eMedicine Specialties > Orthopedic Surgery > Shoulder

Osteonecrosis, Shoulder

Michael Levine, MD, Chairman, Department of Orthopedic Surgery, Western Pennsylvania Hospital
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

Updated: Mar 24, 2009

Introduction

Background

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.

Shoulder osteonecrosis stage II disease.

Shoulder osteonecrosis stage IV disease.

Shoulder hemiarthroplasty in a patient with shoulder osteonecrosis.

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 Procedure

The 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.^1,2

Problem

Osteonecrosis 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 weightbearing 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.

Frequency

The 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.

Etiology

The 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.^1,3

Pathophysiology

The 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.² 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 similar 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.

Presentation

The traumatic form of shoulder osteonecrosis can occur at any age in the face of 3-part, 4-part, or anatomic neck fractures and/or dislocations.
The atraumatic form usually occurs in patients aged 20-60 years with appropriate risk factors.
Presentation depends on etiology. Typically, pain is poorly localized and severe. Night and rest pain are present and are escalated with activity. Range of motion (ROM) is preserved in early disease; however, motion causes pain. Crepitation and locking are noted following subchondral collapse. With arthritic changes, ROM decreases mechanically.

Indications

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–weightbearing joint. However, in the face of severe pain and/or mechanical symptoms, conservative and surgical options are available.

Relevant Anatomy

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.

Contraindications

No specific contraindications to treatment exist, other than those pertaining to high surgical risk situations. Infection or severe systemic disease may preclude surgical intervention.

Workup

Laboratory Studies

Laboratory studies are typically not indicated in the diagnosis of osteonecrosis. Tests can be utilized to identify inciting factors, such as the following:
- Sickle cell disease in African Americans
- Lipid profile to reveal if there is underlying hyperlipidemia
- Coagulopathies - Protein S and protein C deficiencies, factor V Leiden disease

Imaging Studies

Radiographs help establish the diagnosis in most cases. Essential radiographic views include the following:
- Anteroposterior (AP)
- True AP
- Axillary

Shoulder osteonecrosis stage II disease.

Shoulder osteonecrosis stage IV disease.

Shoulder hemiarthroplasty in a patient with shoulder osteonecrosis.

Bone scan⁴
- Can be helpful when disease is suggested but not apparent on radiographs
- Not commonly used because of the increased success rates of MRI
MRI⁴
- Diagnostic modality of choice in the face of normal radiographs and clinical suspicion
- Sensitivity and specificity greater than 98%
- Extent of humeral head necrosis a good predictor of future collapse⁵
Tomography - Helpful in stage II disease to further define lesion

Other Tests

Biopsy can be performed at the time of surgery (eg, core decompression), but the diagnosis usually is based on clinical and radiographic findings.
Venography
Intraosseous pressure measurements

Histologic Findings

The 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.

Staging

Osteonecrosis of the humeral head has been staged by Ficat and Arlet (modified for the shoulder).⁶

Stage I - Normal
Stage II - Cystic and/or osteosclerotic lesions; normal contour of humeral head (see Image 1)

Shoulder osteonecrosis stage II disease.

Shoulder osteonecrosis stage IV disease.

Stage III - Subchondral collapse or crescent sign
Stage IV - Narrowing of joint space; secondary osteoarthritic changes of the glenoid fossa and the glenohumeral head, such as cysts, marginal osteophytes, and destruction of cartilage (see Image 2)

Treatment

Medical Therapy

Removal 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–weightbearing joint. Physical therapy that 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

Core decompression: A central core of bone is removed or drilled from the humeral head into the necrotic zone.⁷
Arthroscopy: Arthroscopic debridement of chondral lesions is performed.
Hemiarthroplasty: Humeral head prosthetic replacement is performed (see Image 3).^8,9,10

Shoulder hemiarthroplasty in a patient with shoulder osteonecrosis.

Total shoulder arthroplasty: The humeral head is replaced with glenoid resurfacing.^8,10

Preoperative Details

The 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

Core decompression: Place the patient in the beach-chair position with the arm over the edge of the table. Perform core decompression with the use of image intensification. Make a small incision in the lateral deltoid. Place a Kirschner wire (K-wire) into the necrotic lesion, and use a cannulated drill to take a core of bone.
Hemiarthroplasty: Place a humeral head prosthesis, usually through a long deltopectoral incision. For idiopathic osteonecrosis, the procedure is technically easier to perform than hemiarthroplasty for advanced arthritis, as there is usually minimal-to-no soft-tissue contracture and head deformity. By using the excised head as a sizer, near-perfect replacement of the articular surface can be achieved.
Total shoulder arthroplasty: Multiple prostheses are available. The glenoid is resurfaced, usually with an all-polyethylene component. Total shoulder arthroplasty is indicated in individuals with stage IV disease.

Postoperative Details

Core decompression and muscle pedicle grafting: Immediate ROM exercises can be initiated. Some limitations on ROM may be placed in cases of muscle pedicle grafting. Patients with core decompression are started on immediate passive ROM exercises, with active ROM as tolerated. Once full ROM is achieved, strengthening exercises can be initiated.
Hemiarthroplasty and shoulder arthroplasty: Immediate passive ROM is initiated, with limitation of external rotation to 45° for 6 weeks to allow for repair of the subscapularis from the surgical approach. Active ROM can be started as tolerated, with the same limitation in the absence of rotator cuff repair, which is rare. Strengthening usually is initiated at 6 weeks postsurgery.

Follow-up

Core decompression: Studies of core decompression have shown good and excellent results in up to 90% of cases of stage I and stage II disease.^11,12 Core decompression also can be successful in stage III disease, with a 30% failure rate requiring subsequent arthroplasty. Failure occurs in all cases of stage IV or V disease; the procedure is palliative only.⁷
Muscle pedicle grafting: Limited experience with this procedure has shown no significant difference from core decompression alone, with increased morbidity. Further studies are required.¹³
Arthroscopy: Limited studies are available for review. Arthroscopy has no effect on the disease process, but it may be helpful in dealing with mechanical symptoms.
Arthroplasty: A 90% success rate has been reported in advanced-stage disease, with most patients regaining full ROM.^8,10

Complications

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 Prognosis

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 Controversies

Disease prevention is the key. Identifying those at risk and defining preventive measures is helpful. Fortunately, many cases can be treated successfully 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.

Multimedia

Media file 1: Shoulder osteonecrosis stage II disease.

Media file 2: Shoulder osteonecrosis stage IV disease.

Media file 3: Shoulder hemiarthroplasty in a patient with shoulder osteonecrosis.

References

Cruess RL. Steroid-induced avascular necrosis of the head of the humerus. Natural history and management. J Bone Joint Surg Br. Aug 1976;58(3):313-7. [Medline].
Cruess RL. Experience with steroid-induced avascular necrosis of the shoulder and etiologic considerations regarding osteonecrosis of the hip. Clin Orthop Relat Res. Jan-Feb 1978;86-93. [Medline].
Cushner MA, Friedman RJ. Osteonecrosis of the Humeral Head. J Am Acad Orthop Surg. Nov 1997;5(6):339-346. [Medline].
Mont MA, Ulrich SD, Seyler TM, Smith JM, Marker DR, McGrath MS, et al. Bone scanning of limited value for diagnosis of symptomatic oligofocal and multifocal osteonecrosis. J Rheumatol. Aug 2008;35(8):1629-34. [Medline].
Sakai T, Sugano N, Nishii T, Hananouchi T, Yoshikawa H. Extent of osteonecrosis on MRI predicts humeral head collapse. Clin Orthop Relat Res. May 2008;466(5):1074-80. [Medline].
Ficat RP, Arlet J. Necrosis of the femoral head. In: Hungerford DS. Ischemia and necrosis of bone. Baltimore, MD: Williams & Wilkins; 1980:171-82.
Soohoo NF, Vyas S, Manunga J, Sharifi H, Kominski G, Lieberman JR. Cost-effectiveness analysis of core decompression. J Arthroplasty. Aug 2006;21(5):670-81. [Medline].
Feeley BT, Fealy S, Dines DM, Warren RF, Craig EV. Hemiarthroplasty and total shoulder arthroplasty for avascular necrosis of the humeral head. J Shoulder Elbow Surg. Sep-Oct 2008;17(5):689-94. [Medline].
Smith RG, Sperling JW, Cofield RH, Hattrup SJ, Schleck CD. Shoulder hemiarthroplasty for steroid-associated osteonecrosis. J Shoulder Elbow Surg. Sep-Oct 2008;17(5):685-8. [Medline].
Tauber M, Karpik S, Matis N, Schwartz M, Resch H. Shoulder arthroplasty for traumatic avascular necrosis: predictors of outcome. Clin Orthop Relat Res. Dec 2007;465:208-14. [Medline].
LaPorte DM, Mont MA, Mohan V, Pierre-Jacques H, Jones LC, Hungerford DS. Osteonecrosis of the humeral head treated by core decompression. Clin Orthop Relat Res. Oct 1998;254-60. [Medline].
Mont MA, Maar DC, Urquhart MW, Lennox D, Hungerford DS. Avascular necrosis of the humeral head treated by core decompression. A retrospective review. J Bone Joint Surg Br. Sep 1993;75(5):785-8. [Medline].
Kawamura K, Kawate K, Yajima H, Kobata Y, Takakura Y. Vascularized scapular grafting for treatment of osteonecrosis of the humeral head. J Reconstr Microsurg. Nov 2008;24(8):559-64. [Medline].
Basmania CJ, Jaramillo JC, Wirth MA. Treatment of posttraumatic versus atraumatic avascular necrosis of the shoulder [abstract]. J Bone Joint Surg Orthop Trans. 1997;11:277.
Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg Br. Jan 1985;67(1):3-9. [Medline].
Iannotti JP, Williams GR. Osteonecrosis: Pathophysiology, classification and pathoanatomy. In: Disorders of the Shoulder: Diagnosis and Management. Lippincott Williams and Wilkins;1999:439-46.
Loebenberg MI, Plate AM, Zuckerman JD. Osteonecrosis of the humeral head. In: Zuckerman JD. Instructional course lectures. Rosemont: American Academy of Orthopaedic Surgeons;1999: 349-58.
Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. Mar 1995;77(3):459-74. [Medline].
Neer CS. Avascular necrosis of the humeral head. In: Shoulder Reconstruction. WB Saunders;1990:194-9.
Petri M, Baker J, Goldman D. Risk factors for osteonecrosis in SLE [abstract]. Arthritis Rheum. 1992;35 Suppl:S110.

Keywords

shoulder osteonecrosis, aseptic necrosis, avascular necrosis, osteonecrosis of the humeral head

Contributor Information and Disclosures

Author

Michael Levine, MD, Chairman, Department of Orthopedic Surgery, Western Pennsylvania Hospital
Michael Levine, MD 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
Disclosure: encore medical Consulting fee Consulting; glaxo smith kline Honoraria Speaking and teaching

Coauthor(s)

Amar Rajadhyaksha, MD, Resident, Department of Orthopedic Surgery, New York Medical College
Disclosure: Nothing to disclose.

Michael Mont, MD, Associate Professor, Department of Orthopaedic Surgery, Johns Hopkins Medical Institution
Michael Mont, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons
Disclosure: Stryker Orthopaedics Consulting fee Consulting; Wright Medical Technology, Inc. Consulting fee Consulting

Medical Editor

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
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Pekka A Mooar, MD, Associate Professor, Department of Orthopedic Surgery, Temple University School of Medicine
Pekka A Mooar, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons
Disclosure: Nothing to disclose.

CME Editor

Dinesh Patel, MD, FACS, Associate Clinical Professor of Orthopedic Surgery, Harvard Medical School; Chief of Arthroscopic Surgery, Department of Orthopedic Surgery, Massachusetts General Hospital
Dinesh Patel, MD, FACS is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Association of Physicians of Indian Origin, American College of International Physicians, and American College of Surgeons
Disclosure: Nothing to disclose.

Chief Editor

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
Mary Ann E Keenan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Orthopaedic Foot and Ankle Society, American Society for Surgery of the Hand, and Orthopaedic Rehabilitation Association
Disclosure: Nothing to disclose.

Further Reading

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Posterior Glenohumeral Instability

Clinical guidelines

ACR Appropriateness Criteria® shoulder trauma. American College of Radiology - Medical Specialty Society. 1995 (revised 2005). 6 pages. NGC:004632

Shoulder complaints. American College of Occupational and Environmental Medicine - Medical Specialty Society. 1997 (revised 2004). 31 pages. NGC:004752

Clinical trials

Bone Repair Cell (BRC) Treatment of Patients With Osteonecrosis of the Femoral Head

Mesenchymal Stem Cell for Osteonecrosis of the Femoral Head

MBCP Safety and Performance in the Osteonecrosis of Femur Head

Proposal For The Development Of A Well Defined Database For Patients With Oral Bisphosphonate-Related Osteonecrosis

Molecular Genetic Study of Avascular Necrosis of the Femoral Head