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- Most common causes up to 90% are associated with alcohol and steroids
- Idiopathic
- Secondary -
- Systemic disease
- SLE causing vasculitis and venous outflow issues ➔ increased intraosseous pressure
- Sickle cell anemia ➔ abnormal shaped RBCs obstruct blood flow
- Radiation ➔ vasculitis
- Hyperlipidemia, Alcohol ➔ theorized to increase lipid levels
- Caisson's decompression disease (release of nitrogen gas bubbles into body)
- Trauma disrupting blood supply - NOF #, talus #
- Tamponade of blood supply - compressive causes
- Steroids leading to fat hypertrophy and increased intraosseous pressure
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- Systematic review by Michael Mont et al. found 59% of patients with asymptomatic AVN progress to symptomatic disease which is usually due to collapse of femoral head
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- Etiology
- Sickle cell highest 73% > Alcohol 47% > Renal failure 46% > Idiopathic 38% > Steroids 26% … Lowest is SLE 7%
- Size of lesion - this paper did not use Kerboul angles but utilized MRI volumetric calculation of head involvement
- >25% involvement - increased risk of collapse
- Involvement of weight bearing area (lateral 2/3 of weight bearing portion of femoral head)
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- Ischemic Phase - the final pathway is the presence of micro-emboli ➔ stasis ➔ increased intraosseous pressure ➔ decreased blood flow ➔ AVN ➔ collapse
- Reparative phase - reactive hyperemia, ingrowth of vascular tissue ➔ creeping substitution of dead bone and new bone formation
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- Sickle cell, SLE can cause micro emboli
- Steroids and Alcohol cause elevated lipid levels
- Renal failure - Pathogenesis in CRF unclear
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- Up to 80%!
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- 2 mechanisms
- 1. The theory is that fat cell hypertrophy within bone marrow increases femoral head pressure → sinusoidal vascular collapse → necrosis of femoral head.
- 2. Steroids also create an intravascular hyperlipidemic state
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- Steinberg Classification
- 0 = XR normal, no pain
- 1 = MRI positive
- 2 = XR increased density (Sclerosis)
- 3 = Crescent sign = subchondral collapse WITHOUT flattening
- 4 = Flattening of femoral head (4 for flattening)
- 5 = OA without acetabular involvement
- 6 = OA with acetabular involvement
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- Initially described in 1974 - was an XR calculation on AP and lateral XR (essentially determining if angle is < or > than 200°)
- Ha 2006 JBJS modified to use MRI: (Modified Kerboul Angle)
ha2006.pdf422.5 KB
- Study of 37 hips, followed for 3 years.
- Combined necrotic angle on mid-coronal and mid-sagittal cuts.
- < 190° = low risk - non-collapsed
- 190-240° = moderate risk - 50% collapsed
- > 240° = high risk - all collapsed
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- XR - Crescent sign
- MRI - Double line sign - A serpentine line paralleled by inner and outer hyperintense lines
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- Weight-bearing status (FWBAT/PWBAT/NWB) shows no difference in outcomes (Mont 1996 systematic review in CORR)
- Provide analgesia, physical therapy to maintain hip ROM, allow full weight-bearing as tolerated, and consider reducing high-impact activities
- Bisphosphonates remain controversial—I don't recommend them. While Agarwala's group reported positive results, no other RCTs have confirmed these findings
CORR 1996.pdf697.8 KB
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- No consensus exists
- Agarwala published in JBJS and JOA (not an RCT; no control group) with 8-10 year follow-up studies. They found clinical improvement and potential delay to arthroplasty when administered for 3 years
agarwala2011.pdf646.2 KB
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- Outcomes? Fairbank et al. showed survival rates corresponding to initial severity: FICAT 1 - 90%; 2 - 66%; 3 - 23%. About 50% progressed by 1 stage
- Various graft types can be inserted
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- Supine position → image intensifier guidance → 2-3 passes with 3mm Steinmann pin
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- Angular - Transtrochanteric Curved Varus Osteotomy (TCVO) or Intertrochanteric Varus osteotomy
- Rotational - Sugioka Transtrochanteric Rotational Osteotomy (TRO)
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- Lateral position → anterolateral approach → dislocate hip → create trap door → debride to bleeding bone → insert corticocancellous ICBG → replace trap door
- Mont used this technique for Ficat stage 3 with collapse
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- Insert guide wire to the collapsed area
- Overdrill with reamer (e.g., DHS reamer)
- Insert graft—either autograft or metal augment
- Partial weight bearing for 6 weeks to prevent subtrochanteric fractures
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- To decompress intraosseous pressure
- Increase blood flow
- Promote healing response
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- Difficult to remove
- Concerns about retained tantalum debris when converting to THR, though wear rates are not increased at 2-year follow-up.
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- Donor site - great toe flexion contracture (37%), ankle pain, sensory loss, infection
- Graft site - pin migration, heterotopic ossification, fracture
- Why does great toe flexion contracture occur?
- We believe that the loss of muscle origins due to fibular removal causes the contracture and a tenodesis effect of the long-toe flexor tendons.
- Can be very subtle and only visible when the ankle is fully dorsiflexed
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- Consider this a Complex Primary procedure
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- Use templating to address leg length discrepancy (LLD)
- Obtain long leg films to accurately measure LLD
- Plan for hybrid implant system
- For specific etiologies like Sickle Cell, arrange blood transfusions and cell saver on standby
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- Prepare for extensile posterior approach
- Anticipate significant stiffness — you may need to release psoas and gluteus maximus; consider in-situ neck cut
- Exercise caution during rasping and broaching due to compromised bone quality
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- Standard full weight-bearing as tolerated (FWBAT)
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- Higher risks of infection and failure
- Necrotic bone has limited potential for bone ingrowth — use cemented implants
- Bone quality challenges include soft areas (from bone marrow hyperplasia) mixed with dense regions, leading to eccentric reaming and difficult cementless fixation of the cup
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A good man obtains favor from the Lord, but a man of evil devices he condemns. Proverbs 12:2