You are in: eMedicine Specialties > Orthopedic Surgery > SHOULDER Osteonecrosis, ShoulderArticle Last Updated: Oct 19, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: Michael Levine, MD, Clinical Instructor of Orthopedic Surgery, University of Pittsburgh School of Medicine, Chief of Orthopedic surgery, West Penn Hospital, Chair, Section of Orthopedic Surgery, Forbes Regional Hospital Michael Levine is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Hip and Knee Surgeons, American Medical Association, Orthopaedic Research Society, Pennsylvania Medical Society, Pennsylvania Orthopaedic Society, and Phi Beta Kappa Coauthor(s): Amar Rajadhyaksha, MD, Resident, Department of Orthopedic Surgery, New York Medical College; Michael Mont, MD, Associate Professor, Department of Orthopaedic Surgery, Johns Hopkins Medical Institution Editors: Mark D Lazarus, MD, Associate Professor of Orthopedic Surgery, Medical College of Pennsylvania-Hahnemann University, Chief of Shoulder and Elbow Service, Department of Orthopedic Surgery, Hahnemann University Hospital; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Pekka A Mooar, MD, Associate Professor, Department of Orthopedic Surgery, Temple University School of Medicine; Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital; Mary Ann E Keenan, MD, Professor, Vice Chair for Graduate Medical Education, Department of Orthopedic Surgery, University of Pennsylvania School of Medicine; Chief of Neuro-Orthopedics Program, Department of Orthopedic Surgery, Hospital of the University of Pennsylvania Author and Editor Disclosure Synonyms and related keywords: aseptic necrosis, avascular necrosis, osteonecrosis of the humeral head INTRODUCTIONSection 2 of 12
  Osteonecrosis of the humeral head is a disorder that involves osteocytes and marrow and is characterized by bone death. Osteonecrosis of the humeral head consists of 2 forms: traumatic and atraumatic. Osteonecrosis of the hip has been researched more thoroughly and is therefore better understood than osteonecrosis of the shoulder. Most of the information regarding osteonecrosis of the humeral head is extrapolated from the research findings of the disorder of the hip. The major difference between osteonecrosis of the hip and osteonecrosis of the humeral head is that the shoulder bears less weight than the hip. History of the ProcedureThe earliest literature on osteonecrosis involves that of the hip. The first significant data came from Cruess in 1976 and then in 1978. The information Cruess published in 1978 provided data from which the current classification system originated. ProblemOsteonecrosis of the humeral head ultimately can result in collapse of the humeral head articular surface and joint destruction. The shoulder is not subjected to the same weight-bearing forces as the hip. The glenoid is less constrained and therefore accepts greater deformity of the humeral head. Also, the blood supply about the shoulder is abundant, and the scapula can compensate for some of the glenohumeral motion loss. Traumatic osteonecrosis results from disruption of the blood supply caused by fracture or dislocation of the proximal humerus. Atraumatic osteonecrosis also is believed to involve abnormalities of humeral head blood flow from multiple etiologies. Atraumatic osteonecrosis often involves the hip as well as other bones. FrequencyThe incidence of both forms of osteonecrosis of the shoulder, particularly the atraumatic form, is difficult to determine. However, it definitely appears to occur less often than in the hip. The traumatic form has been reported in up to 34% of 3-part fractures and 90% of 4-part fractures, as well as nearly all fractures of the anatomic neck. EtiologyThe traumatic form occurs secondary to disruption of the vascular supply, which is secondary to fracture or dislocation of the humeral head. Atraumatic necrosis has multiple associated risk factors. Steroid use and alcohol abuse predominate, but dysbarism, hemoglobinopathies, coagulopathies, Gaucher disease, connective tissue disorders, and idiopathic disorders have been identified as risk factors. PathophysiologyThe initiating insult appears to differ on the basis of causation. Traumatic disruption of the proximal humeral vasculature is a mechanical disruption. Several theories of steroid-induced disease exist. One proposed theory is that increased intraosseous fat cell size results in increased intraosseous pressure and fat embolism. Alcohol abuse appears to work in a manner similarly to that of steroids. Caisson disease or dysbarism causes cell death via air bubbles, with resultant congestion and ischemia. Sickle cell disease causes infarcts in the subchondral bone via infarcts of diseased red blood cells. Following the initial insult, the pathogenesis of the disease is the same, despite etiology. Death of cells and marrow occurs. During the healing phase, bone resorption occurs to eliminate necrotic tissue. During this phase, the bone is weakened. Therefore, the forces across the subchondral plate of the weakened bone can result in microfractures and subsequent collapse. With progressive deformity of the humeral head, the glenoid becomes involved secondary to mechanical factors, with resultant arthritic changes. Clinical
INDICATIONSSection 3 of 12
First, eliminate the inciting factor if it is recognized. Eliminating the inciting factor if and when it is recognized is important; however, it does not reverse the course of the disease process. Treatment often is delayed or is not required because the shoulder is a non–weight-bearing joint. However, in the face of severe pain and/or mechanical symptoms, conservative and surgical options are available. RELEVANT ANATOMYSection 4 of 12
The major blood supply to the humeral head is from the ascending branch of the anterior humeral circumflex artery, which enters the humeral head through the bicipital groove. The posterior humeral circumflex artery pierces the rotator cuff attachments and provides a small amount of collateral flow. Collateral flow about the proximal humerus is minimal, putting the head at risk through trauma or other circulatory insults. Glenoid involvement is believed to occur secondarily to deformity of the humeral head. Intraosseous blood supply to the head arises from the arcuate artery. CONTRAINDICATIONSSection 5 of 12
No specific contraindications to treatment exist, other than those pertaining to high surgical risk situations. Infection or severe systemic disease may preclude surgical intervention. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
Other Tests
Histologic FindingsThe first phases involve cell and marrow necrosis. The reparative phase occurs as the dead bone is removed and replaced by healthy bone. During this period, the bone is weak and subject to subchondral collapse. Following collapse of the subchondral plate, damage to the articular cartilage occurs with resultant arthritic changes to the joint. StagingOsteonecrosis of the humeral head has been staged by Ficat and Arlet (modified for the shoulder).
TREATMENTSection 7 of 12
Medical therapyRemoval of the offending agent, if possible, is the first line of treatment. Nonsurgical options often are more successful in cases of shoulder osteonecrosis because the shoulder is a non–weight-bearing joint. Physical therapy to include modalities for pain control and ROM exercises with subsequent strengthening is helpful in all stages, particularly in stage I and stage II. Studies have shown that treatment with alendronate can possibly prevent a collapse of the femoral head caused by osteonecrosis; however, no research has been published regarding its effectiveness in treating osteonecrosis of the shoulder. Surgical therapy
Preoperative detailsThe decision for a given surgical procedure is based on preoperative staging. Core decompression, muscle pedicle grafting, and arthroscopy are indicated in cases prior to collapse of the humeral head. These procedures can be helpful in stage I, stage II, and stage III disease. Once irregularity of the joint surface occurs, arthroplasty is most beneficial. Intraoperative details
Postoperative details
Follow-up
COMPLICATIONSSection 8 of 12
Common surgical complications include infection and neurovascular injuries, which are particularly rare in these procedures. When performing core decompression, care must be taken to avoid the axillary nerve anteriorly. Avoidance of penetration of the humeral head during core decompression is key. The cephalic vein is at risk during the approach for arthroplasty. Problems with arthroplasty include prosthetic loosening, dislocation, and intraoperative fracture. Fortunately, these problems are rare in avascular necrosis. OUTCOME AND PROGNOSISSection 9 of 12
The shoulder joint bears less weight than the joints of the lower extremity; therefore, symptoms can be mild, even in those with advanced disease. Many patients obtain good results when conservatively treated with analgesics and/or physical therapy for extended periods of time. Surgery can be reserved for those with severe pain, as patients with early-stage disease often do not progress radiographically. FUTURE AND CONTROVERSIESSection 10 of 12
Disease prevention is the key. Identifying those at risk and defining preventive measures is helpful. Fortunately, the disease can be treated successfully in many cases without surgical intervention. Prosthetic fixation in those with osteonecrosis of the shoulder often can be performed without cement because of good bone quality. Clinical identification of disease progression is critical to recognize and treat symptomatic disease in the early stages, thereby avoiding arthroplasty. MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
Osteonecrosis, Shoulder excerpt Article Last Updated: Oct 19, 2006 | ||||||||||||||||||||||||||
