Osteonecrosis of the humeral head

Abstract

A 20-year-old man with a 5-year history of acute lymphoblastic leukemia (ALL) was admitted to our hospital for severe pains in his bilateral groin and right shoulder. He had experienced these pains for 16 months. He underwent allogeneic stem cell transplantation in his second complete remission 13 months prior to hospitalization. He had received corticosteroid therapy both for ALL and for graft versus host disease for a long period (more than 13 months in total), and the total dose of corticosteroids exceeded 20 g in prednisolone equivalent at the time of the hospitalization. X-ray films of the hip joints revealed collapse of bilateral femoral heads. In addition, a subarticular radiolucent line (''crescent sign'') was also observed in an X-ray film of the right shoulder joint (Fig. 1). He was diagnosed with osteonecrosis of the femoral and humeral heads. A magnetic resonance image (MRI) showed a geographical high-intensity area spread to diaphysis, suggesting necrotic changes affecting an extensive area (Fig. 2). He was treated with narcotics for pain. Corticosteroids were reduced as rapidly as possible and maintained at a low dose to treat his adrenal insufficiency. However, his range of motion gradually decreased. Longterm corticosteroid use has been reported to be a risk factor for osteonecrosis of the humeral head, as well as the hip joint. The pathogenesis of steroid-induced osteonecrosis remains unclear, but ischemia from lipocyte hypertrophy or fat embolism has been postulated. The interval between corticosteroid administration and onset of symptom has been reported as between 6 and 18 months. Although the humeral head is the second most commonly affected site in osteonecrosis, it is often unrecognized, and its initial symptoms are often nonspecific. Removal of risk factors can reduce the risk of osteonecrosis to other joints. Thus,

Arthroscopically assisted retrograde drilling of the humeral head with a guiding device

“…The necrotic area is still visible on imaging scans, although the degree of bone marrow oedema has been reduced substantially. This result, however, is to be expected if we consider the slow healing capacity of the humeral head; indeed, numerous studies have demonstrated the late onset of AVN up to two or more years after relevant trauma or causes [1,5,12,19,22,28,34].…”

Humeral Head Avascular Necrosis

“…One mechanism relates to alterations in lipocytes, leading to microemboli in the blood supply to the humerus and subsequent ischemia 43 . Another mechanism suggests that adipocyte hypertrophy and hyperplasia of the bone marrow compartment of convex joints results in elevated intraosseous pressure by blocking venous outflow causing ischemia to the bone 6,31,37,38,44 . A third theory suggests that disruption to vascular endothelial cells results in stasis and a subsequent increase in intraosseous pressure leading to eventual ischemia 45 .…”

“…Patients receiving chronic high-dose corticosteroids are well known to be at increased risk for AVN 1,4,6,20,22,29,30,31,32,33,34,35,36,37,38,39,40 . The prevalence of AVN at any location with corticosteroid use ranges from 21% to 37% 41 .…”

Bilateral idiopathic osteonecrosis of the major tubercle of the humerus

“…The humeral head is the second most common site for osteonecrosis after the femoral head. Osteonecrosis is associated with corticosteroid use, trauma, sickle cell disease, alcoholism, dysbarism (caisson disease), Gauchers disease and other systemic conditions [9, 12].…”