A 45-year-old woman presents with a 5-month history of fatigue, poor exercise tolerance, clumsiness, and numbness of her lower extremities. She previously underwent an uneventful laparoscopic Roux-en-Y gastric bypass (RYGB) procedure 4 years ago. Over the first 18 months postoperatively, she was adherent to taking all of her prescribed nutritional supplements and followed a high-protein, low-carbohydrate diet. She lost 76 lb (equivalent to 33% of her preoperative weight) and was able to discontinue all of her oral antidiabetic medications. Feeling well, the patient has not returned to the office since her 2-year postoperative visit. She also stopped taking her prescribed vitamin and mineral supplements for the past 12 months. Medications: None. Supplements: none.
On examination, weight 190 lb, height 5′5″, body mass index (BMI) 31.7 kg/m2, respiratory rate (RR) 14, blood pressure (BP) 126/84, and heart rate (HR) 98. Pale conjunctiva; abdomen, well-healed laparoscopy scars; neurological examination, impaired perception of position and vibration; positive Romberg test.
The heightened awareness of the multiple health benefits of metabolic and bariatric surgery has led to a steady increase in the number of procedures performed. Although many centers for metabolic and bariatric surgery have introduced multidisciplinary care teams to optimize the perioperative care for their patients, all patients return to their healthcare professional (HCP) after surgery for ongoing, long-term care which may include collaboration with the surgical team. As a result, HCPs may be the first to evaluate medical and nutritional conditions which arise because of these procedures.
The salient role of metabolic and bariatric surgery in providing durable weight loss and the resolution of multiple obesity-related comorbidities is well established and supported by a rapidly expanding body of evidence. For example, the surgically induced, gastrointestinal (GI) physiological changes that include increases in postprandial levels of GI hormones contribute to improvement in diabetes control and, in some patients, full remission. However, the anatomic and physiologic alterations can also lead to unintended consequences which may result in nutrient deficiencies.1,2
Permanent foregut anatomic revisions alter nutrient bioavailability and absorption as a result of reduced gastric acid secretion and changed food exposure to duodenal and proximal jejunal mucosal transporters. The importance of the normal foregut as it relates to nutrient absorption is summarized in Figure 10.1 where sites of nutrient absorption in the GI tract are illustrated. Of additional clinical importance are the adaptive changes which occur after surgery and their effect on preservation of carbohydrate and protein absorption. As a rule, the frequency of nutritional and metabolic consequences of these procedures are directly related to the extent of the alterations in foregut anatomy leading to the greatest impact on weight loss. For example, purely restrictive procedures like the adjustable gastric band (AGB) are associated with the least weight loss and a lesser risk of nutritional and metabolic concerns, whereas malabsorptive procedures like the biliopancreatic diversion (BPD) have the steepest weight loss trajectory and the highest risk of these complications. HCPs should be familiar with the anatomic details of the procedures which will, in turn, facilitate the medical evaluation of surgery-related complications. These details are provided in Chapter 9. This chapter will review the medical, metabolic, and nutritional management of patients who undergo metabolic and bariatric surgery with an emphasis on recognition of complications, current management, strategies for prevention, and close collaboration with the surgical multidisciplinary center.3
FIGURE 10.1 Sites of nutrient absorption in the gastrointestinal tract.
EARLY POSTOPERATIVE MANAGEMENT (<3 MONTHS)
Since the advancement of laparoscopic techniques, improved anesthesia, and postoperative pain management through the early recovery after bariatric surgery (ERABS) protocols, patients are discharged, on average, 1 to 2 days following surgery. While this is beneficial for the patient, it is important for the HCP to become more familiar with the different bariatric surgery procedures performed as well as the potential complications in the early postoperative period.
With the advent of centers of excellence and improved laparoscopic techniques, the incidence of an anastomotic leak postoperatively is extremely low.4 However, when they occur, signs and symptoms usually become apparent on postoperative day 3 or 4, often after the patient has been discharged from the hospital. Anastomotic leaks are more common in patients undergoing RYGB but can occur with the sleeve gastrectomy (SG). HCPs should be familiar with the signs and symptoms of an anastomotic leak and, most importantly, be in contact with the bariatric surgeon for management. This condition is a surgical emergency and requires a high level of suspicion.
The cardinal signs of an anastomotic leak include
tachycardia greater than 120 beats per minute
respiratory rate greater than 22 per minute
extravasation of contract on computed tomography (CT) scan or upper gastrointestinal series
The cardinal symptoms of an anastomotic leak include
shortness of breath
While the suggested workup for a suspected anastomotic leak should be to obtain a CBC with differential and comprehensive metabolic panel and order a CT scan of the abdomen with contrast, the most important next step, if an anastomotic leak is suspected or diagnosed, is prompt communication and transfer to the bariatric surgeon. With early detection, conservative management with endoscopic stenting and parenteral antibiotics is often sufficient in managing these patients. This again underscores the need for the HCP‘s collaboration with the bariatric surgery team to ensure the best possible outcomes for their patients.
Nausea and Vomiting
Nausea and vomiting can occur following any of the bariatric surgery procedures.5 Although most commonly unrelated to obstruction or anatomical defect of the surgery, if the patient is not able to keep anything down by mouth for 24 hours, an evaluation is warranted. Nausea alone is most common. It can most often be managed by antiemetic agents such as ondansetron hydrochloride 4 mg orally and hydration. Similar to suspicion of an anastomotic leak, patients with persistent nausea or vomiting should be evaluated by the bariatric surgery team.
One important sequela of persistent nausea and vomiting is Wernicke encephalopathy.6 This is truly the only “medical emergency” that the HCP should be familiar with and facilitate treatment even before referring to the surgical team. Patients with persistent vomiting may deplete their thiamine stores in just a few days. The signs and symptoms of thiamine deficiency (Wernicke encephalopathy) are
Ataxia (unsteady gait)
Nystagmus (repetitive, uncontrolled movements of the eyes)
Mental confusion (disoriented, hard time focusing or making decisions)
Due to altered GI anatomy from the metabolic and bariatric surgery as well as persistent vomiting, vitamin B1 (thiamine) levels fall. Moreover, with the common addition of dextrose in intravenous hydration, vitamin B1 is driven intracellularly which further depletes stores. The HCP should have a high index of suspicion for Wernicke encephalopathy and a low threshold for treatment. If left untreated, Wernicke encephalopathy can lead to an irreversible pontine stroke. If treated early, symptoms should resolve quickly without sequelae. Depending on the severity of deficiency, treatment should consist of7
Intravenous (IV) administration of 200 mg of thiamine three times per day, or
Oral administration 500 mg once or twice daily for 3 to 5 consecutive days followed by 250 mg for the next 3 to 5 days, or
Intramuscular (IM) administration of 250 mg daily for 3 to 5 days or 100 to 150 monthly.
Once the patient can tolerate oral intake, 100 mg of thiamine supplementation is recommended for at least 30 days. Of note, often Wernicke encephalopathy is mistaken for vitamin B12 deficiency due to ataxia, but unfortunately, vitamin B12 supplementation will have no effect on treating Wernicke encephalopathy. The bottom line, anytime a bariatric surgery patient presents with persistent nausea and vomiting, thiamine supplementation should strongly be considered.
Thiamine deficiency is a medical emergency. Any bariatric surgical patient who presents with persistent vomiting and signs/symptoms of Wernicke-Korsakoff syndrome should be empirically treated with thiamine supplementation.
INTERMEDIATE MEDICAL MANAGEMENT AFTER BARIATRIC SURGERY (<6 MONTHS)
As discussed in Chapter 9, metabolic and bariatric surgery is the most effective long-term treatment approach for patient with severe obesity or moderate obesity with a medical complication. As a result of the weight loss and associated anatomical and physiological changes, there is an improvement or resolution of the patients’ chronic obesity-related medical problems such as diabetes mellitus, obstructive sleep apnea, fatty liver disease, hypertension, and dyslipidemia. This section will review optimal medical management following metabolic and bariatric surgery.
Metabolic and bariatric surgery has been shown to be a safe and effective treatment option for patients with type 2 diabetes mellitus (T2D). For reasons not entirely clear, improvements in insulin sensitivity can occur immediately after metabolic and bariatric surgery and even before any appreciable weight loss has occurred.8 For this reason, the dose of any preoperative antidiabetic medications must be reduced or discontinued early after surgery in order to avoid hypoglycemia. For patients who are managed with insulin, the daily insulin regimen can be often held and replaced by using a sliding correction factor as needed, particularly for patients who undergo RYGB or BPD. Moreover, since dietary intake is significantly reduced both in volume and time of consumption, longer acting agents like insulin glargine are usually better tolerated if post-op insulin is needed.
Depending on the level of preoperative glycemic control, patients adequately controlled with only oral agents may require little, if any, glucose-lowering medication, especially in the immediate postoperative period (7 to 10 days). If an RYGB patient requires resumption of oral medications, regular release and crush or liquid rather than sustained release/extended release formulations are recommended in order to maximize absorption.3 Patients undergoing an SG may not require changes in their formulation. Metformin, both regular and extended release, may not be well tolerated due to its GI intolerance with either procedure within the first 30 days of surgery. The thiazolidinediones (TZDs) may be better tolerated than metformin; however, because of their propensity to cause weight gain or retard weight loss, they should be prescribed judiciously. Sulfonylureas, although better tolerated from the GI standpoint, can produce significant hypoglycemia and therefore should be either discontinued entirely or used at a lower dose with frequent monitoring of blood glucose. Newer classes of medications have been approved for the treatment of T2D. These medications typically do not cause hypoglycemia, are relatively well tolerated, and may also augment weight loss. The glucagon-like peptide-1 (GLP-1) agonists and the sodium glucose co-transporter 2 (SGLT2) inhibitors are both approved for glycemic control, and some agents in these therapeutic classes have been shown to reduce cardiovascular events.9,10,11
For a variety of reasons, blood pressure routinely is decreased in the immediate postoperative period. This, in turn, necessitates using reduced doses of antihypertensive medications. Usually medication dosages can be cut in half, and angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) that are held 48 hours prior to surgery can be restarted postoperatively at a reduced dose. Diuretic agents are typically discontinued following surgery to avoid dehydration and electrolyte abnormalities. As discussed previously, medications that are prescribed in RYGB patients should be in the regular release and crushed/liquid formulation to ensure maximum absorption.
Due to the potential withdrawal effect with abruptly stopping psychotropic medications (particularly antidepressant drugs), they should be continued postoperatively as soon as the patient is able to tolerate p.o. intake. Similar to other medications, they should also be prescribed in the regular release, crushed/liquid form for RYGB patients. Medications that may cause weight gain, such as tricyclic antidepressants and mirtazapine, should be discontinued if possible and replaced with an alternative drug if possible.
Depression and quality of life usually improves in the weeks to months following metabolic and bariatric surgery. However, the HCP should continuously reassess the patient for a recurrence of depression or development of new-onset depression. Untreated depression can contribute to postoperative weight gain. Patients exhibiting major depressive symptoms should be considered for referral to a mental health specialist. In a recent meta-analysis, metabolic and bariatric surgery patients were about four times more likely than matched controls to commit suicide or attempt self-harm.12
Although not as immediate as the improvement in insulin sensitivity/glycemic control, blood lipid profiles have been shown to significantly improve from 3 to 12 months after metabolic and bariatric surgery. Since statin agents may cause nausea in the immediate postoperative period and liver transaminase levels may increase with rapid weight loss, consideration for holding lipid-lowering medications for the first 12 weeks after surgery and reevaluating their need may outweigh the risk of restarting in the immediate postoperative period. However, for patients who are prescribed statin agents for secondary prevention of acute coronary events, the medication should be continued in the immediate postoperative period.
Aspirin and Nonsteroidal Anti-Inflammatory Management
Due to the increased risk of postoperative ulcers, strictures, and bleeding, the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided in RYGB patients.3 Numerous studies have demonstrated increased complications, especially with concomitant tobacco use. If chronic anti-inflammatory use cannot be avoided, consideration for a bariatric procedure without the risk of marginal ulceration, such as the SG, may be in the patient’s best interest. In RYGB patients, short courses (3 to 10 days) of anti-inflammatory therapy such as ibuprofen or naproxen for acute gouty attacks, migraine headaches, and acute musculoskeletal strain are usually well tolerated but should be taken with food to lessen the effect of direct mucosal irritation. It is generally considered safe for patients to resume low-dose aspirin therapy for antiplatelet cardioprotective benefits after the first 30 days of their surgery.
Oral Contraceptive Management
Due to improvement in insulin sensitivity and estrogen metabolism immediately after metabolic and bariatric surgery, ovulatory rates often improve soon after the bariatric surgical procedure despite little, if any, weight loss. However, pregnancy is not recommended for at least 12 months after surgery due to the increased catabolism and increased risk of nutritional deficiencies.13 Like other medications, oral contraception absorption may be inconsistent in RYGB patients, and therefore, an alternative barrier method of birth control should be recommended. This becomes an important issue to discuss with patients, particularly for those who have polycystic ovarian syndrome (PCOS) or amenorrhea with resultant infertility for many years prior to surgery and are under the mistaken impression that they will not be able to conceive.
Medications such as medroxyprogesterone acetate (Depo-Provera) injections may be effective to prevent pregnancy, but also can inhibit weight loss after surgery and should be avoided if possible. Intrauterine devices may be a consideration as an alternative method of birth control. Also, the use of patches for contraception in women with a BMI greater than 35 kg/m2 should be used with caution due to the significant loss of effectiveness and unreliability.
Obstructive Sleep Apnea Management
Obstructive sleep apnea (OSA), as measured by the apnea-hypopnea index (AHI) and daytime sleepiness, often improve after bariatric surgery. Many patients may need the face mask readjusted as the contours of their face change with weight loss. While many patients simply stop using continuous positive airway pressure (CPAP) or oral devices, it is recommended that a repeat sleep study be performed prior to the decision of discontinuing CPAP to ensure that treatment is no longer necessary.14 Changing the prescription to AutoPAP, which detects the lowest amount of inhalation pressure needed throughout the night and adjusts accordingly, may be an option as well. Although there is no specific guidelines for the timing of reevaluation, several high-volume bariatric surgery programs recommend a repeat sleep study after 30% to 40% weight loss or 6 to 8 months after surgery.
LONG-TERM CONSEQUENCES OF METABOLIC SURGERY (>6 MONTHS)
Metabolic Bone Disease After Bariatric Surgery
Obesity was originally felt to strengthen bone because of the long-term weight-bearing burden on bone. However, more recent evidence suggests that obesity may not be as protective on bone health. Factors which contribute to the site-specific fracture risk in obesity include adipokine effects on bone physiology, systemic inflammation, reduced mobility, and vitamin D deficiency.
The prevalence of vitamin D deficiency in individuals with obesity varies from 20% to 85%. Mechanisms include lack of sufficient sun exposure to convert 7-dehydrocholesterol (7-DHC) to vitamin D3 and sequestration of vitamin D in adipose tissue.15 In patients with overweight and obesity, modest weight loss has been shown to result in small decreases in bone density of the hip with sparing of the spine. With greater degree of weight loss, metabolic and bariatric surgery is associated with a deterioration in bone health with specific effects shown in Table 10.1.
TABLE 10.1 Clinical Findings Showing the Deterioration in Bone Health After Metabolic Surgery
EFFECTS OF METABOLIC SURGERY ON BONE HEALTH
Alterations in bone remodeling with increase in markers of remodeling
Increased rates of bone loss
Bone loss by quantitative imaging (DEXA)
Alterations in bone strength
Microarchitectural deterioration related to increased PTH levels
Due to greater malabsorption, the RYGB and BPD procedures are associated with the greatest risk of bone loss and fracture risk compared to the SG or the AGB. The pathogenesis of bone loss after metabolic and bariatric surgery is multifactorial. Malabsorptive surgery results in reduced intestinal absorption of calcium and vitamin D. Reduced gastric acid production related to surgery and antacid use will further reduce calcium absorption, leading to hypocalcemia which is a stimulus for parathyroid hormone (PTH) release and a diagnosis of secondary hyperparathyroidism. This in turn increases bone loss. Evidence also suggests that bone loss after bariatric surgery correlates with the amount of weight loss and the rate at which it occurs due to increased activation of the calcium-PTH axis. Surgery has also been shown to increase the bone turnover markers, N-terminal telopeptide of type I collagen (NTX), bone-specific alkaline phosphatase (BSAP), and osteocalcin. One important marker, sclerostin, is produced in osteocytes, and its main function is to inhibit bone formation. Mechanical unloading of bone after weight loss has been associated with an increased level of sclerostin resulting in significant loss in bone mineral density (BMD). Monitoring of bone health in postoperative patients undergoing all types of bariatric procedures is critical for its preservation. Guidelines for monitoring are summarized in Table 10.2.16
Biochemical indices for diagnostic testing for metabolic bone disease include serum calcium, phosphorus, magnesium, 25(OH)D (and 1,25(OH)D if renal function is compromised), BSAP or osteocalcin, PTH, and a bone marker of resorption such as urine n-telopeptide (NTX), 24-hour urinary calcium excretion, and albumin and prealbumin. Routine monitoring should include only PTH, 25(OH)D every 3 to 6 months for the first year and annually thereafter for patients undergoing AGB, SG, or RYGB. For those who have undergone BPD with or without switch, the following are recommended: PTH and 24-hour urine calcium monitoring every 6 to 12 months, urine N-telopeptide annually, and osteocalcin as needed3 (Table 10.3).
TABLE 10.2 Laboratory Screening and Monitoring for Bone Health After Surgery
GUIDELINES FOR MONITORING BONE HEALTH AFTER METABOLIC SURGERY
Laboratory tests used in the evaluation of bone health
Calcium, phosphorous, magnesium
25(OH) vitamin D (and 1,25(OH) vitamin D if renal function is impaired)
Dual-energy x-ray absorptiometry (DEXA) is the gold standard for measuring bone density; the results are reported in T- and Z-score. The Z-score should be used for premenopausal women and men younger than 50 years. This score is the patient’s BMD expressed in standard deviations (SDs) from the mean in an age- and sex-matched reference population. A low Z-score (below -2.0) is a concern for less bone mass compared to similar aged matched individual. Whereas the T-score is also calculated as an SD from the mean, the comparison group is that of young healthy adults. The World Health Organization (WHO) classifies T-scores above -1 SD as normal, between -1 and -2.5 SD as osteopenia, and below -2.5 SD as osteoporosis. Guidelines recommend DEXA 2 years postoperatively for both men and women after any type of metabolic and bariatric surgery. HCPs should evaluate each postoperative surgical patient based on risk factors which include age, baseline vitamin D and PTH status, weight loss trajectory, and activity level for decisions related to assessment of bone density.17
An abnormal DEXA scan may be indicative of both primary and secondary disease. In the post-bariatric surgery patient, one should first suspect secondary bone disease due to nutritional deficiencies. The etiology of confirmed vitamin D deficiency, hypocalcemia, hypomagnesemia, hypophosphatemia, elevated alkaline phosphatase, secondary hyperparathyroidism, and even protein or vitamin B12 deficiency should be clearly defined and appropriately treated. Treatment should also include weight-bearing exercise and resistance training to mitigating bone loss after surgery.
TABLE 10.3 Routine Monitoring for Metabolic Bone Disease for Bariatric Surgery Patients
BPD w/wo DS
Every 3-6 months for the first year and annually thereafter:
DEXA monitoring may be indicated at baseline and at about 2 years
Every 3 months for the first year, every 3-6 months thereafter:
DEXA monitoring may be indicated at baseline and at about 2 years
BPD w/wo DS, biliopancreatic diversion with or without duodenal switch; DEXA, dual-energy x-ray absorptiometry; RYGB, Roux-en-Y gastric bypass; SG, sleeve gastrectomy.
For treatment of vitamin D deficiency, The Endocrine Society recommends a dose two to three times higher (6,000 to 10,000 IU/day) for patients with obesity, patients with malabsorptive syndromes, and patients on medications affecting vitamin D metabolism. A maintenance therapy of at least 3,000 to 6000 IU/day is recommended. Correction of vitamin D deficiency in bariatric surgery patients generally requires higher doses, particularly in the malabsorptive procedures. Repletion has been recommended for as high as 50,000 to 150,000 IU of D2 or D3 daily for one to 2 weeks. A maintenance dose of up to 50,000 IU one to three times per week may be required. Cholecalciferol (D3) has demonstrated superiority at maintaining 25(OH)D levels and has been recommended particularly if dosing is less than once weekly. It is recommended that both D2 and D3 be taken with a meal containing some fat to maximize absorption.
For patients with persistently low bone density on DEXA with clinical and biochemical evidence of bone disease, additional pharmacologic treatment with a bisphosphonate should be considered. Current recommendations include intravenous therapy with zoledronic acid, 5 mg once a year, or ibandronate, 3 mg every 3 months, due to higher risk of anastomotic ulceration and decreased absorption in RYGB patients. Patients without concerns for risk of ulceration or lack of absorption can be supplemented by mouth using alendronate 70 mg/week, risedronate 35 mg/week (or 150 mg/month), or ibandronate 150 mg/month.
Nephrolithiasis After Bariatric Surgery
An increase in the incidence of nephrolithiasis after metabolic and bariatric surgery has been clearly established, particularly in BPD and RYGB patients, where the calcium oxalate stone risk is threefold that of age-matched controls. A recent study also revealed a 7.6% incidence of nephrolithiasis after any bariatric surgery with a post-RYGB kidney stone incidence at 8.1%. Stone development after malabsorptive (BPD/RYGB) and restrictive (SG) bariatric procedures are largely caused by changes in 24-hour urine profiles, such as increased urinary oxalate, decreased urine volume, and reduced urinary citrate levels leading to increased risk of kidney stones.18 Increased oxalate absorption and a hyperoxaluric state is facilitated by increased colonic oxalate related to increased colonic fatty acid and bile salts as well as alterations in the gut microflora.
The most important factor in preventing stone formation is increasing fluid intake since a greater urinary volume provides a dilutional effect leading to decreased supersaturation ratios. Patients should strive to maintain a daily urine production of at least 2 L by increasing fluid intake, limit dietary oxalate (<150 mg/day) and fat intake (<40 g/day), and consume the Recommended Daily Allowance of calcium (1,000 to 1,200 mg/day).19 Supplemental calcium is also recommended as it binds oxalate, leading to excretion in feces. Postoperative patients who develop symptomatic stones should have an evaluation and intervention by a urologist.
Postprandial Hyperinsulinemic Hypoglycemia
An important unintended metabolic complication which has become increasingly recognized is postprandial hyperinsulinemic hypoglycemia (also called post-bypass hypoglycemia or PBH), which is characterized by hypoglycemic symptoms developing 1 to 3 hours after a meal, in association with a low blood glucose level of <54 mg/dL and relieved by the ingestion of carbohydrate. PBH is distinct from a condition called dumping syndrome where vasomotor symptoms occur within minutes to 1 hour after a meal of calorie-dense food, caused by rapid hyperosmotic food entry into the jejunum which induces fluid shifts into the small intestine.20 Dumping usually occurs early after surgery, most commonly after RYGB, whereas classic PBH commonly develops between 1 and 4 years after surgery.
As PBH has become increasingly recognized, additional studies with larger patient numbers suggest that this condition is most commonly associated with RYGB but has been described after BPD with DS and GS as well. The exact prevalence of this disorder remains unclear, but with increased number of patients undergoing bariatric surgeries, HCPs will likely encounter such patients.