Iron Deficiency Anemia
A lack of iron leading to a reduced number of healthy red blood cells, causing fatigue and weakness.
Emergency Management: Severe, life-threatening symptomatic anemia (e.g., Hgb < 7.0 g/dL with myocardial ischemia or hemodynamic instability) requires immediate Packed Red Blood Cell (PRBC) transfusion.
Iron Deficiency Anemia (IDA) is the most common nutritional disorder worldwide, characterized by a decrease in total red blood cell mass due to inadequate iron stores required for hemoglobin synthesis.
Detailed Overview
Iron is an essential component of the heme molecule in hemoglobin, which carries oxygen to tissues. When iron stores are depleted (due to bleeding, malabsorption, or poor diet), the bone marrow produces smaller, less pigmented red blood cells. In adult men and postmenopausal women, IDA must be considered a sign of occult gastrointestinal malignancy until proven otherwise.
Epidemiology & Demographics
Affects over 1.2 billion people globally. Most common in women of childbearing age (menorrhagia) and young children in developing nations.
Etiological Mechanism
Blood loss (overt or occult), inadequate dietary intake, decreased intestinal absorption, or increased physiologic demand (pregnancy).
Primary Causes
Menorrhagia (heavy menstrual bleeding) - most common cause in premenopausal women
Gastrointestinal bleeding (peptic ulcers, NSAID use, colon cancer) - most common cause in adult men
Malabsorption (Celiac disease, post-gastric bypass surgery)
Pregnancy and lactation (increased demand)
Iron balance is tightly regulated by absorption in the duodenum, controlled by the hormone hepcidin. There is no excretory pathway for iron; loss occurs only through bleeding or mucosal sloughing. When losses exceed absorption, iron stores (ferritin) are first depleted. Next, serum iron falls and transferrin (TIBC) increases. Finally, the bone marrow lacks iron to synthesize heme. Erythropoiesis is impaired, resulting in a microcytic (low MCV), hypochromic anemia.
Diagnostic Criteria & Guidelines
Microcytic anemia (Low Hgb, Low MCV < 80 fL) confirmed by low serum ferritin (<30 ng/mL is diagnostic, <15 ng/mL is highly specific), low serum iron, and elevated Total Iron Binding Capacity (TIBC).
Oral Iron therapy: Ferrous sulfate 325 mg (contains 65 mg elemental iron) PO every other day or once daily. (Recent data shows alternate-day dosing improves absorption and reduces GI side effects by minimizing hepcidin spikes). Take with Vitamin C (ascorbic acid) to enhance absorption. Avoid taking with calcium, antacids, or tea/coffee.
Second-Line & Adjunctive Therapy
Intravenous (IV) Iron (e.g., Iron Sucrose 200 mg IV per dose, or Ferric carboxymaltose 750 mg IV). Indicated for patients intolerant to oral iron (severe GI distress), severe malabsorption (gastric bypass, active IBD), or requiring rapid correction (severe anemia in late pregnancy).
Surgical & Procedural Management
Surgery is directed entirely at the underlying cause (e.g., colon resection for cancer, hysterectomy for fibroids causing intractable menorrhagia).
Patient Counseling & Advice
Warn patients that oral iron will turn their stools black or dark green (normal side effect) and can cause constipation, requiring over-the-counter stool softeners.
Follow-Up & Monitoring Schedule
Recheck CBC and reticulocyte count in 2-4 weeks. Reticulocytes should peak in 7-10 days. Hemoglobin should increase by 1 g/dL every 2-3 weeks. Continue iron therapy for 3-6 months AFTER hemoglobin normalizes to replenish ferritin stores.
Preventive Strategies
Prophylactic iron supplementation in pregnancy. Universal screening for infants at 9-12 months. Treating underlying bleeding disorders.
Excellent with proper supplementation and identification of the root cause. Failure to respond usually indicates non-compliance, continued unrecognized bleeding, or an incorrect diagnosis.