NLE Hematologic Nursing — Bleeding, Clotting and Hematologic MalignanciesRevision Notes

Exam Tips

• Memorize the three platelet thresholds: 50K = trauma risk, 20K = spontaneous risk, 10K = life-threatening. These numbers appear directly in NLE questions.
• Any question that says 'patient is on heparin and now has a falling platelet count' = suspect HIT = STOP heparin immediately.
• Bleeding precautions are universal nursing interventions for ALL platelet disorders — always a safe answer when in doubt.

Key Points

• Normal platelet count: 150,000–400,000/µL. Below this is thrombocytopenia.
• Critical threshold: Below 50,000/µL = bleeding risk with trauma; below 20,000/µL = spontaneous bleeding risk; below 10,000/µL = severe, life-threatening hemorrhage (including intracranial bleeding).
• Hemostasis requires THREE components: adequate platelets, functional clotting factors, and intact blood vessels. Failure in any one causes bleeding.
• Causes of thrombocytopenia: (1) Decreased production — bone marrow failure, chemotherapy; (2) Increased destruction — immune/autoimmune, DIC; (3) Sequestration — splenomegaly traps platelets.
• Heparin-Induced Thrombocytopenia (HIT): paradoxical immune reaction to heparin causing both a FALLING platelet count AND clotting (thrombosis). Priority action: STOP all heparin immediately.
• Nursing priority for thrombocytopenia: BLEEDING PRECAUTIONS — soft toothbrush, electric razor, avoid IM injections, avoid aspirin and NSAIDs, apply pressure to puncture sites.

Definitions

Section Title

Normal Hemostasis and Thrombocytopenia

Common Mistakes

• Confusing the platelet count thresholds: many students mix up 20,000 (spontaneous bleeding) with 10,000 (life-threatening/intracranial). Remember: 'the lower you go, the more you bleed.'
• Administering aspirin or NSAIDs for pain/fever in a thrombocytopenic patient — these inhibit platelet function and worsen bleeding.
• Forgetting that HIT causes BOTH low platelets AND clotting — students sometimes expect only bleeding.
• Giving IM injections to a patient with thrombocytopenia — always use IV or oral routes when platelet count is low.

Exam Tips

• The NLE loves to ask about the FIRST-LINE treatment for ITP: the answer is CORTICOSTEROIDS (prednisone).
• If a question asks about nursing management, 'avoid aspirin and NSAIDs' is almost always part of the correct answer for any platelet disorder.
• Headache + visual changes in a thrombocytopenic patient = EMERGENCY — suspect intracranial hemorrhage and notify the physician immediately.

Key Points

• ITP is an AUTOIMMUNE disorder: the body produces antibodies (IgG) that coat platelets, which are then recognized as foreign and destroyed by macrophages in the SPLEEN.
• Classic presentation: petechiae (pinpoint red dots), purpura (larger bruising), ecchymoses (bruising), mucosal bleeding (gum bleeding, epistaxis/nosebleed), and menorrhagia in women.
• Labs: LOW platelet count with NORMAL WBC and hemoglobin (only platelets are affected). Bone marrow shows INCREASED megakaryocytes (the body tries to make more platelets).
• Management stepladder: (1) Corticosteroids (prednisone) — first-line, suppress immune response; (2) IV Immunoglobulin (IVIG) — for rapid platelet rise (pre-surgery, crisis); (3) Anti-D immunoglobulin — for Rh-positive patients only; (4) Thrombopoietin receptor agonists (eltrombopag, romiplostim); (5) Splenectomy — for refractory/chronic ITP (removes the site of platelet destruction).
• Nursing priority nursing diagnoses: Risk for Bleeding r/t decreased platelet count; Deficient Knowledge r/t disease management.
• Patient education: avoid aspirin/NSAIDs, use soft toothbrush and electric razor, avoid contact sports, wear medical alert bracelet, report any headache or visual changes (signs of intracranial bleeding) IMMEDIATELY.

Definitions

Section Title

Immune Thrombocytopenic Purpura (ITP)

Common Mistakes

• Confusing ITP (immune destruction of platelets) with DIC (consumption of both platelets AND clotting factors). In ITP, only platelets are low; WBC and Hgb are normal.
• Forgetting that anti-D immunoglobulin works ONLY in Rh-positive, non-splenectomized patients — giving it to Rh-negative patients is incorrect.
• Not recognizing that increased megakaryocytes in the bone marrow is a compensatory response, NOT a sign of worsening disease.

Exam Tips

• PRIORITY INTERVENTION in DIC: Treat the underlying cause (e.g., treat the sepsis, deliver the baby). This is always the first nursing/medical priority.
• The NLE may present a septic patient who suddenly develops bleeding from all IV sites — think DIC.
• Remember the lab picture as 'EVERYTHING goes the wrong way': everything you want HIGH (platelets, fibrinogen) is LOW; everything you want SHORT (PT, aPTT) is LONG; D-dimer (which you want low) is HIGH.
• Cryoprecipitate = fibrinogen replacement. FFP = all clotting factors. Platelets = for thrombocytopenia. Know which product does what.

Key Points

• DIC is ALWAYS SECONDARY — it never occurs alone. There is always a trigger. It is NOT a primary disease.
• Pathophysiology: An underlying trigger → massive, widespread activation of the clotting cascade → microthrombi form throughout the body → platelets and clotting factors are CONSUMED → the patient is LEFT with NO clotting ability → paradoxical uncontrolled BLEEDING.
• Think of DIC as: 'Clot everywhere, then bleed everywhere.' Both processes happen simultaneously — this paradox is the key concept.
• Major triggers (memorize): SEPSIS (most common trigger), obstetric emergencies (placental abruption, amniotic fluid embolism, retained dead fetus), massive trauma or burns, malignancy (especially AML), and hemolytic transfusion reactions.
• Clinical presentation SIMULTANEOUSLY shows: (A) CLOTTING signs — organ ischemia, skin necrosis, acral cyanosis (blue/black fingertips and toes); (B) BLEEDING signs — oozing from ALL venipuncture and IV sites, petechiae, purpura, hematuria, GI bleeding, frank hemorrhage.
• CLASSIC LAB PATTERN (must memorize all 5): LOW platelets + LOW fibrinogen + PROLONGED PT + PROLONGED aPTT + ELEVATED D-dimer and fibrin degradation products (FDPs).
• D-dimer is elevated because clots are being formed AND broken down simultaneously.
• DEFINITIVE TREATMENT: TREAT THE UNDERLYING CAUSE — this is always the priority. Without removing the trigger, all other interventions are temporary.
• Supportive replacement therapy: Platelets (for thrombocytopenia), Fresh Frozen Plasma/FFP (replaces ALL clotting factors), Cryoprecipitate (replaces fibrinogen and factor VIII specifically). Packed RBCs for blood loss.
• Heparin use in DIC is controversial and selective — used only when THROMBOSIS predominates over bleeding (e.g., acral ischemia with no active hemorrhage).
• NANDA nursing diagnosis: Risk for Bleeding; Impaired Tissue Perfusion; Ineffective Protection.

Definitions

Section Title

Disseminated Intravascular Coagulation (DIC)

Common Mistakes

• Treating DIC with only blood products and forgetting to address the UNDERLYING CAUSE — the blood products are supportive, not curative.
• Confusing which lab is low vs. high in DIC: ALL of platelets, PT, aPTT, and fibrinogen are abnormally LOW or PROLONGED; D-dimer is HIGH.
• Forgetting that both clotting AND bleeding occur simultaneously — students often think of DIC as only a bleeding disorder.
• Giving lactated Ringer's solution instead of normal saline with blood products — LR contains calcium which can initiate clotting in the IV tubing.

Exam Tips

• Memory aid: Hemophilia A = factor 8 (Eight letters in 'Hemophilia' starts with... just remember A=VIII and B=IX).
• Lab key: aPTT is prolonged + PT is normal = intrinsic pathway problem = hemophilia (or heparin therapy).
• DDAVP is ONLY for mild hemophilia A — if the question mentions hemophilia B or severe hemophilia A, DDAVP is NOT the answer.
• Hallmark sign = hemarthrosis. If a male child presents with recurrent joint swelling after minor trauma, think hemophilia.

Key Points

• Hemophilia is an INHERITED (congenital) X-linked recessive disorder — located on the X chromosome. Males (XY) have only one X chromosome, so they are AFFECTED. Females (XX) have two X chromosomes; if one is defective, the other compensates — females are CARRIERS (usually asymptomatic).
• Hemophilia A = deficiency of Factor VIII (8). This is the MOST COMMON type (~80% of cases).
• Hemophilia B (Christmas disease) = deficiency of Factor IX (9).
• Both factors VIII and IX are part of the INTRINSIC PATHWAY of coagulation.
• CLASSIC LAB PATTERN: PROLONGED aPTT + NORMAL PT + NORMAL platelet count + NORMAL bleeding time. Only the intrinsic pathway is defective.
• Clinical manifestations: prolonged bleeding after minor cuts, dental extractions, or surgery; HEMARTHROSIS (bleeding into joints — especially knees, elbows, ankles) causing pain, swelling, warmth, and limited ROM; deep muscle hematomas; and easy bruising.
• Hemarthrosis is the HALLMARK (most distinctive sign) of hemophilia.
• Chronic repeated hemarthrosis leads to JOINT DESTRUCTION (hemophilic arthropathy) and permanent disability if untreated.
• MANAGEMENT: Replace the missing clotting factor at the FIRST SIGN of bleeding and prophylactically before any procedure. Factor VIII concentrate for hemophilia A; Factor IX concentrate for hemophilia B.
• DDAVP (Desmopressin): Stimulates release of stored factor VIII from endothelial cells. Used for MILD hemophilia A ONLY (not B, and not severe A). Given intranasally or IV.
• For joint bleeds: RICE — Rest, Ice, Compression, Elevation. Apply pressure for external bleeds.
• NEVER give: aspirin, NSAIDs (inhibit platelet function), IM injections (risk of deep muscle hematoma), or NSAIDs.
• Patient and family education: factor self-administration at home, carry medical alert ID, wear protective gear, choose safe activities (swimming vs. contact sports), genetic counseling.

Definitions

Section Title

Hemophilia

Common Mistakes

• Confusing hemophilia A (factor VIII) and hemophilia B (factor IX). Use the memory aid: 'A = 8' (the letter A has 8 lines if you count carefully) or 'B = 9 (B comes after A, 9 comes after 8)'.
• Stating that PT is prolonged in hemophilia — it is NOT. Only aPTT is prolonged because only the intrinsic pathway is affected.
• Thinking females cannot be affected — while rare, a female with two defective X chromosomes (homozygous) can have hemophilia, though this is extremely uncommon.
• Applying RICE incorrectly — Ice should be wrapped in cloth (never directly on skin), applied for 20 minutes at a time to reduce swelling and bleeding in the joint.

Formulas

Exam Tips

• ALL = children; AML = adults. CML = Philadelphia chromosome + imatinib.
• Infection prevention is ALWAYS the top nursing priority in leukemia (it is the #1 cause of death).
• Fever in a neutropenic patient is a MEDICAL EMERGENCY — notify the physician immediately; do not wait for cultures.
• The NLE may ask about which foods to avoid in neutropenic patients: avoid raw/fresh fruits and vegetables (use cooked or canned instead), no fresh flowers in the room.

Key Points

• Leukemia is a MALIGNANT (cancerous) proliferation of IMMATURE white blood cells (BLASTS) in the bone marrow. These abnormal blasts multiply rapidly and CROWD OUT normal blood cell production (hematopoiesis).
• CLASSIC TRIAD OF MANIFESTATIONS (from bone marrow failure — all three result from crowding out of normal cells): 1. ANEMIA (RBC crowded out) → fatigue, pallor, dyspnea, tachycardia 2. NEUTROPENIA (neutrophils crowded out) → recurrent, severe INFECTIONS — the LEADING CAUSE OF DEATH in leukemia 3. THROMBOCYTOPENIA (platelets crowded out) → BLEEDING, bruising, petechiae
• FOUR MAJOR TYPES: • ALL (Acute Lymphocytic/Lymphoblastic Leukemia) — most common in CHILDREN; best prognosis among acute types • AML (Acute Myelogenous Leukemia) — most common acute leukemia in ADULTS • CLL (Chronic Lymphocytic Leukemia) — older adults; often slow/indolent; may not need immediate treatment • CML (Chronic Myelogenous Leukemia) — associated with the PHILADELPHIA CHROMOSOME (t9;22 translocation); treated with tyrosine kinase inhibitors (imatinib/Gleevec)
• DIAGNOSIS: CBC shows abnormal WBC count (can be high, low, or normal) WITH BLASTS visible on peripheral blood smear. BONE MARROW BIOPSY is CONFIRMATORY — shows >20% blasts (AML/ALL).
• MANAGEMENT: (1) Induction chemotherapy — kill all leukemic cells; (2) Consolidation — reinforce remission; (3) Maintenance — prevent relapse. Targeted therapy (imatinib for CML). Hematopoietic Stem Cell Transplant (HSCT) for eligible patients.
• NURSING PRIORITIES (Maslow-based): 1. PHYSIOLOGIC SAFETY — Infection prevention is the TOP PRIORITY (neutropenia = greatest immediate life threat) 2. Protection from bleeding 3. Managing chemotherapy side effects (nausea, mucositis, tumor lysis syndrome, alopecia) 4. Psychosocial support
• Absolute Neutrophil Count (ANC) below 500/µL = SEVERE neutropenia = protective/reverse isolation (private room, HEPA filter, limit visitors, no fresh flowers/fruits, strict hand hygiene).
• Tumor Lysis Syndrome: massive cell death from chemotherapy releases intracellular contents → hyperkalemia, hyperphosphatemia, hyperuricemia, hypocalcemia, and acute kidney injury. Prevent with aggressive IV hydration and allopurinol.

Definitions

Section Title

Leukemia

Common Mistakes

• Stating that leukemia causes HIGH WBC — the WBC can be high, normal, or LOW (aleukemic leukemia). The key abnormality is the BLAST CELLS, not necessarily the total WBC count.
• Prioritizing bleeding over infection — while both are important, INFECTION (due to neutropenia) is the LEADING CAUSE OF DEATH and should be prioritized using Maslow's hierarchy (physiologic safety).
• Confusing protective isolation (protect the immunocompromised patient FROM germs) with contact/droplet/airborne isolation (protect others FROM an infectious patient) — they are opposite in purpose.
• Forgetting that fresh fruits, vegetables, and flowers are contraindicated in neutropenic patients due to mold and bacterial contamination.

Exam Tips

• Reed-Sternberg cells = Hodgkin lymphoma. This association is tested almost every board exam cycle.
• Young adult with painless cervical lymphadenopathy + fever + night sweats + weight loss = HODGKIN LYMPHOMA until proven otherwise.
• B symptoms (Fever, Night sweats, >10% Weight loss) indicate more advanced/worse prognosis in BOTH lymphoma types.
• Hodgkin has BETTER prognosis than most NHL subtypes — it is one of the most curable cancers, especially when caught early.

Key Points

• Lymphomas are cancers of the LYMPHATIC SYSTEM — they start in lymphocytes and primarily involve lymph nodes and lymphoid tissues.
• Both types present most often with PAINLESS LYMPHADENOPATHY — enlarged lymph nodes that do NOT hurt (unlike infectious lymphadenopathy which is tender).
• HODGKIN LYMPHOMA (HL): • Pathognomonic (defining) finding: REED-STERNBERG CELLS on lymph node biopsy — large binucleated cells described as looking like 'owl eyes' • Typically starts in a SINGLE lymph node region (usually CERVICAL — neck nodes) • Spreads in an ORDERLY, PREDICTABLE, CONTIGUOUS fashion (node by node in sequence) • BIMODAL age distribution: peak in young adults (15–35 years) AND again in older adults (>50 years) • GENERALLY GOOD PROGNOSIS, especially when localized (Stage I–II is highly curable with radiation/chemo) • Treatment: ABVD chemotherapy regimen (Adriamycin, Bleomycin, Vinblastine, Dacarbazine) ± radiation
• NON-HODGKIN LYMPHOMA (NHL): • NO Reed-Sternberg cells • Presents with WIDESPREAD, MULTIPLE NODE INVOLVEMENT from the start • UNPREDICTABLE spread pattern (does not follow orderly progression) • More common in OLDER ADULTS and immunocompromised patients • VARIED PROGNOSIS depending on subtype (aggressive vs. indolent types) • Treatment: chemotherapy (CHOP regimen) + immunotherapy (Rituximab — anti-CD20 antibody = R-CHOP); stem cell transplant
• B SYMPTOMS (present in BOTH HL and NHL, indicate advanced disease and WORSE PROGNOSIS): • Fever (unexplained) • Drenching Night Sweats (soaking the sheets) • Significant Weight Loss (>10% of body weight in 6 months) Memory aid: 'FNS' — Fever, Night sweats, Significant weight loss
• STAGING uses the Ann Arbor system (I–IV): Stage I = single node region; Stage II = two or more regions, same side of diaphragm; Stage III = both sides of diaphragm; Stage IV = disseminated (bone marrow, liver, etc.)
• NURSING CARE: infection prevention during treatment, manage fatigue (schedule rest), teach about long-term radiation effects (hypothyroidism, secondary cancers), and emotional support.

Definitions

Section Title

Lymphoma: Hodgkin vs. Non-Hodgkin

Common Mistakes

• Confusing Hodgkin and Non-Hodgkin lymphoma: remember HL = Reed-Sternberg cells, orderly spread, young adults, good prognosis. NHL = no Reed-Sternberg, widespread, older adults, varied prognosis.
• Thinking B symptoms are unique to Hodgkin lymphoma — B symptoms occur in BOTH Hodgkin AND non-Hodgkin lymphoma.
• Confusing painless lymphadenopathy (lymphoma) with painful lymphadenopathy (infection/lymphadenitis) — the PAINLESS nature is the red flag for malignancy.

Exam Tips

• CRAB = hyperCalcemia, Renal failure, Anemia, Bone lesions. This mnemonic covers 90% of multiple myeloma NLE questions.
• Nursing priority: PUSH FLUIDS (3–4 L/day). This is the most unique and tested nursing intervention for multiple myeloma.
• Bone pain (especially back pain) + elderly patient + anemia + hypercalcemia + renal failure = think MULTIPLE MYELOMA.
• The NLE may ask about the test for Bence Jones protein — it is found in the URINE (urine protein electrophoresis), NOT in the serum.

Key Points

• Multiple myeloma (MM) is a malignant proliferation of PLASMA CELLS in the bone marrow. Plasma cells are B lymphocyte-derived cells that normally produce antibodies. In MM, malignant plasma cells produce massive amounts of abnormal, non-functional immunoglobulin called M PROTEIN (paraprotein).
• The classic mnemonic for MM manifestations is CRAB: • C = hyperCalcemia (from bone destruction releasing calcium) • R = Renal failure (from light chain deposition — Bence Jones protein — and hypercalcemia damaging kidneys) • A = Anemia (bone marrow replaced by plasma cells, suppressing RBC production) • B = Bone lesions (lytic/punched-out lesions from plasma cell infiltration and osteoclast activation; pathologic fractures)
• BONE PAIN (especially BACK PAIN) is the most common presenting symptom — caused by lytic bone lesions and vertebral compression fractures.
• PATHOLOGIC FRACTURES: fractures from minimal trauma due to bone weakening by lytic lesions — spine (vertebral collapse), ribs, hips.
• HYPERCALCEMIA signs: BONES (pain/fractures), GROANS (GI symptoms: nausea, constipation), STONES (renal calculi), PSYCHIC MOANS (confusion, depression) — 'bones, groans, stones, psychic moans'.
• RECURRENT INFECTIONS: the abnormal M protein is non-functional; normal antibody production is suppressed → immunocompromised.
• BENCE JONES PROTEIN: light chains of M protein filtered into the urine; their detection on urine protein electrophoresis is diagnostic.
• DIAGNOSIS: M protein on serum/urine protein electrophoresis (SPEP/UPEP), Bence Jones proteinuria, bone marrow biopsy showing >10% plasma cells, lytic lesions on skeletal survey X-rays ('punched-out' lesions).
• MANAGEMENT: (1) Chemotherapy — bortezomib (proteasome inhibitor) + lenalidomide (immunomodulator) + dexamethasone; (2) Bisphosphonates (zoledronic acid, pamidronate) — prevent further bone destruction, treat hypercalcemia; (3) Autologous stem cell transplant for eligible patients; (4) Supportive: pain management, transfusions.
• TOP NURSING PRIORITIES: 1. HYDRATION — push 3–4 L/day of fluids to prevent renal failure and help excrete calcium and Bence Jones protein (kidneys cannot concentrate urine if tubules are damaged) 2. MOBILITY — ambulation stimulates bone remodeling, prevents hypercalcemia worsening, and prevents VTE 3. Fall/fracture prevention — careful handling (log-rolling for spine involvement), no heavy lifting 4. Infection prevention 5. Pain management
• NANDA nursing diagnoses: Chronic Pain r/t bone lesions; Risk for Injury (fractures); Impaired Urinary Elimination; Risk for Infection; Deficient Fluid Volume.

Definitions

Section Title

Multiple Myeloma

Common Mistakes

• Forgetting that AMBULATION (mobility) is a key nursing intervention in myeloma — students often think the patient should be on bed rest due to fracture risk. Ambulation is essential to prevent hypercalcemia worsening and VTE.
• Not pushing adequate fluids — 3–4 liters per day is much higher than typical nursing interventions. This large volume is critical to protect the kidneys from Bence Jones protein damage.
• Confusing multiple myeloma (plasma cell cancer) with leukemia (WBC blast cancer) — in MM, the CBC may show anemia but the key is the plasma cell proliferation and M protein.
• Missing the CRAB mnemonic components — practice: C=calcium, R=renal, A=anemia, B=bone.

Exam Tips

• UNIVERSAL RULE for any reaction: STOP the transfusion FIRST, then keep vein open with NSS using NEW tubing, then notify.
• Most DANGEROUS reaction = Acute Hemolytic (ABO incompatibility). Most COMMON reaction = Febrile Non-Hemolytic.
• TACO vs. TRALI: Blood pressure is the key differentiator. TACO = HIGH BP + JVD + crackles → sit up + diuretics. TRALI = normal/LOW BP + bilateral infiltrates → respiratory support, NO diuretics.
• The only reaction where transfusion CAN be resumed = mild allergic reaction (urticaria only, no other symptoms, resolved with antihistamine).
• Anaphylaxis in transfusion = IgA-deficient patient. Treatment = EPINEPHRINE (not antihistamine alone).
• 4-hour rule: complete each transfusion unit within 4 hours. Memorize this — NLE tests it directly.

Key Points

• PRE-TRANSFUSION VERIFICATION (two-nurse bedside check — RA 9173 mandate for safe nursing practice): 1. Patient IDENTITY using TWO identifiers (name + hospital ID/birthdate) 2. Blood TYPE and RH FACTOR of unit vs. patient 3. CROSSMATCH/COMPATIBILITY number and unit serial number 4. EXPIRATION DATE and integrity of the bag (no leaks, clots, discoloration) 5. Obtain INFORMED CONSENT before transfusion
• EQUIPMENT: • Large-bore IV catheter: 18–20 gauge (smaller gauges cause RBC hemolysis from pressure) • Blood administration tubing with IN-LINE FILTER (170–260 micron filter to remove clots and debris) • Y-set tubing (allows flushing with saline)
• IV FLUID COMPATIBILITY — ONE RULE: Only 0.9% NORMAL SALINE (NSS) may be piggybacked or used to flush blood transfusion lines. • NEVER dextrose solutions (5%D/W, D5NSS etc.) — dextrose causes RBC CLUMPING and hemolysis • NEVER Lactated Ringer's (LR) — calcium in LR initiates the clotting cascade in the tubing
• TRANSFUSION RATE AND MONITORING: • Obtain BASELINE VITAL SIGNS before starting • Start at SLOW RATE (~2 mL/min or ~25–50 mL over the first 15 minutes) • REMAIN WITH THE PATIENT for the FIRST 15 MINUTES — most severe reactions occur within this window • Recheck vital signs at 15 minutes, then per hospital policy (typically every 30–60 minutes) • Complete each unit within 4 HOURS (bacterial proliferation risk beyond 4 hours; return unused blood to blood bank if not started within 30 minutes of issue)
• TRANSFUSION REACTIONS — IMMEDIATE ACTION FOR ANY SUSPECTED REACTION: 1. STOP the transfusion IMMEDIATELY 2. Keep the IV line open with 0.9% NSS using NEW TUBING (do not use the old blood tubing) 3. Notify the physician AND blood bank immediately 4. Check and record vital signs 5. Send the blood bag + tubing + blood samples (from the patient) + urine sample to the laboratory 6. Document all findings and actions
• TYPES OF TRANSFUSION REACTIONS: A. ACUTE HEMOLYTIC REACTION • MOST DANGEROUS/DEADLIEST • Cause: ABO INCOMPATIBILITY — almost always a CLERICAL/IDENTIFICATION ERROR • Onset: Within MINUTES of starting the transfusion (first 50 mL) • Signs: Fever, chills, LOW BACK/FLANK PAIN (hallmark), hypotension, tachycardia, dyspnea, HEMOGLOBINURIA (red-brown/port wine-colored urine) • Progression: Shock, DIC, acute kidney injury, death • Management: Stop transfusion, IV fluids (maintain urine output >30 mL/hr), vasopressors if shocked, send samples to lab B. FEBRILE NON-HEMOLYTIC REACTION (FNHTR) • MOST COMMON transfusion reaction • Cause: Recipient antibodies react against DONOR LEUKOCYTES (white cells in the blood product) • Signs: Fever (>1°C rise) and chills WITHOUT signs of hemolysis; no back pain, no hemoglobinuria • Management: Stop or slow transfusion, antipyretics (acetaminophen), notify MD • Prevention: Use LEUKOCYTE-REDUCED (leukodepleted) blood products C. MILD ALLERGIC REACTION • Cause: Recipient reacts to DONOR PLASMA PROTEINS (allergens) • Signs: URTICARIA (hives) and PRURITUS (itching) — no fever, no respiratory distress • Management: SLOW OR STOP transfusion, administer ANTIHISTAMINE (diphenhydramine); transfusion may be RESUMED slowly if symptoms are MILD and RESOLVE completely • Note: This is the ONLY reaction where transfusion may potentially be resumed after treatment D. ANAPHYLACTIC REACTION • Cause: Recipient is IGA-DEFICIENT and has antibodies against IgA in donor plasma • Signs: SUDDEN, SEVERE — wheezing, bronchospasm, hypotension, shock, stridor, urticaria — within first few mL • Management: Stop transfusion, maintain AIRWAY, give EPINEPHRINE (1:1000 IM), IV fluids, corticosteroids • Prevention: Use WASHED red cells (plasma removed) or IgA-deficient donor products in future transfusions E. CIRCULATORY OVERLOAD (TACO — Transfusion-Associated Circulatory Overload) • Cause: Too much volume infused too quickly, especially in elderly or cardiac patients • Signs: DYSPNEA, crackles/rales (pulmonary edema), HYPERTENSION, distended neck veins (JVD), cough, headache • Management: SLOW or STOP transfusion, SIT PATIENT UPRIGHT (high Fowler's), give DIURETICS (furosemide), oxygen • Prevention: Transfuse slowly, give diuretics between units in high-risk patients F. TRANSFUSION-RELATED ACUTE LUNG INJURY (TRALI) • Cause: Donor antibodies react against recipient leukocytes, causing pulmonary capillary leak • Signs: Acute respiratory distress within 6 hours, non-cardiogenic pulmonary edema, fever, hypoxia, bilateral infiltrates on chest X-ray • Management: Supportive respiratory care (oxygen, possibly mechanical ventilation); no diuretics (unlike TACO) • Key distinction from TACO: TRALI has NORMAL or LOW blood pressure; TACO has HIGH blood pressure G. DELAYED REACTIONS • Delayed hemolytic reaction: occurs days to weeks later; mild hemolysis from alloantibodies to minor antigens • Graft-Versus-Host Disease (GVHD): donor lymphocytes attack recipient tissues — in immunocompromised patients • Iron overload: from chronic transfusions; treat with iron chelation (deferoxamine) • Transfusion-transmitted infections: HIV, hepatitis B/C, CMV (screened but not zero risk)

Definitions

Section Title

Blood Transfusion: Administration and Reactions

Common Mistakes

• Using D5W or lactated Ringer's with a blood transfusion — ONLY normal saline (NSS) is compatible. This is a medication error that can cause hemolysis or clotting in the line.
• Leaving the patient after starting the transfusion — the FIRST 15 MINUTES require the nurse to STAY WITH THE PATIENT (this is when most severe reactions occur).
• Treating TRALI with diuretics — diuretics are for TACO (volume overload), NOT TRALI (immune lung injury). Giving diuretics to a TRALI patient who is already hypotensive is dangerous.
• Resuming a transfusion after ANY severe reaction — the transfusion may only be resumed (cautiously) after a MILD ALLERGIC reaction that completely resolves with antihistamines.
• Not changing tubing when reacting — when stopping due to a reaction, the new NSS flush MUST use NEW tubing (not the blood-contaminated old tubing).