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Transfusion Medicine Fellowship > Apheresis - Practicals > Flashcards

Apheresis - Practicals Flashcards

1
Q

What volumes are normally exchanged for TPEs? Harvests?

A

TPE: 1-1.5x TPV
Harvests: 2-6x TPV

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2
Q

What replacement fluids can be used for apheresis?

A

Saline, albumin, plasma, RBCs

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3
Q

In which circumstances should a red cell prime be used?

A

When ECV or ERCV exceeds 15% of TBV/RCV or when the intraoperative crit would drop below 24%. Or, to constitute a simple transfusion otherwise.

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4
Q

What is the “best” central line site?

A

No best choice.
Femoral: there is no risk to the mediastinal structures, but infection risk is higher.
IJ: Right is preferred over Left (more straight path, less chance of traversing the azygos root)

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5
Q

How are the two lines on a dialysis catheter distinguished?

A

The red catheter is shorter and thicker and is meant for drawing (inlet). The blue catheter is longer and is meant for return.

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6
Q

Can the same arm be used for both inlet and return when performing apheresis over PIVs?

A

Yes, but the return should be downstream of the inlet.

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7
Q

How should central lines be maintained?

A

The dressing should be kept clean and changed often. Heplocks should be used (if >1000u used, draw off before use to avoid systemically anticoagulating patient).

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8
Q

What is recirculation? How much is normally tolerated?

A

Direct re-draw of blood coming on from the return line. Up to 10% is typical and tolerable.

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9
Q

How do reactions to ethylene oxide present? How should they be managed?

A

Burning sensation in the eyes with periorbital edema. Prevent by better priming the circuit with saline or using an ethylene-oxide-free kit.

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10
Q

What effect does apheresis have on clotting factors?

A

Reduces clotting factors by 40-70%; most factors recover in 1-2 days but fibrinogen takes 2-3.

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11
Q

What is Gilcher’s rule of 5s?

A

Consider an athletic man: 75mL blood/kg bodyweight. Subtract 5mL for normal>thin>obese, and another 5mL for female sex.

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12
Q

How are citrate and heparin metabolized in apheresis?

A

Citrate normally has very high first-pass effect, but it may accumulate in patients with hepatic disease (monitor iCa). Heparin is more slowly metabolized.

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13
Q

How should exchange in cryoglobulinemic patients be handled?

A

Used blood warmers, blanket the patient, use warmed components… Warm everything up.

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14
Q

How does pregnancy affect volumes, and how does it affect apheresis procedures?

A

TBV increases by 40%, but TPV increases by 45-55% resulting in RCV going up by only 20-30% and the crit actually decreasing. Lay patients on their left sides to prevent uterine compression of the ICV.

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15
Q

What drug metabolisms should be considered during apheresis?

A

Antihypertensives, anticonvulsants, antiarrhythmics, pressors (to a lesser extent; most are short-lived)

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16
Q

What drives hypocalcemia in apheresis?

A

Binding by calcium, but also binding by replacement albumin (“stripped albumin”). Alkalosis can also make it worse.

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17
Q

Compare and contrast calcium gluconate and calcium chloride for replacement.

A

Calcium chloride has more calcium per gram (272mg/g) than calcium gluconate (93mg/g) but requires central line administration and cardiac monitoring.

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18
Q

How do plasma proteins redistribute to and from the extravascular space?

A

Enter extravascular space via simple diffusion but moreso pinocytosis. Leave extravascular space via lymphatics or pinocytosis.

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19
Q

Compare and contrast the catabolic pattern of IgG and IgM.

A

IgG is metabolized in a first-order fashion (rate of metabolism is dependent on concentration). IgM is metabolized in a zero-order fashion (concentration-independent, amount per unit time)

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20
Q

Why do exchanges in paraproteinemias tend to appear less efficient than expected?

A

Paraproteins tend to increase the intravascular volume due to oncotic forces. The TPV is often underestimated.

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21
Q

Compare and contrast the distribution of IgG, IgA, and IgM.

A

IgG is 45% intravascular.
IgA is 42% intravascular.
IgM is 76% intravascular.

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22
Q

How quickly does complement recover in plasma? Coagulant proteins?

A

Complement mostly recovers in 1 day, as do most coagulation factors. Fibrinogen takes a bit longer (2-3 days).

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23
Q

In what patients should plasmapheresis be performed with plasma as the replacement fluid?

A

Patients at risk of hemorrhage, and patients with thrombotic microangiopathies (eg. TTP).

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24
Q

How are electrolyte levels affected by plasma exchange?

A

Urate and potassium tend to fall. Glucose and bicarbonate do not. Sodium and chloride stay the same due to isotonicity of replacement fluid.

25
Q

How does plasma exchange affect red cell, white cell, and platelet counts?

A

Red cells may fall slightly (happens with 5% albumin but not with plasma?). White cells transiently increase due to dislodging of marginated pool. Platelets experience a 25-33% reduction and take 2 days to recover.

26
Q

How many rounds of exchanges should be performed to treat an IgG-mediated disease? An IgM-mediated disease? How long should you wait between procedures?

A

IgG: 4-6 times, every 1-2 days
IgM: 3-4 times, every day

27
Q

Why does citrate bind calcium?

A

Citrate has 3 negatively charged carboxyl groups, two of which can complex with cations.

28
Q

How is body calcium mostly stored? In what forms is plasma calcium found?

A

Mostly in bones as hydroxyapatite. Plasma calcium is 40% albumin/protein bound, 13% complexed, and 47% ionized (free).

29
Q

What are some possible severe complications of citrate toxicity?

A

From hypocalcemia: Spasms (carpopedal, Chvostek/Trousseau), laryngospasm, QT prolongation.
Note: Hypomagnesemia can also result, but this isn’t usually an issue.

30
Q

What is the effect of citrate infusion on acid balance?

A

Citrate binds free hydrogen, causing a metabolic alkalosis. This is worse in renal failure or with plasma replacement (more citrate).

31
Q

At what WB:AC ratio does platelet clumping occur?

A

18:1

32
Q

What is the usual prime volume of an apheresis circuit?

A

170-200mL.

33
Q

What proteins may be activated by filtration surface contact?

A

Complement, kinins

34
Q

What are the most common side effects resulting from apheresis procedures?

A 
Citrate toxicity
Vasovagal effects (bradycardia, hypotension, diaphoresis, sometimes nausea/vomiting, defecation, and convulsions).
35
Q

What are the side effects of hetastarch?

A

Weight gain, anemia, abnormal coags. Never really clears bone marrow…

36
Q

How much protein is removed in a typical 1x TPV TPE?

A 
110g albumin (-15g with 5% albumin)
40g of other proteins
37
Q

What is the rationale behind rheopheresis?

A

Removal of proteins to affect blood viscosity and cellular aggregation to affect circulation in microvasculature. Used for prevention of wet AMD in Europe but not well-proven.

38
Q

How does immunoadsorption work?

A

Nonspecifically remove antibodies usually using staph protein agarose columns.

39
Q

What conditions may be treated by immunoadsorption?

A

In the US? None. But literature has described use in…

  • Renal transplant (pre and post)
  • Coagulation factor inhibitors
  • Dilated cardiomyopathy (associated with autoantibodies)
40
Q

What is the primary downside of immunoadsorption?

A

Because of serious contact activation, most patients will experience side effects including nausea/vomiting, hypotension, pain…mercury poisoning?

41
Q

What different immunoadsorption instruments are in use?

A

Ig-Therasorb (sheep anti-IgG column)
Selesorb (dextran sulfate column)
Immusorba (tryptophan/phenylalanine column)

42
Q

What is the only specific immunoadsorption column in use?

A

Glycosorb: Removes isohemagglutinins for pre-transplant. Europe only.

43
Q

Why is TPE not the best for treating familial hypercholesterolemia?

A

Removes LDL, but also removes cardioprotective HDL.

44
Q

What are the indications to treat familial hypercholesterolemia with LDL pheresis?

A 
Homozygous patients (with >500 LDL)
Heterozygous patients (with >300 failing medication or with evidence of coronary artery disease)
45
Q

What are the indications for LDL pheresis besides hypercholesterolemia?

A

FSGS, sudden sensorineural hearing loss, maybe acute stroke/MI?

46
Q

What are the 5 methods available for LDL pheresis?

A 
Dextran column (liposorber LA-15)
Dextran direct perfusion (liposorber D)
HELP (heparin precipitation)
Immunoadsorption (sheep anti-human-LDL)
DALI (polyacrylamide column)
47
Q

What methods of LDL pheresis are approved for use in the USA?

A

Dextran-sulfate column (all around better)

HELP

48
Q

What is the mechanism of removal of LDL using HELP?

A

Heparin precipitates out ApoB100 and Lp(a) at acidic pH (5.12).

49
Q

How much LDL is removed with a 3x TPV exchange using DS-A column? Other proteins?

A

85% of LDL and Lp(a)
5% of HDL
Fibrinogen not significantly reduced.

50
Q

What are McLeod’s criteria?

A

REquirements to indicate for apheresis: 1. Need clear understanding of pathophysiology, 2. Abnormality should be correctable by apheresis, 3. Clinical evidence demonstrates improved outcomes.

51
Q

How is intraprocedural hematocrit calculated?

A

(Patient crit * TBV) / (TBV + ECV)

52
Q

What are the 4 major goals of apheresis?

A

Remove a pathogenic substance
Replace a missing substance
Modulate cellular function
Collect a product

53
Q

What is the difference between plasma exchange and plasmapheresis?

A

Plasma exchange is larger volume (>1L).

54
Q

What needle gauges are needed to perform apheresis over peripherals?

A

17ga access

18ga return

55
Q

In what settings is heparin anticoagulation preferable to ACD?

A

Small children
Patients with metabolic alkalosis
Patients in renal failure

56
Q

What adverse reactions may be seen during apheresis?

A 
Citrate toxicity
Allergic reaction
Respiratory difficulty (TRALI, anaphylaxis, ethylene oxide?)
Hypotension
Coagulopathy, hemolysis... (rare)
57
Q

What effect does ECP have on the adaptive immune system?

A

Induces monocyte differentiation into dendritic cells
Alters T-cell subsets
Alters cytokine profiles

58
Q

How does the citrate content of FFP compare to 5% albumin?

A

About 4 times the citrate load.

Transfusion Medicine Fellowship (34 decks)

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