Introduction:
Mild and transient platelet activation is a well-documented phenomenon that occurs during hemodialysis (HD). In rare cases, this can lead to the formation of adherent white thrombi. The tunnelled cuffed catheter (TCC) is a widely used as blood access for hemodialysis. Platelet activation and subsequent white thrombus formation can result in TCC malfunctions. We present our experience in diagnosing and managing this complication. To our knowledge, this is the first study reporting this specific complication.
Methods:
we conducted a retrospective study at Tawam hospital from January 2015 to July 2024 after ethical approval. We included HD patients with recurrent malfunction of TCC that were diagnosed with platelet activation. Clinical data were analyzed, and management outcomes were reviewed using descriptive analysis.
Results:
We identified five patients with a mean age of 59.2 years (range: 12 to 75 years), predominantly female (60%). Four adult patients had long-standing diabetes mellitus leading to end-stage kidney disease (ESKD). One pediatric patient required HD due to congenital nephrotic syndrome. Other comorbidities in adult patients included ischemic heart disease (100%), atrial fibrillation (100%), and hypertension (100%). The median duration between the initiation of HD and the diagnosis of platelet thrombi was 2.5 years. All patients experienced recurrent TCC malfunctions characterized by excellent blood flow at the start of the HD session, followed by a progressive decline in blood flow after 60 to 90 minutes, often leading to early termination of the session. Alteplase lock solution was frequently used with minimal effect. Across all patients (n=5), a total of 23 catheter exchanges were performed. Four patients (80%) experienced malfunction of new HD catheters within the first 24 hours after insertion. One adult patient, who was on aspirin for secondary prevention of atherosclerotic cardiovascular disease, developed progressive thrombocytopenia after starting HD. His TCC blood flow decreased each time aspirin therapy was withheld and improved significantly with its reinitiation. The mean of platelet count of all patients (n=5) decreased from a baseline of 226.2 x 10^9/L to 174.6 x 10^9/L during episodes of catheter malfunction. The diagnosis of TCC malfunction due to platelet activation was proposed after excluding other causes and observing the above findings. Patients were started on 100 mg aspirin, with some receiving an increased dose of LMWH by 10 mg IV per session. This led to a resolving the TCC malfunction completely, confirming the diagnosis. Given that our adult patients had chronic atrial fibrillation, three were started on apixaban 2.5 mg BID in addition to 100 mg aspirin. The pediatric patient, diagnosed with an atrial thrombus attached to the catheter tip, she was started on therapeutic LMWH along with aspirin. Following this treatment, she did not require a catheter change, and two months later, she underwent a successful kidney transplantation.
Conclusions:
Recurrent TCC malfunction occurring 60 to 120 minutes into HD sessions, with no significant improvement after catheter exchange, should prompt nephrologists to consider platelet activation and white thrombi as potential causes. We propose the following diagnostic criteria for this phenomenon: exclud other causes, the blood flow at the start of the HD session is excellent, then start to decrease after an avarge of 60 to 90 minutes, decreasing platelet count, persistent TCC malfunction despite new catheter insertion, and positive response to antiplatelet therapy with or without increasing the dose of HD anticoagulant. In rare occasion white thrombi could be seen adherent to the catheter extension. Multicenter studies are needed to validate these diagnostic criteria and the treatment protocol.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.