Basic plasmapheresis prof. dr. montasser zeid

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Basic Plasmapheresis

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3. Plasma exchange is the removal of plasma from a
patient and replacement by fresh-frozen or stored
plasma.
The terms "plasma exchange" and
"plasmapheresis" are often used inter-changeably.
Basic Plasmapheresis

4. Mechanism Example of diseases
Removal of circulating pathologic factors
Antibodies Antiglomerular basement membrane
disease
Immune complexes Lupus nephritis
Cryoglobulin Cryoglobulinemia
Myeloma protein Myeloma cast nephropathy
Prothorombotic factors Hemolytic uremic syndrome /
thrombotic thrombocytopenic purpura
Possible mechanisms of action
of plasmapheresis

5. Mechanism Example of diseases
Replacement of deficient plasma factors
Antithrombotic or fibrinolytic factor HUS/TTP
Possible mechanisms of action
of plasmapheresis
Effects on the immune system
Removal of complement products Lupus nephritis
Effect on immune regulation Transplantation
Improvement in reticuloendothelial function Cryoglobulinemia

6. Techniques of Plasmapheresis
1. Centrifugal cell separators
 Withdraw plasma from a spinning bowel with
either continuous or intermittent return of
blood cells to the patient.
 Can be done through a single needle in the
anticubital vein.

12.  Centrifugation takes advantage of the different
specific gravities inherent to various blood
products, such as red blood cells (RBCs), white
blood cells (WBCs), platelets, and plasma.

13. Techniques of Plasmapheresis
2. Membrane Plasmafiltration:
 Uses highly permeable membranes through
which blood is pumped at 100-150 ml/min.
Plasma passes through the membrane pores,
whilst the cells are simultaneously returned to
the patient.

14. Techniques of Plasmapheresis
2. Membrane Plasmafiltration:
 All immunoglobulins will cross the membrane
IgG more efficiently than IgM, however some
large immune complexes and some
cryoglobulins may not be adequately cleared.

15.  Membrane plasma
separation uses
differences in particle size
to filter plasma from the
cellular components of
blood.

16.  Secondary membrane plasma fractionation can
selectively remove undesired macromolecules,
which then allows return of the processed plasma to
the patient instead of donor plasma or albumin.
 Examples of secondary membrane plasma
fractionation include cascade filtration,
thermofiltration, cryofiltration, and low-density
lipoprotein pheresis.

17. Anticoagulation:
Either heparin or citrate.
Heparin requirement are double that for HD due
to loss in plasma.
• loading 70-80 units/kg followed by
• 1500 units/h infusion.

18. Anticoagulation:
Citrate anticoagulation
• continuous infusion
• as acid citrate dextrose ACD
• Patients should receive IV calcium.

19. Estimation of plasma volume
35-40 mL/kg body weight
Kaplan's equation
[0.065 x weight (kg)] x (1- Hct)

20. Replacement fluids:
1. Human albumin 5%
2. Fresh frozen plasma FFP.

21. Choice of replacement solution
Solution Advantage Disadvantage
Albumin • No risk of hepatitis
• Allergic reactions rare
• No concern about ABO
blood group
• Expensive
• No coagulation factors
• No immunoglobulins
Fresh frozen
plasma
• Coagulation factors
• Immunoglobulins
• “Beneficial” factors
complement
• Risk of hepatitis
• Allergic reactions
• Must be ABO
compatible
• Citrate loaad

22.  Myriad conditions that fall into this category (including
neurologic, hematologic, metabolic, dermatologic,
rheumatologic, and renal diseases, as well as
intoxications) can be treated with plasmapheresis.)
Indications

23.  The Apheresis Applications Committee of the American
Society for Apheresis periodically evaluates potential
indications for apheresis and categorizes them from I
to IV in the basis of the available medical literature.
 The following are some of the indications, and their
categorization, from the society’s 2010 guidelines.
Indications

24.  Category I (disorders for which apheresis is accepted
as first-line therapy, either as a primary standalone
treatment or in conjunction with other modes of
treatment) are as follows:
 Guillain-Barre syndrome
 Myasthenia gravis
 Chronic inflammatory demyelinating polyneuropathy.
Indications

25.  Hyperviscosity in monoclonal gammopathies
 Thrombotic thrombocytopenic purpura
 Goodpasture syndrome (unless it is dialysis-
dependent and there is no diffuse alveolar
hemorrhage).
 Hemolytic uremic syndrome (atypical, due to
autoantibody to factor H)
 Wilson disease, fulminant
Cont.……

26. Category II (disorders for which apheresis is accepted as
second-line therapy, either as a standalone treatment or in
conjunction with other modes of treatment) are as follows:
 Lambert-Eaton myasthenic syndrome
 Multiple sclerosis (acute central nervous system
emyelination disease unresponsive to steroids)
 RBC alloimmunization in pregnancy
 Mushroom poisoning
Indications

27.  Acute disseminated encephalomyelitis
 Hemolytic uremic syndrome (atypical, due to
complement factor mutations)
 Autoimmune hemolytic anemia (life-threatening cold
agglutinin disease)
 Systemic lupus erythematosus (severe)
 Myeloma cast nephropathy
Indications

28. Category III (optimum role of apheresis therapy is not
established; decision-making should be individualized) are
as follows:
 Posttransfusion purpura
 Autoimmune hemolytic anemia (warm autoimmune
hemolytic anemia)
 Hypertriglyceridemic pancreatitis
 Thyroid storm

29. Category IV (disorders in which published evidence
demonstrates or suggests apheresis to be ineffective or
harmful; institutional review board [IRB] approval is
desirable if apheresis treatment is undertaken in these
circumstances) are as follows:
 Stiff person syndrome
 Hemolytic uremic syndrome (typical diarrhea-associated)
 Systemic lupus erythematosus (nephritis)
 Immune thrombocytopenia

30. Contraindications
Plasmapheresis is contraindicated in the following patients:
 Patients who cannot tolerate central line placement
 Patients who are actively septic or are hemodynamically
unstable
 Patients who have allergies to fresh frozen plasma or
albumin depending on the type of plasma exchange
 Patients with heparin allergies should not receive heparin
as an anticoagulant during plasmapheresis.

31. Contraindications cont.…..
 Patients with hypocalcemia are at risk for worsening of
their condition because citrate is commonly used to
prevent clotting and can potentiate hypocalcemia
 Patients taking angiotensin-converting enzyme (ACE)
inhibitors are advised to stop taking the medication for
at least 24 hours before starting plasmapheresis

32. Complications of plasmapheresis
1. Related to vascular access
 Hematoma
 Pneumothorax
 Retroperitoneal bleed.
2. Related to the procedure
 Hypotension
 Bleeding
 Edema
 Loss of cellular elements (platelets)
 Hypersensitivity reactions

33. Complications of plasmapheresis
3. Related to anticoagulation:
 Bleeding
 Hypocalcemic symptoms
 Tingling and numbness
 Arrythmias
 Hypotension
 Metabolic alkalosis from citrate.

34. Complications
 Patients may also be at further risk for developing
hypotension if they have a history of taking
angiotensin-converting enzyme (ACE) inhibitors, in
particular while undergoing column-based
plasmapheresis.

35. Complications
 The suspected mechanism is related to increased
bradykinin levels caused by use of ACE inhibitors. This
accumulation of kinins leads to hypotension, flushing,
and gastrointestinal symptoms.
 Patients are therefore advised to stop all ACE inhibitors
at least 24 hours before starting plasmapheresis.

36. General orders for plasmapheresis
1. Calculate the plasma volume
2. Measure PT, PTT, platelets
3. When feasible, measure the plasma level of the
substance targeted for removal (e.g.
antiglomerular basement membrane antibody titre,
acetylcholine receptor antibody, cryoglobulin)
4. Space treatments approximately 24 h apart.

37. General orders for plasmapheresis
6. Myeloma with cast nephropathy
7. Crescentic IgA glomerulonephritis
8. For heparin anticoagulation 50 units/kg initially
then, 1000 units/hr
Target Activated clotting time 180-220 sec
(baseline 145 sec)

38. General orders for plasmapheresis
8. For citrate anticoagulation, use ACD-A
at 1:15 to 1:25 dilution with blood.
Use calcium infusion if necessary
Cardiac monitor
9. Administer scheduled medications only at the
end of the session.
10.Catheter care as routine.

39. Performance of Plasma filtration
Priming:
1. Heparinized isotonic saline 5000 IU/L
2. Deareation
3. In the blood compartment discard the initial 300
ml of the liquid
4. In the filtrate compartment at least 500 ml saline
solution should be filtered across the membrane
and discarded.
5. Attach the filtrate tubing system at the upper
filtrate port prior to the connection of the blood
line system.

40. Performance of Plasma filtration
Patient connection:
1. Connect the arterial blood tubing system.
2. Allow blood to flow until all saline solution
expelled.
3. Blood flow rate 100 mL/min.
4. Connect the venous blood tubing system.
5. Circulate blood for approximately 3 min without
filtration.
6. Filtrate flow should not exceed 20% of the blood
flow rate.

41. Performance of Plasma filtration
Termination of plasma filtration:
 The blood should be completely reinfused with
saline to the patient. (Pump max 100 mL/min)
 Return rates of blood product are on the order of
1.5 mL/kg/min, as opposed to the standard 70
mL/min flat rate used in adults.

42. Performance of Plasma filtration
Main problems.
Hemolysis
 Indicated by red colouration of filtrate.
 TMP should be decreased under 80 mmHg.
 reduce filtrate flow.
 reduce blood flow.
Blood leak
 Allow blood to recirculate for some minutes without
filtration.
 In case of a larger blood leak, the filter must be
exchanged.

43.  Sepsis causes disturbances of homeostasis that lead to
excessive coagulation, systemic inflammation, and
impaired fibrinolysis. In addition, blood flow to organs
can be reduced despite adequate cardiac output because
an imbalance occurs between coagulation and
fibrinolysis, resulting in impaired tissue perfusion.
ADJUNCTIVE USE OF PLASMAPHERESIS AND INTRAVENOUS
IMMUNOGLOBULIN THERAPY IN SEPSIS: A CASE REPORT

44.  A newer therapy, administration of drotrecogin alfa
(activated), treats the pathophysiological consequences
of severe sepsis: inflammation, coagulation, and
impaired fibrinolysis.
 but use of the agent increases the risk of bleeding and
so its appropriateness must be determined on an
individual basis.
ADJUNCTIVE USE OF PLASMAPHERESIS AND INTRAVENOUS
IMMUNOGLOBULIN THERAPY IN SEPSIS: A CASE REPORT

45.  Institutional indications for plasmapheresis in patients
with necrotizing soft tissue infection
Patient must have one of the following:
 White blood cell count >30.0 x 109/L
 Serum creatinine level >177 µmol/L (2 mg/dL) at time of
admission
 Hypotension with systolic blood pressure <90 mm Hg
or dependence on inotropes and/or vaopressors
 Acute respiratory failure

46.  Plasmapheresis removes large, harmful molecules such
as pathogenic autoantibodies, endotoxins, and
proinflammatory cytokines.
 If IV Ig is used, it should be given after plasmapheresis,
because it would be removed during plasmapheresis.
 Intravenous immune globulin provides passive, temporary
immunity for patients with sepsis, who frequently have serum
globulin levels in the low normal range.

47.  Most of the research available on use of
plasmapheresis and IV Ig in patients with NSTI and/or
toxic shock syndrome indicates that this combination
provides some improvement in these patients.
 However, no large controlled trials have been done
that would provide statistical support for the clinical
efficacy of this combination of therapies.