Blood transfusion complication

PHUNG HUY HOANG
RESIDENT IN INTERNAL MEDICINE
PHAM NGOC THACH UNIVERSITY OF MEDICINE July 2017
BLOOD TRANSFUSION
COMPLICATIONS

IMMEDIATE DELAYED
IMMUNOLOGIC
• Acute hemolytic transfusion
reactions
• Febrile nonhemolytic transfusion
reactions
• Allergic, anaphylatic reaction
• TRALI
• Delayed hemolytic
transfusion reactions
• TaGVHD
• Posttransfusion purpura
NON-IMMUNOLOGIC
• Transfusion-transmitted infections
• TACO
• Massive transfusion related
• Viral infection
• Iron overload
CLASSIFICATION

Dzieczkowski J. S., Anderson K. C. (2016), Harrison's Principles of Internal Medicine, Anthony S. Fauci Dennis L. Kasper, Stephen L. Hauser, Editor, McGraw Hill Education, pp. 138e1-6

OVERVIEW
• Risks associated with the transfusion of any specific unit of blood: low
• Risks must be weighed against the benefits at the time each transfusion
• Classification: immunologic and nonimmunologic; immediate and delayed
• Severe complications (including death): develop within a few minutes of initiating transfusion
 close attention and early vital sign assessments: at the beginning and within 15
minutes of starting a transfusion

Isbister J. P. (2014), Oh’s Intensive Care Manual, Andrew D Bersten , Neil Soni, Editors, Elsevier, pp. 973-986

IMMUNOLOGIC REATIONS
• Stimulation of antibody production by foreign alloantigens (transfused red cells, leukocytes,
platelets, or plasma proteins)  immunologically mediated reactions in the future.
• Hemolytic reactions: red cell incompatibility
• Febrile or pulmonary reactions: leukocytes and platelet antigens
• Allergic or anaphylactic reactions: antibodies reacting with soluble antigens (plasma
proteins, in transfused material)
• GVHD: engraftment of transfused lymphocytes in immunosuppressed recipients

NON-IMMUNOLOGIC REACTIONS
• Physical or chemical properties of the transfused blood products
• Contaminating infectious agents

Coil C. J., Santen S. A. (2016), Tintinalli’s Emergency Medicine - A Comprehensive Study Guide, Judith E. TintinalliJ, Stephan Stapczynski, O. John Ma, Editors, McGraw Hill, pp. 1518-1523.

Acute hemolytic reactions (AHTR)
PHUNG HUY HOANG
PHAM NGOC THACH UNIVERSITY OF MEDICINE

OVERVIEW
• Most serious and immediately life-threatening
• Rare, human error related
• Soon (<24h), intravascular hemolysis
• ABO incompatibility, other red cell antigens (Jka, K, Fya)
• anti-A and anti-B antibodies: predominantly IgM, binding complement
• Have been reported in association with apheresis platelets (containing abnormally high titer
(>1:250) antiA or anti-B antibodies in the plasma)

SEVERITY
• 47%: no eﬀects (even afer receiving a whole unit)
• 41%: symptoms of AHTR
• Mortality: ~ 2%
Severity ~ volume of red cells infused

PATHOPHYSIOLOGY
• Interaction between antibody and red cell membrane  immune complexes, activation of
complement  release of C3a, C5a (anaphylatoxic activity, coagulation mechanism via cytokines
IL-1,6,8, TNF-α and factor XII  both consumptive coagulopathy and generation of
bradykinin)
• Vasomotor mediators implicated in the transfusion reaction: histamine, serotonin, cytokines
 shock
• Renal failure: poorly understood etiology (primarily ischemic  hypotension, vasoconstriction via
nitric oxide inactivation by Hb, intravascular coagulation, antigen-antibody complex deposition)
• Free hemoglobin once thought to be the major cause of renal failure (precipitating in and
obstructing the renal tubules): adequate evidence to discount this hypothesis!!

MANIFESTATION
• Sudden change clinically
• Fever with or without chills: most common
• Hypotension, shock
• Anaphylaxis
• Anxiety, chest or back pain, flushing, dyspnea with wheezing (bronchospasm), tachycardia
• Hematuria or hemoglobinuria
• Bleeding (consumptive coagulopathy)
Acute renal failure, shock, and intravascular coagulation

LABORATORY
• DAT: detect antibody-coated red cells (Negative DAT occurs in rare cases when all
transfused RBCs are lysed)
• Repeat ABO and Rh typing of the patient and the transfused blood
• Repeat antibody screen and crossmatch may be helpful.
• Intravascular coagulation (esp DIC)
• Renal function
• Urinary hemosiderin or free hemoglobin (post‐transfusion sample of urine)
• Reduced serum haptoglobin, or hyperbilirubinemia
• Further samples of blood (6 hours and/or 24 hours after transfusion): blood count,
bilirubin, free haemoglobin, methaemalbumin

Galel S. A., fontaine M. J., Viele M. K., et al. (2014), Wintrobe's Clinical Hematology, John P. Greer, Daniel A. Arber, Bertil Glader, Editors, Wolster Kluwer, pp. 547-586

MANAGEMENT (1)
• Transfusion must be discontinued immediately (on any suspicious!)
• General ABCs, cardiac and oxygen monitoring
• Maintaining vascular access (slowly NaCl infusion)
• Recheck of the patient’s identity + information on the discontinued blood unit  rule out
bedside identification errors
• Report to the blood bank without delay (a posttransfusion blood sample and the
discontinued bag of blood  sent to the blood bank for investigation)

• Hydration (immediately)  prevent renal failure
• Infusion of normal saline: maintain BP,  urine flow rate to 100 ml/h in 24 hours (without
contraindications)
• Diuretics
• Severe cases of hypotension: IV dopamine (dilates renal vasculature and increases
cardiac output)
• Renal failure: fluid restriction, management of electrolyte balance, dialysis.
• Coagulopathy and active bleeding: platelets, fresh-frozen plasma, or cryoprecipitate
• Shock or anaphylaxis: Hydrocortisone 100mg (IV), antihistamine (parenteral),
epinephrine (0.3 mL of 1:1000 SC), Acetaminophen PO/IV
• Excretion of free Hb: alkalinization of urine (pH ≥ 7.5)
MANAGEMENT (2)

Mosley J. C., Blinder M. A. (2012), The Washington Manual of Critical Care Marin H. Kollef ,
Warren Isakow, Editors, Lippincott Williams & Wilkins, pp. 505-510

PREVENTION
Most common basis for AHTRs is a clerical error resulting from
• mistakes in identifying the patient
• labeling the pretransfusions sample
• identifying the correct red cell unit for the patient

Delayed hemolytic reactions (DHTR)
PHUNG HUY HOANG

OVERVIEW
• Much milder
• Predominantly extravascular: IgG-coated red cells are removed by the reticuloendothelial
system
• 2 to 10 days after a transfusion
• DAT: often positive (transient, may be missed if performed too late, reverts to negative as the
incompatible red cells are removed from the circulation)
• Almost always represent secondary, or anamnestic, antibody responses (secondary
exposure to antigens) = A subsequent transfusion causes recall of the antibody followed by a
falling hematocrit 5 to 10 days later
• Antibodies to Kidd (Jk) antigens and to antigens of the Rh: major offenders (anti-Kell and
anti-Duffy (Fy) implicated in most other delayed reactions)

MANIFESTATION
• Usually no symptoms
• New red cell antibody and positive DAT detected incidentally
• Fever, falling hematocrit, jaundice, and, infrequently, hemoglobinemia and
hemoglobinuria
• Rarely dramatic: renal failure uncommon, but fatalities been reported
• Hemolysis may be noted only by a more rapid decline than usual in the patient’s
hemoglobin level or by an absence of the expected rise in hemoglobin

INVESTIGATION
• DAT  antibodies should be eluted from the red cells and identified
• Give patient a card indicating the presence of the antibody

MANAGEMENT
• No specific therapy is necessary
• Crossmatch-compatible blood negative for the offending antigen(s) for further transfusion
• Physician and patient should be informed
• Prednisone (1 to 2 mg/kg/day) is indicated for more severe reactions

PSEUDOHEMOLYTIC TRANSFUSION REACTIONS
• Conditions that mimic hemolytic transfusion reactions: clinical syndrome consistent with
intravascular hemolysis >< no blood group incompatibility can be identified
• ETIOLOGY:
• Bacterial contamination with organisms such as Yersinia
• Resorption of large hematomas
• Hemolysis caused by drug reactions or vascular prostheses
• Pretransfusion hemolysis of donor blood (mechanical trauma, freezing, heat, or hypotonic
solutions)
Beauregard P., Blajchman M. A. (1994), Transfus Med Rev, 8 (3), pp. 184-99

Febrile Nonhemolytic Transfusion
Reactions (FNHTRs)
PHUNG HUY HOANG

OVERVIEW
• 0.5-3.0% transfusion
• Most commonly encountered transfusion reactions
• More common in multiply transfused patients, multiparous women (exposed to foreign
blood antigens)
• More likely to occur following transfusion of platelets than RBCs
• Typical: chill  fever of 1°C or greater, during or within a few hours of the transfusion (up to
4-6 hours)
• Headache, nausea, and vomiting: may occur
• Usually mild, resolve completely within 1 to 2 hours afer the transfusion is discontinued
• Diagnosed when other causes of fever in the transfused patient are ruled out (underlying
patient condition, bacterial contamination of the unit, acute hemolytic transfusion reaction)

Triulzi D. J. (2009), Anesth Analg, 108 (3), pp. 770-6

ETIOLOGY
• Alloimmunization to antigens on leukocytes and platelets:
• most common
• HLA antibodies, platelet-specific antibodies, granulocyte-specific antibodies: in
common order
• Activation of donor leukocytes by anti-HLA or other antibodies in the recipient, activation
of recipient leukocyte and endothelial cells by transfused donor leukocytes or plasma
constituents
• Transfusion of cytokines developed during product storage ( with the age of the platelet
concentrate and the leukocyte concentration in the product)  apheresis platelets:
leukoreduced  reduced cytokine levels
• Bacterial contamination

MANAGEMENT
• Febrile transfusion reaction  transfusion should be discontinued until the patient has been
carefully assessed by a physician and the blood bank alerted (hemolytic or bacterially
contaminated transfusion ruled out)
• If a febrile reaction occurs in a first-time transfusion: should be treated as an extravascular
hemolytic reaction until proven otherwise
• Antipyretic such as acetaminophen
• Hydrocortisone: severe reactions
• Meperidine: decrease or stop severe shaking chills
• Antihistamines: only if allergic symptoms

PREVENTION
• Transfusing leukoreduced RBCs and/or platelets stored in additive solution
• Prestorage leukocyte reduction
• Premedication with antipyretics (acetaminophen): NOT helpful
• Marti-Carvajal A. J., Sola I., Gonzalez L. E., et al. (2010), Cochrane Database Syst Rev, (6), pp. CD007539
• Tobian A. A., King K. E., Ness P. M. (2008), Transfusion, 48 (11), pp. 2274-6

Transfusion-related Acute Lung Injury
(TRALI)
PHUNG HUY HOANG

OVERVIEW
• Leading cause of transfusion-related deaths
• Severe respiratory distress of sudden onset
• Within 6 hours of transfusion
• A syndrome of noncardiogenic pulmonary edema
• Usually resolves with supportive care within 48 to 96 hours without sequelae (80-90%
patients)
• Usually a complication of fresh frozen plasma or platelet transfusion

PATHOGENESIS
• ‘Two-hit’ hypothesis
• Transfusion of potential granulocyte primers that bind recipient leukocytes (inflammatory
cytokines, active lipids, and/or alloantibodies)
• Event linked to the patient (i.e., underlying sepsis, hematologic disease, and/or postsurgical
status, mechanical ventilation, chronic alcohol abuse, severe liver disease)  a necessary first
hit, leading to adherence of primed neutrophils to the pulmonary endothelium
• Agglutination of granulocytes and complement activation in pulmonary vascular bed 
capillary endothelial damage, fluid leak into the alveoli
• Most common mediators: antibodies specific for either class II HLA or for human
neutrophil antigens (HNAs)

• Triulzi D. J. (2009), Anesth Analg, 108 (3), pp. 770-6
• Silliman C. C., Ambruso D. R., Boshkov L. K. (2005), Blood, 105 (6), pp. 2266-73

MANIFESTATION
• Chills, fever, chest pain, hypotension, and cyanosis, as well as the usual manifestations
of pulmonary edema
• ALI (acute lung injury): PaO2/FiO2 ≤ 300 mmHg
• Bilateral infiltrates on frontal chest radiograph
• NO evidence of circulatory overload

Kleinman S., Caulfield T., Chan P., et al. (2004), Transfusion, 44 (12),
pp. 1774-89

Marino P. L. (2014), Marino's the ICU Book, Wolters Kluwer, pp. 349-368

MANAGEMENT
• Stop transfusion immediately at the first signs of respiratory difficulty
• Supportive measures for the pulmonary edema and hypoxia, including ventilatory support if
required
• Hemodynamic  fluid overload (if not, diuretics: no proven value)
• IV ﬂuid and vasopressors for hypotension (if indicated)
• Glucocorticoids may provide beneft

PREVENTION
• Avoid further transfusion of plasma-containing products from implicated donors found to
have anti-HLA or antigranulocyte antibodies
• Minimize the production of high-plasma-content components (plasma products, pheresis
platelets) from donors at risk for alloimmunization (e.g., women with a history of pregnancy)

Allergic transfusion reactions (ATR)
PHUNG HUY HOANG

OVERVIEW
• Common
• Wide range: urticarial lesions (hives), other skin rashes, bronchospasm, angioedema,
anaphylactic shock
• Whole blood and plasma > concentrated red cells
• Dose related, incidence ~ volume of plasma transfused
• Recipient IgE to proteins or other soluble substances in donor plasma  release of
histamine from mast cells and basophils
• Usually begin during or within an hour of starting a transfusion, but may not become evident
until several hours later.
• Fever is usually absent

IgA-RELATED
• Severe anaphylactoid or anaphylactic reactions: antibodies reacting with IgA in donor plasma
should be considered
• Incidence of genetically determined IgA deficiency (normal population): high, 1:400-500
• 20% to 25% of such patients produce antibodies to IgA, generally class-specific (i.e.,
reacting with all IgA molecules)
• Many patients with normal IgA levels have antibodies that react with some, but not all, IgA
molecules (incidence may be higher in multiply transfused patients)

GRADING
• Grade I:
o skin manifestations
• Grade II:
o mild to moderate hypotension
o gastrointestinal disturbances (nausea)
o respiratory distress
• Grade III:
o severe hypotension, shock
o bronchospasm
• Grade IV:
o cardiac and/or respiratory arrest
Isbister J. P. (2014), Oh’s Intensive Care Manual, Andrew D Bersten , Neil Soni, Editors, Elsevier, pp. 973-986

MANAGEMENT
• Most ATRs: mild, self-limited and respond well to transfusion discontinuation
• Maintaining vascular access
• Antihistamine
• Steroids: usually NOT helpful in acute crises ± required in severe cases
• In cases limited to urticaria: transfusion may be resumed immediately after symptoms
resolve
• Severe symptoms: epinephrine, bronchodilators
• For patients with repeated allergic reactions: premedication with an H1-blocking
antihistamine
• Reducing the plasma content of the transfused blood product (centrifuging the product
and removing almost all the plasma or by red cell washing)
• Severe IgA deficiency: only IgA-deficient plasma and washed cellular blood components

Posttransfusion Purpura (PTP)
PHUNG HUY HOANG

OVERVIEW
• Rare
• Development of life-threatening thrombocytopenia
• Formation of allowantibodies against platelet antigens
• Both the transfused and recipient platelets are destroyed by the immune complexes
• Most common: HPA-1a (polymorphic epitope of GPIIIa)
• HPA-1a/1b negative multiparous women or previously transfused patients
• Within 7-10 days of transfusion
• Confirmation: detection of platelet alloantibodies
• Spontaneous platelet recovery eventually

MANAGEMENT
• IVIG (neutrolize antibodies)
• High dose corticosteroid
• Plasmapheresis (remove antibodies)
• Additional platelet transfusions: can worsen the thrombocytopenia  should be avoided

Transfusion-associated Graft-versus-
Host Disease (TaGVHD)
PHUNG HUY HOANG

OVERVIEW
• Most cellular blood products (red cell, platelet, granulocyte products): contain viable,
immunocompetent T lymphocytes
• Occur in:
• Immunoincompetent recipients
• Also been reported in immunocompetent patients (esp receive transfusions from family
members or from random donors who share HLA antigens  recipient not recognize
donor cells as foreign  allowing the transfused lymphocytes to proliferate
• Most cases: transfusion of leukocyte or platelet concentrates or fresh blood
• A few reports of spontaneous resolution
• Fatal in approximately 90% of aﬀected patients

Galel S. A., fontaine M. J., Viele M. K., et al. (2014), Wintrobe's Clinical
Hematology, John P. Greer, Daniel A. Arber, Bertil Glader, Editors,
Wolster Kluwer, pp. 547-586

PRESENTATION
• Most common: fever
• Typical erythematous, maculopapular skin rash (begins centrally and spreads peripherally to
the hands and feet)
• Abnormalities of hepatic function
• Nausea
• Bloody diarrhea
• Leukopenia followed by pancytopenia due to marrow failure: quite common in TA-GVHD,
most often 2 to 3 weeks after the onset of symptoms

PRESENTATION
• Histological confirmation: skin biopsy
• Laboratory confirmation: demonstrating the presence of donor lymphocytes in the patient
(HLA typing, cytogenetic analysis, analysis of DNA microsatellite polymorphisms or
variable-number tandem repeats)
• Most common cause of death: severe systemic infections (within 3 to 4 weeks from the
time of the implicated transfusion)

MANAGEMENT
• Corticosteroids, antithymocyte globulin, cyclosporine, growth factors: minimal
success
• Current approach: combinations of immunosuppressant medications with lymphocyte-
directed antibody therapy (anti-CD3, anti–interleukin-2 receptor, antithymocyte globulin)
• Prevention: pretransfusion irradiation of all blood products administered to patients at risk
• inhibits proliferation of donor lymphocytes with little significant adverse effect on red cell,
platelet, or granulocyte function
• Changes in the red cell membrane  increased loss of potassium from the cell  limiting
the storage time of irradiated red cells to 28 days
• 2,500 cGy (center of the irradiation field), minimum dose of 1,500 cGy (any point in the
field)

Hoffbrand A. V., Moss P. A. H. (2016), Hoffbrand’s Essential Haematology, John Wiley & Sons, pp. 333-345

Transfusion-associated Circulatory
Overload (TACO)
PHUNG HUY HOANG

• Blood components: excellent volume expanders (compared to similar volumes of crystalloid
fluids)
• At risk:
• Elderly patients with limited cardiac reserve
• Severely anemic patients in congestive heart failure
• Affect by: infusions rates, the volume of infused blood product, and/or an underlying
cardiac, renal, and/or pulmonary pathology
• Fluid volume transfused: may be less important than the infusion flow rate and the patient’s
ability to process the fluid
• Signs such as rales, hypertension, and jugular vein distention  differentiate TACO from
TRALI
OVERVIEW

• Supplemental oxygen
• Diuretic therapy and other measures to manage heart failure
• Partial exchange transfusion
• Transfusion: slowly (1 to 4 ml of blood/kg/hour)
• Mechanical ventilation may be required (non-invasive, invasive)
• Close monitoring of the patient’s vital signs
MANAGEMENT

Transfusion-Related Sepsis
PHUNG HUY HOANG

• Usually from platelet units that are stored at room temperature (Staphylococcus,
Enterobacteriaceae)
• Red cells, stored at refrigerator temperatures, are very rarely contaminated by unusual cold-
growing organisms (e.g., Yersinia, Serratia, Pseudomonas, Acinetobacter, and Escherichia)
• Potential sources:
• asymptomatic bacteremia in the donor
• bacteria from the donor’s skin
• Fever (>38.5°C), rigors, marked hypotension, abdominal pain, vomiting, diarrhea, and the
development of profound shock
• Gr (-) > Gr (+): severity
• Gram stain, culture of the transfused component

Viral Infections
PHUNG HUY HOANG

• All blood products: screened for hepatitis B, hepatitis C, human immunodeficiency virus
1 and 2, and human T-lymphotropic virus I and II.
• Other infectious risks: viruses that are not screened for (CMV, parvovirus B19, prion
transmitted Creutzfeldt–Jacob disease)

Goodnough L. T. (2016), Goldman-Cecil Medicine, Lee Goldman , Andrew I. Schafer, Editors, Elsevier Saunders, pp. 1191-1198

Galel S. A., fontaine M. J., Viele M. K., et al. (2014), Wintrobe's Clinical Hematology, John P. Greer, Daniel A. Arber, Bertil Glader, Editors, Wolster Kluwer, pp. 547-586.

Iron Overload
PHUNG HUY HOANG

• Long term red cell transfusion support for
chronic anemias (e.g bone marrow failure,
Thalassemia)
• Each unit of red cells = 0.2-0.25 g of iron
 deposition of iron initially in
reticuloendothelial tissue at the rate of
200–250mg/unit of red cells
OVERVIEW
• Stigmata of transfusion siderosis: impaired growth, failure of sexual maturation, myocardial
and hepatic dysfunction, hyperpigmentation, and, often, diabetes
• Endocrine, hapatic, cardiac

Goal: serum ferritin level between 1000 and 1500μg/L
• Deferasirox
• Deferiprone
• Deferoxamine
IRON CHELATION THERAPY

Massive transfusion
PHUNG HUY HOANG

• Replacement of the circulating volume in 24 hours
• >4 units of blood in 1 hour with continuing blood loss
• Transfusion of 10 units of red cells in 24 hours
• loss of 50% of circulating blood volume within 3–4 hours.
DEFINITION

Pham H. P., Shaz B. H. (2013), Br J Anaesth, 111 Suppl 1,
pp. i71-82.

PATHOPHYSIOLOGY
Pham H. P., Shaz B. H. (2013), Br J Anaesth, 111 Suppl 1, pp. i71-82.

• Citrate toxicity
• Acid-base disturbance
• Electrolyte disturbance (Ca,K, Na)
• Hypothermia
• Coagulopathy
• Hyperbilirubinaemia
 coagulation parameters, platelet count, and metabolic status (acid-base, electrolyte)
ADVERSE EFFECTS

• Citrate binds free ionized calcium
• Citrate: metabolised by the Krebs cycle in ALL nucleated cells (esp liver)  bicarbonate
• Citrate metabolism impaired: hypotension, hypovolaemia, hypothermia and liver disease
• Toxicity potentiated by alkalosis, hyperkalaemia, hypothermia and cardiac disease
•  free calcium concentration ± metabolic alkalemia ( hypokalemia)
• A warm, well-perfused adult patient with normal liver function can tolerate a unit of blood each
5 minutes without requiring calcium
• Rate of transfusion: more signifcant than total volume transfused
• Perioral and digital paresthesias and nausea; rarely: tetany and cardiac arrhythmias
ADVERSE EFFECTS Citrate toxicity (1)

• Maximum citrate infusion rate (mmol/kg per min) = (mmol citrate per mL of blood x mL of
blood infused per min) ÷ wt (kg)
• mL of blood infused per min = (0.02 ÷ 0.015) x wt (kg) = 1.33 x wt (kg)
• Maximum citrate infusion rate should be 0.02 mmol/kg per minute (maximum rate of citrate
metabolism)
• Citrate concentration in whole blood is 15 mmol/L (0.015 mmol/mL), ~ 450ml/unit
ADVERSE EFFECTS Citrate toxicity (2)

• Management: Perioral and digital paresthesias and nausea; rarely: tetany and cardiac
arrhythmias
• If 10 percent calcium gluconate is used, 10 to 20 mL should be given intravenously (into
another vein) for each 500 mL of blood infused.
• If 10 percent calcium chloride is used, only 2 to 5 mL per 500 mL of blood should be given
• Calcium chloride may be preferable to calcium gluconate (in the presence of abnormal liver
function: citrate metabolism   slower release of ionized calcium)
ADVERSE EFFECTS

• Stored bank blood contains an appreciable acid load (citric acid of the anticoagulant and
lactic acid generated during storage)
• Routine use of sodium bicarbonate: unnecessary, generally contraindicated! (Alkali:
further shifts the oxygen dissociation curve to the left, provides a large additional sodium
load, depresses the return of ionised calcium to normal following citrate infusion)
• Citrate  bicarbonate  alkali
ADVERSE EFFECTS Acid-base disturbance

•  K+ content of stored red cells (RBC leakage during storage)  hyperkalemia: rarely
(Risk: renal failure, shock with acidosis, hemolysis)
• Citrate  excess bicarbonate generated  alkalemia  driving potassium into the cells 
hypokalemia
ADVERSE EFFECTS Potassium
McEvoy C., Murray P. T. (2015), Principles of Critical Care, Jesse B. Hall, Gregory A. Schmidt, John P. Kress, Editors, McGraw Hill, pp. 943-974

• Sodium content of whole blood and fresh frozen plasma: higher than the normal blood level
(due to the sodium citrate)
• Caution: large volumes of plasma infused into patients with disordered salt and water
handling (e.g. renal, liver, cardiac disease)
ADVERSE EFFECTS Sodium

• One of the most common
• Large volume of cold blood is infused rapidly
• Neonates and the elderly are particularly sensitive
• Effect:
• Affects the way the liver metabolizes citrate
• Contributes to the associated coagulopathy, interferes with platelet function and clotting
• Cardiac dysrhythmias  exposing the sinoatrial node to cold fluid
• Blood-warming devices: recommended > 3 units are transfused (careful: overheated 
hemolysis)
ADVERSE EFFECTS Hypothermia

• Dilutional coagulopathy
• Citrate toxicities, hypothermia
• Abnormalities of PT, aPTT, thrombocytopenia
• Factor VIII activity may rise: response to stress
• Factor V: falls, but rarely to dangerous levels
• Should include plasma to correct the levels of coagulation factors, followed by platelet
products (1 U RBC/1 U plasma/1 random donor unit of PLTs: controversial)
• THRESHOLD: PT, aPTT  1.5x; PLT < 50x109.
ADVERSE EFFECTS Coagulopathy

Pham H. P., Shaz B. H. (2013), Br J Anaesth, 111 Suppl 1, pp. i71-82.

Hypotensive reaction
PHUNG HUY HOANG

• Transient hypotension: noted among transfused patients who take angiotensin-converting
enzyme (ACE) inhibitors
• Blood products contain bradykinin (degraded by ACE) ACE inhibitors may have increased
• bradykinin levels  hypotension
• Blood pressure typically returns to normal without intervention

Pandey S., Nambiar A. (2014), Irwin & Rippe’s Manual of Intensive Care Medicine, Richard S. Irwin, Craig M. Lilly, James M. Rippe, Editors, Lippincott Williams & Wilkins, pp. 724-731

Blood products SUMMARY
PHUNG HUY HOANG

SAFE TRANSFUSION
Isbister J. P. (2014), Oh’s Intensive Care Manual, Andrew D Bersten , Neil Soni, Editors,

Hoffbrand A. V., Moss P. A. H. (2016), Hoffbrand’s Essential Haematology, John Wiley &
Sons, pp. 333-345

Watson H. G., Craig J. I. O., Manson L. M. (2014), Davidson’s Principles and Practice of Medicine, Brian R. Walker, Nicki R. Colledge, Stuart H. Ralston, Editors, Churchill Livingstone
Elsevier, pp. 989-1056

• Platelet count <5000/mm3 (<5 × 109/L)
• Platelet count <20,000/mm3 (<20 × 109/L) with a coagulation disorder, low-risk procedure, or
during outpatient treatment
• Platelet count <50,000/mm3 (<50 × 109/L) with active bleeding or invasive procedure within
4h
• Platelet count <100,000/mm3 (<100 × 109/L) with neurologic or cardiac surgery
• As part of a massive transfusion protocol
PLATELETS TRANSFUSION: General indications

• Reversal of warfarin overanticoagulation (not the primary agent)
• Bleeding with multiple coagulation defects
• Correction of coagulation defects for which no specific factor is available
• As a component of a massive transfusion protocol
• As part of plasma exchange when treating thrombotic microangiopathies or neurologic
• disorders
FFP TRANSFUSION: General indications

• Bleeding with a fibrinogen level of <100 milligrams/dL (< 1 g/L)
• Dysfibrinogenemia
• Bleeding in some subtypes of von Willebrand’s disease that are unresponsive to
desmopressin, and factor VIII concentrates are unavailable
CRYOPRECIPITATE TRANSFUSION: General indications

PHUNG HUY HOANG
July 2017
BLOOD TRANSFUSION
COMPLICATIONS

1. Beauregard P., Blajchman M. A. (1994), "Hemolytic and pseudo-hemolytic transfusion reactions: an overview of the hemolytic
transfusion reactions and the clinical conditions that mimic them", Transfus Med Rev, 8 (3), pp. 184-99.
2. Coil C. J., Santen S. A. (2016), "Transfusion Therapy", Tintinalli’s Emergency Medicine - A Comprehensive Study Guide, Judith E.
TintinalliJ, Stephan Stapczynski, O. John Ma, Editors, McGraw Hill, pp. 1518-1523.
3. Dzieczkowski J. S., Anderson K. C. (2016), "Transfusion Biology and Therapy", Harrison's Principles of Internal Medicine,
Anthony S. Fauci Dennis L. Kasper, Stephen L. Hauser, Editor, McGraw Hill Education, pp. 138e1-6.
4. Emery M. (2014), "Blood and Blood Components", Rosen’s Emergency Medicine: Concepts and Clinical Practice, John A. Marx,
Robert S. Hockberger, Ron M. Walls, Editors, Elsevier Saunders, pp. 75-80.
5. Galel S. A., fontaine M. J., Viele M. K., et al. (2014), "Transfusion Medicine", Wintrobe's Clinical Hematology, John P. Greer,
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