RBC, Plasma and Platelet Transfusions

Transfusion - RBC Indications

• Red blood cell transfusions are indicated when there is evidence of tissue ischemia due to impaired oxygen transport.
• Symptomatic anemia and hypovolemic shock/bleeding are reasons for RBC transfusion.
• Hemoglobin less than 7 g/dL (or <8 g/dL in cardiovascular compromised patients) suggests RBC transfusion.
• One unit of RBCs should increase hemoglobin by 1g/dL or hematocrit by 3%.

Plasma and Platelets

• Plasma is a source of coagulation factors; 10-15 ml/kg of plasma replaces about 20% of a patient's clotting factors.
• Plasma transfusion is given in cases of massive hemorrhage.
• It is given prior to surgical procedures for patients with INR >1.6.
• It is given when factor replacement is needed if specific factor concentrates aren't available.
• It is given for plasma exchange.
• Platelets only last about a week after donation.
• Platelet transfusion will increase platelet count by 25-50 per unit given.
• Platelet transfusions are indicated in cases of:
  • Massive hemorrhage
  • Platelet count < 10K
  • Prior to procedure when plt < 50K
  • Active bleeding when plt < 50K
  • CNS or intraocular bleeding when plt < 100K
  • When numbers above are not met but patient is on antiplatelet therapy
  • Congenital platelet dysfunction and bleeding

Cryoprecipitate

• Cryoprecipitate contains fibrinogen and von Willebrand Factor.
• Cryoprecipitate is given in cases of massive hemorrhage.
• Cryoprecipitate is an option for hemophilia A and von Willebrand disease.

Transfusion - ABO and Rh Considerations

• ABO Antigens
• A and B are codominant, thus people can have blood types A to A, B to B, AB to AB and O (meaning lack of A and B)
• Antibodies
• The body naturally makes antibodies to antigens it doesn't possess
  • A has antibodies to B
  • B has antibodies to A
  • AB has NO antibodies (universal recipient)
  • O has antibodies to A and B (O- universal donor)
  • O+ can only go to other +'s
• Rh
• If D-antigen presence is positive, it is present in about 85% of population
• Unlike ABO, an Rh negative person only develops Anti-D antibodies after exposure to Rh positive blood
• A big concern is pregnancy.
• When a mother is Rh negative and is exposed to Rh positive fetal blood, she can develop Anti-D antibodies which can cause Hemolytic Disease of the Fetus and Newborn (HDFN).
• Retest at 28 weeks.
• Pregnancy complications can be prevented with Rh immune globulin (RhoGAM). The anti-D IgG antibodies clear fetal Rh positive cells from the maternal bloodstream, preventing development of maternal Rh antibodies.
• Other concerns are of course transfusion reaction
• Type and Screen
• Includes ABO type, Rh type, and screens for other antibodies.
• Oversimplification: take patients blood, mix it with some antibodies and see what sticks.
• Crossmatching is similarly oversimplified: take some of the recipient blood, mix with some of donor blood- see if they hate each other
• Generally only needed if screen is positive for antibodies
• Donating blood is good, do it if you can

Religious and Personal Blood Transfusion Considerations

• Jehovah's Witnesses generally object to receiving blood products due to their interpretation of certain passages in the Bible related to the sanctity of blood.
• Do not assume patient will refuse blood, have an honest, private, and respectful convo with the patient
• In pediatric cases, practitioner decisions that run contrary to parent wishes have been protected but know hospital policy and contact the ethics committee
• Heparin
• Heparin is derived from porcine intestinal mucosa; consider if patients have dietary restrictions (Vegetarian / Vegan / Islam / Judaism)
• Have an honest conversation with your patient.

Thrombosis and Thrombophilia

• Thrombus: an aggregate of coagulated blood containing platelets, fibrin, and entrapped cellular elements (a blood clot that forms in a blood vessel).
• Thrombosis: formation of a thrombus that either partially or fully obstructs a blood vessel.
• Arterial thrombosis examples: myocardial infarction, stroke, peripheral arterial thrombosis
• Venous thrombosis examples: DVT, PE
• Embolus: Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
• Fat embolus: can happen after a fracture.
• Air embolus: frothy clotty mass with lots of inflammatory response.
• Amniotic fluid embolism: amniotic fluid or fetal tissue that is rare, but has high mortality and intense inflammatory response.
• Thromboembolus: thrombus formed in one location that detaches from vessel wall and travels to a distant site.
• Venous Thromboembolism (VTE): DVT, PE, cerebral venous sinus thrombosis.
• Outcomes
• Lysis: activation of the fibrinolytic system can lead to rapid and total lysis of recent thrombi, can be ineffective otherwise
• Propagation (growth of a thrombus): accumulation of more platelets and fibrin, leading to occlusion
• Embolization
• Organization: induces inflammation/fibrosis with invasion of connective tissue elements, thrombus becomes firm, grayish-white.
• Canalization: formation of a new lumen, lined by endothelium, within the organized thrombus.
• Virchow's Triad
• Conditions that contribute to thrombosis:
• Cancer
• COVID
• Pregnancy
• Circulatory status
• Turbulent flow: turbulence around an aneurysm or at bifurcation sites; major factor for arterial thrombosis.
• Stasis (slowed flow) in narrowed vessels: major factor for venous thrombosis.
• Venous examples:
• Prolonged immobilization, foreign bodies, CHF, pregnancy, dehydration, atrial fibrillation, valve stenosis, ventricular dysfunction, and polycythemia/sickle cell.
• Endothelial Injury
• The big start for clotting cascade
• Atherosclerosis is a major cause.
• Other causes: hyperlipidemia, phlebitis/vasculitis, foreign body, trauma, bacterial infection, smoking, radiation.
• Hypercoagulability
• Inherited etiologies:
• Factor V Leiden: factor Va inactivation slows
• Leiden mutation on factor V gene (2-15% of Caucasians) produces an abnormal factor V which is not deactivated by protein C.
• Normally, thrombomodulin produced by the endothelium, using protein C as a cofactor, down-regulates the activation of factor V. Mutated factor V cannot be deactivated, causing loss of an antithrombotic pathway. Occurs in 20-60% of adults with strong family histories: - Homozygous condition is single greatest risk factor for DVT (increased 50-100 fold), heterozygous risk for DVT increases 4-6 fold
• Protein C or S deficiency
• Severe congenital protein C deficiency is a rare genetic defect found in 1-2 neonates for every one million births
• Complete absence of protein C results in abnormally high numbers of clots causing fatality - Symptoms typically appear soon after birth with widespread clotting
• Protein C concentrate (Ceprotin(R)) is indicated via protein C efficiency, adult/pediatric/neonatal patients
• hyperhomocysteinemia
• Marked hyperhomocysteinemia (plasma homocysteine level > 100 umol/L) occurs in children homozygous for cystathionine-beta-synthetase deficiency (severe developmental disability, lens and skeletal defects, atherosclerotic and thromboembolic disease at early age)
• Moderate elevation of homocysteine levels (16-100 umol/L) occurs in patients heterozygous for this enzyme deficiency or if deficient in vitamin B12, folic acid, or pyridoxine
• Normal metabolic pathways for homocysteine include its: - conversion to methionine (B12 and folate required) - cystathionine (requires pyridoxine)
• Mild/moderate hyperhomocysteinemia is an independent risk factor for CAD, PVD, and DVT
• Homocysteine toxicity results in: - Direct damage to endothelium - increased platelet adhesion - Loss of thrombolysis

Thrombosis and Thrombophilia- VTE and DVT

• VTE: pulmonary embolism most common, 100 - 300K deaths/year
• Sudden death occurs in about 25% of cases with PE Survivors of DVT may have long-term complications (post thrombolytic):
  • Pain, swelling, scaling, discoloration
• Risk Factors
• Include: genetics, male, obesity, smoking, surgery, immobilization, foreign body, estrogen, hormone therapy
• Deep Vein Thrombosis (DVT)
• Stasis: CHF, chronic venous insufficiency, immobilization: "economy class syndrome”- for individuals traveling on flights: Risk- over 4 hours-1 in 4600/ over 8 hours- 1 in 200:
  • Generally, occur asymptomatically/ fatal PE /symptomatic DVT
• Injury: includes trauma, surgery, and childbirth
• Clinical Features
• Propagation may involve proximal larger veins/ embolize to lungs
• More than 90% of all cases occur in superfical/deep leg veins: BK +remainder in pelvis Superficial Thrombi: include local congestion/tenderness/edema, occur in saphenous system:
• Lead to varicose ulcers
• Deep thrombi lead leg veins at /above knee (femoral, iliac, popliteal)
• Venous obstruction may be offset rapidly:
• Impairment leads to chronic deep vein insufficiency, failure of vein drainage
• Asymptomatic in half: they are recognized until embolization

Pulmonary Embolism

• PE: origins in deep veins of low extremities, most fatal- iliofemoral
• Distribution to lungs in around 65%, right lung in 25%, left lung in 10%: Most lower lobes, 65%/ + intermediate arteries, 35% to smaller
• Mechanism: obstructs micro circulation/ arterioles/ capillaries
• Leads to pulmonary hypertension / increase pulmonary vascular resistance
• Usually obstructs P. arteries with primary thrombi: Secondary is caused by vasoconstriction with hypoxemia /humoral: can cause vasodilation, hypertension, ventricular failure
• PE Manifestations
• In absence of disease involving >50- 75% : requires cardigeninc shock, from arteriovenous vasculature
• EKG
• Includes: Tachycardia/ T-wave inversion leads
• Diagnostics: CXK, Arterial Blood gases, Hypoxemia is common

Thrombocytopenia

• Diagnosed as :PLT count <1000/ul/ spontaneous risk with PLT - 10000-2000/ul Three main mechanisms:
  • Decreases in marrow, accelerated destruction from production
• Thromboctyopenia : Damage/ suppression of caused by cytoxin, nutritional differences, infection; or abnormalities relating to maturity.
• Management: Test and treat:
• History of physical evaluation : CBC, with platelet
• For thrombocytopenia caused by a production decrease - Bone Marrow production is useful.

ITP

Definition: Autoimmune, where IgG antibodies which leads to platelet destruction by the spleen

• Usually due to proteins
• Mostly in children/ often follows illness , and is easily self limited

Leukocytosis

Increase in white blood count past normal limits Neutrophilia - Absolute C>100.ul Most secondary.Reactive primary increase Lymphocytosis: C Causes: Infection, stress, Steroids, splenertomy, reactive for viral cause : Viral infection and increase and production

Overview of red blood cell transfusion indications related to tissue ischemia and anemia. Covers plasma transfusion for coagulation factors and hemorrhage. Explains platelet transfusions and their effect on platelet count.