SKIN AND SOFT TISSUE INFECTION DUE TO UNCONTROLLED PREDNISOLONE USE. CLINICAL CASE

ABSTRACT

A common treatment for a number of illnesses is the use of glucocorticoids to lower stress and immunological activation. However, like any strong drug, they are not without side effects. Since glucocorticosteroids reduce local immunity and prevent infection, it is thought that uncontrolled use of these medications can result in the development of secondary skin infections. The article describes the consequences of uncontrolled intake of prednisolone as a factor in the development of necrotizing infection of the skin and soft tissues.

Keywords: glucocorticoids, necrotizing skin and soft tissue infections, rheumatoid arthritis.

Introduction. Endocrine, neuropsychiatric, gastrointestinal, musculoskeletal, cardiovascular, dermatological, or immunological side effects are all associated with glucocorticoids. Up to 90% of individuals who use glucocorticoids for longer than 60 days may experience a variety of negative side effects. Depending on the route of administration, adverse effects may occur at a variety of doses. Even patients on low doses (≤7.5 mg/d) may have some of these side effects. [1, 2]

Clinical case. Patient K., 44 years old, on 12/20/2024, contacted the City Clinical Hospital No. 4, Perm, in serious condition with complaints of constant, aching pain in the left gluteal region, left thigh, in the hypogastric region, and an increase in temperature to 38.0 °C. According to the patient, she was diagnosed with rheumatoid arthritis in 2016. Oral prednisolone therapy was prescribed. The patient was not observed on an outpatient basis and took prednisolone at a dose of about 20 mg once a day until hospitalization. She adjusted the dosage independently depending on her well-being. The patient did not provide any certificates or papers, as well as data in the electronic medical documentation regarding rheumatoid arthritis, prescription for basic therapy was not found. On 12/16/2024, a bluish-colored formation similar to a hematoma with vesicles containing serous-hemorrhagic contents appeared in the left gluteal region. The patient denies any injury. The process progressively spread to the left thigh, groin area, and left iliac region.

On admission, extensive skin necrosis measuring 24x30 cm was observed locally on the left gluteal region, occupying the entire gluteal region, developing skin necrosis along the posterolateral surface of the left thigh, and developing necrosis in the left inguinal region. There were also multiple bullae with serous-hemorrhagic discharge on the left thigh. No fluctuations were observed by palpation. After examination, the patient was hospitalized in the intensive care unit for further examination and treatment. CT scan of the abdominal cavity and pelvic organs on 12/19/24 revealed thickening and infiltration of the subcutaneous fat of the gluteal region (more on the left) due to diffuse linear fluid impregnation. Conclusion: CT signs of panniculitis of the left gluteal region. Necrectomy of the skin and soft tissues of the left gluteal region, left thigh, gluteal region, and left groin was performed. A bacteriological examination of the discharge and a histological examination of the resected material were also performed: at the level of the epithelial layer, there is a necrosis zone with weakly expressed neutrophilic infiltration, edema at the level of the dermis, and uneven blood filling of the vessels. Conclusion: skin necrosis at the level of the epidermis and dermis.

After necrectomy, intensive therapy, daily bandaging was performed in conditions of the intensive care unit. Specialist consultations were held with treatment adjustments. Staged necrectomy (4), tracheostomy were performed. Despite the treatment, the condition gradually worsened, systemic multiple organ failure with a predominance of cardiovascular, respiratory, and renal failure developed. On 01/05/25, against the background of progression of MODS, circulatory arrest occurred, full resuscitation measures were ineffective. Biological death was confirmed.

Discussion. Treatment with corticosteroids is a crucial part of many illness treatments. Endocrine, neuropsychiatric, gastrointestinal, musculoskeletal, cardiovascular, dermatological, or immunological side effects are all associated with glucocorticoids. Before starting corticosteroid therapy, doctors should educate patients about the frequency of different side effects and be knowledgeable about both short- and long-term adverse effects. They should also keep a close eye on patients in case any new side effects appear. The proper use of corticosteroids, the introduction of corticosteroid-sparing therapy, and the slow tapering of corticosteroids to the lowest effective dose can all enhance the risk-benefit ratio of corticosteroid therapy. Additional immunomodulatory therapy should be taken into consideration when systemic corticosteroid medication is expected to be administered for a long period of time.

Long-term treatment with systemic corticosteroids suppresses cellular immunity and predisposes patients to intracellular infections. It also alters monocyte function, which resolves rapidly when the drugs are stopped. The effect of corticosteroids on the immune system is dose-dependent, and with short-term treatment the risk of infection remains unchanged. High-dose corticosteroid treatment makes patients vulnerable to viral, bacterial, fungal, and parasitic infections, and increases the risk of reactivation of latent infections such as tuberculosis. Classic manifestations of infection may also be masked by corticosteroid use, making their diagnosis difficult. [2, 3]

Corticosteroids act on keratinocytes and prevent the secretion of collagen and hyaluronic acid by fibroblasts in the dermis. This inhibits cell proliferation, and with prolonged use of glucocorticoids, thinning of the skin occurs, skin fragility increases, telangiectasias and spontaneous skin hematomas appear. This is called dermatoporosis, comparable to osteoporosis in the elderly. In the final stage, the loss of the skin barrier function is life-threatening and requires hospitalization with skin grafting. Systemic glucocorticoid use for more than one year, even at low doses (equivalent to less than 5 mg/day prednisone), causes skin atrophy, ecchymoses, and erosions in approximately 5% of patients. The catabolic effects of corticosteroids cause atrophy, striae, and delayed wound healing, while decreased vascular integrity results in purpura and easy bruising. [3]

Conclusion. In summary, knowledge of the short- and long-term side effects of glucocorticoids is important when managing a patient taking glucocorticoids for a long time. In our case report, a patient with probable rheumatoid arthritis and no other underlying medical conditions had been taking glucocorticoids for over 9 years and adjusting the dosage without medical supervision. This most likely resulted in side effects (immunosuppression, dermatoporosis), extensive hematoma formation, and subsequent infection, sepsis, and death. To prevent such cases, patients should be informed about what to expect from glucocorticoid therapy, encouraged to have regular visits, and reported any side effects to the physician. If the strategies outlined above are followed, problems from long-term glucocorticoid therapy can be minimized.

 

References:

1. McDonough AK, Curtis JR, Saag KG. The epidemiology of glucocorticoid-associated adverse events. Curr Opin Rheumatol. 2008 Mar;20(2):131-7.
2. Curtis JR, Westfall AO, Allison J, et al. Population-based assessment of adverse events associated with long-term glucocorticoid use. Arthritis Rheum. 2006;55:420–426.
3. Kaya G. New therapeutic targets in dermatoporosis. J Nutr Health Aging. 2012 Apr;16(4):285-8.