The thoracic outlet contains the neurovascular structures to the upper limb and can be divided onto three separate anatomical regions. Medially, the scalene triangle is the space occupied by the three scalene muscles (Scalenus anterior, medius and posterior). This space contains the brachial plexus and subclavian artery, which lie in the interval between the anterior and middle scalenes. The subclavian vein is not contained in this space because it lies anterior to the scalene muscles (Fig. 35.1). The costoclavicular space is the segment bounded by the clavicle superiorly, first rib inferiorly, scalenus muscles medially and pectoralis minor laterally. The retropectoralis minor (subcoracoid) space is lateral [9, 10].

Thoracic outlet syndrome (TOS) may affect the vascular, as well as neurological, structures to the upper limb. Iatrogenic vascular TOS has been reported following plate fixation of clavicle fractures [11–13].

Iatrogenic TOS most commonly occurs in the costoclavicular space , as distinct from TOS of other aetiologies, which usually occurs more medially in the scalene triangle [9]. Compression of the vascular structures produces variable symptoms of discolouration, swelling and temperature changes, whilst brachial plexus compression produces variable pain, weakness and sensory disturbance. Significant callus formation may encroach upon the costoclavicular space (Fig. 35.2). In this situation, mobilisation and fixation of fragments may further reduce the volume of the costoclavicular space , to the point of a clinically apparent TOS [11, 12, 14].

The subclavian vessels are in close proximity to the medial two-thirds of the clavicle (Fig. 35.3). Injury to the subclavian vein has been reported following fixation of an acute clavicle fracture [15] and revision fixation for clavicular non-union [16]. The vein is thin walled, making it easily distendable but difficult to repair (Fig. 35.4). It is located a mean 5 mm from the posterior aspect of the medial clavicle, but can be directly adherent to the periosteum [17]. In contrast, the subclavian artery has comparatively thick walls and is relatively protected by the overlying scalenus anterior muscle.

A pseudoaneurysm is an extravascular haematoma that freely communicates with the intravascular space through a defect in the vessel wall [18] (Fig. 35.5). The wall of a pseudoaneurysm is made up of compressed tissues surrounding the haematoma, rather than the three distinct layers of a true vessel wall [19, 20].

They are a result of penetrating trauma, with the most common iatrogenic cause being endovascular cannulation procedures. However, pseudoaneurysms have also been reported in the shoulder in association with prominent clavicular metalware [8, 21–23] (Fig. 35.6) and the following coracoid transfer procedures [2].

Pseudoaneurysms may be clinically silent for many years – a case associated with a prominent screw was reported as presenting 10 years following clavicle fixation [22] (Fig. 35.5). Intermittent, subacute ischaemic symptoms occur distal to the artery due to compression of the surrounding vessels. Thrombotic events can also occur, which may precipitate acute limb-threatening ischaemia.

Arteriovenous (AV) fistulae are a result of injury to both the artery and an adjacent vein [24]. Like pseudoaneurysms they are commonly associated with penetrating injury.

With time AV fistulae dilate and the pressure in the venous side of the lesion increases, causing venous engorgement and swelling. Persistent, untreated, venous hypertension can cause congestive heart failure or limb-threatening ischaemia.

An air embolism occurs when air or gas is admitted into the vascular system [25] and it most commonly occurs with central venous catheterisation. It is also well recognised in posterior cranial fossa surgery [26], total hip arthroplasty and in spinal surgery in the prone position [27, 28]. Fatal air embolism has been reported following subclavian vein injury sustained during plate fixation of a clavicle fracture [15] (Fig. 35.4).

The surrounding soft tissues adherent to the vein can prevent it from collapsing, and the lumen of the vein has a negative pressure due to the negative intrathoracic pressure. Therefore, any breach of the vessel wall will potentially allow air to be sucked through the defect and into the vessel lumen [29].

Once air enters the subclavian vein , it can have several pathophysiologic consequences. The heart is designed to pump fluid, and struggles to pump the compressible air (“air lock”[30]), which can lead to hypoperfusion and even complete cardiovascular collapse [25, 27, 28, 31]. As in an embolism from any other cause, air in the pulmonary circulation leads to pulmonary vasoconstriction, release of inflammatory mediators, bronchoconstriction and ventilation/perfusion mismatch [27]. If there is a patent foramen ovale, the embolus has the potential to enter the cerebral circulation [27]. The lethal volume of air is estimated to be 200–300 ml (3–5 ml/kg). The closer the vein to the right heart, the smaller this volume [27].

Deep vein thrombosis (DVT) is caused by the classic Virchow triad of vessel wall injury, altered blood flow and hypercoagulability [32]. Surgery and immobility are well known to increase the risk of DVT . There is one reported case of DVT following clavicle fixation [32]. However, it is unclear whether the DVT was due to the initial injury, the surgery or an underlying Paget–Schroetter syndrome. This is a form of thoracic outlet syndrome characterised by venous thrombosis [21, 32]. The risk of pulmonary embolism following upper limb DVT (3–36 %) is similar to that in the lower limb. However, the majority are asymptomatic and it is rarely fatal [33].

The subclavian vessels are at risk during procedures on the medial and middle thirds of the clavicle. The subclavian artery is posterior to, and thus relatively protected by, the scalenus anterior muscle. In contrast the subclavian vein is anterior to this muscle and directly posterior to the medial clavicle. It lies a mean 5 mm from the bone but may directly appose to the posterior periosteum [17]. The vein wall is thin and can be injured by sharp bone fragments, retractors or drills and screws (Fig. 35.4).

The anatomical boundary between the subclavian and axillary vessels is the lateral border of the first rib. The axillary vessels converge and lie postero–inferior to the middle third of the clavicle at mean distance of 13–17 mm [17]. Pseudoaneurysms and AV fistulae of these vessels have been reported due to prominent metalware in this region.

The axillary artery descends on the chest wall to the lower border of teres major, where it becomes the brachial artery. Both axillary vessels are at risk in anterior approaches to the shoulder, particularly revision procedures where the anatomical relationships are distorted by scar tissue.

Anterior dislocation of the glenohumeral joint may cause the humeral head to be directly apposed to the axillary artery (Fig. 35.7). This alone may result in either early or late presenting vascular injury [34]. If an anatomic closed reduction cannot be achieved, then a vascular examination is mandatory to ensure that the artery is not interposed between the articular surfaces. Open reduction may be required in chronic cases, and special care must be taken to identify and protect the artery as it will be displaced into the surgical field.

Clavicular surgery warrants particular attention due to the close proximity of these major vessels to the operative field. Care must be taken when drilling to ensure that, wherever possible, the placement of drill holes should be along a trajectory that avoids the vessels. In the medial third of the clavicle, this safe trajectory is in a superior to inferior direction; and in the middle third, it is anterior to posterior [17]. Dissection around the medial two-thirds of the clavicle must be in the sub-periosteal plane to prevent injury to an adherent subclavian vein . The potential morbidity from compromised blood supply to the clavicle due to this dissection is far less than the morbidity of compromising blood flow to the upper limb or the right atrium due to a vascular injury .

Nerves may be injured by traction, compression or division. Division may be the result of blunt force (laceration), traction (avulsion) or contact with a sharp surface (incision). The extent of injury depends on the magnitude and duration of the provoking stimulus.

Traction injury occurs when attempts are made to mobilise, distract or retract a nerve, or structures surrounding a nerve, without adequately releasing adjacent tether points. These tethers may be the result of normal anatomy, such as where a nerve passes between two muscle heads, or pathological processes, where the nerve is adherent by scar to adjacent structures. Increasing the resting length of a nerve by 8 % has been reported to cause venous obstruction, with ischaemia occurring at 15 % [35].

Compression injuries may arise from inadvertent placement of retractors, interposition between a fixation plate and the bone or suture entrapment. Compression injury can also occur to prominent nerves that are outside of the shoulder region due to positioning of the patient without adequate padding.

Two commonly used classification systems for nerve injury are based on the pathoanatomical lesion present. Seddon [36] classified nerve injury into three groups, depending on the integrity of the axon and the nerve. Sunderland [37] further delineated these groups according to the integrity of the various anatomical layers of the nerve (Table 35.2).

The common feature of all cases of neurological injury is nerve dysfunction. If all axons are involved the lesion is complete, and if any axons are spared the lesion is partial.

Pain is a feature of acute partial nerve injury. In cases where the patient has a persisting noxious stimulus to the nerve – such as an encircling suture or sustained traction over a short segment – the patient may wake from surgery with intense pain in the affected region [38, 39].

The prognosis of the dysfunction is related to the pathoanatomical lesion present in each nerve fibre, that is, the Sunderland class. This in turn directs the management of the injury. The pathoanatomy is influenced by the intensity and the duration of the injury mechanism.

Neurological lesions are usually transient and self-limiting, although permanent injuries have been reported. The brachial plexus or the axillary nerve are the most commonly affected structures. Recovery from a “transient” brachial plexus injury may take 6 months or longer, presenting a significant burden to the patient. Furthermore, it should be noted that the greater the degree of injury to the nerve, the less potential there is for recovery without surgical intervention.

A summary of the major nerves at risk, the areas where they are vulnerable and the reported mechanisms of injury is given in Table 35.3.