ArticleCEN case reports2026
Non-catheter-adherent right atrial mural thrombus in a patient with systemic sclerosis undergoing hemodialysis: a case report.
Article in CEN case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Catheter-related right atrial thrombosis is a rare, potentially fatal complication of central venous catheterization. While most reported cases involve thrombi attached to the catheter tip or mobile intracardiac masses, systemic sclerosis (SSc) is associated with endothelial injury and impaired vascular repair, presenting a unique risk profile characterized by increased susceptibility to thrombus formation. A 56-year-old woman on maintenance hemodialysis for 20 years for IgA nephropathy has had SSc for 10 years after developing digital ulcers. One year before presentation, she developed steal syndrome, causing the closure of her arteriovenous access. Consequently, a tunneled dialysis catheter was inserted via the right internal jugular vein. Transthoracic echocardiography performed 1 year later revealed a right atrial mass, prompting referral for further evaluation. Anticoagulation with warfarin was initiated for a suspected right atrial thrombus. However, the mass enlarged progressively, raising suspicion of a neoplastic lesion. Surgical resection identified a 20 × 20 mm mass attached to the posterior-inferior right atrial wall, which was confirmed as an organized thrombus on histopathological examination. Although the catheter tip was not adherent to the thrombus, repetitive contact between the catheter tip and the right atrial wall occurred during atrial motion. Thus, thrombus formation was attributed to chronic mechanical irritation from the catheter tip, exacerbated by systemic sclerosis-related endothelial vulnerability. This case highlights that chronic mechanical irritation from a deeply positioned dialysis catheter tip can cause a non-catheter-adherent mural right atrial thrombus. SSc-associated endothelial vulnerability may have contributed to impaired recovery from chronic endothelial injury.
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