eMedicine Specialties > Emergency Medicine > Rheumatology

Costochondritis

Lynn K Flowers, MD, MHA, FACEP, Assistant Professor, Department of Emergency Medicine, Emory School of Medicine; Clinical Faculty, Department of Emergency Medicine, Emory University Hospital

Updated: Aug 25, 2009

Introduction

Background

In contrast to myocardial ischemia or infarction, costochondritis is a benign cause of chest pain and is an important consideration in the differential diagnosis. Although the term costochondritis often is used interchangeably with fibrositis and Tietze syndrome, these are distinct diagnoses.

Pathophysiology

Costochondritis is an inflammatory process of the costochondral or costosternal joints that causes localized pain and tenderness. Any of the 7 costochondral junctions may be affected, and more than 1 site is affected in 90% of cases. The second to fifth costochondral junctions most commonly are involved.

Frequency

United States

The exact prevalence of a musculoskeletal etiology for chest pain is not known, although overall prevalence of a musculoskeletal etiology for chest pain was approximately 10% in one study. In a 1994 ED study, 30% of patients with chest pain had costochondritis.1

Mortality/Morbidity

The condition's course generally is self-limited, but the patient often experiences recurrent or persistent symptoms.

Sex

In Disla's costochondritis study, women comprised 69% of patients with costochondritis versus 31% in the control group.1

Clinical

History

  • The onset of costochondritis is often insidious. Chest wall pain with a history of repeated minor trauma or unaccustomed activity (eg, painting, moving furniture) is common. Pain may be described as follows:
    • Exacerbated by trunk movement, deep inspiration, and/or exertion
    • Lessens with decreased movement, quiet breathing, or change of position
    • Sharp, nagging, aching, or pressurelike
    • Usually quite localized but may extend or radiate extensively
    • May be severe
    • May wax and wane

Physical

  • Pain with palpation of affected costochondral joints is a constant finding in costochondritis.
    • The second through the fifth costochondral junctions typically are involved. More than 1 junction is involved in more than 90% of patients.
    • Surprisingly, patients may not be aware of the chest wall tenderness until examination.
  • The diagnosis should be reconsidered in the absence of local tenderness to palpation.
    • Tietze syndrome is characterized by nonsuppurative edema.2
    • Costochondritis has no palpable edema.

Causes

The etiology of costochondritis is not well defined. Repetitive minor trauma has been proposed as the most likely cause. Bacterial or fungal infections of these joints occur uncommonly, usually in patients who are intravenous drug users or who have had thoracic surgery.3 Costochondritis, among others, is a common cause of atypical chest pain (chest pain not caused by myocardial ischemia) in athletes.4

Differential Diagnoses

Abdominal Trauma, Blunt
Herpes Zoster
Acromioclavicular Injury
Myocardial Infarction
Anxiety
Neoplasms, Lung
Gout and Pseudogout
Sternoclavicular Joint Injury

Other Problems to Be Considered

Pericarditis
Pleurodynia
Polychondritis
Fibromyalgia

Workup

Laboratory Studies

  • No specific studies exist for costochondritis. The clinical scenario and the most likely differential diagnoses should guide which laboratory tests are obtained.

Imaging Studies

  • Obtain a chest radiograph in the workup of the differential diagnoses.
  • Some case reports exist where bone (gallium) scans have been used in the United States to confirm the clinical diagnosis, although these are not ED studies.

Treatment

Prehospital Care

Prehospital care should follow standard local protocols for patients with chest pain.

Emergency Department Care

Reassuring the patient of the benign nature of the condition and adequate pain control are the important objectives. Narcotic analgesics generally are not required.

Medication

The goal of therapy is to reduce inflammation. To accomplish this goal, nonsteroidal anti-inflammatory drugs (NSAIDs) are useful.

Nonsteroidal anti-inflammatory drugs

These agents are typically used for the relief of mild to moderate pain and inflammation. Although the effects of NSAIDs in the treatment of pain and inflammation tend to be patient specific, ibuprofen usually is the DOC for initial therapy. Other options include flurbiprofen, mefenamic acid, ketoprofen, and naproxen.


Ibuprofen (Ibuprin, Advil, Motrin)

Usually DOC for treatment of mild to moderate pain if no contraindications exist.
Inhibits inflammatory reactions and pain, probably by decreasing the activity of the enzyme cyclooxygenase, which results in inhibition of prostaglandin synthesis.

Dosing

Adult

400-800 mg PO q4-6h; not to exceed 3200 mg/d

Pediatric

10 mg/kg/dose PO qid

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase 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; high risk of bleeding; because of potential cross-sensitivity to other NSAIDs, do not administer to patients hypersensitive to aspirin, iodides, or other NSAIDs

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 congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy


Flurbiprofen (Ansaid)

Has analgesic, antipyretic, and anti-inflammatory effects. May inhibit cyclooxygenase enzyme, causing inhibition of prostaglandin biosynthesis that, in turn, may result in analgesic and anti-inflammatory activities.

Dosing

Adult

200-300 mg/d PO divided bid/qid

Pediatric

Not established

Interactions

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

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studies 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 drug


Ketoprofen (Oruvail, Orudis, Actron)

Used for relief of mild to moderate pain and inflammation. Initially, administer small dosages to patients with a small body size, the elderly, and those with renal or liver disease. Doses >75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patients' responses.

Dosing

Adult

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

Pediatric

<3 months: Not established
3 months to 14 years: 0.1-1 mg/kg PO q6-8h
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase 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 congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy


Naproxen (Anaprox, Naprelan, Naprosyn)

Used for relief of mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing the activity of the enzyme 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 risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase 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; 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

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 drug

Follow-up

Further Outpatient Care

  • NSAIDs for pain control
  • Local heat
  • Local infiltration of local anesthetic, steroid, or intercostal nerve block (reserved for refractory cases)
  • Biofeedback
  • Gentle stretching of the pectoralis muscles 2-3 times a day may be beneficial
  • Primary care follow-up with persistent symptoms

Deterrence/Prevention

  • Avoid repetitive misuse of muscles.
  • Modify improper posture or ergonomics of the home or work place.

Prognosis

  • The prognosis for patients with costochondritis is excellent.
  • After 1 year, about half of patients still may have discomfort; approximately one third report tenderness with palpation.

Patient Education

  • Reassure patients of the benign nature of the problem, and instruct them regarding avoidance of provoking activities.
  • Provide patients with a good understanding of the proper use and potential adverse effects of NSAIDs.
  • For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center and Muscle Disorders Center. Also, see eMedicine's patient education articles, Costochondritis and Chronic Pain.

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnose a myocardial ischemia or infarction
  • Failure to look for an intrathoracic pathology via chest radiography
  • Failure to palpate for local tenderness with assignment of the diagnosis of costochondritis
  • Failure to adequately control pain
  • Failure to realize that angina and costochondritis can coexist and treat accordingly
  • Failure to diagnose sternoarticular septic arthritis or osteomyelitis in patients who are intravenous substance users
  • Extensive and expensive negative workups
  • Consider costochondral infection in intravenous drug abusers

References

  1. Disla E, Rhim HR, Reddy A, Karten I, Taranta A. Costochondritis. A prospective analysis in an emergency department setting. Arch Intern Med. Nov 14 1994;154(21):2466-9. [Medline].

  2. Fam AG, Smythe HA. Musculoskeletal chest wall pain. CMAJ. Sep 1 1985;133(5):379-89. [Medline].

  3. Gotway MB, Marder SR, Hanks DK, Leung JW, Dawn SK, Gean AD, et al. Thoracic complications of illicit drug use: an organ system approach. Radiographics. Oct 2002;22 Spec No:S119-35. [Medline].

  4. Sik EC, Batt ME, Heslop LM. Atypical chest pain in athletes. Curr Sports Med Rep. Mar-Apr 2009;8(2):52-8. [Medline].

  5. Bayer AS, Chow AW, Louie JS, Guze LB. Sternoarticualr pyoarthrosis due to gram-negative bacilli. Report of eight cases. Arch Intern Med. Aug 1977;137(8):1036-40. [Medline].

  6. Fam AG. Approach to musculoskeletal chest wall pain. Prim Care. Dec 1988;15(4):767-82. [Medline].

  7. Ikehira H, Kinjo M, Nagase Y, Aoki T, Ito H. Acute pan-costochondritis demonstrated by gallium scintigraphy. Br J Radiol. Feb 1999;72(854):210-11. [Medline].

  8. Physician's Desk Reference. Motrin. In: Physician's Desk Reference. 50th ed. Medical Economics Co: Montvale, NJ; 1996:2526-27.

  9. Semble EL, Wise CM. Chest pain: a rheumatologist's perspective. South Med J. Jan 1988;81(1):64-8. [Medline].

  10. Trentham DE, Le CH. Relapsing polychondritis. Ann Intern Med. Jul 15 1998;129(2):114-22. [Medline].

  11. Wadhwa SS, Phan T, Terei O. Anterior chest wall pain in postpartum costochondritis. Clin Nucl Med. Jun 1999;24(6):404-6. [Medline].

  12. Wolf E, Stern S. Costosternal syndrome: its frequency and importance in differential diagnosis of coronary heart disease. Arch Intern Med. Feb 1976;136(2):189-91. [Medline].

Keywords

costochondritis, costal chondritis, costochondral joints, costosternal joints, costal cartilage, chest pain, fibrositis, Tietze syndrome

Contributor Information and Disclosures

Author

Lynn K Flowers, MD, MHA, FACEP, Assistant Professor, Department of Emergency Medicine, Emory School of Medicine; Clinical Faculty, Department of Emergency Medicine, Emory University Hospital
Lynn K Flowers, MD, MHA, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gino A Farina, MD, Program Director, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine
Gino A Farina, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, University Hospitals, Case Medical Center
Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

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