Chronic osteomyelitis and sinus tract

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

Chronic osteomyelitis is persistent or recurrent infection within bone, often maintained by necrotic fragments, a sinus, implants, non-union or an ischaemic soft-tissue envelope. Establish the original mechanism: haematogenous infection, open fracture, fixation, pressure injury, neuropathic ulcer or prior surgery. Construct a timeline of every operation, culture, antimicrobial and symptom-free interval. Ask specifically whether drainage has stopped, changed colour, begun bleeding or developed an enlarging edge, because both acute obstruction and malignant transformation can alter a previously stable pattern.

Examine the whole patient for sepsis and treatment fitness, then the limb for alignment, stability, perfusion, neuropathy, ulceration, scars and reconstructive options. Document each sinus without probing it, including site, output, surrounding skin and any mass. Assess adjacent joints, limb length and function. Palpate for fluctuance and abnormal motion and inspect pressure areas and footwear. Record diabetes control, renal disease, vascular disease, smoking, nutrition, immune suppression and anticoagulation because host optimisation materially affects union, coverage and antibiotic safety.

Separate acute rescue from planned diagnosis. Sepsis requires immediate medical assessment, blood cultures, parenteral antibiotics and drainage of threatening collections. A physiologically stable patient should not receive empirical treatment before specialist review and deep sampling. Prior agents can suppress cultures; BOASt fracture-related infection guidance advises discussing the antibiotic-free interval with microbiology and using at least two weeks in non-acute infection when safe. This is a deliberate diagnostic strategy, not a rule applied to deterioration, spreading cellulitis or bacteraemia.

Plain radiographs are the initial anatomical map: look for cortical thickening, sclerosis, lucency, sequestrum, involucrum, cloaca, deformity, non-union, implant loosening and fracture. Compare serial studies. MRI with contrast where appropriate defines marrow, abscess, sinus and adjacent soft tissue but postoperative change and metal artefact reduce specificity. CT shows cortical sequestra and union detail. Ultrasound can guide aspiration of a superficial collection. Nuclear imaging is reserved for a defined specialist question when standard imaging remains equivocal.

Microbiology must reflect the infected compartment. Do not use a superficial sinus swab to design curative therapy. At planned debridement, obtain at least five representative deep tissue or bone samples with a fresh sterile instrument for each and no-touch technique; take two histology specimens for chronic infection. Label exact sites and tell the laboratory about prior organisms, antibiotics, implants and slow-growing pathogens. If malignancy is possible, obtain properly oriented tissue from the suspicious margin through an oncologically safe biopsy plan rather than an unplanned excision.

A curative operation is more than curettage. Excise sequestra and all non-viable or infected tissue to a viable margin while preserving critical structures, open every communicating cavity, remove unsuitable implants, restore fracture stability and manage the residual dead space. Coordinate orthopaedic and plastic surgeons so vascularised soft-tissue coverage is timely. Local antimicrobial carriers may support dead-space management but do not replace systemic therapy or viable cover. When union is not achieved, staged stabilisation and later bone reconstruction may be required.

Start broad-spectrum systemic antibiotics after samples and narrow promptly when culture and histology return. Review empirical treatment by 48 hours with preliminary results. The infection specialist documents agent, route, dose, interactions, monitoring and duration in relation to surgical completeness, remaining implants and organism. There is no universal oral or intravenous course that overrides anatomy. Rifampicin-containing therapy may be selected for susceptible staphylococcal implant biofilm only in combination and with stringent interaction review; it is not a treatment for an unsampled draining sinus.

Some patients cannot undergo complete eradication because reconstruction is disproportionate, perfusion cannot be restored or host risk is extreme. A documented suppression or palliation plan should state goals, likely failure signs and review responsibility rather than allowing indefinite unmonitored antibiotics. Follow wound closure, recurrence, CRP when informative, union, implant integrity, renal and hepatic toxicity, function and pain. Recurrent drainage after treatment reopens the source-control question. Smoking cessation, nutrition, vascular intervention, diabetes care and pressure relief are part of infection treatment rather than optional extras.

Key points

Chronic osteomyelitis is an anatomical disease of sequestrum, biofilm, dead space, instability and inadequate soft-tissue cover; antibiotics alone rarely correct all five.
A draining sinus communicating with bone strongly supports infection, but a superficial sinus swab usually reflects colonisers and should not select definitive therapy.
If septic, take blood cultures and start parenteral treatment immediately. If stable, avoid empirical antibiotics and preserve deep-sample yield for a planned bone-infection pathway.
Define previous injuries, implants, organisms, antibiotics, operations, union, perfusion, smoking, diabetes and every change in the sinus before choosing tests or surgery.
Initial radiographs assess sequestrum, involucrum, cloaca, deformity, fracture, non-union and implants; MRI maps marrow and soft tissue, while CT better defines cortical sequestra for planning.
Definitive sampling comes from multiple separately instrumented deep bone or interface specimens with histology, not a superficial swab; coordinate any tumour concern with biopsy planning.
Curative surgery removes infected and non-viable tissue, restores stability, manages dead space and provides vascularised cover, followed by culture-directed antimicrobials and rehabilitation.
Inspect a long-standing sinus for bleeding, everted edges, fungation or mass at every review because malignant transformation may present as a change in an otherwise familiar wound.

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

Residual acute infection

Inadequately eradicated haematogenous infection leaves devitalised bone or an undrained focus that persists after systemic symptoms settle.

Post-traumatic contamination

Open fracture, devascularised tissue and repeated fixation introduce organisms and create unstable, poorly perfused anatomy favourable to chronic infection.

Contiguous spread

Pressure injury, neuropathic ulcer, vascular ulcer or deep soft-tissue infection can extend directly into cortex and medulla.

Haematogenous recurrence

Bacteraemic seeding of previously injured bone is less common but should be considered when infection appears remote from trauma or ulceration.

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

1
Sequestrum formation
Ischaemic infected bone separates from viable host bone, creating an avascular fragment that systemic antibiotics cannot reliably sterilise.
2
Involucrum and cloaca
Reactive new bone encases the focus while a cortical channel allows pus to escape, producing the characteristic intermittent sinus.
3
Biofilm persistence
Organisms on necrotic bone or implants adopt slow-growing protected communities that evade host immunity and tolerate otherwise active antimicrobials.
4
Dead space and instability
Cavities, poor soft-tissue envelope and motion at non-union impair vascular delivery and repeatedly disrupt healing after incomplete debridement.
5
Chronic epithelial injury
Long-standing inflammation and repeated epithelial turnover in a sinus can produce dysplasia and Marjolin-type squamous carcinoma.

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

Intermittent sinus

A tract that repeatedly drains and closes suggests communication with a persistent bone focus even when fever and CRP are absent.

Sequestrum pattern

Dense devitalised bone within surrounding lucency and reactive involucrum on imaging supports long-standing infection and predicts incomplete medical sterilisation.

Infected non-union

Persistent pain, abnormal motion, broken or loose implants and absent progression to union should trigger infection sampling even without drainage.

Acute-on-chronic flare

Sudden pain, swelling, fever or stopped sinus output suggests blocked drainage, new abscess or bacteraemia requiring urgent reassessment.

Malignant transformation

Bleeding, fungation, everted margins, mass, new odour or altered pain in a mature sinus requires urgent tissue diagnosis.

Compromised host

Poor pulses, neuropathy, hyperglycaemia, smoking, malnutrition and renal disease predict impaired clearance and reconstruction and must be actively treated.

Red flags requiring action

Fever, hypotension, spreading erythema, escalating deep pain or abrupt cessation of drainage with swelling suggests acute-on-chronic abscess or sepsis and needs urgent source-control assessment.
New deformity, mechanical pain, abnormal mobility or inability to load raises concern for infected non-union or pathological fracture and requires protection and urgent imaging.
A sinus that bleeds, enlarges, becomes everted or fungating, develops a mass or changes after years of drainage requires urgent biopsy planning for squamous carcinoma.
Coldness, pulse change, new motor or sensory deficit, or extensive soft-tissue loss demands immediate vascular, nerve and reconstructive assessment alongside infection care.

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
Initial plain radiographsFirst step
Why
Assess chronic bone architecture, union and implant status.
Interpretation and limitations
Sequestrum, involucrum, sclerosis, cortical defects, lucency and implant failure guide planning; absence of dramatic change does not exclude a sinus-linked focus.
02
FBC, CRP, ESR and organ profile
Why
Measure systemic activity, alternative disease and treatment safety.
Interpretation and limitations
Normal inflammatory markers are compatible with indolent infection; renal, hepatic, glucose and nutritional findings shape reconstruction and antimicrobials.
03
Blood cultures during systemic illness
Why
Identify bacteraemia in an acute flare.
Interpretation and limitations
Take before antibiotics if this causes no delay; persistent S. aureus bacteraemia requires investigation for endocardial and metastatic infection.
04
MRI for extent
Why
Map medullary infection, abscess, sinus and soft-tissue involvement.
Interpretation and limitations
Postoperative oedema and metal artefact reduce specificity, so interpret with radiographs, clinical anatomy and planned samples.
05
CT for cortex and union
Why
Define sequestra, cloacae, cortical defects and mechanical reconstruction.
Interpretation and limitations
CT is particularly useful when dense sclerosis or metal limits MRI but is less sensitive to early marrow and soft-tissue inflammation.
06
Five deep microbiology samples
Why
Recover representative organisms from distinct infected sites.
Interpretation and limitations
Use new instruments and no-touch technique after a safe antibiotic-free interval; concordant deep cultures outweigh superficial sinus flora.
07
Two histology specimens
Why
Confirm chronic inflammation, identify organisms or exclude tumour.
Interpretation and limitations
Request infection histology and urgent oncological review for sinus dysplasia or mass; sampling route must not compromise definitive excision.

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

Primary bone tumour

Pain, destructive imaging, mass and pathological fracture may mimic infection; biopsy must be planned through the definitive surgical team.

Neuropathic arthropathy

Fragmentation, deformity and warmth in an insensate limb may be sterile Charcot change, infection or both, requiring ulcer and MRI correlation.

Sterile inflammatory osteitis

Chronic recurrent multifocal osteomyelitis produces relapsing sterile lesions, often multifocal and without concordant deep cultures or a draining bacterial focus.

Foreign-body reaction

Suture, cement or other material can produce drainage and granuloma, but deep infection must still be excluded before attributing the sinus.

Squamous carcinoma

New mass, bleeding, pain or altered drainage within a chronic sinus indicates malignant transformation until biopsy proves otherwise.

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

01FlareRescue systemic and structural threatsFirst stepSepsis, spreading infection, abscess, neurovascular compromise or threatened fracture complicates chronic disease.

1Stabilise physiology, obtain blood cultures and start immediate parenteral therapy when septic.
2Protect an unstable bone segment and obtain urgent radiographs and source-focused cross-sectional imaging.
3Drain pus and remove immediately life-threatening necrosis while preserving multiple deep cultures and histology where possible.
4EscalationEscalate new sinus mass or bleeding through sarcoma or skin-cancer pathways rather than routine wound excision.

02StableBuild the eradication plan before antibioticsChronic pain, sinus or infected non-union is present without systemic instability.

1Withhold empirical antibiotics and discuss a safe minimum two-week antibiotic-free period in non-acute infection with microbiology.
2Define host, perfusion, union, implants, soft tissue and disease extent with radiographs and targeted MRI or CT.
3Plan orthopaedic, plastic, infection, radiology and rehabilitation input in the bone-infection multidisciplinary team.
4At surgery obtain five deep culture samples and two histology samples before antimicrobials and irrigation.

03DefinitiveRemove persistence and restore mechanicsDefinitiveDeep microbiology, histology and reconstructive feasibility have been established.

1Excise sequestra and infected non-viable tissue, open cavities and manage all dead space.
2Remove unnecessary or unstable metalwork, reconstruct stability and obtain vascularised soft-tissue coverage.
3Start broad-spectrum therapy after sampling, review at 48 hours and narrow to a documented specialist course.
4Monitor healing, union, toxicity and recurrence, or define explicit goals and surveillance for suppression when cure is not feasible.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Provides systemic treatment while the debrided anatomy and independent deep specimens establish definitive microbiology.

Post-sampling empirical antimicrobial therapy

After five deep cultures and histology are obtained, give the full adult regimen in the trust's chronic bone-infection protocol, then review with preliminary results at 48 hours and replace it with an organism-, surgery- and organ-function-specific prescription.

Do not start empirically in a stable unsampled sinus; record allergy, renal and hepatic function, prior resistance, QT risk and interactions, and do not use prolonged therapy as a substitute for sequestrum removal, stability or cover.

May add biofilm activity when an effective companion drug, controlled bacterial burden and a defined implant strategy are present.

Rifampicin-containing therapy when specifically selected

Use only as one component of an infection-specialist regimen for a proven susceptible staphylococcal infection with retained implant or biofilm relevance, after adequate debridement and wound control; never prescribe rifampicin alone.

Check warfarin, direct oral anticoagulants, hormonal contraception, antiepileptics and all other interactions, liver function and resistance risk; a persistently draining wound or rifampicin monotherapy promotes failure.

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

Recurrent sepsis

A contained focus can flare after sinus blockage, immunosuppression or further surgery and produce bacteraemia or systemic organ dysfunction.

Infected non-union

Bone loss, instability and microbial persistence prevent union and create a cycle of implant failure, deformity and repeated reconstruction.

Pathological fracture

Cortical destruction and stress concentration weaken the segment, sometimes fracturing with minimal trauma and contaminating new tissue planes.

Squamous malignancy

Long-standing sinus epithelium can transform into aggressive squamous carcinoma requiring staging and often radical excision or amputation.

Amputation and disability

Uncontrolled infection, malignancy, non-reconstructable perfusion or massive tissue loss may make amputation the safest durable option.

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

Track fever, pain, sinus output, erythema, wound closure and any new mass or bleeding at every contact.
Follow union, alignment, implant integrity and sequestrum or dead-space reconstruction on planned serial radiographs.
Review culture and histology concordance in the bone-infection multidisciplinary team and document contaminants and prior antibiotic effects.
Monitor renal, hepatic and marrow indices and interaction-sensitive medicines throughout prolonged antimicrobial treatment.
Reassess pulses, neuropathy, glucose control, pressure loading, nutrition and smoking because host failure predicts recurrence.
Measure pain, mobility, work and self-care goals and coordinate orthotics, rehabilitation or prosthetic care after radical surgery.

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

The sinus is evidence, not the sample

A communicating tract is clinically important, but its surface organisms are unreliable substitutes for separately collected deep bone specimens.

A closed sinus can be worse

Stopping drainage with increasing pain or swelling may mean retained pus rather than cure and deserves urgent reassessment.

Union and infection are linked

Motion sustains inflammation and impaired healing, while infection prevents union; definitive strategy must address both simultaneously.

Normal CRP does not sterilise bone

Indolent biofilm and avascular sequestra can persist with little systemic inflammatory response.

Biopsy routes matter

A suspicious sinus mass needs planned tissue diagnosis because an ill-placed biopsy can contaminate reconstructive planes and compromise cancer surgery.

Suppression needs an endpoint

When cure is impossible, long-term treatment still needs explicit goals, toxicity monitoring, failure criteria and ownership.

11Common pitfallsFrequent interpretation and management errors.

01
Prescribing repeated empirical oral courses for sinus drainage before obtaining meaningful deep specimens.
02
Treating a superficial sinus swab as the infecting bone microbiology.
03
Performing limited curettage without a plan for dead space, stability and vascularised coverage.
04
Using normal inflammatory markers to dismiss infected non-union or implant loosening.
05
Failing to examine a chronic sinus for malignant change or biopsying a mass through an unsafe route.
06
Calling indefinite antibiotics conservative care without toxicity surveillance and documented failure triggers.