Special Feature
Costochondritis: Take a Scientific Stand in the Emergency Department
By Michael Felz, MD
Few complaints are as challenging and complex for the emergency department (ED) physician as the evaluation of acute chest pain. Although the dramatic symptoms, ECG findings, and laboratory data in acute myocardial infarction (MI) often are straightforward, other pain syndromes may be poorly characterized, creating much diagnostic uncertainty. Costochondritis (CC) represents a surprisingly frequent cause of chest pain in the ED—one that often is not considered until other etiologies have been excluded. This review of the current literature is intended to place the entity of CC on firm scientific footing and in proper priority for physicians treating patients with acute chest pain.
Anatomic Considerations
The costal cartilages serve as elastic struts enabling compliant chest wall excursions during respiration and trunkal movement.1 The first seven ribs articulate individually with the sternum, whereas ribs 8-10 share a conjoint anterior junction known as the costal arch.2 Ribs 11 and 12 terminate freely in the upper abdominal wall. A closely applied collagenous perichondrium provides vascularity to these hyaline articulations. Most of the chest wall innervation derives from intercostal nerves.
Clinical Presentation and Pathogenesis
The dominant feature of CC is the demonstration of localized anterior chest wall pain at chondrosternal articulations that can be duplicated by focused palpation at the same sites. No soft-tissue swelling is evident. A similar but quite rare disorder, Tietze’s syndrome (TS) is an inflammatory condition resembling CC in that localized chest pain is reproducible by the examiner, but soft tissue swelling also is present at the tender foci.3 CC usually affects multiple sites, whereas TS is unifocal.
The etiology of CC may involve minor trauma that result in small tears in costosternal ligaments, as may be caused by coughing, sneezing, or excessive trunkal movements.4 Others have documented rare occurrences of infection with Staphylococcus, Streptococcus pneumoniae, Mycobacterium tuberculosis, and Candida species.5 TS, in contrast, has been linked to Coxsackie A and B viral infections. Biopsy studies from 24 cases of TS have revealed infiltration of lymphocytes, with pathologic changes not in cartilage but in surrounding soft tissues.6
Differential Diagnosis and Management
Both CC and TS must be distinguished from other causes of acute or recurrent anterior chest wall pain, such as trauma, pyogenic infection, osteomyelitis, herpes zoster, neoplasm, rheumatoid arthritis, and fibromyalgia. Even teenagers with tenderness in the thorax will elicit concern about "heart trouble" and require careful evaluation.7 How can ED physicians accurately identify CC (or the more uncommon TS) in patients with acute chest pain? Without doubt, the first priority must be to consider MI or some other life-threatening cardiopulmonary condition. In an effort to stratify risk for coronary artery disease (CAD) syndromes, Lee and associates assessed 596 patients (average age 56 years) who presented with anterior chest pain to a Boston ED.8 Parameters were clinical exam, ECG, enzymes, and technetium cardiac scanning. Final diagnoses included 104 patients (17%) with MI, 143 (24%) with unstable angina, and 349 (59%) with other disorders (including 158 patients with reproducible chest wall tenderness). They observed three statistically significant clinical predictors of low-risk status for CAD: sharp or stabbing pain, absence of prior documented CAD, and pain reproduced by chest wall palpation or positional trunk movement.
In a study of 100 patients (mean age 51 years) with chest pain and previously normal coronary angiography, Wise and associates found 69% had tenderness of the neck, shoulder, or thorax, whereas 23% displayed tenderness of the costosternal region that reproduced pain symptomatology.9 They concluded that chest wall palpation evoking typical chest pain symptoms is a common, specific finding in patients known to be free of CAD.
A prospective analysis of 122 patients with chest pain in a New York ED revealed a diagnosis of MI in seven (6%) patients compared to 36 (30%) found to have CC, of which 17 (15%) had tenderness, which precisely duplicated original symptoms.10 Interestingly, the diagnosis of MI (28%) was far more frequent in a control population. The authors concluded that CC is a common etiology for acute chest pain in the ED and that such patients are distinguished by reproducible symptoms and a lower frequency of MI, despite similar risk factors.
Mukerji and colleagues studied 40 patients (average age 43 years) who had chest pain and normal coronary angiography, and found that 30% had fibromyalgia, 10% had CC, and 3% had rheumatoid arthritis.11 This contrasted with 40 controls with proven CAD, of which one (3%) had fibromyalgia and none had CC. They emphasize, as do others,12 that rheumatologic conditions are common in patients with angiographically normal coronary arteries. The frequency of simultaneous CC and CAD is rare (3-5%) according to two clinical series with a total of 916 patients.4,8
From the standpoint of a busy office, Klinkman and associates analyzed 399 outpatients with chest pain in a Michigan primary care research network and found relative frequencies of 20% for musculoskeletal conditions, 13% for gastroesophageal reflux disease, 13% for CC, 10% for stable angina, and only 1.5% for MI.13 These diverse studies, all emphasizing the value of chest wall palpation, were further clarified and affirmed in a recent, extensive clinical review.14 Finally, timely testing for troponin15 and D-dimer16 has been shown to be of considerable value for confirming or excluding acute CAD events in the ED and office settings.
Diagnostic confirmation of TS is possible by CT scanning of tender, swollen costochondral junctions. Findings include erosions, calcification, and subchondral sclerosis, and exclude similar disorders such as neoplasm, tuberculosis, and occult fracture.17 CC has been reported in elderly males, with confirmation by gallium uptake,18 and in postpartum females as confirmed by radionuclide bone scanning or SPECT imaging.19
Management of CC and TS usually centers on analgesics, local heat, and patient reassurance, although no placebo-controlled trials are available. One investigator has documented the utility of lidocaine and steroid injections for acute pain relief in TS, correlating with an 82% reduction in echogenicity and cartilage broadening by serial ultrasound assessment.20 Historically, pain relief by local steroid injection was felt to have diagnostic value in excluding CAD.4 Curiously, one 52-year-old patient has been described whose reproducible tenderness over the right 10th costochondral junction resolved with a shift in the beltline position of his beeper.21
Conclusions
Costochondritis is a far more common occurrence, by two- to 15-fold, than CAD events in the ED or office setting. Of all chest pain patients, 10-30% will be found to have CC or chest wall syndromes upon final diagnosis. Diagnostic certainty is enhanced by demonstration of precise replication of original symptoms by palpation. Non-evocative chest wall tenderness is a helpful but less specific finding and may be present in a minority (3-5%) of patients with underlying CAD. Normal ECG tracings and enzyme levels, especially if they span 4-6 hours, are helpful for exclusion of ischemic events in patients with presentations suggestive of CC, TS, or other atypical entities for chest pain.
My own anecdotal experience with roughly 200 patients thought to have CC is consistent with the published data regarding this common occurrence in acute chest pain patients, particularly young healthy females who fear a "heart attack." NSAIDs and heat seem to provide dependable pain relief within our academic family medicine practice. I am impressed with the frequency of reproducible chest wall tenderness among our primary care patients admitted from the office or ED for "rule out MI" protocols, in which the vast majority have CAD excluded. On about 10 occasions, I have injected tender costochondral junction regions with 2 cc of 1% lidocaine with gratifying, instant results in pain resolution and diagnostic confirmation.
Perhaps a memorable statement from 25 years ago pertains to ED management of CC today: "If local pressure applied to the anterior part of the chest wall becomes a routine procedure in the physical examination of all patients with precordial pain, a surprisingly large number of cases of costosternal syndrome will be discovered."4 Sounds to me like a good place to start, and stand, in the ED.
References
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3. Ontell FK, et al. The costal cartilages in health and disease. Radiographics 1997;17:571-577.
4. Wolf E, Stern S. Costosternal syndrome: Its frequency and importance in differential diagnosis of coronary heart disease. Arch Intern Med 1976;136:189-191.
5. Meyer CA, White CS. Cartilaginous disorders of the chest. Radiographics 1998;18:1109-1123.
6. Kayser HL. Tietze’s syndrome. Am J Med 1956;21:982-989.
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8. Lee TH, et al. Acute chest pain in the emergency room. Identification and examination of low-risk patients. Arch Intern Med 1985;145:65-69.
9. Wise CM, et al. Musculoskeletal chest wall syndromes in patients with noncardiac chest pain: A study of 100 patients. Arch Phys Med Rehabil 1992;73:147-149.
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11. Mukerji B, et al. The prevalence of rheumatologic disorders in patients with chest pain and angiographically normal coronary arteries. Angiology 1995;46: 425-430.
12. Ghaffari S. Detection and management of coronary artery disease in patients with rheumatologic disorders. Rheum Dis Clin North Am 1999;25:657-669.
13. Klinkman MS, et al. Episodes of care for chest pain: A preliminary report from MIRNET. J Fam Pract 1994;38:345-352.
14. Jouriles NJ. Atypical chest pain. Emerg Med Clin North Am 1999;17:717-731.
15. Ebell MH, et al. A systematic review of troponin T and I for diagnosing acute myocardial infarction. J Fam Pract 2000;49:550-556.
16. Bayes-Genis A, et al. D-dimer is an early diagnostic marker of coronary ischemia in patients with chest pain. Am Heart J 2000;140:379-384.
17. Jurik AG, et al. Radiographic findings in patients with clinical Tietze’s syndrome. Skeletal Radiol 1987;16: 517-523.
18. Ikehira H, et al. Acute pan-costochondritis demon-strated by gallium scintigraphy. Br J Radiol 1999; 72:210-211.
19. Wadhwa SS. Anterior chest wall pain in postpartum costochondritis. Clin Nucl Med 1999;24:404-406.
20. Kamel M. Ultrasonographic assessment of local steroid injection in Tietze’s syndrome. Br J Rheumatol 1997;36:547-550.
21. Kleinman I. Beeper costochondritis [letter]. JAMA 1992;267:56.
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