Introduction

The high congruency of the bony structures forming the elbow, make the elbow an inherently stable joint. The stabilizing system provided by the osseous architecture and the balanced intact musculature which provides dynamic or active joint stability, is supported by strong capsule-ligamentous structures on the lateral and medial side of the elbow joint.^1–6 In full flexion and extension of the elbow, the primary stability is provided by the osseous articulation, whereas the capsule-ligamentous stabilizers are the primary stabilizers in all semi-flexed positions, providing maximal stability at 90° of joint flexion.^3,5–8

Posttraumatic instability of the elbow can be divided into osseous or ligamentous instability or a combination of both. When fractures of the olecranon, radial head or coronoid process heal with displacement, there is a risk of chronic instability. This type of osseous instability is, in general, easily recognized by standard radiography. This is in contrast to ligamentous damage, which is often not recognized in the acute phase, and may result in longstanding, unrecognized chronic posttraumatic instability. It is important to realize that joint instability does not equal laxity. Instability is often described as a non-physiological motion and it is usually symptomatic. Laxity on the other hand is physiological and asymptomatic. Both elbow laxity and elbow instability can be classified with regard the direction of forces displacing the elbow. Simple patterns of laxity or instability include varus and valgus motion, but over the past 15 years more complex patterns of posterolateral rotatory and postero-medial rotatory instability have also been described. Understanding the mechanism of injury is obviously important for appreciating a classification, interpreting the clinical and radiographic findings, instituting the correct treatment, anticipating complications and providing adequate follow-up care.

The most common cause of ligamentous injury of the elbow joint resulting in instability is an elbow dislocation. In adults, the elbow joint is the second most commonly dislocated major joint after the shoulder and is the most commonly dislocated joint in the paediatric age group. The incidence of elbow dislocation in the general population is estimated to be 6/100 000.⁴

Posttraumatic chronic ligamentous instability can be divided into medial or valgus instability, postero-medial instability and posterolateral rotatory instability (PLRI). As the signs and symptoms of these entities are often subtle, the examiner must have a high index of suspicion and a thorough knowledge of the symptoms and expected findings at physical examination in order to make the diagnosis. Persistent insufficiency of the lateral collateral ligament complex (LCLC) (especially the ulnar part – the lateral ulnar collateral ligament (LUCL)) results in PLRI (Fig. 26.1A). Insufficiency of the medial collateral ligament (MCL), in particular the anterior part or AMCL, results in valgus instability (Fig. 26.1B).

Figure 26.1 (A) The lateral collateral ligament complex (LCLC). This complex consists of:

1.Anterior capsule.

2.Radial collateral ligament (RCL).

3.Annular ligament (AL).

4.Interval between annular ligament and lateral ulnar collateral ligament (LUCL).

5.LUCL.

6.Anterior capsule.

The accessory collateral ligament is defined as the most inferior fibres in the AL extending down and inserting with the fibres of the LUCL.

(B) The medial collateral ligament complex (MCLC). This complex consists of:

1.Anterior medial collateral ligament (AMCL).

2.Posterior medial collateral ligament (PMCL).

3.Transverse ligament.

Posterior elbow dislocations should be reduced in supination to clear the coronoid under the trochlea, thereby minimizing additional trauma to the medial soft tissues that have not yet been disrupted. It is preferably to perform the reduction under general anaesthesia as this enables the stability of the elbow to be assessed. However, in general practice this is not always possible. If a reduction is performed under local anesthesia and the post reduction radiograph shows a complete and adequate reduction, assessment of stability can be performed a week after the injury. The elbow, in both situations, is examined for valgus, varus and posterolateral rotatory instability. Both valgus and varus testing is performed in full extension and in varying degrees of flexion up to approximately 40° in order to unlock the olecranon from the fossa.

Instability in a posterolateral direction is tested with the pivot shift test and drawer sign, both of which will be described later. This chapter will focus on insufficiency of the LCLC. It will cover the basic science of lateral instability, the clinical signs and symptoms, the causes of injury to the LCLC and the detection of persistent insufficiency. In addition an overview of conservative and surgical treatment options will be provided. Finally the results and complications of surgical treatment will be described.

Background/aetiology

The trauma mechanism of posterolateral dislocation of the elbow is a fall on the outstretched hand. During the fall the elbow experiences an axial compressive force during flexion. As the body approaches the ground, the body rotates internally resulting in an external rotation on the forearm, which is fixed to the ground. A valgus moment results from the fact that the mechanical axis lies lateral to the elbow joint. The combination of valgus, external rotation and axial compression is the mechanism that causes a posterolateral dislocation or subluxation of the elbow joint.

During a posterolateral dislocation of the elbow joint, rupture of the ligamentous complex occurs in a circle from lateral to medial, as described by O’Driscoll et al; in stage I, the LUCL is disrupted; in stage II, the other lateral ligamentous structures as well as the anterior and posterior capsule are torn. In stage III disruption of the medial collateral ligament can be partial with disruption of the posterior bundle only (IIIA) or complete (IIIB).⁴

In the majority of cases the rupture of the LCLC occurs at its humeral insertion while in the minority a mid-substance injury is seen.

Disruption of the lateral collateral ligament can occur after trauma such as a posterolateral dislocation, a fracture dislocation, an elbow subluxation or a sprain. In all cases of instability it is important to realize that there is a complex interplay between the LCLC and the other stabilizing structures of the elbow, particularly the coronoid process and the radial head. Chronic attenuation of the lateral complex has also been described in patients with cubitus varus deformity following malunion of distal humeral fractures and in patients who are chronic crutch users, i.e. paraplegics.

In a cubitus varus deformity the triceps contraction has been hypothesized to result in asymmetrical loading of the joint resulting in attenuation of the LCLC (Fig. 26.2). If surgical reconstruction is considered in these cases of complex instability a LCLC reconstruction alone will not restore stability. A valgus osteotomy to correct the varus deformity, in addition to a LCLC reconstruction, should be considered and is essential if the varus deformity is more than 20°. Experimental data in cadavers have shown increased strain on the LCLC with more than 25° of varus angulation and increased opening of the joint line space with more than 20° of varus angulation. In the preoperative work-up an assessment of the malunion in three directions is mandatory. Evaluation with a computed tomography (CT) scan of the injured and the uninjured complete humerus is necessary to determine the rotational deformity.

Figure 26.2 A posttraumatic varus deformity can result in a chronic, asymmetrical loading of the triceps tendon resulting in a chronic attenuation and finally insufficiency of the lateral collateral ligament complex. This insufficiency finally can result in posterolateral rotatory instability.

During surgery, the deformity is corrected in valgus, flexion or extension and rotation, depending on the preoperative assessment. Finally, iatrogenic injury as a result of surgery to the lateral side of the elbow or repeated steroid injections can result in injury to the LCLC (Table 26.1).

Table 26.1 Aetiology of lateral collateral ligament insufficiency

Iatrogenic lesions primarily occur after release of the common extensor tendon to treat chronic lateral epicondylitis. The ligament complex is particularly at risk in cases where ‘minimal invasive techniques’ or percutaneous techniques have been used as the surgical procedure. It is of utmost importance that surgeons are aware of the ligamentous anatomy, in order to preserve the ligament during elbow surgery. If transsection of the LCLC occurs during surgery or release of the insertion of the LCLC is necessary during a surgical procedure, the surgeon should repair the ligament as anatomically as possible. The LCLC is the primary capsular-ligamentous stabilizer of the elbow joint to varus and external rotation.^3–9

The mean length of the LCLC from its origin to the annular ligament is 20 mm, and the width is approximately 8 mm.¹⁰ The insertion point on the lateral epicondyle is at the isometric point for the flexion and extension axis, and therefore the ligament is uniformly taut in the entire flexion axis.^2,10 The functional anatomy of the ligament indicates that there is a superior and inferior part to the ligament and only complete division induces clinically significant joint laxity.^5,6,8 The ligament complex is covered by the anconeus muscle, the supinator tendon and the musculo-tendinous insertion of the extensor carpi ulnaris and the extensor digitorum.^9,10 Cohen and Hastings showed that the musculo-tendinous insertion of the extensor carpi ulnaris and the extensor digitorum covered the ligament and provided an additional stabilizing effect for the LCLC.⁹

A broad band originates from the undersurface of the lateral epicondyle and inserts fan-shaped into the annular ligament. This band constitutes the LCL and the LUCL. The fibres of the LUCL component, being the most posterior, pass through the annular ligament and insert on the ulna with fibres from the most inferior part of the annular ligament, inconsistently named the accessory collateral ligament.^2,8,9,11,12 The insertion on the proximal part of the supinator crest, is separated from the annular ligament by a small triangular space.^5,8,11 The annular ligament originates from the anterior and posterior margins of the lesser sigmoid notch and passes around the radial head, maintaining contact between the radial head and the ulna.¹⁰ In PLRI, the proximal radioulnar joint is intact. Laxity or avulsion of the ulnar part of the lateral collateral ligament leads to an increase in external rotation of the ulnohumeral joint.⁵ This increase in external rotation results in a secondary posterior subluxation of the radial head. This secondary subluxation, with an intact proximal radioulnar joint, must be differentiated from isolated posterior head subluxation with disruption of the proximal radioulnar joint and an intact ulnohumeral joint.¹³

Associated injuries with elbow dislocations are common; radial head and neck fractures occur in 5–10%, avulsions of fragments from the medial or lateral epicondyle occurs in 12% and fractures of the coronoid process occur in 10% of all dislocations. The reverse is also true and fractures around the elbow can be associated with ligamentous injury. Van Riet and Morrey in a study of an American population noted injury to the LCLC in 35 of 88 patients with radial head fractures¹⁴ and similar results were also noted in a Dutch study.¹⁵ The incidence of associated, ligamentous injuries in radial head fractures is high, especially in Mason type 3 and 4 injuries. The treating physician should be aware of this and should perform a thorough physical examination of the upper limb in every patient with a radial head fracture.

Presentation, investigation and treatment options

Clinical signs and symptoms of patients with an insufficiency of the LCLC vary depending on the severity of the instability, associated injuries such as radial head or coronoid fractures, and activity levels. In rare cases of LCLC insufficiency recurrent frank elbow dislocations occur. However, more often the symptoms and clinical signs of insufficiency are more subtle. It is important therefore, if an accurate diagnosis is to be made, that the surgeon is fully aware of the clinical symptoms and signs of LCLC insufficiency.^16,17

Most commonly patients complain of lateral-sided elbow pain with clicking, snapping or locking, particularly when the elbow is actively extended with the forearm supinated. Daily activities such as pushing to stand up from a chair or lifting objects in supination induce symptoms. In some patients these activities are even impossible to perform due to ‘apprehension’. A minority of patients complain of ‘subjective feelings of instability’ but are often unable to describe in what direction the elbow feels unstable or under which circumstance these feelings of instability occur. Classically patients with a LCLC insufficiency report a history of trauma or surgery. In postsurgery cases differentiation between preoperative symptoms and postoperative symptoms is essential. Were the preoperative signs and symptoms corrected by the surgery or did the surgery induce symptoms that did not exist preoperatively? Patients with locking symptoms after ‘enthusiastic’ lateral elbow surgery may suffer from an insufficiency of the LCLC.