Introduction

Recurrence of instability represents the leading complication of arthroscopic shoulder stabilization.¹ Recurrence following anteroinferior instability surgery can be clearly defined as a further dislocation or any subjective complaint of subluxation. In our opinion, it is appropriate to also include a “persistent apprehension” that causes functional limitation or pain in the throwing position, as an additional factor that can be considered as a treatment failure. In our experience, a patient who is practicing any sport that needs abduction-external rotation of the arm (throwing movement), with or without contact, will not be able to return to the same level of practice if he or she still presents with anterior apprehension of the shoulder.

In the nineties, arthroscopic Bankart repair became the standard of care for recurrent anterior shoulder instability in many surgical centers. However, in the last years, it has become clearer that this unique surgical procedure could not, by itself, stabilize all shoulders with recurrent anterior instability. Because revision surgery results in a poorer outcome for the patient than a primary procedure,² it is appropriate that the principal focus of attention be directed towards the prevention of failure. By identifying patient factors that predispose to failure and performing a precise preoperative and intraoperative assessment of potential structural lesions, the correct surgical treatment may be tailored to the patient. The current evidence regarding common reasons for failure following instability surgery must be explored under the headings of preoperative history, examination, and radiographic findings, such that “at risk patients for arthroscopic Bankart” may be identified in a systematic manner. Although difficult to quantify, additional factors such as surgical technique and surgeon experience have an undeniable impact on the probability of failure following instability surgery.

In this chapter, we analyze the common reasons of anterior instability treatment failure (i.e., recurrent instability after arthroscopic Bankart) and detail how a careful clinical and radiologic examination can prevent such failures by allowing a choice in the appropriate surgical technique tailored for a specific patient. For the purpose of this chapter, we have excluded discussion of potential causes of treatment failure related to postoperative complications such as stiffness, nerve injury, subscapularis failure, or postcapsulorrhaphy arthropathy.

Determination of risk factors associated with instability recurrence following arthroscopic bankart repair

The risk factors associated with instability recurrence after arthroscopic Bankart repair must be evaluated during the preoperative history and clinical examination and by performing appropriate radiologic investigations.

Preoperative history

Patient age

Although no clear age limit has been defined, younger patients are at greater risk of recurrence following surgery for instability. The age of onset of instability is predictive of the redislocation rate. Patients experiencing single dislocations have a mean age of 43 years compared with 23 years in recurrent cases.³ Greater soft tissue laxity, higher activity levels, and possibly less compliance with postoperative regimens are cited as the principal explanations for the increased risk of surgical failure in the younger age group.⁴ Patients over 40 years of age with recurrent anterior instability must be suspected of having associated rotator cuff tears.

Sporting activity

Certain sports confer an increased risk of recurrent instability following surgical treatment, as does participation at a high competitive level. Contact and forced overhead sports (such as rugby, American football, judo, kayaking, gymnastics) appear to carry the least favorable prognosis. The level of sports practice appears to be another additional risk factor: those who are practicing at a competitive level have a higher risk of failure after arthroscopic Bankart repair because of the higher demand placed on their shoulder and the greater number of glenoid and/or humeral bone lesions.

Hyperlaxity/capsular deficiency

Poor quality soft tissues caused by multiple previous operations, multiple dislocations, or connective tissue disorders may jeopardize the outcome following instability surgery. Capsular distention have been shown to be irreversible ⁵ and directly related to the number of dislocations or subluxations. In our experience, the number of subluxations is clearly underestimated by patients who mainly recall the true dislocations but seem to forget the episodes of subluxation.

Bilateral symptoms ⁶ should alert the surgeon to the possibility of a hyperlaxity diathesis. Patients with connective tissue disorders, such as Marfan syndrome or Ehler-Danlos disease, have joint hyperlaxity and hypermobility.⁷ In such cases, relatively minor trauma may be sufficient to trigger instability episodes.

Previous shoulder stabilization surgery

Failed arthroscopic thermal capsulorrhaphy may result in severe attenuation and/or loss of capsular structures.⁸ Patients with previous open Bankart or Bristow-Latarjet may have a deficient subscapularis muscle-tendon unit, which in itself represents a surgical challenge. Although we have excluded such cases from discussion in this chapter, surgeons should realize that they may be a source of instability treatment failure. When contemplating revision surgery, these potential problems may be identified in advance and anticipated by obtaining the operations notes from prior interventions.

Examination findings

Signs of shoulder hyperlaxity

The finding of “shoulder hyperlaxity” must be considered as a factor in the evaluation of recurrent anterior instability. Shoulder hyperlaxity can be anterior, inferior, posterior, or combined (so-called multidirectional instability). Anterior hyperlaxity of the shoulder is present if the examiner can easily subluxate the humeral head out of the socket in the anteroposterior direction on drawer testing or if there is greater than 85 degrees of passive external rotation with the patient’s arm by his or her side ⁹ (Fig. 34-1). Inferior hyperlaxity is assessed with sulcus sign testing and the hyperabduction test,¹⁰ which we consider to be positive when there is a minimum of 20 degrees of asymmetric abduction at the glenohumeral joint¹¹ (Fig. 34-2). Finally, a gynecoid morphologic aspect of the patient, as well as skin striae, can be subtle but useful findings suggestive of a predisposition towards soft tissue laxity.

FIGURE 34-1 Anterior hyperlaxity with bilateral external rotation of greater than 85 degrees.

FIGURE 34-2 Inferior hyperlaxity with asymmetry of greater than 20 degrees when performing the hyperabduction test.

Radiographic findings

Glenoid bone loss

It is important to distinguish between those patients with loss of contour of the glenoid rim and those with glenoid bony avulsion fractures ¹² (Fig. 34-3). Patients with loss of glenoid contour without any identifiable bony fragment will often have significant attenuation of the anterior band of the inferior glenohumeral ligament and the anterior capsular structures (Fig. 34-4). The deficiency in these structures allows recurrent subluxations or dislocations that effectively erode and compress the anterior glenoid. By contrast, in a study of factors influencing recurrence following arthroscopic Bankart repair, avulsion fractures did not represent an identifiable risk factor.¹³ A possible explanation is that in the setting of avulsion fractures, failure occurs acutely through the bony surface of the glenoid with relative preservation of the attached soft tissues (Fig. 34-5). Although in many instances a bony avulsion fragment will be resorbed over time (Fig. 34-6), if present, it is frequently possible to incorporate the bone fragment into the Bankart repair at the time of surgery.

FIGURE 34-3 Glenoid profile on anteroposterior (AP) radiography. A, Normal shoulder. B, Glenoid avulsion fracture. C, Glenoid loss of substance.

FIGURE 34-4 Glenoid bone loss with attenuation of anterior capsular structures.

FIGURE 34-5 A, Glenoid avulsion fracture. B, Loss of bony substance (often associated with a deficient capsule).

FIGURE 34-6 A, Acute glenoid fracture. B, Over time the bony fragment is resorbed.

Large osseous defects of the glenoid will result in instability regardless of the quality of the capsulolabral repair by altering the glenohumeral contact area and the function of the static glenohumeral restraints.¹⁴ Although, several authors reported different preoperative or intraoperative approaches to qualify the orientation or quantify the area of the glenoid bone loss and their thresholds to maintain glenohumeral joint stability, there is consensus on the critical role played by an intact glenoid articular arc in maintaining shoulder stability and function.¹⁵

In both primary and revision surgery, high rates of failure have been encountered when large defects of the glenoid have not been addressed appropriately at the time of surgery.

Garth’s apical oblique and the Bernageau profile are specific radiographic views that may assist in the assessment of glenoid bone deficiency, although the most accurate indicator is the en face view of the glenoid visualized on sagittal computed tomography (CT) or magnetic resonance imaging (MRI).

Humeral bone loss

Larger posterosuperior humeral head impression fractures (Hill-Sachs lesions) may precipitate recurrent postoperative instability despite adequate soft tissue capsulolabral reconstruction.¹⁶ Combined abduction and external rotation of the arm may bring the Hill-Sachs lesion in contact with the anterior rim of the glenoid. These so-called “engaging Hill-Sachs lesions” run parallel to the face of the glenoid in the abducted externally rotated position of apprehension allowing the humeral head to sublux or dislocate anteriorly (Fig. 34-7).