NLE Hematologic Nursing — Hematologic Assessment and the AnemiasDetailed Explanation

Overview of the Hematologic System and Hematopoiesis

Blood is a specialized connective tissue made up of plasma (the liquid portion, about 55%) and formed elements (cells and cell fragments, about 45%). All blood cells originate in the red bone marrow through a process called hematopoiesis. Think of the bone marrow as a 'blood cell factory' that continuously produces cells under the regulation of hormones and growth factors. The three main formed elements are: 1. ERYTHROCYTES (Red Blood Cells / RBCs): The most numerous cells in blood. Their primary job is to carry oxygen from the lungs to all body tissues using a protein called hemoglobin (Hgb). Each hemoglobin molecule contains iron — this is why iron is so critical for oxygen transport. RBCs are produced in response to erythropoietin (EPO), a hormone secreted by the kidneys when they detect low oxygen levels (hypoxia). RBCs live approximately 120 days. Aged and damaged RBCs are filtered and destroyed by the spleen. 2. LEUKOCYTES (White Blood Cells / WBCs): The immune system's soldiers. There are five types: neutrophils (most numerous, fight bacteria), lymphocytes (fight viruses, produce antibodies), monocytes (become macrophages, clean up debris), eosinophils (fight parasites and allergic reactions), and basophils (involved in allergic responses). Normal WBC count: 5,000–10,000/µL. 3. THROMBOCYTES (Platelets): Tiny cell fragments that initiate clot formation when a blood vessel is injured. Normal range: 150,000–400,000/µL. Key organs involved: - BONE MARROW: Site of hematopoiesis (blood cell production). - SPLEEN: Filters aged RBCs, stores about one-third of the body's platelets, and is part of the immune system. - LIVER: Produces most clotting factors (fibrinogen, prothrombin, and others); stores vitamin B12, iron, and folate.

Hematologic Assessment: History and Physical Examination

As a nurse, your first step in any hematologic problem is a thorough assessment. The nursing process begins with data collection — always use a systematic, head-to-toe approach. HEALTH HISTORY (Subjective Data): Ask the patient about: - Fatigue, weakness, and decreased exercise tolerance (tissue hypoxia from anemia) - Dyspnea on exertion and palpitations (compensatory cardiac response) - Dizziness, headache, and difficulty concentrating (cerebral hypoxia) - Bleeding: heavy menstrual periods, blood in stool or urine, easy bruising, nosebleeds - Recurrent infections (neutropenia risk) - Diet history: iron-rich foods, B12 sources (animal products), folate sources (green vegetables) - Medications: anticoagulants (warfarin, heparin), NSAIDs (GI bleeding), chemotherapy, chloramphenicol (bone marrow toxicity) - Family history: sickle cell disease, thalassemia, G6PD deficiency — common in the Philippines among Visayans, Bicolanos, and other groups - Past medical history: gastrectomy (no intrinsic factor = B12 malabsorption), chronic kidney disease, malabsorption syndromes PHYSICAL ASSESSMENT (Objective Data): Assess by body system: Skin and Mucous Membranes: - PALLOR: Best assessed in the conjunctiva (inner lower eyelid), nail beds, palms, and oral mucosa — these sites are reliable in all skin tones including dark-skinned Filipino patients - JAUNDICE: Yellow discoloration of sclera and skin — seen in hemolytic anemia (excess bilirubin from RBC breakdown) - PETECHIAE: Pinpoint red dots on skin — thrombocytopenia - PURPURA and ECCHYMOSES: Larger areas of bruising — coagulopathy or thrombocytopenia Nails: - KOILONYCHIA (spoon nails): The nail becomes concave/spoon-shaped — classic sign of chronic iron-deficiency anemia Mouth and Tongue: - GLOSSITIS: Smooth, beefy-red, sore tongue — seen in iron deficiency AND pernicious anemia (B12 deficiency) - ANGULAR CHEILITIS: Cracking at the corners of the mouth — iron deficiency - BLEEDING GUMS: Thrombocytopenia Cardiovascular: - TACHYCARDIA: Heart beats faster to compensate for reduced oxygen-carrying capacity - SYSTOLIC FLOW MURMUR: Turbulent blood flow due to decreased blood viscosity in anemia - BOUNDING PULSE: Hyperdynamic circulation Respiratory: - TACHYPNEA and DYSPNEA: Compensatory increase in breathing to deliver more oxygen Neurologic: - PARESTHESIAS (tingling/numbness of hands and feet), ATAXIA, impaired balance and proprioception: SPECIFIC to B12 (pernicious anemia) — NOT seen in iron deficiency or folate deficiency alone Abdomen: - SPLENOMEGALY: Enlarged spleen — hemolysis, lymphoma, portal hypertension - HEPATOMEGALY: Liver enlargement — liver disease, heart failure, malignancy - LYMPHADENOPATHY: Enlarged lymph nodes — infection or malignancy

Interpreting the Complete Blood Count (CBC)

The Complete Blood Count (CBC) is the single most important hematologic laboratory test in nursing practice. Every nurse must be able to identify abnormal values and understand what they mean clinically. NORMAL CBC VALUES (Memorize These for NLE): | Parameter | Normal Range | Clinical Significance | |---|---|---| | Hgb (male) | 13–18 g/dL | Oxygen-carrying capacity | | Hgb (female) | 12–16 g/dL | Lower due to menstruation | | Hct (male) | 42–52% | Roughly 3× the Hgb value | | Hct (female) | 37–47% | | | RBC count | 4.2–6.1 million/µL | | | WBC count | 5,000–10,000/µL | Immune function | | Platelets | 150,000–400,000/µL | Clotting initiation | | MCV | 80–100 fL | Cell size (classify anemia) | | Reticulocytes | 0.5–2% | Marrow response | THE 3× RULE: Hematocrit is approximately 3× the hemoglobin value. So Hgb 10 g/dL → Hct ~30%. This is a quick bedside calculation. USING MCV TO CLASSIFY ANEMIA: MCV (Mean Corpuscular Volume) tells you the average size of RBCs: - MCV < 80 fL = MICROCYTIC (small cells) → Think: Iron deficiency, thalassemia - MCV 80–100 fL = NORMOCYTIC (normal size) → Think: Aplastic anemia, acute blood loss, anemia of chronic disease - MCV > 100 fL = MACROCYTIC (large cells) → Think: B12 deficiency (pernicious), folate deficiency This classification is the FIRST STEP in differentiating anemias. RETICULOCYTE COUNT — The Marrow Response Indicator: Reticulocytes are immature RBCs released from the bone marrow. They indicate how hard the marrow is working: - HIGH reticulocyte count (> 2%): Marrow is responding — seen in blood loss, hemolytic anemia (marrow compensating) - LOW reticulocyte count (< 0.5%): Marrow is NOT responding — seen in aplastic anemia (marrow failure), iron/B12/folate deficiency (nutritional supply problem) WBC DIFFERENTIAL AND ABSOLUTE NEUTROPHIL COUNT (ANC): - NEUTROPHILS (normal: 55–70% of WBCs) are the primary defense against bacteria - A 'LEFT SHIFT' means there are increased immature neutrophils (bands) in circulation — this indicates acute bacterial infection - ANC < 500/µL = SEVERE NEUTROPENIA — extremely high risk for life-threatening infection; requires protective/reverse isolation - ANC calculation: Total WBC × % neutrophils (segs + bands) SERUM FERRITIN AND TIBC (Iron Studies): - SERUM FERRITIN: Best single test for iron stores. Low ferritin = depleted iron stores = iron deficiency - TIBC (Total Iron-Binding Capacity): Measures transferrin's ability to bind iron. When iron stores are low, the body makes MORE transferrin to capture any available iron → TIBC goes HIGH - In iron deficiency: Low ferritin + Low serum iron + HIGH TIBC PERIPHERAL BLOOD SMEAR: A microscopic examination of RBC morphology: - Hypochromic microcytes = iron deficiency - Macro-ovalocytes + hypersegmented neutrophils = B12/folate deficiency - Sickle-shaped cells = sickle cell disease - Blasts (immature WBCs) = leukemia

Blood Typing and Transfusion Compatibility

Before any blood transfusion, the nurse must understand ABO and Rh blood group systems to prevent potentially fatal transfusion reactions. This is also a commonly tested NLE topic. ABO BLOOD GROUP SYSTEM: RBCs carry antigens (proteins) on their surface. The immune system produces antibodies AGAINST antigens it does NOT have. If incompatible blood is transfused, the antibodies attack the transfused RBCs, causing an acute hemolytic transfusion reaction — a medical emergency. | Blood Type | Antigens on RBC | Antibodies in Plasma | Can Receive From | Can Donate To | |---|---|---|---|---| | A | A antigen | Anti-B antibody | A, O | A, AB | | B | B antigen | Anti-A antibody | B, O | B, AB | | AB | A and B antigens | NONE | A, B, AB, O (universal recipient) | AB only | | O | NONE | Anti-A and Anti-B | O only | A, B, AB, O (universal donor) | MEMORY TIP: AB = 'ALL BLOOD accepted' (universal recipient). O = 'Only O' can donate or receive from itself for RBC concentrates, but O-negative is the universal donor. Rh FACTOR: - The Rh factor is another antigen on RBCs — most important is the D antigen. - Rh-POSITIVE (Rh+): RBCs carry the D antigen (about 85% of people) - Rh-NEGATIVE (Rh-): RBCs do NOT carry the D antigen - Unlike ABO antibodies, Rh-negative individuals do NOT automatically have anti-D antibodies. They only form anti-D AFTER being EXPOSED to Rh-positive blood (via transfusion or pregnancy). - CLINICAL IMPORTANCE: An Rh-negative mother carrying an Rh-positive fetus → mother forms anti-D after delivery → in subsequent pregnancies, anti-D crosses the placenta and destroys fetal RBCs → HEMOLYTIC DISEASE OF THE NEWBORN (HDN). Prevent with RhoGAM (anti-D immunoglobulin) at 28 weeks and within 72 hours after delivery. UNIVERSAL DONOR AND RECIPIENT: - TYPE O-NEGATIVE = Universal Donor: Has NO A, B, or D antigens → can be given to anyone without triggering a reaction. Used in emergency/trauma before crossmatch is available. - TYPE AB-POSITIVE = Universal Recipient: Has A, B, and D antigens → has NO anti-A, anti-B, or anti-D antibodies in plasma → can receive any blood type. PRE-TRANSFUSION TESTING: 1. TYPE AND CROSSMATCH: Determines patient's ABO/Rh type and tests patient's serum against donor RBCs for compatibility. This is the standard pre-transfusion test. 2. COOMBS (ANTIGLOBULIN) TEST: - DIRECT COOMBS (DCT): Tests the patient's OWN RBCs for antibodies already attached to them. Positive = autoimmune hemolytic anemia or hemolytic transfusion reaction. - INDIRECT COOMBS (ICT): Tests the patient's SERUM for free antibodies against donor RBCs. Used in crossmatching and prenatal screening. NURSING RESPONSIBILITIES DURING TRANSFUSION: 1. Check physician's order and patient consent 2. Verify blood type, unit number, expiration date with TWO nurses at the bedside 3. Use ONLY 0.9% NaCl (normal saline) with blood — never D5W or lactated Ringer's (can cause hemolysis or clotting) 4. Use blood administration set with in-line filter (170–260 micron) 5. Infuse PRBCs within 4 hours of removal from refrigerator 6. STAY AT BEDSIDE for the FIRST 15 MINUTES — most severe reactions (acute hemolytic, anaphylactic) occur early 7. Vital signs: baseline, then 15 min after start, then per protocol 8. TRANSFUSION REACTION SIGNS: fever, chills, back/flank pain, hives, dyspnea, hypotension, hemoglobinuria (dark/red urine) 9. If reaction suspected: STOP transfusion immediately, keep IV line open with NS, notify physician, send unit and blood samples to blood bank

Iron-Deficiency Anemia

Iron-deficiency anemia (IDA) is the MOST COMMON anemia worldwide and the most common nutritional deficiency in the Philippines, particularly among women of reproductive age, pregnant women, infants, and toddlers. It is a primary focus of the Philippine National Nutrition Council and DOH programs. PATHOPHYSIOLOGY: Iron is essential for hemoglobin synthesis — specifically, iron is part of the heme group that carries oxygen. When iron stores become depleted, hemoglobin production decreases. The bone marrow produces smaller, paler RBCs (microcytic, hypochromic). This is why IDA classically produces a LOW MCV and LOW MCH (mean corpuscular hemoglobin) on CBC. CAUSES (from most to least common in adults): 1. CHRONIC BLOOD LOSS: The #1 cause in adults - Heavy menstruation (menorrhagia) — most common in women of reproductive age in the Philippines - GI bleeding: peptic ulcer disease, esophageal varices, colorectal cancer (IMPORTANT — always investigate occult GI bleeding in adults, especially men and postmenopausal women) - Other: hematuria, repeated phlebotomy 2. INADEQUATE DIETARY INTAKE: Common in infants, toddlers, and poverty-affected communities 3. MALABSORPTION: Celiac disease, gastrectomy, bariatric surgery 4. INCREASED DEMAND: Pregnancy, infancy, rapid growth in adolescence CLINICAL MANIFESTATIONS: General anemia signs: fatigue, pallor, tachycardia, dyspnea SPECIFIC to IDA: - KOILONYCHIA: Spoon-shaped nails (nails become concave) - GLOSSITIS: Smooth, sore tongue - ANGULAR CHEILITIS: Cracks at corners of mouth - PICA: Craving for non-food items, especially ice (pagophagia), dirt, clay — ask Filipino patients directly - RESTLESS LEG SYNDROME: Uncomfortable urge to move legs at night LABORATORY FINDINGS: - LOW Hgb and Hct - LOW MCV (< 80 fL) — microcytic - LOW serum ferritin (MOST SENSITIVE early indicator of iron depletion) - LOW serum iron - HIGH TIBC (body makes more transferrin to capture scarce iron) - Peripheral smear: small, pale RBCs (hypochromic microcytes) - LOW reticulocyte count (marrow cannot produce RBCs without iron) MANAGEMENT — ORAL IRON THERAPY: First-line treatment. Key nursing teaching points: 1. PREPARATION: Ferrous sulfate 325 mg (65 mg elemental iron) — 1–3 times daily 2. TIMING: Take on an EMPTY STOMACH for best absorption (1 hour before meals or 2 hours after) 3. VITAMIN C ENHANCES ABSORPTION: Take with orange juice (orange juice / kalamansi juice) — vitamin C reduces iron to its absorbable ferrous form 4. AVOID: Milk, antacids, calcium supplements, tea, coffee, and high-fiber foods at the same time — these INHIBIT iron absorption 5. SIDE EFFECTS: Black/dark tarry stools (harmless but alarming), constipation (encourage high-fiber diet and fluids), GI upset/nausea (take with small amount of food if severe, though this reduces absorption) 6. LIQUID IRON: Give through a STRAW to prevent teeth staining; rinse mouth after 7. DURATION: Continue for 3–6 months AFTER Hgb normalizes — to replenish iron stores MANAGEMENT — PARENTERAL IRON: Used when oral iron fails, is poorly tolerated, or malabsorption is present. - Types: Iron dextran (IV/IM), iron sucrose (IV), ferric gluconate (IV) - IM injection: Z-TRACK TECHNIQUE — use a 2–3 inch needle, pull skin 1–2 inches laterally, inject slowly, release skin, do NOT massage — this prevents skin staining and tissue irritation - Iron dextran IV: ALWAYS give a test dose first (0.5 mL over 30 minutes) and monitor for ANAPHYLAXIS for 30–60 minutes after; have epinephrine and resuscitation equipment ready - Do NOT massage the injection site after IM iron INVESTIGATE THE CAUSE: In adults (especially men and postmenopausal women), ALWAYS investigate GI bleeding as the source — fecal occult blood test, endoscopy if indicated. Do not just treat the anemia — find and treat the source.

Pernicious Anemia and Vitamin B12 Deficiency

Pernicious anemia is a specific type of Vitamin B12 deficiency caused by an autoimmune destruction of gastric parietal cells, leading to loss of INTRINSIC FACTOR — a protein produced by parietal cells that is required for B12 absorption in the terminal ileum. Without intrinsic factor, no matter how much B12 the patient eats, it cannot be absorbed. PATHOPHYSIOLOGY: Vitamin B12 (cobalamin) is essential for: 1. DNA SYNTHESIS: B12 is required for normal cell division. Without it, cells (especially rapidly dividing bone marrow cells) cannot divide properly — they grow large but cannot split normally, producing MEGALOBLASTS (abnormally large, immature RBCs) 2. MYELIN SYNTHESIS: B12 is required to maintain myelin sheaths around nerve fibers. Deficiency causes PROGRESSIVE DEMYELINATION — explaining the neurologic manifestations CAUSES OF B12 DEFICIENCY: - PERNICIOUS ANEMIA: Autoimmune destruction of parietal cells → no intrinsic factor → no B12 absorption (most common cause in the elderly) - GASTRECTOMY or GASTRIC BYPASS: Surgical removal of parietal cells - ILEAL DISEASE (Crohn's disease, ileal resection): Damages the site of B12 absorption - STRICT VEGAN DIET: B12 is found ONLY in animal products (meat, fish, dairy, eggs) — vegans who do not supplement are at risk (note: this is not 'pernicious anemia' — this is dietary B12 deficiency) CLINICAL MANIFESTATIONS: General anemia signs: fatigue, pallor, dyspnea SPECIFIC to B12/pernicious anemia: - GLOSSITIS: Smooth, beefy-red, sore tongue (similar to iron deficiency, but larger cells) - NEUROLOGIC SIGNS (the key distinguishing feature!): - Paresthesias: Tingling, numbness of hands and feet (like pins and needles) - Ataxia: Unsteady gait, difficulty walking - Impaired proprioception: Cannot feel position of limbs with eyes closed - Impaired vibration sense: Cannot feel tuning fork vibration - If SEVERE: Spasticity, weakness, DEMENTIA, psychosis ('megaloblastic madness') - These neurologic signs are IRREVERSIBLE if B12 deficiency is prolonged — this is why EARLY TREATMENT is critical DIFFERENCE FROM FOLATE DEFICIENCY: Folate deficiency ALSO causes macrocytic/megaloblastic anemia with the same hematologic picture, BUT: - Folate deficiency does NOT cause neurologic signs (no demyelination) - IMPORTANT CLINICAL DISTINCTION: If you give folate to a patient with B12 deficiency (misdiagnosing as folate deficiency), the blood picture improves but the neurologic damage CONTINUES — potentially causing permanent harm. ALWAYS check B12 levels before treating with folate alone. DIAGNOSTIC TESTS: - CBC: Low Hgb, MCV > 100 fL (macrocytic) - Peripheral smear: MACRO-OVALOCYTES (large oval-shaped RBCs) and HYPERSEGMENTED NEUTROPHILS (neutrophils with 5+ lobes — pathognomonic finding) - Low serum B12 level - SCHILLING TEST (historical): Administered radiolabeled oral B12, measured urinary excretion. If absorption improved when intrinsic factor was added → pernicious anemia confirmed. Now largely replaced by anti-intrinsic factor antibodies and anti-parietal cell antibodies testing. - Anti-intrinsic factor antibody: Positive in most cases of pernicious anemia (highly specific) MANAGEMENT: - PERNICIOUS ANEMIA: LIFELONG IM Vitamin B12 (cyanocobalamin) injections - Initial phase: Daily or weekly injections for 1–2 weeks (loading phase) - Maintenance: Once monthly IM injection (for life) - Since the problem is ABSORPTION, oral B12 will NOT work in pernicious anemia — the route MUST be parenteral (IM) - Exception: Very high-dose oral B12 (1,000–2,000 µg/day) can achieve small amounts of passive absorption even without intrinsic factor — used in some cases - DIETARY B12 DEFICIENCY (vegans): Oral B12 supplementation is effective - EARLY TREATMENT is critical — neurologic damage may be partially or fully irreversible; the anemia recovers faster than the neurologic damage - Patient teaching: Emphasize treatment is LIFELONG; stopping injections leads to recurrence and worsening neurologic damage

Aplastic Anemia

Aplastic anemia is a serious, potentially life-threatening condition in which the bone marrow fails to produce enough blood cells of ALL THREE types — RBCs, WBCs, AND platelets. This is called PANCYTOPENIA. The bone marrow becomes hypocellular (mostly fat, with very few blood-forming cells), hence the term 'aplastic' (without formation). PATHOPHYSIOLOGY: In most cases, the immune system (autoreactive T-lymphocytes) attacks and destroys the hematopoietic stem cells in the bone marrow. Without stem cells, the 'blood cell factory' shuts down. Since ALL cell lines are affected, the patient suffers simultaneously from: 1. Anemia (low RBCs) — fatigue, pallor, dyspnea 2. Leukopenia (low WBCs) — recurrent, severe infections 3. Thrombocytopenia (low platelets) — bleeding, petechiae, ecchymoses CAUSES: - IDIOPATHIC: Unknown cause — the most common (about 70% of cases) - DRUGS AND CHEMICALS: - CHLORAMPHENICOL (an antibiotic still used in some developing settings) — most classic drug cause - BENZENE (industrial solvent) — occupational exposure - Chemotherapy and radiation therapy - Some NSAIDs, sulfonamides, anticonvulsants (phenytoin, carbamazepine) - VIRAL INFECTIONS: Hepatitis, Epstein-Barr virus (EBV), CMV, parvovirus B19 - AUTOIMMUNE: Associated with lupus, rheumatoid arthritis - RADIATION EXPOSURE CLINICAL MANIFESTATIONS: Since all three cell lines are affected, think of THREE SETS of symptoms: 1. From ANEMIA: Fatigue, pallor, weakness, dyspnea, tachycardia 2. From LEUKOPENIA: Recurrent bacterial/fungal infections; fever; frequent mouth ulcers (candidiasis); pneumonia 3. From THROMBOCYTOPENIA: Petechiae (pinpoint red dots); purpura (larger purple bruising); ecchymoses; bleeding from gums, nose, and GI tract; prolonged bleeding from minor cuts The RBCs that ARE produced are normocytic and normochromic (normal size and color) — because the problem is QUANTITY, not quality. DIAGNOSIS: - CBC: PANCYTOPENIA — low Hgb, low WBC, low platelets, all three lines affected - MCV: Normal (normocytic, normochromic anemia) - LOW reticulocyte count — the marrow is not responding - BONE MARROW BIOPSY (definitive test): Shows HYPOCELLULAR marrow — mostly fat cells, very few or absent hematopoietic cells MANAGEMENT: 1. REMOVE THE CAUSATIVE AGENT: Stop the offending drug or remove exposure to chemicals/radiation — this may allow marrow recovery 2. SUPPORTIVE TRANSFUSIONS: - Packed RBCs for symptomatic anemia - Platelet transfusions for bleeding when platelets < 20,000/µL - WBCs cannot be transfused effectively — use other means 3. IMMUNOSUPPRESSIVE THERAPY: For patients who are not candidates for stem cell transplant - Anti-thymocyte globulin (ATG) + Cyclosporine — suppresses the autoreactive T-cells attacking the marrow - Eltrombopag — thrombopoietin receptor agonist (stimulates platelet production) 4. HEMATOPOIETIC STEM CELL TRANSPLANT (HSCT) / BONE MARROW TRANSPLANT: THE ONLY POTENTIAL CURE for eligible patients (typically younger patients with a matched donor); under the PhilHealth Z-benefit package in the Philippines NURSING PRIORITIES (using NANDA and Maslow): 1. PHYSIOLOGIC (Maslow Tier 1): Oxygenation — monitor and manage anemia 2. SAFETY (Maslow Tier 2): - INFECTION PREVENTION (highest priority in neutropenia): - PROTECTIVE/REVERSE ISOLATION (private room, HEPA filter, mask for visitors) - Strict hand hygiene (most important infection prevention measure) - Avoid fresh flowers, plants, and raw fruits/vegetables in the room - Monitor temperature — fever ≥ 38.3°C in a neutropenic patient is a MEDICAL EMERGENCY - Administer prescribed prophylactic antibiotics, antifungals - BLEEDING PRECAUTIONS (thrombocytopenia): - Soft-bristle toothbrush - Electric razor (no straight razors) - Avoid IM injections when possible; if necessary, apply prolonged pressure - No rectal temperatures, suppositories, or enemas - Handle patient gently; padded side rails - Apply pressure for 5–10 minutes after any venipuncture

Hemolytic Anemia

Hemolytic anemia occurs when RBCs are destroyed PREMATURELY — faster than the bone marrow can replace them. The 'blood cell factory' (bone marrow) works overtime (high reticulocyte count), but cannot keep up with the destruction. CAUSES — Two Major Categories: A. INHERITED / INTRINSIC (defect IN the RBC): - SICKLE CELL DISEASE (HbS): RBCs sickle under hypoxia/stress and get destroyed - THALASSEMIA (Alpha or Beta): Defective hemoglobin chains; RBCs are fragile and destroyed early - G6PD DEFICIENCY: Enzyme deficiency making RBCs vulnerable to oxidative stress (triggered by certain medications, infections, or fava beans); prevalent in certain Filipino ethnic groups - HEREDITARY SPHEROCYTOSIS: RBCs are sphere-shaped instead of biconcave; trapped and destroyed in the spleen B. ACQUIRED / EXTRINSIC (something OUTSIDE the RBC destroys it): - AUTOIMMUNE HEMOLYTIC ANEMIA (AIHA): Antibodies attack the patient's own RBCs (positive direct Coombs test) - TRANSFUSION REACTIONS: Incompatible blood transfusion → acute hemolysis - DRUGS: Certain antibiotics (dapsone, penicillin), antimalarials - INFECTIONS: Malaria (Plasmodium directly infects and destroys RBCs — highly relevant in Philippine endemic areas) - MECHANICAL: Prosthetic heart valves shear RBCs PATHOPHYSIOLOGY — What Happens When RBCs Are Destroyed: When RBCs are lysed, hemoglobin is released and broken down: - Hemoglobin → BILIRUBIN (indirect/unconjugated) → excreted by the liver - Excess indirect bilirubin causes JAUNDICE (icterus) - Hemoglobin in the blood binds to HAPTOGLOBIN → haptoglobin levels FALL (low haptoglobin = hemolysis marker) - Excess free hemoglobin in blood → excreted in urine as HEMOGLOBINURIA (dark/reddish-brown urine) - The enzyme LDH (lactate dehydrogenase) is released from destroyed RBCs → ELEVATED LDH - Chronic bilirubin overload → PIGMENT GALLSTONES (cholelithiasis) - Spleen works overtime filtering damaged RBCs → SPLENOMEGALY CLINICAL MANIFESTATIONS: General anemia signs + HEMOLYSIS-SPECIFIC signs: - JAUNDICE (yellow skin, scleral icterus) — elevated indirect bilirubin - DARK URINE (hemoglobinuria) — hemoglobin in urine - SPLENOMEGALY — enlarged spleen from increased filtering - ELEVATED INDIRECT BILIRUBIN and ELEVATED LDH - LOW HAPTOGLOBIN - HIGH RETICULOCYTE COUNT — marrow responding to RBC loss - Positive DIRECT COOMBS TEST (in immune-mediated hemolysis) SICKLE CELL DISEASE — Special Focus: Sickle cell disease (SCD) is an inherited hemoglobinopathy in which the hemoglobin S (HbS) gene causes RBCs to deform into a crescent/sickle shape under low oxygen conditions. TRIGGERS OF SICKLING (Vaso-occlusive Crisis): - HYPOXIA (low altitude exposure, respiratory illness) - DEHYDRATION (the most preventable trigger — emphasize hydration) - INFECTION (triggers hypoxia and inflammation) - COLD TEMPERATURE (causes vasoconstriction, reduces O2 to tissues) - ACIDOSIS - Physical or emotional STRESS COMPLICATIONS: - VASO-OCCLUSIVE (PAIN) CRISIS: Sickled cells block capillaries → ischemia → severe pain in bones, joints, and organs; dactylitis (hand-foot syndrome) in young children - ACUTE CHEST SYNDROME: Vaso-occlusion in pulmonary vasculature → chest pain, fever, respiratory distress — can be fatal - STROKE: Cerebral vaso-occlusion - SPLENIC SEQUESTRATION CRISIS: Sudden trapping of blood in the spleen — can cause hypovolemic shock - APLASTIC CRISIS: Parvovirus B19 infection temporarily stops RBC production — severe anemia - CHRONIC ORGAN DAMAGE: Kidneys (renal failure), eyes (retinopathy), heart, liver - CHOLELITHIASIS: Pigment gallstones from chronic hemolysis - IRON OVERLOAD: From chronic transfusions MANAGEMENT OF VASO-OCCLUSIVE CRISIS: 1. HYDRATION: IV fluids (NS or LR) at high rates — dilutes blood, reduces viscosity, and improves flow through capillaries. PRIORITY intervention. 2. OXYGEN: Via face mask/nasal cannula — reverses hypoxia that triggers further sickling 3. PAIN MANAGEMENT: IV opioids (morphine, oxycodone) — sickle cell crises cause SEVERE pain; do not undertreat 4. TREAT THE PRECIPITANT: Antibiotics for infection; warming measures for cold exposure 5. BLOOD TRANSFUSION: In severe anemia, acute chest syndrome, stroke 6. HYDROXYUREA: Oral medication that increases FETAL HEMOGLOBIN (HbF) production — HbF does not sickle, so increasing HbF reduces crisis frequency and severity. Used for PREVENTION. PATIENT TEACHING for Sickle Cell Disease: - HYDRATION: Drink 8–10 glasses of water daily; carry water at all times - AVOID TRIGGERS: Cold environments, high altitude travel (airplanes, mountains), strenuous exercise without adequate hydration - INFECTION PREVENTION: Vaccination (pneumococcal, meningococcal, influenza, Haemophilus influenzae); daily penicillin prophylaxis in young children - RECOGNIZE COMPLICATIONS: Teach to seek care for fever, chest pain, severe pain, neurologic changes

STEP-BY-STEP ANALYSIS: (1) Classify the anemia using MCV: 72 fL < 80 fL = MICROCYTIC → think iron deficiency or thalassemia. (2) Confirm with iron studies: LOW ferritin (depleted stores) + HIGH TIBC (body making more transferrin to catch scarce iron) = IRON DEFICIENCY CONFIRMED. (3) Identify cause: heavy periods (menorrhagia) = chronic blood loss = most common cause in women of reproductive age. Also assess for GI bleeding as a secondary cause. (4) Priority nursing diagnosis under NANDA: 'Activity intolerance' is appropriate because Hgb 9.5 g/dL reduces oxygen delivery to tissues, causing fatigue. However, if dyspnea at rest or tachycardia ≥ 120 bpm is present, consider 'Impaired gas exchange' as higher priority. Teaching: iron absorption optimization is the key patient education intervention.

This patient has DIETARY B12 DEFICIENCY (not pernicious anemia, since he is vegan and presumably has intact gastric function). Key indicators: MCV > 100 (macrocytic), low serum B12, hypersegmented neutrophils on smear (pathognomonic), AND neurologic signs. The combination of macrocytic anemia + neurologic signs (paresthesias + ataxia + cognitive changes) = B12 deficiency until proven otherwise. CRITICAL NURSING ACTION regarding the folate order: Under RA 9173, nurses must exercise professional judgment and clarify potentially harmful orders. Administering folate without B12 in this case could cause irreversible neurologic damage to continue while the blood count falsely improves. This is a PATIENT SAFETY issue — document the concern and seek medical clarification before administering.

ANC CALCULATION: The formula is: Total WBC × (percentage of segmented neutrophils + percentage of band neutrophils). Here: 1,200 × (20% + 5%) = 1,200 × 25% = 300/µL. ANC < 500/µL = SEVERE NEUTROPENIA. ANC 300/µL is critically low — even common organisms (like E. coli, Pseudomonas, Candida) can cause fatal infection. FEBRILE NEUTROPENIA is defined as a single oral temperature ≥ 38.3°C OR temperature ≥ 38.0°C sustained for 1 hour in a neutropenic patient — it is treated as an ONCOLOGIC EMERGENCY. The '1-hour rule' for antibiotics has been shown to improve survival. Blood cultures MUST be collected BEFORE antibiotics to identify the organism. Protective isolation prevents introducing new pathogens to a patient with no immune defense.

ACUTE HEMOLYTIC TRANSFUSION REACTION is a TYPE II hypersensitivity reaction triggered by ABO incompatibility. The patient's antibodies (e.g., anti-B antibodies in a type A patient) bind to the incompatible donor RBCs, activating complement, leading to MASSIVE INTRAVASCULAR HEMOLYSIS. Signs develop within MINUTES to the first hour: FEVER, CHILLS, BACK/FLANK PAIN (from renal ischemia), HEMOGLOBINURIA (dark urine from hemoglobin in urine), HYPOTENSION, TACHYCARDIA. This is LIFE-THREATENING — mortality from this complication can be significant. The nurse MUST ACT IMMEDIATELY. Stopping the transfusion is the FIRST and MOST IMPORTANT action — this limits the volume of incompatible blood infused. Note: the IV line must stay open with NORMAL SALINE (not the blood tubing) to allow medication administration and fluid resuscitation.

Z-TRACK TECHNIQUE RATIONALE: Iron dextran is a dark, irritating solution that permanently stains skin and subcutaneous tissue. The Z-track method creates a 'zigzag' track through tissue layers — when the needle is withdrawn and skin is released, the track closes, preventing the medication from seeping backward into upper tissue layers. This is why NO MASSAGE after IM iron is a strict nursing rule. TEST DOSE FOR IRON DEXTRAN: Iron dextran (especially high molecular weight form) has been associated with anaphylactic reactions. The test dose protocol is: administer 0.5 mL (25 mg) IV or IM slowly, observe for 30–60 minutes. If no reaction, proceed with the full therapeutic dose. Newer iron preparations (iron sucrose, ferric gluconate, ferric carboxymaltose) have lower anaphylaxis risk and may not require a test dose — but iron dextran specifically REQUIRES one. Always have EPINEPHRINE 1:1,000 (0.5 mL SQ) and resuscitation equipment at the bedside.