Acute hemolytic transfusion reaction

An acute hemolytic transfusion reaction (AHTR) is a type of transfusion reaction that is associated with hemolysis. It occurs very soon after the transfusion, and within 24 hrs post-transfusion.[1] It can occur quickly upon transfusing a few milliliters, or up to 1–2 hours post-transfusion.[2]

It is also known as an "immediate hemolytic transfusion reaction".[3] This is a medical emergency as it results from rapid destruction of the donor red blood cells by host antibodies (IgG, IgM). It is usually related to ABO blood group incompatibility - the most severe of which often involves group A red cells being given to a patient with group O type blood. Properdin then binds to complement C3 in the donor blood, facilitating the reaction through the alternate pathway cascade. The donor cells also become coated with IgG and are subsequently removed by macrophages in the reticuloendothelial system (RES). Jaundice and disseminated intravascular coagulation (DIC) may also occur. The most common cause is clerical error (i.e. the wrong unit of blood being given to the patient).

Epidemiology

In the USA in 2011 there were 48 episodes of acute hemolysis due to a mismatch in ABO blood type (1 in 495,207 blood components transfused) and 168 episodes of hemolysis due to other causes (1 in 124,525 blood components transfused).[4] In the UK in 2014 there were 18 episodes of hemolysis due to other causes (1 in 147,972 blood components transfused).[5]

Types

Acute hemolytic transfusion reactions are divided into two types.

Intravascular haemolysis

The most common cause of this reaction is ABO blood groups incompatibility, secondary to human errors. In this process, the donor's red blood cells are destroyed by recipient's preformed antibodies through the activation of complement system. Thus, the donor's red blood cells break open and releases haemoglobin into the blood. The haemoglobin is then excreted into urine, causes haemoglobinuria. Meanwhile, haemoglobin can also pass through the liver system and process into bilirubin, which accumulates under the skin, causing jaundice. The release of red blood cell debris and the activation of complement system causes uncontrolled clotting (disseminated intravascular coagulation) and circulatory shock.[6]

Extravascular haemolysis

In this case, the donor's red blood cells are recognised and bound to IgG antibodies. Macrophages then recognise these IgG antibodies and engulf these red blood cells, removing the red blood cells from the blood circulation into liver and spleen. These red blood cells are then destroyed by macrophages in these organs. Anti-Rh antibodies most commonly directed this type of reaction. This process is much more controlled when compared with intravascular haemolysis. Liver has adequate capacity in processing the bilirubin. Therefore, jaundice rarely occurs.[6]

Signs and symptoms

Early signs are fever, low blood pressure, anxiety, and red-colored urine.

Late signs are generalized bleeding, caused by disseminated intravascular coagulation, and low blood pressure.

Laboratory assessment is based on a positive Direct Antiglobulin Test (DAT), a decrease in serum haptoglobin, and an increase in blood levels of the enzyme lactate dehydrogenase and indirect bilirubin levels.[7]

Pathophysiology

Immune mediated

This may be caused by preformed IgM anti-A, anti-B or both. It may also be caused by other non-ABO IgG antibodies such as Rh, Kell, or Duffy. The former results in a severe intravascular hemolysis and the latter typically causes extravascular hemolysis. The reactions are mediated by cytokines like TNF, IL-8, monocyte chemoattractant protein, IL-1 etc.

Non-immune mediated

These occur when RBCs are damaged before transfusion, resulting in hemoglobinemia and hemoglobinuria. Clinical symptoms are nil or milder.

Diagnosis

Differential diagnoses

Management

  • In case of antibody-mediated acute hemolytic transfusion reactions,
    • Immediately discontinue the transfusion while maintaining venous access for emergency management.
    • Anticipate low blood pressure, kidney failure, and DIC.
    • Prophylactic measures to reduce the risk of renal failure may include low-dose dopamine, vigorous hydration with intravenous crystalloid solutions (e.g., lactated Ringer's solution or normal saline), and osmotic diuresis with mannitol.
    • If DIC is documented and bleeding requires treatment, transfusions of frozen plasma, pooled cryoprecipitates for fibrinogen, and/or platelet concentrates may be indicated.
  • In case of non-antibody mediated AHR
    • This does not require rigorous management.
    • Diuresis induced by an infusion of normal saline until the intense red color of hemoglobinuria ceases is usually adequate treatment.[8]

Prognosis

The major complication is that the hemoglobin, released by the destruction of red blood cells, may cause acute kidney failure (also known as the "oliguric phase"). About 20 deaths occur annually in the US due to AHTR.[9]

Epidemiology

  • Acute hemolytic, immune mediated (fatal)-1 per 250,000-600,000
  • Acute hemolytic, immune mediated (nonfatal)-1 per 6000-33,000
  • Acute hemolytic, nonimmune-Infrequent

References

  1. ↑ Covin RB, Evans KS, Olshock R, Thompson HW (2001). "Acute hemolytic transfusion reaction caused by anti-Coa". Immunohematology. 17 (2): 45–9. PMID 15373591.
  2. ↑ Hoffbrand, A. V.; P.A.H. Moss; J.E. Pettit (2006). Essential Haematology: 5th Edition. Blackwell Publishing. ISBN 1-4051-3649-9.
  3. ↑ Molthan L, Matulewicz TJ, Bansal-Carver B, Benz EJ (1984). "An immediate hemolytic transfusion reaction due to anti-C and a delayed hemolytic transfusion reaction due to anti-Ce+e: hemoglobinemia, hemoglobinuria and transient impaired renal function". Vox Sang. 47 (5): 348–53. doi:10.1111/j.1423-0410.1984.tb04138.x. PMID 6438912.
  4. ↑ "The 2011 National Blood Collection and Utilization Survey Report" (PDF). Department of Health and Human Services. Retrieved 21 January 2016.
  5. ↑ Bolton-Maggs, PHB; Poles, D; et al. (The Serious Hazards of Transfusion (SHOT) Steering Group) (2015). The 2014 Annual SHOT Report (2015) (PDF). SHOT. ISBN 978-0-9558648-7-2. Archived from the original (PDF) on 2016-01-27. Retrieved 2017-10-14.
  6. 1 2 Laura, Dean (2005). Blood Groups and Red Cell Antigens. Bethesda, United States: National Center for Biotechnology Information. Retrieved 4 October 2017.
  7. ↑ Harrison's Principles of Internal Medicine (18th ed.). p. 954.
  8. ↑ "Transfusion Reactions". Retrieved 19 November 2012.
  9. ↑ "Complications of Transfusion: Transfusion Medicine: Merck Manual Professional".
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