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Complications of Massive Blood Transfusion Edgar J. Pierre, M.D. Assistant Professor of Anesthesia, Surgery and Critical Care Ryder Trauma Center University of Miami Someone needs blood every 3 seconds One in ten hospitalized patients needs blood

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complications of massive blood transfusion
Complications of Massive Blood Transfusion

Edgar J. Pierre, M.D.

Assistant Professor of Anesthesia,

Surgery and Critical Care

Ryder Trauma Center

University of Miami


Someone needs blood every 3 seconds

  • One in ten hospitalized patients needs blood
  • 4.5 million lives are saved by blood transfusions/year
  • One unit of blood saves three lives

90% water

  • albumin – the chief protein
  • fibrinogen
  • globulins
  • other clotting proteins
  • one white cell
  • forty platelets
  • six hundred red cells

Blood makes up 7% of the body’s weight

55% plasma

45% cell mass


1818 – first recorded human transfusion

Treats postpartum hemorrhage using patient’s husband as donor

James Blundell, MD


Karl Landsteiner, MD

The breakthrough – blood typing

1901 – Landsteiner discovers the first three human blood groups – A,B,C (later O)

1902 – colleagues Alfred Decastello and Adriano Sturli add AB

1930 – Landsteiner receives the Nobel Prize for Medicine

crystalloid replacement scheme

“3” buckets


Insensible loss


  • 4 cc/Kg for 1st 10Kg of weight
  • 4 cc/Kg for minimal trauma
  • 2 cc/Kg for 2nd 10Kg of weight
  • 6 cc/Kg for moderate trauma
  • 1 cc/Kg for the remaining weight
  • 8 cc/Kg for severe trauma
Crystalloid replacement scheme:

Hourly maintenance x number of hours NPO

estimation of blood volume
Estimation of Blood Volume
  • Most commonly used methodology bases estimation on weight, age, and gender
massive blood transfusion
Massive blood transfusion
  • As the replacement of a patient’s total blood volume in less than 24 hours
  • In a normal adult, this is 10-20 units
  • As the acute administration of more than half the patient’s estimated blood volume per hour
43 y o white female s p uterine rupture with intra abdominal bleeding for exploratory laparotomy
43 y/o white female s/p uterine rupture with intra-abdominal bleeding for exploratory laparotomy
  • Starting hematocrit = 43
  • Weight = 90 Kg
  • Allowable hematocrit = 25

ABL = 90 Kg x 70 cc/Kg x [(43-25)/34] = 3,335 cc

hemodynamic stability is the key indicator
Hemodynamic stability is the key indicator
  • If Hgb > 10g/dl transfusion is rarely indicated
  • If Hgb < 7g/dl transfusion is usually necessary
  • With Hgb between 7-10 g/dl, clinical status are helpful in defining transfusion requirements
    • Blood pressure
    • Heart rate
    • Extraction ratio
transfusion requirements should be based on the patient s physiologic needs
Transfusion requirements should be based on the patient’s physiologic needs
  • Oxygen demand (consumption)
    • CO × (CaO2-CvO2)
  • Oxygen delivery
    • CO × CaO2
  • Extraction Ratio
    • CaO2-CvO2/CaO2
risks of blood component therapy
Risks of blood component therapy
  • Transfusion reactions
  • Hemolytic
    • Donor blood contains an antibody, usually against the patient's HLA or leukocyte specific antigens
  • Non-hemolytic
    • Febrile, urticaria, anaphylactic, purpura
hemolytic reactions
Hemolytic reactions

Acute hemolytic reactions

Are usually due to ABO blood type incompatibility

Occur approximately 1 in 25,000 transfusions

Often very severe and accounts for 50% of deaths related to transfusions

Fatal hemolytic reaction 1:600,000 transfusions

Severity of the reaction depends in the amount of blood given

acute hemolytic reactions
Acute hemolytic reactions
  • Symptoms
    • Chills, fever, nausea, chest pain in awake patients
    • Rise in temperature, unexplained tachycardia, hypotension, hemoglobinuria, DIC, shock and renal failure in anesthetized patients
  • Management
    • Stop transfusion immediately, re-check the unit, test for hemoglobin in plasma and urine
    • Facilitate osmotic diuresis and support hemodynamic
hemolytic reactions18
Hemolytic reactions

Delayed hemolytic reactions

Caused by antibodies to non-D antigens of the Rh system or foreign alleles

1-1.6% chance of developing antibodies following a normal compatible transfusion

Takes weeks or months to happen- and by that time, the original transfused cells have already been cleared

Re-exposure can then cause an immune response

delayed hemolytic reactions
Delayed hemolytic reactions
  • Symptoms
    • Mild and include malaise, jaundice, fever, fall in hematocrit despite transfusion
    • Diagnosis may be facilitated by the direct Coombs test ( detect antibodies on the membranes of red cells
  • Management
    • Generally supportive
    • Occurs in approximately 1 in 2,500 transfusions and most often in females with previous exposure secondary to pregnancy
non hemolytic reactions
Non-hemolytic reactions




Graft versus Host


Immune Suppression

non hemolytic reactions21
Febrile reactions

1-3% of all transfusions

Rise in temperature without evidence of hemolysis

Should receive leukocyte poor transfusions

Use of a filter traps most contaminants

Urticarial Reactions

1% of all transfusions

Erythema, hives without fever

PBRC has decreased the likelihood of this problem

Treatment is with antihistamines

Non-hemolytic reactions
non hemolytic reactions22
Graft vs Host

Immunocompromised patients

Lymphocyte s can mount an immune response against the recipient

Irradiation of transfusions to inactivate the lymphocytes prior to transfusion

Post-transfusion purpura

Common with the development of platelets antibodies

Lead to profound thrombocytopenia

Plasmapheresis is the recommended treatment

Non-hemolytic reactions
non hemolytic reactions23
Non-hemolytic reactions
  • Pulmonary edema
  • Transfusion related acute lung injury – 13% of all transfusion deaths
  • Donor blood contains an antibody, usually against the patient's HLA or leukocyte specific antigens
  • Dyspnea, hypotension and fever within 1-2 hours after transfusion
  • CXR – diffuse, non-specific infiltrates
  • Treatment involves respiratory support as needed
non hemolytic reactions24
Non-hemolytic reactions
  • Anaphylactic reaction
  • Rare and occur in about 1 of 150,000 transfusions
  • Occur in IgA deficient patients with anti IgA antibodies
  • IgA deficiency occurs in 1 of 600-800 patients in the general population
  • Patients should receive thoroughly washed PRBC
  • Treatment involves fluids, epinephrine, corticosteroids and supportive measures
non immune complications
Non-immune complications
  • Infectious complications
    • Viral ( hepatitis, HIV, CMV, HTLV)
    • Parasitic and bacteremia
  • Physiologic complications
    • Coagulopathy
    • Citrate toxicity
    • Hypothermia
    • Acid-base disturbances
infectious complications

Asymptomatic or mild systemic disease

Immunocompromised patients are susceptible to CMV and should receive CMV negative units only


Leukemia and lymphoma retro-viruses associated with transfusion

Current risk is estimated at 1:250,000 to 2,000,000

Infectious complications

Risk of hepatitis A from transfusion is estimated to be 1:100,000

1:30,000 to 250,000 for Hepatitis B

1:30,000 to 1:150,000 for Hepatitis C


All blood is tested for the anti-HIV antibody

6-8 week period required for a person to develop antibody after they are infected therefore infectious units can go undetected

Current risk for HIV infection due to transfusion is estimated to be 1:200,000 to 2,000,000

risks of blood component therapy29
Risks of blood component therapy
  • Infectious risks per unit
  • Viral contamination
  • HIV <1:1,900,000
  • Hepatitis C <1:1,000,000
  • Hepatitis B <1:137,000
  • HTLV I + II <1:641,000
  • Bacterial contamination
  • <1:542 six unit platelets pool
  • <1:777 aphaeresis platelets
  • <1:38,565 PRBC units

Most common cause of bleeding following large volume transfusion: dilutional thrombocytopenia

At least 1.5 times blood volume must be replaced for this to become a clinical problem

Thrombocytopenia can occur following smaller transfusions if DIC or there is pre-existing thrombocytopenia

citrate toxicity
Citrate Toxicity

Citrate in the transfused blood binds to calcium

each unit of blood contains 3 grams of citrate

transfusion rates higher than one unit/5 minutes may lead to citrate toxicity

At least 1.5 times blood volume must be replaced for this to become a clinical problem

Treatment is with intravenous calcium administration if there is biochemical, clinical or electrocardiographic evidence of hypocalcemia


Leads to reduction of citrate and lactate metabolism

−hypocalcemia and metabolic acidosis

Increase affinity of hemoglobin for oxygen,

Leads to platelet dysfunction, and increase tendency for cardiac dysrhythmias

Massive transfusion is an absolute indication for the warming of all blood to body temperature as it is being given

acid base disturbances
Acid/Base Disturbances

Most common abnormality is a metabolic alkalosis

−lactic acid in stored PRBC (30-40mmol/l)

−citrate and lactic acid metabolized to bicarbonate

Final acid/base status being dependent on tissue perfusion, rate of administration and citrate metabolism

management of massive transfusion
Management of Massive Transfusion

Hypotension should be treated speedily. Do not delay fluid administration

Initial red cell replacement is in the form of packed red cells

Blood should be taken for group and crossmatch, these must be properly labeled and identified in all situations

management of massive transfusion36
Management of Massive Transfusion

For extreme emergencies group O blood should be supplied first

Type specific blood should be available in 5-10 minutes and switch promptly

Continue transfusing blood on this basis until crossmatch blood is available

complications of massive blood transfusion38
Complications of Massive Blood Transfusion

Edgar J. Pierre, M.D.

Assistant Professor of Anesthesia,

Surgery and Critical Care

Ryder Trauma Center

University of Miami