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

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

• 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

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

 

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

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

 History

 

• Mechanism of  injury
• Pain
• Swelling
• Treatment taken

 

Examination

 

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

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

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 thickened, bone gap palapable, implant palpable
• No local tenderness at fracture site
• No e/o infection in the form of

1. local rise of temperature,
2. puckered adherent scar & sinuses,
3. 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

 

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

1. Atrophy of hypothenar eminence
2. Weakness of FCU, FDP,ADM, Interossei
3. Sensory d
4. Palpate ulnar nerve
5. Tinel’s sign at-
6. 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