Giant cellulitis-like Sweet syndrome mimicking cellulitis
Sweet syndrome (acute febrile neutrophilic dermatosis) is a rare inflammatory condition. It is marked by the sudden emergence of painful, edematous, and erythematous papules, plaques, or nodules on the skin. Furthermore, it is implicated in a wide range of illnesses caused by neutrophilic dermatoses. Sweet syndrome is classified into three categories based on its cause: classical (after upper respiratory tract infections), malignancy-associated, and drug-associated. However, there are less common forms, such as giant cellulitis-like Sweet syndrome. That causes the formation of huge infiltrating inflammatory plaques.
This case presents the rare gigantic cellulitis-like variation of Sweet syndrome, which is distinguished by huge, infiltrating plaques in unusual locations such as the chest, neck, and arm. This clinical variation can be confused with cellulitis. Because patients have an initial onset of massive erythematous plaques, fever, and leukocytosis with neutrophil predominance. Furthermore, this variation is commonly related to systemic inflammatory and neoplastic diseases.
Case Report
A 60-year-old Ethiopian male patient came to the accident and emergency (A&E) department with a 5-day history of fever, chills, sweating, and rigor. As well as a slight reddish skin color change around the anterolateral region of the right chest wall. He also complained of soreness in his right upper extremity and chest.
He has been weary and sleepy since his symptoms first appeared. Four days previously, he was hurt in the proximal area of his right index finger by a metallic object. While working on an automobile.
On presentation, he had a blood pressure of 90/60 mmHg, a pulse rate of 100, a respiratory rate of 26, an oxygen saturation of 75% with room air, and a temperature of 35.8°C. His random blood sugar level was found to be 45 mg/dL. Upon examination, erythematous, indurated sensitive plaques with ill-defined borders covered the right antero- and posterolateral chest wall, extending to the lateral region of the right neck and medial aspect of the right arm.
Investigations
The initial values were as follows: white blood cell count (WBC) 17.59 × 103/μL with neutrophilia and lymphopenia, platelet count 88 × 103/μL, C-reactive protein 200 mg/L, blood urea nitrogen 114.58 mg/dL, and creatinine 1.59 mg/dL. Liver function tests revealed increased levels of alanine aminotransferase, as well as total and direct bilirubin. His serum salt level was 115 mmol/L, his hemoglobin A1C was 6%, and he had no HIV antibodies.
Soft tissue ultrasonography demonstrated increased echogenicity and thickening/edema of the right lateral chest and abdominal wall subcutaneous tissue, which appeared cobblestone-like. Color Doppler sonography revealed slightly increased flow as well as inflammatory alterations in the soft tissue of the right lateral chest and abdomen wall, which were suggestive of cellulitis. The chest X-ray indicated a right-sided pleural effusion.
Management
As we suspected chest wall cellulitis, we started him on ceftriaxone 1 g intravenous twice daily and vancomycin 750 mg every 48 hours (renal adjusted dose). But there was no improvement after 48 hours. After admission, the skin lesion had spread from the chest wall to the abdomen wall and the upper portion of the thigh.
Therefore, doses of vancomycin and ceftriaxone were adjusted for maximal effect. This treatment was continued for 14 days, but there was no noticeable change. During this period of treatment, the histological investigation of the skin sample revealed a parakeratotic and moderately acanthotic epidermis atop substantial edema of the papillary dermis coupled with a pattern of nodular and widespread dermatitis. In the absence of vasculitis, the inflammatory cells consisted of many neutrophils and leukocytoclastic neutrophil debris mixed with lymphocytes, a few eosinophils, and plasma cells. The infiltrates spread down to the subcutaneous fat, suggesting Sweet syndrome.
The plaque’s unusual location, lack of early response, significant subcutaneous edema, and serous leaking all indicated an unsatisfactory response to antibiotics alone. Following the skin biopsy, the patient was diagnosed with Sweet syndrome and started on 1 mg/kg/day prednisone. One week after commencing steroids, the subcutaneous edema was completely resolved. And there was a considerable decrease in leaking. As well as improved general well-being and independence with everyday activities.
Conclusion
We should be cautious when diagnosing Sweet syndrome in patients who have erythematous plaque-like skin lesions in unusual areas of the body with uneven distribution. This case demonstrates the diagnostic hurdles and effective treatment strategy for a rare type of Sweet syndrome. A 60-year-old Ethiopian man presented with skin plaques, fever, and systemic symptoms that first resembled cellulitis. However, it did not respond to standard treatments.
A skin sample revealed the characteristic neutrophilic infiltrate, which confirmed the diagnosis. The condition improved rapidly with corticosteroid medication, highlighting the necessity of examining Sweet syndrome in patients with atypical cellulitis-like symptoms. That does not respond to usual therapies.
