This presentation talks about the various types of pathological fractures that can occur and the fixation methods for different regions

1. Pathological Fractures

2. • Pathologic fractures occur 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 bones predisposed 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 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.

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 of mass
• 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 and C-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
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

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 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.

17. 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

18. • 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

19. • 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.

21. • 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

23. • 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.

24. 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.

25. • 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.

26. • 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.

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 1 2 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 with score 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 risk is 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
• 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.

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
• 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.

36. Options
• Proximal, total humeral 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
• 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

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 IV lesions-
• Pelvic discontinuity
• Saddle prosthesis or resection arthroplasty.

43. 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.

44. 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.

45. 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.

47. 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.

48. 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.

49. A 58-year-old man with 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 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.

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.