Osteonecrosis of the femoral head is a disease caused by impaired blood flow to the bone. It can result from traumatic or non-traumatic causes like steroid use, alcoholism, or sickle cell disease. Diagnosis involves imaging like x-rays, MRI, or bone scan. Treatment ranges from conservative options like restricted weight bearing to surgical procedures like core decompression or joint replacement depending on the stage of disease. Joint preserving surgeries like core decompression or vascularized bone grafts can help early stages but progression often requires hip replacement.
Osteonecrosis of the femoral head is a disease caused by impaired blood flow to the bone. It can result from traumatic or non-traumatic causes like steroid use, alcoholism, or sickle cell disease. Diagnosis involves imaging like x-rays, MRI, or bone scan. Treatment ranges from conservative options like restricted weight bearing to surgical procedures like core decompression or joint replacement depending on the stage of disease. Joint preserving surgeries like core decompression or vascularized bone grafts can help early stages but progression often requires hip replacement.
Osteonecrosis of the femoral head is a disease caused by impaired blood flow to the bone. It can result from traumatic or non-traumatic causes like steroid use, alcoholism, or sickle cell disease. Diagnosis involves imaging like x-rays, MRI, or bone scan. Treatment ranges from conservative options like restricted weight bearing to surgical procedures like core decompression or joint replacement depending on the stage of disease. Joint preserving surgeries like core decompression or vascularized bone grafts can help early stages but progression often requires hip replacement.
Osteonecrosis of the femoral head is a disease caused by impaired blood flow to the bone. It can result from traumatic or non-traumatic causes like steroid use, alcoholism, or sickle cell disease. Diagnosis involves imaging like x-rays, MRI, or bone scan. Treatment ranges from conservative options like restricted weight bearing to surgical procedures like core decompression or joint replacement depending on the stage of disease. Joint preserving surgeries like core decompression or vascularized bone grafts can help early stages but progression often requires hip replacement.
Pathogenesis Up to 4 month, the femoral head is supplied by (1) metaphyseal vessel penetrate growth disc (2) lateral epiphyseal vessel- run in retinaculum (3) vessel in ligamentum teres The metephyseal supply gradually declines until, by the age of 4 yrs, it has disappeared By age of 7, vessel in ligamentum teres have developed. Between 4-7 yrs, femoral head blood supply entirely on LEV.
Effusion cause stretching & pressure to
LEV. No enough pressure to block arterial flow but cause venous stasis resulting raise in intraosseous pressure and subsequent ischemia. (Lin & Ho 1991)
(1)metaphyseal vessel penetrate growth disc
(2) lateral epiphyseal vessel- run in retinaculum (3) vessel in ligamentum teres
#NOF Dislocation
Incidence of osteonecrosis is 11% in undisplace #
15-50% in displaced # Prevalence after dislocation: 10-15% If reduction is delayed by more than few hours the figure rise to 40%
Corticosteriods
20mg/day is associated with increased risk
Relative risk goes up 4-6 fold for every 10 mg/day increase
Alcohol
>400ml/week increase the relative risk 8-9 fold
Sickle cell disease
: the prevalence of osteonecrosis is
4-2%. Age- dependent :33-50% of patients by age 35
SLE
incidence :15-44%:high dose (>30mg/d) AVN 44%
develops very early after starting high dose corticosteroid treatment. Annals of Rheumatic Diseases.2001;60(12):1145-8.
52 pt. AVN femoral head 11% (20%) AVN in 10 months MRI screening in the first year
Etiology
Ferrari P, et al.
Homozygous 4G/4G PAI-1 genotype.
Ries MD.
HIV infection (risk factor of AVN)
Association between human immunodeficiency virus and
osteonecrosis of the femoral head. J Arthroplasty 2002 Feb: 17(2):135-9
Pathogenesis
Infarction theory Fat embolism theory Accumulative cell stress theory Progressive ischemia theory Immunologic reaction
Pathophysiology of sickle cell disease 6 Glu
Val
Deoxy Hb S polymer forms with low
O2, depends on Hgb S concentration, low pH, high temperature, high 2,3DPG Under a variety of circumstances, different organs are susceptible: spleen, renal medulla (papillary necrosis), & many other complications
Gaucher's disease
hereditary deficiency of the enzyme
glucocerebrosidase (also k/s acid glucosidase). glucocerebroside accumulates in the spleen, liver, kidneys, lungs, brain and bone marrow.
HAEMODYNAMIC PRINCIPLE IN AVN
(1) arterial insufficiency
e.g. FON#, dislocation,
sufe
(2) venous occlusion
(3) intravascular capillary occlusion
e.g.venous drainage of the
femoral head is also reduced in Perthes disease .(Green & Griffin) e.g. sickle cell disease clumping of abnormal red cell lead to decreased capillary perfusion. (Rickles & OLeary1974) e.g. caission disease : rapid atm decompression cause release of N 2 bubbles. e.g. alcohol & steriod cause intraosseous fat embolism due to hyperlipidaemia.
(4) intraosseous capillary tamponade
e.g. bone infection e.g. Gauchers disease -autosomal recessive trait -lack of enzyme -glycosidase -osteonecrosis is due to compression of the marrow capillaries & sinusoids by mass of large macrophages stuffed with glycocerebroside. (Jaffe, 1972) e.g. alcohol & steriod: marrow fat cell is significantly increased. (Solomon) e.g. Cushing syndrome & familial hyperlipidaemia e.g. cassion disease: fat cell swelling contribute to the ischemic changes. (Pooley & Walder)
Diagnosis
History Physical examination Laboratory test CBC, ESR R/O infection Cortisol level No specific biochemical marker for high alcohol intake ( Whitehead, Clarke and Whitefield)
Elevation of four of the following is highly suggestive
An associated risk factor The most common presenting symptom is a deep pain in the groin Exacerbated by activity
Physical examination
Pain on internal rotation
Decrease ROM Hip abductor weakness (G. medius) Shortening of limb
Plain film X-ray
AP pelvis, frog leg
Crescent sign Secondary OA change
Conventional radiograph of the right femur in the frog-leg
position obtained with the patients thigh abducted and flexed shows subchondral area of hyperlucency (arrows) in the anterolateral aspect of the proximal femoral head.
Specimen radiograph of a coronally sectioned femoral head segment
reveals a subchondral fracture (arrows), which manifests as the crescent sign. Note the fragmentation and compaction of the subchondral cancellous trabeculae, which weakens the articulating surface.
Anteroposterior radiograph of the left humeral head
in a patient being treated with high-dose corticosteroids shows multiple subchondral areas of hyperlucency (arrowheads) that are indicative of stage III AVN.
Technetium bone scan (Tc
99) Preradiographic phase AVN Decrease uptake Sensitivity and specificity < MRI SPECT (Single-photon emission computed tomography) sensitivity 100% in renal transplant pt.
BONE SPECT
32 AVN of femoral head
SPECT detect 32/32 -> 100% sensitivity
MRI detect 21/32 -> 66% sensitivity
(The Journal of Nuclear Medicine. 2002;43(8):1006-1011)
MRI
Investigation of choice Decrease signal Screening T1 coronal scan
CT scan Arthroscopic examination
Ficats staging Clinical
Plain film
MRI
Stage O
No pain
normal
abnormal
Stage I
pain
normal
Stage II
crescentsign
Stage III
Collapsed femoral head
Stage IV
Narrow joint space+aceta bulum
normal
sclerotic
Crescent sign
Collapse
Acetabular involvement
Severe joint destruction
Treatment
Conservative
Temporally non-weight bearing Electrical stimuli
Surgery Joint preserving procedure prosthetic replacement
Treatment
Conservative treatment
stage I-II NWB with crutches (6 wks) analgesic+exercise F/U 2 years 80% poor result
Musso, et al. Result of conservative management of osteonecrosis
of the femoral head. A retrospective review. Clin Orthop 1986 June; 207: 209-215
Treatment Options AVN, Hip
Non-weight bearing Core decompression Core decompression + vascularized fibular graft Core decomp + non-vascularized fibular graft Core decomp+ autologous bone marrow cells Osteotomy Resurfacing arthroplasty Bipolar arthroplasty Total hip arthroplasty
Result of nonoperative Rx
55 AVN / nonoperative Rx
92% radiographic progression
84% arthroplasty, Av. Time 21 months (Steinberg. Clin Orthop;1989)
Increase venous drainage Promote vascular ingrowth Bone graft, autologous bone marrow Treatment of choice stage I-II
Core Decompression
Result of core decompression
133 AVN, stage I+II, F/U 9.5 years
90% successful clinical result 79% no radiographic progression (Ficat. JBJS;67B:3-9:1985)
204 AVN, F/U 3 years
no additional operative Rx was necessary 96% stage I 77% stage II 60% stage III (Zizic and Hungerford. Textbook of Rheumatology
Ed 2, Vol.2:1689-1710)
Electrical stimulation
Goal: Enhance bone formation and fracture
healing
Alone or as an adjunct to other surgical
procedure PEMF (pulsing electromagnetic fields) -more effective than symptomatic Rx in precollapse and minimally collapse -as effective as core decompression in precollapse -more effective as core decompression in minimally collapse
Osteotomy
Shift the necrotic segment out of
the region of major weight bearing and replace it with normal bone and cartilage Early to intermediate stage that acetabular cartilage is unaffected
Femoral Osteotomy
Candidate < 40 years old Small lesion (< 200 degrees) Mobile hip No longer taking steroid Difficulty for THR Removal of implants after union
Result of Ostetomy
Sugioka Y (CORR. 1984) 1984
158 hip (success rate
86-95 % (1992 , 295 pts, 79%, avn F/U 11 yrs)
Treatment
Vascularized bone graft
- fibular, iliac crest - revascularized
Vascularized bone graft
Goal:
Decompress the femoral head
Remove necrotic bone Fill necrotic defect with osteoinductive cancellous bone graft Support subchondral bone with strut graft
Enhance revascularized process
Vascularized bone graft
Disadvantage: Technical demand A few centers have significant experience with this technique Well-trained microvascular surgeon More complication
Vascularized bone graft
Advantage: The result is better than
core decompression in stage II, III (Ficat classification)
Result of Vascularized bone
graft
Urbaniak JR (JBJS. 77-A.1995)
mean survival rate= 88%
Patients. stage I , II Judet H (CORR.2001) FU 18 Year Found that 80% of patients 60. stage I,II It works well.
Prosthetic replacement surgery
Limited resurfacing arthroplasty Resurfacing arthroplasty Hemiarthroplasty Total hip replacement
Limited Resurfacing Arthroplasty
Hemisurface arthroplasty
Hemisurface or partial resurfacing arthroplasty
Time-buying procedure for young and
active patient
Adequated bone quality and relative normal
articular cartilage Bone stock preservation and intact intramedllary canal Survivorship 81% at 5.1 years Survivorship 61% at 10 years
(Amstutz HC. Semin Arthroplasty ;9:261,1998)
Hemiarthroplas ty
Treatment
Total hip arthroplasty
- femoral head + acetabulum - stage IV - survivorship in young patient is less than in older patient
