Causes of Increased PMN in Cerebrospinal Fluid
Bacterial meningitis is the most critical cause of elevated PMN in CSF and must be ruled out immediately, as PMN counts typically exceed 250 cells/mm³ with sustained elevation beyond 24 hours, unlike viral meningitis where PMN predominance shifts to lymphocytes within 24-48 hours. 1, 2
Primary Infectious Causes
Bacterial Meningitis
- Bacterial meningitis characteristically produces sustained PMN elevation with absolute neutrophil counts often exceeding 1,000-5,000 cells/mm³ that remain elevated beyond 36 hours of symptom onset 1
- The PMN percentage typically ranges from 70-83% and persists throughout the illness course, distinguishing it from viral etiologies 1
- Common organisms include E. coli, Klebsiella pneumoniae, and Streptococcus pneumoniae 3
Viral Meningitis (Early Phase)
- Aseptic meningitis can paradoxically show PMN predominance in 57% of cases, contrary to traditional teaching 2
- The PMN predominance in viral meningitis occurs predominantly in the first 24 hours but can persist beyond 24 hours in 51% of cases 2
- The absolute neutrophil count in aseptic meningitis typically ranges from 79-182 cells/mm³, significantly lower than bacterial causes 1
- Varicella zoster virus (VZV) can produce recurrent PMN pleocytosis even without rash, often accompanied by increased red blood cells 4
Tuberculous Meningitis
- TB meningitis typically presents with lymphocytic predominance, but early infection can show PMN elevation 3
- CSF adenosine deaminase (ADA) levels >27 U/L suggest tuberculous peritonitis with high sensitivity 5
Non-Infectious Causes
Traumatic Tap/Blood Contamination
- Even minimal blood contamination can introduce PMNs into CSF, with the degree of PMN elevation strongly correlated with CSF red blood cell count 6
- Specimens with ≥100 RBCs/mm³ had PMNs present in 47% of cases, with 6 or more PMNs commonly seen 6
- Correction formula: subtract 1 white blood cell for every 700 RBCs in CSF to account for blood contamination 3
Chemical/Inflammatory Meningitis
- Post-neurosurgical or post-traumatic patients may develop PMN elevation without infection 7
- Hemorrhagic conditions can cause reactive PMN pleocytosis 3
Malignancy
- Peritoneal carcinomatosis can elevate PMN counts, though typically with SAAG ≤1.1 g/dL 5
- Leptomeningeal carcinomatosis may produce mixed cellular responses
Critical Diagnostic Algorithm
Immediate Assessment
- Obtain CSF cell count with differential, glucose, protein, Gram stain, and culture before any antibiotics 3
- Measure simultaneous plasma glucose to calculate CSF:plasma glucose ratio 3
- Document time from symptom onset to lumbar puncture, as this affects interpretation 1, 2
Interpretation Framework
- PMN >250 cells/mm³ with clinical signs of infection = presumed bacterial meningitis requiring immediate empiric antibiotics 3
- PMN predominance with normal glucose and protein in first 24 hours = consider viral meningitis, but bacterial infection cannot be excluded 2
- PMN elevation with elevated RBCs = consider traumatic tap, VZV infection, or hemorrhagic conditions 4, 6
- PMN <250 cells/mm³ with lymphocyte predominance >50% = consider TB, fungal, or late viral meningitis 5
Key Pitfalls to Avoid
- Do not rely solely on PMN predominance to exclude bacterial meningitis, as 57% of viral meningitis cases show PMN predominance 2
- Do not delay antibiotics waiting for culture results if PMN count is elevated with clinical suspicion of bacterial infection 3
- Do not dismiss PMN elevation as "just blood contamination" without correcting for RBC count and assessing clinical context 6
- Do not assume PMN predominance will shift to lymphocytes within 24 hours in viral meningitis, as this occurs in only 49% of cases 2
Additional Testing When Diagnosis Unclear
- CSF lactate >2 mmol/L strongly suggests bacterial over viral meningitis 3
- CSF ADA levels if TB suspected, particularly with lymphocytic predominance developing after initial PMN elevation 5
- VZV and CMV testing if recurrent PMN pleocytosis with increased RBCs 4
- Flow cytometry for PMN phenotype and ROS production may help distinguish infected from non-infected CSF in post-neurosurgical patients 7