Blood Transfusion Reactions - Introduction to General Medicine - Lecture Slides, Slides of Medicine

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Blood Transfusion Reactions

Objectives

 Early identification of common

transfusion rxns.

 Differentiate life threatening reactions

from benign transfusion rxns.

 Manage common immunologic tranx

rxns.

Non immune mediated reactions

 Physical reactions: thermal i.e. heat or cold induced

 Infectious; Hepatitis B/C, malaria, HIV, CMV,

Chagas dx, CJ Virus, West Nile virus

 Chemical; citrate toxicity, hypo/hyperkalemia, iron

overload

 Acute hypotensive reaction: mediated by

bradykinins and occurs in patients with faulty

bradykinin metabolism on ACE I

 Osmotic injury

 Congenital and acquired hemolytic anemia

Immunologic rxns

classic blood tranx rx ns are usually im m unologic and occur 2/ 2

to interactions of inherited/ acquired Ab w ith foreign Ag from

transfused blood

Incidence of rxns

SHOT trial (serious hazards of tranx)

-most common cause is tranx of non-matched blood

mostly 2/2 to clerical error

-2x more common in infants than adults

-more common in pxts with hematological and

oncological conditions

Prevention

• Leukoreduction: evidence is scarce but few studies have shown a

decrease in number of reactions.

• Although tylenol and antihistamine premedication is widely used

there are no evidence to support that their use actually prevents

rxn.

Acute hemolytic rxns

 Medical emergency

 Occurs due to rapid transfused RBC destruction by

preformed recipients Abs

 Mostly 2/2 to ABO incompatibility-typically type O

receiving non O blood. May occur with other blood

types

 IgM mediated complement fixation leading to rapid

intra vascular hemolysis

 Most common causes are clerical or procedural

errors

 Complications includes DIC, shock, ARF 2/2 to ATN

Delayed hemolytic transfusion rxns

Generally occurs within 2-10 days of tranx Usually due to senescent Ab response on re-exposure to a foreign red cell Ag History of previous pregnancy, transfusion or transplant Usually extra vascular and is less severe than acute Other Abs often Rh and Kidd

Clinical presentation Falling HCT, low grade fever, slight increase in indirect bili, spherocytes on blood smear

Diagnosis New +DAT and new Ab test when new blood is ordered

Txt None in the absence of rapid hemolysis Avoid offending Ag in future tranx

Anaphylactic reactions

• life threatening emergency -Occurs within a few seconds to minutes following tranx -Characterized by rapid onset of anaphylaxis -Can occur with all blood products but generally unseen with serum albumin, plasma protein fractions or coagulation factors

Incidence 1 in 20-50 thousand

Mechanism Presence of class specific IgG and anti IgA abs in pxts who are IgA def -Selective IgA def is fairly common, occurring in 1/300-500 people but majority of them do not develop Abs -Ahaptoglobinemia with antihaptoglobin Abs is similar and occur primarily in East Asian

Treatment As in all cases of anaphylaxis: stop tranx, epi 0.3ml of 1.1000 soln IM Consider IV epinephrine drip ABC +/- pressor support

 Very rare (0.1-1%) complication seen in Immuno-compromised individuals esp in solid tumor cancer pxts on chemo, but can occur with acute/chronic leukemia, lymphomas, new borne with erythroblastosis fetalis and transplant pxts

 Different from transplant GVHD by it’s effect on bone marrow (BM aplasia)

 It occurs in immuno-compromised recipients of blood products from donors with identical HLA haplotypes. They are heterozygous for a HLA haplotype for which the donor is homozygous .e.g. genetically identical relatives

HLA ag are shared by donor and recipient, thus donor lymphocyte are engrafted by recipient because they are the only Ag seen by the host.

On the flip side the donor lymphocytes view the recipient’s tissues as foreign leading to immunologic activation and GVHD.

 Bone marrow aplasia is the primary cause of death

Transfusion associated

GVHD

Clinical presentation

Skin : Swollen, erythroderma and bullae formation- most

common

GI : Diarrhea and abdominal cramps

Liver: Elevated LFT and Hyperbilirubinemia

Heme : Bone marrow aplasia, persistent thrombocytopenia

Sk in m anifestation of GVHD Generalized sw elling, erythroderm a and bullous form ation

Transfusion related acute

lung injury

 New acute lung injury occurring during or within 6

hour of blood product tranx

 All blood products have been implicated

 May progress to ARDs

 Immune mediated non cardiogenic pulm edema

Risk factors

No definite risk factors but prolonged storage of

blood products, massive tranx, cytokine txt,

multiparity, thrombocytopenia and active infections

have been implicated in a number of studies.

Pathogenesis

-Abs against HLA -2 hit hypothesis: 1 st^ hit is an underlying pulm pathology that leads to localization of neutrophils in the pulm vasculature 2 nd^ hit is the transfusion of blood products containing sensitized neutrophils Ab leading to release of vasoactive Cytokine and pulm edema

 Leading cause of transfusion related fatalities in the USA

 1 case for every 1000-2400 units transfused

 6-9% mortality rate

Epidemiology

(a) Bilateral patchy alveolar infiltrate in TRAL (b) Complete resolution

a b

Criteria for the diagnosis of TRALI

• No acute lung injury immediately before transfusion
• New acute lung injury:
  1. acute onset lung injury,
  2. no circulatory overload or PA pressures <18mmHg,
  3. bilateral pulm infiltrate on Cxr,
  4. Hypoxemia:Pa02/FiO2 <300, or sat <90% on RA.
• Onset within 6 hours after transfusion
• No temporal relation to an alternate risk factor for acute lung injury

Popovsky TP et al TRALI; definition and review. Crit care Med 2005

Ddx includes  Acute fluid overload: ↑ JVP, ↑SBP and widened pulse pressure during dyspneic episode, ↑ pulm vascular markings on CXR  Hemolytic transfusion rxns  IgA mediated anaphylaxis in IgA def patients

Management

-Mostly supportive with abrupt resolution in symptoms within a few days

-A majority of patients may require mechanical ventilation

-Diuretics play no role in management since it is microvascular damage and not due to volume. It has been shown to actually worsen TRALI

Prognosis

Increased risk of recurrence if they receive products from the implicated

donor but no risk from other donors