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June 27, 2024Contents Name of bone
Location/Articulation
Muscle and ligament attachments
Surface anatomy
Radiography
Physical examination
Embryology
Anomalies
Injuries/Disorders
Name of bone
Distal phalanges of the foot
Location/Articulation
The distal phalanges of the foot, also known as the the ungual phalanges, correspond to the distal phalanges of the fingers. However, the bones in the foot are smaller and flattened from above downward, and each presents an expanded distal extremity to support the nail and end of the toe. The first distal phalanx articulates with the first proximal phalanx. The second through fifth distal phalanges articulate with the intermediate phalanges.
Figure 1. AP view of the distal phalanges of the foot.
Figure 2. Medial view of the first distal phalanx.
Figure 3. Lateral view of the distal phalanges.
Muscle and ligament attachments
Surface anatomy
Radiography
Physical examination
Embryology
Anomalies
Injuries/Disorders
Attachments: phalanges.png (image/x-png) medial foot dp.PNG (image/png) lateral foot dp.PNG (image/png) ap foot dp.PNG (image/png) [...] Read more...
June 27, 2024Origin Anterior inferior iliac spine and the exterior surface of the bony ridge which forms the iliac portion of the acetabulum Insertion Inserts into the patellar tendon as one of the four quadriceps muscles Action(s) Knee extension, hip flexion Nerve Supply Femoral nerve Arterial Supply Lateral femoral circumflex artery Physical Exam Enter physical examination maneuvers for muscle Clinical Importance Enter clinical importance of muscle Disease States Enter links to pages where muscle involved Discussion Functions:
-Hip Flexion -Knee Extension
The rectus femoris is the only muscle in the quadriceps group that is involved in hip flexion, since it is the only one that originates in the pelvis and not the femur.
The rectus femoris is a weaker hip flexor when the knee is extended because it is already shortened and thus suffers from active insufficiency. In essence: the action of raising a straightened leg will recruit more iliacus, psoas major, tensor fasciae latae, and the remaining hip flexors than it will the rectus femoris.
Similarly, the rectus femoris is not dominant in knee extension when the hip is flexed since it is already shortened and thus suffers from active insufficiency. In essence: the action of extending a leg from a seated position is primarily driven by the vastus lateralis, vastus medialis, and vastus intermedius, and less by the rectus femoris.
The rectus femoris is considered a direct antagonist to the hamstrings. The hamstrings oppose the rectus femoris at the hip joint through extension and at the knee joint through flexion. The rectus femoris can be torn which can be very painful. Figures
Click thumbnail for larger image Credits:
From Wikipedia:
Rectus femoris Attachments: Rectus femoris.png (image/png) [...] Read more...
June 27, 2024Introduction
Define/describe the condition
Anatomy
Describe the pertinent anatomy
Pathogenesis
Describe the biomechanics/biologic basis of the disorder or the mechanism of injury
Natural History
Describe the natural history, epidemiology and prognosis
Clinical Presentation
Describe the means to elicit the most useful information from the patient history and physical examination as well as the relevant findings
Imaging and Diagnostic Studies
Describe appropriate radiologic and other diagnostic studies
Classification
Include a list with links to relevant conditions
Treatment
Include:
Medical therapy
Nonoperative treatment
Operative treatment – include links to pages with detailed surgical techniques
Indications and contraindications
Outcome
Include functional and prosthetic survivorship data as applicable
Complications
Include overview of complications
Pearls and Pitfalls
Tips and problems to avoid
Controversy
Include current controversies in diagnosis or treatment
References
Insert selected references and landmark articles [...] Read more...
June 27, 2024Indications
Discuss indications and more general concerns.
Preoperative Planning
Material to be reviewed and conditions to be addressed before surgery. Include any exams preformed under anesthesia
Positioning
Describe and provide OR photos to illustrate positioning
Approach
Consider the various approaches. Provide links to relevant anatomy and surgical approaches.
Techniques
Step by step description to illustrate surgical technique
Pearls and Pitfalls
Tips and problems to avoid
Postoperative Care
Include immediate postoperative care and rehabilitation
Outcome
Include functional and prosthetic survivorship data as applicable
Complications
Include overview of complications
References
Include limited reference list [...] Read more...
Reviews
Recent resources from OrthopaedicsOne Review for Residents and Review for Medical Students spaces.
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June 27, 2024An orthosis is a device that provides support to or improves the function of a moveable part of the body and essentially they control abnormal movement or allow restricted normal movement. Orthosis is a Greek word meaning to make straight
Purpose of Splints
To immobilise or stabilise joints (static splints)
Protection
To put joints to rest
To decrease inflammation
To decrease pain
To prevent undesired motion
To resolve fixed joint contracture, e.g. serial casting
To substitute for lost muscle function
To substitute for loss of a digit For mobilisation or traction to joints (dynamic splints)
To resolve tendon tightness
To resolve joint contracture
To increase activity range on motion to given joints
To increase muscle strength Dynamic Splints
Dynamic splinting to gain motion is most appropriate to use during the proliferative stage of wound healing as increased cellular activity occurs at the healing site, the gentle prolonged force of dynamic splinting influences the direction and alignment of collagen fibres
To be effective a dynamic splint must not be applied until the inflammatory stage is subsiding so that the dynamic forces do not prolong the inflammatory response
Also the tension must be of such low magnitude so as not to tear or force the tissues and thus stimulate the inflammatory response, causing more oedema and then more fibrosis
Precautions
Pressure areas over bony prominences
Insensate hands or limbs
Thin skin, e.g. Rheumatoid Arthritis
Vascular insufficiency
Edema Aims and demands of knee orthoses
Prophylactic or support devices that support the injured knee or weak ligaments
Rehabilitation devices used after surgery
Functional devices that stabilise and support the deformed joint
Experiments show the centre of rotation remains practically unchanged up to almost 90 of flexion scarcely rising or falling and only moves backwards.The height of the centre of rotation above the knee is 20 mm +/- 3 mm
On X-Rays the compromise axis lies in the middle of the intercondylar notch approximately at the proximal insertion of the posterior cruciate ligament [...] Read more...
June 27, 2024Stage 1
Synovitis
Proliferation of synovium, infiltration of subsynovial layer with inflammatory cells, capsular thickening, villous formation of synovium, cell rich effusion
Painful swollen tender joints
Mobility is maintained
X-Ray : extra / juxta-articular osteoporosis secondary to increased vascularity
Acute inflammation
1 – 3 days : increases small blood vessels
3 – 7 days : synovial cells proliferate
14 days : focal accumulation of T lymphocytes & increased interstitial fluid Chronic Inflammation
Increased synovial surface area (villi)
Increased blood vessels, lymphocytes, tissue fluid
Radiologically apparent erosions after 8 weeks Stage 2
Destruction
Persistent chronic inflammation and pannus formation
Periarticular erosions secondary to release of proteolytic enzymes, pannus and osteoclastic resorption of bone
Similar changes occur around tendons
X-Ray : Marginal bony erosions, reduced joint space, especially proximal joints of the hands, feet, wrists and AC joints
Stage 3
Deformity
Secondary to articular destruction, capsular laxity and ligament ruptures
Joint instability and deformity.
Inflammation may have subsided.
Deal with mechanical and functional aspects of the joint
X-Ray : Articular destruction and joint deformity usually obvious. Cervical spine is affected, may see subluxation of Atlanto-Occipital or mid cervical levels. [...] Read more...
June 27, 2024Intraoperative
Arterial damage
Rare
Both direct surgical injury and tourniquet-induced atherosclerotic embolism happen
Tourniquet should not be used if there is :
Documented atherosclerotic disease
Absent distal pulses
Radiographic arterial calcification Peroneal nerve damage
3%
Most common in correction of combined flexion – valgus deformity
Can occur intra or post-operatively due to :
Direct injury
Traction
Hematoma
External pressure from splint or dressing Majority of cases gain partial recovery
50% achieve full recovery
80% if there has been partial nerve palsy
35% if there has been complete nerve palsy Exploration of peroneal nerve is indicated if no recovery by 3 months Blood loss
1000-1500 ml Fat embolism
3%
Associated with stemmed intra-medullary components and guides
Bilateral one stage TKR increases the chance
Perioperative
Wound healing problems
RA
Diabetes
Haematoma
Low albumin
Leukopenia
Malnutrition
Obesity Infection
Affects 1 – 2.5% of TKRs
Classification
Acute infection
< 3 weeks from operation
Confined to joint space
Usually infection has not invaded bone-implant interface Chronic infection : >3 weeks from operation
Hematogenous
May happen years after operation
Source of infection is a remote, usually hidden site Increased incidence in
RA
Obesity
UTI
Previous knee surgery
Accompanying skin ulcer Presents with
Persistent effusion and pain
Loosening
Local inflammatory signs
Drainage
Sepsis Diagnosis
Culture
The gold standard
Intra-operative results are more reliable
25% false negative result for aspiration CRP, ESR, WBC
Usually raised in acute infections
Generally not reliable for making diagnosis, but normalisation of previously raised amounts is a positive indicator for re-implantation Indium and tri-phasic bone scans are helpful Bacteriology
35 – 40% due to Staph aureus
Low virulent organisms :
Staph epidermidis (methicillin sensitive, non glycocalyx forming)
Staph aureus (methicillin sensitive, non glycocalyx forming)
ß hemolytic strep
Anerobic strep High virulent organisms :
Gram negative organisms; E. coli, Pseudomonas, Proteus and Entero-cocci
Staph epidermidis (methicillin resistant, glycocalyx forming)
Staph aureus (methicillin resistant, glycocalyx forming) Others: Corynobacterium, Group B strep, Strep faecalis Treatment
Long term antibiotic suppression if :
Prosthesis removal not feasible
Low virulence or highly sensitive organisms
Prosthesis not loose
Medically unfit patient for operation
Antibiotic therapy can be continued orally and indefinitely Debridement, irrigation and suction
Good choice if :
<4 weeks passed operation
Well-fixed prosthesis
Gram positive, sensitive organism
No sinus tract Poly insert should be removed and a new one replaced later
Some propose complete synovectomy as well
4-6 weeks of IV antibiotic therapy recommended
Success rate
90% if <3 weeks
20-30% if >3 weeks Resection arthroplasty
Good choice If :
There is excessive bone loss
Low demand patient with limited rehab potential
Resistant case Requires prolonged cast/bracing
Results are unpredictable
Aim for 7° valgus and 15° flexion
If unhappy, proceed to arthrodesis Arthrodesis
Painless stable extremity with usually 2 – 8 cm shortening
Often difficult, due to bone loss
Resurfacing implants need less bone loss
75% fusion rate with external fixation
80% fusion rate with internal fixation, e.g. IM nail, plating
Internal fixation requires a clean wound
Fusion usually takes 4 – 6 months Amputation
Life threatening infection
Multiple failed attempts
Elderly, non ambulatory patient Immediate one stage re-implantation
35% success rate Two stage re-implantation Implants removal, followed by 6 weeks antibiotic therapy and re-implantation in a second stage
Insert an antibiotic impregnated spacer
Re-implant prosthesis between 6 weeks and 3 months after debridement
Wait until operation site and inflammatory indices appear normal
Re-implantation is difficult after about 3 months due to :
Soft tissue contracture
Extensor lag
Poor power is the most common post-operative problem Good or excellent results in 75% Postoperative
DVT and PE
Asymptomatic DVT is evident on venography of 50 – 70% of patients
Asymptomatic PE in 15% of patients
Symptomatic PE in 1-3% of patients
A combination of both mechanical and pharmacological prophylaxis is the most effective
Prophylaxis with Warfarin brings down complication rate to 17% Loss of Quadriceps power
Decreased ROM
Defined as <90 flexion
The single most important predictor of post operative ROM is pre-operative ROM
Post-op ROM is equal to pre-op ROM ± 10°
Usual range is 0-110° Fixed Flexion Deformity (FFD)
Will not stretch out automatically, if not addressed at the time of surgery
Most post-op FFDs are result of hamstring spasm
Post-operative FFD <30° usually resolves by 2 years CPM
Has no proven benefit for increasing overall ROM
It may improve early ROM and prevent DVT Flexion <90° at 6 weeks may need MUGA
Arthrofibrosis is the usual culprit
Adhesions occur in medial and lateral gutters Fractures
1%
Occurs within 15 cm of the prosthesis or adjacent to prosthesis stem
Femur > Tibia
More common in
Revision surgery
Osteoporosis
Presence of stress risers; e.g. femoral notching ORIF should be reserved for patients in whom
There is no osteopenia
Stable fixation can be achieved
There is a well-fixed implant
Fracture has disrupted implant interface
Satisfactory closed reduction cannot be maintained Problems of the patella
The most common complication after TKR
Occur in 10% of TKR patients
Comprise 50% of all TKR complications Patellar clunk (tethered patella syndrome)
Impingement of a fibrous nodule developed at the junction of patella and quadriceps tendon in intercondylar notch
The cause of nodule formation is not clear
Nodule impinges in flexion, prevents extension and is released at 30-45° of extension with a clunk
Only happens in posterior stabilised implants
Manage with arthroscopic debridement Fractures of the patella
Secondary to :
AVN
Direct trauma
Under resection (marked stresses over the patella)
Over resection (weak patella)
Patellar pegs create stress risers (some use multiple small pegs rather than one large peg) Treatment
Minimal displaced fracture : treat in extension splint for 6 weeks
Displaced fracture with a well-fixed patellar component : ORIF
Displaced fracture plus loose component : remove implant as bone stock is usually too poor for re-implantation
Severely comminuted facture : partial or total patellectomy Patella baja
Caused by raised joint line
Limits knee flexion due to patellar impingement
Commonly seen in patients who have had :
Previous tibial osteotomy
Previous proximal tibial fracture
Tibial tubercle transfer Managed by :
Lowering joint line
Augment femoral side and resect tibial side
Gives partial relief Placing the patellar insert superiorly
Trimming patellar and tibial poly inserts
Patellectomy Patellar tendon avulsion
Increased risk in
Revision
Prior HTO Treat with
Primary repair plus protective cerclage wiring
Use graft in irreparable cases
Knee fusion is the last resort Patello-femoral instability
Causes include :
IR of tibial or femoral component
Medial translation of femoral component
Lateral placement of the patellar component
Residual valgus deformity
Raised joint line
Inadequate resection of bone in resurfacing (too thick patella) Treatment
If there is malrotation of components, perform revision surgery
If there is no malrotation :
Lateral release
Medial reefing Rarely distal realignment becomes necessary Loosening
The most common long-term complication
Incidence increases with time
More associated with constrained prostheses
Accelerating factors :
Malalignment
Poor cement techniques Debris–induced, macrophage-initiated osteolysis and loosening are considerably rare in TKR, but may be a problem with patellar prostheses
Threefold larger wear particles are produced in a shearing, less-conforming environment of knee
Large particles are less likely to induce a macrophage response and lead to a lower rate of aseptic loosening References
Di Cesare : Knee. In Spivak JM, Di Cesare PE, Feldman DS : Orthopedics; A Study Guide; 1999
McPherson EJ : Adult Reconstruction. In Mark D. Miller : Review of Orthopedics; 2008 [...] Read more...
June 27, 2024Muscle dystrophies : Areas of degeneration and regeneration due to a primary defect in the muscle (Duchenns & Becker’s)
Muscle atrophies : Cells showing degeneration within areas of normal tissue, where the muscle changes are secondary to changes in innervation
Pathological changes demonstrable biochemically, electrically and histologically in the affected muscle groups can be of use in distinguishing the primary myopathies from neurogenic disorders
Features of myopathy are
Marked variations in fibre size
Fibre splitting
Central migration of the sarcolemmal nuclei
Areas of fibre atrophy
Formation of nuclear chains
Areas of necrosis and infiltration with fat cells and connective tissue However, denervated muscle may develop these changes secondarily. Differentiation between the two is not absolute
Duchenne Muscular Dystrophy
Most common of all muscular dystrophies (80% of cases)
Inheritance
X-linked recessive
Only boys affected and girls carriers
Up to 50% may be new mutations
Incidence
1:3,000 males
Clinically
Presents with delayed motor milestones and variable delay in psychomotor function
Steady relentless progression of muscle weakness
Patient going from crisis to crisis with abilities lost one by one
Power of distal muscles is generally retained longer than the proximal muscles
Becomes apparent during first 3 years of life
Muscular weakness accompanied in the early stages by enlargement of the calf’s and other muscle groups (pseudo hypertrophy)
Gowersmanoeuvre on rising from the floor
Extension lag of quadriceps
"Slip through" sign (pick up under arms)
By age 10 the child is unable to walk and rarely survives into adult life
Walking can be prolonged about 2 years by release of contractures, but eventually will be wheel chair bound by the age of 12 years
Once lost ambulation, scoliosis develops with 95% of boys developing curves of greater than 50 by the time they die
Axial rotation of the spine and pelvis occurs to produce a severe deformity
Pelvic obliquity makes sitting painful
Usually bed ridden by the age of 16 years
Limbs slowly develop contractures
Myocardium is also affected
20 – 30% are retarded
Death is usually due to frequent respiratory infections, secondary to weakness of respiratory muscles
Only 25% celebrate their coming of age
If survive greater than age 22, probably has a different condition, e.g. Becker’s
Typical walking posture : head is flexed, shoulders are retracted, spine is lordotic, hips and knees are flexed and feet are in equinus
Investigations
Dystrophin (protein) deficiency can be measured
Creatinine kinase elevated (may be several thousand)
Carriers may have minimal calf hypertrophy and muscle changes
70% of the carriers of Duchenne dystrophy show increased CPK
About 20% of the female carriers will exhibit mild features of muscular dystrophy at some time in their lives
Rule out treatable muscle diseases
Coleman Block test differentiates fixed from non fixed heel varus by placing a block under the foot
Treatment
Maintenance of useful mobility is the major priority
Surgery should be undertaken only with great circumspection
During ambulatory phase some recommend the use of high dose steroids to slow progression
Benefit from active exercise and conversely, rest is detrimental
Release contractures which are preventable and reversible to some extent through physical therapy
Contracture of 20 need surgical release
Contracture of 20° – 40 need serial casting prior to surgical release plus post-operative casting
If contracture is greater than 45° surgery is contraindicated
PETA and division of ilio-tibial band are commonly required
Anaesthesia should be avoided, especially muscle relaxants
Braces
Use KAFO to stabilise knee
Use spine support to slows progression of curve
Should be commenced when power insufficient to maintain the normal erect posture and a kyphosis develops Spinal fusion needed if scoliosis > 35° or vital capacity is 40% (whichever comes first)
Use Galveston technique to stabilise pelvis or new fixation methods
Prophylactic stabilisation surgery from T4 to sacrum is necessary
Pulmonary complications are seen in
50% if FVC is less than 35%
9% if FVC is greater than 35% Stabilisation has no effect on the rate of deterioration of respiratory function
Prognosis
Slow and inevitable progression
Death usually occurs within 20 years
Obese children with obese parents have the worse prognosis
Becker’s Muscular Dystrophy
Allelic with Duchenne muscular dystrophy, but is less severe
Incidence
1:10,000 males
Clinically
Average age at onset of symptoms is approximately 11 years
Loss of ability to walk by 27 years
Death at 42 years on average
Investigations
CPK is elevated between 25 and 200 times normal
Dystrophin present in 5% of cases
Limb Girdle Dystrophy
Inheritance
Autosomal recessive inheritance
Incidence
Rarer than Duchenne type and much less disabling
Clinically
Milder than Duchenne dystrophy
Symptoms usually start in late adolescence (second or third decade)
Pelvic girdle weakness causes waddling gait and difficulty in rising from a low chair
Pectoral girdle weakness makes it difficult to raise the arms above the head
Disease is slowly progressive and by the 5th decade disability is usually marked
Walking may be retained until middle life
Investigations
CPK may be increased up to ten times normal
Treatment
Physiotherapy and splinting to prevent contractures
Surgical correction may be indicated
Facioscapulohumeral Dystrophy
Inheritance
Autosomal dominant
Wide variation in the expression of the disorder
Clinically
Usually presents in early adult life
Facial muscle weakness
Winging of the scapula
Slight pelvic girdle weakness
Deterioration is slow
Life span normal
Investigations
CPK often normal
Scapuloperoneal Myopathy
Inheritance
Autosomal dominant and X-linked variants
Incidence
Both varieties are vary rare
Clinically
Present with foot drop which may mimic Charcot Marie Tooth disease
The dominant variety presents later in life than the X-linked variety
Hereditary Motor and Sensory Neuropathies
Classified by Dyck and Lambert (1968)
Type 1
Autosomal dominant
Consists of :
Hypertrophic form of CMT
Hereditary areflexic dystaxia (Roussy-Levy Syndrome) Clinically
Present in the 2nd decade
Compared to type 2, these patients have a greater tendency to show weakness of the hands, upper limb tremor and ataxia, generalised tendon areflexia, more distal sensory loss, more frequent foot and spinal deformities
Foot
Cavus
Clawing of toes
Wasting of all muscles distal to knee may cause drop foot Upper limb
Progressive wasting of intrinsics and later forearm muscles
Difficulty with fine motor skills Investigations
Motor nerve conduction velocities < 1/2 normal, due to repetive demyelination and remyelination of the peripheral nerve
Histology : "onion bulb " cross-sectional appearance Type 2
Autosomal dominant
Consists of the neuronal form of CMT
Clinically
Present later in the 2nd or 3rd decade
More profound distal lower limb weakness than type 1, upper extremity involvement is less pronounced
Characteristic stork-leg appearance
Flail foot develops a calcaneocavus deformity Investigations
Conduction velocities slightly decreased or normal Type 3
Autosomal recessive
Consists of the hypertrophic neuropathy of infancy (Dejerine-Sottas disease)
Clinically
Present in infants/young children with delayed lower limb milestones
Pes cavus and drop foot common
Sensory loss in stocking/glove distribution
Significant spinal deformity in most
Wheelchair by 3rd or 4th decade Investigations
Markedly slow conduction velocities
Sural nerve biopsy shows onion bulb formation with frequent segmental demyelination Type 4
Autosomal recessive
Consists of Refsums disease, rare
Clinically
Presents in childhood – puberty
Characterised by remissions and relapses
Associated with
Anosmia
Progressive deafness
Night blindness
Hypertrophic neuropathy
Areflexia
Scoliosis
Pes cavus
Equinus Investigations
Elevation of serum phytanic acid is pathognomonic
Elevation of CSF protein levels
Motor nerve conduction velocities low
Nerve biopsy shows onion bulb formation [...] Read more...
June 27, 2024Introduction
Osteonecrosis of the proximal femoral epiphysis in a growing child
Reported by Legg (USA, 1909), Calve (France, 1910) and Perthes (Germany, 1910)
Waldenstrom (1906) reported the features, but related them to TB
Phemister (1920) described pathology of necrotic bone
Epidemiology
Male : Female 4:1
Onset usually 2 – 12
The majority are 5 – 8
Mean 7 years 10 – 15% are bilateral
Anatomy
The ossific nucleus is covered by 3 layers of cartilage (in addition to the articular cartilage):
Superficial zone (lies just deep to the layer of articular cartilage)
Middle zone (zone of epiphyseal cartilage)
Deep zone
**The superficial and middle zones receive nutrition from the synovial fluid.
Etiology
Exact cause of Perthes disease is unknown
There is a 2-20% incidence of family history
some studies have shown it to be associated with:
low birth weight
lower socioeconomic groups
urban communities
children with ADHD
delayed skeletal age/shorter stature
Abnormal somatomedin levels (raised somatomedin A)
incomplete anastomotic network at the proximal femur
Abnormal Type II collagen has been demonstrated in familial, bilateral cases
Thrombophilia – controversial
Potential abnormalities include:
Protein C and S deficiency
Factor V Leiden
Anticardiolipin antibodies
Antithrombin III deficiency Vascular Embarrassment as a Possible Cause:
Alteration in blood supply to femoral head with fetal supply from metaphyseal vessels, lateral epiphyseal vessels running in the retinaculum up the neck and small supply from the ligamentum teres
Metaphyseal supply gradually decreases (by the age of 4)
Vessels in the ligamentum teres are not developed until about the age of 7
Between the age of 4 and 7, blood supply to the head may depend solely on lateral epiphyseal vessels, which are susceptible to external pressure
External pressure may occur from an effusion related to retinacular vessel occlusion, increased intra-capsular pressure, intra-epiphyseal thrombosis, vascular irregularities or increased vascularity
Kemp et al (1971) showed an effusion in the hip can decrease blood supply and cause ischaemia of the femoral head
Effusion may be enough to tip the balance in susceptible individuals
Repeated episodes are necessary to result in AVN of the bone and increased severity of disease may reflect increased number of ischemic events
Pathology
Pathological stages take 2 – 4 years to complete
Salter and Thompson description of events :
Osteonecrosis of femoral head
Temporary cessation of growth of epiphysis
Revascularisation from periphery
Resorption of avascular bone and production of woven bone
Pathological fracture
Resorption of underlying bone and replacement by biologically plastic (woven) bone
Subluxation
Deformity Stages of Perthes Disease
Stage I: Initial (increased radiodensity)
All or part of the bony femoral undergoes osteonecrosis
X-Ray are normal
The head stops enlarging, but the cartilage still nourished by diffusion continues to grow, showing increased apparent joint space
Cessation of growth lasts 6 – 12 months Stage II: Fragmentation
Lasts ~ 1 year
Crescent sign is seen early in fragmentation stage
Trabeculae in dead bone may fracture in subchondral region making tangential line
New bone laid down on dead trabeculae results in increased density on xray Hyperaemia and re-vascularization lead to bone resorption and head becomes rarefied / cystic
Resorption usually complete by 12 – 17 months Stage III: Reossification
Lasts 3-5 years
If repair / re-vascularization has been rapid, the head may maintain its shape
The head may collapse with further flattening / fragmentation
Abnormal stresses transmitted to the growth plate may cause distortion or growth arrest
Lateral portion of head often becomes uncovered
Normal bony architecture will return, but alteration in shape persists, leading to early degenerative changes
Resolution usually takes 6 – 24 months, either heal or residual deformity
As the physis is nourished by the epiphysis, AVN of the epiphysis also causes AVN of the physis to some extent and hence, growth arrest or retardation
There is a direct correlation between severity of physeal involvement and deformity of the head
Coxa magna secondary to premature physeal arrest and hypertrophy of epiphyseal cartilage
The clinical picture varies depending on the age of the child, the stage of the disease and the amount of head involved Stage IV: Healed
residual deformity may be present Clinically
5 – 8 years of age
Many patients appear younger than their actual age
Insidious onset limp, often painless and intermittent
Pain usually in the groin or inner thigh, but may radiate to knee
Limitation of abduction, internal rotation
Thigh, calf, buttock atrophy secondary to disuse
Possibly a positive Trendelenberg sign Limb length discrepancy of 1 to 2.5cm
Investigations
Laboratory:
In light of evidence that coagulopathies may play a role in pathophysiology, some reccommend screening for:
Protein C and S deficiency
Factor V Leiden
Anticardiolipin antibodies
Antithrombin III deficiency Imaging:
X-Rays : AP and lateral (Lauenstein)
At-risk signs:
Gage sign: radiolucency in the lateral epiphysis and metaphysis and mineralization lateral to the epiphysis
poor prognositic indicator; sign of early ossification in enlarged epiphysis Radiolucent lesions in the epiphysis
sign of potential disturbance of the physis
Subluxation
horizontal physis Whole head involvement Residual deformities:
Relative overgrowth of greater trochanter
Coxa breva
Hanging rope sign is characteristic of old Perthes MRI
Very sensitive in detecting infarction
Role yet to be determined Arthrography
Can be used to determine if the head and acetabulum are congruent when deciding upon surgical treatment Classification
*Disease must reach the fragmentation stage before it can be classified and there is large inter-observer variation
Herring (Lateral Pillar)
Interobservor agreement is best with the Herring classification
Femoral head on the AP radiograph is divided into 3 parts with the lateral pillar occupying the lateral 15 – 30%, the central pillar ~ 50% and the medial pillar 20 – 35%
Stage determined at the end of the fragmentation phase
Group A
No involvement of the lateral pillar
There may be lucency and collapse in the central and medial pillars Group B
Greater than 50% of lateral pillar height maintained Group C
Less than 50% of lateral pillar height maintained Catterall
Stage 1
Antero-medial portion of head involved
No collapse
Metaphyseal changes do not occur
Epiphyseal plate is not involved
Heals without significant sequelae Stage 2
More head involved
May have fragmentation of the involved segment
The involved segment shows increased density
Uninvolved pillars of normal bone prevent significant collapse
Regenerates without much loss of height
The end result is usually good
Metaphyseal reaction is localised Stage 3
Collapse of the head seen, as uninvolved pillars not large enough to prevent collapse
May show head within a head
The metaphysis is usually diffusely involved, causing broad neck
The epiphyseal plate is unprotected and usually involved
Results are poor Stage 4
Whole head involvement
Severe collapse occurs early
Restoration of the femoral head usually less complete
The metaphyseal changes may be extensive
The epiphyseal plate is often involved, leading to abnormal growth (coxa magna, coxa breva, coxa vara and coxa valga) Salter – Thompson
Stage A
Lateral portion of femoral capital epiphysis present (Catterall 1 & 2)
Less than 50% head involved Stage B
Lateral portion of femoral capital epiphysis absent (Catterall 3 & 4)
More than 50% head involved
Lateral margin of epiphysis protects epiphysis from stress Ponseti
Those with less than 50% of head involvement
Those with more than 50% of head involvement
Differential Diagnosis
Multiple epiphyseal dysplasia
Other causes of Osteonecrosis
Sickle cell disease
Corticosteroid therapy Gauchers disease
Traumatic AVN
Infection
Treatment
Observation:
Indicated for patients with a good prognosis, including:
Patients younger than 6
Pillar A
Salte-Thompson A
Catterall group 1 Conservative modalities may also be employed
Includes range of motion exercises, night time abduction splinting, home traction
Bracing is rarely used today
Prolonged immobilization, bed rest, and protected weight bearing do not influence course of disease Medical Treatment:
Promising results have been demonstrated with bisphosphonate therapy
Surgical containment:
Indications:
Patients with poor prognosis in the initial stage or fragmentation stage
Hips that are containable:
full range of motion
femoral head/acetabular congruity Options:
proximal femoral varus osteotomy
varus angle must be less than 110 degrees postoperatively innominate osteotmy
shelf
triple Combination femoral and acetabular osteotomy
combination osteotomies not typically performed Salvage procedures
Indications
Patients with significant residual deformity Options:
Valgus, extension osteotomy
Cheilectomy
Chiari osteotomy to cover the femoral head
Lateral shelf arthroplsty
Arthrodesis at skeletal maturity. Should be reserved for patients with severe functional impairment Other Treatment Algorithms:
Treatment by Catterall stage: (Apley)
Stage I : No treatment needed
Stage II & III
No treatment needed if less than 7 years of age, unless head at risk signs present
Aged more than 7 years or head at risk signs, proceed to containment therapy for about 6 – 14 months or until signs of recalcification of head
Full range of movement should exist before using abduction device Stage IV
At any age : containment unless undue force required
Choice between operative and non-operative treatment may not alter natural history of disease
Pelvic or femoral osteotomies have similar results Treatment recommended by Herring (JBJS 76A 448-458, 1994)
Patient less than 6 years old
No evidence that any form of treatment alters the growth potential of the physis or the outcome
Principle is symptom relief Patient 6 – 8 years old
All group A and those group B patients with bone age of less than 7
No alteration of outcome by treatment
Symptomatic relief only Those group B with bone age 7 or over
Better outcome with containment
No difference between method of containment Those in group C
Effect of treatment not known
Currently advocates containment Patient 9 years old or older
Difficult to manage
Tend to get more severe disease
Do not tolerate bracing well, thus more likely to have surgery over bracing
Group A : Symptomatic only
Group B+C : Advocates containment by whatever means Treatment of the child with significant femoral head deformity
Defined significantly involved if :
Femoral head is at least 4 mm out of round
Overly symptomatic Salvage procedures
Cheilectomy or chiari osteotomy to cover the femoral head
Valgus osteotomy to increase abduction and bring more normal medial femoral head into the weight bearing area
Arthrodesis at about skeletal maturity. Should be reserved for patients with severe functional impairment If planning for containment therapy :
Perform arthrogram
Determine if containment can be achieved
Determine optimal position Brace / POP
Operate if :
Failure of bracing
Intolerant of brace Prognosis
70-90% of patients are free of pain 20-40 years after the onset of symptoms despite abnormal radiographs.
Clinical determinants
Increased age at onset harbors worse prognosis (age less than 6-8 do well)
Total head involvement has poor prognosis
Prolonged disease duration
Females have poorer prognosis (possibly due to earlier skeletal maturity and less remodeling potential)
The most important factor for long-term outcomes after the patient has reached the healed stage is degree of deformity of the femoral head and congruency between the femoral head and acetabulum
Mose (Acta Orthop Scand, supp 169, 1977)
Rings of increasing diameter (2 mm)
If head conforms to a single ring in both X-Ray planes, has good prognosis
If head varies from perfect circle by no more than 2 mm, has fair results
If head varies by more than 2 mm in any plane, has poor results Stulberg’s Classification of Residual Deformity: (JBJS 63A: 1095-1108, 1981)
Class 1: Normal hip joint
Class 2: Spherical femoral head, with one or more of the following:
Coxa magna
Coxa breva
Increased acetabular index Class 3: Aspherical, but not flat femoral head (Ovoid or mushroom-shaped) and:
Coxa magna
Coxa breva
Increased acetabular index Class 4: Flat femoral head and abnormal head, neck and acetabulum
Class 5: Flat femoral head and a normal neck and acetabulum
Stulberg’s results
Spherical congruency (class 1+2) : No risk of OA
Aspherical congruency (class 3+4) : Mild-moderate OA in late adulthood
Aspherical incongruency (class 5) : Severe OA before age 50
Conclusion
These results showed that lack of sphericity alone was not the only predictor of a poor outcome (Mose)
As many as 50% do well without treatment
Most of the remaining 50% do well into the 5th decade, despite CE angles less than 20 and Mose sphericity more than 2 mm out of round
No follow up study of sufficient length exists to show containment has altered the natural history of the condition
Radiological determinants
Extent of head involved, i.e. grade of disease
At risk factors
Herring group :
Group A : 100% are Stulberg 1 or 2
Group B
Less than 9 years old at onset
92% are Stulberg 1+2
8% Stulberg 3 More than 9 years old at onset
30% are Stulberg 2
50% Stulberg 3
20% Stulberg 4 Group C
29% are Stulberg 2
52% Stulberg 3
19% Stulberg 4 [...] Read more...
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Recent resources from OrthopaedicsOne PORT Notes, MSK Medicine for Medical Students, and Atlas of Musculoskeletal Oncology spaces.
Recently Updated
June 28, 2024DEFINITION AND PATHOGENESIS
A tumor of unknown origin
IMPORTANCE
No bony counterpart has been reported
Intermediate malignant potential counterpart must be ruled out
CLINICAL FEATURES
Usually present as a slow growing, small painless, well circumscribed subcutaneous or muscular mass
Has been reported presenting as a scalp cyst M:F = 2:1
Median age 50 yrs (21-81)
Reported in the subcutaneous tissue of the head of a 2-yr-old
Retroperitoneal location reported ina 6-yr-old girl with paraspinal extension and disease free 9 yrs after resection Median duration of sxs = 4 yrs
?? alk?
RADIOLOGIC FEATURES
Radiographs may be normal
Peripheral ossification can occur ? uptake on BS
MRI with a well defined mass, with heterogeneous signal
Unusual location
Ethmoid sinus
Parotid/zygomatic arch region
Mediastinum GROSS PATHOLOGY
Tumor size 0.7-17 cm (median 3- cm)
Fibrous capsule with incomplete peripheral shell of mature bone reported
HISTOLOGIC AND MOLECULAR FEATURES
Round to oval cells in cords or nests within a myxoid matrix ± transition to hyaline fibrosis and focal osteoid
Few or no mitotic activity
Higher mitotic activity reported (suggests the malignant counterpart
Mitotic activity reported from 0-50hpf ± necrosis (17%) (suggests the malignant counterpart
± vascular invasion (11%) (suggests the malignant counterpart
± stromal cyst formation Incomplete capsular shell of mature bone
Moderate amounts of myxocollagenous matrix
± focal peripheral metaplastic bone formation
Central zone bone formation has been reported
40% with bone present Background cells can include histiocytes, lymphocytes, and mast cells
Immunohistochemisty
+ S-100 in 6094% reported
Pancytokeratin (10%)
SMA (%)
Desmin (13%)
Collagen II (%)
Glial fibrillary acidic protein positivity reported
Vimentin positivity reported
Neurofilament and neuron specific enolase positivity reported suggesting neural origin
+ synaptophysin reported EM
Abundant intermediate filaments, primitive cell junctions, focally present external lamina reported (suggesting neural origin)
Cytoplasmic dense-core granules measuring 100-200nm Ctyogenetics
42 approximately 46,XY,-Y,add(1)(q42),add(6)(p21),t(10;18)(q26;q11),der(11)t(11;15)(q23;q15),add(12)(q13),ins(14;?)(q13;?),-15,+mar reported
45,XY, der(6;14)(p10;q10),add(12)(q24.3) reported DIFFERENTIAL CLINICOPATHOLOGIC DIAGNOSIS
Calcifying hematoma
Aponeurotic fibroma
Nodular fasciitis
Neurilemoma
Epithelioid" type Myoepithelioma
Mesenchymal hamartoma
Ossifying epithelioid hemangioendothelioma
Chondromyxoid fibroma
Osteosarcoma of soft tissue
Malignant schwannoma
Low-grade fibromyxoid sarcomas
Malignant ossifying fibromyxoid tumor (the malignant counterpart
DISEASE COURSE AND TREATMENT
22-30% LR (may result in amputation)(esp in large tumors, ? cellularity, ? mitoses)
LR usu ? 10 yrs
Subcutaneous LR reported
Chest wall LR reported after only 1 yr > 2 mitotic figures/50 HPFs risk for LR Wide resection with clear margins indicated because of the indistinct differentiation between the benign and malignant counterparts
One report associated with pulmonary metastases extending into the L atrium has been reported representing the malignant counterpart
FIGURES There are no images attached to this page. REFERENCES
Adamek D, Stachura J, Katuza J: Recurrent ossifying fibromyxoid tumour of soft parts. Immunohistochemical profile and ultrastructure. Pol J Pathol 1998;49(3):179-82.
Akai M, Azuma H, Ohno T, Kimura H, Sugano I, Nagao K: Case report 685: ossifying fibromyxoid tumor of the soft parts of the upper arm. Skeletal Radiol 20:608-12,1991.
Al-Brahim N, Dashti MA: Ossifying fibromyxoid tumor of soft parts. Report of a rare tumor in Kuwait. Med Princ Pract 2008;17(4):340-2.
Barrett TL, Skelton HG, Smith KJ, O’Grady TC, Proctor-Shipman L: Ossifying fibromyxoid tumor of soft parts: a case report and review. J Cutan Pathol 1996 Aug 23(4):378-80.
Donner LR: Ossifying fibromyxoid tumor of soft parts: evidence supporting Schwann cell origin. Hum Pathol 1992 Feb;23(2):200-2.
Ekfors TO, Kulju T, Aaitonen M, Kallajoki M: Ossifying fibromyxoid tumour of soft parts: report of four cases including one mediastinal and one infantile. APMIS 1998 Dec;106(12):1124-30. Enzinger FM, Weiss SW, Liang CY: Ossifying fibromyxoid tumor of soft part: a clinicopathological analysis of 59 cases. Am J Surg Pathol 13:817-27,1989. Pubmed
Fisher C, Hedges M, Weiss SW: Ossifying fibromyxoid tumor of soft parts with stromal cyst formation and ribosome-lamella complexes. Ultrastruct Pathol 1994 Nov-Dec;18(6):593-600.
Folpe AL, Weiss SW: Ossifying fibromyxoid tumor of soft parts: a clinicopathologic study of 70 cases with emphasis on atypical and malignant variants. Am J Surg Pathol 2003 Apr;27(4):421-31. Pubmed
Fukunaga M, Ushigome S, Ishikawa E: Ossifying subcutaneous tumor with myofibroblastic differentiation: a variant of ossifying fibromyxoid tumor of soft parts? Pathol Int 1994 Sep;44(9):727-34.
Hanski W, Lewicki Z: New observations on three cases of ossifying fibromyxoid tumor of soft parts. Pol J Pathol 1994;45(3):231-8.
Holck S, Pedersen JG, Ackermann T, Daugaard S: Ossifying fibromyxoid tumour of soft parts, with focus on unusual clinicopathological features. Histopathology 2003 Jun;42(6):599-604.
Ijiri R, Tanaka Y, Misugi K, Sekido K, Nishi T: Ossifying fibromyxoid tumor of soft parts in a child: a case report. J Pediatr Surg 1999 Aug;34(8):1294-6.
Kawashima H, Ogose A, Umezu H, Hotta T, Tohyama T, Tsuchiya M, Endo N: Ossifying fibromyxoid tumor of soft parts with clonal chromosomal aberrations. Cancer Genet Cytogenet 2007 Jul 15;176(2):155-60.
Kilpatrick SE, Ward WG, Mozes M, Miettine M, Fukunaga M, Fletcher CDM: Atypical and malignant variants of fibromyxoid tumor: Clinicopathologic analysis of six cases. Am J Surg Pathol 19:1039-46,1995. Pubmed
Kiryu H, Hashimoto H, Hori Y: Ossifying epithelioid hemangioendothelioma. J Cutan Pathol 1996 Dec;23(6):558-61.
Lax SF, Ratschek M, Steindorfer P, Langsteger W, Harms D, Beham A: Ossifying fibromyxoid tumour of the neck clinically mimicking a primary neoplasm of the thyroid gland. Pathol Res Pract 1995 Feb;191(1):57-60.
Martinez-Rodriguez M, Subramaniam MM, Calatayud AM, Ramos D, Navarro S, Llombart-Bosch A: Ossifying fibromyxoid tumor of soft parts mimicking a schwannoma with uncommon histology: a potential diagnositic pitfall. J Cutan Pathol 2009 Jan;36(1):71-3.
Matsumoto K, Yamamoto T, Min W, Yamada N, Asano G, Moriyama M, Matsumoto T: Ossifying fibromyxoid tumor of soft parts: clinicopathologic, immunohistochemical and ultrastructural study of four cases. Pathol Int 1999 Aug;49:742-6.
McCormack D, Lane H, Bennett D, Fenelon G: Ossifying fibromyxoid tumour of soft parts. Ir J Med Sci 1997 Jul-Sep;166(3):130-1.
Miettinen M: Ossifying fibromyxoid tumor of soft parts. Additional observations of a distinctive soft tissue tumor. Am J Clin Pathol 1991 Feb;95(2):142-9.
Michal M, Miettinen M: Myoepitheliomas of the skin and soft tissues. Report of 12 cases. Virchows Arch 1999 May;434(5):393-400.
Michal M, Sokol L: Benign polymorphous mesenchymal tumor (mesenchymal hamartoma) of soft parts. Report of two cases. Am J Dermatopathol 1997 Jun;19(3):271-5.
Miettinen M, Finnell V, Fetsch JF: Ossifying fibromyxoid tumor of soft parts–a clinicopathologic and immunohistochemical study of 104 cases with long-term follow-up and a critical review of the literature. Am J Surg Pathol 2008 Jul;32(7):996-1005. Pubmed
Nakayama F, Kuwahara T: Ossifying fibromyxoid tumor of soft parts of the back. J Cutan Pathol 1996 Aug;23(4):385-8.
Nishio J, Iwasaki H, Ohjimi Y, Ishiguro M, Isayama T, Naito M, Okabayashi H, Kaneko Y, Kikuchi M: Ossifying fibromyxoid tumor of soft parts. Cytogenetic findings. Cancer Genet Cytogenet 2002 Mar;133(2):124-8. Pubmed
Oda N, Yasui W, Ito H, Tahara E: Ossifying fibromyxoid tumor of soft parts: a case report. Jpn J Clin Oncol 1993 Feb 23(1):64-8.
Orosz Z, Sapi Z, Szentirmay Z: Unusual benign neurogenic soft tissue tumour. Epithelioid schwannoma or an ossifying fibromyxoid tumour? Pathol Res Pract 1993 Jun;189(5):601-5; discussion 605-7.
Raith J, Ranner G, Schaffier G, Groll R, Lindbirchier F, Fritz K, Weybora W: Bone scan in ossifying fibromyxoid tumor of soft parts. Clin Nucl Med 1998 Apr;23(4):262-4.
Sarraj A, Duarte J, Dominguez L, Pun YW: Resection of metastatic pulmonary lesion of ossifying fibromyxoid tumor extending into the left atrium and ventricle via pulmonary vein. Eur J Echocardiogr 2007 Oct;8(5):384-6.
Schofield JB, Krausz T, Stamp GW, Fletcher CD, Fisher C, Azzopardi JG: Ossifying fibromyxoid tumour of soft parts: immunohistochemical and ultrastructural analysis. Histopathology 1993 Feb;22(2):101-12.
Seykora JT, Kutcher C, van de Rijn M, Dzubow L, Junkins-Hopkins J, Ioffreda M: Ossifying fibromyxoid tumor of soft parts presenting as a scalp cyst. J Cutan Pathol 2006 Aug 33(8):569-72.
Sovani V, Velagaleti GV, Filipowicz E, Gatalica Z, Knisely AS: Ossifying fibromyxoid tumor of soft parts: report of a case with novel cytogenetic findings. Cancer Genet Cytogenet 2001 May;127(1):1-6.
Velasco-Pastor AM, Martinez-Escribano J, del Pino Gil-Mateo M, Quecedo-Estebanez E, Fortea-Baixauli JM, Allaga-Boniche A: J Cutan Pathol 1996 Aug;23(4):381-4.
White WL: Self assessment–1993. Non-ossifying variant of ossifying fibromyxoid tumor of soft parts. J Cutan Pathol 1994 Dec;21(6):571-3.
Williams RW, Case CP, Irvine GH: Ossifying fibromyxoid tumour of soft parts–a new tumour of the parotid/zygomatic arch region. Br J Oral Maxillofac Surg 1994 Jun;32(3):174-7.
Williams SB, Ellis GL, Meis JM, Heffner DK: Ossifying fibromyxoid tumour (of soft parts) of the head and neck: a clinicopathological and immunohistochemical study of nine cases. J Laryngol Otol 1993 Jan;107(1):75-80. Pubmed
Willamson ME, Dallimore N: A new bony lump for general surgeons: ossifying fibromyxoid tumour of soft parts. Case report. Eur J Surg 1994 Jan;160(1):53-4.
Yang P, Hirose T, Hasegawa T, Gao Z, Hizawa K: Ossifying fibromyxoid tumor of soft parts: a morphological and immunohistochemical study. Pathol Int 1994 Jun;44(6):448-53.
Yoshida H, Minamizaki T, Yumoto T, Furuse K, Nakadera T: Ossifying fibromyxoid tumor of soft parts. Acta Pathol Jpn 1991 Jun;41(6):480-6.
Zamecnik M, Michal M, Simpson RH, Lamovec J, Hlavcak P, Kinkor Z, Mukensnabl P, Matejovsky Z, Betlach J: Ossifying fibromyxoid tumor of soft parts: a report of 17 cases with emphasis on unusual histological features. Ann Diagn Pathol 1997 Dec;1(2):73-81. Pubmed [...] Read more...
June 28, 2024Opportunity is missed by most people because it is dressed in overalls and looks like work." Thomas Alva Edison [...] Read more...
June 28, 2024DEFINITION AND PATHOGENESIS
Neuroectodermal origin
IMPORTANCE
Rare
CLINICAL FEATURES
Most commonly involves the trunk
RADIOLOGIC FEATURES
GROSS PATHOLOGY
Well-circumscribed purple mass
HISTOLOGIC FEATURES
Small round cells
DIFFERENTIAL CLINICOPATHOLOGIC DIAGNOSIS
Extraskeletal Ewing sarcoma
Rhabdomyosarcoma
DISEASE COURSE AND TREATMENT
Metastases to bone, bone marrow, LN, lung
Chemotx + wide resection
SPECIAL CONSIDERATION CONGENITAL PERIPHERAL NEUROEPITHELIOMA Has been reported as a hand mass in an infant REFERENCES
Bolen JW, Thorning D: Peripheral neuroepithelioma: a light and electron microscopic study. Cancer 46:2456-62,1980.
Cavazzana AO, Niufo V, Roberts J, Triche TJ: Peripheral neuroepithelioma: a light microscopic, immunocytochemical, and ultrastrctural study. Mod Pathol 5:71-8,1992.
Erdmann D, Brown RE, Rumbolo PM: Congenital neuroepithelioma in an infant hand. J Hand Surg 21B:117-21,1996.
Llombart-Bosch A, Terner-Lacombe MJ, Peydro-Olaya A, Contesso G: Peripheral neuroectadermal sarcoma of soft tissue (peripheral neuroepithelioma): a pathologic study of ten cases with differential diagnosis regarding other small, round-cell sarcomas. Hum Pathol 20:273-80,1989.
Pappo AS, Douglass EC, Meyer WH, Marina N, Parham DM: Use of HBA 71 and Anti-2-microglobulin to distinguish peripheral neuroepithelioma from neuroblastoma. Hum Pathol 24;880-5,1993.
Silliman CC, Mierau GW, Strain JD, : Peripheral neuroepithelioma of the soft tissues: a retrospective analysis of 15 pediatric patients. Am J Ped Hematol/Oncol 15:299-305,1993.
Voss BL, Pysher TJ, Humphrey GB: Peripheral neuroepithelioma in childhood. Cancer 54:3059-64,1984. [...] Read more...
June 28, 2024Whatever is worth doing at all is worth doing well." Lord Chesterfield [...] Read more...
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June 29, 2024What’s New
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Tumor Cases
17 year old female with painful right arm mass 43 yr old male with a thigh mass 50 yr old Soft Tissue Sarcoma 57 yr old with multiple exostoses 78 yr old with a thigh mass and lymphadenopathy A 61-year-old male with 7-year history of joint pain, weakness, and multiple fractures Chondroblastoma – Recurrent Chondrosarcoma Compress Fixation Results Destructive Bone Lesion in a Eucalcemic Patient with Primary Hyperparathyroidism Failed Type II Pelvic Reconstruction Fibrous dysplasia with pathological fracture of proximal femur in a 25 year old lady Gaucher’s Disease Glomus Tumor as a Cause of Severe Thigh Pain Metastatic Ewing’s Sarcoma Humerus Recurrent Chondroblastoma Recurrent Giant Cell Tumor Right hip pain and bone infarction Sixty-one year old male with history of joint pain, weakness, and multiple fractures Use of Spare Parts in Musculoskeletal Oncology [...] Read more...
June 29, 2024Select Case Type Select the type of case template to use and enter the title of the case on the next page. [...] Read more...
June 29, 2024History 68 yr old, 52kg female underwent TKA for OA knee 8 years ago. She had polio in the past and has no quadriceps function. Her knee was placed in slight hyperextension and she did well walking without aids or braces. In November 2008, she fell while in Mexico. She sustained a high supracondylar fracture, initially managed with an external fixator. This was later converted to a supracondylar retrograde nail.
Physical Examination The patient was seen 7 months later with a stiff, painful, swollen and warm knee. She had been on intravenous antibiotics and was taking oral cephalosporins at the time. ESR was 37 and CRP was 20.5. Her cell count was 7750, with 90%polys. Antibiotics were stopped and she was aspirated 3 weeks later, no growth.
Initial Imaging Diagnosis (Click to see answer) Treatment Discussion References Attachments: _7202204.jpg (image/jpeg) _7202206.jpg (image/jpeg) _7202211.jpg (image/jpeg) _7202216.jpg (image/jpeg) _7202219.jpg (image/jpeg) _7202222.jpg (image/jpeg) _7202226.jpg (image/jpeg) 1.jpg (image/jpeg) munoz 2 arthrodesis.jpg (image/jpeg) nonunion1.jpg (image/jpeg) nonunion2.jpg (image/jpeg) primary knee2.jpg (image/jpeg) primary knee.jpg (image/jpeg) primary knee2.jpg (image/jpeg) primary knee2.jpg (image/jpeg) primary knee.jpg (image/jpeg) final1.jpg (image/jpeg) final1.jpg (image/jpeg) final 2.jpg (image/jpeg) final.jpg (image/jpeg) final3.jpg (image/jpeg) [...] Read more...
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June 29, 2024Case Conferences are interactive case based learning modules following a standardized history, physical exam, diagnostic workup approach. Create one for CME credits. [...] Read more...
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June 29, 2024Program Information Residency Program: Wayne State University Orthopaedic Surgery Residency Program Program Director: Robert Teitge, MD Number of Residents: 4 per year Number of Staff: 22 Accredited: Accredited Length of Program: 5 Start Dates: July Program Contact Information Name: Colleen M Sturr, MA Address: Oakwood Heritage Hospital
Orthopaedic Surgery Program
10000 Telegraph Rd City: Taylor State/Province: Zip/Postal code 48180 Phone: (313) 375-7227 Fax: (313) 375-7225 Email: [email protected] Website: http://orthosurgery.med.wayne.edu Program Highlights
Conferences
Twice-weekly didactic sessions
Monthly M&M Program Gallery Program Curriculum
PGY-1: General surgery, trauma, vascular surgery, plastic surgery, ICU, anesthesia, orthopaedic surgery, physical medicine and rehabilitation, emergency medicine, MSK radiology
PGY-2: Adult reconstruction, hand, pediatrics, trauma
PGY-3: Spine, general orthopaedics, research, trauma, foot/ankle
PGY-4: Pediatrics, sports medicine, research, adult reconstruction, trauma
PGY-5: Hand, general orthopaedics, trauma, elective
Program Hospitals
Wayne State University School of Medicine – Detroit, MI
Veterans Affairs Medical Center (Detroit) – Detroit, MI
Oakwood Heritage Hospital – Taylor, MI
University of Michigan Hospitals and Health Centers – Ann Arbor, MI
St John Hospital and Medical Center – Detroit, MI
Oakwood Hospital – Dearborn, MI [...] Read more...
June 29, 2024Program Information Residency Program: Boston University Orthopaedic Surgery Residency Program Program Director: Paul Tornetta, III, MD Number of Residents: 25 Number of Staff: 46 Accredited: Accredited Length of Program: 5 Start Dates: June Program Contact Information Name: Lynnette St. Louis Address: Boston University Medical Center
Dowling 2 North
850 Harrison Ave City: Boston State/Province: Massachusetts Zip/Postal code 02118 Phone: (617) 638-8934 Fax: (617) 414-4003 Email: [email protected] Website: http://www.bumc.bu.edu/orthopaedics Program Highlights
One 6-year research position offered per year
Dedicated year of basic science research between PGY-2 and PGY-3
Complete 2 manuscripts for publication and present research at conferences 10 hours per week dedicated to didactic conferences
Grand Rounds
Anatomy
Sports medicine
Adult reconstruction
Basic science
Pathology
Lecture series by Dr. Robert E. Leach
Foot and ankle
Hand
Trauma
Spine
Pediatrics
Daily board rounds
Monthly journal club
Monthly hands-on bioskills lab Program Gallery Program Curriculum
PGY-1: Orthopaedic surgery, general surgery, trauma, critical care, radiology, emergency medicine, anesthesia, vascular surgery
PGY-2: Fracture, foot/ankle, pediatrics, hand, orthopaedic oncology
PGY-3: Pediatrics, sports medicine, fracture, reconstruction
PGY-4: Pediatrics, VA, general, sports, hand, spine
PGY-5: Lahey Clinic, fracture, pediatrics, hand, reconstruction, sports
Program Hospitals
Boston Medical Center – Boston, MA
Shriners Hospitals for Children (Springfield) – Springfield, MA
Massachusetts General Hospital – Boston, MA
Veterans Affairs Medical Center (Boston) – Boston, MA
Lahey Clinic – Burlington, MA [...] Read more...
June 29, 2024Program Information Residency Program: Ohio State University Hospital Orthopaedic Surgery Residency Program Program Director: Joel Mayerson, MD Number of Residents: 5 per year Number of Staff: 31 Accredited: Accredited Length of Program: 5 Start Dates: July Program Contact Information Name: Julia A Panzo Address: Ohio State University Medical Center
4118 Cramblett Hall
456 W 10th Ave City: Columbus State/Province: Ohio Zip/Postal code 43210 Phone: (614) 293-6194 Fax: (614) 293-3596 Email: [email protected] Website: http://www.ortho.ohio-state.edu/ Program Highlights
One 6-year research position available per year
Rotations in the following subspecialties:
Foot and ankle
General orthopaedics
Hand
Infection
Joints
Oncology
Pediatrics
Shoulder
Spine
Sports
Trauma Conferences:
Educational conferences specific to each affiliated hospital
Weekly fracture conference
Weekly Grand Rounds
Monthly journal club
Monthly teaching conferences Program Gallery Program Curriculum
Program Hospitals
Ohio State University Hospital – Columbus, OH
Riverside Methodist Hospitals (OhioHealth) – Columbus, OH
Grant Medical Center (OhioHealth) – Columbus, OH
Nationwide Children’s Hospital – Columbus, OH [...] Read more...
June 29, 2024Program Information Residency Program: Rush University Medical Center Orthopaedic Surgery Residency Program Program Director: Walter W Virkus, MD Number of Residents: 25 Number of Staff: 34 Accredited: Accredited Length of Program: 5 Start Dates: July Program Contact Information Name: Phyllis J Velez Address: Rush University Medical Center
Rm 201 Orthopedic Bldg
1653 W Congress Pkwy City: Chicago State/Province: Illinois Zip/Postal code 60612 Phone: (312) 942-5850 Fax: (312) 942-2101 Email: [email protected] Website: http://www.rush.edu/professionals/gme/orthopedics/index.html Program Highlights
Subspecialty areas:
Adult reconstruction
Pediatric orthopaedics
Orthopaedic oncology
Sports medicine, cartilage restoration, shoulder
Hand surgery
Spine surgery
Foot and ankle
Trauma Didactic education
Weekly core curriculum
Weekly grand rounds
Weekly subspecialty conferences in sports, joint replacement, fracture, tumor, pediatrics, foot/ankle Residents actively involved in all areas of patient care: diagnosis, pre-op, post, rehab
Program Gallery Program Curriculum
PGY–I: 1-month rotations in general surgery, neurosurgery, plastic surgery, trauma/intensive care, rheumatology, radiology, vascular surgery, orthopaedics
PGY–II: 10-week rotations in sports medicine, joint replacement, spine, hand/foot/ankle, trauma
PGY–III: 10-week rotations in sports medicine, joint replacement, hand/foot/ankle, pediatrics/tumor/trauma, research
PGY–IV: 10-week rotations in hand/foot/ankle, trauma, pediatric spine, general pediatrics
PGY–V: 10-week rotations in joint replacement, spine, sports medicine, trauma, tumor/trauma/pediatrics
Program Hospitals
Rush University Medical Center – Chicago, IL
North Shore Skokie Hospital – Skokie, IL
John H Stroger Hospital of Cook County – Chicago, IL
OSF St Anthony Medical Center – Rockford, IL
Shriners Hospitals for Children (Chicago) – Chicago, IL [...] Read more...
June 29, 2024Program Information Residency Program: Carolinas Medical Center Orthopaedic Surgery Residency Program Program Director: Steven L Frick, MD Number of Residents: 15 Number of Staff: 35 Accredited: Accredited Length of Program: 5 Start Dates: July Program Contact Information Name: Sherry Weeks Address: Carolinas Medical Center
PO Box 32861 Suite 300
1025 Morehead Medical Dr City: Charlotte State/Province: North Carolina Zip/Postal code 28232 Phone: Fax: (704) 334-2177 Email: [email protected] Website: http://www.carolinasmedicalcenter.org Program Highlights
One-on-one instruction
Clinic assignments based on current rotation
Extensive operating room experience
Two research projects required, one each in PGY-3 and PGY-5
Educational experience
Twice-weekly core curriculum
Weekly trauma conference, Grand Rounds, journal club
Weekly anatomy/surgical skills
Monthly M&M conference One instructional meeting per year
PGY-1: Orthotics and Prosthetics Course in Chicago (often also attend Southeastern Fracture Consortium meeting)
PGY-2: Orthopaedic Trauma Association Residents Fracture Course
PGY-3: Pediatric Review Course, Montreal
PGY-4: American Academy of Orthopaedic Surgeons Annual Meeting
PGY-5: Residents’ Board Review Course Program Gallery Program Curriculum
PGY-1: Orthopaedics, trauma surgery, intensive care, emergency medicine, plastic surgery, internal medicine, pediatric surgery, neurosurgery, general surgery
PGY-2: Pediatric orthopaedics, trauma, spine, sports, foot/ankle
PGY-3: Adult reconstruction, trauma, tumor, hand, pediatrics
PGY-4: Pediatrics, hand, sports, foot/ankle, spine, adult reconstruction
PGY-5: Chief Resident, trauma, adult reconstruction, tumor, sports
Program Hospitals
Carolinas Medical Center – Charlotte, NC
Carolinas Medical Center-Mercy – Charlotte, NC [...] Read more...
At A Glance
OrthopaedicsOne is more than a “Wikipedia for Orthopaedics” or a “Living Orthopaedic Textbook”. OrthopaedicsOne is a knowledge sharing portal for orthopaedics and musculoskeletal health. OrthopaedicsOne consists of Spaces that provide different features as outlined below. Spaces with networking functionality require a FREE membership.
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Tumor Library – An Atlas of Musculoskeletal Oncology
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Browse Articles by Topic
OrthopaedicsOne Contents forms an outline of the knowledge of orthopaedics and musculoskeletal health. Each section shows the structure of its subject and serves as a table of contents for its coverage on OrthopaedicsOne. For more information on writing for OrthopaedicsOne, please review our Instructions for Authors and Available Topics on OrthopaedicsOne.
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Take the Feature Tour to learn about all the features/services OrthopaedicsOne provides.
Editor’s Choice
Introduction
Define/describe the condition
Anatomy
Describe the pertinent anatomy
Pathogenesis
Describe the biomechanics/biologic basis of the disorder or the mechanism of injury
Natural History
Describe the natural history, epidemiology and prognosis
Clinical Presentation
Describe the means to elicit the most useful information from the patient history and physical examination as well as the relevant findings
Imaging and Diagnostic Studies
Describe appropriate radiologic and other diagnostic studies
Classification
Include a list with links to relevant conditions
Treatment
Include: Medical therapy Nonoperative treatment Operative treatment – include links to pages with detailed surgical techniques Indications and contraindications
Outcome
Include functional and prosthetic survivorship data as applicable
Complications
Include overview of complications
Pearls and Pitfalls
Tips and problems to avoid
Controversy
Include current controversies in diagnosis or treatment
References
Insert selected references and landmark articles [...] Read more...
Indications
Discuss indications and more general concerns.
Preoperative Planning
Material to be reviewed and conditions to be addressed before surgery. Include any exams preformed under anesthesia
Positioning
Describe and provide OR photos to illustrate positioning
Approach
Consider the various approaches. Provide links to relevant anatomy and surgical approaches.
Techniques
Step by step description to illustrate surgical technique
Pearls and Pitfalls
Tips and problems to avoid
Postoperative Care
Include immediate postoperative care and rehabilitation
Outcome
Include functional and prosthetic survivorship data as applicable
Complications
Include overview of complications
References
Include limited reference list [...] Read more...
Classification
Small: 160 degrees or less
Medium: 161 – 199 degrees
Large: 200 or more degrees
Explanation
The Kerboul angle, also known as the “combined necrotic angle,” is a system used to quantify the size of a lesion. To calculate, first identify the center of the femoral head. Two lines are then drawn from this point to the borders of the lesion on both AP and lateral radiographs. The sum of the angles on the AP and lateral radiographs is the Kerboul angle. Lesions are classified as small, medium, or large.
Figures
Reference(s)
Provide the citation for the landmark article and recent review articles describing the classification
Attachments: Kerboull_Radiologic_Classification.jpg (image/jpeg) [...] Read more...
Introduction
Developmental dysplasia of the hip (DDH) is an umbrella term that encompasses a wide range of congenital problems of alignment of the head of the femur and the acetabulum
These may be teratogenic or sporadic
Pathogenesis
The pathophysiology of DDH is poorly understood, especially non-teratogenic forms
Pre-natal factors : mostly play a mechanical role
Constrained uterine environment, particularly in the last trimester
Excess birth weight
Oligohydramnios
Breech presentation Post-natal factors : perhaps account for the geographic and ethnic differences in DDH
Swaddling techniques Aetiology
Malalignment of the developing hip and femur prevents correct development either in the intrauterine or extra-uterine environment
Correct alignment is essential for proper development of the acetabulum
Without proper intervention, the resultant joint space will be malformed and will lead to greater disability and dysfunction as the child develops I think that theories about swaddling techniques are very interesting, but I imagine that intrauterine factors (especially space-limiting conditions that would directly affect limb rotation and alignment) are the most compelling factors in disease development
Nutritional factors
Maternal nutrition may play a role in allowing a child a proper intrauterine growth environment
In particular, gestational diabetes can lead to extreme increases in fetal size, which would restrict intrauterine space and may play a role in preventing proper limb rotation during the 3rd trimester
Risk factors
Breech position
Positive family history
Female sex
Firstborn
Oligohydramnios
Natural History
DDH prevalence in unscreened populations is estimated to be 1.3 per 1000 live births
There is much geographic variation in prevalence
Lowest 1.7/1000 in Sweden
Highest 188.5/1000 in one region of Manitoba, Canada Post-natal risk factors, e.g. swaddling techniques, may account for such a wide variation
Clinical Presentation
Children with DDH may present with
Asymmetric thigh folds
Excessive hip motility or flexibility
Asymmetric leg length Hip instability or true dislocation may be evoked by the Barlow or the Ortolani manoeuvres
The Barlow manoeuvre adducts the flexed hip and pushes the thigh posteriorly to attempt to dislocate the hip joint
The Ortolani test is the reverse; the examiner tries to reduce a dislocated hip Late presentation
Children whose hips escape examination or in whom DDH is not detected, may present with
Limping
Obvious leg-length discrepancy
Waddling gait
Excessive lordosis, to accommodate the leg length difference These children have far more difficult disease to treat, due to the obvious deformities in the femur and acetabulum
They require more invasive treatment in order to correct the problem
Psychosocial impact of disease
No parent wants to have a child with a disease or malformation
Treatments for DDH usually involve serial casting, braces or corrective surgeries, all of which may traumatize or stigmatize children and their parents
Untreated disease can result in serious orthopaedic deformities and limping, both of which can be very stigmatizing
Imaging and Diagnostic Studies
There can be some degree of perceived hip instability in newborns in up to 1 in 100 live births
Because DDH encompasses a wide variety of hip defects, their common presentation is one of perceived hip instability either through the Ortolani or Barlow maneuver
Many centers (especially those in Europe) now routinely ultrasound infants’ hips to elucidate true DDH from normal variation of mobility and stability
X-ray
Best reserved for children over 6 months of age, to allow ossification of the bones to happen
Less operator dependent than US, though they do expose children to radiation
Assess the alignment of the hip and its position within the joint according to landmarks
Hilgenreiner’s line
Perkin’s line
Shenton’s line Ultrasonography
In children under 6 months the best imaging modality is ultrasound, as the joints are primarily carilagenous and are not visible on X-Ray
On ultrasound, a truly dislocated hip will appear outside of the acetabular fossa
Ultrasonographic screening may be the best method of routinely assessing newborns for DDH
This is routinely done in most of continental Europe
Ultrasound, being relatively inexpensive and non-invasive, may prevent future expensive and invasive interventions and therefore represents a beneficial intervention to do on most infants
Laboratory evidence
Teratogenic hip dislocation may have other associated lab abnormalities, however the vast majority of DDH children are otherwise healthy
Treatment
Cases detected early are usually treated with braces to properly align the hip and avoid future surgical intervention
Outcome
Braces work!
A significant portion of people requiring total-hip-replacements under 60 years of age suffer from long term consequences of DDH
4.8% for congenital hip disorders
24.0% for DDH Complications
The risks of serial splinting and braces are mostly minor
Skin irritation
Muscular irritation or contraction
Disuse weakness Castings tend to be short-term (weeks rather than months) and, at least here in the US, most children with DDH do well in the short- and intermediate-term
Surgical risk include osteonecrosis, especially in the older child
Related Topics
Native American and Eastern European cultures routinely swaddle their infants in positions that bring the hips into extension, putting tension on the developing joint and possibly explaining these two population’s high prevalence of DDH [...] Read more...
Septic arthritis
Viral arthritis
Lyme disease
Mycobacterial arthritis
Fungal arthritis
Parasitic arthritis
Rheumatic fever [...] Read more...
Announcements
Exciting News for OrthopaedicsOne Members!
/0 Comments/in Announcements/by [email protected]We’re thrilled to announce the migration of 16 spaces from Confluence to a new content management platform. This move will enhance maintenance and unlock exciting new features for our collaborative knowledge network. Rest assured, we’ve diligently transferred as much vital content as possible. While the look and feel may evolve over the coming months, our […]