The acromioclavicular (AC) joint is a pivotal construct for scapular and shoulder function. The articulation of the acromion and clavicle, when healthy and stable, allows fluid scapular and humeral motion to be achieved, force to be generated, and functional tasks to be executed. When the AC joint becomes compromised anatomically, function of the scapula and/or arm will be compromised. Nontraumatic/atraumatic and traumatic conditions can affect the integrity and function of the AC joint.
Osteolysis, the pathologic destruction of bone, has been shown to occur at the AC joint. Although the cause can occasionally be connected to a metabolic disease, repetitive microtrauma from excessive loading has been identified as the most common etiology. , Repetitive microtrauma that occurs with loading activities, such as weight training, places loads and forces within and across the AC joint, which in turn creates an inflammatory response. The frequent presence of inflammatory mediators compounds over time, resulting in a degrading of the acromioclavicular articulation ( Fig. 21.1 ). , The differential diagnosis of osteolysis may include infection, hyperparathyroidism, rheumatoid arthritis, and scleroderma, especially with bilateral involvement. Local processes that can resemble classic osteolysis are massive osteolysis (Gorham-Stout disease), infections, primary bone tumors such as multiple myeloma, and metastatic malignancy.
AC joint arthritis may also occur and manifest as osteoarthritis (OA) ( Fig. 21.2 ), rheumatoid arthritis ( Fig. 21.3 ), or crystal arthopathy (e.g., gout). Similar to the mechanism related to osteolysis development, repetitive microtrauma with a resultant inflammatory response can lead to the development of OA, which is likely why it is the most prevalent of the three forms of arthritis. In addition to repetitive microtrauma, OA development has been attributed to macrotrauma, acromion shape, and age-related degeneration. However, critical review of the literature has revealed that this information is often incomplete. Patient demographic information is often underreported, with little to no mention of patient activity, occupation, and/or a complete injury history. Without these details, it is difficult to determine the exact pathophysiology of the AC joint OA. Furthermore, multiple investigators have found discrepancies between radiographic evidence of arthritis and clinical symptoms. Collectively, these reports suggest that joint alteration as a stand-alone finding may not guide clinicians toward making a proper diagnosis, which in turn would negatively affect treatment decisions. However, the most accepted theory supporting OA development at the AC joint is micro/macrotrauma creating excessive joint laxity and inflammation. Symptoms could result from bone-on-bone contact due to the arthritis or from the acquired ligament laxity or both.
Surgically related (iatrogenic) joint injury
AC ligament integrity can also be compromised by procedures directed at alleviating AC joint arthritis symptoms. Resection of 5 to 7 mm of bone risks injury to the attachment sites of the posterior and superior AC ligaments, and resection of 10 to 11 mm risks injury to the trapezoid ligament attachment site. In addition, actual damage to the ligaments can also occur. The shortening of the bone may compromise clavicle strut function, increase posterior impingement, and compromise ligament integrity leading to anterior/posterior and rotational instability. , , This can be evaluated clinically by the presence of impingement symptoms upon arm cross-body horizontal adduction and anterior/posterior laxity on clinical testing.
In addition to repetitive microtrauma or iatrogenic joint injury, high-energy macrotrauma can also negatively affect the AC joint. Tackling sports such as American football and rugby, and contact sports such as wrestling and ice hockey, have the greatest incidence of traumatic AC joint injury. Under these circumstances, the AC and coracoclavicular (CC) ligaments and the attachments of the deltoid and trapezius muscles are susceptible to partial or complete tearing or avulsion. The incidence of AC joint separations or dislocations ranges from 1.7 to 9.2 per 10,000 individuals. In specialized populations, such as collegiate and professional football players as well as military cadets, the incidence increases to 3.3 to 26 per 10,000 individuals. , The literature has consistently reported larger male to female ratios with males sustaining anywhere from 2.2 to 8.5 more AC joint separations compared to females. , , Low-grade separation (Rockwood types I and II) occur much more often compared to high-grade separations (Rockwood types III and higher), ranging from 4% to 11%. , ,
Pathoanatomy and pathomechanics of traumatic acromioclavicular joint injury
The mechanism of the traumatic AC injury is a progression of loading due to imposed trauma. The large majority of injuries occur from a force from posterior-superior to inferior-medial, most commonly in a fall ( Fig. 21.4 ). Studies have demonstrated the progression of the initial anatomic disruption from the posterior and superior AC ligaments to the anterior AC ligaments. , These ligaments are avulsed off their clavicular attachments ( Fig. 21.5 ) and create horizontal and rotational instability, , and the loss of the lateral tension band. Progression of the disruption can occur through the inferior capsule into the substance of the trapezoid and conoid ligaments ( Fig. 21.6 ). This 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.
Clinical presentation, clinical evaluation, and treatment options in traumatic acromioclavicular joint injury
Clinical symptoms, function, and dysfunction will vary depending on the amount of ligament disruption and the alteration of shoulder mechanics. The exact diagnosis, encompassing the extent of the anatomic injury and the altered scapulohumeral rhythm (SHR) mechanics, is key to formulating treatment. Types I and II AC ligament sprains will usually result in localized temporary pain and swelling, and can be managed by rest, a short period of immobilization, and gradual resumption of activities.
Complete tears of the AC ligament can result in horizontal (i.e., anterior-to-posterior) and lateral instability of the scapula/acromion in relation to the clavicle. There will be pain and swelling at the joint; pain upon arm horizontal adduction, flexion, or abduction; and sometimes weakness in these motions. There may be a slight prominence of the distal clavicle due to the lateral tilt of the acromion in relation to the clavicle. Anterior/posterior joint integrity can be assessed, and laxity and symptomatic instability identified by stabilizing the clavicle in one hand, grasping the acromion with the other hand, and performing an anterior/posterior translatory force ( Fig. 21.7 ). Due to the intact CC ligaments, scapular kinematics are minimally uncoupled so that resting scapular position and dynamic scapular motion with arm movement are observed to be symmetrical to the uninjured side. Imaging may demonstrate slight AC joint widening, but the CC distance should not be widened. Clinical findings associated with these injuries would be classified as type II in the Rockwood classification. If the ligament sprain heals, as most will, the AC joint complex anatomic integrity is restored, and rehabilitation can be expected to restore three-dimensional SHR mechanics and function. Incomplete ligament sprain healing can occur with continued mechanical dysfunction and clinical symptoms; surgical repair and reconstruction of all components of the AC ligaments may therefore be required.
The ligament disruption can continue into the CC ligaments. Some injuries will involve complete tears of the trapezoid ligament, with stretching or no injury to the conoid ligament. In these cases, there will be some alteration of the suspensory function and more lateral and downward acromial tilt. This would be clinically observed as prominence of the distal clavicle and “step-off” of the acromion. Pain and weakness may be seen with symptoms of impingement due to the acromial position. Anterior/posterior AC joint laxity will be present. Imaging will usually demonstrate AC joint widening, altered acromial position, and some CC space widening. These findings are usually classified as Rockwood type III injuries.
Type III injuries have generated much controversy, with varying opinion about pathoanatomy and treatment. , Treatment of these injuries has been advocated as “individualized” with few concrete guidelines other than continued patient symptoms. There is minimal correlation of imaging and symptoms with the currently used classification systems or with published outcomes. , , Studies have found that patients classified with type III injuries may demonstrate either altered or normal scapular kinematics. , An International Society of Arthroscopy, Knee Surgery, and Orthopaedic Sports Medicine (ISAKOS) consensus statement proposed dividing type III injuries into types IIIa and IIIb, with the differentiation due to absence or presence of altered scapular kinematics on clinical examination or imaging. But there is still minimal consensus how these findings relate to the clinical problem. Precise clinical evaluation, knowledge of the pathoanatomy, and observation of the pathomechanics may provide the basis for better understanding. The CC ligament injuries have the capability of disrupting the screw axis and three-dimensional mechanics. Many injuries that have been classified as type III, due to the prominence of the distal clavicle, have an intact conoid ligament and will not demonstrate loss of control of scapular motion. 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 intact conoid ligament. The disrupted three-dimensional mechanics can be difficult to evaluate with standard two-dimensional imaging. Specialized radiographs, such as the Basamania medial stress view, can demonstrate the altered scapular motion, and magnetic resonance imaging can demonstrate the extent of the ligamentous disruption ( Fig. 21.8 ). Clinical observation of scapular dyskinesis, with prominence of the inferior or medial scapular border, demonstrates the scapular internal rotation and lateral translation that accompanies disruption of both CC ligaments ( Fig. 21.9 ).
Therefore, type III injuries may actually encompass a wide variation in pathoanatomy and pathomechanics, and this variety may explain the difficulty in developing treatment options. The majority of type III injuries without evidence of loss of scapular control (ISAKOS type IIIa) can be managed nonoperatively, emphasizing periscapular strengthening to optimize scapular retraction. Many patients with type III injuries with evidence of loss of scapular control (ISAKOS type IIIb) do not respond to strengthening, with ongoing clinical symptoms, and subsequent surgical treatment. In an updated follow-up study of 48 patients treated for traumatic AC joint injury, 8 demonstrated no scapular dyskinesis and responded well to nonoperative treatment. Conversely, 40 patients demonstrated scapular dyskinesis, with 36 failing nonoperative treatment leading to surgery. This suggests that the type III classification as it currently exists is not adequate to accurately group patients by pathoanatomy or pathomechanics and is not capable of reliably indicating treatment.
Complete disruption of the AC and CC ligaments creates the 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. Clinical symptoms include pain, muscle weakness, impingement, and inability to optimally achieve overhead arm position. These clinical findings are usually classified as type V injuries. Two-dimensional radiographic imaging demonstrates wide separation of the AC and CC distances ( Fig. 21.10 ). There is a prominent acromial step-off and distal clavicle position. Resting scapular position, either on clinical examination or by Basamania medial stress views is inferior and medial to the clavicle. Occasionally, the AC joint may be reduced by movement of the arm and acromion laterally and superiorly, with a decrease in clavicle prominence, normalization of scapular position, modification of impingement symptoms, and improvement in arm motion.
The anatomical injuries and resulting impairment of mechanics and function are frequently not well treated by nonoperative protocols. Periscapular strengthening may be helpful, but optimal muscle function demands joint stability and clavicular strut function in order to be effective. A 4- to 6-week period of rehabilitation can be prescribed, but ongoing symptoms may indicate surgical treatment.
Traumatic AC joint injuries exist on a spectrum of pathoanatomy and consequent pathomechanics. Clinical presentation and symptoms can vary depending on how these anatomical and mechanical disruptions affect SHR and interact with each patient’s needed or desired function. Precise knowledge of the pathoanatomy and pathomechanics are key elements in the establishment of the diagnosis that will guide treatment. The current Rockwood classification of injuries has not been shown to be effective as an accurate and reliable diagnostic tool, and several modifications have been proposed. A diagnostic method based on pathoanatomy and pathomechanics may provide more information for guiding evaluation and suggesting treatment options ( Table 21.1 ). This method organizes type I and II injuries based on the amount of AC ligament injury and healing, and organizes the type III and V injuries based on the amount of mechanical disruption from the combined AC and CC ligament injuries, with alteration of scapular position and motion, and disruption of SHR. All injuries with no scapular prominence and minimal alteration of SHR are considered low grade and those with scapular prominence and alteration of SHR are considered high grade.
|Injury||Clinical Findings||Imaging||Treatment Options|
|Isolated AC ligaments: type I and II with normal healing (low-grade)||Joint pain, no instability||Radiograph: no step-off, no widening||Protection, rehabilitation|
|Isolated AC ligaments with continued symptoms: type II (low-grade)||Joint pain, anterior/posterior instability, impingement||Radiograph: no step-off, ± widening |
MRI: Swelling, ligament injury
|Protection, rehabilitation, possible AC ligament repair/reconstruction|
|Combined AC/CC ligaments: type IIIA (low-grade)||Joint pain, weakness, lateral acromial tilt, step-off, prominent distal clavicle, no scapular dyskinesis via radiograph or clinical examination||Radiograph: mild CC widening |
MRI: AC ligament injury combined with trapezoid ligament injury
|Protection, periscapular rehabilitation, possible AC and CC anatomic reconstruction|
|Combined AC/CC ligaments: type IIIB/V (high-grade)||Joint pain, weakness, impingement, decreased arm motion, lateral acromial tilt, step-off, prominent distal clavicle, inferior medial scapular/acromial position via radiograph and clinical examination||Radiograph: AC and CC widening >2 cm |
MRI: AC ligament injury combined with trapezoid and conoid ligament injury
|Protection, periscapular rehabilitation, possible AC and CC anatomic reconstruction|
AC ligament disruptions may be isolated injuries. Depending on the extent of the disruption to the posterior, superior, and anterior components, the AC joint may be stable or exhibit excessive anterior/posterior and rotational instability on testing. There may be a slight joint step-off, but minimal scapular dyskinesis. Treatment is directed at joint symptoms. Most will heal like sprains, but ongoing joint instability may require longitudinal repair and reconstruction of the posterior, superior, and anterior AC ligaments.
Combined AC and CC ligament disruptions may result in varying pathoanatomy and pathomechanics. Due to the CC ligament injury, there will be a joint step-off with distal clavicle prominence, clinical symptoms related to disruption of SHR, and two-dimensional radiographic imaging findings of variable amounts of widening of the AC and CC spaces. It appears that a group of these patients have less disruption of the three-dimensional functional mechanics, demonstrated by no loss of control of scapular position or motion on Basamania medial stress views or by clinical testing of scapular motion. The pathoanatomy on magnetic resonance imaging in these patients is more related to trapezoid ligament injury, with an intact conoid ligament. There is a higher rate of resolution of clinical symptoms following nonoperative treatment, and the need for surgical intervention occurs infrequently. These may be regarded as low-grade AC joint injuries, which would include most Rockwood type II and the ISAKOS type IIIa injuries.
The group of patients who have more disruption of the three-dimensional functional mechanics demonstrate loss of control of scapular motion and position. The pathoanatomy on magnetic resonance imaging or at surgery is related to the disruption of both trapezoid and conoid ligaments. These have a higher rate of failure following nonoperative treatment. These injuries may be regarded as high-grade AC joint injuries. This would include Rockwood type V and ISAKOS type IIIb injuries.
A period of nonoperative treatment is frequently advocated for all AC joint injuries. It is helpful to allow a period of protected healing, the reinstitution of periscapular muscle strength and control, restoration of glenohumeral joint motion, and evaluation of arm motion, all of which create optimal SHR. Failure of nonoperative treatment is a helpful indicator of the need for surgical treatment.
A conservative plan of care should be undertaken for osteolysis of the distal clavicle, at least initially. The cornerstone of treatment is rest and activity modification, even going so far as to completely discontinue participation in weight-training programs that are undertaken to maximize athletic performance and vigorously encouraged by coaches and strength and conditioning specialists. Nonsteroidal antiinflammatory medication can be prescribed, and from time to time, during the course of recovery, it may be reasonable to perform a corticosteroid injection. Although it can require 6 to 12 months, instances of relatively atraumatic osteolysis of the distal clavicle are capable of recovery of comfort, function, and bone integrity with nonoperative treatment. , , When nonoperative treatment is deemed a failure, excision of the lateral clavicle has been shown to terminate the process and, in nearly all cases, results in a good or excellent outcome. ,
Considering AC joint arthritis is an inflammation-derived condition, therapeutic injection has been thought to be a reasonable treatment modality. However, as of 2010, it was noted that there were no systematic reviews, meta-analyses, or randomized controlled trials regarding therapeutic injections specific to the AC joint. The results of intra-articular corticosteroid injections have been shown to vary but usually result, at the least, in short-term pain relief and improvement in range of motion. However, the effectiveness of injection has been shown to be negatively impacted by a lack of accuracy during injection administration ( Fig. 21.11 ). One group reported that only 15 of 41 corticosteroid injections were confirmed to be intraarticular, an accuracy of 36.5%. Furthermore, cohort studies with various follow-up times have found that (1) one-third of patients reported relief of symptoms 1 month following injection with the relief maintained after 18 months, (2) 25% of patients had symptom reduction for 1 year but significant deterioration was observed at 5 years, and (3) relief of pain occurred within 1 week but returned to baseline pain by 3 weeks. , Taken together, these results suggest that an AC joint injection does not appear to be a viable long-term solution as relief is achieved in a small percentage of patients, and it can dissipate over time.
After rest and activity modification recommendations have been followed and symptoms have been reduced (and possibly eliminated), an attempt at rehabilitation can be made. Physiological deficits and/or impairments (strength, flexibility, endurance, etc.) identified on physical examination may be addressed; however, a progressive program should be used. For example, avoiding maneuvers that will excessively load, stress, or move the compromised AC joint is recommended. This can be achieved through the use of short-lever exercises that can be performed with the arms in an adducted position (i.e., the arms positioned against the thorax) rather than positions that require the arms to be in an elevated or abducted position. Examples of exercises that may be used initially include conscious correction of the scapula (also known as scapular squeezes), “sternal lifts,” and “low rows.” Maneuvers, such as scapular shrugging or elevation, and scapular proprioceptive neuromuscular facilitation, should be avoided in the first phase of rehabilitation (approximately the first 4 to 6 weeks) because of the excessive movement and stress that occurs at the AC joint during their performance. Once the patient has demonstrated that the initial exercises can be performed without exacerbating the previous symptoms, progression into more dynamic motions such as the “lawnmower,” “robbery,” and “fencing” exercises may be added to the treatment progression. Ideally, patients should be provided an exercise volume that begins with 1 to 2 sets of 5 to 10 repetitions with no external resistance. Additional sets and repetitions can be added based on symptoms and exercise tolerance, with an end goal of 5 to 6 sets of 10 repetitions without worsening symptoms. Resistance may be added next beginning with light free-weights (2 to 3 lb maximum) and then progressing to elastic resistance bands. The stability of free weights allows such devices to be utilized prior to resistance bands. In the later phases of the treatment program, long-lever maneuvers can be incorporated, but only when the previous maneuvers have been mastered by the patient and have demonstrated little to no symptom exacerbation.
Parallel conclusions from a recent Cochrane Review and a current concepts review have noted that the available evidence for treating acute AC separations/dislocations is of poor quality and is not robust enough to conclude that there is evidence to support any form of treatment for patients with AC separations/dislocations. Many retrospective case series have been published on this topic; however, within and between studies, patient populations and injury patterns are heterogeneous, treatment methods utilized lack details (i.e., rehabilitation program specifics), and few randomized studies exist to draw definitive conclusions. These issues are further compounded by the variation in outcome assessment with a variety of patient-reported outcome measures being used within the literature. , , , However, considering that one of the tenets of evidence-based medicine is to utilize the best available evidence, some recommendations can be provided.
Treatment for low-grade injury
Common recommendations per the literature can be found in Table 21.2 . For low-grade injuries, a reduction of symptoms can be achieved through nonoperative treatment methods. Time lost from sport can be relatively minimal, ranging from 10 to 12 days. , It should be noted that the ligamentous injury does not completely resolve. A decrease in symptoms and impairments can be achieved but, in some cases, residual deficits in function exist. For example, it has been shown that symptoms can persist from 6 months to 5 years following injury ; however, more than 90% of the time, the symptoms remain insignificant or reasonably well tolerated. , Previous work has shown that patients receiving nonoperative care for low-grade injuries could expect symptoms to resolve by 12 months; however, patients with symptoms at 6 months correlated with those who were symptomatic beyond 1 year. Additionally, other investigators identified a higher incidence of unfavorable outcomes with nonoperative treatment, which led them to suggest that adverse outcomes were underestimated. A long-term follow-up study found that more than half of patients will experience symptoms and obtain noticeably lower functional scores when compared with the uninjured shoulder approximately 10 years after type I or II injuries. While joint dimensional differences were detected by ultrasonography, radiographic degenerative changes were not observed. This suggests that although joint health appeared unremarkable from a two-dimensional assessment, three-dimensional function remained negatively affected.