eMedicine Specialties > Sports Medicine > Shoulder

Acromioclavicular Joint Injury: Treatment & Medication

Author: L. Edward Seade, MD, Chief of Shoulder Service, Orthopaedic Specialists of Austin
Coauthor(s): Reed L Bartz, MD, Consulting Staff, Division of Sports Medicine, Nebraska Orthopaedic and Sports Medicine PC; Robert Josey, MD, Consulting Staff, Department of Orthopedic Surgery, Orthopaedic Specialists of Austin
Contributor Information and Disclosures

Updated: Oct 27, 2008

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

Acromioclavicular joint injuries are painful and the patient often lacks full range of motion after the injury. Physical therapy plays a role in the treatment of these patients. The author routinely starts therapy within the first couple of weeks in acromioclavicular joint sprains. 

For fractures of the acromioclavicular joint, wait until evidence of healing is apparent either clinically or radiographically before starting formal therapy. Therapy for degenerative joint disease of the acromioclavicular joint has not been proven to be successful.

Surgical Intervention

Acromioclavicular joint sprains do well with conservative management. Type I and II injuries never necessitate surgical care to reconstruct the injured ligaments. These injuries may need further care if the acromioclavicular joint becomes arthritic from the injury (see Image 4 or below). 

Postoperative coracoclavicular ligament reconstru...

Postoperative coracoclavicular ligament reconstruction. The clavicle is back to its normal position. The anchor in the clavicle keeps the allograft tendon from coming off of the clavicle. Also note the distal clavicle has been excised, because it had traumatic arthritis from the injury.

Postoperative coracoclavicular ligament reconstru...

Postoperative coracoclavicular ligament reconstruction. The clavicle is back to its normal position. The anchor in the clavicle keeps the allograft tendon from coming off of the clavicle. Also note the distal clavicle has been excised, because it had traumatic arthritis from the injury.



Surgical intervention may be an option in type III acromioclavicular joint sprains, but only after the patient's condition has failed a good trial of conservative treatment with physical therapy and medication. The procedure for these patients is reconstruction of the torn coracoclavicular ligaments with either local tissue or an allograft. In the past, surgeons have used screws, sutures, suture tape, synthetic grafts, and Kirschner (K)-wires to try to repair the defect. These have all fallen out of favor, and the current criterion standard is to reconstruct the torn ligaments as mentioned above.

Fractures in and around the acromioclavicular joint are mostly treated conservatively in a sling. The few times surgery needs to be considered are when there is a moderate amount of displacement of the fracture fragments. Surgery is indicated for open fractures, neurovascular injury, and for those cases in which the skin is compromised and may rupture from the pressure of the prominent bone.

Injuries that lead to arthritis of the acromioclavicular joint are also treated with conservative measures first. Anti-inflammatory medication and intra-articular steroid injections work well for degenerative changes in the acromioclavicular joint. In cases that have failed conservative therapy, excision of the distal clavicle can be performed with a minimally invasive arthroscopic procedure.

Consultations

If the athlete has sustained concomitant rib fractures with shortness of breath, good quality chest radiographs are indicated. A consult from a pulmonary physician or cardiovascular chest surgeon may be necessary.

Medication

The initial treatment of degenerative arthritis of the acromioclavicular joint may include the use of nonsteroidal anti-inflammatory drugs (NSAIDs), along with occasional corticosteroid injections.

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well; these may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.


Ibuprofen (Motrin, Ibuprin, Advil)

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

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.

Coadministration with aspirin increases the risk of inducing serious NSAID-related side 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

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

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


Ketoprofen (Oruvail, Actron, Orudis)

For relief of mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease.

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

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.

Coadministration with aspirin increases the risk of inducing serious NSAID-related side 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

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

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


Naproxen (Naprelan, Anaprox, Naprosyn)

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

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

Coadministration with aspirin increases the risk of inducing serious NSAID-related side 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

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

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.


Indomethacin (Indocin, Indochron ER)

Rapidly absorbed. Metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. Inhibits prostaglandin synthesis.

Adult

25-50 mg PO bid/tid

75 mg SR PO bid; not to exceed 200 mg/d

Pediatric

1-2 mg/kg/d divided PO bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Coadministration with aspirin increases the risk of inducing serious NSAID-related side 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

Documented hypersensitivity; GI bleeding or renal insufficiency

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, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur; discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs


Diclofenac (Voltaren, Cataflam)

Inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which in turn decreases the formation of prostaglandin precursors.

Adult

Persistent night pain or morning stiffness: Up to 100 mg hs may help to relieve pain; not to exceed total daily dose of 200 mg

Pediatric

>12 years: Administer as in adults.

<12 years: Not established

Coadministration with aspirin increases the risk of inducing serious NSAID-related side 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

Documented hypersensitivity; do not administer into the CNS; do not give to patients with peptic ulcer disease, recent GI bleeding or perforation, or renal insufficiency; do not administer to those at high risk of bleeding.

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, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs


Sulindac (Clinoril)

Decreases the activity of cyclooxygenase and in turn inhibits prostaglandin synthesis. Results in a decreased formation of inflammatory mediators.

Adult

150-200 mg PO bid or 300-400 qd; not to exceed 400 mg/d

Pediatric

Not established

Coadministration with aspirin increases the risk of inducing serious NSAID-related side 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

Documented hypersensitivity; patients in whom aspirin, iodides, or other NSAIDS induce hypersensitivity; gastrointestinal (GI) bleed; renal insufficiency

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, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases the risk of acute renal failure in preexisting renal disease or compromised renal perfusion; low white blood cell counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia occurs; caution in persons with anticoagulation defects or in those receiving anticoagulant therapy

Corticosteroids

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body's immune response to diverse stimuli.


Hydrocortisone (Solu-Cortef, Hydrocortone phosphate)

Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Adult

Small joints: 10-25 mg intralesional

Large joints: 25 mg intralesional

Pediatric

Not established

Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia

Documented hypersensitivity; viral, fungal, or tubercular skin infections

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 the presence of hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis; abrupt discontinuation of glucocorticoids may cause adrenal crisis.


Triamcinolone (Aristospan Intra-Articular, Aristocort Forte, Kenaject-40)

For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Adult

2-20 mg intra-articularly q3-4wk

Pediatric

Not established

Coadministration with barbiturates, phenytoin, and rifampin decreases the effects of triamcinolone.

Documented hypersensitivity; fungal, viral, and bacterial skin infections

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

Multiple complications (eg, severe infections, hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression) may occur; the abrupt discontinuation of glucocorticoids may cause adrenal crisis.

More on Acromioclavicular Joint Injury

Overview: Acromioclavicular Joint Injury
Differential Diagnoses & Workup: Acromioclavicular Joint Injury
Treatment & Medication: Acromioclavicular Joint Injury
Follow-up: Acromioclavicular Joint Injury
Multimedia: Acromioclavicular Joint Injury
References

References

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Further Reading

Keywords

acromioclavicular joint injury, shoulder pain, shoulder injury, shoulder dislocation, shoulder separation, acromioclavicular joint separations, dislocated shoulder, AC joint injury, AC separation, AC joint disruption, acromioclavicular disruption, shoulder joint

Contributor Information and Disclosures

Author

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

Coauthor(s)

Reed L Bartz, MD, Consulting Staff, Division of Sports Medicine, Nebraska Orthopaedic and Sports Medicine PC
Disclosure: Nothing to disclose.

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

David T Bernhardt, MD, Director of Adolescent and Sports Medicine Fellowship, Associate Professor, Department of Pediatrics, University of Wisconsin
David T Bernhardt, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Sports Medicine, and American Medical Society for Sports Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Russell D White, MD, Professor of Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City School of Medicine, Truman Medical Center Lakewood
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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