Weak bones predisposed to fractures. Poor callus formation. Slow healing.
Common metastatic cancers- Breast Lung Prostate thyroid kidney Common sites of metastasis- Spine Pelvis Ribs Skull proximal femur Proximal humerus .
History Degree of trauma Presence of prodromal pain- dull aching to intense pain. Exacerbated by weight bearing. Previously diagnosed or treated cancer, h/o radiation Rx Weight loss, fever, night sweats, fatigue.
Factors suggesting path # Spontaneous fracture Fractures after minor trauma Pain at the site before the fracture Multiple recent fractures Unusual # patterns Patient older than 45 years. History of malignancy.
Examination Palpation of mass Identification of obvious deformity Neurovascular examination. Evaluation of possible primary sites(Breast, prostate, lung, thyroid) Lymphadenopathy.
Lab CBC ESR Electrolytes BUN Serum glucose Liver function tests Total protein Albumin Calcium , phosphorus, and alkaline phosphatase.
N- telopeptide and C- telopeptide are markers of bone collagen breakdown measured in serum and urine. C onfirm increased destruction caused by bone metastasis M easure the overall extent of bone involvement A ssess the response of the bone to bisphosphonate treatment Demers LM, Costa L, Lipton A. Biochemical markers and skeletal metastases. Clin Orthop Relat Res. 2003;(415):S138–S147.
Disorders producing Osteopenia Disorder Serum Calcium S. Phosphorous S. Alkaline phosphatase Urine Calcium Osteoporosis N N N N Osteomalacia Low Low High Low Hyperparathyroidism High Low Normal High Renal Osteodystrophy Low High High Pagets disease N N High Hydroxyproline Myeloma N N N Light chains
Associated Medical Problems Limitation of ADL due to pain/pathological fractures. Neurological deficits/ paralysis in spinal fractures. Prolonged recumbency predisposes to hypercalcemia . Anemia Hypercalcemia of malignancy- poor prognosis.
Level of hypercalcemia does not always correlate with the severity of the metastasis. Vigorous volume repletion- treat the tumor directly/ bisphosphonates to reduce osteoclastic activity. All biochemical parameters should be corrected prior to surgery.
Ennekings questions Where is the lesion? Epiphysis/Metaphysis/ Diaphysis Cortex/ Medullary canal Long bone/ Flat bone What is the lesion doing to the bone? Osteolysis - Total/ Diffuse/ Minimal
What is the bone doing to the lesion? Well defined reactive rim- benign/slow growing Intact but abundant periosteal reaction- Aggressive Periosteal reaction that cannot keep up with tumor- Malignant
Clues to tissue type within the lesion- Calcification-Bone infarct/ Cartilage tumor Ossification-Osteosarcoma/ Osteoblastoma Ground glass appearance- Fibrous dysplasia Entire bone to imaged. Pain in the distal sites can have proximal source.
Osteopenia- indicates inadequate bone(osteoporosis) or inadequately mineralised bone( osteomalacia ) Looser lines-compression side radiolucent lines Calcification of small vessels Phalangeal periosteal reaction s/o osteomalacia or hyperparathyroidism
Osteoporosis- Thinning of cortices Loss of normal trabecular pattern Permeative or moth eaten pattern of cortical destruction is highly suggestive of malignancy. >40 yrs - Metastatic carcinoma, myeloma, lymphoma.
Performing biopsy for lytic lesions Solitary bone lesion in a patient with or without history should be done. Needle biopsy is definitive when differentiating carcinoma from sarcoma with adequate immunohistochemistry. When there is pathologic fracture through the lytic lesion, bleeding can occur due to early fracture callus.
Thus these fractures should be stabilised first and then biopsy undertaken. Biopsy should be obtained from a site near but unaffected by fracture. Site should be as small as possible, longitudnally in line with the extremity. Tissues involved in post- biopsy hematoma must be considered as contaminated.
Cultures for all biopsy to rule out infections that may mimic tumors on x rays. If definitive diagnosis present on frozen sections intraop then ideal to fix the fractures, otherwise wait for permanent sections.
Impending pathological fractures Known skeletal mets usually treated by radiation/chemotherapy +/- prophylactic fixation. Radiological assesment of lesion and patient symptoms necessary to calculate the risk. Mirels developed a scoring system based on pain, location, size of the lesion,radiographic appearance.
Lesions with score of less than 7 can be irradiated safely, >8 require prophylactic fixation. Patients treated prophylactically have: Shorter hospitalization More immediate pain relief F aster and less complicated surgery Less blood loss Quicker return to premorbid function Improved survival Fewer hardware complications
Fracture risk is greatest during patient positioning, prepration and draping. Decision making includes: Life expectancy of the patient Patient comorbidities Extent of the disease T umor histology Anticipated future oncologic treatments D egree of pain
Management considerations Treatment of local bone lesion- Surgical stabilisation +/- resection: large lytic lesion at risk of fractures/pathologic fractures. Radiation: Adjuvant local treatment for entire operative field. Functional bracing Bisphosphonates: inhibit osteoclast mediated bone resorption .
Perioperative antibiotics Thromboembolic prophylaxis Nutrition: Serum prealbumin Post operative pulmonary exercises Early mobilisation .
Bracing Indicated in- Limited life expectancies Severe comorbidities Small lesions Radiosensitive tumors Humerus shaft, forearm, tibia Weight bearing should be limited.
Operative treatment Intramedullary device or modular prosthesis provides better stability. Bone cement- Increases the strength of fixation Should not be used to replace segment of bone Goal should be to stabilize as much of the bone as possible.
Periacetabular lesions Harrington classification: Class I lesion- Minor defects, with maintenance of lateral cortex, superior wall, medial wall. Treated with conventional cemented acetabular component. Class II- Major acetabular defect with deficient medial wall and superior dome. Antiprotrusion device/ medial mesh
Class III Massive defects with deficient lateral cortex and superior bone. No substantial peripheral rim for fixation of metal component. Acetabular cage with long screw fixation into remaining pubis,illium or ischium. Bone cement to provide stability and steinmann pins to anchor the construct.
Class IV lesions- Pelvic discontinuity Saddle prosthesis or resection arthroplasty .
Proximal femur Painful lytic lesions should be stabilised - High risk of fracture Ease of surgery Stabilize as much of proximal femur to avoid future implant failure- since lytic process is continous .
Femur neck Cemented prosthesis procedure of choice. Curette all tumour tissue before putting the implant. Use a long stem component for adjacent lesions- cement to be injected in a fairly liquid state after canal prepration .
Intertrochanteric region High failure rate of DHS. Intramedullary device or prosthetic replacement. A cephalomedullary device has an added function of protecting the femoral neck. Cemented calcar replacing prosthesis used for more extensive lesions.
Subtrochanteric region Statically locked nail +/- bone cement. Failed internal fixation/ extensive destruction- modular proximal femur device. Increased risk of dislocation and abductor weakness with megaprosthesis . Bipolar head is used to provide additional stability if acetabulum is not involved. Largest diameter nail used for diaphysis.
Distal femur Difficult to treat due to poor bone stock and communition . Lateral locking plate with cement or modular distal femur prosthesis. For extensive destruction modular prosthesis is the optimum choice as it allows resection en bloc. Retrograde nail- does not stabilize neck, seeding.
A 58-year-old man with a pathologic fracture of the distal femur due to lung cancer
Tibia Proximal tibia- locking plate with cement Diaphysis- Intramedullary nail.
Spine Any cancer patient with back pain- consider mets . Any patient treated for osteoporotic compression fracture should undergo a biopsy when not responding to treatment or when there is excessive destruction of bone. CT guided biopsy.
X ray- Loss of pedicle on the AP view. MRI C omplete replacement of the vertebral segment Multiple vertebral body lesions Pedicle involvement Intact intervertebral disk Bone marrow biopsy.
Indications of surgery P rogression of disease after radiation Neurologic compromise caused by bony impingement Radioresistant tumor within the spinal canal I mpending fracture Spinal instability caused by a pathologic fracture Progressive deformity.