NLE Hematologic Nursing — Hematologic Assessment and the AnemiasRevision Notes

Exam Tips

• NLE questions often test the relationship between kidney disease and anemia — always link EPO deficiency to kidney failure.
• Remember the '120-day rule' for RBC lifespan; this explains why chronic blood loss (not acute) depletes iron stores over time.
• The spleen is the KEY organ for filtering old RBCs — splenomegaly in hemolytic anemia is a compensatory response to increased RBC destruction.

Key Points

• Blood is composed of plasma and formed elements; all formed elements are produced in bone marrow through hematopoiesis.
• Erythrocytes (RBCs) carry oxygen via hemoglobin; they live approximately 120 days and are stimulated by erythropoietin released by the kidneys in response to hypoxia.
• Leukocytes (WBCs) defend the body against infection; types include neutrophils, lymphocytes, monocytes, eosinophils, and basophils.
• Thrombocytes (platelets) initiate hemostasis (clotting); normal lifespan is 8–10 days.
• The spleen filters aged RBCs and stores platelets; the liver produces most clotting factors and stores vitamin B12, iron, and folate.
• Erythropoietin (EPO) is the key hormonal regulator of RBC production — kidney disease reduces EPO, causing anemia of chronic kidney disease.
• Hematopoiesis occurs in the red bone marrow of flat bones (sternum, pelvis, ribs) in adults.

Definitions

Section Title

Overview of the Hematologic System

Common Mistakes

• Confusing the functions of leukocytes and erythrocytes — remember: RBCs carry oxygen, WBCs fight infection, platelets clot.
• Forgetting that erythropoietin is produced by the KIDNEYS, not the bone marrow; students often confuse the site of production with the site of action.
• Overlooking the liver's role — the liver produces clotting factors AND stores B12, iron, and folate, making hepatic disease a contributor to multiple hematologic problems.
• Assuming all blood cells live the same length of time — RBCs: 120 days, platelets: 8–10 days, WBCs: hours to days.

Exam Tips

• NLE clinical scenarios frequently describe a patient with 'pale conjunctiva and spoon-shaped nails' — this is iron-deficiency anemia.
• A scenario describing 'pallor + paresthesias/numbness of hands and feet + beefy red tongue' = pernicious anemia (B12 deficiency).
• The presence of ALL THREE: pallor, recurrent infections, AND petechiae/bleeding = aplastic anemia (pancytopenia).
• In the Philippines, malnutrition and heavy menstrual blood loss are the most common causes of iron-deficiency anemia in the primary health care setting.

Key Points

• A thorough history includes: fatigue, dyspnea, pallor, dizziness, bleeding or bruising, recurrent infections, diet (iron, B12, folate intake), medications (anticoagulants, NSAIDs, chemotherapy), and family history of blood disorders.
• In Filipino patients with darker skin tones, pallor is best assessed at the conjunctiva, nail beds, and palms — NOT solely at the face.
• Jaundice in hematologic conditions signals hemolysis (increased bilirubin from RBC destruction); cyanosis signals severe hypoxia.
• Compensatory signs in anemia: tachycardia, tachypnea, and a systolic flow murmur (increased cardiac output to deliver more oxygen despite low Hgb).
• Petechiae (pinpoint), purpura (larger), and ecchymoses suggest thrombocytopenia or coagulopathy.
• Glossitis (inflamed tongue) and angular cheilitis (mouth corner cracks) indicate iron or B12 deficiency.
• Koilonychia (spoon-shaped nails) is a classic sign of chronic iron-deficiency anemia.
• Neurologic changes (paresthesias, ataxia) specifically suggest vitamin B12 deficiency — NOT iron deficiency.
• Lymphadenopathy and splenomegaly suggest malignancy, hemolysis, or infection.

Definitions

Section Title

Hematologic Assessment: History and Physical Examination

Common Mistakes

• Assessing pallor only on the face in Filipino patients — always check conjunctiva and nail beds for accurate assessment regardless of skin tone.
• Attributing neurologic signs (paresthesias, ataxia) to iron deficiency — these are signs of B12 deficiency ONLY; iron deficiency does NOT cause neurologic damage.
• Missing the significance of a flow murmur in anemia — this is a COMPENSATORY cardiac response, not a primary cardiac problem.
• Confusing petechiae with purpura — petechiae are tiny (pin-point), purpura are larger, but both are non-blanching and suggest bleeding disorders.

Formulas

Exam Tips

• MEMORIZE the critical CBC normals: Hgb Male 13–18, Female 12–16; WBC 5,000–10,000; Platelets 150,000–400,000; MCV 80–100 fL.
• The MCV is your KEY to anemia classification on the NLE: Small cells (microcytic, <80) = iron deficiency; Big cells (macrocytic, >100) = B12 or folate; Normal cells (normocytic, 80–100) = aplastic or acute blood loss.
• If an NLE question asks about a patient's risk for infection, calculate or estimate ANC — platelets tell you bleeding risk, ANC tells you infection risk.
• Low reticulocytes = marrow problem or no raw materials (nutritional deficiency). High reticulocytes = marrow is working overtime (hemolysis or blood loss).

Key Points

• The CBC is the cornerstone diagnostic test for all hematologic conditions and is heavily tested on the NLE.
• Normal Hgb: MALE 13–18 g/dL; FEMALE 12–16 g/dL. Below these values = anemia.
• Normal Hct: Male 42–52%; Female 37–47%. Rule of thumb: Hct is approximately 3× the Hgb value.
• Normal WBC: 5,000–10,000/µL. Below 5,000 = leukopenia; above 10,000 = leukocytosis.
• Normal Platelets: 150,000–400,000/µL. Below 150,000 = thrombocytopenia; below 20,000 = critical bleeding risk.
• Normal MCV: 80–100 fL. MCV classifies anemia: Microcytic (<80), Normocytic (80–100), Macrocytic (>100).
• Normal Reticulocytes: 0.5–2%. Elevated reticulocytes = active marrow response (blood loss/hemolysis). Low reticulocytes = marrow failure or nutritional deficiency.
• A 'left shift' in WBC differential (increased band neutrophils) signals acute bacterial infection.
• Absolute Neutrophil Count (ANC) < 500/µL = severe neutropenia; highest risk for life-threatening infection.
• Peripheral blood smear reveals cell morphology: hypochromic microcytes (iron deficiency), hypersegmented neutrophils (B12/folate deficiency), sickle cells (sickle cell disease).

Definitions

Section Title

Interpreting the Complete Blood Count (CBC)

Common Mistakes

• Memorizing only one normal Hgb value — remember there are DIFFERENT normals for males (13–18) and females (12–16).
• Confusing MCV with MCH — MCV measures SIZE (microcytic/normocytic/macrocytic); MCH measures COLOR/hemoglobin content (normochromic/hypochromic). Both are useful but MCV is more commonly tested.
• Thinking a high reticulocyte count always means the patient is getting better — high retics mean the marrow is RESPONDING to increased demand (blood loss or hemolysis), not necessarily that the condition is resolving.
• Forgetting that normal platelet count is 150,000–400,000/µL — some students incorrectly state 150–400 (without the thousands).

Exam Tips

• NLE memory aid for blood type antibodies: 'You have antibodies AGAINST what you DON'T have.' Type A lacks B antigen → has anti-B. Type O lacks both → has anti-A AND anti-B.
• Emergency transfusion without crossmatch → always use O-NEGATIVE packed RBCs.
• For NLE questions about Rh and pregnancy: Rh-NEGATIVE mother carrying Rh-POSITIVE baby → risk of HDN in subsequent pregnancies → give RhoGAM (anti-D immunoglobulin) within 72 hours after first exposure.
• A positive DIRECT Coombs = immune-mediated hemolytic anemia. Remember: 'D for Direct = Destruction of own cells.'

Key Points

• ABO blood typing is based on antigens present on the RBC surface and the corresponding antibodies in the plasma.
• Type A: has A antigen, anti-B antibodies; can receive from A and O.
• Type B: has B antigen, anti-A antibodies; can receive from B and O.
• Type AB: has both A and B antigens, NO antibodies; can receive from A, B, AB, and O — UNIVERSAL RECIPIENT.
• Type O: has NO antigens, has both anti-A and anti-B antibodies; can only receive from O — UNIVERSAL DONOR (especially O-negative).
• Type O-NEGATIVE is the universal donor for RBC transfusions because it lacks A, B, AND Rh(D) antigens — safe for emergency use before crossmatch.
• Type AB-POSITIVE is the universal recipient for whole blood and packed RBCs.
• The Rh factor: Rh-negative individuals do NOT have anti-D antibodies naturally; they form them only after exposure to Rh-positive blood (sensitization). Critical in pregnancy (hemolytic disease of the newborn — HDN).
• Before elective transfusion: TYPE AND CROSSMATCH is performed to confirm ABO/Rh compatibility.
• The Coombs (Antiglobulin) Test: Direct Coombs detects antibodies already attached to patient's own RBCs (immune hemolytic anemia); Indirect Coombs detects antibodies in patient's serum (used in crossmatching and prenatal screening).

Definitions

Section Title

Blood Typing and Transfusion Compatibility

Common Mistakes

• Confusing universal DONOR and universal RECIPIENT — O-negative DONATES to all; AB-positive RECEIVES from all. Think: 'O gives, AB takes.'
• Stating that type O can receive from anyone — Type O can only receive from type O because they carry BOTH anti-A and anti-B antibodies.
• Forgetting the Rh component — even type O blood that is Rh-POSITIVE can cause reactions in Rh-negative recipients; the universal donor is O-NEGATIVE.
• Mixing up Direct and Indirect Coombs tests — Direct = antibodies ON patient's own RBCs (direct detection on cells); Indirect = antibodies IN patient's serum (indirect, you test the liquid part).

Exam Tips

• Memory aid for iron lab pattern: 'In iron deficiency, everything is LOW except TIBC which is HIGH.' Low ferritin, low serum iron, low Hgb, low MCV, HIGH TIBC.
• NLE questions about iron administration: empty stomach + vitamin C = best absorption; Z-track for IM; straw for liquid; warn about black stools.
• Remember: FERROUS sulfate (Fe2+) is better absorbed than FERRIC (Fe3+); vitamin C keeps iron in the ferrous state for absorption.
• In the Philippine primary care context: malnutrition screening in children (6–59 months) often includes assessment for iron-deficiency anemia as per DOH protocols.

Key Points

• The MOST COMMON anemia worldwide and the most common nutritional deficiency in the Philippines.
• Characterized by MICROCYTIC (small), HYPOCHROMIC (pale/low color) RBCs due to insufficient iron for hemoglobin synthesis.
• Most common cause in adults: CHRONIC BLOOD LOSS (GI bleeding in men and older women; heavy menstruation in reproductive-age women).
• Other causes: inadequate dietary intake (especially in malnourished Filipino infants and children), malabsorption (celiac disease, post-gastrectomy), and increased demand (pregnancy, infancy).
• Key laboratory findings: LOW Hgb/Hct, LOW MCV (<80 fL), LOW serum ferritin (BEST MARKER of iron stores), LOW serum iron, HIGH TIBC (total iron-binding capacity).
• Specific clinical signs: koilonychia, glossitis, angular cheilitis, and PICA (especially pagophagia — craving ice).
• Treatment: Oral FERROUS SULFATE 325 mg (65 mg elemental iron), 1–3 times daily.
• Administration: Take on an EMPTY STOMACH for best absorption; give with VITAMIN C (orange juice) to enhance absorption. If GI upset, may take with food (absorption slightly reduced).
• AVOID: milk, antacids, tea, coffee, and calcium supplements taken at the same time as iron — these inhibit absorption.
• Warn patients about BLACK/TARRY STOOLS (normal, harmless side effect) and constipation; liquid iron must be taken through a STRAW to prevent teeth staining.
• Parenteral iron (iron dextran, iron sucrose) for malabsorption or intolerance; IM iron given by Z-TRACK technique to prevent skin staining; give test dose for iron dextran and observe for ANAPHYLAXIS.
• ALWAYS investigate the SOURCE of blood loss — do not just treat the anemia without finding the cause, especially occult GI bleeding.

Definitions

Section Title

Iron-Deficiency Anemia

Common Mistakes

• Recommending iron with milk or antacids — these DECREASE iron absorption; always pair iron with vitamin C (ascorbic acid).
• Alarming the patient about black stools without explaining it is EXPECTED and HARMLESS — failure to warn leads to patient non-compliance when they see dark stools.
• Forgetting to investigate the CAUSE of iron deficiency — treating only with iron tablets without finding occult GI bleeding is incomplete nursing care.
• Administering IM iron without Z-track technique — this leads to skin tattooing and is a reportable medication error.
• Confusing iron sucrose with iron dextran — only IRON DEXTRAN requires a test dose for anaphylaxis; iron sucrose has a lower anaphylaxis risk but still requires monitoring.

Exam Tips

• NLE key distinction: BOTH B12 deficiency and folate deficiency cause macrocytic/megaloblastic anemia. But ONLY B12 deficiency causes NEUROLOGIC signs (paresthesias, ataxia). This is the most commonly tested differentiating point.
• If the question says 'pernicious anemia' → route must be IM (intramuscular) because oral B12 cannot be absorbed.
• Early treatment is critical — the more neurologic damage that occurs, the less reversible it becomes. NLE scenarios may ask about priority interventions; preventing further neurologic damage is a major goal.
• Remember: Pernicious anemia used to be called 'pernicious' because it was fatal before injectable B12 was discovered.

Key Points

• Pernicious anemia is an AUTOIMMUNE condition where the body destroys gastric parietal cells, causing LOSS OF INTRINSIC FACTOR (IF) production.
• Without intrinsic factor, vitamin B12 CANNOT be absorbed in the terminal ileum regardless of dietary intake.
• Other causes of B12 deficiency: gastrectomy (removal of parietal cells), ileal disease/resection, strict vegan diet (B12 is found only in animal products).
• B12 is needed for DNA synthesis and MYELIN SHEATH formation — deficiency impairs both RBC maturation AND neurologic function.
• Result: MACROCYTIC (large), MEGALOBLASTIC (immature, abnormal large cells) anemia.
• Key CBC findings: elevated MCV (>100 fL), HYPERSEGMENTED NEUTROPHILS (5+ lobes) on peripheral smear, low B12 level.
• UNIQUE clinical features of B12 deficiency NOT seen in folate deficiency: NEUROLOGIC SIGNS — paresthesias (numbness/tingling) of hands and feet, ataxia (unsteady gait), impaired proprioception, and if untreated, IRREVERSIBLE neurologic damage and dementia.
• Beefy red, sore, smooth glossitis is characteristic.
• The SCHILLING TEST historically confirmed pernicious anemia by measuring urinary excretion of radiolabeled oral B12 with and without added intrinsic factor — corrected absorption with IF added = confirms pernicious anemia. Now largely replaced by antibody testing (anti-intrinsic factor antibodies, anti-parietal cell antibodies).
• Treatment: LIFELONG intramuscular (IM) cyanocobalamin (vitamin B12) injections — because oral B12 cannot be absorbed without intrinsic factor.
• Loading doses: daily or weekly injections initially; then MONTHLY for life.
• CRITICAL teaching point: Treatment is LIFELONG. Stopping injections will cause relapse and potentially IRREVERSIBLE neurologic damage.

Definitions

Section Title

Pernicious Anemia and Vitamin B12 Deficiency

Common Mistakes

• Saying folate deficiency causes neurologic problems — FOLATE DEFICIENCY DOES NOT CAUSE NEUROLOGIC SIGNS. Only B12 deficiency causes paresthesias, ataxia, and dementia.
• Assuming oral B12 supplements will work in pernicious anemia — because the defect is ABSENT intrinsic factor (absorption problem), not dietary insufficiency; treatment must be PARENTERAL (IM).
• Forgetting that treatment is LIFELONG — students often say 'continue until B12 levels normalize'; this is wrong because the underlying autoimmune defect cannot be corrected.
• Confusing macrocytic anemia with sickle cell anemia — sickle cell produces NORMOCYTIC, not macrocytic, anemia.

Exam Tips

• NLE priority intervention for aplastic anemia with ANC < 500/µL: INFECTION PREVENTION is the priority using Maslow's Physiological and Safety hierarchy — infection can be rapidly fatal.
• Bleeding precautions for thrombocytopenia: soft-bristle toothbrush, electric razor, NO IM injections (use subcutaneous or IV routes), NO rectal temperature or suppositories, apply prolonged pressure to venipuncture sites.
• If a question asks about the CAUSE of aplastic anemia and lists chloramphenicol — this is correct; it is the most commonly tested drug-induced aplastic anemia example.
• The key difference between aplastic anemia and leukemia on a CBC: both can show low counts, but leukemia shows BLASTS (immature malignant cells) on smear, while aplastic anemia shows a hypocellular marrow with no abnormal cells.

Key Points

• Aplastic anemia is BONE MARROW FAILURE causing suppression of ALL blood cell lines (erythroid, myeloid, megakaryocyte series).
• Result: PANCYTOPENIA — simultaneous anemia, leukopenia, and thrombocytopenia.
• RBC morphology: NORMOCYTIC, NORMOCHROMIC (cells are normal size and color — the problem is that too FEW are being made, not abnormal cells).
• Common causes: IDIOPATHIC (most common — possibly autoimmune T-cell mediated destruction of stem cells), drugs/chemicals (chloramphenicol — a key NLE drug, benzene, chemotherapy), radiation, viral infections (EBV, hepatitis), autoimmune disorders.
• Chloramphenicol is the classic drug associated with aplastic anemia — important in the Philippine context as it is used in typhoid fever treatment.
• TRIPLE THREAT of manifestations (all from pancytopenia): 1) Anemia (fatigue, pallor, dyspnea); 2) Leukopenia (recurrent infections, fever); 3) Thrombocytopenia (petechiae, bleeding, ecchymoses).
• Diagnosis: CBC showing pancytopenia + BONE MARROW BIOPSY showing HYPOCELLULAR (fatty, empty) marrow.
• Management: (1) REMOVE the causative agent; (2) Supportive TRANSFUSIONS (packed RBCs for anemia, platelets for bleeding); (3) IMMUNOSUPPRESSIVE therapy (anti-thymocyte globulin/ATG + cyclosporine); (4) HEMATOPOIETIC STEM CELL TRANSPLANT (HSCT/bone marrow transplant) — the only curative treatment for eligible patients.
• Nursing priority: INFECTION PREVENTION (protective/reverse isolation, hand hygiene, monitor ANC and temperature) and BLEEDING PRECAUTIONS.

Definitions

Section Title

Aplastic Anemia

Common Mistakes

• Describing aplastic anemia cells as microcytic or macrocytic — aplastic anemia cells are NORMOCYTIC because the marrow is making fewer but morphologically NORMAL cells.
• Thinking only the anemia component requires management — ALWAYS address all three: anemia (transfuse), leukopenia (infection precautions), AND thrombocytopenia (bleeding precautions).
• Forgetting chloramphenicol as a causative drug — in the Philippine context, this is highly relevant because chloramphenicol is on the Philippine National Drug Formulary for typhoid fever.
• Confusing protective isolation (for the neutropenic patient) with contact isolation (for infectious patients) — in aplastic anemia, isolation protects the PATIENT from environmental pathogens, not the other way around.

Exam Tips

• Classic NLE scenario for hemolytic anemia: 'Patient has anemia WITH jaundice AND splenomegaly AND dark urine' = hemolytic anemia. The jaundice key differentiates it from other anemias.
• Sickle cell crisis priority interventions in order: (1) Hydration, (2) Oxygen, (3) Pain management (IV opioids), (4) Treat infection. Remember: 'HOPE' — Hydration, Oxygen, Pain control, Eradicate infection.
• Pre-splenectomy vaccines must be given BEFORE surgery — Pneumococcal, Meningococcal, and H. influenzae type B vaccines, because the spleen normally filters encapsulated bacteria.
• Folic acid supplementation in hemolytic anemia is important because rapid RBC turnover consumes large amounts of folate for DNA synthesis in the marrow.

Key Points

• Hemolytic anemia is caused by PREMATURE DESTRUCTION (hemolysis) of RBCs faster than the bone marrow can replace them.
• Causes: INHERITED (sickle cell disease, thalassemia, G6PD deficiency, hereditary spherocytosis) or ACQUIRED (autoimmune, transfusion reactions, drugs, mechanical heart valves).
• Key signs of hemolysis: JAUNDICE (elevated indirect/unconjugated bilirubin from Hgb breakdown), DARK URINE (hemoglobinuria), SPLENOMEGALY (spleen overworked filtering destroyed cells), elevated LDH, LOW HAPTOGLOBIN.
• HIGH RETICULOCYTE COUNT (marrow is compensating by releasing immature cells rapidly).
• POSITIVE DIRECT COOMBS TEST confirms immune-mediated (autoimmune) hemolysis.
• SICKLE CELL DISEASE: inherited autosomal recessive hemoglobinopathy; abnormal hemoglobin S (HbS) causes RBCs to SICKLE (become crescent-shaped) under deoxygenated conditions.
• Sickling triggers: HYPOXIA, DEHYDRATION, INFECTION, ACIDOSIS, COLD TEMPERATURES, physical stress.
• VASO-OCCLUSIVE CRISIS (most common type): sickled cells obstruct small blood vessels → severe bone pain (often in arms, legs, back, chest), organ infarction.
• Management of sickle cell crisis: HYDRATION (IV fluids to prevent sickling), OXYGEN (to relieve hypoxia), PAIN CONTROL (IV opioids — morphine is first-line), TREAT INFECTION (precipitating factor), BED REST and warmth.
• HYDROXYUREA: the primary disease-modifying drug for sickle cell; increases fetal hemoglobin (HbF) production, which does not sickle, reducing crisis frequency.
• General management of hemolytic anemia: treat the cause, FOLIC ACID supplementation (high marrow turnover increases folate demand), transfusions as needed, SPLENECTOMY in some cases (with pre-splenectomy vaccination against Streptococcus pneumoniae, H. influenzae, N. meningitidis).
• Long-term complications of sickle cell disease: cholelithiasis (pigment gallstones), aplastic crisis (triggered by parvovirus B19), chronic organ damage (kidneys, eyes, lungs), and with chronic transfusion therapy — iron overload.

Definitions

Section Title

Hemolytic Anemia and Sickle Cell Disease

Common Mistakes

• Saying hemolytic anemia shows low reticulocytes — hemolytic anemia shows HIGH reticulocytes because the marrow is actively responding. Low retics = marrow failure (aplastic anemia).
• Forgetting to give OXYGEN in sickle cell crisis — hypoxia perpetuates sickling; oxygen is a critical nursing intervention along with hydration.
• Overlooking HYDRATION as a priority in sickle cell crisis — IV fluids reduce blood viscosity and help unsickle cells by improving oxygenation. Ask Filipino patients about fluid intake habits, especially during hot weather.
• Confusing hemolytic jaundice (indirect/unconjugated bilirubin elevated) with obstructive jaundice (direct/conjugated bilirubin elevated) — in hemolysis, the liver has NOT conjugated the excess bilirubin yet, so INDIRECT bilirubin is elevated.

Exam Tips

• Maslow prioritization on NLE: Physiological needs first (oxygen/gas exchange), then Safety (infection/bleeding), then Psychological needs (fear, knowledge deficit). Apply this when choosing 'priority nursing action' in multiple-choice questions.
• When an NLE question asks the FIRST nursing action when a transfusion reaction is suspected: STOP the transfusion IMMEDIATELY, then maintain IV access with normal saline, notify the physician, and monitor vital signs.
• Dietary teaching for Filipino patients: recommend locally available iron-rich foods like malunggay (moringa), kangkong (water spinach), liver, and legumes; for B12, emphasize animal products; for folate, recommend vegetables and fortified rice.
• RA 9173 reference: Section 28 outlines the scope of nursing practice including health teaching and administration of medications — nurses have both a legal and professional responsibility for all the teaching points above.

Key Points

• Apply the NURSING PROCESS systematically; use NANDA-approved nursing diagnoses prioritized by Maslow's Hierarchy.
• Priority NANDA nursing diagnoses in anemia: (1) Activity Intolerance r/t tissue hypoxia AEB fatigue and dyspnea on exertion; (2) Impaired Gas Exchange r/t decreased oxygen-carrying capacity; (3) Risk for Infection (aplastic anemia/neutropenia); (4) Risk for Bleeding/Ineffective Protection (thrombocytopenia); (5) Imbalanced Nutrition: Less than Body Requirements (iron/B12/folate deficiency).
• ACTIVITY MANAGEMENT: Balance activity with rest; cluster nursing care to conserve patient energy; encourage gradual increase in activity as tolerated; assess and document activity tolerance.
• OXYGEN THERAPY: Administer supplemental oxygen for symptomatic hypoxia (SpO2 <90% or severe dyspnea); monitor continuously in severe anemia.
• INFECTION PRECAUTIONS for neutropenic patients (ANC <500): Protective (reverse) isolation, strict hand hygiene by all staff and visitors, restrict visitors with active infections, monitor temperature q4h (fever >38°C is a medical emergency in neutropenia), avoid live plants and fresh flowers (harbor mold/bacteria).
• BLEEDING PRECAUTIONS for thrombocytopenic patients: Soft-bristle toothbrush, electric razor for shaving, avoid IM injections and rectal temperatures/suppositories, minimize venipunctures, apply prolonged pressure (5–10 min) to all puncture sites, pad side rails for fall prevention.
• MEDICATION ADMINISTRATION: Administer prescribed hematinics (iron, B12, folate), growth factors (EPO, G-CSF), or transfusions per physician orders and monitor response.
• DIETARY TEACHING: Iron sources (red meat, organ meats, dark leafy vegetables like kangkong/malunggay, legumes, fortified cereals); B12 sources (animal products: meat, fish, eggs, dairy); folate sources (green leafy vegetables, citrus, legumes, fortified grains).
• TRANSFUSION MONITORING: Monitor vital signs before, 15 minutes after start, and every hour during transfusion; stop immediately and notify physician if fever, chills, back pain, flushing, or hypotension (signs of hemolytic transfusion reaction).
• Under RA 9173, nurses are legally and professionally responsible for safe medication administration, accurate assessment, and patient education — all critical competencies in hematologic nursing.

Definitions

Section Title

Nursing Management: Priority Interventions and Patient Teaching

Common Mistakes

• Prioritizing comfort over safety in neutropenic patients — fever in a neutropenic patient is a MEDICAL EMERGENCY requiring immediate blood cultures and IV antibiotics, not just comfort measures.
• Taking rectal temperature in thrombocytopenic patients — rectal manipulation can cause rectal bleeding; use axillary or tympanic route instead.
• Giving IM injections without considering platelet count — below 50,000/µL, IM injections pose significant hematoma risk; use IV or oral routes whenever possible.
• Forgetting to teach patients about food-drug interactions for iron supplements — specifically that iron must NOT be taken with calcium (milk), antacids, or tannins (tea, coffee).