Increase in cell counts - leucocytosis
Description
- WCC >~11x10^9/L - a finding, not a diagnosis - always characterise by which cell line
- Reactive (secondary) vs clonal (haematological malignancy) is the central distinction
Epidemiology
- Extremely common incidental finding - most is reactive (infection, inflammation, stress, drugs)
- Clonal causes much rarer but higher stakes to identify
Aetiopathogenesis
By cell line
- Neutrophilia - infection (bacterial), inflammation, tissue necrosis (MI, burns), corticosteroids (demargination, not true increase in production), smoking, stress/exercise, CML (clonal), G-CSF
- Lymphocytosis - viral infection (EBV, CMV), pertussis, CLL (clonal, monotonous small lymphocytes), acute stress response
- Eosinophilia - allergy/atopy, parasitic infection, drug reaction (esp. DRESS), CTD (EGPA), hypereosinophilic syndrome, myeloid/lymphoid neoplasm with eosinophilia (rare)
- Monocytosis - chronic infection (TB, endocarditis), CTD, CMML (clonal)
- Basophilia - rare, suggests CML or other myeloproliferative neoplasm
Diagnosis
A. Differential + film
- Blood film - blasts, left shift with toxic granulation (reactive) vs blasts/dysplasia (clonal)
- Left shift with band forms + toxic granulation -> favours infective/reactive
B. Red flags for clonal disease
- Very high WCC (>50x10^9/L), especially with immature myeloid precursors at all stages of maturation (myelocytes, metamyelocytes) -> think CML
- Monotonous small mature lymphocytes -> CLL -> flow cytometry (CD5+CD23+ B cells)
- Splenomegaly, B symptoms, other cytopenias -> raises clonal suspicion
C. Work-up
- Clinical context first (infection screen, drug chart, smoking) - often no further testing needed if clearly reactive
- If atypical/persistent/unexplained: blood film review by haematologist, flow cytometry, BCR-ABL1 if CML suspected, bone marrow if cytopenias/blasts present
Management
Reactive
- Treat the underlying cause (infection, inflammation, stop causative drug)
- No treatment of the leucocytosis itself
Clonal - by diagnosis
- CML - BCR-ABL1 TKI (imatinib and successors)
- CLL - observation if asymptomatic/early stage; targeted therapy (BTK inhibitors, venetoclax) if symptomatic/progressive
- Hypereosinophilic syndrome / organ involvement - corticosteroids +/- targeted therapy, urgent if end-organ damage (cardiac, pulmonary)
- Extreme leucocytosis with hyperviscosity symptoms (leukostasis) - haematological emergency -> urgent cytoreduction (hydroxyurea, leukapheresis in severe AML/CML blast crisis)
Associations
- Smoking - chronic mild neutrophilia
- Corticosteroids - neutrophilia (demargination) + lymphopenia
- Splenectomy - persistent mild neutrophilia/lymphocytosis (loss of splenic clearance)
- Pregnancy - physiological mild neutrophilia
Natural history & complications
- Reactive leucocytosis resolves with the underlying trigger
- Leukostasis (symptomatic hyperviscosity from very high blast/WCC count) - medical emergency, risk of CNS/pulmonary microvascular occlusion
- Persistent unexplained leucocytosis - always warrants specialist review, do not attribute to "stress" indefinitely
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