Transfusion Medicine
Updated: Aug 10
Red Blood Cell Transfusion
RBCs are collected from whole blood donation or by apheresis
How RBC apheresis works:
Venous access → blood enters the apheresis machine → Blood is separated by centrifugation → a predetermined amount of RBCs are collected and remaining components are returned
Why use apheresis?
Collects two units of RBCs from one donor in a singe session
Reduces the recipient's exposure to multiple donors.
Indications:
Patients requiring chronic transfusion (Sickle cell disease, thalassemia)
Collection of rare blood types
O-negative donor collection
Packed RBCs in preservative solution allow up to 42 days (6 weeks) of refrigerated storage (1-6 °C)
Up to 28 days (4 weeks) for irradiated units
Most RBCs in US are leukocyte reduced.
One unit of RBCs raises hemoglobin by roughly 1 g/dL (Hct by ~3%) in a stable adult.
Transfusion indications:
Hb <7 g/dL for most hemodynamically stable hospitalized adults
Hb <8 g/dL for preexisting cardiovascular disease and orthopedic surgery
Active/massive bleeding
Hb alone should not drive transfusion.
Transfuse hypotensive patients before Hb reaches 7.
Symptomatic anemia
Platelet Transfusion
Mostly collected by apheresis
Stored at 20–24 °C with continuous gentle agitation for 5 days
Irradiation does not change storage life (unlike RBCs)
Apheresis donation causes citrate-induced hypocalcemia (perioral tingling, cramping)
In general, spontaneous bleeding is uncommon until platelet count falls below 5,000-10,000
Thresholds for platelet transfusion based on 2025 AABB guideline:
Hypoproliferative thrombocytopenia (chemotherapy, HSCT) in non-bleeding patients: <10,000
Central venous catheter placement: <10,000
Lumbar puncture: <20,000
Consumptive thrombocytopenia without major bleeding: <10,000
Interventional radiology procedures:
Low risk procedures: <20,000
High risk procedures: <50,000
Neurosurgery: <100,000
Platelet transfusion is NOT recommended for:
Consumptive thrombocytopenia due to dengue without major bleeding
Hypoproliferative thrombocytopenia in nonbleeding adults undergoing autologous HSCT or with aplastic anemia
Nonthrombocytopenic patients undergoing cardiovascular surgery (including those receiving cardiopulmonary bypass) in the absence of major hemorrhage
TTP/HIT
May increase thrombotic complications
Reserve for life-threatening bleeding or urgent procedures
ITP
Usually ineffective if not being treated with steroids/IVIG, because transfused platelets are rapidly destroyed
Reserve for life-threatening bleeding or urgent procedures
Uremic platelet dysfunction:
Platelet transfusion does not help because the transfused platelets acquire the same defect.
Treatment:
Dialysis clears uremic toxins
DDAVP 0.3 µg/kg IV/SC works within ~30 min for 6-8 hours
DDAVP may cause tachyphylaxis, hyponatremia with repeat dosing, flushing/hypotension
Cryoprecipitate
Correction of anemia with ESA/RBC shorten bleeding time.
Refractory to platelet transfusion?
Definition: Corrected Count Increment (CCI) <5,000/μL at 1 h after fresh ABO-identical platelets on at least two consecutive transfusions
A raw "before" and "after" platelet counts can look small because the patient is large or the unit contained few platelets. CCI adjusts for body surface area (BSA) and the number of platelets given, so it reflects the true response.
Consult transfusion medicine
Approach based on the response:
If poor rise at 1 hour:
Platelets are destroyed almost immediately → antibodies/ immune causes (<20%)
Test for HLA antibodies. If positive, give HLA-matched apheresis platelets or give antigen-negative units selected to avoid the patient's antibodies. If still refractory despite good HLA matching, test for HPA (platelet-specific) antibodies.
Salvage options: epitope-matched platelets, rituximab, high-dose IVIG, or plasmapheresis.
If good rise at 1 hour, then a drop by the next day:
Platelets survived initially but were used up or trapped → consumption or splenic sequestration/ non-immune causes (>80%) such as sepsis, splenomegaly, DIC, GVHD
Plasma Transfusion
Collected from apheresis/whole blood donations
Contains all clotting factors
Can be stored at -18C for up to 1 year
Indicated if patient has multiple factor deficiencies + active bleeding
Massive hemorrhage/ massive transfusion
Liver disease/acute liver failure with active bleeding
DIC
If patient has actively bleeding or require an invasive procedure
TTP
Plasma is used as the replacement fluid during therapeutic plasma exchange.
This replaces ADAMTS13 while plasma exchange removes the pathogenic autoantibody and ultra-large VWF multimers.
Urgent warfarin reversal if 4-factor PCC is unavailable
4-factor PCC + IV vitamin K is generally preferred for major/life-threatening bleeding because PCC is faster and requires much less volume.
Plasma compatibility is essentially the reverse of RBC compatibility, because we are worried about the antibodies in the donor plasma attacking the recipient's RBCs.
AB blood type = universal plasma donor
Rh matching is generally not required for plasma, because plasma contains essentially no clinically meaningful quantity of RBCs.
Do NOT routinely give plasma for:
Volume expansion
Use crystalloid/other appropriate fluids.
Hypoalbuminemia
Nutritional support
Mildly elevated INR without bleeding
INR of plasma is around 1.1 to 1.4
Routine correction of abnormal coagulation tests before a low-bleeding-risk procedure
Warfarin reversal when 4-factor PCC is available and indicated
Cryoprecipitate Transfusion
Storage:
Stored frozen at ≤ −18°C for up to 1 year
After thawing, stored at room temperature
Must be transfused within 6 hours of thawing
Cannot be refrozen.
Contains:
Fibrinogen (factor I)
Factor VIII
Factor XIII
vWF
Fibronectin
Indications:
Hypofibrinogenemia/dysfibrinogenemia with bleeding or high bleeding risk
Fibrinogen level:
<100 mg/dL: commonly used threshold before an invasive procedure
<150 mg/dL: consider replacement with active bleeding
<200 mg/dL: may be targeted in life-threatening/massive hemorrhage
Factor XIII deficiency if factor XIII concentrate is unavailable
Fibrinogen replacement in settings such as DIC or massive hemorrhage when fibrinogen is low

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