19.1 Apheresis and Extracorporeal Circulation

19.1 Apheresis and Extracorporeal Circulation

Quick Answer: Donor apheresis collects a component and returns the rest to a healthy donor. Therapeutic apheresis removes a pathogenic blood constituent from a patient. ASFA publishes indication Categories I–IV; Category I means accepted first-line therapy. Classic Category I examples at BB level are TTP (plasma exchange with plasma replacement for ADAMTS13), hyperviscosity, anti-GBM / Goodpasture, selected myasthenia gravis, and RBC exchange for specified sickle-cell indications. Leukapheresis and thrombocytapheresis are classic cytoreductive indications; the official ASFA category is published and edition-specific. Replacement is albumin for most TPE and plasma when the patient needs ADAMTS13. Citrate causes ionized hypocalcemia. CPB, ECMO, and dialysis raise heparin and dilutional coagulopathy; irradiation is not routine just because blood is in a circuit.

This is June 9, 2026 outline V.D. Chapter 4.4 told you what an apheresis product is. Chapter 2 told you donor intervals. This section is procedure and indication: who is on the machine, what is removed, what goes back, and what a circuit does to hemostasis. If a stem asks TTP replacement fluid, ASFA first-line, citrate tetany, ECMO heparin, or “irradiate the bypass circuit,” answer it here.

Donor apheresis is not therapeutic apheresis

Donor (preparative) apheresis takes a healthy volunteer, anticoagulates the draw, separates one or more components, and returns everything else. The output is a licensed blood component or an HCT/P: platelets, plasma, double red cells, granulocytes, concurrent combinations, or mobilized HPC-A. Eligibility, intervals, and QC live in Chapters 2 and 4. The donor is not being treated.

Therapeutic apheresis treats a patient. A pathogenic substance is removed: autoantibody and ADAMTS13-deficient plasma (TPE), immunoglobulin that is making plasma syrup-thick (hyperviscosity), anti-GBM antibody, hemoglobin S–containing red cells, blasts that are sludging the microcirculation, or a platelet count so high that the patient is clotting or bleeding from acquired von Willebrand syndrome. The patient may receive a replacement fluid. The blood bank’s job is product selection, replacement inventory, vascular-access coordination, and recognition of citrate and volume complications.

Do not call every machine procedure “plasmapheresis.” Plasmapheresis / therapeutic plasma exchange (TPE) removes plasma. RBC exchange (erythrocytapheresis) removes red cells and returns donor red cells. Leukocytapheresis and thrombocytapheresis are cytapheresis. Photopheresis and LDL apheresis exist clinically; BB items stay with TPE, RBC exchange, and cytapheresis unless the stem names another modality.

ASFA categories are published — do not invent them

The American Society for Apheresis (ASFA) publishes the indication guideline. Each indication is assigned a category and a grade of evidence.

• Category I — first-line therapy, alone or with other treatment
• Category II — second-line; used when first-line fails or as adjunct
• Category III — role not established; decision-making individualized
• Category IV — ineffective or harmful in published evidence

The exam tests the concept and a short list of classic first-line examples. It does not ask you to recite an unpublished ASCP category table. If you are not sure of a category, say ASFA publishes it and do not invent a number.

Classic Category I examples BB expects:

• TTP — daily TPE with plasma replacement. You are removing autoantibodies and ultra-large vWF multimers and replacing ADAMTS13. Albumin does not supply ADAMTS13. Platelets are withheld unless life-threatening bleed (17.3). Caplacizumab and immunosuppression sit alongside TPE; they do not replace the first TPE run.
• Hyperviscosity (Waldenström macroglobulinemia, some myelomas) — TPE to drop IgM/IgG viscosity before therapy that can flare viscosity.
• Anti-GBM disease (Goodpasture) — TPE to remove anti-GBM antibody, especially with pulmonary hemorrhage or a salvageable kidney, plus immunosuppression.
• Myasthenia gravis, selected presentations (moderate–severe crisis, pre-thymectomy in many ASFA listings) — TPE to remove acetylcholine-receptor or MuSK antibody.
• Sickle cell disease, specified indications — RBC exchange for acute stroke and for stroke prophylaxis in patients who meet protocol criteria. Units are hemoglobin S–negative and at least C/c, E/e, K matched (17.2). A common protocol target is post-exchange HbS < 30% — that is a clinical target, not an ASCP statute.

Leukocytapheresis for symptomatic hyperleukocytosis (leukostasis: hypoxemia, CNS change, usually AML/ALL with very high blast counts) and thrombocytapheresis for symptomatic extreme thrombocytosis are classic BB cytoreductive indications. ASFA’s published category is indication- and edition-specific (cytoreduction is often second-line rather than automatic Category I). Treat them as accepted machine indications when the patient is symptomatic; do not invent a category number, and do not leukapherese a number without leukostasis just because the WBC is high.

Guillain-Barré (AIDP) is another widely published Category I TPE indication. IVIG is an alternative; the blood bank still must be ready to supply albumin if TPE is chosen.

Replacement fluids — albumin versus plasma

Most TPE is replaced with 5% albumin (sometimes albumin plus saline). Albumin maintains oncotic pressure and does not transmit viruses or TRALI antibodies. It also does not replace ADAMTS13, fibrinogen, other clotting factors, or immunoglobulins. After a 1–1.5 plasma-volume exchange with albumin, factor levels fall; schedule invasive procedures with that in mind.

Plasma (FFP, PF24, or thawed plasma per inventory) is the replacement when the patient needs a plasma protein you just removed — first and foremost TTP. Plasma is also used when the patient is already coagulopathic or when the service’s protocol calls for plasma at the end of an albumin exchange to restore fibrinogen. Plasma replacement carries TRALI, allergic, and citrate-load risks that albumin does not.

RBC exchange is replaced with donor red cells, not albumin. Cytapheresis often needs little more than saline or a small albumin bolus because the removed buffy-coat or platelet volume is modest compared with a plasma-volume exchange.

Citrate toxicity

Almost every apheresis circuit is anticoagulated with ACD-A. Citrate chelates ionized calcium. The donor or patient feels perioral tingling, distal paresthesias, chest tightness, nausea, then carpopedal spasm, QT prolongation, hypotension, and arrhythmia if ionized calcium keeps falling. Risk rises with high inlet rates, large-volume procedures, plasma return (returned plasma and replacement FFP are themselves citrated), liver failure (citrate is metabolized by the liver), and small patients.

Management is slow the inlet, give oral calcium, and, when symptoms persist or the ionized calcium is critically low, give IV calcium gluconate (or chloride via a central line per protocol). Do not “push through” tetany. Heparin is an adjunct or alternative in some HPC and specialized circuits; it is not the default community-donor anticoagulant.

Citrate also appears in massive transfusion (18.2). Same ion, same treatment idea, different setting.

Extracorporeal circuits the blood bank supports

Cardiopulmonary bypass (CPB) takes the entire cardiac output through an oxygenator. The circuit is primed with crystalloid ± colloid/albumin ± red cells, so the patient starts with dilutional coagulopathy and a drop in hematocrit and platelet count. Anticoagulation is unfractionated heparin titrated to ACT, then protamine reversal. Residual heparin, hypothermia, contact activation, hyperfibrinolysis, and platelet dysfunction all look like “the blood bank issued bad plasma.” They are circuit physiology. Cell salvage and antifibrinolytics (TXA) belong in the OR plan (19.3).

ECMO is a days-to-weeks circuit. Patients consume platelets and factors, hemolyze in the pump, and remain anticoagulated (heparin or a direct thrombin inhibitor such as bivalirudin). The blood bank issues frequent small doses, watches for circuit-related hemolysis (DAT-negative, rising plasma hemoglobin), and does not irradiate every unit just because an oxygenator is in line.

Hemodialysis / CRRT uses heparin or regional citrate. Blood-bank issues are mostly chronic anemia (ESA, iron — 19.3), occasional urgent red cells, and not mistaking a citrate bath for a TPE indication.

Irradiation is not routine for a circuit. TA-GVHD risk follows recipient immunity and product type (4.3, 17.2), not the presence of CPB tubing. Neonatal ECMO, congenital immunodeficiency, and HPC transplant patients still get irradiated cellular products for the usual indications. Do not irradiate an HPC graft (below).

HPC collection — blood-bank issues, not a red-cell dose

HPC-A is G-CSF–mobilized (± plerixafor) peripheral blood collected by large-volume leukapheresis. The product is an HCT/P (21 CFR 1271), dosed by CD34+ cells, often cryopreserved in DMSO (4.4, 11.4). Typical clinical collection targets are in the 2–5 × 10^6 CD34+ cells/kg range — protocol numbers, not ASCP official cutoffs.

Blood-bank work is ABO/Rh of graft versus recipient, plasma or red-cell reduction for major/minor ABO mismatch, citrate management during a long run, and supportive transfusion of the recipient. Irradiate the blood components the patient receives. Do not irradiate the HPC product — that would inactivate the graft you just collected.

Worked scenario. A 34-year-old with TTP has platelet count 12 × 10^9/L and neurologic change. Order daily TPE with plasma replacement, not albumin, and do not issue prophylactic platelets. The same machine used tomorrow for a Waldenström patient with epistaxis and a serum viscosity of 6 will be TPE with albumin.

Exam traps. Donor apheresis ≠ therapy. TTP replacement is plasma, not albumin. ASFA categories are published — do not invent them. Citrate = ionized hypocalcemia. Circuit coagulopathy is heparin + dilution, not a new antibody. Do not irradiate because of CPB alone, and never irradiate the stem-cell bag.