Contents

• Orientation: The Shoulder Girdle as a Suspensory System
• Part I - The Clavicle: Anatomy, Mechanism, and Classification
  • 1.1 Epidemiology and the unique nature of the bone
  • 1.2 Mechanism, deforming forces, and associated injuries
  • 1.3 Classification
• Part II - Management of Clavicle Fractures
  • 2.1 Midshaft fractures: the great operative controversy
  • 2.2 Lateral and medial clavicle fractures
  • 2.3 Complications
• Part III - The Acromioclavicular Joint
  • 3.1 Anatomy and the two planes of stability
  • 3.2 The Tossy-Rockwood classification (types I-VI)
  • 3.3 Treatment and the type III controversy
• Part IV - The Sternoclavicular Joint
  • 4.1 Anatomy: an incongruent joint held by ligaments
  • 4.2 Classification, mechanism, and the posterior dislocation emergency
  • 4.3 Treatment of the posterior dislocation
• Part V - Fractures of the Scapula
  • 5.1 A rare fracture and a marker of high energy
  • 5.2 Anatomy and imaging
  • 5.3 Classification
  • 5.4 Treatment
• Part VI - The Suspensory Complex, the Floating Shoulder, and Scapulothoracic Dissociation
  • 6.1 The superior shoulder suspensory complex and double disruption
  • 6.2 The floating shoulder
  • 6.3 Scapulothoracic dissociation
• Part VII - Chest-Wall (Thoracic Cage) Injuries
  • 7.1 Rib fractures: a marker, and a risk in their own right
  • 7.2 Associated thoracic injuries
  • 7.3 Flail chest
  • 7.4 Management
• Part VIII - A Synthesis: How to Reason Through Shoulder-Girdle and Chest-Wall Trauma
• References

Orientation: The Shoulder Girdle as a Suspensory System

The injuries gathered under this topic, fractures of the clavicle and scapula, dislocations of the acromioclavicular and sternoclavicular joints, and trauma to the thoracic cage, are united by a single idea: the upper limb is suspended from the axial skeleton rather than rigidly bolted to it. The only true bony articulation between the arm and the trunk is the sternoclavicular joint, a small, incongruent joint that bears almost none of the load directly.[1] Everything lateral to it (the clavicle, the acromioclavicular joint, the scapula with its glenoid, and the muscular envelope) forms a sprung, mobile linkage that trades stability for the enormous range of motion the shoulder enjoys. The clavicle is the strut that holds the shoulder out from the chest, the scapula is the mobile platform on which the glenohumeral joint sits, and the ligaments of the two clavicular ends are the suspension cables.

Two consequences follow, and they organise the whole topic. First, because the girdle is a ring-and-strut system, its components fail in predictable patterns. A laterally directed force can break the clavicle, dislocate the AC joint, or dislocate the SC joint, the three “weak links” in the same chain.[2] Second, because the scapula and the upper ribs lie buried in muscle against a high-energy-absorbing chest wall, a fracture of the scapula or of the first ribs is less important for itself than as a marker that great force has been delivered to the thorax, with all the lethal visceral injury that implies. The candidate who keeps the suspensory model in mind will understand why a floating shoulder is unstable, why a posterior sternoclavicular dislocation is a mediastinal emergency, and why a scapular fracture should prompt a hunt for a pneumothorax rather than a cast.

Part I - The Clavicle: Anatomy, Mechanism, and Classification

1.1 Epidemiology and the unique nature of the bone

Clavicle fractures account for about 2.6% of all fractures and are concentrated in the young and active, particularly in high-speed-fall sports such as cycling and motorcycling and in collision sports.[3] Their incidence is rising: a Swedish register recorded an increase from 36 to 59 per 100,000 person-years between 2001 and 2012, with a striking 705% rise in surgical fixation over the same period, a number that captures the modern shift toward operative treatment discussed below.[4] The distribution by site is examinable and clinically decisive: the midshaft (middle third) accounts for 80-85%, the lateral (distal) third for 15-20% (these favour the elderly after simple falls), and the medial third for only 0-5%, the rarest and the most ominous.[5]

The clavicle is a genuinely unusual bone. It is the first bone in the body to ossify, in the fifth embryonic week, and its medial (sternal) epiphysis is the last of all the long-bone epiphyses to fuse, often not until 23-25 years and occasionally as late as 31.[6] This single fact resolves a recurring diagnostic trap. In a patient under 25, what looks like a sternoclavicular dislocation or a medial clavicle fracture is frequently a physeal (Salter-Harris) injury through that late-closing growth plate.[7] The bone’s S-shape gives it its name (from clavicula, a small musical key). Its middle third is the weakest point, being the thinnest, the most sharply curved, and the only segment with no muscular or ligamentous attachment to buttress it.[8]

The familiar teaching that the clavicle is the only long bone to ossify by intramembranous (rather than endochondral) ossification is correct and worth knowing, though the mined sources state only that it is the first bone to ossify and do not use that exact phrase.[9]

1.2 Mechanism, deforming forces, and associated injuries

The dominant mechanism is a direct blow to the point of the shoulder, in a fall or a tackle; the once-cited “fall on the outstretched hand” is now questioned.[10] The resulting deformity is three-dimensional and predictable from the muscle pulls: the medial fragment is pulled up and back by the sternocleidomastoid, while the lateral fragment is drawn down by the weight of the arm and the deltoid and medially by the pectoralis major, producing the typical shortened, drooped, anteriorly rotated shoulder.[11] A different, traction mechanism, the arm violently pulled or pinned, produces the far graver picture of scapulothoracic dissociation, recognisable on the radiograph because the fracture is distracted and widely separated rather than shortened and overlapped.[12]

The subclavian vessels and the brachial plexus lie immediately beneath the bone, the plexus closest to the clavicle in its midportion, yet acute neurovascular injury is surprisingly uncommon. When it occurs it is usually a traction injury to the cervical roots with a poor prognosis, most often in the setting of scapulothoracic dissociation, the “closed forequarter amputation”.[13] More routinely, high-energy clavicle fractures keep dangerous company: ipsilateral rib and scapular fractures, pneumothorax, and, in polytrauma series, a mortality of 20-34% driven by the associated head and chest injuries.[14] An open clavicle fracture, rare given the subcutaneous position, is a particular red flag for serious concomitant injury and warrants antibiotics and usually operative stabilisation.[15]

1.3 Classification

Four schemes are in use. The oldest, Allman, simply divides the bone into thirds (middle, lateral, medial).[16] The Neer classification of distal-third fractures is the one that changes management, because it hinges on the coracoclavicular ligaments:[17]

• Type I: fracture lateral to intact CC ligaments, minimally displaced and stable.
• Type II: the CC ligaments are detached from the medial fragment, so the medial fragment is unstable and the nonunion rate is high (subdivided by Rockwood into IIA, with both conoid and trapezoid on the distal fragment, and IIB, with the conoid torn).
• Type III: an intra-articular fracture extending into the AC joint.

The Robinson (Edinburgh) classification, the most prognostically useful, was derived from over 1,000 patients and confusingly reverses the numbering: type 1 is medial, type 2 is diaphyseal, type 3 is lateral, each subdivided by displacement and articular involvement.[18] Finally the AO/OTA scheme codes the clavicle as segment 15 (medial, shaft, lateral) with the usual simple/wedge/complex diaphyseal subdivisions.[19]

Imaging is usually a single AP film, ideally taken upright (gravity maximises the deformity) with a 20° cephalad tilt to clear the thoracic cage. A supine trauma film underestimates displacement by nearly 90% compared with an upright film, enough to change the treatment recommendation.[20] Shortening is measured against the uninjured side, and CT is reserved for the medial third, where plain films are notoriously unreliable.[21]

Part II - Management of Clavicle Fractures

2.1 Midshaft fractures: the great operative controversy

For decades the clavicle was the textbook “benign” fracture. Neer reported only 3 nonunions in 2,235 middle-third fractures and Rowe 0.8% in 566, and malunion was dismissed as a radiographic curiosity.[22] Those figures, it is now recognised, were inflated by selection bias (complex fractures were operated), incomplete follow-up, and the inclusion of children with their excellent remodelling.[23] Modern, patient-oriented data on displaced midshaft fractures tell a very different story. Hill found 15% nonunion and 31% unsatisfactory results, Zlowodzki’s meta-analysis confirmed a 15.1% nonunion rate with nonoperative care, and Robinson reported up to 21% nonunion in displaced comminuted fractures.[24] Even united fractures can disappoint. Nowak found 46% of patients still symptomatic at ten years despite only 7% nonunion, and McKee documented measurable strength and endurance deficits, establishing symptomatic malunion as a real entity.[25]

The decisive evidence came from randomised trials. The Canadian Orthopaedic Trauma Society (COTS) trial of 2007, the first published RCT, showed that primary plate fixation of completely displaced midshaft fractures reduced nonunion and symptomatic malunion and improved function.[26] Zlowodzki’s review found plating cut nonunion from 15.1% to 2.2% (an 86% relative reduction), McKee’s meta-analysis of six RCTs found nonunion-plus-symptomatic-malunion fell from 23% to 1.4%, and the large Clavicle Trial (Ahrens) found 11% nonunion with a sling versus 1% with a plate plus better early function.[27] The honest balance, stated by both source texts, is that the functional advantage of surgery is real but modest, on the order of 10 points on a 100-point scale. Some trials show equivalent long-term scores with a higher reoperation rate in the surgical group (largely for hardware removal), and “the operative pendulum should not swing into indiscriminate fixation.”[28]

The accepted fracture-specific indications for surgery are therefore complete displacement (no cortical contact), shortening greater than 2 cm, marked comminution or a segmental pattern, an open fracture or threatened skin, plus the associated indications of vascular injury, progressive neurological deficit, a floating shoulder, bilateral fractures, multiple ipsilateral rib fractures, and polytrauma needing early arm use.[29] When surgery is chosen, a 3.5-mm compression or precontoured plate is the gold standard (reconstruction-type plates are too weak and fail by fatigue), with union rates of 94-100%.[30] Intramedullary fixation (or an elastic titanium nail) gives a smaller scar and less prominence but controls length and rotation poorly. It is therefore reserved for simple transverse or short-oblique patterns and must never be used for comminuted fractures, which telescope. Smooth wires and pins are contraindicated about the shoulder because of the lethal risk of migration.[31] High-level evidence finds no difference in outcome between plating and nailing, with more hardware removals after nailing and slightly more major complications after plating.[32]

Nonoperative treatment is a simple sling; a figure-of-eight bandage is no better and is less comfortable, and if applied too tightly it can cause a transient lower-trunk plexus palsy.[33]

2.2 Lateral and medial clavicle fractures

Displaced lateral (Neer II) fractures have a high rate of delayed and non-union, variously reported at 22-40%, yet that nonunion is often minimally symptomatic. Robinson found only 14% eventually came to surgery among displaced lateral fractures, which is the modern argument for treating most of them nonoperatively.[34] When fixation is needed (severe displacement, high demand, or symptomatic nonunion), the challenge is purchase in the small distal fragment. Options include an anatomic distal-clavicle locking plate, coracoclavicular augmentation, or a hook plate (whose hook sits in the subacromial space and which routinely needs removal to regain full elevation).[35]

Medial-third fractures are rare and ominous. One series found them in middle-aged men after motor-vehicle trauma with a 20% mortality from associated head and chest injury, so the fracture itself is mostly treated nonoperatively while the patient is investigated for those associated injuries.[36] The literature genuinely disagrees about the demographic, one paper linking medial fractures to elderly osteoporotic falls and another to high-energy trauma. In the young, the late medial physis again means many are physeal injuries best defined by CT.[37]

2.3 Complications

Four complications dominate after midshaft fractures. Nonunion is failure to heal by six months; the risk factors are complete displacement, shortening over 2 cm, comminution, female sex, advanced age, and refracture, and the treatment is compression plating with bone graft. Malunion is governed chiefly by shortening and is corrected by osteotomy and plating. Hardware prominence is the commonest reason for reoperation. Finally there are the rare but serious late neurovascular problems, chiefly thoracic-outlet compression from hypertrophic callus, for which corrective osteotomy, not “removing the bump”, is the treatment.[38] Plates should not be removed routinely, and not before two years after union, to avoid refracture.[39]

Part III - The Acromioclavicular Joint

3.1 Anatomy and the two planes of stability

The acromioclavicular joint is stabilised in two orthogonal planes by two different ligament systems, and this is the single most important fact for understanding its injuries. The acromioclavicular (capsular) ligaments, of which the superior is the strongest, control horizontal (anteroposterior) stability.[40] The coracoclavicular ligaments, the conoid (more medial, on the conoid tubercle) and the trapezoid (more lateral), control vertical (superoinferior) stability and are the prime suspensory ligaments of the upper limb.[41] Overlying both is the deltotrapezial fascia, the last structure to fail. Once the distal clavicle buttonholes through it, the dislocation becomes irreducible.[42] The normal coracoclavicular distance is 1.1-1.3 cm, and an increase of 50% over the normal side signifies a complete dislocation.[43]

The mechanism is a fall onto the point of the shoulder with the arm adducted, driving the acromion down and medially and tearing the ligaments in sequence, AC ligaments first, then CC ligaments, then the deltotrapezial fascia.[44] A common misconception is worth correcting here. The clavicle does not “ride up”. Rather the whole shoulder girdle droops downward once its suspension fails, and only the slight upward pull of the trapezius lifts the clavicle.[45]

3.2 The Tossy-Rockwood classification (types I-VI)

The six-type classification grades the progressive injury to the AC ligaments, the CC ligaments, and the muscle attachments:[46]

• Type I: a sprain of the AC ligaments; ligaments intact, radiographs normal.
• Type II: the AC ligaments are torn but the CC ligaments only sprained; the joint is unstable horizontally but vertically intact, and the CC distance equals the normal side.
• Type III: both AC and CC ligaments are torn, a complete dislocation, with a 25-100% increase in the CC distance.
• Type IV: the distal clavicle is displaced posteriorly into or through the trapezius, best seen on the axillary view.
• Type V: a severe type III, with the clavicle stripped of its deltotrapezial attachments and lying subcutaneously, the CC distance increased more than 100% (100-300%).
• Type VI: the rare inferior dislocation, the clavicle lodged in a subacromial or subcoracoid position.

Imaging uses the Zanca view (a 10-15° cephalad tilt at half the usual penetration) with bilateral comparison, and the axillary view to detect the posterior displacement of a type IV.[47] The once-standard weighted stress views are no longer recommended, because they do not change the grade or the treatment and are painful.[48]

3.3 Treatment and the type III controversy

There is firm consensus that types I and II are treated nonoperatively and that types IV, V, and VI are treated operatively in the active patient.[49] Type III is the long-standing controversy. The pendulum swung from conservative (1930s-40s) to operative (1950s-70s) and back again. Modern surveys show most surgeons favour initial nonoperative care, randomised trials show quicker recovery and fewer complications without surgery (Bannister found an operative advantage only in the subgroup displaced more than 2 cm), and the chapter concludes bluntly that “no high-quality prospective study has demonstrated surgical benefit for type III injuries.”[50] The reasonable default is a trial of nonoperative care for six to eight weeks, reserving surgery for failures, overhead athletes, heavy labourers, and polytrauma.[51]

The widely taught ISAKOS subdivision of type III into IIIA (stable) and IIIB (unstable), used to guide which type III injuries merit surgery, is standard teaching but was not present in the mined chapter.[52] When reconstruction is required, the modern operation is an anatomic coracoclavicular ligament reconstruction with a tendon graft through clavicular tunnels at the conoid and trapezoid insertions. This is biomechanically superior to the older modified Weaver-Dunn transfer of the coracoacromial ligament, which restores only about a quarter of native CC strength and leaves up to 30% recurrent instability.[53] Across all techniques, the historical lesson is the same as for the clavicle: transarticular pins and smooth wires must be avoided because of migration and reported deaths.[54]

Part IV - The Sternoclavicular Joint

4.1 Anatomy: an incongruent joint held by ligaments

The sternoclavicular joint is a saddle-type diarthrodial joint with less than 50% bony congruity, so that, as with the AC joint, its stability comes almost entirely from its ligaments: the intra-articular disc, the costoclavicular (rhomboid) ligament, the interclavicular ligament, and above all the capsule.[55] The capsular ligament is the strongest structure and the most important restraint to upward displacement, and within it the posterior capsule is the single most important structure preventing both anterior and posterior translation.[56] As already noted, the medial epiphysis is the last to fuse (23-25 years, occasionally to 31), so in young patients SC “dislocations” are often physeal injuries.[57] The clinical danger of this joint lies entirely behind it. A curtain of vital structures (the brachiocephalic (innominate) artery and vein, trachea, oesophagus, vagus and phrenic nerves, and the great veins) lies immediately posterior to the medial clavicle.[58]

4.2 Classification, mechanism, and the posterior dislocation emergency

SC injuries are graded as sprain, subluxation, or dislocation, and classified by direction into anterior (much the commoner) and posterior (retrosternal) dislocation.[59] The mechanism is usually indirect: a force compressing and rolling the shoulder forward produces a posterior dislocation, and rolling it backward produces an anterior one; a direct blow to the anteromedial clavicle drives it posteriorly into the mediastinum.[60]

The anterior dislocation is benign. Closed reduction is usually unstable but the residual prominence is well tolerated, and chronic anterior instability is best managed by “skillful neglect.”[61] The posterior dislocation is a true emergency, because the displaced clavicle can compress or lacerate the structures behind it, producing dyspnoea, dysphagia, venous congestion, a weak pulse, hoarseness, or pneumothorax. One literature review found mediastinal complications in 27% of posterior dislocations.[62] CT (of both joints and the medial clavicles) is the imaging modality of choice, supplemented if needed by the serendipity view, and CT angiography if vascular injury is suspected.[63]

4.3 Treatment of the posterior dislocation

The treatment of choice is closed reduction, and it should be performed in an operating theatre with a cardiothoracic team and bypass capability on standby, because reduction can re-open a vessel the clavicle was tamponading.[64] Reduction is by abduction-traction on the arm with a bolster between the scapulae, lifting the medial clavicle with the fingers or, if needed, a sterile towel clip around the clavicular shaft. Most reduce within 48 hours and are then stable.[65] If open treatment is required, the medial clavicle is stabilised by capsular repair or a figure-of-eight tendon graft, and the costoclavicular ligament must be preserved or reconstructed. Smooth pins and K-wires across the SC joint are absolutely contraindicated because of fatal migration.[66] A distinction matters in the young. An asymptomatic, irreducible posterior physeal injury may be observed, since it will remodel, whereas a true dislocation will not.[67]

Part V - Fractures of the Scapula

5.1 A rare fracture and a marker of high energy

Scapular fractures are rare, only 0.4-0.9% of all fractures and 3-5% of shoulder-girdle injuries, because the bone is protected by a thick muscular envelope and rides on an elastic chest wall.[68] Their importance is largely as a marker of high-energy trauma. Associated injuries occur in 80-95% of operative series, including rib fractures (up to 65%), thoracic and pulmonary injuries (up to 67%), head injuries (up to 42%), and a mortality of 2-11% driven by intrathoracic injury.[69] The practical lesson is that finding a scapular fracture should trigger a deliberate search for the injuries that accompany it. The great majority of scapular fractures, especially isolated body fractures, are treated nonoperatively, with good results.[70]

5.2 Anatomy and imaging

The scapula’s load is carried by two thick pillars, the lateral pillar (lateral border to inferior angle) and the spinal pillar (glenoid to spine base), connected by the thin medial border. The central body is only a few millimetres thick.[71] The suprascapular nerve, running through the scapular notch and around the spinoglenoid notch, is at risk both in surgical-neck fractures and during surgery.[72] CT with three-dimensional reconstruction is the gold standard, and four measured parameters drive the surgical decision: the glenopolar angle (GPA), medio-lateral displacement (lateral border offset), angulation, and articular step or gap.[73] The GPA, the angle between the glenoid axis and a line to the inferior scapular angle, has a normal range of roughly 30-45°, and a low value (below about 20-22°) indicates significant deformity.[74]

5.3 Classification

Fractures are divided anatomically into glenoid (intra-articular), neck, body, and processes (in Bartoníček’s 375-case series, body fractures were the commonest at 50%, glenoid 24%, processes/borders 20%, and neck only 6%).[75] The named classifications worth knowing are the Ideberg classification of intra-articular glenoid fractures (type 1 anterior rim, type 2 inferior through the neck, type 3 superior through the coracoid base, type 4 horizontal through neck and body, type 5 type-4-plus-a-neck-fracture) and its Goss modification (which splits the rim into anterior Ia and posterior Ib and adds a type VI for comminution).[76] The AO/OTA scheme codes the scapula simply as processes, body, and glenoid (or fossa, body, processes), and the Ada-Miller and Ogawa schemes are also in use.[77]

5.4 Treatment

Intra-articular glenoid fractures are fixed when there is an articular step or gap (the threshold ranges across authors from 2 to 10 mm, most settling on about 4-5 mm) together with involvement of roughly 20-30% of the surface or persistent glenohumeral subluxation.[78] Extra-articular neck and body fractures are operated for severe displacement, the criteria being roughly 100% translation, 30-45° angulation, lateral-border offset of 1-2 cm, or a GPA below 20-22°. The exact numbers vary between authors and the sources openly disagree (for example, the critical GPA is given as ≤20° in Rockwood and ≤22° by Cole in Skeletal Trauma).[79] The workhorse exposure for the body, neck, and posterior glenoid is the posterior Judet approach, while the anteroinferior glenoid rim is reached through a deltopectoral approach.[80] Scapular fractures heal in 6-8 weeks and nonunion is very rare.[81]

Part VI - The Suspensory Complex, the Floating Shoulder, and Scapulothoracic Dissociation

6.1 The superior shoulder suspensory complex and double disruption

Goss conceptualised the superior shoulder suspensory complex (SSSC) as a bony-and-soft-tissue ring (the glenoid, coracoid, coracoclavicular and coracoacromial ligaments, distal clavicle, AC joint, and acromion) slung between two bony struts: the superior strut, the middle third of the clavicle, and the inferior strut, the junction of the lateral scapular body and spine.[82] A single break in the ring is generally stable because the remaining structures hold the parts in place. A double disruption (two breaks in the ring, or one break plus a fractured strut) is potentially unstable and prone to displacement, delayed union, and malunion.[83]

6.2 The floating shoulder

The floating shoulder, classically an ipsilateral fracture of the clavicle and the scapular neck, is the best-known double disruption.[84] Its management is genuinely contested. Williams showed biomechanically that the shoulder only truly “floats” once the CC and CA ligaments are also disrupted, because until then the glenoid remains tethered to the acromion and clavicle.[85] Skeletal Trauma (Cole) treats a displaced double lesion as a surgical entity and recommends fixing both the clavicle and the scapula when both are displaced more than 1 cm, observing that fixing the clavicle alone can leave a malunited, drooping scapula.[86] Rockwood (Bartoníček) is more sceptical, arguing that many reported “neck” fractures are actually infraspinous body fractures that do not destabilise the glenoid, and that a midshaft clavicle fracture is largely irrelevant to glenoid position.[87] The reasonable synthesis is that the genuinely displaced double lesion warrants fixation, that fixing the clavicle is often the key step, and that the older blanket recommendation to operate on every floating shoulder was too aggressive.[88]

6.3 Scapulothoracic dissociation

At the extreme end of the spectrum is scapulothoracic dissociation, a rare, devastating, high-energy injury in which the whole shoulder girdle is laterally distracted from the chest wall, a closed forequarter avulsion.[89] It combines shoulder-girdle disruption (SC dislocation, clavicle fracture, or AC dislocation), massive muscle tearing, subclavian or axillary vascular injury, and partial or complete brachial plexus avulsion, with the skin usually intact. Mortality is about 11%.[90] The Zelle classification grades it by the associated injury (type 1 musculoskeletal only, 2A with vascular injury, 2B with incomplete neurological injury, 3 with both, 4 with complete plexus avulsion). The extent of the plexus injury is the dominant prognostic factor: a complete avulsion is functionally an amputation, and early above-elbow amputation may give the best result.[91]

Part VII - Chest-Wall (Thoracic Cage) Injuries

7.1 Rib fractures: a marker, and a risk in their own right

Up to 39% of patients with blunt chest trauma sustain rib fractures, and the number of broken ribs is an independent predictor of morbidity and mortality.[92] The mechanism is the pain-splinting cascade: pain causes shallow breathing and suppressed coughing, leading to atelectasis, retained secretions, and pneumonia.[93] The location of the fractures carries specific warnings. Fractures of the first three ribs, well protected behind the scapula, mark very high energy; the classic teaching that they flag great-vessel, brachial-plexus, or head injury is standard, though the mined orthopaedic text states only that ribs 1-3 indicate high energy.[94] Fractures of the lower ribs (8-12) point to intra-abdominal injury. A right-sided fracture at or below the eighth rib carries a 19-56% chance of liver injury, and a left-sided fracture a 22-28% chance of splenic injury, with three or more ribs raising the relative risk of splenic injury to 6.2.[95] In the elderly, a less compliant chest wall fractures with less energy and tolerates it far worse. Each additional rib fracture raises mortality by about 19% and pneumonia risk by 27%, and the odds of death are roughly 2.5 times higher above 64 years than in young adults.[96]

7.2 Associated thoracic injuries

Rib fractures keep dangerous company, and the candidate must be able to define the immediately life-threatening injuries. Tension pneumothorax is the classic emergency: air trapped under pressure shifts the mediastinum and obstructs venous return. Its bedside diagnosis (tracheal deviation away from the side of injury, distended neck veins, absent breath sounds, hypotension) and its treatment (immediate needle decompression followed by a chest tube) are core ATLS teaching. This orthopaedic chest-wall chapter describes only the principle that a small pneumothorax can become a tension pneumothorax under positive-pressure ventilation, requiring urgent tube thoracostomy.[97] Massive haemothorax (the standard thoracotomy thresholds of an initial 1500 mL drained or ongoing 200 mL/hr are also ATLS rather than this orthopaedic text) requires a large-bore (≥32F) chest tube.[98]

Pulmonary contusion is the injury that most often determines the outcome of chest-wall trauma. It is a parenchymal injury with alveolar and capillary haemorrhage that reduces compliance and increases shunt. It develops over hours (it may be invisible on the initial film and take up to 48 hours to appear, though CT shows it at once) and drives respiratory failure and ARDS: a contusion involving more than 20% of lung volume produces ARDS about 82% of the time versus 22% below that threshold.[99] Cardiac contusion and tamponade, aortic and tracheobronchial injury, and diaphragmatic rupture complete the list of associated injuries to be excluded.[100]

7.3 Flail chest

A flail chest is, anatomically, a segment of chest wall that has lost continuity with the rest, classically three or more consecutive ribs each fractured in two or more places (the sources disagree on the exact count, Skeletal Trauma using four consecutive unilateral ribs).[101] Clinically it produces paradoxical motion, the segment sucking inward on inspiration and bulging outward on expiration. One caveat matters: a radiographic flail with undisplaced fractures or one splinted by muscle or hidden under the scapula need not show paradoxical motion.[102] The pivotal historical insight is that the respiratory failure of flail chest is driven less by the mechanical instability than by the underlying pulmonary contusion. Trinkle’s landmark work in 1975 showed that treating the lung injury (analgesia, pulmonary toilet, selective ventilation) rather than obligatorily ventilating every flail chest to “internally splint” it dramatically reduced ventilator days, complications, and mortality.[103]

7.4 Management

The three pillars of nonoperative care, which apply from a single painful rib to a flail chest, are multimodal analgesia (with regional techniques, the thoracic epidural the most effective), aggressive pulmonary toilet and physiotherapy, and selective mechanical ventilation guided by gas exchange rather than by chest-wall instability.[104] Ventilation is for respiratory failure, not for the flail itself, and should be weaned as fast as possible. Strapping or binding the chest is abandoned because it worsens the very atelectasis it was meant to prevent.[105]

Surgical stabilisation of rib fractures (SSRF) has grown rapidly (from under 1% of cases before 2010 to about 10% after) and is now indicated chiefly for flail chest with respiratory failure or failure to wean, a severely displaced chest-wall deformity, ribs impaling viscera, or intractable pain or nonunion, and opportunistically when a thoracotomy is being done for another reason.[106] The evidence in flail chest, three small RCTs and several meta-analyses, points consistently to fewer ventilator days, less pneumonia, fewer tracheostomies, shorter ICU stays, and probably lower mortality, though the trials are small and used dated implants, and a large definitive RCT is awaited.[107] Two cautions recur. Severe pulmonary contusion may abolish the benefit of fixation (a disputed relative contraindication), and ribs 1-2 (hard to reach) and the floating ribs 11-12 (which add no stability) are generally not fixed.[108] The optimal window is within about four to five days of injury.[109]

Sternal fractures are not detailed in the mined orthopaedic chapter beyond the concept of a central or “sternal” flail; standard teaching is that they arise from a direct blow (the steering wheel) or deceleration, are associated with cardiac contusion (warranting an ECG and observation), and are managed nonoperatively unless markedly displaced, unstable, or ununited.[110]

Part VIII - A Synthesis: How to Reason Through Shoulder-Girdle and Chest-Wall Trauma

Five habits of thought carry the candidate through this topic. First, think of the girdle as a suspensory ring: identify which link has failed (clavicle, AC joint, SC joint, scapular strut) and whether a second link has also failed, because a single break is usually stable and a double break (a floating shoulder, a double SSSC disruption) is not. Second, treat the rare and the buried fractures as messengers: a scapular fracture, a first-rib fracture, or a sternoclavicular injury is a flag for high-energy thoracic and visceral trauma, so the reflex should be to image the chest and abdomen, not to apply a sling. Third, respect the two true emergencies of this region, the posterior sternoclavicular dislocation, which can throttle the mediastinum, and the tension pneumothorax, which can arrest the circulation. Both are recognised clinically and treated before imaging is complete. Fourth, let ligaments, not bones, define stability at the two clavicular joints: the AC ligaments hold the horizontal plane and the CC ligaments the vertical, the SC posterior capsule holds both, and operative plans that ignore these soft tissues fail. Fifth, know where the evidence is genuinely unsettled: the displaced midshaft clavicle (operate or not), the type III AC dislocation (almost always not), the floating shoulder (fix one bone or both), and the role of rib fixation in the contused flail chest. Present these as the live controversies they are rather than as settled rules.

The recurring theme is that the shoulder girdle and the thoracic cage are not isolated mechanical structures but the bony shell over the great vessels, the brachial plexus, and the lungs. The fractures in this chapter are frequently trivial in themselves and frequently lethal in their company, and the examiner is testing whether the candidate looks past the obvious broken bone to the danger behind it.

References

1. Rockwood & Green’s Fractures in Adults, p.1576 (the SC joint is the only true articulation between the upper extremity and the axial skeleton).

2. Rockwood & Green’s Fractures in Adults, p.1696 (with lateral compression of the shoulder girdle the clavicle is the main strut, and the system fails at the AC joint, the clavicle, or the SC joint).

3. Rockwood & Green’s Fractures in Adults, p.1693.

4. Rockwood & Green’s Fractures in Adults, p.1716 (Swedish Hospital Discharge Register).

5. Rockwood & Green’s Fractures in Adults, p.1694; Skeletal Trauma, pp.1700-1701.

6. Rockwood & Green’s Fractures in Adults, p.1548; Skeletal Trauma, pp.1694-1695.

7. Rockwood & Green’s Fractures in Adults, pp.1571-1572, p.1744.

8. Skeletal Trauma, pp.1694-1695.

9. The statement that the clavicle is the only long bone formed by intramembranous ossification is standard embryological teaching; the mined Rockwood and Skeletal Trauma extracts state that it is the first bone to ossify (fifth embryonic week) and describe its membranous origin and late medial physis, but do not use the verbatim phrase. Included for completeness, not falsely page-cited.

10. Rockwood & Green’s Fractures in Adults, p.1696; Skeletal Trauma, p.1701.

11. Rockwood & Green’s Fractures in Adults, pp.1697, 1713.

12. Rockwood & Green’s Fractures in Adults, p.1703.

13. Rockwood & Green’s Fractures in Adults, p.1714; Skeletal Trauma, p.1702.

14. Rockwood & Green’s Fractures in Adults, pp.1700, 1703.

15. Rockwood & Green’s Fractures in Adults, pp.1705-1706.

16. Rockwood & Green’s Fractures in Adults, p.1708.

17. Rockwood & Green’s Fractures in Adults, p.1708; Skeletal Trauma, p.1700.

18. Rockwood & Green’s Fractures in Adults, pp.1708-1709. The full alphanumeric Robinson subgroups (e.g. 2A undisplaced/cortical-alignment versus 2B displaced, with the 1A/1B and 3A/3B subdivisions) are presented in the source as a figure rather than transcribed in the text; the type 1/2/3 framework and the displacement/comminution subdivision are given. The detailed subgroups are standard teaching (Robinson, JBJS Br 1998).

19. Rockwood & Green’s Fractures in Adults, pp.1708-1709; Skeletal Trauma, p.1701.

20. Rockwood & Green’s Fractures in Adults, p.1706 (Backus: 89% increase in displacement on upright films).

21. Rockwood & Green’s Fractures in Adults, pp.1706-1707.

22. Rockwood & Green’s Fractures in Adults, p.1694; Skeletal Trauma, p.1703.

23. Rockwood & Green’s Fractures in Adults, pp.1718, 1751.

24. Rockwood & Green’s Fractures in Adults, pp.1694, 1718, 1751.

25. Rockwood & Green’s Fractures in Adults, pp.1710, 1718, 1751, 1754.

26. Rockwood & Green’s Fractures in Adults, p.1768; Skeletal Trauma, pp.1703, 1716.

27. Rockwood & Green’s Fractures in Adults, pp.1695, 1718, 1751.

28. Rockwood & Green’s Fractures in Adults, pp.1696, 1718, 1768; Skeletal Trauma, p.1703.

29. Rockwood & Green’s Fractures in Adults, pp.1719-1720; Skeletal Trauma, p.1703.

30. Rockwood & Green’s Fractures in Adults, pp.1735-1736; Skeletal Trauma, p.1703.

31. Rockwood & Green’s Fractures in Adults, pp.1722-1723, 1727; Skeletal Trauma, p.1706.

32. Rockwood & Green’s Fractures in Adults, pp.1694, 1727.

33. Rockwood & Green’s Fractures in Adults, p.1718.

34. Rockwood & Green’s Fractures in Adults, pp.1742-1743; Skeletal Trauma, pp.1699, 1709.

35. Rockwood & Green’s Fractures in Adults, pp.1738-1743.

36. Rockwood & Green’s Fractures in Adults, p.1694.

37. Skeletal Trauma, p.1700; Rockwood & Green’s Fractures in Adults, p.1744.

38. Rockwood & Green’s Fractures in Adults, pp.1751-1762; Skeletal Trauma, pp.1711-1713.

39. Rockwood & Green’s Fractures in Adults, pp.1738, 1762; Skeletal Trauma, p.1713.

40. Rockwood & Green’s Fractures in Adults, pp.1573, 1575.

41. Rockwood & Green’s Fractures in Adults, pp.1573-1575.

42. Rockwood & Green’s Fractures in Adults, pp.1542, 1569.

43. Rockwood & Green’s Fractures in Adults, p.1565.

44. Rockwood & Green’s Fractures in Adults, p.1542.

45. Rockwood & Green’s Fractures in Adults, p.1542.

46. Rockwood & Green’s Fractures in Adults, pp.1562-1564, 1569.

47. Rockwood & Green’s Fractures in Adults, pp.1543, 1553, 1557.

48. Rockwood & Green’s Fractures in Adults, p.1549.

49. Rockwood & Green’s Fractures in Adults, pp.1578, 1590.

50. Rockwood & Green’s Fractures in Adults, pp.1579-1581, 1589.

51. Rockwood & Green’s Fractures in Adults, pp.1580-1581, 1590.

52. The ISAKOS subdivision of Rockwood type III into IIIA (stable, non-operative) and IIIB (unstable, consider surgery) is standard modern teaching (ISAKOS Upper Extremity Committee consensus, 2014) but is not present in the mined Rockwood chapter, which discusses the type III controversy without it. Included for completeness, not falsely page-cited.

53. Rockwood & Green’s Fractures in Adults, pp.1590-1591, 1593-1600.

54. Rockwood & Green’s Fractures in Adults, pp.1590, 1619.

55. Rockwood & Green’s Fractures in Adults, pp.1576-1577.

56. Rockwood & Green’s Fractures in Adults, p.1578 (Bearn; Spencer et al.).

57. Rockwood & Green’s Fractures in Adults, pp.1548, 1571.

58. Rockwood & Green’s Fractures in Adults, pp.1575-1576.

59. Rockwood & Green’s Fractures in Adults, p.1571.

60. Rockwood & Green’s Fractures in Adults, pp.1543-1544.

61. Rockwood & Green’s Fractures in Adults, pp.1582-1583.

62. Rockwood & Green’s Fractures in Adults, pp.1545-1546, 1549, 1621 (Worman & Leagus: 16 of 60, 26.7%).

63. Rockwood & Green’s Fractures in Adults, pp.1549, 1558, 1560-1561.

64. Rockwood & Green’s Fractures in Adults, pp.1583-1584.

65. Rockwood & Green’s Fractures in Adults, pp.1584-1586.

66. Rockwood & Green’s Fractures in Adults, pp.1604-1605, 1610, 1615.

67. Rockwood & Green’s Fractures in Adults, pp.1587-1589.

68. Rockwood & Green’s Fractures in Adults, p.1641.

69. Rockwood & Green’s Fractures in Adults, p.1646; Skeletal Trauma, pp.1718-1719.

70. Rockwood & Green’s Fractures in Adults, p.1660; Skeletal Trauma, p.1740.

71. Rockwood & Green’s Fractures in Adults, p.1642.

72. Rockwood & Green’s Fractures in Adults, p.1644; Skeletal Trauma, p.1729.

73. Rockwood & Green’s Fractures in Adults, pp.1648-1651; Skeletal Trauma, pp.1719-1720.

74. Rockwood & Green’s Fractures in Adults, pp.1650-1651.

75. Rockwood & Green’s Fractures in Adults, pp.1653-1654.

76. Rockwood & Green’s Fractures in Adults, p.1652.

77. Rockwood & Green’s Fractures in Adults, p.1652; Skeletal Trauma, pp.1721-1722.

78. Rockwood & Green’s Fractures in Adults, p.1662; Skeletal Trauma, p.1727.

79. Rockwood & Green’s Fractures in Adults, pp.1663, 1650; Skeletal Trauma, p.1727.

80. Rockwood & Green’s Fractures in Adults, pp.1663-1666; Skeletal Trauma, pp.1729-1734.

81. Rockwood & Green’s Fractures in Adults, p.1668.

82. Rockwood & Green’s Fractures in Adults, p.1642; Skeletal Trauma, p.1722.

83. Rockwood & Green’s Fractures in Adults, p.1675; Skeletal Trauma, pp.1722, 1727.

84. Rockwood & Green’s Fractures in Adults, p.1675.

85. Rockwood & Green’s Fractures in Adults, p.1676.

86. Skeletal Trauma, pp.1740-1741.

87. Rockwood & Green’s Fractures in Adults, pp.1676-1679.

88. Rockwood & Green’s Fractures in Adults, p.1748.

89. Rockwood & Green’s Fractures in Adults, p.1679.

90. Rockwood & Green’s Fractures in Adults, p.1679.

91. Rockwood & Green’s Fractures in Adults, p.1680.

92. Rockwood & Green’s Fractures in Adults, p.2893; Skeletal Trauma, p.1745.

93. Rockwood & Green’s Fractures in Adults, pp.2902, 2905.

94. Rockwood & Green’s Fractures in Adults, p.2892. The association of first/second-rib fractures with great-vessel, brachial-plexus, and head injury is standard trauma teaching; the mined extract states only that fractures of ribs 1-3 indicate high-energy trauma. The vascular/plexus association is included as standard teaching, not falsely page-cited.

95. Rockwood & Green’s Fractures in Adults, p.2897; Skeletal Trauma, p.1746.

96. Skeletal Trauma, p.1753.

97. Rockwood & Green’s Fractures in Adults, p.2907 (the extract: a small pneumothorax can become a tension pneumothorax under positive-pressure ventilation, needing urgent tube thoracostomy). The classic clinical tetrad of tension pneumothorax and the needle-decompression technique (second intercostal space mid-clavicular line, or fifth intercostal space anterior axillary line) are standard ATLS teaching, not detailed in this orthopaedic extract; included for completeness.

98. Rockwood & Green’s Fractures in Adults, pp.2906, 2918. The massive-haemothorax thoracotomy thresholds (≥1500 mL initial output or ≥200 mL/hr ongoing) are standard ATLS teaching and are not stated in the mined extract, which gives chest-tube removal thresholds (<100-400 cc/day) instead.

99. Rockwood & Green’s Fractures in Adults, pp.2895-2897, 2904.

100. Rockwood & Green’s Fractures in Adults, p.2894.

101. Rockwood & Green’s Fractures in Adults, p.2892; Skeletal Trauma, pp.1745-1746.

102. Rockwood & Green’s Fractures in Adults, pp.2892, 2898-2899.

103. Rockwood & Green’s Fractures in Adults, pp.2904-2905.

104. Rockwood & Green’s Fractures in Adults, pp.2905-2907; Skeletal Trauma, pp.1745-1746.

105. Rockwood & Green’s Fractures in Adults, pp.2904-2905.

106. Rockwood & Green’s Fractures in Adults, pp.2908-2909; Skeletal Trauma, pp.1746-1747.

107. Rockwood & Green’s Fractures in Adults, pp.2920-2921; Skeletal Trauma, p.1753.

108. Rockwood & Green’s Fractures in Adults, pp.2909-2910, 2924-2925; Skeletal Trauma, pp.1746, 1752.

109. Rockwood & Green’s Fractures in Adults, p.2910.

110. The mined extract addresses the sternum only as a source of central/sternal flail (Rockwood & Green’s Fractures in Adults, p.2901; Skeletal Trauma, p.1746); the mechanism (direct blow/deceleration), the cardiac-contusion association, the predominantly nonoperative management, and the operative indications for displacement/instability/nonunion are standard teaching not detailed in this extract, included for completeness.

111. Rockwood & Green’s Fractures in Adults, pp.1576, 1696.

112. Rockwood & Green’s Fractures in Adults, p.1694; Skeletal Trauma, pp.1700-1701.

113. Rockwood & Green’s Fractures in Adults, pp.1694-1695, 1718-1720, 1768.

114. Rockwood & Green’s Fractures in Adults, p.1708.

115. Rockwood & Green’s Fractures in Adults, pp.1573-1575, 1542.

116. Rockwood & Green’s Fractures in Adults, pp.1562-1564, 1578-1590.

117. Rockwood & Green’s Fractures in Adults, pp.1545-1546, 1583-1586, 1605.

118. Rockwood & Green’s Fractures in Adults, p.1646; Skeletal Trauma, pp.1718-1719.

119. Rockwood & Green’s Fractures in Adults, pp.1642, 1675-1676; Skeletal Trauma, pp.1722, 1740.

120. Rockwood & Green’s Fractures in Adults, pp.2892, 2904-2905.

121. Rockwood & Green’s Fractures in Adults, pp.2905-2910, 2920-2921; Skeletal Trauma, pp.1746-1747, 1753.

122. Standard ATLS teaching; the mined orthopaedic extract (Rockwood & Green’s Fractures in Adults, p.2907) describes only that a small pneumothorax can become a tension pneumothorax under positive-pressure ventilation, needing urgent tube thoracostomy. The clinical tetrad and needle-decompression technique are core ATLS and are included for completeness.

123. Rockwood & Green’s Fractures in Adults, pp.1679-1680.

124. Rockwood & Green’s Fractures in Adults, p.2897; Skeletal Trauma, p.1746.