Spontaneous Severe Hip Pain Manifesting As Bilateral Femoral Insufficiency Fracture – Metabolic Sequelae Following Bariatric Surgery

Presentation Number: SUN 306
Date of Presentation: April 2nd, 2017

Pei Shan Yeo*1 and Huiling Liew2
1Tan Tock Seng Hospital, Singapore, Singapore, Singapore, 2Tan Tock Seng Hospital, Singapore, Singapore



Metabolic bone disease (MBD) can occur after bariatric surgery. Its pathophysiology is often multifactorial including pre-operative existing calcium and vitamin D deficiency in the obese individual; post-operative mechanical off-loading of bones; altered micronutrients absorption and parathyroid hormone (PTH) regulation. These patients may hence be at heightened risk of increased bone loss through varied processes including osteomalacia and osteoporosis. These can lead to fractures.

Clinical Presentation

We present a 47-year-old Chinese male with sudden onset debilitating bilateral hip pain resulting in inability to ambulate for a week.

His significant past medical history included bilio-pancreatic bypass surgery for morbid obesity 18 years ago. He had defaulted endocrine reviews and micronutrient replacements including calcium and Vitamin D supplements for the last 2 years. Upon admission, he was found to have multiple electrolyte derangement including hypocalcemia, hypophosphatemia and hypokalemia. He was also deficient in micronutrients including Vitamin A, D, zinc and folate. Importantly, his adjusted calcium level was 2.10 mmol/L (Reference Index: 2.15 – 2.58 mmol/L) and Vitamin D levels were undetectably low at <9ug/dL (RI: >20 ug/dL).

Magnetic Resonance Imaging (MRI) of his hips revealed bilateral subarticular undisplaced fracture lines are seen in both the femoral heads with marrow edema suggestive of femoral head insufficiency fractures. Dual Energy X-ray Absorptiometry (DXA) showed a BMD of the lumbar spine at 0.992 g/cm2, and Z-score of +0.1 and BMD of the femoral neck at 0.704 g/cm2, and Z-score of -0.8. There was a significant bone loss exceeding the least significant change (LSC) range compared to 2 years ago.

He was referred to the orthopaedic team. The sites of fracture were, however, not amendable to surgical fixation. He was prescribed with 6 weeks of non-weight bearing status to allow for fracture healing. He was aggressively replaced with Vitamin D and calcium simultaneously with both intra-muscular Vitamin D injection and subsequent daily oral Vitamin D capsules.

At 6 month’s post fracture, our patient had recovered uneventfully and able to weight bear and ambulate independently. He had been adequately replaced with calcium and Vitamin D supplements with latest laboratory measurement of 25 ug/dL at his review visit.


MBD can occur after bariatric surgery, particularly those resulting in malabsorption. Fractures resulting from MBD severely affect one’s quality of life and mobility. Obese patients are at risk of Vitamin D and calcium deficiency at baseline. Notwithstanding bariatric surgery being an effective therapy for obesity, this case underscored the importance of patient education on the metabolic sequelae and the need for lifelong micronutrients replacement which are essential for bone health.


Nothing to Disclose: PSY, HL