Hip



Coxa Vara

Localised bony dysplasia of the femoral neck
Characterised by a decreased neck shaft angle and the presence of a triangular ossification defect (Fairbanks Triangle) of the inferior femoral neck and results in decreased length of the involved limb
The normal neck shaft angle in a child is ~ 160o which decreases to about 120o in the adult

 

Classification

Congenital
assumed to be a limb bud abnormality occuring in the developing embryo
may be difficult to differentiate from DDH
Significant varus present at birth - but - usually minimal progression during growth
Associations PFFD, Congenital short femur, Congenital bowed femur

Developmental
Normal at birth, develops coxa vara in early childhood, progressive with growth

Acquired
Due to neck bending due to bone softening or due to fracture

softening
children- rickets, bone dystrophies, Perthes, fibrous dysplasia,SUFE
adults- osteomalacia,
elderly- osteoporosis, Pagets
any age- infection -TB or pyogenic
fracture
children- eg through bone cyst; adult- eg malunion of # NOF

Incidence

rare- 1/ 25000 live births, M=F, R=L, Bilat in 30%
an autosomal dominant inheritance pattern has been described
may be more common in negroes

 

Aetiology

Histological abnormalities havebeen found in Bx of the femoral necks- in width of the growth plate

absenceof normal orderly progression of cartilage columns
(similar to appearance of Blounts Dx)
current theory - deformity due to a primary ossification defect in the inferior femoral neck. Physiologic shearing stresses in weight bearing fatigue the abnormal bone ® progressive deformity

 

Clinically

Most present with a progressive gait deformity bw walking age and ~ 6 yo
pain is rare
unilateral dx- present with gait 2o to abductor weakness and a LLD
bilateral dx - present with waddling gait similar to that of DDH

 

examination
prominent and elevated greater trochanter
+ve Trendelenberg
LLD - usually mild, av 2.5 cm
FFD with ­ ROM - esp abduction and IR

XRay ­ neck- shaft angle
more vertical position of the physeal plate- defined by the angle bw Hilgenreiners line and the line through the epiphyseal plate- normally 25o or less
Fairbanks triangle - a triangular metaphyseal fragment in the inferior femoral neck surrounded by an inverted radiolucent Y ( represents a zone of abnormal osification with an interposed triangular segment of dystrophic bone)
­ in normal anteversion of the prox femur ( may become retroverted)
coxa breva
rarely mild acetebular dysplasia

 

Natural History

( Weinstein etal, J Paediatr Orthop 1984; 470)
The determining factor for progression is the epiphyseal angle
- if remains less than 45�- usually spontaneously heal femoral neck defect and do not progress
- if more than 45� progression, ultimately resulting in the development of a stress fracture related nonunion of the femoral neck as well as premature degenerate changes in the hip jt by late teens

 

Treatment

aims
  1. correct neck-shaft angle to a more physiologic range
  2. change load from shear to compression at physis
  3. correct LLD
  4. restore proper length -tension relation for the abductors

Conservative treatment of no value
Surgery valgus proximal femoral osteotomy either intertrochanteric or subtrochanteric - internally fixed to maintain correction
combine with adductor release to allow easier correction of the deformity at the osteotomy

Indications

  1. Epiphyseal angle 45-60� - observe- if progresses ® operation
  2. >60� ® operation
  3. Shaft- neck angle less than ~ 90�
  4. Development of Trendelenberg gait
    aim is to overcorrect to a neck- shaft angle of more than 160�, an epiphyseal angle of 30� or less

Operate when child is younger - do not wait- remodelling better in young pt

 

Prognosis

spontaneous healing of metaphyseal defect within 3-6 mths if adequate valgus achieved
50- 89% - operated hips develop premature closure of the prox femoral physis- usually within 2 yrs of surgery- if it occurs, need to mnitor for recurrence of deformity or LLD. To prevent recurrence of deformity due to premature closure of physis, greater trochanteric apophyseodesis or advancement can be performed

If recurrent deformity, repeat osteotomy

 

[ Back to the Top ]



DDH

Developmental dysplasia of the hip refers to a broad spectrum of conditions characterised by instability of the hip with subluxation or dislocation due to acetabular or femoral dysplasia.

 

Incidence

6.4 per 1000 births in Australia
7.4 per 1000 births in SA 1986 - 1990
Females more than Males (females ® 80% of all dislocations)
Breech female ® 1 in 35 chance of DDH
60% of DDH are the first born child
Siblings of affected children ® 10 times increased risk of DDH
Left hip more than Right hip (60% left, 20% right and 20% bilateral)

 

Aetiology

Genetic predisposition Joint laxity- dominant inheritance
Acetabular dysplasia- polygenic inheritance
41% concordance with monozygotic twins, 2.8% with dizygotic

 

Assoc. with:
torticollis
metatarsus adductus
calcaneovalgus feet
congenital recurvatum or disloc. knee

 

Racial:
Aborigines-­ incidence
Lapps, Navajo, Italians of Sth Tyrol- � incidence (may be due to swaddling in extension)

 

Environmental:
Hormonal influence ® joint laxity and reason for lower incidence in boys as male hormones reduce effect (hormonal effect lasts about 10 days- Oestrogens inhibit collagen cross linking® laxity)

 

Intra uterine malposition-
10 fold � risk with breech
assoc with oligohydramnios
Increased incidence among first born children

 

Teratologic:
Associated with other conditions eg Arthrogryposis, chromosomal abnormalities and sacral agenesis

 

Acquired:
sepsis ( TB or pyogenic) - the head and neck of the femur may be destroyed ® pathological dislocation (difficult to reconstruct)
Traumatic
Unbalanced paralysis particularly adductor spasm (CP, Spina bifida, Polio)

 

Pathology

Acetabulum and femoral head develop from primitive mesenchymal cells and at 7 weeks gestation a cleft develops in pre-cartilaginous cells
The normal development of the acetabulum is dependant on the presence of the femoral head
There is little remodelling capacity of the acetabulum after the age of 7 - 8 years and if the head is not contained in the developing acetabulum ® false acetabulum develops
Femoral neck usually short and excessively anteverted
Capsule remains intact and may ® hour glass restriction due to indentation by psoas tendon
Cartilaginous labrum often large and may be folded into the joint
Ligamentum teres is often unduly thick and may limit reduction
Muscles arising from pelvis ® adaptive shortening
Rate of growth in first year rapid - if hip dislocated during this time neither develop normally
Transverse acetabular ligament displaced superiorly resulting in possible block to reduction
Subluxation of the hip will result in more rapid degeneration of the hip and earlier development of OA than frank dislocation

Blocks to reduction:

  • Inverted limbus
  • Hour-glass constriction of capsule (psoas tendon over acetabular inlet) or capsular adhesions
  • Deformation of head or neck of femur
  • Thick ligamentum teres or hypertrophy of transverse ligament
  • Acetabular floor filled with fibro-fatty tissue (the pulvinar)
  • Tight adductors or psoas
    The transverse acetabular ligament

 

Clinically

Neonatal history important (breach, assisted delivery etc)
Hips may be asymptomatic
Clicky hips may be evident or limitation of abduction on nappy changes
Asymmetrical skin creases
Leg may be slightly short and externally rotated
Delayed walking not usually a feature
Limp or asymmetry evident after walking commences but bilateral dislocation may be less apparent
Bilat dislocation- no assymetry, is an abnormally wide perineal gap
Decreased abduction in flexion esp

Ortolanis' test
reported in 1937 (test hip reduced by manoeuvre- gentle abduction+ anterior translation)

Barlows' test
reported in 1962 is a two stage test

  1. is the hip dislocated
  2. is the hip dislocatable ?

60% of unstable hips at birth are stable at 1 week, 88% stable at 3/12 (only 12% remain unstable)- hip flexed to 90%, slight abduction- pressure over gt trochanter may reduce a dislocated hip, pressure over lesser trochanter may dislocate an unstable hip

Galleazzi sign
® the affected limb short in the thigh when the knee is flexed to 90o with the hips flexed to 45o and the heels at the same level
Even with screening a significant number are presenting late

X-Rays
Earliest X-Rays of value at 6 weeks to 3 months
Associated with delayed appearance of the epiphysis
Hilgenreiners horizontal line through triradiate cartilage and Perkins vertical line from outer edge of acetabulum- should have head medial to vertical line and below horizontal line)
Acetabular angle (index) normal is <27.5o and> 30o indicates dysplasia, significant if> 40o
Von Rosen's line described in 1956 (with hips abducted 45o and 25o internally rotated line up the shaft of the femur should intersect acetabulum and not ilium above it)
Shentons line should be continuous
Centre edge angle (Wiberg) < 20o indicates dysplasia, ~ 30o is normal

 




Investigation

Clinical examination

U/S:
in the very young (reliable up to the age of 1 year) with 90% sensitivity
Graf pioneered using static measurements taken from coronal scans -described 4 types of hip based on 3 lines and 2 angles:

 

  1. baseline-line
    along outer ilium to the point where perichondrium unites the with the ilium

     

  2. inclination line-
    from the point where the perichondrium unites with the ilium to the acetabular labrum

     

  3. acetabular roof line
    from the lower edge of the ilium at the triradiate cartilage to the point where perichondrium unites with ilium

     

a- between 1 and 2 above
b- between 1 and 3 above

Ref: Boeree and Clarke JBJS 76B:525-533, 1994
a combination of clinical screening and US in 26, 952 infants in Southampton
Pavlik harness treatment in only 4.4/1000
17 cases with risk factors but normal clinical exam identified on US
late presentation rate .22/1000 births

ref: Marks etal JBJS 76B: 534-538, 1994
Routine US screening program of all neonates in Coventry - 14,050 1989-92
no late cases since program began
5 cases with normal clinical exam and no risk factors identified on US
Arthrogram and EUA for delayed or resistant cases (define optimal position for correction ® femoral or acetabular procedure) indicates sphericity of femoral head and congruency with the joint

May need CT to delineate bony anatomy or femoral anteversion and location of uncovered femoral head ® assist in planning osteotomy

 

Classification

Type 1 Developmental - Occur in the perinatal period and respond well
Type 2 Acquired - Neuromuscular origin
infection
Type 3 Teratologic disorders

Based on Presentation:
Early
Late

Classification by degree:
Type 1: Hip stable
Type 2: Hip subluxable
Type 3: Hip dislocatable
Type 4: Hip dislocated

Radiological: (Tonnis)
Type 1: Femoral capital epiphysis medial to Perkins line and below Hilgenreiners line
Type 2: Epiphysis below Hilgenreiners line but lateral to Perkins
Type 3: Epiphysis lateral to Perkins line at the level of the acetabular margin
Type 4: Epiphysis lateral to Perkins line and above the acetabular rim

Classification of AVN in DDH: (Kalamchi)
Grade 1: Involvement of the femoral capital ossific nucleus only due to a transient deficiency of the blood supply ® normal head or slight loss of height
Grade 2: Epiphysis and lateral physis involved ® head in valgus with short lateral portion of neck and lateral growth plate may close prematurely
Grade 3: Epiphysis and central physis involved
Grade 4: Epiphysis and all of physis involved ® coxa breva or coxa vara and trochanteric overgrowth

Differential Diagnosis: (of a painless limp since infancy)
Infantile coxa vara
Pathological dislocation (illness in childhood and X-Ray ® femoral head not there)
Polio-myelitis with evidence of paralysis ® limp

 

Treatment

1: Before weigh bearing
Splint in the safe zone (90o - 120o flexion and half way between full abduction and dislocation, usually about 60o abduction)
Reassess at six weeks and usually splint to three months at which time ® X-Ray
Duration of splintage related to the age at diagnosis, development of the acetabulum and stability of the hip (rough guide splint for twice the age of the patient when splint applied)
If only a dysplastic hip and no frank dislocation six weeks may be enough
Unreducible hips ® pre-operative traction (Pughs)

Adelaide experience with the DB splint ® 2.5% AVN radiologically
Progressive growth deformity occurred in only one of 240 cases

2: After weight bearing (crawling)
Principle is to reduce and hold the hip in the joint until it is stable
Traction may be required to restore normal station of the hip prior to surgery to reduce the risk of AVN (Weinstein ® no difference in AVN rate without traction)
The majority of orthopaedist would use traction and continue for an average of three weeks but the efficacy of pre-operative traction remains questionable
In children older than 3 years traction before open reduction has been reported to produce poorer results than femoral shortening (Schoenecher & Strecker, JBJS 1984)
Continuation of attempts at closed reduction for more than four weeks is very unlikely to succeed and will only accentuate the pathological process
Closed reduction alone ® high incidence of AVN
Examine under anaesthetic and ® arthrogram, may need adductor release and if reduced ® spica for 6/52 - 3/12 and follow with X-Rays

If concentric reduction not achieved or "unsafe" ® open reduction may need derotation femoral osteotomy +/- femoral shortening +/- acetabular procedure (acetabulo-plasty, Salter, etc or shelf)
More than 2 years ® traction ® CR ® open reduction
More than 4 years ® open reduction and femoral shortening
More than 8 years no scope for femoral or acetabular remodelling ® salvage procedures

3. Treatment after Age limit
ie above treatment of the dislocation is unwise over a certain age as complications of treatment outweigh the benefits at this point
Age limit for bilateral dislocation 4 years (lower as the risk of intervention is doubled and partial failure leads to asymmetry)and for unilateral dislocation possibly 6 years and definitely 8 years after which ® salvage procedures
Trochanteric advancement may ® improve gait restore function
Treatment should be completed by the age of 5 years

4. Acetabular dysplasia
1 year old splint as for DDH but after 1 year ® operation if head remains uncovered (femoral, Salter, Chiari or shelf)

Indications for open reduction

  1. Failure to achieve reduction, femoral head persistently above triradiate cartilage or femoral head will not enter acetabulum
  2. Position required to maintain reduction extreme
  3. If arc of reduction and re-dislocation < 20o (small safe zone)
  4. Failed previous reduction
  5. Age: Children> 3 years old generally accepted in association with femoral shortening
  6. Inverted limbus

Reconstruction procedures if;

  1. Continued subluxation or instability
  2. Failure of adequate acetabular development
    Varus rotation osteotomy best done before age of 4 years because of the limited ability of the acetabulum to remodel after this age

After the age of 4 years acetabular procedures are thought to be more effective than femoral
Reconstruction procedures- all redirect acetabulum (except Pemberton)
: medialise- Chiari, Sutherland
: lateralise- Steele ( also decreases abductor distance)

Sutherland- like Salter but also osteotomise through pubic body®� freedom of movement at medial point of rotation

 

Pemberton-
change direction/shape of acetabular roof at triradiate cartilage
must be done in young child so that acetabulum can remodel
risks- � stiffness as distortion of acetabular roof
� acetabular pressure (­ volume of acetabulum
® greater correction esp for those with true acetabular dysplasia

 

Salter-
cover by rotation of acetabulum on symphysis pubis
improves acetabular index by ~10o
lengthens by ~ 1cm ®may need to shorten as well as do varus/derotation

 

Dial-
periarticular acetabular osteotomy- osteotomise outside capsule
risks- vascular damage, sciatic nerve damage

 

Steele-
Great latitude in correction

Salvage procedures
Chiari- described 1955 for acet. dysplasia assoc with DDH
osteotomy just above jt capsule angled 10� up and inward, displace at least 50% of pelvic thickness
complications- cut too high or too low, sciatic n. injury

15 yr follow up-
good result 75%, fair 9%, poor 16%
better result if pt less than 4 yo at operation
adequate medialisation

 

Shelf- (Wilson + Staheli)
allows coverage with congruity, leaves hip lateral

Trochanteric Transfer/ contralat epiphyseodesis
Ref: Porat etal JBJS 76B:463-467, 1994
15 pts with trochanteric relative overgrowth due to prox femoral physeal arrest following treatment for DDH- good results with trochanteric transfer in eliminating limp, can be combined with contralat epiphyseodesis to manage LLD

Complications:
Pavlic harness fails to reduce the hip in as many as 8% of cases
AVN occurs in as many as 2.4% of cases splinted in the safe zone
AVN increased incidence in open procedures with an incidence of ~ 8% for antero-lateral approaches, 10% for inguinal approaches, 17% for the Ludloff (medial) approach and 5% when shortening femoral osteotomy was combined with open reduction.

Salter (1969) indicators of AVN;

  1. Failure of appearance of the ossific nucleus 1 year after reduction
  2. Failure of growth of an existing nucleus 1 year after reduction
  3. Broadening of femoral neck 1 year after reduction
  4. Increased radiographic density of the femoral head followed by radiographic appearance of fragmentation
  5. Residual deformity of head and neck when re-ossification is complete (coxa vara, coxa magna, coxa plana and short broad femoral neck, [coxa breva])

Pre-reduction traction and adductor tenotomy did not decrease the incidence of AVN and abduction into the frog position was the incriminating factor ® compression of vessels of the trochanteric anastomosis and retinacular vessels
Long term growth defect occurred in 0.7%

Prognosis:
Dysplastic acetabulum with CE angle < 20o ® tendency for hip to subluxate ® restricted
abduction and flexion
Estimated that 20 - 50% of degenerate OA is secondary to subluxation of the hip or dysplasia as measured by a reduction in the CE angle
Pavlik harness ® 98% sucess for acetabular dysplasia and 85% success in the treatment of DDH

ref: Malvitz and Weinstein JBJS 76A 1777-1792, 1994
152 dislocated hips in 119 pts , av FU 30 yrs , treated with closed reduction
Hips reduced younger do best
AVN with growth disturbance occurred in 60% - in some did not become obvious for many yrs. The young infant who does get AVN tends to get a more severe form of it, however, the younger infants have a much less chance of AVN
65 hips ( 43% ) had XR evidence of OA
17 hips had THR when pt av age of 36 yrs
Noted that function tended to decrease with time and state that prognosis is guarded for these patients


[ Back to the Top ]



Irritable Hip (Transient Synovitis)

Most common cause of a painful hip in children

 

Incidence

Male : Female 2:1
Average age at onset 5 - 6 years

 

Aetiology

Viral infection probably the most likely (evidence of infective or reactive aetiology - URTI within 2 week period prior to onset in 70%)
Allergic reaction
Trauma

 

Clinically

Usually present with painful limp of acute or insidious onset
Child rarely appears ill and is usually afebrile
All movements are limited ® discomfort
Irritability subsides quickly

X-Rays:
Normal
Exclude Perthes disease

Investigations:
Need to exclude infection ® ESR, CRP, WCC and ? bone scan
ESR usually normal or minimally elevated
Fluid aspiration of the joint ® appears turbid but is sterile on culture

 

Differential Diagnosis

Must rule out sepsis
Slipped epiphysis
Perthes disease
Inflammatory arthritis (pauciarticular rheumatoid)
Early TB

 

Prognosis

? prerequisite to Perthes disease
1% of Perthes patients present with a transient synovitis of this type

 

[ Back to the Top ]



Perthes Disease

Osteonecrosis of the proximal femoral epiphysis in a growing child caused by poorly understood non genetic factors
Reported by Legg (USA, 1909), Calve (France, 1910) and Perthes (Germany, 1910)
Waldenstrom (1906) reported the features but related them to TB
Phemister (1920) described pathology of necrotic bone

 

Incidence

Male : Female 4:1
Onset usually 2 - 12 (the majority are 4 - 8 and mean 7 years)
~ 10 - 12% are bilateral
Birth weight usually lower than normal children
Skeletal age often delayed

 

Aetiology

Familial incidence ? and increased incidence in lower socioeconomic groups
Associated with delayed bone age and shorter children
? Disproportionate growth and abnormalities in skeletal growth, ? abnormal somatomedin levels ( raised somatomedin A)

 

Pathophysiology

Alteration in blood supply to femoral head with foetal supply from metaphyseal vessels, lateral epiphyseal vessels running in the retinaculum up the neck and small supply from the ligamentum teres
Metaphyseal supply gradually decreases (by the age of 4) vessels in the ligamentum teres are not developed until about the age of 7 and between the age of 4 and 7 blood supply to the head may depend solely on lateral epiphyseal vessels which are susceptible to external pressure from an effusion
Aetiology ? related to retinacular vessel occlusion, increased intra-capsular pressure, intra-epiphyseal thrombosis, vascular irregularities or increased vascularity
Kemp et al (1971) showed an effusion in the hip can ® decreased blood supply and ischaemia of the femoral head
Effusion may be enough to tip the balance in susceptible individuals
Repeated episodes are necessary to result in AVN of the bone and increased severity of disease may reflect increased number of ischaemic events

Salter and Thompson:
AVN of femoral head
Temporary cessation of growth of epiphysis
Revascularisation from periphery
Resorption of avascular bone & production of woven bone
Pathological #
Resorption of underlying bone and replacement by biologically plastic (woven) bone
Subluxation
Deformity

 

Pathology

Pathological stages ® 2 - 4 years to complete

Stage I: (Ischaemia)
All or part of the bony femoral head dies at which time the X-Ray remains normal
The head stops enlarging but the cartilage still nourished by diffusion continues to grow ® increased apparent joint space
Cessation of growth lasts 6 - 12 months

Stage II: (Resorption)
Trabeculae in dead bone may fracture in subchondral region ® tangential line
New bone layed down on dead trabeculae ® increased density
Hyperaemia and re-vascularization ® bone resorption ® head becomes rarefied / cystic
Resorption usually complete by 12 - 17 months

Stage III: (Resolution / recalcification)
If repair / re-vascularization has been rapid the head may maintain its shape
The head may collapse ® further flattening / fragmentation
Abnormal stresses transmitted to the growth plate may ® distort or ® growth arrest
Lateral portion of head often becomes uncovered
Normal bony architecture will return but alteration in shape persists ® early degenerative changes
Resolution usually 6 - 24 months ® heal or residual deformity
As the physis is nourished by the epiphysis AVN of the epiphysis also ® AVN of the physis to some extent ® growth arrest or retardation. There is a direct correlation bw severity of physeal involvement and deformity of the head
Coxa magna secondary to premature physeal arrest and hypertrophy of epiphyseal cartilage
The clinical picture varies depending on the age of the child, the stage of the disease and the amount of head involved

 

Clinically

Limp often painless and intermittent
Pain usually in the groin, inner thigh but may ® knee
LLD averages 2.14cm
Limitation of abduction (hinge abduction) particularly in flexion

 

Investigations

AP and lateral (Lauenstein) plain XRs
Bone scan-
helpful in early stages of disease when diagnosis is in doubt
not of use in determining extent of involvement and hence prognosis
MRI-
Very sensitive in detecting infarction- role yet to be determined
Arthrography
best position to splint the leg ie position of containment
planning for osteotomy

X-Rays
Head at risk signs:

  1. Prolonged decrease ROM
  2. Whole of head involved
  3. Lateral subluxation of head (head partially uncovered)
  4. Calcification lateral to epiphysis
  5. Metaphyseal change
  6. Gage's sign (Radiolucency in the lateral epiphysis and metaphysis)

Relative overgrowth of greater trochanter and coxa breva
Hanging rope sign characteristic of old Perthes

Classification

Disease must reach the fragmentation and collapse phase before it can be classified and there is large inter-observer variation
Catterall:
Stage 1:
Antero-medial portion of head involved and no collapse, metaphyseal changes do not occur and the epiphyseal plate is not involved
Heal without significant sequelae

 

Stage 2:
More head involved and may ® fragmentation of the involved segment
The involved segment shows increased density and uninvolved pillars of normal bone prevent significant collapse ® regeneration without much loss of height and the end result is usually good. Metaphyseal reaction localised

 

Stage 3:
More of the head involved ® collapse as uninvolved pillars not large enough t prevent collapse
May show head within a head
The metaphysis is usually diffusely involved ® broad neck and the epiphyseal plate is unprotected and also usually involved ® results poorer

 

Stage 4:
Whole head involvement and severe collapse occurs early and restoration of the femoral head usually less complete

The metaphyseal changes may be extensive
The epiphyseal plate is often involved ® abnormal growth (coxa magna, coxa breva, coxa vara and coxa valga)

Salter - Thompson:

Stage A:
Lateral portion of femoral capital epiphysis present
(Catterall 1 & 2) less than 50% head involved

 

Stage B:
Lateral portion of femoral capital epiphysis absent
(Catterall 3 & 4) more than 50% head involved
(Lateral margin of epiphysis protects epiphysis from stress)

Ponseti:
Those with less than 50% of head involvement
Those with more than 50% of head involvement

Herring
note that interobservor agreement is best with the Herring classification
Femoral head on the AP radiograph is divided into 3 parts with the lateral pillar occupying the lateral 15 - 30%, the central pillar ~ 50% and the medial pillar 20 - 35%

 

Group A:
No involvement of the lateral pillar but there may be lucency and collapse in the central and medial pillars

 

Group B:
Greater than 50% of lateral pillar height maintained

 

Group C:
Less than 50% of lateral pillar height maintained

 

Differential Diagnosis

Morquios
Cretinism
Multiple epiphyseal dysplasia
Sickle cell disease
Gauchers disease
Traumatic AVN
Infection

 

Treatment

Treatment is controversial but the aim is for resolution of symptoms and a spherical, well covered femoral head

 

Resolution of symptoms
Bed rest while hip irritable with skin traction
Partial weight bearing on crutches
Use of NSAIDS

Treatment with prolonged bed rest and immobilisation does not change the radiological course of the disease

Options for longer term treatment are:

  1. Supervised neglect ® activities as tolerated with regular checks and if recurrence ® RIB
  2. Containment in abduction splint or broomstick plasters or operative ® osteotomy of femur or pelvis

Treatment by Catterall stage: (Apley)

Stage I:
No treatment needed
Stage II & III:
No treatment needed if less than 7 years of age unless head at risk signs present
Aged more than7 years or head at risk signs ® containment for about 6 - 14 months or until signs of recalcification of head
Full range of movement should exist before ® abduction device
Stage IV:
At any age ® containment unless undue force required
Choice between operative and non-operative treatment may not alter natural history of disease
Pelvic or femoral osteotomies ® similar results

 

Treatment recommended by Herring (JBJS 76A 448-458, 1994)

Pt less than 6 yo:
No evidence that any form of treatment alters the growth potential of the physis or the outcome ®\ principle is symptom relief
Pt 6,7 or 8 yo:
All group A and those group B pts with bone age of less than7 yo - no alteration of outcome by treatment ® symptom relief only
Those group B with bone age 7 or over - better outcome with containment - no difference bw method of containment
Those in group C - effect of treatment not known- currently advocates containment
Pt 9 or older: difficult to manage- tend to get more severe disease; do not tolerate bracing well, thus more likely to have surgery over bracing

Gp A - symptomatic only
Gp B+C - advocates containment by whatever means

 

Bracing

Yes or No? - controversial
2 recent studies have concluded that bracing has not changed the natural history of the disease-
1. Meehan et al JBJS 74A 2-12, 1992
2. Martinez etal JBJS 74A 12-21, 1992

How long long to brace?- until definite signs of XR of reossification® wean from brace

 

Treatment of the child with significant femoral head deformity

eg Mose - at least 4 mm out of round should be mainly symptomatic.

Salvage procedures
eg Cheilectomy,chiari osteotomy to cover the femoral head, valgus osteotomy to increase abduction and bring the more normal medial femoral head into the weight bearing area, arthrodesis at about skeletal maturity -should be reserved for pts with severe functional impairment

If need to contain:

  1. Arthrogram - determine if containment can be achieved - determine optimal position
  2. Brace/ POP
  3. Operation if
    a. failure of bracing
    b. nontolerance of brace

 

Prognosis

Clinical determinants:
  1. Increased age at onset ® worse prognosis ( less than 6 do well and more than 10 do poorly)
  2. Females worse than males, increased involvement of the femoral head
  3. Persistent hip irritability with reduction in ROM ® worse prognosis

Radiological determinants:

  1. Extent of head involved- ie grade of disease
  2. At risk factors
  3. Herring (1992):
    1. 100% Stulberg 1 or 2
    2. less than9 yo at onset- 92% Stulberg 1+2, 8% Stulberg 3
      more than9 yo at onset- 30% Stulberg 2, 50% Stulberg 3, 20% Stulberg 4
    3. 29% Stulberg 2, 52% Stulberg 3, 19% Stulberg 4

Mose: (Acta Orthop Scand, supp 169, 1977)

Rings of increasing diameter (2mm)
If head conforms to a single ring in both X-Ray planes ® good prognosis
If head varies from perfect circle by no more than 2mm ® fair results
If head varies by more than 2mm in any plane ® poor results

Stulberg: (JBJS 63A: 1095-1108, 1981)

class 1:
normal hip jt
class 2:
a spherical femoral head but with one or more of -
  1. coxa magna
  2. shorter than normal femoral neck
  3. abnormally steep acetabulum

class 3:
a nonspherical but not flat femoral head (ovoid, mushroom shaped)
abnormalities of acetabulum corresponding to head
class 4:
a flat femoral head - abnormal acetabulum corresponding to head
class 5:
a flat femoral head and a normal neck and acetabulum

Stulbergs results
Spherical congruency (class 1+2)= no risk of OA
Aspherical congruency(class 3+4)= mild-mod OA in late adulthood
Aspherical incongruency (class 5)= severe OA before age 50

These results showed that lack of sphericity alone was not the only predictor of a poor outcome (cf Mose)

As many as 50% do well without treatment and most of the remaining 50% do well into the 5th decade despite CE angles less than 20o and Mose sphericity more than 2mm out of round
? contained head ® altered disease / prognosis at 50 years
No follow up study of sufficient length to show containment has altered the natural history of the condition

 

[ Back to the Top ]



Slipped Epiphysis

Progressive displacement of the femoral head relative to the neck through an open growth plate

 

Incidence

2 per 100,000 people or 3 - 4 per 100,000 less than 25 years
Male : Female 2.5:1
Mean age for males 13.5 years and females 11.5 years
More common on the left than the right (2:1)
More common in Negroes than Caucasians

 

Aetiology

Risk factors ( Spear, 1982)
1. � physeal ht
2. planar physis
3. � load
4. abnormal physeal inclination
5. defic physeal components

Disorders associated with slipped epiphysis

Endocrine:
Cryptorchidism
Hypothyroidism, Hyperparathyroidism, Hypo-oestrogen states
Adiposogenital syndrome, Acromegaly
Pan-hypopituitarism, Pituitary tumours
Genetic:
Kleinfelters syndrome
Downs syndrome
Marfans disease
Iatrogenic:
Radiation therapy
Chemotherapy
Growth hormone therapy
Metabolic:
Rickets
Renal disease
Osteodystrophy
Other:
Coxa vara
Intracranial tumours

usually occurs just before puberty and may show evidence of endocrine abnormalities

Experiments on rats-
oestrogens � strength of growth plate
GH ­ strength of growth plate
plate strength more thanin female than male; ­ in both sexes about puberty
Familial-
~ 5% of pts with SCFE have parents with evidence of SCFE

 

Theory

Growth hormone ® stimulate growth of the physis ready for the pubertal growth spurt. Sex hormones play a part in converting cartilage to bone. If the sex hormones fail to keep up there is too much un-ossified cartilage unable to resist stress imposed by increased body weight

 

Pathology

Resembles a stress fracture
During growth the proximal femoral epiphysis becomes increasingly more oblique and therefore more liable to displacement following injury
Underlying abnormality suggested by the gradual onset in 70% and as it often occurs bilaterally (20%)
Slip is associated with an increased width of the physis with a reduction in the proportion in the resting zone (60 - 70% decreasing to 15 - 30%) and increased size of the hypertrophic zone (15 - 30% increasing to 60 - 80%) and the slip occurs between the proliferative and hypertrophic zone
NB: growth plate fractures occur between the hypertrophic zone and the zone of calcification
Chondrocytes are often clustered instead of the usual columnar arrangement
Synovitis associated with slipped epiphysis ® immune complex found in the synovial fluid of a good number of cases (? significance)

 

Clinically

70% occur gradually and 30% are acute or acute on chronic
Nearly 50% present with knee or lower thigh pain
Most marked limitation of abduction and internal rotation
May present with an antalgic gait
Classically ® external rotation in flexion
Often a history of hip strain, even in chronic slip (50%) and acute slips may follow a fall
Pain sometimes in the groin but often only thigh and knee but limp occurs early and is more a consistent feature
May be 1 -2cm short (LLD) which is proximal to the greater trochanter
The joint may be irritable and may be Trendelenburg positive
Two thirds are unduly fat, sexually underdeveloped and skeletal age lags behind actual age by as much as 20 months
One third are tall and thin and sexual development normal
Bilat disease is present or develops in 20 - 30% and is commoner with endocrine abnormalities

 

Investigations

U/S can differentiate acute and acute on chronic slips from chronic slips by the presence of an effusion, epiphyseal step and remodelling of the metaphysis and an indication of the degree by the size of the step (Adelaide, 1991)
Acute slips ® pre-operative bone scan to assess vascularity of head prior to treatment and this should be repeated post-operatively
X-Rays
Growth disc wide and woolly on the metaphyseal side
Trethowans sign - Line up superior margin of neck should intersect epiphysis (usually 20% of the femoral head lateral to this line)
Capeners sign -AP view in the normal hip the posterior acetabular margin cuts across the medial corner of the upper femoral metaphysis. With slipping the entire metaphysis is lateral to the posterior acetabular margin

 

 

Classification

Extent or severity:
Minimal
Less than 1/3 or 30o slip angle (~ 56%)
Moderate
Between 1/3 and 2/3 or 30 - 50o slip angle (~ 25%)
Severe
Greater than 2/3 or more than 50o slip angle (~ 19%)

Onset type:

Acute:
Sudden onset of symptoms less than or equal to 2/52 (~ 11%)
Chronic:
Symptoms existing for greater than 2/52 (~ 60%)
Acute on Chronic:
Symptoms for greater than 1/12 with acute (~ 23%) exacerbations
Pre slip:
Widening of epiphyseal plate with no real slip (~ 6%) associate with weakness or ache of the limb with exertion

 

Treatment

Primary:
Fixation in situ- single cannulated screw
Aim is to stabilise the epiphysis against further slipping
In acute and acute on chronic slips reduction should be accomplished by either skeletal traction with internal rotation or gentle manipulation at the time of surgery (contraversial, many would say all should be pinned in situ)
(Update 3) ® restore hip to pre injury position and pin there
Forceful manipulation must be avoided
Chronic slips ® pin in situ
Avoid pinning into supero-lateral quadrant where postero-superior retinacular vessels enter

Secondary:

  1. Manipulation- not in chronic slips
    gentle reduction preceded by traction only in cases of severe acute or acute on chronic slips
    risk is of AVN
  2. Osteotomies
    should be reserved for realignment of the hip after healing of the slipped epiphysis has taken place due to the high incidence of complications when performed acutely. The slip will remodel for several years and the pt will gradually achieve a more normal range of motion due to this- therefore defer osteotomy for at least a year

Dunn intra-capsular neck osteotomy via a lateral approach requires meticulous technique (removal of posterior beak and trimming of the neck, the head is reduced on the neck and then pinned), growth plate must be open and high incidence of AVN (2.5% in chronic slips and greater in acute slips, other results ® increased rate)

Open reduction + osteotomy of the femoral neck should not be performed
Southwick biplane sub-trochanteric osteotomy ® correct s
subsequent deformity in two planes by measuring the slip angle in the AP film and the varus tilt on the lateral film (the difference in the head / shaft angle on the AP and Lateral films from that on the normal side ® size of the biplanar wedge excised). Advantage - far from blood supply of head (low risk AVN).
Disadvantage- less correction as is far from primary deformity; unexplained incidence of chondrolysis following operation

Tertiary (salvage)
not contemplated during adolescence unless complications of AVN or chondrolysis occur and severe functional problems remain despite prolonged conservative management. Include:

  1. Osteotomy- eg for AVN
  2. Arthroplasty- rarely suitable
  3. Arthrodesis- is treatment of choice for unilateral hip destruction in young patients

 

Complications

AVN: incidence decreased by pinning in situ and the use of narrow threaded pins (use only one pin and certainly no more than 2), more common in acute than chronic slips ? related to effusion or haemarthrosis ® increased joint pressure

AVN associated with manipulation of the epiphysis (especially in chronic slips), intra- capsular osteotomies and open reduction of the epiphysis

Incidence of AVN:
25% Moderate and severe slips
4% Mild slips
1.5 - 2% Insitu pinning
20% Closed reduction
27% Open reduction and pinning
33% Femoral neck osteotomies
10% Trochanteric osteotomies

Chondrolysis:
affects about 8%- in vast majority assoc with pin penetration
is more common in females than males and in blacks than whites
® reduced joint space, weight relief may ® restoration of joint space ? but ROM may not return (? only related to perforation of the joint)
® benign form in ~1/3 ® spontaneous resolution
recalcitrant form ® progressive loss of joint space and OA in ~ 2/3
Treatment of chondrolysis ® remove the pin, mobilise the joint and may require capsulotomy and manipulation under anaesthetic

Coxa Vara:
if displacement not reduced, the physis fuses in the deformed position
painless, pt may limp, predisposes to OA
treatment- osteotomy

 

Prognosis

Minor slips:®90% good
Moderate slips:®50% good
Severe slips:®30% good

Osteoarthritis
is inevitable if AVN results
deformity characteristic of old SCFE has been described in ~40% of pts with OA undergoing reconstructive surgery (Murray etal: the aetiology of primary OA of the hip. Br J Radiol 38: 810, 1965). It is thought that in most hips with SCFE, OA will eventually develop.

Bilateral slippage - in up to 25%- not routine to pin prophylactically
( only if specific risk factor eg identifiable endocrinopathy)
ref: Jerre etal JBJS 76B: 563-567, 1994
32 yr FU of 61 pts with unilat SUFE - 41% had evidence of bilat slip

recommend
not to prophylactically pin
3 mthly XR surveillance until maturity

 

[ Back to the Top ]