Case Presentation: A 69-year-old male with a history of hypertension, hyperlipidemia and single left functional kidney presented with a five-day history of worsening generalized weakness and multiple episodes of watery, non-bloody diarrhea. Days before admission, he was treated for a suspected sinus infection. Upon admission, he exhibited azotemia and a positive nucleic acid amplification test (NAAT) for Clostridium difficile. His creatine kinase (CK) was notably high at 11,000. He was treated with oral fidaxomicin for C. difficile and intravenous (IV) fluids. After 5 days of antibiotics and resolution of diarrhea, his generalized weakness persisted. His CK levels increased to 15,000 raising suspicion of inflammatory myositis. His myositis panel returned positive for anti-JO-1, anti-SSA-52, anti-Smith-RNP, and Scl-100, prompting treatment with IV pulse dose steroids, which initially improved his symptoms. However, upon switching to oral steroids, his weakness worsened. The patient developed acute respiratory distress with inability to clear secretions, that prompted intubation. His CXR suggested pneumonia that progressed to septic shock and ARDS. Despite all aggressive measures, he was persistently acidotic. An emergent laparotomy revealed global intestinal hypoperfusion. Given the prognosis of a nonsurvivable bowel injury, the family opted for comfort measures. Subsequently, the patient passed away shortly after the discontinuation of life support measures.
Discussion: Idiopathic inflammatory myopathies (IIM) are a heterogenous group of autoimmune disorders usually characterized by chronic inflammation of the muscle with varying clinical manifestations, treatment responses and prognoses. (2) Our case was particular because our patient presented AKI with ongoing Clostridium difficile infection and elevated CK levels. Infectious agents that have been proposed to be triggers of myositis include Coxsackie B virus, parvovirus, enterovirus, and human immunodeficiency virus (HIV). (2) Even more limited data is available about C. difficile as a possible trigger for inflammatory myositis. However, some case reports have reported induced rhabdomyolysis from this infection, with some reporting a toxin-mediated mechanism. As far as we are concerned, our case is the first report of a patient with inflammatory myositis with superimposed C. difficile infection. IIM, most of the time, have an indolent course but our case questions if the superimposed C. difficile infection was the cause of such a rapid progression.Also, IIM can involve other organs. Respiratory complications are significant sources of morbidity and mortality. In addition, the inflammatory process can obviously involve respiratory muscles, but prevalence data is scarce. (5) Diaphragmatic involvement can be subtle and, most of the time, asymptomatic. Our patient had evidence of respiratory muscle involvement, which was the most significant risk factor for developing a fatal lung infection.
Conclusions: Despite the many immunosuppressive agents used to treat IIM, a prompt diagnosis maximizes these patients’ ability to recover muscle, achieve better outcomes, and reduce mortality. Clinicians must remain vigilant regarding the significant clinical variability seen in these conditions, as well as potential triggers and factors that may lead to poor prognosis.