Common Avascular Necrosis Symptoms & Causes
Early-stage AVN may be asymptomatic, detected incidentally on imaging. As the condition progresses, symptoms include deep, aching shoulder pain that worsens gradually over weeks to months, pain initially with activity that progresses to pain at rest, significant pain with overhead activities and reaching, night pain disrupting sleep, progressive stiffness limiting range of motion, weakness developing as pain worsens, grinding or catching sensations once collapse occurs, and rapid functional decline once humeral head collapses. Unlike arthritis developing gradually over years, AVN can progress rapidly from minimal symptoms to severe disability in months. Causes include traumatic injuries—shoulder fractures (particularly displaced proximal humerus fractures) and fracture-dislocations disrupting blood supply to humeral head; chronic corticosteroid use for conditions like asthma, rheumatoid arthritis, lupus, or organ transplants (dose and duration dependent); excessive chronic alcohol consumption; sickle cell disease and other hemoglobinopathies causing vascular occlusion; systemic lupus erythematosus and other autoimmune conditions; decompression sickness (the bends) in divers and pilots; radiation therapy to shoulder region; chemotherapy; coagulopathy and clotting disorders; and idiopathic AVN where cause remains unknown despite thorough evaluation.
Schedule Your ConsultationWho's at risk for developing Avascular Necrosis?
Several factors increase risk of developing avascular necrosis of the shoulder. Understanding risk factors enables early detection and prevention strategies:
Corticosteroid Use
+Chronic corticosteroid use is the leading non-traumatic cause of AVN. Risk increases with doses exceeding 20mg prednisone daily, treatment duration longer than several months, and cumulative lifetime dose. Patients taking steroids for asthma, autoimmune diseases, organ transplants, or inflammatory conditions face elevated risk. Even short-term high-dose steroids can trigger AVN in susceptible individuals. The mechanism involves fat emboli and direct bone cell toxicity.
Trauma and Fractures
+Displaced proximal humerus fractures, particularly 3-part and 4-part fractures, disrupt blood supply to the humeral head causing AVN in 15-30% of cases. Fracture-dislocations carry highest risk. Even with optimal surgical treatment, AVN may develop months later. High-energy trauma with significant soft tissue injury increases risk. Previous shoulder surgery disrupting vascular anatomy can predispose to AVN.
Alcohol and Substance Abuse
+Chronic excessive alcohol consumption (typically over 400ml per week or binge drinking) significantly increases AVN risk through fat emboli, direct cellular toxicity, and coagulopathy. Smoking compounds risk by further reducing blood flow. Combined alcohol and tobacco use dramatically elevates AVN likelihood. The condition often affects multiple joints simultaneously in chronic alcoholics.
Medical Conditions
+Sickle cell disease causes vascular occlusion with recurrent infarcts leading to AVN. Systemic lupus erythematosus increases risk through disease itself and corticosteroid treatment. Gaucher's disease, coagulation disorders, radiation exposure, chemotherapy, HIV infection, organ transplantation, decompression illness, and hyperlipidemia all elevate risk. Patients with AVN in one joint (particularly hip) should be screened for shoulder AVN as bilateral and multi-joint involvement is common.
Avascular Necrosis Prevention
Prevention focuses on minimizing modifiable risk factors and early detection. Use corticosteroids at lowest effective dose for shortest duration possible—work with physicians to minimize steroid exposure when treating chronic conditions. Avoid excessive alcohol consumption and stop smoking—both significantly increase AVN risk. For patients requiring chronic steroids, consider bone-protective medications and regular monitoring. After shoulder fractures, especially displaced proximal humerus fractures, maintain close follow-up with imaging to detect early AVN when intervention may prevent progression. Ensure anatomic fracture reduction and stable fixation minimizing AVN risk. Divers and pilots should follow proper decompression protocols preventing decompression sickness. Patients with sickle cell disease require comprehensive management preventing vascular crises. For patients with AVN in other joints (hip, knee), screen shoulder with MRI even if asymptomatic—early detection enables intervention before collapse. Once diagnosed with early-stage AVN, immediate treatment maximizes chances of preventing progression. Regular monitoring with MRI tracks disease progression allowing timely intervention. Advanced-stage AVN with collapse cannot be prevented from progressing to arthritis—focus shifts to joint replacement planning.
How is Avascular Necrosis Diagnosed?
Diagnosis requires high clinical suspicion, particularly in patients with known risk factors. Comprehensive history documents risk factors including corticosteroid use (dose, duration), alcohol consumption, previous shoulder trauma or surgery, medical conditions predisposing to AVN, and symptom onset and progression. Physical examination in early stages may be relatively normal or show mild limitation. Advanced stages demonstrate significant motion restriction, pain with all movements, crepitus, and weakness.
X-rays may appear normal in early AVN—this is why high clinical suspicion is critical. As disease progresses, X-rays show subchondral lucency (crescent sign indicating subchondral fracture), flattening or collapse of humeral head, sclerosis (increased bone density), cysts, and eventual secondary arthritis. MRI is the gold standard for early diagnosis, detecting AVN before X-ray changes appear. MRI shows characteristic patterns including "double line sign" (pathognomonic for AVN), extent of humeral head involvement (percentage of head affected predicts prognosis), bone marrow edema, subchondral fracture, and degree of collapse. Staging systems (Ficat, Cruess, or modified classifications) based on imaging guide treatment. CT scan provides detailed assessment of structural collapse and surgical planning for advanced disease. Bone scan may detect AVN but is less specific than MRI. Early diagnosis when imaging shows AVN without collapse provides best treatment outcomes. Bilateral shoulder imaging recommended as AVN is often bilateral.
What treatment is best for Avascular Necrosis?
Treatment depends critically on AVN stage at diagnosis. Early intervention before humeral head collapse provides best outcomes. Once structural collapse occurs, joint-preserving options are limited. Treatment selection considers stage, symptoms, age, activity level, and bilateral involvement. Stage-appropriate treatment is essential.
Conservative Management and Monitoring
+For very early-stage AVN (pre-collapse), protected weight-bearing, activity modification, and close monitoring with serial MRI may allow spontaneous healing in some cases. Discontinue corticosteroids if possible. Eliminate alcohol and tobacco. Treat underlying medical conditions. Pain management with NSAIDs. This approach is limited to earliest stages and requires close surveillance—progression to collapse necessitates surgical intervention.
Core Decompression
+For early-stage AVN before collapse, core decompression involves drilling into the humeral head to reduce intraosseous pressure, stimulate new blood vessel formation, and promote healing. Most effective in early stages (Ficat I-II) with success rates of 60-80% preventing progression. Combined with biological augmentation (bone graft, bone marrow aspirate) may improve outcomes. Ineffective once collapse occurs.
Biological Augmentation Techniques
+Advanced biological treatments for early AVN include bone marrow aspirate concentrate delivering stem cells and growth factors, platelet-rich plasma, bone grafting (vascularized fibular graft or other techniques), and various experimental approaches. These are often combined with core decompression. Success rates vary and long-term data is limited. Reserved for early stages in younger patients attempting to delay joint replacement.
Shoulder Replacement
+For advanced AVN with humeral head collapse and secondary arthritis, total shoulder replacement (hemiarthroplasty or total arthroplasty depending on glenoid involvement) provides definitive treatment. Success rates exceed 90% for pain relief and functional improvement. Most appropriate for older patients (over 50-60). Younger patients face challenges with implant longevity but severe symptoms often justify surgery. Earlier intervention prevents secondary glenoid damage.
Avascular Necrosis Treatment in Cleveland, Ohio
Cleveland Shoulder Institute specializes in diagnosing and treating avascular necrosis of the shoulder at all stages. We utilize high-resolution MRI protocols specifically optimized for early AVN detection. Our team has expertise in both joint-preserving interventions for early-stage disease and joint replacement for advanced collapse. We participate in research evaluating biological augmentation techniques for AVN treatment.
Treatment planning is stage-appropriate and individualized. For early-stage AVN, we offer core decompression with biological augmentation attempting to preserve the native joint. For advanced stages with collapse, we specialize in shoulder replacement using latest implant technology. Our surgeons perform over 150 shoulder replacements annually including complex AVN cases. We understand AVN often affects younger patients requiring thoughtful discussion of treatment options, realistic expectations, and long-term planning. Located in Cleveland with comprehensive imaging capabilities, same-day urgent consultations for suspected AVN, and multidisciplinary care ensuring optimal outcomes.
Schedule Your ConsultationMeet our Shoulder Specialist Team
Dr. Gobezie is a fellowship-trained shoulder and elbow surgeon specializing in complex shoulder conditions including avascular necrosis. He completed advanced training in shoulder arthroplasty and reconstruction, maintaining expertise in both joint-preserving techniques for early AVN and joint replacement for advanced disease. Dr. Gobezie stays current through active research participation evaluating AVN treatment outcomes and novel biological interventions.
Supporting Dr. Gobezie are board-certified radiologists with expertise in musculoskeletal MRI for AVN diagnosis, specialized physical therapists understanding unique challenges of AVN rehabilitation, and dedicated medical staff. This collaborative approach ensures early accurate diagnosis, stage-appropriate treatment selection, expert surgical technique when needed, and optimal outcomes. Our team understands the devastating impact of AVN on younger, active individuals and provides compassionate care while offering advanced treatment options from joint preservation to replacement.
What Our Patients Say About Avascular Necrosis Treatment
Real experiences from patients who successfully treated shoulder avascular necrosis:
"My AVN was caught early on MRI after taking steroids for lupus. Dr. Gobezie performed core decompression with bone graft. Three years later, my shoulder is stable with no progression. Early detection and treatment saved my joint. Very grateful for his expertise."
— Jennifer Russell
"I developed AVN after a complicated shoulder fracture. By the time it was diagnosed, my humeral head had collapsed. Dr. Gobezie was honest that replacement was necessary. The surgery went well and I have excellent pain relief and function now. He made a difficult situation manageable."
— Christopher Hughes
"At 45, learning I needed shoulder replacement due to AVN from chronic steroid use was devastating. Dr. Gobezie thoroughly explained why earlier intervention wasn't possible in my case. Two years post-surgery, I'm pain-free and back to normal activities. The replacement was the right decision."
— Patricia Sanders
Avascular Necrosis Frequently Asked Questions
Can avascular necrosis be reversed or cured?
+Early-stage AVN before collapse may respond to treatment with core decompression and biological augmentation, potentially halting progression and allowing healing. However, once humeral head collapse occurs, the damage is irreversible and joint replacement becomes inevitable. Early detection and intervention provide the only opportunity to preserve the native joint. Advanced AVN cannot be reversed—only replaced.
How quickly does avascular necrosis progress?
+Progression varies widely. Some patients progress from early AVN to collapse within months, while others remain stable for years. Factors affecting progression include extent of humeral head involvement, continued corticosteroid use, alcohol consumption, and individual biological factors. Without treatment, most cases eventually progress to collapse and arthritis. This is why early detection and intervention are critical.
Will I develop AVN in my other shoulder or joints?
+AVN is often bilateral and multi-joint. If you have AVN in one shoulder, you have increased risk in the opposite shoulder and other joints (particularly hips and knees). Risk factors like corticosteroid use and alcohol consumption affect the entire body. Your doctor should screen other joints with MRI even if asymptomatic. Early detection in other joints enables intervention before symptoms develop.
Is it the steroids or my disease causing AVN?
+Both contribute. Certain diseases like lupus and rheumatoid arthritis independently increase AVN risk, but corticosteroids used to treat these conditions significantly compound the risk. Higher doses and longer duration increase likelihood. Some patients develop AVN from disease alone, but steroids are the strongest modifiable risk factor. Minimizing steroid exposure while managing disease is the goal.
Am I too young for shoulder replacement?
+AVN often affects younger patients (30s-50s) creating difficult decisions. While shoulder replacements have limited lifespans (15-20 years), severe AVN causing collapse and arthritis leaves few alternatives. Joint-preserving options work only in early stages before collapse. Quality of life improvement may justify replacement despite young age and eventual need for revision. Your surgeon discusses all options and realistic expectations.