MAMC Journal of Medical Sciences

: 2022  |  Volume : 8  |  Issue : 1  |  Page : 82--84

Sequential Fracture of Neck of Femur of Both Sides in a Patient with Psychosis: A Diagnostic Dilemma

Dhananjaya Sabat1, Prerna Kukreti2,  
1 Department of Orthopedics, Maulana Azad Medical College and Lok Nayak Hospital, New Delhi, India
2 Department of Psychiatry, Lady Hardinge Medical College, New Delhi, India

Correspondence Address:
Dhananjaya Sabat
Department of Orthopedics, Room no 610, Department of Orthopedics, Lok Nayak Hospital, New Delhi 110002


The authors describe the case of an adult male patient with psychosis developed fractures of neck femur of both sides sequentially at a year interval following trivial trauma. In addition, the patient was found to have hyperthyroidism. The rare presentation, possible complex etiopathogenesis for the problem and difficulties in treatment are discussed.

How to cite this article:
Sabat D, Kukreti P. Sequential Fracture of Neck of Femur of Both Sides in a Patient with Psychosis: A Diagnostic Dilemma.MAMC J Med Sci 2022;8:82-84

How to cite this URL:
Sabat D, Kukreti P. Sequential Fracture of Neck of Femur of Both Sides in a Patient with Psychosis: A Diagnostic Dilemma. MAMC J Med Sci [serial online] 2022 [cited 2022 Aug 14 ];8:82-84
Available from:

Full Text


Metabolic bone-disease-associated fractures have varied presentation. The present case describes an adult male patient with psychosis who had sequential fractures of neck of femur at 1 year interval later on found to have associated hyperthyroidism. Such presentation is not reported till date in literature.

 Case Report

A 37-year-old male presented to the emergency department with history of fall from stairs and injury to the left hip. Radiographs of the left hip showed a transcervical fracture of the neck of femur. The pulse rate was 82 per minute and blood pressure 134/84 mmHg. The patient had hemoglobin of 12.4 g%, a normal renal function test, and electrocardiograph. It was noted that the patient had fractured his right neck of femur 12 months back after a fall from bicycle and underwent a closed reduction and internal fixation with three 7-mm cannulated cancellous screws which got united in mild varus.

He was posted under anesthesia and the fracture fixation was carried out with three 7-mm cannulated cancellous screws after achieving a closed reduction. The immediate postoperative period was uneventful.

The rare presentation of sequential fracture of neck femur in an adult male aroused suspicion of some associated disorder which may have contributed to his fractures occurring with low energy trauma. On detailed history, the patient was under treatment for psychotic episodes since last 3 years from psychiatric department of a tertiary care hospital and was on the following drugs: tablet Risperidone 2 mg at night, tablet Trihexyphenidyl 2 mg in the morning, and tablet Clonazepam 0.5 mg at night. The reports of the previous treatment revealed that in the initial treatment, he had received tablet Risperidone 6 mg at night, tablet Amisulpride 100 mg BD, tablet Fluoxetine 20 mg in the morning for first 2 years. His wife informed that patient lost weight rapidly over the last 3 years though had increased appetite; and his psychotic behavior was under control with treatment.

Detailed clinical evaluation also revealed a fine tremor in hands and brisk deep tendon reflexes. Further investigations revealed a serum calcium level of 7.90 g/dL (normal: 8.2–10.4 g/dL) by indirect (ISE) method, serum phosphate level of 2.70 mg/dL (normal: 2.5–4.6 mg/dL) by phosphomolybdate method, serum alkaline phosphatase (ALP) level of 542.00 IU/L (normal: 39–117 IU/L) and serum parathyroid hormone level 303.300 pg/mL (normal: 12–72 pg/mL) suggestive of osteomalacia. Thyroid profile was free T3: 10.99, free T4: 6.289 ng/dL (normal: 0.950–2.250 ng/dL) and thyroid-stimulating hormone (TSH) 0.004 μIU/mL (normal: 0.200–5.100 μIU/mL), suggesting a hyperthyroid state. Ultrasonogrphy of thyroid with 14 mHz linear probe showed size of right lobe 1.9 × 2.2 cm and left lobe 2.3 × 1.7 mm, with peak systolic velocity in right inferior thyroid artery 54 cm/second and left inferior thyroid artery 51 cm/second suggestive of Graves disease. A 5-mCi 99mTc pertechnetate scan of thyroid showed overall increased intake with mildly enlarged both lobes with homogenous distribution of tracer. There was no hot or cold nodule or retrosternal extension or pyramidal lobe. In 20-minute 99mTc pertechnetate scan also showed increase uptake to total 34.2% (right lobe: 18.2%; left lobe: 16.0%; normal: 0.2–3%).

With the diagnosis of Graves disease and osteomalacia, antithyroid treatment was started with tablet Carbimazole 10 mg 2/2/2, tablet Propranolol 40 mg 1/1/1 along with tablet Cholecalciferol 60000 IU, 1 tablet weekly a total of 10 tablets and calcium supplementation 1000 mg/day. Antipsychotic treatment was tapered off. The patient improved clinically and TSH value gradually improved. But the left fracture neck femur started showing signs of delayed union with progressive varus in alignment of neck femur in spite of limited nonweight-bearing ambulation [Figure 1].{Figure 1}

At 5 months follow-up; patient was off antipsychotics. His calcium, phosphate, and ALP levels as well as thyroid profile were normal with medications. He was advised a valgus osteotomy for his ununited fracture of neck femur on left hip which patient refused. Patient continued to remain a household ambulator with a stick and did not opt for further surgical intervention till last follow-up of 16 months [Figure 2].{Figure 2}


Metabolic bone disease has variable presentations and association of endocrinopathy is common. Making the diagnosis is difficult when the definitive clinical signs are not clear. On the other hand, drug-induced derangements in metabolism of bone can further complicate the evaluation of the disease and thus formulating a single hypothesis for the cause and effect in such cases is not always possible.

In this case, the association of sequential fractures of both sides neck of femur can be attributed to variety of factors. Firstly, hyperthyroidism can itself affect bone metabolism. One of the first reports of hyperthyroid bone disease was in 1891 when von Recklinghausen described the “worm eaten” appearance of the long bones of a young woman who died from hyperthyroidism.[1] Overt hyperthyroidism is associated with accelerated bone remodeling, reduced bone density, osteoporosis, and an increase in fracture rate.[2],[3] These changes in bone metabolism are associated with negative calcium balance, hypercalciuria, and, rarely, hypercalcemia.[4],[5],[6] Bone density measurements have demonstrated that bone loss is common in patients with overt hyperthyroidism and to a lesser extent in those with subclinical hyperthyroidism. The extent of reduction in bone density in patients with hyperthyroid ranges from 10% to 20%.[7],[8],[9] Also osteomalacia is known to be associated with thyrotoxicosis. In hyperthyroidism, subclinical vitamin D deficiency may get precipitated into an overt form. Osteomalacia may coexist with thyrotoxicosis, but may remain undiagnosed, unless clinically suspected and biochemically confirmed.[10] Despite the variable bone density findings, a history of overt hyperthyroidism is a risk factor for hip fracture later in life.[3],[11] The mechanism by which these happen is unclear. Possible mechanisms include direct stimulation of osteoclastic activity or indirect stimulation through increased osteoblastic activity by T3 or TSH or interleukin-6.[12] In overt hyperthyroidism, osteoclastic resorption is stimulated out of proportion to osteoblastic remineralization.[13] At result, the normal cycle duration of approximately 200 days is halved, and each cycle is associated with a 9.6% loss of mineralized bone.

Secondly, psychosis and depression can be the cause even the first presentation of hyperthyroidism. Clinical case reports reveal that hyperthyroid individuals may manifest psychosis and depression. The prevalence of clinical hypothyroidism in psychiatric patients ranges from 0.5% to 8%.[14],[15],[16],[17],[18]

Thirdly, long-term use of psychotropic medications may be associated with adverse effects on bone metabolism. Risperidone is known to increase prolactin levels, which in turn suppresses gonadotropin-releasing hormone release leading to impaired gonadal steroidogenesis in men and women. Long-term hyperprolactinemia may lead to decrease bone mineral density in both sexes.[19],[20],[21] Patients with psychiatric disorders frequently have other predisposing factors for osteoporosis, such as poor nutrition, history of smoking, low activity level, and amenorrhea.

The possible etiopathology of the fractures in this case can be a combined deleterious effect of all the mechanisms described earlier. Whether the effects are additive or multiplicative, that remains a matter of further research. But it can be safely concluded that adequate calcium (at least 1500 mg/day) and vitamin D (400–800 IU/day) supplementation must be given to patients of hyperthyroidism and patients on antipsychotic drugs. In addition, periodic screening with DEXA scans may also be recommended.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1von Recklinghausen FD. Die Fibröse oder deformierende Ostitis, die Osteomalazie und die osteoplastische Carzinose in ihren gegenseitigen Beziehungen. Festchrift Rudolf Virchow [in German]. Berlin: George Reimer; 1891. p. 1.
2Meunier PJ, S-Bianchi GG, Edouard CM. Bony manifestations of thyrotoxicosis. Orthop Clin North Am 1972;3:745-74.
3Cummings SR, Nevitt MC, Browner WS. Risk factors for hip fracture in white women. N Engl J Med 1995;332:767-73.
4Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormones on bone and mineral metabolism. Endocrinol Metab Clin North Am 1990;19:35-63.
5Frizel D, Malleson A, Marks V. Plasma levels of ionised calcium and magnesium in thyroid disease. Lancet 1967;I:1360-1.
6Krolner B, Jorgensen JV, Nielsen SP. Spinal bone mineral content in myxoedema and thyrotoxicosis. Effects of thyroid hormone(s) and antithyroid treatment. Clin Endocrinol 1983;18:439-46.
7Nielsen HE, Mosekilde L, Charles P. Bone mineral content in hyperthyroid patients after combined medical and surgical treatment. Acta Radiol Oncol Radiat Phys Biol 1979;18:122-8.
8Linde J, Friis T. Osteoporosis in hyperthyroidism estimated by photon absorptiometry. Acta Endocrinol (Copenh) 1979;91:437-48.
9Diamond T, Vine J, Smart R, Butler P. Thyrotoxic bone disease in women: a potentially reversible disorder. Ann Intern Med 1994;120:8-11.
10Goswami R, Shah P, Ammini AC. Thyrotoxicosis with osteomalacia and proximal myopathy. J Postgrad Med 1993;39:89-90.
11Wejda B, Hintze G, Katschinski B. Hip fractures and the thyroid: a case control study. J Intern Med 1995;237:241-7.
12Reddy PA, Harinarayan CV, Sachan A, Suresh V, Rajagopal G. Bone disease in thyrotoxicosis. Indian J Med Res 2012;135:277-86.
13Eriksen EF. Normal and pathological remodeling of human trabecular bone: three dimensional reconstruction of the remodeling sequence in normals and in metabolic bone disease. Endocr Rev 1986;7:379-408.
14Sabeen S, Chou C, Holroyd S. Abnormal thyroid stimulating hormone (TSH) in psychiatric long-term care patients. Arch Gerontol Geriatr 2010;51:6-8.
15Marian G, Nica EA, Ionescu BE, Ghinea D. Hyperthyroidism—cause of depression and psychosis: a case report. J Med Life 2009;2:440-2.
16Snabboon T, Khemkha A, Chaiyaumporn C, Lalitanantpong D, Sridama V. Psychosis as the first presentation of hyperthyroidism. Intern Emerg Med 2009;4:359-60.
17Benvenga S, Lapa D, Trimarchi F. Don’t forget the thyroid in the etiology of psychoses. Am J Med 2003;115:159-60.
18Bahls SC, de Carvalho GA. The relation between thyroid function and depression: a review. Braz J Psychiatry 2004;26:41-9.
19Misra M, Papakostas GI, Klibanski A. Effects of psychiatric disorders and psychotropic medications on prolactin and bone metabolism. J Clin Psychiatry 2004;65:1607-18.
20Pack AM, Gidal B, Vazquez B. Bone disease associated with antiepileptic drugs. Cleve Clin J Med 2004;71:S42-8.
21Beerhorst K, Huvers FC, Renier WO. Severe early onset osteopenia and osteoporosis caused by antiepileptic drugs. Neth J Med 2005;63:222-6.