Anemia of Chronic Disease (ACD)

Sort ACD from iron deficiency before treating it - Ferritin is a positive acute-phase reactant and transferrin a negative one, so ACD shows a normal-to-high ferritin with low serum iron and low transferrin, while true iron deficiency shows a low ferritin. Getting this backwards means prescribing oral iron that hepcidin will not let the gut absorb.

Baseline workup - CBC with MCV, corrected reticulocyte count, iron studies, and a creatinine with eGFR. ACD is usually normocytic (MCV 80-100 fL) but can be microcytic, so a low MCV does not rule it out.

Find the disease underneath - Anemia is a presentation, not a diagnosis. Chronic infection, malignancy, renal failure, endocrine failure (hypothyroidism, hypopituitarism), and marrow disorders all produce it, and each brings its own anesthetic problems.

Use the elective window - Treatment is directed at the underlying disease; erythropoiesis-stimulating agents plus iron are the treatment of choice for renal ACD. IV iron bypasses the hepcidin block on gut absorption that makes oral iron unreliable here.

Judge tolerance by onset and comorbidity, not by the number alone - Chronic anemia is compensated and symptoms typically begin below about 7 g/dL, but that floor moves up in patients with cardiovascular disease and in any state of increased oxygen demand. Ask about exercise tolerance, dyspnea, palpitations, and angina.

No reserve for surgical loss - The patient starts the case with reduced oxygen-carrying capacity and nothing to give away. Plan blood conservation up front and have products available rather than sent for on a case with real EBL.

Protect delivery intraoperatively - Tachycardia, hypoxemia, and hypovolemia all cost more in a patient already short on carrying capacity. Keep heart rate controlled, saturation solid, and volume where you want it rather than chasing them after the fact.

Anemia of chronic disease is a hypoproliferative, usually normocytic normochromic anemia driven by inflammation rather than by blood loss or true iron deficiency. IL-6 released during chronic infection, inflammation, or malignancy drives hepatic production of hepcidin, itself a positive acute-phase reactant. Hepcidin binds ferroportin on duodenal enterocytes and reticuloendothelial macrophages and targets it for lysosomal degradation, so dietary iron absorption falls and stored iron stays locked inside macrophages as ferritin. Serum iron drops despite adequate total-body stores.

Erythropoietin levels are elevated but lower than the degree of anemia should produce — a relative EPO deficiency — and in chronic kidney disease the deficiency becomes absolute, with anemia appearing as GFR falls below 60 and worsening from there. The result is a chronically low hemoglobin, a corrected reticulocyte count under 2%, and reduced oxygen-carrying capacity without any acute volume loss.