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The considerable morbidity imposed by degenerative joint disease of the ankle has driven new approaches to the treatment of ankle arthritis. Compared with the other major lower extremity joints, the ankle possesses unique anatomic, biomechanical, and biologic characteristics that make it resistant to primary arthritic degeneration and susceptible to posttraumatic arthritis after innocuous-appearing trauma, leading to a lower overall prevalence than in the hip or knee.
A variety of nonoperative and surgical options are available to managing ankle arthritis. Evaluation with radiographs, advanced imaging, and selective injection helps guide treatment selection. Bracing and injection therapy can postpone need for surgery. Allograft resurfacing distraction arthroplasty and distal tibial realignment provide options for joint preservation. Minimally invasive techniques and improved fixation options have made fusion more reliable. The recognition of risk factors for nonunion and judicious application of autologous bone graft or recombinant bone growth–stimulating molecules can reduce the need for revision surgery.
Determining the prevalence of ankle osteoarthritis in a population faces numerous challenges. Relying on clinical symptoms for identification of cases results in under-reporting due to the inconsistent correlation between joint degeneration and the clinical syndrome of osteoarthritis. The cost and logistical challenges to obtaining unbiased imaging or cadaveric samples of a populations limits large-scale studies of osteoarthritis prevalence.
Autopsy studies provide useful information, particularly highlighting differences in prevalence of degeneration among different joints. Generally, in all joints, cartilage fibrillation is more frequently observed than full-thickness defects, and the prevalence of macroscopic cartilage changes increases with age. However, the lack of information concerning symptoms associated with the joints being studied make it unclear if observed degenerative changes are associated with clinical osteoarthritis.
Meachim et al examined knee, shoulder, and ankle joints at autopsies performed on adults and found full-thickness chondral defects in 1 of 20 ankle joints from men older than 70 years ( Fig. 22-1 ). Huch et al graded the cartilage of 36 knees and 78 ankles from both limbs of 39 organ donors to evaluate the prevalence of ankle osteoarthritis using a 5 point scale described by Collins ( Table 22-1 ) and found grade 3 and 4 degenerative changes in 5 of 78 (6%) ankle joints and in 9 of 36 (25%) knee joints. In a series of investigations, Muehleman et al examined seven joints, including the knee and ankle of both lower legs in 50 cadavers with a mean age of 76 years (see Fig. 22-1 ). Sixty-six percent of the knee joints had grade 3 and 4 degenerative changes compared with 18% of the ankle joints. Both Huch and Muehleman observed that the medial compartments of both the knees and the ankles were more commonly involved than the lateral compartments. Radiographs often showed no evidence of degenerative changes despite direct examination of the joints showing regions of full-thickness cartilage erosion.
Grade 0 | Normal gross appearance |
Grade 1 | Fraying or fibrillation of the cartilage |
Grade 2 | Fibrillation and fissuring of the cartilage and osteophytes |
Grade 3 | Extensive fibrillation and fissuring with frequent osteophytes and 30% or less full-thickness chondral defects |
Grade 4 | Frequent osteophytes and greater than 30% full-thickness chondral defects |
Overall, the autopsy studies demonstrate that advanced degenerative changes are at least three times more prevalent in the knee than in the ankle, and the prevalence of degenerative changes in both joints increases with increasing age (see Fig. 22-1 ). However, limitations include relatively small numbers of joints examined, lack of random or systematic sampling of populations, and lack of correlation to radiographic findings or clinical symptoms.
Attempts to evaluate the prevalence of ankle arthritis by plain radiographs alone have limited value. Although epidemiologic studies based on radiographs generally document an increase in degeneration in all joints with increasing age, most have not focused on the ankle osteoarthritis specifically. Evaluation of ankle articular cartilage thickness is particularly difficult on radiographs that were not performed in a standardized fashion, and cadaver studies have shown that ankle radiographs often do not show signs of joint degeneration even when the ankle joint has regions of full-thickness erosion of articular cartilage.
Further, radiographic studies of the ankle joint are limited by the lack of strong correlation between formation of radiographic signs of osteoarthritis and development of clinical symptoms. Van Der Schoot et al followed 88 patients after tibial fractures for 15 years and found 3 of 56 (5%) had ankle pain with no radiographic findings of osteoarthritis and similarly 2 of 32 (6%) had ankle pain with radiographic findings. Conversely, the 4% rate of knee pain without radiographic osteoarthritic changes increased to 24% having knee pain when radiographic findings were present.
Very few studies of the prevalence of osteoarthritis have included patients with ankle osteoarthritis. The available information suggests that knee osteoarthritis is likely more than five times more common than ankle osteoarthritis. However, in the United States, knee replacements are performed approximately 10 times more often than ankle replacements and ankle fusions combined.
It is unclear if this disparity suggests the rate of clinically symptomatic ankle arthritis is lower than estimates from cadaver or radiographic studies. Using surgical volumes to estimate clinical prevalence, however, may underestimate disease burden of ankle arthritis. Variability in symptom severity and functional limitation in the ankle relative to the knee, lack of comfort with surgical treatment options for ankle arthritis among physicians, and the relative efficacy of nonsurgical treatments for ankle osteoarthritis would all attenuate the frequency of surgical treatment of ankle osteoarthritis relative to that of knee replacement.
The vast majority of ankle arthritis is a result of prior ankle fractures or ligamentous injury. In a consecutive series of 639 patients with Kellgren-Lawrence grade 3 and 4 ankle arthritis over 13 years, Saltzman et al found 445 (70%) had posttraumatic etiology while only 23 (3.6%) were diagnosed with primary ankle osteoarthritis without associated deformity ( Table 22-2 ). In a similar study of 406 patients with end-stage ankle arthritis over 10 years, Valderrabano et al found that posttraumatic arthritis was the most common presenting etiology (78%), followed by arthritis secondary to other causes including associated deformity (19%) and primary osteoarthritis without associated deformity (2%) (see Table 22-2 ). Many patients identified with idiopathic ankle osteoarthritis have malalignment of the tibial plafond or hindfoot and for our purposes are considered a separate category of secondary ankle arthritis. In Mann’s series, 10 of 77 patients classified as having primary arthrosis, the average age was 69 years (range, 59–78) compared with 52 years for patients with secondary ankle arthritis ( P < 0.05). These studies emphasize the intrinsic resistance of the uninjured ankle joint to primary articular degeneration.
Type of Arthritis | N | Percentage of Total | Age | Gender Male/Female |
---|---|---|---|---|
Posttraumatic | 742 | 71.0% | 52 ± 14 | 49%/51% |
Rheumatoid | 98 | 9.4% | 59 ± 13 | 23%/77% |
Congenital or acquired deformity | 54 | 5.2% | 67 ± 12 | 68%/32% |
Primary (no deformity) | 32 | 3.1% | ||
Neuropathic | 31 | 3.0% | 54 ± 14 | |
Osteochondritis dissecans | 24 | 2.3% | 45 ± 13 | 33%/67% |
Hemophiliac | 18 | 1.7% | 24 ± 17 | 100%/0% |
Avascular necrosis | 17 | 1.6% | 50 ± 15 | 100%/0% |
Postinfection | 13 | 1.2% | 57 ± 17 | 67%/33% |
Hemochromatosis | 11 | 1.1% | 73%/27% | |
Gout | 5 | 0.5% | 46 ± 18 |
Injuries to the bones and supporting ligaments around the ankle resulting in instability or joint incongruity frequently lead to posttraumatic arthritis. The most common causes of posttraumatic arthritis are rotational ankle fractures (43%), followed by history of ankle sprain (26%) and tibial plafond fracture (13%) ( Table 22-3 ). Even a single ankle sprain may result in posttraumatic arthritis.
Type of Trauma | N | Percentage of Total | Age |
---|---|---|---|
Rotational ankle fracture | 321 | 43.3% | 51 ± 14 |
Ankle sprain | 191 | 25.7% | 58 ± 13 |
Plafond fracture | 98 | 13.2% | 43 ± 12 |
Tibia fracture | 58 | 7.8% | 49 ± 16 |
Talar fracture | 47 | 6.3% | 50 ± 15 |
Combined fractures | 27 | 3.6% | 55 ± 12 |
Posttraumatic ankle osteoarthritis is hypothesized to result from elevated contact stress that exceeds the capacity of the articular cartilage to repair itself or adapt. According to this hypothesis, the development of posttraumatic ankle osteoarthritis progresses through overlapping stages: articular cartilage injury, chondrocyte response to tissue injury, and decline in chondrocyte function.
The cartilage injury resulting in posttraumatic ankle arthritis frequently results from the energy of the initial trauma. After injury, some patients rapidly develop joint degeneration even without apparent articular surface damage or joint instability, while other patients with articular surface incongruity or an unstable joint do not develop arthritis. This variable response after cartilage injury results from a cascade of inflammatory cytokine release, which may end in recovery or lead to apoptotic chondrocyte death and opens the door to exciting interventions to reverse the apoptotic process. The initial presence or lack of articular cartilage damage after injury is not apparent by routine radiographic evaluation. Instead, the severity of bone and soft tissue injury may provide clues to the amount of energy absorbed by the articular cartilage. Fortunately, advances in magnetic resonance imaging (MRI) techniques hold promise for diagnosing these traumatic cartilage injuries and following their course.
Posttraumatic cartilage injury may also be the consequence of accumulated pathologic contact stresses related to joint malalignment and instability. These elevated contact stresses may result from intraarticular joint incongruity such as by displaced intraarticular fractures. Alternatively, or synergistically, instability created by damage to bony and ligamentous constraints also elevates articular surface contact stresses. Common examples of posttraumatic ankle joint instability include widening of the distal tibiofibular syndesmosis, shortening and rotation of the fibula, or capsuloligamentous laxity.
Over 25% of patients with ankle arthritis have identifiable, nontraumatic etiologies (see Table 22-3 ). The most common secondary causes are rheumatoid arthritis, followed by overload associated with acquired or congenital deformity, neuropathic (Charcot) arthropathy, and sequelae of osteochondral defects. Hemophilia, avascular necrosis (AVN), postinfectious arthritis, hemochromatosis, and gout together make up about 6% of cases.
Thirty percent of patients with rheumatoid arthritis will develop symptoms in the ankle or foot. The ankle is the most frequently affected joint below the knee, and females are affected more commonly than males. The presence of ankle symptoms suggests a more severe level of rheumatoid disease activity and is an independent marker for nonremission. While joint tenderness is a nonspecific sign of disease activity, imaging with MRI or ultrasound may detect synovial hypertrophy and effusion and help identify active disease requiring medical treatment. Other inflammatory and crystal deposition arthropathies behave similarly, though rheumatoid arthritis affects gait parameters more than gout or psoriatic arthritis. Once signs of joint erosion and degradation are evident on standard radiographs, more definitive treatment may be required even if patients achieve remission of their inflammation.
Multiple intraarticular hemorrhages often leads to arthritis in patients with hemophilia. Patients with neuropathic arthropathy of the ankle and degenerative disease after necrosis of the talus with collapse of the articular surface make up a small portion of the patients with degenerative disease of the ankle.
The relative rarity of primary osteoarthritis of the ankle suggests unique characteristics of the joint relative to other large joints are chondro-protective. In the uninjured state, anatomic factors leading to congruency and stability, tensile properties of the ankle’s articular cartilage, and metabolic characteristics of ankle chondrocytes combine to protect the joint from premature wear.
On the other hand, the thinness of ankle articular cartilage and the small contact area, leading to higher contact stresses for a given force, seem to make the joint more susceptible to posttraumatic arthritis. The thinner, stiffer articular cartilage of the ankle may be less able to adapt to articular surface incongruity and increased contact stresses than the thicker articular cartilage of the hip and knee. The thickness of ankle articular cartilage ranges from less than 1 mm to slightly less than 2 mm, compared with 3 to 6 mm in the hip or knee. When loaded, the human ankle joint has a contact area averaging 350 mm 2 , compared with 1120 mm 2 for the knee and 1100 mm 2 for the hip. The ankle’s smaller contact area leads to larger contact stress for a given force. Ankle contact stresses are further increased by factors such as ligamentous instability, ankle position, and torque.
The bony and ligamentous anatomy of the ankle joint confers a high degree of stability and congruence protecting the articular cartilage from damaging shear forces. Ankles exhibit a reproducible axis of joint rotation particular to each individual. In ankles with intact bone and soft tissue structures, including joint capsule and ligaments, translation of the talus relative to the mortise outside of this axis is minimized.
The distal tibia and the medial malleolus, together with the lateral malleolus, form the ankle mortise, which contains the talus. These bony structures support three sets of opposing articular surfaces. The tibial medial malleolus and the medial facet of the talus form the medial articulation, or medial gutter. The fibular lateral malleolus and the talar lateral articular surface form the lateral articulation, or lateral gutter. The distal tibia and the superior dome of the talus form the primary weight-bearing articular surface of the neutrally aligned ankle ( Fig. 22-2 ). The distal tibial articular surface has a longitudinal convexity that matches a concavity on the surface of the talus, which divides the tibiotalar articulation into the medial and lateral compartments for evaluation of ankle loading and degenerative changes.
Medial and lateral ligamentous complexes and the ankle joint capsule stabilize the relationship between the talus and the mortise. Firm anterior and posterior ligaments bind the distal tibia and fibula together to form the distal tibiofibular syndesmosis. The talus and mortise widen slightly from posterior to anterior. Thus when the talus is maximally dorsiflexed, the tibiofibular syndesmosis spreads, and the wider portion of the talar articular surface locks into the ankle mortise, allowing little or no rotation between the talus and the mortise.
Ankle joint articular cartilage differs from that of other major weight-bearing joints in thickness and tensile properties. These differences help to explain the relative resistance of the ankle to development of primary osteoarthritis.
Cartilage strength and stiffness provides resistance to cartilage wear as joints are subject to repetitive loads during gait and activity. While cartilage thickness and collagen and proteoglycan content adapt favorably to physiologic contact stresses, loss of strength and stiffness is seen in early osteoarthritis as collagen and proteoglycan concentration decreases, even before macroscopic changes are evident. These changes lead to an 80% reduction of energy dissipation potential in arthritic cartilage samples.
A more gradual decline in tensile properties of ankle articular cartilage compared with other large weight-bearing joints helps explain the vulnerability of the hip and knee to degenerative changes as one ages and the relative resistance of the ankle to development of primary osteoarthritis. The tensile fracture stress and tensile stiffness of ankle articular cartilage deteriorate less rapidly with age than those of the hip ( Figs. 22-3 and 22-4 ). While the tensile fracture stress and stiffness of hip femoral articular cartilage are initially greater than that of talar articular cartilage, with age they decline exponentially in the hip but linearly in the ankle. As a result, beginning in middle age, ankle articular cartilage can withstand greater tensile loads than hip articular cartilage.
The age-related declines in articular cartilage tensile properties result from a complex loss of cellular function and alteration in extra-cellular matrix properties, subchondral bone, and joint fluid composition leading to weakening of the collagen fibril network. This is an area of active study given the enormity of the problem arthritis poses and the potential that intervention may slow or reverse the process at an early stage.
Ankle articular cartilage differs from that of other joints in the expression and response to cytokines that regulate chondrocyte activity and extracellular matrix composition. The catabolic cytokine interleukin-1 (IL-1) inhibits proteoglycan synthesis by chondrocytes in knee articular cartilage more effectively than in ankle articular cartilage perhaps due to a greater number of IL-1 receptors in the chondrocytes of knee articular cartilage. Furthermore, the anabolic response of chondrocytes after removal of IL-1 and administration of osteogenic protein 1 (OP-1) is accentuated in ankle cartilage compared with knee cartilage. Messenger ribonucleic acid (mRNA) for neutrophil collagenase (matrix metalloproteinase-8 [MMP-8]) is found in chondrocytes of human knee articular cartilage but not in those of ankle articular cartilage. While these observations need further study, they suggest that metabolic differences exist between knee and ankle articular cartilage, which might help to explain the relative rarity of primary ankle osteoarthritis.
Ankle arthritis severely impacts the lives of affected individuals. A variety of functional outcome measures and gait analyses highlight the severity of this impact and establish a baseline for the functional limitations of patients with end-stage arthritis of the ankle.
Ankle osteoarthritis patients have similar degree of disability to patients with arthritis of other large lower extremity joints and to patients with severe chronic medical conditions. Glazebrook et al prospectively compare patients with end-stage ankle and hip arthritis and found patients with ankle arthritis had SF-36 scores equivalent in severity to patients with end-stage hip arthritis, and they were two standard deviations below patients without arthritis. Ankle osteoarthritis patients also have similar degree of disability based on SF-36 scores to patients with end-stage renal disease and congestive heart failure. Agel et al showed that patients with ankle arthritis scored three times worse than control patients on the Musculoskeletal Functional Assessment (MFA), and Segal et al found that patients with ankle arthritis had reduced function based on both SF-36 and MFA scores. In addition, these patients showed reduced ankle motion, ankle plantar flexion moment, peak ankle power absorbed, and peak ankle power generated in the affected limb when compared with the normal contralateral limb. Peruccio et al found patient factors such as obesity and lower education levels may adversely affect Health Related Quality of Life subscales in ankle osteoarthritis patients to a greater extent than knee osteoarthritis patients.
The first step in evaluating patients with suspected ankle arthritis is taking a thorough history and physical exam. Clues to etiology such as prior trauma or history of sprains may lead to concerns for posttraumatic arthropathy; a history of multiple joint swelling and stiffness or gout may suggest inflammatory etiology; and a history of steroid use or alcoholism could suggest AVN. Examination should focus on the ankle as well as the whole lower extremity to account for overall alignment as well as adjacent joint and contralateral limb disease.
When evaluating the patient with ankle pain and apparent arthritis, one of the first tasks of the clinician is to determine whether the problem is global (affects the majority of the joint) or focal (affects a specific region of the joint). Inflammatory arthritides such as rheumatoid disease and seronegative spondyloarthropathies are, by definition, global processes. Similarly, hemophiliac, gouty, crystalline deposition, and septic arthropathies are diffuse joint processes. Intraarticular pilon fractures and neuroarthropathic fractures that cause ankle arthritis generally induce a global arthritic response, especially with multiple fracture lines involving the tibiotalar joint. Conversely, tibial shaft malunions, ankle instability, and foot malalignment that lead to ankle cartilage loss initially often cause well-localized focal problems.
Taking a good history and performing a careful physical examination are essential. Understanding the time course, location, and quality of pain can help differentiate ankle arthritis from painful joints in the hindfoot or midfoot or pain emanating from tendons or nerves. First, determine if there is a history of trauma contributing to the development of ankle arthritis. Although a past fracture is the most common cause of ankle degeneration, recurrent sprains or even a single major sprain can also be responsible. Determine if there is a history of other joint stiffness and swelling. While ankle arthritis is usually not the first manifestation of generalized inflammatory arthritis, it certainly is common in patients with severe multiarticular disease. Eliciting a history of hemophilia, gout, talar AVN, or infection could also explain the etiology of end-stage arthritis and may affect treatment plans.
Next, determine which activities cause ankle pain or limit function. This will help define the extent to which the problem disables the patient and what their posttreatment expectations may include and helps focus in on what anatomy is leading to pain. Walking uphill causes bony impingement in the anterior ankle or the talonavicular joints. Pain caused by downhill walking suggests a problem at the back of the ankle and can include posterior soft tissue impingement, trigonal problems, or synovial chondromatosis. Pain in the posterior ankle and hindfoot walking on uneven ground can indicate subtalar joint disease. Hindfoot pain associated with hindfoot malalignment might not be from the ankle or subtalar joints themselves but might be due to secondary bony impingement of the calcaneus on the lateral process of the talus or fibula or to peroneal or posterior tibial tendon tears.
The examination is done with the patient sitting and standing. In the seated position, a careful vascular and neurologic assessment is made and points of maximal tenderness are identified. Joint motion of the ankle, hindfoot, midfoot, and first ray are compared with the opposite side. The ligamentous stability around the ankle is tested. All major extrinsic tendons should be palpated to determine if there are associated tendinopathies and strength tested in major joint planes. Careful attention should be given to the skin and nails: patients with rheumatoid arthritis may show punctate infarcts suggestive of ongoing vasculitis, signs of venous statis or arterial insufficiency may be evident, and psoriatic plaques could suggest an inflammatory disease. Axial rotational alignment should be explored if standing/walking foot progression angle is asymmetric. It is best tested with the patient seated or lying prone and the knees bent.
The standing and walking examinations complement the seated examination. Alignment of the foot should be evaluated with weight bearing. Patients with recurrent instability often have a declinated first ray, whereas patients with severe flatfeet and secondary ankle disease often have clinical instability of the medial column. Alignment of the hindfoot is assessed from behind, noting excessive varus or valgus angulation of the heel. Correction of heel valgus with toe rise suggest a competent hindfoot joint complex while lack of correction may indicate the ankle arthritis is associated with hindfoot arthritis, incompetent posterior tibial tendon, or hindfoot coalition. Restriction of ankle dorsiflexion can lead to early heel rise or back-knee gait. The posture of the forefoot upon striking the ground should be noted. Patients who load the lateral part of the foot might have fixed varus deformity of the ankle or transverse tarsal region.
Plain radiographs should be taken with the patient standing whenever possible as this reveals considerable additional information about joint spaces and foot alignment when physiologically loaded. Even with the expectation of weight bearing, a patient’s ability to apply weight to the affected limb during radiography varies by up to 10% but is improved by specific instruction to bear 50% of their weight on each limb.
At the minimum we obtain a standing ankle anteroposterior, lateral, and mortise views. Beam angle may need to be altered to accommodate for lower leg deformity to obtain true images of the joint. Any patient with altered alignment or preparing to undergo surgery also has a hindfoot alignment view ( Fig. 22-5 ) and long leg alignment view ( Fig. 22-6 ). These are very helpful to define if coronal or sagittal plane malalignment is supramalleolar, intraarticular, or in the hindfoot. Standing views of the entire foot are important if there is suggestion the patient’s disease extends into the transverse tarsal joints, midfoot, or forefoot.
MRI is a very useful adjunct for imaging the ankle ( Fig. 22-7 ). It is excellent in delineating abnormalities of soft tissues around the ankle joint and is sensitive for patients with early ankle joint arthropathy and osteochondral injury. It has clinical correlation with disease impact in rheumatoid arthritis and hemophilia. However, MRI findings may be distorted by hardware near the ankle joint and may not find all lesions compared with intraoperative inspection. In addition, the articular surfaces of the ankle are naturally closely packed and congruous, making visualization of articular cartilage defects difficult, though traction during scan acquisition helps improve visualization. MRI coil strength also correlates with the ability to detect cartilage lesions, making detection of cartilage irregularity difficult at strengths below 3 Tesla. New sequences such as T1rho may improve the ability to detect early cartilage wear in the ankle.
Ultrasound imaging for arthritis of the ankle is most useful for diagnosing and following synovitis and effusion related to inflammatory arthropathy. Forty-four percent of rheumatoid arthritis patients in a cross-sectional study had signs of ankle synovitis, suggesting the ankle should be considered in early evaluation of patients suspected of inflammatory arthritis. Ultrasound is an effective tool for this screening since synovial hyperplasia detection correlates well with MRI findings.
Computed tomography (CT) helps define the bony architecture of arthritic ankle joint, surrounding joints, and adjacent soft tissue. Talar dome flattening and extensive subchondral cysts may drive decisions toward fusion versus total ankle replacement ( Fig. 22-8 ). Dual-energy techniques and postacquisition processing allows rendering of bony and soft tissue structures in two or three dimensions to highlight any feature of interest (e.g., bone, tendons, cartilage) and allow for minimizing artifact due to adjacent metal. Intraarticular injection of contrast material enhances the accurate visualization of ankle articular features. CT scan, however, requires a high radiation dose and may be associated with small but measurable increased rates of cancer in a pediatric population.
Bone scan uses a gamma counter to record uptake of an injected radiopharmaceutical tracer, typically technetium ( 99m Tc) combined with a precursor to bone formation such as methylene diphosphonate, to demonstrates areas of high bone turnover. The technique is sensitive but not specific for ankle arthritis ( Fig. 22-9 ). The SPECT-CT combines single photon emission computed tomography with a traditional CT scan to superimpose morphologic and biologic information, improving the specificity of the bone scan and helping to show exactly which bones and joints may be involved in ankle and foot arthritis when multiple joints are affected ( Fig. 22-10 ). Both intra- and inter-observer reliability to identify arthritic joints in the foot and ankle is higher using SPECT-CT than with CT or bone scan alone. This can be particularly useful in localizing active arthritis in the multiple, closely confined joints of the ankle and foot, and can lead to improved diagnostic accuracy in nearly 40% of cases.
Selective injections are used to help identify the source of pain for patients who have clinical or radiographic findings that suggest more than one focal source of pain. Either before or shortly after the injection, the patient is asked to perform activities that are known to cause the pain (e.g., walk on uneven ground, walk up or down stairs, run), and degree of improvement is recorded. There is some overlap in joint coverage depending on where the injection is placed. For example, subtalar joint injection was found to extravasate into the ankle in nearly 25% of cases. To increase accuracy, diagnostic injections may done under fluoroscopic or ultrasound control, and preinjection with contrast for confirmation of needle placement may be considered.
Selective injection may improve outcomes by focusing surgical planning on the most symptomatic joints. In a clinical study comparing arthritis severity based on CT scan imaging with pain relief after injection, less than half of the time the degree of pain relief experienced correlated with the degree of radiographic arthritis, prompting changes to surgical planning in these patients. In a study of foot and ankle fusion patients, Khoury et al reported that the reduction in pain after an intraarticular injection correlated to the response from surgery.
Little has been written about the nonoperative treatment of diffuse ankle arthritis. Nonoperative treatment is based on provider experience and patient preferences.
A variety of nonsteroidal antiinflammatory drugs (NSAIDs) are available for treating pain and inflammation associated with ankle arthritis, with varying efficacy and risk profile. Care must be exercised when prescribing these medications because of substantial side effects including gastrointestinal ulceration and risk of life-threatening bleeding, cardiovascular risk, and risk of renal impairment. Topical antiinflammatory preparations as well as capsaicin topical cream also provide relief from arthritic pain compared with placebo. Glucosamine chondroitin combination therapy is noninferior to celecoxib with similar safety profile in a large prospective randomized controlled multicenter trial of knee osteoarthritis patients. Beneficial effects were seen in pain, stiffness, swelling, and functional improvements over 6 months. Minimal side effects were noted.
Judiciously timed injection of the joint with corticosteroid preparations can help a patient enjoy important life events, and at times can provide months or years of relief. Repeated injections should be used judiciously to avoid attenuation of surrounding soft tissues. They should also be used sparingly in patients with mild arthritic changes due to their chondrotoxic properties, particularly when combined with local anesthetics.
A variety of alternative injections have generated interest in the treatment of ankle arthritis over the last decade. Hyaluronic acid is a naturally occurring component of joint fluid that is theorized to improve the intraarticular environment and reduce pain in arthritic joints. The benefit and safety of hyaluronic acid viscosupplementation injections for ankle arthritis has been suggested through systematic review of a number of randomized controlled trials and prospective clinical series, though bias from industry funding of such studies should be considered when interpreting the results. In some series, this improvement was similar to control saline injection, though there does not appear to be any significant adverse events associated with the injections. The safety profile of this treatment suggests it is a viable option for patients that have failed other treatments and hope to avoid surgery and repeat steroid shots, though discussion with the patient regarding the lack of high-quality evidence to support its clinical use is recommended.
Platelet-rich plasma injection involves centrifugation of a patient’s blood to separate out a concentrated layer of platelets and plasma for injection into various body parts. Its use in ankle arthritis has scant evidence in small prospective series that have demonstrated efficacy and safety without adequate control groups. Prospective, randomized, and controlled trials are eagerly anticipated. The safety profile of this treatment suggests it is a viable option for patients that have failed other treatments and hope to avoid surgery and repeat steroid shots, though discussion with the patient regarding the lack of high-quality evidence to support its clinical use is recommended.
Injection of mesenchymal stem cell preparation taken from autologous bone marrow aspiration similarly has scant evidence lacking control group comparison. Recommendation for this treatment awaits further evidence of efficacy to justify the morbidity of bone marrow aspiration.
The standard nonoperative treatment for end-stage ankle arthritis is mechanical unloading and addition of a rocker sole to shoe wear. If patients accept the cosmetic and functional limitations of an ankle–foot orthosis (AFO), they often obtain partial pain relief and may find they are able to walk farther or stand longer. A custom AFO that can be molded to the contour of the posterior calf muscles may permit some additional unloading of the ankle. A low-profile posterior-based AFO with Velcro tibial strap can remain in a shoe after doffing and is easy to don even for patients with arthritic hands. A contoured, lace-up “Arizona” type brace may be better tolerated by younger active patients due to its better cosmesis ( Fig. 22-11 ). Adding a solid ankle cushion heel (SACH) or a rocker sole can help by further limiting ankle motion while allowing roll-off, creating a more normal gait. These shoe modifications should be used cautiously with patients with poor balance to prevent falls. A cane or other assistive devices can also be very helpful.
An exciting addition to bracing options for ankle arthritis are a new style of custom, energy-absorbing AFOs that partially bypasses the arthritis ankle, allowing greatly improved function up to and including running. One such brace, the Intrepid Dynamic Exoskeletal Orthosis (IDEO), demonstrates improved functional levels on validated tests of agility, power, and speed when worn compared to a variety of more traditional braces. These results have been validated in a multicenter study of 81 patients over one year, demonstrating high satisfaction and improvement in function, though not to the level of unaffected control subjects.
The decision to operate on ankle arthritis requires a clear assessment of the patient’s functional needs and a complete understanding of the cause of the patient’s problem. Keeping in mind the general concept of achieving a stable, painless, plantigrade foot helps direct treatment decisions. Malalignment secondary to trauma, ligamentous instability, or foot deformity frequently coexists with painful and arthritic ankles. Reestablishing normal foot alignment encourages improved foot function and helps to maintain residual natural adjacent joint motion, especially in the subtalar joint, which can delay the development of secondary hindfoot arthritis.
The indications for surgery continue to evolve as techniques change and evidence for effectiveness accumulates. The emergence of several alternative strategies to treat end-stage ankle arthritis has given the surgeon options to individualize patient care. Supramalleolar osteotomies hold promise of prolonging ankle function by redistributing forces across joints. Ankle joint distraction with tensioned wires can similarly prolong ankle function. Ankle replacement is emerging as a viable alternative for selected patients. Of all the surgical techniques, though, ankle fusion remains the mainstay of surgical reconstruction.
The high success rate and low complication rate of a well-performed ankle fusion continue to make ankle arthrodesis an attractive choice for treating end-stage ankle arthritis. The loss of joint motion is typically well tolerated if the remaining hindfoot and midfoot joints are supple, though long-term results are diminished by development or progression of arthritis in other joints of the hindfoot.
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