Gangguan Penyambungan Tulang
Published on September 10, 2026
Risk Factors
Malunion
Inadequate reduction, poor immobilization, loss of follow-up, fractures managed conservatively without close monitoring
Non-Union
Smoking, diabetes, NSAIDs use, infection, inadequate blood supply (e.g., scaphoid waist, femoral neck), open fractures, soft tissue interposition, excessive gap or motion at fracture site
Etiology
Malunion
Fracture heals in a non-anatomical position (abnormal angulation, rotation, or shortening)
Non-Union
Fracture fails to heal; cessation of all reparative processes without bone union by 6 to 9 months, or no radiographic progress over 3 consecutive months
Presentation
Malunion
Visible deformity, limb-length discrepancy, altered gait, pain with activity, decreased range of motion, early secondary osteoarthritis of adjacent joints
Non-Union
Persistent pain and motion at the fracture site well beyond the expected healing window, functional impairment, inability to bear weight
Classic Exam
Malunion
Angular or rotational deformity of the limb, limb shortening on measurement, abnormal joint mechanics
Non-Union
Tenderness at the fracture site, palpable motion or crepitus at the fracture gap, possible warmth/swelling (hypertrophic type) or no callus palpable (atrophic type)
Diagnostics
Malunion
Radiographs showing healed fracture in malalignment (angulation, shortening, rotation); CT for precise rotational assessment
Non-Union
Radiographs showing a persistent fracture line, absent or inadequate bridging callus, sclerotic bone ends, or a gap; CT for detailed evaluation of bony bridging
Management
Malunion
Corrective osteotomy with internal fixation if functionally significant; observation if deformity is minor and asymptomatic
Non-Union
Hypertrophic: rigid internal fixation alone. Atrophic: bone grafting combined with stable fixation. Infected: debridement, antibiotics, staged reconstruction
Keywords
Malunion
"Healed in poor alignment," "angular deformity after fracture," "limb-length discrepancy post-fracture," "malrotation"
Non-Union
"Fracture line still visible at 9 months," "persistent pain at fracture site," "motion at fracture," "no callus formation," "sclerotic bone ends," "elephant foot callus"
01Pathophysiology
Normal fracture healing proceeds through a well-orchestrated sequence: hematoma formation, inflammatory response, soft callus (cartilaginous) formation, hard callus (woven bone) formation, and finally remodeling into mature lamellar bone. Disruption at any stage of this cascade leads to abnormal healing outcomes.
Malunion occurs when the fracture proceeds through all healing phases but consolidates in a non-anatomical position. The bone unites with residual angulation, rotation, or shortening. This happens because the fracture fragments were either inadequately reduced at the time of initial treatment or because the reduction was lost during the healing period due to insufficient immobilization. The resulting deformity alters the normal biomechanical axis of the limb, leading to abnormal load distribution across adjacent joints. Over time, this eccentric loading accelerates cartilage wear and produces secondary degenerative arthritis. Rotational malunion is particularly problematic in the lower extremity because even small degrees of malrotation significantly alter gait mechanics.
Non-union represents a complete failure of the biological healing process. The fracture site becomes a pseudarthrosis, essentially a false joint where fibrous tissue or fibrocartilage fills the gap instead of bone. The pathophysiology diverges based on the biological activity at the fracture site, which is the foundation of the Weber and Cech classification system.
In hypertrophic non-union, the biology is intact. The periosteum and surrounding tissues maintain adequate vascularity and are actively attempting to heal. The problem is purely mechanical: excessive motion at the fracture site prevents the soft callus from maturing into hard callus. Radiographically, this produces abundant callus that flares outward from the bone ends (the classic "elephant foot" appearance), but the callus never bridges the gap. The key concept here is that the biology is willing but the mechanical environment is hostile.
In atrophic non-union, the problem is fundamentally biological. The bone ends are avascular and metabolically inert. There is no osteogenic activity, no callus formation, and the bone ends become rounded, sclerotic, and often osteopenic. The medullary canal may seal off with sclerotic bone. This type is associated with devascularization from the initial injury (periosteal stripping in open fractures or high-energy trauma), smoking-induced microvascular compromise, and metabolic factors that impair osteoblast function. The bone simply has no capacity to heal without biological augmentation.
Oligotrophic non-union sits between these two extremes. There is some biological capacity, but an insufficient inflammatory response was mounted at the fracture site, often because of excessive fracture gap or displacement that prevented the initial hematoma from bridging the fragments.
Understanding this mechanical versus biological distinction is the single most important concept for management decisions and is the principle most frequently tested.
02Classification and Clinical Manifestation
Malunion Classification
Angular (Varus/Valgus)
Description
Fracture heals with abnormal coronal plane angulation
Clinical Consequence
Altered mechanical axis, asymmetric joint loading, accelerated osteoarthritis
Angular (Apex Anterior/Posterior)
Description
Fracture heals with sagittal plane angulation (recurvatum or procurvatum)
Clinical Consequence
Abnormal gait mechanics, cosmetic deformity
Rotational
Description
Fracture heals with torsional malalignment
Clinical Consequence
Altered foot progression angle, compensatory hip/knee strain, functionally significant even at small degrees
Shortening
Description
Fracture heals with overlap or bone loss causing limb-length discrepancy
Clinical Consequence
Gait disturbance, compensatory pelvic obliquity, secondary scoliosis if greater than 2 cm
Combined
Description
More than one plane of deformity
Clinical Consequence
Compound biomechanical disturbance; typically requires multiplanar corrective osteotomy
Type of Deformity | Description | Clinical Consequence |
|---|---|---|
Angular (Varus/Valgus) | Fracture heals with abnormal coronal plane angulation | Altered mechanical axis, asymmetric joint loading, accelerated osteoarthritis |
Angular (Apex Anterior/Posterior) | Fracture heals with sagittal plane angulation (recurvatum or procurvatum) | Abnormal gait mechanics, cosmetic deformity |
Rotational | Fracture heals with torsional malalignment | Altered foot progression angle, compensatory hip/knee strain, functionally significant even at small degrees |
Shortening | Fracture heals with overlap or bone loss causing limb-length discrepancy | Gait disturbance, compensatory pelvic obliquity, secondary scoliosis if greater than 2 cm |
Combined | More than one plane of deformity | Compound biomechanical disturbance; typically requires multiplanar corrective osteotomy |
Non-Union Classification (Weber and Cech)
Viable (Hypertrophic)
Subtype
Elephant foot
Vascularity
Rich blood supply
Callus
Abundant, exuberant
Radiographic Appearance
Large, flaring callus at bone ends without bridging
Key Feature
Adequate biology, inadequate stability
Viable (Hypertrophic)
Subtype
Horse hoof
Vascularity
Moderate blood supply
Callus
Moderate callus
Radiographic Appearance
Less exuberant callus, still no union
Key Feature
Moderate biological response with mechanical failure
Viable
Subtype
Oligotrophic
Vascularity
Adequate blood supply
Callus
Minimal to absent callus
Radiographic Appearance
Fracture line visible, no sclerosis, little callus
Key Feature
Inadequate fracture reduction or gap; biology present but not activated
Non-viable (Atrophic)
Subtype
Torsion wedge
Vascularity
Poor blood supply
Callus
No callus
Radiographic Appearance
Intermediate necrotic fragment with sclerotic ends
Key Feature
Devascularized intermediate fragment
Non-viable (Atrophic)
Subtype
Comminuted
Vascularity
Poor blood supply
Callus
No callus
Radiographic Appearance
Missing intermediate fragments, sclerotic ends
Key Feature
Bone loss from injury or debridement
Non-viable (Atrophic)
Subtype
Atrophic
Vascularity
Absent blood supply
Callus
No callus
Radiographic Appearance
Rounded, sclerotic, osteopenic bone ends, sealed medullary canal
Key Feature
Completely inert bone ends
Type | Subtype | Vascularity | Callus | Radiographic Appearance | Key Feature |
|---|---|---|---|---|---|
Viable (Hypertrophic) | Elephant foot | Rich blood supply | Abundant, exuberant | Large, flaring callus at bone ends without bridging | Adequate biology, inadequate stability |
Viable (Hypertrophic) | Horse hoof | Moderate blood supply | Moderate callus | Less exuberant callus, still no union | Moderate biological response with mechanical failure |
Viable | Oligotrophic | Adequate blood supply | Minimal to absent callus | Fracture line visible, no sclerosis, little callus | Inadequate fracture reduction or gap; biology present but not activated |
Non-viable (Atrophic) | Torsion wedge | Poor blood supply | No callus | Intermediate necrotic fragment with sclerotic ends | Devascularized intermediate fragment |
Non-viable (Atrophic) | Comminuted | Poor blood supply | No callus | Missing intermediate fragments, sclerotic ends | Bone loss from injury or debridement |
Non-viable (Atrophic) | Atrophic | Absent blood supply | No callus | Rounded, sclerotic, osteopenic bone ends, sealed medullary canal | Completely inert bone ends |
Infected Non-Union (Special Category)
Feature | Description |
|---|---|
Pathogenesis | Biofilm formation on bone or hardware prevents healing and perpetuates inflammation |
Clinical Signs | Draining sinus, erythema, persistent wound drainage, fever, elevated inflammatory markers |
Microbiology | Staphylococcus aureus is the most common organism; polymicrobial in open fractures |
Key Principle | Must eradicate infection before definitive reconstruction can succeed |
03Diagnostic Workup
Plain Radiographs (AP and Lateral)
Purpose
Best initial test for both conditions
Findings in Malunion
Healed fracture in abnormal alignment; measure angulation and shortening
Findings in Non-Union
Persistent fracture line, sclerotic bone ends, absent or inadequate bridging callus
CT Scan
Purpose
Most accurate test for structural assessment
Findings in Malunion
Precise measurement of rotational deformity (comparison with contralateral limb); 3D reconstruction for surgical planning
Findings in Non-Union
Detailed assessment of bony bridging vs. fibrous union; identifies subtle callus that plain films may miss
Full-Length Standing Films (Scanogram)
Purpose
Limb-length and mechanical axis assessment
Findings in Malunion
Quantifies limb-length discrepancy and mechanical axis deviation
Findings in Non-Union
Not routinely needed
Bone Scan (Technetium-99m)
Purpose
Assesses biological activity at fracture site
Findings in Malunion
Not typically indicated
Findings in Non-Union
Distinguishes hypertrophic (increased uptake) from atrophic (decreased or absent uptake) non-union
Laboratory Studies (ESR, CRP, WBC, Blood Cultures)
Purpose
Rule out infection
Findings in Malunion
Not typically needed unless symptomatic
Findings in Non-Union
Elevated inflammatory markers suggest infected non-union
Bone Biopsy and Culture
Purpose
Gold standard for infected non-union
Findings in Malunion
Not indicated
Findings in Non-Union
Confirms organism identity and guides antibiotic therapy; at least 3 to 5 intraoperative tissue samples recommended
Test | Purpose | Findings in Malunion | Findings in Non-Union |
|---|---|---|---|
Plain Radiographs (AP and Lateral) | Best initial test for both conditions | Healed fracture in abnormal alignment; measure angulation and shortening | Persistent fracture line, sclerotic bone ends, absent or inadequate bridging callus |
CT Scan | Most accurate test for structural assessment | Precise measurement of rotational deformity (comparison with contralateral limb); 3D reconstruction for surgical planning | Detailed assessment of bony bridging vs. fibrous union; identifies subtle callus that plain films may miss |
Full-Length Standing Films (Scanogram) | Limb-length and mechanical axis assessment | Quantifies limb-length discrepancy and mechanical axis deviation | Not routinely needed |
Bone Scan (Technetium-99m) | Assesses biological activity at fracture site | Not typically indicated | Distinguishes hypertrophic (increased uptake) from atrophic (decreased or absent uptake) non-union |
Laboratory Studies (ESR, CRP, WBC, Blood Cultures) | Rule out infection | Not typically needed unless symptomatic | Elevated inflammatory markers suggest infected non-union |
Bone Biopsy and Culture | Gold standard for infected non-union | Not indicated | Confirms organism identity and guides antibiotic therapy; at least 3 to 5 intraoperative tissue samples recommended |
The workup begins with plain radiographs in at least two orthogonal views (anteroposterior and lateral). This is the best initial test for both malunion and non-union. For malunion, the films demonstrate the healed fracture in its malaligned position and allow measurement of angular deformity. For non-union, the hallmark finding is a persistent fracture line with absence of progressive callus formation on serial imaging over time. Hypertrophic non-union shows abundant callus without bridging, while atrophic non-union shows sclerotic, rounded bone ends with no callus whatsoever.
CT scanning is the most accurate test for detailed structural assessment. In malunion, CT with comparison to the contralateral extremity is the definitive method for quantifying rotational deformity, which is notoriously difficult to assess on plain films. In non-union, CT provides cross-sectional detail to determine whether partial bony bridging exists (which may change the classification from true non-union to delayed union) and is essential for preoperative planning.
When non-union is identified, the critical next step is to determine whether the non-union is viable or non-viable and whether infection is present. A technetium bone scan can help differentiate: hypertrophic non-union demonstrates increased radiotracer uptake reflecting active biological turnover, whereas atrophic non-union shows diminished uptake reflecting biologically inert bone.
Laboratory investigation for infection should be performed in any non-union, particularly in patients with a history of open fracture, prior surgical fixation, or clinical signs of infection (drainage, erythema, persistent pain). ESR and CRP are sensitive screening markers. If infection is suspected, intraoperative tissue culture (not swab cultures) is the gold standard for identifying the causative organism.
An important clinical pearl: delayed union and non-union exist on a spectrum. Delayed union means the fracture is progressing toward healing but at a slower rate than expected. Non-union means healing has ceased entirely. The distinction is made by serial radiographs showing lack of any progression over at least 3 months. Do not diagnose non-union based on a single radiograph.
04Management and Treatment
Malunion (Asymptomatic, Minimal Deformity)
Treatment Approach
Observation, physical therapy
Key Principle
Not all malunions require surgical correction
Malunion (Symptomatic or Functionally Significant)
Treatment Approach
Corrective osteotomy with internal fixation
Key Principle
Re-create the fracture in a controlled fashion, realign, and stabilize
Hypertrophic Non-Union
Treatment Approach
Rigid internal fixation alone (compression plating or exchange nailing)
Key Principle
Biology is adequate; the problem is mechanical, so provide stability
Atrophic Non-Union
Treatment Approach
Bone grafting (autologous iliac crest graft) combined with stable internal fixation
Key Principle
Biology is deficient; must supply osteogenic, osteoinductive, and osteoconductive elements along with mechanical stability
Oligotrophic Non-Union
Treatment Approach
Stable fixation with or without bone graft depending on gap size
Key Principle
Activate the dormant biological response through stable mechanical environment
Infected Non-Union
Treatment Approach
Staged approach: (1) debridement and hardware removal, (2) culture-directed antibiotics for 6 to 8 weeks, (3) definitive reconstruction after infection clearance
Key Principle
Eradicate infection first; union cannot occur in the presence of active infection
Adjunctive Therapies
Treatment Approach
Low-intensity pulsed ultrasound (LIPUS), electrical bone stimulation
Key Principle
May be used as supplements but not as primary treatment
Condition | Treatment Approach | Key Principle |
|---|---|---|
Malunion (Asymptomatic, Minimal Deformity) | Observation, physical therapy | Not all malunions require surgical correction |
Malunion (Symptomatic or Functionally Significant) | Corrective osteotomy with internal fixation | Re-create the fracture in a controlled fashion, realign, and stabilize |
Hypertrophic Non-Union | Rigid internal fixation alone (compression plating or exchange nailing) | Biology is adequate; the problem is mechanical, so provide stability |
Atrophic Non-Union | Bone grafting (autologous iliac crest graft) combined with stable internal fixation | Biology is deficient; must supply osteogenic, osteoinductive, and osteoconductive elements along with mechanical stability |
Oligotrophic Non-Union | Stable fixation with or without bone graft depending on gap size | Activate the dormant biological response through stable mechanical environment |
Infected Non-Union | Staged approach: (1) debridement and hardware removal, (2) culture-directed antibiotics for 6 to 8 weeks, (3) definitive reconstruction after infection clearance | Eradicate infection first; union cannot occur in the presence of active infection |
Adjunctive Therapies | Low-intensity pulsed ultrasound (LIPUS), electrical bone stimulation | May be used as supplements but not as primary treatment |
Malunion Management
Not every malunion warrants surgery. The decision to intervene depends on the degree of deformity, the patient's symptoms, functional limitations, and the risk of progressive joint degeneration. Accepted angulation thresholds vary by anatomical location:
Tibial shaft: up to 5 degrees of varus/valgus, 10 degrees of apex anterior/posterior, 10 degrees of rotation, and 1 cm of shortening are generally tolerable in adults.
Femoral shaft: less tolerance for angular deformity due to the larger lever arm.
Forearm: very low tolerance for malunion because rotation is critical for pronation and supination; even 10 degrees of angular deformity in the forearm can significantly limit rotational function.
When intervention is indicated, the treatment is a corrective osteotomy. The surgeon cuts through the malunited bone at the site of maximal deformity (or at the center of rotation of angulation, abbreviated as CORA), realigns the fragments, and stabilizes them with a plate and screws or an intramedullary nail. Preoperative planning using CT-based 3D reconstruction and templating is standard. For limb-length discrepancy greater than 2 cm, gradual correction with an external fixator (Ilizarov or Taylor Spatial Frame) using distraction osteogenesis may be preferred.
Non-Union Management
The treatment of non-union is dictated by the Weber and Cech classification, and this is the highest-yield management concept for examination purposes.
Hypertrophic non-union has viable biology. The callus is present and active, but the fracture is not healing because there is too much motion. The treatment is purely mechanical: provide rigid stabilization. This is typically achieved with compression plating (applying compressive force across the fracture site) or exchange nailing (replacing the existing intramedullary nail with a larger-diameter nail to achieve greater stability and also stimulates the endosteal surface). Bone grafting is generally unnecessary because the biological environment is already favorable.
Atrophic non-union has no viable biology. Treatment requires both mechanical stabilization and biological augmentation. The gold standard biological augmentation is autologous iliac crest bone graft, which provides all three elements necessary for bone healing:
Osteogenic cells (mesenchymal stem cells and osteoblasts from the graft)
Osteoinductive factors (bone morphogenetic proteins and growth factors within the graft matrix)
Osteoconductive scaffold (the trabecular architecture of the graft serves as a lattice for new bone formation)
The surgical technique involves opening the non-union site, debriding the sclerotic bone ends, opening the medullary canals, applying the bone graft, and achieving rigid fixation. In cases with bone loss, structural grafting or the use of induced membrane technique (Masquelet technique) may be necessary.
Infected non-union demands a staged protocol. The first stage involves radical debridement of all necrotic and infected tissue, removal of existing hardware, and collection of at least 3 to 5 deep tissue cultures. Temporary stabilization is achieved with an external fixator. A local antibiotic-impregnated cement spacer (typically polymethylmethacrylate loaded with vancomycin and/or gentamicin) is placed in the defect. Systemic culture-directed intravenous antibiotics are administered for 6 to 8 weeks. Inflammatory markers (ESR and CRP) are monitored serially. Once infection is confirmed to be eradicated clinically and by normalized laboratory values, the second stage proceeds with definitive reconstruction using bone grafting and stable internal fixation.
Adjunctive Therapies
Low-intensity pulsed ultrasound (LIPUS) at 20 minutes per day and electrical bone stimulation are FDA-approved adjuncts for non-union treatment. Evidence supports their use in augmenting fracture healing, though they are not substitutes for appropriate surgical management. They are most commonly used for early delayed union or as postoperative supplements.
Risk Factor Modification
Smoking cessation is critical. Nicotine directly impairs osteoblast function and causes microvascular vasoconstriction, reducing blood flow to the fracture site. Patients should also discontinue NSAIDs during fracture healing, as prostaglandin inhibition interferes with the inflammatory phase of bone repair. Nutritional optimization (calcium, vitamin D, adequate protein intake) and glycemic control in diabetic patients are important supportive measures.
05Differential Diagnosis and Distractors
Delayed Union
Why It Is Similar
Patient presents with persistent pain at fracture site and incomplete healing on radiograph, similar to non-union
Key Discriminator
Delayed union still shows some radiographic progression (callus formation advancing, fracture line becoming less distinct) on serial films; non-union shows no progression over 3 or more months and may show sclerotic, sealed bone ends
Stress Fracture
Why It Is Similar
Localized bone pain with activity, possible visible fracture line on imaging
Key Discriminator
History of repetitive overuse rather than a prior acute fracture event; no prior history of trauma requiring treatment; periosteal reaction pattern differs
Osteomyelitis
Why It Is Similar
Persistent pain at a previous fracture site, elevated inflammatory markers, may coexist with non-union
Key Discriminator
Osteomyelitis can exist without a fracture gap; imaging shows cortical destruction, involucrum, and sequestrum rather than the non-union pattern of sclerotic bone ends with a persistent fracture line. However, always consider infected non-union as a combined diagnosis
Pathologic Fracture Through a Bone Lesion
Why It Is Similar
Fracture that fails to heal, raising concern for non-union
Key Discriminator
Radiographs show an underlying lytic or blastic lesion (tumor, metastasis) at the fracture site; the bone was abnormal before the fracture occurred
Refracture
Why It Is Similar
New pain and radiographic fracture line at a previously healed fracture site
Key Discriminator
History of a new traumatic event after documented prior union; the fracture line is acute (sharp, without sclerosis) rather than the chronic appearance of a non-union
Complex Regional Pain Syndrome (CRPS)
Why It Is Similar
Persistent pain and functional limitation after a fracture, may mimic non-union clinically
Key Discriminator
CRPS shows burning pain out of proportion to injury, allodynia, autonomic changes (color and temperature changes), and trophic changes; radiographs may show patchy osteopenia (Sudeck atrophy) but the fracture itself has healed
Hardware Failure
Why It Is Similar
Pain at the fracture site after fixation, raising concern for non-union
Key Discriminator
Radiographs show broken plate, bent screws, or broken nail; hardware failure is often the consequence of non-union (cyclic loading on hardware without bony support) rather than the primary diagnosis, so always assess for underlying non-union when hardware fails
Differential | Why It Is Similar | Key Discriminator |
|---|---|---|
Delayed Union | Patient presents with persistent pain at fracture site and incomplete healing on radiograph, similar to non-union | Delayed union still shows some radiographic progression (callus formation advancing, fracture line becoming less distinct) on serial films; non-union shows no progression over 3 or more months and may show sclerotic, sealed bone ends |
Stress Fracture | Localized bone pain with activity, possible visible fracture line on imaging | History of repetitive overuse rather than a prior acute fracture event; no prior history of trauma requiring treatment; periosteal reaction pattern differs |
Osteomyelitis | Persistent pain at a previous fracture site, elevated inflammatory markers, may coexist with non-union | Osteomyelitis can exist without a fracture gap; imaging shows cortical destruction, involucrum, and sequestrum rather than the non-union pattern of sclerotic bone ends with a persistent fracture line. However, always consider infected non-union as a combined diagnosis |
Pathologic Fracture Through a Bone Lesion | Fracture that fails to heal, raising concern for non-union | Radiographs show an underlying lytic or blastic lesion (tumor, metastasis) at the fracture site; the bone was abnormal before the fracture occurred |
Refracture | New pain and radiographic fracture line at a previously healed fracture site | History of a new traumatic event after documented prior union; the fracture line is acute (sharp, without sclerosis) rather than the chronic appearance of a non-union |
Complex Regional Pain Syndrome (CRPS) | Persistent pain and functional limitation after a fracture, may mimic non-union clinically | CRPS shows burning pain out of proportion to injury, allodynia, autonomic changes (color and temperature changes), and trophic changes; radiographs may show patchy osteopenia (Sudeck atrophy) but the fracture itself has healed |
Hardware Failure | Pain at the fracture site after fixation, raising concern for non-union | Radiographs show broken plate, bent screws, or broken nail; hardware failure is often the consequence of non-union (cyclic loading on hardware without bony support) rather than the primary diagnosis, so always assess for underlying non-union when hardware fails |
06Traps and High-Yield Pearls
The most common way students answer questions on this topic incorrectly is by failing to distinguish the type of non-union before selecting a treatment. The question stem will describe a patient with a fracture that has not healed and then ask for the next best step in management. Students who memorize "non-union equals bone grafting" will choose bone graft for every non-union, but this is wrong for hypertrophic non-union, which only needs rigid fixation. The radiographic description in the question stem is your guide: abundant callus without bridging points to hypertrophic non-union and the answer is mechanical stabilization; absent callus with sclerotic bone ends points to atrophic non-union and the answer is bone grafting plus fixation.
A second common trap involves hardware failure. When a question describes a broken plate or nail, students often focus on replacing the hardware. The correct reasoning is to recognize that hardware failure is usually a sign of underlying non-union. The metal failed because the bone never healed and the hardware bore all the mechanical load until fatigue failure occurred. The next step is not simply to replace the hardware but to address the non-union itself.
Another frequently tested concept is the role of modifiable risk factors. A vignette may describe a smoker on chronic NSAIDs with a delayed or non-healing fracture. Before jumping to surgical intervention, identify and address reversible contributors: smoking cessation, NSAID discontinuation, metabolic workup (vitamin D, calcium, thyroid function, nutritional status), and glycemic optimization.
Finally, know the distinction between delayed union and non-union. This is a timeline-based and radiographic-progression-based diagnosis. The question will present serial radiographs. If there is slow but ongoing callus formation, the answer is continued observation or non-invasive stimulation. If there is no radiographic progression over 3 consecutive months (or failure to heal by 6 to 9 months), the diagnosis shifts to non-union and surgical intervention becomes appropriate. Getting the timing wrong leads to either premature surgery (operating on a delayed union that would have healed) or delayed intervention (watching a true non-union that will never heal on its own).
The core competency being tested is the ability to integrate radiographic findings with clinical context to classify the healing complication correctly, and then match the classification to the appropriate treatment principle: mechanical solution for mechanical problems, biological solution for biological problems, and infection control before reconstruction.