Avascular necrosis of femoral head

Overview
Introduction Anatomy Epidemiology Etiology & risk factors Pathology Pathophysiology Diagnosis Classification & staging Treatment

Introduction
Common cause of musculoskeletal disability Major diagnostic and therapeutic challenge. Accounts for 5-10% of THR No universally satisfactory therapy inspite of early diagnosis by MRI Early diagnosis have impact on prognosis

History
Konig first described the condition in 1888 In 1925, Haenish - first case of idiopathic ischemic necrosis of the femoral head In 1940, arterial occlusion postulated as the cause AVN following steroid therapy described first by Pietrograndi in 1957

Anatomy

Etiology
Idiopathic Traumatic

Non-traumatic
Genetic Environmental

Etiology
Traumatic
Common cause of AVN Can occur within 8 hours Damage to superior retinacular vessels, nutrient artery, artery of the ligamentum teres Intracapsular hematoma tamponade effect Hip dislocation Fracture neck femur

Etiology
Non traumatic
Steroid Alcohol Haemoglobinopathies Dysbarism Gaucher disease Irradiation Metastatic disease Pancreatic disease Dialysis Hemophilia Hypercoagulable states Legg-Calv-Perthes (LCP) disease Slipped capital femoral epiphysis Congenital dislocation of the hip Fatty liver

Epidemiology
Morbidity Severe joint destruction-- 3 years following diagnosis in 50% of patients Head collapse -- 2 years after development of hip pain Race SCD- African American population Beta thalassemia Southern Europeans and Southeast Asians.

Sex- M : F

4:1

Age third-to-fifth decades

Frequency
Incidence
15,000 cases per year Bilateral in 30-70% of patients at the time of initial presentation Incidence by associated conditions Trauma
Transcervical and subcapital fractures - 11-45% Displaced femoral head fractures (27-30%) undisplaced fractures (16%) Posterior femoral head dislocation - 10-26% Anterior femoral head dislocation - 3-9% Dislocation longer than 12 hours - 52% Dislocated hips reduced within 12 hours - 22%

Frequency
Excessive alcohol intake 40% of all cases of AVN Bilateral in 73% Renal transplantation

40% of recipients 54-80% -- bilateral

Steroid use

5-25% in high doses over a long term

Systemic lupus erythematosus 5-40%

Frequency
Sickle cell disease SS disease 4-12% SC disease, 20-68% Hemophilia - 3% Rheumatoid arthritis- 12% Slipped capital femoral epiphysis < 7% in hips reduced within 24 hours 17% after 24 hours Legg-Calv-Perthes disease 15-20%

Alcoholism
direct toxic effect fat deposition in the liver low-grade asymptomatic fat emboli hydrolyzed to free fatty acids-endothelial

damage

Amount of alcohol

Steroid
fat emboli from the liver- occlusion of vessels increase in the size of the intramedullary fat cells without an equivalent compensatory loss of trabecular and cortical bone increased intraosseous pressure Free fatty acids- toxic to vascular endothelium- intravascular coagulation Angiogenesis inhibition

direct toxic effect osteogenic cells

Dose

Steroid
More severe than AVN caused by other conditions b`coz of demineralization and accelerated osteolysis Systemic lupus erythematosus (SLE) and renal allograft recipients prednisone doses greater than 100 mg/d within the first month following transplantation increased with chronic renal disease dialysis and medical management significantly reduces the incidence systemic lupus erythematosus - vasculitis

Decompression sickness (Caisson disease)

Risk factors pressure greater than 17 lb per square inch. depth of the dive the number of dives uncontrolled decompression low oxygen concentrations

Intravascular bubbles of nitrogen obstructs capillaries.

Extravascular nitrogen compresses intramedullary vessels. Arteriolar spasm Fat cells have a 5-fold ability to absorb dissolved nitrogen.--increases their volume within the nonexpandable confines of the bony trabeculae and cortex,

Metastatic disease
increased intramedullary pressure

steroid therapy

local radiation therapy

Pancreatic disease
Lipolytic enzymes ------breakdown of the fat----- free
fatty acids---- toxic to endothelium-----intravascular coagulation. Release of intracellular fat from fat-laden hepatic cells.

Hemoglobinopathies
Hyperviscosity
Vascular occlusion Chronic anemia--- bone marrow hyperplasia

Etiology
Gaucher disease Glucocerebroside accumulation in the reticuloendothelial cells within the bone marrow---- increased intramedullary pressure

Dialysis
Elevated levels of parathormone ---increased subchondral bone turnover--- replacement by disorganized bone matrix unable to support normal weightbearing, resulting in microfractures and increased intramedullary pressure

Etiology
Irradiation
Arteritis ----fibrosis and endothelial proliferation Doses exceeding 30 Gy.

Hemophilia
Repeated microhemorrhages ---increased intramedullary pressure Capsular distension----tamponade effect

Hypercoagulable states
Inherited disorders
Deficiencies of specific protein inhibitors (protein C,protein S) Structural abnormalities of factor V Disorders of the fibrinolytic system Hyperfibrinogenemia

hyperlipoproteinemia (types II and IV) smoking diabetes oral contraceptives

Acquired disorders Pregnancy

Legg- Calv- Perthes disease

Most common cause of AVN in children Time of onset 3-10 years, highest incidence 68 years Vascular anatomy of the proximal femur in a transitional stage
Artery of the ligamentum teres does not penetrate the epiphysis until 9 or 10 years Epiphyseal growth plate prevents communication between the blood supply of the epiphysis and metaphysis

Venous tamponade Nonspecific synovitis

Slipped capital femoral epiphysis

Superolateral displacement and external rotation of the femoral metaphysis----twisting and kinking the lateral epiphyseal vessels

HIV infection
Multifactorial etiologies Hypertriglyceridemia

Steroid use
Caloric deprivation--- irreversible deposition of acid mucopolysaccharides in the marrow

Pathophysiology
Thrombosis or embolization

Structural damage to the arterial or venous walls from vasculitis

Increased intraosseous pressure from enlargement of intramedullary fat cells or aspects

Pathophysiology
Multifactorial End result of a number of different factors with the final common pathway resulting in bone death and collapse of the femoral head.

Final common pathway Intravascular coagulation Vasoconstriction Impaired fibrinolysis Intramedullary hemorrhages Infarction

Pathology
Gross pathology Cancellous bone -- irregular areas of yellow necrosis Patchy zone of softening Microfractures Articular sequestrum Collapse Destruction of the articular cartilage Marginal osteophytes

Pathology
Histopathology
Cell necrosis Vascular poliferation in adjacent normal bone Vascular proliferation in necrotic bone Diferentiation of mesenchyme in osteoblast & fibroblast Remodelling Resorption of subchondral bone & invasion of articular cartilage

Clinical features
High index of suspicion Pain

Click
Range of motion Gait

Investigations
Plain radiography CT scan Single-photon emission computed tomography MRI Bone scan Bone scintigraphy using pinhole collimation Planar scintigraphic imaging using quantitative bone scan

Anatomy
CT anatomy Physiologic thickening of bone trabeculae in the center of the femoral head appears similar to a star--Asterisk sign

Anatomy
MRI anatomy Fatty marrow femoral capital epiphysis and the greater trochanter > 2 yrs high signal on T1 and T2 Hematopoietic marrow femoral neck, intertrochanteric region, and acetabulum low signal on T1 & high signal on T2

Plain radiography
AP view Frog leg lateral view Sclerosis, cysts Flattening Crescent sign

CT scan
Analysis of morphologic features
Sensitivity 55% Extent Detection of subchondral or cancellous fractures and collapse

MRI
Most sensitive means of diagnosing Noninvasive More sensitive than CT scanning, scintigraphy 99% sensitive & specific Single density line on T1 Double density line on T2

MRI
Classification of the AVN lesion into 4 types according to alterations in central avascular segment signal
Class A:

Increased signal on T1WI Intermediate-to-high signal on T2WI Increased signal both T1WIs and T2WIs Decreased signal on T1WI Increased signal on T2WI
Central osteonecrotic focus fluid Central osteonecrotic focus-- blood

Central osteonecrotic focus fat

Class B:

Class C:

Class D: Central osteonecrotic focus -fibrous tissue

Decreased signal on both T1WIs and T2WIs

MRI
Correlation of clinical symptoms with MRI class
class A lesions-- 54% asymptomatic classes B and C lesions 11% asymptomatic class D lesions-- 67% asymptomatic

Single-photon emission computed tomography

Early, may demonstrate avascular focus in presence of normal MRI findings Sensitivity of 85% High-resolution sensitivity 97% Images in 3 dimensions As an alternative to MRI

Differentials
Clinical Plain film radiography
Malignancy Osteomyelitis Transient osteoporosis of the hip Advanced DJD Insufficiency fractures Epiphyseal dysplasia Bone metastases

Differentials
Bone scintigraphy Infection Plasma cell myeloma Skeletal metastasis Radiation therapy Arthritis Sympathetic dystrophy Bone marrow edema syndrome Bone metastases

Differentials
CT
Degenerative disease Insufficiency fracture Malignancy Infection Plasma cell myeloma Bone metastases

Differentials
MRI
Transient osteoporosis of the hip Transient bone marrow syndrome Bone bruise Epiphyseal stress fracture Infection Infiltrative neoplasm Insufficiency fracture Bone metastases

Transient osteoporosis T1 image

Ficat & arlet

Steinberg
Stage 0 - Abnormal MRI findings, normal radiograph findings, and normal bone scan findings Stage 1 - Abnormal bone scan findings, mild groin pain, and normal radiographs findings Stage 2 - Osteoporosis, groin pain, and mottled sclerotic and/or cystic areas Stage 3 - Crescent line, pain with subchondral fracture activity, and no femoral head flattening Stage 4 - Segmental flattening, pain with femoral head activity, no acetabular involvement, and normal joint space Stage 5 - Joint space narrowing, resting pain, and acetabular degeneration (DJD)

University of Pensylvania system of calssification & staging

0 normal or nondiagnostic radiograph, bone scan, MRI 1 normal radiograph, abnormal bone scan &/or MRI 2 lucent & sclerotic changes in femur head 3 subchondral collapse without flattening 4 flattening of femur head 5 joint narrowing &/or acetabular changes 6 advanced degenerative changes Each stage 3 types A - <15% involvement B 15 30% involvement C - >30% involvement

Other classification systems

Marcus
Association Research Ciculation Osseous Japnese Investigation Committee

Sequelae of AVN
Minimal disease: small area and not adjacent to an articular surface, may be asymptomatic may heal spontaneously, may remain undetected or be discovered More severe disease: repair at the interface between viable and necrotic bone. Ineffective resorption of dead bone Dead bone is reabsorbed only partially. Reactive and reparative bone The incomplete resorption of dead bone mixed sclerotic and cystic appearance

Sequelae of AVN
Mechanical failure at the interface between dead and viable bone microfractures do not heal as within dead bone. crescent sign collapse of the articular cartilage degenerative joint disease (DJD) and joint dissolution.

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