Overweight and obesity increase morbidity and mortality because of associated complications such as type 2 diabetes mellitus, hyperlipidaemia and hypertension, all of which ultimately may lead to coronary artery disease, stroke and an increased risk for malignancies.1 It is estimated that 3.4 million adults die each year as a result of being overweight or obese.2 In 2008, the World Health Organization (WHO) assumed that, worldwide, 300 million men and 200 million women were classified as obese.2
The prevalence of morbid obesity, as defined by a body mass index (BMI) above 40 kg/m2, has likewise increased considerably to 4.9% of the general population in the United States of America (USA).3 In addition, studies have shown that the prevalence of obesity in the USA increased from 22.9% in 1988–1994 to 30.5% in 1999–2000 to 34.9% in 2011–2012, and worldwide, between 1980 and 2013, from 28.8% (95% uncertainty interval 28.4–29.3%) to 36.9% (36.3–37.4%) in men, and from 29.8% (29.3–30.2%) to 38.0% (37.5–38.5%) in women.4,5 Since dietary and behavioural interventions in these patients have been shown to be largely ineffective, bariatric surgery has become the preferred therapeutic option since it has proven to be the most effective and durable method to achieve weight loss and reduce obesity-related comorbidities and even mortality. The Swedish Obese Subjects (SOS) study demonstrated the benefits of bariatric surgery over conservative treatment of morbid obesity with regard to reducing the incidence of cardiovascular events and type 2 diabetes mellitus for over 15 years.6 Owing to the multiple favourable metabolic effects, and, in particular, the remission of type 2 diabetes mellitus, bariatric surgery is quite often referred to as ‘metabolic surgery’. However, long-term success of bariatric surgery relies on the treatment by an interdisciplinary team to prevent acute perioperative and chronic side-effects, which are mostly related to multiple nutritional deficiencies.7 These include common deficiencies, such as insufficient quantities of iron, vitamin D and vitamin B12, and more rare deficiencies, such as inadequate quantities of thiamine and trace elements.8
Bariatric surgery is indicated for patients with a BMI > 40 kg/m2 or for individuals with a BMI > 35 kg/m2 and significant obesity-associated comorbidities such as type 2 diabetes mellitus. These criteria were determined by the National Institutes of Health (NIH) in 1992 and are still valid.9 Although there are reports about favourable results in less obese or even overweight subjects, especially for type 2 diabetes mellitus remission, bariatric surgery should only be performed in the context of controlled clinical trials in this population, as, at the moment, long-term study results regarding the benefit–risk ratio for patients with BMI < 35 kg/m2 are lacking.10,11
Furthermore, patients should be between 16 and 65 years of age, the operative risk must be acceptable and there must be a documented failure of non-surgical approaches for long-term weight loss. For very severe obesity, bariatric surgery can also be performed in younger subjects after careful consideration. In this regard, psychological evaluation is of greatest importance and the social setting regarding support has to be carefully evaluated. In addition, the patient must have the ability to attend regular aftercare visits. Apart from medical reasons, exclusion criteria are psychological instability, ongoing alcohol or substance abuse, severe active psychosis and untreated severe depression.12 In addition, it is mandatory to exclude endocrine diseases such as Cushing’s disease or untreated hypothyroidism before surgery.
Since its introduction in the 1950s, the frequency of bariatric surgery procedures has increased steadily, especially in the last decade. Bariatric surgery is classified into pure restrictive, pure malabsorptive or combined procedures (see Figure 1). At present, most procedures performed in Europe and North America are malabsorptive and restrictive, such as Roux-en-Y gastric bypass (RYGB), or purely restrictive, such as laparoscopic gastric banding.13 Sleeve gastrectomy, which consists of the resection of the fundus thereby forming a sleeve, was originally developed as surgical technique as the first step for super-obese patients to promote weight loss, when the risk for a more invasive RYGB was too high. However, as many patients achieved good weight loss results via this procedure alone, and because of a much lower rate of nutritional deficiencies, sleeve gastrectomy has become, more and more, a stand-alone modality for many obese patients.14 In addition, sleeve gastrectomy is much easier and quicker to perform than RYGB, leading to fewer complications.15 Considering the surgical technique, sleeve gastrectomy can also be regarded as a restrictive technique, but studies and experience demonstrate a malabsorptive component. In addition, the loss of ghrelin-producing cells in the fundus inhibits hunger signals and thus alters appetite regulation. Like with malabsorptive procedures, glucagon-like peptide (GLP-)1 and peptide tyrosine tyrosine (PYY), which act as satiety hormones, exhibit a more rapid release and at higher levels following meal ingestion than those who have not had surgery thereby promoting weight loss.16
In RYGB, the stomach is divided and the resulting pouch provides a volume of less than 30 ml. The location of the jejunojejunal anastomosis determines the length of the Roux limb and, equally important, the length of the common channel which extends from this anastomosis to the ileocaecal valve. The length of the common channel regulates the malabsorptive component of the procedure. RYGB is a complex surgery with a multitude of possible post-operative complications such as anastomotic leak or bowel strangulation due to an internal hernia and, hence, the most important factor for a successful operation is an experienced, well-trained surgeon.
Restrictive procedures are the laparoscopic adjustable gastric banding (LAGB), intragastric balloon and vertical banded gastroplasty, which reduce food intake as a result of the smaller volume of the stomach. In LAGB, an inflatable band is placed to form a 15- to 20-ml superior gastric pouch. The band connects to a self-sealing reservoir (port) beneath the skin, which allows adjustment to increase or reduce food passage. There are some procedure-specific complications which are higher than originally thought, such as band slippage, band erosion, oesophageal dilatation and port migration.17 Furthermore, weight loss is not maintained to the same extent as seen with RYGB or even sleeve gastrectomy.18 Increasing experience with LAGB has shown a high long-term failure rate with severe complications, most of which require reoperation (e.g. oesophageal dilatation or band erosion). However, removal of the laparoscopic gastric band often leads to rapid weight gain.19 Therefore, LAGB is largely abandoned in most countries and failed LAGB is usually converted to RYGB. However, these conversion surgeries have much higher complication rates than primary RYGB and should be performed only by an experienced surgeon in a specialized centre. Therefore, careful choice of the appropriate surgical procedure is a prerequisite for long-term success.
In a few special situations, such as super-obesity, severe malabsorptive procedures, such as biliopancreatic diversion with or without jejunal switch, can be indicated. This surgical method leads to substantial and long-lasting weight loss because of a shortening of the small intestine to decrease nutrient absorption. However, severe malabsorption, the main mechanism for this procedure, can be life-threatening. Therefore, use of this procedure is quite limited.
The patient with morbid obesity is at increased risk for intra- and post-operative complications. In addition to the routine pre-operative programme before any other major abdominal surgery, pre-operative assessment should include evaluation for:
sleep apnoea syndrome and pulmonary dysfunction
metabolic and endocrine disorders (uncontrolled type 2 diabetes mellitus and disturbed thyroid function, Cushing’s disease)
gastro-oesophageal disorders (e.g. Helicobacter pylori infection)
cardiac function (echocardiogram)
bone mineral density
evidence for gall stones (ultrasound)
nutritional status, body composition.
Patients with morbid obesity have an increased peri-operative risk. Anaesthesia itself is more difficult and carries more risk in obese patients than in non-obese patients. The risk of venous thromboembolic events is increased in patients undergoing bariatric surgery despite use of the laparoscopy and aggressive prophylactic anticoagulation strategy.20 In a retrospective analysis of 668 patients undergoing bariatric surgery, patients with thrombosis prophylaxis (enoxaparin) had fewer pulmonary embolisms than patients without.21 Therefore, bariatric surgery is an indication for a longer thrombosis prophylaxis. Furthermore, patients with morbid obesity more often have complications regarding wound healing and infections at the surgical site than lean patients.22
Surgical complications and nutritional deficiencies after bariatric surgery differ in their prevalence and are dependent on the surgical procedure used. The most common complication is peritonitis caused by leakage of the anastomosis, followed by intestinal strangulation caused by an internal hernia or, in rare cases, pancreatitis.23,24 The reported incidence of leakage after bariatric surgery varies from 0.6% to 5.6%.25,26 Usually, ultrasound or abdominal computerised tomography scans (using water-soluble contrast media) are used for diagnosis before exploratory laparoscopy is performed. Treatment can range from a conservative approach using endoluminal fibrin glue to immediate laparoscopy.27–30 In a recent review, however, the authors concluded that patients with apparent symptoms of leakage after RYGB should undergo immediate operative intervention without further diagnostic evaluation.31
Other common post-operative complications after bariatric surgery are explained below.
Dysphagia and emesis
In general, vomiting is a common problem after bariatric surgery and, in particular, after RYGB. For the most part, it is caused by ingestion of too much solid food or fluids; however, it can also point to a marginal ulceration or stenosis of the proximal anastomosis. Therefore, continued vomiting despite nutritional intervention requires prompt gastroscopy.
Dehydration, especially in the first weeks after surgery, is a serious problem as many patients are not able to ingest the necessary volumes of fluid. In addition, frequent emesis might aggravate this problem. Therefore, patients are advised to chew extensively and to eat often but only small quantities of food. Water should be ingested separately.
Following RYGB, vomiting can be caused by a small intestinal obstruction (internal hernia or intussusception), obstruction of the biliopancreatic limb or acute gastric distension.32 Vomiting of bile should never occur after RYGB and prompts immediate surgical intervention.
If vomiting is accompanied by abdominal pain, an ulceration or ischaemia of the gastrojejunal anastomosis must be suspected. Ulcers of the gastrojejunal anastomosis are categorized as marginal, ischaemic or anastomotic and occur in 0.6% to 16% of all patients who undergo gastric bypass surgery, depending on the definition and the screening method used.33–35 The pathogenesis of these ulcers is still a subject of debate. The main factors seem to be the size of the pouch, as a larger gastric pouch leads to more acid production, the tension at the anastomosis and the use of foreign suture material.35,36 Furthermore, type 2 diabetes mellitus, smoking and the use of anticoagulation and non-steroidal anti-inflammatory drugs favour the development of ulcers. The impact of H. pylori infection is still not clear.35,37
Dumping syndrome and hypoglycaemia
Post-prandial hypoglycaemia is a potentially dangerous complication of gastric bypass and sleeve gastrectomy, and is increasing in prevalence. While in most cases hypoglycaemia can be treated and prevented by dietary modification, a subset of individuals develop life-threatening neuroglycopenia with loss of consciousness and seizures with potentially fatal consequences, such as motor vehicle accidents. Those patients require complex nutritional and medical management strategies to reduce post-prandial insulin secretion and stabilize glucose excursions, sometimes also by using medications, including acarbose [Glucobay® (Europe and China), Precose® (North America) and Prandase® (Canada); Bayer Healthcare Pharmaceuticals, Montville, NJ, USA], octreotide and diazoxide, and frequent monitoring of glucose values.38 Unfortunately, however, medical intervention is not effective in most cases.
In a Swedish registry, data regarding the frequency of hypoglycaemia after bariatric surgery and potentially related symptoms (loss of consciousness, syncope, seizures, accidental death) were evaluated.39 Marsk et al.39 found a low absolute but a two- to sevenfold increased relative risk. Furthermore, this study could assess only severe hypoglycaemia because patients with mild and moderate hypoglycaemia would not attend a hospital or an emergency unit and less severe hypoglycaemia may be much more prevalent.
Hypoglycaemia typically occurs 2 to 3 hours after a meal with inappropriately high insulin levels accompanied by low glucose levels especially after gastric bypass, but, to a lesser extent, also after sleeve gastrectomy. The symptoms of the patients vary from no symptoms to sweating, shaking, emesis and loss of consciousness. Interestingly, this complication usually starts 2–3 years after surgery, indicating that it is not solely linked to the rapid improvement of insulin sensitivity. One hypothesis for post-gastric bypass hypoglycaemia is the increase in GLP-1 with expansion of insulin-producing islet cells.40 Regarding the frequency of post-prandial hypoglycaemia following bariatric surgery, all patients should specifically be asked about symptoms of hypoglycaemia and undergo an extended oral glucose or mixed-meal tolerance test when appropriate. Patients with hypoglycaemia need intensive counselling by a dietitian focusing on the intake of complex carbohydrates.
Many studies have demonstrated that patients who regularly attend aftercare visits have greater weight loss and fewer complications, especially regarding malnutrition.41 Furthermore, it is widely accepted that non-adherence to nutritional supplement recommendations is a critical causal factor for nutritional deficiency after bariatric surgery. Data about adherence are, unfortunately, scarce. Most studies demonstrate that 6 months after bariatric surgery only about one-third of the included patients are adherent to their vitamin supplementation.42–44
In addition, sufficient fluid uptake after surgery might be a major issue. During the period of rapid loss of fat mass, patients also lose muscle mass. Thus, there is an increase in purines, which must be eliminated by the kidneys. Therefore, fluid intake is of utmost importance, especially for patients with elevated urine acid before surgery. In addition, in all patients who had a restrictive or combined malabsorptive and restrictive surgery, food and fluid uptake must be strictly separated as, otherwise, because of the small stomach, patients are not able to drink enough. Therefore, it is recommended not to drink before and until 20 minutes after eating.
An important issue in the phase of rapid weight loss after surgery is protein deficiency. Even well-informed and motivated patients have difficulties in ingesting 40 grams of protein per day, which is well below the recommended daily intake (0.8 g/kg body weight). Since an intake of at least 60 grams of protein per day is necessary to avoid symptoms of malnutrition, many patients must add protein powder to their diet to maintain sufficient protein levels.45 Protein deficiency is a serious complication after bariatric surgery, especially for patients with a short common channel with subsequent relative protein malabsorption. The first symptom of protein deficiency might be hair loss, and the presence of oedema is always a signal for severe protein deficiency. Long-term protein deficiency can include signs of muscle mass wasting.46 Severe protein deficiency, like Kwashiorkor, is particularly prevalent after distal gastric bypass.47 In severe cases of protein deficiency, surgical revision must be considered. The severity of protein deficiency and the amount of lean tissue mass loss is dependent not only on protein intake but also on the bariatric procedure performed.48–50 Diagnosis of protein deficiency is established by measurement of serum albumin. Since albumin is also an acute phase reactant, it should not be assessed in the context of inflammation.
Micronutrients are essential dietary factors, which have various functions in biochemical and metabolic processes. Micronutrients are divided into fat-soluble vitamins, water-soluble vitamins, trace elements and essential minerals.
Vitamin B1 (thiamine)
Thiamine plays an essential role in the tricarboxylic acid cycle and in the pentose phosphate pathway in humans. It is important for neuronal communication, immune system activation, and signalling and maintenance processes in cells and tissues, as well as cell membrane dynamics.51 Vitamin B1 deficiency is quite common (up to 49% depending on the operation procedure) after bariatric surgery because of decreased uptake, malabsorption and, especially during the first weeks after bariatric surgery, frequent vomiting.52 Furthermore, body storages of thiamine are relatively small and usually suffice for only 18–20 days.53 Clinical presentation of severe vitamin B1 deficiency is mostly neuropsychiatric (Wernicke’s encephalopathy, neurological ‘dry’ beriberi) but might also include high-output cardiac ‘wet’ beriberi or gastroenterological symptoms. Patients with Wernicke’s encephalopathy may have auditory and visual hallucinations, nystagmus, ataxia or confusion and may behave aggressively. Patients with neurological ‘dry’ beriberi may present with numbness, muscle weakness, convulsions, pain in the upper and lower extremities and exaggerated tendon reflexes. Patients with ‘wet’ beriberi manifest with tachycardia, right ventricular dilatation and leg oedema as a consequence of high-output failure. Finally, patients with gastrointestinal symptoms may develop delayed gastric emptying as well as nausea, vomiting and constipation.54 The European Federation of Neurological Societies recommends follow-up of thiamine status for, at least, up to 6 months after bariatric surgery.55 Usually, thiamine deficiency is corrected by oral vitamin B1 supplementation. The standard dose would be 100 mg twice a day. If this is not successful, in most cases the thiamine deficiency is associated with bacterial overgrowth (‘bariatric beriberi’) and antibiotic therapy might be necessary to correct thiamine deficiency.56
Vitamin B2 (riboflavin)
Riboflavin is present in the flavo-coenzymes, which play a role in a number of metabolic pathways, e.g. the proper functioning of the glutathione peroxidase and reductase.57 Previously, riboflavin deficiency after bariatric surgery was described as only a biochemically but not a clinically relevant phenomenon.58 However, in patients without bariatric surgery, vitamin B2 deficiency causes stomatitis, scaly dermatitis, a sore throat and a normochromic, normocytic anaemia. Riboflavin can be supplemented orally with 5–10 mg of riboflavin a day.
Vitamin B12 (cobalamin)
Vitamin B12 deficiency is – second to iron deficiency – the most common cause of anaemia after bariatric surgery. The prevalence of vitamin B12 deficiency after RYGB and biliopancreatic diversion is 4–62% after 2 years and increases up to 19–35% after 5 years.58–61 However, because of the long-lasting storage of vitamin B12 in the liver and kidneys, up to 3 years, vitamin B12 deficiency can present in the few years after bariatric surgery. Therefore, guidelines recommend that vitamin B12 levels should be checked annually in patients who underwent surgical procedures excluding the lower part of the stomach.45 The reason for vitamin B12 deficiency is probably multifactorial, but one main mechanism is the exclusion of a significant part of the stomach from contact with nutrients after gastric bypass or biliopancreatic diversion. Therefore, production of the intrinsic factor, which is necessary for the absorption of vitamin B12, is diminished. Vitamin B12 cannot be supplemented orally and must be administered by intramuscular injection or intravenously. Interestingly, the amount of the necessary supplementation differs individually. In addition, intranasal and sublingual application of vitamin B12 bypasses the need for the intrinsic factor and is an alternative to intramuscular or intravenous application.62 In patients with suspected vitamin B12-induced anaemia, homocysteine or holotranscobalamin should be assessed as they have a higher sensitivity than vitamin B12 levels. Cobalamin deficiency presents with pernicious anaemia, depression and potentially irreversible peripheral polyneuropathy, as well as concentration difficulties, memory disturbances and myelosis funicularis.
Folic acid plays a crucial role in the synthesis of thymidine and purine as well as in the metabolism of several amino acids. Folic acid deficiency is common and must be supplemented. It is of utmost importance when patients are planning a pregnancy after bariatric surgery, since folic acid deficiency in pregnancy can lead to severe complications in the fetus (neural tube defects).63 Body stores of folate are minimal, thus the deficiency may occur at an early post-operative stage. Folic acid is well absorbed throughout the small intestine (and colon), so the deficiency is thought to be predominantly because of decreased intake rather than malabsorption and can easily be corrected by oral vitamin supplementation. Therefore, folic acid deficiency is a good marker for general adherence to vitamin supplementation of a patient.64 However, in patients with folic acid deficiency after bariatric surgery, small intestinal bacterial overgrowth must also be considered.56 In those patients, clinicians should also exclude other malabsorptive disorders such as coeliac disease. Treatment of folic acid deficiency consists of daily oral supplementation with 1–5 mg folate.
Vitamin C (ascorbic acid)
Ascorbic acid plays a crucial role in a multitude of biochemical pathways such as the hydroxylation of proline and lysine and it is a cofactor for the iron-dependent dioxygenases and copper-dependent monooxygenases. Vitamin C deficiency results in scurvy, characterized by early symptoms such as malaise, myalgias and petechiae, and might progress to degeneration of capillaries, bone and connective tissue. However, up to now, only biochemical evidence but no clinical reports of vitamin C deficiency after bariatric surgery exist.58 Treatment of vitamin C deficiency consists of daily oral 200 mg ascorbic acid.
Vitamin A includes provitamins such as beta-carotene and retinols. In high doses, vitamin A can be toxic and cause liver damage, headaches, diplopia, vomiting, dryness of mucous membranes and abnormalities of the bones. Vitamin A requires micelle formation with conjugated bile acids and is mainly absorbed in the proximal jejunum.65 Therefore, the potential cause of vitamin A deficiency after bariatric surgery might be because of a relative deficiency in bile acids as they are bypassed and to deconjugated bile acids as a result of bacterial overgrowth. The prevalence of vitamin A deficiency after gastric bypass is about 8–11%.66,67 Clinical presentation of vitamin A deficiency is impaired vision, especially poor night vision, pruritus and dry hair. Previously, guidelines did not recommend prophylactic vitamin A supplementation, but there are studies indicating that supplementation of 10 000 international units (IU) per day might be beneficial.68 In manifest vitamin A deficiency, guidelines recommend 10 000–25 000 IU/day.69
Vitamin D is known to be the key regulator of calcium and bone metabolism. Firstly, it regulates intestinal absorption and renal secretion of calcium and phosphate, and, secondly, it stimulates and inhibits osteoclast activity in order to optimize bone formation. Thus, lack of vitamin D causes inadequate calcium absorption and utilization.70 Furthermore, observational studies indicate inverse associations of circulating 25-hydroxyvitamin D with risk of death as a result of cardiovascular disease and cancer.71 Secondary hyperparathyroidism, vitamin D deficiency and bone loss are frequent complications after bariatric surgery, which can result in long-term morbidity, leading to bone loss and fractures.72 The prevalence of increased serum parathyroid hormone levels is present in about 53% of all patients after gastric bypass surgery.73 In a retrospective analysis of patients after gastric bypass, 80% demonstrated vitamin D deficiency, which persisted in 45% despite supplementation.74 However, vitamin D deficiency is also very frequently present before surgery with a prevalence of about 54%.75 Vitamin D deficiency should be corrected before surgery to minimize the risk of developing osteoporosis. Vitamin D deficiency is most severe after biliopancreatic diversion, followed by gastric bypass surgery. However, patients who undergo sleeve gastrectomy are also likely to suffer from vitamin D deficiency. Therefore, regular screening of vitamin D and parathyroid hormone levels is essential to prevent bone loss and its sequelae. Dual energy X-ray absorptiometry scanning should be considered, especially in patients at high risk of osteoporosis such as post-menopausal women.
A recent meta-analysis shows that 25-hydroxy vitamin D levels greater than 60 nmol/l are optimal for patients after bariatric surgery.76 However, there are studies indicating that 75 nmol/l is more beneficial.77 Supplementation of vitamin D should be started with oral vitamin D (ergocalciferol 50 000 IU) once weekly. Vitamin D levels should be checked 8–12 weeks afterwards. However, there are currently no evidence-based recommendations for the supplementation of vitamin D and individuals might need much higher doses to prevent bone mineral disorders.
Vitamin E comprises tocopherols and tocotrienols. Vitamin E is important for the prevention of lipid peroxidation. Vitamin E deficiency after bariatric surgery is not well studied and is characterized by neurological symptoms such as ataxia, muscle weakness and peripheral neuropathy.78 Furthermore, unexplained anaemia might be linked to vitamin E deficiency. For initial treatment, oral vitamin E supplementation at 800–1200 IU should be taken daily.
Vitamin K acts as a key factor for the formation of prothrombin and other factors involved in blood clotting. Vitamin K is mainly absorbed in the distal jejunum and ileum. Like other fat-soluble vitamins, vitamin K requires micelle incorporation for absorption and has a small body store because of rapid turnover. The absence of reports in the literature indicates that this deficiency might be rare. However, there is a study with intracranial haemorrhage in five neonates after gastric bypass of the mothers, suggesting that subclinical vitamin K might be present after gastric bypass surgery.79 Vitamin K deficiency should be supplemented with 10 mg intramuscularly at the beginning, followed by 1–2 mg/week orally or parenterally after gastric bypass or biliopancreatic diversion.
Anaemia is a common complication after bariatric surgery with a prevalence ranging from 17% after sleeve gastrectomy to 30% after biliopancreatic diversion and gastric bypass 2 years after surgery, and 45% after 5 years (for RYGB or biliopancreatic diversion).61,80–82 Gastric banding differs from the other procedures as anaemia is present in only 1.5% of cases 5 years after bypass surgery.83 The main reasons are reduced iron absorption because of the induced dissociation of the resorptive area (duodenum) from the chyme by the surgical procedure. In addition, intolerance to red meat and reduced gastric acid secretion might be important cofactors for developing iron deficiency. To enable deoxidation of ferrous iron (Fe2+) to ferric iron (Fe3+), patients should always take some ascorbic acid together with iron supplementation. However, a study demonstrated that even when combining ascorbic acid and iron tablets, iron absorption was significantly decreased throughout the study period.84 To improve resorption rate, iron tablets should not be taken at the same time as calcium tablets, since calcium increases the pH value and this reduces iron resorption, and they should ideally be taken 1 hour before or 2 hours after a meal. After identification of iron deficiency, other potential causes such as gynaecological causes (especially in young women) and gastroenterological disorders (e.g. coeliac disease) should be excluded. Patients with iron deficiency after bariatric surgery should supplement 150–200 mg iron daily in combination with vitamin C. Parenteral supplementation can be necessary, especially after malabsorptive procedures. In general, potential iron deficiency must be evaluated before surgery and can be taken into consideration when choosing the appropriate bariatric procedure.
Calcium is a meaningful mineral in normal cell physiology. Bones and teeth are the main stores in the human body. Calcium ions crossing cell membranes are an important signal for a multitude of cellular processes. Long-term calcium deficiency leads to osteoporosis and increases the risk of fractures.
Increasing evidence demonstrates an association between an elevated risk for fractures and bariatric surgery, especially after gastric bypass.85 This association is not observed following laparoscopic gastric banding86 if participants are also matched for weight. Thus, many of these data on bone loss after bariatric surgery seem to be related to gastric bypass.87
Interestingly, prior fracture is not predictive for post-operative fracture, indicating that apart from the operation procedure patients with obesity can be regarded as distinct from the general population, in which prior fracture is a strong predictor for a subsequent fracture.88 In bariatric patients, calcium and vitamin D levels must be closely monitored, especially after malabsorptive procedures such as gastric bypass or biliopancreatic diversion. In patients with hypoalbuminuria, measurement of ionized calcium levels should be considered. In addition, alkaline phosphatase levels and 24-hour urinary calcium are determined every 6–12 months in patients after gastric bypass surgery. However, the use of diuretics might influence calcium levels in the urine. If elevated, alkaline phosphatase and parathyroid hormone should be measured for diagnosis of metabolic bone disease which requires aggressive correction of calcium and vitamin D deficiency. Calcium should be supplemented by oral administration of at least 1.2 g calcium daily.
Zinc plays an important role as a cofactor of enzymatic reactions in cell growth, cell proliferation, immunity and wound healing.89 In addition, zinc can reduce the development of toxic radicals because of an antagonistic effect on iron and copper.90
The main symptoms of zinc deficiency are hair loss, nail dystrophy, glossaries and, in more severe cases, acrodermatitis, enteropathy and hypoalbuminuria. Even though clinical reports of zinc deficiency after bariatric surgery are lacking, hypozincaemia has been reported.91 Hypozincaemia can be initially treated with 220 mg zinc sulphate taken every other day, or with 50 mg zinc gluconate taken every other day.
Copper is an important component of proteins involved in neurotransmitter synthesis well as in cytochrome oxidase. Patients with hypocupraemia suffer from anaemia, neutropenia, optic neuropathy and myelopathy.92,93 The neurological symptoms usually occur more than 10 years after bariatric surgery and even after oral copper supplementation patients do not fully recover from the neurological symptoms induced by hypocupraemia.94,95 Furthermore, the clinical picture of copper deficiency is similar to that of vitamin B12 or iron deficiency, so that copper deficiency is often misinterpreted. Guidelines recommend oral copper supplementation of 2 mg/day included in routine multivitamin supplementation after bariatric surgery. In severe cases with neurological symptoms copper should be administered intravenously 2 mg to 4 mg for 5–6 days.45
Selenium is essential for the enzyme glutathione peroxidase, which protects cells from damage caused by free radicals. Clinical presentation of selenium deficiency includes cardiac myositis and in severe cases cardiomyopathy (Keshan disease) with subsequent heart failure.96,97 One case report describes life-threating cardiomyopathy 9 months after biliopancreatic diversion leading to 100 kg weight loss caused by selenium deficiency. In that patient, cardiac function improved dramatically after 3 weeks following correction of selenium deficiency and other nutritional deficiencies.96 The prevalence of selenium deficiency after bariatric surgery is about 11–15%.98 For treatment of selenium deficiency, sodium selenite (100 µg) should be taken orally.
Owing to the increasing prevalence of obesity and, in particular, morbid obesity worldwide, the frequency of bariatric procedures will increase drastically over the next decades. Bariatric surgery has been proven to reduce comorbidities and mortality in morbid obese patients. It has been shown that long-term success relies on good adherence to follow-up investigations, proper supplementation and medical treatment. Especially after malabsorptive procedures, severe nutritional deficiencies need to be considered and prevented. However, at the moment, strong scientific evidence in terms of double-blind randomized controlled studies investigating the best post-operative care with regard to macro- and micronutrients supplementation is lacking. In addition, recognition of nutritional deficiencies which have been rare in the developed world during the last decades and are now increasing because of bariatric surgery requires special attention and ongoing education. Standardized vitamin supplementation as well as post-operative treatment regimens are of major importance and need to be tailored to the bariatric procedure. Table 1 provides an overview of essential parameters to be considered and the corresponding control schedule following various bariatric procedures. In future, research should allow generating evidence-based guidelines for the appropriate perioperative care of bariatric patients.
|1 month||3 months||6 months||12 months||18 months||24 months||Annually|
|RYGB, sleeve gastrectomy|
|Full blood count||x||x||x||x||x||x|
|24-Hour urine calciumb||x||x||x|
|Biliopancreatic diversion, duodenal switch|
|Full blood count||x||x||x||x||x||x||x|
|24-Hour urine calciumb||x||x||x|