduced intake of meat, diminished contact of food with gastric
acid 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 supplementation of up to 300 ug elemental iron daily is effective in the majority of patients with iron
deciency anaemia, and may be enhanced by addition of vitamin C, but non-adherence to supplements
is a major risk factor for ongoing iron deciency. In those not responding to oral iron supplements,
intravenous iron administration may be necessary.
Vitamin A deciency 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-vitamin
preparations also contain vitamin A, but there is no consensus on a recommended prophyllactic
dose vitamin A intake after bariatric surgery. In case of deciencies, doses of 10,000e25,000 IU of
vitamin A daily until clinical improvement, which may take up to 3 weeks. In women who want to
become pregnant, supplements of vitamin A should be used cautiously as hypervitaminosis A has
teratogenic effects.
Zinc deciency has been reported to increase with 6% per year after bariatric surgery. Moreover, up
to 30% of patients have abnormally low serum zinc levels prior to bariatric surgery, and this was
attributed to sequestration in adipose tissues [27]. These numbers indicate a high risk for zinc deciency after bariatric surgery, but there is no consensus on routine supplementations of zinc postoperatively although it has been reported that zinc content of multi-vitamin supplement preparations
is insufcient in patients after bariatric surgery. In case of deciency, the recommended dose is 60 mg
of elemental zinc taken orally twice daily. Administration of zinc may deplete copper stores, and hence
this should be considered and measured when administering zinc supplements.
Copper deciency has been reported in up to 18% of patients after bariatric surgery, usually several
months after the intervention [27]. Copper deciency manifests itself with haematological (anaemia,
leucopenia) and neurological signs (neuropathy, myelopathy, ataxia) and can be treated by one week of
6 mg of elemental copper orally daily, followed by a week of 4 mg daily and then 2 mg daily as
maintenance 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.

Conclusion
Bariatric surgical procedures provide effective weight loss but may have a number of consequences
that physicians should be aware of and consider in a pre- and postoperative management plan. The risk
of gastro-esophageal reux is a factor that may drive the choice for type of bariatric intervention. A
strict follow-up plan with administration of multi-vitamin supplements and assessment of serum
levels must be implemented in all patients, and preoperative assessments of potential nutritional
deciencies is also highly recommended. Finally, clinicians should be aware of the symptoms of
dumping syndrome and its diagnosis and management options.
Conict of interest
None declared.
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