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Isolated corticosteroid myopathy of the gluteal muscles.

Abstract: Corticosteroid myopathy is a severe side effect of corticosteroid application. Although the risk usually increases with drug dosage, even a single dose can lead to substantial muscular damage. Usually the tissue recovers over time after discontinuation of the responsible drug. We report local corticosteroid myopathy in a patient who had been given corticosteroid injections because of chronic hip pain. In this case, the patient's myopathy in the left hip region had not improved after 6 months.

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Corticosteroid myopathy is one of the most important drug-induced myopathies (Bannwarth, 2002). Chronic administration of corticosteroids can result in progressive muscle atrophy, predominantly affecting the proximal limbs (Mitsui et al., 2002). However, even a single low-dose epidural steroid injection can induce severe steroid myopathy (Boonen, Van Distel, Westhovens, & Dequeker, 1995; Mitsui et al.). A total cumulative oral maintenance dosage of more than 400 mg is sufficient to cause steroid myopathy (Bielefeld, 1996). According to Owczarek, Jasinska, and Orszulak-Michalak (2005) corticosteroid myopathy is caused more often by the use of potent fluorinated steroids, such as dexamethasone, than by the use of nonfluorinated steroids, such as hydrocortisone. Usually, drug-induced myopathies reverse themselves after discontinuation of the responsible drugs (Coquet, Bannwarth, & Henin, 2001).

This article describes a patient who developed severe palsy of the hip abductor following repeated corticosteroid injections into the left gluteal muscles for treatment of chronic hip pain. Local corticosteroid myopathy was suggested as the etiology.

Case Report

The department of neurology admitted a 55-year-old woman to evaluate her progressive difficulty in walking. She reported that she had been living with pain in her left hip region for more than 2 years. During this period, she had received corticosteroid injections into the left buttock almost monthly. The exact drug and the dosage were unknown. This treatment had slightly relieved the pain, but the patient had noted progressive difficulty with abduction and internal rotation of her left hip.

The patient did not report any relevant diseases or injuries, except for obesity. The neurologic examination demonstrated severe paresis of left hip abduction (3/5) and internal rotation. A positive left-sided Trendelenburg's sign was noted as a consequence.

Laboratory examination demonstrated normal muscle-enzyme levels. Electromyography (EMG) of the left gluteus medius and minimus muscles showed no spontaneous activity. The motor unit potentials had normal amplitudes, but they were shorter and steeper than normal. That finding is consistent with myopathty. Nerve conduction studies revealed no abnormalities.

Magnetic resonance imaging (MRI) of the left hip region demonstrated a fatty degeneration of the left gluteus muscles. The gluteus maximus muscle was smaller than on the right side; the left gluteus minimus muscle was almost completely atrophied. The left gluteus medius muscle showed atrophic and hypertrophic parts. There were no other pathological MRI findings (Fig. 1).

[FIGURE 1 OMITTED]

The application of corticosteroids was stopped due to the radiologic findings. To manage the persistent hip pain, physical therapy was initiated.

At follow-up 6 months later, the patient had experienced no progression. Clinical and radiologic findings were identical to the earlier findings. Future improvement of muscular strength cannot be completely ruled out. However, considering the time elapsed and failure of physical therapy to improve symptoms, the prognosis is poor.

Discussion

The main functions of the gluteus medius, gluteus minimus, and tensor fascia lata muscles are the abduction and the internal rotation of the leg (Donofrio, Bird, Assimos, & Mathes, 1998; Willick, Margherita, & Carter, 1998). These muscles are innervated by the superior gluteal nerve (SGN), which contains only motor and no sensory fibers and derives from nerve roots L4, L5, and S1.

There are a number of causes for a lesion of the SGN or its supplied muscles in the hip region. Among the most important are direct nerve injuries due to needle injections into the gluteal region, hip surgery, and myopathy (Eksioglu, Uslu, Gudemez, Atik, & Tekdemir, 2003; Willick et al., 1998). Eksioglu et al. underlined the necessity to define a safe access area to avoid SGN damage during hip surgery. Other, less common etiologies for an isolated SGN lesion are nerve ischemia in diabetes and hypotension (Willick et al.). A rare cause is entrapment syndrome of the SGN as a result of compression by tendinous fibers of the piriformis muscle (Kountouris & Okur, 1982; Plihal, Saudan, Vischer, & Roth, 1989; Rask, 1980). The SGN can also be compressed by an abdominal mass such as an aneurysm of the iliac artery (Grisold, Karnel, Kumpan, Hitzenberger, & Zifko, 1999). In most reported cases of isolated SGN lesions, the nerve recovered within 3-4 months, although some patients have shown incomplete recovery even longer than I year after the damage (Donofrio et al., 1998; Eksioglu, Uslu, Gudemez, Atik, Tekdemir, 2003).

Corticosteroids can cause two different types of myopathy. The rare acute form results in a general atrophy with rhabdomyolysis; the chronic form shows a symmetric myopathy accompanied by diffuse myalgia (Rosener, Martin, Zipp, Dichgans, & Martin, 1996). In this case, multiple local corticosteroid injections appeared to have caused the corticosteroid myopathy.

After drug injection, the solution might have spread into the selected muscle and the space between the different muscle parts (e.g., medial and minimal gluteal muscle), leading to chronic local tissue damage. This hypothesis is supported by the fact that at a follow-up 3 months after discontinuation of the corticosteroid injections, the patient's symptoms had not worsened. In addition, the MRI results showed a fatty degeneration in the left hip region, indicating long-lasting chronic damage only present in the medial and minimal gluteal muscle. Therefore, a systemic muscle disease was quite unlikely. Considering that the EMG findings did not show any sign of denervation, a primary neurogenic process also was unlikely. Therefore, an isolated lesion of the SGN due to drug injection was the probable cause of the isolated myopathy.

The risk of permanent damage from corticosteroid injections can be reduced in a number of ways. The use of intramuscular injections should be reduced to an absolute minimum because of risks, such as myopathy, infection, and necrosis. Safe areas for intramuscular injection must be defined in clinical practice to keep complications to the lowest possible level (Small, 2004). Patients should be made aware of the possible side effects of corticosteroids and of alternative treatment options. The occurrence of any side effect should be reported immediately to the medical staff.

Summary

Local corticosteroid myopathy of the medial and minimal gluteal muscle can occur following repeated buttock injections. Indications for intragluteal injection, selection of the applied drug, the place of injection, and hygiene factors should be carefully considered to minimize all risks. In particular, the necessity for repeated corticosteroid injections should be carefully evaluated.

References

Bannwarth, B. (2002). Drug-induced myopathies. Expert Opinion on Drug Safety, 1(1), 65-70.

Bielefeld, P. (1996). [Present status of cortisone myopathy]. La Revue de Medicine Interne, 17(3), 255-261.

Boonen, S., Van Distel, G., Westhovens, R., & Dequeker, J. (1995). Steroid myopathy induced by epidural triamcinolone injection. British Journal of Rheumatology, 34, 385-386.

Coquet, M., Bannwarth, B., & Henin, D. (2001). [Drug-induced and toxic myopathies]. La Revue du Praticien, 51(3), 278-283.

Donofrio, P. D., Bird, S. J., Assimos, D. G., & Mathes, D. D. (1998). Iatrogenic superior gluteal mononeuropathy. Muscle & Nerve, 21, 1794-1796.

Eksioglu, F., Uslu, M., Gudemez, E., Atik, O. S., & Tekdemir, I. (2003). Reliability of the safe area for the superior gluteal nerve. Clinical Orthopaedics and Related Research, 412, 111-116.

Grisold, W., Karnel, F., Kumpan, W., Hitzenberger, P., & Zifko, U. (1999). Iliac artery aneurysm causing isolated superior gluteal nerve lesion. Muscle and Nerve, 22, 1717-1720.

Kountouris, D., & Okur, H. (1982). [Isolated superior gluteal nerve injury caused by an injection]. Zeitschrift fuer Allgemeinmedizin, Stuttgart, 58, 1155-1156.

Mitsui, T., Azuma, H., Nagasawa, M., Iuchi, T., Akaike, M., Odomi, M., et al. (2002). Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle. Journal of Neurology, 249, 1004-1009.

Owczarek, J., Jasinska, M., & Orszulak-Michalak, D. (2005). Drug-induced myopathies: An overview of the possible mechanisms. Pharmacological Reports, 57(1), 23-34.

Plihal, E., Saudan, Y., Vischer, T. L., & Roth, G. (1989). [Superior gluteal nerve entrapment neuropathy]. Schweizerische Rundschau fuer Medizin Praxis, 78, 326-329.

Rask, M. R. (1980). Superior gluteal nerve entrapment syndrome. Muscle & Nerve, 3, 304-307.

Rosener, M., Martin, E., Zipp, F., Dichgans, J., & Martin, R. (1996). [Neurologic side effects of pharmacologic corticoid therapy]. Nervenarzt, 67, 983-986.

Small, S. P. (2004). Preventing sciatic nerve injury from intramuscular injections: Literature review. Journal of Advanced Nursing, 47(3), 287-296.

Willick, S. E., Margherita, A. J., & Carter, G. T. (1998). Isolated superior gluteal nerve injury: Two case reports. Muscle & Nerve, 21, 951-953.

Questions or comments about this article may be directed to Astrid S. Peters, MD, astrid.peters@neuro.imed.uni-erlangen.de. She is a medical resident in the Department of Neurology, University of Erlangen-Nuremberg Hospital, Erlangen, Germany.

Brigitte Stemper, MD, is a medical resident in the Department of Neurology, University of Erlangen-Nuremberg Hospital, Erlangen, Germany. Stefan Leis, MD, is a medical resident in the Department of Neurology, University of Erlangen-Nuremberg Hospital, Erlangen, Germany.

Rolf Janka, MD, is a medical resident in the Department of Neurology, University of Erlangen-Nuremberg Hospital, Erlangen, Germany.

Josef G. Heckmann, MD, is a professor in the Department of Neurology, University of Erlangen-Nuremberg.
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Author:Peters, Astrid S.; Stemper, Brigitte; Leis, Stefan; Janka, Rolf; Heckmann, Josef G.
Publication:Journal of Neuroscience Nursing
Geographic Code:1USA
Date:Oct 1, 2006
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