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Avascular Necrosis of The Hip

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Epidemiology

• 200,000-300,000 estimated new cases each year in the United States
• Cause of approximately 10% of total hip replacements
• Mean age at time of diagnosis is < 50 years

 

Pathogenesis and Etiologies

Current thoughts on exact mechanisms are an area of hot debate, but include:

• Genetic predisposition
• Metabolic factors
• Vascular factors
  • Vascular damage
  • Increased intraosseous pressure
  • Mechanical stresses

80% of all atraumatic cases of AVN are due to:

• Glucocorticoid Use
  • Theories
    • Microemboli in the arteries of the bone from alterations in lipid metabolism
    • Increased bone marrow adipocyte size and number causing decreased venous outlow
    • Changes venous endothelial cells of the bone leading to stasis and necrosis
  • Dose of prednisone < 15-20 mg/day has lowest risk of developing AVN (<3%)
• Alcohol Use
  • Causes fat emboli, venous stasis, elevated cortisol, and adipocyte hyperrophy
  • While not considered an absolute risk factor, it is associated with up to 31% of AVN cases

 

Trauma can also predispose patients to develop AVN and most commonly associated with:

• Femoral neck fracture
• Hip dislocations

 

Other atraumatic causes of AVN include sickle cell disease, Gaucher disease, decompression disease, treatment for ALL, and transplantation

 

Signs and Symptoms

• Pain
  • Groin, thigh, and/or buttock pain
  • Worse with weightbearing or motion
    • Although 2/3^rd may have rest pain
    • 1/3^rd may have night pain
  • Decreased ROM with forced internal rotation and abduction
  • Limp

 

Imaging

• Plain Radiographs
  • May not see any changes early in disease course
  • Progression of changes
    • Decreased density –> sclerosis –> subchondral radiolucency (crescent sign) and collapse
    • 
• Magnetic Resonance Imaging
  • Much more sensitive than plain films
    • May see early changes undetectable on plain radiographs
      • T1 – Signal low-density line differentiating healthy and ischemic bone
      • T2 – Second high-density line showing hypervascular granulation
  • 

 

Classification and Staging

In 1993, The Association of Research Circulation Osseous (ARCO) staging system for AVN was developed to unify descriptions for treatment and research purposes.

 

Treatment

The goal of treatment is to preserve the native joint for as long as possible.

• Nonoperative Management
  • Generally ineffective at halting the process
  • Includes bed rest, partial weightbearing, and pharmacotherapeutics
    • Bisphosphonates
      • Slows bone resorption
    • Vasodilators
      • Decrease intraosseous pressure and improve blow flow
    • Statins
    • Anticoagulants
• Joint-Preserving Procedures
  • Core Decompression
    • Drills holes into femoral neck decrease pressure and allow for neovascularization
    • 
    • http://www.ibji.com/education/patient-information/hip-pelvis/Core-Decompression-Avascular-Necrosis#vm_A_16a25645
  • Vascularized Fibular Graft
    • Larger core decompression with bone graft placed
    • 
• Total Joint Replacement

 

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Slipped Capital Femoral Epiphysis (SCFE)

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Definition

• Displacement of the capital femoral epiphysis from the neck of the femur through the physeal plate anterolaterally and superiorly

 

Risk Factors

• Obesity is #1 risk factor
  • > 60% of patients in > 90^th percentile for weight
• Renal failure
• History of radiation therapy
• Endocrine abnormalities
  • Hypothyroidism, GH deficiency

 

Signs and Symptoms

The most common clinical presentation of SCFE are pain and altered gait, but can be divided into four presentation patterns:

• Preslip
  • (+) pain, but no radiographical displacement of epiphysis
  • May show widening of the physis
• Acute
  • < 3 weeks duration
  • (+) joint effusion but no metaphyseal remodeling
  • 10-15% of initially presentation of hip pain and often associated with trauma
• Acute-on-chronic
  • Worsening symptoms in known SCFE
• Chronic
  • Most common pattern of presentation
  • Vague, intermittent symptoms > 3 weeks
  • (+) metaphyseal remodeling but no effusion

Pain is classically characterized as dull, aching in the hip, groin, thigh, or knee.  Physical exam reveals decreased internal rotation and abduction ROM with increased pain.  Passively flexing the affected hip while the leg is extended will cause external rotation and abduction.

 

Stability

• Stable Slips
  • Walking and weightbearing still possible with or without crutches
• Unstable Slips
  • No ability to weightbear, even with crutches
  • No examination of the ROM of the hip should occur until orthopaedic consultation

 

Radiographic Evaluation

Most SCFE are diagnosed by plain radiography and have characteristic findings on each view:

• AP view
  • Mild, widening, lucency, and irregularity of the physis
  • Blurring of the junction between metaphysis and growth plate
  • Klein’s Line
    • Normal = intersecting lateral portion of femoral head from superior femoral neck
    • SCFE = line passes outside of epiphysis
    • 
• Lateral View
  • Usually obtained via frog-leg or cross-table
    • Unstable SCFE should have true lateral
  • Posterior displacements are best seen on lateral views

 

Grading of Severity

2 ways to grade severity: Displacement of femoral neck or Angle of Southwick.

• Displacement
  • Mild = < 1/3^rd the diameter of the femoral neck
  • Moderate = > 1/3^rd, but < 2/3^rd the diameter of the femoral neck
  • Severe = > 2/3^rd the diameter of the femoral neck
• Angle of Southwick
  • Mild = < 30^o
  • Moderate = 30-60^o
  • Severe = > 60^o

 

Treatment

All SCFEs must be repaired surgically and the goals of surgery are to stabilize the diseased physis to prevent further slippage and avoid complications (AVN).  Treatment of choice is a single cannulated screw placed in the center of the epiphysis.

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References

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