eMedicine Specialties > Physical Medicine and Rehabilitation > Traumatic Brain Injury

Posttraumatic Heterotopic Ossification: Treatment & Medication

Author: Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver
Contributor Information and Disclosures

Updated: Jul 28, 2008

Treatment

Rehabilitation Program

Physical Therapy

The treatment of heterotopic ossification (HO) often is quite challenging and, in many cases, unsatisfactory. Therefore, emphasis should be placed on the importance of understanding the natural history of HO in developing treatment strategies. Most cases of HO occur within 3 months after spinal cord injury. Most roentgenographic evaluation occurs during a 6-month period, and the progress of HO is related to the severity of injury. In patients with severe injuries, roentgenographic progression has been found to subside by 6 months and serum alkaline phosphatase and bone scan activity to become normal or significantly decreased. In patients with more severe deficits, larger amounts of bone formation that progressed for more than 1 year has been seen, and elevated alkaline phosphatase levels and increased bone scan activity have been observed for up to 2 years or longer.

The role of physical therapy in patients with HO is controversial. The major goal of treatment is to maintain ROM and thereby preserve function; however, opinions differ regarding ROM exercises for patients with HO.

Several authors have reviewed the literature that compares opposing philosophies. One theory is that an aggressive regimen of passive ROM exercises may predispose the patient to the development of HO because of microtrauma or local hemorrhage. Several authors suggest that passive stretching and ROM exercises are contraindicated after HO is suggested, but they recommend active exercise within the pain-free range. Other authors stress the importance of ROM exercises to maintain joint mobility and to prevent or retard fibrous ankylosis. They found no evidence for increased HO or decreased ROM with passive ROM exercises.

Forceful manipulation of joints with preexisting HO under anesthesia helps to maintain useful joint ROM and to prevent ankylosis. A study by Garland and colleagues found that 64% of affected joints maintained or gained ROM with rehabilitation after manipulation.5 Some patients required repeated manipulations; none had a detectable increase in HO. The literature generally supports the common use of active ROM exercises and gentle, passive ROM exercises to maintain available joint motion and to avoid progressive contractures. If ankylosis seems inevitable despite exercises, it is best for the patient if it occurs in the most functional position.

Medical Issues/Complications

In a patient with a severe head injury, problems (such as deforming spasticity and contracture) often have time to develop because of the time needed to handle prolonged complications in acute care (eg, craniotomy facial bone surgeries, cholecystitis, pneumonia or other infections). In addition, if the head-injury patient displays a low level of responsiveness during much of the hospital course, this often casts doubt in the mind of acute care personnel about the individual's suitability for rehabilitation. Aggressive measures to prevent deformities may be given a lesser priority, especially if staff members are dealing with complications that have a greater medical priority. The resulting deformities may be quite advanced by the time the patient reaches acute rehabilitation, making intervention more difficult.

Surgical Intervention

In cases of heterotopic ossification (HO), surgery for removal of ectopic bone should be undertaken only for clear functional goals, such as for improved standing posture or ambulation or for independent dressing and feeding. In general, surgery is not undertaken earlier than 18 months after injury.

Excision should be considered for patients in whom shoulder motion is severely limited by extensive heterotopic bone, especially if dynamic electromyography studies reveal volitional capacity for the various shoulder muscles. Excision also may be undertaken to improve passive shoulder functions.

HO that restricts elbow motion is excised surgically at maturation. Maturation of HO is determined by the radiographic appearance of a defined cortex and by a normal level of serum alkaline phosphatase. Additional prognostic indicators for successful HO excision are good cognitive recovery (Rancho scale level VI or greater) and selective motor control in the extremity. Time since onset of brain injury alone is not an accurate prognosticator.6,7

lf joint deformity from HO results in significant functional limitations, such as difficulty with hygiene, sitting, or ambulation, surgical resection of HO may be indicated. Surgery also may be appropriate if an underlying bone mass contributes to repeated pressure sores. Various recommendations have been made for the timing of surgery. Surgery is contraindicated in patients with clinical, laboratory, or radiographic evidence of active ossification. Waiting for the maturation of heterotopic bone before operating may take 1-2 years. Heterotopic bone should be excised when it significantly restricts joint ROM and limits function and rehabilitation. Other authors have said that the process is stabilized after 6-8 months and that surgery is of benefit after that time, although the authors did not state whether radiation treatments were given to the patients studied.

Traditionally, surgery should be delayed for 18 months after brain injury. Patients with good neurologic recovery, good motor control, normal or slightly elevated levels of alkaline phosphatase, and a mature lesion may be candidates for surgery before the 18 months. In more severely compromised patients, if motor control is still improving and laboratory test values still indicate abnormalities, surgery should be delayed longer than 18 months. With such patients, the major indication for surgery is limb positioning. Once HO has matured, at 12-18 months or more after injury, it can be removed surgically or partially resected if clinically indicated. Postexcision, low-dose radiation or the use of etidronate disodium (EHDP) can prevent its recurrence.8,9,10,11,12,13

However, several case series suggest that earlier resection results in improved function without significant risk of recurrence. Although diphosphonates are an effective means of prophylaxis if initiated shortly after the trauma, mineralization of the bone matrix resumes after drug discontinuation, making this traditional practice also controversial.

Consultations

  • Physiatrists - To plan the best rehabilitative approach
  • Neurologists - To rule out other neurologic impairments
  • Orthopedic surgeons - If any surgical treatment is necessary

Other Treatment

Forceful joint manipulation appeared to enhance formation of HO, and it has been postulated that the force generated by muscle spasticity may promote its development.

Medication

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Nonsteroidal anti-inflammatory drugs

Nonsteroidal anti-inflammatory drugs (NSAIDs) have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.11,14,15,16,17,18,19,20,21


Indomethacin (Indocin, Indochron E-R)

An indoleacetic acid derivative and NSAID, indomethacin is related structurally and pharmacologically to sulindac. Theoretically, indomethacin decreases inflammation associated with heterotopic ossification (HO) and quiets the spastic muscles driven by pain. The effect is thought to be due to inhibition of the synthesis of prostaglandin. Indomethacin is known to be highly potent in preventing HO after total hip replacement, due to one of the most potent inhibitors of the cyclooxygenase enzyme, which catalyzes the formation of prostaglandin precursors (endoperoxides) from arachidonic acid.

Adult

25 mg PO tid for 3 mo after surgery

Pediatric

1 mg/kg PO tid for 3 mo after surgery

Risks of bleeding increase with concomitant NSAIDs, anticoagulant or heparin therapy, or alcohol ingestion; decreases anti-hypertensive effects of alpha-adrenergic blocking agents; serum levels of indomethacin are decreased slightly by concomitant aspirin and increased by concomitant probenecid; renal elimination decreased and serum levels and toxic effects of methotrexate and lithium increased by concomitant administration; GI absorption delayed by food and milk; antihypertensive effects of thiazide diuretics antagonized by indomethacin; antagonizes prostaglandin-mediated natriuretic effects of loop diuretics

Documented hypersensitivity; complete or partial syndrome of nasal polyps, angioedema, or bronchospastic reactivity to aspirin or other NSAIDs

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur; discontinue if there is persistent leukopenia, granulocytopenia, or thrombocytopenia

Bisphosphonate derivatives

Analogs of pyrophosphate, these act by binding to hydroxyapatite in bone-matrix, thereby inhibiting the dissolution of crystals. Bisphosphonate derivatives prevent osteoclast attachment to the bone matrix and inhibit osteoclast recruitment and viability.8


Etidronate disodium (Didronel)

The role of etidronate disodium (EHDP) in preventing heterotopic ossification (HO) has been studied extensively. The literature to date does not adequately support the efficacy of its use in patients with brain injuries. EHDP is a bisphosphonate that reportedly retards formation, growth, and dissolution of hydroxyapatite crystals; therefore, it is thought to limit ectopic soft-tissue calcification by preventing conversion of calcium phosphate compounds in hydroxyapatite crystals. EHDP often is used to retard HO once it is discovered; the drug is thought to be more effective if given prophylactically or in the earlier stages of formation. EHDP does not dissolve established calcification.

An active HO process is often painful, and treatment with agents such as EHDP is often effective in reducing the inflammatory aspects of the HO process and in quieting the spastic muscles driven by pain. Therefore, EHDP is the mainstay of drug treatment, reducing the incidence and severity of ectopic bone formation with minimal side effects. Effective prophylactic treatment should be initiated as soon as possible. Optimal drug dose and length of treatment have not been established adequately in TBI.

Adult

Not established; 20 mg/kg/d PO for 3 mo, followed by 10 mg/kg/d PO for 3-6 mo for a total of 6-9 mo suggested

Pediatric

Not established

Coadministration with calcium-containing products and other multivalent cations decrease absorption

Documented hypersensitivity, hypocalcemia, and renal impairment

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Because effect on normal bone healing is questionable, EHDP caution in long-bone fractures; GI side effects (eg, diarrhea, nausea) are infrequent and can be minimized by dividing total daily dose

More on Posttraumatic Heterotopic Ossification

Overview: Posttraumatic Heterotopic Ossification
Differential Diagnoses & Workup: Posttraumatic Heterotopic Ossification
Treatment & Medication: Posttraumatic Heterotopic Ossification
Follow-up: Posttraumatic Heterotopic Ossification
Multimedia: Posttraumatic Heterotopic Ossification
References
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Further Reading

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Keywords

posttraumatic heterotopic ossification, heterotopic calcification, heterotopic ossification, HO, posttraumatic brain injury heterotopic ossification, traumatic brain injury, TBI, post-TBI heterotopic ossification, etidronate disodium, EHDP

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Contributor Information and Disclosures

Author

Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver
Auri Bruno-Petrina, MD, PhD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Canadian Association of Physical Medicine and Rehabilitation, College of Physicians and Surgeons of British Columbia, and International Society of Physical and Rehabilitation Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert L Sheridan, MD, Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School
Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, and American College of Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consort
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

 
 
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