Can avascular necrosis be fatal: Your Hip Pain May be the Sign of a Rare Condition
Avascular necrosis of bone in severe acute respiratory syndrome
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Clin Radiol. 2004 Jul; 59(7): 602–608.
Published online 2004 Jun 18. doi: 10.1016/j.crad.2003.12.008
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AIM: To report the incidence of avascular osteonecrosis (AVN) in severe acute respiratory syndrome (SARS) patients.
MATERIALS AND METHODS: Sixty-seven SARS patients who had large joint pain between March 2003 and May 2003 underwent both plain radiographs and magnetic resonance imaging (MRI) examination on the same day. All patients received steroids and ribavirin treatment. All plain radiographs and MR images were analysed by two experienced musculoskeletal radiologists. Any abnormalities, location, extent, morphology, the number, size and signal intensity of lesions were evaluated.
RESULTS: Twenty-eight patients were identified with AVN, The mean time to diagnosis of AVN was 119 days after the onset of SARS, or 116 days after steroid use. Three patients had early bilateral AVN of the femoral head, four patients of one femoral head, five patients of the bilateral hips and knees, four patients of the ipsilateral hip and knees, 10 patients of the knee(s), one patient of the right proximal fibula, and one patient of the knees and talus. Results of hip, knee and ankle plain radiographs were negative.
CONCLUSION: AVN can occur in the patients with SARS. AVN had a strong association with steroid use. More studies are required to confirm whether the virus itself can also lead to AVN.
Keywords: Bones, Necrosis, Magnetic resonance, Steroids
Severe acute respiratory syndrome (SARS) is a newly recognized disease that was first reported in Guangdong province, People’s Republic of China, in November 2002, and it has rapidly spread to other Asian countries, North America, and Europe. By 12 August, 2003, more than 8000 individuals have been infected with SARS, of which 812 were fatal.1., 2. It has been shown that a previously unknown coronavirus is the primary cause of SARS.3., 4., 5., 6.
Avascular osteonecrosis (AVN) is a well-recognized condition of unknown aetiology whereby the circulation of the blood to an area of bone is impaired.7 Eventually the involved area of bone dies and necrosis develops. It may be idiopathic or associated with a number of diseases, such as trauma, use of steroids, sickle cell disease, and vasculitis. Risk factors include the use of steroids and alcohol abuse. Intravascular fat embolism or thrombosis, coagulopathy, venous congestion and development of intra-osseous hypertension have been postulated as aetiological factors.8., 9. The early diagnosis of AVN is important as surgical core decompression may arrest the progress of the condition and prevent subsequent femoral head collapse.10
About 23–32% of SARS patients become critically ill,11 so corticosteroids are frequently prescribed. Corticosteroids have long been regarded as a predisposing factor for the development of AVN. AVN has not been previously reported in patients with SARS so the present study was undertaken to investigate the incidence of AVN in SARS patients.
Sixty-seven patients (age range 21–55 years; mean age 32.3 years) consisting of 55 women (age range 21–55 years; mean age 32.9 years) and 12 men (age range 21–52 years; mean age 28.5 years) who fitted the WHO case definition for SARS,12 and who had also reported large joint pain during or after hospitalization were included in our study group. None of the patients had pre-SARS joint pain. The joint pain was discovered in a retrospective review of the notes, and occurred 12–120 days after the onset of SARS (average 60.73 days). Except for one patient, all patients were hospital staff, and the majority were nurses.
They were screened with plain radiographs of the affected joints. If no suitable reason was found for the pain (such as osteoarthritis or fractures), magnetic resonance imaging (MRI) examination was undertaken on the affected joint (hip, knee or ankle) on the same day as plain radiograph. Informed consents were obtained from all the patients, and they could withdraw at any time.
The antiviral agent, ribavirin, was administered to all patients, 750 mg daily for about 2 weeks, then taken orally 250 mg daily for 1 week. All patients were treated with intravenous methylprednisolone (80–800 mg daily) for 3–20 consecutive days, 1–11 days after the diagnosis of SARS was made, then oral prednisolone was given, they were managed conservatively with stepwise steroid withdrawal. The cumulative dosage of therapeutic doses was 4117.33 mg (range 640–20,000 mg).
None of the patients were alcoholics or intravenous drug users.
2.2. MRI protocol
MRI was performed using a 1.5 T Signa CVi imager (GE Medical Systems, Milwaukee WI, USA). A phased-array body coil was used. All MRI examinations were performed by using preset protocols, as follows: for the hip, coronal T2-weighted fast spin-echo sequence (3400 ms/100 ms (repetition time/echo time), 5 mm section thickness, 0. 5 mm section gap, echo train length of 16, 256×224 matrix, 400 mm field of view) followed by a coronal short tau inversion recovery (STIR) fat-suppressed T2-weighted sequence (3420/100, 5 mm section thickness, 0.5 mm section gap, echo train length of 16, 256×224 matrix, 400 mm field of view) and a coronal T1-weighted spin-echo sequence (460/8.3, 5 mm section thickness, 0.5 mm section gap, 256×224 matrix, 400 mm field of view).
For the knee, coronal T2-weighted fast spin-echo sequence (3140 ms/100 ms (repetition time/echo time), 5 mm section thickness, 1.5 mm section gap, echo train length of 16, 256×224 matrix, 400 mm field of view) followed by a coronal STIR fat-suppression sequence (3420/100, 5 mm section thickness, 1.5 mm section gap, echo train length of 16, 256×224 matrix, 400 mm field of view) and a coronal T1-weighted spin-echo sequence (400/8.3, 5 mm section thickness, 1.5 mm section gap, 256×224 matrix, 400 mm field of view).
2.3. MR Image evaluation
AVN was diagnosed using MRI as interpreted by two experienced musculoskeletal radiologists (N. H, X.K.D), who separately evaluated all the MR images; agreement was reached by consensus. Established MRI criteria and staging systems were used for the diagnosis of AVN.14 The following characteristics, such as location, extent, morphology, the number, size and signal intensity of lesions on T1-weighted, T2-weighted and fat-suppressed T2-weighted MR images were evaluated.
No abnormality could be found on the plain radiographs of all of the patients. The diagnosis of AVN was based on MR findings. Twenty-eight of 65 SARS patients between April 2003 and August 2003 were identified as having AVN (). Among them, there are 22 women (age range, 23–50 years; mean age, 31.8 years) and six men (age range, 21–52 years; mean age, 29.2 years). The mean time to diagnosis of AVN was 119 days after the diagnosis of SARS, or 116 days after steroid administration. Three patients had bilateral AVN of the hips (), four patients of one femoral head (), five patients of the bilateral hips, distal femur and proximal tibia, four patients of the ipsilateral hip and knees, 10 patients of the knee(s), one patient of right proximal fibula, and one patient of knees and talus (). However, many small patchy areas of AVN involving the subchondral areas of the medial, lateral femoral condyle and tibia plateau were found ().
Clinical characteristics of patients with severe acquired respiratory sydrome (SARS) complicated by avascular necrosis (AVN)
|Patient No.||Age||Sex||AVN||Mean time to diagnosis of AVN after:|
|SARS (days)||Steroid use (days)|
|1||36||F||Bilateral distal femur, proximal tibia and left talus||108||99|
|2||21||M||Bilateral distal femur and right proximal tibia||93||91|
|3||47||F||Bilateral distal femur||109||108|
|4||33||F||Left hip and bilateral distal femur||104||103|
|6||28||M||Bilateral hips and right distal femur||100||96|
|7||24||M||Right proximal fibula||125||125|
|8||22||F||Left distal femur||135||131|
|10||30||F||Right distal femur||111||110|
|11||49||F||Bilateral hips, distal femur and left proximal tibia||109||109|
|12||34||F||Bilateral hips, distal femur and left proximal tibia||130||127|
|14||52||M||Right femur neck, distal femur and bilateral proximal tibia||111||107|
|16||25||F||Bilateral hips, distal femur and proximal tibia||122||122|
|18||24||F||Right distal femur and proximal tibia||116||114|
|19||30||F||Right hip, bilateral distal femur and left proximal tibia||118||116|
|20||24||F||Right hip, left distal femur and bilateral proximal tibia||118||117|
|22||24||F||Right distal femur and bilateral proximal tibia||135||134|
|23||26||M||Left distal femur and right proximal tibia||120||115|
|24||31||F||bilateral distal femur||122||120|
|25||36||F||Bilateral hips, distal femur and right proximal tibia||145||143|
|26||24||M||Left distal femur and right proximal tibia||124||123|
|28||50||F||Right distal femur||128||118|
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MR images of pelvis of patient 7. (a) Coronal T2-weighted and (b) coronal T2-weighted fat-suppressed and (c) coronal T1-weighted MR images showing bilateral AVN of the femoral heads.
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MR images of pelvis of patient 21. (a) Coronal T2-weighted and (b) coronal T2-weighted fat-suppressed and (c) coronal T1-weighted MR images showing AVN of the left femoral head.
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MR images of the knee and left ankle of patient 1. (a) Coronal T2-weighted and (b) coronal T2-weighted fat-suppressed and (c) coronal T1-weighted and (d) coronal T2-weighted and (e) coronal T1-weighted and (f) sagittal T1-weighted MR images showing AVN of the bilateral distal femurs, left proximal tibia and left talus.
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MR images of knee of patient 19. (a) Coronal T2-weighted and (b) coronal T2-weighted fat-suppressed and (c) coronal T1-weighted MR images showing AVN of the subchondral areas of the bilateral femoral condyle and left tibia plateau.
SARS is a new disease that was first reported in Guangdong Province, People’s Republic of China in November 2002, from where it rapidly spread throughout Asia, North America and Europe. Coronavirus was found to be the primary cause of SARS.3., 4., 5., 6.
AVN represents compromised circulation of the blood to an area of bone.7 As a result haematopoietic cells, which are sensitive to anoxia, usually die within 6–12 h after reduction or removal of the blood supply, bone cells usually die within 12–48 h, and marrow fat cells usually die within 5 days.13 Many mechanisms have been postulated as causes of AVN, including the following: trauma; idiopathic causes, such as Legg-Calvé-Perthes disease; renal transplantation; increase in endogenous steroid levels; use of immunosuppressants and other drugs, such as exogenous steroids; collagen vascular disorders, such as systemic lupus erythematosus; haemoglobinopathies, such as sickle cell disease, haemophilia; alcohol use; and others. Existing hypotheses for its pathogenesis include vascular thrombosis, fat embolism, or vasculitis.14
Early diagnosis of AVN is important, as suitable treatment may prevent its progress and subsequent bone collapse. However, the early diagnosis of AVN is difficult using plain radiographs, as radiographs usually appear normal at stage 1, but radiography can identify the latter stages of AVN. Bone scintigraphy and MRI improve the diagnostic accuracy.15 MRI is the most sensitive diagnostic technique for the diagnosis of AVN at any stage,7., 16., 17., 18. particular in the early stage, with a sensitivity of 93–100%.15., 19. It aids staging, estimating prognosis and surgical planning.20., 21. In our study, no abnormalities were seen on the plain radiographs or computed tomography (CT), but AVN was diagnosed using MRI, so MRI is the imaging technique of choice for the early diagnosis of AVN.
The association of AVN with steroid use has long been recognized. AVN can occur from 6 months to 10 years after the use of steroid.22 The pathogenesis of steroid-induced AVN is unknown, but it maybe due to the increase in the size of marrow fat cells or to fat embolism, so that the intra-osseous pressure is increased. 23 As about 23–32% of SARS patients become critically ill,11 corticosteroids, either intravenously and/or orally, are frequently prescribed. In our study, all the SARS patients received steroids. Some studies show that there is no relation between AVN and the cumulative dosages of therapeutic doses,24., 25. but other studies show a strong correlation between the mean daily total steroid dose and AVN.26., 27. A study by Rademaker et al.28 shows that 700 mg prednisolone is the threshold for developing AVN. In our study, only one patient received prednisolone below this threshold (640 mg), and at the time of writing this patient has not developed AVN.
It is said that body weight gain might also be a risk factor for the development of AVN, but this is controversial.14., 25. Body weight gain might be an independent risk factor for AVN, as it did not correlate with the use of steroids.29
It is unknown why AVN occurred 91–143 days after the steroid use, which is shorter than is generally recognized for patients receiving chronic steroid therapy. 22., 30. Also why many patchy areas of AVN involving the subchondral areas of the distal femoral condyle and tibia plateau were found. As MRI is more sensitive than plain radiography, this could be one reason to explain the anomalies in the present study; but as we know little about this new coronavirus, whether the virus itself or in combination with steroid use could lead to these phenomenon, still needs to be studied. Further study is needed to follow up those SARS patients without joint pain to investigate whether they develop AVN in the future.
In conclusion, we have documented the incidence of AVN in association with SARS. Corticosteroids could be the major predisposing factor in the development of AVN in SARS patients. This risk of the development of AVN should be borne in mind, and steroids should be administrated cautiously.
1. World Health Organisation. Cumulative number of reported probable cases of SARS. Available at: http: www.who.int/csr/sars/countr/2003_06_09/en. Accessed 11 June, 2003. Accessibility verified 23 June, 2003.
2. World Health Organisation Severe acute respiratory syndrome (SARS) Wkly Epidemiol Rec. 2003;78:81–83. [PubMed] [Google Scholar]
3. Ksiazek T.G, Erdman D, Goldsmith C.S. A novel coronavirus associated with severe acute respiratory syndrome. N Engl J Med. 2003;348:1953–1966. [PubMed] [Google Scholar]
4. Drosten C, Gunther S, Preiser W. Identification of a novel coronavirus in patients with severe acute respiratory syndrome. N Engl J Med. 2003;348:1967–1976. [PubMed] [Google Scholar]
5. Peiris J.S, Lai S.T, Poon L.L. Coronavirus as a possible cause of severe acute respiratory syndrome. Lancet. 2003;361:1319–1325. [PMC free article] [PubMed] [Google Scholar]
6. Kuiken T, Fouchier R.A, Schutten M. Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome. Lancet. 2003;362:263–270. [PMC free article] [PubMed] [Google Scholar]
7. Imhof H, Breitenseher M, Trattnig S. Imaging of avascular necrosis of bone. Eur Radiol. 1997;7:180–186. [PubMed] [Google Scholar]
8. Chernetsky S.G, Mont M.A, LaPorte D.M, Jones L.C, Hungerford D.S, McCarthy E.F. Pathologic features in steroid and non-steroid associated osteonecrosis. Clin Orthop. 1999;368:149–161. [PubMed] [Google Scholar]
9. Jones J.P., Jr. Intravascular coagulation and osteonecrosis. Clin Orthop. 1992;277:41–53. [PubMed] [Google Scholar]
10. Ryu J.S, Kim J.S, Moon D.H. Bone SPECT is more sensitive than MRI in the detection of early osteonecrosis of the femoral head after renal transplantation. J Nucl Med. 2002;43:1006–1011. [PubMed] [Google Scholar]
11. Peiris J.S, Chu C.M, Cheng V.C. Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study. Lancet. 2003;361:1767–1772. [PMC free article] [PubMed] [Google Scholar]
12. World Health Organisation. Case definitions for surveillance of severe acute respiratory syndrome (SARS). Available at: http://www.who.int/csr/sars/casedefinition/en. Accessed 18 August, 2003.
13. Burgener F.A, Meyers S.P, Tan R.K, Zaunbauer W. Thieme Stuttgart; New York: 2002. Musculoskeletal system. In Differential diagnosis in magnetic resonance imaging. [Google Scholar]
14. Tang S, Chan T.M, Lui S.L, Li F.K, Lo W.K, Lai K.N. Risk factors for avascular bone necrosis after renal transplantation. Transplant Proc. 2000;32:1873–1875. [PubMed] [Google Scholar]
15. Tervonen O, Mueller D.M, Matteson E.L, Velosa J.A, Ginsburg W.W, Ehman R.L. Clinically occult avascular necrosis of the hip: prevalence in an asymptomatic population at risk. Radiology. 1992;182:845–847. [PubMed] [Google Scholar]
16. Bluemke D.A, Zerhouni E.A. MRI of avascular necrosis of bone. Top Magn Reson Imaging. 1996;8:231–246. [PubMed] [Google Scholar]
17. Usher B.W, Friedman R.J. Steroid-induced osteonecrosis of the humeral head. Orthopedics. 1995;18:47–51. [PubMed] [Google Scholar]
18. Gogas H, Fennelly D. Avascular necrosis following extensive chemotherapy and dexamethasone treatment in a patient with advanced ovarian cancer: case report and review of the literature. Gynecol Oncol. 1996;63:379–381. [PubMed] [Google Scholar]
19. Arlet J. Non-traumatic avascular necrosis of the femoral head. Past, present, and future. Clin Orthop. 1992;277:12–21. [PubMed] [Google Scholar]
20. Wright D.G, Adelaar R.S. Avascular necrosis of the talus. Foot Ankle Int. 1995;16:743–744. [PubMed] [Google Scholar]
21. Schweitzer M.E. Magnetic resonance imaging of the foot and ankle. Magn Reson Q. 1993;9:214–234. [PubMed] [Google Scholar]
22. Blacksin M.F, Kloser P.C, Simon J. Avascular necrosis of bone in human immunodeficiency virus infected patients. Clin Imaging. 1999;23:314–318. [PubMed] [Google Scholar]
23. Wang G.J, Sweet D.E, Reger S.I, Thompson R.C. Fat-cell changes as a mechanism of avascular necrosis of the femoral head in cortisone-treated rabbits. J Bone Joint Surg Am. 1977;59:729–735. [PubMed] [Google Scholar]
24. Fryer J.P, Granger D.K, Leventhal J.R, Gillingham K, Najarian J.S, Matas A.J. Steroid-related complications in the cyclosporin era. Clin Transplant. 1994;8:224–229. [PubMed] [Google Scholar]
25. Han D, Kim S, Chang J, Kim S. Avascular necrosis following renal transplantation. Transplant Proc. 1998;30:3034–3035. [PubMed] [Google Scholar]
26. Zizic T.M, Marcoux C, Hungerford D, Dansereau J.V, Stevens M.B. Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus. Am J Med. 1985;79:598–604. [PubMed] [Google Scholar]
27. Isono S.S, Woolson S.T, Schurman D.J. Total joint arthroplasty for steroid-induced osteonecrosis in cardiac transplant patients. Clin Orthop. 1987;217:201–208. [PubMed] [Google Scholar]
28. Rademaker J, Dobro J.S, Solomon G. Osteonecrosis and human immunodeficiency virus infection. J Rheumatol. 1997;24:601–604. [PubMed] [Google Scholar]
29. Johnson C.P, Gallagher-Lepak S, Zhu Y. R. Factors influencing weight gain after renal transplantation. Transplantation. 1993;56:822–827. [PubMed] [Google Scholar]
30. Enright H, Haake R, Weisdorf D. Avascular necrosis of bone: a common serious complication of allogeneic bone marrow transplantation. Am J Med. 1990;89:733–738. [PubMed] [Google Scholar]
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Avascular Necrosis (AVN or Osteonecrosis): Symptoms, Causes, Treatment
Written by Mary Anne Dunkin
Medically Reviewed by Dan Brennan, MD on October 25, 2022
- What Is Avascular Necrosis?
- Symptoms of Avascular Necrosis
- Causes and Risk Factors for Avascular Necrosis
- Who Gets Avascular Necrosis?
- Avascular Necrosis Diagnosis
- Avascular Necrosis Treatment
- Caring for Avascular Necrosis at Home
- Prognosis for Avascular Necrosis
Avascular necrosis (AVN) is the death of bone tissue due to a loss of blood supply. You might also hear it called osteonecrosis, aseptic necrosis, or ischemic bone necrosis.
If it isn’t treated, AVN can cause the bone to collapse. AVN most often affects your hip. Other possible sites are the shoulder, knees, and ankles.
In its earliest stages, AVN may have no symptoms, but as the disease progresses it typically becomes very painful. At first, it might only hurt when you put pressure on the affected bone. Then, pain may become constant. If the bone and surrounding joint collapse, you may have severe pain that makes you unable to use your joint. The time between the first symptoms and bone collapse can range from several months to more than a year.
Things that can make avascular necrosis more likely include:
- Alcohol. Several drinks a day can cause fat deposits to form in your blood, which lower the blood supply to your bones.
- Bisphosphonates. These medications that boost bone density could lead to osteonecrosis of the jaw. This could be more likely if you’re taking them for multiple myeloma or metastatic breast cancer.
- Medical treatments. Radiation therapy for cancer can weaken bones. Other conditions linked to AVN include organ transplants, like kidney transplants.
- Steroid drugs. Long-term use of these inflammation-fighting drugs, either by mouth or in a vein, leads to 35% of all cases of nontraumatic AVN. Doctors don’t know why, but longtime use of medications like prednisone can lead to AVN. They think the meds can raise fat levels in your blood, which lowers blood flow.
- Trauma. Breaking or dislocating a hip can damage nearby blood vessels and cut the blood supply to your bones. AVN may affect 20% or more of people who dislocate a hip.
- Blood clots, inflammation, and damage to your arteries. All of these can block blood flow to your bones.
Other conditions associated with nontraumatic AVN include:
- Decompression sickness, which causes gas bubbles in your blood
- Gaucher disease, in which a fatty substance collects in the organs
- Long-term use of drugs called bisphosphonates to treat cancers like multiple myeloma or breast cancer, which can lead to AVN of the jaw.
- Pancreatitis, inflammation of the pancreas
- Radiation therapy or chemotherapy
- Autoimmune diseases such as lupwww.webmd.com/lupus/arthritis-lupusus
- Sickle cell disease
As many as 20,000 people develop AVN each year. Most are between ages 20 and 50. For healthy people, the risk of AVN is small. Most cases are the result of an underlying health problem or injury.
Your doctor will start with a physical exam. They’ll press on your joints to check for tender spots. They’ll move your joints through a series of positions to check your range of motion. You might get one of these imaging tests to look for what’s causing your pain:
- Bone scan. The doctor injects radioactive material into your vein. It travels to spots where bones are injured or healing and shows up on the image.
- MRI and CT scan. These give your doctor detailed images showing early changes in bone that might be a sign of AVN.
- X-rays. They’ll be normal for early stages of AVN but can show bone changes that appear later on.
Treatment goals for AVN are to improve the joint, stop the bone damage, and ease pain. The best treatment will depend on a number of things, like:
- Your age
- Stage of the disease
- Location and amount of bone damage
- Cause of AVN
If you catch avascular necrosis early, treatment may involve taking medications to relieve pain or limiting the use of the affected area. If your hip, knee, or ankle is affected, you may need crutches to take weight off the damaged joint. Your doctor may also recommend range-of-motion exercises to help keep the joint mobile.
- Medications. If the doctor knows what’s causing your avascular necrosis, treatment will include efforts to manage it. This can include:
- Blood thinners. You’ll get these if your AVN is caused by blood clots.
- Nonsteroidal anti-inflammatory drugs (NSAIDs). These will help with pain.
- Cholesterol drugs. They cut the amount of cholesterol and fat in your blood, which can help prevent the blockages that lead to AVN.
- Surgery. While these nonsurgical treatments may slow down the avascular necrosis, most people with the condition eventually need surgery. Surgical options include:
- Bone grafts. Removing healthy bone from one part of the body and using it to replace the damaged bone
- Osteotomy. Cutting the bone and changing its alignment to relieve stress on the bone or joint
- Total joint replacement. Removing the damaged joint and replacing it with a synthetic joint
- Core decompression. Removing part of the inside of the bone to relieve pressure and allow new blood vessels to form
- Vascularized bone graft. Using your own tissue to rebuild diseased or damaged hip joints. The surgeon first removes the bone with the poor blood supply from the hip, then replaces it with the blood-vessel-rich bone from another site, such as the fibula, the smaller bone in your lower leg.
- Electrical stimulation. An electrical current could jump-start new bone growth. Your doctor might use it during surgery or give you a special gadget for it.
You can do these things to help:
- Rest. Stay off the joint. This can help slow damage. You might need to hold back on physical activity or use crutches for several months.
- Exercise. A physical therapist can show you the right moves to get range of motion back in your joint.
To lower your risk of AVN:
- Cut back on alcohol. Heavy drinking is a leading risk factor for AVN.
- Keep your cholesterol in check. Small bits of fat are the most common thing blocking blood supply to you bones.
- Use steroids carefully. Your doctor should keep tabs on you while you’re taking these medications. Let them know if you’ve used them in the past. Taking them over and over again can worsen bone damage.
- Don’t smoke. It boosts your AVN risk.
More than half the people with this condition need surgery within 3 years of diagnosis. If a bone collapse in one of your joints, you’re more likely to have it happen in another.
Your outlook depends on several things:
- Disease stage at the time you were diagnosed
- If you have an underlying condition
You’re less likely to do well if:
- You’re over 50.
- You’re at stage III or higher when you’re diagnosed.
- More than a third of the bone’s weight-bearing area is dead.
- The damage goes past the end of the bone.
- You have a long history of cortisone treatments.
Avascular Necrosis (AVN)/Osteonecrosis – together by St. Jude
Other names: OH, aseptic necrosis, ischemic bone necrosis
What is avascular necrosis (AVN)?
Avascular necrosis (osteonecrosis) is a condition in which part of the bone dies due to poor blood supply. Avascular necrosis may be a side effect of certain cancers or treatments.
Children at high risk are those receiving high doses of corticosteroids (dexamethasone and prednisone).
Avascular necrosis may be mild and improve after treatment is completed, or it may be severe, accompanied by severe pain and long-term disability.
Avascular necrosis in children with cancer
Avascular necrosis (AVN) is a common side effect of treatment for leukemia and lymphoma. Nearly half of children treated for acute lymphoblastic leukemia (ALL) suffer from some degree of avascular necrosis. In addition, the high-risk group includes children who have undergone bone marrow transplantation.
In children with cancer, avascular necrosis often occurs at the ends of long bones, at a site called the epiphysis.
This disease can affect any bone. However, in children with cancer, avascular necrosis often occurs at the ends of long bones, at a site called the epiphysis.
Avascular necrosis can be accompanied by pain and affect joint function, especially knee, hip, shoulder and ankle. Damage to the bone and joint can lead to long-term problems such as joint destruction and arthritis.
In cancer treatment, avascular necrosis is more common in older children and adolescents than in young children or adults. In children younger than 10 years, this condition is less common.
Avascular necrosis can be difficult to diagnose in its early stages. The patient may not experience pain or other symptoms until severe bone damage develops. The condition of high-risk children should be monitored throughout the course of treatment.
Treatment of avascular necrosis depends on the severity of the pain and the degree of bone destruction. Pain relief and physical therapy can help manage symptoms. Some patients may require surgery to improve blood flow and relieve pressure within the bone. In case of severe damage or destruction of the joint, the patient may eventually need arthroplasty.
Symptoms of avascular necrosis
Some patients may not show symptoms at all, especially in the early stages. As the condition worsens, pain in the joint or bone may appear. Family members may notice that the child has begun to limp, tries not to use the affected joint, stiffness or limitation of range of motion may become noticeable. Occasionally, avascular necrosis can lead to bone destruction, with the pain escalating dramatically.
Avascular necrosis can develop in one place or in several bones at once (multifocal course). Chemotherapy affects the entire body, so when treating childhood cancer, avascular necrosis usually occurs in several joints, most commonly in the knee and/or hip. Other joints, such as the shoulder and ankle, may also be affected.
In general, the presence of pain and disability depends on the following factors:
- Which parts of the bone are affected
- How severe is the avascular necrosis
- How quickly progresses
- To what extent the bone is able to regenerate
However, pain cannot be considered a reliable indicator of the severity of avascular necrosis. Avascular necrosis in a small area can be very painful. At the same time, other patients may not have pain at all, despite the very large area affected by avascular necrosis.
Symptoms of avascular necrosis
- Pain (may be temporary or permanent)
- Joint stiffness or “stuck”
- Lameness or change in gait
- Tendency not to use the affected joint or avoidance of certain activities
- Problems getting up or down stairs
Factors that increase the risk of developing avascular necrosis
- High doses of dexamethasone or prednisone as part of cancer treatment
- Age over 10 years
- Sickle cell disease
- High-dose bone irradiation
- Treatment with asparaginase and dexamethasone
- Congenital genetic changes
Causes of avascular necrosis
Avascular necrosis is a complex process. The main reason for the development of avascular necrosis is a decrease in blood flow to the bone. If the blood vessels are too thin, damaged, or clogged, nutrients and oxygen cannot reach the bone, causing bone cells to begin to die.
Cancer treatments, including chemotherapy and radiation, can cause bone cell death and/or affect bone repair. As a result, the bone can break down faster than it has time to recover from damage. In addition, the treatment may affect the blood supply to the bones, leading to avascular necrosis.
Many children receive corticosteroid drugs (eg, dexamethasone, prednisone) for chemotherapy. These drugs are also used to combat side effects such as nausea and swelling. However, corticosteroids can increase the level of fatty substances (lipids) in the blood. Accumulation of fats in blood vessels can lead to blockage. In addition, these drugs can cause changes in the cells that line the walls of blood vessels, thereby thinning and weakening blood vessels.
Chronic high-dose dexamethasone is associated with a higher risk of developing avascular necrosis than prednisone or intermittent dexamethasone. Some drugs, such as asparaginase, can also interfere with the action of dexamethasone and increase the risk of developing avascular necrosis because these drugs interact with each other. Other drugs (eg, methotrexate) can also cause bone damage and increase the risk of avascular necrosis, especially when used with corticosteroids.
Diagnosis of avascular necrosis
Different medical centers have different approaches to identifying patients at risk and monitoring their condition. Imaging methods are used to identify areas of avascular necrosis (sometimes called foci). Magnetic resonance imaging (MRI) is the most sensitive diagnostic imaging modality for diagnosing avascular necrosis. X-rays are less sensitive, but may be useful for monitoring progression and for monitoring the patient’s condition in the postoperative period. Less commonly, other methods such as bone scintigraphy and computed tomography (CT) are used.
Some clinics screen children at high risk to detect avascular necrosis even if they are asymptomatic. As a rule, such screening is part of a clinical or scientific research program and is mainly carried out for the knee and hip joints. When screening high-risk patients who are asymptomatic, the most common finding of avascular necrosis is on diagnostic imaging of the knee. As a rule, necrosis is observed on both sides of the knee joint (femoral and tibial), the knee may be the only affected joint. However, if avascular necrosis is found in the hip joint, the knees are also most commonly affected.
Avascular necrosis associated with high doses of corticosteroids usually becomes visible on MRI within the first year of therapy. If a patient does not show signs of avascular necrosis on MRI after 12 months of therapy, then even continued use of corticosteroids will most likely not cause the development of this condition.
Physicians are constantly looking for more accurate diagnostic methods through the use of more sensitive imaging techniques. In addition, research is underway in the field of predicting the development of avascular necrosis.
Progression of avascular necrosis
The course of avascular necrosis is difficult to predict. Lesions may grow, remain stable, or disappear. Progression can be fast or slow.
The severity (or stage) of avascular necrosis is important to know for treatment planning. Doctors consider two main factors:
- Size of lesions
- Is the bone on which the articular surface rests damaged
If the damaged bone cannot support the joint surface, the bone tissue under the cartilage will begin to break down. The normally smooth layer of cartilage that lines the joints begins to flake off. This leads to problems in the joint, including arthritis, pain and decreased mobility of the joint.
Joint destruction is more likely if the lesion is:
- close to the surface of the joint
- large, occupies 30% or more of the entire surface
- located in a weight-bearing joint (thigh, knee)
Since the knee and hip joints work under weight load, in severe cases of avascular necrosis, their destruction is quite common. If the focus of avascular necrosis in the hip joint occupies more than 30% of the joint surface, joint destruction usually occurs within 2 years.
Treatment of avascular necrosis
Treatment of avascular necrosis is always individual. Doctors take into account the following factors:
- Patient age
- Patient health and cancer stage
- Cancer treatment used and chemotherapy schedule
- Stage of avascular necrosis
- What bones and joints are affected
- Severity of pain
The main treatment is to relieve pain, keep the joint functioning and prevent further damage.
Treatment strategies may include the following:
Your doctor may prescribe pain medications, including NSAIDs (meloxicam, celecoxib) or acetaminophen. However, some painkillers put the patient at risk for bleeding, kidney or liver problems, or worsening the side effects of chemotherapy. Family members should check with their doctor before giving a child any medications, even over-the-counter medications, as they may interact with other medications or increase side effects.
Research is underway to prevent or treat avascular necrosis with drugs that affect blood flow, blood clotting, inflammation, fat metabolism, and/or bone cells. However, it has not yet been possible to achieve sustainable positive results.
Physiotherapy is an important part of the treatment of avascular necrosis. The physiotherapist will recommend how to reduce the weight load or eliminate painful activities. They may also prescribe special treatments, including:
- Exercises to help with the patient’s limitations (muscle weakness, joint stiffness, or trouble walking).
- Aids (walkers, crutches or canes) to aid mobility and reduce weight bearing on the affected joint. The physiotherapist will select the appropriate option and teach the patient how to walk with their help.
- Orthoses and support bandages (foot, knee or arm) support the affected joint and help reduce pain during daily tasks
- Instructions for home care, including gymnastics, recommendations for exercise and treatment with heat and/or cold
Avascular necrosis and weight-bearing effects
Reduced weight-bearing is recommended to avoid joint damage, severe pain and healing after surgery. However, many doctors and physiotherapists recommend that the patient perform light activities, as far as pain allows. Physical activity is important for increasing blood circulation, improving bone healing, and strengthening muscles, which reduces stress on the joints.
Patients with avascular necrosis should avoid high impact activities such as running, jumping and contact sports. This is especially important in patients with severe avascular necrosis to avoid joint destruction due to trauma.
Complementary or integrative therapies
The patient may benefit from psychosomatic therapies (eg, massage, acupuncture, biofeedback, and relaxation techniques). Special techniques help to cope with pain, reduce stress, reduce muscle tension and improve blood flow. Before using any new treatments, the patient’s family should consult with their physician to ensure they are safe and appropriate for the patient.
Adjustment of chemotherapy
In the case of severe avascular necrosis, the treatment team may recommend changing the chemotherapy plan to reduce the body’s exposure to corticosteroids. Such decisions should be made taking into account the risks to the health of patients in general.
Some patients require surgery to treat avascular necrosis. The operation will speed up the healing of the bone and prevent its further damage. Joint replacement may also be required. The following types of procedures are possible:
- Bone decompression – This procedure is performed to reduce pressure within the bone, increase blood flow and thereby improve healing speed. With this decompression, the surgeon drills small holes in the bone, cracking open the damaged tissue. After the dead tissue is removed, the voids can be filled with a bone graft. This is a minimally invasive surgery requiring only a small incision. It usually takes several weeks of rest or weight-bearing to heal. Typically, patients recover quickly and report less pain and improved joint function.
- Bone graft is a surgical procedure performed for avascular necrosis to replace and restore bone tissue with a bone graft. In this case, the transplanted tissue can be taken from the patient himself (from another bone, autograft) or from a donor (allograft). In addition, artificial materials can be used. If the cartilage is damaged, a combined bone and cartilage graft may be used. In some cases, blood vessels are also transplanted along with the bone tissue. This material is called a vascularized bone graft. It can help improve the blood supply to the joint. In avascular necrosis, bone grafting is most often used in conjunction with bone decompression.
- Arthroscopy is a type of minimally invasive procedure in which a miniature camera and fine surgical instruments are inserted through small incisions. In patients with avascular necrosis, arthroscopy may be used to repair torn cartilage, smooth the surface of a bone, or remove debris from inside a joint. This can relieve symptoms such as pain, stiffness, and a “stuck” joint.
- Osteotomy – This surgical operation is used to reduce the weight load on the affected area by reshaping or repositioning the bone. During this procedure, a wedge-shaped incision is made in the bone, after which the bone can be rotated, thereby changing the load on it. In the new position, the bone is held by plates, staples or screws until it heals. Osteotomy can help prevent joint destruction, delaying or eliminating the need for a joint replacement.
- Arthroplasty (Arthroplasty) – Joint replacement surgery may be required for severe bone disease. During this operation, the affected bone is removed and replaced with an artificial joint. Endoprosthetics may be needed for young patients after joint destruction. However, arthroplasty is also a common operation for adult cancer survivors who suffer from arthritis or who complain of worsening joint function years after treatment ends. Patients who have undergone joint replacement at an early age are likely to have to undergo repeated surgery in the future. Early diagnosis and treatment of avascular necrosis is important to prevent or delay arthroplasty.
Managing Avascular Necrosis: Tips for Patients and Families
Know your risks. Talk to your doctor about the patient’s cancer treatment (including doses received) and other risk factors.
Monitor your symptoms and get recommended tests. Seek medical attention if you develop pain or problems with your joints, especially if symptoms have not been observed before or if they worsen. Once your treatment is over, ensure that bone health is adequately addressed in your rehabilitation plan.
Stay physically active. Adjust your physical activity to reduce weight bearing and pay attention to pain as it will tell you what level of activity is acceptable. Avoid activities that involve pushing and falling, as well as contact sports – take care of bones and joints. If you’re not sure if a particular sport is okay to play, ask your doctor or physical therapist.
Wear shoes that provide support and use your prescribed orthoses and assistive devices. This is important as it helps to maintain proper joint alignment and function. Proper footwear also helps prevent falls and joint injuries.
Bone health and overall well-being depend on a healthy lifestyle:
Eat healthy foods, stay physically active, maintain a healthy weight, and don’t smoke.
Modified January 2019
Avascular necrosis. Description of the disease, methods of treatment
Avascular necrosis (osteonecrosis or bone infarction) is the death of bone tissue due to blockage of the blood supply. Hematopoietic cells are most sensitive to low oxygen levels and are the first to die after reduced blood flow (usually within 12 hours). This starts the process of bone marrow death and subsequent destruction of the entire bone.
The most common is avascular necrosis of the femoral head. Basically, the hip joint suffers from a combination of unreliable blood supply and high stress in this area while standing.
Symptoms and causes of avascular necrosis of the femoral head
At the initial stage of the disease, symptoms do not appear. Gradually, joint pain may develop, limiting the ability to move. With a complication, there is a risk of destruction of the bone or the nearby surface of the joint.
Major risk factors are bone fractures, hip dislocation, alcoholism and high dose steroid use. Sometimes avascular necrosis can develop as a side effect of radiation therapy, chemotherapy, or organ transplantation. Osteonecrosis is also associated with diseases such as cancer, lupus, sickle cell anemia, HIV infections, Gaucher’s disease, and decompression sickness.
Examination for avascular necrosis of the femoral head
In the early stages of avascular necrosis of the bone, bone scintigraphy and MRI are the preferred diagnostic methods. X-rays at this stage of the disease often show no abnormalities. In the later stages, the picture looks less transparent than usual.
Treatment of avascular necrosis of the femoral head
Various methods are used to treat avascular necrosis of the femoral head. The most common approach is a total hip replacement.
Endoprosthetics for avascular necrosis of the femoral head is an effective method for the elderly. When installing a prosthesis in young patients, over time, a second operation may be required due to the expiration of its expiration date.
Other treatments include bisphosphonates. These are drugs that slow down the rate at which bone breaks down. Sometimes decompression (tunnelization) of the core of the affected hip bone is performed. The internal pressure of the bone is relieved by drilling a hole in it and implanting living bone tissue and an electrical device to stimulate new vascular growth.
A microvascular free fibula graft can also be placed for avascular necrosis. In this procedure, a portion of the fibula, along with its blood supply, is removed and transplanted into the head of the femur.