A 19-yr-old man with traumatic brain injury from a motor vehicle accident was admitted to a rehabilitation unit after 2 mos of acute care hospitalization. His initial Glasgow Coma Scale score was 6. The patient had a prolonged period of coma and had undergone ventriculoperitoneal shunting for increased intracranial pressure. At admission, the patient was confused and inappropriate (Rancho Los Amigos level V). He had a left spastic hemiplegia, left hip and knee flexion deformities, and a left ankle plantar-flexion contracture. Range of motion in the left hip, knee, and ankle joints was limited and painful. A hard, nontender mass was palpable in the right quadriceps muscle. Heterotopic ossification (HO) was clinically suspected. Plain radiographs revealed minimal soft tissue calcification near the right mid-femur but did not show ectopic bone or other bony abnormality around the left hip. Serum alkaline phosphatase level was elevated at 143 units/liter (normal, 37–107 units/liter). A triple-phase bone scan showed a diffuse but irregular increase in radiopharmaceutical uptake inferior to the left hip joint and medial to the right mid-femur on the delayed images (Fig. 1). These findings were consistent with active HO. Rehabilitation included aggressive range-of-motion exercises to the left hip, knee, and ankle joints and serial casting to increase knee extension. Oral antispasticity medication was administered to reduce spastic hypertonia. Indomethacin was used to treat/prevent HO and to reduce pain.
HO is the formation of new bone in soft tissue. The prevalence of clinically significant HO in the traumatic brain injury population is estimated to be 10–20%. Major risk factors for HO development include immobility, limb spasticity, and prolonged coma. HO does not develop intra-articularly, and in traumatic brain injury, it tends to occur in decreasing frequency around the hips, elbows, shoulders, knees, and at times, in the thigh. HO may present with range-of-motion limitation, pain, swelling, erythema, or other features of inflammation. Bony ankylosis, nerve and vascular compression, or lymphedema may also occur. These findings are nonspecific, and diagnostic testing (plain radiographs, triple-phase bone scan, serum alkaline phosphatase) is usually required for confirmation.
Early diagnosis of HO in the traumatic brain injury population is essential so as to limit additional disability and pain. Nonsteroidal antiinflammatory drugs, etidronate sodium, range-of-motion exercises, and spasticity management may be used to prevent HO development or progression. Treatment of established, severe, functionally limiting HO includes surgical resection and forceful manipulation.
Radionuclide triple-phase bone scan is particularly sensitive for detection of early HO. Positive phase I (dynamic blood flow) and phase II (blood pool) scans may precede a positive phase III (delayed) scan by 2–4 wks. A positive phase III scan can precede radiographic findings of ossification by 1–4 wks. This test can also provide a measure of bone maturity. Serial scans can be used to gauge progression of the process and also to guide the timing of possible surgical resection, which is usually done when the HO is mature.