Pathologic Fracture Management

A pathologic fracture occurs through bone weakened by pre-existing disease, typically with minimal trauma that would not fracture normal bone. The underlying pathology compromises the structural integrity and mechanical properties of the bone.

Recognising it. Five features set it apart from an ordinary fracture:

• A low-energy mechanism: normal activities or a minor fall
• A pre-existing bone lesion on imaging
• Pain preceding the fracture, for weeks to months
• An abnormal fracture pattern or location
• Poor healing potential unless the underlying pathology is addressed

The diagnosis rests on correlating the clinical presentation, mechanism, imaging characteristics and patient risk factors, which is what separates it from an insufficiency fracture or an occult traumatic injury.

Causes. The underlying pathology falls into five groups:

• Malignant: metastatic disease (50%), multiple myeloma (20%), primary bone sarcoma (10%)
• Benign: fibrous dysplasia, enchondroma, simple bone cyst, aneurysmal bone cyst
• Metabolic: osteoporosis, osteomalacia, hyperparathyroidism
• Infection: chronic osteomyelitis with bone destruction
• Other: Paget's disease, radiation necrosis

Several systems are in use, and each answers a different question.

Mirels' score is the most clinically relevant of them. Each of four variables scores 1 to 3 points:

The total is read against fracture risk:

• 7 or less: low risk, observation acceptable
• 8: intermediate risk, an individualised decision
• 9 or more: high risk (33% fracture rate), prophylactic fixation indicated
• 10-12: very high risk (fracture rate over 50%), urgent intervention

Why sources quote 8 or 9. The score was derived from a retrospective study of 78 metastatic long-bone lesions and has become the most widely used tool for this decision. Mirels' original paper described a score of 8 or higher as a prelude to fracture, and a score of 7 or lower as safe to irradiate. The threshold taught today treats 8 as a borderline, individualised score and 9 or higher as a clear indication to fix, so different sources quote either 8 or 9 as the cut-off, and both trace back to the same study.

What the score is good at. Mirels has a negative predictive value of 86-100% but a positive predictive value of only 23-70%, and a systematic review of femoral fracture-risk methods concludes that it leads to overtreatment. A low score is therefore a reliable reason not to operate; a high score identifies a group in which the majority of lesions still would not have fractured.

Use the score to decide who needs closer assessment - axial cortical involvement on CT, tumour type, expected survival, the consequence of fracturing at that site - not as an automatic operative indication.

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Stratifying risk drives the central decision between observation with serial imaging and prophylactic stabilisation before the fracture occurs.

The lesion. Features that raise the risk of fracture:

• Lytic rather than blastic or mixed
• Size over 2.5-3 cm
• Cortical destruction over 50%
• Subtrochanteric or femoral neck location
• Pain that persists despite radiotherapy
• Progressive enlargement on serial imaging

The patient. Primary tumour type matters (renal, thyroid, lung, breast, melanoma), as do multiple skeletal metastases and failed radiotherapy. Ongoing chemotherapy impairs healing, limited life expectancy affects the choice of reconstruction, and activity level and ambulatory status count too.

The mechanics. Risk is higher in regions of tensile stress and in the high load-bearing bones, the femur and tibia. Eccentric loading, a reduced cross-sectional area and loss of trabecular architecture add to it; the biomechanics are set out under Pathophysiology.

The tumour type. Fracture risk varies with the lesion:

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Osteolysis. Tumour cells secrete RANKL (receptor activator of nuclear factor kappa-B ligand), which binds RANK on osteoclast precursors and drives massive osteoclast activation and differentiation. Resorption outpaces formation, the cortex thins, the trabeculae are destroyed and the bone loses its structural integrity.

The osteoblastic response. Some tumours (prostate, breast) stimulate osteoblast activity and produce mixed lesions. The new bone is disorganised, mechanically inferior woven bone without lamellar structure: more of it, but of poorer quality, and still prone to fracture under physiological loads.

The metastatic cascade. Destruction and tumour growth feed each other in sequence:

1. Tumour cells preferentially metastasise to red marrow-rich areas
2. Adhesion molecules facilitate colonisation of bone
3. A tumour microenvironment is established
4. A "vicious cycle" of bone destruction and tumour growth sets in
5. Cytokines (IL-6, PTHrP) amplify osteoclast activity
6. Structural compromise progresses

Primary bone tumours. Tumour replaces normal bone directly, and its expansion thins the cortex, though periosteal reaction may add some strength. Pathologic fracture occurs through the lesion in 5-10% of osteosarcomas and significantly worsens the prognosis through local contamination.

This understanding guides the timing of adjuvant therapy, and explains why radiotherapy or systemic therapy alone rarely prevents fracture once critical bone loss has occurred.

Osteoporosis. Resorption outpaces formation, with loss of trabecular connectivity, cortical thinning and porosity, microarchitectural deterioration and reduced bone mineral density. Fractures occur with minimal trauma: these are insufficiency fractures.

Osteomalacia. Mineralisation is defective, from vitamin D deficiency or resistance, so unmineralised osteoid accumulates and the bone loses stiffness and strength. Looser zones (pseudofractures) appear in stress regions, and true fractures occur through the weakened bone.

Hyperparathyroidism. Excessive PTH stimulates osteoclasts and produces focal osteolysis with haemorrhage; haemosiderin deposition gives the brown tumour its name. These cystic lesions weaken the bone, can mimic primary bone tumours, and fracture.

Paget's disease. Excessive turnover, both resorption and formation, lays down a disorganised mosaic pattern of lamellar bone, so the bones are enlarged but mechanically weak, with increased fracture risk in both the lytic and sclerotic phases. The bone has a chalky consistency that makes fixation difficult, and carries a 1% risk of sarcomatous transformation.

The metabolic aetiology determines the treatment: addressing the underlying disorder may prevent further fractures, but healing through pathologic bone remains challenging.

Stress concentration. A focal lesion that creates a cortical defect concentrates stress at its edges, according to the stress concentration factor Kt = 1 + 2(a/b), where a is the defect depth and b the defect width. A circular hole creates a threefold stress concentration and an elongated defect an even higher one, which explains why lytic lesions fracture more readily than blastic lesions.

Critical defect size. Loss of cortical continuity sets the risk:

• Less than 25% cortical involvement: generally stable
• 25-50%: intermediate risk, depending on location and loading
• Over 50%: high fracture risk
• Over 75%: impending fracture imminent

Bending. The femur experiences primarily bending moments during gait, which puts the lateral cortex in tension, the highest-risk region, and the medial cortex in compression, which is more tolerant of defects. The subtrochanteric region has the highest bending moments, which is why subtrochanteric lesions score highest in Mirels.

Torsion. Torsional strength relates to the polar moment of inertia, J, which for a hollow cylinder is J = π(R⁴ - r⁴)/2. Cortical destruction therefore dramatically reduces torsional resistance: a 50% cortical defect reduces torsional strength by more than 60%.

Stiffness. The elastic modulus falls as tumour takes over:

• Normal cortical bone: 17-20 GPa
• Tumour-infiltrated bone: 5-10 GPa
• Pathologic fracture healing, if it occurs: 2-5 GPa

The reinforcement required therefore exceeds that of normal fracture fixation. These principles guide implant selection: the construct must compensate for the complete loss of the bone's contribution to load-bearing.

Views. AP and lateral radiographs of the affected bone, including the joints above and below, with the contralateral limb for comparison and additional obliques if needed to characterise the lesion.

Features of a pathologic fracture. Look for:

• A lytic or sclerotic lesion at the fracture site
• Cortical destruction or erosion
• Pathological periosteal reaction
• A soft-tissue mass
• Bone expansion
• Matrix mineralisation
• Geographic, moth-eaten or permeative destruction

Characterising the lesion. The Lodwick classification grades the pattern of destruction:

A narrow zone of transition means a slow-growing lesion and a wide one an aggressive lesion, and a cortical breach suggests malignancy. Note the periosteal reaction (onion-skin, sunburst, Codman triangle), any soft-tissue component, and the matrix: rings and arcs for chondroid, cloud-like for osteoid.

Skeletal survey. Indicated when myeloma is suspected, in the metastatic work-up, for assessing metabolic bone disease, and in polyostotic fibrous dysplasia. It identifies synchronous lesions that affect prognosis and may reveal the primary tumour site. The standard views:

• Skull: AP and lateral
• Spine: AP and lateral cervical, thoracic and lumbar
• Pelvis: AP
• Chest: PA and lateral
• Both humeri and femora: AP
• Hands, if myeloma is suspected

CT. CT gives superior cortical bone detail: it assesses cortical destruction, identifies a cortical breach not visible on radiographs, and characterises periosteal reaction and matrix mineralisation. It is used for surgical planning (implant sizing, 3D reconstruction), to guide the biopsy trajectory and in the complex anatomy of pelvic and spinal lesions, and CT chest looks for lung metastases.

Its limitations are radiation exposure, beam-hardening artefact from metal, poor soft-tissue contrast, and missing lesions confined to the bone marrow.

MRI. MRI is preferred for soft-tissue extent, marrow involvement (oedema, tumour), the relationship to neurovascular structures, skip lesions, spinal cord compression and joint involvement. The sequences:

• T1-weighted: anatomical detail and marrow fat
• T2-weighted: oedema and tumour, which are bright
• STIR: sensitive to marrow oedema
• T1 with gadolinium: tumour vascularity and enhancement pattern

Whole-body MRI is an emerging technique for the metastatic survey. It detects marrow involvement before cortical destruction, has a higher sensitivity than bone scan for many tumours, and is useful in myeloma staging.

Bone scintigraphy. Tc-99m MDP identifies metabolically active bone lesions as "hot spots" of increased turnover, surveying the whole body in a single study. Sensitivity is high (90%) but specificity low. It is useful for metastatic screening.

PET-CT. 18F-FDG PET-CT shows metabolically active, glucose-avid tumours and combines anatomical with metabolic information; it is superior to bone scan for many malignancies. It guides biopsy to the most active areas and monitors treatment response, but not all tumours are FDG-avid, and infection and fracture give false positives.

Choose by the clinical question: CT for bone detail and surgical planning, MRI for soft tissue and marrow, nuclear medicine for the systemic survey.

Finding the primary. For suspected metastatic disease:

• CT chest, abdomen and pelvis: lung, renal, gastrointestinal and retroperitoneal primaries
• Mammography: breast cancer
• PSA: prostate, if appropriate
• Thyroid ultrasound, if the history or examination suggests it
• Urinalysis: haematuria from renal cell carcinoma

Laboratory studies. These look for myeloma, metabolic bone disease and metastatic burden:

• Full blood count (anaemia, myeloma, leukaemia)
• Comprehensive metabolic panel (renal function, calcium)
• Liver function tests (metastatic burden)
• Alkaline phosphatase (bone turnover)
• Serum protein electrophoresis with immunofixation (myeloma)
• Urine protein electrophoresis (Bence-Jones protein)
• PTH and vitamin D (metabolic bone disease)
• TSH (thyroid disorders)

Suspected primary bone tumour. When the radiographs suggest a primary sarcoma, stage with chest CT for pulmonary metastases, MRI of the entire bone for extent and skip lesions, and a bone scan or PET-CT for distant bone metastases. ALP and LDH are prognostic in osteosarcoma.

Unknown primary. When the fracture occurs and the primary tumour is unknown, in 10-15% of cases, the sequence is:

1. Complete imaging staging (CT chest, abdomen and pelvis; PET-CT)
2. Basic laboratory work-up
3. Biopsy of an accessible lesion
4. MDT discussion
5. Stabilisation may proceed while the work-up continues
6. Histology often guides further investigation
7. Some primaries are never identified (occult tumour, patient death)

The examiner's question. "Before you operate on any pathologic fracture, convince me you know the diagnosis. What is your systematic approach to identifying the underlying pathology? When is it safe to stabilise first and biopsy later versus mandatory to establish diagnosis before instrumentation?" A structured answer runs:

1. Clinical assessment (age, history, presentation)
2. Imaging characterisation, radiographs first
3. Staging investigations (identify the primary and systemic involvement)
4. Biopsy strategy: when, where, how
5. MDT discussion (oncology, radiation oncology, radiology)
6. A definitive treatment plan: stabilisation and definitive management

The sequence balances the urgency of managing the fracture against the need for a diagnosis to guide definitive treatment and prognosis.

When biopsy is mandatory. Before any treatment:

• Suspected primary bone tumour
• A solitary bone lesion without a known primary
• Indeterminate radiographic features
• A young patient, in whom sarcoma is more likely than metastasis
• A lesion inconsistent with the known primary tumour

Before instrumentation, biopsy is also needed if there is any possibility of primary sarcoma, if infection cannot be excluded clinically, for a benign aggressive lesion that needs intralesional treatment, and for legal and documentation purposes (a tissue diagnosis).

Timing relative to stabilisation. Which comes first depends on the fracture, the patient and how certain the diagnosis is:

When stabilisation comes first, the biopsy can be taken through or adjacent to the incision. The decision balances diagnostic necessity against clinical urgency, with multidisciplinary input whenever possible.

Core needle biopsy is preferred. It is minimally invasive, can be done under local anaesthesia, has a complication rate under 1%, leaves a smaller contamination zone, and gives adequate tissue for diagnosis in 80-90%. Its weaknesses are sampling error from a small sample, possible crush artefact, too little tissue to subtype some tumours, and the need for an experienced pathologist. The technique:

• Image guidance, CT or fluoroscopy
• A direct approach that does not transgress neurovascular structures, avoiding the joint, the neurovascular bundle and major muscle groups
• A longitudinal track in line with the definitive incision
• Multiple cores (3-5 samples)
• Fresh tissue for cytogenetics, and for culture if infection is considered

Open biopsy is used when a core biopsy is inadequate or non-diagnostic, when tissue is needed for special studies, for a primary bone tumour that needs a generous sample, and when biopsy is taken at the time of stabilisation. The principles:

• The smallest possible incision, placed longitudinally in line with the definitive resection
• An extensile approach if resection is possible at the same sitting
• Meticulous haemostasis, because haematoma spreads contamination
• Watertight closure
• Mark the biopsy tract with a suture or clip
• Avoid drains, which create a contaminated tract

Choosing the site. Take the extraosseous component if there is one, which is easier and safer, and avoid critical structures. In the anterior thigh, stay away from the medial side (femoral vessels) and the posterior side (sciatic nerve); an anterolateral approach is generally safe.

When biopsy goes wrong. Poor technique contaminates adjacent compartments, which worsens prognosis, and risks neurovascular injury, propagation of a pathologic fracture, haematoma formation and spread, infection and non-diagnostic tissue.

Stabilising without prior biopsy. Four clinical scenarios permit it:

1. Known widely metastatic disease. An established metastatic cancer with multiple skeletal metastases and a lesion consistent with the known primary leaves an extremely low probability of an alternative diagnosis; biopsy at the time of stabilisation or after.
2. Life- or limb-threatening emergency. A pathologic fracture with neurovascular compromise, impending cord compression requiring immediate decompression, or massive haemorrhage from a vascular tumour; the biopsy is performed during the stabilisation.
3. Obvious benign lesion. A classic radiographic appearance (a unicameral bone cyst, for example) in a young patient at a characteristic location, which can be managed intralesionally with a low risk of misdiagnosing malignancy.
4. Damage control. A polytrauma patient or medical instability, where stabilisation is temporary only and definitive treatment follows once the diagnosis is established.

Medicolegal considerations. Proceeding without a tissue diagnosis requires clear documentation of the clinical reasoning, MDT discussion when feasible, an informed consent discussion with the patient, tissue obtained at surgery when safe, and a low threshold for intraoperative frozen section if there is doubt.

The "never operate without biopsy" rule has appropriate exceptions, but they should be conscious decisions with clear justification rather than oversights.

Observing an impending fracture. Non-operative treatment is reasonable when:

• The Mirels score is 7 or less (low risk)
• The patient is non-ambulatory or non-weight-bearing
• Life expectancy is very limited (weeks)
• Medical comorbidities prohibit surgery
• The patient prefers it after an informed discussion
• The lesion is in the upper limb, where biomechanical demand is lower

Monitor with serial radiographs at 4-6-week intervals, assessing pain, functional status and signs of progression, with a low threshold for surgery if anything changes.

A completed fracture without surgery. This is rarely appropriate. It is considered for a minimally displaced upper limb fracture in acceptable alignment for the patient's functional demands, a prognosis measured in weeks (hospice), medical contraindications to anaesthesia, or a patient who declines surgery.

Care then consists of multimodal analgesia, often requiring opioids; immobilisation with a splint, brace or protected weight-bearing; nursing care (skin, DVT prophylaxis, bowel and bladder); palliative care involvement; counselling the family about expectations; and a focus on quality of life.

What it costs. Non-operative treatment risks persistent, often severe, pain and the complications of immobility (pneumonia, DVT, deconditioning). It also risks nonunion, because healing through tumour is unlikely, progressive deformity, contractures and pressure sores, reduced independence and quality of life, and psychological harm (helplessness, depression).

Shared decision-making is essential, with a realistic discussion of both the surgical and the non-surgical trajectory.

As primary treatment. Radiotherapy is a primary treatment for impending fractures in these situations:

• Radiosensitive tumours (myeloma, lymphoma, small cell lung)
• Small lesions (under 2-3 cm)
• A Mirels score of 6-7
• Pain control as the primary goal

It reduces the risk of progression by promoting sclerosis.

What it achieves. The expected results:

• Pain relief in 60-80% of patients
• Time to effect: typically 2-4 weeks
• Lesion stabilisation: 30-50% show sclerosis
• Fracture prevention: a modest effect, not reliable for high-risk lesions

Its limits. Bone is temporarily weakened during the first 2-4 weeks (osteoclast activation), and radiotherapy does not restore lost bone immediately, so fracture can occur during or after treatment. Subsequent fixation is more difficult because healing is compromised, and wound complications increase if surgery follows radiotherapy.

After stabilisation. Adjuvant radiotherapy is given for radiosensitive tumour types, to reduce the risk of local progression, to improve bone healing around the implant and to palliate pain. It is typically started 2-3 weeks after surgery, to allow wound healing; it can be delayed if adjuvant chemotherapy takes priority, and is coordinated with the oncology team.

Dose. The regimens in use:

• Palliative regimens: 8 Gy single fraction or 20 Gy in 5 fractions
• Definitive regimens: 30-40 Gy in multiple fractions
• Stereotactic body radiotherapy (SBRT): emerging for oligometastatic disease

Effects on healing. Radiotherapy impairs osteoblast function, reduces angiogenesis, increases the risk of infection and delays fracture healing, and may lead to radiation-induced fractures years later. It is a useful adjunct but rarely sufficient as the sole treatment of a high-risk impending or a completed pathologic fracture.

Bisphosphonates. They inhibit osteoclast-mediated bone resorption and reduce skeletal-related events (fracture, pain, hypercalcaemia), and reduce fracture risk by 30-40% in metastatic disease. Zoledronic acid is the most commonly used (4 mg IV monthly); watch renal function and the risk of osteonecrosis of the jaw.

Denosumab. A RANKL inhibitor that blocks osteoclast activation, given as 120 mg subcutaneously monthly. It is superior to bisphosphonates for fracture prevention and particularly effective in breast cancer and myeloma; the risks are hypocalcaemia, ONJ and rebound hypercalcaemia if it is stopped.

Tumour-directed therapy. Treating the tumour itself takes three forms:

• Chemotherapy is tumour-specific: bortezomib, lenalidomide and dexamethasone for myeloma, and hormonal or chemotherapy for breast cancer according to receptor status. It reduces tumour burden and promotes healing, and its timing around surgery is individualised because of infection risk.
• Hormonal therapy (tamoxifen or aromatase inhibitors for breast cancer, androgen deprivation for prostate cancer) can produce dramatic responses with bone sclerosis, but takes months to act and is not a means of preventing an acute fracture.
• Targeted therapy acts on tumour-specific molecular targets, such as tyrosine kinase inhibitors for renal cell carcinoma and radioactive iodine for differentiated thyroid cancer, with variable skeletal efficacy.

Metabolic bone disease. Treatment is vitamin D and calcium supplementation, teriparatide (anabolic) for severe osteoporosis, bisphosphonates or denosumab for osteoporosis, and treatment of the underlying endocrinopathy (hyperparathyroidism, hyperthyroidism).

Where it fits. Systemic therapy complements but does not replace surgical stabilisation of a high-risk lesion. Surgery provides immediate stability, systemic therapy addresses the underlying disease and radiotherapy provides local control; the multimodal approach improves both function and survival.

Core principles. Six concepts shape the construct:

1. Stabilise the entire bone (nail versus plate length)
2. Bypass the lesion by at least 2 cortical diameters
3. Augment with cement when possible
4. Make the fixation durable enough to outlive the patient's prognosis
5. Restore weight-bearing early, for quality of life
6. A single operation if possible, to reduce morbidity

Prognosis first. The Katagiri score predicts survival in skeletal metastases from the primary tumour site, visceral or cerebral metastases, performance status, previous chemotherapy, multiple skeletal metastases and abnormal laboratory data. Expected survival then sets the construct:

The goal is to match surgical invasiveness and construct durability to a realistic prognosis, avoiding both under- and over-treatment.

Intramedullary nailing. The load-sharing nail is preferred over the load-bearing plate. It prophylactically stabilises the entire bone against skip lesions, does not depend on healing, is inserted closed with little soft-tissue trauma and allows early full weight-bearing. It does not preclude radiotherapy, and allows better delivery of it than a plate. The technique is modified for tumour:

• Lock proximally and distally, prophylactically, to prevent fracture through other lesions
• Consider cement augmentation of the proximal screws for enhanced fixation
• Ream aggressively, which removes tumour and allows a larger nail
• Capture the fracture site with multiple interlocking screws
• Consider exchange nailing to a larger diameter

Cement with a nail. Cement is injected through drill holes before the screws are inserted. It improves screw purchase in osteoporotic or tumour-involved bone and enhances rotational stability, at the risk of extravasation into the fracture site or soft tissues; its thermal necrosis is beneficial as tumour kill but can harm normal bone.

Plate fixation. The plate is preferred for periarticular metaphyseal lesions, when the lesion is to be curetted and grafted directly, where the anatomy is unsuitable for a nail (proximal humerus, distal radius), and in the upper limb, where lower loads tolerate plate biomechanics. The construct:

• Locking plates, for angular stability and better hold in osteoporotic bone
• Span the lesion by at least 3-4 screw holes on each side
• Unicortical screws through the lesion are acceptable if the proximal and distal screws are bicortical
• Consider double plating (90-90) for large defects
• Cement augmentation dramatically improves the construct

PMMA augmentation. Polymethylmethacrylate gives immediate mechanical support, hardening in minutes, and its exothermic reaction reaches 70-80°C, causing thermal tumour necrosis. It improves screw purchase in weak bone, fills the void after curettage, and is radiographically visible, so loosening can be monitored. The steps:

1. Curettage of the tumour (intralesional excision)
2. A high-speed burr to create margins
3. Pulse lavage
4. Pack the cavity with cement in the doughy phase
5. Insert the screws or nail before it hardens completely
6. Avoid extravasation into the joint or neurovascular structures

Beyond the leakage, thermal and embolic complications described under Complications, cement prevents MRI follow-up and is difficult to revise if the construct fails.

Endoprosthetic replacement. Indicated for:

• Periarticular lesions with joint involvement
• Massive, unreconstructable bone destruction
• Failed previous fixation
• Expected survival over 1 year
• Acetabular metastases (Harrington classification III-IV)

Proximal femur. A modular tumour prosthesis with a cemented stem, long enough to bypass diaphyseal lesions, with calcar replacement if the subtrochanteric region is involved. Reconstruction of the abductor mechanism is crucial for gait. The complications are dislocation (15-20%), infection (5-10%) and aseptic loosening.

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Proximal humerus. Reverse shoulder arthroplasty is used because the rotator cuff is often non-functional, and a standard stemmed hemiarthroplasty if the cuff is intact. Tuberosity reattachment is challenging (cement augmentation). The functional goals are pain relief and hand-to-mouth function; active elevation is limited without a cuff.

Distal femur. A hinged or rotating-hinge total knee prosthesis, with long stems and augments for massive bone loss, preservation or reconstruction of the extensor mechanism, and early range of motion to prevent stiffness. It has a higher failure rate than proximal femoral reconstruction because the stresses are greater.

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Allograft-prosthetic composite. A structural allograft provides bone stock, a prosthetic stem is inserted through it, the host bone-allograft junction is fixed with a plate, and tendons can be reattached to the allograft. The advantages are bone stock restoration, soft-tissue reattachment sites and the potential for biological fixation. The disadvantages:

• Allograft availability and cost
• Fracture (20-30%)
• Nonunion at the host-graft junction (15-25%)
• Infection (10-15%)
• Prolonged protected weight-bearing

In metastatic disease it is generally reserved for younger patients in whom longer survival is expected, for pathologic fractures through a previous allograft, and for revision of a failed endoprosthesis.

Resection without reconstruction. Rarely indicated: the fibula, which is usually tolerated (the peroneal nerve must be preserved at the proximal fibula), limited rib resections and non-weight-bearing areas. It is generally avoided because of major functional compromise, limb-length discrepancy, instability and poor patient acceptance.

Amputation. The indications in pathologic fracture:

• Uncontrolled pain despite attempts at reconstruction
• Fungating tumour with ulceration or bleeding
• Unsalvageable neurovascular compromise
• Life-threatening sepsis in the setting of tumour
• Patient preference (rare)

Palliative amputation has a significant psychological impact, prosthetic rehabilitation is often poor in the metastatic population, and it offers no survival benefit because it does not affect the systemic disease. Wheelchair mobility may exceed prosthetic ambulation. Consider it only when the limb has become a non-functional liability.

The choice of reconstruction balances functional restoration, durability, surgical morbidity and a realistic prognosis, through multidisciplinary discussion.

Haemorrhage. The risk comes from hypervascular tumours (renal cell, thyroid), large lesions with soft-tissue extension, coagulopathy (liver metastases, chemotherapy) and vascular injury during the approach. Prevent it with preoperative embolisation of hypervascular lesions, crossmatched blood, a cell saver if the tumour burden is low, meticulous haemostasis, and a tourniquet considered for extremity lesions.

Control bleeding with direct pressure and packing, bipolar or monopolar cautery, bone wax for cortical bleeding, and gelfoam or other haemostatic agents. Massive haemorrhage calls for damage control: pack, stabilise temporarily and resuscitate in ICU.

Cement extravasation. Cement can penetrate the joint (arthrotomy, synovitis), compress neurovascular structures (nerve palsy, vascular injury) or extrude into the soft tissues (wound complications). Prevent it with careful attention to cement viscosity and fluoroscopic monitoring.

Thermal injury. Excessive necrosis of normal bone raises the risk of fracture, extruded cement can burn the skin, and heat conduction can injure nerves. Irrigate during polymerisation and minimise contact with the soft tissues.

Fracture propagation. Iatrogenic fracture can occur during reduction manoeuvres, reaming for an intramedullary nail, or implant insertion in difficult anatomy. Prevent it with gentle technique and image guidance, and consider prophylactic cerclage wires.

Neurovascular injury. Direct injury during the approach (anatomy altered by tumour), compression by cement or haematoma, and ischaemia from prolonged tourniquet or retraction. Prevention is careful dissection, frequent neurovascular checks and appropriate retraction.

Anticipation and prevention matter most, because intraoperative complications in oncological surgery often have limited salvage options.

Wound complications. Prior radiotherapy, malnutrition (cancer cachexia), immunosuppression (chemotherapy, steroids), hypoalbuminaemia and previous surgery or biopsy are the risk factors. The problems are dehiscence (5-10% in irradiated fields), haematoma (higher risk with tumour vascularity), infection and skin necrosis from a poor soft-tissue envelope.

Prevention means minimising tension on the closure, considering plastic surgery involvement (flap coverage), preoperative nutritional optimisation, and delaying radiotherapy after surgery as described above. Drains are controversial here: a contamination tract against the prevention of haematoma.

Infection. Infection complicates 5-15% of pathologic fracture surgery. It is more likely with immunosuppression (chemotherapy), malnutrition, concurrent radiotherapy, a large tumour burden and cement use (biofilm formation). Staphylococcus aureus is the most common organism, Gram-negative bacilli appear in the immunosuppressed, and polymicrobial infection follows an open fracture or poor soft tissues.

Management is difficult. The challenges are a limited life expectancy (a palliative approach), chemotherapy interruption if systemic treatment is needed, implant removal that is often not feasible because of fracture instability, long-term suppressive antibiotics, and balancing infection treatment against cancer treatment priorities.

Thromboembolism. Malignancy (a hypercoagulable state), immobility, pelvic or lower limb surgery and some prothrombotic chemotherapy agents raise the risk. Prevention combines chemical prophylaxis (LMWH, apixaban), mechanical prophylaxis (SCDs), early mobilisation and extended prophylaxis for 4-6 weeks.

Treat DVT or PE with therapeutic anticoagulation, and consider an IVC filter if anticoagulation is contraindicated; metastatic disease in the brain or liver carries a risk of bleeding.

Persistent pain. The causes are incomplete stabilisation, tumour progression, nerve injury or compression, the implant itself (prominence, soft-tissue irritation), referred pain from spinal metastases and a psychological component (anxiety, depression). Management:

• Multimodal analgesia
• Adjuvant radiotherapy if the tumour is progressing
• Revision surgery for mechanical failure
• Neuropathic pain medication
• Palliative care or pain team involvement
• Attention to psychological needs

The postoperative period needs close monitoring and a low threshold for intervention, balanced against the priorities of cancer treatment.

Mechanical failure. Implant breakage occurs in 5-15% at 1 year. The risk factors are under-fixation, disease progression, long survival and inadequate bypass of the lesion, and load-bearing constructs (plates) carry a higher risk than load-sharing ones (nails). Progressive deformity presents as loss of reduction, varus or valgus collapse, subsidence into osteoporotic bone and cement fragmentation. Loosening shows as screws backing out (inadequate purchase), failure of the cement-bone interface and progressive osteolysis.

Nonunion is expected. Tumour precludes normal fracture healing, radiotherapy impairs osteoblast function, chemotherapy delays healing, and metabolic abnormalities such as hypercalcaemia add to it. Healing is therefore neither expected nor required: the construct must provide stability without biological incorporation, and cement provides immediate, permanent stability. "Union" may occur at the periphery of the lesion.

Revision. The indications are painful implant failure, progressive deformity affecting function, nonunion with implant failure (a rare indication) and survival that exceeds the durability of the original construct. The options are exchange to a larger or longer nail, conversion of a plate to an endoprosthesis, cement augmentation of the existing construct, and allograft or bone graft where there is healing potential.

Revision is contraindicated by very limited life expectancy (weeks to months), prohibitive medical comorbidity, infection (suppression rather than reconstruction), disseminated disease progression and the patient's preference.

Local disease progression. Tumour growth despite initial treatment, new lesions in the same bone (skip metastases), increasing soft-tissue extension and pathologic fracture through adjacent bone. The responses:

• Adjuvant radiotherapy if not previously given
• Optimisation of systemic therapy
• Extended fixation (a longer nail, additional plates)
• Conversion to an endoprosthesis
• Amputation, very rarely, as salvage only

The natural history of pathologic fractures includes high rates of mechanical complications, so constructs are designed for durability rather than for dependence on biological healing.

Primary tumour type is the most important factor:

Burden of disease. A solitary skeletal metastasis carries a better prognosis and multiple skeletal sites an intermediate one. Visceral metastases mean a poor prognosis, and spinal cord compression brings worse outcomes.

Performance status. Ambulatory, independent patients have better survival and quality of life, those who need assistance sit in between, and bedridden patients have a poor prognosis and limited benefit from surgery.

Laboratory markers. A raised alkaline phosphatase indicates a worse prognosis, anaemia is associated with reduced survival, hypoalbuminaemia reflects malnutrition and poor outcomes, and hypercalcaemia reflects advanced disease and is a poor prognostic sign.

Lower limb. 75-85% regain ambulatory status, and the median time to weight-bearing is 3-7 days. Walking may not return to its previous level, walking aids are often required, and systemic disease progression limits rehabilitation.

Upper limb. More than 90% achieve functional use. The return to activities of daily living is earlier, pain relief more consistent and overall satisfaction better.

What surgery gives. Pain reduction is the most consistent benefit. It also brings independence in activities of daily living, a psychological sense of control, reduced caregiver burden, the ability to receive oncological treatment, and hospice care at home rather than in hospital.

What limits recovery. Disease progression (new metastases, visceral involvement), complications (infection, nonunion, implant failure), deconditioning, the side effects of chemotherapy, depression and anxiety, and inadequate social support.

Reading the table. Surgery does not prolong survival, because the systemic disease determines longevity, but it dramatically improves quality of life. The functional outcomes justify the surgical morbidity in appropriate candidates, and patient selection is critical: avoid surgery in the moribund. The goals are palliation, function and independence, not cure.

The evidence supports surgical stabilisation for functional restoration and quality of life even when the prognosis is limited, provided the patient is medically fit for anaesthesia.

The Harrington classification of acetabular metastases grades the defect and points to the reconstruction:

Fixation or arthroplasty. The decision depends on:

1. The class of acetabular involvement
2. Whether there is a femoral head or neck lesion
3. Expected survival (over 6 months for THA)
4. The patient's ambulatory status and goals
5. The severity of hip pain

For an isolated periacetabular lesion without articular involvement, percutaneous screw fixation with cement augmentation may suffice.

Non-operative management. Suited to lesions in non-weight-bearing areas (iliac wing, sacrum), non-ambulatory patients, very limited life expectancy and medical contraindications. The adjuvants are radiotherapy for pain control, systemic therapy, and interventional radiology (embolisation, ablation).

Percutaneous stabilisation. Fluoroscopic or CT-guided screws with cement augmentation (a cementoplasty or vertebroplasty technique), for limited periacetabular lesions and poor surgical candidates. Pain improves in 60-80%; the procedure is minimally invasive with a quick recovery, and may delay the need for arthroplasty.

Acetabular reconstruction. The historical Harrington technique passed Steinmann pins across the ilium into the ischium, laid a cement mantle over them and cemented a cup into it; loosening rates were high and it has been largely abandoned. Modern techniques are cup-cage constructs for structural support, custom (patient-specific) triflange implants, augments and jumbo cups, and cement with mesh for Class II defects.

Saddle prosthesis. A salvage procedure for massive pelvic destruction where reconstruction is not feasible. The prosthesis "saddles" the remaining ilium on a long femoral stem, with no acetabular fixation, and so provides stability without acetabular reconstruction. Pain relief is generally good, limb-length discrepancy is common and the dislocation risk moderate; it provides palliation when other options are exhausted.

Pelvic lesions are some of the most challenging reconstructions in oncological orthopaedics, and often require subspecialty expertise and custom implants.