Orthopaedics made easy

Acute Osteomyelitis

2008-01-13T23:00:00.000+05:30

Acute osteomyelitis ia a commonly tested topic in orthopedic examinations. So I would now summarise the key points in the pathogenesis, clinical diagnosis and management of this common orthopedic condition- Acute osteomyelitis.

Definition

Osteomyelitis is an inflammation of the bone caused by an infecting organism.

Classification of osteomyelitis

1. Duration--

acute (less than 2 weeks),
subacute ( 2-6weeks)
chronic (>6 weeks)

2. Mechanism--

exogenous
hematogenous.

Exogenous osteomyelitis is caused by open fractures, surgery (iatrogenic), or contiguous spread from infected local tissue. The hematogenous form results from bacteremia.

3. Host response to the disease --

pyogenic
nonpyogenic.

4. Cierny and Mader classification system for chronic osteomyelitis based on host factors and anatomical criteria.

Acute Hematogenous Osteomyelitis

· the most common type of bone infection

· usually is seen in children.

· M > F.

. age distribution- bimodal,< 2 years & 8 to 12 years.

Pathogenesis of acute osteomyelitis

Acute hematogenous osteomyelitis is caused by a bacteremia, which is a common occurrence in childhood. Bacteriological seeding of bone generally is associated with other factors such as localized trauma, chronic illness, malnutrition, or an inadequate immune system.

In children the infection generally involves the metaphyses of rapidly growing long bones.

Bacteremia-->Sluggish flow of blood in hair pin like loops of vessels in highly vascular metaphysis -->Bacteria settle in metaphysis--> inflammatory reaction -->à local ischemic necrosis of bone --> abscess formation -->abscess enlarges --> intramedullary pressure increases -->cortical ischemia --> allow purulent material to escape through the thin cortex into the subperiosteal space --> subperiosteal abscess.

If left untreated -->extensive sequestra formation and chronic osteomyelitis.

The metaphysis is commonest site of osteomyelitis, because-

· Is highly vascular

· Has a hair pin like arrangement of capillaries

· Has sluggish blood flow

· has relatively fewer phagocytic cells than the physis or diaphysis, allowing infection to occur more easily in this area

· thin cortex

In children younger than 2 years, some blood vessels cross the physis and may allow the spread of infection into the epiphysis.

A resulting abscess will break through the thin metaphyseal cortex, forming a subperiosteal abscess.

The diaphysis rarely is involved, and extensive sequestration occurs infrequently except in the most severe cases.

In children older than 2 years of age, the physis effectively acts as a barrier to the spread of a metaphyseal abscess to epiphysis.

because the metaphyseal cortex in older children is thicker, the infection spreads into the diaphysis --> endosteal blood supply may be jeopardized.

With a concurrent subperiosteal abscess, the periosteal blood supply is damaged and can result in extensive sequestration and chronic osteomyelitis if not properly treated.

Hematogenous seeding of bone in adults usually is seen in a compromised host. generally the vertebral bodies are affected. In these patients, abscesses spread slowly, and large sequestra rarely form.

Spread of infection to a contiguous joint

In children younger than 2 years of age,

the common blood supply of the metaphysis and epiphysis crosses the physis .

metaphyseal abscess --> epiphysis --> joint.

The hip joint is the most commonly affected in young patients;

physes of the proximal humerus, radial neck, and distal fibula also are intraarticular, and infection in these areas can lead to septic arthritis as well.

In severe infection, epiphyseal separation can occur in children younger than 2 years of age.

In older children this common circulation is no longer present and septic arthritis is rare.

After the physes are closed, infection can extend directly from the metaphysis into the epiphysis and involve the joint. Therefore septic arthritis due to acute hematogenous osteomyelitis generally is seen only in infants and adults.

Causative microbes in acute osteomyelitis

· Staphylococcus aureus is the most common infecting organism found in older children and adults with osteomyelitis.

· Gram-negative bacteria -vertebral body infections in adults.

· Pseudomonas -- intravenous drug abusers.

· Fungal osteomyelitis-- chronically ill patients receiving long-term intravenous therapy or parenteral nutrition.

· Salmonella osteomyelitis- SS or SC hemoglobinopathies. tends to be diaphyseal

· In infants -S. aureus (mc),group B streptococcus & gram-negative coliforms . S. aureus or gram-negative organisms - orthopaedic infections found in premature infants

· Group B streptococcus - otherwise healthy infants 2 to 4 weeks of age.

· Haemophilus influenzae-6 months and 4 years.

DIAGNOSIS of acute osteomyelitis

In infants, the elderly, or immunocompromised patients, clinical findings may be minimal. Fever and malaise/ pain and local tenderness / Swelling/ compartment syndrome has been reported in children.

· WBC count often normal,

· ESR and CRP level elevated.

· The CRP is a measurement of the acute phase response and is especially useful in monitoring the course of treatment of acute osteomyelitis because it normalizes much sooner than the ESR.

· Skeletal changes, such as periosteal reaction or bony destruction, generally are not seen on plain films until 10 to 12 days into the infection.

· Technetium 99m bone scans can confirm the diagnosis as early as 24 to 48 hours after onset in 90% to 95% of patients.

· Gallium scans and indium 111–labeled leukocyte scans also can aid in diagnosis when used in conjunction with technetium scanning.

· MRI can show early inflammatory changes in bone marrow and soft tissue.

· The causative organism can be identified in approximately 50% of patients through blood cultures.

· Bone aspiration usually gives an accurate bacteriological diagnosis and should be performed with a 16- or 18-gauge needle in the area of maximal swelling and tenderness, usually the long bone metaphysis. The subperiosteal space should be aspirated first by inserting the needle to the level of the outer cortex. If no purulent material or fluid is encountered, the needle is placed through the cortex to obtain a marrow aspirate.

· CT or ultrasound-assisted aspiration in suspected hip or vertebra OM

TREATMENT of acute osteomyelitis

It has been well established that sequestered abscesses demand surgical drainage. However, areas of simple inflammation without abscess formation can be treated with antibiotics alone.

Nade's principles for the treatment of acute hematogenous osteomyelitis:

1. an appropriate antibiotic will be effective before pus formation;

2. antibiotics will not sterilize avascular tissues or abscesses and such areas require surgical removal;

3. if such removal is effective, antibiotics should prevent their reformation and therefore primary wound closure should be safe;

4. surgery should not further damage already ischemic bone and soft tissue;

5. antibiotics should be continued after surgery.

general supportive care--- IV fluids, analgesics, and comfortable positioning of the affected limb.

If no abscess (by subperiosteal or bone marrow aspirate) then intravenous antibiotics based on the gram stain should be started.

Empirical antibiotic coverage for the most likely infecting organism should be started if gram stain is negative, and the patient then should be carefully monitored. The CRP should be checked every 2 to 3 days. If no appreciable clinical response within 24 to 48 hours, then occult abscesses must be sought and surgical drainage considered.

Surgery for acute osteomyeilitis

Indications

· an abscess requiring drainage

· failure to improve despite appropriate IV antibiotic treatment for 48 hours.

Objective

· to drain any abscess cavity and

· remove all nonviable or necrotic tissue.

Surgical Procedure for acute osteomyelitis

· Do not exsanguinate the limb with an elastic bandage if infection is present

· When a subperiosteal abscess is found in an infant, several small 4 mm holes should be drilled through the cortex into the medullary canal.

· If intramedullary pus is found, then a small window of bone is removed.

· The skin is then closed loosely over drains, and the limb is splinted.

· The limb is protected for several weeks to prevent pathological fracture.

· 2 weeks IV antibiotics,à4 weeks oral antibiotics

I hope this simplifies your study of acute osteomyelitis.

Technorati Tags: acute osteomyelitis,clinical diagnosis,management,surgery,orthopedics,microbes,pathogenesis

Congenital Muscular Torticollis (CMT)

2008-01-09T08:00:00.001+05:30

del.icio.us Tags: congenital muscular torticollis,wry neck,treatment,natural history,prognosis,unipolar release,bipolar release,sequelae,causes

Congenital muscular torticollis is a common cause of wry neck. This is also a common clinical case in orthopedic examinations for students, interns & residents. In this post, I try to summarize the most salient features of this disease.

What is Congenital muscular torticollis?

It is wry neck caused by fibromatosis within the sternocleidomastoid muscle.

What is the natural history ?

presents as mass in neck most commonly near clavicular attachment of sternoclaviculomastoid muscle
at birth or in first 2 weeks.
right >left.
attains maximal size within 2 months and then remains so or regresses
usually it diminishes and disappears within a year.
If it fails to disappear, the muscle becomes permanently fibrotic and contracted and causes torticollis that is also permanent unless treated.

What are common Associations?

· difficult delivery.

· metatarsus adductus,

· developmental dysplasia of the hip 7% to 20%, and

· talipes equinovarus.

Why does it happen?

· malposition of the fetus in utero,

· birth trauma,

· infection, and

· vascular injury

. sequela of an intrauterine or perinatal compartment syndrome.

clinical groups:

· sternomastoid tumor group (those with a clinically palpable sternomastoid tumor)-needs surgery more often

· muscular groups (those with clinical thickening and tightness of the sternocleidomastoid muscle), and

· postural torticollis (those with postural head tilt and clinical features of torticollis but without tightness or tumor of the sternocleidomastoid muscle)-corrects with stretching

Does ultrasonography help?

· helps predicting which infants would require surgical treatment.

· if fibrotic change is limited to lower third sternocleidomastoid muscle ,most patients recover without surgery

· whole muscle fibrotic involvement requires surgical release

Does non-operative treatment help?

· Yes, during infancy.

· parents should stretch the sternocleidomastoid muscle by manipulating the child's head manually.

· effective in about 95% before the age of 1 year.

· more likely to be successful if the restriction of motion was less than 30 degrees and no facial asymmetry or the facial asymmetry was noted only by the examiner.

What is the Surgical treatment?

· Unipolar release

.Bipolar release

When to operate? Why?

. operation be delayed until the child is between the ages of 1 and 4 years.

. CMT did not resolve spontaneously if it persisted beyond age of 1 year.

· Nonoperative therapy after the age of 1 year was rarely successful.

· Children who were treated during the first year of life had better results

· surgery should be delayed until evolution of the fibromatosis is complete,

· Surgery performed before the age of 6 to 8 years may allow remodeling of any facial asymmetry and plagiocephaly. Helpful upto 12 years of age.

· tethering of the scar to the deep structures is common before the age of 1 year

UNIPOLAR RELEASE

. It is release of sternal and clavicular attachments of the sternocleidomastoid muscle

. It is appropriate for mild deformity

· Skin incision: 5 cm long just superior to and parallel to the medial end of the clavicle

Incise the tendon sheath of sternocleidomastoid muscle longitudinally and resect 2.5 cm of tendon ends.

· Next, with the child's head turned toward the affected side and the chin depressed, & divide remaining bands of contracted muscle or fascia until the deformity can be overcorrected.

· If overcorrection is not possible, do a bipolar release by a small transverse incision inferior to the mastoid process. Avoid damaging the spinal accessory nerve.

BIPOLAR RELEASE

. It is release of sternocleiodmastoid muscle at both its attachments

. It is suitable for moderate /severe deformity, after failed operation or in patients older than 6 years of age

· For this, make a short transverse proximal incision behind the ear

. divide the sternocleidomastoid muscle insertion transversely just distal to the tip of the mastoid process.

· Next, make a distal incision 4 to 5 cm long in line with the cervical skin creases, a fingerbreadth proximal to the medial end of the clavicle and the sternal notch.

· Cut the clavicular portion of the muscle transversely and perform a Z-plasty on the sternal attachment so as to preserve the normal V-contour of the sternocleidomastoid muscle in the neckline.

Postoperative protocol?

· Syres’s traction for 1 week

· At 1 week, manual stretching to maintain the overcorrected position is begun.

· Manual stretching should be continued three times daily for 3 to 6 months

· Molded cervical orthosis for 6-12 weeks.

What are possible complications of surgery?

tethering of the scar to the deep structures
reattachment of clavicular or sternal head
failure to correct the tilt of the head
failure of facial asymmetry to correct.
damage to anterior and external jugular veins and the carotid vessels
damage to spinal accessory nerve
recurrence
loss of v-contour of neck

Which cases have Bad prognosis

· established facial asymmetry

· limitation of motion of more than 30 degrees at the beginning of treatment

· rotation deformity of more than 15 degrees

· clinical group (sternomastoid tumor)

· older age at presentation

What are the possible Sequelae of no treatment/

· torticollis slowly becomes worse during growth.

· head becomes inclined toward the affected side and the face toward the opposite side.

· If the deformity is severe, the ipsilateral shoulder becomes elevated

· frontooccipital diameter of the skull may become less than normal.

Shoulder-Surgical Approaches

2008-01-05T21:05:00.000+05:30

Technorati Tags: surgical Approaches,shoulder

Approach	Skin incision	Superficial interval	Deep interval	Risks
Anterior(Henry)	10-15cm incision in line of delto-pectoral groove from tip of coracoid or anterior axillary skin fold incision	deltoid (axillary)& pectoralis major ( medial and lateral pectoral )	Medial retraction of conjoint tendon or coracoid tip osteotomy + subscapularis tenotomy + glenohumeral capsulotomy	Musculocutaneus nerve axillary nerve second part of axillary artery Cephalic vein
Anterolateral	transverse, from anterolateral corner of acromion to just lateral to coracoid process	detach deltoid from AC joint & 1cm of anterior aspect of acromion + split deltoid for 5 cm	detach coracoacromial ligament from both ends & excise	Axillary nerve
Lateral	5cm long incision from the tip of the acromion down the lateral aspect of the arm	split deltoid in line with its fibres from acromion down for 5 cm	acromion could be split in coronal plane to expose full length of supraspinatus	Axillary nerve lies 7cm from tip of the acromion
Posterior	linear incision along entire length of spine of scapula extending to posterior corner of acromion	detach deltoid from scapular spine + develop plane in deltoid & infraspinatus + retract deltoid inferiorly	teres minor (Axillary) & infra-spinatus (Supra-scapular)	Axillary nerve & posterior circumflex artery in quadrangular space suprascapular nerve

Hip- Surgical Approaches

2008-01-04T18:52:00.000+05:30

Technorati Tags: Hip,Surgical Approaches

Approach	Skin incision	Superficial Interval	Deep Interval	Risks
Anterior (Smith Peterson	Along anterior 1/2 of iliac crest to ASIS then 10cm vertically to lateral side of patella	sartorius (femoral) & tensor faciae latae (superior gluteal)	rectus femoris (femoral) & gluteus medius (superior gluteal)	Lateral cutaneous nerve of thigh ascending branch of lateral femoral circumflex artery
Anterolateral (Watson Jones)	15cm straight longitudinal incision centered on greater trochanter	tensor faciae latae (superior gluteal) & gluteus medius (superior gluteal)	Trochanteric osteotomy OR Partial detachment of Gluteus medius	Femoral nerve descending branch of lateral femoral circumflex artery
Lateral (Hardinge)	10-15 cm incision centered on tip of greater trochanter with hip 0 deg flexed	tensor faciae latae (superior gluteal) & gluteus maximus (inferior gluteal)	Split gluteus medius (superior gluteal) & vastus lateralis (femoral)	superior gluteal nerve femoral nerve
Posterior (Moore-Southern)	10 - 15 cm curved incision (straight with hip flexed 30) centred over posterior aspect of greater trochanter	split gluteus maximus (inferior gluteal)	Tenotomy of short external rotators & posterior capsulotomy	Sciatic nerve Branches of the inferior gluteal artery
Medial (Ludloff)	From 3cm below the pubic tubercle over adductor longus as long as required	adductor longus & gracilis (both anterior division of obturator )	adductor brevis (anterior division of obturator) & adductor magnus (posterior division of obturator & sciatic)	anterior and posterior divisions of obturator nerve medial femoral circumflex artery

HIP EXAMINATION PROFORMA

2008-01-02T20:51:00.001+05:30

Performed in standing, supine and lateral positions

Inspection

lumbar lordosis
attitude of limb
levels of ASIS, patellae, malleoli
swelling--gluteal region ,Scarpa’s triangle, trochanteric region
scars, sinuses
skin over the joint
muscle wasting

Palpation

temperature
tenderness-anterior joint line, posterior joint line
trochanteric palpation

level
trochanteric tenderness- superficial /deep / transtrochanteric
trochanteric surface--thickening / irregularity

palpable swelling

hard : femoral head, bony neoplasm
firm : soft tissue neoplasm
soft : cold abscess

Vascular sign of Narath

Movements

Thomas’ test for flexion deformity of the hip
determination of abduction / adduction deformity
Flexion
Extension
Abduction
Adduction
External & internal rotation in hip extension (prone) & with hip flexed 90 degrees
active/passive
lag/deformity/arc
compare with opposite side
Differential rotation
Knee to axilla sign

MEASUREMENTS

apparent length
true length-

supratrochanteric

Bryant’s triangle
Nelaton’s line
Shoemaker’s line

infratrochanteric segmental lengths- femur, tibia

thigh & calf girth
Gluteal wasting
Galeazzi test

Special tests

Trendelenburg test
Trendelenburg sign
telescopy

Other tests

Gait
Function-ambulation distance, walking, sitting, squatting,stairs
Other joints-Hip, SI joint , knee joint
lymph nodes (inguinal,external iliac group)
Per abdomen examination
Per rectal examination

KNEE EXAMINATION PROFORMA

2008-01-02T20:05:00.001+05:30

Inspection

Alignment
Attitude
Swelling/contours / abnormal shifts / prominence
wasting
scars/ sinuses
patellar shape/size/position

Palpation

Local temperature
Local tenderness- patellar grate, retropatellar tenderness, fibular head, femoral & tibial condyles, tibial tuberosity
Synovium thickening
bony palpation-L/E femur, U/E Tibia & fibula
effusion-patellar tap/cross fluctuation
Patello-femoral joint - apprehension test for patellar subluxation, patellar tilt, patellar grind
Popliteal fossa examination- swelling: pulsatile + changes with flexion/extension +

Movements

Flexion
Extension
active/passive
lag/deformity/arc
compare with opposite side

Measurements

Length of femur & tibie
thigh & calf girth
Q angle
intercondylar distance/ intermalleolar distance
lateral thigh-leg angle
Tibial torsion

Special Tests

Meniscus

McMurray’s test
Apley’s grinding test

ACL

anterior drawer test
Lachman test
pivot shift test

PCL

posterior drawer test
sag sign

MCL and LCL

varus and valgus stress test at 30 degrees
alpeys distraction test

Other tests

Neuro-vascular deficit- peroneal nerve palsy
Lymph nodes- popliteal , inguinal
Opposite knee, ipsilateral hip & ankle
Gait
Function-ambulation distance, walking, sitting, squatting,stairs

ELBOW EXAMINATION PROFORMA

2008-01-02T19:35:00.001+05:30

Inspection:

Attitude
Alignment of the elbow & forearm
Swellings around the elbow-besides the triceps tendon on either sides,Over Olecranon process,In front /antecubital fossa
Scars , sinuses
Muscular wasting

Palpation:

Temperature
Tenderness-Humero-radial joint line
Confirmation of inspection findings.
Swelling &cross fluctuation test
Palpation of bones--- L/3 Humerus, U/E & head of Radius , U/E ulna & Olecranon,
3 point bony relationship

Range of movements:

Flexion
Extension
Supination
Pronation
Deformity
Block- Springy (elastic) / bony
any change of arc

Instability

Varus-valgus stress test in 15 elbow flexion & shoulder maximally IR/ER respectively.
Pivot shift test—posterolateral rotatory instability - Reider 97

Measurements:

3 bony relationships
Arm length & girth
Forearm length & girth
carrying angle

lymph nodes:axillary, supratrochlear/epitrochlear

other joints in the same extremity.-ROM of Wrist ,Hand,Shoulder.

DNVD

Special tests

Yamamoto test
Cozen’s test
Mill’s manoeuvre
finger hyperextension

Genu varum

2008-01-01T00:15:00.000+05:30

Diagnosis

Bilateral symmetrical genu vara of 20 deg
without generalised liagamnet laxity
of 6 months duration
with probable etiology being rickets
with active signs of rickets
in a 5 year old schoolgoing girl
presently concerned with cosmeis & awkard gait

History

onset
duration
progression
treatment taken
trauma/infection/surgery
diet
family history

Examination

Bilateral /unilateral
symmetrical/asemmetrical genu vara with
lateral thigh leg angle of-20 deg
intercondylar distance -
site of deformity
Knee-range
ligamentous laxity
fibula level
Tibial torsion
Signs of rickets
stature
Limb mength discrepancy
Gait +lateral thrust + foot progression angle
other joints

Osteoarthritis of Knee

2007-12-30T20:11:00.000+05:30

Diagnosis

Bilateral symmetrical tricompartmental osteoarthritis of the knees
With 20 deg flexion deformity with further flexion upto 90 deg
With 30 deg varus deformity
With varus instability
in a 60 year old retired postman
disabled due to pain, difficulty sqauatting & using stairs

History

mechanical pain
grating sensation with movement
progressive bowing
clicking, locking
disability-squatting/walking, cross-leg sitting/stairs
treatment taken-supervised physiotherapy
Ask for intermittent claudication ( associated lumbar canal stenosis)

Examination

Bilateral varus deformity of 30 deg
tenderness at medial & joint line & at margins of patella
osteophytes are palpable at joint line
local temp not raised
knee joint effusion: patellar tap+ cross fluctuation+
synovial hypertrophy+
patellar glide painful
patellar grind test +
normal patellar tracking
ROM: 20 deg flexion deformity , further flexion to 90 deg
entire range painful with crepitus
extensor lag of 20 deg
varus laxity ++
McMurray's test -
thigh wasting of 2 cm
popliteal fossa normal to examination
no distal neurovascular deficit
opposite knee: as mentioned
Hip, spine, 1st carpometacarpal joint normal

Technorati Tags: osteoarthritis,knee,genu varum,deformity

Congenital Talipes Equinovarus

2007-12-25T19:20:00.000+05:30

Diagnosis

Left sided
Neglected/ recurrent/ resistant
Idiopathic/ non-idiopathic
Partially correctible
Congenital talipes equinovarus deformity
With out associated anomalies
In a 3 year old first born male walking child
Currently brought due to parental concern of deformity

History

Present since birth
Traetment taken- castings ( number, done by, frequency, when stopped, correction achieved, what braces used, how long), surgery ( when, postoperative immobilization, braces, correction achieved)
Family history
Associated anomalies

Examination

Left foot is smaller
With concave medial border facing up with a deep crease
With convex lateral border facing down
With callosity over dorsal aspect of fifth metatarsal
With deep crease on posterior aspect
With absence of fine crease over tendo achilles
With posterior tuberosity of calcaneum difficult to palpate

There is a bony prominence over dorso-lateral aspect of foot
1 cm calf atrophy
There is compensatory genu valgum & in-torsion of tibia
Normal hip & spine & neurological examination
Other joints normal

Sprengel's Shoulder

2007-12-25T18:19:00.000+05:30

Diagnosis

Right sided
Sprengel's deformity
In a 2 year old right hand dominant male child
Who is a product of full term normal delivery
With no other associated congenital anomalies
With restricted shoulder range of motion
Currnetly brought by parental concern of deformity

History

Present since birth
Any progression
Other anomalies
Family history/ other sibling

Examination

As compared to left scapula,the right scapula is

elevated
Hypoplastic
With decreased height to width ratio
With supraspinous portion tilted forward
With medial border tilted medially
Without omovertebral bar

Right clavicle is tilted up & hypoplastic

Right shoulder has ROM= (glenohumeral & combined)

Wasting/ weakness of deltoid

Spine & limbs are normal to examination

There are no associated anomalies

Cubitus Valgus

2007-12-25T18:18:00.000+05:30

Cubitus valgus

Diagnosis

Right sided
cubitus valgus deformity of 20 deg
with tardy ulnar nerve palsy
due to nonunion of lateral condyle humerus fracture
of 1 year duration
in a 12 year old right handed male school-going boy
presently disabled due to weakness of right hand & cosmetic deformity

History

Injury ( time, mechanism, open/closed, treatment taken,)
h/o massage done
Deformity ( when noticed, progression)
Pain
Siffness
Tingling, numbness, weakness

O/E

Nonprogressive Cubitus valgus deformity of 20 deg,
3-bony point relationship disturbed with increased distance between olecranon & lateral epicondyle
Thickened lateral supracondylar ridge
Abnormal mobility of lateral condyle fragment/ pain on stressing lateral condyle
E/O tardy ulnar nerve palsy in the form of

Atrophy of hypothenar eminence
Weakness of FCU, FDP,ADM, Interossei
Sensory d
Palpate ulnar nerve
Tinel's sign at-
Sensory deficit in ulnar nerve distribution

There is 20 deg flexion deformity with further flexion possible upto100 deg with a bony block, the range is associated with pain & crepitus
There is 40 deg supination & 50 deg pronation possible

Arm length is reduced by 2 cm
2 cm arm wasting of arm 7 forearm
e/o valgus instability

Nonunion

2007-12-25T18:14:00.000+05:30

Diagnosis

Aseptic/ septic ( with active infection/ with e/o old infection or with no e/o infection)
Mobile/ stiff
Nonunion of right tibia (or ulna or femur or humerus or clavicle) shaft at M/3- L/3 junction
In an operated case
With 4 cm limb length discrepancy/ gap
With 20 deg varus deformity
With knee stiffness
Of 1 year duration
In a 40year old male labourer
Presently disabled due to inability to weightbear

History

mechanism of injury,
time,
open/closed,
treatment taken,
time of treatment,
compliance with treatment,
Weightbearing
Smoker/ alcoholic
Diabetic

Examination

Abnormal painless/ painful mobility in anteroposterior & lateral directions
Absence of transmitted rotations
Bone ends are tickened, bone gap palapable, implant palpable
No local tenderness at fracture site
No e/o infection in the form of

local rise of temperature,
puckered adherent scar & sinuses,
irregular thickened bone

20 deg varus deformity ( fixed/ mobile)
4 cm shortening of leg
2 cm calf wasting
Knee stiffness with 0 to 90 painless range, normal ankle range
No lymphadenopathy
No distal neurovascular deficit
Gait & ambulation status in lower limb
prehensile function in upeer limb
Check for scars of bone grafting

Tendo Achilles Ruture

2007-12-24T23:03:00.000+05:30

Tendo Achilles Rupture

Diagnosis

Left/right sided
Degenerative/ posttraumatic
Neglected/ treated
tear of tendo achilles
of 3 months duration
in a 65 year old retired male postman/ 25 year old labourer
currently disabled with difficulty walking on uneven surfaces, running & climbing stairs

H/o

Mechanism of injury
Pain
Swelling
Treatment taken

O/E

There is e/o TA rupture in the form of-

Palpable defect of 4cm length , 2cm above calcaneal tuberosity
Inability to tiptoe
Increased passive dorsiflexion
Thomson's test
Calcaneus gait
Calf wasting of 2 cm

Cartilaginous tumours

2007-12-22T02:06:00.000+05:30

Tumor	Age	Location	Clinical presentation	Pathology	Radiology	Treatment	Prognosis	DD
Enchondroma	10 - 50 yrs	metaphyseal.> 50% - small bones of the hands and feet.15% femur ,12% humerus. originating within the medullary cavity Periosteal form originates in the periosteum and erodes into the cortex	60% pathological fracture, lump or as incidental finding.75% solitary.Olliers disease ->more cellular and 50% ->malignant transformation.Mafuccis disease -> multiple haemangiomata , 100% malignant change	Macro - bluish white well demarcated, well encapsulated and often lobulated gritty tissue. Micro - hypocellular; nests of mature cartilage cells, nuclei are small and uniform, no atypia + calcification. Periosteal form less common , more cellular. Predilection for proximal humerus near deltoid insertion.	X-Rays Scalloped erosions on endosteal surface. flecks of calcification - sometimes called 'ground glass'. Periosteal form (juxtacortical) -shallow crater lined by rim of mature reactive bone, lifts periosteum	Observe - x-ray 6 months & 1 year after presentation. Curettage and grafting if latent. If active -> recurrence but this may be better than morbidity of en block excision.Periosteal form -> en bloc excision (with a margin)	Good	x
Chondroblastoma	10-20yrs, M>F	epiphyseal but may expand into metaphysis.Usually affects proximal humerus, proximal tibia or femur	ache progressive	Arises from chondroblasts.Usually active benign lesion (Stage 2).Histology ->pinkish grey tissue, lobulated, may be haemorrhagic, richly cellular multinucleate giant cells with polyclonal or round chondroblasts	Open physis. Well defined area of rarefaction eccentrically placed in the epiphysis or across the growth plate.No reaction in surrounding bone 50% show central calcification. 50% show linear periosteal reaction.Bone scan increased uptake at margins	Curettage & bone grafting (15% recurrence). avoid joint penetration because chondroblastoma cells will grow in joint fluid..Use cryotherapy if extension intra capsular to avoid excision of joint	no chance of malignant change	GCT (adults) ABC (histology similar) clear cell chondrosarcoma epiphyseal osteomyelitis
ChondroMyxoid Fibroma	10 - 30 years	eccentric metaphyseal lesions 75% lower extremity and 50% tibia	chronic ache	variable amounts of chondroid, fibromatoid & myxoid elements.May develop from a remnant of the growth plate ?.histo- firm lobulated jelly like areas of mucoid with condensations of cells on the periphery.areas of chondroid and myxomatous tissue. Contains giant cells, macrophages and monocytes.usually no bone osteoid	Rounded or oval rare area.Usually eccentric.May cross the growth plate. Sharp outline and sclerotic rim.Scalloped margin and thin cortex	Extra capsular marginal excision ->almost no recurrence.If skeletally immature wait until maturity	Malignant change has been reported, thus where possible it should be excised	x
Osteochondroma	under 20 yrs	metaphyseal area of any endochondral bone /50% are distal femur, upper tibia or proximal humerus	lump or interference of tendon function. sessile or pedunculated. Active growth during skeletal growth ->become latent.Move towards diaphysis with growth and usually angle away from the growth plate.Trevor's Disease: Osteochondroma on epiphyseal side of the growth plate	Normal bone covered by a cap of normal cartilage which resembles growth plate but more disorganized. Binucleate chondrocytes in lacunae.Covered with a thin layer of periosteum.Diaphysial Aclasis- Autosomal dominant. Disordered endochondral growth. Multiple osteochondromas and disordered metaphyseal growth. Short stature and bowing of limb. Malignancy Risk = ~ 20% overall or 0.2% per lesion	hallmark is blending of tumour into underlying metaphysis. well defined metaphyseal excrescence of bone with a mottled density Cartilaginous cap displays irregular areas of calcification . Bone scan -during growth period activity at the tip.increased activity after maturity suggests malignant change	Nil required unless symptomatic (persistent irritation (from bursitis or tendon) or neurovascular compromise. Extra capsular marginal excision Including the cartilaginous cap & overlying perichondrium.Deep bony base has minimal activity & may be removed piecemeal.cartilaginous cap should not be traumatised during removal.Recurrence = <>	malignancy ~ 0.2% in a solitary lesion. low grade.Evidence- Cartilaginous cap thicker than 1 cm in an adult (in child may be 2-3 cm thick) Cartilage cap > 8cm diameter. Fluffy outline. Bone scan - Marked increase in uptake in an adult. CT/MRI - soft tissue mass or displacement of a major neurovascular bundle	Myositis ossificans, Parosteal osteosarcoma

Other tumours

2007-12-22T01:55:00.001+05:30

Tumor	Age	Location	Clinical presentation	Pathology	Radiology	Treatment	Prognosis	DD
EWINGS TUMOUR	10 - 30 yrs.M>F	.Diaphyseal.60%- long tubular bones (also pelvis ribs and scapula) .considered a systemic disease	pain + limp. Pain is throbbing, worse at night and often severe. ill, pyrexial. a tender palpable lump with an ill defined edge .Pathological fracture is rare.30% have mets at presentation - Lung & Lymph Nodes .Serology-Anaemia .Increased ESR & WCC & serum Alkaline Phosphatase	poorly demarcated .soft tissue extension common .Macro- tissue is grey and brain like or like red currant jelly if haemorrhagic.Micro -homogenous population of densely packed small, round, neoplastic cells with large oval hyperchromatic nuclei.Cells may form a ring of 7-8 cells around a central area of necrosis= "rosette".haemorrhage and necrosis are typically present .pread to distant sites via the blood and lymphatics (? multi centric from the onset)	"onion skin" periosteal reaction.Rarefied area in medulla, but bone marrow infiltration is often not obvious on plain x-ray.Often the cortex is perforated .Appearance varies widely .MRI is essential to elucidate the soft tissue involvement .T1 - the tumour has low intensity compared to the normal high intensity of bone marrow .T2 - tumour is hyper intense compared to muscle.Bone Scan-increased uptake	Best results with combined therapy.Relatively radio sensitive.12 wks induction chemotherapy with VAC (vincristine, actinomycin D & cyclophosphamide) are used preoperatively -> re-evaluate and restage -> surgical resection .Wide surgical excision & limb salvage, usually. Radiotherapy -> whole of bone .Usually stop 2 - 4 weeks prior to surgery	50% 5 year survival (30-60% depending on mets) .14% of long term survivors -> secondary tumours and 1 - 2% are malignant (eg leukaemia or osteosarcoma).Young males and pelvic lesions -> worse prognosis.If 10% viable tumour after chemotherapy =80% cure ;If not =20-30% cure	Osteomyelitis Lymphoma (Reticulum cell sarcoma) Osteosarcoma Chondrosarcoma Neuroblastoma Metastatic Ca
EOSINOPHILIC GRANULOMA	<10> M=F	any bone. skull (10%), femur and spine most commonly .Metaphyseal or diaphyseal	spectrum of Langerhan's cell histiocytosis( histiocytosis X.) EG.Sub-types-Hand Schuller Christian disease -children > 3 yrs,traid of skull lesions, exophthalmos, & diabetes insipidus , minority - wide spread visceral involvement (liver, spleen, pituitary).cranial lesions are always present Letterer-Siwe disease -lymphomatous proliferation of poorly differentiated histiocytes,<3>	arise from the reticulo endothelial system.Glistening reddish tissue with flecks of yellow .mixture of pale lipid filled histiocytes, eosinophils, & some giant cells, plasma cells, & neutrophils . Langerhan's giant cells - grooved or coffee bean shaped nucleus and abundant pale staining cytoplasm	Mottled lytic defect usually no sclerotic rim.May destroy cortex.Usually endosteal or periosteal reaction.Lesions in flat bones and ribs appear punched out .May appear loculated due to sparing of large trabeculae .Rapid destructive bone lesion .Spinal lesions -> collapse (vertebra plana) which may heal .May be no localised bone lesion but generalised osteoporosis.Bone scan usually hot but variable	Usually heal spontaneously.curettage and grafting -> diagnosis.May be able to diagnose by aspiration rather than open operation .Steroids Radiotherapy for aggressive lesions or for inaccessible disease	LSD -> worse prognosis often fatal in infancy .HSC: excellent prognosis if there is no extra-osseous disease.Soft tissue involvement -> worse prognosis .Liver involvement -> 50% die.Lung involvement usually not fatal .Anaemia -> increased mortality and indicates poor prognosis Skeletal lesions only do not -> death	Ewings Osteomyelitis Lymphoma Leukaemia
LYMPHOMA OF BONE (NON-HODGKIN'S)( reticulum cell sarcoma)	middle aged or elderly	femur and pelvis in >20 yrs. 40 -50% around the knee	pain and swelling / Pathological fracture.CBC & blood smears to rule out leukaemia Bone marrow aspirates CT Abdominal exploration -> splenectomy -> staging	Histo- sheets of poorly differentiated cells with irregular nuclei.Usually composed of cells of a mixture of types, reticulum cells, lymphocytes and lymphoblasts.Hodgkins -> Reed-Sternberg cells histologically (large, sharply delineated cells with abundant cytoplasm and a double nucleus)	Early -> vague mottled lucent areas .Diffuse destructive lytic lesion with little periosteal reaction .Usually combination of patchy sclerosis and mottled destruction .Hodgkins disease -> ivory vertebrae	Surgery (wide excision) radiotherapy for localised lesions Chemotherapy for systemic involvement	Lymphoma of bone has the best prognosis of all primary malignant bone tumors.44% 5 year survival .Pure Hodgkins disease or lymphocytic disease -> worse prognosis	Osteosarcoma Ewing's sarcoma Osteomyelitis Metastatic Ca

Bone cysts

2007-12-22T01:54:00.000+05:30

Tumor	Age	Location	Clinical presentation	Pathology	Radiology	Treatment	Prognosis	DD
Unicameral (Simple) Bone Cyst (UBC)	5-15 yrs, M>F	proximal humerus (67%), proximal femur (15%),unusual sites (e.g. calcaneum, pelvis) in patients >17 years	Asymptomatic.Usually presents as a pathological fracture (~ 65%).Active cysts neargrowth plate, but move away with growth and become inactive (latent)	thin walled cavities filled with blood tinged fluid. lining cells are cuboidal, but are not an endothelium. endosteal osteoclastic activity and periosteal new bone formation.Aetiology- Unknown/Venous obstruction leading to a transudate of fluid/ Fluid contains high levels of IL-1 & IL-6, which stimulate osteoclasts	Well defined, central osteolytic area with a thin sclerotic margin.Metaphyseal in young - moves towards diaphysis with growth. fills and slightly expands the juxta epiphyseal metaphysis.CT not helpful unless the UBC is in the pelvis	goal is to minimise fracture risk until the cyst heals (but this can take years).Steroid inj. 60-80% success rate /Curettage and bone graft - 50% recurrence rate and possibility of damage to the growth plate .Bone marrow aspirate has recently been used
Aneurysmal Bone Cyst (ABC)	<20>M	any bone in the body.most common- metaphysis of the lower extremity long bones. vertebral bodies or arches of the spine. pelvis	Swelling, tenderness and pain. Limited ROM due to joint obstruction.Spinal lesions can cause cord compression.Pathological fractures are rare due to the eccentric location of the lesion	Macro- blood filled sponge with a thin periosteal membrane. Soft, fibrous walls separate spaces filled with friable blood clot.Micro- cystic spaces filled with blood. fibrous septa have immature woven bone trabeculae as well as macrophages filled with haemosiderin, fibroblasts, capillaries and giant cells.Aetiology- Unknown,/ a reactive process to trauma or vascular disturbance/ secondary to increased venous pressure that leads to haemorrhage which causes osteolysis. This osteolysis can in turn promote more haemorrhage causing amplification of the cyst/ secondary ABC-- common precursor GCT, (19-39%), osteoblastoma, angioma, and chondroblastoma. fibrous dysplasia,NOF,CMF, UBC, fibrous histiocytoma, eosinophilic granuloma, and osteosarcoma.	eccentrically in the metaphysis and appears osteolytic. periosteum is elevated and the cortex is eroded to a thin margin. expansile nature of the lesion is often reflected by a "blow-out" or "soap bubble" appearance .'Pencil-in-cup' appearance.CT scan can help delineate lesions in the pelvis or spine. can narrow theDDs by demonstrating multiple fluid-fluid levels within the cystic spaces.MRI can also confirm the multiple fluid-fluid levels	A slow growing, indolent ABC has been observed to regress spontaneously.Most lesions can be treated with curettage and application of a high-speed burr.Recurrence--Wide resection and limb-sparing reconstructions Curettage and bone graft can be complicated by profuse bleeding from the lesion.Radiation has been used in some cases where operative treatment is not possible, but this adds the additional risk of malignancy
GCT	20-30 yrs, F>M, after closure of physes	distal femur, proximal tibia and the distal radius.Most common tumour to occur in the distal phalanx.meta/epiphyseal.	Pain, swelling,Pathological fracture.Benign, usually solitary and locally aggressive.Egg shell crackling	Soft, friable tumour.Cut surface tan in colour, with areas of necrosis and haemorrhage.Numerous multinucleated giant cells. stromal cells are homogenous mononuclear round/ovoid with large nuclei. nuclei of the stromal cells are identical to the nuclei of the giant cells.Up to 50% have soft tissue extension but does not indicate malignancy	Usually well defined lesion in the epiphysis extending up to the joint surface without marginal sclerosis, cortex thinned and sometimes ballooned soap bubble appearance.Junction with normal bone poorly defined	Intralesional excision by "extended" curettage.Curettage alone has a high local recurrence rate (50%) and the curettage is "extended" into the bone by a few millimetres by either using a burr, liquid nitrogen or phenol. resulting cavity can be filled with bone graft or cement.En-bloc resection is possible if the bone is expendable e.g. proximal fibula, proximal radius.Amputation reserved for massive local recurrence, malignant change or infection.Radiotherapy reserved rare cases of unresectable tumours because of increased risk of secondary malignancy	Sarcomatous transformation in 5 - 10%.Recurrence following simple curettage 50%. Recurrence following simple curettage plus adjuvant treatment (cryo etc) 17%. Malignancy more common in recurrent GCT

Fibrous Tumours

2007-12-22T01:49:00.000+05:30

Tumor

Age

Location

Clinical presentation

Pathology

Radiology

Treatment

Prognosis

Fibrous Cortical defect (Non-ossifying fibroma)	Children, M>F	metaphyseal	Usually an incidental finding in children. Most heal spontaneously.Larger ones may -> pathological fracture (common presentation)	whorled fibrous tissue, foam cells.occasionally, small elongated giant cells Jaffe-Campanacci syndrome: multiple FCDs., cafe-au-lait spots,mental retardation,hypogonadism, ocular & cardiovascular abnormalities.	Lucent. in the cortex of a long bone.metaphyseal eccentric.Margin well defined, sometimes scalloped and often sclerosed	Most spontaneously resolve or move to the diaphysis of the bone with growth.Pathological fractures: usually heal with a normal amount of callus, but resolution of the fibroma may or may not occur.intracapsular curettage is usually sufficient to promote healing of lesion, however, the defect may be supplemented with bone grafts +/- stabilisation		malignant fibrous histiocytoma eosinophilic granuloma osteosarcoma histiocytic lymphoma pyogenic osteomyelitis
Fibrous dysplasia	children adolescents, onset 8 yrs. M > F. (Albrights - F> M)	Ribs commonest (40%) Lower limbs more than upper limbs	Relatively common and usually monostotic.Craniofacial -> skull deformity. Epiphyses usually spared.McCune - Albrights Syndrome- Polyostotic disease, pain, fracture (85%), deformity (unilateral usually),Skin pigmentation-cafe au lait spots with serrated borders (called "coast of Maine") that tend to stop abruptly at the midline of the body .Precocious puberty (endocrinopathy). usually presents earlier, may be unilateral or widespread, affecting long bones, hands, feet & pelvis.Malignant transformation (chondrosarcoma or osteosarcoma) is about 4 %;	Bone replaced by firm, whitish tissue of gritty consistency.Vascular tumour with poorly orientated bone trabeculae separated by fibrous tissue. Bone is woven rather than lamellar . lack of osteoblastic rimming of trabeculae	Lucent lesion in medullary space. Sclerotic margin with no discernable matrix.Ground glass appearance typical. No periosteal reaction Shepherds crook deformity of proximal femur.Variable appearance with expansion of cortex	Monostotic -> curettage and grafting if symptomatic. Polyostotic -> symptomatic treatment.May require osteotomy for deformity or lengthening / shortening procedures	Monostotic lesions cease activity at puberty but may be reactivated by pregnancy.Polyostotic - 85% -> pathological fracture.malignant change occurs after radiotherapy	Pagets disease/ FCD Hyperparathyroidism osteoblastoma osteosarcoma
Malignant Fibrous Histiocytoma	>30yrs. M > F	metaphyseal knee 40%	pain, swelling.15%pathological fracture. May arise in Pagets, fibrous dysplasia, long standing osteomyelitis or irradiated bone. Mets to the lung, and other bones via the blood	Discrete greyish white rubbery tumour. Irregular bony margins.Composed of a fibroblasts, myofibroblasts & large plump foamy histiocytes fibrous component is in a "storeiform pattern" (radiating).Cell of origin- histiocytic cell/ fibroblasts/multipotent mesenchymal cell .Classification-- Myxoid/ Non Myxoid	bone often mottled or moth eaten with extension into soft tissue.Osteolytic lesion may be surrounded by reactive bone.Destructive appearance radiologically.Usually little periosteal reaction	Radical excision / Amputation or radiotherapy if not amenable to resection. reports of increased survival with neo adjuvant chemotherapy (doxorubicin, vincristine, methotrexate, T10)	Better in young.If initial procedure a wide or radical excision = more than 80% 4yr survival	mets
FIBROSARCOMA			25% have metastasised at presentation		Osteolytic lesion.Margins can range from well-defined to ragged and moth-eaten.Periosteal reaction is seen with cortical destruction Extension into the soft tissue is common	Stage 1A - limb salvaging excision with wide margin.Stage 2B - radical or wide margins with adjuvant chemotherapy or radiation therapy Classically considered radio-resistant. useful as adjuvant to surgery and chemotherapy. irradiation of lung secondary deposits not accessible to surgery	Stage 2 fibrosarcoma is guarded	Mets multiple myeloma MFH leiomyosarcoma

Bone forming tumours

2007-12-22T01:43:00.000+05:30

Tumor	Age	Location	Clinical presentation	Pathology	Radiology	Treatment	Prognosis	DD
Osteoid osteoma	5-25yrs, M:F-2:1	Any endochondral bone,tibia & femur- 50%. spine - post elements	Pain worse at night relieved by aspirin. 10% spine -> scoliosis. joint effusion, LLD, synovitis self limiting. surgery for pain relief Pain decreases as it matures lasting 18 - 30 months . healed by 3 - 7 years	Nidus < style="text-decoration: underline;">osteoblastic tissue surrounded by vascular fibrous tissue finally surrounded by mature reactive cortical bone. Contains fibroblasts, osteoblasts and osteoclasts, no marrow element. calcified centre in nidus	Lytic nidus surrounded by sclerotic bone (which may mask the nidus) Centre of nidus may be calcified CT or tomograms -> diagnosis Hot spot on bone scan	NSAIDs/ Nidus excision with intact rim of reactive bone.Intraop localisation with Bone scan/Tetracycline/ CT/ X-Ray .( dumbbell nidus)./Percut radiofrequency coagulation
Osteoblastoma	10 - 35 yrs	spine (post elements), / long bones or phalanges	Less intense pain than osteoid osteoma. often with scoliosis	More organised &larger size (2 - 10 cm) Less reactive bone.. Vascular stroma, abundant irregular areas of mineralised bone and osteoid. Vascular tumour +/- haemorrhage and +/- calcification. Texture gritty and friable.Spectrum of aggressiveness	Well demarcated osteolytic lesion sometimes containing flecks of calcification.May be aggressive.metaphyseal/ enlarges bone. periosteum intact. no soft tissue mass. Bone scan - intense activity	Intra capsular resection -> 20% recurrence En bloc resection -> no recurrence Use cryotherapy (PMMA) as adjuvant		ABC osteoid osteoma (spine) Giant cell tumour Osteosarcoma (if more aggressive)
Osteosarcomas	10 - 20 & 50 - 70 yrs, M>F	distal femur or around the knee. metaphyseal	Pain-constant and worse at night. Pathological fracture rare. tender lump which may lack a definite edge and may be attached to muscle may pulsate and feel warm. Telangiectatic-osteolytic-path # of femur tibis diaphysis.	Pleomorphic and anaplastic cells ,abundant fibrous and chondroid matrix. Stroma of spindle cells with numerous mitoses. high grade aggressive tumours. 50% osteoblastic, 25% chondroid, 25% fibroblastic. 20% are secondary (eg Pagets, enchondromas, osteochondromas, chronic osteomyelitis, irradiation, fibrous dysplasia, osteopetrosis, 100% of bilateral retinoblastomas and bone infarction). In the metaphysis, initially extends within medulla, perforates the cortex, raise periosteum -> Codman's triangle.As the tumour mass expands new bone forms along vascular channels -> appearance of sunray spicules. Mets via blood to lung , bones. oncogenes - Retinoblastoma gene and P53	Variable with combination of bone destruction and bone formation. Sun ray spicules (Radial ossification) and Codmans triangle (lifting of periosteum).Cortical breach common. Adjacent soft tissue mass.Joint space rarely involved.25% Lytic, 35% Sclerotic, 40% Mixed	primary by en bloc excision and microscopic disease by chemotherapy (Methotrexate -> 80% response).T10 regimen (methotrexate, vincristine, adriamycin). for 12 months. Radiotherapy- local pain /surgically inaccessible lesions / painful mets. Relatively radio-resistant, pre-operatively to decrease the size and vascularity. Sx- Wide resection / Amputation. Reconstruction -Allografts/Endoprosthesis/ expendable bone (fibula, ilium)/ Rotationplasty	Untreated -> 95% death in 2 years.10% have macro-metastases at presentation; 90% have micro-metastases.metastatic (Stage 3) disease 5 year survival now 30 - 40% (10-20% with surgery alone). adults /big/secondary tumor/proximal/telangiectatic/high grade is bad. Parosteal / Intra osseous (classical) osteosarcoma -> good prognosis.Pathological fracture does not affect prognosis	callus / myositis ossificans Stress fracture Osteomyelitis or syphilis Benign bone tumour Ewings
Parosteal Osteosarcoma	30 - 50 yrs. F>M	posterior aspect of distal femur, juxtametaphyseal	constant ache or lump		Well circumscribed mass.May be separated from cortex by a lucent line (30%).Broad based tumour with mottled calcification. Cortex not eroded Does not invade medullary cavity . Tends to encircle bone	Chemotherapy or radiotherapy not effective in preventing recurrence -> wide surgical resection	better than classical osteosarcoma. 70-80% 5 year survival.not different in relation to stage at presentation	Osteochondroma Myositis ossificans

Recurrent Shoulder dislocation

2007-12-15T21:57:00.000+05:30

Diagnosis-

Right sided,
traumatic/non-traumatic,
recurrent anterior shoulder dislocation
with uni-directional/ multi-directional instability
with 6 dislocations in last 6 months
in a 20 year old right handed male bowler
currently disabaled due to pain & instability

History-

h/o repeated episodes of shoulder dislocations since 6 months.

First dislocation --

time,
traumatic/ atraumatic,
mechanism of injury,
Rx taken (reduced sponateously or by doctor, was anaestheisa given, post-reduction immobilisation-duration & method.)

Subsequent episodes-

number,
mechanism-trivial trauma,
h/o Rx taken (as for first episode)

O/E

E/o anterior shoulder instability in the form of

+ apprehension test with apprehension reduced by relocation
+ anterior drawer test
+ Lachman's test

E/o posteriosr instability in the form of

+posterior drawer test
+Lachman's +
+Jerk test.

E/o inferior laxity in the form of

+ sulcus sign at 0 & 45 degrees &
+ Flagin test.

- drop arm test
- Neers impingement test

On ROM testing, there is restriction of abduction & external rotation.

+wasting of suprapinatus & infraspinatus fossae & deltoid

e/o axillary nerve palsy in form of badge sign & deltoid weakness

Opposite shoulder is normal

no e/o generalised ligamentous laxity

Cases for study

2007-12-10T17:16:00.000+05:30

Hip

AVN

Perthes

Ank Spond

NU # ITNF

NU # TCNF

CDH

RA -Protrusio

Spondyloarthropathy

Post-septic

SCFE

Old unreduced dislocation

SPINE

PID-lumbar

LCS

TB spine

Scoliosis

Spondylolisthesis

Kyphosis

Cervical myelopathy

Paediatrics

CTEV

CDH

CMT

Rickets

Genu valgum

Genu varum

PPRP

Sprengels

CPT

Cong. Dislocn patella

Osteogenesis imperfecta

Radial club hand

Ulnar club hand

AMC

CVT

Cong constriction bands

Scurvy

Tibia vara

SHOULDER

Recurrent dislocation

Old unreduced dislocn

Frozen shoulder

Impingement -RC tear

Stiff (post-traum arthritis)

Knee

Chronic synovitis

Stiff knee

ACL-Medial meniscus

Recurrent dislocation patella

PCL

Quadriceps contracture

Intra-articular LB

Charcoat`s joint

Haemophilic arthritis

PVNS

Foot

Pes cavus

Pes planus

Painful heel

Hallux valgus

Ankle

Subtalar Arthritis-malunited #calcaneum

TA tear

Malunited Potts

Tumors

OGS

Ewings

GCT

ABC/UBC

Osteochondroma

Fibrous dysplasia

Others

Osteomyelitis

Leprosy

RSD

MND

Muscular dystrophy

Amputation-AK/BK

Osteomalacia

Maduramycosis

Diabetic foot

Elbow

C.varus-MU # SCH

C.valgus-NU lat condyle

Stiff elbow

Old unreduced dislocation

Old unreduced Monteggia

Malunited # TY humerus

Tennis elbow

Wrist

Malunited # LE radius + DRUJ instability

Synovitis-TB / RA

Carpal tunnel syndrome

Madelung`s deformity

Kienbock`s

NU # scaphoid

Hand

VIC

Dupuytrens

Kaplan`s

1st MC jt arthritis

Trigger finger

Ganglion

Syndactyly

Polydactyly

Nerve injuries

Ulnar NP

Radial NP

Brachial plexus

Common Popliteal NP

Median NP

Combined

OBPP

Thoracic outlet syndrome

Trauma

NU-Tibia shaft

Humerus

R-U

Femur-shaft

Clavicle