Case of the Month

Fig 5: Axial T2 WI shows effusion in the talonavicular, subtalar joints with destruction of the talonavicular joint.  

Discussion

Avascular necrosis (AVN) of the navicular bone occurs commonly in children, typically affecting ages two to nine years- also known as Köhler’s disease. 

It can also occur in adults- known as Müller-Weiss disease- often due to trauma, repetitive stress, or systemic factors like chronic corticosteroid use, excessive alcohol consumption, or vascular conditions. 

It leads to persistent midfoot pain, swelling and tenderness, stiffness, and difficulty in walking often exacerbated by weight-bearing activities. 

The navicular bone’s blood supply is particularly susceptible to compromise due to its unique vascular anatomy, predisposing it to AVN (1). Tubercular osteomyelitis of the navicular bone is exceedingly rare, representing a small fraction of osteoarticular tuberculosis cases. Foot and ankle tuberculosis accounts for less than 1% of all bone tuberculosis instances (2).

Radiologically, early stages may show subtle sclerosis, progressing to fragmentation, collapse, and a characteristic “comma-shaped” deformity of the navicular bone. (3) Avascular necrosis (AVN) of the navicular bone presents with distinct radiological findings depending on the stage and chronicity of the condition.(4)

1. Early Stage- 

Radiographs

• Sclerosis of the navicular bone due to impaired vascular supply.

• Loss of the normal trabecular pattern.

• Subtle flattening or increased radiodensity.

CT Scan

• Early cortical irregularity or subchondral fractures may be visible.

• Sclerosis is more conspicuous.

MRI

• T1-weighted images: Decreased signal intensity in the navicular due to ischemia.

• T2-weighted images: Variable signal changes; may show edema or fluid signal surrounding the navicular.

• Contrast-enhanced MRI may show diminished or absent enhancement, indicating necrosis.

2. Advanced or Chronic Stage

Radiographs

• Collapse of the navicular bone, leading to fragmentation.

• Flattening of the bone ("wafer-like" appearance in severe cases).

• Joint space narrowing or secondary arthritis in adjacent joints.

CT Scan

• Bone collapse, fragmentation, and deformity.

• Subchondral cysts or sclerosis in advanced stages.

MRI

• Persistent low signal intensity on T1-weighted images, indicating chronic necrosis.

• Surrounding joint effusion or bone marrow edema in secondary arthritis.

Early imaging, especially with MRI, is critical to detect changes and initiate treatment to prevent progression.

This case illustrates an exceptional location of osteoarticular TB and supports diagnostic difficulties encountered: imaging is not specific, lesions are paucibacillary, and the peripheral location of the Koch bacillus within the lesion dictates surgical biopsy rather than percutaneous puncture (5).

Early diagnosis through imaging and microbiological studies is crucial for effective management, typically involving prolonged anti-tubercular therapy. Delayed treatment can lead to joint destruction and deformities, underscoring the importance of considering tuberculosis in the differential diagnosis of navicular bone lesions, especially in endemic regions (6). Conservative treatment with anti-tubercular therapy has shown excellent results without complications in cases of navicular bone tuberculosis (7).

Conclusion-

While AVN of the navicular bone presents with specific clinical and radiological features, the rare occurrence of tubercular etiology should be considered, particularly in regions with high tuberculosis prevalence. Timely diagnosis and appropriate therapy are vital to ensure favorable outcomes (8).