Apheresis, Blood Administration, and Patient Blood Management

Three laboratory duties share one chapter. Therapeutic apheresis removes a pathologic blood constituent through an extracorporeal circuit. Blood administration moves an issued component into the patient under safeguards that survive the journey from the transfusion service to the vein. Patient blood management pairs every transfusion decision with the laboratory work and clinical alternatives that might make the transfusion unnecessary.

The apheresis circuit

Apheresis withdraws blood, separates a target component, diverts or collects it, and returns the remainder. Centrifugation separates by density: red cells pack outward first, then white cells and platelets, then plasma. Two flow patterns cover most instruments. Intermittent-flow centrifugation processes one bowl of blood at a time, drawing, separating, collecting, and reinfusing in cycles, typically 6 to 8 cycles for a plateletpheresis procedure; it can run from a single needle, which suits donors, but its extracorporeal volume is generally higher than continuous-flow systems. Continuous-flow centrifugation draws, separates, and reinfuses simultaneously through two venous sites or a dual-lumen central catheter, and newer platforms support single-needle operation. Membrane filtration passes plasma through pores that retain cells, producing cell-free plasma for collection or exchange.¹

Citrate is the standard apheresis anticoagulant. It chelates ionized calcium and halts the calcium-dependent coagulation steps inside the circuit. Citrate metabolism returns calcium to the circulation, and parathyroid hormone responds to any ionized-calcium dip by mobilizing bone calcium and increasing intestinal absorption and renal reabsorption. When citrate delivery outpaces that response, perioral or distal paresthesia appears, and severe reduction progresses to tetany and arrhythmia. Fluid that shifts into the circuit can produce hypovolemic hypotension. The extracorporeal volume of an apheresis procedure is generally kept at or below 15% of estimated total blood volume under the device’s validated limits and the facility procedure; the 10.5 mL/kg collection limit governs whole-blood donation, a separate question from apheresis extracorporeal volume. A distinct vasovagal reaction produces parasympathetic bradycardia and hypotension, most often in younger patients, and remains a recognized event during therapeutic procedures as well as donations.¹

Donor-side apheresis, including donation intervals, yields, and donor-reaction management, is covered in the Donor Qualification, Collection, and Reactions page.

Therapeutic apheresis principles

Therapeutic apheresis removes a pathogenic constituent more efficiently than the body’s clearance mechanisms can. Procedures divide by target: cytapheresis selectively removes red cells, white cells, or platelets, and plasmapheresis or plasma exchange removes plasma when the pathologic substance circulates there. The American Society for Apheresis assigns each disease, indication, and modality a category: category I means apheresis is accepted as first-line therapy, category II accepts it as second-line therapy, category III leaves the optimum role undefined and individualized, and category IV applies when evidence shows apheresis is ineffective or harmful, with institutional-review-board approval desirable before any use.²

The blood bank medical director acts as a consulting physician. Responsibility is shared in writing: the treating clinician manages vascular access and overall care, the apheresis team controls the procedure and its anticoagulation, and laboratory monitoring and replacement-fluid choice follow the delineated plan. Written informed consent is required.¹

Cytapheresis procedures

Therapeutic plateletpheresis treats symptomatic thrombocytosis, generally above 1,000,000/µL with thrombosis or hemorrhage, and lowers the count 30% to 60% per session as a bridge until cytoreductive medication takes effect.¹

Therapeutic leukapheresis treats hyperleukocytosis, generally a white-cell or blast count above 100,000/µL with pulmonary or cerebral leukostasis risk, more common in acute myeloid leukemia than in acute lymphoblastic leukemia; it also lowers the count 30% to 60% per session.¹

Erythrocytapheresis (red-cell exchange) replaces the patient’s red cells with donor cells while holding the volume constant. For sickle cell disease it removes HbS-containing cells and replaces them with compatible red cells that are relatively fresh, under 10 days old, leukoreduced, HbS negative, and matched for Rh and K antigens, aiming for an HbS fraction below 30% during acute complications.^1,3 Red-cell exchange also treats severe malaria or babesiosis parasitemia above 10% and removes incompatible transfused red cells after an ABO-mismatched transfusion.

Hematopoietic progenitor cell collection harvests CD34-positive mononuclear cells from the buffy-coat layer after growth-factor mobilization, sparing the patient a marrow harvest under anesthesia. Photopheresis treats leukapheresis-collected leukocytes with 8-methoxypsoralen and UVA light, which crosslinks DNA and drives apoptosis; it is FDA-approved for cutaneous T-cell lymphoma with additional use in graft-versus-host disease and solid-organ transplant rejection.¹

Plasma exchange, immunoadsorption, and replacement fluid

Plasma exchange removes the patient’s plasma and replaces it with albumin, plasma, or a combination. Thrombotic thrombocytopenic purpura is the classic category I indication, and plasma supply supports the exchange; the plasma components themselves carry the same transfusion-reaction risks described in the Transfusion Reactions and Transfusion-Transmitted Infections page. Immunoadsorption perfuses separated plasma through a ligand-coated column, historically staphylococcal protein A, that binds IgG and immune complexes and removes pathogenic antibody without any replacement fluid.¹

Replacement-fluid choice is a laboratory responsibility with clinical consequences. Albumin is the standard oncotic replacement because it carries no antibody, needs no compatibility testing, and carries minimal infection risk under modern viral inactivation. Fatal apheresis events are rare, predominantly cardiac or respiratory, and disproportionately involve plasma as the replacement fluid, a pattern that supports reserving plasma for thrombotic thrombocytopenic purpura and hemolytic uremic syndrome and using albumin for routine oncotic replacement.¹

Adverse effects of apheresis

Apheresis complications overlap with donor-collection physiology. Citrate toxicity and hypocalcemia lead the list, with the signs and the parathyroid response described above; oral or intravenous calcium follows the facility procedure under medical direction. Vascular-access complications include hematoma, infection, and pneumothorax after central-line placement. Vasovagal reactions and hypovolemia follow, the latter more frequent with intermittent-flow instruments. Allergic reactions occur, most often to plasma replacement and occasionally to albumin. Mechanical hemolysis follows equipment malfunction such as a kinked line. Air embolism is rare. Repeated plasma removal depletes clotting factors and immunoglobulins, and coagulation testing before and after exchange guides whether plasma must replace part of the albumin volume.¹

Administration safeguards

Positive identification repeats at every stage: at collection, in the laboratory during testing and again at issue, and at the bedside immediately before infusion, as detailed in the Pretransfusion Testing page. Clerical error at the bedside remains the leading preventable cause of fatal ABO-incompatible transfusion, which is why the final check matches the recipient, the unit label, and the compatibility record together.^1,3

Every component is administered through a sterile, pyrogen-free filter that removes clots and aggregates, generally a standard 150- to 260-micron filter. Start slowly and observe the patient for the first 10 to 15 minutes, then infuse as rapidly as tolerated, and finish within 4 hours after entering the container because room-temperature storage beyond that invites bacterial growth; order smaller aliquots when the rate must stay slow. Monitor pulse, respiration, blood pressure, and temperature periodically throughout.³

Laboratory indication thresholds

Transfusion thresholds pair a laboratory value with the clinical setting. For most hemodynamically stable hospitalized adults, current international guidance suggests a restrictive red-cell threshold of 7 g/dL. Hospitalized adults with acute myocardial infarction are the defined exception, where the 2025 guideline suggests a liberal strategy below 10 g/dL on low-certainty evidence.^4,5 Platelet thresholds follow the values in the component therapy page, with prophylaxis below 5,000 to 10,000/µL and bleeding support at higher counts. Plasma is considered for active bleeding with PT or PTT elevation or an INR above 1.5, and cryoprecipitate for fibrinogen or factor XIII deficiency. The Circular of Information adds the ceiling: plasma is withheld from a minimally elevated INR of 1.7 or less in a nonbleeding patient, because roughly 30% factor activity remains and a standard dose may leave the INR unchanged.³

Worked example. A stable adult on the medical ward has a hemoglobin of 6.8 g/dL with no bleeding, no cardiac disease, and a gradually declining trend. The restrictive threshold of 7 g/dL applies, so the laboratory value supports considering one red-cell unit with a posttransfusion hemoglobin check. A second patient the same day has a hemoglobin of 9.4 g/dL the morning after an acute myocardial infarction. The general threshold would withhold transfusion, and the myocardial-infarction guideline instead supports considering transfusion below 10 g/dL, with the treating team weighing ischemic symptoms and volume-overload risk.

Patient blood management

Transfusion decisions weigh patient-specific laboratory and clinical data together. Patient blood management programs pair transfusion practice with alternatives that remove the need: iron repletion for iron-deficiency anemia, erythropoietic support where indicated, preoperative optimization of hemoglobin and anticoagulant management, and intraoperative blood conservation. The laboratory contributes the iron studies, blood counts, and coagulation results that make those decisions, and the facility’s transfusion guidelines and audit data show whether each transfusion met a documented indication.¹