hip clinical conditions part 1 (bursitis to SCFE) Flashcards by JOANN ENRICKE BALBOA

between iliopsoas and iliopectineal eminence

communicates with joint cavity

Iliopectineal or Iliopsoas bursitis

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Clinical features of Iliopectineal or Iliopsoas bursitis

tenderness over anterior hip at the middle of inguinal ligament

Hip held in flexed, abducted and ER (action of iliopsoas)

Extending, adducting and IR the hip elicits pain

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Differential diagnosis of Iliopectineal or Iliopsoas bursitis

Femoral hernia, psoas abscess (pain in psoas in posterior), synovitis and septic arthritis

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Bed rest in traction, hot compress

Cellulitis or frank infection necessitates antibiotic treatment
Subsides within several weeks

Treatment of Iliopectineal or Iliopsoas bursitis

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Behind greater trochanter and in front of tendinous portion of gluteus maximus

Deep trochanteric bursitis

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Clinical features of Deep Trochanteric Bursitis

Tenderness behind greater trochanter

LE held in abducted and ER position to relax the tension from gluteus maximus and bursa

Pain may radiate to back of thigh

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Differential diagnosis of Deep Trochanteric Bursitis

septic arthritis hip, osteomyelitis proximal femur

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rest and heat
- Hot Packs, ultrasound, NSAIDS

If bursa is infected - antibiotic therapy and possible drainage

Treatment of Deep Trochanteric Bursitis

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Between GT and skin and subcutaneous tissue

Superficial trochanteric bursitis

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Clinical features of Superficial trochanteric bursitis

Tenderness and swelling over the area of the bursa

Pain on extreme adduction of the hip

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same with deep trochanteric bursitis

Treatment of Superficial trochanteric bursitis

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Located superficial to the ischial tuberosity

AKA weaver’s bottom (develops in tailors, boatmen - occupation necessitates prolonged sitting on hard surfaces)

Ischiogluteal bursa

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Clinical features of Ischiogluteal bursa

Tenderness over the ischial tuberosity
Pain radiates down the posterior thigh mimicking a herniated disc

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rest and heat

Use of pillow or cushioned seat to prevent recurrence

Steroid + anesthetic injection (to lessen inflammation)

Excision of bursa if persistent

Treatment of Ischiogluteal bursa

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results from impairment of the blood supply to the femoral head

Osteonecrosis

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It may involve entire head (Total) or incomplete (spotty distribution or limited to one segment of the femoral head)

Pathology of Osteonecrosis

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Etiology of Osteonecrosis

Trauma to the major blood vessels supplying the femoral head

Impairment of circulation occurring in small vessels and sinusoids of the femoral head

Idiopathic

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Stages of Osteonecrosis

Degeneration and disappearance of osteocytes from their lacunae is seen in the bone trabeculae

Marked hyperemia of tissues adjacent to the infarct

Revascularization

Osteoclastic resorption of dead trabeculae and osteoblastic repair with new bone occurs

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invasion of the infarcted area by new blood vessels and young connective tissue

Revascularization

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process of removal of dead bone and replacement of new bone

Creeping substitution

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results from a subchondral fracture due to osteoclastic activity

collapse of the entire head causes flattening of the femoral head

Crescent sign

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Signs and symptoms vary
Children
limp and slight spasm of the hip are the first manifestations
Pain referred to thigh or knee on weight bearing
Pain worse on standing and walking, relieved by rest
Atrophy (hip or thigh muscles)
Limited Abduction and internal rotation

Clinical features of Osteonecrosis

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protect the hip joint in abduction until reconstitution (healing) of the head is complete

Treatment of Osteonecrosis for CHILDREN

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surgery often needed (give cane or crutch to lessen weight)

core decompression
derotation osteotomy
arthrodesis (joint fusion)
arthroplasty (joint replacement) - treatment of choice in older less active patients

Treatment of Osteonecrosis for ADULT

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idiopathic form (unknown cause) of osteonecrosis in children AKA Coxa Plana as osteonecrosis often results in flattening of the head Previously thought to be tuberculosis of the hip

Legg-Calve Perthes Disease (LCPD)

Characteristics of LCPD

Age: 3-12 years old (majority < 7 yo) Boys, young thin and short (80%) > Girls Unilateral (85%) > Bilateral Short stature No evidence of being hereditary but occasionally more than 1 family member is affected

Etiology of LCPD

Not clearly established

injury or disease of the blood supply to the head increased intra-articular pressure occluding retinacular vessels extensive metaphyseal changes affecting metaphyseal- epiphyseal vessels

Theories of LCPD

Pathology of LCPD

Self limited over a period of 2-3 years Necrosis of the bone and marrow of the epiphysis Severe involvement may involve physis causing growth disturbance - leads to a broad and short femoral neck - If it affect epiphyseal plate, poorer chance of recovery

Clinical features of LCP

Limp Pain Limited hip abduction and IR Atrophy of hip, thigh and leg muscles Thickening of joint capsule which becomes palpable posteriorly as having a boggy feel OA is a late complication

most common sign of LCPD associated with muscle spasm with or without pain worsens as disease progresses

Limp

Pain of LCPD is often referred to the

knee

Radiographic Stages of LCP

Initial stage Fragmentation stage Reossification or reparative stage Remodeling stage

sclerotic, smaller proximal femoral ossific nucleus

Initial stage

segmental collapse (resorption) of the capital femoral epiphysis follows, with increased density of the epiphysis

Fragmentation stage

necrotic bone is resorbed with subsequent reossification of the capital femoral epiphysis

Reossification or reparative stage

remodeling begins when the capital femoral epiphysis is completely re-ossified

Remodeling stage

Self limited with tendency towards spontaneous recovery

Prognis of LCPD

best prognosis

Catterall Group I

better chance to recover

Younger children

Good prognosis of LCPD

Catterall Group I (best prognosis) Younger children (better chance to recover) Slender than heavier children (move heavy, can be easily broken) Boys > Girls

radiographic changes that indicate poorer prognosis

“Head at risk”

Defect or lytic area at the lateral border of the epiphysis with underlying metaphyseal resorption

Gage’s sign

only anterior part of the head is involved, best prognosis

Group I

1/2 head involved & collapse of central portion

Group II

Most of head involved, metaphyseal resorption maybe present

Group III

total head involvement

Group IV

most important factor in preventing hip deformity

Containment of the femoral head within the acetabulum

Non-surgical treatment for children under 4 yo with partial involvement

periodic observation

relief from deforming forces of weight bearing, muscular tension and subluxation must be done Traction Abduction Brace

Non-surgical Treatment for older px of LCPD

in early stages, for 1-2 weeks when spasm subsides

Traction

maintains hip in abduction and slight internal rotation to keep the femoral physis completely within the acetabulum, for 1-2 years

Abduction brace

reserved for hips with poor prognosis (i.e older than 6 yo, total or near total head involvement) Varus osteotomy at the subtrochanteric level Tilting acetabulum laterally (Salter innominate osteotomy)

Surgical intervention of LCPD

AKA Developmental or Infantile Coxa Vara Usually not detected at birth and becomes evident as the child begins to walk

Congenital Coxa Vara

Etiology of Congenital Coxa Vara

Congenital or growth defect of the femoral neck

Painless waddling gait if bilateral affectation, if unilateral patient lurches to affected side Trendelenburg test (+) due to inefficient gluteus medius action Abduction and internal rotation limited, while adduction and external rotation is increased Prominent greater trochanter on palpation Leg length shortening of 2-4cm (shortening depends on the extent of depression of the head and neck relative to the shaft)

Clinical features of Congenital Coxa Vara

Radiograph Congenital Coxa Vara

Decreased neck shaft angle triangular area of bone in the lower side of the neck close to the head inverted Y ossification defect upward prominence of the GT and proximal shaft

Diagnosis of Congenital Coxa Vara

Clinical features + Radiographs showing decreased neck shaft angle

protected weight bearing is adequate but must be followed up regularly to detect progression

Treatment for MILD DEFORMITIES of Congenital Coxa Vara

to correct fixed adduction deformity

Abduction osteotomy thru the GT or subtroch for Congenital Coxa Vara

equalize the leg length in children with unilateral involvement and residual leg length discrepancy even after osteotomy

Leg Lengthening procedure for Congenital Coxa Vara

Obese children 10-16 yo less common in tall and thin children Boys > Girls average age of onset is about 2 years earlier in girls than boys coinciding with the earlier bone maturation in girls Bilateral in 25% of cases History of trivial trauma or strain

Slipped Capital Femoral Epiphysis

Types of Slips

Acute Acute Superimposed on Chronic Chronic

least common, symptoms are severe usually follows severe trauma (fall from a height) not preceded by significant symptoms

Acute Slip

mild hip and knee discomfort followed by sudden onset of severe pain and disability acute symptoms associated with mild trauma (stumbling or tripping)

Acute Superimposed on Chronic Slip

gradual onset slowly increasing symptoms for weeks to months no history of trauma symptoms often mild, aching, fatigue and feeling of stiffness after standing or walking limp (with a gait pattern/leg length discrepancy) early diagnosis often missed as pain is frequently referred to the knee

Chronic Slip

Etiology and Pathology of SCFE

Unknown Combination of rapid growth, obliquity of physis and minor trauma Endocrinopathies Head slips at the epiphyseal plate due to disruption in the hypertrophic zone Direction of slip of the head: downward and backward on the neck

important stabilizer of the physis thins out during adolescence and yields to shear forces associated with increased body weight and a vertical slope of the physis

periosteum

Direction of slip of the head SCFE

downward and backward on the neck

difficult to spot on AP xray because direction of initial displacement to posterior Lateral view is essential

Early slippage

determines prognosis

widening only of the physis, barely detectable displacement AKA Pre-slipping

Minimal slip

displacement between minimal and one third of femoral neck diameter

Mild slip

1/3 to 1/2 diameter of the neck

Moderate slip

> 1/2 displacement

Severe slip

Diagnosis should be suspected in any adolescent with limp accompanied by hip or knee discomfort with restriction of internal rotation Affected limb gradually becomes shorter and smaller ROM especially IR and abduction is restricted “Obligatory external rotation”

Other clinical features of SCFE

flexion of the hip accompanied by adduction and ER

“Obligatory external rotation

Signs of SCFE

Widening of epiphyseal line Displacement of the neck upward and forward on the head Remodeling causes neck to be bowed or curved → results in a form of coxa vara

Nearly half of pain referred to knee or medial side of thigh - thus often misdiagnosed Xrays confirm the diagnosis lateral view is essential

Diagnosis of SCFE

Differential Dx of SCFE

LCPD, Congenital coxa vara, RA, fractures and tuberculous infection

Complications of SCFE

Osteonecrosis Chondrolysis Osteoarthritis

cartilage necrosis

Chondrolysis

directly related to severity of the slip

Osteoarthritis

slipping itself after attempts of reduction of a chronic slip after surgical correction at the proximal neck

Osteonecrosis

related to early detection and treatment and the degree of slipping

Prognosis

Good prognosis of SCFE if

slip is treated early, slip is minimal or mild

Treatment for ACUTE SCFE

Reduction by gradual traction Manipulation under anesthesia + pinning (using 3 threaded pins) to fix the reduction

Treat for > 3 wks duration

manipulation should not be attempted, may disrupt retinacular vessels leads to osteonecrosis pinning in situ osteotomy at the subtrochanteric region

Treatment for mild to moderate slip

pinning in situ (pinning is temporary, can be removed eventually)

Treatment for mild to severe slip

osteotomy at the subtrochanteric region corrects the ER, adduction and extension deformities

Prophylactic pinning indicated for

high risk patients (younger age, very obese male)

treatment for obese patients

Weight reduction Monitoring of opposite hip since bilaterality is common