Duke Orthopaedics
presents
Wheeless' Textbook of Orthopaedics

Osteonecrosis of the Humeral Head

 

Co-authors:  Milford H. Marchant Jr., M.D., Allston Stubbs, M.D., Carl J. Basamania, M.D.

March 15, 2005

       - Background:
             - Definition:  In situ death of bone within the humeral head due to disruption of blood supply
             - Other Names:  Avascular Necrosis or Aseptic Necrosis
             - Initially described in the Humeral Head in 1960 by Heimann and Freiberger (NEJM)
             - 2nd Most common site of Osteonecrosis (Femoral Head = 1st)
             - Knowledge based largely on extrapolated data from the Femoral Head
                    - Similar Etiology - Different Disease
                    - Non-Weight Bearing Joint
                    - Greater Vascular Watershed
                    - Functional capacity of shoulder is more forgiving
                    - Glenohumeral Joint is Less Constrained
             - Progressive  Osteoarthritis of Glenohumeral Joint (5%)

      - Etiology / Associated Diseases:
             - Primary
                    - Posttraumatic (Fracture / Dislocation)
                    - Corticosteroid therapy
                    - Hemoglobinopathies - Sickle Cell Disease
                    - Alcohol Abuse / Smoking
                    - Dysbarism (Decompression Sickness)
                    - Gaucher Disease
             - Other
                    - Septic Osteonecrosis                 - Connective Tissue Disorders
                    - Hypercoagulable Disease           - Chemotherapy
                    - Peripheral Vascular Disease       - Chronic Dialysis
                    - Hyperlipidemia                          - SLE
                    - Cushing's Syndrome                  - Pregnancy
                    - Hyperuricemia                           - Myxedema
                    - Radiation Therapy                     - Pancreatitis

      - Anatomy / Blood Supply:
             - Humeral Head is directly supplied by the Anterior & Posterior Humeral Circumflex arteries
             - Several Anastomotic contributions
                    - Suprascapular a.
                    - Thoracoacromial a.
                    - Subscapular a.
             - Primary = Anterolateral branch of the Anterior Humeral Circumflex Artery
             - Course:
                    - Branch off Axillary Artery
                    - Joins Surgical Neck of Humerus at the inferior border of Subscapularis Tendon
                    - Anterolateral Branch travels proximal and lateral to Intertubercular groove
                    - Enters Head at transition from Intertubercular groove to Greater Tuberosity
                    - Arcuate Artery of Laing = artery within the humeral head
             - Microvasculature
                    - Subchondral bone is especially vulnerable
                    - Arterioles become sinusoids which make 180 degree turns to return to the              
                    intraosseous circulation
                    - Vulnerable to thrombotic/embolic events

      - Pathogenesis:
             - Humeral Head Blood Supply Compromised
                    - Etiology of Compromise (Mankin, et al. (1992))
                           1. Mechanical Disruption of Blood Vessels
                           2. Arterial Obstruction = Thrombosis / Embolism
                           3. Injury or Compression of Arterial Walls
                           4. Venous Outflow Obstruction (Chandler's Disease)
                          - Nontraumatic necrosis of bone (osteonecrosis).

                    - Site of Compromise  (Hungerford (1981))
                           1. Intraosseous - Extravascular (Intraosseous Pressure)
                           2. Intraosseous - Arterial
                           3. Extraosseous - Arterial
                           4. Venous 
                          - Pathogenetic considerations in ischemic necrosis of bone.
             - Trauma
                    - Fracture / Dislocation / Shoulder Surgery can physically disrupt blood supply
                    - Greatest risk:   4-part fractures
                           - Fractures involving the Anatomic Neck
                    - Incidence variable = 15% - 30% of 4-part fractures (Lee and Hansen (1981))
                           - Low compared to similar injuries in the hip
                                  - Creeping Substitution:  New bone is deposited on dead trabecular scaffold
                                  - Rich Vascular supply in Soft Tissues surrounding the joint 
                            - Post-traumatic avascular necrosis of the humeral head in displaced proximal humeral fractures. 
             - Corticosteroids
                    - Most Common reported cause of non-traumatic Osteonecrosis
                    - Occurs most commonly with high-dose administration or long-term use
                    - Several Case reports of varying duration of use, dose, and route of administration
                    - Impossible to predict:
                           - Occurrence
                           - Timing (6 - 18 months)
                           - Joint involvement
                           - Confounding variable in certain diseases
                    - Mechanism is still obscure
                           - Vasculitis
                           - Stress Fractures
                           - Hypercoagulopthy
                           - Alterations in fat metabolism: Enhanced Lipid Production
                    - Theories
                           - Intraosseous - Extravascular
                                  - Increased Intraosseous Adipocyte Size
                                  - Leads to increased intraosseous pressure and ischemia
                           - Intraosseous - Arterial
                                  - Fatty changes in liver & Increased serum lipids
                                  - Fat Embolism and Coagulation Abnormalities
                                  - Cadaveric & Biopsy Studies demonstrated fat emboli in subchondral vessels
                    - Animal Model (Motomura, et al. (2004)
                           - Rabbits given High Dose Methylprednisolone
                           - Treatment with Warfarin and Probucol
                           - Pathology: Statistically significant reduction in size of Adipose Cells in Bone Marrow
                           - Results:  Statistically significant ecrease incidence of Osteonecrosis 
                           - Combined effects of an anticoagulant and a lipid-lowering agent on the prevention of steroid-induced osteonecrosis in rabbits.
             - Hemoglobinopathy
                    - The most common cause of Osteonecrosis World-Wide (Milner, et al. (1993))
                           - Sickle Cell Disease is most prevalent
                           - Sickle Cell Disease & alpha-thalesemia have highest incidence of Osteonecrosis
                                  - Higher baseline HCT
                    - Proposed Mechanisms
                           1. Emboli cause microinfarcts in subchondral bone
                           2. Chronic Hemolytic Anemia causes Bone Marrow Hyperplasia  
                                  - Results in increased marrow pressure and ischemia
                    - Sickle Cell Disease (Milner et al. (1993) & David, et al.  (1993))
                           - 2524 pts with Sickle Cell Disease
                           - Prevalence of Humeral Head Osteonecrosis = 5% - 28%
                           - 2.9 cases per 100 patient years
                           - 67% developed Bilateral Disease 
                     - Osteonecrosis of the humeral head in sickle cell disease.
                     - The shoulder in sickle-cell disease.
             - Dysbarism
                    - Nitrogen gas bubbles
                    - Air embolism - Arterial congestion and Ischemia
                    - Damage to adipose tissue & Release of Vasoactive substances
                           - Promotion of Thrombosis
             - Gaucher Disease
                    - Lipid Lysosomal Storage Disease - Autosomal Recessive
                    - Defect in Beta-glucosidase
                    - Accumulation of Glycolipid "Glucosylceramide" in liver, spleen, and bone marrow
                           - Excess Glycolipid within Marrow Cells  (Gaucher Cells)
                    - Leads to increase in intraosseous pressure and vascular occlusion
                    - Damaged macrophages release substances which cause vasospasm
             - Alcohol Abuse / Smoking
                    - Proposed Mechanism is similar to corticosteroids
                    - Alcohol use leads to fatty changes in liver
                    - Compounded - Alcohol increases systemic cortisol
                    - Smoking causes vasoconstriction which further increases risk for developing osteonecrosis

      Biomechanics:
             - Lesion Location:  Superior Central Portion of Humeral Head is most common
             - Corresponds to Glenohumeral contact region:
                    - 60 degrees of Humeral Elevation
                    - 90 degrees of Forward Flexion / Abduction
             - Zone of Injury - Disease Progression
                    - Ischemic Bone Injury
                    - Vascular ingrowth at the periphery of the lesion
                    - Focal Osteopenia
                    - Migration of Mesenchymal stem cells into necrotic cancellous bone
                    - Macrophages resorb dead tissue and osteoblasts lay down new bone
                    - Interspersed Thickened Trabeculae surround lesion
                    - Resorption occurs faster than Restoration
                    - Weakened Subchondral bone
                    - Microfractures (18 - 24 months)
                    - Collapse of articular surface under normal stresses of joint motion = Flattening
                    - Articular Cartilage Degeneration

Classification / Radiology:
      - Cruess Classification System (Cruess (1978))
                    - Modified from Ficat & Arlet Classification of Femoral Head osteonecrosis
                    - No clinical or functional parameters - based solely on bony change on Plain Radiographs
             Stage I
                    - Changes not yet visible on Plain Radiographs
                    - Can be detected on MRI
                    - Clinical Signs and Symptoms are diffuse
             Stage II
                    - Sclerosis:  Wedge Shaped, Mottled,Diffuse
                    - Area of Osteopenia
                    - Sphericity Maintained
             Stage III
                    - "Crescent Sign" = Subchondral Fracture
                    - Minimal Depression of Articular Surface
             Stage IV
                    - "Flattening" = Collapse of Joint Surface and Subchondral bone
                    - Fragmentation
                    - Loose Bodies
                    - Secondary Arthritis
             Stage V
                    - Degenerative Disease Extends to Involve Glenoid
             - The current status of avascular necrosis of the femoral head.
      - MRI
             - Useful for identifying and quantifying pre-collapse disease (Radiographic Stage I & II)
             - Provides No Advantage once diagnosis has been made
             - Exception - May identify disease in symptomatic contralateral shoulder with normal x-rays

Clinical Evaluation / Natural History:
      - Presentation
             - Patients are younger than most arthritis patients
             - Insidious onset of Shoulder Pain - Prevents normal ADL
             - Night Pain / Difficulty Sleeping
             - Painful Click / Crepitus
      - Physical Examination
             - Active / Passive ROM often preserved until late stage disease
             - Discomfort greatest at 90 degrees of elevation / abduction
      - Evaluation
             - H&P
             - Risk Factor Assessment
             - Labs to rule out infection +/- serology testing
             - Shoulder X-rays
             - Evaluate for Additional Site Disease
      - Additional Site Disease (L'Insalata, et al. (1995))
             - Reviewed 42 patients / 65 shoulders with Humeral Head Osteonecrosis
             - Women > Men / Avg. Age at Diagnosis = 46y
             - 55% had Bilateral Humeral Disease
             - 76% had osteonecrosis at other sites
             - 69% Hip
             - 29% Femoral Condyle
             - 9% Talus 
             - Humeral head osteonecrosis: clinical course and radiographic predictors of outcome.

      - Natural History
             - Variable - appears to be slow
             - Many patients present with late stage disease
                    - Non-weight bearing joint with soft tissue constraints
             - Etiology dictates progression
                    - Sickle Cell Patients have most benign course symptomatically
                           - Low requirement for surgery even with advanced disease
                    - Corticosteroid users have variable course
                           - Dependent on stage of presentation
                    - Post-Traumatic patients often require surgical intervention

Treatment
      - Goals
             - Preserve Shoulder Function
                    - Strength
                    - ROM
                    - ADL's
             - Halt progression of disease
             - Decrease symptoms
             - Decision for Surgical Intervention based on Radiographic Stage & Clinical Symptoms

      - Conservative Treatment = Stage I & II Disease
             - Patient Education
             - Reduction of Risk Factors
                    - Stop Alcohol / Tobacco use
                    - Judicious use of corticosteroids
             - Physical therapy
                    - Preserve Shoulder Motion
             - Activity Modification
             - Avoiding Overhead Activities
             - NSAIDs may provide some symptom relief

      - Surgical Treatment
             - Indications:
                    - Failure of Non-op tx:  Core Decompression vs. Arthroplasty
                    - Traumatic Osteonecrosis(Basamania, et al.  Abstract 64th AAOS Meeting. 1997)
                           - Treatment of post-traumatic versus non-traumatic osteonecrosis of the shoulder
                           - Non-operative treatment of post-traumatic osteonecrosis was unsuccessful
                           - 41% of non-traumatic pts were treated successfully with Therapy & activity modification

             - Core Decompression
                    - Goal:  Reduce intraosseous - extravascular pressure to reestablish blood flow
                    - Adapted from use in the Femoral Head
                    - Best used in treatment for non-traumatic early stage disease (Stage I, II, III)
                    - Varying success rates (40% - 90%)
                    - Success may be similar to Natural History of disease
                    - Original Technique (Mont, et al.):
                           - 2cm to 3cm Incision Axillary Fold
                           - Deltopectoral Approach to humeral metaphysis
                           - Guide Wire advanced to within 1cm of subchondral surface
                           - Position checked under Fluoroscopy
                           - 5mm coring device lateral to bicipital sulcus
                           - 1 to 3 biopsies performed depending on lesion size
                           - Post-op Sling 3 - 5 days - activity advanced gradually
                    - Results
                           - Mont, et al. (1993) Retrospective Review
                                  - 30 decompressions - 20 pts atraumatic osteonecrosis
                                  - Patients failed conservative tx after avg. 9.6 months
                                  - Varying stages of disease
                                  - Over-all 73% Good-Excellent Results Post-op UCLA Shoulder Scores
                                  - Stages I & II :  14/14 shoulders G-E
                                  - Stage III :  7/10 shoulders G-E
                                  - Stage IV :  1/6 shoulders G-E 
                        - Avascular necrosis of the humeral head treated by core decompression. A retrospective review.

                           - L'Insalata et al. (1996) 
                                  - 5 Stage III patients
                                  - Pre-op:  0 - 1 mm of articular incongruity
                                  - All had clinical progression of disease
                                  - 4/5 required arthroplasty within 3 years 
                                  - Humeral head osteonecrosis: clinical course and radiographic predictors of outcome.

                           - LaPorte, et al (1998) 
                                  - Assessed Long-term outcome of Core Decompression
                                  - 43 patients / 63 shoulders with mean f/u 10 years
                                  - Avg. Age:  36 (22 - 76)
                                  - Atraumatic Osteonecrosis
                                         Stage I :  94% (15/16) successful
                                         Stage II :  88% (15/17) successful
                                         Stage III :  70% (16/23) successful
                                         Stage IV :  14% (1/7) successful
                                  - Average Time to Failure = 24 months 
                                  - Osteonecrosis of the humeral head treated by core decompression.
             - Arthroplasty
                    - Prosthetic replacement of damaged articular surface
                    - Useful when treating later stage disease (III, IV, V) - especially post-collapse disease
                    - Osteonecrosis represents approximately 5% of patients requiring arthroplasty
                    - Reliable means of restoring range of motion and providing pain relief
                           - 90% to 100% Pain relief reported in literature for osteonecrosis
                           - Good results for ROM in non-traumatic diseasae
                    - Hemi-arthroplasty vs. Total Shoulder Arthroplasty remains controversial
                    - Most Agree to Press Fit Humeral Component
                    - Glenoid resurfacing in Stage V disease with intact or reparable Rotator Cuff



Original Text by Clifford R. Wheeless, III, MD.

Last updated by Data Trace Staff on Monday, January 7, 2013 1:40 pm

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