Hemolytic transfusion reactions (HTR) are adverse reactions to blood transfusions that can range from subclinical to lethal. They occur when a patient receives incompatible red blood cells and their immune system mounts an immune response that destroys the transfused red blood cells. The summary discusses preventive strategies like electronic verification systems and protocols to avoid incompatible transfusions, as well as treatments for different types of reactions like acute HTR, delayed HTR, and passenger lymphocyte syndrome in transplant recipients. Effective prevention and management requires understanding the pathophysiology and risk factors for different transfusion reactions.

1. Hemolytic transfusion
reaction
Dr Shreyas kate

2. Transfusion Reactions
TRANSFUSION
REACTIONS
Acute Hemolytic
reactions
Non Hemolytic
Febrile Reactions
Allergic Reactions
Delayed Hemolytic
Reaction

5. Article
• Journal: The New England Journal of Medicine
• Published : July 11, 2019
• Authors: Sandhya R. Panch, M.D., M.P.H., Celina Montemayor-Garcia,
M.D., Ph.D., and Harvey G. Klein, M.D.

6. INTRODUCTION
• 15℅ of inpatients receive blood transfusion
• 1 ℅ of them suffer severe adverse effects
• 5℅ – Hemolytic transfusion reaction
• Bystander Hemolysis

7. HISTORY
• Mid 17 th Century – First documented reaction
• Landsteiner’s discovery of ABO blood groups in 1900
• Ottenberg- Routine pretransfusion testing
• Development of anticoagulant–preservative
• Combination of serologic techniques and molecular identification of
the corresponding red-cell genes (compatibility testing)

8. Epidemiologic Features
• Hemolysis was the most common cause of transfusion-associated
death during the 1976–1985
• Least common fatal complications (1/1,972,000) red-cell units
transfused in 2016
• “Wrong blood in the tube”
• Delayed hemolytic reaction- 1 in 500 to 1 in 1000

10. PATHOPHYSIOLOGY
• Acute hemolytic reactions:
• Pre-existing IgM, and less commonly IgG
• Complement Activation (C5 through C9)
• Hemolysis
• Increased free Hgb
• ATN

13. Pathophysiology
• Delayed hemolytic reaction:
• Incomplete complement activation (C3a and C5a)
• Proinflammatory cytokines
• Bradykinin and Kallikrein system activation
• Vasodilation, Hypotension DIC

14. • severe hemolytic reactions
• long-term transfusions
• part by the release of cell-free hemoglobin,
• activates leukocyte-driven
• inflammasome pathways and causes endothelial
• dysfunction through nitric oxide scavenging
• post-transfusion haemoglobin levels falling below the pretransfusion values
Pathophysiology

15. • Passenger lymphocyte syndrome
• solid-organ transplantation
• Incompatibility between the donor’s plasma and the recipient’s red cells,
“minor ABO incompatibility”
• viable donor B lymphocytes, termed “passenger lymphocytes,”
• develop 5 to 14 days after heart– lung, liver, kidney, intestinal
transplantations, as well as after hematopoietic stem-cell infusions
Pathophysiology

17. CLINICAL
Suspected AHTR
Signs & Symptom: Fever,chills,rigor, flank pain reddish urine
,hypotension, dyspnea, sense of “impending doom,”
oliguria, anuria, bleeding Timing: minutes to hours after
transfusion
Stop transfusion immediately,
repeat clerical check
• Ancillary tests: positive DAT, hemoglobinemia,
hemoglobinuria, low haptoglobin, high LDH, elevated direct
or indirect bilirubin, high D-dimers, increased fibrinogen, PT
or PTT (if DIC is present), BUN, or creatinine
Repeat and confirm ABO,
Rh, antibody compatibility;
repeat DAT
Immune-mediated hemolysis:
aggressive hydration Severe cases:
pressor support, renal consultation,
management of coagulopathies
Perform Gram's stain and blood
cultures to rule out acute
Infections Rule out drug-induced
hemolysis, nonimmune causes

18. CLINICAL
Suspected DHTR
Signs and symptoms: fatigue, pallor, jaundice
Timing: 2 days to 1 month after transfusion
or infusion
Obtain detailed patient history: record of
multiple or recenttransfusions, including IVIG,
platelets, plasma; HSCT; history of
alloimmunization, pregnancies, or
transplantation
Ancillary tests: new positive antibody screen, incompatible
cross-match, decreased hemoglobin, positive DAT or IAT, low
haptoglobin, high LDH, elevated indirect bilirubin, spherocytes
or microspherocytes on peripheral smear, reticulocytosis
Management: cautious transfusion with antigen-negative,
cross-match– compatible units In severe cases: immune
modulators (glucocorticoids, IVIG, rituximab, erythropoietin-
stimulating agents)

20. Management
• Supportive care
• Prompt interruption of the transfusion
• Saving of the remaining blood in the unit for testing
• Blood and Urine sampling
• ICU along with a renal consultation (dialysis)

21. • Vigorous hydration with isotonic saline
• Maintain urine output at a rate above 0.5 to 1 ml/kg/hr
• ? Mannitol
• Supplemental diuretics
• Sodium bicarbonate (130 mmol per liter in 5% dextrose) at a starting
at 200 ml /hr to achieve a urinary pH >6.5
• Hyperkalemia
• Vasopressor : dopamine infusion (2 - 10 μg /kg/min)
Management

22. • In DIC (bleeding, platelets, FFP and cryoprecipitate)
• platelet >20,000 per cubic ml
• INR < 2.0
• fibrinogen > 100 mg/Dl
• No evidence supports the routine use of therapeutic high-dose
glucocorticoids, intravenous immune globulin, or plasma exchange
Management

23. • Transfusion of incompatible units
• prophylaxis with glucocorticoids (hydrocortisone at a dose of 100 mg,
administered just before transfusion and repeated 24 hours later)
• IV IG (1.2 to 2.0 g /kg, administered over a period of 2 to 3 days, with the first
dose given just before the incompatible transfusion)
Management

24. • Sickle cell disease:
• Glucocorticoids
• IV Ig
• Rituximab
• Erythropoiesis-stimulating agents
• Life-threatening hemolysis:
• Plasma exchange
• Hemoglobin based red-cell substitutes
• eculizumab,
• Tocilizumab
• anti–IL 6 monoclonal antibody
Management
Newer agents : Heme scavengers
1.haptoglobin
2. hemopexin

25. • Preventing passenger lymphocyte syndrome
• A recipient with blood group A receiving a transplant from a group O donor
should receive group O red cells and group AB plasma
• Prophylactic plasma reduction in the donor graft, partial red-cell exchange
Management

26. Prevention
• “zero tolerance” policies
• accepting blood samples without core identifiers
• Electronically generated labels
• Identification bands
• Repeating ABO checks
• Centralized transfusion databases

27. • Patients who are already heavily alloimmunized and require long-
term transfusion support, Prophylactic
• Rituximab (1 to 2 gm iv)
• Inj methylprednisolone
• Patients with sickle cell disease
• glucocorticoids
• intravenous immune globulin
• rituximab
• erythropoiesis-stimulating agents
Prevention

28. SUMMARY
• HTR are important cause of transfusion-associated reactions and may
be subclinical, mild, or lethal
• Electronic verification systems
• Other reactions
• Delayed hemolytic transfusion reactions,
• Hyperhemolysis
• Passenger lymphocyte syndrome in transplant recipients
• Preventive strategies
• Systematic protocols

29. THANK YOU