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Eosinophil activation in the cerebrospinal fluid of children with shunt obstruction
Sabrina M Heidemann1, Michael Fiore, Sandeep Sood
1Department of Pediatrics, School of Medicine, Wayne State University, Detroit, Mich., USA. sheidema@med.wayne.edu
Insights
In shunt obstruction, activated eosinophils release cationic proteins like ECP and EDN. Elevated ECP in cerebrospinal fluid is linked to shorter ventriculoperitoneal shunt survival.
Area of Science:
- Neuroscience
- Immunology
- Pediatric Surgery
Background:
- Ventriculoperitoneal shunts are crucial for treating hydrocephalus in children.
- Shunt malfunction and failure are significant complications, necessitating further surgical interventions.
- The role of inflammatory markers, such as eosinophils and their products, in shunt failure is not fully understood.
Purpose of the Study:
- To investigate eosinophil activation and release of cationic proteins (ECP and EDN) in cerebrospinal fluid (CSF) during shunt obstruction.
- To determine if these proteins are associated with ventriculoperitoneal shunt failure.
Main Methods:
- Prospective observational study in a pediatric intensive care unit.
- Analysis of CSF for cell counts, ECP, and EDN concentrations in children (0-18 years) with suspected shunt malfunction.
- 6-month follow-up to assess shunt failure.
Main Results:
- Eosinophilia (≥ 5% eosinophils in CSF) was observed in 17% of patients.
- Patients with CSF eosinophilia showed significantly higher concentrations of ECP and EDN.
- Elevated CSF ECP levels correlated with an increased need for shunt revisions within 6 months.
Conclusions:
- Eosinophils are activated in the CSF of pediatric patients with malfunctioning ventriculoperitoneal shunts.
- The release of ECP and EDN by eosinophils occurs during shunt obstruction.
- Elevated ECP is a potential biomarker associated with reduced ventriculoperitoneal shunt longevity.
Objective:
To determine if eosinophils are activated to release the cationic proteins, eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) in shunt obstruction, and to find out if these proteins are associated with ventriculoperitoneal shunt failure.
Patients And Methods:
This was a prospective observational study carried out in a 20-bed tertiary pediatric intensive care unit. Patients studied were children aged 0-18 years with suspected ventriculoperitoneal shunt malfunction requiring shunt revision. No interventions were performed. Cerebrospinal fluid (CSF) was analyzed for cell count and EDN and ECP concentrations. Patients were prospectively followed for 6 months to evaluate shunt failure.
Results:
In a 2-month period, 56 shunt revisions were performed on 56 children. Three children had culture-proven infection. Eosinophilia, defined as ≥ 5% eosinophils in the CSF, was present in 9 out of 53 children (17%). The 3 patients with infection did not have eosinophilia and were excluded from further analysis. Patients with CSF eosinophilia had higher concentrations of ECP (1.38 ± 0.66 vs. 0.41 ± 0.15 ng/ml; p = 0.013) and EDN (16.94 ± 5.83 vs. 4.69 ± 1.33 ng/ml; p = 0.011). Patients with CSF eosinophilia did not have more ventriculoperitoneal shunt revisions within 6 months (6 of 9) compared to those who did not have eosinophilia (21 of 44; p = 0.50). However, patients with higher levels of ECP in the CSF required more shunt revisions within 6 months of their surgeries (p < 0.05).
Conclusions:
In patients with malfunctioning ventriculoperitoneal shunts, CSF eosinophils are activated and release ECP and EDN. The presence of ECP is associated with a shorter shunt life.
