CHAPTER 24 AVASCUIAR NECROSIS 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 bone, in this should be understood by any practitioner treating instance the talus, as a closed compartment. An pathology of the foot and ankle. Its pathogenesis is increase in marrow pressure causes a decrease in such that if it is not diagnosed early and treated perfusion 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 death 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 femoral head 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 osteomyelitis, suppurative arthritis of the ankle joint, 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 lupus 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 rheumatoid arthritis 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 current 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 cartilage, 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 infarction 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 osteocytes.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 Corticosteroid 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, osteoporosis, 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 osteoarthritis." 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 radiography. The radiographic changes correlate stages. First, there is an interruption of intracellular