**2. Micronutrient deficiencies prior to bariatric surgery**

Nutritional deficiencies often exist prior to BS [3–5]. Subjects with obesity typically adopt an unhealthy high calorie, low quality diet with unbalanced nutritional composition [6]. For instance, one study showed that in female BS candidates, despite consumption of high-caloric diet (2801 ± 970 kcal/day), 66% of them had at least a single micronutrient deficiency [7]. Prior to BS, low iron, ferritin, vitamin B12 and hemoglobin were observed among 12.6%, 8.7%, 10.6% and 7.7%, of patients respectively [7]; and the incidence of folate deficiency before BS was 26.8% [8]. Vitamin D deficiency is the most common deficiency in patients undergoing BS with a prevalence as high as 78.8% [7, 8].

Research found that low preoperative levels of hemoglobin, vitamin B12, and ferritin were independently associated with reduction in the levels of micronutrients postoperatively [8]. Moreover, vitamins D and B1 and albumin deficiencies before BS predicted deficiencies one year after surgery [8].

Such findings highlight the need for complete nutritional assessments and adequate correction of pre-existing deficits before BS. Therefore, all BS candidates must undergo appropriate nutritional evaluation, including micronutrient measurements at least once preoperatively. Screening should include iron studies, and vitamins D and B12 and folic acid levels. The repetition of the tests until surgery should be individualized as clinically indicated [9, 10]. In comparison with purely restrictive procedures, more extensive nutritional evaluations are required for malabsorptive procedures. For instance, thiamine and vitamins A and E levels may be assessed in patients prior to Roux en Y gastric bypass (RYGB) and biliopancreatic diversion with duodenal switch (BPD/DS) [10].

Deficiencies found on screening prior to BS should be treated accordingly to avoid worsening of the symptoms post-surgery [9]. For vitamin D, there is a lack of solid evidence regarding the cutoff value where treatment should be started. A group of experts advocated supplementation in all patients with values below 20 ng/mL, and in an individualized manner for values between 21 and 30 ng/mL [9].

#### **3. Micronutrient deficiencies post bariatric surgery**

#### **3.1 Causes of micronutrient deficiencies post bariatric surgery**

Several factors and mechanisms contribute to the development of nutritional deficiencies post BS. Below are some examples:

*Nutritional Deficiencies Post Bariatric Surgery: A Forgotten Area Impacting Long-Term Success... DOI: http://dx.doi.org/10.5772/intechopen.95123*

## *3.1.1 Non-compliance with nutritional supplementation*

Nonadherence to the recommended nutritional supplementation is recognized as a critical factor that leads to nutritional deficiency after BS. Compliance with multivitamins tends to be good in the early post-surgery period and decreases on the long term. For instance, a study of 16,620 patients post BS showed that the pharmacy dispensing of micronutrient supplements by patients significantly decreased between the first and fifth years for iron (from 27.7 to 24.5%), calcium (from 14·4 to 7·7%), but increased for vitamin D (from 33·1 to 34·7%) [11]. Barriers to vitamin adherence post BS include forgetting to take the supplementation and difficulty in swallowing the pills [12].

#### *3.1.2 Lack of follow up*

Despite clear international guidelines, long-term follow-up after BS is poor. A study assessed the follow up with the bariatric surgeon after RYGB and demonstrated a significant increase in the time between follow ups (13.3 ± 7.8 vs. 86.9 ± 39.9 months) in the long-term [13]. The same study demonstrated that a shorter time since last surgeon visit was independently predictive of multivitamin use (p = 0.001) [13]. Research also reported that male sex, younger age, absence of type 2 diabetes and poor 1-year follow-up were predictors of poor 5-year follow-up [11].

#### *3.1.3 Other causes*

Other contributing factors include pre-operative deficiencies, post-surgery food intolerance, poor eating habits, vomiting, changes in taste and eating patterns [14].

#### **3.2 Mechanisms of micronutrient deficiency after bariatric surgery**

The underling mechanisms that contribute to micronutrient deficiency following BS include reduced food intake due to restrictive effect of surgery, rerouting of nutrient flow which affect absorption, and changes in gastrointestinal anatomy/ physiology post-surgery. It is important to note that the anatomical changes and the mechanisms of action of the various procedures dictate the frequency and severity of nutritional deficiencies after BS. For instance, micronutrient deficiencies are less common in restrictive procedures such as gastric banding (LAGB) and laparoscopic sleeve gastrectomy (LSG), where there are no alterations of the intestinal continuity and normal digestive processes. However, micronutrient deficiencies are more common after surgical procedures that cause malabsorption such as RYGB, oneanastomosis gastric bypass (OAGB), single anastomosis duodeno–ileal bypass with sleeve gastrectomy (SADI-S) and BPD/DS [10, 15].

#### **3.3 Water soluble vitamin deficiency post bariatric surgery**

#### *3.3.1 Vitamin B1 (thiamin)*

Vitamin B1 is absorbed in the jejunum and therefore may be excluded from absorption after RYGB and BPD/DS [16]. Additionally, the storage of thiamine is low in the human body and can become rapidly devoid without regular and adequate intake [8]. These characteristics might explain why thiamin deficiency is observed subsequent to a short period of persistent vomiting after surgical complications such as band slippage post LAGB [17], stomach oedema after LSG [18],


*Nutritional Deficiencies Post Bariatric Surgery: A Forgotten Area Impacting Long-Term Success... DOI: http://dx.doi.org/10.5772/intechopen.95123*


*laparoscopic sleeve gastrectomy, RYGB Roux en Y gastric bypass, BPD/D biliopancreatic diversion.*

#### **Table 1.**

*Summary of common micro and micro nutritional deficiencies.*

or stoma stenosis after RYGB [19]. Cases of thiamine deficiencies have also been reported after BPD/DS [20].

The manifestations of thiamine deficiency include peripheral neuropathy, Wernicke's encephalopathy (WE), Korsakoff's psychoses and cardiomyopathy [14, 10] (**Table 1**). These clinical conditions could be severe or even fatal if they are not recognized and treated promptly**.** Borderline deficiency may cause less severe symptoms that could be missed. Therefore, oral or parenteral thiamine supplementation should be initiated in any bariatric patient presenting with persistent vomiting severe enough to interfere with adequate nutrition, even before obtaining confirmatory laboratory data [10, 14]. In symptomatic patients, oral supplementation may be used only after 1–2 weeks of parenteral administration and continued until symptom resolution [10].

In severely malnourished patients receiving nutrition support, empiric thiamine supplementation along with fluid and electrolyte monitoring and replacement are indicated to avoid exacerbation of thiamin deficiency and refeeding syndrome [10]. Refeeding syndrome is a condition that results from fluid and electrolyte imbalances, particulalry hypophosphatemia, causing serious complications such as cardiac arrhythmias [21]. Empiric thiamine supplementation is also indicated for high-risk bariatric patients and patients with risk factors for thiamine deficiency such as females, African Americans, patients not attending the dietitian clinic, patients with gastrointestinal symptoms, heart failure, persistent vomiting, or on parenteral nutrition and those with excessive alcohol use [10]. The recommended dose for prevention and treatment of thiamin deficiency is summarized in **Table 1**.

**Wernicke Encephalopathy:** is a serious complication of thiamin deficiency. It is an acute neuropsychiatric syndrome characterized by ataxia, ophthalmoparesis, nystagmus, and confusion. WE most commonly occurs during the first weeks to months following BS [17]. Among patients who were diagnosed with WE, 52% had RYGB and 21% had LSG [15]. Symptoms of WE are typically preceded by malnutrition, which results from persistent prolonged vomiting, although vitamin noncompliance or increased alcoholism are also risk factors [15]. Radiologic imaging of the brain especially magnetic resonance imaging can be used to support the diagnosis of WE, but is not always sensitive to WE symptoms. Findings include hyperintensities in the thalamic region, the mammillary bodies, and the region around the third and fourth ventricle [22]. The recommended treatment is 500 mg of parenteral thiamine three times daily until symptoms of acute WE resolute [10]. The treatment is lifesaving and has the potential to reverse this acute neuropsychiatric syndrome. Recovery typically occurs within 3–6 months of initiation of therapy if the symptoms are recognized early [23]. Studies have shown that patients who received suboptimal thiamin dose or had more than one acute symptom were more likely to progress later into a permanent neurologic deficits (Korsakoff's syndrome) [17]. Korsakoff's syndrome is neuropsychiatric disorder characterized by severe amnesia, executive problems, and confabulations, leading to lifelong impairment [17].
