Letters to the Editor

MRI for Confirmation of Suspected Scaphoid Fracture

to the editor: I read with great interest the article by Phillips and colleagues in the September 1, 2004 issue of American Family Physician,¹ and would like to share our experience with a different management technique for patients with clinically suspected scaphoid fracture and negative initial radiographs. As stated in the article,¹ there is great variability in the accuracy of initial radiographs to detect scaphoid fractures immediately after injury, and 15 to 65 percent may remain radiographically occult.² The clinical examination also has a great deal of variability in detecting scaphoid fractures, usually showing acceptable sensitivity (around 90 percent), low specificity (rarely above 50 percent), and poor positive predictive value (weighted average of approximately 20 percent).³ Thus, the standard of care suggested for using only positive clinical examination and negative radiographs as a screening tool to justify wrist immobilization may result in unnecessary casting in about one half of patients.⁴ At our institution, we recommend additional imaging in this situation to avoid overtreatment, to decrease the rate of complications, and to increase the quality of life for the patient. Magnetic resonance imaging (MRI) has been advocated as the modality of choice because of its excellent sensitivity and specificity, especially when T1-weighted images are coupled with coronal short tau inversion recovery images. Ultrasonography may be an alternative because it is more readily accessible, less expensive, and less time consuming. We usually suggest limited wrist MRI protocol at presentation of patients with a clinically suspected scaphoid fracture and negative initial radiographs. Practicality naturally precludes the use of MRI as a first-line diagnostic study in some cases. If an experienced radiologist is readily available, ultrasonography may be performed after negative radiographs, and only negative studies referred to early MRI. This approach adds little in terms of financial costs compared with standard immobilization and radiographic follow-up.^3,5,6 When losses of productivity and quality of life caused by unnecessary immobilization are considered, early additional imaging is favored, especially MRI. Opinions may vary because data are subject to interpretation and the availability of imaging equipment is not uniform. The literature on this subject demonstrates the level of continuing debate about this seemingly well-understood clinical problem. Personally, I think that there is sufficient support to encourage more use of early MRI and ultrasonography in patients with clinically suspected scaphoid fracture and negative initial radiographs.

carlos frederico arend, m.d.

Radimagem Diagnostico por Imagem
Rua Cristóvão Colombo, 1691
Porto Alegre-RS Brazil

REFERENCES

in reply: Dr. Arend makes an excellent point concerning the poor sensitivity of the clinical examination and plain radiographs to diagnose scaphoid fractures. We support his opinion that an early magnetic resonance imaging (MRI) approach can be a preferred method for evaluating patients with a suspected scaphoid fracture and normal radiograph. Additionally, wearing a thumb spica cast for two weeks is problematic for many patients. A number of studies^1-3 have shown that early MRI is a cost-effective approach, and early MRI may soon become the preferred approach.

Nevertheless, it may be premature to completely abandon the traditional approach of casting patients for two weeks and then re-evaluating them. There are two reasons for this. First, in our review of the literature it was suggested, but not specifically determined, that MRI is 100 percent sensitive in detecting occult fractures. Because many of the studies failed to identify a specific “gold standard” when using an MRI to detect fractures, we ask the reasonable question: Will any fractures be missed by an MRI, and what will the clinical consequences be? With the traditional approach, there are theoretically no consequences to missing an early fracture because the patient would be treated empirically with definitive treatment for a nondisplaced fracture. Can the same be said for an early MRI approach in which a patient with a negative MRI would not be casted? We were unable to find any outcome studies that addressed this issue.

Second, the availability of immediate MRI is variable, and practical system issues need to be addressed when introducing a new “standard.” For example, at our institution it can take up to a week to get an outpatient MRI, and MRIs are not available at night or on weekends, so not all patients can be offered an early MRI approach.

We are certainly in agreement that an early MRI approach is reasonable and preferred under many clinical situations, but would not recommend completely abandoning the standard approach.

T. Grant Phillips, M.D.
Andrew Reibach, M.D.
W. Paul Slomiany, M.D.

The Washington Hospital Family Practice Residency Program
95 Leonard Ave.
Washington, PA 15301

REFERENCES

Case Report: Drug Interactions Between Statins and Azole Antifungals

to the editor: Physicians are using statins more often for the treatment of hyperlipidemia, and they should be aware of the potentially serious interaction between statins and azole antifungals. We report a case of rhabdomyolysis resulting from the addition of itraconazole (Sporanox) to a stable medication regimen that included simvastatin (Zocor).

The patient is a 67-year-old woman with dyslipidemia, diabetes mellitus, hypertension, and coronary artery disease. Her medications included simvastatin, enalapril (Vasotec), isosorbide dinitrate (Sorbitrate), atenolol (Tenormin), and insulin. Three weeks before presentation, she was prescribed itraconazole for onychomycosis. Two weeks after starting this medication, the patient presented to her primary physician with complaints of weakness in her arms and legs. Her symptoms were progressive, leading to the inability to walk without assistance. She was referred to the emergency department for further evaluation. Her examination was significant for upper and lower extremity proximal muscle weakness and the inability to rise from a sitting position. Laboratory tests revealed a total creatine kinase of 17,439 U per L and urine myoglobin of 130 mg per dL. Serum electrolytes and renal function were normal. Hepatic function revealed an aspartate transaminase of 805 U per L and alanine transaminase of 421 U per L. Hepatitis serologies were negative. Rheumatologic evaluation for myositis included antinuclear antibody screen, centromere antibody, rheumatoid factor, JO-1 autoantibody, SCL-70 autoantibody, all of which were negative.

The patient was admitted for rhabdomyolysis and was treated with intravenous hydration; urinary alkalinization was not performed. During the seven-day hospitalization, the patient regained her baseline motor strength. The creatine kinase peaked at 20,740 U per L and then normalized. The hepatic transaminases also normalized, and the patient’s renal function and urine remained normal. The patient was discharged and continues to follow with her primary physician.

The statins atorvastatin (Lipitor), cerivastatin (Baycol), lovastatin (Mevacor), and simvastatin are metabolized by the cytochrome P450 system, primarily CYP3A4.¹ Pravastatin (Pravachol) is not appreciably metabolized² and fluvastatin (Lescol) is primarily metabolized by CYP2C9.³ Rosuvastatin (Crestor) is excreted in the feces unchanged (90 percent), and the remainder undergoes metabolism by CYP2C9.⁴ The azole antifungals: fluconazole (Diflucan), itraconazole, ketoconazole (Nizoral), and miconazole (Monistat) are potent inhibitors of CYP3A4. Inhibition of CYP3A4 results in markedly increased plasma statin levels, which increase the risk for myopathy. Lovastatin and simvastatin have the greatest potential for this interaction.⁵

Because statins remain some of the most commonly prescribed pharmaceuticals,⁶ physicians are challenged to identify concomitant agents that inhibit their metabolism, namely CYP3A4 inhibitors. The reader is referred to Bottorff and Hansten¹ for a concise review and a complete list of CYP3A4 and 2C9 substrates and inhibitors. For physicians facing this issue, it may be prudent to employ a drug holiday for the duration of antifungal therapy, choose a statin that does not have this interaction, or use another class of antifungal.

brandon wills, d.o., m.s.

Toxikon Consortium

John H. Stroger Jr. Hospital of Cook County

University of Illinois Medical Center
Rush University Medical Center
Illinois Poison Center
1528 Hull Ave.
Westchester, IL 60154-3643

Trevonne thompson, m.d.

Department of Emergency Medicine
John H. Stroger Jr. Hospital of Cook County
Chicago, IL

steve aks, d.o.

Toxikon Consortium
Department of Emergency Medicine
John H. Stroger Jr. Hospital of Cook County
Chicago, IL

REFERENCES

Send letters to Jay Siwek, M.D., Editor, American Family Physician, 11400 Tomahawk Creek Pkwy., Leawood, KS 66211-2672; fax: 913-906-6080; e-mail: afplet@aafp.org.

Please include your complete address, telephone number, fax number, and e-mail address. Letters should be submitted on disk, double-spaced, fewer than 500 words, and limited to one table or figure and six references. Please submit a word count.

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