MOD 1 - Avascular Necrosis

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48 Terms

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Epiphyseal Pathologies Covered

  • Ischemic Necrosis

  • Leg-Calve-Perthes Disease

  • Osteochondritis

  • Freiberg Kohler’s Disease

  • Kohler’s Disease

  • Osgood Schlatter’s Disease

  • Kienbock’s Disease 

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Ischemic necrosis (adults) - Classification

depends on the cause

  • idiopathic 25%

  • secondary disease (trauma)

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Ischemic necrosis (adults) - Description

  • following trauma, particularly with joint dislocation and joint capsule tear

  • common in hip, shoulder, scaphoid, knee, ankle

  • 30-60 y/o

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Ischemic Necrosis (adults) - Pathogenesis

micro fractures in early stages → fragmentation, compression and resorption in later stages → left untreated can lead to collapse of bone and/or arthritis

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Ischemic Necrosis (adults) - Signs and Symptoms

  • pain

  • limp

  • loss of function

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Ischemic Necrosis (adults) - Radiographic Appearance

  • MRI, CT and Nuclear scans are better at detecting early stages

  • Crescent sign = radiolucent subcortical band representing a fracture line

  • Later Stages = flat femoral head, combo of sclerotic (dense) and lytic (translucent) regions

<ul><li><p>MRI, CT and Nuclear scans are better at detecting early stages</p></li><li><p><strong>Crescent sign </strong>= radiolucent subcortical band representing a fracture line</p></li><li><p>Later Stages = flat femoral head, combo of sclerotic (dense) and lytic (translucent) regions</p></li></ul><p></p>
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Ischemic Necrosis (adults) - Treatment

  • analgesics and NSAID

  • exercise, physiotherapy

  • immobilization, rest

  • surgery

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Legg-Calvé-Perthes Disease - Definition

  • Temporary loss of blood supply at the femoral head ossification center

  • Affects the epiphyseal plate before closure of the growth plate, thus affects peds

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Legg-Calvé-Perthes Disease - Classification

hereditary, traumatic, inflammatory, metabolic

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Legg-Calvé-Perthes Disease - Etiology

  • cause is obscure

  • avascular necrosis

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Legg-Calvé-Perthes Disease - Common Age Group

  • children 3-12 (peak 5-7)

  • predominately males 4:1

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Legg-Calvé-Perthes Disease - Pathogenesis

  1. Early/Avascular

    • loss of blood supply to the FH leading to decrease in size

    • increased joint space, lateral femoral displacement

  2. Fragmentation (of epiphyses)

    • crescent sign

    • blurred FH outlines

  3. Repair

    • return of blood supply

    • new bone deposits

    • wide short femoral neck

  4. Healed/Deformity

    • enlarged and flattened FH

    • enlarged GT

<ol><li><p>Early/Avascular</p><ul><li><p>loss of blood supply to the FH leading to decrease in size</p></li><li><p>increased joint space, lateral femoral displacement</p></li></ul></li><li><p>Fragmentation (of epiphyses)</p><ul><li><p>crescent sign</p></li><li><p>blurred FH outlines</p></li></ul></li><li><p>Repair</p><ul><li><p>return of blood supply</p></li><li><p>new bone deposits</p></li><li><p>wide short femoral neck</p></li></ul></li><li><p>Healed/Deformity </p><ul><li><p>enlarged and flattened FH</p></li><li><p>enlarged GT</p></li></ul></li></ol><p></p>
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Legg-Calvé-Perthes Disease - Signs and Symptoms

  • include vague groin pain extending down towards knee

  • limping

  • decreased ROM

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Legg-Calvé-Perthes Disease - Radiographic Appearance

  • FH = flat, small

  • Epiphyseal Plate = increased density, widening

  • FN = widened and decreased length

  • GT = enlarged

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Legg-Calvé-Perthes Disease - Treatment

  • no cure, have to let it run thru all stages

  • casting, traction, bedrest

  • osteotomy, internal fixation

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Osteochondritis Dissecans - Description

name should be Osteochondroses as there is no primary inflammation

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Osteochondritis Dissecans - Classfication

Traumatic, causing avascular necrosis of the end of a bone

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Osteochondritis Dissecans - Pathogenesis

  • Idiopathic, traumatic

  • Small fragments of subchondral bone necrotize if displaced, undisplaced frags may reattach and revascularize

  • frags are known as “joint mice”

  • high incidence in medial condyle 75%

<ul><li><p>Idiopathic, traumatic</p></li><li><p>Small fragments of subchondral bone necrotize if displaced, undisplaced frags may reattach and revascularize</p></li><li><p>frags are known as <strong>“joint mice”</strong></p></li><li><p>high incidence in medial condyle 75%</p></li></ul><p></p>
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Osteochondritis Dissecans - Common Group

  • age 11- 20 yrs

  • active in sports

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Osteochondritis Dissecans - Signs and Symptoms

  • joint effusion

  • clicking

  • locking

  • tenderness

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Osteochondritis Dissecans - Radiographic Appearance

  • cartilage fragments are only seen on CT, MRI, NM

  • aim is to assess location of frag within joint space and origin

  • requires tunnel/notch view for best assessment

<ul><li><p>cartilage fragments are only seen on CT, MRI, NM</p></li><li><p>aim is to assess location of frag within joint space and origin </p></li><li><p>requires tunnel/notch view for best assessment </p></li></ul><p></p>
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Osteochondritis Dissecans - Treatment

  • joint arthroscope to remove joint mice and/or secure loose cartilage

  • drilling to stimulate healing of subchondral bone

  • Non surgical: protected WB or immobilization

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Freiberg Kohler’s Disease - Classfication

Traumatic, causing avascular necrosis of the end of a bone

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Freiberg Kohler’s Disease - Etiology

  • avascular necrosis of 2nd MT head (smt 3rd)

  • disruption of growth plate due to trauma or increased stress

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Freiberg Kohler’s Disease - Common Group

  • teen athletes who land with impact on the balls of their feet and young teen females who regularly wear high heeled shoes

  • adolescence females 5:1 (age 13-18 yrs)

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Freiberg Kohler’s Disease - Pathogenesis

Growing epiphyseal site experiences avascular necrosis due to repeated micro fractures where the middle of the metatarsal meets the growth plate

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Freiberg Kohler’s Disease - Signs and Symptoms

  • tenderness and pain

  • localized

  • aggravated with activity

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Freiberg Kohler’s Disease - Radiographic Appearance

  • Bone scan and MRI are better for early stages

  • Initial Stage

    • articular cortex irregularity

    • sclerosis/lucency

    • altered joint space

  • Later Stage

    • enlarged, flattened and fragmented head

    • altered joint space

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Freiberg Kohler’s Disease - Treatment

  • no known treatment

  • conservative:

    • reduced activity

    • non WB

  • invasive:

    • surgery for excision

    • osteochondral transplant

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Kohler’s Disease - Classification

traumatic

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Kohler’s Disease - Etiology

  • trauma - usually compression type injury

  • avascular necrosis of navicular bone

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Kohler’s Disease - Pathogenesis

compression and/or injury during development phase, thus predom affects children 3-7 yrs (males)

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Kohler’s Disease - Signs and Symptoms

  • midfoot pain and swelling

  • pt walks with increased weight on lat. side of foot

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Kohler’s Disease - Radiographic Appearance

  • patchy and/or homogenic sclerosis (increased density)

  • severe cases bone collapses and fragments

  • abnormal architecture evident into adulthood

<ul><li><p>patchy and/or homogenic sclerosis (increased density)</p></li><li><p>severe cases bone collapses and fragments</p></li><li><p>abnormal architecture evident into adulthood</p></li></ul><p></p>
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Kohler’s Disease - Treatment

  • resolves with time

  • pain killers

  • cast for 6-8 weeks

  • arch supports

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Classification - Osgood Schlatter’s

  • inflammatory

  • can be traumatic

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Etiology - Osgood Schlatter’s

  • repetitive strain

  • commonly seen in active teens  

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Pathogenesis - Osgood Schlatter’s

traction force of the patellar tendon causes inflammation and fragmentation of the immature tibia

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S&S - Osgood Schlatter’s

  • swollen tibial tuberosity area

  • painful on resisted knee extension

  • limping

  • pain

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Rad - Osgood Schlatter’s

  • ST swelling

  • loss of sharp patellar tendon margins

  • tibial tub fragmentation

<ul><li><p>ST swelling</p></li><li><p>loss of sharp patellar tendon margins</p></li><li><p>tibial tub fragmentation</p></li></ul><p></p>
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Treatment - Osgood Schlatter’s

  • rest

  • ice

  • physical therapy

  • NSAID

  • surgery (rare)

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Classification - Kienbock’s disease

  • traumatic

  • degenerative

  • idiopathic

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Etiology - Kienbock’s disease

  • exact cause is unknown

  • however, association seen between negative ulnar variance (rly short ulna compared to radius)

  • repetitive trauma/load to the lunate

  • lack of blood supply 

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Pathogenesis - Kienbock’s disease

  • stage 1 = x-ray appears normal, osteonecrosis only seen on MRI or bone scane

  • 2 = sclerosis of lunate

  • 3a = lunate collapse (no carpal instability → radioscahpoid angle <60)

  • 3b= lunate collapse (carpal instability → radioscahpoid angle >60)

  • 4 = lunate collapse with degenerative arthritis

<ul><li><p>stage 1 = x-ray appears normal, osteonecrosis only seen on MRI or bone scane</p></li><li><p>2 = sclerosis of lunate</p></li><li><p>3a = lunate collapse (no carpal instability → radioscahpoid angle &lt;60)</p></li><li><p>3b= lunate collapse (carpal instability → radioscahpoid angle &gt;60)</p></li><li><p>4 = lunate collapse with degenerative arthritis</p></li></ul><p></p>
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Rad - Kienbock’s disease

  • best seen on MRI

  • dense/brighter lunate (sclerosis)

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S&S - Kienbock’s disease

  • center wrist pain

  • swelling

  • stiffness

  • crepitation (creaking/crackling sound with movement)

  • irreg. lunate shape

  • changes in carpal alignment

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Treatment - Kienbock’s disease

  • no definitive cure

  • NSAIDS, immoblization

  • occupational therapy 

  • surgery (proximal row carpectomy, fusion/arthodesis)