Case Presentation: A 46-year-old woman with uncontrolled type 2 diabetes mellitus and monoclonal gammopathy of undetermined significance (MGUS-monoclonal IgG Kappa paraproteinemia) diagnosed 4 years ago presented with right knee pain and swelling 3 days after a minor fall. She reported 3-4 episodes of “cellulitis” after minor trauma over the past 4 years. During her prior admission, skin biopsy showed inflammatory panniculitis and improved with a short course of colchicine and prednisone. She remained well until this fall. On presentation, she was febrile to 103.3° with a HR of 129. Exam showed erythema, warmth, and swelling over the posterolateral knee, a mild effusion, and lateral joint line tenderness. Laboratory evaluation revealed a C-reactive protein of 324 mg/L (reference ≤5.0 mg/L), erythrocyte sedimentation rate of 114 mm/hr (≤27.0 mm/hr), and white blood cell count of 24.64 K/uL (4.0-10.0 K/uL). She was empirically started on intravenous antibiotics for presumed sepsis. Synovial fluid was negative for crystals and organisms on gram stain. After 2 days of IV antibiotics without improvement, a repeat punch biopsy was done. Histopathology again showed mild superficial perivascular inflammatory infiltrate with unremarkable epidermis and dermis. Subcutaneous fat demonstrated focal fat necrosis with a lobular neutrophilic and eosinophilic infiltrate, and stains and cultures were negative for bacteria and fungi. Antibiotics were switched to oral agents and colchicine 0.6 mg bid, and fever and erythema gradually improved.She was discharged on colchicine twice daily and counseled on trauma avoidance. Over 2 months of follow-up, she had a few mild episodes of post-traumatic inflammation responsive to continued colchicine and topical triamcinolone. Based on our findings, we felt her diagnosis was trauma-induced inflammatory panniculitis with MGUS as a contributor to her exaggerated inflammatory response.
Discussion: Trauma-induced inflammatory panniculitis is a rare, self-limited disorder defined as ‘changes in the subcutaneous fat at a site of blunt injury’, often unrelated to the severity of trauma [1,2,4]. It presents clinically as indurated, erythematous, and warm subcutaneous lesions and is treated symptomatically [1,3,4]. In patients with underlying conditions such as MGUS, inflammatory responses to tissue injury may be amplified [5]. A variety of cutaneous manifestations of MGUS have been documented, including neutrophilic dermatosis like Sweet’s Syndrome [6]. The underlying pathophysiology is direct pathogenic activity of the monoclonal immunoglobulin leading to neutrophil recruitment and activation, often described as autoinflammatory with dysregulation of innate immune pathways and cytokine networks – driving neutrophil-mediated tissue injury [5,6]. Clinical history of minor trauma and histopathologic findings of lobular panniculitis with focal fat necrosis and perivascular inflammatory infiltrate were essential for establishing the diagnosis. These features narrowed the differential by distinguishing it from panniculitides driven by vasculitis or with predominantly septal involvement. Negative stains and cultures excluded infection, while the absence of granulomas or vasculitis ruled out autoimmune etiologies.
Conclusions: Recognizing trauma-induced inflammatory panniculitis is crucial, as it is often mistaken for cellulitis, leading to unnecessary antibiotic use and delayed targeted therapy
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