I upload for my future reference.
Feel free to download if you need a fast reference or feel free to edit and improve if you need to do your presentations.
For undergraduate medical students.
Referred from Apley's.
I upload for my future reference.
Feel free to download if you need a fast reference or feel free to edit and improve if you need to do your presentations.
For undergraduate medical students.
Referred from Apley's.
This presentation gives a brief idea of Acute osteomyelitis, its cause, predisposing factors, pathogenesis, signs and symptoms, investigation and its management. It also explain Nades principle.
Title: Understanding Giant Cell Tumor of Bone: A Comprehensive Overview
Introduction:
Giant Cell Tumor of Bone (GCTB) is a rare but potentially aggressive bone tumor that primarily affects young adults. While typically benign, it can be locally destructive and lead to significant morbidity if not managed appropriately. This presentation aims to provide a comprehensive understanding of GCTB, including its epidemiology, pathogenesis, clinical presentation, diagnostic modalities, treatment options, and prognosis.
Epidemiology:
GCTB accounts for approximately 5% of all primary bone tumors, with a peak incidence in the third and fourth decades of life. It shows a slight female predilection and commonly arises in the epiphyseal regions of long bones, particularly around the knee.
Pathogenesis:
The exact etiology of GCTB remains elusive, but it is thought to arise from mesenchymal stromal cells. Genetic alterations, including mutations in the H3F3A gene, have been implicated in its pathogenesis. Additionally, dysregulation of the RANK/RANKL/OPG pathway plays a crucial role in the development and progression of GCTB.
Clinical Presentation:
Patients with GCTB typically present with localized bone pain, swelling, and limited range of motion at the affected joint. Pathologic fractures may occur, especially in larger lesions. Rarely, patients may present with systemic symptoms such as fever and weight loss.
Diagnostic Modalities:
Diagnostic evaluation of GCTB includes imaging studies such as plain radiographs, which often show characteristic lytic lesions with well-defined margins and cortical thinning. Magnetic resonance imaging (MRI) provides detailed soft tissue evaluation and aids in surgical planning. Biopsy remains the gold standard for definitive diagnosis.
Treatment Options:
The management of GCTB is challenging and requires a multidisciplinary approach. Treatment options include curettage with or without adjuvant therapy (such as adjuvant bone cement, phenol, or cryotherapy), en bloc resection for aggressive or recurrent tumors, and denosumab therapy for unresectable or metastatic disease. Close surveillance is essential due to the risk of local recurrence.
Prognosis:
The prognosis of GCTB is generally favorable, with a low incidence of metastasis. However, local recurrence rates range from 10% to 50%, depending on the extent of surgical resection and the use of adjuvant therapy. Long-term follow-up is necessary to monitor for recurrence and late complications.
Conclusion:
In conclusion, Giant Cell Tumor of Bone poses a significant clinical challenge due to its potential for local recurrence and morbidity. Early diagnosis, appropriate staging, and a tailored treatment approach are crucial for optimizing patient outcomes. Continued research into the molecular mechanisms underlying GCTB pathogenesis and the development of targeted therapies are essential for improving treatment strategies and patient prognosis. Giant Cell Tumor of Bone (GCTB)
Similar to Osteomyelitis and Septic arthritis.pptx (20)
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.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
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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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
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Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
1. Osteomyelitis and Septic arthritis
prepared by: Alazar (OSR-2)
moderator : Dr. Birhanu Ayana
(Consultant pediatric orthopedic surgeon)
May, 2022
2. Outline
Part 1: Osteomyelitis
• definition
• history & epidemiology
• pathogenesis
• classical & modern concepts
• classifications
• AOM
• subacute OM
• COM
• treament principles
• prongs of Rx in COM
• complications
• special forms of OM
Part 2: Septic Arthritis
• routes of spread
• risk factors
• pathophysiology
• classification
• clinical features, labs & imaging
• ddx
• treatment principles
• sequelae in ped hips
4. Definition & History
primary infection of the BM --> subsequent infection of the
cortex & periosteum “Nelaton, 1844”
fractured spine of dimetrodon Pemian reptile, 291-250 million
yrs ago
5. Epidemiology & Pathogenesis
incidence
• acute hematogenous OM decreasing
• due to direct inocultion /contiguous focus increasing
Older theories
Hobo’s
• metaphysis: “poor phagocytic activity”
Trueta, 1968
• sluggish flow through “hair-pin bends”
• 3 clinical stages
• 3 types of OM
6. stage 1 “boil” in the bone
• severe constant pain & tenderness; absent
inflammatory ssx
stage 2
• pus in medulla & subperiosteal space;
systemic ssx appear
stage 3
• inflammation spreads to STs
challenged recently by findings of pus
w/n 48hrs beneath the periosteum
his view of no/late inv’t of diaphysis
also not supported
7. infantile childhood adults
transphyseal blood supply physis & epiphysis spared often due to contiguous spread
diaphysis rarely involved diaphysis is at greater risk
(endosteal thrombosis)
long bone inv’t in hematogenous
rare
thin & weak bone
• give way to pus under
pressure
no extensive devascularization &
large sequesterum
metaphyseal cortex is thicker
extensive devascularization & large
sequestrum (“cylinderical
sequestrum”)
infected bone resorbed leaving
behind a cavity
high regenerating potency of
periosteum --> large involucrum
growth disturbance rare whole bone inv’t & chronic OM
common
joint inv’t if
• metaphysis is intracapsular
• iatrogenic seeding while
drainage
8. Starr from Toronto
• progression & course of abscess
Wilenski concept
• site of bone inv’t depends on occlusion at
particular site by septic embolus
Morrisey & Haynes
• concept of “trauma as focalizing influence”
• delicate metaphyseal circ --> hematoma formation
9. Modern concept & understanding
A. Alteration of homeostasis of the body
• close interaction of host factors, bacteriological factors & env’t
B. terminal metaphyseal vessels
open ended (NOT looped/“hair-pin bends”)
• chondrotropic bacteria adhere to cartilage cells at junction
b/n metaphy and physis “homing of bacteria”
sluggish flow not important
C. centripetal concept of developing infection
lodging in periosteal circulation --> subperiosteal abscess -->
involve the cortical circ --> thrombosis of nutrient aa --> dev’t
of characteristic AOM
10. biofilms are permanent
source of virulent pathogens
insensitive to immune system
& progressively resistant to
Abx
rush to surface --> thrive --> review mechanisms for inc proliferation (quorum
sensing) --> grow into mushrooms & columns --> interval shedding of “planktonic
form” --> host immunity “confused” mounts a common inflammatory rxn
• ineffective (Th2 humeral response against pseudomonas)
• self damaging & misdirected (Th1 & Th17 cell mediated response against S. Aureus) --> further
tissue damage and inc adhesion
11. Classification
13 d/t classification systems (Hotchen et al.)
• most important variables
• bone inv’t
• antimicrobial resistance patterns
• need for ST coverage
• host status
12. traditional
classfication
acute, subacute, chronic time of onset
manner of clinical presentation
response to Rx
depending on duration of ssx
• arbitrary (<2 weeks, 2 wks-3 mo; >3 smo)
• identification of sequestrum on xray 4-6wks
Meier acute, acute with x-ray changes, chronic localized, chronic systemic
Lew & Waldvogel hematogenous/endogenous
, contiguous/exogenous,
vascular insufficiency,
chronic
by cause not useful for guiding Rx
or determining Px
based on host
response
pyogenic or nonpyogenic
Cierny & Mader based on host factors & anatomic criteria
Trueta neonatal, infantile, early
child hood, late childhood,
adolescent
based on age & dev’t helpful in identifying
causative organism &
clinical manifestation
13. PTO (post-traumatic OM)
Kelly hematogenous, # healing w/ OM, # nonunion w/ OM, no # OM
Gordon et al. • type A: tibia defect & nonunion; no segmental loss
• type B: tibia defect >3 cm; fibula intact
• type C: tibia defect >3 cm; involving both tibia & fibula
Mayet al. • type 1: tibia & fibula intact and load bearing stable
• type 2: fibula intact; tibia continuous but need bone graft
• type 3: fibula intact; tibia defect <= 6cm
• type 4: fibula intact; tibia defect > 6cm
• type 5: tibia defect > 6 cm; fibula #
Schmidt et al. • classified by 8 items
• source of infection
• anatomical region, stability
• FB
• infection range
• activity of infection
• microorganism,
comorbidity
• good for clinical classification of
PTO
• complex; limits its use in clinic
14. CCHOM
Lauschke based on onset
• early acute: <= 3 days
• late acute: 4-5 days
• chronic: >=6 days
peds doesnt recognise more
extensive dz
progression (not
applicable to majority
of CCHOM seen in
clinical practice)
Beit CURE
classification
comments on both
sequestrum & involucrum
• useful tool in
planning
designed in countries where readily available
CT & MRI are not there
Solagberu’s pre-invasion to compound
chronic
based on
progressionof dz
subjectivity of grading
makes reproducibility
difficult
15. Cierny-Mader classification
University of Texas Medical Branch
(UTMB) clinical staging system
• for adult OM (Cierny et al.)
• part of affected bone, physiological status &
risk factors affecting immunity, metabolism &
vascularity
• doesn’t recognize chronic form of bone
infection
(but best suited for classifying chronic OM)
helps in determining if Rx
should be
• simple Vs complex
• curative Vs palliative
• limb sparing Vs
ablative
16. draw back
• relatively subjective
• reliant on clinical judgement,
interpretation of radiology & asst
of host status
• created to classify OM in adults
• less transferable to peds
• most children are normal hosts
with localized OM (3A) -->
limited application
17. Beit CURE classification
Type A Brodie’s abscess
Type B Sequestrum
involucrum
B1: localized cortical sequestrum
B2: sequestrum with structural
normal involucrum
B3: sequestrum with sclerotic
involucrum
B4: sequestrum w/o structural
involucrum
Type C sclerotic
physeal damage indicated by the addition of “P”: proximal or “D”:
distal
Jones et al.
solely for use in CCHOM
explicit use of plain
radiograph
has been assessed for intra-
& inter-observability
comments on both
sequestrum & involucrum
• useful tool in planning
18.
19. Acute hematogenous OM
• most common type & usu seen in peds
• metaphyses of rapidly growing long bones
• bimodal age destribution in peds
• < 2yrs & between 8-12yrs
• much less common after physis are closed
• in adults, often seen in immunocompromised host
• predilcation for vertebral bodies
20.
21. in peds: clinical diagnosis
• localized bone pain & fever
• presumed OM till proven otherwise
(upto 40% peds afebrile on admission)
• pain & local tenderness are common findings
• other typical ssx (refusal to bear weight, malaise, limited ROM, redness,
warmth, swelling)
in infants, elderly or immunocompromised
• ssx minimal
22. in adults: high index of suspicion
• hx open #
• nonhealing ulcers
• contiguous sites of infection
• predisposing factors
• C/f
• tenderness to deep palpation
• thrust tenderness (vertebral OM)
• painful ROM
24. TC/DC
• WBC normal in >50%; elevated in only 35%
ESR (90%) & CRP (98%)
• elevated & sensitive; non-specific
• ESR peaks 3-5 days; normalizes by 3wks
• CRP rises w/n 6hrs, peaks in 2 days; normalizes by 7-10 days
Blood culture
• +ve in 50% of AOM in peds; commonly -ve in adults
• despite low yield always obtain prior to Abx (if +ve, repeat q48hrs until clear)
Bone aspirate/contiguously infected joint aspirate culture
• identification of causative only ~50-60%
25. X-rays
1cm & 30-50% dec in mineral
content for noticable change
limited role in AOM
48-72hrs: muscle swelling &
blurring of ST planes
26. periosteal thickening, lytic
lesions, endosteal scalloping,
osteopenia, loss of trabecular
structure
• 5-7 days in children; 10-14
days in adults
27. USG
• detect concurent SA & differentiates from SA,
pyomyositis, ST abscess, cellulitis & malignant bone
tumors
• earliest sign (w/n 48hrs): deep ST swelling
• thin layer of subperiosteal fluid, subperiosteal abscess
& perosteal rxn (hypoechoic & anechoic shadow)
• doppler: detect hyperemia around periosteum &
surrounding ST abscess
• Labbe et al.: dx accuracy 64% on admission; 84% on
2nd day
MRI
• sn: 98%, sp: 75%
• show early inflammatory changes in BM &
ST
• changes in marrow evident w/n 3-5 days
• short tau-inversion sequence & T1 spin
echo
• highest sensitivity & specificity
• marrow change as early as 1-2 days
• detects intraosseous & subperiosteal
abscesses
28. T-99 bone scan
• can confirm dx 24-48hrs after onset in 90-95%
• negative scan rules out dx
• role in multifocal dz/nonlocalized esp. in infant/toddler where
sedation is unwanted
• gallium & 111-labeled leukocyte scans inc specificity
• use has dec with inc use of MRI
29. Chronic OM
>6 wks; devitalized bone
usu persistence of AOM
incomplete Rx, trauma, implant related, open #
may develop de novo
• infection with chronic persisting type of microbes, OM ass with DM
foot/vascular dz
r/f for polymicrobial OM: advanced age, GA type 3 injuries, need for
blood transfusions & multiple debrima
30. sequestrum: hallmark
• 10 days histopathologically
• seen on xray by 3 weeks
• 2-3 month for sequestrum to separate
from parent bone
involurum
• rough inner & smooth outer surface
• physiologically seen in infants
Cloacae
31. Sequestrum
shape consistency color
pencil like or cylinderical/tubular:
infants
coke like: TB black:
• amputation stump
• long exposure of necrotic
bone to air
• fungal infection
• actinomycosis
ring: ex-fix pins, schanz screws,
ilizarov wires
feathery: syphilis
conical/annular: amputation
stumps
sand like (coarse): TB in
metaphysis green - pseudomonal OM
trapezoid & irregular: adolescents sand like (fine): viral OM
coralliform: perthes
flake like: TB
button sequestrum: calvarium
32.
33. intermittent acute
exacerbations for years
• w/c responds to rest & Abx
ssx: nonspecific
pain
• Walenkamp phenomena (gradually inc bcm
unbearable & suddenly relaxes w/ opening
up of sinus & pus discharge)
tenderness on deep palpation
irregulary thickened
muscle atrophy
characteristic ones
• adherent sinus tract with
discharging pus/bone pieces
• nonhealing wound exposing
surgical hardware
• nonhealing wound/ulcer
overlying exposed bone
34. labs
• WC: elevated in only 35%
• ESR & CRP: elevated in most pts
X-ray
• periosteal reaction , involucrum formation, sinus tracts, ST fistulas,
sequestrum formation, cortical destruction
CT
• superior in demonstrating
• sequestrum, cloacae, involucrum or intraosseous gas
• beam hardening effect in presence of implants (losing resolution)
• nature & magnitude of bone defect
35. Sinography
• valuable adjunct to surgical planning
MRI
• extent of inv’t & activity of dz
• sequestrum & ossified periosteal shell: low intensity on all sequences
• surrounding granulation tissue & pus: high signal on T2 & STIR
• “rim sign”: well-defined rim of high signal intensity surrounding focus
of active dz
36. nuclear imaging/3-phase bone scintigraphy
• as early as 48hrs; high sensitivity; low specificity; inc uptake in all 3 phases
• gallium: intense uptake in infection, aseptic inflammatory conditions & malignancy
• Indium-111: improv in specificity
• FDG-PET: highest accuracy for confirming/excluding; vertebral lesions better
evaluated
Bone biopsy
• >5 neutrophils/HPF (specificity 93-97%)
• useful before proceeding with reconstruction/during repeated debrima
• high -ve yield of culture from “biofilm” infections
• even with sonication/subcultures
37. Subacute hematogenous OM
less common than AHO; incidence increasing
inc host resistance & dec virulence of bacteria
or
administration of Abx before onset of ssx
onset insidious & as a rule no systemic features of infection
38. remitting pain
• mild to moderate
• prominent after activity
• night pains (relief from ASA)
localized tenderness & swelling (may even be absent)
peds: metaphysis > diaphysis (equal distribution in adults)
• metaphyseal equivalents: pelvis, vertebrae, calcaneum, clavicle & talus
• multifocal rarely
• ddx: Ewing’s, Largerhans, osteosarcoma, chondroblastoma, ABC, GCT, PVNS,
NOF, chondromyxoid fibroma, osteoid osteoma, intracortical hemangioma
39. Robert et al. (modified Gledhill
classification)
• 6 types (morphology, location &
bone rxn)
40. labs: often not helpful
• WBC normal; ESR inc in 50% only
• blood cultures -ve
xray
• nonsensitive & non-specific
• characteristic lesion: lytic cavity surrounded by sclerosis
• Serpentine sign of Letts
MRI
• better characterization & differentiation of spinal lesions
• Penumbra sign: Brodie’s abscess
Tissue dx (FNAC/trephine bx)
• must for documentation & diagnosis
• yield is +ve only 60%
41. Principles of treatment in AOM
• until 1920’s, surgical Rx was the only Rx for OM
(ubi pus ibi evacua)
• currently, Abx is the basis for Rx of AOM
• Nade principles (pertaining to Abx use) for managment of AOM
• Abx is effective before pus/abscess formation (<48hrs)
• Abx can’t sterilize avascular tissue/abscess
• Abx prevent reformation of pus once evacuated
• Evacuation of pus restores periosteum & blood flow
• Abx should be continued following surgery
42. surgical indications in AOM
• abscess formation (strongest indication)
• concomitant septic arthritis
• some recommend in proximal femur OM (even absent SA)
• persistence w/o improv after 48hrs of Abx Rx
• slow progression as clinically deemed after 72hrs of Abx Rx
• multifocal OM with pus formation esp. in an ill, moribund child
• delayed presentation >7-10 days
• bone more/less dead & immediate pus evacuation should be done to preserve as
much bone
43. Abx
• 1st line
• b-lactams (1st gen cephalosporins)
• efficacy against MSSA, K.kingae, Strep. pyogens, Strep. pneumo
• clindamycin
• concern for MRSA & allergic to B-lactams
• inactive against K.kingae
• vancomycin
• pt clinical status, regional resistance patterns
• comparatively less effective against MSSA
• gm negative coverage
• neonates, HAI
44.
45. historically, long course IV
• to prevent compx or relapses
• randomized, controlled,
multicenter trial in UK
• 1054 patients
• Rxed for complex bone &
joint infections
• sequential IV/PO
noninferior to entirely IV
with fewer IV related compx
& lower financial costs
46. initial 5-7 days: IV
• normal temp, improved c/f, resolving CRP
• minimum of 3 days
3-4 wks: PO
total duration arbitrary
• cont Rx for 4wks
• revascularization of bone takes that much time
• <3 wk Rx associated with higher rates of relapse/recurrence
• depends on extent of infection & clinical and lab responses
47. supportive Rx
• immobilization/comfortable positioning, hydration, electrolyte replacement,
protein rich diet & adeq analgesia
frequent serial examinations
• daily clinical condition and limb girth
• CRP q2-3 days
clinical improvement occurs w/n 24-48hrs
• fever settles w/n 2-3 days
• erythema & swelling settle & range and rhytm of mov’t recover
by 1 wk
• WBC decline
• ESR reduce by minimum of 20%
• CRP reduce by 50%
48. Principles of treatment in SOM
controversial
• prolonged IV Abx in peds (Hamdy & Colleagues)
• surgical Rx in adults
• agressive looking lession: Bx & curette --> Abx
• simple abscess: No Bx. IV Abx*48hrs --> 6wk PO Abx
surgical indications
• poor response to Abx
• doubtful lesions that appear as potential threats
• impending joint inv’t
• subperosteal pus/synovitis
49. Principles of treatment in COM
based on oncologic approach
• radical surgical eradication of affected bone & ST
+ reconstruction for stable limb function
• systemic & local Abx and adjuvant therapy to eradicate infection
• retain limb function
immunocompromised host
• might not survive extensive surgical stress required to eradicate
• limited surgical debrima + suppresive Abx + nutritional support
• goal: limit the freq of sinus drainage & pain
50.
51. timing the intervention
prerequisites for surgery in symptomatic pt
acute phase should subside (no fever)
D/C Abx 1 week before
sequestrum should have separated from parent bone
involucrum strong enough for supporting the bone w/o need of
supportive fixation
• seen in 3/4 cortices on 2 perpendicular views; minimum of 70% circumferential
on CT
• may take 2-8 mo to form
salvagable limb
• use Klemm’s triad for assessing
pt willing for multiple operations
• on average # of op required is 4
52. 5 Rx prongs
bone & ST debridement w/ removal of infected & necrotic tissue and
drainage (wound toileting)
removal of metal implants, hardware & FB
stabilization of the bone throughout
local Abx therapy
dead space mgm’t
• reconstruction of the ST
• reconstruction of the osseous defect
53. 1. Tissue debridment ‘’excision of focus’’
aid in identification of nonviable tissue
& sequesterum
• methylene blue: stains viable gray; nonviable
blue
• sulfous blue: color all tissue green; devitalized
remains uncolored
• intra-op lased doppler: cumbersome & not very
accurate
sinus tract excised, infected granulation
tissue curetted out
sequestrae inspected for completeness
& not fractured while removal
if bone window needs to be created for
removing sequestrum
• oval fashion; 10-15% more length than
measured length of sequestrum
progressive nibbling of involucrum &
bone till punctate bleeding bone
saucerization
• burred to have smooth borders that aren’t
undermined; akin to “wide resection”
margin of 5mm recommended
54. sclerotic bony blocks in the
medullary cavity should be opened
ST debridment
• all grossly visible necrotic tissue &
slough excised
thorough irrigation
splint limb till wound heals
• prevents pathological #
NWB ROM excercises
Abx continued
repeated q48 hrs till samples taken
from wound return normal/local
conditions of wound looks healthy
55. 2. Bone Stabilization
Ex-fix
• cumbersome to pt for prolonged duration
• possibility of pin site infection
slab/cast
• often inadequate
• has to be changed frequently
56. 3. Local Abx Rx
advantages of local Abx over
systemic?
advantages of biodegradable over
nonbiodegradable?
57. PMMA (antibiotic loaded bone cement)
current gold standard
high compression strength
• good structural strength; an advantage in membrane induced technique
Abx elution approaches 75% @ 30days
• maintaing >100*MIC & approaching/exceeding MBEC conc
implantation short Vs intermediate to long term
• short term: removed within 10 days (bead pouch technique)
• intermediate term: removed by 2-3wks
• long term: kept for 3wks & pulled daily at a rate of 1 bead/day that extends to 2-
3wks
• for upto 80 days
59. Bead-pouch technique
• beadson circlage wire
• covered with adhesive sheet (2 layers)
• “closed bead-hematoma-Abx env’t”
• dressing & bead pouch change repeated q48-72hrs
• depending on fluid accumulation
• debride till healthy granulating bed
• when satisfactory, ST coverage planned
*** suction drainage: ineffective & counterproductive
60. IM Abx cement nail
• recent alternative to external
fixation
• removal of standard nail --> I&D
of IM canal (RIA) --> Abx PMMA
nail + systemic Abx
• NWB in cast for 6-8wks
• exchanged with standard nail
after clearance of infection
61. biodegradable systems
useful when instability is not an issue & ST coverage is adequate
• bone graft & bone substitutes
• protein-based materials (natural polymers)
• synthetic polymers
• miscellaneous material
elution
• for water soluble agents depends on SA of carrier & initial conc
• for insoluble agents depends on porosity of the matrix
62. closed suction drains
• modified Lautenbach method (success rates of ~85% reported)
• adv
• allows change in local Abx delivery based on culture results
• aids in gradual dec in the size of ST dead space
• disadv
• frequent occlusions (steptokinase solves this)
• prolonged hospitalization required
• risk of secondary contamination
63. 4. Dead space (cavity) mgmt
Dead space managment
leave to heal of its own
(not preferred)
secondary intention
mobilize local tissue
(usu done)
mm flaps (myoplasty)
myocutaneous flaps
osteomyocutaneous flaps
microvascular
reconstruction
mm flap
osteomyofasciocutaneous
flaps
using foreign material
(mainly bone cement)
biodegradable
non-biodegradable
Autogenous cancellous
bone graft
64. A. Reconstruction of the osseous defect
Autogenous cancellous bone grafts
prerequisite
• critical defect of 6-7cm
• optimal vascular situation in ST & bone
• optimal contact b/n cancellous graft & living cancellous bone
• infection-free bone bed in defect
65. Rhinelander-Papineau technique
• open bone grafting of vascularized bone bed defect
3 stages
1st stage (debrima & stabilization)
debrima repeated till deemed healthy
wound packed with Abx soaked dressings/bead-pouch
technique
nailing (original recommendation)/Ex-fix (commonly used)
• Rhinelander used POP cast
delay 2nd stage till healthy granulation is obtained
66. 2nd stage (cancellous autografting)
cancellous iliac bone graft
• pack tightly concentrically to SC level
ends of bones petalled (inc SA of contact)
pack with Abx-soaked dressings
• changing after 4-5 days (when graft stabilize &
incorporate)
• freq dressings till granulation tissue engulfs the
grafts & surrounding skin covers them
VAC (Archdeacon & Messerschmitt)
• hasten healing & remove serous discharge
in b/n edges refreshed if epithelium dig
into grafts
3rd stage (skin closure)
for large wound defects (>3-4cm)
• prolonged time for spontaneous
epithelization
providing wound coverage
• skin grafts, mm pedicle flaps or free
microvascular flaps
In mini-papineau
• after bone grafting --> local mm
pedicle flap
• incorporation is faster
• skin coverage provided early
67. Reconstruction of segmental bone defects
Wiese defined CSD
• loss of length of segmental bone that exceeds the diameter of affected
bone by a factor of 2 to 2.5 (Wiese & Pape, 2010)
open bone grafting
• small-moderated bone defects (up to 3cm) in peds
71. bone stabilized by Ex-fix/IMN
• internal fixators (locked plates): for smaller bones of forearm & hand
spacer removed after 8 wks
bone formation & union in ~ 8-9 months
adv
prevention of encroachment by adjacent ST into bone defects
stable placement of graft in place
prevention of resorption of graft/local production of osteoinductive
substances
• maintain graft volume & helps in augmenting bone formation
72. animal studies
• membrane have histologic
characteristics & local factors
(VEGF, TGFB-1, BMP-2) that
facilitate bone healing
73. 24 adult crossbred ewes (mean age of 5.6 +/- 0.4 yrs; mean wt 55
+/- 5 kg)
allocated into 3 groups (empty ctrl, 100% allograft, 67%
allograft/33% autograft)
• For ctrl group, ST closed over an empty defect
• For graft material groups, defect was filled w/ PMMA prior to closure
4 wks after surgery, sheeps of gr 2&3, reanesthesized and sample
taken from fibrous capsular tissue surrounding PMMA for
histological and immunohistochemical evaluation
Patterns of expression including distribution & intensity of staining
summarized
74. retrospective series
single center experiece of 21 pts w/ infected nonunion/underlying
OM
20/21 went to solid union at mean time of 5.6mo (range 2-10mo)
• average time to healing of 1.21mo/cm of defect
success rate of 95.23%
75. prospective study, case series
19 pts (12 posttraumatic OM, 4 infected nonunion, 3 COM)
most had large bone defects & multiple previous surgical
intervenions
• 4.1 previous operations (range, 2-11 failures)
most had >1 debrima before graft application
overall success (union) rate reported to be 85.71% (18 in 21
cases)
76. Callus-distraction & distraction histiogenesis
(Ilizarov method)
many different techniques
• Monorail (Wagner type)
• lengthening over IMN (rail-road lengthening)
• Unilateral Ex-fix & hybrid fixators
• Three dimensional fixators (for multi-plane deformity correction)
• Ring fixators (classic Ilizarov technique)
77. considered today gold
standard
• esp if defect >4cm but <15cm
DO with ring fixation over an IMN:
reported for defects upto 13cm
• the combined method improved ex-fix
period & consolidation index
• the earlier removal of ex-fix: inc pt
comfort, dec compx rate & convinient &
rapid rehab
DO with monolateral Ex-fix: defects ranging
from 6-18.5cm
• union 34/35 with no reinfection
• average length of fixator wear 17mo
78. adv
bone formation in distraction zone is autogenic & healthier
single low risk surgical procedure
deformity correction can be simultaneously done
resultant increase in vascularity improves surrounding ST & ctrls
infection
early weight bearing can be allowed
disadv
time required to achieve solid union
high incidence of associated compx
impact on patient’s mental health
79. problem analyzing data from
literature
• infected & noninfected cases often
presented together making clear
discrimination & analysis difficult
evaluated use of Ilizarov in Rx of infected nonunions
of tibia & femur
the only review exclusively dealing w/ infected cases
24 studies, 590 patients (mean age 22.7 yrs)
many had multiple procedures in the past (average of
3.64)
mean bone defect of 6.7 cm (femur: 8.05 cm; tibia: 6.54
cm)
mean f/u: 3 yrs
overall union rate 97.26%
overall time with the fixation: 10.69mo
low compx and adverse effects
81. Microvascular graft osteosynthesis
“vascularized grafts”
defects > 6 cm
• reconstruction up to 26 cm reported
adv
good healing (due to vascularity & simultaneous cortical support)
previously failed cases tried w/ cancellous grafts
can be used in pts w/ poor ST envelop
maintain mass, architecture & strength
with endurance of load undergo remodelling & hypertrophy
82. vascularized fibula (commonly)
vascularized rib, scapula or ilium grafts
disadv
needs skill & expertise in microvascular surgery
• otherwise success rate is low
arteriogram should be done before fibula harvest
• peroneal arteria magna (5%) --> peroneal aa is the dominant aa of foot -->
harvesting leads to severe ischemia of foot
83. Huntington’s procedure
(ipsilateral fibula transfer, tibialization of fibula)
Rx posttraumatic tibial defects, OM produced defects and congenital
deformities
original procedure 2 steps (now done in 1)
• 1st: distal part of fibula osteotomized & inserted into medullary canal of
tibia/fixed to the surface
• 2nd: done at 2-4mo; proximal portion of fibula cut and approximated to tibia
surface
bone union around ~ 6 mo
• till then protection by slab or Ex-fix
84. adv
less expertise than free
microvascular fibula transfer
bone remodels w/ weight
bearing & hypertrophies
union & bone uptake more
certain than avascular fibula
graft
union bypasses stage of
creeping substitution
85. B. Reconstruction of the ST defect
planning of cover done during initial surgical planning
• carried out when infection undergoes remission (usu after 6-8 days)
ST coverage options depend on the ff criteria (Heppert et al.)
• type of osteosynthesis
• site & size of ST defect
• local vascular status
• pt compliance
spectrum of Rx
• localized muscle flap --> microvascular free-tissue transfer
success rate of 66-100% reported
86. NPWT
• VAC system (Kinetic Concepts,
Inc., San Antonio, TX)
• PICO (Smith & Nephew,
Mepmphis TN)
• canister-less, single-use device
• Avelle (ConvaTec, Oklahoma
City, OK)
efficacy in Rx of
complex wounds well reported
(helpful in prevention of OM)
little information in Rx of OM
87. continous/intermittent application of sub-atm pressure to
wound
• reduce edema
• enhance granulation tissue
• maintain a moist & viable env’t
increased mechano-transduction
• inc collagen organization
• inc expression of FGF-2 & VEGF
• contracture of the wound & inc angiogenesis
88. Amputation
reserved for
• unrelenting & multiply failed cases where no possibility of reconstruction
or
• reconstructed limb will fare worse than prosthetic fitted amputated limb
other indications
• OM associated with
• malignant change
• aa insufficiency
• major nn paralysis
• joint contractures & stiffness that make a limb nonfunctional
should be fully logically supported & only prescribed when all options
have been exhausted
89. Adjuvant Rx
Hyperbaric oxygen
elevated atm pressure (2-2.5 atm)
90-120 mins
beneficial physiologic effects
• osteoblasts & osteoclasts inhibited by oxygen deficient envt partially reversed
• synergistic effect w/ Abx on infection ctrl
• stimulating angiogenesis
• suppressing anaerobic organisms
not evidenced based; no destinct benefit of therapy
90. Compx of OM
AOM
COM
SA, AVN
growth disturbance
septicemia & multisys inv’t
DVT & PE
ADR
• neutropenia, rash, hepatitis,...
COM
recurrence & relapses; residual stage
LLD, pathological #, infected
nonunion
implant failure
SA, septicemia
DVT
joint stiffness, ST contractures
ST abscess formation & cellulitis
amyloidosis
SCC of the sinus tract (0.2-1.6%)
91. Some special forms of OM
Sclerosing OM of Garre
thickening of bone cortex in irregular fashion
• w/o suppuration, sequesteration, sinus formation
chronic low grade infective pathology
• no organism have been isolated
peds & young adults
pain with activity or @ night; Ssx of inflammation absent
92. xray
inc bone density
complete obliteration of medullary cavity
marked cortical thickening
lamellated periosteal rxn
Rx
course of Abx
in few, decompression of meduallary canal
• in extreme unusual cases, surgical removal of a segment of bone + recon
93. Brodie’s abscess
most common subtype of subacute OM
• nonorthopedic literature refer this as chronic form of OM
Sir Benjamin Brodie (St George Hospital, London, U.K), 1832
• dark colored pus surrounded by whiter & harder dense bone
• inner surface of the cavity appeared highly vascular
typically in peds & boys
metaphysis in peds; metaphy-epiphy area in adults
rarely cross physis/physeal scar
intermittent pain of long duration + local tenderness
94. xray
lytic oval lesion (oriented along the long axis)
surrounded by thick dense rim of reactive sclerosis
pathognomonic feature: lucent tortuous channel (“serpentine sign”)
• extending toward physis
MRI best characterizes pathology
“target sign” Marti-Bonmati et al.
• central 2 rings & peripheral halo
“penumbra sign”
• 4 sections
• central core (abscess cavity): low intensity on T1 & high on T2 & STIR
• 1st layer (grannulation tissue): isointense
• 2nd layer (reactive new bone formation): hypointense on all sequence
• outermost layer: peripheral halo of low intensity on T1
• ddx: benign cystic lesions, chondrosarcoma, eosinophilic granuloma,
intraosseous ganglion
95. Neonatal OM
2 forms
severely ill with septicemia
• B-hemolytic streptococci & S. Aureus
• common source is umblical cord
mildly affected
• fever usu absent
• pseudoparalysis & local ssx of inflammation
Rx
• standard
• should be followed for angular deformities
96. CNO/CRMO
subacute & chronic features
etiology unknown
• cultures -ve; autoimmune (genetic); imbalance b/n pro- & anti-inflammatory cytokine
peds (peak age 10 yrs); F>M
xray
• osteolytic & sclerotic with minimal/no subperiosteal bone formation; bilaterally symmetric
• spine, tibia, femur, clavicle
• dx of exclusion
• Abx are of no use
• an episode subsides by 6wks; continue to recur over 2yrs
• little or no sequelae & self limiting
98. large joints more commonly
• esp. knee & hip (60%)
monoarticular is the rule
• polyarticular in <20%
usu hematogenous
most frequently in adults but most serious
sequelae in peds
transepiphyseal vessels
• patent in peds <18 mo; open up again near
puberty
• septic arthritis from AOM more common in
infants & adults
• less common in older children
99. r/f (systematic review by Mathews et al.)
joint rendered structurally abnormal (underlying
inflammatory/degenerative arthritis)
prosthetic joint
IVDU, alcoholism
DM
prev intra-articular steroid injections
cutaneous ulcers
Male sex
age <5
concomitant infections
inc susceptibility to infections
100. poor px
delayed presentation & suboptimal mgmt
• longer than 5 days
underlying RA
presence of OM
elderly, multiple comorbidities
prostethic joints
101. pathophysiology
why the prediliction for joints?
collagen receptors on S.aureus adhere to synovial cartilaginous junctions
lack of limiting basement membrane
synovial fibroblasts inhibit phagocytosis
delayed/inadequate Rx
fibrinous adhesions/fibrous ankylosis
articular erosion by pannus (chondrolysis)
destruction of stabilizing ligaments
102. culprits
macophages, PMN, synovial cells release (the host inflamm response)
• cytokines (IL-1b, IL-6 & TNF-a), immunoglobulin G, lysosomal enzymes (MMPs)
bacterial endotoxins & direct baterial invasion of synovium
inc intra-articular pressure
experimental model in rabbit knees (after S.aureus injection)
PG subunit loss
• 30% at 48 hrs
• 50% at 5 days
• 80% at 3 wks
• collagen degradation starts by 3 wks
103. Bacterial arthritis
commonly monoarticular
• polyarticular: 5-8% peds & 10-19% adult
gonococcal or nongonococcal
type of organism
• depend on age, immune status, habits, pre-existing arthropathy
104. Gonococcal arthritis
most common cause of acute monoarthritis in sexually active
young adults
2 forms
• disseminated gonococcal infection
• fever, chills, vesiculopustular skin lesions, tenosynovitis &
polyarthragia
• blood culture +ve; synovial culture -ve
• purulent arthritis
• knee, wrist & ankle
• synovial culture +ve
• acute onset of pain & swelling
105. nongonococcal
• Gm +ve: 80%
< 3mo 3mo-5yr 6-10 yr >10 yr
Bacteria GBS S. aureus S. aureus S.aureus
Gm- ve bacilli K. kingae N. gonorrhea
MRSA S. pneumo,
GABHS
candida H.inf
(unvaccinated)
106. ill-appearing child
+ atraumatic limitation of mobility
+ joint irritability
other c/f
fever (absent in elderly)
inability to bear weight/limp
malaise, poor appetite, irritability, progressive reluctance to use affected limb
warmth & tenderness of affected joint
joint effusion
limited active & passive ROM
107. SA Vs OM
• presence of irritable joint w/c is provoked by gentle passive motion
• joint motion doesn’t substantially provoke ssx in OM
SA Vs transient synovitis (hip)
Kocher & colleagues
• fever > 38.5 (best predictor)
• hx of NWB
• ESR > 40 mm/h
• WBC > 12k
• CRP > 20 mg/L (added by Caird et al., 2006)
Luhmann
• only 59% probability when all 4 +
• fever, WBC, prev health care visit: only 71%
• advised for adjunct USG & arthrocentesis
Predictive probability
Kocher Caird
0 predictors 0.2% 16.9%
1 predictors 3% 36.7%
2 predictors 40% 62.4%
3 predictors 93.1% 82.6%
4 predictors 99.6% 93.1%
5 predictors N/A 97.5%
108. WBC, ESR & CRP: +ve
Blood culture +ve: 50% cases
Synovial fluid aspiration: most valuable test
• fluid analysis
• cloudy/turbid
• CRP > 10.5 mg/dl
• WBC > 50k
• PMN %: >90%
• Gm staining: +ve in only 50%
• Culture positivity ranges 30-70%
• joint fluid may inhibit growth of certain bacteria
109. Xray
• nonspecific
• joint space widening, periarticular osteopenia, enlargement of ST shadows,
displacement of fat pads
• joint space narrowing
• periosteal rxn appear late (3-4wks)
• not as prominent as in OM
U/S
• non-echo free effusion with synovial thickening
• differentiates from bursitis & cellulitis by plane of collection
MRI
• no better advantage over clinical judgement
• TB arthritis in axial locations
110. Principles in mgm’t
adeq drainage + resection of infected tissue
Abx
• uncomplicated SA: duration ~ 3wks
• guided by normalization of ESR
resting the joint in stable position
• joint mobilization & weight bearing encouraged early (based on pain
tolerance)
low dose IV corticosteroid
111.
112. 123 peds
low dose IV dexa + Abx Vs Abx alone
113. SA of hip in peds
Poor prognostic factors (Choi et al.)
< 22wks of age
prematurity
ssx > 4 days
disability after acute septic arthritis
pain: incongruous articulae surfaces/pathologic dislocation
stiffness: partial/complete ankylosis
deformity: abnormal angulation or shortening
instability: destruction of prox femur/pathologic dislocation
SA of infancy “Tom-Smith’s arthritis”
affection of hip joint in peds (not only restricted to infants)
114. Neonatal period & infancy
Most common in this group
Classic ssx not seen (fever, chills, rigor,
prostration)
High index of suspicion
• Refusal to feed & cyanosis during feeding
• Abdominal distention
• Presence of focus of infection
• Edema of LE/buttock
• Crying on handling
• Not able to use lower limb actively
• Abnormal position of femur
(flexion & abduction)
Children
Unwell
Febrile
Intense pain
Restriction of all hip joint movt (esp.
rotation)
Tenderness over Scarpa’s triangle
115. If pus aspirated, hip joint promptly drained
Anterior approach
• Avoid damage to vascular supply
• Reduce chance of post-op dislocation
Immobilization until infection is controlled
116. Compx of acute septic arthritis of hip
Pathological dislocation
Prompt aggressive treatment
ST contracture haven’t formed
• Reduction at time of drainage
If damaged head
• Heavy skeletal traction to bring head to acetabulum
• then reduce by abduction & gentle rotation
Immobilized in spica till stable or fibrous/bony ankylosis
117. Complete resorption of the head
• May be replaced by new bone of vascularity is restored
Pelvic abscess
Persistent infection
• Characterized by excessive scarring & draining sinuses
Ankylosis of hip
OM of proximal femur
Myositis ossificans
Contractures & deformities
Coxa breva/magna
118. Post septic hip sequelae in peds
residual deformity
• Dx not established early &
proper Rx not instituted
• severe infection
myriad presentation
• great mimicker
needs in-depth Hx, detailed
clinical & radiological
assessment
Pain
Limp
LLD
Stiffness
Sinus
119. Classification systems
Hunka (1982)
Based on observation of pts that he treated
Type 1: absent/minimal head change
Type 2: Deformity of head
• A: intact physis; B: premature fusion
Type 3: Pseudoarthrosis of neck
Type 4: Complete destruction of
prox femoral epiphysis
• A: stable neck segment; B: unstable neck segment
Type 5: Complete destruction to the IT line + dislocation
120. Choi et al. (1990)
modification of Hunka
detailed description of the anatomical alteration of the
proximal femur
Type 1
• 1A: normal xray; 1B: AVN
Type 2 (invt of epi, phy, metaphy)
• 2A: Coxa breva; 2B: Coxa vara/valga
Type 3 (only femoral neck)
• 3A: Coxa vara/valga +/- excessive version
• 3B: pseudoarthrosis of neck
Type 4 (loss of femur head & neck)
• 4A: Segment of neck preserved
• 4B: No neck remnant
121. Johari (2002)
uniqueness: classified dislocations where CFE is present
Group 1: loss of CFE/neck, metaphy spike; stable
Group 2: loss of CFE & neck; unstable
Group 3A: CFE present; dislocation; unstable
Group 3B: CFE present; subluxation; unstable
Group 4: articular incongruity; AVN; coxa magna; physeal
disturbance (coxa breva, vara, valga & trochanteric
overgrowth); stable
Group 5: Pseudoarthrosis of neck; stable/unstable
122. Forlin & Milani (2008)
simpler, more reliabe & useful for prognosis & Rx selection
based on instability & destruction of femur head
Grade 1: head/neck wn acetabulum
• A: head (total/part) present
• B: absent
Grade 2: Hip dislocated
• A: head present
• B: absent
123. Principles & algorithms of reconstructive
procedures
aim
hip stability & conc reduction of hip
correction of LLD
preservation of articular cartilage
remnants & reorientation of the axis
of normal physiologic load
adequate containment of femoral
head
correction of other deformities
Rx options
patient’s ssx & needs
extent of inv’t
affordability
active or quiescent
age of patient
degree of residual deformity
124. Management algorithm according to Choi
type 1: observation
type 2: mechanical issues &
containment (subluxation)
addressed
type 3: derotation; + grafting
for 3B
type 4A
<6 yr: Open reduction + modified
Harmon operation/ distal transfer of GT
(if fail salvage done)
>6 yr: treated as 4B
type 4B
<6 yr: GT arthroplasty + fem varus
osteotomy + acetabuloplasty (if fail
salvage done)
> 6yr or all salvage cases: Ilizarovs hip
reconstruction osteotomy
126. Symptomatic approach
painful joint degeneration:
• PSO, THR, resection, arthrodesis
abductor insufficiency
• GT growth arrest, GT transfer
(RNL/ANL), PSO, arthrodesis
LLD
• ST release, epiphysiodesis,
lengthening, PSO w/
lengthening
instability
• open reduction, GT arthroplasty,
PSO, arthrodesis, THR, pelvic
osteotomy
loss of motion
• ST release
malpositioned extremity
• realignment osteotomy, THR
non-union
• bone grafting, valgus osteotomy
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