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From Inflammatory Arthropathy to Toxic Shock Syndrome: A Case of Colonization and Complication

Christopher Fontela

Pro | Internal Medicine

Presented at: Florida Society of Rheumatology

Date: 2024-07-11 00:00:00

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Summary: Title: Severe Invasive Streptococcal Infection Leading to Streptococcal Toxic Shock Syndrome and Necrotizing Fasciitis in a Patient with Rheumatoid Arthritis and Sjogren's Syndrome Abstract: Background: Septic arthritis and streptococcal toxic shock syndrome (STSS) are severe manifestations of invasive streptococcal infections, leading to significant morbidity and mortality if not promptly recognized and treated. Patients with underlying inflammatory arthritis, such as rheumatoid arthritis (RA), are particularly susceptible to infections due to chronic inflammation, frequent intra-articular corticosteroid injections, immunosuppressive medications, and an overall suppressed immune system. Case Report: A 57-year-old female with RA and secondary Sjogren's Syndrome (SS) was brought to the emergency department following a witnessed syncopal episode. Over the past month, she experienced fatigue, difficulty ambulating, intermittent fever and chills, and cognitive decline. Initial laboratory tests revealed neutrophilic leukocytosis, thrombocytopenia, hyperkalemia, acute kidney injury, transaminitis, and anion gap metabolic acidosis. Imaging of the brain, chest, abdomen, and pelvis did not reveal acute pathology or source of infection. Despite a clinical picture highly suspicious for sepsis, the absence of an obvious infection source prompted further investigation. Management included intravenous fluid resuscitation, empiric antibiotics, and electrolyte correction. However, 24 hours post-admission, the patient decompensated and experienced a brief cardiac arrest. Blood cultures subsequently grew Group A Streptococcus (Strep pyogenes), confirming sepsis; however, the source remained unidentified. Further inquiry revealed the patient had hip pain and sicca symptoms for approximately eight months. Laboratory tests showed positive rheumatoid factor and SSA antibody. A hip MRI performed five days prior to admission, the results of which had yet to be received, eventually revealed a massive complex left hip joint effusion, extensive synovitis suggestive of septic joint superimposed on inflammatory arthropathy, and iliopsoas bursitis with a large complex collection likely communicating with the hip joint. The family later revealed the patient was treated approximately one month prior for a large cellulitis of the left thigh with apparent resolution, identifying the initial source of infection. Conclusion: This case highlights the intricate challenges posed by septic arthritis, especially in a patient infected with Streptococcus pyogenes, leading to subsequent STSS. Initial treatment included Rocephin and Clindamycin, coupled with thorough irrigation of the affected joint. Despite these efforts, the patient developed necrotizing fasciitis affecting all extremities, necessitating the amputation of both legs and the right upper extremity. Following multiple extensive debridements, the patient stabilized sufficiently for transfer to a long-term acute care facility for rehabilitation. Given the high mortality of STSS, this underscores the critical importance of prompt and aggressive management in severe cases of septic arthritis.