Aetiology

Almost all clavicle fractures are caused by acute trauma; stress fractures of the clavicle are rare. Among otherwise healthy adults, sport injuries, high-energy trauma, falls, and assaults are the main causative factors.

A direct fall on the shoulder (e.g., while playing sports) is the most common mechanism of injury in the population as a whole (87%), and especially in younger age groups (<30 years) and in males.[5][6]​​​[14]​​​​[15][16]​​​​​​ Road traffic accidents are another common cause.[3][5][6]​​​[16]​​​​​ In one study of clavicle fractures, of those resulting from a road traffic accident, 39% occurred in cyclists, 26% in car drivers or their passengers, 17% in motorcyclists, and 17% in pedestrians.[3]

A direct blow to the clavicle and a fall on the outstretched hand (6%) are less typical mechanisms of injury.[14][15]

Pathophysiology

Acute fracture causes moderate to severe pain, as well as impairment of function. Fractures may be associated with bleeding from the bone itself and from injured soft tissues and nearby vessels. Although this bleeding can be severe and even life-threatening (e.g., when a major vessel is lacerated), the haematoma that forms around the ends of the fracture serves as the start of the fracture healing process. Acute inflammatory mediators and cells head to and proliferate in and about the haematoma. While this may lead to local swelling and pain, the inflammatory response is an important part of healing.

The fracture haematoma also serves as a scaffold for subsequent callus formation. Within 8 hours of injury, increased cell division occurs in the periosteum and throughout the injured bone. Over the next few days, this increased cell division becomes more localised to the area of the fracture, and this continues for several weeks. In addition, mesenchymal stem cells are recruited to the fracture site, where they multiply and differentiate into osteogenic cells. This leads to the development of a soft cartilaginous callus between the fracture ends and superficial to the periosteum. This occurs about 7-10 days after the injury and starts to stabilise the fracture. Simultaneously, a central, hard callus starts to form subjacent to the periosteum, between the ends of the fracture.

Multiple growth factors allow for the development and ingrowth of new blood vessels to provide an adequate blood source for the ongoing work of healing. Hard cartilaginous callus formation peaks by around day 14 post injury, and this cartilage starts to become replaced by woven bone. This remodelling process starts 3-4 weeks post injury, and is implemented by osteoclasts resorbing the hard callus and osteoblasts depositing lamellar bone. Eventually, the external aspect of the callus becomes lamellar bone and the internal aspect is re-formed into a medullary cavity.[17]

Assuming proper stabilisation and adequate blood supply, fractures achieve union in around 6-12 weeks (with a faster healing time for children). Functional recovery of long bone fractures may take months beyond the point at which clinical and radiographic union occur, and the process of remodelling may not be fully complete for years.

Classification

Allman classification[1]

The Allman classification describes the location of a clavicle fracture, dividing the clavicle into thirds, with group I in the middle third, group II in the lateral third distal to the coracoclavicular (CC) ligaments, and group III in the medial third.

  • Group I: middle third of the clavicle

  • Group II: distal third of the clavicle

  • Group III: medial third of the clavicle

Neer classification[2]

The Neer classification divides distal clavicle fractures into three types based on the relationship of the fracture line to the CC ligaments and acromioclavicular (AC) joint.

Type I and III fractures occur distal to the CC ligaments, while type IIA fractures occur medial to the CC ligaments and type IIB occur between or lateral to the CC ligaments. Neer type II distal clavicle fractures are inherently less stable than types I and III.

Robinson[3]

Robinson developed a classification from a series of 1000 clavicle fractures reviewed over 6 years. It considers fracture location, displacement/angulation, and articular involvement/fragmentation. It divides fractures into three types (based on fracture location along the bone), with subgroups A and B (depending on displacement of the major fragments), and two further subgroups based on comminution.

Robinson’s classification defines displacement as more than 100% translation of the fracture fragments.[4]​

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