Barrons Independent

Clavicle fractures represent approximately 5% of all adult fractures and are among the most common injuries of the shoulder girdle. While colloquial explanations often attribute these fractures to falls onto an outstretched hand (FOOSH), contemporary clinical and biomechanical evidence reveals a more nuanced interplay of anatomical vulnerabilities and force transmission mechanisms.

This report synthesizes current research to clarify the pathophysiology of clavicle fractures, evaluate the validity of common mechanistic assumptions, and explain why the clavicle serves as the "weak link" in traumatic shoulder injuries.

Anatomical Foundations Of Clavicular Vulnerability

Structural Characteristics

The clavicle is an S-shaped bone that functions as a strut between the sternum and the glenohumeral joint, maintaining shoulder girdle stability while protecting underlying neurovascular structures. Its midshaft - the junction of the medial and lateral curvatures - is the thinnest and least muscularly protected segment, making it the fracture site in 80% of cases. This anatomical bottleneck creates a stress concentration point during force transmission.

The bone’s cortical thickness decreases by 35% at the midshaft compared to its medial and lateral thirds, reducing bending resistance. Furthermore, the midshaft lacks direct ligamentous attachments, unlike the distal clavicle, which is stabilized by the coracoclavicular and acromioclavicular ligaments. These factors render the midshaft disproportionately vulnerable to failure under load.

Muscular And Ligamentous Forces

Six muscles exert dynamic forces on the clavicle:

• Proximal pull: Sternocleidomastoid and trapezius
• Distal pull: Pectoralis major, deltoid, and subclavius

During trauma, these muscles create opposing vectors that displace fracture fragments. For example, proximal fragments typically elevate due to sternocleidomastoid traction, while distal fragments depress under the weight of the arm. Ligamentous constraints at the sternoclavicular and acromioclavicular joints further modulate force distribution during impacts.

Mechanisms Of Injury: Direct Vs. Indirect Trauma

Direct Impact (Primary Mechanism)

Fall onto the lateral shoulder accounts for 81-94% of clavicle fractures. This mechanism delivers compressive force directly to the acromion, which propagates along the clavicular axis.

Biomechanical studies demonstrate that a 1,526 N axial load - equivalent to the force generated in a 1.5-meter fall - suffices to fracture cadaveric midshaft clavicles. The S-shaped morphology converts these axial loads into bending stresses, with failure initiating at the superoanterior cortex (tension side) and propagating posteriorly.

Indirect Mechanisms (FOOSH And Rare Scenarios)

While FOOSH injuries are frequently implicated in patient narratives, they account for only 6% of clavicle fractures. In such cases, force transmits from the hand through the radius, humerus, and glenohumeral joint before reaching the clavicle.

This indirect pathway more commonly causes distal humerus or wrist fractures (e.g., Colles’ fractures). When clavicular fractures do occur via FOOSH, they typically involve:

• Lateral compression: The humeral head impacts the glenoid, creating a lever arm that stresses the clavicle.
• Muscular recoil: Sudden trapezius contraction during arm hyperabduction generates torsional forces on the clavicular midshaft.

Comparative studies show indirect mechanisms produce less fracture displacement than direct impacts due to energy dissipation through adjacent joints and soft tissues.

Why The Clavicle Fails: Biomechanical And Epidemiological Factors

Stress Distribution And Failure Patterns

Finite element analyses reveal that clavicular stress under axial load peaks at the midshaft’s superoanterior cortex, correlating with clinical fracture patterns. The bone’s curvature increases bending moments by 22% compared to a straight strut, exacerbating tension forces on the convex surface. During direct shoulder impacts, the clavicle sustains 65% of the total force transmitted through the shoulder girdle, versus 15-20% in FOOSH mechanisms.

High-Risk Populations And Activities

• Contact sports: Football, hockey, and rugby players experience clavicle fractures at 3× the general population rate due to lateral shoulder impacts.
• High-energy trauma: Motor vehicle collisions and falls from height account for 18% of cases, often causing comminuted or bilateral fractures.
• Pediatric injuries: Clavicle fractures represent 10-15% of childhood fractures, typically from FOOSH mechanisms but with lower displacement due to robust periosteum.

Clinical Implications And Treatment Considerations

Diagnosis Challenges

While 90% of clavicle fractures are diagnosable via anteroposterior radiographs, computed tomography (CT) becomes critical for:

• Assessing posteriorly displaced medial fractures risking vascular injury.
• Evaluating coracoclavicular ligament integrity in distal fractures.

Conservative Vs. Surgical Management

Non-displaced fractures (<100% displacement, <2 cm shortening) heal successfully with sling immobilization in 92% of cases. However, displaced midshaft fractures(>2 cm shortening) have a 15-30% nonunion rate with conservative treatment due to persistent muscular deforming forces. Surgical indications include:

• Open fractures or neurovascular compromise
• Comminuted fractures with >20 mm displacement
• Polytrauma patients requiring early mobilization

Biomechanical comparisons of fixation techniques show:

• Pre-contoured plates reduce clavicular strain by 40% versus intramedullary nails.
• Dual-plating (superior + anterior) improves stability in oblique fractures but increases soft tissue dissection.

Debunking The "Weak Link" Hypothesis

The clavicle’s propensity to fracture stems not from inherent weakness but from its role as the primary load-bearing structure in the shoulder girdle. During direct impacts, it absorbs 70% of the kinetic energy that would otherwise injure the brachial plexus or subclavian vessels. Its fracture represents a protective failure mode - analogous to a mechanical fuse - that prevents more severe neurovascular damage.

While FOOSH mechanisms can theoretically transmit force to the clavicle, kinetic energy studies show 85% dissipates at the wrist and elbow during such falls. Thus, clavicle fractures via this route are uncommon except in high-velocity scenarios (e.g., cycling crashes at >30 km/h).

Conclusion

The clavicle’s anatomical configuration and biomechanical role make it susceptible to fracture during direct shoulder impacts - not primarily from FOOSH mechanisms. Its S-shaped morphology and midshaft cortical thinning create natural stress risers, while muscular forces exacerbate post-traumatic displacement.

Understanding these principles allows clinicians to educate patients about injury mechanisms, advocate for sport-specific protective gear, and select optimal treatment strategies. Future research should explore personalized fixation approaches based on fracture morphology and load-sharing requirements.