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Home , Avascular necrosis, Femoral head

CHAPTER 24 AVASCUIAR OF THE TALUS

./oel W. Brook, D.P.M. Micbael S. Douney, D.P.M.

Avascular necrosis (A\,T{) of the talus is a topic that extravascular compromise considers , in this should be understood by any practitioner treating instance the talus, as a closed compartment. An pathology of the and ankle. Its pathogenesis is increase in marrow causes a decrease in such that if it is not diagnosed early and treated to the osteoc),tes and creates a "marrow properly, it may result in sequelae with a high compaftment syndrome." This can occur in degree of morbidity. The literature on A\N is infectious processes where the infectious by-prod- extensive, and illustrates the fact that it is a ucts increase the intraosseous pressure. complex, progressive disease that defies simple Vascular disruption is another etiologic categorization. It is most easily defined as the mechanism. Traumatic vascular disruption is self- of bone cells secondary to complete interruption or explanatory, and occurs most frequently with a significant decrease in the vascular supply to talar neck fractures. Disruption due to vascular bone.' Synonyms for the process include ischemic compression refers to an increase in soft tissue necrosis, osteonecrosis and aseptic necrosis."3 The volume and/or pressure which may occur either latter is actually a misnomer, and will subsequently intraosseously or extraosseously, and again, is most be discussed in the section on etiology. commonly a sequela of infection. Intraluminal It is important to discern between the etiology obstruction occurs with any embolic process. and pathogenesis of A\N in that a working The majority of literature dealing with A\N knowledge of both contribute to the diagnosis of reflects the disease process as it effects the femoral the disease. The etiology of AVN encompasses the head.6,' The factors predisposing a patient to factors or conditions that predispose the patient to developing A\N in general, and of the develop the pathology. Its significance often lies in are numerous, and beyond the scope of this paper. the information rendered from the patient's history. Bone infarcts in the talus have been repofied in The pathogenesis of A\N is the physiologic process patients with sickle cell anemia, Gaucher's disease resulting in the production of a bone infarct, and is (i.e. familial splenic anemia), hematogenous diagnostically significant with respect to the , suppurative arthritis of the ankle , changes seen on various imaging modalities. and in patients undergoing renal dialysis.6'7 The factors most often responsible for predisposing a ETIOLOGY patient to developing A\N of the talus are: systemic erythematosus (SLE), exogenous administra- The determinant underlying all classifications or tion of cofiicosteroids, infection, and trauma. predisposing conditions is the interruption of blood supply to the bone. The etiology of A\N may be subdivided into mechanisms and predisposing Table 1 factors. The mechanisms can involve the anatomic location of the circulatory compromise or vascular - disruption. These are academic classification ETIOLOGY MECHANISMS systems whose component parts overlap (Table 1). Extraosseous afierial compromise includes Location of Circulatory Vascular Disruption5 such phenomena as trauma, alheromata, and Compromise' microemboli. Intraosseous arterial obstruction is Extraosseous Arterial Traumatic seen with fat emboli and in systemic disease Intraosseous Arterial Vascular Compression processes, such as and Intraosseous Intraluminal systemic lupus erythematosus (SLE). Intraosseous Extravascular Obstruction 144 CHAPTER 24

Although SLE is associated with AVN, it is not trauma, which damages the vessels supplying the thought to be a primary cause for its development. talus. The primary blood supply to the body of the SLE is an autoimmune disease with a diverse array talus is the artery of the tarsal cana| a branch of the of clinical manifestations including: Raynaud's posterior tibial artery. Secondary supplies are from phenomenon, vasculitis/vasculopathy, hyper- the deltoid artery and the afiery of the sinus tarsi, lipidemia, and antiphospholipid syndrome (.a branches of the artery of the tarsal canal and disease process associated with venous and arterial anterior tibial artery, respectively.",'u Although the thrombosis). Patients with SLE are often treated literature repofts a case of an isolated A\N to with systemic steroid therapy.B It is believed that, as the head of the talus,l' A\N almost exclusively a result of these factors, patients with SLE develop involves the body of the talus. In addition to the A\N at lower and/or less frequent doses of steroids tenuous blood supply of the talus, the majority of the compared to patients taking steroids for other bone is covered with articular , a conditions such as rheumatoid arthritis, chronic relatively avascular tissue.115 The Hawkins' classifica- obstructive pulmonary disease, and status-post tion for talar neck fractures has classically been used organ transplantation.5,e'' to predict the incidence of onset of A\N, and is Infection is also not a primary cause of AVN. based upon the seyerity of the fracture and concomi- This explains why the term aseptic necrosis is a tant dislocations of the peritalar joint complexes." misnomer. Infection results in an inflammatory Subsequently, various studies have reported inci- response which ultimately results in the direct dences which can be summarized as follows: Type I: destruction of bone. A\N is a bone 0-73o7ot Type II: 2O-500/o; Type lII: 84-7000/o.1821 caused by compromising the blood supply to the Type IV talar neck fractures as first described by bone. The increase in pressure from the local Canale and Kelly are reported too infrequently in the accumulation of fluids and exudates can result in literature to accurately quantitate the likelihood of either intraosseous or extraosseous vascular the development of subsequent A\N.22 Szyszkowitz compression, which disrupts the blood supply to devised a system of classifizing fractures of the entire the .lo Therefore, infection by way of the talus, not just the neck, and related them to the onset inflammatory process and its sequelae, secondarily of various complications including A\N. In his results in the development of A\N. classification scheme, only general statements induced AVN was first concerning the onset of A\N are proposed. For described by Pietrograde." Currently, the use of example, in fractures of the proximal neck or body, systemic colticosteroids is the leading cause of necrosis seldom occurs, whereas in fractures of subchondral A\N in adults." Steroid use is rarely, the proximal neck with ankle and/or subtalar however, the sole factor involved in the develop- dislocation, A\N neady always occurs.'3 In general, ment of A\N, but is implicated in causing A\DJ with A\N is reported to occur in 50o/o of talar neck certain systemic diseases." Several mechanisms fractures.le20'23'21 Daniels'5 reported a composite have been proposed for steroid-induced AVN. incidence of 37o/0. A number of authors rcpol| a These include a steroid-induced hypercoaguable significantly lower incidence of A\N following talar state, fatty emboli, , and increased neck fraclurec.26-2e A lower incidence of 75o/o to 750/o intramedullary lipocyte size. has been attributed to early open reduction with The length of time of cofticosteroid usage internal fkation with protection of the blood supply reportedly necessary to produce AVN varies from the deltoid artery. Talar neck fractures are not markedly in the literature from one week to several the only injury pattern where A\N of the talus months." Most authors now agree that it is occurs. Goldner et a1.30 repoft a 330/o onset of talar necessary to take large doses of steroids over body A\N with late segmental collapse in Gustillo several months, as it takes time for the pathologic Type 3 open subtalar joint dislocations. changes to occur, specifically the increase in Idiopathic A\N of the talus has been repofted, intramedullary lipocyte size resulting in an increase btrt it is rare.3' According to Kenzora, idiopathic A\N in intramedullary pressure.5e,ln The reason why occurs due to an accumulated stress theory, where certain patients have this apparent increased conditions associated with A\T{ produce a bone cell sensitivity to steroids remains unknown." sickness. As the sickness progresses or other decom- Of the predisposing factors, the only one pensating factors such as steroid use are added, a which directly results in the production of AVN is critical stress is reached. and A\N occurs.a,3' CHAPTER 24 145

PATHOGENIESIS the stage of the disease.' Of the three types of bone infarct: medullary, intracortical, and subchondral, A bone infarct occurs when there is death of the only the latter occurs in the talus. This type of marrow fat cells. Of the three cellular components infarct develops in a predictable pattern. The of bone, hematopoietic, osteocltes, and marrow fat insidious onset of symptoms parallels those seen in cells, the latter is least sensitive to the effects of patients with ." anoxia, and takes up to five days to die after the AVN has been classically diagnosed by onset of anoxia. Bone death from anoxia occurs in . The radiographic changes correlate stages. First, there is an interruption of intracellular with secondary to repair, and are enzymes. This is followed by an alteration or not detectable until 5 to tZ weeks after the insult cessation of intracellular metabolic activity. In the has occurred.3'1.6'31r-36 A talus with AVN presents with third stage there is irreversible disruption or sclerotic densities involving all or part of the body. dissolution of intracellular nuclear and cytoplasmic In cases where pat of the body of the talus is ultrastructure resulting in cell death.6 spared, it usually occurs medially, in the area of Understanding the pathogenesis of bone blood supply from the deltoid artery.:'- Bobechko infarction, facilitates identification of an infarct via and Harris38 reported that radiographic sclerosis various imaging modalities. Vhen considering the seen in avascular bone is due to viable bone being three dimensional infarct, there are four zones deposited on necrotic bone, osteoporosis of which need to be considered.6 An outer rim of surrounding from disuse and the hyperemia normal tissue surrounds an inflammatory zone of of repair, and calcification of necrotic active hyperemia. The hyperemia produces a further increasing . \7hen attempting localized area of and a relative increase to diagnose A\N radiographically, it is important to in radiographic density of the innermost zone of understand that the talar body is normally more infarcted bone. The central zone of celI death and radiodense compared to the talar neck, and that the its contiguous zone of ischemic injury are both overlapping shadows of the malleoli also increase contained within the zone of hyperemia. Repair of the density of the body compared to surrounding the infarcted tissue begins along the outer structures.3e perimeter of the ischemic tissue, thereby creating Hawkins' sign is a subchondral radiolucency in the hyperemic zone of granulation tissue. It is this the dome of the talus which appears 6 to B weeks progressive margin between ischemic and viable after injury, suggesting bone resorption during tissue that is sensitive to detection with the use of revascularization.'8 The presence of Hawkins' sign is magnetic resonance imaging.a 33 a good indicator that the vascularity of the talus is intact, and that A\N will not occur.2e Hawkins' sign DIAGNOSIS is often seen medially on the anteroposterior radiograph of the ankle, and again correlates with deltoid artery.4 It can also A\N of the talus is diagnosed using a combination the blood supply of the lateral view is made more of information gained from the history and physical been seen on the but presence the malleoli. is exam, and from various imaging studies. As difficult by the of It the absence of Hawkins' sign previously mentioned, the history gives clues as to important to note that indicator that A\N will occur.'e the etiologic factors predisposing a patient to is not a reliable scintigraphic studies are more develop the disease. In addition to traurirra, Although systemic illnesses, infection, and the use of sensitive than radiography in the detection of AVN, glucocorticoids, a history positive for rearfoot or they are not specific. There will be a decreased after injury which reflects ankle surgery may also result in A\N of the talus. uptake immediately the The information extracted from the history is more the disruption of the vascular supply to the bone. valuable than that from the physical examination It must be remembered though, that if vascular because symptoms experienced by patients with disruption is secondary to trauma, the cold area in A\N are nonspecific. Patients have pain with active the talar body could be obscured by the increased or passive range of motion of the subtalar or ankle uptake at the fracture site. 'Weeks to months after revascularize, joint, tenderness) mild eryzthema, local edema, and the injury, when the bone begins to may have joint clicking or locking, depending on an increase in uptake may be expected.a'"'3a This is 146 CHAPTER 24 not particularly useful from a diagnostic standpoint. zone of hyperemia.4'x'47 Mitchell et a1. referred to Despite this, it may have some prognostic value for this as the "Double Line Sign," which is diagnostic predicting the onset of A\N in iniury patterns for A\T{.41'17'1e consistent with its development. Canale and Kelly Brody et a1.50 found that on T1-weighted have used scintigraphy to determine the length of images changes could be seen within the first week treatment following the onset of A\N. They found of clevascularizalion. By days 1.6 and 23, areas of increased uptake in the entire talat body, patchy an<1 more homogeneous decreased signal representing revasculaization, and continued intensity could be seen, respectively. The detection treatment until the scan began to show a decrease of changes to the fat cells themselves is variable. in activity.'e Should the practitioner have a high However, the changes cause an increase in degree of suspicion for the development of A\N vascularity, inflammation and the production of a based on a positive history or injury pattern along granulation tissue interface. As discussed in the with bone scan uptake patterns consistent with section on pathogenesis, MRI is very sensitive in A\N, they may choose to use more aggressive detecting the presence of this granulation tissue therapy or perform a more specific diagnostic interface. modality. Computed tomography (CT) has also been COMPLICATIONS investigated as a diagnostic modality. The vast majority of research has been done on A\N of the The complications of AVN of the talus ate femoral head. CT can be used to assess the subtle summarized in Table 2 The production and changes in trabecular patterns and cortical integrity. revascularization of osteonecfotic bone can occur Overall though, the effectiveness of computed without symptoms or morbid changes, and are tomography is currently questionable. usually diagnosed incidentally. Bone is unique in Conversely, magnetic resonance imaging that an infarction of osseous tissue can completely (MRI) is currently the gold standard for the early revascularize and repait itself." Therein lies the and most specific non-invasive diagnosis of AVN' mechanism responsible for producing the morbid Coleman et al.4' reported MRI to be sensitive to complications associated with AVN of the talus. The detecting A\N of the in asymptomatic patients hyperemia is an inherent part of the repair process. when radiographic studies were negative. As the bone repairs itself there is a transient Hendersona'repofied a case however, where serial structural weakness involving the trabeculae MRI scans failed to show AVN of the talus in a supporting the subchondral bone in the dome of patient with a negative Hawkins' sign' Although the talus. If the biomechanical stresses of rare, false negatives of A\N have been reported.*'15 bearing are superimposed upon the talus during The hallmark MRI finding is the appearance of a this stage of hyperemia and compromised reactive interface representing a layet of fibromes- structural integrity, the trabeculae may fracture, and enchymal tissue at the margin between viable and the collapse of the subchondral bone and the over- infarcted medullary bone.a6'a7 This presentation lying articular cartrlage may ensue. relates to the previously described three dimensional layers of a bone infarct. The images process' correlate with the stages of the disease Table 2 Early in the process, a line or arc of decreased signal intensify can be seen on T1-weighted COMPLICATIONS OCCURRING This represents granulation tissue replacing images. SECONDARY TO A\/I\[ OF THE TALUS fat and is the transition between normal and ischemic bone.133'46'18 On T2-weighted images, this None line or arc demonstrates a bilaminar appearance Collapse of articular surfaces characterized by an outer border of decreased Ankle or subtalar DJD signal intensity, and an inner layer of increased Intra-articular loose bodies signal intensity, the latter of which represents the Infection CHAPTER 2,i 147

Catto described a phenomenon known as Adelaar,51 Delee," and Pennal" also agfee that "late segmental collapse," in which there is a protected weight-bearing should be instituted, This fracture along the sclerotic bone rim with collapse is significant because these authors feel that it is of the entire remaining infarct into the zone of both unreasonable and impractical to prescribe revascularization.ll Delee found that one in three such a long treatment of non-weight bearing. patients with total body O'Brien et a1.55 and Hawkins'u believe that weight experienced collapse of the ankle or subtalar bearing does not necessarily result in collapse. joint.22 Degenerative joint disease of the ankle Hawkinsls and Gillquist et a1.56 state that even if and/or subtalar joint, and the production of collapse occurs, it is well tolerated by most intra-articular loose bodies are a direct result of the patients, and rarely requires reconstrLlctive surgery. collapse of the articular surfaces. Infection is rare, This conclusion is not supported by many authors, but is mentioned since any necrotic tissue can including Monkman et a1.,5t w-ho indicate that late provide an environment which can serve as a nidus segmental collapse following AVN is a poor for infection." prognostic sign. Additional consetwative therapy involves a modification of activity level. In TREATMENT symptomatic patients, a decrease in activity will usually be self-imposed because of pain. Dictating There are two primary goals of treatment. The first specific changes in activity leve1s or exercise is to prevent the onset of the previously mentioned routines, such as a change over to swimming from complications. Early diagnosis translates into a running, will decrease the potentiai risk of articular better prognosis.a The key is to have a high level of collapse. suspicion for A\N by fully understanding the There are currently no reports in the literature etiologic factors and the pathogenic process. This that address the use of electric bone stimulation as knowledge will guide the practitioner to order the a modality for the treatment of A\N of the talus. appropriate studies in a timely manner. Once A\N There are however, studies that address A\N of the has been diagnosed, the practitioner mlrst choose a femoral head. The rationale for using electric bone treatment plan appropriate to the patient which stimulation is based on the loss of structural al1ows the second goal of treatment to occur, integrity during the repair process of AVN, and the namely, revascularization of the talus. Full revascu- increase in bone formation that is induced with larization of the talus may take two or more years, electric stimulation.5E Electric bone stimulation has and coirelates with the previously described dense also been shown to decrease osteoclastic bone sclerc'tic talar body.zo':; If the revascularization resorption in vitro.te Since structural integrity is occurs in a slow homogenous way, collapse of the compromised because of an increase in the amount talar domr: does not occur. When revascularization of bone resorption compared to new bone occurs rapidly in a patchy distribution there is formation, this could potentially be a viable collapse alcng the interface of avascular trabeculae treatment for subchondral A\N of the talus. Aaron and the invadrrrg vascular granulation tissue. Penny et al. showed a decreased incidence of clinical and and Davis felt this is due to the devitalized bone radiographic progression of femoral head A\N in being reabsorbed faster than the new bone is being patients treated with pulsed electric magnetic fields deposited, resulting in structural weakness.'o (PEMF) bone stimulation.6o PEMF and implanted Most authors currently recommend protected direct current bone stimulation have been shown weight-bearing. Controversy arises with respect to to be successful in decreasing the progression the degree of protection as well as the time for of A\N, while electrical bone stimulation via therapy. Borner,i' Zllch,t' and Kazars3 believe non- capacitive coupling has apparently not added any weight bearing should be instituted for 6 to 18 therapeutic value.tE Steinberg et a1. found no months when treating AVN. Canale and Kelly found indication that the addition of capacitive coupling that in their patients, those who remained non- gave better results than and grafting weight bearing for at least B months had the most alone.6' Finally, Mont and Hungerford accurately favorable results. Those patients treated by means state that electric bone stimulation for the treatment of protected weight-bearing with a patellar tendon- of A\D{ of the femoral head is currently still bearing brace also had good outcomes, but less so. experimental, and that it has not yet been I48 CHAPTER 24 approved by the Food and Drug Administration for clinician can recognize the characteristic changes the treatment of A\T{.aS However, as a result of the as they present on various imaging studies. Though positive data concerning the use of PEMF and isolated incidents of false-negative studies have implantable direct current bone stimulation, studies been reported, magnetic resonance imaging is evaluating the use of such modalities for the treat- currently the gold standard for early and accurate ment of A\N of the talus are justified. diagnosis. Once the diagnosis is made, prompt Theories justifying surgical intervention as a aggressive treatment consisting of protected primary treatment for AVN of the talus are based weight-bearing or non-weight bearing is necessary upon the premise of creeping substitution revascu- in order to prevent the onset of morbid complica- larization from surrounding well-vascul arized bone tions, namely the collapse of the talar dome. into avascular areas, in this case within the talus. Surgical treatment should be reseryed for two with either subtalar or triple conditions associated with A\N of the talus. The arthrodesis has been attempted and advocated by first addresses decreasing the chances of many authors.6'67 Boyd6' theorized, however, that developing A\N with early open reduction and the revascularization process occurring from an internal fixation of fracture dislocations patterns arthrodesis procedure would extend only 3 to 4 predisposing to A\N. Secondly, should late stage millimeters into the body of the talus. Supporting collapse occur rendering the patient symptomatic, Boyd's hypothesis, various authors have proven afthrodesis of the affected is indicated. that primary arthrodesis is unsuccessful at causing more rapid revascularization of an osteonecrotic REFERENCES talus.'S'O Penny and Davis'O recommended a Blair fusion consisting of advancement of a cofiicocan- 1 Zlzlc TM: Osteonecrosis. Curr Opin Rbeumatol 3G)481-189, cellous strut from the distal into the neck of 1c;c)1. the talus, once the talar body has been removed. 2 Trott A\f: Developmental Disorders. 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