ORTHOPAEDICS

MR findings reveal loss of marrow fat of lunate bones on these sequences.

Diagnosis is Avascular necrosis of lunate (Kienbock’s disease).

Discussion

Introduction
Existence of avascular necrosis of various growth centers within the body has long been recognized. In children or adolescents, such changes are frequently referred to as ischaemic necrosis and usually are associated with temporary interruption of blood supply. Such conditions are, as a result, self-limiting.

In the case of avascular necrosis of the carpal lunate, the condition frequently occurs during adult life. Secondary to an injury, and as a result of the injury, the blood supply is often permanently lost. This condition has been referred to in the literature as "Kienbock's disease".

Avascular necrosis occurs in other bones too, particularly:

Humeral head,  Femoral head & condyles, tibial plateau, talus, and scaphoid

Causes (common):
Trauma (femoral neck fractures, or posterior hip dislocations)

Sickle cell anemia

Corticosteroids

Deconpression sickness (embolization with nitrogen bubbles)

Gaucher`s disease

Diabetes

Pathogenesis
Infarction causes marrow edema and venous outflow obstruction, increasing pressure and widening the area of infarction; Hyperemia of the surrounding bones causes osteoporosis of living bone, while infarcted bone retains its density and thus appears whiter or denser on roentgenogram. Though this bone is eventually revascularized, resorption can lead to mechanical failure, with subcondral fractures (crescent sign). The result is flattening of the bone with joint incongruity and progression of secondary osteoarthritis.

The cause of Kienbocks disease is unknown. The disease sometimes begins with a simple fracture or multiple compression fractures caused by repeated stresses across the wrist. Trauma may or may not precede symptoms. The loss of blood supply to the lunate has been attributed to many factors, including traumatic interference with circulation, ligament injury with degeneration and collapse, primary circulatory or vascular problems, and solitary or chronic injuries resulting in vascular impairment.

Kienbocks disease is commonly associated with negative u1nar variance, in which the ulnar head lies more proximal than the radial head on posteroanterior x-ray. (Neutral ulnar variance means the distal surfaces of the radius and ulna are level.)

Clinical Findings
Usually, pain progresses in severity. Physical exam typically reveals a moderately swollen wrist with limitation of dorsiflex ion and palmar flexion as well as reduction in grip strength of at least 50%. (Grip strength is usually lost later in the disease process.) Pronation and supination are not affected. Carpal tunnel syndrome is found in 10% to 15% of patients.

Imaging

X-rays of the wrist help to determine the presence of avascular necrosis and u1nar variance. X-rays in early Kienb6ck-'s disease may be completely normal. The earliest indication of avascular necrosis on plain radiographs is increased lunate density ac-companied by flattening, but chronic pain may be present before x-ray findings appear.

Computed tomography (CT) has gained wide acceptance in the early diagnosis and evaluation of Kienbock’s disease.

Bone scintigraphy using Tc-99m phosphate is a highly sensitive, albeit nonspecific, modality for identifying metabolic bone changes. It has a role as a screening tool in patients who have wrist pain of unknown origin and normal radiographs.

Magnetic resonance imaging: MRI very effectively helps detect early avascular necrosis in various bones, including the lunate, by revealing loss of bone marrow fat. It can detect abnormalities in the lunate when plain radiographs are normal.

Classification
Stage I is an acute injury with x-rays showing normal lunate density and structure A compression fracture may exist at this stage but may only be detected with tomography or CT.

Stage 2 is characterized by increased radiographic density in the lunate relative to the other carpal bones. The lunate retains its size, shape, and anatomic relationship to the other carpal bones.

Stage 3 Kienbock's disease is characterized by lunate collapse and proximal migration of the capitate. Scapholunate dissociation is a prominent feature on anteroposterior radiographs.

Stage 4 disease is characterized by established osteoarthritis of the wrist, with degenerative cysts, subchondral scle-rosis, and joint space narrowing.

Treatment
Immobilization was initially advocated for all stages of the disease. The results, however, have generally been unsatisfactory, with progressive collapse common. Based on clinical experience, though, immobilization in a cast until symptoms resolve for stage 1 disease is still reasonable to decrease the vascular injury and allow the lunate to heal.

Patients with negative ulnar variance may benefit from an equalization of the distal articular surfaces of the radius and ulna. Excellent results have been reported with ulnar-lengthening and radial-shortening osteotomies. These operations should not be used when the lunate has collapsed, as in stage 3 or 4 disease.

In stage 3 disease, triscaphe (scaphoid-trapezium-trapezoid) and scaphocapitate fusion

Salvage procedures for stage 4 disease include proximal row carpectomy and wrist arthrodesis.

Contribution
Dr. Deepak Patkar, MRI Centre, Nanavati Hospital, Mumbai