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A 23-Year-Old Male Patient With History of Severe Traumatic Brain Injury Presents to Inpatient Rehabilitation With Left Hip Pain and Decreased Range of Motion

Meriggi, Jenna DO; Weppner, Justin DO

American Journal of Physical Medicine & Rehabilitation: December 2019 - Volume 98 - Issue 12 - p e142–e143
doi: 10.1097/PHM.0000000000001186
RFS – Teaching Images

From the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.

All correspondence should be addressed to: Justin Weppner, DO, 3471 Fifth Ave, Pittsburgh, PA 15213.

Jenna Meriggi and Justin Weppner are in training.

Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.

Online date: March 28, 2019

A 23-yr-old man admitted to inpatient rehabilitation unit after a severe traumatic brain injury secondary to motor vehicle accident. The patient's 71-day acute hospital course was complicated by prolonged coma, respiratory failure requiring tracheostomy placement, pneumonia, sepsis, dysphagia with percutaneous endoscopic gastrostomy placement, spastic left hemiplegia, and bilateral lower extremity deep vein thromboses. Passive range of motion (ROM) of the left hip was limited and painful. Heterotopic ossification (HO) was clinically suspected, and an x-ray of the pelvis revealed left hip joint space narrowing with HO present medially and laterally about the hip joint (Fig. 1). Serum alkaline phosphatase level was elevated at 267 U/l (44–147 U/l). Comprehensive rehabilitation included ROM exercises, dantrolene to reduce spasticity, and indomethacin for pain. The patient continued to experience impairments in mobility, transfers, and activities of daily living despite medical management. At 18 mos after injury, a triple-phase bone scan revealed mature left hip HO and the patient subsequently underwent surgical resection. After surgery, the patient had immediate improvement in left hip passive ROM with gradual improvements in active ROM and function over a course of physical therapy (Fig. 2).





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Heterotopic ossification is the formation of mature, lamellar bone in extraskeletal soft tissue where bone does not usually exist. The acquired form is most common and typically precipitated by musculoskeletal trauma or neurologic injury.1

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Heterotopic ossification develops in 10%–20% of patients with closed head injury with 10% of those cases resulting in clinically significant joint immobility.1 In spinal cord injuries, the incidence ranges from 20% to 30%, and once HO develops, there is up to a 35% chance of significant limitations in joint ROM.1 The most common location of HO in traumatic brain injury patients is the hip with other affected joints including the shoulder, elbow, and knee.2,3

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Heterotopic ossification is thought to be associated with local inflammation and the differentiation of mesenchymal stem cells present in soft tissues into osteoprogenitor cells.4

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Risk Factors

The risk factors are muscle spasticity, pressure ulcers, deep vein thrombosis, edema, prolonged coma, immobilization, and long bone fractures.3

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Clinical signs and symptoms appear between 3 to 12 wks after the inciting event and include swelling, redness, warmth, low-grade fever, pain, and loss of ROM.1

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Differential Diagnosis

The different diagnosis are deep vein thrombosis, cellulitis, thrombophlebitis, septic arthritis, abscess, hematoma, fracture, and tumor.

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Serum alkaline phosphatase can be used as a screening tool for HO.1 Levels become abnormal 2 wks after injury and increase to 3.5 times the normal value by 10 wks after injury. Plain radiographs are specific for HO but not sensitive in early formation of HO.3 When positive, radiographs show circumferential bone formation near a joint. Plain films may not be positive until 2 to 4 wks after HO appears on bone scan. Conventional radiography is economical and commonly used as an initial evaluation of patients with clinical symptoms of HO. In cases when HO is suspected early in the clinical course or when radiographs are negative despite a high clinical suspicion for HO, a triple-phase bone scan is the most sensitive test. A triple-phase bone scan can reveal HO during flow studies and blood-pool images as early as 2.5 wks after injury. Delayed phase images become positive 1 wk later approximately 3.5 wks after injury.1

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Prophylactic treatment includes ROM exercises, nonsteroidal anti-inflammatory medications, and bisphosphonates.3

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Current treatment recommendations include joint mobilization with ROM exercises and surgical resection.3 If the patient continues to have impaired function with deficits in mobility, transfers, hygiene, or activities of daily living despite nonsurgical management, surgical resection should be considered and is the most effective mode of treatment.3 After initial surgery, 20% develop recurrent HO symptoms such as decreased ROM and 6% of patients require repeat resection of HO.5 Timing of surgery is controversial with one single-site retrospective study advocating for early surgical intervention, whereas other studies advocate for delayed surgical resection until HO has fully matured to minimize recurrence.1,5 Additional prospective, multisite studies are needed to better understand timing of surgical resection and with lack of consensus guidelines the timing of surgery may be institution specific.

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Learning Points

  • Risk factors for HO include muscle spasticity, pressure ulcers, presence of deep vein thrombosis, edema, severity of traumatic brain injury, prolonged coma, immobilization, and long bone fractures.
  • Triple-phase bone scan is the most sensitive test for HO and can reveal HO as early as 2.5 wks after injury. Plain film radiographs are specific for HO but may be falsely negative early after injury until the HO has matured.
  • A triple-phase bone scan may be used to determine the maturity of HO before surgery.
  • Prophylaxis includes ROM exercises, nonsteroidal anti-inflammatory drugs, and bisphosphonates. Treatment includes joint mobilization with ROM exercises and surgical resection.
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1. Shehab D, Elgazzar AH, Collier BD: Heterotopic ossification. J Nucl Med 2002;43:346–53
2. Garland DE, Blum CE, Waters RL: Periarticular heterotopic ossification in head-injured adults. Incidence and location. J Bone Joint Surg Am 1980;62:1143–6
3. Aubut JA, Mehta S, Cullen N, et al: A comparison of heterotopic ossification treatment within the traumatic brain and spinal cord injured population: an evidence based systematic review. NeuroRehabilitation 2011;28:151–60
4. Fredrick SK, Glaser DL, Hebela N, et al: Osteogenic gene expression correlates with development of heterotopic ossification in war wounds. Clin Orthop Relat Res 2014;472:396–404
5. Almangour W, Schnitzler A, Salga M, et al: Recurrence of heterotopic ossification after removal in patients with traumatic brain injury: a systematic review. Ann Phys Rehabil Med 2016;59:263–9
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