Atraumatic Pantalar Avascular Necrosis in a Patient With Alcohol Dependence

Atraumatic Pantalar Avascular Necrosis in a Patient With Alcohol Dependence

The Journal of Foot & Ankle Surgery xxx (2015) 1–2 Contents lists available at ScienceDirect The Journal of Foot & Ankle Surgery journal homepage: w...

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The Journal of Foot & Ankle Surgery xxx (2015) 1–2

Contents lists available at ScienceDirect

The Journal of Foot & Ankle Surgery journal homepage: www.jfas.org

Case Reports and Series

Atraumatic Pantalar Avascular Necrosis in a Patient With Alcohol Dependence Fayaz Callachand, Dip SEM(UK), MSc, FRCS (T&O) 1, David Milligan, MB BCh, BaO, BSc (Hons) 2, Alistair Wilson, FRCS (T&O) 1 1 2

Orthopaedic Surgeon, Musgrave Park Hospital, Belfast, Northern Ireland Doctor, Ulster Hospital, Dundonald, Northern Ireland

a r t i c l e i n f o

a b s t r a c t

Level of Clinical Evidence: 4

In the United States, an estimated 10,000 to 20,000 new cases of avascular necrosis are diagnosed each year. We present an unusual case of atraumatic avascular necrosis with widespread hindfoot and midfoot involvement. A 62-year-old female with a history of alcohol dependence and smoking, who had previously been treated for avascular necrosis of the knee, presented with right-sided foot pain and difficulty weightbearing. Imaging studies revealed extensive avascular necrosis of the hindfoot and midfoot, which precluded simple surgical intervention. The patient was followed up for 18 months. In the last 8 months of the 18-month period, the patient managed her symptoms using an ankle-foot orthosis. A diagnosis of avascular necrosis should be considered in patients with atraumatic foot and ankle pain, especially in the presence of risk factors such as alcohol excess and smoking. Ó 2015 by the American College of Foot and Ankle Surgeons. All rights reserved.

Keywords: alcoholism aseptic necrosis hindfoot midfoot osteonecrosis

In the United States, an estimated 10,000 to 20,000 new cases of avascular necrosis (AVN) are diagnosed each year (1). Avascular necrosis of the talus is a known complication of severe trauma to the ankle (2,3). A small number of documented cases of atraumatic AVN of the talus have been reported (4), with some investigators stating associations with hemophilia (5), corticosteroids (6), and alcoholism (7). Alcoholism tends to cause AVN in the hip and shoulder (8). However, we describe a case predominantly involving the talus, with extensive involvement of the hindfoot and midfoot. Case Report We report the case of a 62-year-old female patient who presented with atraumatic AVN predominantly of her right talus but also involving the calcaneus, midfoot, and distal tibia. The patient was a heavy smoker with a history of alcohol dependence. Our patient initially complained of right ankle pain and difficulty weightbearing in February 2013, 5 weeks after elective right total knee arthroplasty. She had undergone knee arthroplasty after an 11-month history of knee pain and imaging studies that revealed Financial Disclosure: None reported. Conflict of Interest: None reported. Address correspondence to: Fayaz Callachand, Dip SEM(UK), MSc, FRCS (T&O), Musgrave Park Hospital, Stockmans Lane, Belfast BT9 7JB, Northern Ireland. E-mail address: [email protected] (F. Callachand).

multiple areas of necrosis of both the femur and the tibia, with varus collapse. The patient had previously been employed as a hairdresser and for a number of years had suffered from alcohol dependence. She was at the time a heavy smoker, smoking 40 cigarettes per day, and had recently been hospitalized for treatment of pneumonia. Clinical examination of the ankle revealed tenderness over the right talar neck and tibiotalar joint, anterior ankle impingement, and hindfoot stiffness. After a full history and clinical assessment, the patient had plain radiographs taken of the right ankle, which showed widespread bony sclerosis, collapse, and degeneration (Fig. 1). Magnetic resonance imaging of the affected foot showed widespread AVN of the talus, calcaneus, navicular, cuboid, second and third metatarsal bases, medial and middle cuneiforms, and distal tibia (Fig. 2). The patient was followed for 18 months and managed her symptoms with an ankle-foot orthosis and analgesia for the last 8 months of the 18-month period. At the last follow-up visit, the patient was coping well and has continued conservative treatment, with close monitoring using regular radiographic and magnetic resonance imaging surveillance. Discussion The talus is especially prone to AVN for several reasons (2,9). First, a large percentage of its surface is covered by articular

1067-2516/$ - see front matter Ó 2015 by the American College of Foot and Ankle Surgeons. All rights reserved. http://dx.doi.org/10.1053/j.jfas.2015.07.024

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Fig. 1. (A) Anteroposterior and (B) lateral radiographs of right ankle showing marked sclerosis, collapse, and degenerative changes, in keeping with extensive avascular necrosis of the talus.

cartilage, and only a small percentage of the surface area remains available for arterial infiltration. In addition, the nutrient vessels are small in caliber, and the collateral circulation is not extensive, increasing the likelihood of AVN in the event of arterial insufficiency. Alcohol dependence is an important factor in the development of AVN. The exact mechanism remains unclear; however, studies have shown that increased alcohol intake can directly induce the deposition of fat cells in the bone marrow, reducing the levels of osteogenesis and increasing the risk of AVN (8). Other findings have indicated that the pathogenesis can result from fat embolism linked to coexisting hyperlipidemia in the alcoholic patient (10). Smoking, too, can play an important role in the development of AVN. This can be directly from the increased atherosclerotic load of the peripheral vascular system (11), leading to a chronically reduced arterial supply to an already undersupplied region of the body. It has been shown that patients who smoke, when adjusted for age, sex, and medical comorbidities, have a relative risk of 3.9 for developing atraumatic AVN of the femoral head (12). Thus, it follows that this increase in relative risk should apply to other areas. Other risk factors for the development of AVN include long-term corticosteroid use (4). It has also long been established that trauma to the talus, in particular, a displaced fracture, can lead to AVN (3). In a recent study by Issa et al (13), of 85 patients with ankle AVN, 35.6% had a history of alcohol abuse and 29% had a history of smoking. Also, 40% had previously presented with AVN of another large joint and, of these, the knee was the most common, accounting for 37%. The present patient had a high risk of AVN because of her alcohol dependence and smoking and clearly had multifocal disease. In conclusion, this is an unusual presentation of AVN, which should be considered in patients presenting with atraumatic ankle pain and a history of alcohol dependence and smoking. References 1. Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 77:459, 1995. 2. Pearce D, Mongiardi CN, Fornasier VL, Daniels TR. Avascular necrosis of the talus: a pictorial essay. Radiograph 25:399–410, 2005. 3. Halvorson JJ, Winter SB, Teasdall RD, Scott AT. Talar neck fractures: a systematic review of the literature. J Foot Ankle Surg 52:56–61, 2013. 4. Delanois RE, Mont MA, Yoon TR, Mizell M, Hungerford DS. Atraumatic osteonecrosis of the talus. J Bone Joint Surg Am 80:529–536, 1998.

Fig. 2. Sagittal slices from magnetic resonance imaging scan of right foot and ankle showing widespread bony necrosis on both (A) T1- and (B) T2-weighted sequences. Extensive necrosis was present in the talar body and dome, with fracture of the talar neck and depression of the articular surface at the tibiotalar joint. 5. Macnicol MF, Ludlam CA. Does avascular necrosis cause collapse of the dome of the talus in severe haemophilia? Haemophilia 5:139–142, 1999. 6. Tasic V, Traikovski Z, ZAfrovski G, Gucev Z, Trompeter RS. Aseptic necrosis of both tali in a child with steroid dependent nephrotic syndrome. Nephrol Dialysis Transplant 21:1702–1704, 2006. 7. Harris RD, Silver RA. Atraumatic aseptic necrosis of the talus. Radiology 106:81–83, 1973. 8. Wang Y, Li Y, Mao K, Li J, Cui Q, Wang GJ. Alcohol-induced adipogenesis in bone and marrow: a possible mechanism for osteonecrosis. Clin Orthop Relat Res 410:213–224, 2003. 9. Kelly PJ, Sullivan CR. Blood supply of the talus. Clin Orthop 30:37–44, 1963. 10. Jacobs B. Alcoholism-induced bone necrosis. NY State J Med 92:334–338, 1992. 11. Jones JP. Intravascular coagulation and osteonecrosis. Clin Orthop Relat Res 277:41–53, 1992. 12. Matsuo K, Hirohata T, Sugioka Y, Ikeda M, Fukuda A. Influence of alcohol intake, cigarette smoking, and occupational status on idiopathic osteonecrosis of the femoral head. Clin Orthop Relat Res 234:115–123, 1998. 13. Issa K, Naziri Q, Kapadia BH, Lamm BM, Jones LC, Mont MA. Clinical characteristics of early stage osteonecrosis of the ankle and treatment outcomes. J Bone Joint Surg Am 96:e73, 2014.