CASE REPORT |
https://doi.org/10.5005/jp-journals-10040-1289 |
Idiopathic AVN of Calcaneus: A Case Report
1,3Department of Pediatric Orthopedic Surgery, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India
2Department of Orthopedics, Prasad Ortho Care Clinic, Bengaluru, Karnataka, India
4Department of Orthopedic, Srinivas Speciality Hospital, Bengaluru, Karnataka, India
Corresponding Author: Chandan Kulkarni, Department of Orthopedics, Prasad Ortho Care Clinic, Bengaluru, Karnataka, India, e-mail: cuk146@gmail.com
Received: 02 December 2022; Accepted: 10 January 2023; Published on: 30 December 2023
ABSTRACT
Introduction: Calcaneus is an uncommon location for avascular necrosis (AVN) due to its robust vascular supply.
Case description: We present a case of isolated idiopathic AVN diagnosed after excluding the common etiologies. The patient presented to us with heel pain and inability to bear weight, for which he was investigated; plain radiographs and magnetic resonance imaging (MRI) of the foot revealed a lytic lesion in the body of the calcaneum. Excision biopsy of the lesion was carried out by a lateral approach, and the lesion was thoroughly curetted out. Infective etiologies were suspected after intraoperative (intra-OP) assessment of the material obtained after the biopsy and were sent for culture sensitivity and histopathology. The cavity was left in situ as there was good surrounding bone, and the limb was stabilized with a below knee slab.
Results: The culture revealed no growth and tested negative for tuberculosis, and histopathology revealed features of AVN of the calcaneus, which was confirmed by two experienced pathologists. The patient was kept non weight bearing for 6 weeks. At 6 weeks, he was pain free and started full weight bearing. There was radiological evidence of healing of the lesion at 3 months and he is being followed up regularly.
Conclusion: Thus, AVN of the calcaneum can be a rare cause of heel pain and has to be kept in mind when evaluating a patient with heel pain without a history of trauma.
How to cite this article: MS RP, Kulkarni C, Pai P, et al. Idiopathic AVN of Calcaneus: A Case Report. J Foot Ankle Surg (Asia-Pacific) 2024;11(1):46–49.
Source of support: Nil
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
Keywords: Avascular necrosis, Calcaneum, Case Report, Heel pain, Idiopathic
BACKGROUND
Calcaneus is an uncommon location for AVN. This is possibly due to its triple blood supply, robust anastomosis, and cancelous architecture. Several etiological factors have been described, including posttraumatic, sickle cell anemia, thalassemia, steroid therapy, ethambutol abuse, pancreatitis, caisson disease, trauma, and infections as possible causes of AVN.1 Idiopathic AVN of the talus is a relatively unknown entity and very few cases have been reported in the literature regarding the same.
Here we present a case of isolated idiopathic AVN, diagnosed after excluding the common etiologies. We have also reviewed the causes of osteonecrosis of the calcaneus and proposed a plan of management of the lesion.
CASE DESCRIPTION
A 41-year-old male presented to the outpatient department with a history of diffuse, dull, and aching pain in the right heel for 2 months. The pain was aggravated by weight bearing. He experienced no relief with anti-inflammatory drugs. He did not have any constitutional symptoms. There was no history of trauma, steroid intake, or chronic illnesses.
Initial physical examination revealed no local signs of inflammation around the heel or ankle. Diffuse tenderness was noted on palpation of the heel. He had unrestricted movements at the ankle and subtalar joints.
Plain radiographs revealed a well-defined lytic lesion in the anterior aspect of the body of calcaneum without surrounding sclerosis and a nidus. MRI and computed tomography (CT) scans were done to assess the lesion further. They revealed a benign, well-defined intraosseous cystic lesion measuring 2 × 2 cm in the anterior aspect of the body of the calcaneum and sclerosis, without surrounding edema (Figs 1 and 2). The differentials included bone cysts, osteoid osteoma, intraosseous lipoma, and osteomyelitis.
Fig. 1: T2-weighted sagittal MRI showing a well-defined intramedullary cystic lesion in the anterior aspect of the calcaneum. There is no surrounding bony edema or cortical disruption
Figs 2A to D: (A and B) A coronal image of CT of the heel showing a lytic lesion in the body of the calcaneus with nidus noted in the cavity; (C and D) Similar findings noted on the sagittal section of the CT of the heel
An excision biopsy of the lesion was planned. The lesion was reached through a lateral extensile approach. The wall of the cystic lesion was defined and a bony window was created to reach the cavity. The cavity was visualized completely. It contained minimal fluid, fatty necrotic bony tissue at the center, and a thin layer of granulation tissue lining the cavity. The margins of the cavity were curetted out thoroughly with different-sized curettes, with care being taken not to perforate the medial wall. The bony walls appeared healthy and were not excised (Figs 345). The cavity was not filled with cement due to a possible infectious etiology. The curetted material was sent for Gram and Ziehl–Neelsen (ZN) staining, culture, sensitivity, and histopathology. He was started on empirical antibiotic therapy and was immobilized in a below knee slab.
Fig. 3: The lesion was exposed by lateral approach, and the lateral wall of the cyst was excised to visualize the cavity
Fig. 4: Walls of the cavity visualized after complete excision of the contents, which were sent for Gram staining, ZN staining, culture, and histopathological evaluation
Fig. 5: Yellow arrow showing intact inferior cortex confirmed by intra-OP radiography using C-arm while performing excision biopsy
The Gram stain, ZN stain, and culture revealed no signs of infection. Histopathology revealed dead bone that stained blue and deep blue compared to the normal bone and the adjacent marrow showed fat necrosis—consistent with the picture of AVN of the bone (Fig. 6). There were no features of acute or chronic infection. The histopathology slides were examined by two experienced pathologists and their findings concurred.
Fig. 6: Histopathology revealed dead bone that stained blue and deep blue compared to the normal bone, and the adjacent marrow showed fat necrosis—consistent with the picture of AVN of bone
The patient was kept nonweight bearing for 3 weeks postoperative (post-OP), and the immediate range of movements (ROM) was started as tolerated. Sutures were removed at 2 weeks post-OP and the wound was healthy. There was radiological evidence of healing at 6 weeks and weight bearing was initiated. The patient was pain free from 3 weeks post-OP and had full ROM at the ankle joint (Figs 7 and 8).
Fig. 7: Post-OP 6 weeks after the slab removal—wound healed perfectly, with no evidence of discharge
Fig. 8: Plain radiographs of the heel taken at 3 months post-OP shows radiological signs of healing of the cyst. No breach in the cortex or lysis was noted, as shown by the arrow
Full weight bearing was started at 3 months postsurgery. The patient was followed up regularly every 2 months till 6 months, and 6 monthly thereafter. He remained asymptomatic at 1 year of follow-up.
We retrospectively approached two senior radiologists with plain radiographs and the CT with MRI films to discuss the possibility of the lesion having features of AVN of the calcaneum. They were of the opinion that the lesion radiologically was consistent with a bone cyst, osteoid osteoma, intraosseous lipoma, or an old AVN of the calcaneum forming a benign cyst in the body. There were no features suggestive of acute or chronic inflammation or infections.
DISCUSSION
Avascular necrosis (AVN) of the calcaneum is very rare as there is a rich blood supply, and the literature reports <10 cases with varied etiologies causing osteonecrosis. Systemic steroid intake, blood dyscrasias, embolization from cocaine injections or intraarterial thrombolysis, trauma, and infections are the common causes of AVN of the calcaneum described in the literature. We report a case of idiopathic AVN after the above etiologies were looked for and thoroughly ruled out.2-8
Avascular necrosis (AVN) of the calcaneum has been described in the literature following intraarticular fracture of the calcaneum. In a case report by Bui-Mansfield and Clayton, they described such a case of calcaneal fracture managed conservatively and developing rest pain on follow-up. They investigated and found a lytic lesion much similar to our case, with a biopsy confirming the diagnosis of idiopathic AVN of the calcaneum.
Avascular necrosis (AVN) has been reported in 3% of transplant recipients, and multiple bones are affected as the steroid therapy given to the recipients caused hypertrophy of fat cells in the bone marrow, leading to intramedullary hypertension and subsequent venous occlusion.5,7 AVN of the calcaneum was also reported in a heart transplant patient on long-term steroid therapy. The lesion resolved after 6 months.4
Avascular necrosis (AVN) of the calcaneum has been reported in cases of sickle cell anemia, with 24% of the patients having symmetrical bilateral bony infarcts. The possible etiology is attributed to the sickle cells clumping together to cause an arteriolar occlusion, leading to sterile bony infarcts. A case report of AVN of the calcaneum reported in a case of sickle cell anemia, revealed the involvement of bilateral calcanei in the posterior aspects on nuclear imaging, and the biopsy results and cultures were negative for infective etiologies.2 Thus, the lesions were attributed to veno-occlusive disease.
In a patient with known thalassemia, AVN of the calcaneum was diagnosed on ankle MRI imaging; however, unlike our case, the patient had multiple foci of AVN in the anterior and posterior aspects of the calcaneum.6
Isolated infarct in the calcaneum has been described previously as a complication of embolization.3 Hartley and Earnshaw reported such a complication in a patient who initially presented with thrombotic occlusion of the posterior tibial artery for which a plasminogen activator was administered and the condition resolved. The patient had presented to the clinic 4 months after the embolization with local cellulitis around the heel. He was further investigated and a radiograph revealed sclerosis of the calcaneum secondary to osteonecrosis, and the biopsy of the specimen led to the isolation of Staphylococcus aureus from the sequestra. The etiology of osteonecrosis, in this case, was suspected to be secondary to the embolization, which got infected subsequently. Calcaneal infarction has also been reported after cocaine injection into the foot intravenously.8
Avascular necrosis (AVN) is commonly seen in bones with a single dominant arterial supply, which, when disrupted by etiologies mentioned above, leads to osteonecrosis, common sites being the talar neck, femoral and humeral neck, and scaphoid. The calcaneum has a robust and dual blood supply, which makes it a very uncommon site for osteonecrosis. The vascular supply of the calcaneus consists of the penetrating vessels at the nonarticular sites, which at the center of the bone form recurrent branches. These branches are anastomose with the epiphyseal arterial branches. Given the vascular anatomy, there exists a watershed zone in the body of the calcaneus in the otherwise well-vascularized bone.5 The watershed zone in the body of the calcaneus is, therefore, more prone to AVN when subjected to various insults as described above, unlike our case where there was no detectable etiology for the same.
CONCLUSION
Idiopathic AVN of the calcaneum is a cause of persisting heel pain in an adult. AVN of the calcaneum, though not as common as bony cysts, osteoid osteomas, lipomas, or infections, must be considered as a differential for a cystic lesion in the calcaneal body. Excision biopsy must be planned to rule out other causes. This condition has a good prognosis and the patients make a full recovery.
ORCID
Chandan Kulkarni https://orcid.org/0000-0002-5801-5411
Puneeth Pai https://orcid.org/0000-0002-6141-4544
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