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Pathological fractures
Pathological fractures occur in abnormal, weakened bones, often due to systemic conditions like osteomalacia or metastatic cancers. Symptoms may include spontaneous fractures, pain before fractures, and multiple recent fractures, particularly in patients over 45 or with a history of malignancy. Treatment includes stabilization of lesions, possible surgical intervention, and assessment based on Mirel's criteria, with consideration for patient comorbidities and expected oncological treatments.
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Introduction and definition of pathological fractures due to abnormalities in bone.
Classification into correctable (like renal osteodystrophy) and uncorrectable causes (like osteoporosis).
Characteristics of weak bones, poor healing, and signs indicating pathological fractures, especially in older patients.
Various examination methods, lab tests, and biochemical markers to assess the condition and extent of bone involvement.
Differentiation of disorders causing osteopenia with their serum and urine biochemical profiles.
Associated problems like pain, neurological deficits, and hypercalcemia and their clinical features.
Clinical management strategies for hypercalcemia in cancer patients and the importance of imaging.
Guidelines for biopsy procedures in bone lesions, with emphasis on avoiding complications.
Mirel’s scoring system for assessing pathological fracture risk based on various factors.
Management strategies including surgical stability and implant considerations for lesions.
Classification and management of acetabular and proximal femur lesions, emphasizing repair techniques.
Approach to spine-related pathological fractures in cancer patients, discussing imaging and treatment options.
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Pathological fractures
- 1.
- 2. • Pathologic fracturesoccur in abnormal bone. • Weakened bone predisposes the patient for failure during normal activity or after minor trauma.
- 3. Systemic- non neoplastic Correctable •Renal osteodystrophy • Hyperparathyroidism • Osteomalacia • Disuse osteoporosis Uncorrectable • Osteogenesis imperfecta • Polyostotic fibrous dysplasia • Postmenopausal osteoporosis • Paget disease • Osteopetrosis
- 4. • Weak bonespredisposed to fractures. • Poor callus formation. • Slow healing.
- 5. • Common metastatic cancers- –Breast – Lung – Prostate – thyroid – kidney • Common sites of metastasis- – Spine – Pelvis – Ribs – Skull – proximal femur – Proximal humerus.
- 6. History • Degree oftrauma • 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.
- 7. 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.
- 8. Examination • Palpation ofmass • Identification of obvious deformity • Neurovascular examination. • Evaluation of possible primary sites(Breast, prostate, lung, thyroid) • Lymphadenopathy.
- 9. Lab • CBC • ESR •Electrolytes • BUN • Serum glucose • Liver function tests • Total protein • Albumin • Calcium, phosphorus, and alkaline phosphatase.
- 10. • Anemia, hypercalcemia,increased ALP- widespread metastasis. • Serum and urine electrophoresis- multiple myeloma • Microsopic hematuria- RCC • TFT, CEA, CA-125, PSA.
- 11. • N-telopeptide andC-telopeptide are markers of bone collagen breakdown measured in serum and urine. – Confirm increased destruction caused by bone metastasis – Measure the overall extent of bone involvement – Assess 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.
- 12. Disorders producing Osteopenia DisorderSerum 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
- 14. 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.
- 15. Hypercalcemia- Clinical features •Neurologic- Headache, confusion, irritability, blurred vision. • GI- Anorexia, Nausea, Vomiting, Weight loss. Constipation, abdominal pain. • MSK- Fatigue, Weakness, joint and bone pain, unsteady gait. • Urinary- Nocturia, polydipsia, polyuria.
- 16. • Level ofhypercalcemia 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.
- 17. Ennekings questions • Whereis the lesion? – Epiphysis/Metaphysis/ Diaphysis – Cortex/ Medullary canal – Long bone/ Flat bone • What is the lesion doing to the bone? – Osteolysis- Total/ Diffuse/ Minimal
- 18. • What isthe 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
- 19. • Clues totissue 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.
- 21. • Osteopenia- indicatesinadequate 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
- 23. • Osteoporosis- – Thinningof 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.
- 24. Performing biopsy forlytic 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.
- 25. • Thus thesefractures 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.
- 26. • Cultures forall 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.
- 27. 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.
- 28. Mirel’s Criteria Variable 12 3 Site Upper extremity Lower extremity Peritrochanteric Pain Mild Moderate Severe Lesion Blastic Mixed Lytic Size <1/3rd diameter 1/3rd-2/3rd >2/3rd
- 29. • Lesions withscore of less than 7 can be irradiated safely, >8 require prophylactic fixation. • Patients treated prophylactically have: – Shorter hospitalization – More immediate pain relief – Faster and less complicated surgery – Less blood loss – Quicker return to premorbid function – Improved survival – Fewer hardware complications
- 30. • Fracture riskis greatest during patient positioning, prepration and draping. • Decision making includes: – Life expectancy of the patient – Patient comorbidities – Extent of the disease – Tumor histology – Anticipated future oncologic treatments – Degree of pain
- 31. Management considerations • Treatmentof 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.
- 32. • Perioperative antibiotics •Thromboembolic prophylaxis • Nutrition: Serum prealbumin • Post operative pulmonary exercises • Early mobilisation.
- 34. Bracing • Indicated in- –Limited life expectancies – Severe comorbidities – Small lesions – Radiosensitive tumors • Humerus shaft, forearm, tibia • Weight bearing should be limited.
- 35. Operative treatment • Intramedullarydevice 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.
- 36. Options • Proximal, totalhumeral endoprosthesis. • Humerus shaft- locked intramedullary nails, intercalary allograft. • Distal humerus- flexible intramedullary nail, bicondylar fixation, resection with modular distal femur reconstruction. • Radius/ Ulna- Flexible rods, rigid plate fixation,radial head resection, curettage.
- 38. Periacetabular lesions • Harringtonclassification: • 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
- 41. • 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.
- 42. • Class IVlesions- • Pelvic discontinuity • Saddle prosthesis or resection arthroplasty.
- 43. Proximal femur • Painfullytic 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.
- 44. Femur neck • Cementedprosthesis 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.
- 45. Intertrochanteric region • Highfailure 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.
- 47. Subtrochanteric region • Staticallylocked 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.
- 48. Distal femur • Difficultto 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.
- 49. A 58-year-old manwith a pathologic fracture of the distal femur due to lung cancer
- 50. Tibia • Proximal tibia-locking plate with cement • Diaphysis- Intramedullary nail.
- 51. Spine • Any cancerpatient 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.
- 52. • X ray-Loss of pedicle on the AP view. • MRI – Complete replacement of the vertebral segment – Multiple vertebral body lesions – Pedicle involvement – Intact intervertebral disk • Bone marrow biopsy.
- 53. Treatment • Radiation • Corticosteroids+/- bracing • Kyphoplasty/ vertebroplasty • Adjuvant radiation.
- 54. Indications of surgery •Progression of disease after radiation • Neurologic compromise caused by bony impingement • Radioresistant tumor within the spinal canal • Impending fracture • Spinal instability caused by a pathologic fracture • Progressive deformity.
Editor's Notes
- #21 permeative sclerotic lesion in the mid-diaphysis of the right femur. There is significant new bone formation and periosteal reaction. Note the Codman triangle RCC