eMedicine Specialties > Sports Medicine > Shoulder

Shoulder Dislocation

L. Edward Seade, MD, Chief of Shoulder Service, Orthopaedic Specialists of Austin
Robert Josey, MD, Consulting Staff, Department of Orthopedic Surgery, Orthopaedic Specialists of Austin

Updated: Dec 8, 2008

Introduction

Shoulder dislocations may occur from a traumatic injury or from loose capsular ligaments. Different conditions may affect the stabilizing structures of the shoulder and, thus, negatively affect patients with shoulder dislocations.¹

Background

This article focuses on glenohumeral joint dislocation. Although acromioclavicular (AC) joint separations are sometimes called shoulder dislocations by nonmedical persons, these are not true shoulder dislocations. Shoulder dislocations occur when the head of the humerus comes out of its socket, the glenoid.

For excellent patient education resources, visit eMedicine's Breaks, Fractures, and Dislocations Center and Sports Injury Center. Also, see eMedicine's patient education articles, Shoulder Dislocation and Shoulder Separation.

Frequency

United States

• The shoulder is the most commonly dislocated joint in the body.^1,2,3
• Although most shoulder dislocations occur anteriorly, they may also occur posteriorly, inferiorly, or anterior-superiorly.
• Patients with a previous shoulder dislocation are more prone to redislocation.
• Other factors that show a clear correlation to redislocation are the age of the patient and concomitant rotator cuff tears and fractures of the glenoid.
  • Younger patients (teenagers and those aged 20 years) have a much higher frequency of redislocation than patients in their 50s and 60s.⁴ Many physicians believe that age is less of a predisposing risk factor for redislocation than activity level.
  • Patients who tear their rotator cuffs or fracture the glenoid during their shoulder dislocation have a higher incidence of redislocation than patients without these problems.

Functional Anatomy

Shoulder stability is maintained by the glenohumeral ligaments, the joint capsule, the rotator cuff muscles, the negative intra-articular pressure, and the bony/cartilaginous anatomy.

The main stabilizers of the shoulder joint are the ligaments and the capsule complex. Multiple ligaments are present, but the inferior glenohumeral ligament is the most important and the one most commonly injured during an anterior shoulder dislocation. The injury may be a tear of the ligament/capsule off one of its bony attachments, and/or it may cause a stretch injury to these structures.

Tears in the rotator cuff muscles may also lead to shoulder instability. Four rotator cuff muscles are present in the shoulder. They are found superficial to the glenohumeral ligaments and the bones. Large tears may lead to shoulder instability, even with intact glenohumeral ligaments. Instability of the shoulder can also occur from injury to the nerves that control the shoulder muscles, specifically the axillary nerve.

Sport-Specific Biomechanics

The shoulder is a very mobile joint; therefore, it is often placed in awkward positions during sports. Thus, the force from a fall or a blow may be sufficient to cause shoulder damage. If the force is strong enough, the athlete tears the ligaments/tendons, fractures the glenoid or humerus, and dislocates the shoulder.

Clinical

History

Patients with a dislocated shoulder report a myriad of symptoms to their physician.

• Because most dislocations happen from trauma, patients report feeling the shoulder pop out during the incident. Different shoulder positions during the dislocation tear different ligaments. Thus, trying to determine the shoulder position at the time of the injury is important. The most common dislocation is anterior. In an anterior dislocation, the patients report having their arm abducted and externally rotated.
• Ask the patient if they had to go to the emergency department to have the shoulder reduced. If they did, they should have a radiograph of the dislocated shoulder. If they did not go to the emergency department, did the patient pop the shoulder back in or did it just go back in by itself?
• Patients with very loose joints (hyperlaxity) report feeling like their joint rolls out of the socket. These patients can usually "roll" the shoulder back in.
• Remember that patients with previous shoulder dislocations are more apt to redislocate, so ask about any previous dislocations.
• Some patients feel stingers or numbness run down their arm at the time of the dislocation.

Physical

The physical examination in a patient suspected of having a dislocated shoulder should confirm what the clinician picked up from the history of the injury.

• If the patient has a dislocated shoulder, range of motion (ROM) is poor and the patient is in a lot of pain. If the shoulder is anteriorly dislocated, the arm is in slight abduction and external rotation. In patients who are thin, the prominent humeral head can be felt anteriorly and the void can be seen posteriorly in the shoulder.
• Posterior shoulder dislocations can be easy to miss, because the patient usually keeps his or her arm in internal rotation and adduction (ie, the patient holds the arm up against his or her abdomen). In patients who are thin, the prominent head can be seen and palpated posteriorly. Poster shoulder dislocations can be missed, because the patient appears to only be guarding the extremity. If the proper radiographs are not obtained, the diagnosis will be missed (see Imaging Studies).
• Performing a detailed neurovascular examination before and after the shoulder has been reduced is imperative. Injury to the axillary nerve during shoulder dislocation has been reported to be as high as 40%. 

Causes

Approximately 95% of shoulder dislocations result from a major traumatic event, and 5% result from atraumatic causes. Distinguishing the type and severity of the event is important to determine the true etiology of the dislocation. This distinction is necessary to determine the treatment.^1,2,5,6,7

With a traumatic dislocation, the cause is obvious; however, atraumatic dislocations can result for different reasons. Ligamentous lax shoulders may dislocate with little or no trauma. Patients with lax ligaments may have 2 loose shoulders, but only 1 may be symptomatic. Congenital causes, such as excessive retroversion of the humeral head or malformation of the glenoid, can lead to instability. Neuromuscular causes, such as injury to the axillary nerve or cerebral palsy, have also been associated with shoulder instability.

Differential Diagnoses

Acromioclavicular Joint Injury
Bicipital Tendonitis
Clavicular Injuries
Rotator Cuff Injury
Shoulder Dislocation
Swimmer's Shoulder

Other Problems to Be Considered

Glenoid labrum tear

Workup

Laboratory Studies

• Laboratory studies are not necessary to diagnose shoulder dislocation injuries.

Imaging Studies

• Radiographs
  • When dealing with shoulder instability, obtaining 2 orthogonal views of the shoulder is imperative. 
  • The author suggests routinely ordering an anteroposterior (AP) view of the shoulder and an axillary lateral view. If an axillary lateral radiography cannot be obtained, then a scapular Y view may be taken in its place. If good radiographs cannot be obtained, order a computed tomography (CT) scan. This study can be performed quickly and is not expensive.
  • Posterior shoulder dislocations can look like a normal shoulder on the AP view. If an orthogonal view radiograph is not obtained, the diagnosis may be missed.
• Magnetic resonance imaging (MRI)
  • Glenohumeral ligament tears can be visualized with an MRI. They are better seen with the injection of contrast into the joint before the MRI evaluation. The bony architecture on these studies can also be appreciated.
  • Patients older than 45 years tend to tear the rotator cuff tendons when the shoulder is dislocated. The tendons are less elastic and do not stretch out during the incident and thus tear. Proper diagnosis is necessary to get these patients back to their preinjury status. If the patient is older than 45 years and has marked weakness in the strength testing of the rotator cuff muscles, an MRI is a great tool to assess for tears.

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Specialty Site Radiology

Procedures

• The most important treatment of an acute shoulder dislocation is prompt reduction of the glenohumeral joint.^1,6,8 Numerous reduction techniques have been described that can be performed after administering an intra-articular injection or after putting the patient under conscious sedation. After determining the direction of the dislocation, the physician must remember that the most important aspect of reduction is relaxation of the shoulder musculature. Once reduction has been accomplished, postreduction radiographs are necessary to verify reduction.
• Shoulder reduction techniques are as follows:
  • For the more common anterior dislocations, one of the oldest methods of reduction is the Hippocratic method, in which the physician's foot is placed in the patient's axilla while gentle longitudinal traction is applied. Internal or external rotation of the shoulder may facilitate reduction.
  • The Stimson technique involves having the patient lie prone on an examining table, allowing the affected arm to hang off the bed. Again, longitudinal traction and internal or external rotation are applied to the arm. Weights can also be added to the patient's wrist to facilitate reduction.
  • The Milch maneuver is one in which abduction and external rotation are applied to the affected extremity while the physician's thumb disengages the humeral head. This technique can also be attempted with the patient in the prone position.
  • Finally, one of the simplest maneuvers is passive forward elevation of the arm while the physician maneuvers the humeral head with the opposite hand.
• Differentiating a posterior from an anterior dislocation is important, because the reduction maneuvers differ. If reduction cannot be achieved with the patient under conscious sedation, general anesthesia may be needed for adequate relaxation. The patient should be in the supine position. The affected arm should be adducted with the application of gentle traction. The humeral head should be maneuvered anteriorly by the examiner's hand. The arm should not be rotated externally because the presence of a humeral fracture is possible.

Related eMedicine topic:
Joint Reduction, Shoulder Dislocation, Anterior

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

In the acute phase of a dislocated shoulder, therapy should be limited. The arm should be immobilized in a sling and swathed for 1-3 weeks. Active or passive shoulder abduction with shoulder internal rotation is permissible, and removing the arm from the sling to work in a neutral internal-external rotation position is desirable, because a neutral position may actually improve positioning of the torn anterior capsule to the glenoid. During this time, the patient should perform elbow, wrist, and hand ROM exercises.

A good adage during the first 3 weeks after a shoulder dislocation is to "keep the hand in view." While looking forward, the patient should never let his or her hand be placed in a position outside the line of vision. This instruction assures a midrange position that does not compromise apposition of the torn or stretched anterior capsular structures to the glenoid.

Surgical Intervention

The recurrence rate for shoulder instability is highly dependent on the age of the patient. Nonoperative care should be performed first before entertaining the thought of surgery. Most patients are able to rehabilitate their shoulder with rest and physical therapy.^1,5  

In patients who have recurrent shoulder instability, operative care should be highly considered.^2,6,7  Numerous studies have shown the increased likelihood of traumatic glenohumeral arthritis in patients with multiple shoulder dislocations. Operative care may consist of both open or arthroscopic treatment of the cause of instability.

Recovery Phase

Rehabilitation Program

Physical Therapy

After the initial period of immobilization, passive ROM exercises should begin. Older individuals should begin performing ROM of the shoulder after 1 week of immobilization, because these patients are prone to shoulder stiffness. Passive ROM exercises should include shoulder pendulum exercises and an overhead pulley system for the shoulder. Goals for passive ROM should be 30° of external rotation and 90° of flexion for the first 3 weeks, followed by 40° of external rotation and 140° of flexion for the second 3 weeks.

The rotator cuff may also have been injured during the dislocation, so the therapist should be cognizant of the status of the rotator cuff during the early phase of rehabilitation.

Surgical Intervention

Athletes who demonstrate symptomatic instability during guarded physical therapy should be considered for an MRI evaluation and probable arthroscopic or open anterior shoulder tissue repair.

Maintenance Phase

Rehabilitation Program

Physical Therapy

More vigorous therapy can be initiated after full passive ROM has been regained, usually after 6 weeks. Rotator cuff strengthening exercises can be initiated with the use of rubber tubing or weights. Because the rate of shoulder redislocation is so much higher in young adults, vigorous training and strengthening should be delayed until approximately 3 months after the injury. Swimming is an ideal exercise to regain shoulder strength and should be encouraged once strengthening exercises have begun.

Medication

Shoulder dislocations are extremely painful events. If relocation is not accomplished within an hour, anesthesia via conscious sedation is necessary in the emergency department setting. Medications for this technique are not discussed in this article.

Oral narcotic analgesics are reasonable for a period of days, but prolonged use is categorically inappropriate.

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Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma. A 3- or 4-day supply of hydrocodone or similar schedule III narcotic should be provided following shoulder relocation.

Related eMedicine topic:
Toxicity, Narcotics

Hydrocodone and acetaminophen (Lortab, Norcet, Vicodin)

Drug combination for moderate to severe pain.

Dosing

Adult

1-2 tab or cap PO q4-6h prn

Pediatric

<12 years: 10-15 mg/kg/dose acetaminophen PO q4-6h prn; not to exceed 2.6 g/d acetaminophen

>12 years: 750 mg acetaminophen PO q4h; not to exceed 10 mg hydrocodone bitartrate per dose or 5 doses/d

Interactions

Coadministration with phenothiazines may decrease the analgesic effects; the toxicity increases with CNS depressants or TCAs

Contraindications

Documented hypersensitivity; high altitude cerebral edema (HACE) or elevated intracranial pressure (ICP)

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

The tablets contain metabisulfite, which may cause hypersensitivity; caution in patients who are dependent on opiates, because this substitution may result in acute opiate-withdrawal symptoms; caution in the presence of severe renal or hepatic dysfunction

Hydrocodone and ibuprofen (Vicoprofen)

Drug combination for short-term (<10 d) relief of moderate to severe acute pain.

Dosing

Adult

1-2 tab PO q4-6h prn; not to exceed 5 tab/d

Pediatric

Not established

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; monitor PT duration closely (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; third trimester of pregnancy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with impaired renal function, peptic ulcer disease, impaired thyroid function, asthma, hypertension, edema, heart failure, increased ICP, and erosive gastritis; duration of action may increase in elderly persons

Acetaminophen and codeine (Tylenol With Codeine [# 3])

Indicated for mild to moderate pain.

Dosing

Adult

30-60 mg/dose based on codeine PO q4-6h or 1-2 tab q4h; not to exceed 4 g/d of acetaminophen

Pediatric

0.5-1 mg/kg/dose PO based on codeine q4-6h; 10-15 mg/kg/dose based on acetaminophen; not to exceed 2.6 g/d of acetaminophen

Interactions

The toxicity of codeine increases with CNS depressants, TCAs, MAOIs, neuromuscular blockers, phenothiazines, and narcotic analgesics.

Rifampin can reduce the analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase the hepatotoxicity of acetaminophen.

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients who are dependent on opiates, because this substitution may result in acute opiate-withdrawal symptoms; caution in the presence of severe renal or hepatic dysfunction.

Hepatotoxicity with acetaminophen is possible in individuals with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses and exceed recommended the maximum dose.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also exist, such as leukotriene synthesis inhibition, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions. During rehabilitation, shoulder discomfort may interfere with sleep or basic ADLs. Oral NSAIDs should decrease the discomfort. NSAIDs do not speed recovery and should not be used to accelerate physical therapy goals.

Related eMedicine topic:
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Ibuprofen (Motrin, Ibuprin)

DOC for mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

<6 months: Not established

6 months to 12 years: 4-10 mg/kg/dose PO tid/qid

>12 years: Administer as in adults.

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy

Naproxen (Naprosyn, Anaprox, Naprelan, Aleve)

For mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Dosing

Adult

500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

<2 years: Not established

>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of the drug.

Ketoprofen (Orudis, Oruvail, Actron)

For mild to moderate pain and inflammation. Small initial doses are indicated in small and elderly patients and in those with renal or liver disease.

Doses >75 mg do not increase the therapeutic effects. Administer high doses with caution and closely observe the patient for response.

Dosing

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

<3 months: Not established

3 months to 12 years: 0.1-1 mg/kg PO q6-8h

>12 years: Administer as in adults.

Interactions

Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of coagulation abnormalities or during anticoagulant therapy

Follow-up

Return to Play

Return to play in patients following a shoulder dislocation is determined when full ROM and strength have been regained. Return to play is usually sooner for older adults than for younger athletes, because the fear of redislocation is much lower in older adults. Usually, older adults can return to play within 3 months. With younger adults, conditioning can continue through shoulder rehabilitation; however, decisions about returning to play should be more conservative than those in older adults. Again, absolute criteria are full ROM and full strength.

When determining a patient's return to competitive sports, the author uses the following criteria:

• Scapular stability through full ROM
• Normal scapulohumeral rhythm
• Full active and passive ROM
• Rotator cuff strength at 80% of opposite side
• Pain-free activities of daily living (ADLs)

Complications

The most common complication of an acute shoulder dislocation is recurrence. This complication occurs because the capsule and surrounding ligaments are stretched and deformed during the dislocation. Age is the most important indicator for prognosis; dislocations recur in approximately 90% of teenagers.

Another common complication following dislocation is fracture. The most common type is a Hill-Sachs lesion or compression fracture of the posterior humeral head. Fractures of the proximal humerus, greater tuberosity, coracoid, and acromion have also been described.

Rotator cuff tears also commonly occur as a result of shoulder dislocations, and the frequency of this complication increases with age. This complication can be expected in 30-35% of patients aged 40 years or older. Slow progression in return to active function following shoulder dislocation in a middle-aged patient should warrant a workup for a rotator cuff tear.

Vascular injuries are rare, but they do occur, especially in older patients. Vascular injuries are more common with inferior dislocations and usually involve a branch of the axillary artery.

Nerve injuries are much more common than vascular injuries, especially with anterior or inferior dislocations. The axillary nerve is the nerve injured most often and may be crushed between the humeral head and the axillary border of the scapula or injured by traction from the humeral head. Axillary nerve injury has been reported in as many as 33% of acute anterior dislocations.

Prognosis

Age at dislocation is the most important prognostic indicator for recurrence of shoulder dislocations. Younger age at initial injury increases the likelihood for future dislocation. The recurrence rate is thought to be 90% if the initial episode occurs in the teen years. In patients aged 40 years or older, the recurrence rate is 10-15%. Most redislocations occur within 2 years of the primary injury. Persons with axillary nerve injuries can be expected to recover completely within 3-6 months.

Education

Educate the patient on the importance of strength training following shoulder dislocation. The patient must understand that recurrence is possible and therapy should be used to prevent recurrence.

References

1. Matsen FA III, Thomas SC, Rockwood CA Jr. Anterior glenohumeral instability. In: Rockwood CA Jr, Matsen FA III, eds. The Shoulder. Vol 1. Philadelphia, Pa: WB Saunders Co; 1990:526-622.

2. Dodson CC, Cordasco FA. Anterior glenohumeral joint dislocations. Orthop Clin North Am. Oct 2008;39(4):507-18, vii. [Medline].

3. Blasier RB, Guldberg RE, Rothman ED. Anterior shoulder stability: Contributions of rotator cuff forces and the capsular ligaments in a cadaver model. J Shoulder Elbow Surg. 1992;1:140-50.

4. Hovelius L, Augustini BG, Fredin H, et al. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am. Nov 1996;78(11):1677-84. [Medline].

5. Burkhead WZ Jr, Rockwood CA Jr. Treatment of instability of the shoulder with an exercise program. J Bone Joint Surg Am. Jul 1992;74(6):890-6. [Medline]. [Full Text].

6. Schenk TJ, Brems JJ. Multidirectional instability of the shoulder: pathophysiology, diagnosis, and management. J Am Acad Orthop Surg. Jan-Feb 1998;6(1):65-72. [Medline].

7. Cox CL, Kuhn JE. Operative versus nonoperative treatment of acute shoulder dislocation in the athlete. Curr Sports Med Rep. Sep-Oct 2008;7(5):263-8. [Medline].

8. Cofield RH, Kavanagh BF, Frassica FJ. Anterior shoulder instability. Instr Course Lect. 1985;34:210-27. [Medline].

9. Jouve F, Graveleau N, Nove-Josserand L, Walch G. [Recurrent anterior instability of the shoulder associated with full thickness rotator cuff tear: results of surgical treatment] [French]. Rev Chir Orthop Reparatrice Appar Mot. Nov 2008;94(7):659-69. [Medline].

10. Pouliart N, Gagey O. Consequences of a Perthes-Bankart lesion in twenty cadaver shoulders. J Shoulder Elbow Surg. Nov-Dec 2008;17(6):981-5. [Medline].

11. Reeves B. Acute anterior dislocation of the shoulder. Clinical and experimental studies. Ann R Coll Surg Engl. May 1969;44(5):255-73. [Medline]. [Full Text].

Keywords

shoulder dislocation, dislocated shoulder, shoulder pain, rotator cuff muscles, shoulder injury, anterior shoulder dislocation, dislocation of the glenohumeral joint, glenohumeral dislocation, glenohumeral subluxation, glenohumeral joint dislocation, posterior shoulder dislocation, acromioclavicular joint injury, humerus, glenoid, glenohumeral ligaments, glenoid labrum, negative intra-articular pressure

Contributor Information and Disclosures

Author

L. Edward Seade, MD, Chief of Shoulder Service, Orthopaedic Specialists of Austin
Disclosure: Nothing to disclose.

Coauthor(s)

Robert Josey, MD, Consulting Staff, Department of Orthopedic Surgery, Orthopaedic Specialists of Austin
Robert Josey, MD is a member of the following medical societies: American Medical Association, Phi Beta Kappa, and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Joseph P Garry, MD, Director of Sports Medicine and Sports Medicine Fellowship, Associate Professor of Family Medicine and Exercise and Sport Science, Department of Family Medicine, East Carolina University Brody School of Medicine
Joseph P Garry, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Heart Association, American Medical Society for Sports Medicine, North American Primary Care Research Group, and North Carolina Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Henry T Goitz, MD, Fellowship Director, Sports Medicine, Department of Orthopedic Surgery, Henry Ford Hospital
Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons and American Orthopaedic Society for Sports Medicine
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD, Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Sports Medicine Fellowship Director, Medical College of Wisconsin
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa, and Wilderness Medical Society
Disclosure: Nothing to disclose.

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