Terri Sandi Susyanto, dr

Preceptor:
Prof. Dr. Darmadji Ismono, dr, SpB,SpOT(K), FICS

Orthopedic and Traumatology Division

Padjajaran University Medical Faculty
Hasan Sadikin Hospital
2017
Outline
 Introduction

 Epidemiology

 Pathophysiology

 Clinical evaluation

 Management
Introduction
 Metastasis- spread of a cancer or other disease from one organ or
part of the body to another without being directly connected with it

 Minor trauma or during normal activity

 5th decade most prevalent

 Metastases 2nd most common cause of pathologic fractures

 F: breast and lungs – 80%

 M: prostate and lungs – 80%

 10% - no primary tumor found

Epidemiology
Primary Site % metastasis to Bone
Breast 50-85
Lung 30-50
Prostate 50-70
Hodgkin’s 50-70
Kidney 30-50
Thyroid 40
Melanoma 30-40
Bladder 12-25
Pathophysiology
 Most spread is hematogenous

 Few tumors due to contiguous spread

 Most common osteolytic via osteoclast stimulation

 Prostate – commonly osteoblastic

 Breast – mixed

 Theories explaining predilection of bone for metastasis

Paget’s fertile soil hypothesis
 1889

 Sites of secondary growths are not a matter of chance

 Some organs provide a more fertile environment for the growth

of certain metastases

 Example: breast cancer to liver, Krukenberg tumor

 Prostate cancer to bone

 Hart and fielder later proved this using radioactive labelling

Ewing’s circulation theory
 1928

 Metastatic deposits dependent on route of blood and

lymph flow

 Organs though to be passive receptacles

 Organs with prominent venous systems have more

secondaries

 Baston plexus of spine responsible for prostate secondaries

Red marrow theory
 In descending order of frequency:
 Spine
 Pelvis
 Ribs
 Proximal appendicular skeleton
 Marrow sinusoids more susceptible to tumor cell
penetration
 Sudden change from arterioles to sinusoids favours
tumor cell entrapment
 Ewing’s and Paget’s theories not mutually exclusive
Molecular level
 Cells from primary enter blood vessels

 Attachment and penetration of basement membrane,

neovascularisation

 Type 1 collagen shown to be chemotactic to tumor cells

 RANK ligand produced by tumor cells stimulating osteoclast activity

 PTHrP produced by breast and lung cancer cells stimulates osteoclasts

 Prostate cancer cells produce BMPs, IGF1, TGFβ2 which stimulate

osteoblasts
Clinical evaluation: History
 Pain – most common, preceding fracture, night, constant,
dull, aggravated by activity

 Trauma – usually minimal for type of fracture

 Constitutional – anorexia, night sweats, weight loss, fatigue

 Previous cancer

 Carcinogen – smoking, radiation, occupational toxins

Factors suggesting pathologic
fracture
 Spontaneous fracture

 Minor trauma

 Pain at site preceeding fracture

 Multiple recent fractures

 Age > 45 yrs

 Prior history of malignancy

Associated problems
 Lowered Quality of life:
 Debilitating pain

 Immobility

 Neurologic deficits – spine mets

 Anaemia

 Hypercalcemia
Hypercalcemia
 Neurologic: headache, confusion, irritability, blurred vision

 Gastrointestinal: anorexia, nausea, vomiting, abdominal

pain, constipation, weight loss

 Musculoskeletal: fatigue, weakness, joint and bone pain,

unsteady gait

 Urinary: nocturia, polydypsia, polyuria, urinary tract

infections
Clinical evaluation: examination
 Local: mass, deformity, tenderness, contiguous
skeleton, neurologic exam

 Systemic: cachexia, pallor, lymphadenopathy, entire

skeletal system

 Primary: breast, thyroid, prostate, lung, pelvic

Clinical evaluation: Laboratory
 TBC – anaemia of chronic disease

 Calcium – elevated

 Alkaline phosphatase – elevated, non specific

 Tumor markers – PSA, CEA, CA125, TFTs

 N-telopeptide + C-telopeptide – markers of bone

destruction, determine extent of skeletal involvement,
assess response to bisphosphonates
Imaging: plain radiographs
 Enneking’s questions:

 Location: diaphysis, metaphysis, epiphysis, cortical or

medullary

 Effect: osteoblastic vs. osteolytic or mixed

 Reaction: sclerotic rim, periosteal reaction, codman

triangle

 Isolated avulsion of lesser trochanter – imminent femoral

neck fracture
Osteolytic, diaphyseal medullary,
periosteal reaction
Osteoblastic mets to bone
Codman triangle
Osteolytic lesion in lesser trochanter
Radiology: CT scans
 Most sensitive for detecting bone destruction

 Determines extent of cortical involvement

 Also used to search for primary lesion in pelvis,

abdomen or chest
Mixed lesion in lung mets
Radiology: MRI
 Most sensitive for assessment of the anatomic extent of
a lesion

 Most adequate for spinal metastases to determine

neurologic structure involvement

 Can determine extraosseous spread of a mass

Bone scanning
 Technetium-99m (99m Tc) bone scanning:

 Sensitive for detection of occult lesions

 Assessment of the biologic activity of lesions

 Identification of other sites

 Assessing response to therapy

Biopsy
 Indicated to rule out primary tumor of bone

 Immunohistochemistry can determine primary

 Biopsy at fracture site complicated by bleeding and callus

formation

 Needle vs incisional

 Oncological surgical principles adhered to

 Cultures to rule out infection

Impending pathologic fractures
 Prophylactic stabilisation before radiotherapy can be
performed for pain

 Radio and chemotherapy without stabilisation also an

option

 Decision to stabilise difficult

 Mirel’s criteria useful to determine which lesions at

high risk of fracture
Mirel’s criteria
VARIABLE SCORE
SITE Upper Limb Lower Limb Peritrochanteric
PAIN Mild Moderate Severe
LESION Blastic Mixed Lytic
SIZE <1/3 1/3 – 2/3 >2/3

Size is the diameter of cortex involved on plain radiographs

A score of 8 or more is an indication for prophylactic stabilisation
Advantages
 Prophylactic stabilisation:
 Shorter hospital stay

 More immediate pain relief

 Faster and less complex surgery

 Quicker return to premorbid function

 Improved survival
Management objectives
 Decrease pain

 Restore function

 Maintain/restore mobility

 Limit surgical procedures

 Minimize hospital time

 Early return to function (immediate weightbearing)

Non operative management
 Bisphosphonates – modifies bone resorption by
osteoclasts, shown to reduce risk of skeletal metastasis

 Hematologic – correction of anaemia, coagulopathy, DVT

prophylaxis

 Hypercalcemia – hydration, calcium restriction,

bisphosphonates, mithramycin

 Analgesia

 Radiation – most useful in spinal metastases

Radiotherapy
 Used to reduce pain secondary to bone metastases

 Partial in 80%. Complete in 50 – 60%

 Halts progression of bony destruction

 Allows healing of an impending pathologic fracture

 Postoperative local tumor control

Bracing
 Patients with limited life expectancies, severe
comorbidities, small lesions, or radiosensitive tumors

 Upper extremity lesions particularly amenable

 Adjuvant radiotherapy of suscepible tumors required

Operative: principles
 Durable, weight bearing impalnts needed

 PPMA augmentation of construct useful incl. prosthesis

 Bone graft less useful due to prolonged healing time

 Prophylactically stabilise as much bone as possible

 Anticipate hemorrhage due to neovascularisation

 Thus tourniquet, preoperative embolisation

Upper extremity
 Scapula, clavicle – non operative

 Proximal humerus – prosthesis (long stem), intramedullary

nail with multiple screws

 Humerus Diaphysis – locked IM nail > plating

 Distal humerus – prosthesis, retrograde flexible IM nails >

bicondylar plating

 Forearm – Rare. IM nails or plating

Lower extremity
 Acetabular – reconstruction with appropriate
prosthesis
 Femoral neck – hemi- or THR. Cemented. Long stem
 Intertrochanteric – recon nail or prosthesis > DHS
 Subtrochanteric – locked IM nail
 Femur shaft – locked IM nail preferably
cephalomedullary
 Around the knee – locked plating > retrograde nailing
Spinal fractures
 Commonly present with compression fracture

 MRI to differentiate from osteoporosis

 Lesion involving body and pedicle sparing disc highly

suggestive

 Radiotherapy, steroids if no neurodeficits or

impending fracture
Spinal fractures
 Surgery:
 Progression of disease after radiation
 Neurologic compromise
 Impending fracture
 Spinal instability due to pathologic fracture
 Progressive deformity due to pathologic fracture
 Options:
 Minimally invasive kyphoplasty/vertebroplasty
 Decompression and instrumentation
Controversies and future trends
 Optimal length of femoral component of THR
 Criteria for impeding fracture
 Wide resection of solitary metastases – RCC
 Radiofrequency ablation
 Cryotherapy
 Acetabuloplasty – percutaneous PMMA injection
 RANK L modification
 Angiogenesis inhibitors
Summary
 Diagnosis and treatment requires a multidisciplinary
approach

 Aggressive surgical treatment relieves pain, restores

function, and facilitates nursing care

 Biopsy all solitary lesions or refer appropriately

 Understand tumor biology and tailor treatment

THANK YOU