apheresis joshua daniel new
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1. Removal of whole blood from a donor or a patient
2. Separation into blood components
3. Retention of desired component
4. Return of the remaining elements to the donor or patient
5. Can be used to collect a component intended fortransfusion or remove a pathologic component
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Centrifugation
Types of separation
Membrane Filtration
Continuous Process
Types of Machines
Intermittent Process
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Inlet Pump Plasma Pump
Desired
component
Return to Patient
ACD
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Plasma
Packedred cells
Buffycoat
Granulocytes1.085*
Monocytes1.065*
Lymphocytes1.071*
Platelets1.048*
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APHERESIS
DONORAPHERESIS
THERAPUTICPLASMA
EXCHANGE
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Red cell pheresis
Plateletpheresis
Plasmapheresis
Granulocytopheresis
Stem cell pheresis
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Collecting only packed red cells from the donor
Up to 2 units of red cells can be collected from a
single donor
Interval between 2 units donation is 6 months
Desired Hb% 14 gms, weight > 60 Kgs
Useful in corporate setups where finding donors isdifficult
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Plateletpheresis is the process of collecting onlyplatelets
Random donor Platelets > 5.5 x 1010
plateletsin 50 - 70 ml of plasma
Single Donor platelet 3 x 1011 platelets in
~300 ml of plasma
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High quality product with better post transfusion plateletincrements
Leuko-Reduced product
Reduced donor exposure therefore reduced TTIs and
Alloimmunization
Less time consuming and can be harvested from a singledonor
Donor can donate 2 times a week
Single unit transfusion increases post transfusion 30 40thousand
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Severe neutropenia (ANC
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Patients with bone marrow failure where neutrophilrecovery is not anticipated to recur spontaneously and
no further active treatment is planned
Sepsis in the absence of either neutropenia or knownneutrophil dysfunction
Pyrexia of unknown origin (PUO)
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Granulocytes are transfused daily untilthe patient's infection clears or until the
neutrophil count exceeds 500/l
Dosage: 1x 1010
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Process of harvesting circulating blood stem cellsto use in bone marrow transplantation.
Can also be collected and separated from thebone marrow
Stem cell marker is CD 34
Minimum dosage 2x106 per kg body weight of thepatient
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Aplastic anemia Sickle cell anemia, thalassemia
Fanconis anemia, Pure red cell aplasia
Congenital immune deficiency syndromes Glycogen and lipid storage disorders
PNH, Radiation injury
Leukemia's Lymphomas
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Erythrocytopheresis
Thrombocytopheresis
Leukopheresis
Plasmapheresis
o LDL Pheresis
o Immuno Adsorption
o Photopheresis
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RBC PlasmaWBC PLT
Sickle Cell Dis.
Malaria
Leukemias
Cell Therapies
Thrombocytosis
Guillain Barrie Synd.
Myasthenia Gravis
Good pastures Synd.Acute liver failure
Drugs overdose
Poisoning
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Extracorporeal blood purification techniquedesigned to remove large molecular weight
substances from the plasma.
Examples: pathogenic auto antibodies,immune complexes, cryoglobulins, myelomalight chains, endotoxin, and cholesterolcontaining lipoproteins.
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The substance to be removed should be
Sufficiently large(mol wt greater than 15,000)which cannot be easily removed by less expensivepurification techniques like hemofiltration or high-fluxhemodialysis.
Must have asufficiently long half-life, so thatextracorporeal removal is much more rapid thanendogenous clearance pathways.
Must be acutely toxic and resistant toconventional therapy, so that the rapid eliminationfrom the extracellular fluid by TPE is indicated.
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Plasma Volume Exchange Percent Removed
0 0%
0.5 39.3%
1.0 63.2%
1.5 77.7%
2.0 86.5%
2.5 91.8%
3.0 95.0%
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Category I: Standard acceptable first line therapy
Category II: Generally accepted in a supportive role
Category III: Not clearly indicated based oninsufficient evidence.
Category IV: Demonstrated to have a lack of efficacyClinical applications should be undertaken onlyunder an approved research protocol.
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Neurological:
Guillain Barre synd Myasthenia Gravis
CIDP Paraprotein associated
poly neuropathy
Hematological: TTP
Sickle cell crisis ABO mismatch Marrow
transplant
Others:
Cutaneous T cellLymphoma
Leukocytosis Thrombocytosis
Good pasteur synd Hypercholestrolemia
Phytanic acid storagedisease
Amanita phalloidespoisoning
Cryoglobinemia
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Neurological: Multiple sclerosis Eaton lambert synd Acute CNS inflamatory
demyelinating disease
Pediatric autoimmuneneropsychiatry disorder
Hematological: ITP
Maternal-fetal Rhincompatability Coagulation factors
inhibitors Hyperviscosity synd
Renal & Others:
RPGN
Acute renal failure dueto cast nephropathy Graves disease Digitalis toxicity
Pemphigus vulgaris Bullous pemphigoid Toxic epidermonecrolysis
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Neurological:
Stiff man syndrome
Multiple sclerosis
Paraneoplastic synd
Polymyositis
Hematological:
Posttransfusion
Purpura Aplastic anemia
Autoimmune
hemolytic anemia
Renal & others: Hepatic failure
Recurrent focalglomrulosclerosis
HUS
Renal transplantrejection
Heart transplantrejection
Drugs over dose
Poisoning
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Examples: AIDS, amyotrophic lateralsclerosis, lupus nephritis, psoriasis, renaltransplant rejection, schizophrenia,
rheumatoid arthritis
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Acute progressive paralyzing illness affecting both
motor and sensory peripheral nerves .Etiopathology: Ab to Basic Myelin protein whichcauses destruction of myelin (Demyelination).
Clinical features: Rapidly progressive symmetricalmuscle weakness, and paresthesias, respiratory andoropharyngeal muscles may involve in more severecases requiring mechanical ventilation
Autonomic dysfunction (BP & HR) seen in 25% ofpatients.
long-term neurologic deficits in 75%.
Mortality 5%.
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Most effective when initiated within 7 days of diseaseonset.
Can accelerate motor recovery, decrease time on theventilator, and speed attainment of other clinical
milestones.
Median time to wean from mechanical ventilation andthe time to walk without assistance are comparable or
sometimes better than IV IGPatients with axonal involvement reported greaterpotential benefit than IVIG
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Nerve
Muscle
Anti-AchRAbAcetylcholine (Ach)
AchR
Auto-Ab directed against the acetylcholine receptors
on the motor end plate prevents the normal functioningof the receptors by increasing the receptor turnover,blocking the binding of acetylcholine, and fixingcomplement with degradation of the receptor.
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1) Acetylcholine esterase inhibitors :Increases the amount
of acetycholine at the motor end plate eg., pyridostigmine,neostigmine
2) Immuno-suppressive medications : Decreases theantibody production eg., cortico-steroids or azathioprine.
3) IVIg give beneficial effects.
4)TPE: is specially useful during1) crisis and 2) Before
thymectomy for early recovery from surgery 3) Managementof severe disease refractory cases unresponsive toconventional therapy 4) Rapid resolution of clinical signs,5) Lower incidence of complications
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Causes: Hepatitis ( viral, autoimmune)Drug toxicity ( Acetaminophen)
Ingestion of hepatotoxins
Wilsons diseaseFulminant liver failure:
Mortality rate is 50 90 % caused by acute
metabolic disturbances, hepaticencephalopathy, severe coagulopathy
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Removes albumin bound and large mol.wt toxins like aromaticamino acids, endotoxins, indols, mercaptan , phenol
Most studies show improved cerebral & hepatic blood flow,mean arterial pressure, cerebral perfusion pressure andcerebral metabolic rate
Improves laboratory parameters cholinesterase activity &galactose activity
Restores coagulation factors and removes activated clottingfactors, tissue plasminogen activator, FDP
In some patients, liver regenerates during TPE
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Mushroom ( Amanita phyllode)
Paraquat
Anti digoxin antibodies
Vincristine
Eltroxin
Cysplatin.
Carbamazepine
Tricyclic anti-depressants
Methanol
Ethanol
Heavy metal ( mercury )
Verapamil
Diltiazem,
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Drug removal is most dependent on percentage ofprotein binding and volume of distribution. Drugs witha high percentage of protein binding and a relatively
modest volume of distribution will have the greatestlikelihood of being removed by TPE
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Not significantly removed:
Prednisolone
Minimal removal:Cyclophosphamide
AzathioprineAminoglycosidesTobramycinDigoxinVancomycin
Post treatment supplement needed:Phenytoin
Acetylsalicylic acidPropranololThyroxine
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THANK YOU