Urosepsis-triggered acute polymyositis with Inflammatory Subcutaneous Edema-a rare combo
Arti Yadav, Jasmeet Kaur, Amrinder Singh, Navneet Gupta
Polymyositis usually has a gradual progression, no cutaneous involvement, and sometimes a viral infection as the trigger. Here, we present a case of severe Polymyositis presenting acutely with inflammatory subcutaneous edema triggered by bacterial sepsis. Polymyositis is a chronic autoimmune inflammatory myopathy typically characterized by symmetrical proximal muscle weakness that progresses over time. A 28-year-old woman came in with a history of low-grade fever and proximal weakness in all four limbs for one month. In emergency investigations, neutrophilic leucocytosis, deranged renal function tests, elevated serum creatine phosphokinase levels (7387 U/L), elevated serum lactate dehydrogenase levels (3378 U/L), and a full field of pus cells with positive nitrite test on urinalysis were revealed. Ultrasound of the soft-tissue neck and arms showed inflammation in the subcutaneous plane/ inflammatory subcutaneous edema. Empirical antibiotics (IV ceftriaxone) gradually lead to the resolution of fever, leucocytosis, sepsis, and serum creatinine. Further testing revealed a negative Antinuclear Antibody, Rheumatoid factor, Antineutrophil Cytoplasmic Antibodies, and Extractable Nuclear Antigen Antibodies (ENA) Panel. Muscle atrophy, muscle fiber necrosis, and endomysial lymphocytic infiltration were seen in the muscle biopsy, indicating Polymyositis. The patient began to recover symptomatically, with oropharyngeal dysphagia, muscular weakness, and subcutaneous edema resolving quickly within a week after starting steroids. A gradual fall in serum creatine phosphokinase levels was also noted. During the outpatient follow-up, prednisolone was decreased to a low dose, and oral Azathioprine was begun as a steroid-sparing medication. Prednisolone was discontinued at subsequent outpatient visits, and the patient continued to be asymptomatic on oral Azathioprine.