Anemia nursing reference: types, interventions, and NCLEX review

Anemia is one of the most common conditions nurses encounter across every clinical setting — from med-surg and oncology to obstetrics and primary care. The term describes a reduction in the oxygen-carrying capacity of the blood, most often measured as a hemoglobin below 12 g/dL in women or below 13.5 g/dL in men. Behind that single lab value lies a broad family of disorders with different mechanisms, lab signatures, treatments, and nursing priorities.

This reference covers all major anemia types in a single document — pathophysiology, lab diagnostics, medical management, nursing assessment, diagnoses, and interventions — along with 6 NCLEX-style practice questions. For a focused look at sickle cell disease, see the companion sickle cell disease nursing reference.

Fast-scan summary

Pathophysiology overview

Red blood cells (RBCs) carry hemoglobin, the protein that binds oxygen in the lungs and releases it to tissues. Anemia impairs this oxygen-delivery system in one of three ways: RBCs are lost faster than they can be replaced, fewer RBCs are produced, or RBCs are destroyed prematurely.

Defining thresholds (WHO/NIH criteria):

• Men: hemoglobin <13.5 g/dL or hematocrit <41%
• Women: hemoglobin <12.0 g/dL or hematocrit <36%
• Pregnant women: hemoglobin <11.0 g/dL (any trimester)

When hemoglobin falls, tissues become hypoxic. The body compensates by increasing heart rate and respiratory rate, redistributing blood to vital organs, and stimulating erythropoietin (EPO) release from the kidneys to drive RBC production. These compensatory mechanisms produce the classic clinical signs — tachycardia, tachypnea, dyspnea on exertion, pallor — and explain why nursing assessment of the cardiovascular and respiratory systems is essential for every patient with anemia.

Mean corpuscular volume (MCV) is the single most useful initial classifier. A low MCV points to iron deficiency or thalassemia; a high MCV points to B12 or folate deficiency; a normal MCV points to hemolysis, bone marrow failure, or anemia of chronic disease.

Classification by mechanism

Types of anemia: deep dive

Iron deficiency anemia

Iron deficiency anemia (IDA) is the most common anemia worldwide, affecting roughly 1–2 billion people. It develops when iron stores are depleted to the point that hemoglobin synthesis is impaired.

Causes: Chronic blood loss (most common in adults — GI bleeding, menorrhagia), inadequate dietary intake (common in infants, toddlers, vegetarians), malabsorption (celiac disease, post-gastrectomy), increased demand (pregnancy).

Lab findings: Low MCV (<80 fL), low serum ferritin (<12 ng/mL — earliest marker of depletion), low serum iron, elevated total iron-binding capacity (TIBC), low transferrin saturation (<16%). Peripheral smear shows microcytic, hypochromic RBCs.

Symptoms: Fatigue, pallor, koilonychia (spoon-shaped nails), pica (craving ice, clay, or starch — called pagophagia when specifically ice), glossitis, angular cheilitis, restless legs syndrome.

Medical management: Ferrous sulfate 325 mg orally two to three times daily with vitamin C to enhance absorption; IV iron (iron sucrose, ferric carboxymaltose) for patients who cannot tolerate oral iron, have active malabsorption, or have persistent bleeding. Reticulocyte count rises within 7–10 days of treatment. Hemoglobin normalizes in 4–8 weeks; iron stores require 3–6 months to replete.

For relevant GI bleeding context, see the GI bleed nursing reference.

B12 deficiency anemia (pernicious anemia)

Vitamin B12 (cobalamin) is essential for DNA synthesis and myelin formation. Deficiency produces megaloblastic anemia — large, abnormally shaped RBCs that cannot divide normally — and, uniquely among the anemias, causes irreversible neurological damage if untreated.

Cause of pernicious anemia: Autoimmune destruction of gastric parietal cells eliminates intrinsic factor (IF), a glycoprotein that binds dietary B12 and enables its absorption at the terminal ileum. Without IF, B12 cannot be absorbed regardless of dietary intake.

Other causes of B12 deficiency: Strict vegan diet (B12 is found only in animal products), terminal ileum resection or disease (Crohn’s disease), prolonged metformin or proton pump inhibitor use, gastric bypass surgery.

Lab findings: Elevated MCV (>100 fL), low serum B12 (<200 pg/mL), elevated methylmalonic acid (MMA) and homocysteine (sensitive markers of cellular B12 deficiency), hypersegmented neutrophils and large ovalocytes on peripheral smear.

Neurological symptoms (key differentiator from folate deficiency): Subacute combined degeneration of the spinal cord — symmetrical paresthesias (tingling, numbness in hands and feet), proprioception loss, ataxia, weakness, and in severe cases, cognitive impairment and psychosis. These neurological changes may be irreversible if treatment is delayed.

The Schilling test was historically used to distinguish pernicious anemia from other B12 deficiency causes by measuring radiolabeled B12 absorption with and without IF. It is rarely performed today; anti-parietal cell and anti-intrinsic factor antibodies are the preferred diagnostic tests.

Medical management: IM cyanocobalamin 1,000 mcg — daily for one week, then weekly for 4–8 weeks, then monthly for life. Because intrinsic factor is permanently absent in pernicious anemia, oral supplementation is ineffective unless given in pharmacological doses (1,000–2,000 mcg/day) that allow passive absorption. High-dose oral B12 is an acceptable alternative for motivated, adherent patients.

Folate deficiency anemia

Folate (vitamin B9) is required for RBC maturation and fetal neural tube development. Like B12 deficiency, it produces megaloblastic changes. Unlike B12 deficiency, it does not cause neurological damage.

Causes: Poor dietary intake (most common; folate-rich foods include leafy greens, legumes, citrus), alcohol use disorder (alcohol impairs folate absorption and increases renal excretion), malabsorption, medications (methotrexate, trimethoprim, phenytoin block folate metabolism), pregnancy (increased demand).

Lab findings: Elevated MCV, low serum folate (<4 ng/mL), low RBC folate (more reliable marker of tissue stores), elevated homocysteine — but methylmalonic acid is normal (this distinguishes folate deficiency from B12 deficiency).

Medical management: Oral folic acid 1 mg/day; women of childbearing age should receive 0.4–0.8 mg/day prophylactically to prevent neural tube defects.

Aplastic anemia

Aplastic anemia is a life-threatening condition in which the bone marrow fails to produce sufficient blood cells of all three lines — RBCs, white blood cells, and platelets. The result is pancytopenia.

Cause: In most cases, autoreactive T-lymphocytes attack hematopoietic stem cells. Triggers include certain medications (chloramphenicol, NSAIDs, sulfonamides), viral infections (hepatitis, EBV, CMV, parvovirus B19), radiation and chemotherapy exposure, and inherited disorders (Fanconi anemia). Approximately 70% of cases are idiopathic.

Lab findings: CBC shows low RBC, WBC (particularly neutropenia), and platelets — pancytopenia. Reticulocyte count is very low (hypoproliferative pattern). Bone marrow biopsy is diagnostic and shows a hypocellular marrow replaced by fat cells.

Clinical presentation: Fatigue and pallor (anemia), infection susceptibility and fever (neutropenia), petechiae, ecchymosis, and mucosal bleeding (thrombocytopenia).

Medical management: Allogeneic hematopoietic stem cell transplantation (HSCT) is curative and preferred for younger patients with a matched sibling donor. For those who are not transplant candidates: antithymocyte globulin (ATG) plus cyclosporine (immunosuppressive therapy), eltrombopag (thrombopoietin receptor agonist), and supportive transfusions. Patients receiving immunosuppressive therapy are at high infection risk — neutropenic precautions are mandatory.

Hemolytic anemia

Hemolytic anemia results from premature RBC destruction. RBC lifespan normally is 120 days; hemolysis shortens this dramatically. The bone marrow compensates by increasing production (elevated reticulocyte count), but in severe hemolysis, production cannot keep pace.

Lab findings common to all hemolytic anemias: Elevated LDH (released from lysed cells), elevated indirect (unconjugated) bilirubin (product of heme breakdown), low haptoglobin (haptoglobin binds free hemoglobin and is consumed), elevated reticulocyte count, variable MCV (often normocytic).

Intrinsic (intracorpuscular) causes

G6PD deficiency: X-linked disorder in which RBCs lack glucose-6-phosphate dehydrogenase, an enzyme that protects RBCs from oxidative damage. Exposure to oxidative stressors — infections, certain medications (primaquine, dapsone, nitrofurantoin, high-dose aspirin), fava beans — triggers hemolytic episodes. Peripheral smear shows bite cells and Heinz bodies. Management centers on avoiding triggers; transfusion for severe acute episodes.

Hereditary spherocytosis: Autosomal dominant structural defect in the RBC membrane (usually spectrin or ankyrin) causes spherical, fragile RBCs that are destroyed in the spleen. Hallmark findings: splenomegaly, jaundice, and spherocytes on smear. Osmotic fragility test is positive. Splenectomy reduces hemolysis significantly.

Extrinsic (extracorpuscular) causes

Autoimmune hemolytic anemia (AIHA): Antibodies target RBC antigens. Warm AIHA (IgG, active at 37°C) is most common; associated with SLE, CLL, and certain drugs (methyldopa, penicillin). Cold AIHA (IgM, active at <37°C) is associated with Mycoplasma pneumoniae infection and lymphomas. Direct Coombs test (DAT) is positive. Warm AIHA is treated with corticosteroids; refractory cases may require splenectomy or rituximab.

Microangiopathic hemolytic anemia (MAHA): RBCs are physically sheared by damaged or narrowed vasculature. Peripheral smear shows schistocytes (fragmented RBCs). Causes include thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), and HELLP syndrome (in pregnancy — for which see the HELLP syndrome nursing reference).

Anemia of chronic disease (ACD) / Anemia of inflammation

ACD is the second most common anemia worldwide and develops in the setting of chronic inflammatory states — including rheumatoid arthritis, chronic kidney disease, malignancy, HIV, and inflammatory bowel disease.

Mechanism: Elevated inflammatory cytokines (particularly IL-6) stimulate hepatic production of hepcidin, a hormone that blocks iron release from storage sites (macrophages, liver) and reduces intestinal iron absorption. Iron becomes trapped inside cells and unavailable for erythropoiesis, even when total body iron stores are adequate or elevated. EPO response is also blunted.

Lab findings (key differentiator from IDA): Low serum iron, but also low TIBC (distinguishes from IDA where TIBC is high), and normal to elevated ferritin (ferritin is an acute-phase reactant — it rises with inflammation). Transferrin saturation is low. MCV is usually normocytic, occasionally mildly microcytic.

Medical management: Treating the underlying condition is the primary intervention. Erythropoiesis-stimulating agents (ESAs — epoetin alfa, darbepoetin alfa) are used in CKD patients to reduce transfusion dependence. IV iron supplementation is appropriate when true iron deficiency coexists. For kidney disease context, see CKD and ESRD nursing.

Clinical presentation by severity

Diagnostic workup

Integrating lab values into clinical decision-making is a core nursing competency. For a comprehensive review of normal ranges across all major lab panels, see the nursing lab values cheat sheet.

Medical management

Iron supplementation

Oral iron: Ferrous sulfate 325 mg (contains 65 mg elemental iron) two to three times daily, ideally on an empty stomach to maximize absorption. Vitamin C (ascorbic acid) taken simultaneously enhances non-heme iron absorption. Calcium, antacids, dairy, coffee, and tea inhibit absorption. Common side effects: constipation, dark stools, nausea — take with a small amount of food if GI distress occurs. Stools will turn black; educate patients this is expected and benign.

IV iron: Indications include intolerance to oral iron, malabsorption (celiac disease, inflammatory bowel disease, post-bariatric surgery), active or ongoing blood loss that outpaces oral replacement, and CKD patients on hemodialysis. Formulations include iron sucrose (Venofer), ferric gluconate (Ferrlecit), and ferric carboxymaltose (Injectafer). Monitor for hypersensitivity reactions during infusion; anaphylaxis risk is low with newer formulations but resuscitation equipment should be available.

Blood transfusion

Packed red blood cell (pRBC) transfusion is indicated when:

• Hemoglobin <7 g/dL in stable, non-bleeding patients (restrictive threshold — supported by TRICC trial evidence)
• Hemoglobin <8 g/dL in patients with cardiac disease or active myocardial ischemia
• Any level in actively bleeding, hemodynamically unstable patients

Each unit of pRBCs raises hemoglobin by approximately 1 g/dL. Monitor for transfusion reactions: febrile non-hemolytic (most common), allergic, acute hemolytic (ABO incompatibility — medical emergency), transfusion-related acute lung injury (TRALI), and transfusion-associated circulatory overload (TACO — particularly in elderly and cardiac patients).

Erythropoiesis-stimulating agents (ESAs)

Epoetin alfa (Epogen, Procrit) and darbepoetin alfa (Aranesp) stimulate the bone marrow to produce more RBCs by mimicking EPO. Primary indications: anemia of CKD, anemia related to chemotherapy, and anemia in myelodysplastic syndromes. Adequate iron stores are required for ESAs to be effective — assess iron studies before initiation. Risks include hypertension (monitor BP closely), increased risk of thromboembolism, and — in malignancy — potential tumor progression.

B12 and folate replacement

IM cyanocobalamin for pernicious anemia (see B12 section above). High-dose oral B12 (1,000–2,000 mcg/day) is appropriate for dietary deficiency without malabsorption. Oral folic acid 1 mg/day for folate deficiency; 4–5 mg/day is used in women with a prior neural tube defect-affected pregnancy.

Nursing assessment

Systematic assessment covers multiple body systems because impaired oxygen delivery has widespread effects.

Cardiovascular: Heart rate and rhythm (tachycardia is a key early compensatory sign), blood pressure, presence of a flow murmur (a systolic ejection murmur caused by high-velocity, low-viscosity blood flow — expected in significant anemia), and signs of cardiac decompensation (S3 gallop, JVD, peripheral edema). For patients with known cardiac disease, assess for angina or worsening heart failure — see heart failure nursing.

Respiratory: Respiratory rate, oxygen saturation (SpO2), dyspnea at rest versus exertion, use of accessory muscles.

Hematologic / skin: Pallor of the conjunctivae, nail beds, and oral mucosa (more reliable than skin pallor in dark-skinned patients). Jaundice (scleral icterus) in hemolytic anemias. Petechiae and ecchymosis in thrombocytopenic states (aplastic anemia). Koilonychia (IDA). Angular cheilitis, glossitis (IDA, B12/folate).

Neurological: Paresthesias, gait instability, proprioception deficits, and cognitive changes (specifically associated with B12 deficiency — can be the presenting complaint before anemia becomes apparent). Use of the GCS assists in documenting neurological baseline.

Gastrointestinal: Assess for overt or occult bleeding — hematemesis, melena, hematochezia, and guaiac-positive stools. Splenomegaly (percuss and palpate carefully) in hemolytic anemias and hereditary spherocytosis.

Activity tolerance: Baseline functional status, exercise tolerance, and impact on activities of daily living. Activity intolerance is often the chief complaint that brings patients to care.

Nutritional status: Dietary history — iron-rich foods, B12 sources (animal products), folate sources (leafy greens, legumes). Dietary pattern (vegan, vegetarian, food insecurity). Alcohol use.

Nursing diagnoses

Nursing interventions

Activity intolerance

• Assess activity tolerance before and after any activity; monitor heart rate, respiratory rate, and SpO2 during exertion.
• Implement activity pacing — cluster care to allow rest periods; prioritize essential activities.
• Assist with ADLs during periods of symptomatic anemia; maintain safety during position changes (orthostatic hypotension risk).
• Administer supplemental oxygen as ordered when SpO2 falls below 94% or the patient is symptomatic.
• Administer prescribed blood products or EPO-stimulating agents; reassess activity tolerance as hemoglobin improves.
• Encourage gradual resumption of activity as hemoglobin rises; set realistic goals with the patient.

Rationale: Pacing prevents excessive oxygen demand on a system already operating at reduced capacity. Incremental activity increases as hemoglobin improves builds tolerance without precipitating cardiac stress.

Ineffective tissue perfusion

• Monitor vital signs every 4 hours or per protocol; report heart rate >100 bpm, systolic BP <90 mmHg, or new rhythm changes.
• Administer pRBC transfusions per order; monitor for transfusion reactions for the first 15 minutes of each unit and per institutional protocol.
• Assess peripheral perfusion: capillary refill, skin temperature, pulse quality.
• Position patient with head of bed elevated to reduce work of breathing; avoid Trendelenburg in anemia (worsens dyspnea).
• Monitor hemoglobin, hematocrit, and reticulocyte count trends; report values consistent with worsening anemia or inadequate treatment response.

Rationale: Early recognition of hemodynamic instability prevents progression to high-output cardiac failure, which is a recognized complication of severe untreated anemia.

Imbalanced nutrition

• Assess 24-hour dietary recall for iron, B12, and folate content; identify deficiency-specific gaps.
• Administer oral iron with vitamin C-rich foods or juice; separate from calcium-rich foods, antacids, and coffee by at least 2 hours.
• Administer IM cyanocobalamin per order for pernicious anemia; document injection site rotation.
• Refer to a registered dietitian for individualized meal planning; involve the patient’s family or caregivers where appropriate.
• Teach dietary sources specific to the deficiency (see patient education table).

Risk for infection (aplastic anemia / neutropenia)

• Implement protective isolation (neutropenic precautions) when absolute neutrophil count (ANC) <500/mm³: private room, restrict visitors with illness, limit fresh flowers and raw produce.
• Perform meticulous hand hygiene before and after all patient contact; reinforce with all visitors.
• Assess for subtle signs of infection in neutropenic patients — fever >38°C may be the only sign (neutropenia blunts typical inflammatory response); report immediately.
• Administer prophylactic antibiotics, antifungals, or antiviral agents per order.
• Avoid rectal temperatures, rectal suppositories, and IM injections when platelet count is critically low.

Risk for bleeding (thrombocytopenia)

• Institute bleeding precautions: soft toothbrush, electric razor, avoid aspirin and NSAIDs, no flossing.
• Apply prolonged pressure (at least 5 minutes) to venipuncture sites; document site assessment.
• Assess for petechiae, ecchymosis, and mucosal bleeding at each assessment.
• Monitor platelet count; anticipate platelet transfusion orders when count falls below 10,000–20,000/mm³ or if active bleeding occurs.
• Educate patient to avoid straining (increases intracranial pressure risk with low platelets) and to use stool softeners.

Deficient knowledge

• Assess health literacy and preferred learning style before teaching.
• Teach the specific type of anemia, its cause, and why the prescribed treatment works.
• Explain the importance of treatment adherence — particularly for B12 (lifelong) and iron (months of supplementation needed to replete stores).
• Review side effects of iron supplementation: black stools (expected), constipation (manage with adequate hydration and fiber), nausea (take with small meal if needed).
• Provide written materials that reinforce verbal teaching.

Patient education

NCLEX-style practice questions

Question 1

A patient with iron deficiency anemia asks why the nurse is giving their iron supplement with orange juice instead of milk. What is the best response?

A) “Milk interacts with the iron and can cause liver damage.” B) “Vitamin C in orange juice enhances non-heme iron absorption; calcium in milk inhibits it.” C) “Orange juice coats the stomach and prevents nausea from the supplement.” D) “Milk is too thick and will slow down the medication’s absorption into the bloodstream.”

Correct answer: B

Rationale: Vitamin C (ascorbic acid) reduces dietary non-heme iron from the ferric (Fe³⁺) to the ferrous (Fe²⁺) state, which is far more readily absorbed by enterocytes. Calcium — abundant in milk — directly competes with iron for the same intestinal transport proteins and significantly reduces iron absorption. Orange juice does not coat the stomach or affect absorption speed in any clinically meaningful way. Understanding iron absorption enhancers and inhibitors is a high-yield nursing pharmacology topic.

Question 2

A nurse is caring for a patient newly diagnosed with pernicious anemia. The patient asks why they cannot simply take an oral B12 pill every day. What is the most accurate explanation?

A) “Oral B12 is too expensive and your insurance will not cover it.” B) “Oral B12 causes too many side effects in this condition.” C) “Your stomach no longer produces the protein needed to absorb B12 from the gut.” D) “The injections work faster and only need to be given once.”

Correct answer: C

Rationale: Pernicious anemia results from autoimmune destruction of the gastric parietal cells that produce intrinsic factor (IF). Without IF, dietary and oral supplemental B12 cannot be absorbed at the terminal ileum. IM cyanocobalamin bypasses gastrointestinal absorption entirely, delivering B12 directly into the bloodstream. Cost and side effects are not the reason. High-dose oral B12 (1,000–2,000 mcg/day) can achieve some passive absorption and is sometimes used, but the standard treatment remains lifelong IM injections.

Question 3

The nurse is reviewing lab results for a patient with chronic rheumatoid arthritis who appears pale and fatigued. The CBC shows hemoglobin 9.8 g/dL, MCV 82 fL. Iron studies show: serum iron low, TIBC low, ferritin elevated. Which type of anemia do these findings most suggest?

A) Iron deficiency anemia B) Folate deficiency anemia C) Anemia of chronic disease D) Aplastic anemia

Correct answer: C

Rationale: Anemia of chronic disease (ACD) classically presents with low serum iron AND low TIBC — this distinguishes it from iron deficiency anemia, where TIBC is elevated (the body upregulates transferrin production to capture any available iron). Ferritin is an acute-phase reactant and is elevated in inflammatory conditions, even when functional iron availability is impaired. The normocytic MCV is also consistent with ACD. Folate deficiency would show macrocytosis; aplastic anemia would show pancytopenia.

Question 4

A patient with aplastic anemia has an ANC of 320/mm³. Which nursing intervention is the highest priority?

A) Administer a ferrous sulfate supplement as ordered. B) Prepare to transfuse two units of pRBCs. C) Implement neutropenic precautions and monitor for fever. D) Obtain a serum B12 level before starting any treatment.

Correct answer: C

Rationale: An ANC below 500/mm³ places the patient at severe risk for life-threatening infection. Neutropenic precautions — private room, strict hand hygiene, restricting ill visitors, avoiding raw produce and fresh flowers — are the priority. In neutropenic patients, fever >38°C is a medical emergency requiring immediate evaluation. Iron supplementation is not the priority intervention for aplastic anemia (which involves all cell lines, not iron deficiency). pRBC transfusion may be warranted for symptomatic anemia but is not the highest priority when infection risk is the immediate threat. B12 testing is irrelevant here.

Question 5

A nurse is preparing to administer the first unit of packed RBCs to a patient with severe iron deficiency anemia. During the first 15 minutes of the infusion, the patient develops fever, chills, and lower back pain. What is the priority action?

A) Slow the infusion rate and administer diphenhydramine. B) Stop the infusion immediately, keep the IV line open with normal saline, and notify the provider. C) Complete the transfusion rapidly before the reaction worsens. D) Document the reaction and monitor closely; these symptoms are expected with transfusion.

Correct answer: B

Rationale: Fever, chills, and lower back pain during a blood transfusion are the classic triad of an acute hemolytic transfusion reaction (AHTR), most often caused by ABO incompatibility. This is a life-threatening emergency. The nurse must stop the transfusion immediately, maintain IV access with a new NS line (do not disconnect the IV), notify the provider, and prepare to support blood pressure and urine output. The blood unit and tubing are saved for the blood bank to investigate. Slowing the rate or completing the transfusion risks massive hemolysis and acute kidney injury. These symptoms are never expected or acceptable.

Question 6

A patient with G6PD deficiency is prescribed trimethoprim-sulfamethoxazole (TMP-SMX) for a urinary tract infection. What is the nurse’s priority action before administering this medication?

A) Administer the medication as ordered; G6PD deficiency does not affect drug metabolism. B) Hold the medication and notify the provider, as sulfonamides are a known trigger for hemolytic episodes in G6PD deficiency. C) Administer the first dose and monitor for hemolysis over the next hour. D) Substitute the medication with a lower dose of the same drug.

Correct answer: B

Rationale: G6PD deficiency renders RBCs unable to neutralize oxidative stress. Sulfonamides, including TMP-SMX, are a well-documented oxidative trigger for hemolytic episodes in G6PD-deficient patients. Administering the medication could precipitate acute hemolytic anemia. The nurse must hold the dose and contact the prescriber to request an alternative antibiotic. Monitoring after administration is insufficient — prevention is the standard of care. Dose reduction does not eliminate the oxidative risk. This question tests the nurse’s role as the last safety check in the medication administration process.

Key takeaways

Anemia spans a wide clinical spectrum — from the common and correctable (iron deficiency with oral supplementation) to the rare and life-threatening (aplastic anemia requiring bone marrow transplantation). The unifying thread for nursing practice is understanding the mechanism behind each type, because the mechanism determines the lab pattern, the treatment, and the nursing priorities.

Use the MCV as your first classifier: low MCV directs you toward iron deficiency; high MCV toward B12 or folate; normal MCV toward hemolysis, marrow failure, or chronic disease. Layer in ferritin, TIBC, reticulocyte count, and peripheral smear to sharpen the picture. From there, nursing care follows logically — manage oxygen delivery, prevent complications of pancytopenia, replace the deficient nutrient, and educate the patient to prevent recurrence.

For electrolyte considerations in critically ill patients with anemia, see the electrolyte imbalances reference. For kidney disease-related anemia and EPO management, see CKD and ESRD nursing. For sepsis-related anemia of critical illness, see the sepsis nursing reference.