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.
Hip resurfacing has emerged as a viable alternative to replacement for arthritis in young patients. Selected individuals will benefit by Hip resurfacing arthroplasty offered by the Madras Joint replacement center in India. See if you qualify for this procedure.
Hip resurfacing has emerged as a viable alternative to replacement for arthritis in young patients. Selected individuals will benefit by Hip resurfacing arthroplasty offered by the Madras Joint replacement center in India. See if you qualify for this procedure.
Newer advances in the field has made surgeons once again looking at Core decompression as an important procedure for treating avascular necrosis of the femoral head. The talk is about the newer development in the field of the Core decompression and how the newer techniques are transforming the way the surgeons take care of this important problem.
Safe surgical dislocation for femoral head fractures.dr mohamed ashraf,dr rah...drashraf369
femoral head fractures are very complex fractures that need immediate and prompt surgical intervention.conventional surgical appproaches to hip may lead to short and long term complications.dr mohamed ashraf ,dr rahul thampi et al are presenting their experience with gantz safe surgical dislocation approach to surgical management of femoral head fractures
Orthobiologics - PRP, BMC the real story so far!Vaibhav Bagaria
A basic presentation on the role of orthobiologics, PRP, Bone marrow aspirate concentrate in orthopaedics. Insights, and future research directions in a rapidly evolving field.
a simplified version of periprosthetic fractures, easy to learn and understand with lots of images and classification. It includes hip, shaft of femur, knee, shoulder
This is a short presentation on avascular necrosis of femoral head. This presentation gives brief description of causes of AVN, investigations and modes of treatment options available.
AVN TREATMENT IN HYDERABAD
Core decompression for AVN
Stem cell treatment for AVN
Surgery for AVN
Avascular necrosis treatment options
Hip replacement in hyderabad
Hip specialist in hyderabad
Hip surgery in hyderabad
Total hip replacement in hyderabad
cemented hip replacement
uncemented hip replacement in hyderabad
ceramic hip replacement
delta motion hip
ceramic on ceramic hip replacement
metal on poly hip replacement
affordable hip replacement in hyderabad
Newer advances in the field has made surgeons once again looking at Core decompression as an important procedure for treating avascular necrosis of the femoral head. The talk is about the newer development in the field of the Core decompression and how the newer techniques are transforming the way the surgeons take care of this important problem.
Safe surgical dislocation for femoral head fractures.dr mohamed ashraf,dr rah...drashraf369
femoral head fractures are very complex fractures that need immediate and prompt surgical intervention.conventional surgical appproaches to hip may lead to short and long term complications.dr mohamed ashraf ,dr rahul thampi et al are presenting their experience with gantz safe surgical dislocation approach to surgical management of femoral head fractures
Orthobiologics - PRP, BMC the real story so far!Vaibhav Bagaria
A basic presentation on the role of orthobiologics, PRP, Bone marrow aspirate concentrate in orthopaedics. Insights, and future research directions in a rapidly evolving field.
a simplified version of periprosthetic fractures, easy to learn and understand with lots of images and classification. It includes hip, shaft of femur, knee, shoulder
This is a short presentation on avascular necrosis of femoral head. This presentation gives brief description of causes of AVN, investigations and modes of treatment options available.
AVN TREATMENT IN HYDERABAD
Core decompression for AVN
Stem cell treatment for AVN
Surgery for AVN
Avascular necrosis treatment options
Hip replacement in hyderabad
Hip specialist in hyderabad
Hip surgery in hyderabad
Total hip replacement in hyderabad
cemented hip replacement
uncemented hip replacement in hyderabad
ceramic hip replacement
delta motion hip
ceramic on ceramic hip replacement
metal on poly hip replacement
affordable hip replacement in hyderabad
Avascular necrosis of Hip - treatment modalities and current concepts.pptxVivek Jadawala
Slide 1 - Treatment modalities of Avascular Necrosis of Hip
JOURNAL CLUB PRESENTATION
Dr. Vivek Jadawala
PGY-3, Dept. of Orthopaedics,
JNMC, DMIHER
Slide 2 - image
slide 3 - image
slide 4 - Osteonecrosis of Hip - Osteonecrosis is death of living elements of involved bone (cells including marrow) with progressive destruction and alteration of bone architecture as a result of compromised vascularity.
Usually aseptic but may be incited by loss of vascularity from infection.
Slide 5 - Epidemiology - Male > Female
Average age group – 35 to 50 years
Bilateral Hip joints – 80 % of the cases
Most common site – Antero-lateral aspect of femoral head
Slide 6 - Blood supply of femoral head
Slide 7 - Classification of AVN: Ficat and Arlet -STAGE 0 :
X-ray : normal
MRI: normal
clinical symptoms: nil
STAGE I :
X-ray : normal or minor osteopenia
MRI: edema
bone scan: increased uptake
clinical symptoms: pain typically in the groin
Slide 8 - Stage I
Slide 9 - Stage II -
X-ray: mixed osteopenia and/or sclerosis and/or subchondral cysts, without any subchondral lucency (crescent sign)
MRI: geographic defect
Bone scan: increased uptake
clinical symptoms: pain and stiffness
Slide 10 - Stage III - X-ray: Crescent sign and eventual cortical collapse
MRI: same as plain radiograph
clinical symptoms: pain and stiffness +/- radiation to knee and limp
Slide 11 - Stage IV - X-ray: end-stage with evidence of secondary degenerative change
MRI: same as plain radiograph
clinical symptoms: pain and limp
Slide 12 - Stage IV
Slide 13 - image
Slide 14 - Steinberg staging of AVN
Slide 15 - Steinberg staging - STAGE 0:
- normal or non-diagnostic radiographs, MRI and bone scan of at risk hip (often contralateral hip involved, or patient has risk factors and hip pain)
STAGE I:
normal radiograph, abnormal bone scan and/or MRI
STAGE II:
- cystic and sclerotic radiographic changes
STAGE I AND II
A, mild: <15% head involvement as seen on radiograph or MRI
B, moderate: 15% to 30%
C, severe: >30%
Slide 16 - STAGE III:
- subchondral lucency or crescent sign
A, mild: subchondral collapse (crescent) beneath <15% of articular surface
B, moderate: crescent beneath 15% to 30%
C, severe: crescent beneath >30%
STAGE IV:
flattening of femoral head, with depression graded into
A, mild: <15% of surface has collapsed and depression is <2 mm
B, moderate: 15% to 30% collapsed or 2-4 mm depression
C, severe: >30% collapsed or >4 mm depression
Slide 17 - STAGE V:
- joint space narrowing with or without acetabular involvement
STAGE VI:
- advanced degenerative changes
Slide 18 - Association Research Circulation Osseous classification
Slide 19 - image
Slide 20 - Kerboul angle - Original classification was proposed on radiographs where he divided the necrotic region into small, medium and large regions:
Small - less than or equal to 160°
Medium - 161 to 199°
Large - 200 or more degrees.
Slide 21 - Modified Kerboul angle - based on MRI has much higher values as the MRI overestimates the necrotic region
Tensor fascia lata[tfl] muscle pedicle grafting for avn hip dr mohamed ashraf...drashraf369
slide presentation of a very promising surgical technic for a very elusive condition called avascular necrosis of femoral head.good clinical and surgical demo by dr mohamed ashraf,HOD, govt TD medical college ,alleppey,kerala, india
it comprises of the anatomy, epidemiology, mechanism of injury and management options.
there is also the fracture classifications
management was grouped into operative and conservative
there is also a section for children.
Hip fractures in elderly - general aspectsappumaalu
This is prepared to present before doctors from different specialities. Hence here discussiuon comes only in a general practitioner's aspect. It is not going deep into the orthopaedic aspects
This is short Presentation on avascular necrosis of femoral head.This presentation gives brief description of introduction, causes investigation and treatment for AVN of hip.
Splenic trauma - Causes, Complications, ManagementVikas V
Splenic Trauma - A detailed Presentation about Splenic Trauma, anatomy of the spleen, Causes of Trauma, Mechanism of Injury, Diagnosis, Management, Surgical management, Steps of Splenectomy, and Complications
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
3. theories on the pathogenesis
1. direct cellular toxicity
2. coagulopathic states
3. hyperlipidemia with fat emboli
4. vascular interruptions or abnormalities
5. elevated bone marrow pressure
• None of these theories can fully account for the variety of
causes.
• Most patients with the risk factors just mentioned never
develop osteonecrosis
• many patients without identifiable risk factors do acquire
the disease.
• process is most likely multifactorial.
6. DIAGNOSIS
• Patients are typically asymptomatic early
• eventually have groin pain on ambulation.
• Plain radiographs should be obtained
– AP and frog-leg lateral views
• Radiographic changes
• normal in the early stages
• increased density or lucency in the femoral head.
• the pathognomonic crescent
– best seen on frog-leg lateral views
• In the end stages of the disease
– femoral head collapse
– severe arthritic changes
7. Bone scanning
• useful, especially in assessing the status of
multiple joints
• The uptake of technetium-99m
– decreased in the very early stage of disease
– variable or increased at a stage when symptoms
occur
• there is no relationship between the
scintigraphic appearance of the femoral head
and the pain and function of the hip
8. MRI
• earlier diagnosis
• allow determination of the exact stage and extent of the
pathological process without use of invasive methods.
• Differentiation between transient osteoporosis and
osteonecrosis
• useful in following the progression of the disease
• evaluating the efficacy of treatment.
• When plain radiographs show changes in only one joint
– define clearly the extent of the disease in the symptomatic hip
– evaluate the asymptomatic hipallow detection of the disease
in the early stages when most treatments are more effective
9. TREATMENT
• the rate of progression is high, especially in symptomatic
patients
• Asymptomatic osteonecrosis
– the lesion < 30% of the area of the femoral head remain
asymptomatic in most patients (95%) for > 5 years
– lesion size increased the percentage of painful osteonecrosis
increased up to 83% in hips with large lesions (>50% of the
area of the femoral head)
• When subchondral collapse occurs and joint space is lost
inevitable progressive osteoarthritis
• extremely poor prognosis, with a rate of femoral head
collapse of greater than 85% at 2 years in symptomatic
patients (stage I or II disease)
10. core decompression
• The theoretical advantage
– relieves intraosseous pressure caused by venous
congestion improved vascularity possibly
slowing the progression of the disease
• the results of core decompression are better
than the results of nonoperative treatment
• the earlier the stage of the diseasethe
better the results
• the best results reported in stage I hips
11. core decompression
• INDICATIONS:
– Ficat stage I and IIA
– small central lesions in young
– Non obese patients who are not taking steroids
• ADVANTAGES:
– relatively simple to perform
– a very low complication rate
– The surgical field for subsequent total hip arthroplasty, if needed, is
not substantially altered
• For more advanced Ficat stages (IIB or III):
– the results of core decompression are much less predictable,
– so alternative treatment methods should be explored
• > 30% of patients, even with early-stage disease, will likely require
THA within 4 to 5 years of core decompression surgery
12.
13. POSTOPERATIVE CARE
• Partial weight bearing (50%) on crutches for at
least 6 weeks
– protect the cortical window
• In patients with advanced disease, protected
weight bearing is prolonged.
14. CORE DECOMPRESSION—
PERCUTANEOUS TECHNIQUE
• using multiple small drillings with a 3.2-mm
Steinmann pin
• lower rate of femoral head collapse
• low morbidity
• few or no surgical complications.
15.
16. POSTOPERATIVE CARE
• Physical therapy
– Gait reconditioning with a cane or crutches
• Protected weight bearing (approximately
50%) for 5 to 6 weeks then advanced to full
WB as tolerated
• High-impact loading such as jogging or
jumping is not permitted for 12 months
17. BONE GRAFTING
• Successful results after core decompression with
structural bone grafting 50% to 80%
• No difference between tibial or fibular
autogenous grafts and fibular allografts
• comparing vascularized and nonvascularized
fibular grafts for large lesions (>30% of the
femoral head)
– better clinical results and more effective prevention
of femoral head collapse with vascularized grafting
18. • nonvascularized bone grafts
– less than 2 mm of femoral head depression
– core decompression failed
– no acetabular involvement (Ficat stage I or II)
• The bone grafts technique
– standard core track technique, “trapdoor”
technique
– “lightbulb” technique
19.
20. VASCULARIZED FIBULAR GRAFTING
• good results in 80% to 91%
• reasonable option for patients younger than 50
years without collapse of the femoral head
• for patients older than 50 THA is indicated if
symptoms warrant surgical intervention
• Concurrent steroid use is not a contraindication
for this procedure
• not indicated for patients with asymptomatic
early-stage osteonecrosis because the results of
core decompression are equally effective for this
group of patients.
21.
22. PROXIMAL FEMORAL OSTEOTOMY
• move the involved necrotic segment of the
femoral head from the principal weight-bearing
area. These procedures have achieved
• best results for small-sized or medium-sized
lesions (<30% femoral head involvement) in
young patients(<55Y) in whom it is optimal to
delay a THA
• idiopathic or posttraumatic osteonecrosis did
better than alcohol-induced or steroid-induced
necrosis.
23. • A valgus-extension intertrochanteric
osteotomy combined with curettage of the
avascular segment and autogenous bone
grafting was reported to have an 87% success
rate at 65 months.
25. RESURFACING HEMIARTHROPLASTY
• If osteonecrosis involves >30% of the head
• an attractive alternative for young patients
with advanced osteonecrosis because very
little bone is sacrificed
26. TOTAL HIP ARTHROPLASTY AND
BIPOLAR HEMIARTHROPLASTY
• Most series that have examined unipolar and
bipolar hemiarthroplasty for the treatment of
osteonecrosis have reported uniformly poor
results.
• The results of primary total joint replacement
for osteonecrosis are now approaching the
results reported for osteoarthritis in age-
matched patients.