Key Insights On Treating Atraumatic Osteonecrosis Of The Talus

Osteonecrosis, also called avascular necrosis or ischemic necrosis, is a pathologic condition in which the cells in bone tissue die due to a lack of blood supply.^1,2 There are between 10,000 and 20,000 cases of avascular necrosis diagnosed in the United States each year but only a small percent involve the talus.^1,2 Delanois and colleagues treated 37 ankles in 24 patients between 1974 and 1996 for atraumatic osteonecrosis of the talus.³ This group represented only 2 percent of the 1,056 total patients treated for osteonecrosis throughout this time period.³ This highlights the rarity of atraumatic osteonecrosis in the general population. Accordingly, talar osteonecrosis can be difficult to diagnose and challenging to treat, especially in the absence of an inciting event.    

Researchers believe the cause of atraumatic osteonecrosis is a combination of genetic, metabolic and local factors that affect the body’s blood supply, leading to vascular damage, increased intraosseous pressure and mechanical stresses on the foot.¹ In addition, there are many associated risk factors, including alcohol dependence, prolonged glucocorticoid use, smoking, pregnancy, systemic lupus erythematous, antiphospholipid antibodies, hyperlipidemia and hyperuricemia.^1,3 Of these associated risk factors, glucocorticoids and alcoholism account for 80 percent of all cases of atraumatic osteonecrosis.¹

The true mechanism of atraumatic osteonecrosis is still unknown but several hypotheses have emerged. Authors believe that prolonged glucocorticoid use and alcoholism lead to changes in circulating lipids, which can subsequently result in microemboli to the vessels supplying the bone.^1-2,4 One study performed by Wang and colleagues examined the effect alcohol had on rabbit and mouse bone marrow following intragastric alcohol allocation.⁴ The authors noted fat cell proliferation and hypertrophy as well as diminished hematopoiesis in the femoral head, thus leading to an increased risk of avascular necrosis.

Physicians should maintain a high level of suspicion for this in patients with underlying systemic disease, a history of prolonged glucocorticoid use or a history of alcohol substance abuse. With atraumatic osteonecrosis of the talus, patient complaints are often vague.^1,5 Ankle pain is the most common complaint upon initial presentation.⁵ Patients may describe a deep aching pain or a sharp pain, which may or may not bother them at rest. Rarely, patients will complain of pain that keeps them awake at night. Early on in the course of the disease, the physical examination may be unremarkable.⁵ There may or may not be edema in the ankle. In later stages of the disease, patients may experience joint pain and crepitus with loss of motion due to talar dome collapse.⁵       

Early diagnosis is the key to preventing breakdown of the talus.^1,5-6 Unfortunately, many patients with atraumatic talar avascular necrosis present late in the course of the disease, which may have already progressed to fractures or collapse.¹

A Guide To Diagnosis And Treatment

Researchers recommend obtaining plain film radiographs in all cases of suspected osteonecrosis.⁵ Radiographic imaging will show increased density and sclerosis to the talus. In some cases, subchondral cystic changes and/or articular collapse may be visible on X-rays.^1,5 Following positive radiographs or if X-rays are negative but suspicion remains high for osteonecrosis, one may order magnetic resonance images (MRI) or computed tomography (CT) scans. These imaging modalities are more sensitive than plain film radiographs and are better at identifying pathology.⁶ Magnetic resonance imaging is the gold standard for early diagnosis of avascular necrosis. Changes on MRI are often visible before changes on X-rays or CT can become apparent.⁶ A CT scan can better assess trabecular patterns and cortical integrity.       

One can first attempt conservative treatment. This includes either partial weightbearing or complete non-weightbearing of the affected extremity.^6-7 If conservative treatment fails, surgical treatment options may be options. Physicians can utilize core decompression for Stage I or Stage II avascular necrosis of the talus.⁷ Core decompression decreases intraosseous pressure within the talus and boosts revascularization. To perform core decompression, one would make multiple perforations in the avascular area of the talus with a small 1.5-mm to 2.0-mm drill.⁷       

Although bone stimulation is not widely studied, it may be a viable option. Holmes and colleagues demonstrated successful treatment of talar osteonecrosis with arthroscopic drilling, bone grafting and the use of an internal bone stimulator.⁸

In more advanced cases of osteonecrosis, one can perform debridement of avascular bone with subsequent packing or placement of autograft or allograft bone.⁷ In the later stages III or IV of avascular necrosis in which there is substantial collapse of the talus, arthrodesis or salvage procedures may be warranted. These include the possibility of subtalar joint arthrodesis, ankle joint arthrodesis or tibiocalcaneal arthrodesis.⁷       

Note that surgical intervention is not always necessary following collapse of the talus. One should reserve these procedures for symptomatic patients.⁶ Many patients remain pain-free despite collapse of the talus.⁶       

Case Study: Addressing Atraumatic Osteonecrosis In A Patient With Chronic Ankle Pain

A 75-year-old Caucasian female presented to the clinic in moderate distress with a chief complaint of diffuse ankle pain and swelling in her right foot that has persisted over the last 12 months. She described her pain as a dull ache but admitted the pain had caused some difficulty with walking. The patient denied any history of trauma or ankle sprains. She attempted conservative treatment (including rest, ice and warm water soaks) at home without significant relief of her discomfort. The patient saw her family physician, who prescribed her compression stockings and meloxicam (Mobic, Boehringer Ingelheim) 7.5 mg once a day, but the patient admits these treatments have not helped with her pain.       

The patient is 5’5” and weighs 203 lbs. Her social history is unremarkable. She denies a history of smoking and alcohol intake. She currently lives independently at home. Her past medical history is significant for diabetes mellitus, hypercholesterolemia, hypertension, macular degeneration and hepatitis, but the patient could not relate which type of hepatitis she had. Her current medications include ramipril (Altace, Pfizer), pioglitazone (Actos, Takeda Pharmaceuticals), pravastatin (Pravachol, Bristol-Myers Squibb), vitamin D, omega 3 and Bayer aspirin.       

The lower extremity physical examination showed her skin temperature and color were within normal limits. Pedal pulses were palpable and hair was present on the dorsal digits. She had a slightly diminished sensation of the right foot and ankle in comparison with the left, but did not complain of any significant paresthesias. The vibratory sensation was decreased to the right hallux interphalangeal joint. Her protective sensation was absent to the toes on the right but intact at the level of the metatarsal heads. The patient has +3/4 pitting edema on the right foot and ankle in comparison to the left, which demonstrates only +1/4 pitting edema. Range of motion at the ankle joint was lower on the right in comparison to the left. She had diffuse pain to palpation and pain with range of motion of the ankle joint on the right. Subtalar joint range of motion was decreased but without pain.       

Radiographs demonstrated increased density and sclerosis throughout the entire talar body, neck and head (see images 1 and 2). Some arthritic spurring was visible at the talar neck. A subtle cortical defect was present in the talar neck although it was difficult to determine if that was a new or old finding. There were no appreciable cystic changes to the talar body on X-rays. The alignment of the ankle joint appeared to be adequate without collapse.       

Following a review of radiographic findings, a local radiologist recommended a CT scan (see images 3-5), which revealed significant cystic changes throughout the talar body. Fractures to the talar neck with fragmentation were present. In addition, there appeared to be a fracture to the talar body with slight plantar compression.

The patient wore a controlled ankle motion (CAM) boot with a walker to allow her to ambulate with light touchdown to the right foot. Given her age, size and independent lifestyle, we do not believe she is a good candidate to be fully non-weightbearing. We are awaiting follow up with the patient to review the results of her CT scan and discuss possible surgical interventions if these become warranted in the future.    

References

1. Jones LC, Mont MA. Osteonecrosis of bone. UpToDate. Available at https://www.uptodate.com/contents/osteonecrosis-avascular-necrosis-of-bone . Published Sept. 22, 2014.
2. Callachand F, Milligan D, Wilson A. Atraumatic pantalar avascular necrosis in a patient with alcohol dependence. J Foot Ankle Surg. 2015; epub Sept. 17.
3. Delanois RE, Mont MA, Yoon TR, et al. Atraumatic osteonecrosis of the talus. J Bone Joint Surg. 1998; 80(4):529-36.
4. Wang Y, Li Y, Mao K, et al. Alcohol-induced adipogenesis in bone and marrow: a possible mechanism for osteonecrosis. Clin Orthop Rel Res. 2003; 410:213-224.
5. Chiodo C, Herbst SA. Osteonecrosis of the talus. Foot Ankle Clin. 2004; 9(4):745-755.
6. Brook JW, Downey MS. Avascular necrosis of the talus. McGlamry’s Comprehensive Textbook of Foot and Ankle Surgery, Second Edition, Chapter 24, Lippincott, Williams and Wilkins, Philadelphia, 1997, pp. 143-150.
7. Horst F, Gilbert BJ, Nunley JA. Avascular necrosis of the talus: current treatment options. Foot Ankle Clin. 2004 9(4):757-773.
8. Holmes GB. A unique treatment for talar osteonecrosis: placement of an internal bone stimulator. J Bone Joint Surg. 2015; 5(1):1-5.