Clinical Applications ofTherapeutic Apheresis   Raul H. Morales-Borges, MD         Medical Director          Blood Service...
Origin of the Word “APHERESIS”   Greek   Means “Withdrawal   Blood components are separated by    centrifugation accord...
Density of blood components   Plasma 1.025-1.029   Platelets 1.040-1.045   Lymphocytes 1.050-1.061   Granulocytes 1.08...
Blood Component Separation
Definition of TPE•Removal of large volumes of patient plasma and replacement of the plasma with appropriatefluids.Specialt...
Therapeutic Apheresis (TA)   Whole blood is removed from the patient    into an instrument that separates its    componen...
TA Technologies       Membrane             Centrifugation   Prisma Gambro BCT   Asahi Plasma Flow   Cascade apheresis f...
Apheresis in Clinical Practice    Sickle Cell Dis.    Malaria                   Thrombocytosis             RBC        WBC ...
Bloodletting and Plasmapheresis
“When it comes to bloodletting four        questions must be answered”   Who?   When?   How much?   Which Fluids?
Removed with                   Plasma•Immune complexes•Immunoglobulins (IgG, IgM, IgA)•Abnormal/increased amounts of plasm...
Access   Plamapheresis is an extracorporeal theapy    and as such is dependent on adequate    central vascular access.  ...
A “perfect” apheresis catheter: Dual lumen Staggered ports Large-bore lumens Minimal length Sufficient firmness Biocompati...
How much?   Volume of exchange    • 1-1.5 plasma volume         Calculation depends on numerous factors    • Frequency o...
Important Formulas   Total Blood Volume= 0.065 x Kg   Plasma Volume=(0.065 x Kg) x (1 –    Hct in decimal number)   Red...
Efficiency of Plasmapheresis   What is being                  Efficiency of Plasmapheresis    removed?                  7...
Frequency of                ProceduresDisease specific:     IgM removal: Predominantly     intravascular Procedure may be ...
Exchange Fluids   5% Albumin    • Best choice    • Dilute only with saline   Combination of saline and albumin   FFP  ...
Replacement FluidCrystalloids: Contain no protein. Normalsaline 0.9%   Ex: in combination with albumin   replacementColloi...
Anticoagulant•ACD-A:   Binds to Ca++.      Lowers pH of the blood. Inhibits platelet clumping.   Acts as an extracorporeal...
Diseases Treated with TA             Guillain-Barre Syndrome 11%             Guillain-Barre Syndrome 11%               Mya...
American Society for Apheresis         (ASFA) Guidelines   Indications by Category (there are 4    categories).   There ...
Category I: Apheresis is considered primaryor standard.Category II: There is sufficient evidence tosuggest efficacy, usual...
Renal and metabolic diseases:  Antiglomerular basement  membrane antibody disease (cat.  I)  Rapidly progressive  glomerul...
Hematologic diseases:  ABO-mismatched marrow transplant  (cat. II)  Thrombotic thrombocytopenia purpura  (cat. I)  Myeloma...
Neurologic disorders:  Guillain-Barré syndrome (Acute  inflammatory demyelinating  polyradiculoneuropathy)(cat. I)  Chroni...
Modified McLeod’s Criteria for     Evaluation of Efficacy of      Therapeutic Apheresis  Evidence        Mc Leod’s    Expl...
ASFA 2010 Indication Categories                for TA   There are 68 diseases.   There are many TA accordingly to the di...
General Issues to be ConsideredWhen Evaluating a New patient for         Initiation of TA   Rationale   Impact   Techni...
Risks / Side effects of TA            The overall rate is < 5%.   Transfusion Reactions   Nausea/Vomiting   Hypotension...
Use of Calcium in           Preventing Symptoms   TUMS 1000 mg po 30 minutes prior    the procedure and halfway of the   ...
Use of Magnesium   IV Magnesium as per an article from    FDA, NIH, Walter Reed ARMY    Institute of Research (Salim Hadd...
Metabolic Alkalosis due to TPE   It’s common in patients with    decreased renal function.   Secondary to large sodium c...
Blood Component Collection by Apheresis   Began in the 1970’s.   Platelet donors are limited to 24    collections during...
Use in Hematopoietic Stem Cell      Transplatation as Mobilization &          Collection of PBHPC’s   Last Standards & Ru...
TTP – A Thrombotic Microangiopathy   Microvascular Occlusive Disorder   Platelet thrombi   Thrombocytopenia   Mechanic...
TTP – hyaline thrombi in      glomerolus
TTP – Mortality Rate 90% 80% 70% 60% 50% 40% 30% 20% 10%  0%Before Plasma Exchange   After Plasma Exchange
Pathophysiology of TTP   Presence of Unusually Large von    Willebrand Factor Multimers    (ULvWFM)   Absence or low lev...
Plasma Exchange in TTP          FFP as exchange fluid   Removal of auto-antibodies to vWF    multimers cleaving enzyme  ...
Pathophysiology of TTP          Normal                                     TTPCleaved von Willebrand Factormultimers      ...
Diagnosis            From Pentad to Triad   Thrombocytopenia         Thrombocytopenia   MAHA                     MAHA...
Conditions Associated with TTP   Primary (idiopathic)   Secondary    • Systemic autoimmune           • Drugs      disord...
Treatment of TTP   Daily plasma exchange   Exchange fluids    •   FFP    •   Cryopoor plasma    •   Detergent treated pl...
Treatment of persistent TTP   Plasma exchange   Corticosteroids   Vincristine   Rituximab   Splenectomy
Treatment of relapsing TTP   Plasma exchange   Treat beyond improvement   Consider adding medications   Splenectomy  ...
TTP/HUS (Hemolytic Uremic             Syndrome)   HUS    • MAHA    • Renal failure   Classic HUS    • Childhood, Escheri...
Rapidly Progressive Glomerulonephritis    (RPGN); Crescentic Glomerulonephritis   Subacute deterioration of renal    func...
Rapidly Progressive Glomerulonephritis    (RPGN); Crescentic Glomerulonephritis   Goodpasture’s syndrome (Anti-Glomerular...
Goodpasture’s syndrome   Anti-GBM antibodies crossrective    with alveolar basement membrane
Goodpasture’s Syndrome   Clinical presentation    •   RPGN    •   Pulmonary hemorrhage    •   Anti-GBM antibodies   Trea...
Antineutrophil Cytoplasmic               Antibodies•   ANCA by immunofluorescence    methods     • c-ANCA = Wegener’s     ...
Vasculitis
ANCA positive Pauci Immune                  RPGN   Clinical presentation    •   RPGN with or without pulmonary hemorrhage...
Immune Complex RPGN (MPGN)
Immune Complex RPGN   Clinical presentation    •   RPGN    •   Membranoproliferative GN (MPGN)   Associations    •   Hep...
Acute Inflammatory Demyelinating                Polyradiculoneuropathy (AIDP)                             ‘               ...
Anti-myelin Antibodies
GBS Clinical Course                        GBS courseSymptom severity                            Time
Myasthenia Gravis                      NerveAcetylcholine (Ach)      AchR                     Anti-AchR Ab                ...
Myasthenia Gravis   Clinical picture    • Variable degrees of weakness; improved by      rest    • Thymoma in 15% of pati...
Myasthenia Gravis   Plasmapheresis    • Acute myasthenic crisis    • Respiratory insufficiency    • Failure to respond to...
Myasthenia GravisBefore plasmapheresis          After Plasmapheresis
Hyperviscosity Syndrome   Causes    • Wadenstrom’s macroglobulinemia 50%    • Multiple myeloma 5%   Clinical presentatio...
Systemic Lupus Erythematosus                (SLE)   Systemic autoimmune disease with the    presence of autoantibodies an...
Red Cell Exchange   Sickle Cell Disease   Malaria   Babesiosis
Sickle Cell Disease   Clinical picture    • Chronic genetic anemia    • Hgb S instead of Hgb A alters the erythrocytes an...
Malaria   Cause    • Plasmodium falciparum, vivax, ovale, malariae    • Transmitted by female anopheline mosqito    • Inf...
White Cell Depletion                   Leukapheresis   Leukocytosis    •   Acute Myelogenous Leukemia (AML)    •   Chroni...
Plateletpheresis   Thrombocytosis (>1,000 x 10 /L)        9    • Essential    • Polycytemia vera   Clinical picture    •...
Rheumatoid Arthritis   Chronic inflammatory autoimmune disease    • Arthritis    • Rheumatoid nodules    • Serum rheumato...
Protein A binds IgG
Protocols for Reducing anti-HLA    antibodies in positive CXM and                  AMR   IVIG alone   Plasmapheresis and...
Protocols for Reducing anti-HLA antibodies in positive CXM and AMR                                        30% rejectionIVI...
LDL Apheresis   Using Liposorber or HELP system   For LDL > 300 mg/dl or LDL > 200    mg/dl plus CAD   Can be used in s...
Extracorporeal photopheresis   Immunomodulatory effect   Cellex or TheraKos   Using 8MSO 0.6 mg/kg   For:    • CTCL   ...
Quality & Audit Management   cGMP, cGTP, SOP’s, CFR   FDA requirements & AABB standards   OSHA, CMS, Joint Commission ...
Summary   Therapeutic Apheresis is an    outpatient or inpatient procedure    that usually takes two to three hours    an...
References   Journal of Clinical Apheresis, Vol.15,    No.1/2, 2000, Special Issue, Clinical    Applications of Therapeut...
Cont. References   R Bambauer, R Latza, R Schiel: Therapeutic Apheresis in the Treatment of    Hemolytic Uremic Syndrome ...
Dr. Raúl H. Morales Borges                    Hematólogo/Oncólogo   Cruz Roja                                Ashford Med...
Gracias
Clinical Applications Of Therapeutic Apheresis
Clinical Applications Of Therapeutic Apheresis
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  • 18
  • Clinical Applications Of Therapeutic Apheresis

    1. 1. Clinical Applications ofTherapeutic Apheresis Raul H. Morales-Borges, MD Medical Director Blood Services American Red Cross of Puerto Rico
    2. 2. Origin of the Word “APHERESIS” Greek Means “Withdrawal Blood components are separated by centrifugation accordingly to relative density.
    3. 3. Density of blood components Plasma 1.025-1.029 Platelets 1.040-1.045 Lymphocytes 1.050-1.061 Granulocytes 1.087-1.092 Erythrocytes1.078-1.114
    4. 4. Blood Component Separation
    5. 5. Definition of TPE•Removal of large volumes of patient plasma and replacement of the plasma with appropriatefluids.Specialty areas: •Renal and metabolic diseases •Hematologic diseases •Neurologic disorders
    6. 6. Therapeutic Apheresis (TA) Whole blood is removed from the patient into an instrument that separates its components via a centrifugation process. The goal is to selectively remove a substancial proportion of one or more components causing disease while returning the remaining components to the patient, with or without replacement of the removed component.
    7. 7. TA Technologies Membrane Centrifugation Prisma Gambro BCT Asahi Plasma Flow Cascade apheresis for selective plasma component removal Specialized devices
    8. 8. Apheresis in Clinical Practice Sickle Cell Dis. Malaria Thrombocytosis RBC WBC PLT Plasma Leukemias TTP Cell Therapies Guillain Barre Syn. Myasthenia Gravis Goodpasture’s Syn. Waldenstrom’s
    9. 9. Bloodletting and Plasmapheresis
    10. 10. “When it comes to bloodletting four questions must be answered” Who? When? How much? Which Fluids?
    11. 11. Removed with Plasma•Immune complexes•Immunoglobulins (IgG, IgM, IgA)•Abnormal/increased amounts of plasma protein•Cholesterol••Plasma metabolic waste products•Plasma protein bound poisons
    12. 12. Access Plamapheresis is an extracorporeal theapy and as such is dependent on adequate central vascular access. As plasmapheresis results in profound immunosuppression, a tunnelled line is preferred. Baxter/Edwards Bloodlines are used. Apheresis/dialysis-compatible catheter vendors include MedComp, Quinton Intruments, Vascath, Arrow, and Vaxcel.
    13. 13. A “perfect” apheresis catheter: Dual lumen Staggered ports Large-bore lumens Minimal length Sufficient firmness Biocompatibility Infection resistance
    14. 14. How much? Volume of exchange • 1-1.5 plasma volume  Calculation depends on numerous factors • Frequency of procedures • Duration of therapy
    15. 15. Important Formulas Total Blood Volume= 0.065 x Kg Plasma Volume=(0.065 x Kg) x (1 – Hct in decimal number) Red Cell Volume= Hct in decimal x TBV
    16. 16. Efficiency of Plasmapheresis What is being Efficiency of Plasmapheresis removed? 70 60 • IgG - mainly 50 40 1 plasma vol 1.5 plasma vol extravascular Percent 30 2 plasma vol 20 • IgM – mainly 10 0 intravascular
    17. 17. Frequency of ProceduresDisease specific: IgM removal: Predominantly intravascular Procedure may be done every other day. IgG removal: Predominantly extravascular Procedure may be done daily.
    18. 18. Exchange Fluids 5% Albumin • Best choice • Dilute only with saline Combination of saline and albumin FFP Cryopoor plasma Cryoprecipitate (vWF mediates in recurrent TTP; also used to avoid fluid overload)
    19. 19. Replacement FluidCrystalloids: Contain no protein. Normalsaline 0.9% Ex: in combination with albumin replacementColloids: Contain protein 5% albumin Ex: Guillian-Barré, myasthenia gravisFresh frozen plasma/cryo-poor plasma Ex: TTP, HUS (thrombotic microangiopathies)6% hetastarch, pentastarch
    20. 20. Anticoagulant•ACD-A: Binds to Ca++. Lowers pH of the blood. Inhibits platelet clumping. Acts as an extracorporeal anticoagulant. May cause hypocalcemia.•Heparin: Complexes with antithrombin and increases its activity which inactivates thrombin and other factors and prevents thrombus formation.* Acts as a systemic anticoagulant. There are individual sensitivities and elimination rates. Can cause heparin induced thrombocytopenia.*Essentials of hemostasis and thrombosis drugs used inmanagement of thrombosis.
    21. 21. Diseases Treated with TA Guillain-Barre Syndrome 11% Guillain-Barre Syndrome 11% Myasthenia Gravis 12% Myasthenia Gravis 12% CIDP 8% CIDP 8% Cryoglobulinemia 30% Cryoglobulinemia 30% Anti-GBM Disease 30% Anti-GBM Disease 30% Pauci-immune RPGN 13% Pauci-immune RPGN 13% SLE nephropathy 10% SLE nephropathy 10% Myeloma kidney 7% Myeloma kidney 7% Recurrent FSG 5% Recurrent FSG 5% Renal transplantation 5% Renal transplantation 5%
    22. 22. American Society for Apheresis (ASFA) Guidelines Indications by Category (there are 4 categories). There are 3 levels of evidence. There are 2 grade recommendations.
    23. 23. Category I: Apheresis is considered primaryor standard.Category II: There is sufficient evidence tosuggest efficacy, usually in an adjunctiverole.Category III: Insufficient data to determineeffectiveness. Isolated published studieshave indicated that it may be of benefit as a“last-ditch” effort.Category IV: Controlled trials have notshown benefit.
    24. 24. Renal and metabolic diseases: Antiglomerular basement membrane antibody disease (cat. I) Rapidly progressive glomerulonephritis (cat. II) Familial hypercholesterolemia (cat. II) Cryoglobulinemia (cat. II)
    25. 25. Hematologic diseases: ABO-mismatched marrow transplant (cat. II) Thrombotic thrombocytopenia purpura (cat. I) Myeloma, paraproteins, or hyperviscosity (cat. II) Coagulation factor inhibitors (cat. II)
    26. 26. Neurologic disorders: Guillain-Barré syndrome (Acute inflammatory demyelinating polyradiculoneuropathy)(cat. I) Chronic inflammatory demyelinating Polyradiculoneuropathy (cat. I) Myasthenia gravis (cat. I) Cryoglobulinemia with polyneuropathy (cat. II)
    27. 27. Modified McLeod’s Criteria for Evaluation of Efficacy of Therapeutic Apheresis Evidence Mc Leod’s Explanation CriteriaMechanism Plaussible Clear Pathogenesis RationaleCorrection Better Blood Meaningfully CorrectedClinical Effect Perkier Clinically Patients Worthwhile
    28. 28. ASFA 2010 Indication Categories for TA There are 68 diseases. There are many TA accordingly to the diseases. Few of the procedures are: • Total Plasma Exchange (TPE) • RBC Exchange • Extracorporeal Photopheresis (ECP) • Immunoadsorption (IA) • Thrombocytapheresis & Leukocytapheresis • Selective removal methods • Adoptive Cytapheresis • Membrane differential filtration • Cryofiltration apheresis
    29. 29. General Issues to be ConsideredWhen Evaluating a New patient for Initiation of TA Rationale Impact Technical Issues Therapeutic Plan Clinical and/or laboratory end-points Timing & Location
    30. 30. Risks / Side effects of TA The overall rate is < 5%. Transfusion Reactions Nausea/Vomiting Hypotension, hypovolemia, fluid overload Vasovagal reactions Pallor, tachycardia, respiratory distress, muscle spasm, chills, rigors Hematomas, venous sclerosis, thrombosis, bleeding, infection Hypocalcemia from citrate
    31. 31. Use of Calcium in Preventing Symptoms TUMS 1000 mg po 30 minutes prior the procedure and halfway of the procedure (As recommended by Medical Directors Consensus from ARC) Or Use Calcium Gluconate as always.
    32. 32. Use of Magnesium IV Magnesium as per an article from FDA, NIH, Walter Reed ARMY Institute of Research (Salim Haddad et al: Transfusion June 2005; 45: 934-944).
    33. 33. Metabolic Alkalosis due to TPE It’s common in patients with decreased renal function. Secondary to large sodium citrate load given during the procedure. Can be prevented when using 3% albumin and cryoprecipitate rather than FFP’s Pearl RG, Rosenthal MH: American Journal of Medicine 1985 Sep; 79(3): 391-393.
    34. 34. Blood Component Collection by Apheresis Began in the 1970’s. Platelet donors are limited to 24 collections during a rolling 12-month period. RBC’s donors are limited to donate 2 units every 16 weeks. Single whole blood or one PRBC’s unit donor every 8 weeks.
    35. 35. Use in Hematopoietic Stem Cell Transplatation as Mobilization & Collection of PBHPC’s Last Standards & Rules by FDA on 11/24/2004 and effective on 05/25/2005. Goal: To achieve the Product CD34+ cell counts appropriate for infusion to the recipient.
    36. 36. TTP – A Thrombotic Microangiopathy Microvascular Occlusive Disorder Platelet thrombi Thrombocytopenia Mechanical damage to erythrocytes 70% of patients are women
    37. 37. TTP – hyaline thrombi in glomerolus
    38. 38. TTP – Mortality Rate 90% 80% 70% 60% 50% 40% 30% 20% 10% 0%Before Plasma Exchange After Plasma Exchange
    39. 39. Pathophysiology of TTP Presence of Unusually Large von Willebrand Factor Multimers (ULvWFM) Absence or low levels of ADAMTS13 (vWF cleaving metalloprotease) Presence of auto-antibodies to ADAMTS13
    40. 40. Plasma Exchange in TTP FFP as exchange fluid Removal of auto-antibodies to vWF multimers cleaving enzyme Infusion of vWF multimers cleaving enzyme
    41. 41. Pathophysiology of TTP Normal TTPCleaved von Willebrand Factormultimers Platelet aggregatevWF-CleavingEnzyme Auto-antibody to vWF-Cleaving Uncleaved unusually Enzyme large vWF multimers Endothelial Cell Endothelial Cell
    42. 42. Diagnosis From Pentad to Triad Thrombocytopenia  Thrombocytopenia MAHA  MAHA CNS symptoms  LDH elevation Renal insufficiency Fever
    43. 43. Conditions Associated with TTP Primary (idiopathic) Secondary • Systemic autoimmune • Drugs disorders  Ticlopidine  SLE  Clopidrogel  Rheumatoid arthritis  Cyclosporine A  Scleroderma  Tacrolimus  Polyarteritis nodosa  Quinine • Infectious diseases • Neoplastic diseases  HIV infection • Surgeries  Bacterial endocarditis  Cardiovascular  Intestinal • PBSC transplantation • Pregnancy
    44. 44. Treatment of TTP Daily plasma exchange Exchange fluids • FFP • Cryopoor plasma • Detergent treated plasma Treat until clinical symptoms improve and laboratory values normalize Avoid platelet transfusions
    45. 45. Treatment of persistent TTP Plasma exchange Corticosteroids Vincristine Rituximab Splenectomy
    46. 46. Treatment of relapsing TTP Plasma exchange Treat beyond improvement Consider adding medications Splenectomy Look for other disease association
    47. 47. TTP/HUS (Hemolytic Uremic Syndrome) HUS • MAHA • Renal failure Classic HUS • Childhood, Escherichia coli 0157:H7 association Adult HUS • Renal disease is more severe • Difficult to differentiate from TTP Platelet – fibrin thrombi Normal ADAMTS 13 (vWF cleaving enzyme) levels No auto-antibody to ADAMTS Response to plasma exchange – equivocal results
    48. 48. Rapidly Progressive Glomerulonephritis (RPGN); Crescentic Glomerulonephritis Subacute deterioration of renal function Crescents in glomeruli Various etiologies
    49. 49. Rapidly Progressive Glomerulonephritis (RPGN); Crescentic Glomerulonephritis Goodpasture’s syndrome (Anti-Glomerular Basement Membrane Disease or Anti-GBM Disease) Pauci immune RPGN (Wegener’s Granulomatosis or microscopic polyarteritis with antineutrophil cytoplasmic antibodies (ANCA) RPGN with granular immune complex deposits sometimes associated with systemic vasculitis
    50. 50. Goodpasture’s syndrome Anti-GBM antibodies crossrective with alveolar basement membrane
    51. 51. Goodpasture’s Syndrome Clinical presentation • RPGN • Pulmonary hemorrhage • Anti-GBM antibodies Treatment • Immunosuppressive drugs  Cyclophosphamide  Corticosteroids  Azathioprine • Plasmapheresis (ASFA Category I)  Daily pheresis for 14 days with 5% albumin, 1-1 ½ plasma volume  Finish procedure with 1 liter of FFP in cases with pulmonary hemorrhage and /or renal biopsy
    52. 52. Antineutrophil Cytoplasmic Antibodies• ANCA by immunofluorescence methods • c-ANCA = Wegener’s disease (60% to 90%) • p-ANCA = microscopic polyangiitis (MPA) (50% to 80%), UC (40% to 80%), Crohn’s (10% to 40%)Hoffman GS. Arth Rheum. 1998;41(a):1521–1537.
    53. 53. Vasculitis
    54. 54. ANCA positive Pauci Immune RPGN Clinical presentation • RPGN with or without pulmonary hemorrhage • Perinuclear (p-ANCA)-systemic microvasculitis • Internuclear (c-ANCA)-Wegener’s granulomatosis Treatment • Immunosuppressive drugs • Plasmapheresis (ASFA Category II) may benefit patients with severe renal disease (Cr 9) and dialysis dependent patients
    55. 55. Immune Complex RPGN (MPGN)
    56. 56. Immune Complex RPGN Clinical presentation • RPGN • Membranoproliferative GN (MPGN) Associations • Hepatitis C • Cryoglobulinemia Treatment • Antiviral drugs • Corticosteroids • Plasmapheresis (ASFA Category II)
    57. 57. Acute Inflammatory Demyelinating Polyradiculoneuropathy (AIDP) ‘ Guillain-Barre Syndrome (GBS) Pathogenesis • Anti-myelin (gangliosides) antibodies GM1, GM1b, GD1a Clinical presentation • Ascending paralysis • “albuminocytologic dissociation”  High CSF protein  No CSF pleocytosis • 10-23% require assisted ventilation • Nerve conduction studies show demyelination • dysautonomia Treatment • Supportive care • IVIG 400mg/kg x 5 days • Plasmapheresis (ASFA Category I)  Start within 14 days of onset  5-6 Q.O.D. procedures, 1-1 1/2 plasma volume exchange with 5% albumin
    58. 58. Anti-myelin Antibodies
    59. 59. GBS Clinical Course GBS courseSymptom severity Time
    60. 60. Myasthenia Gravis NerveAcetylcholine (Ach) AchR Anti-AchR Ab Muscle
    61. 61. Myasthenia Gravis Clinical picture • Variable degrees of weakness; improved by rest • Thymoma in 15% of patients Treatment • Mestinon • Prednisone • Imuran or other immunomodulatory meds • Plasmapheresis (ASFA Category I) • IVIG 400 mg/kg x 5 days • Thymectomy
    62. 62. Myasthenia Gravis Plasmapheresis • Acute myasthenic crisis • Respiratory insufficiency • Failure to respond to medications • Side effects of medications (prednisone) • Before and after surgery (thymectomy)
    63. 63. Myasthenia GravisBefore plasmapheresis After Plasmapheresis
    64. 64. Hyperviscosity Syndrome Causes • Wadenstrom’s macroglobulinemia 50% • Multiple myeloma 5% Clinical presentation • Neurologic symptoms • Bleeding diathesis • Retinal hemorrhage and papilledema • Hypervolemia • Congestive heart failure Treatment • Plasmapheresis (ASFA Category II) • Chemotherapy
    65. 65. Systemic Lupus Erythematosus (SLE) Systemic autoimmune disease with the presence of autoantibodies and immune complexes (anti-DNA, anti-DS-DNA) Multiple organ involvement including the kidneys Controlled clinical trials failed to show benefit from plasmapheresis in lupus nephropathy Plasmapheresis (ASFA Category III)
    66. 66. Red Cell Exchange Sickle Cell Disease Malaria Babesiosis
    67. 67. Sickle Cell Disease Clinical picture • Chronic genetic anemia • Hgb S instead of Hgb A alters the erythrocytes and their membranes (sickle red cells) • Increased blood viscosity • Microvascular occlusion  Infarcts in brain, lungs, retina  Pain crisis  Priapism  Acute chest syndrome  Stroke • Treatment  Red cell transfusions  Hydroxyurea  Red cell exchange (ASFA Category I) • Aims to maintain Hgb S <30
    68. 68. Malaria Cause • Plasmodium falciparum, vivax, ovale, malariae • Transmitted by female anopheline mosqito • Infected RBC adhere to endothelial cells of capillaries and postcapillary venules via surface knobs • Microvascular obstruction of brain, kidneys,lungs Clinical picture • Fever, malaise, headache • Neurologic impairment • Renal failure • ARDS Traetment • Chloroquine, quinine, quinidine • Red cell exchange (ASFA Category III) • Plasmapheresis for removal of cytokines to prevent or treat lactic acidosis, hypoglycemia (NR)
    69. 69. White Cell Depletion Leukapheresis Leukocytosis • Acute Myelogenous Leukemia (AML) • Chronic Myelogenous Leukemia (CML) • Acute Lymphocytic Leukemia (ALL) • Chronic Lymphocytic Leukemia (CLL) Clinical picture • Hyperviscosity with microvascular occlusion  CNS symptoms  Hemorrhage  Pulmonary insufficiency Treatment • Combination chemotherapy (tumor cell lysis leads to metabolic imbalance and ARDS) • Leukapheresis (ASFA Category I)  Ptreatment of leukocytosis  Prevention of tumor cell lysis syndrome
    70. 70. Plateletpheresis Thrombocytosis (>1,000 x 10 /L) 9 • Essential • Polycytemia vera Clinical picture • Microvascular occlusion  CNS symptoms  Hemorrhage  Pulmonary insufficiency Treatment • Chemotherapy • Plateletpheresis (ASFA Category I)
    71. 71. Rheumatoid Arthritis Chronic inflammatory autoimmune disease • Arthritis • Rheumatoid nodules • Serum rheumatoid factor Treatment • DMARD (Disease Modifying Anti Rheumatic Drugs) • Anti-TNF alpha monoclonal antibodies • Apheresis  Plasmapheresis (ASFA Category IV)  Lymphoplasmapheresis (ASFA Category II)  Prosorba column (ASFA Category II)
    72. 72. Protein A binds IgG
    73. 73. Protocols for Reducing anti-HLA antibodies in positive CXM and AMR IVIG alone Plasmapheresis and IVIG Plasmapheresis, IVIG and anti-CD20 antibody (splenectomy) AmJTransplant 4(7):1033-1041, 2004
    74. 74. Protocols for Reducing anti-HLA antibodies in positive CXM and AMR 30% rejectionIVIG 42 patients episodes 89% graft survival at 2 yearsPlasmapheres 62 patients 94.2% graftis and IVIG survival at 3 years AmJTransplant 4(7):1033-1041, 2004
    75. 75. LDL Apheresis Using Liposorber or HELP system For LDL > 300 mg/dl or LDL > 200 mg/dl plus CAD Can be used in severe hypertriglyceridemia.
    76. 76. Extracorporeal photopheresis Immunomodulatory effect Cellex or TheraKos Using 8MSO 0.6 mg/kg For: • CTCL • Graft vs. Host Disease • Solid organ transplant rejection • Crohn’s Disease • Scleroderma
    77. 77. Quality & Audit Management cGMP, cGTP, SOP’s, CFR FDA requirements & AABB standards OSHA, CMS, Joint Commission CAP CLIA Foundation for the Accreditation of Cellular Therapy (FACT)
    78. 78. Summary Therapeutic Apheresis is an outpatient or inpatient procedure that usually takes two to three hours and the blood components causing illness are removed from circulation saving lifes. The risks or side effects are manageable or preventable. Its under used. Future review of the guidelines is recommended & encouraged.
    79. 79. References Journal of Clinical Apheresis, Vol.15, No.1/2, 2000, Special Issue, Clinical Applications of Therapeutic Apheresis Journal of Clinical Apheresis 2000-2006 APHERESIS, Principles and Practice, 2nd & 3rd Editions from 2003 & 2010 respectively, Bruce C. McLeod Editor, AABB Press
    80. 80. Cont. References R Bambauer, R Latza, R Schiel: Therapeutic Apheresis in the Treatment of Hemolytic Uremic Syndrome in View of Pathophysiological Aspects. Ther Apher Dial 15(1): 10-19, 2011. ZM Szczepiorkowski et al: Guidelines on the use of therapeutic apheresis in clinical practice-evidence based approach from the Apheresis Applications Committee of the American Society for Apheresis. Jounal of Clinical Apheresis 25: 83-177, 2010. SG Shelat: Practical Considerations for Planning a Therapeutic Apheresis Procedure. The American Journal of Medicine 123(9): 777-784, 2010. Lamont Williams (AABBR Staff Writer): Plasma exchange in Organ Transplantation. AABB News, 8-19, April 2010. K. El-Gharini & DJ. Unsworth: Therapeutic apheresis – pasmapheresis. Clinical Medicine, 6(4): 343-347, July/August 2006. RB Striker, RG Miller & DD Kiprov: Role of plasmapheresis in acute disseminated (postinfectious) encephalitis. J Clin Apher 7(4):173-179, 1992.
    81. 81. Dr. Raúl H. Morales Borges Hematólogo/Oncólogo Cruz Roja  Ashford Medical Americana de PR Center • Servicios de Sangre • Suite # 107 • Ubicados en el • Condado, San Juan Centro Medico de • Tel. 787-722-0412 PR • Fax 787-723-0554 • Tel. 787-759-8100 • Cel. 787-354-0758 • Ext. 3873 • ihoa@coqui.net • Dir. 787-993-3873 • www.ihoapr.com • Cel. 787-505-5814 • MoralesBorgesR@usa.redcross.org
    82. 82. Gracias

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