Pathological fracture

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Tumour weakens bone by stimulating osteoclast resorption, replacing normal marrow and cortex or, less often, producing disorganised osteoblastic bone. Load-bearing structures then fail under ordinary force. Metastatic breast, prostate, lung, renal and thyroid cancers and myeloma are common causes; primary bone tumours and severe osteoporosis, Paget disease or osteomalacia remain important alternatives.

Impending fracture is the opportunity to prevent catastrophe. Ask about focal pain at rest and during weight bearing, analgesic escalation, limping, difficulty transferring and a sudden change in independence. Functional pain in a femur or humerus with substantial cortical destruction is concerning even before a visible fracture line. Do not ask the person to demonstrate walking when failure is plausible.

At presentation, support the limb in its found position, give prompt analgesia and document distal pulse, colour, temperature, capillary refill, power and sensation. Look for open skin, bleeding, compartment tension and signs of spinal or pelvic injury. Check the mechanism because a seemingly minor fall may also cause head injury or an ordinary osteoporotic fracture that still requires treatment.

Radiograph the whole bone in two planes and include the joints above and below. Imaging should describe lesion site, lytic or blastic character, cortical involvement, fracture pattern and other lesions. CT helps plan fixation and assess the pelvis; MRI defines marrow, soft tissue and neural relation. Bone scan, PET-CT or staging CT assesses burden according to tumour type; local structural imaging remains necessary.

Diagnosis must precede definitive reconstruction when the lesion is uncertain. Review prior histology and whether imaging fits the known cancer. A solitary lesion, atypical pattern or no cancer diagnosis may represent a primary sarcoma or infection. Biopsy should be planned by the team that would perform definitive tumour surgery, with the tract placed so it can later be excised.

Surgical planning balances expected survival, bone healing potential, anatomical load and the patient's goal. Metastatic fractures often do not unite normally, so constructs should work immediately and last for the person's lifetime. Intramedullary fixation may span the whole bone; joint-destroying or proximal lesions may need endoprosthetic replacement. Embolisation can reduce bleeding from highly vascular renal or thyroid metastases.

Postoperative or primary palliative radiotherapy reduces local pain and progression, but an unstable completed long-bone fracture usually needs mechanical assessment before radiation alone. Antiresorptive treatment reduces later skeletal-related events in selected cancers. Rehabilitation should start early with explicit permitted weight bearing, transfer technique, thrombosis and pressure prevention and equipment for home.

For a person in the last days, transfer and major surgery may offer no meaningful recovery. This does not make the fracture untreatable: use a comfortable splint or positioning plan, pre-empt movement pain, provide personal-care instructions, prevent pressure damage and discuss whether sedation for otherwise intolerable movement is acceptable.

Key points

A pathological fracture occurs through bone weakened by metastasis, myeloma, primary tumour, osteoporosis or another metabolic lesion, sometimes after minimal or no trauma.
New focal weight-bearing pain, night pain, functional decline or pain despite analgesia can signal an impending fracture before displacement occurs.
Sudden pain, deformity, inability to use the limb, shortening or crepitus requires immediate immobilisation, neurovascular assessment, analgesia and orthopaedic review.
First-line imaging is two-view plain radiography including the entire affected bone and adjacent joints; image before forcing movement or weight bearing.
CT defines cortical destruction and fixation anatomy, while MRI best shows marrow and soft-tissue extension; staging imaging establishes whether disease is solitary or widespread.
A solitary destructive lesion without secure cancer diagnosis needs orthopaedic-oncology planning before biopsy, because an incorrectly placed tract can compromise definitive surgery.
Mirels scoring supports assessment of impending long-bone fracture, but progressive functional pain and specialist judgement matter more than a threshold used in isolation.
Prophylactic stabilisation of a high-risk lesion is generally safer and restores function more predictably than operating after a displaced fracture.
Fixation or endoprosthetic replacement is followed by oncology review and often radiotherapy; bisphosphonate or denosumab reduces future skeletal events but does not repair an acute break.
When surgery is unlikely to benefit, provide stable positioning, pressure care, rapid analgesic access, practical transfer planning and an honest discussion of expected mobility.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Osteolytic metastasis

Breast, lung, renal, thyroid and other tumours activate osteoclasts, destroy cortex and reduce the load required for structural failure.

Myeloma bone disease

Plasma-cell cytokines increase focal resorption and suppress repair, producing punched-out lesions, vertebral collapse and long-bone fracture.

Primary skeletal tumour

Sarcoma or other primary bone neoplasm can first present with pain or fracture and requires protected biopsy planning.

Metabolic fragility

Osteoporosis, osteomalacia, Paget disease and treatment-related bone loss can cause fragility fracture alongside or independent of cancer.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Cortical load loss
Tumour replaces and erodes cortical bone, reducing cross-sectional strength and allowing ordinary bending or torsion to propagate a crack.
2
Trabecular disruption
Marrow infiltration removes internal load-sharing architecture, particularly in vertebrae, pelvis and the ends of long bones.
3
Abnormal remodelling
Osteoclast and osteoblast signalling becomes uncoupled, producing either destructive lysis or dense but mechanically poor tumour-associated bone.
4
Impaired union
Persistent tumour, radiotherapy, malnutrition and systemic treatment limit healing, so fixation must not rely on ordinary fracture biology.
5
Pain sensitisation
Periosteal stretch, microfracture, inflammatory mediators and muscle spasm create rest pain and severe incident pain during loading or care.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Impending long-bone failure

Increasing focal pain with loading, analgesic escalation, limp or transfer difficulty over a destructive lesion suggests high fracture risk.

Completed fracture

Sudden severe pain, loss of function, deformity, shortening, abnormal rotation or crepitus after minimal force indicates structural failure.

Axial fracture

New vertebral or pelvic pain, height loss, inability to sit or neurological symptoms may reflect collapse in load-bearing axial bone.

Aggressive solitary lesion

Progressive night pain, swelling, soft-tissue mass and a destructive radiographic pattern without established metastasis raises primary bone tumour.

Vascular metastasis

Renal and thyroid deposits can be highly vascular, increasing operative blood loss and making preoperative embolisation relevant.

Threatened limb or compartmentRed flag

Absent pulse, increasing tense swelling, pain on passive stretch, pallor or progressive sensory and motor loss requires immediate orthopaedic and vascular action.

Red flags requiring action

A pulseless, pale or cold limb or progressive motor and sensory loss indicates neurovascular compromise.
Pain out of proportion, tense swelling or pain on passive stretch suggests compartment syndrome.
An open wound over a fracture risks contamination and tumour or bone exposure and needs emergency care.
Pelvic fracture with hypotension, abdominal distension or falling haemoglobin may conceal life-threatening haemorrhage.
Back pain with weakness, sensory change or sphincter dysfunction moves immediately to the MSCC pathway.
A solitary aggressive lesion must not undergo unplanned biopsy or fixation before bone-tumour specialist review.
New weight-bearing pain in known metastasis can be an impending fracture even when the initial radiograph shows no complete break.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line whole-bone radiographsFirst stepFirst line
Why
Obtain orthogonal views of the entire affected bone including both adjacent joints without unsafe loading or manipulation.
Interpretation and limitations
Fracture line, lesion character, cortical loss and additional lesions guide protection and urgent orthopaedic planning.
02
CT for structural anatomy
Why
Define cortical destruction, joint involvement, complex pelvis or vertebral anatomy and dimensions for fixation or replacement.
Interpretation and limitations
CT is the reference map for bone hardware planning but cannot characterise every marrow or neural abnormality.
03
MRI for marrow and soft tissue
Why
Assess intramedullary extent, soft-tissue mass, neurovascular relation and occult fracture when radiography is inconclusive.
Interpretation and limitations
MRI best defines local tumour extent and is essential when spinal canal or a primary bone tumour is suspected.
04
Staging imaging
Why
Use CT, bone scintigraphy or tumour-appropriate PET to identify systemic disease and other weight-bearing lesions.
Interpretation and limitations
Widespread versus solitary disease changes biopsy, reconstruction, oncology and prognosis decisions; dedicated local imaging is still required.
05
Mirels-supported risk assessment
Why
Combine site, pain, lesion nature and size for long-bone metastasis with functional pain, cortical involvement and specialist judgement.
Interpretation and limitations
A score around 9 or more supports prophylactic-fixation referral, but the score is not a stand-alone diagnostic or treatment threshold.
06
Planned histological diagnosis
Why
Biopsy a solitary or atypical destructive lesion after orthopaedic-oncology imaging and tract planning.
Interpretation and limitations
Histology is the diagnostic gold standard when identity is uncertain; an unplanned tract can contaminate tissue needed for limb-sparing surgery.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Ordinary traumatic fracture

Adequate trauma and otherwise normal bone suggests a conventional fracture, although cancer and osteoporosis can lower the required force.

Bone infection

Fever, inflammatory change, ulceration or bacteraemia with a destructive lesion suggests osteomyelitis, which can also cause structural failure.

Primary bone sarcoma

A solitary aggressive lesion, periosteal reaction or soft-tissue mass without matching metastatic pattern requires specialist tumour-centre assessment before biopsy.

Avascular necrosis

Steroid exposure and joint-centred pain with subchondral collapse may mimic proximal metastatic disease and changes reconstruction planning.

Severe bone pain without fracture

Metastasis, arthritis, radiculopathy and muscle injury can cause major pain without mechanical discontinuity but may still indicate impending failure.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Completed fractureProtect, image and stabiliseFirst stepSudden pain, deformity or functional loss indicates a pathological fracture.

1Immobilise in a comfortable position, provide rapid analgesia, document neurovascular findings, assess blood loss and obtain whole-bone radiographs.
2Contact orthopaedics promptly and define cancer diagnosis, prognosis, comorbidity, previous radiotherapy and the functional outcome important to the patient.
3Use fixation or replacement designed for immediate function and expected lifetime, followed by oncology, radiotherapy and rehabilitation planning.

02Impending fractureStabilise before the bone failsA destructive weight-bearing lesion causes progressive functional pain or substantial cortical loss without complete fracture.

1Restrict unsafe loading, provide aids and analgesia and obtain radiographs with CT or MRI as required; assess other skeletal sites.
2Use a risk tool only as support and arrange orthopaedic-oncology review for prophylactic fixation or replacement before displacement.
3Coordinate postoperative radiotherapy and systemic or bone-targeted treatment and state permitted weight bearing and rehabilitation goals.

03Uncertain lesionProtect diagnosis before fixationA solitary, atypical or aggressive lesion lacks a secure matching cancer diagnosis.

1Do not perform routine curettage, biopsy or intramedullary fixation; protect the limb and refer to the regional bone-tumour service.
2DefinitiveComplete local MRI and staging selected by the tumour team and plan a biopsy tract that can be removed during definitive surgery.
3Base reconstruction, radiotherapy and systemic treatment on histology, extent, prognosis and the informed preference of the patient.

04Non-operative comfortMake movement and care tolerableSurgery is declined or recovery burden exceeds likely functional benefit near the end of life.

1Agree a comfortable splint or supported position, handling restrictions and realistic mobility plan with orthopaedic and palliative input.
2Provide regular and pre-emptive movement analgesia, bowel care, pressure prevention and equipment for toileting, turning and transfers.
3Explain expected change to patient and carers and review rapidly if pain remains intolerable, skin fails or care at the chosen place becomes unsafe.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Reduces severe incident pain sufficiently for essential care while mechanical stabilisation or a comfort handling plan is arranged.

Pre-emptive opioid for fracture movement

Give an immediate-release opioid dose before imaging, turns or transfers, selected from current opioid exposure and renal function; titrate the regular regimen from documented rescue use and prescribe bowel care.

Monitor sedation, respiratory rate, delirium and myoclonus and avoid repeatedly moving an unstable limb simply because analgesia has reduced warning pain.

Reduces subsequent pathological fractures and other skeletal-related events but does not mechanically stabilise the current fracture.

Denosumab for future skeletal-event reduction

For an eligible solid tumour with bone metastases, use the commissioned oncology regimen, commonly 120 mg subcutaneously every four weeks, with calcium and vitamin D management tailored to renal and calcium status.

Check calcium, vitamin D, dental health and jaw symptoms; severe hypocalcaemia is more likely in kidney failure and jaw osteonecrosis risk rises with cumulative exposure.

Reduces skeletal events and may contribute to bone-pain management in selected cancers after acute fracture care is addressed.

Zoledronic acid for selected metastatic bone disease

Use the tumour-specific oncology protocol, often 4 mg intravenously every three to four weeks with infusion and dose adjustment based on renal function and indication.

Renal injury, hypocalcaemia, acute-phase reaction and jaw osteonecrosis require renal, calcium and dental review; it cannot replace fixation of unstable bone.

Reduces venous thromboembolism risk during fracture-related immobility and postoperative recovery when the balance is favourable.

Thrombosis prophylaxis around immobility and surgery

Use the local orthopaedic or cancer low-molecular-weight heparin regimen after individual bleeding, platelet, renal, anaesthetic and procedural timing assessment.

Coordinate with surgery, neuraxial anaesthesia and bleeding risk and avoid automatic continuation when active bleeding or a last-days comfort plan makes harm greater.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Neurovascular injury

Displaced fragments or expanding tumour can damage vessels and nerves, causing ischaemia, bleeding, paralysis or compartment syndrome.

Loss of mobility

Pain and mechanical failure remove walking and transfer ability, accelerating thrombosis, pressure damage, chest infection and dependency.

Fat embolic or thrombotic events

Long-bone injury and immobility can cause respiratory and neurological deterioration from fat embolism or venous thromboembolism.

Fixation failure

Progressive tumour, inadequate construct length or survival beyond implant durability can produce loosening, breakage, pain and repeat surgery.

Persistent movement pain

Non-operative instability makes turning, toileting and transfers repeatedly painful and can require pre-emptive opioid or proportionate sedation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat distal pulse, capillary refill, power and sensation after splinting, transfer, reduction or any increase in pain or swelling.
Monitor pain at rest and during a defined movement such as turning or transfer and use rescue requirement to refine the regimen.
Check skin under splints and pressure points and prevent heel, sacral and device-related injury during immobility.
After surgery monitor wound, blood loss, infection, thrombosis, implant alignment and the stated weight-bearing instruction.
Track the patient-important function expected from treatment, such as sitting out, transferring or walking to the bathroom.
During antiresorptive treatment monitor renal function, calcium, vitamin D context, dental symptoms and cumulative treatment burden.
Review other painful weight-bearing sites and new spinal symptoms rather than treating one fracture as the only skeletal risk.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Functional pain predicts failure

Pain during weight bearing or ordinary use often matters more than lesion appearance alone when deciding prophylactic stabilisation.

The implant must outlast the patient

Metastatic bone may not unite, so reconstruction is chosen for immediate durable load rather than hoped-for biological healing.

Biopsy has an anatomy

The path of a needle can seed tumour and must lie within tissue that definitive surgery can remove.

Radiotherapy is not a splint

It can reduce tumour pain and progression but does not immediately restore mechanical integrity to a displaced unstable fracture.

Prevention is usually less burdensome

Prophylactic fixation often requires a smaller operation and preserves function better than emergency surgery after completion.

Non-operative is still active

Position, pre-emptive analgesia, handling instructions, equipment and skin care form a treatment plan rather than therapeutic absence.

11Common pitfallsFrequent interpretation and management errors.

01
Asking a patient with a painful femoral lesion to demonstrate weight bearing before imaging.
02
Radiographing only the visible fracture instead of the whole bone and adjacent joints.
03
Using a Mirels score as an automatic operation decision without specialist judgement.
04
Biopsying a solitary aggressive lesion before tumour-centre planning.
05
Assuming radiotherapy alone will stabilise a displaced long-bone fracture.
06
Selecting fixation that depends on union in bone unlikely to heal.
07
Forgetting preoperative embolisation assessment for highly vascular metastasis.
08
Starting bone-targeted medicine without calcium, renal and dental review.
09
Providing analgesia but no instructions for transfers, toileting or pressure relief.
10
Promising restoration of walking when the agreed operation targets pain-free transfers only.