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Complications of Blood Transfusion - Part 1 of 2: Immune Complications, Hemolytic and Non-Hemolytic

(Originally posted 13 September 1999 on About Anesthesiology)

Of all the blood given to patients, the largest percentage is administered in the operating room and therefore, most of this is given by anesthesiologists to patients under their care. It is important, therefore, to be aware of the possible complications of blood transfusion. This is a brief summary of these possible complications.

The complications can be broadly classified into two categories:

    • Immune Complications
    • Non-immune Complications

We will cover the immune complications this week in part one of our feature and cover the non-immune reactions in part two.

Immune Complications

Immune complications can further be classified into two categories:

    • Hemolytic (acute and delayed)
    • Non-Hemolytic (includes febrile, urticarial, anaphylactic, purpura, etc.)

These are primarily due to the sensitization of the recipient to donor blood cells (either red or white), platelets or plasma proteins. Less commonly, the transfused cells or serum may mount an immune response against the recipient. The immune complications are easily classified into hemolytic and non-hemolytic reactions.

Hemolytic reactions usually involve the destruction of transfused blood cells by the recipient's antibodies. Less commonly, the transfused antibodies can cause hemolysis of the recipient's blood cells. There are acute (also known as intravascular) hemolytic reactions and delayed (also known as extravascular) hemolytic reactions.

Acute hemolytic reactions are usually due to ABO blood type incompatibility - in other words, human error plays a large part in these reactions. Blood given to the wrong patient has been attributed to physician error approximately 20% of the time, the operating room is the most common site of this error, and the anesthesiologist is the most commonly implicated physician. This type of reaction has been reported to occur approximately 1 in 25,000 transfusions - but it is often very severe and accounts for over 50% of reported deaths related to transfusion. The severity of the reaction often depends in the amount of blood given.

Symptoms of acute hemolytic reactions include chills, fever, nausea, chest pain and flank pain in awake patients. In anesthetized patients, you should look for rise in temperature, unexplained tachycardia, hypotension, hemoglobinuria, oozing in the surgical field, DIC, shock and renal shutdown.

Management of acute hemolytic reactions mandates that the transfusion be stopped immediately. The unit should be re-checked. Blood from the recipient patient should be drawn to test for hemoglobin in plasma, repeat compatibility testing and coagulation tests. A foley catheter should be placed to check for hemoglobin in the urine. Osmotic diuresis with mannitol and fluids should be utilized (low-dose dopamine may help renal function and support blood pressure). With rapid blood loss, platelets and fresh frozen plasma may be indicated.

Delayed hemolytic reactions are generally mild in comparison. These are caused by antibodies to non-D antigens of the Rh system or to foreign alleles in other systems such as the Kell, Duffy or Kidd antigens. Following a normal, compatible transfusion there is a 1-1.6% chance of developing antibodies to these foreign antibodies. This takes weeks or months to happen - and by that time, the original transfused cells have already been cleared.

Re-exposure to the same foreign antigen can then cause an immune response. Thus the reaction is typically delayed from two to twenty-one days after transfusion.

Symptoms are generally mild and include malaise, jaundice, fever, a fall in hematocrit despite transfusion, and an increase in unconjugated bilirubin. Diagnosis may be facilitated by the direct Coombs test which can detect the presence of antibodies on the membranes of red cells.

Treatment is generally supportive. These reactions occur in approximately 1 in 2,500 transfusions and most often in females with previous exposure secondary to pregnancy.

Non-Hemolytic reactionsare due to sensitization of the recipient to donor white cells, platelets or plasma proteins. These reactions include:

    • Febrile
    • Urticarial
    • Anaphylactic
    • Pulmonary Edema (non-cardiogenic)
    • Graft vs. Host
    • Purpura
    • Immune Suppression

Febrile reactions are typically due to white cell or platelet sensitization. This reaction is relatively common occurring in 1-3% of all transfusions. The presenting symptom is a rise in body temperature without evidence of hemolysis. Patients with a history of this reaction that require additional transfusions should receive leukocyte poor transfusions. Use of a filter traps most contaminants.

Urticarial reactions are characterized by erythema, hives and itching without fever. Again, this is a relatively common reaction and occurs in about 1% of all transfusions. It is thought to be due to sensitization against plasma proteins. The use of packed red blood cells rather than whole blood has decreased the likelihood of this problem. Treatment is with antihistamines for symptomatic relief.

Anaphylactic reactions are rare and occur in about 1 of 150,000 transfusions. These are severe reactions that can occur with very small amounts of blood (a few milliliters). Typically, these reactions occur in IgA-deficient patients with anti-IgA antibodies. These antibodies react to transfusions containing IgA. Treatment is with epinephrine, fluids, corticosteroids and supportive measures. IgA deficiency occurs in 1 of 600-800 patients in the general population. Patients with known IgA deficiency should receive thoroughly washed packed red blood cells, deglycerolized frozen red cells or IgA free blood units.

Some patients can develop pulmonary edema and present with a picture that looks like adult respiratory distress syndrome (ARDS). This is a rare but serious complication that is thought to be due to the transfusion of antileukocyte antibodies that interact with the patient's white blood cells causing them to aggregate in the pulmonary circulation. Subsequent damage to the alveolocapillary membrane triggers the syndrome. Treatment involves respiratory support as needed.

Graft versus Host disease is seen exclusively in immunocompromised patients where cellular blood products containing lymphocytes are given. These lymphocytes can mount an immune response against the compromised recipient. Irradiation of transfusions can be utilized to inactivate the lymphocytes prior to transfusion.

Post-transfusion purpura is common with the development of platelet antibodies. The external purpura signal a reaction that may lead to profound thrombocytopenia which usually occurs about one week post transfusion. Plasmapheresis is the recommended treatment.

Immune suppression is a debatable complication. The transfusion of leukocyte-containing blood products appears to be immunosuppressive causing a decrease in Natural Killer cell function, decreased phagocytosis and decreased helper to suppressor cell ratios. The reason for this is unclear. The effect was first seen in renal transplant patients in whom preoperative blood transfusions appeared to improve graft survival. The clinical significance of this effect on such things as cancer recurrence and post-operative infection is still unclear.

That's it for the immune mediated complications of blood transfusion. In part two, we'll talk about the non-immune complications - those associated with massive blood transfusion and infectious problems.


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