Avascular necrosis of femoral head.Causes for AVN, Investigations and tratments

1. Avascular Necrosis Of Femoral
Head
Dr. Garaka Jayasuriya.
Registrar in Orthopaedics
NH - Kandy
22/12/2022

2. Outline
• Introduction.
• Classification
• Etiology
• Pathogenesis
• Clinical presentation
• Investigations
• Management
• Prognosis

4. • Also known as Hip Osteonecrosis.
• It represents a condition caused by reduced blood flow to the
femoral head secondary to a variety of risk factors such as a
• Traumatic event,
• Sickle cell disease,
• Steroid use
• Alcoholism,
• Autoimmune disorders,
• Hypercoagulable states

5. • Accounts for 10% of total hip arthroplaty.
• Male > females.
• Bilateral hips involved 80% of cases.

6. Pathogenesis
1. Traumatic AVN of Hip
2. Idiopathic AVN of Hip

7. Traumatic AVN
• Due to injury of femoral head blood supply.
(medial femoral circumflex)
• AVN rates of specific traumatic injuries
Femoral head fracture: 75-100%
Basicervical fracture: 50%
Cervicotrochanteric fracture: 25%
Hip dislocation: 2-40% (2-10% if reduced within 6 hrs)
Intertrochanteric fracture: rare

8. • Higher risk of AVN with greater initial displacement and poor
reduction.
• Decompression of intracapsular hematoma may reduce risk.
• Quicker time to reduction may reduce risk.

9. Idiopathic AVN
• Coagulation of the intraosseous microcirculation
• Venous thrombosis
• Retrograde arterial occlusion
• Intraosseous hypertension
• Decreased blood flow to femoral head
• AVN of femoral head
• Chondral fracture and collapse

10. Risk factors
Direct causes indirect causes
Irradiation
Trauma
Hematologic diseases (leukemia,
lymphoma)
Dysbaric disorders (decompression
sickness, "the bends") - caisson disease
Marrow-replacing diseases (e.G.
Gaucher's disease)
Sickle cell diseas
alcoholism
hypercoagulable states
steroids (either endogenous or
exogenous)
systemic lupus erythematosus (SLE)
transplant patient
virus (CMV, hepatitis, HIV, rubella,
rubeola, varicella)
protease inhibitors (type of HIV
medication)
idiopathic

11. Clinical Presentation
Symptoms
• Insidious onset of pain
• Pain with stairs, inclines, and impact
• Pain common in anterior hip
O/E
• Mostly normal initially
• Advanced stages similar to hip oa (limited motion, particularly
internal rotation

12. Investigations
• Diagnosis can be made with radiological imaging.
• X rays - Moderate/late disease.
– Ap hip
– frog-lateral of hip
– AP and lateral of contralateral hip
• MRI - To detect early or subclinical osteonecrosis.
– Highest sensitivity (99%) and specificity (99%)
• Bone scan

13. Ficat classification
Stage Clinical features Plain radiograph
X ray
MRI Bone scan
0 nil normal normal
I pain typically in
the groin
normal or minor osteopenia edema increased
uptake
II pain and stiffness mixed osteopenia and/or
sclerosis and/or subchondral
cysts, without any subchondral
lucency
geographic
defect
III pain and stiffness
+/- radiation to
knee and limp
crescent sign and eventual
cortical collapse
same as plain
radiograph
IV pain and limp end-stage with evidence of
secondary degenerative
change
same as plain
radiograph

15. Management
Goals of Treatment-
1. observation with management of the underlying systemic
conditions.
2. Operative management is indicated for advanced disease
with presence of……
- Subchondral collapse
- Femoral head flattening
- Degenerative joint disease

16. Non operative Management
Bisphosphonates
• Indicated for pre collapse AVN (ficat stages 0-II).
• Lack of evidence.
• Alendronate, Zolindranate etc..

18. Operative managements
1. Core decompression with or without bone grafting.
2. Rotational osteotomy.
3. Curettage and bone grafting through mont trapdoor
technique or merle d'aubigne lightbulb technique.
4. Vascularized free-fibula transfer.
5. Total hip replacement.
6. Total hip resurfacing.
7. Hip arthrodesis.

19. Core decompression with or without bone
grafting.

21. Vascularized free-fibula transfer.

22. Rotational osteotomy.

23. Total hip resurfacing

24. Total hip replacement

25. Hip arthrodesis

26. Post op plan…

27. Prognosis
• Risk of femoral head collapse with osteonecrosis is based on
the modified Kerboul combined necrotic angle.
• calculated by adding the arc of the femoral head necrosis on a
mid-sagittal and mid-coronal MR images.

28. • Low-risk group = combined necrotic angle less than 190°
• Moderate-risk group = combined necrotic angle between 190°
and 240°
• High-risk group = combined necrotic angle of more than 240°

29. Case - 1
• 47 years old female
• C/o
L/ Hip Pain for 6/52
Hx of fall 3/12
No constitutional symptoms
No PMH
• O/E
Antalgic limping gait
No LLD
Painful passive movements

30. • Blood Ix
Esr 37
RF 18

31. • X rays

32. • MRI

35. Case - 2
15 y old boy.
C/o
L/ Hip pain and difficulty in walking -3 /12
Hx of slipped and fall 3/12
No constitutional symptoms
PMH - none

36. O/E
Limping gait.
LLD- 4cm R>L.
painful passive joint movements.
Ix
FBC, CRP, ESR – normal

37. X Ray

38. • Diagnosis.
Perthes disease.
Management
shelf osteotomy

39. Summary
• AVN is diagnosed always retrospectively.
• Therefore no primary preventive measures.
• Early diagnosis may reduce collapse of articular surface.
• Management will be depended on…
• Severity of AVN
• Age of the Patient
• Demand of the Patient
• Comorbidities