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9.06.2009. МРТ плечевого сустава. Жалобы на боль.

Пациент 1976 г.р. жалуется на боли в правом плечевом суставе, "как будто мышцы перетрудил", в течение 4-5 месяцев. Травм не было. После исследования пациенту мной был задан ряд вопросов. Возможно вы их зададите  мне? Не буду раскрывать карты раньше времени...

 

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МРТ плечевого сустава.

Хотел написать, но автор пока отговорилa )))).

Случай редкий! Подумаем вместе?

 
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Уважаемая автор, а

Уважаемая автор, а рентгенограмм нет?

 
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Не может это быть "сухой

Не может это быть "сухой костоедой"?

 
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 могу сказать тоже самое

 могу сказать тоже самое случай редкий ))) а вот какие вопросы задавали, не знаю. Обычно спрашиваю про стнадартные причины, которые могут привести к таким изменениям ))

 
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Рентгенограмм нет. А спросила

Рентгенограмм нет. А спросила я его, не принимал ли кортикостероидов. Ответ был положительный. Оказывается, пациент считает себя излечившимся от лимфогранулематоза (может быть, так оно и есть, я на это надеюсь, но бумаг никаких нет). В апреле была последняя "химия", в ходе лечения назначали и кортикостероиды. А теперь какие варианты?

Мысль с костоедой интересная, честно говоря, в голову не пришло. На МРТ не видела никогда (да и не на МРТ тоже!). При таком поверхностном расположении, теоретически, должен развитьс туберкулезный артрит? Или нет? 

 
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Туберкулеза здесь нет - и при

Туберкулеза здесь нет - и при таком расположении, конечно уже должен быть туб. артрит, а костоеда идет из слизистых сумок большого и малого бугорков.

Классика ограниченного асептического некроза головки плечевой кости. Изменения по-типу рассекающего остеохондрита. Дифференцировать в принципе не с чем, такая картина - участок некроза, полулунной формы в субхондральных отделах суставной головки с зонами отграничения, первая остеолиз (повышенный сигнал на STIR), вторая ободок склероза (пониженный сигнал на Т1) и регионарный отек кости - патагномонична для постановки диагноза асептического некроза.

 
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 Совершено согласна с

 Совершенно согласна с seven_ray! В плане течения заболевания - должна быть в меньшей степени выражена деформация, нагрузка ведь совсем не такая, как в тазобедренном суставе. И, следовательно, более благоприятный исход. Задумалась над стадийностью, деформации-то нет! Какая, по вашему мнению? А еще меня смутила неоднородность сигнала от костного мозга. Диффузные изменения костного мозга? Или я это уже "притягиваю" к основному заболеванию?

 
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 неоднородность сигнала от

 неоднородность сигнала от костного мозга за счет остеопороза головки. Главное, что на Т1 и STIR нет признаков инфильтрации костного мозга. Поэтому можно притягивать к основному заболеванию, если им считать системный остеопороз на фоне приема глюкокортикоидов. 

 
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Спасибо за обсуждение. Может,

Спасибо за обсуждение. Может, еще по стадии свое мнение кто-нибудь выскажет?  

 
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MPT Асептический некроз....

Опередили! А обещали до завтра не "колотся"! Мой ответ Анне один в один совпал с ответом Андрея, конечно асептический некроз головки плечевой кости на фоне приёма кортикостероидов.  Классификацию можно посмотреть здесь:
Wheeless' Textbook of Orthopaedics http://www.wheelessonline.com/ortho/Humeral_Head_Osteonecrosis

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. NEJM. 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)

                    - Site of Compromise   (Hungerford. Can J. Surg. 1981.)
                            1. Intraosseous - Extravascular (Intraosseous Pressure)
                            2. Intraosseous - Arterial
                            3. Extraosseous - Arterial
                            4. Venous
              - 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 & Hansen. J of Trauma. 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
              - 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. Arthritis and Rheumatism. 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
              - Hemoglobinopathy
                    - The most common cause of Osteonecrosis World-Wide (Miner et al. Clin. Orthop. 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.   Clin Orthop. 1993. & David et al.   JBJS-Br. 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
              - 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 (CORR 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

      - 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.   JSES.   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

      - 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. JBJS-Br.):
                            - 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. JBJS-Br. 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

                            - L'Insalata et al. JSES. 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

                            - LaPorte & Mont et al. CORR 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
              - 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.

   
       
 

 
 

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