Perioperative management of bariatric surgery patients: Focus on metabolic bone disease

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ABSTRACTChronic vitamin D deficiency, inadequate calcium intake, and secondary hyperparathyroidism are common in obese individuals, placing them at risk for low bone mass and metabolic bone disease. After bariatric surgery, they are at even higher risk, owing to malabsorption and decreased oral intake. Meticulous preoperative screening, judicious use of vitamin and mineral supplements, addressing modifiable risk factors, and monitoring the absorption of key nutrients postoperatively are essential in preventing metabolic bone disease in bariatric surgery patients.


  • Metabolic bone disease in obese patients is multifactorial: causes include sequestration of vitamin D in the adipocytes, inadequate nutrition due to chronic dieting, and lack of physical activity.
  • Before bariatric surgery, one must look for and treat preexisting nutritional deficiencies.
  • In the immediate postoperative period, aggressive strategies (ie, giving multivitamins and minerals intravenously and orally) can prevent nutritional deficiencies and secondary bone disease.
  • Postoperatively, many bariatric patients require chewable or liquid supplements to facilitate adequate absorption.
  • Clinical suspicion, timely interventions, and lifelong monitoring can prevent metabolic bone disease in bariatric surgery patients.



A 56-year-old woman who underwent Roux-en-y bariatric surgery because of morbid obesity 6 years ago presents to her primary care physician with vague complaints of fatigue, myalgias, arthralgias, and weakness that have slowly been getting worse. Before surgery she weighed 340 pounds (154 kg), and in the first 2 years afterward she lost 160 pounds (72.5 kg). She is postmenopausal, has no history of fractures, nephrolithiasis, or thyroid disease, and does not smoke or consume alcohol. She gives herself monthly intramuscular vitamin B12 injections, and takes a multivitamin tablet, calcium carbonate 500 mg, and vitamin D 400 IU daily.

After her surgery she returned for her first two postoperative appointments, but because she was feeling well, was losing weight, and had returned to work full-time, she cancelled all subsequent appointments with the surgeon, bariatrician, and dietitian.

On physical examination, the patient’s weight is stable at 187 pounds (84.5 kg), her height is 165.1 cm, and her body mass index is 31. Her head, eyes, ears, nose, throat, heart, lungs, and abdomen are normal. Her upper legs are weak, requiring her to use her arms in rising from a chair, and she feels discomfort when the proximal muscles of her arms and legs are palpated. She has mild osteoarthritis of the hands and knees. Her neurologic examination is normal.

Pertinent laboratory data:

  • Calcium 8.1 mg/dL (reference range 8.5–10.5)
  • Albumin 3.7 g/dL (3.4–4.7)
  • Magnesium 1.9 mg/dL (1.7–2.6)
  • Phosphorus 2.7 mg/dL (2.4–4.5)
  • Alkaline phosphatase 240 U/L (40–150)
  • Intact parathyroid hormone 215 pg/mL (10–60)
  • 25-hydroxyvitamin D < 7.0 ng/mL (31–80)
  • 24-hour urine volume 2,310 mL
  • Urine creatinine normal
  • Urine calcium 25.4 mg/24 hours (100–300).

Dual-energy x-ray absorptiometry (DXA) data, lumbar spine:

  • Bone mineral density 0.933 g/cm2
  • T score –2.0
  • Z score –0.8.

Left total hip:

  • Bone mineral density 0.628 g/cm2
  • T score –2.6
  • Z score –2.4.


This is a classic presentation of metabolic bone disease in a bariatric surgery patient lost to follow-up. Many patients have non-specific and vague symptoms for many months or years that are often incorrectly diagnosed as fibromyalgia, rheumatoid arthritis, polymyalgia rheumatica, Paget disease, or depression.1 They typically have low serum and urine calcium levels, very low or undetectable 25-hydroxyvitamin D levels, high alkaline phosphatase levels, secondary hyperparathyroidism, and a clinical picture consistent with both osteomalacia and osteoporosis.1

This case underscores the importance of monitoring nutrients and biochemical markers at baseline and on an ongoing basis to detect early indicators of malabsorption and ultimately prevent the development of metabolic bone disease and fragility fracture, with its risks of disability and even death. It also illustrates the essential role that primary care physicians play in the continuing care of these patients.


Although we used to think that morbid obesity protected against metabolic bone disease, in fact, vitamin D and calcium deficiencies and elevated parathyroid hormone (PTH) levels are common in extremely obese people, placing them at risk of low bone mass.2–6 More than 60% of candidates for weight-loss surgery are deficient in vitamin D,5,7 and 25% to 48% have elevated PTH levels.5,6

And that is before bariatric surgery: afterward, severely restricted oral intake and significant weight loss, coupled with a procedure that bypasses the major site of calcium absorption, place many patients at extremely high risk.5,8

After combination restrictive and malabsorptive procedures (eg, the popular Rouxen-y procedure, in which the stomach is reduced in size—”restricted”—and the proximal duodenum is bypassed so that less food is absorbed), as patients lose weight their PTH levels rise and 25-hydroxyvitamin D levels decrease, although corrected calcium levels usually remain within normal limits.3,9 Secondary hyperparathyroidism has been documented as soon as 8 weeks after bariatric surgery, and osteomalacia after gastric bypass surgery is not uncommon.1,7,10–13

Exclusively restrictive procedures such as gastric banding, formerly presumed not to alter bone metabolism, now also appear to place patients at risk of metabolic bone disease due to inadequate intake of calcium and vitamin D in the immediate postoperative period.10

Numerous reported cases further illustrate the ever-present risk of metabolic bone disease in this population if adequate supplementation of calcium and vitamin D is not given. In these cases, significant bone disease occurred from 8 weeks to 32 years after bariatric surgery, often with devastating consequences.1,4,8,11–14


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