Signature ✍️
- Acute anemia: ↑ symptoms/HR, ⊖ transfusion response, ↑ reticulocytes
- Chronic anemia: ⥀ symptoms/HR, ⊕ transfusion response, ↓ reticulocytes
DDx 🏳️🌈
- Iron deficiency
- Thalassemia
- Lead poisoning
- Sideroblastic anemia
- Hyperproliferative
- Hemorrhage
- Hemolysis
- Hypersplenism
- Hypoproliferative
- Anemia of inflammation
- Anemia of CKD
- Anemia of hypothyroidism
- Anemia of marrow failure
- Megaloblastic
- Pathophys: ↓ DNA synthesis → megaloblastic marrow changes (hypercellular, large erythroblasts a.k.a megaloblasts, cytosolic sideroblasts) → cytopenias → intramedullary hemolysis +/- TMA
- B12 & Folate
- Cu
- Hydroxyurea (urea analog blocks DNA synthesis)
- Methotrexate (folate depletion + direct precursor toxicity)
- Azathioprine (metabolism into 6-mercaptopurine → ↓ purine synthesis)
- Nitrous oxide (N2O, subacute combined degeneration)
- Non-megaloblastic
- Reticulocytosis (e.g. > 10%)
- EtOH & liver disease
- MDS
Principles❗️
2 Guiding Principles
Concurrent cytopenias? The presence of multiple cytopenias increases the probability of marrow issue rather than peripheral issue
Tempo? In acute anemia, etiologies of hemoglobin loss should be suspected prior to consider decreased synthesis, except in cases of acute marrow dysfunction, which can be due to common causes (medications, toxins, sepsis) & can’t miss causes (aplastic anemia, chronic hemolysis + acute crisis)
What about the MCV? This is much less helpful than tempo, because concurrent processes may lead to varying MCVs & even MCV normalization. For example, a patient with chronic microcytic anemia from thalassemia may have normal MCV if they develop megaloblastic anemia. However, observing an MCV trend from in a new direction can inform emergent pathology occurring on that part of the MCV spectrum
Helpful Resources 📚
References 📚
- Principles borrowed from @rabihmgeha
- Framework adapted from @AndreMansoor
- B12 testing principles from @WilliamAird4
