AVASCULAR NECROSIS
A | Waist of scaphoid | |
B |
Neck of femur |
|
C |
Neck of talus |
|
D |
Surgical neck of humerus |
Post traumatic avascular necrosis is seen all of the following fractures except?
A |
Waist of scaphoid |
|
B |
Neck of femur |
|
C |
Neck of talus |
|
D |
Surgical neck of humerus |
Avascular necrosis is commonly seen in Fracture femoral neck, fracture neck of talus, fracture waist of scaphoid and lunate, fracture neck of talus.
A 45 year old was given steroids after renal transplant. After 2 years he had difficulty in walking and pain in both hips. Which one of the following is most likely cause?
A |
Primary Osteoarthritis |
|
B |
Avascular necrosis |
|
C |
Tuberculosis |
|
D |
Aluminum toxicity |
Difficulty in walking and pain in both hips after 2 years of steroid intake is suggestive of avascular necrosis.
Avascular necrosis is NOT seen in:
A |
Fracture neck of femur |
|
B |
Fracture neck of scaphoid |
|
C |
Fracture neck of talus |
|
D |
Dislocation of lunate |
Avascular necrosis is common in fracture of femoral neck (including slipped capital femoral epiphysis, posterior dislocation of hip), fracture neck of talus, fracture waist of scaphoid and lunate (dislocation).
Regions notorious for AVN: Head of femur, body of talus, proximal part of scaphoid and lunate.
In fracture neck femur the more proximal the lesion, more are chances of avascular necrosis. So subcapital fracture neck of femur has maximum chances of AVN (worst prognosis).
Ref: Apley’s Orthopedics 8/e, page 570 ; Maheshwari 3/e, page 40-41, 270
Avascular necrosis of bone is most common in
A |
Scapula |
|
B |
Scaphoid |
|
C |
Calcaneus |
|
D |
Cervical spine |
Ans: B i.e. Scaphoid
They are:
l. The head of the femur (after fracture of the femoral neck or dislocation of the hip).
2. The proximal part of the scaphoid (after fracture through its waist).
3′ The lunate (following dislocation)
4. The body of the talus (after fracture of its neck)
Following are the common sites of Avascular necrosis, EXCEPT:
A |
Proximal half of scaphoid |
|
B |
The body of talus |
|
C |
Patella |
|
D |
Head of the femur |
C i.e. Patella
Avascular necrosis is common in head of femur, proximal scaphoid and body of talusQ
The most common site of fracture neck of femur that causes avascular necrosis is
A | Sub-capital | |
B |
Intertrochanteric |
|
C |
Trans-cervical |
|
D |
Basal |
A i.e. Subcapital
Malunion is rarest complication of fracture neck femur (almost not seen) because intracapsular fracture neck femur almost never unite unless thay are anatomically reduced and stabliy fixed.
Most common complications of intracapsular fracture neck femur are nonunioin & fixation failure (more common in most series of displaced fractures) and avascular necrosis (more common in most series of undisplaced fractures). Shortening is seen in almost all cases of nonunion & AVN.
Chances of avascular necrosis (AVN) and nonunion increases as the fracture site becomes more proximal Q.
The more proximal the fracture located the worse the prognosis. Chances of AVN & nonunion (or worseness of prognosis)
in decreasing order is
- Subcapital Q > transcervical > basal > intertrochanteric
- Transphyseal > transcervical > cervicotrochanteric > intertrochanteric (in children)
Complications of Hip Fractures
|
Intracapsular Fracture Neck Femur |
Extracapsular Fracture Intertrochanteric Femur |
Most |
– Non union (in |
MalunionQ |
common |
displaced fracture) |
|
|
– Avascular |
|
|
(Osteo) necrosis |
|
|
(in undisplaced fracture) |
|
Least common |
MalunionQ |
NonunionQ |
Nonunion is second most common complication (after avascular necrosis) of undisplaced fracture neck femurQ. The probable causes of nonunion in fracture neck femur are –
– Cambium layer of periosteum which produce callus is missing. There fore femoral neck must heal via direct endosteal healing only. There is no contact with soft tissues which could promote callus formation.
Precarious blood supply: by tearing the ascending cervical branches or retinacular vessels the injury deprives head of its main blood supplyQ.
Synovial fluid interfere with fracture healing as it prevents clotting of fracture hematoma and release angiogenic inhibiting factors.
– Inadequate reduction and improper immobilization.
* It is important to note that avascular necrosis and nonunion are independent events, because AVN is based on vascular supply of femoral head, whereas nonunion is based on the healing process. So AVN can occur even in united fractures.
* Femoral neck fractures should unite by 6 months. If there is no evidence of healing or patient continued to have pain at 3 – 6 months after surgery then a delayed (3 months) or non union ( 6 months) should be contemplated.
* AVN is a late complication and ischemic collapse usually occur with in 2 -years of fracture.
According to anatomical location of fracture neck femur the chances of AVN & nonunion in decreasing order are: subcapital (transepiphyseal in children) > TranscervicalQ > Basicervical.
– Temponade effect of intracapsular hematoma causing floating of both fracture ends and making reduction difficult.
March 2012
A |
Cuboid |
|
B |
Calcaneum |
|
C |
Navicular |
|
D |
Talus |
Ans: D i.e. Talus
Because of the poor blood supply, after a fracture through the neck, the body of talus becomes avascular
Best diagnostic modality to diagnose avascular necrosis is:
March 2007
A |
MRI scan |
|
B |
CT scan |
|
C |
X-ray |
|
D |
USG |
Ans. A: MRI Scan
- Alcoholism
- Excessive steroid use
- Post trauma
- Caisson disease (decompression sickness)
- Vascular compression
- Vasculitis
- Thrombosis
- Damage from radiation
- Bisphosphonates (particularly the mandible)
- Sickle cell anaemia
- Gaucher’s Disease
- Idiopathic (no cause is found).
Rheumatoid arthritis and lupus are also common causes of AVN.
Avascular necrosis most commonly affects the head of femur. Other common sites include the talus, scaphoid and the jaw. Avascular necrosis usually affects people between 30 and 50 years of age.
When it occurs in children at the femoral head, it is known as Legg-Calve-Perthes syndrome.
It is most oftenly diagnose clinically.
Because early X-rays are usually normal in the early stage of the disease, bone scintigraphy and MRI are the diagnostic modality of choice since both can detect minimal changes at early stages of the disease.
Late radiographic signs include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity