Avascular Necrosis of the Lunate

AVASCULAR NECROSIS OF THE LUNATE

Hollevoet N.

Dept. Of Orthopaedics, University Hospital Gent, Belgium

Aetiology

The aetiology of avascular necrosis of the lunate or Kienböck’s disease remains unknown and may be multifactorial.

Ulnar variance: Hultènreporten in 1928 that the percentage of wrists with a negative ulnar variance was much higher in Kienböck’s disease than in controls. This finding was supported by other studies and radial shortening or ulnar lengthening osteotomies became methods of treatment. However, ulnar variance can change with the position of the wrist and shoulder, and increases with age. Most studies using standardized X-rays and age-matched controls could not demonstrate an association between Kienböck’s disease and ulnar variance.

Geometry of the distal radius: In patients with Kienböck’s disease radial inclination has been reported to be less than in controls.

Trauma: An acute fracture of the lunate can lead to avascularnecorsis, but in most instances a fracture is the consequence of avascular necrosis and the causative factor. Repetitive loading (e.g. working with vibrating tools) may produce microfractures which casuse vascular injury and aseptic necrosis. Traumatic carpal instability has been reported to result in Kienböck’s disease, but in most cases carpal instability is secondary to lunate collapse.Avulsion of capsular structures can cause avascular necrosis, but less than 1% of the lunate dislocations progress to avascular necrosis.

Morphology of the lunate and trabecular pattern: Three different types of lunates have been described by Zapico, but no association with Kienböck’s has been shown.

Vascular anatomy of the lunate: In 8 % of the lunates there is only one single nutrient vessel. Individuals with this pattern of blood supply may be more at risk for Kienböck’s disease during trauma, abnormal carpal loading or disease. Autoimmune diseases, vasculitis and steroid intake have been reported to increase the risk for avascular necrosis.

Venous stasis: A higher intraosseous pressure has been measured in lunates with avascular necrosis. Impaired venous drainage may be responsible for this. It has also been shown that intraosseous pressure increases with extension of the wrist. Abnormal loading or position of the wrist can cause venous stasis, as in cerebral palsy.

Incidence

The incidence of Kienböck’s disease is unknown.

Natural history

Radiographic changes are progressive in nature: there is a lunate collapse and eventually arthritic changes with reactive synovitis, grip weakness and pain.

Clinical presentation

Avascular necrosis of the lunate is more common in men than in women and more frequently involves the dominant hand. Patients complain of wrist pain, weakness and loss of mobility. The first symptoms of Kienböck’s disease usually occur in patients between 20 a 40 years old. Clinical examination may show a limited motion of the wrist. Pressure on the lunate is painful and swelling may be present.

Diagnosis

The diagnosis can be made on plain X-rays. Bone scanning and magnetic resonance imaging show changes before X-rays become positive. CT-scans are superior to plan X-rays in disclosing lunate fractures.

Classification

Staging in Kienböck’s disease is important because it forms the base of treatment. The Lichtman classification is generally used: stage 1: normal X-ray or fracture in the necrotic subcorticaltrabeculae, stage2: relative increase in bone density, stage 3A: lunate collapse, stage 3B: lunate and carpal collaps, stage 4: arthritic changes.