Acromioclavicular joint injuries revisited: Pathoanatomy, pathomechanics, and clinical presentation

Abstract

Multiple papers have described aspects of treatment of acromioclavicular (AC) joint injuries. Most have emphasized aspects of surgical treatment, and some papers have addressed non-operative treatment. Few papers have highlighted the specific pathoanatomy of an AC joint injury or have described methods of evaluating the 3-dimensional pathomechanics resulting from the pathoanatomical injury. This paper is based on 3 observations: (1) AC joint injuries exist and present on a spectrum of pathoanatomy; (2) The effect of the pathoanatomy on normal AC joint mechanics to produce pathomechanics is dependent on the extent of the pathoanatomy; and (3) Treatment protocols should be developed to address the specific pathoanatomy to optimize the mechanics. A comprehensive clinical approach emphasizing the evaluation of the extent of the anatomic injury and understanding its mechanical consequences regarding shoulder and arm function is a key in the development of guidelines for developing operative or non-operative treatment protocols and for establishing outcomes of the treatment protocols.

Introduction

Injury to the acromioclavicular (AC) joint complex has 2 major consequences. The first is the actual injury to the structures that comprise the joint. The second is that the injury has the potential to affect the normal 3-dimensional mechanics and function of scapulohumeral rhythm (SHR), the coupled motions of the trunk, shoulder girdle, and arm that allow production of effective task-specific functions and activities. A comprehensive clinical approach emphasizing the evaluation of the extent of the anatomic injury and its physiological and mechanical consequences is fundamental for development of operative or non-operative treatment protocols for optimal restoration of SHR and shoulder function. It can also help to clarify the traditional Rockwood type I-VI classification system for AC joint injuries and improve the understanding, evaluation, and treatment of the type III AC joint injury.

This paper will present an approach for evaluating the AC joint injury which is based on understanding the pathoanatomy of the AC joint injury and the resulting pathomechanics as they affect the clinical presentation and symptoms, and which can suggest guidelines for treatment indications and techniques. It is based on 3 observations: (1) AC joint injuries exist and present on a spectrum of pathoanatomy, and techniques for precise determination of the pathoanatomy need to be developed and refined; (2) The pathoanatomy is only one aspect of the clinical presentation. The effect of the pathoanatomy on normal AC joint mechanics to produce pathomechanics, and the effect on 3-dimensional SHR, are dependent on the extent of the pathoanatomy. Techniques, including a detailed and comprehensive clinical evaluation, for the precise determination of the specific 3-dimensional pathomechanics of the individual case and its role in clinical shoulder dysfunction need to be developed, especially in the case of the type III injury; and (3) Treatment protocols should be developed to address the pathoanatomy to optimize the mechanics, along with concise determination of the goals and outcomes of the treatment.

Anatomy and pathoanatomy

The AC joint is a relatively stiff structure, with strong posterior, superior, and anterior ligament components that are thicker on their acromial insertions than their clavicular insertions, and coracoclavicular (CC) ligaments that augment the stiffness. ¹ The main functions of the ligaments as restraints to AC joint motion and facilitators of coupled rotational motions of the scapula and clavicle are illustrated in Figure 1. During arm motion, the AC ligaments as a unit provide major restraint to anterior/posterior and rotational joint forces and motions and the superior AC ligament component acts as a tension band to constrain lateral tilt motions of the acromion in relation to the clavicle that occur due to the force produced by the weight of the arm and scapula.^2–4 AC joint stability and stiffness is also maintained by the CC ligaments, whose main restraints are to joint motion in the inferior/superior direction, as well as their suspensory function of the scapula on the clavicle. In addition, the CC ligaments act as torque transducers, transmitting force developed around the scapula and transferring scapular motion to the clavicle to produce coupled clavicular motions. This stiffness creates a strong and stable link that allows rotational and elevation motions produced by the scapula or clavicle to be efficiently transmitted to the other bone of the articulation, creating an efficient screw axis between the 2 bones. ⁵ Efficient upper limb mechanics and SHR requires these coupled motions of the clavicle and acromion through the screw axis during the full range of arm motions, with the AC joint acting as a limited motion link. Varying amounts of injury to the AC and CC ligaments has the potential to change the normal linkage between the scapula and the clavicle and can result in alterations in scapular position and motion patterns during limb movement and consequent alterations in SHR.

Figure 1.

Acromioclavicular (AC) joint ligamentous anatomy and mecahnics: (A) AC ligament anterior/posterior translation; (B) AC ligament lateral tilt (acromion on clavicle); (C) coracoclavicular (CC) ligament suspension (scapula on clavicle); (D) CC ligament torque transfer (scapula to clavicle). Anatomical image used and adapted with permission from Lennard Funk, shoulderdoc.co.uk.

AC joint injury and pathoanatomy exist on a spectrum based on the amount of applied force to the AC joint complex. It may range from a first-degree mild sprain or ‘stretch’ of the AC ligaments by themselves to complete joint disruption involving disruption of the AC and CC ligaments and alteration in the relative position of the bones of the articulation.

Most AC joint injuries occur from a force directed from posterior-superior to inferior-medial, most commonly in a fall. Studies have demonstrated that with increasing amounts of force the anatomic disruption may progress from the posterior and superior AC ligaments to the anterior AC ligaments.^2,6–8 These ligaments may then be avulsed off their clavicular attachments, creating instability of the acromion on the clavicle and create horizontal and rotational laxity^2,9 as well as the loss of the lateral tilt tension band function. The disruption can continue through the inferior capsule and progress successively into the substance of the trapezoid and conoid ligaments. ¹⁰ Complete disruption of both trapezoid and conoid ligaments creates the vertical instability of the scapula on the clavicle and the loss of the optimal force and motion transfer between the scapula and clavicle. ⁸

Pathomechanics and the question of the type III injury

The spectrum of pathoanatomy will result in a spectrum of pathomechanics. The comprehensive diagnosis, which will encompass the extent of the pathoanatomy and the specific pathomechanics, is key to formulating a prognostically valuable classification scheme that aids in guiding subsequent treatment. This can be summarized in Table 1.

Table 1.

Acromioclavicular (AC) joint examination clinical findings.

Pathoanatomy	Inspection/palpation	Provocative maneuver	Observation	Corrective maneuver	Imaging	Treatment options
Isolated AC ligament sprain grade 1–2, Rockwood type I	( − ) deformity ( + ) pain	( − ) laxity	( + ) decreased arm motion	( − ) SAT ( − ) SRT	( − ) step-off ( − ) widening	Rest Immobilization Activity Modification Rehabilitation
Isolated AC ligament sprain grade 3, Rockwood type II	( + ) swelling ( + ) pain	( + ) A/P laxity	( + /−) scapular protraction at rest ( + ) pain with arm motion	( + ) SAT	( − ) step-off ( + /−) widening	Rest Immobilization Activity Modification Rehabilitation Possible topical/oral NSAIDS Possible cortisone injection Possible AC ligament repair/reconstruction for continued joint symptoms
‘Low grade’ AC joint injury: AC ligament tear with CC ligament tear (trapezoid ligament), Rockwood type III/ISAKOS type IIIA	( + ) distal clavicle prominence ( + ) pain	( + ) A/P laxity ( − ) S/I laxity	( + /−) scapular protraction at rest ( − ) scapular dyskinesis with arm movement	( + ) SRT	( + ) step-off increasing with weighted views ( + ) widening <2 cm ( + ) AC and trapezoid injury via MRI	Rest Immobilization Activity Modification Rehabilitation Possible AC and CC anatomic reconstruction if conservative measures fail
‘High grade’ AC joint injury: AC ligament tear with CC ligament tear (trapezoid and conoid ligaments), Rockwood type III–V/ ISAKOS type IIIB	( + ) distal clavicle prominence ( + ) pain	( + ) A/P laxity ( + ) S/I laxity	( + ) scapular protraction at rest ( + ) scapular dyskinesis with arm movement ( + ) inferior medial acromial position relative to clavicle	( + ) SRT ( + ) joint reduction with decreased arm elevation	( + ) step-off increasing with weighted views ( + ) widening >2cm ( + ) AC, trapezoid, and conoid injury via MRI ( + ) inferior medial acromial position	Rest Immobilization Activity Modification Rehabilitation Possible AC and CC anatomic reconstruction to restore anatomy and scapulohumeral rhythm

SAT = scapular assistance test; SRT = scapular retraction test; A/P = anterior/posterior; NSAIDS = non-steroidal anti-inflammatory drugs; CC = coracoclavicular; ISAKOS = International Society of Arthroscopy, Knee Surgery, and Orthopaedic Sports Medicine; MRI = magnetic resonance imaging; S/I = superior/inferior; cm = centimeter.

Mild injuries confined to the AC ligaments and defined as grade 1 and 2 sprains will usually not create altered joint mechanics. Clinical findings associated with these injuries would be classified as type I in the Rockwood classification.^11,12

More involved injuries confined to the AC ligaments, defined as grade 3 sprains, with anatomic disruption of the fibers, can result in some horizontal (i.e., anterior-to-posterior) laxity and lateral tilting of the scapula/acromion in relation to the clavicle, which can produce the clinical appearance a mild step off. Due to the intact CC ligaments, scapular kinematics are minimally uncoupled from clavicle kinematics so that resting scapular position and dynamic scapular motion with arm movement are most frequently observed to be symmetrical to the uninjured side. Clinical findings associated with these injuries would be classified as type II in the Rockwood classification.^11,12

 Further progression of the injury can produce complete tears of the trapezoid ligament, with stretching or no injury to the conoid ligament.^8,10 In these cases, there will be some alteration of the suspensory function and more lateral and downward acromial tilt, clinically observed as prominence of the distal clavicle and ‘step off’ of the acromion. Imaging will usually demonstrate AC joint widening, altered acromial position, and some CC space widening and these injuries are usually classified as Rockwood type III injuries (Table 1).^11,12

Rockwood type III injuries are the source of much controversy. Studies have documented that there is little consensus or reliability on precise guidelines for determination of a type III injury or on describing which factors are best utilized to identify patients who may be more suitable for operative versus non-operative treatment, which has resulted in little precision regarding treatment indications for this injury.^13–15 A major problem is that there is a variety of pathoanatomy that may produce the clinical pathomechanics that has been clinically identified as a type III injury. ¹⁵ One possible method of improvement is to evaluate the effect of the injury on the coupled SHR. Studies have found that patients classified with type III injuries may demonstrate either altered or normal scapular kinematics.^16,17 An International Society of Arthroscopy, Knee Surgery, and Orthopedic Sports Medicine (ISAKOS) consensus statement proposed dividing type III injuries into type IIIA and type IIIB, with the differentiation due to absence or presence of altered scapular kinematics on clinical examination or imaging (Table 1). ¹⁵ Many injuries that have been classified as Rockwood type III, due to clinically or radiographically observed prominence of the distal clavicle, have intact conoid ligaments and so may not demonstrate loss of dynamic control of scapular motion in SHR. Since control of scapular motion is a crucial element in SHR, a key diagnostic step would involve methods to identify altered scapular mechanics as an indicator of an injured conoid ligament including the clinical observation of scapular dyskinesis, with prominence of the inferior or medial scapular border (i.e., scapular internal rotation and lateral translation) that accompanies disruption of both CC ligaments. Many type III injuries without evidence of loss of scapular control (ISAKOS type IIIA) can be managed non-operatively emphasizing periscapular strengthening to optimize scapular retraction. Many patients with type III injuries with evidence of loss of scapular control (ISAKOS type IIIB) fail to respond to strengthening, with ongoing clinical symptoms, and are often recommended for surgical treatment (Table 1). ¹⁵

Complete disruption of the AC and CC ligaments creates the complete pathoanatomy that results in loss of all suspensory and force transmission functions of the ligaments, disruption of the strut function of the clavicle in relation to the scapula, and alteration of the screw axis and SHR. This results in anterior, inferior, and medial translation of the acromion in relation to the clavicle, with the clinically observed ‘bump’ of the distal clavicle and protraction of the scapula. The pathoanatomy and the consequent pathomechanics create a clinical presentation of a combination of pain, weakness, and movement related pain during arm elevation, with frequent difficulty in achieving effective overhead arm positions and motions. These injuries are classified as Rockwood type IV-VI, most commonly type V. The anatomical injuries and resulting impairment of mechanics and function are frequently not well treated by non-operative protocols. Periscapular strengthening may be helpful, but optimal muscle function demands joint stability and clavicular strut function in order to be effective.^15,18

Based on these concepts, a classification method of the spectrum of AC joint injury can be created that is based on the 3-dimensional pathomechanics of AC joint injury that can be observed and clinically and radiographically evaluated: ‘low grade’ injury, defined as a stable scapula with preserved biomechanics and SHR, relatively normal radiographs, and no clinical evidence of scapular dyskinesis; and ‘high grade’ injury, defined as an unstable protracted scapula, with altered biomechanics and SHR, altered appearance on radiographs and evidence of scapular dyskinesis; the latter subtype is less amendable to non-operative care (Table 1).

Clinical evaluation

Both the ISAKOS classification system, including the type IIIA and IIIB, and the ‘low grade/high grade’ system, require a comprehensive clinical evaluation to establish the true pathoanatomy and pathomechanics, to better identify the treatment options. The exam comprises visualization/inspection/palpation, provocative maneuvers, observation of motion, and corrective maneuvers that may alter the clinical symptoms (Table 1) and may be augmented with appropriate imaging. For acute AC joint injuries, the exam should be performed both at the initial visit but also 3–6 weeks after the injury, to allow for reduction in pain and better ability to evaluate motions. This would be especially valuable in type III injuries.

Visualization and inspection should be accomplished by direct evaluation of the symptomatic joint and comparison, if possible, to the asymptomatic contralateral joint. The most common visualized alterations may include varying amounts of prominence of the distal clavicle due to an apparent superior position relative to the inferiorly and medially displaced acromion in low grade or high grade AC separations or altered posture of the scapula and arm into protraction due to muscle weakness or imbalance associated with AC ligament sprains.

Palpation often reveals the location of the symptomatic pathology. The clavicle should be palpated along its entire length from the sternoclavicular joint to the AC joint. Point tenderness along the bone, especially near the AC joint, will suggest bony involvement. The acromion and its extension into the scapular spine, and the coracoid and CC ligament area can also be palpated, and pain in these areas can be differentiated from other anatomic areas around the joint. Finally, direct palpation of the AC joint, making sure that the palpation pressure is localized to the joint and not to the bone, can elicit pain that can confirm the joint is a potential source of some of the clinical symptoms.

Provocative maneuvers may be utilized to reproduce the clinical symptoms and provide information about the anatomic structures that may be involved. The maneuvers most commonly used in clinical practice ¹⁹ include the active compression test, ²⁰ cross body adduction test, ²¹ and AC shear test. ^22,23 The active compression test is a resisted test that was designed to help distinguish between labral injury and AC joint abnormality. It is important to understand that ‘abnormality’ is a broad term which could include instability, joint derangement, and/or arthritis/arthrosis. The lack of specificity of this maneuver is the likely reason for the variation in clinical utility values reported in the literature.^20,24–26 The cross body adduction test is a passive maneuver that is used often in clinical practice ¹⁹ but has small positive likelihood ratios for detecting AC injury.^24,25,27 However, moderate positive likelihood ratios have been reported when the active compression test and cross body adduction are used as a cluster. Cadogan et al. found a positive likelihood ratio of 6 when the cluster of these 2 maneuvers with the addition of the Hawkins-Kennedy test ²⁸ and AC joint tenderness are positive whereas Chronopolous et al. found a positive likelihood ratio of 8 with these 2 maneuvers plus the AC resisted extension test being positive. ²⁴ Interestingly, there are no clinical utility values in the literature for the AC shear test, yet this test may provide valuable information regarding specific ligament integrity. In the AC shear test, the clavicle and acromion may be grasped and mobilized in several directions to load, unload, and shift the loads, and to place stress on the ligaments. The clavicle and acromion may be translated in vertical (inferior/superior) and horizontal (anterior/posterior or rotational) directions. In low grade (Rockwood/ISAKOS I, II, IIIA) AC injuries, with mainly AC ligament injuries, most of the demonstrated laxity will be in the horizontal direction and be graded by the traditional sprain classification types 1–3, depending on the amount of translation. High grade (Rockwood/ISAKOS IIIB, IV, V) AC injuries will demonstrate laxity in the vertical as well as horizontal directions. In addition, in the high grade injuries, the horizontal adduction maneuver will pull the acromion inferior and medial to the clavicle, resulting in the characteristic posture of clavicle prominence, even though the true altered motion is the acromial displacement. The lack of maneuver specificity suggests that the active compression test and cross body adduction test are better for low grade injury when an obvious deformity is not present. The AC shear test is ideal for identifying specific ligament involvement in low and high grade injury.

A thorough and dynamic scapular examination is key to assess the functional consequence of the AC joint injury on arm function rather than identifying the injury itself (Figure 2). The effect of AC joint pathoanatomy on SHR can be assessed by observation of the motions of the arm, scapula, and clavicle ²⁹ during arm flexion and abduction and load bearing. In high grade AC separations the resulting pathomechanics can include dynamic increase in inferior and medial positioning of the scapula under the clavicle resulting from loss of ligament and suspensory function and will be seen as excessive scapular protraction, which can be clinically observed as an asymmetrical scapular position at rest or medial border prominence upon arm motion in elevation and/or descent. Maintenance of symmetrical scapular position during motion indicates a low grade injury with less pathoanatomical injury and pathomechanical deficit and suggests better outcomes from non-operative treatment.

Figure 2.

Scapular examination algorithm.

The exam can include scapular corrective maneuvers, which can be helpful to indicate the effect that modifying the pathoanatomy may have on the symptoms, and also noting any change in the pathomechanics, function, or symptoms. The patient's response to the maneuvers may result from some restoration of more normal joint kinematics or from facilitation of proprioception, strength, or movement strategies, and can give information regarding the patient's place on the spectrum of injury and dysfunction and which may help suggest treatment options. Manual realignment and reduction of the AC joint, conferring joint stability, may sometimes be possible, and may decrease the joint symptoms and may improve the dynamic deficits in normal SHR. This can be accomplished directly by mobilizing the acromion and clavicle, or indirectly by mobilizing the scapula in relation to the stabilized clavicle in the Scapular Assistance Test (SAT) and the Scapular Retraction Test (SRT).^29–31 These maneuvers help place the clinical presentation of the injury in context to possible scapular-based consequences however; the results generated should be supported by other examination components and treatment decisions should be made when piecing together all examination findings. Other strategies for evaluation may include facilitation of distal (rotator cuff) and proximal (kinetic chain) muscle activation. Considering that as many as 20% of patients will demonstrate associated intra-articular pathology most commonly a labral injury and/or glenohumeral instability, an inclusive glenohumeral joint internal derangement exam should also be performed.^32–34

Plain X-rays should be obtained in every case as they can assess bone injury and the 2-dimensional relative positioning of each bone. Measurement of AC and CC distances can be helpful in estimating static vertical bone displacement. High grade or type V injuries will usually demonstrate more than 2 cm of separation in the CC distance. Bilateral views can also be helpful in identifying altered positions. Views with weights held in the hands can accentuate the alteration in suspensory capability. Cross body adduction (Basamania) views can highlight the inferior and medial displacement of the acromion and scapula in relation to the clavicle. Magnetic resonance imaging may not be routinely utilized but is helpful in identifying the location and extent of the ligament injuries, such as low grade AC ligament sprains, AC ligament tear/ trapezoid ligament injury, or AC ligament tear/trapezoid ligament tear/conoid ligament tear.

The results of the evaluation can be used in algorithms regarding decision making for all types of AC joint injuries and can help improve understanding of the type III injuries (Figure 3).

Figure 3.

Acromioclavicular joint injury treatment algorithm developed by Beitzel et al. Arthroscopy 30 (2): 271–278, 2014 (reprinted with permission).

Treatment guidelines

The goals of treatment, either non-operative or operative, are to minimize pain and optimize function, in the context of patient specific activities and demands. In most cases, this would result from restoration of the pathoanatomy. In cases of AC ligament sprains, it most frequently would involve rest and supportive care. In more high grade injuries with more tissue disruption, surgical treatment may be indicated.

Non-operative

A recent systematic review of the literature disseminated information specific to non-operative AC joint treatment, noting that the literature has not been helpful in guiding clinicians on how to best manage AC joint injury conservatively. ¹⁸ The review identified numerous concerns including low quality critical appraisal evidence as well as methodological inconsistencies within (robust detail for operative measures and limited to non-existent detail for non-operative measures) and between studies (injury heterogeneity, surgical technique variations, and variations in outcome measures). The authors recommended an approach to treatment focused on restoring dynamic function rather than cosmetic realignment. The approach advocates using symptom control initially then progressing to a kinetic chain-based treatment program (Table 2). ¹⁸ This framework addresses the SHR component of shoulder function by attempting to keep symptoms from being exacerbated while simultaenously utilizing more motor control principles compared to traditional strengthening principles. ³⁵

Table 2.

Non-operative rehabilitation guidelines.

Guideline	Key points
Rest and activity modification as needed to decrease acute symptoms	Often 1–2 weeks, however no standardized time frame has been identified within the literature
	Interventions such as immobilization or therapeutic modalities can be incorporated but optimal positioning/time of immobilization as well as specific modalities have not been identified within the literature
Begin incorporating therapeutic exercise for addressing proximal segment control	Utilize exercises designed for leg and trunk/core strengthening
	Re-evaluate every few weeks to determine if strength is advancing
Employ exercises for scapular and shoulder mobility and/or lower extremity mobility as needed	Mobility can be addressed simultaenously with proximal segment control interventions
Progress to short-lever interventions beginning with maneuvers that utilize trunk and leg motion to facilitate more optimal scapular positioning and mobility	These maneuvers will be performed sitting or standing and with the arm close to the trunk
	Progress to next guideline with visually observed improved scapular control and when patient can perform 5–6 sets of 10 or more repetitions without early fatigue or symptom exacerbation
Phase out short-lever interventions and phase in long-lever maneuvers	Begin with maneuvers requiring the arm to be slightly flexed or abducted then transition to maneuvers with the arm at or above shoulder height

It should be noted that the literature to date has found that: 1) non-operative treatment often permits earlier improvements in subjective outcomes, but no differences occurring at long-term follow-up after 6 months^36–46; 2) operative treatment results in better joint reduction^{36,38,41,45,47,48}; and 3) non-operative treatments can result in faster return to activities, but residual symptoms such as pain and joint instability may persist.^49–52 These items can serve as the foundation for discussion with patients regarding what is known and general expectations. In brief, non-operative management can be attempted but there is a ceiling effect that will likely occur based on severity of injury. It should be noted that the ligamentous injury will often not completely resolve. Decrease in symptoms and impairments can be achieved but, in some cases, residual deficits in function exist. Furthermore, non-operative efforts will in most cases not affect cosmetic appearance of the disrupted anatomy. Rehabilitation measures are not able to fully realign the dissociated acromion and clavicle but they can attempt to optimize the surrounding scapular muscles in order to re-establish the scapula as a coordinated link in the kinetic chain.^53,54 Although the deformity may be present, scapular control (or lack thereof) and patient feedback should serve as the benchmarks for determining if the outcome is acceptable. The examination results and the patient's self-reported function will help guide the clinical decision-making process.

Operative

Multiple surgical procedures have been developed to address high grade AC joint injuries with fixation materials including hook plates^36,37,44,47; screws or pins^{40,48,49,52,55–57}; wire, graft, tape, or suture^{38,39,41–43,45,50,51,57–60}; and biologic allograft. ⁴⁶ Many have been based on inaccurate understanding of the 3-dimensional mechanics of AC joint function and pathomechanics. The purpose of this paper is not to review the different procedures advocated for this injury. However, more recent understanding of the pathoanatomy and pathomechanics has identified several principles that should guide operative treatment and provide more focused surgical technique. They include: (1) Anatomic reconstruction of the CC ligament attachment sites on the clavicle; (2) Use of biologic augmentation, especially in chronic cases; (3) Anatomic repair or reconstruction of the superior, anterior, and posterior AC ligaments to the clavicle; (4) Complete reduction of the clavicle into the AC joint, and (5) addressing any concomitant intra-articular pathoanatomy.

Summary

AC joint injuries exist and present on a spectrum of pathoanatomy. More precise evaluation of the exact pathoanatomy involving the AC joint structures and the CC ligaments and the effect of the pathoanatomy on the 3-dimensional function of the shoulder and arm through SHR is needed to provide the optimal guidance for the development of treatment protocols that can address the specific injury and restore the optimal mechanics. Specific clinical exam techniques for evaluation of scapular motion and AC joint laxity, complemented by imaging, can define the pathoanatomy and pathomechanics of the specific injury, an allow a more precise diagnosis. This information can be used to develop the guidelines for non-operative and operative treatment and can also be used to establish methods of evaluating outcomes of the treatment. This approach would better delineate the AC injury and provide more focus for treatments.