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HIP DISEASES

Congenital Hip Dislocation
Pathological Dislocation
Avascular Necrosis
Legg - Calve Perthes Disease
Slipped Capital Femoral Epiphysis
Coxa Vara
Coxa Valga
Transient Synovitis
Snapping Hip
Piriformis Syndrome
Bursitis
Tensor Fascia Latae Tightness
Condrolysis
Deeper Acetabulum
Hip Fracture
Total Hip Replacement


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CONGENITAL HIP DISLOCATION

· Different manifestations and approaches tp patient depending on the
      patient’s age
· Common in or among: female (2-3x common)
        Left side (5x common)
        Italy or Japan – the way they carry their babies
        Breech delivery
· Associated with other congenital  conditions like Torticollis, Metatarsus
      Varus, Ligamentous Laxity


· NEWBORN/NEONATAL STAGE (birth less than 6 mos)
-  dislocation of femoral head – is upward and posteriorly
-  positive in PROVOCATIVE TESTS because the hip is still lax (ligaments)

A. Barlow’s Test – move the hip from normal to dislocated; if you want to
      dislocate thehip
        	  - palpable or audible click of DISLOCATION 

B. Ortolani’s Test – to reduce the dislocation, opposite the Barlows
        	  - palpable or audible click of REDUCTION

· As the baby grows old, the provocative tests become negative because of
      the development of some strength of the ligaments and muscles
· Other signs of dislocation: asymmetry of the thigh and inguinal
      crease/folds limitad abduction on the affected side

· GALLEAZI’S test – measures the length of the leg with the knees and hip
      flexed

* the affected is shorter and there’s TELESCOPING or a sensation or pull
* 1st 3 mos- femoral head is not yet visible thru x-ray (confirmatory test)

· INFANCY STAGE up to 2y/o
* px is already sitting
* if bilateral, there’s WADDLING GAIT
* if unilateral – weakness of gluteus medius ( stabilizes the pelvis)

- Shortened length of ms – (+) weak ms, so in standing there’s broadening
      of the buttocks
- (+) weak ms hyperlordosis of the lumbar spine since hip ms also acts on
      the spine
- in walking – (+) lurching, which is a method to decrease the lever arm,
      thereby decreasing the force needed by the gluteus medius to
      prvent tilting
* Negative provocative tests but the other signs ( thigh & inguinal crease
      & limitad abduction ) can still be seen
* (+) galleazi & there’s minimal telescoping 

· 6 y/o & beyond: Limping
* LOM of hip
* Weakness of the gluteus medius
* Negative provocative tests
* Trendelenburg & lurching

· Treatment
* Initial Stage (px is still a baby)
- reduce the femoral head back to the acetabulum through TRACTION
- allow the femoral head to maintain that position until the supporting
      structures develop some strength & the jointr stabilizes thru/by:
- putting the patient in a non-rigid splint
- even if only one side is affected, the splint should still be bilateral
      to stabilized the pelvis which moves in unison
- the position should be 90 deg of flexion and abduction beyond 60 deg
      ( frog leg position )
- ex: Von Rosen, Pavlik Harness ( 6mos ), Ilfeld ( 12-13mos )
- at 9 mos, the patient can now walk but with crutches to decrease wt
      bearing

·Late Stage ( 2-6y/o )
- non-rigid orthosis-can still be tried but usually is not enough
- Surgery
- done after putting  the patient in a flexed and abducted position to
      contain the head
- to improve the fit of the acetabulum and the femoral head

1.Varus Osteotomy – cut a wedge of bone either in the trochanter or the
      femoral neck, then, fuse it. Decreases the neck-shaft angle
2.Salter Innominate Osteotomy – same procedure: surgery done on the pelvis
      if the acetabulum is too shallow to increase the coverage
3.Pemberton – cut the acetabulum at the middle then advance the upper
      segment producing a deeper acetabulum

·Femoral Anteversion or Angle of Torsion of the Femoral Shaft
- since the orientation of the acetabulum is forward, downward and outward,
      the femoral head undergoes torsion in the upper part to fit in the
      acetabulum
- in CHD, (+) excessive anteversion. Treatment: Varus or Salter Osteotomy
      Derotation of the femoral head and neck

·Diagnosis:
            US          
            X-ray  
            Special Test   
            Gait Analysis     
            Dynamic  
            US -whil;e doing Ortolani, (+) dislocation of the femoral head

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PATHOLOGICAL DISLOCATION

·Loosening, subluxation, dislocation of the femoral head from the
     acetabulum
·Reasons 1. Erosion in the femoral head and acetabulum
         2.Weakness and paralysis of the hip ms
- adduction contracture of the hip
- paralysis of the hip abductors

·Dislocating forces – adduction and extension of the hip

·causes: CP, Spina Bifida, Poliomyelitis,  Malignancy, Fracture, TB of the
         hip, Arthritis, Pyogenic Infection ® increase pus® destroy ms,
         ligaments, bones & capsule, Neuropathatic Joint – destroyed
         nerve supply
 
.Treatment:     1. Traction
  	         2. Bracing –in flexed and abducted position
          	 3. Surgery: as that of CHD     

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AVASCULAR NECROSIS

· Disruption of the blood supply to the femoral head ( Posterior
      Retinacular Arteries )
· Most common cause:  fracture of the femoral neck, ( in close proximity
      with the PRA)

· Other causes:
1.Forceful manipulation of the hip ( ex. If beyond  60 deg of abduction,
      in CHD extreme rotation )
2.Forceful reduction of the Slipped Capital Femoral Epiphysis (SCFE)
3.Any abnormality in the blood
a.Sickle-cell anemia – RBC can’t pass thru the small vessels easily because
      they are no longer deformable, if several RBC grouped together ® a
      clot is formed blocking small blood vessels ® prolonged ischemia
      ®NECROSIS
b.Decompression Disease ( Caisson’s Dse ) – occurs among deep sea divers 
- sudden formation of nitrogen bubble follwing sudden ascend which cannot
      be removed ® will impede blood flow.
- can also cause SCI, if nitrogen bubbles formed in the artery supplying
      the spinal cord.

· Idiopathic Causes:		
1. Legg-Calve Perthes Dse – in children
2.Idiopathic Osteonecrosis of the femoral head in adults = 30-60; bilateral
      clotting chronic alcoholism

·Stages:
1.Necrosis – will last for 5 mos
           - bone cells and bone marrow die
           - migration of undifferentiated mesenchymal cells
           - angiogenesis (formation of new blood vessels)

2.Fragmentation – aka Stage of Bone Resorption
           - crescent sign – presence of radioluscent area immediately at
                the subchondral bone, represents a fracture
           - will last 5-7 mos       

3. Re- ossification or Regeneration – new bone cells replace the dead cells
           - called Creeping Substitution – 2-4 years
           - dead cells are resorbed by inflammatory cells
       
 4.   Remodelling – new femoral head establishes
           - if the femoral head involvement is severe, establishment of
                a Normal Head should