Avascular necrosis of femoral head

1. AVASCULAR
NECROSIS
JULY 17, 2019
BY DR OLAGUNJU
OLUWAJUWON
FMC BIRNIN KEBBI, NIGERIA

2. OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• ANATOMY
• ETIOLOGY
• PATHOPHYSIOLOGY
• CLINICAL PRESENTATION

3. • STAGING
• DIFFERENTIAL DIAGNOSIS
• TREATMENT
• COMPLICATIONS
• PROGNOSIS
• REFERENCES

4. INTRODUCTION
Avascular necrosis (AVN) is defined as cellular death of bone
components due to interruption of the blood supply; the bone
structures then collapse, resulting in pain, loss of joint function and
long-term joint damage.

5. • AVN usually involves the epiphysis (end part of a long bone), such as
the femoral and humeral heads and the femoral condyles, but small
bones can also be affected.

9. • In clinical practice, AVN is most commonly encountered in the hip.
• Most available data regarding the natural history, pathology,
pathogenesis, and treatment of AVN pertains to femoral head
necrosis.

11. • Avascular necrosis is also called osteonecrosis, aseptic necrosis, and
ischemic bone necrosis.

12. EPIDEMIOLOGY
• The frequency of AVN depends on the site involved.
• The most common site is the hip;
• other locations include the
• carpals, talus, femur, metatarsal, mandible, and humerus.

13. • In the United States, approximately 15,000 new cases of AVN are
reported each year.
• AVN accounts for more than 10% of total hip replacement surgeries
performed in the United States.

14. • Osteonecrosis of the jaw associated with bisphosphonate has also
been well studied and reported.
• Most patients with osteonecrosis of the jaw also had an ongoing
malignancy and/or had undergone a recent dental procedure.

15. • In most countries, the incidence and prevalence of AVN are not well
reported.

16. • AVN has no racial predilection except for cases associated with sickle
cell disease and hemoglobin S and SC disease, which predominantly
occur in people of African and Mediterranean descent.

17. • With the exception of AVN associated with systemic lupus
erythematosus, AVN is more common in men, with an overall male-
to-female ratio of 8:1.
• AVN is a disease of middle age that most often occurs during the
fourth or fifth decade of life and is bilateral in more than half of
cases.

18. • When it occurs in children at the femoral head, it is known as Legg-
Calve-Perthes syndrome.
• The use of high-dose corticosteroids carries a reported 3-20%
incidence of AVN.

19. ANATOMY

25. ETIOLOGY
• AVN may be primary or idiopathic.
• For AVN that is secondary or associated with an underlying condition
or exposure, the following factors have been identified:
• Systemic corticosteroid use or Cushing disease [12]
• Trauma
• Alcohol abuse

26. • Systemic lupus erythematosus (with or without antiphospholipid syndrome),
as well as other connective-tissue diseases
• Hemoglobinopathies or hemophilic disorders (eg, sickle cell disease,
hemophilia A or B)
• Osteoporosis medications (ie, bisphosphonates, denosumab)

27. • Hyperlipidemia
• Bone disorders (slipped capital femoral epiphysis, congenital dysplasia of the
hip, Legg-Calve-Perthes disease)
• HIV infection
• Renal Transplantation

28. • Allogeneic bone marrow transplantation
• Radiation therapy
• Gaucher disease
• Malignancy (marrow infiltration, malignant fibrous histiocytoma)

29. • Caisson disease (uncommon diving-related decompression illness)
• Pregnancy
• Psoriasis
• Inflammatory bowel disease

30. • Prolonged, repeated exposure to high pressure (as experienced by
commercial and military divers) has been linked to AVN, though the
relationship is not too well understood.

31. PATHOPHYSIOLOGY
• Although the pathophysiology of AVN is not fully understood, the
final common pathway is interruption of blood flow to the bone.
• AVN often affects bones with a single terminal blood supply, such as
the femoral head, carpals, talus, and humerus.

32. • The earliest pathologic characteristics of osteonecrosis are necrosis of
hematopoietic cells and adipocytes followed by interstitial marrow
edema.
• Osteocyte necrosis occurs after approximately 3 hours of anoxia, but
histological signs of osteocyte death do not appear until
approximately 24 to 72 hours after oxygen deprivation.

33. • Interruption of the vascular supply and resultant necrosis of marrow,
medullary bone, and cortex are theorized to be caused by the
mechanisms listed below.
• However, individual patients usually have more than one risk factor;
this indicates that the pathogenesis of AVN is likely multifactorial.

34. • Vascular occlusion:
• This is characterized by the interruption of the extraosseous blood supply via
factors such as direct trauma (eg, fracture, dislocation), nontraumatic stress,
and stress fracture.

35. • Altered lipid metabolism:
• Animal studies have led to the hypothesis that increased levels of serum lipids
leads to lipid deposition in the femoral head, causing femoral hypertension
and ischemia.
• Lipid-level–lowering drugs in animals reverse this process. Corticosteroid
administration was associated with fat emboli in the femoral heads of rabbits.

36. • Intravascular coagulation:
• Disorders of the coagulation system have been implicated in the pathogenesis
of AVN.
• Typically, it is a secondary event triggered by a familial thrombophilia,
hypercholesterolemia, allograft organ rejection, other disorders (e.g,
infection, malignancy), or pregnancy.

37. • Healing process:
• Necrotic bone triggers a process of repair that includes osteoclasts,
osteoblasts, histiocytes, and vascular elements.
• Osteoblasts build new bone on top of the dead bone, leading to a thick scar
that prevents revascularization of the necrotic bone, with resultant abnormal
joint remodelling and joint dysfunction.

38. • Primary cell death:
• Osteocyte death without other features of AVN has been seen in renal
transplant patients, as well as in patients receiving steroids and those who
consume significant amounts of alcohol.

40. CLINICAL PRESENTATION
• Avascular necrosis (AVN) may be asymptomatic and is occasionally
discovered incidentally on radiographs.
• Symptoms depend on the affected joint.
• Medullary infarcts are usually silent, and infarcts of the small bones of the
hands and feet are often symptomatic.

41. • Pain in the affected joint is typically the presenting symptom of AVN,
regardless of the location.
• Patients with AVN of the femoral head often report groin or
anterior thigh pain that is exacerbated by weight bearing.

42. • The pain may initially be mild but progressively worsens over time
and subsequently may be present at rest or at night.
• Large infarcts, such as those due to Gaucher disease and
hemoglobinopathies, are associated with very severe pain.

43. • Initially, the physical examination findings of AVN may be unrevealing.
• Abnormal physical findings depend on the location and severity of disease.
• With progression of AVN of the hip, joint function deteriorates and the
patient may walk with a limp.

44. • AVN of smaller, non–weight-bearing joints typically does not cause
significant disability.
• Findings may include the following:
• Patients with AVN may have tenderness around the affected bone.
• Both active and passive joint movements may be restricted and painful.

45. • A neurologic deficit may be present if a nerve is affected (compressed)
because of necrosis and compression deformity of affected bones.
• Advanced AVN can result in joint deformity and muscle wasting.

46. STAGING
• The French orthopedic surgeon Paul (RP) Ficat (1917-1986) in
association with Professor Jacques Arlet devised a system of staging
idiopathic avascular necrosis of femoral head in the late 1970s based
on two fundamental concepts :

47. • a standard radiograph shows only the shadow of the mineralized
portion of a bone
• bone necrosis is the end result of severe and prolonged ischemia

53. • stage 0
• plain radiograph: normal
• MRI: normal
• clinical symptoms: nil

54. • stage I
• plain radiograph: normal or minor osteopenia
• MRI: edema
• bone scan: increased uptake
• clinical symptoms: pain typically in the groin

55. • stage II
• plain radiograph: mixed osteopenia and/or sclerosis and/or
subchondral cysts, without any subchondral lucency (crescent sign:
see below)
• MRI: geographic defect
• bone scan: increased uptake
• clinical symptoms: pain and stiffness

56. • stage III
• plain radiograph: crescent sign and eventual cortical collapse
• MRI: same as plain radiograph
• clinical symptoms: pain and stiffness +/- radiation to knee and limp

57. • stage IV
• plain radiograph: end-stage with evidence of secondary degenerative
change
• MRI: same as plain radiograph
• clinical symptoms: pain and limp

58. DDX
• Inflammatory synovitis
• Complex regional pain syndrome
• Osteoarthritis
• Soft tissue trauma (e.g., Labral tear)
• Osteomyelitis
• Neoplastic bone conditions
• Osteoporosis

59. DIAGNOSTICS
• No laboratory test findings specifically suggest or confirm the
presence of avascular necrosis (AVN).
• Plain radiographic findings are unremarkable in early stages of AVN.

60. • Nevertheless, the American College of Radiology (ACR) considers x-
ray of the pelvis and hips the most appropriate initial imaging study in
patients at risk for AVN who present with hip pain.

62. • If radiographs are normal or show femoral head lucencies suspicious
for osteonecrosis, magnetic resonance imaging (MRI) of the hips
without contrast is most appropriate.

66. • The ACR advises that MRI is the most sensitive and specific imaging
modality for diagnosis and provides optimal evaluation of the
likelihood of articular collapse.

67. • Additional ACR recommendations include the following :
• Contrast-enhanced MRI may be needed to detect early osteonecrosis of the
hip in pediatric patients, which is indicated by hypoperfusion
• In patients with a contraindication for MRI, alternative imaging modalities are
computed tomography (CT) or bone scintigraphy with single-photon emission
CT (SPECT).

68. • Histology is the criterion standard for diagnosis of AVN.
• However, bone biopsy is not routinely performed because of the
availability of sensitive noninvasive tests such as MRI.

69. TREATMENT
• MEDICAL
• Medical management of avascular necrosis (AVN) primarily depends
on the location and severity of disease, as well as the patient's age
and general health.
• Treatment outcomes correlate directly with the stage of the disease.
• No medical treatment has proven effective in preventing or arresting
the disease process.

70. • Conservative measures include
• limited weight bearing with crutches and pain medications.
• This may be beneficial and is a reasonable initial course of action if the
involved segment is smaller than 15% and far from the weight-bearing region.
Immobilization may be helpful in some cases (eg, AVN of the distal femur or
tibia). In advanced AVN, the disease course is unaffected by activity and will
eventually require surgery.

71. • Treatment with bisphosphonates may be helpful.
• Iloprost, a vasoactive prostaglandin analog that is approved for
inhalational treatment of pulmonary hypertension, has shown clinical
and radiographic benefits in early-stage AVN when administered
intravenously.

72. • Statin therapy to prevent corticosteroid-induced AVN may be helpful.
• Extracorporeal shockwave therapy (ESWT) has shown beneficial
effects in early AVN of the femoral head.
• ESWT may relieve pain and improve hip function of the hip, and
induce regression of AVN.
• ESWT may be combined with alendronate therapy.

73. • SURGICAL MANAGEMENT
• Several surgical procedures have been used in an attempt to treat AVN,
with variable success.
• No surgical procedure is the consensual best among surgeons in the
treatment of AVN.

74. • In early stages of AVN (precollapse), core decompression with or
without bone graft is typically considered the most appropriate
treatment.
• In late stages, characterized by collapse, femoral head deformity, and
secondary osteoarthritis, total hip arthroplasty is the most
appropriate treatment.

75. Core decompression
• Researchers postulate that core decompression improves circulation
by decreasing intramedullary pressure and preventing further
ischemia and progressive joint destruction.
• The best results are obtained when treating patients with early AVN
(precollapse).
• Core decompression is also effective for pain control.

77. Bone graft
• Bone graft options include structural cortical or medullary bone graft
and vascularized bone graft with either a muscle-pedicle bone graft or
free vascularized fibular graft.

78. • Bone grafting is combined with the following:
• Core decompression, which may interrupt the cycle of ischemia
• Excision of sequestrum, which may inhibit revascularization of the femoral
head
• Period of limited weight bearing

81. OSTEOTOMY
• Several osteotomy procedures have been tried with variable success.
• Intertrochanteric osteotomies have been performed in patients with
posttraumatic AVN.

83. Total hip arthroplasty
• Most patients with advanced disease (stage III and above) require
total hip arthroplasty.
• Total hip arthroplasty provides excellent pain relief for many years,
although most young patients require repeat surgery.
• high failure rates (10-50% after 5 years), patients with AVN will
probably need a second total hip arthroplasty during their lifetime.

85. Cell therapy
• The use of stem cells implanted via core decompression has been
studied for the treatment of early-stage (precollapse) AVN of the
femoral head.

86. • Systematic reviews of studies with patient-reported outcomes have
demonstrated clinical benefit with the use of stem cells for hip AVN,
with a low rate of complications, but have highlighted the lack of
standardization with this technique.

87. COMPLICATIONS
• The natural history of AVN involves subchondral necrosis,
subchondral fracture and collapse of bone, deformity of the
articular surface, and osteoarthritis.
• In later stages, sclerosis and total destruction of the joint may occur.
• Nonunion of fracture and secondary muscle wasting are potential
complications.

88. PROGNOSIS
• The prognosis of AVN depends on the disease stage at the time of
diagnosis and the presence of any underlying conditions.
• More than 50% of patients with AVN require surgical treatment
within 3 years of diagnosis.
• Half of patients with subchondral collapse of the femoral head
develop AVN in the contralateral hip.

89. • Poor prognostic factors include the following:
• Age older than 50 years
• Advanced disease (stage 3 or worse) at the time of diagnosis
• Necrosis of more than one third of the weight-bearing area of the femoral
head on MRI

90. • Lateral involvement of femoral head (compared with medial lesions)
• Non-modifiable risk factors such as cumulative dose of corticosteroids
(corticosteroid-induced AVN)

91. CONCLUSION
• Clinical and MRI characteristics need to be evaluated for the critical
diagnosis of ONFH.
• The progression of ONFH has not been well established, therefore it is
difficult to evaluate whether a specific treatment modality changes
the natural course of the disease.

92. • Medical treatment outcomes correlate directly with the stage of the
disease.
• No medical treatment has proven effective in preventing or arresting
the disease process.

93. • Most patients with advanced disease (stage III and above) require
total hip arthroplasty.

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98. THANK YOU FOR LISTENING