AVN Of The Hip (Aspectic Necrosis) (Osteonecrosis) Flashcards

1
Q

How does AVN typically present

A
  1. Bilateral in younger patients
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2
Q

What is the etiology of Intravascular AVN?

A
  1. Femoral head has a poor, terminal blood supply with little collateral development
  2. Vasculitis/vasospams/sickle cell disease/fat or air embolization will block the blood supply
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3
Q

What is the etiology of extravascular AVN?

A
  1. Femoral head is encased in rigid cortical bone
    *leaves no room for expansion within the head
    *expansion may compress blood flow
  2. Repeated micro fractures
  3. Cellular toxicosis (alcoholism)
  4. Trabecular deformation
  5. Disease processes within the joint capsule
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4
Q

What is the pathophysiology of AVN?

A
  1. Occurs in the fatty marrow
  2. Anterolateral portion of the femoral head is most likely effected
  3. Thrombosis/embolization of smaller arteries
  4. Increased intraosseous pressure due to enlargement of intramedullary fat cell or osteocytes
  5. End result of multiple factors terminating in bone death and collapse off the femoral head
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5
Q

What dos thrombosis lead to?

A
  1. Vasoconstriction and impaired fibrinolysis and infaraction due to necrotic vessels
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6
Q

Why does lysis occcur?

A
  1. To correct the intramuscular thrombosis throughout the body
    *a prolonged or repeated thrombotic episode may cause vessel injury and occlusion
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7
Q

How does AVN occur?

A
  1. Happens at the interface between healthy bone and devascularized bone
  2. Necrotic/devascularized bone is only partially reabsorbed and new bone is laid over old bone
    *leads to sclerotic and cystic area with ongoing inflammation
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8
Q

What does AVN progression equal?

A
  1. Mechanical failure of bone
    *microfractures develop in the necrotic portion of the bone and do not effectively heal
    *microfractures lead to subchondral fracture and likely collapse of articular cartilage
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9
Q

What are the stages of AVN?

A

0: preclinical and preradiologic
1: preradiologic
*mild findings seen on MRI
2: reparative phase
*demineralization present
3: early collapse of e oral head
4: progressive degeneration with increased flattening of the femoral head

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10
Q

What are the risk factors of AVN?

A

Age
Trauma
Steroid use
Alcohol use
SLE
Decompression sickest

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11
Q

What is the clinical presentation of AVN of the hip

A
  1. Asymptomatic initially
  2. Insidious onset
    *progressive development of limp along with decreasing ROM and decreasing muscle strength
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12
Q

What will be found on the PE?

A
  1. Decreased ROM
  2. Click May elicited with external rotation of an abducted hip or with rising from a seated position
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13
Q

What is the trendelenburg sign?

A

Sign of weak adductor hip muscles
1. When standing on affected leg, the pelvis on the opposite side drops

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14
Q

What are the diagnostic findings

A
  1. MRIis most sensitive for diagnosing AVN
  2. Plain radiographs
    *can assess later stages of AVN (2,3,4)
    *and flattening of femoral head and joint destruction
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15
Q

What is the prognosis of AVN

A
  1. Early diagnosis is optimal
  2. Mild/minimal/early
    *if lesion is not next to the joint line, it may heal spontaneously or progress slowly
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16
Q

What is the non surgical treatment?

A

Protected weight bearing
*poor prognosis

17
Q

What is the surgical treatment

A
  1. Bone marrow decompression/core decompression
    *drill a hole in the femoral head
    *relieves vascular engorgement and inflammation
    *relieves intramedullary pressure
  2. Bone grafting
    *severe stage 2 pre-collapse lesion
    *early stage 3
    *failed core decompression
  3. Total hip arthroplasty
    *femoral head collapse
    *failed attempt at previous surgical treatment