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ms 1 - 2nd shift > hip clinical conditions part 1 (bursitis to SCFE) > Flashcards

hip clinical conditions part 1 (bursitis to SCFE) Flashcards

1
Q

between iliopsoas and iliopectineal eminence

communicates with joint cavity

A

Iliopectineal or Iliopsoas bursitis

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2
Q

Clinical features of Iliopectineal or Iliopsoas bursitis

A

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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3
Q

Differential diagnosis of Iliopectineal or Iliopsoas bursitis

A

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

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4
Q

Bed rest in traction, hot compress

Cellulitis or frank infection necessitates antibiotic treatment
Subsides within several weeks

A

Treatment of Iliopectineal or Iliopsoas bursitis

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5
Q

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

A

Deep trochanteric bursitis

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6
Q

Clinical features of Deep Trochanteric Bursitis

A

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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7
Q

Differential diagnosis of Deep Trochanteric Bursitis

A

septic arthritis hip, osteomyelitis proximal femur

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8
Q

rest and heat
- Hot Packs, ultrasound, NSAIDS

If bursa is infected - antibiotic therapy and possible drainage

A

Treatment of Deep Trochanteric Bursitis

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9
Q

Between GT and skin and subcutaneous tissue

A

Superficial trochanteric bursitis

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10
Q

Clinical features of Superficial trochanteric bursitis

A

Tenderness and swelling over the area of the bursa

Pain on extreme adduction of the hip

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11
Q

same with deep trochanteric bursitis

A

Treatment of Superficial trochanteric bursitis

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12
Q

Located superficial to the ischial tuberosity

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

A

Ischiogluteal bursa

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13
Q

Clinical features of Ischiogluteal bursa

A

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

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14
Q

rest and heat

Use of pillow or cushioned seat to prevent recurrence

Steroid + anesthetic injection (to lessen inflammation)

Excision of bursa if persistent

A

Treatment of Ischiogluteal bursa

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15
Q

results from impairment of the blood supply to the femoral head

A

Osteonecrosis

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16
Q

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

A

Pathology of Osteonecrosis

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17
Q

Etiology of Osteonecrosis

A

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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18
Q

Stages of Osteonecrosis

A

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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19
Q

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

A

Revascularization

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20
Q

process of removal of dead bone and replacement of new bone

A

Creeping substitution

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21
Q

results from a subchondral fracture due to osteoclastic activity

collapse of the entire head causes flattening of the femoral head

A

Crescent sign

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22
Q

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

A

Clinical features of Osteonecrosis

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22
Q

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

A

Treatment of Osteonecrosis for CHILDREN

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23
Q

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

A

Treatment of Osteonecrosis for ADULT

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24
Q

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

A

Legg-Calve Perthes Disease (LCPD)

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25
Q

Characteristics of LCPD

A

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

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26
Q

Etiology of LCPD

A

Not clearly established

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27
Q

injury or disease of the blood supply to the head

increased intra-articular pressure occluding retinacular vessels

extensive metaphyseal changes affecting metaphyseal- epiphyseal vessels

A

Theories of LCPD

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28
Q

Pathology of LCPD

A

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

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29
Q

Clinical features of LCP

A

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

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30
Q

most common sign of LCPD

associated with muscle spasm
with or without
pain worsens as disease progresses

A

Limp

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31
Q

Pain of LCPD is often referred to the

A

knee

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32
Q

Radiographic Stages of LCP

A

Initial stage

Fragmentation stage

Reossification or reparative stage

Remodeling stage

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33
Q

sclerotic, smaller proximal femoral ossific nucleus

A

Initial stage

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34
Q

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

A

Fragmentation stage

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35
Q

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

A

Reossification or reparative stage

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36
Q

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

A

Remodeling stage

37
Q

Self limited with tendency towards spontaneous recovery

A

Prognis of LCPD

38
Q

best prognosis

A

Catterall Group I

39
Q

better chance to recover

A

Younger children

40
Q

Good prognosis of LCPD

A

Catterall Group I (best prognosis)

Younger children (better chance to recover)

Slender than heavier children (move heavy, can be easily broken)

Boys > Girls

41
Q

radiographic changes that indicate poorer prognosis

A

“Head at risk”

42
Q

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

A

Gage’s sign

43
Q

only anterior part of the head is involved, best prognosis

A

Group I

44
Q

1/2 head involved & collapse of central portion

A

Group II

45
Q

Most of head involved, metaphyseal resorption maybe present

A

Group III

46
Q

total head involvement

A

Group IV

47
Q

most important factor in preventing hip deformity

A

Containment of the femoral head within the acetabulum

48
Q

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

A

periodic observation

49
Q

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

Traction

Abduction Brace

A

Non-surgical Treatment for older px of LCPD

50
Q

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

A

Traction

51
Q

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

A

Abduction brace

52
Q

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)

A

Surgical intervention of LCPD

53
Q

AKA Developmental or Infantile Coxa Vara

Usually not detected at birth and becomes
evident as the child begins to walk

A

Congenital Coxa Vara

54
Q

Etiology of Congenital Coxa Vara

A

Congenital or growth defect of the femoral neck

55
Q

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)

A

Clinical features of Congenital Coxa Vara

56
Q

Radiograph Congenital Coxa Vara

A

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

57
Q

Diagnosis of Congenital Coxa Vara

A

Clinical features + Radiographs showing decreased neck shaft angle

58
Q

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

A

Treatment for MILD DEFORMITIES of Congenital Coxa Vara

59
Q

to correct fixed adduction deformity

A

Abduction osteotomy thru the GT or subtroch for Congenital Coxa Vara

60
Q

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

A

Leg Lengthening procedure for Congenital Coxa Vara

61
Q

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

A

Slipped Capital Femoral Epiphysis

62
Q

Types of Slips

A

Acute

Acute Superimposed on Chronic

Chronic

63
Q

least common, symptoms are severe

usually follows severe trauma (fall from a height)

not preceded by significant symptoms

A

Acute Slip

64
Q

mild hip and knee discomfort followed by sudden onset of severe pain and disability

acute symptoms associated with mild trauma (stumbling or tripping)

A

Acute Superimposed on Chronic Slip

65
Q

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

A

Chronic Slip

66
Q

Etiology and Pathology of SCFE

A

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

67
Q

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

A

periosteum

68
Q

Direction of slip of the head SCFE

A

downward and backward on the neck

69
Q

difficult to spot on AP xray because direction of initial displacement to posterior

Lateral view is essential

A

Early slippage

70
Q

determines prognosis

A

determines prognosis

71
Q

widening only of the physis, barely detectable displacement

AKA Pre-slipping

A

Minimal slip

72
Q

displacement between minimal and one third of femoral neck diameter

A

Mild slip

73
Q

1/3 to 1/2 diameter of the neck

A

Moderate slip

74
Q

> 1/2 displacement

A

Severe slip

75
Q

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”

A

Other clinical features of SCFE

76
Q

flexion of the hip accompanied by adduction and ER

A

“Obligatory external rotation

77
Q

Signs of SCFE

A

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

78
Q

Nearly half of pain referred to knee or medial side of thigh - thus often misdiagnosed

Xrays confirm the diagnosis
lateral view is essential

A

Diagnosis of SCFE

79
Q

Differential Dx of SCFE

A

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

80
Q

Complications of SCFE

A

Osteonecrosis

Chondrolysis

Osteoarthritis

81
Q

cartilage necrosis

A

Chondrolysis

82
Q

directly related to severity of the slip

A

Osteoarthritis

83
Q

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

A

Osteonecrosis

84
Q

related to early detection and treatment and the degree of slipping

A

Prognosis

85
Q

Good prognosis of SCFE if

A

slip is treated early, slip is minimal or mild

86
Q

Treatment for ACUTE SCFE

A

Reduction by gradual traction

Manipulation under anesthesia + pinning (using 3 threaded pins) to fix the reduction

87
Q

Treat for > 3 wks duration

A

manipulation should not be attempted, may disrupt retinacular vessels leads to osteonecrosis

pinning in situ

osteotomy at the subtrochanteric region

88
Q

Treatment for mild to moderate slip

A

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

89
Q

Treatment for mild to severe slip

A

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

90
Q

Prophylactic pinning indicated for

A

high risk patients (younger age, very obese male)

91
Q

treatment for obese patients

A

Weight reduction

Monitoring of opposite hip since bilaterality is common

ms 1 - 2nd shift (13 decks)

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