CSF Pleocytosis Etiological Analysis in a Cohort of Pediatric Patients
DOI:
https://doi.org/10.64149/J.Carcinog.24.1s.53-66Keywords:
CSF, Pleocytosis, Etiological, Analysis, Pediatric, PatientsAbstract
Background:Cerebrospinal fluid (CSF) analysis is one of the most critical diagnostic tools in pediatric medicine, particularly when investigating central nervous system (CNS) infections and inflammatory conditions. Among its parameters, pleocytosis, defined as an abnormal increase in white blood cells in the CSF, serves as an important indicator of underlying pathology. In children, the presence of CSF pleocytosis often signals potentially life-threatening conditions such as meningitis, encephalitis, or autoimmune disorders, necessitating prompt and accurate diagnosis (Dyckhoff-Shen et al., 2024).
The pediatric population presents unique diagnostic challenges due to differences in immune response, susceptibility to infections, and clinical presentation compared to adults. Infants and young children, for instance, may not exhibit classic symptoms of CNS infections, making CSF analysis a cornerstone in clinical decision-making. Identifying the causes of pleocytosis in this age group is therefore crucial for guiding treatment and predicting outcomes (Moon et al., 2023).
Etiologically, CSF pleocytosis can arise from a broad range of conditions, both infectious and non-infectious. Infectious causes include bacterial, viral, fungal, and parasitic agents, with viral infections often being the most common in pediatric cohorts. Non-infectious causes include autoimmune encephalitis, systemic inflammatory diseases, malignancies, and post-vaccination responses. Distinguishing between these etiologies is essential because treatment strategies and prognoses differ widely (Xu et al., 2019).
In bacterial meningitis, CSF pleocytosis is typically marked by a predominance of neutrophils, reflecting the acute inflammatory response. In contrast, viral infections often produce a lymphocytic predominance, although early viral infections may initially mimic bacterial profiles. Such variations highlight the importance of detailed cytological and biochemical analysis of CSF alongside microbiological testing to identify the precise etiology (Prakapenia et al., 2018).




