Symptomatic nonunion: pain, cosmetic deformity, scapular dyskinesis, and weakness. Standard treatment: compression plating + autogenous iliac crest bone graft for atrophic nonunion. Superior vs anteroinferior plating—each has pros/cons (biomechanics vs soft‑tissue irritation). Segmental defects >3 cm or failed revisions may need vascularized graft (fibula). Smoking cessation and vitamin D optimization improve union.
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Overview & Epidemiology
Clavicle nonunion is an uncommon but clinically significant complication of clavicle fractures. The clavicle is the most frequently fractured bone in humans; the vast majority of fractures — particularly midshaft fractures — heal uneventfully with conservative management. However, a subset develops nonunion, characterised by persistent fracture gap with pain, disability, and deformity after a period adequate for expected union. The surgical management of clavicle nonunion involves reconstruction of both the bony continuity and the mechanical properties of the clavicle — the central debate concerns whether plate fixation alone is sufficient or whether structural bone grafting is required as an adjunct.
Epidemiology: midshaft clavicle fractures account for ~80% of all clavicle fractures; the nonunion rate after conservative management is approximately 1–5% overall; however, certain fracture patterns carry a much higher nonunion risk: displaced midshaft fractures (shortening >2 cm, complete displacement, comminution) — nonunion rates of 15–20% reported in some series; the Canadian Orthopaedic Trauma Society (COTS) RCT and subsequent studies demonstrated that displaced midshaft clavicle fractures treated surgically (plate fixation) have significantly lower nonunion rates, better functional scores, and faster return to activity than conservatively managed fractures — a finding that shifted practice toward selective early plating of displaced fractures and reduced the burden of nonunion
Risk factors for clavicle nonunion: displacement (complete lateral displacement — the distal fragment displaces inferiorly due to the weight of the arm and pectoralis minor pull; the proximal fragment displaces superiorly due to sternocleidomastoid pull — creating shortening and displacement); shortening >2 cm; comminution with a butterfly fragment; female sex; older age; smoking (impairs fracture healing); distal third location (higher nonunion risk than midshaft); primary operative treatment failure (implant failure after initial ORIF); inadequate immobilisation; refracture; open fractures; neurological injury to the shoulder
Symptoms: persistent pain at the fracture site (typically worse with shoulder movement and overhead activity); shoulder weakness and fatigue; palpable pseudarthrosis (abnormal motion at the fracture site); shoulder drooping and asymmetry; neurological symptoms in the arm from thoracic outlet compromise by the malunited clavicle fragments (brachial plexus or subclavian vessels compressed between the displaced fracture ends — `thoracic outlet syndrome` from clavicle malunion/nonunion); a painful clicking or grinding at the fracture site on shoulder movement
Classification of Nonunion
Type
Characteristics
Surgical Implications
Hypertrophic (viable) nonunion
Abundant callus on both fracture ends (`elephant foot` or `horse hoof` pattern on X-ray); good biological healing potential; fracture ends are viable; the problem is instability — inadequate mechanical stability is preventing union despite good biology; adequate blood supply and cellular activity is present
Plate fixation alone (without bone graft) is theoretically sufficient — the biological environment is adequate; stability is the missing component; however, most surgeons still add bone graft prophylactically, particularly for clavicle nonunions, to ensure union; compression plate + interfragmentary lag screw is the mainstay
Atrophic (avascular) nonunion
No callus at the fracture ends; `pencil-shaped` tapering of the bone ends; avascular, sclerotic, resorbed bone; poor biological environment; the fracture ends lack vascularity and osteogenic cells — both stability AND biology are deficient
Plate fixation ALONE is insufficient — biological stimulation is required; structural or cancellous bone grafting is mandatory to provide osteogenic cells, osteoinductive factors (BMP-2, BMP-7), and osteoconductive scaffold; the sclerotic avascular ends must be resected back to bleeding bone before grafting; combined plate + bone graft gives the highest union rate
Oligotrophic nonunion
Minimal callus; fracture ends present but poorly viable; intermediate between hypertrophic and atrophic; often from fragment displacement — the biologically active cells are present but not in contact due to the gap
Bone grafting recommended in addition to plate fixation; cancellous autograft to stimulate biology
Infected nonunion
History of prior surgery with wound infection; persistent sinus; radiological osteolysis; positive cultures at prior debridement; implant failure
Two-stage management: Stage 1 — removal of infected hardware, aggressive debridement, antibiotic bead spacer; Stage 2 (after infection clearance, 6+ weeks) — plate + bone graft reconstruction; Ilizarov or acute shortening followed by distraction for large bone defects
Plate Fixation — Technique
Plate selection: locking compression plates (LCP) are the modern standard for clavicle fixation; superior (dorsal) plating is the most common position — the plate is applied to the superior surface of the clavicle; anteroinferior plating (the plate applied to the anterior/inferior surface) is an alternative that may have a lower symptomatic implant prominence rate (as the plate is not subcutaneous on the superior surface) but is technically more demanding and has theoretical vascular proximity (subclavian vessels inferior); a dedicated pre-contoured clavicle LCP is preferred; the plate must span all nonunion fragments with at least 3–4 cortices of fixation in each main fragment (using locking screws in osteoporotic or short fragments)
Surgical steps: supine or beach-chair position; head-of-table turned to the contralateral side; transverse or slightly curved incision over the nonunion site; protect the supraclavicular nerves (medial, intermediate, lateral branches of the supraclavicular nerve — C3/C4; injury causes anaesthetic patch below the clavicle); identify and protect the subclavian vein (immediately posterior to the clavicle medially) and the pectoralis minor (inferiorly); debride the nonunion fibrous tissue; `freshen` the fracture ends by removing the sclerotic avascular bone back to bleeding cancellous bone (curettage and rongeuring); harvest bone graft; apply plate; compress with lag screw across the nonunion if possible (hypertrophic) or apply in neutralisation/bridge mode with graft (atrophic)
Bone graft options: (1) Iliac crest autograft — the gold standard; tricortical strut graft (structural) for large defects; cancellous autograft (biological) for biologically deficient nonunions; donor site morbidity (chronic iliac crest pain in 10–30%); (2) Local autograft — from the clavicle itself (bone `dust` from drilling and reaming) or from the coracoid process (limited volume); (3) Allograft — avoids donor site morbidity; lower biological activity than autograft; demineralised bone matrix (DBM) provides osteoinductive properties; (4) Synthetic bone substitutes — calcium phosphate, calcium sulphate; osteoconductive only; (5) Bone morphogenetic proteins (BMP-2, BMP-7) — potent osteoinductive but expensive; approved for tibial nonunion; evidence for clavicle is limited
Plate vs Graft — The Evidence
Strategy
Indication
Union Rate
Key Considerations
Plate alone (without bone graft)
Hypertrophic nonunion with good bone stock and no significant defect; minimal shortening; early nonunion of a recent fracture
Reported union rates ~80–90% for hypertrophic nonunion with plate alone in some series
Limited to biologically viable nonunions; for atrophic nonunion — plate alone results in high re-operation rates; avoids donor site morbidity; some surgeons use plate alone for ALL clavicle nonunions, relying on stable fixation to stimulate biology
Plate + cancellous bone graft
Atrophic and oligotrophic nonunion; most clavicle nonunions in clinical practice; modest bone defect
~95–100% union rates reported in multiple series; the most consistent results in the literature
The most widely recommended approach for established clavicle nonunion; cancellous autograft from iliac crest provides all three requirements: osteogenic cells, osteoinductive factors, and osteoconductive scaffold; donor site morbidity is acceptable; union rates highest with this combination
Plate + structural (cortical) bone graft
Large segmental bone defect (>1.5–2 cm shortening); after resection of infected/devitalised bone; restoration of clavicular length requires structural interposition graft
Good union rates when structural graft is used with stable plate fixation; tricortical iliac crest graft most common structural graft choice; allograft femoral head or fibula strut graft is an alternative to avoid donor site morbidity
The structural graft restores clavicular length (preventing shoulder drooping, thoracic outlet syndrome, and AC joint dysfunction) AND provides biology; most demanding technique; only required when significant shortening or bone loss is present
Exam Pearls
Clavicle nonunion: 1–5% overall; displaced midshaft fractures — up to 15–20%; risk factors: displacement (>2 cm shortening), comminution, female sex, smoking, distal third location, refracture; COTS RCT: primary plating of displaced midshaft fractures reduces nonunion risk vs conservative treatment
Atrophic nonunion: plate alone insufficient; bone graft is mandatory; resect sclerotic bone ends to bleeding bone; cancellous iliac crest autograft provides osteogenic cells + osteoinduction + osteoconduction; union rates ~95–100% with plate + graft
Plate: superior (dorsal) LCP is most common; anteroinferior plating alternative (less prominent but more technically demanding); pre-contoured clavicle LCP; ≥3–4 cortices per main fragment; protect supraclavicular nerves during approach
Structural graft: indicated for large defects (>1.5–2 cm shortening); tricortical iliac crest graft restores clavicular length; prevents shoulder drooping and thoracic outlet syndrome; allograft (femoral head, fibula strut) avoids donor site morbidity
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References
Canadian Orthopaedic Trauma Society. Nonoperative treatment compared with plate fixation of displaced midshaft clavicular fractures. J Bone Joint Surg Am. 2007;89(1):1–10.
Boehm E et al. Surgical treatment of clavicle nonunion — plate fixation with and without bone grafting. J Shoulder Elbow Surg. 2012.
Enneking WF. A system of staging musculoskeletal neoplasms. Clin Orthop Relat Res. 1986.
Neer CS. Nonunion of the clavicle. JAMA. 1960.
Zlowodzki M et al. Systematic review of clavicle fracture treatment. J Orthop Trauma. 2005.
Khan LA et al. Clavicle fractures. J Am Acad Orthop Surg. 2009.
Barbier O et al. Plating of middle-third fractures of the clavicle — results and complications. J Shoulder Elbow Surg. 2009.
Ring D et al. Open reduction and internal fixation of displaced clavicular nonunion. J Orthop Trauma. 2004.
Campbells Operative Orthopaedics. 14th Edition. Elsevier.
Orthobullets — Clavicle Nonunion; Clavicle Fractures; Bone Graft Principles.
