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Plasmapheresis

Plasmapheresis. Prepared by Dr Majeed H.Shekhany FICMSmed 14/May/2013. Dr Ahmed Akl. Mansoura Urology and Nephrology center. Apheresis from the Greek aphairesis removal Plasmapheresis the removal of plasma from blood Therapeutic Plasma Exchange (TPE): Plasmapheresis +

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Plasmapheresis

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  1. Plasmapheresis Prepared by Dr Majeed H.Shekhany FICMSmed 14/May/2013 Dr Ahmed Akl Mansoura Urology and Nephrology center

  2. Apheresis • from the Greek aphairesis • removal • Plasmapheresis • the removal of plasma from blood TherapeuticPlasmaExchange (TPE): Plasmapheresis + Replacement (FFP, Albumin and/or Saline) Mansoura Urology and Nephrology center

  3. Therapeutic Apharesis Technologies A- Centrifugal plasma separation. B- Membrane plasma separators. Hollow-fiber devices + Standard dialysis equipment * Low TMP (<500 mmHg) to avoid hemolysis. *Blood flow rate: 100-150 ml/min. Mansoura Urology and Nephrology center

  4. Centrifugation • If lower gravity is used more cells and especially platelets will flotate in the plasma compartment. • loss of platelets • Continuous vs sequential • two vs one needle(s) • Continuous: the risk of a drop in BP is less • Anticoagulation: citrate Mansoura Urology and Nephrology center Dr Ahmed Akl

  5. Filtration • diffusion and/or convection/filtration • Two larger veins or double lumen in one larger vein • Anticoagulation: heparin or low molecular weight heparin • Its of 2 types: 1-signle filtration technique 2-double filtration technique Mansoura Urology and Nephrology center Dr Ahmed Akl

  6. Filtration Mansoura Urology and Nephrology center Dr Ahmed Akl

  7. Permeability Of Plasma Filter Mansoura Urology and Nephrology center Dr Ahmed Akl

  8. Double filtration Mansoura Urology and Nephrology center Dr Ahmed Akl

  9. Mansoura Urology and Nephrology center Dr Ahmed Akl

  10. Double filtration • This waste will mainly contain larger molecules • immunoglobulins, immune complex, M-components and LDL-cholesterol • the need of plasma or albumin transfusion is greatly reduced • Anticoagulation: heparin or nafamostate mesilate Mansoura Urology and Nephrology center Dr Ahmed Akl

  11. Mansoura Urology and Nephrology center Dr Ahmed Akl

  12. Double filtration • Hypercholesterolemia • Cryoglobulinemia • hyperviscosity syndroms • mircrocirculatory disorders and antibody mediated diseases

  13. Double filtration • DFPP effectively and safely eliminated anti-ABO antibodies from ABO-incompatible kidney transplantation recipients and contributed to successful ABO-ILKT.

  14. Plasma exchange • the plasma is separated from the blood, discarded in total, and replaced with a substitution fluid • Substitution: albumin, starch and or plasma usually in relation 1:1 to avoid hypotension and hypoperfusion Mansoura Urology and Nephrology center Dr Ahmed Akl

  15. Mansoura Urology and Nephrology center Dr Ahmed Akl

  16. Pharmacokinetic basis for TPE prescription: • Volume: 1 or 2 plasma volumes/session. • Frequency: Daily. • Number of sessions: 5 (can be extended if IgM is the pathogenic AB). • Length of the session : < 2 hours. Estimation of plasma volume: -Approximately 35-40 ml/kg BW - Kaplan’s method: EPV = [0.065 × weight (kg)] × (1 – HCT)

  17. Exchange Fluids • 5% Albumin • Best choice • Dilute only with saline • Combination of saline and albumin • Fresh frozen Plasma (FFP) • starch Mansoura Urology and Nephrology center Dr Ahmed Akl

  18. Indication Dr Ahmed Akl Mansoura Urology and Nephrology center

  19. Plasma exchange • Category I.standard and acceptable, based on controlled or well-designed clinical trials or a broad base of published experience • Category II.generally accepted in a supportive role • Category III.not clearly indicated • Category IV.lack of efficacy Mansoura Urology and Nephrology center Dr Ahmed Akl

  20. Plasma exchange Mansoura Urology and Nephrology center Dr Ahmed Akl

  21. Plasma exchange Mansoura Urology and Nephrology center Dr Ahmed Akl

  22. Plasma exchange Mansoura Urology and Nephrology center Dr Ahmed Akl

  23. Plasma exchange

  24. Plasma exchange

  25. Plasma exchange

  26. Plasma exchange

  27. Emergency indications 1- Anti-GBM disease and/or pulmonary hemorrhage in Goodpasture’s syndrome.: In anti-GBM disease, if plasmapheresis is initiated late in the disease (serum creatinine > 7 mg/dL or after oliguria develops), it is rare that plasmapheresis is effective. 2- Hyperviscosity syndrome with signs and symptoms suggesting impending stroke or loss of vision. 3- Microangiopathic thrombocytopenia [TTP/hemolytic uremic syndrome (HUS)]: TTP with central nervous system (CNS) and renal complications can be a fulminant and rapidly fatal disorder and requires the institution of plasmapheresis as soon as possible.

  28. 4- Patients with very high factor VIII inhibitor levels requiring urgent surgery, to prevent post-surgical bleeding complications. 5- Pulmonary embarrassment in Guillain-Barré Syndrome. 6- Patients with myasthenia gravis and respiratory distress not responding to medication. 7- Acute poisoning with certain mushrooms or with other strongly protein-bound poisons such as parathion or paraquat may require emergency plasmapheresis depending on the severity of the intoxication.

  29. Apheresis in Clinical Practice Sickle Cell Dis. Malaria Thrombocytosis RBC WBC PLT Plasma Leukemias Cell Therapies TTP Guillain Barre Syn. Myasthenia Gravis Goodpasture’s Syn. Waldenstrom’s

  30. Complication

  31. Apheresis • Citrate toxicity • Vascular access complications (hematoma, sepsis, phlebitis, neuropathy) • Vasovagal reactions • Hypovolemia • Allergic reactions • Hemolysis • Air embolus • Depletion of clotting factors • Circulatory and respiratory distress • Transfusion-transmitted disease • Lymphocyte loss • Depletion of proteins and immunoglobulins Denise M. Harmening ,Modern blood banking and transfusion practices, Philadelphia : F.A. Davis, 2005

  32. Plasma exchange • Complications occur more commonly with FFP replacement compared to albumin-saline replacement. • Pruritis and urticaria occur more commonly with FFP • Hypotension occurs more commonly with albumin-saline

  33. TTP – A Thrombotic Microangiopathy • Microvascular Occlusive Disorder • Platelet thrombi • Thrombocytopenia • Mechanical damage to erythrocytes • 70% of patients are women

  34. TTP – hyaline thrombi in glomerolus

  35. TTP – Mortality Rate Before Plasma Exchange AfterPlasma Exchange

  36. 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

  37. Pathophysiology of TTP Normal TTP Cleaved von Willebrand Factor multimers Platelet aggregate vWF-Cleaving Enzyme Auto-antibody to vWF-Cleaving Enzyme Uncleaved unusually large vWF multimers Endothelial Cell Endothelial Cell

  38. Primary (idiopathic) Secondary Systemic autoimmune disorders SLE Rheumatoid arthritis Scleroderma Polyarteritis nodosa Infectious diseases HIV infection Bacterial endocarditis Drugs Ticlopidine Clopidrogel Cyclosporine A Tacrolimus Quinine Neoplastic diseases Surgeries Cardiovascular Intestinal PBSC transplantation Pregnancy Conditions Associated with TTP

  39. Plasma Exchange in TTPFFP as exchange fluid • Removal of auto-antibodies to vWF multimers cleaving enzyme. • Infusion of vWF multimers cleaving enzyme.

  40. 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

  41. Treatment of persistent TTP • Plasma exchange • Corticosteroids • Vincristine • Rituximab • Splenectomy

  42. Treatment of relapsing TTP • Plasma exchange • Treat beyond improvement • Consider adding medications • Splenectomy • Look for other disease association

  43. 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

  44. Rapidly Progressive Glomerulonephritis (RPGN); Crescentic Glomerulonephritis • Subacute deterioration of renal function • Crescents in glomeruli • Various etiologies

  45. Fibrin deposition in Crescents

  46. 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

  47. Goodpasture’s syndrome • Anti-GBM antibodies crossreactivewith alveolar basement membrane

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