Orthopedics

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Case Reports 

Slipped Capital Femoral Epiphysis With Severe Vitamin D Deficiency

Nathan W. Skelley, BS; Derek F. Papp, MD; Rushyuan J. Lee, MD; M. Catherine Sargent, MD

Abstract

Slipped capital femoral epiphysis is a relatively common disorder in late childhood and early adolescence, with an incidence in the United States of approximately 10 per 100,000. Although clinicians have theorized that contributing factors to the development of slipped capital femoral epiphysis include 25-hydroxyvitamin D deficiency and other nutritional deficiencies, the roles of these factors have not been fully analyzed. This article presents a case of a morbidly obese 13-year-old African-American boy who presented with sudden worsening of chronic hip pain and was diagnosed with stable, bilateral, grade-III slipped capital femoral epiphysis and severe vitamin D deficiency. He was initially treated with bilateral single-screw percutaneous fixation, however, after continued pain and nonunion, a right valgus subtrochanteric osteotomy was performed in association with correction of his severe vitamin D deficiency. This procedure led to improvement of his hip function and successful resolution of the pain. Approximately 3 months after the second operation and vitamin supplementation, the patient had signs of union, and his weight bearing progressed without discomfort. Although the osteotomy provided substantial biomechanical advantage by changing the forces across the physis from shear to compressive, correction of the vitamin D deficiency was critical in providing metabolic capacity for bone healing. Vitamin D plays an important role in bone formation and development, but the level of 25-hydroxyvitamin D is not routinely measured during assessment and treatment of slipped capital femoral epiphysis patients. The early detection and proper treatment of vitamin D may assist in the treatment of patients with slipped capital femoral epiphysis.

Slipped capital femoral epiphysis is a relatively common disorder affecting children in late childhood and early adolescence; the incidence in the United States is approximately 10 per 100,000 persons.1 Slipped capital femoral epiphysis is most common in peripubetal children, shows a male predominance, and is thought to be the result of multifactorial biomechanical weakening along the femoral physis.1

Although diagnosis and treatment have been previously well described,1,2 the search for the cause and early detection of slipped capital femoral epiphysis continues. Recent research indicating the effects of nutritional factors on adolescent growth has highlighted vitamin D as one of the most prevalent deficiencies among children.3 The association between severe vitamin D deficiency and slipped capital femoral epiphysis remains unclear and, to our knowledge, has not previously been reported in United States patients.

This article presents a case of an obese 13-year-old African-American boy who presented with stable, bilateral, slipped capital femoral epiphysis and severe vitamin D deficiency.

In 2008, a 13-year-old, morbidly obese,4 African-American boy presented with a sudden worsening of chronic bilateral hip pain. Radiographs revealed severe, bilateral slipped capital femoral epiphysis with varus deformity, as defined by the physeal stability system of Loder et al5 and the Southwick angles found with imaging.2 At presentation, the patient had a body mass index of 37 kg/m2, was above the 97th percentile for weight, and was at the 86th percentile for height at his age. His surgical history included decompression and drainage of a right orbital abscess secondary to sinusitis in 2003 with no complication. He had a family history of diabetes, but no history of other endocrine problems or previous slipped capital femoral epiphyses in his family. He indicated his diet consisted primarily of high-calorie, processed foods, and that he did not take vitamin supplements.

The patient underwent bilateral single-screw percutaneous fixation. During the procedure, no evidence of hardware penetration of the articular surface on the left side was present, and the fixation appeared adequate. The right side, however, could not be adequately imaged because of the patient’s morbid obesity; therefore, a computed tomography scan (CT) was obtained…

Abstract

Slipped capital femoral epiphysis is a relatively common disorder in late childhood and early adolescence, with an incidence in the United States of approximately 10 per 100,000. Although clinicians have theorized that contributing factors to the development of slipped capital femoral epiphysis include 25-hydroxyvitamin D deficiency and other nutritional deficiencies, the roles of these factors have not been fully analyzed. This article presents a case of a morbidly obese 13-year-old African-American boy who presented with sudden worsening of chronic hip pain and was diagnosed with stable, bilateral, grade-III slipped capital femoral epiphysis and severe vitamin D deficiency. He was initially treated with bilateral single-screw percutaneous fixation, however, after continued pain and nonunion, a right valgus subtrochanteric osteotomy was performed in association with correction of his severe vitamin D deficiency. This procedure led to improvement of his hip function and successful resolution of the pain. Approximately 3 months after the second operation and vitamin supplementation, the patient had signs of union, and his weight bearing progressed without discomfort. Although the osteotomy provided substantial biomechanical advantage by changing the forces across the physis from shear to compressive, correction of the vitamin D deficiency was critical in providing metabolic capacity for bone healing. Vitamin D plays an important role in bone formation and development, but the level of 25-hydroxyvitamin D is not routinely measured during assessment and treatment of slipped capital femoral epiphysis patients. The early detection and proper treatment of vitamin D may assist in the treatment of patients with slipped capital femoral epiphysis.

Slipped capital femoral epiphysis is a relatively common disorder affecting children in late childhood and early adolescence; the incidence in the United States is approximately 10 per 100,000 persons.1 Slipped capital femoral epiphysis is most common in peripubetal children, shows a male predominance, and is thought to be the result of multifactorial biomechanical weakening along the femoral physis.1

Although diagnosis and treatment have been previously well described,1,2 the search for the cause and early detection of slipped capital femoral epiphysis continues. Recent research indicating the effects of nutritional factors on adolescent growth has highlighted vitamin D as one of the most prevalent deficiencies among children.3 The association between severe vitamin D deficiency and slipped capital femoral epiphysis remains unclear and, to our knowledge, has not previously been reported in United States patients.

This article presents a case of an obese 13-year-old African-American boy who presented with stable, bilateral, slipped capital femoral epiphysis and severe vitamin D deficiency.

Case Report

In 2008, a 13-year-old, morbidly obese,4 African-American boy presented with a sudden worsening of chronic bilateral hip pain. Radiographs revealed severe, bilateral slipped capital femoral epiphysis with varus deformity, as defined by the physeal stability system of Loder et al5 and the Southwick angles found with imaging.2 At presentation, the patient had a body mass index of 37 kg/m2, was above the 97th percentile for weight, and was at the 86th percentile for height at his age. His surgical history included decompression and drainage of a right orbital abscess secondary to sinusitis in 2003 with no complication. He had a family history of diabetes, but no history of other endocrine problems or previous slipped capital femoral epiphyses in his family. He indicated his diet consisted primarily of high-calorie, processed foods, and that he did not take vitamin supplements.

The patient underwent bilateral single-screw percutaneous fixation. During the procedure, no evidence of hardware penetration of the articular surface on the left side was present, and the fixation appeared adequate. The right side, however, could not be adequately imaged because of the patient’s morbid obesity; therefore, a computed tomography scan (CT) was obtained postoperatively to evaluate screw placement. It was determined that the screw violated the articular surface, and the patient was returned to the operating room for revision fixation with a shorter screw.

Postoperatively, the patient was prescribed restricted weight bearing for 2 weeks, with subsequent limited activity and physical therapy. At approximately 3 months postoperatively, he discontinued the therapy against medical advice. During his early postoperative period, the patient was pain-free. However, 5 months after surgery, he began experiencing moderate hip pain (4 of 10 on a general pain analog scale, greater on the right than on the left) and required intermittent use of crutches. By this time, his body mass index had progressed to 45 kg/m2.

Obtaining adequate radiographs in this obese patient was difficult, so CT imaging was used to assess physeal closure and healing. The scan showed 25% bony bridging at the left physis but minimal bridging at the right physis. Because of the ongoing pain and apparent nonunion of his right slipped capital femoral epiphysis, a right valgus derotational subtrochanteric osteotomy was performed 8 months after his index procedure. The original screw was removed and replaced with a dynamic hip screw and sideplate with 5 screws, with no complication. Perioperatively, nutritional work-up and a sleep study revealed obstructive sleep apnea syndrome and severe 25-hydroxyvitamin D deficiency (11.1 ng/mL). His comprehensive metabolic panel showed low levels of sodium, chloride, calcium, protein, and albumin, and elevated levels of glucose and liver enzymes. His hemoglobin A1c was within normal limits. He had no record of endocrine or thyroid problems, and his hormone levels were within normal limits. The patient was started on continuous positive airway pressure therapy and vitamin supplementation.

Approximately 3 months after the osteotomy and vitamin supplementation, the patient showed signs of union, and weight bearing progressed with no discomfort. At the most recent follow-up in 2010, the patient was undergoing physical therapy to improve mobility and range of motion, and he remained pain-free in both hips.

Discussion

The complicated treatment course and delayed recognition and correction of vitamin D deficiency make our case unique. It is, to our knowledge, the first case report of an association between slipped capital femoral epiphysis and vitamin D deficiency in the United States. In 2004, Brown6 reviewed a national United States database of slipped capital femoral epiphysis patients and discovered an association between seasonal variation and slipped capital femoral epiphysis that he suspected might be related to decreased cutaneous synthesis of vitamin D. His findings were supported by a previous study by Loder.7 Understanding the relationship between vitamin D and slipped capital femoral epiphysis may advance the treatment of patients with slipped capital femoral epiphysis.

Vitamin D plays an important role in bone formation and development.8-10 Serum 1,25-hydroxyvitamin D has been noted to increase during times of increased growth and is involved in bone matrix mineralization of the growth-plate cartilage.8 In a retrospective review of National Health and Nutrition Examination Survey data from 2001 to 2004, Kumar et al3 indicated that 9% of US children are deficient (<15 ng/mL) and 61% are insufficient (15-30 ng/mL) in 25-hydroxyvitamin D. These reference ranges, however, are outdated because more recent reports consider the lower limit of 30.0 ng/mL of 25-hydroxyvitamin D (normal range: 30-100 ng/mL) to be a threshold for optimal health.11,12 A 25-hydroxyvitamin D level between 21 to 29 ng/mL is considered insufficient, and a level of <20 ng/mL is considered deficient.11,12 Our patient’s postoperative 25-hydroxyvitamin D level of 11.1 ng/mL represented a severe vitamin D deficiency. We did not measure midportion parathyroid hormone or preoperative vitamin D level.

To our knowledge, the largest study to date of the relationship between slipped capital femoral epiphysis and vitamin D was reported by Jingushi et al13 in 1997. They analyzed 13 Japanese patients with slipped capital femoral epiphyses and found that 7 had severely deficient 25-hydroxyvitamin D levels, 3 of whom had levels comparable to that of our patient. They also found a positive correlation between low levels of vitamin D and low levels of parathyroid hormone present at the time of diagnosis.13 Midportion parathyroid hormone is 1 of 3 major parathyroid hormone fragments secreted by the parathyroid gland. In their study, the level of midportion parathyroid hormone and vitamin D returned to normal 1 year after coxalgia.13

Although the role of vitamin D in slipped capital femoral epiphyses remains unknown, the measurement of vitamin D is becoming more common in physical assessment and may be beneficial in the initial work-up of patients with slipped capital femoral epiphyses. Treatment of vitamin D deficiency may facilitate postoperative healing in adolescents/children because the peripubetal adolescent experiences an increased nutritional and metabolic demand secondary to increased growth during the developmental period. Many reports suggest that the recommended intake of vitamin D 400 IU is inadequate, and some researchers have indicated that the level should be raised to at least 800 IU of vitamin D3 per day.11 Because it is difficult to achieve such a high level of vitamin D from a well-balanced diet alone, such intake levels usually require the addition of sensible sun exposure and vitamin D supplementation.11

Previous studies have noted numerous complications in nutritionally deficient adolescents,3,9,10 but there is little literature focusing on slipped capital femoral epiphysis and 25-hydroxyvitamin D.3 Endocrine, genetic, geographic, and environmental activities have all been implicated as possible contributing factors in the cause of slipped capital femoral epiphysis.1,6 Our patient had no endocrine abnormalities or family history of slipped capital femoral epiphysis and was not active in athletics. However, the patient was morbidly obese, male, and African-American, which are 3 risk factors associated with slipped capital femoral epiphysis.1 After performing the right valgus subtrochanteric osteotomy (Figure 1) and recognizing and treating his severe 25-hydroxyvitamin D deficiency, an improvement was observed in his bone healing and postoperative recovery (Figure 2). Although the osteotomy provided substantial biomechanical advantage by changing the forces across the physis from shear to compressive, correction of the vitamin D deficiency was critical in providing metabolic capacity for bone healing.

Figure 1: Postoperative AP radiograph of the patient's pelvis before vitamin D repletion Figure 2: One-year postoperative AP radiograph of the patient's pelvis after vitamin D repletion
Figure 1: Postoperative AP radiograph of the patient’s pelvis before vitamin D repletion. Figure 2: One-year postoperative AP radiograph of the patient’s pelvis after vitamin D repletion. Note healing around the right lesser trochanter and increased density at the femoral epiphysis bilaterally.

Additional studies analyzing the association between 25-hydroxyvitamin D and slipped capital femoral epiphysis are necessary to infer any causative relationship, but the role of this vitamin in bone development currently warrants its measurement in slipped capital femoral epiphysis patients. The early detection and proper treatment of vitamin D may assist in the treatment of patients with slipped capital femoral epiphysis. Additional studies are necessary to determine the exact role of vitamin D in the treatment of slipped capital femoral epiphysis patients.

References

  1. Aronsson DD, Loder RT, Breur GJ, Weinstein SL. Slipped capital femoral epiphysis: current concepts. J Am Acad Orthop Surg. 2006; 14(12):666-679.
  2. Kay RM. Slipped capital femoral epiphysis. In: Morrissy RT, Weinstein SL, eds. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:1085-1124.
  3. Kumar J, Muntner P, Kaskel FJ, Hailpern SM, Melamed ML. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001-2004. Pediatrics. 2009; 124(3):e362-e370.
  4. Centers for Disease Control and Prevention. About BMI for children and teens. http://www.cdc.gov/healthyweight/assessing/bmi/childrens_bmi/about_childrens_bmi.html. Accessed June 16, 2010.
  5. Loder RT, Richards BS, Shapiro PS, Reznick LR, Aronson DD. Acute slipped capital femoral epiphysis: the importance of physeal stability. J Bone Joint Surg Am. 1993; 75(8):1134-1140.
  6. Brown D. Seasonal variation of slipped capital femoral epiphysis in the United States. J Pediatr Orthop. 2004; 24(2):139-143.
  7. Loder RT. A worldwide study on the seasonal variation of slipped capital femoral epiphysis. Clin Orthop Relat Res. 1996; (322):28-36.
  8. Chesney RW, Rosen JF, Hamstra AJ, DeLuca HF. Serum 1,25-dihydroxyvitamin D levels in normal children and in vitamin D disorders. Am J Dis Child. 1980; 134(2):135-139.
  9. Seino Y, Ishizuka S, Shima M, Tanaka H. Vitamin D in bone formation. Osteoporos Int. 1993; 3(Suppl 1):196-198.
  10. Suda T, Ueno Y, Fujii K, Shinki T. Vitamin D and bone. J Cell Biochem. 2003; 88(2):259-266.
  11. Holick MF. Vitamin D deficiency. N Engl J Med. 2007; 357(3):266-281.
  12. Rollins G. Vitamin D testing-what’s the right answer? Clin Lab News. 2009; 35(7):1, 6, 8, 9.
  13. Jingushi S, Hara T, Sugioka Y. Deficiency of a parathyroid hormone fragment containing the midportion and 1,25-dihydroxyvitamin D in serum of patients with slipped capital femoral epiphysis. J Pediatr Orthop. 1997; 17(2):216-219.

Authors

Mr Skelley and Drs Papp, Lee, and Sargent are from the Department of Orthopedic Surgery, The Johns Hopkins University, Baltimore, Maryland.

Mr Skelley and Drs Papp, Lee, and Sargent have no relevant financial relationships to disclose.

Correspondence should be addressed to: M. Catherine Sargent, MD, c/o Elaine P. Henze, BJ, ELS, Medical Editor and Director, Editorial Services, Department of Orthopedic Surgery, Johns Hopkins Bayview Medical Center, 4940 Eastern Ave, #A665, Baltimore, MD 21224-2780 (ehenze1@jhmi.edu).

doi: 10.3928/01477447-20101021-27

10.3928/01477447-20101021-27

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