Internal Impingement of the Shoulder

Original Editors - Joshua Caldwell, Phillip Williams, Gary Diekhoff, Bryan McAdams as part of the Texas State University Evidence-based Practice Project,Huart Deborah

Top Contributors - Joshua Caldwell, Phillip Williams, Gary Diekhoff, Bryan McAdams, Rachael Lowe, Kim Jackson, Admin, Evi Jacobs, Deborah Huart, Mandeepa Kumawat, Tarina van der Stockt, Fasuba Ayobami, Katherine Knight, Naomi O'Reilly, Jess Bell, George Prudden, WikiSysop, Wanda van Niekerk, Robin Tacchetti, Jeremy Brady, Jelle Habay and Simisola Ajeyalemi  

Search Strategy

Definition/Description

Internal impingement is commonly described as a condition characterized by excessive or repetitive contact between the posterior aspect of the greater tuberosity of the humeral head and the posterior-superior aspect of the glenoid border when the arm is placed in extreme ranges of abduction and external rotation. (1,2,3,4)     (Level of Evidence: 2A,2A,2A,3A) This ultimately leads to impingement of the rotator cuff tendons (supraspinatus/infraspinatus) and the glenoid labrum.

There are two types of internal impingement: anterosuperieur and posterosuperieur. Anterosuperieur impingement occurs only rarely.(17) (level of Evidence: 5)

Clinically Relevant Anatomy

The scapula is a flat blade lying along the thoracic wall. Because of the wide and thin configuration, it’s possible for the scapula to glide smoothly on the thoracic wall and provides a large surface area for muscle attachments, both distally and proximally.(21) (Level of Evidence: 5)
The coracoacromial arch and the subacromial elements are important elements of anatomy related to internal impingement. As the name implies, the coracoacromial arch is formed by the coracoid and the acromion processes and the connecting coracoacromial ligaments. It protects the humeral head and subacromial structures from direct trauma and superior dislocation of the humeral head. Impingement may occur when the rotator cuff and other subacromial structures become encroached between the greater tuberosity and the coracoacromial arch.

The tendons of the rotator cuff are:
- Subscapularis tendon (anterior)
- Supraspinatus tendon (superior)
- Infraspinatus tendon (posterior)
- Teres minor tendon (posterior)

The rotatorcuff stabililizes the shoulder against the action of the prime movers to prevent excessive anterior, posterior, superior, or inferior humeral head translation.(34) (Level of Evidence: 5)

The rotatorcuff tear is located on the articular side of the rotator cuff, typically at the intersection of the infraspinatus and supraspinatus insertions onto the humeral head. (3) (Level of Evidence: 2A)

The scapulothoracic articulation is a prime example of dynamic stability of the human body. By a lack ligaments, the joint delegates the function of stability fully to the muscles that attach the scapula to the thorax. So their proper function is essential to the normal biomechanics of the shoulder.

These muscles include:
• Serratus anterior
• Trapezius
• Levator scapulae
• Rhomboid major
• Rhomboid minor
• Latisimus dorsi
• Pectoralis major and minor
• Supraspinatus and infraspinatus

The serratus anterior and the trapezius has been suggested to be the most important muscles acting upon the scapulothoracic articulation.(34) (level of Evidence: 5)

Epidemiology /Etiology

Epidemiology

          The majority of patients who have been identified as having internal impingement are overhead athletes. Understanding this patient population, it is not surprising that it typically affects young to middle aged adults. In most major case series of internal impingement, patients are under 40 years of age and participate in activities involving repetitive hyperabduction and external rotation of the arm.  The majority of the research on internal impingement has been done on elite baseball players.  However, non-elite athletes, as well as non-athletes may also be affected by internal impingement.   With the non-elite athletic population, it is important to realize that older patients are more likely to have concurrent shoulder conditions. Since internal impingement is often involved with other pathology of the shoulder the incidence of it in isolation has not been established.

Etiology

          The understanding of the etiology behind internal impingement has gradually evolved but remains incomplete. The lack of a common biomechanical model is largely due to the limited patient population in which the syndrome is seen in as well as the myriad of associated pathologic findings that have been reported.  SLAP lesions, rotator cuff tendon lesions, and anterior GH (glenohumeral) instability are the most commonly cited pathologies that may accompany this syndrome. Unlike subacromial impingement, there is not a single pathomechanical process that is leading to internal impingement, which makes it a more complex syndrome.    Although many different biomechanical explanations have been proposed by numerous investigators, there is a relatively high consensus that the repetitive, extreme ranges of GH (glenohumeral) abduction and external rotation, along with underlying shoulder dysfunction, are likely the prime culprit leading to the development of internal impingement.    There are three common underlying factors seen throughout the literature that have been shown to contribute to this disorder.     

Anterior GH instability: Jobe et al. hypothesized that anterior instability/laxity of the shoulder complex caused by repetitive stretching of the anterior GH capsule led to this type of impingement in throwing athletes.  This laxity allows for increased anterior humeral head translation, ultimately leading to entrapment of the supra/infraspinatus seen with this syndrome.  A case series on 17 patients with internal impingement syndrome who were treated with arthroscopic debridement for under surface tears of the rotator cuff provided the first clinical evidence to support the concept of internal impingement.  

Muscle imbalance and/or improper neuromuscular control of the shoulder complex:   Jobe et al. also reported that malpositioning of the arm relative to the glenoid bone during throwing motions can also lead to impingement of the rotator cuff tendons between the glenolabral complex and the humeral head. Fatigue and/or weakness of the scapular retractors have been shown to cause a decreased force production in all four of the rotator cuff muscles, which would also lead to abnormal positioning of the GH joint.     At the base of this abnormal scapular positioning lies the lack of neuromuscular control of the periscapular musculature as well as muscle imbalances between the rotator cuff and upward rotators of the scapula (serratus anterior, upper trap, lower trap).

Tight posterior GH capsule: The posterior-inferior GH joint capsule is hypothesized to become hypertrophied in the follow-through tensile motion of throwing. After ball release, the resultant force on the glenohumeral joint is one of distraction. The posterior shoulder musculature responds by providing a compressive force (decelerating). The PI capsule is subjected to high tensile forces, resulting in hypertrophy over time. Posterior capsule tightness leads to GIRD (glenohumeral internal rotation deficit), which is a key clinical finding associated with this syndrome.    Also, several cases have reported that a contracture of the PIGHL (posterior-inferior GH ligament), which is often seen in these patients, shifts the contact position of the humeral head and glenoid posteriorly and superiorly, which allows for more external rotation during pitching, thus adding to the impingement condition as well.        

Characteristics/Clinical Presentation

The diagnosis of internal impingement based on history alone is extremely difficult, and symptoms tend to be variable and fairly nonspecific.  Because of the variable nature of internal impingement, understanding the patient population and the clinical presentation is critical to identifying this disorder. A review of the literature does show several common symptoms that most internal impingement patients seem to share.
Internal Impingement patients present with:

Posterior Shoulder Pain

• Chronic- diffuse posterior shoulder girdle pain is the chief complaint in the throwing athletes with internal impingement, but the pain may also be localized to the joint line.  The patient may describe the onset of posterior shoulder pain, particularly during the late-cocking phase of throwing, when the arm is in 90° of abduction and full external rotation. 
• Acute – non-throwing athletes, who present with this syndrome, have a chief complaint of acute shoulder pain following injury

Decrease in throwing velocity - a progressive decrease in throwing velocity or loss of control and performance in the overhead athlete.

“Dead arm” - Some signs of the pathologic process include a so-called “dead arm,” the feeling of shoulder and arm weakness after throwing, and a subjective sense of slipping of the shoulder  

Muscular Asymmetry - Overhead athletes and throwers in particular often have muscular asymmetry between the dominant and the nondominant shoulder.

Muscular/Neuromuscular Imbalance – A common finding is muscle imbalances in the shoulder complex as well as improper neuromuscular control of the scapula.

Increased Laxity - A patient with isolated internal impingement may have an increase in global laxity or an increase in anterior laxity alone of the dominant shoulder.

Anterior Instability - Patients may have instability symptoms, such as apprehension or the sensation of subluxation with the arm in a position of abduction and external rotation.

Rotator Cuff Pathology - Patients may also present with symptoms similar to those associated with other rotator cuff pathologies (tears, other impingements). Younger patients with such symptoms, particularly throwing athletes, should raise the clinician’s index of suspicion for internal impingement. In fact, some authors have identified internal impingement as the leading cause of rotator cuff lesions in athletes.

Jobe Clinical Classification of Internal Impingement
 - Jobe developed a classification scheme to further distinguish between the varying severities of internal impingement. The Jobe classification system focuses on the primary patient population of overhead athletes.

1. Stage I: (Early) Shoulder stiffness and a prolonged warm-up period; discomfort in throwers occurs in the late-cocking and early acceleration phases of throwing; no pain is reported with activities of daily living.
2. Stage II: (Intermediate) Pain localized to the posterior shoulder in the late-cocking and early acceleration phases of throwing; pain with activities of daily living and instability are unusual.
3. Stage III: (advanced) Similar to those in stage II in patients who have not responded to nonoperative treatments.

Differential Diagnosis

In many situations the diagnosis of internal impingement is made through the physical examination along with MRI and radiographs. It is important to understand that the common findings for internal impingement have been found in asymptomatic shoulders so it is key to evaluate the patient's entire clinical scenario.  The patient's age, profession, activity level, symptom severity, degreee of disability & the effects of this condition on their athletic performance need to be part of the clinicians decision making process. When exam findings are somewhat unremarkable, and when the patient presents with signs of numerous pathologies, yet do not seem to fit any one pathology exclusively, this should raise the clinicians suspicion for a case of internal impingement. During the diagnostic process it is helpful to understand that Internal impingement has a similar presentation to numerous pathologic shoulder conditions, including but not limited to:

• Partial- or full-thickness rotator cuff tears
• Anterior or posterior capsular pathologies
• SLAP (Superior Labrum Anterior to Posterior) lesion
• Subacromial Impingement
• Glenoid chondral erosion
• Chondromalacia of the posterosuperior humeral head
• Anterior GH instability
• Biceps tendon lesion
• Scapular Dysfunction

Each of these disorders can exist alone or as concomitant pathological condition.

Examination and Clinical Findings

When evaluating a patient with suspected internal impingement syndrome, it is very important to get a thorough history, as it is an important element of the clinical diagnosis.  However, diagnosing internal impingement on the history alone is extremely difficult as symptoms tend to be variable and non-consistent.  A thorough, complete examination of the shoulder complex must be done to rule in/out any concomitant shoulder pathologies. 

THE BASIC EXAM: 

Clinical Technique	Findings
Palpation of the shoulder complex	TTP (tender to palpation) posterior shoulder/joint line
Observation of muscle symmetry between shoulders	involved shoulder usually has increased muscle bulk and lies lower than unaffected shoulder abnormal scapulothoracic rhythm/scapular movement
Gross strength testing of the shoulder, rotator cuff, and scapular retractor/stabilizer muscles	weak rotator cuff muscles weak middle/lower trap, rhomboids weak serratus anterior
Joint accessory mobility: GH/ST/AC/SC joints	Decreased dorsal glenohumeral glide posterior capsule tightness
Flexibility tests for the shoulder, thoracic, and cervical spine	Variable: General Considerations pec minor/major latissmus dorsi SCM, upper trap, levator scapulae thoracic rotation/extension
ROM: GH/scapulothoracic joints as well as the cervical and thoracic spine as it has been shown that dysfunction in any of these areas can directly impact the shoulder	decreased GH internal rotation: 10-15 degrees increased GH external rotation: 10-15 degrees

SICK Scapula: Burkhart et al. have reported that scapular protraction is also a common finding in these patients.   This is characterized by Scapular malposition, a prominent Inferior medial border, Coracoid pain, and scapular dysKinesia, all of which can be picked up in the basic examination during palpation and observation of the scapula. Tyler et al. reported that scapular retractor muscle fatigue led to an overall decrease in force production of the rotator cuff muscles as well as decreased strength of the scapular stabilizers.

TESTS FOR INTERNAL IMPINGEMENT:   

Recently, a small number of tests were created to help rule in/out the presence of internal impingement.

• "Posterior Impingement Sign": Meister et al. investigated the ability to detect articular sided rotator cuff tears and posterior labral lesions. They reported a sensitivity and specificity of 75.5% and 85% respectively, meaning a negative test is extremely accurate in ruling out posterior rotator cuff tears.  A (+) test is indicated by the presence of deep posterior shoulder pain when the arm is brought nto a position of abduction to 90° to 110°, extension to 10° to 15°, and maximal external rotation.
• Relocation Test: Jobe and colleagues have reported this can be used to identify internal impingement. A positive test would be posterior shoulder pain that was relieved by a posterior directed force on the proximal humerus.

TESTS FOR ASSOCIATED CONDITIONS:

Tests for other shoulder pathologies may be (+) or (-) due to the variable clinical presentation of internal impingement.  Understand that there is no proven combination of test findings that identify internal impingement.    

• Subacromial Impingement: Test Item Cluster
  
• Full/partial thickness rotator cuff tears: Test Item Cluster
  

SLAP Lesions: Although the validity of physical examination tests used to detect SLAP lesions is controversial, the fact that these lesions are a common finding with internal impingement warrants the need to perform at least some combination of the following tests:

• Active compression test
• Crank test
• Speeds test
• Biceps load test II      

Laxity of the anterior GH joint capsule: The following have proven diagnostic accuracy: Generally (+) but may be (-) 

• The apprehension test
• Jobe subluxation/relocation test
• Anterior release test
  

         

Medical Management (current best evidence)

Surgery for internal impingement may be indicated if improvements have not been seen with a prolonged rehab protocol specifically designed to correct any impairments, imbalances, deficiencies and/or pathologic findings. Based on recent literature, arthroscopic interventions are listed as the preferred type of surgery. Prior to any surgical procedure it is highly recommended that a thorough exam under anesthesia (EUA) is done, as well as a diagnostic arthroscopy. Due to the often-confusing physical findings that may be associated with internal impingement, the final therapeutic surgical plan should be aimed at specific pathologic lesions related to patient symptoms that have been identified from an EUA and diagnostic arthroscopy. It’s recommended that the EUA specifically assess for GH ROM, any kind of subluxation, as well as a meticulous analysis for the presence of any instability. 

Non-surgical interventions for internal impingement that are recommended in the literature are rest, ice (cryotherapy), and NSAIDS (or other oral-anti-inflammatory meds). However, physical therapy is the cornerstone of non-surgical interventions and should always be extensively tried before considering surgical interventions.

Physical Therapy Management (current best evidence)

Prevention/Early Management:

One of the early signs of internal impingement, which should be carefully monitored for, is a decrease in pitching ability and quality. In addition to the signs and symptoms previously mentioned, the pitcher or overhead athlete may report feelings of tightness, stiffness, or not loosening up . If these signs or symptoms are observed the pitcher should be removed from participation and started in a rehab program. In this early stage, treatment should include stretching to increase shoulder ROM and decrease posterior capsule tightness, strengthening to rebuild the soft tissue support, and neuromuscular re-education to prevent recurrence .

With the findings from a thorough clinical exam, the clinician should design an individualized impairment based treatment plan with an initial focus on correcting muscle imbalances, instabilities and ROM deficits before beginning more complex dynamic exercises. (see Table 1 for protocol)<span id="fck_dom_range_temp_1291015013156_182" />

• Anterior GH Instability: It’s been reported that if anterior instability is present and not improved through strengthening of the supporting shoulder musculature then operative management reconstructing the anterior capsulolabral area may be warranted. The good news is that many of the exercises used to treat instability are already being employed in many shoulder rehab protocols. One example is closed kinetic chain (CKC) exercises, which can have several therapeutic benefits including the ability to engage the rotator cuff musculature as a single stabilizing unit.  It is recommended that the clinician avoid all GH mobilizations if any amount of instability is present as mobs could potentially contribute to an increase in instability.  
• Tight Posterior GH Capsule: GIRD (Glenohumeral Internal Rotation Deficit) is highly correlated with a tight posterior capsule and is another common finding in all over-head athletes. As an injury prevention measure, research has shown that 90% of throwers could reduce GIRD to an acceptable level in 2 weeks after beginning a posterior capsule stretching program.
• Muscle Imbalance and/or improper neuromuscular control of the shoulder complex: Scapular dyskinesia caused by these imbalances of the shoulder complex are also associated with internal impingement as well as any kind of shoulder injury, especially those seen in over-head athletes. Research looking at 96 overhead athletes with isolated SICK scapula showed a 100% return to pre-injury level of throwing after engaging in a 4 month scapular stabilization program aimed at strengthening the periscapular musculature and the rotator cuff. The subscapularis, the only internal rotator of the 4 rotator cuff muscles, is often over looked but strengthening this muscle has been suggested in order to prevent over-angulation in the late cocking phase of throwing. .
  

Evidence-Based Protocol

In 2008, Cools, et al. published guidelines for rehabbing internal impingement in tennis players based on clinical literature and clinical experience.  Parts of these guidelines are backed by evidence, but many of the treatments discussed have not been validated with medical research, so until that research is conducted these guidelines may provide a foundational starting point for clinicians treating internal impingement.  Realize that this protocol is geared toward the athletic population. However, it can be applied to the non-athletic population as well by incorporating activity-specific functional activities instead of sport-specific.  A non-athlete may also not need to progress all the way to phase 3, which will depend on the activity level they wish to return to. 

Phase one:

• For treatment of GIRD, see additional considerations section after phase 3
• Restore proper muscle balance and endurance: Focus should be on correcting muscle imbalances of the rotator cuff muscles and periscapular muscles (see exercises listed in neuromuscular re-education below). Gradually start to incorporate proprioceptive training and dynamic stability exercises.
• Address instability: Closed chain exercises are suggested because axial compression exercises that put stress through the joint in a weight-bearing position result in joint approximation and improved co-contraction of the rotator cuff muscles.
• Neuromuscular Re-education: Scapular dyskinesia is largely due to decreased activation of the middle trap (MT), lower trap (LT), and serratus anterior (SA) when compared to the upper trap (UT).  4 exercises aimed specifically at the MT and LT are referenced in the table below as well as for SA activation.   

Phase two:

• Improve dynamic stability: Done with progressively more complex and activity specific exercises. With muscle imbalances already addressed, the therapist can begin to add dynamic movements into rehab using “tactile cueing” to ensure patient is engaging the scapular musculature before beginning a movement. Progress to verbal cueing.
• Strengthening exercises: Target all shoulder and scapular musculature. Start introducing eccentric and open kinetic chain exercises in order to begin preparing for specific athletic overhead movements.

Phase three:

• Functional rehabilitation plan: Designed to prepare the athlete to return to full athletic activity. Strengthening exercises are continued and plyometrics are initiated using both hands and limiting external rotation at first, progressing to one handed drills and gradually working into increasing velocity and resistance.

Additional Considerations

Rehabbing the GIRD component:Started immediately upon 1st treatment and continue throughout. Numerous RCT’s have shown that this internal rotation deficit can be decreased by performing stretches aimed at the p

File:Sleeper stretch.JPG

Sleeper stretch applying a downward force to affected arm into internal rotation

osterior capsule; namely the “sleeper stretch” and the “cross body adduction stretch.” 

• The sleeper stretch is performed with the patient lying on their injured side with the shoulder in 90° forward flexion, the scapula manually fixed into retraction, while glenohumeral internal rotation is performed passively. The patient should feel a stretch in the posterior aspect of the shoulder and not in the anterior portion, if they do, then reducing intensity and rotating the trunk slightly backwards can reduce the intensity of the stretch.

File:Cross body stretch.JPG

Cross body stretch

• The “cross-body stretch,”is another popular stretch for the posterior capsule and can be performed by moving the arm into horizontal adduction. This stretch has been shown to be superior for stretching the posterior capsule and for increasing internal ROM.
  

Joint mobilizations (mobs): GH anterior-posterior joint mobs can be used to help stretch the posterior capsule and increase internal rotation, however, if instability is noted on the initial exam, joint mobs should be avoided.  Grade IV, end range, dorsal-glide mobilizations are performed with the patient supine with shoulder placed into 90 abduction, and either in neutral or end range internal rotation of the humerus (refer to pictures).

File:Posterior glide mob.JPG

Posterior directed mob with pt's arm near end range horizontal adduction

File:AP mob.JPG

Posterior directed mob

File:Internal rotation mob.JPG

Posterior directed mob with pt's arm in full internal rotation

File:CT manip.JPG

Cervicothoracic manip

Thoracic and cervicothoracic manipulation: Spinal manipulations can be used to improve mobility in these regions and have proven therapeutic short and long term effects. Several studies have shown a significant improvement in symptoms of shoulder impingement syndrome when a thoracic manipulation was combined with exercise. The benefits of a thoracic or cervicothoracic manipulation for internal impingement have yet to be studied, but based on the similar presentation of these two syndromes and the low-risk to benefit ratio of manipulation, these procedures may add a huge benefit to treatment.

File:Kinetic chain.JPG

kinetic chain exercise

Whole body kinetic chain exercises: Incorporating this early in rehab has been recommended in order to prepare the athletes whole body for return to activity. Core stability, leg balance, and diagonal movement patterns can be used to incorporate the entire kinetic chain whilesimultaneously involving the shoulder as well. One example of this is simply adding a degree of instability to an exercise; doing external rotation exercises while sitting on an exercise ball or while performing a single leg stance by standing on the opposite leg of the arm you are working.

Table 1: Cools et al. protocol

Figure 1 - Rehab guidelines for overhead athletes with internal impingement

Key Research

Hanchard N, et al. The Cochrane Library. (2008)

• Discussed the modified relocation test from Hammer 2000 and the posterior impingement sign from Meister 2004. Explained the testing procedures.

McClure P, et al. Journal of Orthopaedic & Sports Physical Therapy. (2007)

• Compared the effectiveness of the cross body stretch vs. sleeper stretch for posterior capsule tightness. The cross body stretch was greater than the sleeper stretch in improving internal rotation but the small sample size did not allow for statistical significance.

Resources

• http://www.eorif.com/Shoulderarm/Throwing%20Athlete.html
• http://eorif.com/Shoulderarm/internal%20impingment.html
• http://www.throwinginjuries.com/Rotator%20Cuff%20Tears.htm
• Overview of the shoulder complex: Key elements
  

Clinical Bottom Line

           Internal impingement can come across as a very difficult diagnosis to evaluate and treat. However, it is important to realize that this diagnosis, just like most shoulder conditions, is really impairment-based; it just happens to have a name attached to it. That said, an impairment-based treatment approach aimed at the individual clinical findings should be the treatment of choice. The three most common impairments that have been found to contribute to internal impingement, and that need to be addressed from day 1 include:

• Anterior GH instability
• Tight posterior GH capsule
• Muscle imbalance and/or improper neuromuscular control of the shoulder complex

         

Recent Related Research (from Pubmed)

see tutorial on Adding PubMed Feed

Failed to load RSS feed from http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=1pq-4TZ0w1pAinDjEFMq04QbVh58ZTzLSDy-HTvq_RXiuBBsij|charset=UTF-8|short|max=10: Error parsing XML for RSS

References

see adding references tutorial.

ua