1 LU5 Panel Discussion Tan, J. to Yap J. UPCM 2013

2 20 year old female Chief complaint: Right hip pain Onset 3 months PTCPosition Right Hip Precipitating Walking, prolonged standing (-) trauma, forceful contact Palliative Paracetamol + Ibuprofen (minimal relief) Rest (minimal relief) Quality Increasing in severity, causing her to limp Radiation - Systemic (-) fever, malaise, loss of appetite Timing Our patient is a 20 year old female, with no other information provided. She came to the outpatient department with the chief complaint of right hip pain. History of present illness started 3 months ago, with no history of trauma or high-impact activities. Pain was brought about by walking and prolonged standing, intake of Paracetamol + Ibuprofen and rest provided minimal relief. There were no associated symptoms, but since then, the pain has been reported to be increasing in severity, enough for our patient to start limping. Other questions we can ask? 1) Occupation, civil status, religion. 2) Position- pain at side of leg, consider bursitis; pain at buttocks area, consider back pain or spinal problem. Is it radiating anywhere? (in osteonecrosis, radiates to groin, anterior thigh, or knee) Was the pain involving bone, muscle or skin? 3) Precipitating – What distance of walking causes pain? How long is prolonged standing? 4) Quality- persistent vs. resolving; Pain intensity- VAS? Characterize pain. 5) Radiation- does the pain go down a neural pathway or dermatomal level? 6) Loss of sensation? (ito dapat ang S- Sensory sa OPPQRST) 7) Timing- morning pain/stiffness? Unremitting? How long does the pain last after it starts?

3 History Medical Family Personal Social (+) DM: parents (+) PTB: MotherCurrently a student Plays badminton occasionally Took Dexamethasone tabs (3 months) early weight gain The patient has a family history of Diabetes mellitus and pulmonary tuberculosis. Currently a student, she has time to plays badminton occasionally. An attempt to gain weight was also elicited, at the start of the year, when the patient took Dexamethasone tablets for 3 months on the advice of a friend. Ask whether the dexamethasone was taken BEFORE or AFTER the hip pain started? Also, is she still taking the tablets? Further information that could have been elicited- Patient’s medical history- history of surgeries, hospitalizations. Allergies, or other illnesses like Sickle cell disease, Hyperlipoproteinemia, Legg-Calves-Perthes (more predisposed to AVN since there is hyperviscosity of the blood). DM can predispose to Charcot arthropathy. Surgical hx can suggest infection. In addition to Fam Hx provided, whether or not someone else in the family had a similar condition would have been wise to note. As for PSHx, it would’ve been good to quantify the “occasionally” in her badminton exercise, when was the last time she played?); also her diet could have been elicited; if patient smoked, drank, or took illegal drugs; Important to ask alcohol history since alcohol induced osteonecrosis follows same pathogenesis as steroid induced osteonecrosis. Ask about other medications – biphosphonates can also induce osteonecrosis. Also, metabolic disorders such as Cushing’s syndrome are also associated with increased risk of osteonecrosis. OB and sexual history should have been gotten- was the patient pregnant? When was her LMNP?

4 Review of Systems OB HistoryNot provided Systemic symptoms? Menstrual irregularities, amenorrhea? Change in bowel habits, quality of stools? Lower back pain? Radiation of pain? Numbness, tingling, or weakness in the leg or foot? Systemic symptoms: To rule out more dangerous pathologies, always ask about night sweats, fevers, weight loss, or anorexia. Is there any history of stress fractures, menstrual irregularities, or amenorrhea? To rule out abdominal sources of the hip pain, ask about nausea, vomiting, diarrhea, changes in stools, or the presence of blood in stools. To help rule out spinal causes, ask about lower back pain; radiation of pain down the leg into the calf, foot, or toes; and numbness, tingling, or weakness in the leg or foot.

5 Physical Exam Abdomen Globular, (-) masses, tendernessBP 140/ RR HR BMI: 26.67 Skin Slightly pale, thin skin w/ prominent capillary network, (+) facial hirsutism HEENT Cushingoid features Chest & Lungs Clear breath sounds, regular heart rhythm, distinct heart sounds Abdomen Globular, (-) masses, tenderness Upon physical examination, the patient was overweight, hypertensive and borderline tachypneic, but heart rate was still within normal range. Patient had Cushingoid features, of which were specified a buffalo hump, telangiectasia, central obesity (thin arms, globular stomach), thinning of the skin, and hirsutism. Examination of the chest and lungs were unremarkable. Abdomen was also unremarkable, save for its being globular. Other things noted could have been her temperature, which will give a clue about presence of inflammation. Psychological disturbances, ranging from euphoria to psychosis, and behavioural changes could also have been elicited. We should also consider sources of referred pain. The groin should be examined for femoral or inguinal hernias, osteitis pubis, athletic pubalgia, and adductor tendinitis- all of which manifest with pain that mimics that associated with hip disorders.

6 Physical Exam Muskoloskeletal Gait Arms Legs SpineDecrease in stance phase over R hip Arms Thin upper extremities, (-) signs of arthritis Legs R hip decreased ROM  flexion, internal, external rotation Spine (+) Buffalo hump Her gait revealed a decrease in stance phase over the R hip, and likewise the R hip had decreased capacity to flex, and internally and externally rotate. Degrees of limitation were not specified. Other things that could have been noted were: The attitude of the hip at rest: since the hip capsule’s largest potential volume is with the hip flexed, abducted, and externally rotated- patients with synovitis or effusions tend to hold the hip in this position. Presence of lumbar lordosis- there could be verterbral muscle spasm, and excessive lordosis may suggest flexion deformity of the hip. Check motor, sensory and reflex testing; staight-leg testing. Was the reason for the limited ROM due to pain, or did the joint “lock”? Was there Trendelenburg gait (often a good indicator of an intraarticular hip disorder, but also is seen in patients with extraarticular problems)? Was there tenderness around affected bone? Were both active and passive joint movements restricted and painful? Was there a neurologic deficit present (if a nerve is compressed due to necrosis/compression deformity of affected bones). Was there joint deformity and muscle wasting? Was there deficiency in leg length? If there is leg shortening and external rotation has pain, suggest hip fracture (BUT no history of trauma).

7 Summary of the Case History Physical Examination 20 year old female3 month history of R hip pain- no history of trauma or overuse Intake of Dexamethasone for 3 months Cushing symptoms: HTN, hirsutism, buffalo hump, central obesity, thin skin, telangiectasia Right hip: Decrease in stance phase, decreased ROM (flex, int., ext. Rotate) To summarize pertinent findings, we have a 20 year old female with a 3 month history of R hip pain. The patient started taking steroids 3 months ago, and currently has Cushiongoid features (as noted). On physical examination, decreased ROM in the right hip was noted in all ranges. Decrease in the stance phase of the R side during gait was also noted.

8 Given our data, we now proceed to this algorithm care of Harrison’s.First question: Is it articular? *click* At this point, we are not sure whether active and passive movement is affected as it was not clearly stated in the physical examination. We can answer this with both yes and no. With “no” we can rule out trauma *click* since our history denies such event. Fibromyalgia and polymyalgia rheumatica are not top priority *click* because our patient complain of 1 joint area only. With this, we are left with *click* bursitis and tendinitis. If we follow “yes”, *click* then we go down to chronic then non-inflammatory (the patient has been using steroids for some time).

9 We answer the last question with a “no”, and that gives us Osteonecrosis and Charcot Arthritis.However, we will still include osteoarthritis as one of our differentials WHY

10 Differentials Entity Rule In Rule OutAvascular Necrosis (Osteonecrosis) (+) Hip Pain (+) Steroid Use (+) Precipitated by walking, prolonged standing (+) increasing severity of pain AVN often in the femoral head Affects y/o Cannot be ruled out Osteoarthritis of the hip (+) Hip pain (+) Joint pain on motion Female, Overweight (+) minimal relief with NSAIDs, paracetamol and rest May be secondary to AVN Usually affects >50 y/o After that little exercise, let’s look at our differentials, here presented in lessening order of likelihood. AVN is often found in femoral head. Our patient experiences hip pain precipitated by movement and progressively increasing in severity. We take into account the patient’s use of steroids for 3 months which predisposes her to this condition. Although it commonly affects an older age group, we cannot strike this out at the moment. Next, OA is often found at weight-bearing structures or very mobile areas including the hip. Our patient has risk factors like being female and overweight. There is also joint pain on motion and relief with intake of NSAIDs and paracetamol. Although this affects patients much older than she is, we also cannot rule this out. Third, neoplasms: For bone neoplasms, bone pain or noticing a mass is usually the first symptom of the patient. Osteosarcoma is common at the age range, but its predilection site is usually at long bones (though pelvis is a significant location), and it’s also more common in males. (OS also often presents as pain with activity!) Ewing’s is common in adolescents and the 2nd decade of life, and can show up in long or flat bones. Chondrosarcoma is common in flat bones, (especially shoulder and pelvis), but usually presents in older age groups.

11 (Osteosarcoma, Ewing’s, Osteoid Osteoma, chondrosarcoma)Differentials Entity Rule In Rule Out Neoplasm (Osteosarcoma, Ewing’s, Osteoid Osteoma, chondrosarcoma) (+) Hip Pain (+) Pain with activity (OS) (-) weight loss/anorexia Cannot be ruled out Charcot arthopathy (+) family history of DM rapid course patients cannot sense pain commonly occurs at knee, ankle , foot almost always presents with signs of inflammation Charcot arthropathy is a neurogenic/neuropathic arthropathy with progressive joint destruction, often rapid. It develops because of the inability to sense pain. It’s possible from her family history that the patient has DM, which as we know can damage nerves. A good ROS would have been helpful here, because no signs or symptoms of DM were offered. Also, the hip joint isn’t a site it usually affects. Bursitis patients experience chronic, intermittent, aching pain over the lateral hip- like in our case- from repetitive use, trauma, infection, or systemic inflammatory disease. They also present with localized tenderness, edema, erythema, and/or reduced movement, the last of which was seen in our patient. Though patients are predominantly women, this pathology usually hits those older. Other components of the VITAMIN CD: Inflammatory causes – unlikely, given steroid use and NSAID use Infection – No apparent source of infection, meaning no trauma or systemic infection. TB or any other septic arthritis is unlikely, and the joint is not particularly warm or swollen. Traumatic cause – No history, apart from playing badminton. Even then, hip would probably be not as severely affected as ankle or knee. Autoimmune – RA? But we lack criteria for RA, and steroid use should have reduced this. Metabolic/Toxic – Symptoms simply not systemic enough. Congenital – Late onset for this, but I guess it’s possible? Degenerative – Early onset for this, I think.

12 Entity Rule In Rule Out Bursitis (+) Hip pain (+) Decreased ROM and pain with movement female No history of inflammatory disease or trauma 4th-6th decade No signs of inflammation Tendinitis More common in women (-) overuse injury, acute trauma, RA? Repetitious weight-bearing activities

13 Working Impression Avascular Necrosis of the Hip secondary to Steroid Use , to consider secondary Osteoarthritis

14 Algorithm from Kelley’s Textbook of Rheumatology for Osteonecrosis/Avascular Necrosis

15 Conditions Associated with OsteonecrosisMetabolic Diseases-Abnormality in Fat or Other Metabolic Component Gaucher's disease [158] Fat embolism [159] [160] Pancreatitis [62] [64] [161] [162] Chronic liver disease [163] Pregnancy [37] [164] Fabry's disease [165] [166] Gout [167] Hyperparathyroidism [168] Hyperlipidemia 159,160 [159] [160] Hypercholesterolemia [167] Diabetes [169] Dietary, Drugs, and Environmental Factors Corticosteroids [145] [146] Cigarette smoking [22] Dysbaric osteonecrosis [4] [147] Alcohol consumption [22] [148] Lead poisoning [149] [150] Bisphosphonates [98] [15] Musculoskeletal Conditions-Compromise in Structural Integrity Trauma [152] Legg-Calvé-Perthes disease 29,153 [29] [153] Congenital hip dislocation 154,155 [154] [155] Hereditary dysostosis Slipped capital femoral epiphysis [156] [157]

16 Rheumatologic ConditionsAntiphospholipid antibody syndrome [180] Rheumatoid arthritis [181] Systemic lupus erythematosus [61] [97] [182] [183] [184] Infl ammatory bowel disease [185] [186] Necrotizing arteritis [187] Mucocutaneous lymph node syndrome [188] Polymyositis [189] Sarcoidosis [63] Mixed connective tissue disease Infectious diseases HIV infection [190] Osteomyelitis [191] Meningococcemia [173] [176] [192] Hematologic Conditions-Abnormalities in Components of Blood Hemoglobinopathies Sickle cell anemia [38] [170] [171] Thalassemia [172] Disseminated intravascular coagulation 85, [85] [173] [174] [175] [176] Hemophilia [41] [42] [43] Thrombophilia [177] Marrow infiltrative disorders Hypofibrinolysis [178] Thrombophlebitis/venous thrombosis [179] Oncologic Disorders and Their Treatment Organ transplantation [193] [194] [195] [196] [197] [198] Radiation exposure [199] [200] [201] [202] [203] [204] Regional deep hyperthermia [205] Acute lymphoblastic leukemia [206] [207]

17 Diagnostics

18 Lab Exams Little to no value in avascular necrosis of the hipIf suspecting infection – CBC, ESR, CRP may be useful For inflammatory arthritis/spondyloarthropathies – RF, HLA-B27 Specifically for the differential ankylosing spondylithis ESR – may be elevated acutely CBC – leukocytosis may be seen acutely; chronically, normochromic, normocytic anemia RF – negative HLA-B27 – positive in 95% of patients but not everyone will develop disease RF – rheumatoid factor HLA – Human leukocyte antigen

19 Imaging Modalities A. Plain Radiographs B. CT-Scan C. MRI D. Bone Scan w/ SPECT

20 How to select an imaging modality for AVN?

21 Radiographic Findings

22 Flattening of joint surfaceCrescent Sign Snowcapping Areas of lucency Flattening of joint surface CRESENT SIGN Earliest sign of AVN of femoral head Thin radioluscent line beneath articular cortex Best visualized in frog-leg position SNOWCAPPING Diffuse homogenous increase in density Represents deposition of reparative bone Seen without crescent sign or collapse Most commonly seen in head of humerus LUSCENT AREAS– site of resorption of necrotic marrow and trabecular.

23 Crescent Sign

24 Flattening of joint surfaceLuscent areas

25 Flattening Snowcapping Luscent areas

26

27 Magnetic Resonance Imaging (MRI)

28 A. Indication Imaging procedure of choice and most accurateAsymptomatic lesions that are undetectable on plain radiographs and lesions with unknown etiology Most sensitive study Sensitivity: % Specificity: 72-87% Size of the lesion and gross estimates of the stage of disease , specially early AVN Imaging procedure of choice in clinically suspected radiographically occult or acute cases avascular necrosis MRI allows sequential evaluation of asymptomatic lesions that are undetectable on plain radiographs - Most sensitive study (88-100% sensitivity and 72-87% specificity) and most accurate in staging AVN Images clearly depict the size of the lesion, and gross estimates of the stage of disease - Allows assessment of the lesion size and location, which are shown to relate to prognosis and need for treatment

29 B. Advantages Early disease detection: Bone marrow changes (including inflammatory and reactive hyperemic changes) Superior soft tissue contrast Multiplanar imaging Guide interventional procedures; response to treatment; joint effusions and bone edema detection More effective than Bone Scan and SPECT in detecting AVN - Ability to detect bone marrow changes, including inflammatory and reactive hyperaemic changes, enables early detection of disease - Allows assessment of the lesion size and location, which are shown to relate to prognosis and need for treatment - Demonstrates superior soft tissue contrast allowing evaluation of morphologic features. - Multiplanar imaging (axial, sagittal, coronal, or any variation thereof) - May help guide interventional procedures such as core decompression, may demonstrate response of the femoral head to treatment, and may detect the joint effusions and bone edema that often accompany avascular necrosis (AVN) - More effective than SPECT in detecting AVN

30 C. Limitations Expensive and limited availabilityNO: With cardiac pacemakers and intracranial clips; claustrophobic patients Problems in malpositioning Orthopedic hardware in post-surgical patients - Expensive and limited availability - Cannot be performed in patients: with cardiac pacemakers and intracranial clips, claustrophobic patients - Problems in malpositioning: in children, slight pelvic obliquity may cause the normal dark-appearing growth plate to appear in the same axial cut as the contralateral bright-appearing epiphysis; in such cases, the normal growth plate may appear to be abnormal on MRI. - Difficult to detect avascular necrosis (AVN) after surgery to repair a hip fracture because of the presence of orthopedic hardware, which creates significant image distortion.

31 D. Diagnostic Findings Classic Findings: Focal lesion in the anterosuperior portion of femoral head that is well demarcated but is inhomogeneous Early NVA: T1-weighted images: low signal intensities within the lesion T2-weighted images: high signal intensities or fat-suppressed images Bone marrow edema Bone Marrow Edema: - Found typically in focal and subchondral lines. The signal changes are based on the high amount of “free” water in bone marrow, which referred to as bone marrow edema. This is often nonspecific and localized in the medial aspect of the femoral head. In approximately 50% of all patients similar abnormalities can be outlined within the joint, representing accompanying joint effusion

32 T1 WI : Avascular necrosis of both femoral headsT1 WI : Avascular necrosis of both femoral heads. Note the decreased signal intensity in both femoral heads.

33 R A. T1-weighted image: localized hypointensity in right head of hip joint. B T2- weighted image: localized hyperintensity in right head of hip. Result: localized bone marrow edema in right hip. A A 42-year-old female patient. Bad feeling in right hip. Plain X-ray normal. Coronal MRI of both hips. a SE T1-weighted image: localized hypointensity in right head of hip joint. b SE T2- weighted image: localized hyperintensity in right head of hip. Some effusion within the joint. Result: localized bone marrow edema in right hip. T2: Water is white. Take note of the urine in the urinary bladder. It is white. B

34 D. Diagnostic Findings Irreversible NVA:-Necrotic areas are demarcated by fibrovascular tissue and a sclerotic rim (new bone formation) - Pathognomonic: “DOUBLE-LINE SIGN” on T1- and T2-weighted images - consists of two parallel neighboring stripes of hypointensity and hyperintensity -Necrotic areas are demarcated by fibrovascular tissue and a sclerotic rim (new bone formation). In some cases necrosis may lead to condensation of bony trabecles and sclerosis. - The MRI scan shows the almost pathognomonic “double-line” on T1- and T2-weighted images, representing the above-mentioned granulation tissue and reactive bone formation at the rim of the lesion. The sign consists of two parallel neighboring stripes of hypointensity and hyperintensity, respectively.

35 T1 WI of R femoral head (coronal and axial): Double Line SignMRI double-line sign. A (Coronal), B (Blow-up of A) and C (Axial). T1-weighted image : right head of femur-serpiginious parallel lines of hypo- and hyperintensity representing fibrovascular tissue (yellow arrow) and new bone formation (red arrow). Central low intensity mirrors necrosis. No edema around lesion (silent AVN) T1 WI of R femoral head (coronal and axial): Double Line Sign C

36 A B T2 WI of R femoral head (coronal and axial): Double Line SignMRI: A. Double-Line sign; B. SE T2-weighted image coronal: double-line sign on left side and to a minor degree also on right side. Edema and effusion (hyperintensity, red arrow) around demarcated lesion on the left is well outlined.    For Further subchondral microfractures and reactive bone changes (seen as crescent sign): best seen with CT and/or plain radiographs. MRI and bone scans would no longer add any additional important diagnostic information. B

37 Bone Scintigraphy/Scan w/ SPECT

38 A. Indication Technetium-99 methylene-diphosphonate bone-scanningSuperior to plain radiographs but inferior to MRI Approximately 75% sensitive and specific for avascular necrosis. Principle: Increased metabolic/reactive area, increased uptake of isotope, more black

39 B. Advantages Useful screening modalityImproved accuracy with the addition of SPECT Alternative to MRI Provides physiologic data Quantification of uptake in the perfusion and static phases Needs correct computer programming - Useful screening modality if the site of pathology has not been localised. -Improved accuracy with the addition of SPECT - Alternative to MRI when MRI cannot be performed or when MRI results are not clear-cut. - Planar scintigraphic imaging using quantitative bone scanning provides physiologic data that cannot be obtained with other modalities, including MRI; for example, this technique allows quantification of uptake in the perfusion and static phases, but needs correct computer programming is required

40 C. Limitations Poor spatial resolution and less sensitive than MRI in detecting early ANV Difficult to interpret if disease is bilateral Hyperemic areas (increased uptake) may obscure necrotic centers (indicative of AVN) Uniform high level of activity: difficult to distinguish from other ds. (osteoarthritis, fracture, and inflammatory arthritis) - Poor spatial resolution. - Lacks specificity - In early AVN, bone scan is less sensitive than MRI. - Results are difficult to interpret if disease is bilateral. In unilateral disease, the healthy side can be used for comparison. - The ring of increased activity reflecting hyperemia in the early stages and bone healing later obscures the photon-deficient necrotic center within the femoral head, which is indicative of avascular necrosis (AVN). The site may show a uniform high level of activity, making it impossible to distinguish avascular necrosis (AVN) from other causes of increased activity, such as osteoarthritis, fracture, and inflammatory arthritis.

41 D. Diagnostic Findings Early AVN: Increased osteoblastic activity and blood flow DOUGHNUT SIGN: Reactive zone surrounding the necrotic area. Tecnhnical: Photopenic area (cold area) located anterolaterally which is surrounded by an area of increased activity is most consistent w/ dx of avascular necrosis. - In early AVN, osteoblastic activity and blood flow are increased; thus, the sensitivity of radionuclide bone scan is better than that of plain films at this stage. The central area of decreased uptake is surrounded by an area of increased uptake. This phenomenon is known as the doughnut sign and indicates the reactive zone surrounding the necrotic area. In other words, a photopenic area (cold area) located anterolaterally which is surrounded by an area of increased activity is most consistent w/ dx of avascular necrosis.

42 Bilateral central area of diminished uptake surrounded by increased zone of uptakeRadionuclide bone scan of the pelvis in a 68-year-old man with hip pain demonstrates a bilateral central area of diminished uptake surrounded by a zone of increased uptake in the femoral head consistent with avascular necrosis.

43 A B -Reactive hyperemic changes, hypervascularity, and higher turnover in bone metabolism are mirrored by higher uptake in bone scintigraphy -Bone scintigraphy (Tc-99m MDP): higher activity in right head and neck of femur due to hyperaemia and increased new bone formation. Bone Scan (Tc-99m MDP): higher activity in right head and neck of femur due to hyperemia and increased new bone formation Planar bone scan of the pelvis in a patient with bilateral avascular necrosis of the femoral head shows marked increased uptake of radiopharmaceutical agent in both hips.

44 Bone Scan with Single-photon emission CT scanning (SPECT)SPECT scanning eliminates radioactivity resulting from hyperemia about the hip joint and from the underlying acetabulum and adjacent bladder- Vascularity is emphasized Initially, SPECT images reflect vascular integrity; early in the disease, SPECT scans may demonstrate an avascular focus Sensitivity of 85-97% for SPECT scanning SPECT scanning provides images of the radioactivity within the target organ in 3 dimensions. With this modality, overlying and underlying areas of radioactivity may be separated into sequential tomographic planes, thus providing increased image contrast and improved lesion detection and localization, as compared with planar scintigraphy. SPECT scanning eliminates radioactivity resulting from hyperemia about the hip joint and from the underlying acetabulum and adjacent bladder. SPECT scanning is used as an alternative to MRI when MRI cannot be performed or when the results of MRI are indeterminate. Initially, SPECT images reflect vascular integrity; early in the disease, SPECT scans may demonstrate an avascular focus; such findings are missed with MRI unless contrast is used. Collier et al found a sensitivity of 85% for SPECT scanning. With triple-head high-resolution SPECT scanning, Lee et al reported a sensitivity of 97%.

45 Limitations - SPECT scanning demonstrates poor spatial resolution. Artifacts from the bladder are frequently encountered; these artifacts may obscure the photon-deficient region of the femoral head. A number of techniques, such as the use of multihead cameras with shorter acquisition times that improve resolution and increase sensitivity, have been advocated, but none has gained universal acceptance. - SPECT imaging requires a cooperative patient who must remain immobile for up to 45 minutes of acquisition time, thus this modality is difficult to use in children because of the necessity to remain motionless for long periods of time. Children may require sedation. In addition, diagnosing Legg-Calve-Perthes (LCP) in small children may be difficult because of the small size of the femoral epiphysis and associated bladder artifacts.

46 To reinforce the figure in next slideMagnified coronal T2-weighted MRI image of the right knee showing a medial meniscal tear

47 Example of SPECT Images. Used to reinforce Bone Scan findings. Wala akong makitang SPECT SPECT Images of the a patient with right knee medial meniscal tear showing a crescent of increased activity in the medial tibial plateau, which is scintigraphically characteristic feature of a meniscal tear. Example of SPECT Images. Used to reinforce Bone Scan findings.

48 Imaging Comparison X-ray shows collapse of LFHCoronal T1-weighted magnetic resonance image shows decreased signal within LFH Bone scan with technetium-99m hydroxymethylene diphosphonate : Normal (D) fluorine-18 fluorodeoxyglucose positron emission tomography scan : Normal Imaging studies in a patient with avascular necrosis of the left femoral head (LFH). (A) X-ray shows collapse of LFH (3). (B) Coronal T1-weighted magnetic resonance image shows decreased signal within LFH (3). (C) Bone scan with technetium-99m hydroxymethylene diphosphonate and (D) fluorine-18 fluorodeoxyglucose positron emission tomography scan do not show any gross abnormality of LFH.

49 CT Scan

50 CT Scan Detection of AVN Sensitivity in detecting early AVN = 55%Doesn’t demonstrate the early vascular and marrow abnormalities Earliest visible sign: Osteoporosis Provides information essential for planning treatment Useful in evaluating extent of involvement Enables detection of subchondral or cancellous fractures or collapse

51 Asterisk sign - femoral head w/o AVNClumping and distortion of the central trabeculae Low density region (reparative zone) Figure 1 - prominent and thickened but normal trabeculae (arrow) within the femoral head. Asterisk - delicate, sclerotic, raylike branchings emanating in a radial fashion from the central dense band.

52 AVN: Fracture in anterior aspect of femurAVN: degenerative joint disease around the anteromedial and posterolateral aspects of the right hip Figure 2: joint space narrowing, juxta-articular sclerosis, and osteophyte formation.

53 AVN Classification (FICAT System)Stage I conventional radiograph is normal, but MRI or radionuclide imaging findings will confirm AVN Stage II cystic and sclerotic changes are seen on conventional radiographs Stage III crescent sign is seen Stage IV flattening of the femoral head, narrowing of the hip joint, severe joint destruction

54 Management

55 Treatment Goal The treatment goal for avascular necrosis is to prevent further bone loss Management depends on the amount of bone damage Early stages of avascular necrosis may benefit from more conservative treatment, while later stages may require surgery.

56 Non-pharmacological TreatmentNon-operative treatment alone for symptomatic AVN of the hip yields unfavorable results Prognosis for patients with avascular necrosis treated with nonoperative modalities that restrict weight-bearing: Most studies have reported >90% progression of collapse and the need for total hip replacement within 4 years

57 Pharmacologic TreatmentMedical therapy for AVN of the hip is principally indicated for relief of discomfort. No medical treatment has proven effective in preventing or arresting the disease process. NSAIDs and COX-2 inhibitors for pain relief Effects of bisphosphonates, lipid-lowering substances and anticoagulants on delaying disease progression are currently investigated and hold promise.

58 Surgical Management Core Decompression Bone Graft OsteotomyTotal hip arthroplasty

59 Core Decompression Better results if used in early AVN (precollapse)Improves circulation by decreasing intramedullary pressure Prevent further ischemia and progressive joint destruction Effective for pain control

60 Bone graft Options: structural cortical or medullary bone graft and vascularized bone graft with either a muscle-pedicle bone graft or free vascularized fibular graft Bone graft is combined with the following: Core decompression Excision of sequestrum Period of limited weight bearing

61 Osteotomy Done to transfer weight to the healthier cartilageIntertrochanteric osteotomies have been performed in patients with posttraumatic AVN Transtrochanteric rotational osteotomy rotation of the femoral head and neck on the longitudinal axis The necrotic anterosuperior part of the femoral head becomes posterior thus weight bearing is now transferred to the healthier posterior articular surface

62 Hemiarthroplasty For displaced femoral neck fracture which caused AVN and if acetabulum is healthy Replacement of the femoral head and neck with a metal and plastic prosthesis Procedure: Posterior approach to the hip Exposure and entry into the joint capsule Removal of femoral head and resection of femoral neck Insertion of the prosthesis, can be secured with use of polymethylmethracrylate bone cement

63 Total Hip ArthroplastyFor patients with advanced disease, sclerosis and cystic changes on both acetabular and femoral articular surfaces Total hip arthroplasty provides excellent pain relief for many years, although most young patients require repeat surgery

64 Total Hip ArthroplastyProcedure Posterior approach: incision through the lateral proximal hip to expose the posterolateral part of the femur, greater trochanter and muscles Femoral head removal by transecting the femoral neck Reamers and rasps are inserted to create a space for the stem of the femoral prosthesis Articular cartilage from the acetabulum is removed by reamers to the level of good cancellous bone The acetabular prosthesis is attached to a metal cup and then impacted into place Joint is relocated and the wound is closed

65 Best management is surgical, followed by a period of REHABILITATION!

66 Rehabilitation ProgramIncludes exercise, pain control, and joint protection techniques Isotonic exercises, such as straight-leg raising, that distribute the stress through the hip joint must be avoided Gravity-eliminated active assistive exercise, such as pool therapy and isometric exercises, can improve hip ROM and strength

67 Hip Precaution Should be observed for 12 weeks after the procedureThis allows for a pseudocapsule to reform; incidence of dislocation is reduced by > 95% after 12 weeks.

68 Physical Therapy To reestablish basic activities of daily living (ADL) with modifications that keep the patient's ROM within restricted limits To teach joint protection To review fall risks To provide equipment with training

69 Special Devices for Independence in ADLElevated toilet seats Shower seats Shoe horns Eelastic shoe laces Reachers that allow socks to be pulled on

70 Exercises 6-8 weeks after surgery : isometrics and active ROM exercises against gravity >6-8 weeks: resisted open kinetic chain strengthening can start in the place of joint motion with 1-10 lbs

71 Partial Weight-BearingGoals: It allows the soft tissues to heal adequately. It allows for the muscles to reattach firmly to bone or for the trochanteric osteotomy to heal. It allows more adequate time for bone ingrowth to be achieved if the patient received bone-ingrowth prosthesis.

72 References DeAngelis NA, Busconi BD. Assessment and differential diagnosis of the painful hip. Clin Orthop Relat Res. 2003;406:11–18. Fauci, S. et al (2008). Harrison's principles of internal medicine. 17th ed. New York: McGraw-Hill. Harris, ED et al (2004). Kelley's Textbook of Rheumatology. 7th ed. USA: Elsevier Saunders. [accessed November 6, 2010] [accessed November 6, 2010]

73 REFERENCES(MRI & Bone Scan): 1 www. imagingpathways. health. wa. govREFERENCES(MRI & Bone Scan): Department of Health Western Australia 2 H.Imhof, et al. (1997) Musculoskeletal radiology: Imaging of avascular necrosis of bone. Eur. Radiol. 7, 180–186 © Springer-Verlag Tofferi, J.K. & Gilliland, W. (2009. )Avascular Necrosis: Differential Diagnoses & Workup. emedicine 4 Aiello, M.R. (2009). Imaging in Avascular Necrosis of the Femoral Head. emedicine Talamo, G. et al (2005) Avascular Necrosis of Femoral and/or Humeral Heads in Multiple Myeloma: Results of a Prospective Study of Patients Treated With Dexamethasone-Based Regimens and High-Dose Chemotherapy. Journal of Clinical Oncology Vol. 23: No.22 8 Wilfred, C.G. (2009). Ankylosing Spondylitis. 9 Schwart’s Principles of Surgery, 9th ed. 10