Textbook Reading-Rockwood - Chapter 20 Pathologic Fractures p643-p647

Textbook Reading-Rockwood -Chapter 20

Pathologic Fracturesp643-p647

Pathologic Fractures

• Bone weakness with a pre-existing abnormality

• Fractures due to low energy injuries.

• Distored archetecture and distored bone density


• Correctable diseases : renal osteodystrophy, hyperparathyroidism, osteomalacia, and disuse osteoporosis.

• Uncorrectable diseases : osteogenesis imperfecta, poly-ostotic fibrous dysplasia, postmenopausal osteoporosis, Paget's disease, and osteopetrosis.


• A primary goal in the management of patients with any systemic skeletal disease is to prevent disuse osteoporosis, which may lead to additional pathologic fractures.


• 10 million Americans > 50 years osteoporosis• 34 million osteomalacia & risk for osteoporosis• 1.5 million people pathologic fracture related to osteo

porosis each year • 20% elder who sustain a hip fracture die within 1 year • One of every two women > 50 years osteoporosis-rela

ted fracture in lifetime • Other skeletal conditions such as Paget's disease one

million people in USA • 20,000 to 50,000 Americans osteogenesis imperfecta


• The American Cancer Society 1.3 million new cancer cases in 2003 50% skeleton metastasis

• With improved medical treatment of many cancers increased prevalence of bone metastasis increases the chances of pathologic fracture.

• The majority of bone metastases originate from cancers breast, lung, and prostate, followed by the thyroid and kidney.

• The most common sites spine, pelvis, ribs, skull, and proximal long bones.

EVALUATION OF THE PATIENT WITH AN IMPENDING OR ACTUAL PATHOLOGIC

FRACTURE • Clinical• History• Physical Examination • Laboratory Studies • Associated Medical Problems • Radiographic Workup• Plain X-Rays• Nuclear Medicine Studies • Three-Dimensional Imaging/Angiography • When and How to Biopsy

History

• TABLE 20-1 Evaluation of a Patient with a Lytic Bone Lesion

• TABLE 20-2 Factors Suggesting a Pathologic Fracture

TABLE 20-1 Evaluation of a Patient with a Lytic Bone Lesion

• History: thyroid, breast, or prostate nodule • Review of systems: gastrointestinal symptoms, weight loss,

flank pain, hematuria • Physical examination: lymph nodes, thyroid, breast, lungs,

abdomen, prostate, testicles, and rectum • Plain x-rays: chest, affected bone, humerus, pelvis, femur,

spine • 99mTc bone scan/FDG-PET scan: total body • CT scan: chest, abdomen, pelvis • Laboratory: complete blood count, erythrocyte sedimentatio

n rate, calcium, phosphate, urinalysis, prostate-specific antigen, immunoelectrophoresis, and alkaline phosphatase

• Biopsy: needle vs. open• FDG, Fluorine-18 deoxyglucose; PET, positron emission tomography;

CT, computed tomography.

TABLE 20-2 Factors Suggesting a Pathologic Fracture

• Spontaneous fracture

• Fracture after minor trauma

• Pain at the site before the fracture

• Multiple recent fractures

• Unusual fracture pattern (banana fracture)

• Patient >45 years of age

• History of primary malignancy

Physical Examination

• Careful evaluation of the affected skeletal region Palpation of a mass or fracture and a detailed neurologic examination

• All extremities and the entire spine should be evaluated for additional lesions or lymphadenopathy

• Careful evaluation of all possible primary sites (breast, prostate, thyroid) and a stool guaiac test

Laboratory Studies

• Baseline laboratory CBC/DC, ESR, BUN, SUGAR, liver function, protein, albumin, CA, P, and ALP.

• Bone metastases anemia of chronic disease, hypercalcemia, and increased alkaline phosphatase

• U/Amicroscopic hematuria renal cell carcinoma (RCC)

Laboratory Studies

• Serum and urine protein electrophoreses multiple myeloma

• Thyroid function tests, CEA, CA125, and PSA are serum markers for specific tumors

• N-telopeptide and C-telopeptide in serum and urine increased destruction caused by bone metastasis

Laboratory Studies

• Prostate-specific antigen is a sensitive measurement of prostate cancer : < 10 ng/mL excludes bone metastasis

• Remember that serum calcium is a measurement of unbound calcium in the serum, and, therefore, determination of serum protein is necessary to interpret the calcium level.

• Correct Ca(mg/dl)=Total Ca(mg/dl)-0.8×[4.0-albumin(g/dl)] 。

TABLE 20-3 Disorders Producing Osteopenia

Disorder

Laboratory Value

Serum Calcium

Serum Phosphoru

s

Serum Alkaline Phosphatas

e Urine

Osteoporosis Normal Normal Normal Normal Ca

Osteomalacia Normal to low

Normal to low

Normal to high

Low Ca

Hyperparathyroidism

Normal to high

Normal to low

Normal High Ca

Renal osteodystrophy

Low High High

Paget's disease Normal Normal Very high Hydroxyproline

Myeloma Normal Normal Normal Protein

Associated Medical Problems

• Pain unable to ambulate or perform daily activities

• Spinal fractures neurologic deficits

• Prolonged bedrest predisposing hypercalcemia

• 40% hypercalcemia related to malignancy lung, breast, kidney, and genitourinary tract

Associated Medical Problems

• Hypercalcemia poor prognosis 60% : survive < 3 months, and only 20% 1 year

• No reliable correlation between the hypercalcemia and skeletal involvement

• Lung ca hypercalcemia without obvious bone metastases

• Multiple myeloma or breast cahypercalcemia with extent of bone metastases

TABLE 20-4 Signs and Symptoms of 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

Radiographic Workup -Plain X-Rays

• Evaluate a destructive bone lesion or pathologic fracture plain x-ray in two planes.

• Diagnostic clues osteopenia, periosteal reaction, cortical thinning, Looser's lines, and abnormal soft tissue shadows


• Osteomalacia or hyperparathyroidism looser's lines (compression-side radiolucent lines), calcification of small vessels, and phalangeal periosteal reaction.

• Osteoporosis thin cortices and loss of the normal trabecular pattern.


• Osteolytic or osteoblastic lesion tumor inactive, active, or aggressive.

• Small osteolytic lesions without endosteal or periosteal reaction inactive or minimally active (benign) primary bone tumors.

• Cortex erosion but are contained by periosteum active benign or low-grade malignant bone tumors


• Large lesions that destroy the cortex aggressive, malignant lesions

• Permeative or moth-eaten pattern of cortical destruction highly suggestive of malignancy

• > 45 years & destructive bone lesions metastatic carcinoma , multiple myeloma and lymphoma

• Solitary bone lesion primary bone tumor chondrosarcoma, malignant fibrous histio-cytoma, or osteosarcoma


• Osteolytic destruction is most common lung, thyroid, kidney, and colon

• Osteoblastic with sclerosis metastatic prostate cancer

• Metastatic breast cancer mixed osteolytic and osteoblastic

osteolytic & osteoblastic

TABLE 20-5 Evaluation of Plain X-rays

Question Option Interpretation

1. Where is the lesion? Epiphysis vs metaphysis vs diaphysis

Cortex vs medullary canalLong bone (femur, humeru

s) vs flat bone (pelvis, scapula)

2. What is the lesion doing to the bone?

Bone destruction (osteolysis)

-Total -Diffuse -Minimal

3. What is the bone doing to the lesion?

Well-defined reactive rim

Benign or slow-growing

Intact but abundant periosteal reaction

Aggressive

Periosteal reaction that cannot keep up with tumor (Codman's triangle)

Highly malignant

4. What are the clues to the tissue type within the lesion?

Calcification Bone infarct/cartilage tumor

Ossification Osteosarcoma/osteoblastoma

Ground glass Fibrous dysplasia

• Thank you for attention.

Rockwood Chapter 20Pathologic fractures

P.648~652

Report: R3 范姜治澐

Plain X-Rays

• Generalized osteopenia

• Periosteal reaction• Cortical thinning • Looser's lines (compr

ession-side radiolucent lines)

• Abnormal soft tissue shadows

Question Option Interpretation

Where is the lesion? Epiphysis vs metaphysis vs diaphysisCortex vs medullary canalLong bone (femur, humerus) vs flat bone (pelvis, scapula)

Codman's triangle

What is the lesion doing to the bone?

Bone destruction (osteolysis) -Total -Diffuse -Minimal

What is the bone doing to the lesion?

Well-defined reactive rimIntact but abundant periosteal reactionPeriosteal reaction that cannot keep up with tumor (Codman's triangle)

What are the clues to the tissue type within the lesion?

CalcificationOssificationGround glass

Bone infarct/cartilage tumorOsteosarcoma/osteoblastomaFibrous dysplasia

• Osteomalacia or hyperparathyroidism– Looser’s line– Calcification of small vessels – Phalangeal periosteal reaction

• Osteoporosis – Thin cortices– loss of the normal trabecular pattern without o

ther abnormalities

• Osteolytic or osteoblastic lesion

Inactive Small osteolytic lesions surrounded by a rim of reactive bone

Without endosteal or periosteal reaction

Active Lesions that erode the cortex but are contained by periosteum

Aggressive Large lesions that destroy the cortex

“moth-eaten”

• Multiple myeloma and lymphoma – Most destructive bone lesions in patients mor

e than 45 years of age of metastatic carcinoma followed by them

• A solitary bone lesion should be fully evaluated to rule out a primary bone tumor – chondrosarcoma, – malignant fibrous histiocytoma– osteosarcoma

Bone metastasis

Osteolytic lung, thyroid, kidney, and colon

Osteoblastic

with sclerosis

Prostate

Mixed Breast

• Tumor cells secrete factors that interact with host cells in the bone microenvironment and affect the cycle of normal bone turnover

• An isolated avulsion of the lesser trochanter is almost always pathologic

• A cortical lesion in adults is usually a metastasis

Nuclear Medicine Studies

• Technetium bone scintigraphy – detects osteoblastic activity

• Multiple myeloma, occasional metastatic RCC are falsely negative on bone scan

• Fluorine-18 deoxyglucose • Positron emission tomography (PET) scanning

– Gold stadard recently in metabolic imaging

• PET/computed tomography (CT) scanning had higher sensitivity and specificity

• Magnetic resonance imaging (MRI) is not generally used – Useful in the evaluation of patients with spinal

metastasis

• Standard angiogram is still useful when embolizing feeding tumor vessels in vascular lesions – Metastatic RCC – Multiple myeloma

Search for a primary lesion

• examination of the breast, thyroid, and prostate

• chest x-ray and CT scans of the chest, abdomen, and pelvis

• mammogram

• skeletal survey including skull films (MM)

• PET

• A solitary bone lesion in a patient with or without a history of cancer should be biopsied

• Needle biopsy – differentiating a carcinoma from a sarcoma – Immunohistochemical staining – Fracture should be stabilized initially with tract

ion or a cast

• Incisional biopsy – site unaffected by the fracture – as small as possible – longitudinal fashion – hemostasis

• Cultures should always be sent

• Intraoperative frozen section – surgical treatment of the pathologic fracture – best to wait for the permanent sections before

definitively treating the tumor and fracture

IMPENDING PATHOLOGIC FRACTURES • X-ray appearance of the lesion

• Patient's symptoms

• 50% to 75% cortical involvement – Significant pain relief after prophylactic

fixation

• Painful, larger than 2.5 cm, and involves more than 50% of the cortex

Classification

• Mirels developed a scoring system – presence or absence of pain, and the – size, – location– radiographic appearance

• Lesions scoring 8 or higher require prophylactic internal fixation before irradiation

Prophylactic stabilization

• shorter hospitalization (average 2 days)• discharge more likely (40%) • immediate pain relief• faster and less complicated surgery• less blood loss• quicker return to premorbid function• improved survival• fewer hardware complications

• Goals of surgical treatment – alleviate pain– reduce narcotic use– restore skeletal stability– regain functional independence

• Decision-making for operation– life expectancy of the patient – patient comorbidities – extent of the disease – tumor histology– anticipated future oncologic treatments– degree of pain

TREATMENT OPTIONS FOR PATIENTS WITH

METASTATIC OR SYSTEMIC DISEASE

• Local bone lesion can be treated with – nonsurgical management (radiation, functional bracin

g, and bisphosphonates) – surgical stabilization with or without resection

• large lytic lesions at risk for fracture• existing pathologic fractures

• Pathologic long bone fractures – overall rate of fracture healing: 34% – 74% survived > 6 months– Fractures due to MM were most likely to heal

• Ideal reconstruction– Allow immediate weight-bearing – Not require revision

• Load-bearing fixation device are prefered– Poor healing rate, 30~40%– IM device, modular prosthesis

• PMMA– increase the strength of the fixation – improves the bending strength of a fixation

• Autogenous bone graft – Not generally used

• Segmental allografts – Rarely indicated – Require a prolonged healing time

• Cemented prosthesis

• IM nailing– Prophylactically stabilization of entire bone – Femur, humerus, or tibia – Reconstruction nail for stabilize the femoral n

eck

• Hypervascular metastatic cancers – RCC– Thyroid ca– MM

• Tourniquet

• Preoperative angiographic embolization – within 36 hours

Nonoperative treatment

• limited life expectancies

• severe comorbidities

• small lesions

• radiosensitive tumors

• Patients should limit weightbearing on the affected extremity

Upper Extremity Fractures

• 20% bone metastasis

• 50% in the humerus

• Benefits to quality of life – operation prefered

•

Scapula/Clavicle

• Nonoperative treatment– immobilization – radiation– medical management

Proximal Humerus

• humeral head or neck – proximal humeral replaceme

nt • pain relief and local control of t

he tumor • range of motion and stability ar

e often limited

– intramedullary fixation – cement may be required

Humeral Diaphysis

• locked intramedullary fixation

• Intercalary metal spacer – After complete resection of a metastatic lesion – minimizing blood loss – alleviating the need for postoperative radiation

• Plate fixation of the humerus is at risk of failure

Distal Humerus

• flexible intramedullary nails

• bicondylar plate fixation

• resection with modular distal humeral reconstruction

Forearm/Hand

• Unusual • Often from the lung, breast, and kidney • Radius and ulna

– Flexible rods or rigid plate fixation

• Radial head– Resection

• Hand– curettage, internal fixation, and cementation

• Amputation

Rockwood and Green’s Rockwood and Green’s fractures in adultsfractures in adults

Rockwood and Green’s Rockwood and Green’s fractures in adultsfractures in adults

Chapter 20

Pathologic FracturesP652-654

Kristy L. Weber

Presented by R3 Meng-huang Wu

Humeral Diaphysis• IM nailing

– Mechanical and rotational stability– PMMA augment

• Intercalary Metal spacer– Modular reconstruction in

segmental defects or large bone loss

– Minimize blood loss– Alleviate post op RT

• Plate fixation with cement– Extensive exposure– Inability to protect the entire bone– Risk of failure

Distal Humerus

• Flexible intramedullary nails

• Bicondylar plate fixation with cement

• Resection with modular distal humeral reconstruction– massive bone loss involving the condyles

• Curettage of the distal humeral lesion – open reduction in fracture– use PMMA

Flexible intramedullary nails

• Ease of insertion: retrograde via bilat. entry point

• span the entire humerus

• excellent functional recovery

• preservation of the elbow joint

Forearm/Hand

• Metastases distal to the elbow are unusual– lung, breast, and kidney

• Radius and ulna – flexible rods or rigid plate fixation

• Radial head – resection

• Hand– Intralesional curettage, internal fixation, and c

ementation• Distal or extensive

– amputation

Pelvic/Acetabular Fractures

• Bony pelvis– Many bone metastases or pathologic fra

ctures do not affect weight-bearing; not require surgical intervention. • Lesions of the iliac wing, superior/inferior p

ubic rami, or sacroiliac region. • Insufficiency fractures caused by osteoporo

sis: protected weight-bearing until the pain diminishes

Periacetabular lesions

• Affect ambulatory status and often present a difficult surgical problem

• CT scans with 3D reconstructions

Harrington classification

• Minor acetabular defects

• Intact lateral cortices and superior and medial walls

• Conventional cemented acetabular component

•the location and extent of the defect

Class I

Class II

• Major acetabular defects with a deficient medial wall and superior dome.

• Antiprotrusio device or medial mesh

Class III

• massive defects with deficient lateral cortices and superior dome.

• Acetabular cage • The massive bony

defect is filled with PMMA

• A cemented PE cup

Class IV• pelvic discontinuity• resection and reconstr

uction using a saddle prosthesis

• satisfactory pain relief and function: 70% to 75%

• Complications: 20% to 30% of cases

• trabecular metal, tantalum

Lower Extremity Fractures

• Femur: most common• The proximal 1/3 is involved in 50% of cases wit

h the intertrochanteric region accounting for 20% of cases.

• Most painful of all bone metastases• Alter the quality of a patient's life and threaten a

n individual's level of independence. • Painful lesion:

– Prophylactically stabilized whenever possible • high incidence of subsequent fracture and the comparative e

ase of the operation.

Femoral Neck

• Rarely heal and tends to progress

• High incidence of failure if traditional fracture fixation devices

Cemented replacement prosthesis

• Treatment of choice

• THR?: acetabular involvement

• All tumor tissue should be curetted from the femoral canal

• Adjacent lesions in the subtrochanteric region or proximal diaphysis– long-stemmed cemented femoral component– Cement side effect vs stability

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Textbook Reading-Rockwood - Chapter 20 Pathologic Fractures p643-p647