Adv Pathophysiology Unit 4 Page 1 of 18. Learning Objectives for this file:

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1 Adv Pathophysiology Unit 4 Page 1 of 18 Learning Objectives for this file: Topics Include: 1. Overview of clinical hematology get the organization 2. Transfusions components 3. Transfusion reactions 4. Blood types 5. Hemolytic Disease of the Newborn (HDN) 6. Hemapheresis Disorders of clotting pathways in another file in this Unit

2 Adv Pathophysiology Unit 4 Page 2 of 18 HOW TO THINK ABOUT CLINICAL HEMATOLOGY: all on ONE page!! organize material this way the next files go over these areas this is how clinicians think of these conditions A. RBC: anemias and myeloproliferative syndromes ANEMIAS: clinical thinking groups anemias into these 3 categories o IMPROPER PRODUCTION OF RBC: iron deficiency (reduced dietary, overload syndromes), chronic disease anemias, bone marrow failure, B12/FA deficiency anemias. o ABNORMAL DESTRUCTION: autoimmune, isoimmune, traumatic, postinfectious, intrinsic RBC defects (membrane, metabolism & enzymopathies, hemoglobinopathies), extrinsic RBC defects. o BLOOD LOSS: menses, GI, tumor, trauma. MYELOPROLIFERATIVE SYNDROMES (POLYCYTHEMIAS): o Polycythemia vera: rare true overproduction of RBC in bone marrow, etiology unknown. o Secondary Polycythemia: the most common due to low oxygen states (pulmonary & other etiologies). B. HEMORRHAGIC DISORDERS: coagulopathies, & disorders of hemostasis (abnormal bleeding & clotting). Grouped into these 3 categories 1. VASCULAR: Rendu-Osler-Weber (Hereditary Hemorrhagic Telangiectasia), Henoch-Schonlein Purpura (allergic), Ehlers-Danlos (Connective tissue -- Marfans, etc), Scurvy. 2. PLATELET DISORDERS: immune (ITP), heparin induced (monitor CBC for platelets as well as the PT to look for thrombocytopenia in patient on heparin), sepsis, RDS, hypersplenism, TTP, HUS (hemolytic uremic syndrome), von Willebrand's, other acquired. 3. COAGULOPATHIES: Hereditary: hemophilias Acquired: vitamin K deficiency, liver disease, DIC, circulating pathologic anticoagulants. C. DISORDERS OF THE WBC: grouped into these 4 categories 1. LEUKOPENIAS & LEUKOCYTOSES: too little or too many. 2. LEUKEMIAS -- ACUTE & CHRONIC (covered in oncology section) 3. EOSINOPHILIAS: too many eosinophils. 4. LYMPHOCYTE DISORDERS: Plasma cell dyscrasias (Myelomas): disorders of circulating lymphocytes. T-cell disorders: reduced count & function. D. DISORDERS OF TISSUE LYMPHOCYTES: LYMPHOMAS (solid) E. SPLEEN DISORDERS: hypersplenism causing cytopenia, asplenia F. METABOLIC DISORDERS OF PIGMENT METABOLISM: PORPHYRIAS genetic types acquired types

3 Adv Pathophysiology Unit 4 Page 3 of 18 TRANSFUSIONS & CLINICAL IMMUNOHEMATOLOGY: This is an organ transplant since blood is living tissue. 15 million per year. RULE: a transfusion that is not specifically indicated is contraindicated!! Informed consent is usually obtained. Careful consideration of risks/benefits. Safest is autologous transfusion (patient's own blood); collect 3-4 units for several weeks prior to elective surgery. Can also process blood lost during traumatic hemorrhage and surgical blood loss, & transfuse back into the patient. Blood components are separated (fractionated) and stored & used separately to obtain the best use of donated blood; also, special preparations have specific clinical uses. Whole blood is mostly used to provide raw material for components and clinically in special cases (rapid transfusion in acute traumatic blood loss, exchange transfusion in the neonate with hemolytic disease of the newborn). Risks include: o Fe overload, development of antibodies, transmission of blood-borne pathogens & other diseases viral hepatitis, HIV, CMV, HTLV-I (Human T-lymphotrophic virus type I causes lymphoma, leukemia), bacteria, malaria & other parasites. o transfusion reactions & errors.

4 Adv Pathophysiology Unit 4 Page 4 of 18 Immunohematology: (Remember: Blood "type" = the antigen on the RBC) Two systems of genetically determined RBC Ag are ABO & Rh. Antigens on red blood cells are inherited with Mendelian genetics of codominance, use Punnett square. Main Blood Type: Type A (homozygous AA or heterozygous OA) Type B (homozygous BB or heterozygous OB) Type O (homozygous OO) Type AB (heterozygous AB) If the antigen is present on the RBC, this person will not have the corresponding agglutinin (which is an immunoglobulin of IgG or IgM type), but will have the other agglutinins. Therefore, Type A has B-agglutinin, Type-B has A-agglutinin, and Type-AB has no agglutinins. A nice internet page with animations describing how the lab determines blood types: And discusses population phenotypes, Rh factor, and HDN.

5 Adv Pathophysiology Unit 4 Page 5 of 18 Rh-Type (D antigen): another antigen found on RBC that is extremely antigenic a person with this antigen is "Rh-positive" here are other weak Rh-type antigens as well Major blood types: blood type is the antigen located on the Red Blood Cell (RBC). If you have one type of antigen, then you will NOT make an antibody to that antigen. BUT, you WILL make antibodies to the other antigens. Type A: has A antigen, and B antibody Type B: has B antigen, and A antibody Type AB: has BOTH antigens, and NO antibodies (or they would destroy their own RBC). o often called the Universal Recipient. o no antibodies, so can receive either type A (with antigen A), type B (with antigen B), or type AB (withboth antigens A & B), or type O (with no antigen ). Type O: have NEITHER antigen, may produce BOTH antibodies. o often called the Universal Donor. o Anyone receiving these RBC will NOT make antibodies to the donated RBC, since there is no antigen on the RBC cell surface.

6 Adv Pathophysiology Unit 4 Page 6 of 18 Blood Type & Transfusions: Same exact type should be used in transfusion, usually the cells destroyed in a reaction are the DONOR cells. Rh-type: o except in emergencies, Rh-negative patients should always receive Rh negative blood o If they receive Rh+ blood, their plasma antibodies will agglutinate the transfused cells by reacting with the Rh factor on the transfused RBC o Rh-positive can receive either Rh-neg or Rh-pos. Universal donor: in emergencies if no time for blood typing, use type-o, since there are no antigens on donor RBC to react with patient's circulating agglutinins. Universal recipient: if emergency, Type-AB is universal recipient, since the patient has no circulating agglutinins Ab at all to react against the donor blood. Iso-immunization (Maternal-fetal): Rh-neg mother and Rh-pos baby o baby s blood cells crossover into mother s bloodstream and sensitize her (mother makes antibodies to Rh antigen) o Rh-negative mother produces Rh-agglutinins (Rh-Ab) after exposure to her Rh-pos fetus. Usually no maternal-fetal (or transfusion) reaction on the first exposure, since Rh-agglutinins take a while to develop Future Rh-pos fetuses suffer RBC hemolysis in utero This is Hemolytic Disease of the Newborn (HDN), previously called erythroblastosis fetalis Lab: Direct Coomb's test detects Ab coating patient's RBC; would test cord blood of infants of Rh-neg mothers Hemolytic disease of the newborn (HDN) (older term, Erythroblastosis fetalis): o hemolytic anemia of the fetus or neonate o caused by transplacental transmission of maternal antibody o evoked by maternal and fetal blood group incompatibility. o Prevention: passive immunity administration of gamma-globulin to the mother at 28 weeks (before she is sensitized) that destroys any fetal cells that should cross over (mother never sees the Rh antigen). Must be done for any pregnancy (even those that miscarry or are aborted). This immunoglobulin lasts 3-6 months, and therefore repeat at delivery. What is given is Rho-gam or another similar product, which is preformed antibody to passively immunize the mother; usually given at 28 weeks & at birth, and after any pregnancy not carried to term; different protocols & dosing schedules exist. o Treatment: if HDN develops, intrauterine or neonatal exchange transfusions are done. Monitoring mother s anti-rh antibody levels during pregnancy (Coomb s and other lab tests for hemolysis) and baby s results via amniocentesis or neonatal heel-stick bilirubin. SEE MORE BELOW ON HDN

7 Adv Pathophysiology Unit 4 Page 7 of 18 HEMOLYTIC DISEASE OF NEWBORN (HDN): Older term is erythroblastosis fetalis Example of a hospital policy on how to handle this situation: Also, "perinatology.com" is a nice website with accurate information on various perinatology topics ("peri" means "around" -- so any topic relating to end of term pregnancy and the delivery period), see: Terminology? Alloimmunization or Isoimmunization? Alloimmunization results from exposure to a polymorphism in an antigen present in the host, and may be a single amino acid difference in a protein Isoimmunization results from exposure to an antigen not present in the host example is Rh(D) in which a person who is Rh negative is exposed to Rh positive cells through transfusion or pregnancy, since the Rh negative person lacks the RhD protein (antigen)

8 Adv Pathophysiology Unit 4 Page 8 of 18 BLOOD TRANSFUSIONS: 1. BLOOD COMPONENTS FOR TRANSFUSION: Rarely use whole blood, in fact, this is not even available any more at most blood banks Instead, whole blood is fractionated into its parts to achieve greater use from one unit of donated blood Typically, oxygen-carrying capacity is sufficient at patient Hb 10 g/dl (Hct 30%) For purposes of transfusion, anemia is usually defined as <10g/dL PRBC (packed RBC): This is designed to replace Hb which is essentially O2 carrying capacity In a healthy person who is isovolemic, there is adequate O2 carrying capacity at Hb levels down to 7 gm/dl?? How much does one unit raise the Hematocrit? o One unit raises the Hct by 3% (and the Hb by 1gm/dL) (can redo Hct in 15 min) o Reference Wiesen, AR, et al, "Equilibration of hemoglobin concentration after transfusion in medical inpatients not actively bleeding," Ann Intern Med, 1994; 121: At: Indications for PRBC transfusion: o Hemodynamically stable anemia without acute coronary syndrome, Hb trigger <7g/dL (transfusion goal 9-10 g/dl) o Acute hemorrhage with evidence of hemodynamic instability or inadequate oxygen delivery o Symptomatic (e.g. tachycardia, tachypnea, postural hypotension) anemia not explained by other causes o Chronic transfusion dependent bone marrow syndromes at Hb <10g/dL o Transfusion or exchange transfusion for severe sickle syndromes o Hemodynamically stable anemia with ischemic heart disease in ST-segment MI Dosing: o Usually administered as single units then reassess, except for ongoing blood loss with hemodynamic instability o Neonate dose is usually ml/kg o Each unit is approximately hematocrit of 60-80% (average 75%) and mg of iron Frozen thawed RBC: costly, for patients with multiple antibodies and history of transfusion reactions

9 Adv Pathophysiology Unit 4 Page 9 of 18 Washed RBC: citrate preservative is removed by washing can order most transfusion components as washed (plasma, WBC, Platelets) For patients: o with plasma reactions, or WBC Ab (febrile transfusion reactions) o & (because no citrate) for heart surgery & pediatrics (immature liver can't handle citrate) Platelet concentrates: for severe thrombocytopenia (surgical, or for extra-corporeal circulation surgery) One platelet concentrate unit only raises the platelets by 5-10,000 (need 6-8 concentrates) May be immediately consumed by the underlying disease Unit of transfusion: o Usually provided as a platelet pool (a five-pack or six-pack) or one large apheresis unit o Using either of these will raise platelet count by 20,000-40,000 preferred that they are ABO compatible, but this is not mandatory Indications for Platelet transfusion: o Platelet count 10,000/microliter or less o Increased risk of hemorrhage due to mucosal solid tumors, graft vs. host disease, associated coagulopathy with platelet count 20,000 or less o Active hemorrhage with platelet count 50,000 or less o Invasive procedure with significant risk of bleeding with platelet count 50,000 or less o Intracranial or intraocular hemorrhage with platelet count 100,000 or less o Massive transfusion (replacement of blood volume) o Acute trauma resuscitation in conjunction with RBC & plasma transfusion o Microvascular hemorrhage with evidence of platelet dysfunction Relative contraindications to platelet transfusion: (platelets consumed by disease) o Thrombotic thrombocytopenic purpura o Hemolytic uremic syndrome o Heparin induced thrombocytopenia o Immune thrombocytopenic purpura 10 minutes to 1 hour after platelet transfusion, obtain platelet count Cryoprecipitate (factor VIII) & plasma fraction concentrates: Concentrated coagulation factors (clotting factors) o Usually includes Factor VIII, von Willebrand s factor, fibrinogen (250 mg), Factor XIII Indications: o Hypofibrinogenemia (fibrinogen < 200 mg/dl) o Hemorrhage with evidence of dysfibrinogenemia o Factor XIII deficiency o Uremic bleeding used in hemophilias, von Willebrand's disease, DIC, uremic bleeding also to prepare "fibrin glue" for cardiothoracic surgery since it contains fibrinogen although expert opinion does not recommend this use

10 Adv Pathophysiology Unit 4 Page 10 of 18 Fresh frozen plasma (FFP): unconcentrated source of all clotting factors except platelets use in liver failure, bleeding EUD, to supplement RBC in exchange transfusion Dosing: o Dose of 10 ml/kg usually provides coagulation factors to achieve hemostasis o Blood bank may refer to it as FFP plasma Supplementing PRBC with FFP: o Typical transfusion usual ratio is 1:4 (FFP:PRBC) o Massive transfusion (10+ units for an adult, or replacement within 24 hours of a volume of blood equal to or more than one person s blood volume) newer thinking is a 1:1 ratio based on mortality results (Duchesne JC, et al. Review of current blood transfusions strategies in a mature Level 1 trauma center: were we wrong for the last 60 years? J Trauma 2008;65: ) Other indications for plasma transfusion: o Hemorrhage with coagulation factor deficiency (factor level <50% or INR >1.5) o Invasive procedure with significant risk of bleeding and coagulation factor deficiency (factor level <50% or INR >1.5) o Acute resuscitation in trauma o Thrombotic thrombocytopenic purpura o Acute reversal of warfarin Adverse events: o Acute lung injury o Allergic reactions o Volume overload Granulocytes: for chemotherapy patients or sepsis. Whole blood: for rapid massive blood loss although again, most blood banks recommend PRBC and FFP+platelets instead for infant exchange transfusions (in hemolytic disease of newborn)

11 Adv Pathophysiology Unit 4 Page 11 of HEMATOCRIT ASSESSMENT AFTER TRANSFUSION: Each unit of PRBC raises Hb by 1 gm/dl and the Hct by 3% Hb/Hct can be checked 15 minutes after transfusion completed no need to wait 24 hrs as previously thought this is true if the patient is not actively bleeding if actively bleeding, the Hct may continue to drop and the recheck value may not be reliable Reference: Wiesen, AR, Hospenthal, DR, et al. Equilibration of Hemoglobin Concentration after Transfusion in Medical Inpatients after Transfusion, Not Actively Bleeding. Ann Intern Med, 1994; 121: At:

12 Adv Pathophysiology Unit 4 Page 12 of TRANSFUSION REACTIONS & COMPLICATIONS: An immediate transfusion reaction is due to complement activation, delayed reaction to production of IgM antibodies. Prevention with compatibility testing (cross-matching) before transfusion: determines ABO/Rh, tests for any Ab in recipient blood, then tests donor blood for RBC-Ag. Different types of reactions: most common are febrile nonhemolytic and chill-rigor reactions Presentation: chills, rigors, fever, dyspnea, light-headedness, urticaria, itching, and flank pain Protocol: o Stop transfusion, do not restart or use other units that have been issued o keep IV line open with saline o send blood back to blood bank to investigate along with clotted & anticoagulated blood from the patient If urgent need for immediate transfusion, use type O Rh-negative RBCs should be used Most common causes of transfusion related DEATH: o ABO incompatibility (# 1) o Acute lung injury (# 2) Nice overview:

13 Adv Pathophysiology Unit 4 Page 13 of 18 Febrile nonhemolytic reactions: WBC antibodies to WBC HLA appear in patient's plasma after multiple transfusions due to exposure of patient to WBC with multiple foreign Ag o can also occur in multiparous women o can also occur in platelet concentrates due to cytokines released from stored cells o these are not true incompatibility reactions o these then react with WBC in later transfusions Presentation: o temperature increase of 1 C o headache, back pain o sometimes also allergic reactions (urticaria, pruritus) o if fever & chills occur, you must suspect HEMOLYTIC reaction so, you still have to stop the transfusion and investigate the possibility (same diagnostic workup as hemolytic reaction) Treatment: o pretreatment with acetaminophen and diphenhydramine for future transfusions o if patient has had more than one febrile reaction in the past, use leukoreduction filters as well as leukoreduced blood components ( washed or filtered )

14 Adv Pathophysiology Unit 4 Page 14 of 18 Hemolytic reactions acute hemolytic transfusion reactions (AHTR): Why hemolysis occurs: o usually hemolysis of donor RBCs from ABO/Rh incompatibility, plasma antibodies (immunoglobulns), or use of hemolyzed/fragile donor RBC (over-warming stored blood or infusing in hypotonic solutions) o most severe type of hemolysis is due to donor RBC interacting with antibody (immunoglobulin) in recipient plasma o reaction can be acute (within 23 hr) or delayed (1-14 days later) o the hemolysis is INTRAvascular o possibly disseminated intravascular coagulation (DIC) with pink/red color of patient's blood when centrifuged (seeing free Hb in the serum) o hemoglobinuria with acute renal failure as end-organ damage (renal tubular damage from free Hb) Acute Presentation: o may occur immediately, or sometime during the transfusion, occasinaly 1 hour later o symptoms are discomfort and anxiety, dyspnea/fever/chills, facial flushing o may also have severe pain in the lumbar area, nausea/vomiting o shock with rapid/feeble pulse, cold/clammy skin, hypotension o after the hemolysis, jaundice can occur If under ANESTHESIA: o may only see the hypotension o at incision or operative site or mucous membranes, may see bleeding due to the DIC o looking at urine, it may appear dark due to hemoglobinuria Management: o IV fluids to try to flush renal tubules o furosemide to maintain renal function o recheck patient ID and unit ID, STOP transfusion o worry about giving pressor drugs that may reduce renal function (e.g. epinephrine, norepinephrine, high-dose dopamine) usually use low-dose dopamine if needed o if no diuretic response within 2-3 hours, may need dialysis nephrology consult is done immediately once AHTR is suspected Lab diagnostics: o urine Hb (positive) o serum LDH & bilirubin (elevated due to RBC hemolysis) o serum haptoglobin (low because free Hb binds to the haptoglobin) Prognosis: o usually good o renal failure recovery when diuresis is seen o prolonged oliguria and/or shock are poor prognostic signs Delayed hemolytic reaction: o an anamnestic response to RBC antigen o may have slight fever, or more rarely similar severe symptoms as acute AHTR o Hb drops 1-2 weeks after transfusion

15 Adv Pathophysiology Unit 4 Page 15 of 18 Hypersensitivity (HSR Type I) allergic reactions: Hypersensitivity to an unknown component in donor blood (allergens in donor plasma) Presentation: o usually mild o may have pruritis or urticaria o maybe edema, dizziness, headache o rarely spasm of smooth muscle causing wheezing and involuntary voiding o rarely anaphylaxis Pathophysiology: o Often IgA mediated an IgE has been formed as anti-iga Management: o Can pretreat with antihistamine to prevent o during reaction, can use diphenhydramine and steroid (e.g. solucortef) o some patients with more severe reactions need washed RBC, platelets Circulatory (volume) overload: osmotic load increases COP in the vascular space that causes volume overload usually in patients with pre-existing cardiac or renal insufficiency must observe for signs of heart failure (dyspnea, rales) Treatment: loop diuretic (e.g. furosemide) Massive transfusions: Definition: transfusion within 24 hours of a volume of blood equal to or more than one person s blood volume (10 units in a 70-kg adult) Washout: Patient s own blood is washed out o disseminated intravascular coagulation (DIC) o dilutional thrombocytopenia (platelets in whole blood are not functional) o microvascular bleeding (oozing and bleeding from raw and cut surfaces) since patient s clotting factors are washed out o Treatment replaces clotting factors: give 5-10 units of platelet concentrate may also need FFP (fresh frozen plasma) Citrate toxicity & Hypocalcemia: o pediatric & liver failure patients can t metabolize citrate and develop hypocalcemia o Treatment: IV 10% calcium gluconate 10 ml in 100 ml D5W over 10 min Acute lung injury: anti-hla and/or anti-granulocyte antibodies in donor plasma agglutinate and cause degranulation of lung granulocytes Presentation: o noncardiogenic pulmonary edema (adult respiratory distress syndrome) o second most common cause of death, but many cases are mild Treatment: o supportive therapy o avoid diuretics

16 Adv Pathophysiology Unit 4 Page 16 of 18 Altered oxygen affinity: older blood (more than one week old) has reduced 2,3-DPG in the RBC blood older than 10 days has no 2,3-DPG The hemoglobin is shifted to the left with an increased affinity for oxygen and slower release to the tissues Clinically significant in: o infants with exchange transfusion o sickle cell patients with acute chest syndrome & stroke o patients with severe heart failure Within hours, the 2,3-DPG regenerates Risk of Sepsis: must balance rate of infusion so that it is slow enough to avoid rapid volume overload but, can t be overly long due to risk of bacterial growth of blood reaching room temperature Microaggregates: old stored blood develops microaggregates form (platelets, WBC, fibrin) that deposit in recipient patient lungs. Use very fine filters for massive transfusions of blood that has been stored more than 5-6 days. Cold reaction: usually due to rapid transfusion of large amounts of cold blood Presentation: o cardiac arrhythmias o cardiac arrest Prevention: o may need to heat tubing (use IV set with heat-exchange device) o do NOT microwave can cause hemolysis of RBC o do NOT heat the blood bag -- blood returned to lab unused cannot be rechilled, and bacteria will grow rapidly if warmed. Potassium toxicities: renal failure may develop elevated potassium if given blood more than 1 week old (due to potassium accumulation) mechanical hemolysis during transfusion can increase potassium (e.g. transfusing through a small needle/catheter) older RBC (more than 3 weeks old) can take up potassium and recipient develops hypokalemia

17 Adv Pathophysiology Unit 4 Page 17 of 18 Disease Transmission (Infectious complications): RBC units: o bacterial contamination should be rare and RBC units are inspected for color change that can indicate bacteria o refrigeration also limits bacterial growth (except for cryophilic Yersinia sp which can produce endotoxin) Platelet units: o stored at room temperature so more potential for bacteria and endotoxin o storage limited for 5 days for this reason and units are cultured Bloodborne pathogens: o syphilis (serologic tests for syphilis may be negative in early stages of disease, so donors may have disease and still have negative test results) o Viral hepatitis risk is reduced by viral heat inactivation o HIV very very rare (1:2.6 million risk) o CMV (cytomegalovirus) transmission is via WBC more of a problem for immunocompromised recipients who should receive CMV-negative products using filtered (WBC reduced) units o HTLV-I (Human T-lymphotrophic virus type I) causes adult T-cell lymphoma/leukemia, myelopathy, and tropical spastic paraparesis blood is tested for this virus o CJD (Cretuzfeldt-Jakob Disease) not reported, and risk is further reduced by prohibiting donation by those who have received human-derived growth hormone or dura mater transplant or with family member with CJD o mad cow (bovine spongiform encephalopathy risk reduced by prohibiting people who have spent a long time in the United Kingdom o malaria transmitted via infected RBCs donors are asked about travel and medical history Graft vs host disease (GVHD): immunocompetent lymphocytes are transfused into an immunocompromised host and donor lymphocytes attack host tissues (also can occur with blood from close relative due to matching HLA type) Presentation: o fever, serious skin rash (starts at trunk and spreads centrifugally and develops into erythroderma with bullae), vomiting, bloody diarrhea, lymphadenopathy, pancytopenia (from bone marrow aplasia), jaundice & elevated LFTs o occurs several days to a month after transfusion Workup: bone marrow and skin biopsies Mortality: more than 90% (no treatment is available) Prevention: o irradiate blood products to damage DNA of donor lymphocytes o done for immunocompromised patients, if using blood from a first-degree relative, if using HLA-matched components o recipient must be severely immunocompromised (not just taking corticosteroids or other immunosuppressants) to be an indication for irradiation

18 Adv Pathophysiology Unit 4 Page 18 of 18 THERAPEUTIC HEMAPHERESIS: Removal of harmful constituent(s) from patient's blood and then returning the blood to the patient Plasmapheresis: plasma exchange removes plasma components. Plasmapheresis is similar to dialysis, except that plasma exchange can also remove proteinbound toxic substances. Clinical: o experimental use in autoimmune disease multiple sclerosis (MS), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) o proven benefit in other diseases that are also autoimmune myasthenia gravis (MG), Guillain-Barre (GB), thrombocytopenic purpura (TTP). o Multiple complications (citrate reduces Calcium, may need a-v fistula, fluid shifts, reduced needed plasma components). Cytapheresis: (cytoreduction) removes excessive numbers of blood cells. Cytapheresis can reduce pathological elevations in blood cells e.g. o Thrombocytosis (platelets) o Leukocytosis (WBC) o Polycythemia (RBC) Blood is removed and discarded (any abnormal blood cannot be used in transfusions to others) reduces blood tumor burden (used in addition to chemotherapy)