Fragility Fracture (Case 43)

Published on 24/06/2015 by admin

Filed under Internal Medicine

Last modified 24/06/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1507 times

Chapter 51
Fragility Fracture (Case 43)

Paul Sack MD

Case: The patient is a 67-year-old woman with a history of hypertension and osteoarthritis of the knees who presents to the emergency department after falling and fracturing her left hip. She lost her balance in her kitchen after turning and fell on her left hip. She had immediate pain and could not put any weight on her left leg. A radiograph revealed a femoral neck fracture of her left femur. She reports a wrist fracture 3 years ago after falling in her kitchen. This fracture was treated by an orthopedist in the outpatient setting. She has never had a dual-energy x-ray absorptiometry (DXA) scan performed. She occasionally takes a multivitamin, but does not take any additional calcium. She also takes atenolol for her hypertension. She is married and has two children. She went through menopause at the age of 44 years and was only briefly on hormone replacement therapy for 2 years. She has one or two alcoholic beverages on the weekends. She has never smoked tobacco.

Differential Diagnosis

Primary osteoporosis


Multiple myeloma

Secondary osteoporosis

Paget disease


Speaking Intelligently

The most common cause of a fragility fracture, a fracture that occurs with no or minimal trauma, is low bone density or osteoporosis. Unfortunately, osteoporosis does not cause symptoms until a fracture has occurred. Therefore, routine screening with a DXA scan is recommended for all patients at risk. The other main causes of a fragility fracture, such as multiple myeloma, Paget disease, and metastatic cancer, are usually fairly obvious with plain radiographs. Once the diagnosis of osteoporosis has been established, either on the basis of the DXA scan or by a clinical history of an osteoporotic fracture, the focus should be on prevention of the next fracture. This includes educating the patient about how to reduce the risk of a fall, ruling out secondary causes of bone loss, ensuring an adequate amount of calcium and vitamin D intake, and using prescription medications to help rebuild bone density and strength.



Clinical Thinking

• Peak bone mass usually occurs in the third decade of life, and then bone mass diminishes with age.

• Estrogen deficiency accelerates this process, which is why women are more likely to have osteoporosis and osteoporotic fractures.

• Other conditions that can lead to accelerated bone loss or fragility fractures are hyperthyroidism, hyperparathyroidism, steroid excess (either exogenous or endogenous), vitamin D deficiency, and testosterone deficiency (in men).

• Other processes that can result in fragility fractures that are not necessarily due to osteoporosis include metastatic cancer, multiple myeloma, and Paget disease. Therefore, when a patient presents with a fragility fracture, it is important to rule out these other causes.

• Once the diagnosis of osteoporosis has been established and secondary causes have been either excluded or treated, the main goal of therapy is to decrease the risk of a future fracture.


• Osteoporosis is frequently a silent disease until a fracture occurs. As a result, many patients will not have any specific complaints. The history should therefore focus on identifying risk factors as well as potential secondary causes of osteoporosis.

• In a woman, estrogen deficiency is the main cause of osteoporosis. Late menarche, amenorrhea, and early menopause are important risks. If a woman is postmenopausal, determining the age of menopause and how much time (if any) the patient was on estrogen replacement therapy is important.

• In a man with osteoporosis, identifying causes, such as testosterone deficiency, are common. Therefore, specific questions regarding sexual drive (libido), erectile function, shaving habits, muscle strength, and overall energy are essential.

• Ascertain the patient’s intake of calcium and vitamin D; this includes intake of dairy products as well as OTC calcium and vitamins. Sunlight exposure should also be assessed, as lack of sunlight is a major risk factor for vitamin D deficiency. Vitamin D deficiency is also more common in patients with celiac disease, so it is important to note any symptoms of malabsorption.

• Certain medications may cause bone loss. The main offenders are glucocorticoids such as prednisone. Doses of prednisone over 10 mg/day for more than a few months will lead to worsening bone density. Phenytoin (Dilantin) diverts vitamin D to inactive forms, resulting in vitamin D deficiency and decreased calcium absorption. Androgen deprivation therapy medications used for treating prostate cancer will decrease testosterone production.

• Endocrinopathies that cause osteoporosis must be considered. To rule out hyperthyroidism, question patients about tremor, palpitations, heat intolerance, weight loss, and hair loss. Primary hyperparathyroidism is another silent disease, but the patient with hyperparathyroidism may have a history of kidney stones and hypercalcemia. Excessive weight gain, easy bruising, wide abdominal stretch marks, proximal muscle weakness with difficult-to-control diabetes or hypertension suggest Cushing syndrome (excess endogenous steroid production).

• Both smoking and excessive alcohol use, defined as more than three drinks a day, are risks for osteoporosis. A detailed family history for osteoporosis is important. While the family member may not have been officially diagnosed with osteoporosis, he or she may have had a hip fracture or severe kyphosis.

• The patient’s own history of fragility fractures is important. A hip fracture during a car accident is not considered an osteoporotic fracture, but a hip fracture after slipping on ice is. If there has been a vertebral compression fracture, patients will complain of localized, midline, sharp pains that may be disabling. Patients may also have height loss, scoliosis, or kyphosis as the vertebrae compress and change the contour of the spine. Pain is generally not associated with osteoporosis unless a fracture has already occurred.

Physical Examination

• The height measurement is essential when assessing the osteoporotic patient. An attempt should be made to determine if there has been height loss.

• Examine the spine for point tenderness, thoracic kyphosis, and an exaggerated cervical lordosis (dowager’s hump).

• The remainder of the physical exam should be focused on including or excluding the secondary causes of osteoporosis. Signs of hyperthyroidism include proptosis, an enlarged thyroid, tremor, tachycardia, warm and moist skin, and proximal muscle weakness. Cushing syndrome presents with central obesity, thin arms and legs, supraclavicular fat pads, a dorsocervical fat pad, widened purplish abdominal stretch marks, proximal muscle weakness, and hypertension.

Tests for Consideration

25-OH Vitamin D: This is the inactive or storage form of vitamin D. The vitamin D level should be at least above 32 ng/mL, and some experts are arguing for even higher levels. It is not recommended to check the active form (1,25-dihydroxyvitamin D3) in patients with normal kidney function. In patients with vitamin D deficiency as indicated by a low 25-OH vitamin D level, the active vitamin D can sometimes still be in the low normal range.


Intact PTH: In the setting of a normal or low calcium level, an elevated PTH level may indicate vitamin D deficiency.
This is known as secondary hyperparathyroidism. If the PTH is inappropriately elevated in the setting of an elevated calcium level, the diagnosis is primary hyperparathyroidism.


Calcium: The serum calcium concentration is tightly regulated in the body. PTH and vitamin D play an essential role in this regulation. Remember to correct the calcium if the albumin is not within the normal range.


Alkaline phosphatase: An elevated alkaline phosphatase can be found in both Paget disease and severe vitamin D deficiency (osteomalacia).


Testosterone (in men): Testosterone deficiency causes bone loss. A level less than 300 ng/dL should cause some suspicion for hypogonadism. A full evaluation of this should follow, including a free testosterone, FSH, LH, and prolactin.


TSH: A screening TSH level should be ordered in all patients with decreased bone density. Some patients with subclinical or mild hyperthyroidism may not have obvious symptoms, but the increased bone turnover associated with hyperthyroidism can lead to bone loss.


Cushing syndrome evaluation: This evaluation is not done routinely, but if the patient has the classic findings of Cushing syndrome or has unexplained early bone loss, it should be considered. This can be achieved with a 1-mg dexamethasone suppression test, a midnight salivary cortisol level, or a 24-hour urine for free cortisol.

$23, $23, $24

Celiac disease evaluation: If you suspect malabsorption because of symptoms or if the patient continues to have low vitamin D levels despite aggressive replacement, celiac disease should be considered. IgA anti-tissue transglutaminase and IgA endomysial antibody levels are blood tests to evaluate for celiac disease.


Serum protein electrophoresis (SPEP) and/or urine protein electrophoresis (UPEP): If multiple myeloma is suspected, these tests will confirm or exclude the diagnosis.

$15, $25



Buy Membership for Internal Medicine Category to continue reading. Learn more here