ABSTRACT

Bariatric surgery can result in substantial weight loss and significant metabolic improvements. Therefore, postoperatively, clinicians should be prepared to taper treatments for weight-related chronic metabolic diseases. For patients with type 2 diabetes, early and dramatic improvements in glucose homeostasis require anticipatory management. This includes insulin dose reductions, discontinuation of certain oral agents, and close monitoring. Antihypertensive medications should be adjusted to avoid hypotension. Even after postoperative improvements in dyslipidemia, some patients will continue to meet criteria for statin therapy. While many obesity-related diseases will improve, clinicians should also be prepared to manage postoperative medical and nutritional complications. Micronutrient deficiencies are common, and professional guidelines provide recommendations for preoperative screening, universal postoperative supplementation, micronutrient monitoring, and repletion strategies. Changes in gastrointestinal physiology may result in dumping syndrome, and patients may report early gastrointestinal and vasomotor symptoms after eating. In contrast, post-bariatric hypoglycemia is a rare complication of malabsorptive procedures, resulting in insulin-mediated hypoglycemia after carbohydrate-containing meals. Rapid weight loss may increase the risk of cholelithiasis, which can be mitigated by ursodiol. After malabsorptive procedures, enteric hyperoxaluria and other factors may result in nephrolithiasis, which can be addressed with hydration, dietary interventions, and calcium. All bariatric operations induce a high bone turnover state, with declining bone mineral density (BMD) and increased fracture risk. Appropriate strategies include adequate calcium and vitamin D supplementation and targeted BMD screening. Long-term strategies to prevent weight regain include adherence to comprehensive lifestyle interventions and identification and avoidance of medications that promote weight gain and may include weight management medications. In summary, given dramatic physiologic changes with bariatric surgery, clinicians should be prepared to taper treatments for chronic metabolic diseases, to manage postoperative medical and nutritional complications, and to identify and manage risk for weight regain. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.

INTRODUCTION

Bariatric surgery is a highly effective treatment for obesity, inducing substantial and durable weight loss and improvement in obesity-related comorbidities (1). Moreover, it reduces mortality (2-4). The surgical treatment of obesity is discussed in the Endotext chapter entitled “Surgical Treatment of Obesity”, with sections devoted to the modern bariatric surgical procedures including the biliopancreatic diversion with duodenal switch (BPD/DS), Roux-en-Y gastric bypass (RYGB), sleeve gastrectomy (SG), and adjustable gastric band (AGB) (5). This chapter also addresses the benefits of bariatric surgery on obesity-related conditions including type 2 diabetes (5).

As the postoperative bariatric surgery patient population increases with time, endocrinologists and primary care providers must have the training and tools required to meet the population’s medical needs. In this chapter, we first review the postoperative approach to chronic co-morbid medical conditions, focusing on type 2 diabetes, hypertension, and dyslipidemia. We then discuss potential medical and nutritional complications of bariatric surgery (Table 1), including the pathophysiology, screening, and treatment of those potential complications. Psychiatric and behavior disorders, such as depression and substance abuse, associated with bariatric surgery are not discussed in this chapter as they are not usually managed by endocrinologists.

POSTOPERATIVE APPROACH TO CHRONIC METABOLIC CONDITIONS

In the perioperative and early postoperative periods (usually the first 30 to 90 days after surgery), a patient’s surgeon will monitor closely for surgical complications such as anastomotic leak, deep vein thrombosis, and infection. An experienced dietitian generally assists with meal initiation and progression. Later, regular follow-up with the surgeon—including, eventually, annual follow-up for life—is essential for assessing weight loss success and reinforcing necessary lifestyle modifications. The primary care provider or endocrinologist assumes responsibility for the early and later postoperative management of chronic medical conditions, including diabetes, hypertension, and dyslipidemia. This section summarizes the effects of bariatric surgery on those conditions and the recommended approach to management.

PREVENTION AND TREATMENT OF POSTOPERATIVE MEDICAL AND NUTRITIONAL COMPLICATIONS

While a patient’s surgeon monitors closely for postoperative surgical complications, the primary care provider or endocrinologist often identifies and manages postoperative medical and nutritional complications. This section reviews these potential complications (Table 1), with attention to pathophysiology, screening, and therapeutic approach.

Bone Loss and Fracture Risk

Bariatric surgery has a significant impact on bone metabolism. All bariatric procedures induce a high postoperative bone turnover state. For example, after RYGB biochemical markers of bone resorption have been shown to double in the first postoperative year (87-90). Bone mineral density (BMD) assessed by dual-energy X-ray absorptiometry (DXA) decreases (87-90), and while there has been concern about potential unreliability of DXA assessment in the setting of marked weight loss and changing soft tissue composition (91,92), declines in BMD have now been demonstrated clearly using quantitative computed tomography (QCT) at the axial skeleton and high-resolution peripheral QCT at the appendicular skeleton (93-98). Decline in BMD has been most consistently reported after RYGB (88,89,99), but also after BPD/DS (100,101) and SG (96,98,102-104). In one recent study comparing cohorts of adults undergoing RYGB vs. SG, some bone density and microstructural parameters changed less after SG than after RYGB, while for other parameters, where was no evidence of smaller effects after SG (98). After AGB, DXA-assessed BMD decreases modestly at the proximal hip but not at the spine (88,89), with reductions in hip density smaller than those after RYGB (105). While some loss of bone mass may be an appropriate physiological response to weight loss, BMD has been shown to decline progressively after RYGB, even after weight stabilization (94,103,106) and mild weight regain (106). Postmenopausal women appear to have the greatest declines in bone density and microstructure after RYGB (107) and after SG (98).

Ultimately, the important question is whether fracture risk increases after bariatric surgery. Studies have now indicated that fracture risk is indeed higher after bariatric surgery in comparison to obese (108-110), non-obese (109), and general population (111) nonsurgical controls. There may be bias introduced when studies identify obese nonsurgical controls based on the assignment of diagnostic codes for morbid obesity, as those nonsurgical patients may be sicker. However, studies with BMI-matching also demonstrate an increase in fracture risk (112,113). Fracture risk after bariatric surgery appears to vary by bariatric procedure, with the risk most clearly defined for RYGB (112). Fracture risk is higher after RYGB than AGB (114,115). Studies published to date about fracture after SG (110,116) have been shorter-term because the procedure is newer; longer-term data are needed before conclusions can be drawn.

Negative skeletal effects resulting from bariatric surgery appear to be multifactorial (90,117-119). Potential mechanisms include the decreased skeletal loading with weight loss; loss of muscle mass; changes in levels of fat-secreted hormones (adipokines), sex steroids, and gut-derived hormones; changes in bone marrow adipose tissue (120); and, importantly, nutritional factors including vitamin D deficiency, inadequate calcium intake, and calcium malabsorption. Intestinal calcium absorption has been shown to decrease after RYGB even in the setting of optimized vitamin D status (99), presumably because the bypassed duodenum and proximal jejunum are usually the predominant sites of active, transcellular, 1,25-dihydroxyvitamin D-mediated calcium uptake, and the distal intestine is unable to compensate. In response to calcium malabsorption after RYGB, parathyroid hormone (PTH) secretion increases, and the effects of PTH include an increase in bone resorption in order to maintain serum calcium concentration. Meanwhile, bone resorption also increases due to non-PTH-mediated processes like mechanical unloading and changes in the hormonal milieu. This mobilization of calcium from the skeleton may actually dampen the need for greater PTH secretion (Figure 1). A recent study showed that intestinal calcium absorption also decreases after SG, even in the setting of robust vitamin D status, even though it is not a bariatric procedure categorized as malabsorptive (121). Participants with lower postoperative fractional calcium absorption had greater losses of hip BMD, suggesting that calcium malabsorption may contribute to detrimental skeletal effects not only after RYGB but also after SG.

Figure 1.

Effects of RYGB on calcium homeostasis. Reprinted from J Steroid Biochem Mol Biol, Schafer AL, Vitamin D and intestinal calcium transport after bariatric surgery, 173:202-210, 2017 (122), with permission from Elsevier.

Strategies that aim to decrease the risk of postoperative skeletal complications have been included in the AACE/TOS/ASMBS Clinical Practice Guidelines (24) as well as in an additional bone metabolism-focused position statement from the ASMBS (123). A reasonable approach is described in Table 8.

Preoperatively, testing of 25-hydroxyvitamin D level with treatment of vitamin D deficiency is recommended for patients preparing to undergo any bariatric surgical procedure (33). DXA scanning should be performed based on age-appropriate recommendations of the Bone Health and Osteoporosis Foundation (124) or the United States Preventive Services Task Force (125); other patients with risk factors for osteoporosis or fracture, such as postmenopausal women and older men, may be considered for baseline BMD assessment.

Postoperatively, universal supplementation with calcium and vitamin D are necessary after any bariatric surgical procedure, even after procedures without a malabsorptive component; intestinal calcium absorption has been shown to decrease postoperatively not only after RYGB (99) but also after SG (121). Even after AGB, restricted food intake and variety poses a risk for micronutrient deficiencies. After RYGB, SG, and AGB, a total calcium intake of 1200-1500 mg/day from diet and supplements (as needed) is recommended. After BPD/DS, a higher calcium intake may be necessary. Supplemental calcium should be provided as chewable calcium citrate in divided doses. An initial postoperative vitamin D supplement of 3000 IU/day is reasonable for most patients regardless of procedure. Postoperative laboratory monitoring should include 25-hydroxyvitamin D, calcium, albumin, phosphorus, and PTH levels. The vitamin D supplement dose can be titrated to achieve and maintain a 25-hydroxyvitamin D level of at least 30 ng/mL. If secondary hyperparathyroidism is present despite an optimized 25-hydroxyvitamin D level, the most likely cause is inadequate calcium intake or absorption; a low 24-hour urinary calcium level would support this. Increased calcium intake would be appropriate, with follow-up laboratory testing to confirm normalization of PTH level. The PTH level should, of course, be interpreted and targeted based on renal function. Professional organizations have differed in their recommendations about postoperative DXA, in light of the absence of evidence about the utility of such screening. A reasonable approach is to consider DXA after 2 years in those at higher risk for osteoporosis or fracture such as postmenopausal women, older men, and those with other risk factors.

Table 8.

Pre- and Postoperative Skeletal Health Strategies

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Preoperative strategies
	Check 25-hydroxyvitamin D and replete low levels
	DXA based on age-appropriate screening
	Consider DXA in higher-risk individuals such as postmenopausal women, older men, and those with risk factors for osteoporosis or fracture
Postoperative strategies
Supplementation	Calcium, as calcium citrate, to achieve total daily calcium intakes: AGB, SG, RYGB: Calcium 1200-1500 mg/day from diet + supplements BPD/DS: Calcium 1800-2400 mg/day from diet + supplements
	Vitamin D 3000 IU, titrate to ≥30 ng/mL
Lab monitoring	Calcium, albumin, phosphorus, PTH, 25-hydroxyvitamin D after 3 months, then every 6-12 months
	24-hour urinary calcium if additional data is needed (e.g., elevated PTH)
BMD monitoring	DXA based on age-appropriate screening; consider after 2 years in others who are at higher risk such as postmenopausal women, older men, and those with osteoporosis risk factors

Other strategies which may benefit the skeletal health of the bariatric surgery patient include exercise—particularly weight-bearing and muscle-loading exercise—and higher protein intake, as these mitigate loss of bone mass during non-surgical weight loss in older adults. A randomized controlled trial of a multipronged intervention of exercise, calcium, vitamin D, and protein supplementation was shown to attenuate—although not entirely prevent—postoperative increases in bone turnover markers and declines in BMD after RYGB and sleeve gastrectomy (104).

For those who have had bariatric surgery and are found to be at high risk of fracture, there are very few data to guide the use of antiosteoporosis medications. Antiresorptive agents such as bisphosphonates and denosumab should only be considered after appropriate therapy for calcium and vitamin D insufficiency and confirmation that adequate calcium and vitamin D status are maintained. Otherwise, there is a meaningful risk of medication-induced hypocalcemia (126). If pharmacotherapy is prescribed, a parenterally administered agent is recommended due to concerns about adequate gastrointestinal absorption and potential anastomotic ulceration with orally administered bisphosphonates. Research is needed to guide the use of these medications—either for prevention of bone loss or for treatment of osteoporosis—in the postoperative bariatric surgery population.

WEIGHT REGAIN AFTER BARIATRIC SURGERY

Given that obesity is a chronic disease and sustained weight loss requires ongoing management, understanding the durability of weight loss after bariatric surgery is of critical importance. Unfortunately, published studies reporting weight loss after bariatric surgery thus far tend to be short-term (many with < 5 years follow-up), and longer studies often lack high retention rates and/or adequate control groups (127,128). Additionally, the literature on long-term weight loss mostly addresses AGB and RYGB, and the literature on SG is still emerging. Furthermore, methods of quantifying weight change vary across studies, including percentage excess weight loss (%EWL) and percentage weight loss (%WL) (Table 9), making comparisons between studies challenging. Percentage weight loss (%WL) may be the best method for measuring weight change after bariatric surgery (129), as it is least confounded by preoperative BMI and allows surgical studies to be compared to non-surgical interventions. However, this method is not widely used in the surgical literature.

Using RYGB as an example, several studies with long-term follow-up and high retention rates highlight expected weight trajectories (Figure 2 and Table 10). It is important for patients to understand that the amount of weight loss can be highly variable between people, and that soon after achieving a postoperative weight loss nadir, it is not unusual to have a slight weight regain before achieving a new weight stabilization. These findings were highlighted in an analysis from the Longitudinal Assessment of Bariatric Surgery (LABS) Study, a 10-center observational cohort study in the U.S. that followed 2348 participants after RYGB (n=1738) or AGB (n=610). Serial weight measurements were obtained in person for 82.9% of participants up to 7 years after surgery (10). The weight nadir was typically achieved between 6 months and 2 years after this procedure, with a mean weight loss 7 years after RYGB of 28.4% (95%CI, 27.6-29.2) with 3.9% weight regain having been observed between years 3-7. Grouping individuals by similarly modeled weight-loss trajectories identified six distinct patterns (Figure 2). Roughly 75% of individuals achieved a 7-year weight loss of 25% or more from baseline (Groups 3 to 6). Less than 5% lost less than 10% of their initial weight while 13.3% lost 45% or more. These patterns of weight loss closely mirrored achieved weight loss by 6 months and all but one group experienced some weight rebound between postoperative years one to six (10).

Figure 2.

Weight change trajectory groups following RYGB. Lines indicate modeled group trajectories; data markers and median values; bars, interquartile range (IQR) of observed data. Negative value indicates weight loss from baseline (10).

Adams et al. prospectively followed a cohort of 417 subjects undergoing RYGB at a Utah-based surgical group (130) for 6 years, 92.6% of whom had follow-up weights, mostly obtained via in person measurement or medical chart review. Weight change was compared to 2 control groups: those who sought but did not undergo surgery (72.9% follow-up) and matched controls from a local healthcare database (96.9% follow-up). The RYGB group had the greatest mean adjusted weight loss from baseline to postoperative year 2 at 34.9%, decreasing to 27.7% in postoperative year 6. The authors report the absolute difference between these two figures as “percent weight regain” of 7.2%. Additionally, among RYGB patients, 94% had lost >20% of baseline weight at year 2, though 76% had maintained >20% weight loss at year 6. The control groups experienced negligible weight change.

A Veterans Administration (VA) retrospective cohort study evaluated 10-year weight loss outcomes among 1787 individuals who underwent RYGB, comparing these to 5305 non-surgical matches derived from the VA electronic health record (131). Among eligible patients, 81.9% of RYGB patients and 67.4% of non-surgical matches had follow-up data at 10 years. Percentage weight loss in the RYGB group was 31% (n= 1755) at year 1 and 28% (n=564) at year 10. The control group had lost only modest amounts of weight in follow-up, and the difference in weight loss between RYGB and controls was calculated at 30% and 21% in postoperative years 1 and 10, respectively.

Christou et al. of McGill University retrospectively studied 272 patients who had undergone RYGB, 83% of whom were available for in-person or phone follow-up (132). Among all patients, the greatest %EWL was 89% at the 2.5 years postoperative time-point, and this reduced to 68.1% at the 12 years postoperative time-point. Thus, approximately 18% of excess weight loss in the second year was regained by year 12. At 10 years, among patients with a starting BMI <50 kg/m², “excellent” surgical response (postoperative BMI <30 kg/m²) and “good” surgical response (postoperative BMI 30-35 kg/m²) were achieved in 51% and 29%, respectively. Among those with a baseline BMI >50 kg/m², the results were less positive: 13% achieved an excellent response, and 29% achieved a good response. The rates of follow-up were similar between the two groups.

Carbajo et al. of Spain performed a database analysis of 1200 patients who underwent one-anastomosis gastric bypass (a modification of RYGB) and had at least 6 years follow-up (133). Mean preoperative BMI was 46 kg/m² (range, 33-86 kg/m²). Among the 1200, follow-up rates at 6, 8, 10 and 12 years were 87% (n=233), 74% (n=607), 72% (n=759) and 70% (n=839), with roughly half followed up in person and half via electronic correspondence. %EWL was 77% for 6-year follow-up, 73% for 8-year follow-up, and 70% for 10- and 12-year follow-up. Percentage weight loss in the first 5 years of operation was not reported.

Pories et al. of East Carolina University School of Medicine retrospectively evaluated %EWL in patients who underwent RYGB from 1980-1994 (134). Among the 608 operated on, 574 were alive at the time analysis, and 553 of those remained in contact (i.e., 96% follow-up). Among the 553, 49% were examined in person, and the remainder were interviewed by telephone. Mean %EWL values at years 1, 2, 10, and 14 were 69% (n=506), 58% (n=407), 55% (n=158), and 49% (n=10), respectively. Thus, the average excess weight loss at 14 years is 20% less than at year 1.

Overall, among RYGB studies with high retention rates, the greatest average weight loss (nadir) is typically reported in the first two years with %EWL ranging from 69-89% and %WL of 31-35%. In general, about 10-20% of the maximum weight lost after surgery is regained when patients are followed for six years or longer. However, %EWL remains between 49-70% and %WL nearly 30%, which far exceeds any non-surgical weight loss interventions.

In the LABS study, 7-year weight loss after AGB averaged only 15% with 25% losing ≤ 5% of baseline weight and another 5% regaining all their lost weight and more (10). Data on weight loss following SG is still emerging, but typically runs roughly 2% to 5% less than RYGB by either %EWL or %TWL criteria, with greater variability between patients (13,135-138).

CONCLUSIONS

The postoperative management of the bariatric surgery patient requires an interdisciplinary team, including the surgeon, dietitian, endocrinologist and/or primary care provider. It is critical that endocrinologists and primary care providers have the training and tools required to meet the population’s medical needs, which include the management of chronic metabolic conditions and the prevention and treatment of postoperative medical and nutritional complications during lifelong follow-up. The teamwork of informed and experienced clinicians can optimize the long-term benefits of bariatric surgery.

ACKNOWLEDGMENTS

Dr. Kim’s research is supported by the Department of Veterans Affairs (1IK2CX001984).

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