Hematology & Family Medicine & Internal Medicine
Hemoglobin (Hb)
Hemoglobin (Hb) is the tetrameric protein found in red blood cells (erythrocytes), whose main function is to transport oxygen from the lungs to the tissues, and return carbon dioxide to the lungs. It represents around 33 % of the red blood cell's weight, and is made up of four polypeptide subunits (globins), each bearing a heme prosthetic group containing a ferrous iron atom (Fe²⁺) capable of reversibly binding to an oxygen molecule. Hemoglobin concentration in blood is expressed in grams per liter (g/L) or per deciliter (g/dL) - 1 g/dL = 10 g/L. Normal adult values are 130 to 175 g/L for men and 120 to 160 g/L for women, according to Canadian laboratories. Hemoglobin is the reference parameter for diagnosing and classifying the severity of anemia (Hb below normal values, depending on age and sex) and polycythemia (Hb above normal values). It differs from hematocrit in that it measures the hemoglobin concentration itself - and not the volume occupied by red blood cells - making it a more stable parameter, less influenced by variations in mean corpuscular volume (MCV). Hemoglobin electrophoresis can be used to identify pathological structural variants (HbS in sickle cell disease, HbC, HbE) and abnormalities in globin chain synthesis (thalassemias), with major implications for preventive medicine and medical genetics.
Hemoglobin structure, function and variants
- Molecular structure and types of hemoglobin : structure of normal adult Hb (HbA): tetramer of two alpha (α) and two beta (β) chains → formula α₂β₂ → molecular weight: 64,500 Da → each chain carries a heme group (protoporphyrin IX + Fe²⁺) → binding capacity: 1 molecule of O₂ per iron atom → 4 molecules of O₂ per Hb molecule → allosteric cooperativity: binding of one O₂ molecule increases the affinity of the other three sites (sigmoid dissociation curve for oxyhemoglobin) → regulators of affinity for O₂: 2,3-diphosphoglycerate (2,3-DPG): binds to deoxyhemoglobin → decreases affinity for O₂ → promotes release of O₂ to tissues + pH (Bohr effect): low pH + high CO₂ (active tissues) → decreases affinity → release of O₂ + high temperature → decreases affinity → release of O₂; normal age-dependent hemoglobin types: fetal hemoglobin (HbF = α₂γ₂): predominant in utero and in the first weeks of life → high affinity for O₂ (captures O₂ at placenta from maternal circulation) → gradually replaced by HbA after birth: HbF 70-90 % at birth → 1 % in adulthood) under certain conditions: hemoglobinopathies + leukemias + aplasia + normal adult hemoglobin: HbA (α₂β₂): 96-98 % + HbA₂ (α₂δ₂): 2-3.5 % → increased level in beta-thalassemia minor (trait): HbA₂ >3.5 % = diagnostic criterion + HbF: <1 %; pathological forms of hemoglobin: HbS (sickle cell disease): glutamate → valine substitution in position 6 of β chain (β6Glu→Val) + GAG→GTG mutation → deoxygenated HbS polymerizes → RBC sickling + HbC: β6Glu→Lys substitution → crystallizes → moderate hemolysis + HbE: β26Glu→Lys substitution + splicing mutations → microcytosis + frequent in Southeast Asia + other variants: HbD-Punjab + HbO-Arab + Hb Constant Spring (α-chain extension); hemoglobin measurement on modern automatons: cyanmhemoglobin method (ICSH - reference method): RBC lysis + oxidation of Fe²⁺ to Fe³⁺ (methemoglobin) + transformation to cyanmethemoglobin + spectrophotometric reading at 540 nm → but most modern automata (Sysmex XN + Beckman-Coulter DxH) use the cyanide-free method (SLS - sodium lauryl sulfate) → coefficient of variation <1 % → interference: severe lipemia + massive hyperleukocytosis + carboxyhemoglobin → false high Hb if uncorrected
- Normal values, physiological variations and definition of anemia : hemoglobin reference values (Canadian laboratories - venous plasma - calibrated automatons): adult male (18-70 years): 130-175 g/L + adult female (18-70 years): 120-160 g/L + pregnancy: Hb <110 g/L = anemia (WHO) in 1st and 3rd trimester + Hb 70 years): slight physiological decline expected but any Hb <120 g/L (H) or <110 g/L (F) merits investigation + altitude: +10 g/L for 1,000 m altitude above 1,500 m (hypoxia-stimulated EPO) + smoking: slightly higher Hb (carboxyhemoglobin → shift in dissociation curve → relative hypoxia → EPO stimulation) → correct Hb for smoking in population; WHO definition of anemia (2001): adult male: Hb <130 g/L + adult non-pregnant female: Hb <120 g/L + pregnant female 1st + 3rd trimester: Hb <110 g/L + pregnant female 2nd trimester: Hb <105 g/L + child 6 months-5 years: Hb <110 g/L + child 5-11 years: Hb <115 g/L + child 12-14 years: Hb <120 g/L; classification of anemia severity: mild: Hb 100-130 g/L (H) or 100-120 g/L (F) → mild symptoms on exertion + moderate: Hb 70-100 g/L → fatigue + dyspnea on exertion + palpitations + severe: Hb <70 g/L → rest dyspnea + rest tachycardia + high output heart failure + angina + very severe (critical): Hb <50 g/L → life-threatening → indication for near-absolute transfusion
- Hemoglobin electrophoresis and neonatal screening : hemoglobin electrophoresis: method: separation of Hb variants according to their electrical charge in agarose or cellulose acetate gel (alkaline pH 8.6 and/or acid pH 6.2) → HPLC (High Performance Liquid Chromatography): current reference method → separation + quantification of Hb fractions (HbA + HbA₂ + HbF + variants) on cation exchange column → automatic detection → highly sensitive and reproducible → interpretation of fractions: HbA₂ >3.5 %: beta-thalassemic trait (βTA or βTB) → HbA₂ 4-7 % in beta-thalassemia minor → if >7 %: associated hemoglobin D + HbF >5 % in adults: thalassemic syndrome + hereditary persistence of HbF (PHHF) + sickle cell anemia treated with hydroxyurea + hemopathies → presence of an HbS fraction: sickle cell anemia (SS if HbA absent + SA if HbA present = sickle cell trait) + presence of HbC: HbCC (moderate chronic hemolytic anemia) or HbSC (major sickle cell syndrome with moderate phenotype); neonatal screening in Quebec: provincial neonatal screening program (Quebec) → screening for sickle cell disease + major sickle cell syndromes by HPLC on dried blood (blotting paper - «Guthrie test») at D2-J5 of life → indication: high-risk population (sub-Saharan Africa + Caribbean + Mediterranean + India + Southeast Asia) → Programme Québécois de Dépistage Néonatal (PQDN - MSSS) → if screening positive → confirmation by HPLC on venous sample + genotyping → genetic consultation + pediatric hematological follow-up → genetic counseling: if both parents are carriers (trait) → risk 1/4 homozygous form (disease) + 1/2 trait + 1/4 non-carrier child
Anemia, hemoglobinopathies and special clinical situations
| Clinical situation | Assessment and diagnosis | Treatment and follow-up |
|---|---|---|
| Diagnostic approach to low Hb - etiological algorithm VGM - reticulocytes - ferritin - B12 - hemolysis |
Low hemoglobin requires a structured diagnostic approach based on erythrocyte indices, reticulocytosis and biochemical tests; first step - VGM as a morphological orientation tool: microcytic anemia (VGM <80 fL) : martial deficiency (most frequent cause - low ferritin + CST 100 fL) : vitamin B12 deficiency (autoimmune gastric atrophy - Biermer's disease - anti-FI positive + gastrostomy + strict veganism) + folate deficiency (pregnancy + alcoholism + drugs: MTX + carbamazepine + trimethoprim) + alcoholism (direct macrocytosis independent of deficiencies) + hypothyroidism + MDS (myelodysplastic syndrome - macrocytosis + dysplasia on CBC + pancytopenia) + drugs (hydroxyurea + zidovudine + capecitabine); second stage - reticulocytes : regenerative anemia (high reticulocytes - RPN >2) → marrow actively producing → look for hemolysis or bleeding + aregenerative anemia (low reticulocytes - RPN <2) → insufficient production → nutritional deficiency + marrow insufficiency + chronic disease | Biological work-up oriented according to the type of anemia: systematic 1st-line work-up: complete CBC with blood smear (RBC morphology: microcytes + hypochromia + elliptocytes + spherocytes + schizocytes + sickle cells + targets + Howell-Jolly bodies + nucleated RBCs) + reticulocytes + ferritin + CRP (ferritin = acute-phase reactant → interpret with CRP) + vitamin B12 + serum folate + TSH + creatinine + GFR; if regenerative anemia (elevated reticulocytes) → hemolysis workup: LDH (elevated if intravascular or intracorpuscular hemolysis) + haptoglobin (collapsed if intravascular hemolysis - haptoglobin binds to free Hb → complex catabolized by liver) + total bilirubin + indirect (elevated if hemolysis → hemolytic jaundice) + direct antiglobulin test (DAT or direct Coombs): positive if autoantibodies (IgG) or complement (C3d) on RBCs → autoimmune hemolytic anemia (AHAI) → GS Rh + phenotyping + hematology opinion + smear : spherocytes (AHAI + hereditary spherocytosis) + schizocytes (MAT - thrombotic microangiopathy - PTT + SHU + CIVD) + sickle cells + Heinz bodies (after special staining - G6PD deficiency + methemoglobinemia); if aregenerative anemia + macrocytosis: B12 (<148 pmol/L → deficiency) + methylmalonic acid (AMM) + homocysteine : functional markers of B12 deficiency (more sensitive than serum B12 levels) + antiintrinsic factor (Biermer's disease - specificity 95-99 % but sensitivity 50-70 %) + anti-gastric parietal cells (APC - sensitivity 85 % but not very specific) + gastroscopy + gastric biopsy if Biermer's suspected → atrophic fundic gastritis |
| Sickle cell disease - HbSS and major sickle cell syndromes Vaso-occlusive crisis - hydroxyurea - transfusion - transplantation |
Sickle cell disease is the most common monogenic disease in the world - its management has been transformed by hydroxyurea, erythrocyte exchange and new targeted therapies; pathophysiology: deoxygenated HbS polymerizes into rigid fibers → sickling of RBCs → 3 major consequences: chronic hemolysis (lifespan of sickled RBCs : 10-20 days vs 120 days for normal RBCs → severe chronic hemolytic anemia - baseline Hb 60-90 g/L) + vaso-occlusion (sickle + rigid RBCs block capillaries → tissue ischemia → intense pain + organ necrosis) + endothelial dysfunction (intravascular hemolysis → free Hb → NO scavenging → vasoconstriction + hypercoagulability); major sickle cell syndromes: HbSS (homozygous sickle cell disease): most severe → 70-80 % sickle cell RBCs + HbSC (HbS + HbC in trans): moderate phenotype → proliferative retinopathy + thromboembolic complications + Hb often 90-110 g/L + HbSβ⁰-thalassemia: HbS + no β chain → picture close to SS + HbSβ⁺-thalassemia: HbS + little β chain → moderate phenotype; major clinical manifestations: painful vaso-occlusive crisis (CVO): intense osteoarticular pain (back + hips + limbs) → management: level 3 immediately if VAS >7 (morphine IV or SC) + NSAIDs + ketorolac + NaCl 0.9 % (hyperhydration) + local heat → hospitalization if VAS >7 or duration >4h + acute chest syndrome (ACS): pulmonary infiltrate + chest pain + fever + hypoxemia → main cause of sickle cell mortality → treatment: urgent transfusion (single or exchange) + antibiotic (ceftriaxone + azithromycin) + bronchodilators + O₂ + ischemic stroke (20 % of HbSS before age 20 without prevention) + splenic sequestration (especially child <5 years) + priapism + sickle cell nephropathy | Treatment of sickle cell disease - therapeutic options: hydroxyurea (HU): mechanism: increase in HbF (inhibits polymerization of HbS) + reduction in reticulocytes and leukocytes + improvement in RBC hydration → dose: 15-35 mg/kg/d PO + titration to maximum tolerated dose (nadir Platelets >80,000 + PNN >2,000) → proven efficacy: 1995 MSH trial (Charache - NEJM): reduction of CVO by 44 % + of STA by 50 % + of transfusions by 50 % + recommended from 9 months (child) by NHLBI 2014 guidelines + adverse effects: myelosuppression (CBC monitoring every 4-8 weeks) + macrocytosis (benign - compliance marker) + theoretical mutagen but no clinically documented leukemic surrisk + reimbursed RAMQ on drug list + voxelotor (Oxbryta): HbS polymerization inhibitor (increases HbS affinity for O₂) → HOPE 2019 trial (Vichinsky - NEJM): Hb improvement +1.5 g/dL + hemolysis reduction + FDA approval 2019 → under INESSS evaluation in Quebec + crizanlizumab (Adakveo): anti-P-selectin (inhibits sickle cell RBC adhesion to endothelium) → SUSTAIN 2017 trial (Ataga - NEJM): CVO reduction of 45 % vs placebo → FDA approval 2019 + Health Canada 2021 + L-glutamine (Endari): reduces oxidative stress in sickle cell RBCs → FDA approval 2017 + hematopoietic stem cell transplantation (allograft): only curative treatment available → indication: HbSS + recurrent APS + stroke + frequent CVO ± comorbidities + HLA-compatible donor (ideally sibling) → cure rate: 85-95 % if genotypic donor → gene therapy (LentiGlobin bb1111 - Bluebird Bio + CRISPR-Cas9 - Vertex/CRISPR Therapeutics): BCL11A gene editing or direct correction of HbS mutation → FDA approval December 2023 (exagamglogene autotemcel - Casgevy - world's first approved CRISPR therapy) → availability in Canada: under evaluation Health Canada / INESSS 2024-2025 |
| Thalassemias - alpha and beta Thalassemia trait - thalassemia major - iron - Desferal |
Thalassemias are quantitative abnormalities of globin chain synthesis - reduction or absence of production of one or more chains → imbalance → precipitation of excess chains → intramedullary destruction + peripheral hemolysis; beta-thalassemia: mutations in the HBB gene (chromosome 11) → reduction (β⁺) or absence (β⁰) of β-chain synthesis + clinical classification: beta-thalassemia trait (βThal minor or «thalassemia minor»): heterozygous β⁰ or β⁺ → slightly low Hb (100-120 g/L in F) + very low VGM (3.5 % on HPLC → no treatment → important for genetic counseling + thalassemia intermediate (βThal intermediate): genotype β⁺/β⁺ or β⁰/β⁺ + moderate mutations → Hb 70-100 g/L → intermittent transfusion + iron overload possible + thalassemia major (Cooley - βThal major - β⁰/β⁰): Hb <70 g/L requiring regular transfusions + extramedullary erythropoiesis + hepatosplenomegaly + bone deformities (thalassemic facies) → management in specialized center; alpha-thalassemia: deletions of the HBA1/HBA2 gene (chromosome 16) - 4 alleles: 1 deletion (αα/α-): silent carrier → asymptomatic → normal Hb + VGM → 2 deletions (α-/α- or αα/--): alpha-thalassemic trait → low VGM + normal or slightly low Hb + normal HbA₂ (different from beta!) → diagnosis by PCR/genotyping → 3 deletions (--/α-): HbH (β₄) - HbH disease → moderate chronic haemolytic anaemia + haemoglobin H precipitates + Heinz bodies → Hb 80-110 g/L → 4 deletions (--/--): Hb Bart (γ₄) - hydrops fetalis → incompatible with ectopic life → immediate fetal death in utero or neonatal. | Treatment of severe thalassemias: regular transfusions (thalassemia major): goal: maintain pre-transfusion Hb >95-100 g/L → suppression of inefficient erythropoiesis (main source of iron overload) → pheno-compatible RBCs (Rh + Kell at least) → leukodepleted → interval: every 2-4 weeks according to regimen + iron chelation: necessary in all polytransfused patients (iron overload → cardiac + hepatic + endocrine hemosiderosis): deferasirox (Exjade - Jadenu): 10-20 mg/kg/d PO → 1st line → well tolerated → monitor creatinine + hepatic workup + deferoxamine (Desferal): 20-40 mg/kg/d SC nightly infusion × 8-10h → effective but restrictive (nightly SC injection) → reserved if deferasirox CI + deferiprone (Ferriprox): 75-100 mg/kg/d PO × 3/d → useful for cardiac chelation + in combination with deferoxamine if advanced cardiac fibrosis → chelation goal: serum ferritin 20 ms (cardiac siderosis monitoring - CMR method); hematopoietic stem cell transplantation: curative treatment of thalassemia major → cure rate: 85-90 % if genoidentical HLA donor + patient in Pesaro class I (absence of hepatomegaly + no portal fibrosis + regular chelation before transplantation) → betibeglogene autotemcel gene therapy (Zynteglo - Bluebird Bio): lentiviral vector → insertion of a functional copy of the β-globin gene → FDA 2022 approval + Health Canada under evaluation; luspatercept (Reblozyl): traps TGF-β ligands → reduces inefficient erythropoiesis → FDA + EMA approval for transfusion-dependent beta-thalassemia → BELIEVE 2020 trial (Cappellini - NEJM): reduction in transfusion requirement of ≥33 % in 21.4 % vs. 4.5 % on placebo → Health Canada approval 2021 |
| Methemoglobinemia and carboxyhemoglobin - Dysfunctional Hb Methylene blue - CO - co-oximetry - intoxication |
Some forms of hemoglobin are unable to transport oxygen - their accumulation leads to tissue hypoxia despite sometimes normal total Hb; methemoglobinemia: mechanism: oxidation of Fe²⁺ to Fe³⁺ in the heme moiety → methemoglobin (MetHb) unable to bind O₂ + left Bohr effect on the curve of remaining Hb → worsening hypoxia → clinical thresholds: MetHb >10 %: central cyanosis (grey-slate hue) + low SpO₂ pulse saturation (~85 % regardless of actual O₂ level) → «saturation set at 85 % by pulse oximeter» → major diagnostic pitfall as pulse oximeter does not distinguish MetHb from OxyHb + MetHb >20-30 %: headache + dizziness + dyspnoea + confusion + MetHb >50 %: convulsions + coma + life-threatening + MetHb >70 %: potentially fatal; causes of acquired methemoglobinemia: drugs: dapsone ++ + primaquine + nitrates + nitrites (contaminated water + excess nitrite-treated deli meats) + benzocaine + topical lidocaine + chloroquine + metoclopramide + nitrofurantoin + rasburicase → at-risk populations: G6PD deficiency (reduced NADPH oxidase pathway → less reducing power) + infants (50 % + mechanical ventilation; co-oxymetry: reference method for measuring Hb fractions: OxyHb + DeoxyHb + MetHb + COHb + SulfHb → available on blood gas co-oximeters (ABL from Radiometer + EPOC) → do not rely on pulse-oximeter alone if CO intoxication or methemoglobinemia suspected | Carbon monoxide (CO) intoxication and carboxyhemoglobin: CO binds to hemoglobin with 240× higher affinity than O₂ → carboxyhemoglobin (COHb) → displaces O₂ → tissue hypoxia → also blocks mitochondrial cytochrome c oxidase (direct cellular toxicity) → left-shifted dissociation curve (less O₂ delivered to tissues); CO sources: incomplete combustion (gas + fuel oil + wood + coal + propane + gasoline) + fire + engine in enclosed space + motor-driven electric generator; clinical picture according to COHb: COHb 50 %: coma + convulsions + cardiorespiratory arrest + COHb >70 %: fatal; diagnostic pitfall: SpO₂ on pulse-oximeter normal or subnormal (COHb absorbs light like OxyHb at 660 nm → false high saturation) → always assay COHb by co-oximetry if CO intoxication suspected; treatment: O₂ normobaric at 100 % (reservoir mask or intubation) → COHb half-life: ambient air 5-6h → O₂ 100 % 60-90 min → O₂ hyperbaric (HBOT) 2.5-3 ATA → 20-30 min → HBOT indications (Weaver 2002 NEJM): COHb >25 % + pregnancy + loss of consciousness + neurological symptoms + cardiac ischemia → available in Quebec: CHU de Québec + IUCPQ hyperbaric center + SMOH (Service Médical d'Oxygénothérapie Hyperbare) → neurological sequelae: lucid post-interval syndrome (dementia + personality disorders + parkinsonism) → 10-30 % of severe forms → brain MRI: lesions of the pallidums + periventricular white matter. |
| Hemoglobin and pregnancy - Gestational anemia and screening Iron - folates - B12 - screening for hemoglobinopathies - thalassemia |
Pregnancy profoundly modifies hemoglobin and exposes to specific risks that justify systematic screening; physiological modifications of pregnancy on Hb: hemodilution: expansion of plasma volume by 40-50 % in 2nd trimester + increase in erythrocyte mass by 20-30 % → Hb dilutes → «physiological anemia» → minimum acceptable Hb in pregnancy according to WHO: 110 g/L (1st + 3rd trimester) + 105 g/L (2nd trimester) → caution: the 'physiological anemia« of pregnancy should not lead to overlooking a true iron deficiency anemia → ferritin <30 µg/L → martial deficiency → treat + increase needs: iron: iron needs increase from 1 mg/d (outside pregnancy) to 6-7 mg/d at the end of pregnancy → needs covered by a varied diet + systematic supplementation if ferritin <30 µg/L + folates: needs double in pregnancy → systematic pre-conceptional supplementation: folic acid 0.4-5 mg/d (0.4 mg if no particular risk + 4 mg if history of AFTN + valproate + morbid obesity + diabetes) → recommendation Society of Obstetricians and Gynaecologists of Canada (SOGC) 2015 + MSSS Quebec → reduces the risk of neural tube defects by 70 % + vitamin B12: supplementation recommended if strict vegan diet (risk of maternal + neonatal deficiency) → B12 1,000 µg/d PO; screening for hemoglobinopathies in pregnancy in Quebec: SOGC 2008 recommendation (J Obstet Gynaecol Can): Hb electrophoresis recommended for all high-risk pregnant women (African + Caribbean + Mediterranean + Middle Eastern + Asian origin) → in Quebec: universal screening recommended by several pediatric associations → if maternal sickle cell trait (HbAS) → paternal screening → if both parents carriers → genetic counseling + prenatal diagnosis (amniocentesis + villocentesis → HBB + HBA genotyping) → universal neonatal screening available in Quebec if at-risk origin. | Management of anemia in pregnancy: iron-deficiency anemia in pregnancy: 1st-line oral iron: ferrous sulfate 300 mg/d or ferrous fumarate (Palafer) + ascorbic acid → Hb monitoring + ferritin at 4 weeks → if severe anemia (Hb <90 g/L in 2nd-3rd trimester) or intolerance to oral iron + urgent need for correction: IV iron : carboxymaltose iron (Ferinject) → reassuring safety data after 1st trimester (no sufficient data in 1st trimester) → superior efficacy to oral iron for rapid correction of Hb + avoid transfusion in pregnancy unless life-threatening emergency (risk of maternal-fetal erythrocyte alloimmunization); megaloblastic anemia in pregnancy: folate deficiency: folic acid 5 mg/d × 4-6 weeks + B12 deficiency: B12 1,000 µg/d PO or 1,000 µg IM × 7 days (cyanocobalamin or hydroxocobalamin) if malabsorption; prenatal screening for sickle cell risk: if two parents carry a sickle cell trait (HbAS + HbAS) or another risk combination (HbAS + HbAC + HbAS + βThal) → risk: 1/4 affected child → prenatal diagnosis possible: villocentesis (SA 10-13) or amniocentesis (SA 15-18) → HBB genotyping → couple's informed decision → medical genetics consultation (Cliniques de génétique médicale at CHU de Québec + CHUM + CHU Ste-Justine + McGill University Health Centre); postpartum transfusion: postpartum hemorrhage (PPH): major cause of maternal mortality → Hb <70 g/L + hemodynamic instability → packed red blood cells + PFC + cryoprecipitate + tranexamic acid (1 g IV × 2/d - WOMAN Trial 2017 Lancet) → oxytocin + uterotonics → interventional radiology (uterine artery embolization) if possible before surgery |
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The pulse oximeter does not measure hemoglobin: SpO₂ measured by the digital sensor reflects the oxygen saturation of available hemoglobin - but detects neither anemia (low Hb), nor methemoglobinemia, nor CO intoxication. A SpO₂ at 98 % with Hb at 60 g/L represents severe tissue hypoxemia despite normal saturation. Blood gas co-oximetry is the only method for determining OxyHb, DeoxyHb, COHb and MetHb fractions.
Situations requiring urgent medical assessment
Hb <65-70 g/L + dyspnea at rest + tachycardia + hypotension + angina → severe symptomatic anemia → urgent transfusion of packed red blood cells (O- if grouping not available) → simultaneous etiological workup → CBC + reticulocytes + group + IAR + coagulation.
Slate-gray central cyanosis + SpO₂ ~85 % fixed regardless of O₂ administered + exposure to an oxidizing drug (dapsone + benzocaine + nitrates). → methemoglobinemia → co-oximetry on blood gas → methylene blue 1-2 mg/kg IV if MetHb >20 % and symptomatic patient → urgent.
Intense headache + confusion + nausea in an enclosed space or after exposure to incomplete combustion + normal SpO₂ on pulse oximeter → CO intoxication → COHb by co-oxymetry → immediate O₂ 100 % → evaluation for hyperbaric oxygen therapy if COHb >25 % or loss of consciousness → immediate evacuation of source.
Acute anemia + chest pain + fever + hypoxemia in a known sickle cell patient → acute chest syndrome → hematological emergency → transfusion (single or erythrocyte exchange depending on baseline Hb) + ceftriaxone + azithromycin + O₂ → hospitalization.
Consult at Clinique Omicron
Clinique Omicron doctors prescribe and interpret hemoglobin assays as part of blood counts, prenatal check-ups, periodic check-ups and assessment of symptoms of fatigue or shortness of breath. The initial assessment of anemia - including ferritin, vitamin B12, folate and TSH - as well as the management of mild to moderate iron-deficiency anemia, can be performed at several points of service in Quebec, or by teleconsultation. For complex situations - hemoglobinopathies, hemolytic anemias, prenatal screening - coordination with hematology or medical genetics is organized. To book an appointment, visit cliniqueomicron.ca.
The contents of this page are provided for information purposes only and do not replace the advice of a physician or hematologist. Any hemoglobin abnormality must be evaluated in its full clinical context before concluding a diagnosis or initiating treatment.
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