The document discusses avascular necrosis (also known as osteonecrosis), which is the death of bone tissue due to impaired blood supply. It affects over 20,000 new patients per year in the US, most commonly in the ages of 30-60. Common causes include steroid use, alcoholism, trauma, and blood clotting disorders. Diagnosis involves imaging like x-rays, CT, MRI, and bone scans to detect bone changes. Treatment aims to delay disease progression and joint breakdown through nonsurgical methods or sometimes surgery like joint replacement.
Avascular necrosis is a condition which appears when there is a loss of blood supply to the bone, resulting in bone death. Avascular necrosis is also known as aseptic necrosis, ischemic bone necrosis, or osteonecrosis
This document discusses avascular necrosis (AVN), also called osteonecrosis. It defines AVN as bone death caused by sudden obstruction of blood supply to bone. Common causes include trauma, corticosteroid use, and decompression sickness. Sites often affected are the femoral head, scaphoid, and talus. The goal of treatment is to improve joint function, stop further bone damage, and preserve the bone and joint. Methods include nonsurgical options to delay progression and surgical interventions like core decompression or grafts, with joint replacement usually performed later.
Osteonecrosis, also known as avascular necrosis, occurs when bone loses its blood supply and dies. It most commonly affects the femoral head. Early symptoms are often absent. As collapse occurs, pain and loss of function increase. Risk factors include alcoholism, corticosteroid use, trauma, and idiopathic causes. MRI is the most sensitive imaging test, showing changes in signal intensity and double line signs. Staging systems evaluate extent of involvement and prognosis. Treatment depends on stage, with core decompression or hip replacement for late stages with collapse.
The document discusses avascular necrosis (AVN), also known as osteonecrosis, which is the death of bone tissue due to a lack of blood supply. It provides details on:
- The main causes of AVN including trauma, alcoholism, steroid use, decompression sickness, and blood disorders.
- The pathology and progression of AVN, from initial bone cell death, to bone repair attempts, to structural failure and collapse if left untreated.
- Clinical signs and symptoms including pain that worsens with activity and improved with rest, limited range of motion, and characteristic findings on x-rays such as patchy demineralization and sclerosis.
- Staging of AVN
This document discusses avascular necrosis (AVN) of the bone, also known as osteonecrosis. It begins by explaining that AVN results from interrupted blood supply to the bone, which can lead to bone and cell death. The most common sites of AVN are the femoral head, scaphoid, and talus. Non-surgical treatments include limited weight bearing, while surgical options include core decompression, bone grafting, and osteotomies to preserve the joint. More advanced cases may require joint replacement like hip resurfacing or total hip arthroplasty. Risk factors include corticosteroid use, alcoholism, trauma, and various medical conditions.
Avascular necrosis femoral head by DR RAJAT MALOT (MS,DNB, MNAMS,FELLLOWSHIP ...chitrapandey
This document summarizes avascular necrosis of the femoral head, including:
1. It provides an overview of the typical clinical presentation, including gradual onset of hip pain that worsens with activity and is relieved by rest. Range of motion may be limited.
2. It discusses the blood supply of the femoral head and how avascular necrosis occurs when this blood supply is disrupted.
3. It reviews various classification systems for staging avascular necrosis, including the widely used Ficat & Arlet classification system which has 4 stages ranging from preclinical to osteoarthritis.
Osteonecrosis is a condition caused by loss of blood supply to the bone, which can lead to bone tissue death and joint collapse. It is often caused by long term steroid use or heavy alcohol use. Symptoms may include joint pain that worsens with weight bearing. Diagnosis involves x-rays, MRI, or biopsy. Treatment options range from medications and reduced activity to core decompression surgery or joint replacement depending on severity. Preventing osteonecrosis involves limiting steroid use, alcohol, and smoking.
Avascular necrosis is a condition which appears when there is a loss of blood supply to the bone, resulting in bone death. Avascular necrosis is also known as aseptic necrosis, ischemic bone necrosis, or osteonecrosis
This document discusses avascular necrosis (AVN), also called osteonecrosis. It defines AVN as bone death caused by sudden obstruction of blood supply to bone. Common causes include trauma, corticosteroid use, and decompression sickness. Sites often affected are the femoral head, scaphoid, and talus. The goal of treatment is to improve joint function, stop further bone damage, and preserve the bone and joint. Methods include nonsurgical options to delay progression and surgical interventions like core decompression or grafts, with joint replacement usually performed later.
Osteonecrosis, also known as avascular necrosis, occurs when bone loses its blood supply and dies. It most commonly affects the femoral head. Early symptoms are often absent. As collapse occurs, pain and loss of function increase. Risk factors include alcoholism, corticosteroid use, trauma, and idiopathic causes. MRI is the most sensitive imaging test, showing changes in signal intensity and double line signs. Staging systems evaluate extent of involvement and prognosis. Treatment depends on stage, with core decompression or hip replacement for late stages with collapse.
The document discusses avascular necrosis (AVN), also known as osteonecrosis, which is the death of bone tissue due to a lack of blood supply. It provides details on:
- The main causes of AVN including trauma, alcoholism, steroid use, decompression sickness, and blood disorders.
- The pathology and progression of AVN, from initial bone cell death, to bone repair attempts, to structural failure and collapse if left untreated.
- Clinical signs and symptoms including pain that worsens with activity and improved with rest, limited range of motion, and characteristic findings on x-rays such as patchy demineralization and sclerosis.
- Staging of AVN
This document discusses avascular necrosis (AVN) of the bone, also known as osteonecrosis. It begins by explaining that AVN results from interrupted blood supply to the bone, which can lead to bone and cell death. The most common sites of AVN are the femoral head, scaphoid, and talus. Non-surgical treatments include limited weight bearing, while surgical options include core decompression, bone grafting, and osteotomies to preserve the joint. More advanced cases may require joint replacement like hip resurfacing or total hip arthroplasty. Risk factors include corticosteroid use, alcoholism, trauma, and various medical conditions.
Avascular necrosis femoral head by DR RAJAT MALOT (MS,DNB, MNAMS,FELLLOWSHIP ...chitrapandey
This document summarizes avascular necrosis of the femoral head, including:
1. It provides an overview of the typical clinical presentation, including gradual onset of hip pain that worsens with activity and is relieved by rest. Range of motion may be limited.
2. It discusses the blood supply of the femoral head and how avascular necrosis occurs when this blood supply is disrupted.
3. It reviews various classification systems for staging avascular necrosis, including the widely used Ficat & Arlet classification system which has 4 stages ranging from preclinical to osteoarthritis.
Osteonecrosis is a condition caused by loss of blood supply to the bone, which can lead to bone tissue death and joint collapse. It is often caused by long term steroid use or heavy alcohol use. Symptoms may include joint pain that worsens with weight bearing. Diagnosis involves x-rays, MRI, or biopsy. Treatment options range from medications and reduced activity to core decompression surgery or joint replacement depending on severity. Preventing osteonecrosis involves limiting steroid use, alcohol, and smoking.
Osteonecrosis of the femoral head, also known as avascular necrosis, refers to bone cell death caused by disrupted blood flow to the femoral head. It commonly affects young adults and can lead to hip joint replacement. Early diagnosis using MRI is important. Staging systems classify the extent of involvement and structural changes, from pre-collapse changes seen on bone scan to late stage joint space narrowing. While no treatment reliably stops progression, core decompression and bone grafting may delay collapse in early stages. Once collapse occurs, osteoarthritis usually develops, necessitating joint reconstruction or replacement.
This document discusses avascular necrosis of the hip joint, also called osteonecrosis. It defines osteonecrosis as the ischemic death of bone components due to impaired blood flow. Symptoms include dull, progressive pain that worsens at night and with walking, as well as limited hip motion. Diagnosis involves imaging like X-rays, CT scans, and MRI. Imaging findings reflect the stage of the condition according to classifications by Ficat and Arlet and Steinberg, ranging from bone changes to joint space narrowing and collapse. MRI specifically reveals bone marrow edema, a double line sign, collapse of the femoral head, joint effusion, and involvement of the acetabulum.
Osteonecrosis is the death of bone tissue due to a lack of blood supply. It can be caused by trauma or other events that disrupt blood flow, such as fractures or dislocations. Imaging like x-rays and MRIs are used to stage osteonecrosis and monitor for signs of bone death and structural damage over time. The femoral head, humeral head, and scaphoid bone are particularly susceptible to osteonecrosis due to their vascular anatomy. Long term complications can include bone collapse and osteoarthritis. Prevention focuses on minimizing corticosteroid use and maintaining circulation for patients with conditions like sickle cell disease.
A 41-year-old male presented with right hip, knee, and groin pain that began six months ago after a fall. He was previously treated with high-dose corticosteroids for skin lesions, which likely caused his current avascular necrosis (bone cell death due to interrupted blood flow). Imaging showed abnormalities in his right femoral head consistent with avascular necrosis. He was diagnosed with avascular necrosis likely caused by his past prolonged corticosteroid use.
Osteonecrosis is a condition where bone tissue dies due to an interruption of blood supply. It can affect any bone but most commonly affects the hip joint. Symptoms include joint pain and tenderness. Doctors diagnose through x-rays, MRI, CT scans, and bone scans. Treatment depends on the stage of disease and may include medications to improve blood flow, hyperbaric oxygen therapy, electrical stimulation, core decompression surgery, bone grafts, or in severe cases, joint replacement surgery.
This document provides an overview of avascular necrosis (AVN), including:
- AVN is cell death of bone tissue due to interrupted blood supply, causing pain and joint damage. It most commonly affects the hip.
- Risk factors include corticosteroid use, trauma, alcohol abuse, and blood disorders. The condition leads to bone collapse and is diagnosed through imaging like MRI.
- Treatment depends on severity but may include medications, physical therapy, surgery, and in severe cases, joint replacement. Left untreated, it can cause long-term disability.
1. Radiography is the first step in diagnosing avascular necrosis, though it has limitations in detecting early stages. Changes seen on radiography include osteoporosis, sclerosis, fractures, and joint space narrowing.
2. MRI is the most sensitive imaging modality and allows for accurate staging. Changes seen include band forms and double line signs.
3. Different imaging modalities show characteristics of avascular necrosis at various stages. SPECT may show cold spots while radiography shows fractures and joint damage at later stages. Proper staging guides treatment selection and monitoring of progression.
Avascular necrosis of the femoral head
introduction
causes
anatomy of femur
blood supply of femur
Clinical Features
Investigations
Differential Diagnosis
treatments
Surgical Treatment
Prognosis
aseptic necrosis
ischemic necrosis.
Legg-Calvé-Perthes syndrome
Causes Of Avascular Necrosis
Avascular necrosis, also known as osteonecrosis or bone infarction, is the death of bone tissue due to a lack of blood supply. It most commonly affects the femoral head. There are many potential causes including trauma, alcohol use, steroid use, and idiopathic cases. Diagnosis is made through imaging like x-rays, CT scans, MRIs, and bone scans. Treatment depends on the stage of necrosis and other factors, and may include observation, core decompression, vascularized bone grafts, partial or total hip replacement, or hip resurfacing. Staging is important for determining treatment and can range from pre-symptomatic changes visible only on MRI to complete femoral head destruction indistinguishable from osteo
Avascular necrosis is the death of bone tissue due to a lack of blood supply. It most commonly affects the femoral head. Early symptoms include dull, progressive pain in the hip or thigh that worsens with activity or at night. Imaging plays an important role in diagnosis, with plain X-rays initially appearing normal but later showing signs of bone collapse like the crescent sign. MRI is the most sensitive technique and can detect avascular necrosis as early as 48 hours. Staging systems evaluate the extent of bone involvement and deterioration of the joint space to classify the severity of avascular necrosis. Treatment options depend on the stage of the disease.
Presentation1.pptx, radiological imaging of paget disease.Abdellah Nazeer
Paget's disease is a chronic bone disorder characterized by abnormal bone remodeling. It commonly affects the pelvis, spine and skull. Radiography is often used to evaluate Paget's disease and detect characteristic features like thickened bone and osteolytic lesions. While some cases are asymptomatic, complications can include fractures, osteoarthritis, nerve entrapment and rare neoplastic transformations. MRI and bone scintigraphy provide additional information about disease activity and complications.
This document discusses osteonecrosis of the femoral head, including risk factors, pathogenesis theories, classifications, diagnosis, and treatment options. Key points:
- Risk factors include corticosteroid use, smoking, sickle cell anemia and others. Theories on causes include toxicity, vascular issues, but the process is likely multifactorial.
- Diagnosis involves radiographs, bone scans and MRI, which can detect early-stage disease.
- Treatment depends on disease stage and size. Options include core decompression, bone grafting, osteotomies and arthroplasty. Younger patients with smaller lesions may be candidates for bone-preserving options, while larger lesions often require joint replacement.
Imaging of spinal cord acute myelopathiesNavni Garg
This presentation provides a comprehensive review of imaging of causes of acute myelopathies and a systemic approach for narrowing down the differentials
This document discusses Legg-Calvé-Perthes disease (LCPD), a condition where the blood supply to the femoral head is disrupted, causing bone cell death. As the necrotic bone breaks down and is reabsorbed, the femoral head can become misshapen. The summary is:
LCPD involves avascular necrosis of the femoral head, leading to bone resorption and potential deformity. Treatment aims to contain the femoral head within the acetabulum during healing to restore its shape, and may include bracing, osteotomies or arthrodiastasis. Surgical options depend on the stage, extent of involvement and deformity present.
This document discusses three bone conditions: osteochondritis dessicans, caisson disease, and Caffey's disease. Osteochondritis dessicans involves post-traumatic fractures of articular bone that may become detached or loose bodies. Caisson disease is dysbaric osteonecrosis caused by decompression sickness from exposure to hyperbaric environments like diving or space travel. Caffey's disease is an infantile cortical hyperostosis of unknown origin with fever, irritability, and painful soft tissue swelling preceding patchy bone lesions.
infantile cortical hyperostosis :-Infants with tender swelling in the soft tissues and cortical thickenings in the skeleton.Self limited disease with unknown Etiology. it is a genetic mutatic disease present in infants.
A 17-year-old male soccer player presented with nagging left knee pain for several months that was worse with exercise. Examination found pain and crepitus with compression of the medial femoral condyle. MRI revealed a subchondral defect in the medial femoral condyle consistent with osteochondritis dissecans (OCD), a separation of cartilage and subchondral bone from the underlying bone most common in the medial femoral condyle of adolescents. Initial treatment involves immobilization but surgery may be needed if the fragment is loose or detached to prevent premature arthritis.
Caffey disease, also known as infantile cortical hyperostosis, is a self-limited condition characterized by asymmetric thickening of bone cortices in infants less than 5 months old. It presents as fever, soft tissue swelling, and irritability and typically resolves without sequelae within 6-9 months. Osteopetrosis is a rare genetic disorder where bone resorption is impaired, leading to abnormally dense and brittle bones. It can range from mild to lethal depending on the mutated gene. Legg-Calve-Perthes disease involves osteonecrosis of the femoral head epiphysis in children, commonly presenting with hip pain and limping. It is diagnosed based on imaging findings of femoral
This document discusses avascular necrosis (also known as osteonecrosis), which is the death of bone tissue due to impaired blood supply. It affects over 20,000 new patients per year in the US, most commonly males ages 30-60. Risk factors include steroid use, alcoholism, blood clotting disorders, and autoimmune diseases like SLE. Symptoms may include joint pain. Diagnosis involves imaging modalities like x-ray, CT, MRI, and bone scans. Treatment aims to delay disease progression and prevent joint breakdown, and may include nonsurgical options or eventually joint replacement if collapse occurs.
This document discusses biological treatment options for avascular necrosis (AVN) of the femoral head. It provides details on the anatomy and blood supply of the femoral head. AVN occurs when there is interruption of blood flow to the femoral head, leading to bone cell death. Imaging plays an important role in diagnosis and staging of AVN. Conservative options include restricted weight bearing, medications, and physical therapies. Surgical options become necessary with more advanced stages to prevent femoral head collapse. The document covers various classification and staging systems used to determine the appropriate treatment based on the individual case.
Osteonecrosis of the femoral head, also known as avascular necrosis, refers to bone cell death caused by disrupted blood flow to the femoral head. It commonly affects young adults and can lead to hip joint replacement. Early diagnosis using MRI is important. Staging systems classify the extent of involvement and structural changes, from pre-collapse changes seen on bone scan to late stage joint space narrowing. While no treatment reliably stops progression, core decompression and bone grafting may delay collapse in early stages. Once collapse occurs, osteoarthritis usually develops, necessitating joint reconstruction or replacement.
This document discusses avascular necrosis of the hip joint, also called osteonecrosis. It defines osteonecrosis as the ischemic death of bone components due to impaired blood flow. Symptoms include dull, progressive pain that worsens at night and with walking, as well as limited hip motion. Diagnosis involves imaging like X-rays, CT scans, and MRI. Imaging findings reflect the stage of the condition according to classifications by Ficat and Arlet and Steinberg, ranging from bone changes to joint space narrowing and collapse. MRI specifically reveals bone marrow edema, a double line sign, collapse of the femoral head, joint effusion, and involvement of the acetabulum.
Osteonecrosis is the death of bone tissue due to a lack of blood supply. It can be caused by trauma or other events that disrupt blood flow, such as fractures or dislocations. Imaging like x-rays and MRIs are used to stage osteonecrosis and monitor for signs of bone death and structural damage over time. The femoral head, humeral head, and scaphoid bone are particularly susceptible to osteonecrosis due to their vascular anatomy. Long term complications can include bone collapse and osteoarthritis. Prevention focuses on minimizing corticosteroid use and maintaining circulation for patients with conditions like sickle cell disease.
A 41-year-old male presented with right hip, knee, and groin pain that began six months ago after a fall. He was previously treated with high-dose corticosteroids for skin lesions, which likely caused his current avascular necrosis (bone cell death due to interrupted blood flow). Imaging showed abnormalities in his right femoral head consistent with avascular necrosis. He was diagnosed with avascular necrosis likely caused by his past prolonged corticosteroid use.
Osteonecrosis is a condition where bone tissue dies due to an interruption of blood supply. It can affect any bone but most commonly affects the hip joint. Symptoms include joint pain and tenderness. Doctors diagnose through x-rays, MRI, CT scans, and bone scans. Treatment depends on the stage of disease and may include medications to improve blood flow, hyperbaric oxygen therapy, electrical stimulation, core decompression surgery, bone grafts, or in severe cases, joint replacement surgery.
This document provides an overview of avascular necrosis (AVN), including:
- AVN is cell death of bone tissue due to interrupted blood supply, causing pain and joint damage. It most commonly affects the hip.
- Risk factors include corticosteroid use, trauma, alcohol abuse, and blood disorders. The condition leads to bone collapse and is diagnosed through imaging like MRI.
- Treatment depends on severity but may include medications, physical therapy, surgery, and in severe cases, joint replacement. Left untreated, it can cause long-term disability.
1. Radiography is the first step in diagnosing avascular necrosis, though it has limitations in detecting early stages. Changes seen on radiography include osteoporosis, sclerosis, fractures, and joint space narrowing.
2. MRI is the most sensitive imaging modality and allows for accurate staging. Changes seen include band forms and double line signs.
3. Different imaging modalities show characteristics of avascular necrosis at various stages. SPECT may show cold spots while radiography shows fractures and joint damage at later stages. Proper staging guides treatment selection and monitoring of progression.
Avascular necrosis of the femoral head
introduction
causes
anatomy of femur
blood supply of femur
Clinical Features
Investigations
Differential Diagnosis
treatments
Surgical Treatment
Prognosis
aseptic necrosis
ischemic necrosis.
Legg-Calvé-Perthes syndrome
Causes Of Avascular Necrosis
Avascular necrosis, also known as osteonecrosis or bone infarction, is the death of bone tissue due to a lack of blood supply. It most commonly affects the femoral head. There are many potential causes including trauma, alcohol use, steroid use, and idiopathic cases. Diagnosis is made through imaging like x-rays, CT scans, MRIs, and bone scans. Treatment depends on the stage of necrosis and other factors, and may include observation, core decompression, vascularized bone grafts, partial or total hip replacement, or hip resurfacing. Staging is important for determining treatment and can range from pre-symptomatic changes visible only on MRI to complete femoral head destruction indistinguishable from osteo
Avascular necrosis is the death of bone tissue due to a lack of blood supply. It most commonly affects the femoral head. Early symptoms include dull, progressive pain in the hip or thigh that worsens with activity or at night. Imaging plays an important role in diagnosis, with plain X-rays initially appearing normal but later showing signs of bone collapse like the crescent sign. MRI is the most sensitive technique and can detect avascular necrosis as early as 48 hours. Staging systems evaluate the extent of bone involvement and deterioration of the joint space to classify the severity of avascular necrosis. Treatment options depend on the stage of the disease.
Presentation1.pptx, radiological imaging of paget disease.Abdellah Nazeer
Paget's disease is a chronic bone disorder characterized by abnormal bone remodeling. It commonly affects the pelvis, spine and skull. Radiography is often used to evaluate Paget's disease and detect characteristic features like thickened bone and osteolytic lesions. While some cases are asymptomatic, complications can include fractures, osteoarthritis, nerve entrapment and rare neoplastic transformations. MRI and bone scintigraphy provide additional information about disease activity and complications.
This document discusses osteonecrosis of the femoral head, including risk factors, pathogenesis theories, classifications, diagnosis, and treatment options. Key points:
- Risk factors include corticosteroid use, smoking, sickle cell anemia and others. Theories on causes include toxicity, vascular issues, but the process is likely multifactorial.
- Diagnosis involves radiographs, bone scans and MRI, which can detect early-stage disease.
- Treatment depends on disease stage and size. Options include core decompression, bone grafting, osteotomies and arthroplasty. Younger patients with smaller lesions may be candidates for bone-preserving options, while larger lesions often require joint replacement.
Imaging of spinal cord acute myelopathiesNavni Garg
This presentation provides a comprehensive review of imaging of causes of acute myelopathies and a systemic approach for narrowing down the differentials
This document discusses Legg-Calvé-Perthes disease (LCPD), a condition where the blood supply to the femoral head is disrupted, causing bone cell death. As the necrotic bone breaks down and is reabsorbed, the femoral head can become misshapen. The summary is:
LCPD involves avascular necrosis of the femoral head, leading to bone resorption and potential deformity. Treatment aims to contain the femoral head within the acetabulum during healing to restore its shape, and may include bracing, osteotomies or arthrodiastasis. Surgical options depend on the stage, extent of involvement and deformity present.
This document discusses three bone conditions: osteochondritis dessicans, caisson disease, and Caffey's disease. Osteochondritis dessicans involves post-traumatic fractures of articular bone that may become detached or loose bodies. Caisson disease is dysbaric osteonecrosis caused by decompression sickness from exposure to hyperbaric environments like diving or space travel. Caffey's disease is an infantile cortical hyperostosis of unknown origin with fever, irritability, and painful soft tissue swelling preceding patchy bone lesions.
infantile cortical hyperostosis :-Infants with tender swelling in the soft tissues and cortical thickenings in the skeleton.Self limited disease with unknown Etiology. it is a genetic mutatic disease present in infants.
A 17-year-old male soccer player presented with nagging left knee pain for several months that was worse with exercise. Examination found pain and crepitus with compression of the medial femoral condyle. MRI revealed a subchondral defect in the medial femoral condyle consistent with osteochondritis dissecans (OCD), a separation of cartilage and subchondral bone from the underlying bone most common in the medial femoral condyle of adolescents. Initial treatment involves immobilization but surgery may be needed if the fragment is loose or detached to prevent premature arthritis.
Caffey disease, also known as infantile cortical hyperostosis, is a self-limited condition characterized by asymmetric thickening of bone cortices in infants less than 5 months old. It presents as fever, soft tissue swelling, and irritability and typically resolves without sequelae within 6-9 months. Osteopetrosis is a rare genetic disorder where bone resorption is impaired, leading to abnormally dense and brittle bones. It can range from mild to lethal depending on the mutated gene. Legg-Calve-Perthes disease involves osteonecrosis of the femoral head epiphysis in children, commonly presenting with hip pain and limping. It is diagnosed based on imaging findings of femoral
This document discusses avascular necrosis (also known as osteonecrosis), which is the death of bone tissue due to impaired blood supply. It affects over 20,000 new patients per year in the US, most commonly males ages 30-60. Risk factors include steroid use, alcoholism, blood clotting disorders, and autoimmune diseases like SLE. Symptoms may include joint pain. Diagnosis involves imaging modalities like x-ray, CT, MRI, and bone scans. Treatment aims to delay disease progression and prevent joint breakdown, and may include nonsurgical options or eventually joint replacement if collapse occurs.
This document discusses biological treatment options for avascular necrosis (AVN) of the femoral head. It provides details on the anatomy and blood supply of the femoral head. AVN occurs when there is interruption of blood flow to the femoral head, leading to bone cell death. Imaging plays an important role in diagnosis and staging of AVN. Conservative options include restricted weight bearing, medications, and physical therapies. Surgical options become necessary with more advanced stages to prevent femoral head collapse. The document covers various classification and staging systems used to determine the appropriate treatment based on the individual case.
1. Avascular necrosis of the femoral head, also known as osteonecrosis, refers to the death of bone cells in the femur due to interrupted blood supply, leading to structural changes and collapse of the femoral head.
2. It most commonly affects adults aged 30-70 years old and is seen more often in males. Common causes include fractures of the femoral neck, hip dislocations, chronic alcoholism, and steroid use.
3. Early diagnosis is important as imaging like MRI can detect osteonecrosis before changes are evident on x-ray. X-rays may eventually show signs like sclerosis, cysts, flattening of the femoral head. Bone scans can also help detect early changes through decreased
This document discusses avascular necrosis (AVN), also known as osteonecrosis. It begins by defining AVN as the death of bone components due to interrupted blood supply. Key areas that are commonly affected are described. The document then covers the pathophysiology, various causes (traumatic, non-traumatic), clinical presentation, imaging techniques, staging classifications, and management strategies for AVN. Treatment approaches include conservative options, decompression procedures, realignment osteotomies, arthrodesis, and arthroplasty.
This document discusses the investigation and management of discitis/diskitis. Key points include:
- Elevated ESR, CRP, and procalcitonin levels can indicate discitis, along with abnormal findings on imaging like MRI and X-rays. Blood and sputum cultures help identify the infection source.
- MRI is the most sensitive test for discitis, showing abnormalities in the disc space and vertebrae on T1 and T2 weighted images. CT also shows bone destruction.
- Treatment involves intravenous antibiotics for 6-8 weeks, immobilization, and pain management. Surgery may be needed for neurological complications, non-response to treatment, or deformity correction.
-
Discuss the orthopaedic manifestations of sickle cell diseaseSoliudeen Arojuraye
This document discusses the orthopaedic manifestations and their management in sickle cell disease (SCD). It outlines the pathophysiology of SCD, which involves hemoglobin S polymerization and sickling of red blood cells under conditions of hypoxia and acidosis, leading to vaso-occlusion. Common orthopaedic manifestations include vaso-occlusive crises, osteomyelitis, septic arthritis, osteonecrosis, growth disturbances, and osteoporosis. Management involves treating acute complications conservatively while surgical intervention is often needed for chronic complications such as osteonecrosis to prevent joint damage. Specialized multidisciplinary care is important due to increased risks for patients with SCD.
1) The document reviews Paget's disease of bone, discussing its epidemiology, pathophysiology, clinical presentation, diagnosis, and management. It affects bone remodeling and can cause pain, deformity, fractures, and neurological complications.
2) Treatment may involve medications like calcitonin and bisphosphonates to reduce symptoms and prevent complications. Surgery is occasionally needed for deformity correction or joint replacement, with careful attention to bleeding risks.
3) Complications of Paget's disease include arthritis, fractures, neurological problems, and rare malignant transformation. Management involves a multidisciplinary approach with medications, surgery, and lifestyle modifications.
- Ankylosing spondylitis is an inflammatory disorder that primarily affects the axial skeleton including the spine and sacroiliac joints. It has a strong association with the HLA-B27 gene.
- The disease usually begins in young adults and presents as inflammatory back pain. Diagnosis requires radiographic evidence of sacroiliitis along with symptoms of back pain and stiffness.
- While the exact cause is unknown, it is thought to be immune-mediated potentially triggered by intestinal bacteria in genetically susceptible individuals with HLA-B27. Tumor necrosis factor inhibitors can provide relief of symptoms.
Paget's disease is a disorder that causes abnormal bone remodeling. It most commonly affects the pelvis, spine, skull, and thighbones. In the active phase, bone resorption occurs, seen on x-rays as osteolytic lesions. Later, bone formation results in osteosclerosis. Complications can include bone deformity, fractures, neurological problems if the spine is involved, and in rare cases, bone cancer. Diagnosis is based on elevated biomarkers and imaging findings characteristic of the different disease phases.
Neuropathic arthropathy, also known as Charcot arthropathy, is a condition characterized by progressive joint destruction and deformity caused by loss of sensation in the joints. It is most commonly seen in patients with diabetes or neurological disorders. The main theories for its pathophysiology are neurotrauma from repetitive micro-injuries without pain perception, and neurovascular changes that increase bone resorption. Treatment involves initial casting to immobilize the joint, followed by bracing, orthotics, and immobilization over the course of 1-2 years to allow healing. Surgical options like fusion or reconstruction may be used for advanced cases or deformity correction.
Arthritis and arthroplasty- dr. Mahmoud Abdel KareemAhmed-shedeed
This document provides information about osteoarthritis (OA), including its definition, prevalence, risk factors, pathology, diagnosis, natural history, differential diagnosis, and treatment. It notes that OA is the most common form of arthritis, affecting over 20 million people in the US. Risk factors include age, obesity, family history, and previous joint injury or disorder. Diagnosis is typically based on symptoms like pain and stiffness, physical exam findings, and x-ray evidence of cartilage loss, bone spurs, and bone changes. Treatment includes conservative options like medications, exercise, and weight loss, as well as intra-articular injections or surgery for advanced cases.
Degenerative disc disease is a condition characterized by changes in the discs between vertebrae. As discs degenerate they lose water content and height. Fissures can form in the annulus fibrosus and the nucleus pulposus loses structure. This can lead to bulging of the disc and potentially protrusion or extrusion of disc material. Kirkaldy-Willis divided the process into three stages: dysfunction, instability, and stabilization. Symptoms include back pain and pain that may radiate into the legs. Diagnostic imaging includes x-rays, CT, MRI, and discography which can help identify problematic discs.
Rheumatoid arthritis is an autoimmune disease where the immune system attacks the joints, causing inflammation and damage over time. It affects about 2.1 million Americans, especially women. While the exact cause is unknown, genetics and environmental triggers may play a role. Symptoms include pain, stiffness, and swelling in the wrist and small joint areas. Left untreated, it can cause deformities and disability. Treatment involves medications to reduce inflammation and physical therapy to maintain joint mobility and function.
Cervical spondylosis is a common cause of neck pain, radiculopathy, and myelopathy. It involves chronic degenerative changes in the cervical discs and vertebrae due to aging. Common symptoms include neck pain, headaches, and radiating arm pain. Diagnosis involves clinical exam showing signs of radiculopathy or myelopathy as well as imaging like x-rays, CT, and MRI to identify areas of nerve root or spinal cord compression. Treatment options include conservative measures or surgery to decompress the spinal cord if conservative treatment fails.
Complications of fracture.pptx BY DR.BSPbharti pawar
This document discusses various complications that can arise from fractures, classifying them as immediate, early, or late complications. Immediate complications include hypovolaemic shock and injuries to major blood vessels or internal organs. Early complications involve systemic issues like fat embolism, deep vein thrombosis, and crush syndrome, as well as local infections. Late complications are related to imperfect unions, including delayed union, non-union, malunion, and avascular necrosis. Many of these complications require aggressive emergency treatment to stabilize the patient and prevent long-term disabilities.
This document discusses avascular necrosis (AVN), also known as osteonecrosis or bone death. It defines AVN as the sudden obstruction of arterial blood supply to bone. Common causes include trauma, corticosteroid use, and decompression sickness. Sites commonly affected are the femoral head, scaphoid, and talus. The goal of treatment is to improve joint function, stop further bone damage, and preserve the bone and joint. Methods include nonsurgical options to delay progression and surgical interventions like core decompression or grafts, with arthroplasty reserved for later stages.
This document discusses skeletal changes seen in various blood disorders including thalassemia, sickle cell anemia, and hemophilia. Thalassemia causes bone marrow expansion leading to osteoporosis, cortical thinning, and bone deformities. Sickle cell anemia results in bone infarcts, osteonecrosis, and vertebral endplate abnormalities. Hemophilia produces joint hemorrhages, pseudo-tumors, osteoporosis, and eventual joint destruction. Radiographs are useful for identifying characteristic findings in these inherited bleeding and hemolytic disorders.
Osteonecrosis, or avascular necrosis, is the death of bone tissue due to a lack of blood supply. It most commonly affects the femoral head. Interruption of blood flow to an area of bone can be caused by trauma, corticosteroid use, alcoholism, and other medical conditions. Patients experience pain and loss of function in the affected joint. Imaging such as MRI and bone scans can detect osteonecrosis early. Treatment depends on the stage of the disease and may include bisphosphonates, decompression surgery, joint replacement, or fusion.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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4. Ahlback disease: medial femoral
condyle, i.e. SONK
Brailsford disease: head of radius
Buchman disease: iliac crest
Burns disease: distal ulna
Caffey disease: entire carpus or
intercondylar spines of tibia
Dias disease: trochlea of the talus
Dietrich disease: head of metacarpals
Freiberg infraction: head of the
second metatarsal
Friedrich disease: medial clavicle
Hass disease: humeral head
Iselin disease: base of 5th metatarsal
Kienbock disease: lunate
Kohler disease: patella or navicular
(children)
Kummel disease: vertebral body
Legg-Calvé-Perthes disease: femoral
head
Liffert-Arkin disease: distal tibia
Mandl disease: greater trochanter
Mauclaire disease: metacarpal heads
Milch disease: ischial apophysis
Mueller-Weiss disease: navicular
(adult)
Panner disease: capitellum of
humerus
Pierson disease: symphysis pubis
Preiser disease: scaphoid
Sever disease: calcaneal epiphysis
Thiemann disease: base of phalanges
Van Neck-Odelberg
disease: ischiopubic synchondrosis
5. Osteonecrosis has been estimated to affect
20,000 new patients per year in the US
75% of patients are between the ages of 30-
60 years old
25% of patients with the condition are < 25
years of age
The disease is more common in males
7:3 males-females
An important exception to this male-to-female
ratio is SLE
6. pathogenesis
Avascular necrosis result from direct or indirect injury ,or
damage to the vascular flow.
Ciculatory deficiency result in bone and bone marrow
cell death.(osteocyte , haematopoetic cell , adipocyte).
The necrotic tissue triggers repair ,a reactive surface
develops at the boundary with the healthy bone.
Revitalization of the necrosis due to ingrowth of blood
vessel and connective tissue from healthy surroundings
→abnormal and biomechanically weak bone
Small lesions can heal , if not or incomplete →
subchondral bone will break from repeated microtrauma
and various significant defects will result.
7. Cellular ischemia → death of hematopoietic cell in
6-12 hrs, osteocyte in 12-48 hrs and lipocyte in 2-5
days
8. Clinical Presentation
Osteonecrosis can be asymptomatic and found incidentally on
imaging
A high index of suspicion is necessary for patients with risk
factors
Pertinent patient history includes history of steroid use, alcohol
abuse and clotting abnormalities
Pain in the affected joint (although non-specific) is usually the
presenting symptom
The initial physical exam findings may not be useful and are
often non-specific
After osteonecrosis progresses, joint function deteriorates and
the patient may
Have tenderness around the affected bone
Have joint deformity and muscle wasting
May even have a neurologic deficit if a nerve is compressed due to
necrosis and deformity of the affected bones
9. Late Presentation
Unfortunately, most patients present late in the course of disease
In the late stages, you may see highly deteriorated joint function
and a significant limp
Without treatment, the patient would be more likely to present
with severe pain at rest and at night and would have more
restriction and pain with joint movements
Joint deformity, muscle wasting and non union of fracture are
also more common with advanced osteonecrosis
Medullary infarcts usually remain stable over time, while
subchondral infarcts often collapse and may predispose to
severe secondary osteoarthritis
14. the high prevalence and multifocal nature of AVN in
SLE patients during high dose steroid treatment
of disease exacerbation results from the co-
occurrence of two processes
1. Vascular Injury with widespread activation of
endothelium and inflammatory vasculopathy or
thrombosis disrupting the microcirculation
2. Lipid Deposition with interosseous fat
accumulation, secondary to glucocorticoid induced
abnormal lipid metabolism, increasing intramedullary
pressure (i.e. bony compartment syndrome) and
decreasing perfusion
15.
16. Classification of the progress of the disease as
described in the association research circulation
osseous (ARCO)
Initial stage (ARCO 0)
An ischaemic attach.
Still reversible and asymptomatic.
Histologicaly minimal changes can be
found.
Pathological perfusion can be shown by
dynamic contrast MRI.
17. Reversible early stage (ARCO
1)
Edema of the bone marrow with extend
of medullary cavity necrosis.
Start of repair process, with gradual
replacement of necrotic tisssue by
growth of fibrous vascullar tissue.
Still no reactive surface.
MRI
18.
19. Non_reversible early stage
(ARCO 2)
Histological bone process, in the sense of
bone resorption and formation of bone
marrow and the trabecula.
vascular Granulation tissue attempts to
repair the necrotic area inside the
secleretic zone, which is directly opposed
to the area of the vital tissue.
MRI (MR double line
sign)→pathognomonic in t2 ,it corresponds
to reactive interface.
X-ray → blotchy change +seclerotic
changes are visible.
20.
21. Transitional stage (ARCO 3)
Mechanical failure of the affected bone
area lead to the subchonral microfracture.
It usually begins at the margin of the
defect and is consequence of in sufficient
repair.
X-ray → small suchonral crescent sign.
MRI → MRI cresent sign , if subchondral
fracture filled with synovial fluid.
22.
23. Late stage (ARCO 4)
Secondary arthritic lesion (calcification
+resorptive cyst).
Deformity
Detect by any imaging method.
24.
25. AP radiographic view of the pelvis shows flattening of the outer portion of
the right femoral head from avascular necrosis, with adjacent joint space
narrowing, juxta-articular sclerosis, and osteophytes representing
degenerative joint disease (stage IV)
26.
27.
28. Most common sites
Head of humerus
Head of femur
Scaphoid
Femur condyles
Affects bones with a single terminal blood
supply
34. diagnosis
History
Physical examination
investigation
Plain radiography
There is significant delay between infarct onset and development of
radiographic signs. Classic description is of medullary lesion of sheet-
like central lucency surrounded by shell-like sclerosis with serpiginous
border. Discrete calcification and periostitis may also be seen.
CT
Generally does not reveal much more than the plain film.
The best modality for estimating the extent of bone death
It is not as sensitive as MRI
35. MRI
An important feature in differentiating bone infarct from other
medullary lesions is that the central signal usually remains that of
normal marrow. The marrow is not replaced.
T1
serpiginous peripheral low signal due to granulation tissue and to
lesser extent sclerosis
peripheral rim may enhance post gadolinium
central signal usually that of marrow
T2
acute infarct may show ill-defined non-specific area of high
signal
double-line sign: hyperintense inner ring of granulation tissue
and a hypointense outer ring of sclerosis
absence of double-line sign does not exclude bone infarct
central signal usually that of marrow
36. GE (gradient echo)
will also show double-line
oedema obscured by susceptibility
Nuclear medicine
bone scan
Bone scintigraphy is also quite sensitive (~85%) and is the second option
after MRI. It is a choice when multiple sites of involvement must be assessed
in patients with risk factors, such as sickle cell disease. The findings are
different accordingly to the time of the scan:
• early disease: often represented by a cold area likely representing the
vascular interruption
• late disease: may show a "doughnut sign": a cold spot with
surrounding high uptake ring (surrounding hyperaemia and adjacent
synovitis)
no uptake (cold spot) where blood supply absent
mildly increased uptake at periphery during acute phase
37. Biopsy
A biopsy is a surgical procedure in which a tissue
sample from the affected bone is removed and studied.
Although a biopsy is a conclusive way to diagnose
osteonecrosis, it is rarely used because it requires
surgery.
Functional Evaluation of Bone
Tests to measure the pressure inside a bone may be used
when the doctor strongly suspects that a patient has
osteonecrosis, despite normal results of x rays, bone
scans, and MRIs. These tests are very sensitive for
detecting increased pressure within the bone, but they
require surgery.
38.
39.
40. Imaging Method Findings Time to Diagnosis Comments
CT
reactive sclerosis
subchondral
collapse
months
sensitivity poor
specificity OK
radionuclide
imaging
decreased uptake
early, increased
uptake late
weeks
sensitivity good
specificity poor
MRI
decreased signal in a
segmental pattern
days to weeks
sensitivity excellent
specificity good
MRI or PET flow
study
decreased flow
through affected
bone
minutes
theoretically
possible, but not yet
proven
46. Differential
Diagnostic Considerations
Other problems to consider in the differential diagnosis
of avascular necrosis include the following:
Inflammatory synovitis
Complex regional pain syndrome
Labral tears
Osteomyelitis
Neoplastic bone conditions
Differential Diagnoses
Osteoarthritis
Osteoporosis
47. Various methods for treatment and delaying disease
progression
Non surgical –
Appropriate treatment for osteonecrosis is necessary to keep
joints from breaking down. Without treatment, most people with
the disease will experience severe pain and limitation in
movement. To determine the most appropriate treatment, the
doctor considers the following:
the age of the patient
the stage of the disease (early or late)
the location and whether bone is affected over a small
or large area
the underlying cause of osteonecrosis; with an ongoing
cause such as corticosteroid or alcohol use, treatment may not
work unless use of the substance is stopped.
The goal in treating osteonecrosis is to improve the patient’s
use of the affected joint, stop further damage to the bone, and
ensure bone and joint survival. To reach these goals, the doctor
may use one or more of the following surgical or nonsurgical
treatments.
48. Nonsurgical Treatments
Usually, doctors will begin with nonsurgical treatments,
alone or in combination. Unfortunately, although these
treatments may relieve pain or help in the short term, for
most people they don’t bring lasting improvement.
Medications.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are often
prescribed to reduce pain.
People with clotting disorders may be given blood
thinners to reduce clots that block the blood supply to
the bone.
Cholesterol-lowering medications may be used to
reduce fatty substances (lipids) that increase with
corticosteroid treatment (a major risk factor for
osteonecrosis).
Bisphosphonate
Anticoagulants
Vasodilators
Biophysical modalities
49. Reduced weight bearing. If osteonecrosis is diagnosed
early, the doctor may begin treatment by having the
patient remove weight from the affected joint. The doctor
may recommend limiting activities or using crutches. In
some cases, reduced weight bearing can slow the
damage caused by osteonecrosis and permit natural
healing. When combined with pain medication, reduced
weight bearing can be an effective way to avoid or delay
surgery for some patients.
Range-of-motion exercises. An exercise program
involving the affected joints may help keep them mobile
and increase their range of motion.
Electrical stimulation. This treatment has been used in
several centers to induce bone growth, and in some
studies has been helpful when used before femoral head
collapse.
50. Surgical –
A number of different surgical procedures are used to treat osteonecrosis. Most people
with osteonecrosis will eventually need surgery.
Core decompression. This surgical procedure removes the inner cylinder of bone,
which reduces pressure within the bone, increases blood flow to the bone, and
allows more blood vessels to form. Core decompression works best in people who
are in the earliest stages of osteonecrosis, often before the collapse of the joint. This
procedure sometimes reduces pain and slows the progression of bone and joint
destruction.
Osteotomy. This treatment involves reshaping the bone to reduce stress on the
affected area. Recovery can be a lengthy process, requiring several months of very
limited activities. This procedure is most effective for patients with early-stage
osteonecrosis and those with a small area of affected bone.
Vascularised bone graft/muscle pedicle graft.This is the transplantation of
healthy bone from another part of the body. It is often used to support a joint after
core decompression. In many cases, the surgeon will use what is called a vascular
graft, which includes an artery and vein, to increase the blood supply to the affected
area. Recovery from a bone graft can take several months.
Arthroplasty/total joint replacement. Total joint replacement is the treatment of
choice in late-stage osteonecrosis and when the joint is destroyed. In this surgery,
the diseased joint is replaced with artificial parts. Total joint replacement, or
sometimes femoral head resurfacing, is often recommended for people for whom
other efforts to preserve the joint have failed. Various types of replacements are
available, and people should discuss specific needs with their doctor.