Laboratory Medicine & Hematology & Family Medicine
Complete blood count (CBC)
The complete blood count (CBC) - also known as the complete blood count (CBC) or hemogram - is the most widely prescribed blood test in clinical medicine. It provides automated quantification of the three cell lineages of peripheral blood (red blood cells or erythrocytes, white blood cells or leukocytes, and platelets or thrombocytes) and their derived parameters, and is the essential baseline assessment for the vast majority of clinical situations: annual health check-up, investigation of fatigue or weight loss, preoperative assessment, monitoring of chemotherapy, exploration of infection or inflammation, screening for hemopathy. In Quebec, FSC is performed on a venous blood sample taken in an EDTA tube (purple or lavender cap) and analyzed by a hematology analyzer such as Sysmex, Beckman Coulter DxH or Abbott CELL-DYN, which simultaneously measures all parameters by electrical impedance (Coulter method) and laser diffraction. When the automated system detects morphological anomalies or critical values (alarms), a peripheral blood smear is taken manually by a technician or hematologist to confirm and clarify the anomalies. The standard FSC includes erythrocyte parameters (hemoglobin, hematocrit, erythrocyte count, VGM, TGMH, CGMH, IDR), leukocyte parameters (total leukocyte count and differential formula: neutrophils, lymphocytes, monocytes, eosinophils, basophils) and platelet parameters (platelet count, mean platelet volume - MPV). Clinical interpretation of FSC must always be integrated into the clinical context, and can never replace clinical examination - a value slightly outside the reference range may be normal for a given individual, and a value within the limits may mask significant pathology.
Reference values and erythrocyte parameters
- Erythrocyte parameters - normal adult values : hemoglobin (Hb): female 120-160 g/L + male 130-175 g/L - the parameter most commonly used clinically to define anemia (WHO: Hb <120 gl femme + <130 hommeadulte) ; hématocrite (ht) : 0,36–0,46 0,40–0,52 — proportion volumique des érythrocytes dans le sang total numération érythrocytaire (gr) 3,8–5,2 × 10¹² 4,5–5,9 volume globulaire moyen (vgm) 80–100 fl paramètreclé de la classification anémies (microcytaire<80 normocytaire macrocytaire>100 fL); mean globular hemoglobin content (TGMH): 27-33 pg - amount of Hb per erythrocyte - low in martial deficiency + thalassemia (hypochromia); mean globular hemoglobin concentration (CGMH): 320-360 g/L - degree of erythrocyte hemoglobin saturation - low in martial deficiency (hypochromia) + very high in hereditary spherocytosis (>360 g/L); erythrocyte distribution index (RDI or RDW): 11.5-14.5 % - measure of erythrocyte size heterogeneity (anisocytosis) - high in martial deficiency + myelodysplastic syndromes + hemolytic anemia - normal in thalassemia minor (homogeneous microcytosis) - very useful to distinguish martial deficiency (high RDW) vs. thalassemia minor (normal RDW) in microcytosis ; reticulocytes (often requested separately but are part of the extended FSC): normal value 20-100 × 10⁹/L (or 0.5-2.5 %) - high reticulocytes = regenerative anemia (hemolysis + acute hemorrhage + regeneration after treated deficiency) - low or normal reticulocytes in anemia = aregenerative anemia (central = aplasia + bone marrow invasion + deficiency)
- Leukocyte parameters - normal adult values : total leukocytes: 4.0-10.0 × 10⁹/L - leukopenia <4,0 G/L + leucocytose >10.0 G/L; differential leukocyte count - normal values (adult): neutrophils (PNN): 1.8-7.5 × 10⁹/L (50-70 % of leukocytes) - severe neutropenia <0.5 G/L = major infectious risk + moderate neutropenia 0.5-1.0 G/L + mild 1.0-1.8 G/L; lymphocytes: 1.0-4.8 × 10⁹/L (20-40 %) - lymphopenia <1,0 G/L (VIH + corticothérapie + LLC avancée) + lymphocytose >4.8 G/L (viral infections + CLL + lymphoma); monocytes: 0.2-1.0 × 10⁹/L (2-8 %) - monocytosis in chronic infections + CMML (chronic myelomonocytic leukemia); eosinophils: 0.05-0.5 × 10⁹/L (1-5 %) - hypereosinophilia >0.5 G/L: parasitoses + allergies + drugs + clonal hypereosinophilia (FIP1L1-PDGFRA); basophils: 0.01-0.10 × 10⁹/L (<1 %) - basophilia in CML + polycythemia vera + mastocytosis; physiological and ethnic variants of leukocyte count: benign ethnic neutropenia (formerly benign neutropenia of Afro-descendants): neutrophils 1.0-1.8 G/L in pathology-free individuals of African or Yemenite descent - linked to a polymorphism of the DARC gene (Duffy antigen) - no increase in infectious risk - important to know to avoid unnecessary investigations
- Platelet parameters - normal adult values : platelet count: 150-400 × 10⁹/L - thrombocytopenia <150 gl (légère 100–150 + modérée 50–100 sévère <50 l) thrombocytose>450 G/L (reactive vs clonal); mean platelet volume (MPV or MPV): 7-12 fL - high MPV = young, large platelets (peripheral destruction - ITP + TTP) + low MPV = reduced production (aplasia + chemotherapy); platelet aggregates to EDTA: EDTA-dependent false thrombocytopenia (anti-platelet antibodies agglutinating in the presence of EDTA) → confirm on citrate tube → normal result on citrate confirms pseudothrombocytopenia - to be systematically evoked in the presence of any isolated asymptomatic thrombocytopenia without suggestive clinical context; preanalytical - conditions sampling on FSC quality: difficult sampling with hemolysis (falsely low Hb + falsely high CGMH) + coagulated sampling (unusable results) + time between sampling and analysis >4h at room temperature (morphological changes in leukocytes + platelet degranulation) + storage at <4 °c (agglutinines froides artificielles) + hyerleucocytose>100 G/L (interference on Hb measurement by turbidity)
Interpretation of FSC anomalies
| FSC anomaly | Main causes and diagnostic orientation | Additional tests and treatment |
|---|---|---|
| Hypochromic microcytic anemia VGM <80 fL + low TGMH |
Microcytic hypochromic anemia is the most common form of anemia in general practice - its two main causes are martial deficiency and thalassemia minor, which require precise clinical and biological distinction as their treatments are radically different; martial deficiency (iron deficiency): most frequent cause of anemia worldwide - microcytosis + hypochromia + high IDR (>14.5 %) + marked anisocytosis on smear - causes: chronic blood loss (menorrhagia + digestive occult rectorrhagia + intravascular haemolysis) + inadequate intakes (strict veganism + malnutrition) + malabsorption (celiac disease + gastrectomy + prolonged PPIs - PPIs reduce the gastric acidity required to reduce ferric iron to ferrous) - martial status : ferritin (reflection of iron stores - low <15 µg/L in true deficiency - falsely normal or high in inflammatory states) + serum iron (low) + transferrin (high) + transferrin saturation coefficient - TSC (low <15 %) + saturation coefficient = serum iron / total binding capacity × 100; thalassemia minor (thalassemic trait): marked microcytosis + NORMAL IDR (homogeneous RBC population) + Mentzer ratio = GMV / number of RBCs: 13 = probable martial deficiency - normal or elevated ferritin - Hb electrophoresis: Hb A2 >3.5 % = β-thalassemia minor (Hb A2 normal in α-thalassemia - diagnosis by PCR in genetics) - no indication for iron supplementation; anemia of chronic/inflammatory diseases: normocytic or slightly microcytic + elevated or normal ferritin + low iron + low transferrin (in contrast to martial deficiency) + elevated hepcidinemia - context: chronic inflammation + neoplasia + renal failure + autoimmune disease; lead intoxication: microcytosis + basophilic punctations on smear + elevated blood lead + occupational or environmental context | 1st-line workup for microcytic anemia: ferritin (most reliable parameter of iron stores) + serum iron + transferrin + CST + reticulocytes + peripheral blood smear; if ferritin is low (confirmed martial deficiency): search for cause: in women of childbearing age → menorrhagia (most frequent cause) → gynaecological work-up; in any adult without obvious cause → occulted rectal bleeding → digestive work-up (FIT - faecal immunological test + colonoscopy if FIT positive or digestive symptoms) → search for celiac disease (anti-transglutaminase IgA + total IgA antibodies) ; if normal or elevated ferritin + microcytosis + normal IDR → Hb electrophoresis → thalassemia; treatment of martial deficiency: ferrous iron PO (ferrous fumarate + ferrous gluconate + ferrous sulfate 150-200 mg elemental iron/d fasting or 1h before meal) - increase in reticulocytosis in 7-10d (response criterion) + Hb normalization in 4-8 weeks + treatment for 3-6 months after Hb normalization to replenish reserves (ferritin >50 µg/L); IV iron (ferric carboxymaltose - Ferinject + iron sucrose - Venofer): indicated if digestive intolerance to oral iron + malabsorption + severe symptomatic deficiency (Hb <90 g/L) + chronic renal failure on EPO + 2nd-3rd trimester pregnancy + refusal of oral iron - superior efficacy to oral iron in terms of rapid correction of ferritin; monitoring under treatment: CBC + ferritin at 4-6 weeks (expected response) + at 3 months (Hb normalization) |
| Macrocytic anemia VGM >100 fL |
Macrocytic anemia encompasses two mechanistically distinct major categories: megaloblastic macrocytosis (abnormal DNA synthesis due to vitamin B12 or folate deficiency) and non-megaloblastic macrocytosis (various causes without abnormal DNA synthesis); megaloblastic macrocytosis - vitamin B12 (cobalamin) deficiency: VGM often >110-120 fL + macro-ovalocytes + hypersegmentation of neutrophils (≥5 lobes in >5 % of PNN = highly specific criterion) + anemia + pancytopenia possible in severe forms - specific neurological manifestations absent in folate deficiency: peripheral neuropathy (lower limb paresthesias + ataxia) + subacute combined degeneration of the spinal cord (posterior cord + spinocerebellar involvement) - causes: malabsorption (autoimmune atrophic gastritis = Biermer's anemia - antiintrinsic factor + anti-parietal cell antibodies - the most frequent cause of symptomatic low B12) + gastrectomy + ileal Crohn's disease + ileal resection + strict veganism (absence of animal products) + Metformin (reduces ileal B12 absorption) + long-term PPIs; folate deficiency (folic acid = vitamin B9): morphology identical to B12 deficiency - absence of neurological impairment - causes : inadequate intake (alcoholism + anorexia + diet low in green vegetables) + malabsorption (celiac disease) + antifolate drugs (methotrexate + trimethoprim + phenytoin + sulfasalazine) + increased needs (pregnancy - folates are essential for neural tube closure - periconceptional supplementation 0.4-5 mg/d depending on risk factors) + chronic hemolysis; non-megaloblastic macrocytosis - frequent causes: alcoholism (macrocytosis without anemia or morphological abnormality of the smear - direct mechanism on the erythrocyte membrane) + hypothyroidism + chronic liver disease + drugs (hydroxyurea + zidovudine + azathioprine + leflunomide) + myelodysplastic syndromes (MDS - macrocytosis + cytopenia + dysplasia on smear - myelogram mandatory) + bone marrow regeneration (reticulocytosis - reticulocytes larger than mature RBCs) | 1st-line workup for macrocytosis: VGM + blood smear (macro-ovalocytes + PNN hypersegmentation = megaloblastic) + serum B12 assay + erythrocyte folates (erythrocyte folates better reflect folic status than serum folates, which vary with recent intake) + TSH + GGT + liver workup + complete blood count (pancytopenia?) + reticulocytes; if low B12 : search for cause → antiintrinsic factor antibodies (specificity 95 % for Biermer if positive) + anti-parietal cell antibodies (sensitivity 80 % but less specific) + gastroscopy if Biermer suspicion (fundic biopsies - atrophic gastritis + metaplasia) + colonoscopy if digestive symptoms + urinary MMA assay + homocysteinemia (elevated in both B12 and folate deficiencies) - useful in case of borderline B12 values; treatment of B12 deficiency : Oral B12 (cyanocobalamin 1,000 µg/d PO - as effective as IM in most cases if no total malabsorption because a fraction of B12 is absorbed by passive diffusion independently of the intrinsic factor) + IM B12 (cyanocobalamin 1,000 µg IM/d × 7d → weekly × 4 → monthly for life) - if Biermer or total malabsorption → IM or nasal for life; folate deficiency treatment: folic acid 1-5 mg/d PO × 3-4 months + correction of cause - NEVER supplement with folates alone without excluding B12 deficiency (risk of masking the hematological manifestations of B12 deficiency while allowing irreversible neurological damage to progress); MDS: bone marrow work-up (myelogram + bone marrow biopsy + cytogenetics + NGS) + hematology referral. |
| White blood cell abnormalities Leukocytosis + leukopenia + differential formula |
Leukocyte count abnormalities are frequent and their interpretation requires analysis of the complete differential formula and clinical context; neutrophilia (PNN >7.5 × 10⁹/L) : acute bacterial infection (most frequent - increased PNN + toxic granulations + Döhle bodies on smear in severe infections) + leukemoid reaction (PNN >30 G/L with myelemia - severe infections + G- drugs.CSF + neoplastic soliditis) + corticosteroids (PNN demargination - rapid increase in PNN without infection) + smoking (moderate chronic neutrophilia) + physical stress (surgery + infarction) + pregnancy + polycythemia vera + chronic myeloid leukemia (CML - PNN >30 G/L + myelemia + basophilia + spleno - BCR-ABL +) ; neutropenia (PNN 4.8 × 10⁹/L): acute viral infections (EBV + CMV + adenovirus - atypical lymphocytosis with large activated lymphocytes on smear) + pertussis (marked lymphocytosis in catarrhal phase - small mature lymphocytes) + CLL (persistent lymphocytosis + monoclonal + Gumprecht shadows on smear + CD19+CD5+ immunophenotyping mandatory) + leukemic non-Hodgkin's lymphoma; eosinophilia (>0.5 × 10⁹/L) : invasive tissue parasitoses (toxocariasis + filariasis + echinococcosis + hookworm - intraluminal parasites such as pinworms do not give hypereosinophilia) + allergies + asthma + drugs (DRESS) + Churg-Strauss disease (EGPA) + hypereosinophilic syndrome (FIP1L1-PDGFRA if >1.5 G/L persistent → imatinib) + T lymphoma; monocytosis (>1.0 × 10⁹/L) : chronic infections (tuberculosis + brucellosis + endocarditis + leishmaniasis) + CMML (chronic myelomonocytic leukemia - persistent monocytes >1 G/L + dysplasia + myelogram). | Diagnostic approach to leukocyte abnormalities: moderate leukocytosis (10-30 G/L) in obvious infectious or inflammatory context → no immediate further investigation + treatment of cause + FSC check at 4-6 weeks after resolution of context; persistent unexplained leukocytosis >12-15 G/L or >30 G/L → blood smear mandatory → if myelemia (promyelocytes + myelocytes + metamyelocytes) + basophilia → CML → BCR-ABL by PCR or FISH → urgent hematology; persistent lymphocytosis >5 G/L in adults >45 years → lymphocyte immunophenotyping (flow cytometry) → LLC exclusion → if LLC confirmed (CD19+CD5+CD23+ + kappa or lambda restriction) → Binet classification → hematology reference ; isolated neutropenia → complete drug review → follow-up CBC at 3-4 weeks after discontinuation of suspect drug → if persistent → ANA + B12 + folates + HIV serology + ANCA → if unexplained → myelogram + hematology consultation; fever + neutropenia (1.5 G/L → parasite workup (serologies + coproparasitology × 3) + ANA + ANCA + mast cell tryptase + BCR-ABL + FIP1L1-PDGFRA + myelogram → referral to internal medicine or hematology |
| Platelet abnormalities Thrombocytosis + thrombocytopenia |
Platelet abnormalities are frequent at FSC and require a rigorous diagnostic approach taking into account the level of thrombocytopenia and the clinical context; thrombocytopenia <150 G/L - approach by mechanism: false EDTA-dependent thrombocytopenia (pseudo-thrombocytopenia) : always exclude in 1st intention - confirm by sampling on citrate or heparin tube + call laboratory to check platelet aggregates on smear - accounts for 15-30 % of incidental thrombocytopenia discovered on routine workup; thrombocytopenia due to peripheral destruction (regenerative - high MPV - normal reticulocytes): IPT (primary immunological thrombocytopenia): isolated thrombocytopenia <100 G/L + normal smear + exclusion of secondary causes - anti-platelet antibodies (low sensitivity + specificity - not recommended routinely) - diagnosis of exclusion - treatment if platelets 0.1 % + ADAMTS13 450 G/L: reactive (most frequent): martial deficiency + infection + inflammation + post-splenectomy + solid cancer + corticosteroids - benign + treatment of cause; essential (clonal): essential thrombocythemia (ET): persistent thrombocytosis >450 G/L + JAK2 V617F mutation (in 55 % of ETs) + CALR mutation (25 %) + MPL (5 %) → myelogram + molecular biology → hematology → thrombotic + hemorrhagic risk | Clinical thresholds for thrombocytopenia and practical steps to be taken: thrombocytopenia 100-150 G/L: generally asymptomatic - FSC check-up at 4-8 weeks + verification of pseudothrombocytopenia + drug history + HIV serology + TSH + ANA if suggestive context; thrombocytopenia 50-100 G/L : mild to moderate bleeding risk - minor surgery possible if >80 G/L - avoid NSAIDs + aspirin + anticoagulants - active etiological investigation mandatory - refer to haematology if cause not obvious; thrombocytopenia <50 G/L : significant bleeding risk - contraindication to lumbar punctures + deep biopsies without prior platelet transfusion if <50 G/L - contraindication to elective surgery if <50 G/L - hospitalization if <20 G/L or active bleeding; thrombocytopenia <20 G/L without obvious cause → hospitalization + urgent investigation + hematology referral; platelet transfusion: prophylactic threshold (without bleeding): platelets <10 G/L in the context of drug-induced aplasia + <20 G/L if fever or invasive procedure planned + <50 G/L before non-neurosurgical surgery + 50 % or platelets <100 G/L → score 4Ts → discontinue heparin if TIH suspected + switch non-heparin anticoagulant |
| Polyglobulia and polycythemia High hemoglobin and hematocrit |
Elevated hemoglobin and hematocrit may reflect a true increase in erythrocyte mass (polyglobulia vera) or a decrease in plasma volume (relative polyglobulia or pseudo-polyglobulia); relative polyglobulia (pseudo-polyglobulia): Hb and Ht elevated by hemoconcentration without increase in erythrocyte mass - causes: severe dehydration + diuretics + profuse vomiting + extensive burns + Gaisbock syndrome (obese man + hypertension + smoker + stress) - treatment: correction of cause + hydration; true polyglobulia - definition: Hb >185 g/L in men + >165 g/L in women (WHO 2022) OR hematocrit >52 % in men + >48 % in women - classification: secondary polyglobulia (appropriate - chronic hypoxia → EPO increase → compensatory polyglobulia) : COPD + sleep apnea + altitude + smoking + cyanogenic heart disease + high-affinity hemoglobin - serum EPO dosage (high) + O₂ saturation (low if respiratory cause) + PSG if apneas suspected; inappropriate polyglobulia (ectopic EPO secretion): renal cell carcinoma + hemangioblastoma + hepatocarcinoma + uterine fibroids - elevated serum EPO + abdominal imaging; polycythemia vera (PV - clonal myeloproliferative disease): high Hb + Ht + leukocytosis + thrombocytosis + splenomegaly + aquagenic pruritus (pathognomonic) + low EPO + JAK2 V617F mutation (present in 95 % of PV) - major thrombotic risk (stroke + MI + portal vein thrombosis) + risk of transformation into myelofibrosis or AML - treatment: bloodletting (phlebotomy) to maintain Ht <45 % + aspirin 100 mg/d + hydroxyurea (if high risk) + ruxolitinib (anti-JAK2 - if resistance or intolerance to hydroxyurea) | Approach to polycythemia on FSC: step 1: check preanalytical conditions (prolonged tourniquet → pseudo-increased Ht) + exclude dehydration + repeat FSC on fresh sample if in doubt; step 2: if Hb >165 g/L woman or >185 g/L man persists → serum EPO assay + O₂ saturation (SpO₂ rest + effort) + search for JAK2 V617F mutation by PCR; interpretation: JAK2 V617F positive → polycythemia vera → myelogram + osteo-medullary biopsy + thrombotic workup → emergency hematology; JAK2 negative + EPO low → other myeloproliferative mutation (exon 12 JAK2 + CALR + MPL) → myelogram; high EPO + low SpO₂ → secondary respiratory polyglobulia → spirometry + PSG + chest CT + ECG; high EPO + normal SpO₂ → ectopic polyglobulia → abdomino-pelvic CT (renal carcinoma ++) + abdominal ultrasound; emergency treatment if severe symptomatic polyglobulia (Ht >55 % + signs of hyperviscosity: headache + flush + dizziness + tinnitus + erythromelalgia): phlebotomy (150-450 mL) + hydration → hematology |
ℹ️
FSC critical values - laboratory alert thresholds : Quebec laboratories (according to Accreditation Canada + LSPQ standards) automatically transmit the following critical values to the prescribing physician without delay: hemoglobin <70 gl ou>200 g/L - leukocytes <2,0 G/L ou >30 G/L - platelets <50 gl ou>1,000 G/L - presence of circulating blasts. These values require immediate clinical reassessment and medical action within a defined timeframe (critical value protocol). A critical result received by the laboratory must be communicated to the doctor or nurse in charge within 60 minutes, in accordance with Accreditation Canada standards.
FSC results requiring urgent medical action
Circulating blasts + pancytopenia (low Hb + neutropenia + thrombocytopenia) → possible acute leukemia → urgent same-day hematology referral - don't wait.
Thrombocytopenia <20 G/L + schizocytes on smear + hemolytic anemia → MAT (TTP or SHU) → immediate medical emergencies → plasma exchange in specialized hospital setting.
Severe neutropenia <0.5 G/L + fever ≥38.3 °C → febrile neutropenia → medical emergencies → blood cultures + broad-spectrum IV antibiotic therapy without delay.
Consult at Clinique Omicron
Clinique Omicron doctors prescribe and interpret complete blood counts as part of check-ups, chronic disease monitoring and symptom investigation. Abnormalities requiring specialized assessment (hematologist, gastroenterologist, gynecologist) are referred rapidly. Consultations are available at several points of service in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is provided for information purposes only and does not replace a physician's interpretation. A complete blood count abnormality must always be interpreted in the patient's overall clinical context.
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