- All individuals produce antibodies against the ABO blood group antigens A and B through environmental exposure like bacteria, without needing a blood transfusion or pregnancy. These antibodies are usually detectable within 3-6 months of birth. - Newborn infants do not usually have significant levels of anti-A or anti-B antibodies in their plasma, so pretransfusion testing is not required for transfusions in the first 4 months of life, except for infants of alloimmunized mothers who may have antibodies passed through the placenta. - Transfusion complications can be classified as immunological, like hemolytic transfusion reactions, or non-immunological, like circulatory overload. The development of antibodies against red blood cell

3.  ALL IMMUNOCOMPETENT INDIVIDUALS PRODUCE
ANTIBODIES AGAINST THE MISSING ABO(H) BLOOD
GROUP ANTIGENS.
 ANTI-A AND ANTI-B PRODUCTION DOES NOT REQUIRE
RED CELL STIMULATION THROUGH TRANSFUSION OR
PREGNANCY BUT OCCURS PREDOMINATELY
THROUGH ENVIRONMENTAL EXPOSURE, SUCH AS
BACTERIA.
 ANTI-A AND ANTI-B ARE USUALLY DETECTABLE WITHIN
3 TO 6 MONTHS AFTER BIRTH.
 BY THE AGE OF 5 YEARS, THE TITERS OF ANTI-A AND
ANTI-B ANTIBODIES REACH MAXIMUM AND PERSIST
THROUGHOUT ADULTHOOD. THE TITERS OF IGM ANTI-
A ANTI-B ANTIBODIES MAY GRADUALLY DECLINE WITH
ADVANCED AGE.

4.  NEWBORN INFANTS DO NOT USUALLY HAVE A
SIGNIFICANT AMOUNT OF ANTI- A OR ANTI-B IN
THEIR PLASMA; THEREFORE, PRETRANSFUSION
TESTING IS NOT USUALLY REQUIRED FOR
TRANSFUSIONS WITHIN THE FIRST 4 MONTHS OF
LIFE.
 INFANTS BORN TO ALLOIMMUNIZED MOTHERS ARE
AN EXCEPTION TO THIS RULE, AS OTHER SPECIFIC
BLOOD GROUP ANTIBODIES MAY HAVE CROSSED
THE PLACENTA AND MAY BE PRESENT IN THE
INFANT’S CIRCULATION

6.  ON THE RED CELL MEMBRANE, BOTH THE A AND B
TRANSFERASES ADD SUGAR MOIETIES TO A
SUBSTRATE THAT IS ENCODED BY THE H (FUT1)
 GENE. FUT1 IS LOCATED AT CHROMOSOME 19q13.1-
qTER, AND INHERITED IN A MENDELIAN MANNER. TWO
ALLELES HAVE BEEN IDENTIFIED AT THIS LOCUS: H
AND h. THE ALLELE H, encodes for enzyme H
TRANSFERASE TYPE II [A(1,2) FUCOSYL-
TRANSFERASES; FUT1], WHICH ADDS AN L-FUCOSE TO
THE TERMINAL GALACTOSE MOLECULE OF
OLIGOSACCHARIDE CHAINS IN AN A(1–2) LINKAGE.
THIS STRUCTURE IS CALLED H SUBSTANCE, AND IT IS
TO THIS STRUCTURE THAT THE A AND B
TRANSFERASES ADD SPECIFIC SUGARS RESULTING
IN A AND B ANTIGENS.

7.  sometimes inherited at the H locus is h. This h allele
encodes for a nonfunctional transferase.
 If the h allele is inherited in the homozygous state (hh), l-
fucose molecules (H substance) are not present on the red
cell membrane. Without the presence of H substance on the
red cell membrane, the A and B transferases, even when
present, are not able to add the specific sugars that give A
and B antigen specificity..

8. This hh genotype is known as the Bombay
phenotype: Serologically, the red cells group as O;
however, unlike the true O phenotype, which has
large amounts of H antigen on the red cells, red cells
from the Bombay phenotype lack H antigen. The
clinical relevance of the Bombay phenotype relates to
the ability of these individuals to form not only anti-A
and anti-B but also anti-H. The presence of all three
of these antibodies makes it difficult to find
compatible blood if transfusion is required. The only
compatible blood for an individual with the Bombay
(hh) phenotype is blood from another Bombay
individual, and this phenotype is extremely rare.

9. Blood group
system
Antigen Alloantibody Clinical
significance
Rh (D,C/c,E/e) RBC Protein IgG HTR, HDN
Lewis (LeᵅLeᵇ) oligosaccharides IgM/IgG Rare HTR
Kell (K/K) RBC Protein IgG HTR, HDN
Duffy (Fyᵅ, Fyᵇ) RBC Protein IgG HTR, HDN
Kidd (Jkᵅ, Jkᵇ) RBC Protein IgG HTR (often
delayed), HDN
(mild)
I/i Carbohydrate IgM None
MNSsU RBC Protein IgM/IgG Anti-M rare HDN,
anti-S-s, and U
HDN, HTR

11. TRANSFUSION COMPLICATIONS CAN BE CLASSIFIED
AS
 IMMUNOLOGICAL
 NONIMMUNOLOGICAL

14.  ALLOIMMUNIZATION TO TRANSFUSED ANTIGENS
 HEMOLYTIC TRANSFUSION REACTION
ACUTE
DELAYED
 FEBRILE NONHEMOLYTIC TRANSFUSION
REACTION
 TRNSFUSION RELATED ACUTE LUNG
INJURY(TRALI)

15. CONT...
 ALLERGIC TRANSFUSION REACTION
 POST TRANSFUSION PURPURA
 TRANSFUSION ASSOCIATED GRAFT VERSUS HOST
DISEASE(TA-GAVD)
 TRANSFUSIONRELATED IMMUNOMODULATORY
EFFECTS (TRIM)

16.  TRANSFUSION ASSOCIATED CIRCULATORY
OVERLOAD
 MASSIVE TRANSFUSION
METABOLIC
HYPOTHERMIA
DILUTIONAL
 MISCELLANEOUS
PLASTICIZERS
TRANSFUSION HEMOSIDEROSIS

17. HEPATITIS A,B,C,DELTA
HIV 1 ,2
SYPHILIS
CYTOMEGALO VIRUS
WESTNILE VIRUS
PARASITES : MALARIA ,BABESIA ,TRYPANOSOMES
VARIANT CREUTZFELDT JAKOB DISEASE
BACTERIAL CONTAMINATION

18.  LEADING CASUE OF TRANSFUSION RELATED
MORTALITY
 THE DEVELOPMENT OF ANTIBODIES CAPABLE OF
REACTING WITH RED CELL ANTIGENS MAY LEAD
TO RED CELL DESTRUCTION USUALLY INVOLVING
TRANSFUSED RATHER THAN RECIPIENT CELLS.

19.  IMMEDIATE HEMOLYTIC TRANSFUSION REACTIONS
(IHTRS) ARE MOST TYPICALLY ASSOCIATED WITH
ABO INCOMPATIBILITY, BECAUSE ANTI-A AND ANTI-B
ANTIBODIES ARE PREDOMINANTLY IgM AND ARE
CAPABLE OF BINDING COMPLEMENT AND CAUSING
IMMEDIATE DESTRUCTION OF RED CELLS
 USUALLY RELATED TO HUMAN ERROR
 OTHER RED CELL ANTIGEN SUCH AS Jk, K, Fy WHICH
MAY BIND TO COMPLEMENT.

20. CONT....
 IHTRS OCCUR SOON AFTER THE INCOMPATIBLE
TRANSFUSION HAS BEGUN.
 FEVER WITH OR WITHOUT CHILLS IS ONE OF THE
MOST COMMON MANIFESTATION.
ANXIETY
CHEST OR BACK PAIN
FLUSHING
DYSPNEA
TACHYCARDIA
HYPOTENSION.

21. IF THE PATIENT IS UNDER GENERAL ANESTHESIA
SYMPTOMS MAY NOT BE RECOGNIZED;
ONLY SEVERE HYPOTENSION AND EVIDENCE OF
OOZING OR HEMOGLOBINURIA SERVE AS CLUES
TO THE PRESENCE OF A HEMOLYTIC REACTION.

22.  IHTRS MAY BE LIFE-THREATENING, AND
COMPLICATIONS MAY INCLUDE
ACUTE RENAL FAILURE
SHOCK
INTRAVASCULAR COAGULATION.
 IT HAS BEEN ESTIMATED THAT A FATAL IMMEDIATE
HEMOLYTIC REACTION OCCURS IN APPROXIMATELY
1/600,000 RED CELL TRANSFUSIONS .
 THE MORTALITYOF A SEVERE IHTR INCREASES
WITH THE AMOUNT OF BLOOD TRANSFUSED,WITH A
44% MORTALITY RATE IN PATIENTS RECEIVING
MORE THAN1 L OF INCOMPATIBLE BLOOD

23.  PATHOPHYSIOLOGY
 PRIMARY EVENT IN IHTRS IS INTERACTION
BETWEEN
ANTIBODY AND RED CELL MEMBRANE
DEVELOPMENT OF IMMUNE COMPLEX
RELEASE OF C3a AND C5a WITH
ANAPHYLOTOXIC ACTIVITY ,COAGULATION
MECHANISM VIA CYTOKINES AND FACTOR XII

24. CONTU...
 VASOMOTOR MEDIATOR
HISTAMINE
SEROTONIN
CYTOKINES
 RENAL FAILURE OCCURS PRIMARILY ISCHEMIC
CASUED BY COMBINATION OF
HYPOTENSION,VASOCONSTRICTION(NITRIC
ACID INACTIVATION BY HEMOGLOBIN),INTRA
VASCULAR COAGULATION .
 CIRCULATING FREE HEMOGLOBIN PRECIPITATING
AND OBSTRUCTING RENAL TUBULES
RENAL FAILURE

25.  INVESTIGATION
 IN INTRAVASCULAR REACTION FREE PLASMA HB
DETECTED QUICKLY BY CENTRIFUGING TUBE OF
BLOOD WITH EDTA PINK OR RED PLASMA
 RED CELL TYPING REPEATED ON ALL
SPECIMENS
 THE DIRECT ANTIGLOBULIN TEST
 URINARY HEMOSIDERIN OR FREE HEMOGLOBIN
WINE COLOURED URINE IS TYPICAL OF INTRA
VASCULAR HEMOLYSIS
SUPPORTIVE EVIDENCE BY REDUCED SR
HAPTOGLOBIN,
HYPERBILIRUBINEMIA,METHEMALBUMINEMIA

28. MANAGEMENT
 STOP TRANSFUSION IMMEDIATELY AS SEVERITY
RELATED TO VOLUME OF RED CELL TRANSFUSION
 RECHECK PATIENT IDENTITY R/O BEDSIDE
IDENTIFICATION ERRORS
 HYDRATION MUST BEGUN IMMEDIATELY TO
PREVENT RENAL FAILURE.
 INFUSION OF NORMAL SALINE TO MAINTAIN BP,
INCRESAE URINE FLOW RATE 100ML/HR .
 ONCE OLIGURIC RENAL FAILURE IS ESTABLISHED
FLUID CHALLENGES MUST BE RESTRICTED.USE
SUPPORTIVE MEASURES ELECTROLYTES
BALANCE, DIALYSIS

29. MANAGEMENT
 EARLY HEPARINIZATION AT MODERATE
DOSE
 MASSIVE INTRA VASCULAR HEMOLYTIC
REACTION EXCHANGE TRANSFUSION

30.  DHTRS GENERALLY ARE MUCH MILDER THAN
THOSE OCCURRING IMMEDIATELY,AND RED CELL
DESTRUCTION
PREDOMINANTLY EXTRAVASCULAR.
 THE TRANSFUSED RED CELLS ARE DESTROYED
BEGINNING 2 TO 10 DAYS AFTER A TRANSFUSION.

31.  INVESTIGATION MAY REVEAL THE PRESENCE OF A
RED CELL ANTIBODY NOT DETECTED IN THE
PRETRANSFUSION BLOOD SAMPLE. THE DIRECT
ANTIGLOBULIN TEST IS OFTEN POSITIVE, BUT THE
REACTION IS TRANSIENT AND MAY BE MISSED IF IT IS
PERFORMED TOO LATE.
 THE TEST REVERTS TO NEGATIVE AS THE
INCOMPATIBLE RED CELLS ARE REMOVED FROM THE
CIRCULATION

32.  IN DELAYED HEMOLYTIC REACTIONS,
DESTRUCTION OF THE SENSITIZED REDCELLS IS
PREDOMINANTLY EXTRAVASCULAR; THAT IS, THE
IgG-COATED RED CELLS ARE REMOVED BY THE
RETICULOENDOTHELIAL SYSTEM.
SYMPTOMS
 FEVER, FALLING HEMATOCRIT, JAUNDICE,
INFREQUENTLY HEMOGLOBINEMIA AND
HEMOGLOBINURIA
 RARELY, THE REACTIONS MAY BE DRAMATIC;
RENAL FAILURE IS UNCOMMON, BUT FATALITIES
HAVE BEEN REPORTED.

33.  THE ANTIBODIES RESPONSIBLE FOR DHTRS ARE
WELL DEFINED.
 ANTIBODIES TO KIDD (JK) ANTIGENS AND TO
ANTIGENS OF THE RH SYSTEM ARE THE MAJOR
OFFENDERS, WITH ANTI-KELL AND ANTI-DUFFY (FY)
IMPLICATED IN MOST OTHER DELAYED REACTIONS.
 ANTI-KIDD ANTIBODIES ARE PARTICULARLY
TROUBLESOME BECAUSE THE PLASMA
CONCENTRATION OF THESE ANTIBODIES DECLINES
MORE RAPIDLY THAN OTHERS, SO
PRETRANSFUSION TESTS ARE MORE COMMONLY
NEGATIVE IN PATIENTS WHO ARE IN FACT
SENSITIZED.

34.  MANAGEMENT
NO SPECIFIC THERAPY IN MOST INSTANCES
ADEQUATE HYDRATION

35.  MOST COMMON CAUSE ALLOIMMUNIZATION
TO ANTIGENS ON LEUCOCYTES AND
PLATLETS
 HLA ANTIBODIES
 GRANULOCYTE SPECIFIC ANTIBODIES
 PLATELET SPECIFIC ANTIBODIES
 PRESENCE OF CYTOKINES IN BLOOD
COMPONENTS
 MORE COMMON IN MULTI-TRANSFUSED
PTS

36. CLINICAL FEATURES
 CHILLS FOLLOWED BY FEVER OF 1 DEGREE
CENTIGRADE USUALLY DURING OR WITHIN FEW
OF TRANSFUSION
 HEADACHE
 RIGORS
 NAUSEA
 VOMITING
 HYPOTENSION
 SHOCK

37.  ANTIPYRETICS SUCH AS ACETAMINOPHEN
 SEVERE REACTION HYDROCORTISONE
 MEPERIDINE TO DECREASE OR STOP SEVERE
SHAKING CHILLS
CAN BE PREVENTED BY
 LEUCOREDUCED / LEUCODEPLETED BLOOD
COMPONENTS PRE STORAGE b/c REDUCTION
OF LEVEL CYTOKINES

38.  TRALI IS REPORTED BY THE FDA AS THE NUMBER-
ONE CAUSE OF TRANSFUSION-ASSOCIATED
FATALITY .
 INCIDENCE VARIES FROM 1IN 5000 TO 1 IN 557000
DEPENDING ON BLOOD COMPONENT INVOLVED
 TRANSFUSION-RELATED ACUTE LUNG INJURY
(TRALI) MOST COMMONLY PRESENTS AS SEVERE
RESPIRATORY DISTRESS OF SUDDEN ONSET,
CAUSED BY A SYNDROME OF NONCARDIOGENIC
PULMONARY EDEMA RESEMBLINGTHE ADULT
RESPIRATORY DISTRESS SYNDROME.

39. SYMPTOMS & SIGNS
 CHILLS,
 FEVER,
 CHESTPAIN,
 HYPOTENSION,
 CYANOSIS, AS WELL AS THE USUAL
MANIFESTATIONS OF PULMONARY
EDEMA(HYPOXEMIA) MAY BE SEEN

40. “TWO HIT THEORY”
 TRAUMA, SURGERY, SEPSIS MAY FIRST “PRIME”
NATIVE GRANULOCYTES CAUSING SURFACE
ADHESION SITES RESULTING LUNG SEQUESTRATION
 BIOLOGICALLY ACTIVE MEDIATORS THAT ARE
BREAKDOWN PRODUCTS FROM CELLULAR
ELEMENTS IN BLOOD PRODUCTS ACTIVATE
SEQUESTERED LEUKOCYTES
 AGGLUTINATION OF GRANULOCYTES AND
COMPLEMENT ACTIVATION OCCUR IN THE
PULMONARY VASCULAR BED, LEADING TO CAPILLARY
ENDOTHELIAL DAMAGE WITH CONSEQUENT FLUID
LEAK INTO THE ALVEOLI.

41. THE DIAGNOSIS
 TRALI REACTION IS BASED ON THE ONSET OF
ACUTE LUNG INJURY (ALI) WITHIN 6 HOURS OF
TRANSFUSION.
 ALI IS CHARACTERIZED BY AN ACUTE ONSET OF
HYPOXEMIA (OXYGEN SATURATION <90% PATIENT
BREATHING ROOM AIR OR A PAO2/FIO2 ≤300 MMHG),
BILATERALINFILTRATES ON FRONTAL CHEST
RADIOGRAPH
NO EVIDENCE OF CIRCULATORYOVERLOAD.

42. DIFFERENTIAL DIAGNOSIS (D/D)
 CIRCULATORY OVERLOAD (TACO)
 ALLERGIC/ANAPHYLACTIC
 BACTERIAL
 ACUTE HEMOLYTIC REACTION

43.  MANAGEMENT
 SUPPORTIVE MEASURES FOR THE PULMONARY EDEMA AND
HYPOXIA, INCLUDING VENTILATORY SUPPORT IF REQUIRED.
 HEMODYNAMIC MONITORING MAY BE REQUIRED TO
DETERMINE WHETHER FLUID OVERLOAD IS A FACTOR; IF
NOT,
DIURETICS ARE OF NO PROVEN VALUE
 THE AABB REQUIRES EVALUATION OF DONORS IMPLICATED
IN TRALI. DONORS WHOSE PLASMA IS IMPLICATED IN SUCH
REACTIONS SHOULD BE EXAMINED FOR THE PRESENCE
OF GRANULOCYTE-SPECIFIC AND HLA ANTIBODIES
THAT REACT WITH RECIPIENT LEUKOCYTES REPORTED
TRALI CASES

44. URTICARIA
◦ COMMONLY ENCOUNTERED
◦ CHARACTERIZED BY LOCAL ERYTHEMA, HIVES
AND ITCHING, USUALLY WITHOUT FEVER OR
OTHER COMPLICATIONS.
◦ IF LOCALIZED URTICARIA IS THE ONLY
MANIFESTATION, IT IS USUALLY NOT NECESSARY
TO DISCONTINUE THE TRANSFUSION.
◦ ETIOLOGY UNKNOWN
◦ PRE-TREAT WITH ANTIHISTAMINES.

45. ANAPHYLACTIC SHOCK
 OCCURS AFTER THE INFUSION OF ONLY A FEW
MILLILITERS OF BLOOD OR PLASMA AND THE
ABSENCE OF FEVER.
 ONSET CHARACTERIZED BY: COUGHING, BRONCHO
SPASM, RESPIRATORY DISTRESS, CIRCULATORY
COLLAPSE, NAUSEA, ABDOMINAL CRAMPS, VOMITING,
DIARRHEA, SHOCK AND LOSS OF CONSCIOUSNESS.
 MOST ALLERGIC REACTIONS ARE THOUGHT TO BE
MEDIATED BY RECIPIENT IGE TO PROTEINS OR
OTHER SOLUBLE SUBSTANCES IN DONOR PLASMA.
 THE INTERACTION BETWEEN THE ANTIGEN AND IGE
STIMULATES THE RELEASE OF HISTAMINE FROM
MAST CELLS AND BASOPHILs.

46.  REACTIONS MAY OCCUR IN IgA DEFICIENT PATIENTS
WHO HAVE DEVELOPED ANTI-IgA ANTIBODIES AFTER
IMMUNIZATION BY PREVIOUS TRANSFUSION OR
PREGNANCY
 STOP TRANSFUSION IMMEDIATELY–START WORK UP
 SENSITIZED IgA-DEFICIENT PATIENTS MUST BE
TRANSFUSED WITH BLOOD AND BLOOD
COMPONENTS THAT LACK IgA.

47.  POSTTRANSFUSION PURPURA IS THE DEVELOPMENT OF
LIFE-THREATENING THROMBOCYTOPENIA 5 TO 10 DAYS
AFTER TRANSFUSION
 THIS RARE COMPLICATION IS CAUSED BY THE
DEVELOPMENT OF ALLOANTIBODIES DIRECTED AGAINST
PLATELET-SPECIFIC ANTIGENS;
ANTI–HPA-1A IS OFTEN IMPLICATED, ALTHOUGH
ANTIBODIES WITH OTHER SPECIFICITIES HAVE ALSO BEEN
REPORTED
 POSTTRANSFUSION PURPURA IS THOUGHTTO OCCUR AS A
RESULT OF A SECONDARY IMMUNOLOGIC RESPONSE TO
THE PLATELET-SPECIFIC ANTIGEN, MOST PATIENTS HAVING
BEEN SENSITIZED BYPRIOR PREGNANCY OR
TRANSFUSION. THE MECHANISM OF DESTRUCTION OF THE
PATIENT’S OWN PLATELETS IS UNCERTAIN

48.  DIFFERENTIAL DIAGNOSIS
◦ ITP
◦ TTP
◦ ALLOIMMUNIZATION
◦ SEPSIS
◦ DIC
◦ BM FAILURE
◦ DRUG-INDUCED
 TREATMENT/PREVENTION
◦ STEROIDS
◦ PLASMA EXCHANGE
◦ IGIV – HIGH DOSE
◦ PLATELETS TRANSFUSION NOT EFFECTIVE
◦ ANTIGEN-NEGATIVE BLOOD PRODUCT

49.  ALLOGENEIC BLOOD TRANSFUSION RESULTS IN THE
TRANSFER OF NOT ONLYRBCS, BUT ALSO
SIGNIFICANT AMOUNTS OF POTENTIAL IMMUNE
EFFECTOR CELLS, THEIR PRODUCTS (E.G.,
CYTOKINES), AND VARIOUS SUBSTANCES THAT MAY
BE SEEN BY THE HOST IMMUNE SYSTEM AS FOREIGN
ANTIGENS.
 A LARGE BODY OF LITERATURE EXISTS THAT
SUBSTANTIATES THE MODULATIONOF HOST IMMUNE
SYSTEMS BY TRANSFUSED ALLOGENEIC CELLSAND
SUBSTANCES, RAISING THE POSSIBILITY OF THE
DEVELOPMENT OFCLINICAL SYNDROMES GENERALLY
REFERRED TO AS TRANSFUSION-RELATED
IMMUNOMODULATION(TRIM)

50.  BENEFICIAL TRANSFUSION-
RELATEDIMMUNOMODULATORY EFFECTS HAVE
BEEN REPORTED IN RENAL TRANSPLANT
PATIENTS, WOMEN WITH RECURRENT
SPONTANEOUS ABORTIONS, AND PATIENTS WITH
CROHN’S DISEASE.
 A LARGE NUMBER OF CLINICAL STUDIES HAVE
BEEN PERFORMED SPECIFICALLY ADDRESSING
TWO POTENTIAL HARMFUL TRIM-ASSOCIATED
EFFECTS:
 CANCER RECURRENCE
 POSTOPERATIVE BACTERIAL INFECTIONS

51.  MOST CELLULAR BLOOD PRODUCTS, INCLUDING
RED CELL, PLATELET, AND GRANULOCYTE
PRODUCTS, CONTAIN VIABLE, IMMUNOCOMPETENT T
LYMPHOCYTES.
 WHEN TRANSFUSED INTO IMMUNO INCOMPETENT
RECIPIENTS,
THESE DONOR LYMPHOCYTES MAY PROLIFERATE IN
THE PATIENT AND LEAD TO THE CLINICAL
SYNDROME OF TRANSFUSION-ASSOCIATED GRAFT-
VERSUS-HOST

52.  TA-GVHD HAS ALSO BEEN REPORTED IN IMMUNO
COMPETENT PATIENTS, ESPECIALLY THOSE WHO
RECEIVE TRANSFUSIONS FROM FAMILY MEMBERS
OR FROM RANDOM DONORS WHO SHARE HLA
ANTIGENS, AS IS THE CASE WHEN THE DONOR IS
HOMOZYGOUS FOR A SHARED HLA HAPLOTYPE.
 IN THESE CASES, THE RECIPIENT DOES NOT
RECOGNIZE THE DONOR CELLS AS FOREIGN,
ALLOWING THE TRANSFUSED LYMPHOCYTES TO
PROLIFERATE AND CAUSE TA-GVHD.

53. SIGNS/SYMPTOMS
FEVER IS MOST COMMON SYMPTOM
APPEARS WITH IN 1-2 WEEKS OF TRANSFUSION
SKIN – TYPICAL ERYTHEMATOUS ,MACULO
PAPULAR SKIN RASH BEGINS CENTRALLY AND
SPREADS PERIPHERALLY TO HANDS AND FEETS ,
DESQUAMATION
GI  NAUSEA ,BLOODY DIARRHEA
ABNORMALITIES OF HEPATIC FUNCTION
BM  FAILURE LEADING TO
PANCYTOPENIA.AFTER 2-3 WEEKS OF ONSET OF
SYMPTOMS

54. DIAGNOSIS
 BASED ON THE CLINICAL PICTURE AND CAN BE
CONFIRMED HISTOLOGICALLY WITH A SKIN BIOPSY.
 LABORATORY CONFIRMATION THAT THE GVHD IS
TRANSFUSIONINDUCED CAN BE OBTAINED BY
DEMONSTRATING THE PRESENCE OF DONOR
LYMPHOCYTES IN THE PATIENT.
 THIS CAN BE DONE BY HLA TYPING OF PATIENT AND
DONOR CELLS BY DNA METHODS.

55. TREATMENT/PREVENTION
 COMBINATION OF IMMUNOSUPPRESENT MEDICATION
WITH
LYMPHOCYTE DIRECTED ANTIBODY THERAPY (ANTI
CD 3,ANTI INTERLEUKIN 2 RECEPTOR ,ANTI
THYMOCYTE
GLOBULIN)
 GAMMA IRRADIATION
 RENDER T-CELLS INCAPABLE OF REPLICATION
 FDA REQUIREMENT
 MINIMUM OF 2500 CGY TARGET TO THE MIDLINE OF
THE CONTAINER
 MINIMUM OF 1500 CGY TARGET TO ALL OTHER
PART OF COMPONENT

56.  TRANSFUSION OF RED CELL PREPARATIONS OR PLASMA
PRODUCTS MAY RESULT IN TRANSFUSION-ASSOCIATED
CIRCULATORY OVERLOAD (TACO).
 ALL PATIENT WILL EXPERIENCE A TEMPORARY RISE IN BLOOD
VOLUME AND VENOUS PRESSURE FOLLOWING THE
TRANSFUSION OF BLOOD OR PLASMA
 FOR THOSE WHO ARE ACTIVELY BLEEDING. HOWEVER, YOUNG
PEOPLE WITH NORMAL CARDIOVASCULAR FUNCTION WILL
TOLERATE THIS CHANGES PROVIDED IT IS NOT EXCESSIVE.
 PREGNANT WOMEN, PATIENT WITH SEVERE ANAEMIA, ELDERLY
WITH COMPROMISED CARDIOVASCULAR FUNCTION WILL NOT
TOLERATE THE INCREASE IN PLASMA VOLUME AND ACUTE
PULMONARY OEDEMA MAY DEVELOP.

57.  FREQUENTLY DUE TO TRANSFUSION OF A UNIT AT
TOO FAST RATE.
 SIGNS OF CARDIAC FAILURE –
RAISED JVP,
BASAL CREPITATIONS IN BOTH LUNGS,
DRY COUGH,
BREATHLESSNESS

58. MANAGEMENT
 STOP THE TRANSFUSION IMMEDIATELY.
 PROP UP THE PATIENT
 OXYGEN THERAPY
 INTRAVENOUS DIURETICS SHOULD BE USED
APPROPRIATELY.
 IF MORE RAPID VOLUME REDUCTION IS NEEDED,
THERAPEUTIC PHLEBOTOMY CAN BE USED.
 TRANSFUSIONS SHOULD BE ADMINISTERED
SLOWLY, AT
A RATE OF 1 TO 2 ML OF BLOOD/KG OF BODY
WEIGHT PER HOUR UNDER CLOSE MONITORING

59. METABOLIC EFFECTS-HYPERKALEMIA
 STORED BLOOD DIFFERS IN ITS COMPOSITION
FROM THAT CIRCULATING IN THE BODY.
 IF LARGE AMOUNTS OF STORED BLOOD ARE
INFUSED RAPIDLY, ONE MAY OBSERVE ADVERSE
EFFECTS RELATED TO SUCH DIFFERENCES.
 THE ELEVATED K+ CONTENT OF STORED RED
CELLS RARELY LEADS TO HYPERKALEMIA, BUT IT IS
A RISK IN THE PRESENCE OF RENAL FAILURE,
SHOCK WITH ACIDOSIS, OR HEMOLYSIS.

60. HYPOCALCEMIA
 PLASMA CONTAINS A SIGNIFICANT AMOUNT OF
CITRATE AS ANTICOAGULANT; RECIPIENTS WITH
NORMAL CIRCULATORY STATUS PROMPTLY
METABOLIZE THIS IN THE LIVER, BUT DURING
PLASMA EXCHANGE OR IN PATIENTS IN SHOCK OR
SEVERE LIVER FAILURE, CITRATE EXCESS
MAYLEAD TO HYPOCALCEMIA.
 HYPOCALCEMIC REACTIONS CAUSED BY CITRATE
MAY BE TREATED BY INTRAVENOUS CALCIUM
INFUSION.

61.  HYPOTHERMIA MAY OCCUR IF A LARGE VOLUME OF
COLD BLOOD IS INFUSED RAPIDLY.
 HYPOTHERMIA IS ONE OF THE MOST COMMON
COMPLICATIONS OF MASSIVE TRANSFUSION AND
CONTRIBUTES TO THE ASSOCIATED
COAGULOPATHY.
 NEONATES AND THE ELDERLY ARE PARTICULARLY
SENSITIVE TO THIS REACTION.
 CARDIAC DYSRHYTHMIAS CAN RESULT FROM
EXPOSING THE SINOATRIAL NODE TO COLD FLUID.

62.  HYPOTHERMIA INTERFERES WITH PLATELET
FUNCTION AND CLOTTING, BOTH OF WHICH ARE
IMPROVED WHEN THE PATIENT IS WARMED.
 ONE WAY OF APPROACHING THIS PROBLEM IS
WITH THE USE OF WARMED INTRAVENOUS FLUIDS.
 USE OF AN IN-LINE WARMERS WILL PREVENT
HYPOTHERMIA.

63.  IRON OVERLOAD IS A MAJOR PROBLEM IN PATIENTS
WHO REQUIRE LONGTERM RED CELL TRANSFUSION
SUPPORT FOR CHRONIC ANEMIAS DUE TO BONE
MARROW FAILURE.
 EACH UNIT OF RED CELLS CONTAINS
APPROXIMATELY 0.25 G OF IRON. AFTER A LARGE
NUMBER OF RED CELL TRANSFUSIONS, IN THE
ABSENCE OF BLOOD LOSS, THE RECIPIENT
DEVELOPS THE STIGMATA OF TRANSFUSION
SIDEROSIS.
 COMMON AFTER 100 UNITS OF RBCS HAVE BEEN
TRANSFUSED (TOTAL BODY IRON LOAD OF 20gms)

64. SYMPTOMS & SIGNS OF IRON OVER LOAD
 IMPAIRED GROWTH, FAILURE OF
 SEXUAL MATURATION,
 MYOCARDIAL AND
 HEPATIC DYSFUNCTION,
 HYPERPIGMENTATION,
 DIABETES.
 PATIENTS SUCH AS THOSE WITHTHALASSEMIA WHO
ARE AT RISK OF THIS COMPLICATION SHOULD
RECEIVEPROPHYLACTIC AGGRESSIVE IRON
CHELATION THERAPY. CHELATING AGENTS
DEFUROXAMINE AND DEFERASIROX

65.  HEPATITIS
 SYPHILIS
 MALARIA
 CYTOMEGALOVIRUS
 HUMAN IMMUNODEFICIENCY VIRUS
 HUMAN T CELL LEUKAEMIA VIRUSES.
DONOR SELECTION CRITERIA AND SUBSEQUENT
SCREENING OF ALL DONATIONS ARE DESIGNED TO
PREVENT DISEASE TRANSMISSION, BUT THESE DO
NOT COMPLETELY ELIMINATE THE HAZARDS.

68. IS RARELY TRANSMITTED BY TRANSFUSION. ANY
DONOR WHO HAS BEEN IN CLOSE CONTACT WITH
HEPATITIS A PATIENT OR DEVELOPS HEPATITIS A IS
DEFFERED FOR 12 MONTHS.

69.  IS A FREQUENT SEQUEL TO BLOOD
TRANSFUSION. CURRENTLY ALL BLOOD
DONATIONS ARE TESTED FOR HBSAG BY
VERY SENSITIVE THIRD GENERATION
TECHNIQUES ( EG; ELISA ), ABLE TO DETECT
AT LEAST 0.5 IU OF HBSAG PER ML OF SERUM.
IN HUSM, EIA METHOD IS USED WITH 99.9 %
SENSITIVITY.
HBSAG POSITIVE SUBJECTS ARE
PERMANENTLY EXCLUDED FROM DONATIONS

70. ALL DONATED BLOOD ARE TESTED FOR ANTI
– HCV. IMPROVED SCREENING ASSAYS
BASED ON MULTIPLE RECOMBINANT OR
SYNTHETIC ANTIGENS INCLUDING VIRAL
CORE PROTEIN ARE NOW AVAILABLE.
 INDIVIDUALS WITH A HISTORY OF JAUNDICE
MAY BE ACCEPTED AS DONORS 1 YEAR
AFTER THE ILLNESS PROVIDED THEY
TESTED AND NEGATIVE FOR HBSAG AND
ANTI HCV.

71.  THE ORGANISM IS MORE LIKELY TO BE TRANSMITTED
IN PLATELET CONCENTRATE DUE TO THEIR ROOM
TEMPERATURE STORAGE AND SHORT SHELF LIFE.
 TREPONEMA PALLIDUM DOES NOT SURVIVE WELL AT 4º
C AND RED CELL PREPARATION ARE LIKELY TO BE NON
INFECTIVE AFTER 4 DAYS REFRIGERATION. PASSIVE
TRANSMISSION OF THE ANTIBODY TO THE RECEPIENT
MAY CAUSE DIAGNOSTIC CONFUSION.
 ANY DONATIONS WITH POSITIVE RESULT IS
DISCARDED, ANY SUBJECTS WITH POSITIVE TESTS ARE
PERMANENTLY DEFERRED, EVEN AFTER EFFECTIVE
THERAPY.

72.  MALARIAL PARASITES REMAIN VIABLE IN BLOOD
STORED AT 4º C AND EASILY TRANSMITTED BY
BLOOD TRANSFUSION.
 IN SOME ENDEMIC AREAS, ALL RECIPIENTS ARE
TREATED WITH ANTIMALARIAL DRUGS.
 DONORS WHO COME FROM ENDEMIC AREA OR HAVE
HAD AN ATTACK OF MALARIA CAN BE ACCEPTED,
THEIR PLASMA CAN BE USED FOR FRACTIONATION
BUT RED CELLS MUST BE DISCARDED..

73.  POST TRANSFUSION CMV INFECTION IS NOT
UNCOMMON.
 THE INFECTION IS CHARACTERISED BY
FEVER SPLEENOMEGALY, AND ATYPICAL
LYMPHOID CELLS IN THE PERIPHERAL
BLOOD.
 DUE TO ITS BENIGN COURSE, SCREENING
FOR PAST INFECTION AMONG DONORS ARE
NOT NECESSARY.

74. CYTOMEGALOVIRUS
•HOWEVER, THERE ARE PATIENT AT RISK OF
DEVELOPING FATAL PNEUMONITIS OR DISSEMINATED
CMV INFECTION : PREM BABY < 1500G, BM OR AND
OTHER ORGAN TRANSPLANT RECIPIENT, PREGNANT
WOMEN ( RISK TO FETUS ).
•FOR THEM, ANTI – CMV FREE BLOOD & COMPONENTS
SHOULD BE PROVIDED.
•AS AN ALTERNATIVE, SINCE CMV IS CELL ASSOCIATED,
LEUKODEPLETED BLOOD MAY BE USED.

75.  HIV CAN BE TRANSMITTED BOTH IN CELLULAR AND
PLASMA COMPONENTS.
 THE MAJORITY OF RECIPIENT OF BLOOD OR BLOOD
PRODUCTS WHO HAVE BEEN INFECTED IN THE PAST
WERE TRANSFUSED BEFORE 1985 WITH
UNHEATED, NON PASTEURIZED POOLED PLASMA
PRODUCTS, FACTOR VIII AND IX.

76.  WITH SCREENING PROGRAME, HIV TRANSMISSION
STILL OCCUR THROUGH DONATIONS GIVEN IN THE
WINDOW PERIOD OF INFECTIVITY.
 WITH CURRENT ANTIBODY SCREENING TECHNIQUE,
THE ESTIMATED WINDOW PERIOD IS ABOUT 3 WEEKS.
 PCR FOR HIV RNA IS ABLE TO REDUCE THE WINDOW
PERIOD TO APPROXIMATELY 1 WEEK.

77.  HTLV 1 AND II ARE RELATED RETROVIRUSES.
 HTLV 1 IS ENDEMIC IN THE CARIBBEAN, PARTS OF
AFRICA AND IN JAPAN, 3 – 6 % OF THE POPULATION
ARE SEROPOSITIVE.
 HTLV 1 IS ASSOCIATED WITH TROPICAL SPASTIC
PARAPARESIS AND ADULT T CELL – LEUKAEMIA.
 IMPORTANCE OF HTLV II IS NOT CLEAR.
 BOTH HTLV 1 AND II ARE CELL ASSOCIATED AND NOT
TRANSMITTED IN PLASMA.
 CURRENTLY AVAILABLE TEST INCLUDE ELISA AND
GELATIN PARTICLE ASSAY, BUT CONFIRMATION OF
POSITIVE RESULT ARE DIFFICULT DUE TO CROSS
REACTIVITY WITH OTHER RETROVIRUSES.

78.  MOST BACTERIA DO NOT GROW WELL AT COLD
TEMPERATURES, PRBCS AND FFP ARE NOT COMMON
SOURCES OF BACTERIAL CONTAMINATION.
 SOME GRAM-NEGATIVE BACTERIA CAN GROW AT
1–6°C. YERSINIA, PSEUDOMONAS, SERRATIA,
ACINETOBACTER, AND ESCHERICHIA SPECIES HAVE
ALL BEEN IMPLICATED IN INFECTIONS RELATED TO
PRBC TRANSFUSION.
 PLATELET CONCENTRATES, WHICH ARE STORED AT
ROOM TEMPERATURE, ARE MORE LIKELY TO CONTAIN
SKIN CONTAMINANTS SUCH AS GRAM-POSITIVE
ORGANISMS, INCLUDING COAGULASE-NEGATIVE
STAPHYLOCOCCI.

79.  RECIPIENTS OF TRANSFUSION CONTAMINATED WITH
BACTERIA MAY DEVELOP FEVER AND CHILLS, WHICH
CAN PROGRESS TO SEPTIC SHOCK AND DIC.
 THESE REACTIONS MAY OCCUR ABRUPTLY, WITHIN
MINUTES OF INITIATING THE TRANSFUSION, OR
AFTER SEVERAL HOURS.
 THE ONSET OF SYMPTOMS AND SIGNS IS OFTEN
SUDDEN AND FULMINANT, WHICH DISTINGUISHES
BACTERIAL CONTAMINATION FROM AN FNHTR.
 THE REACTIONS, PARTICULARLY THOSE RELATED TO
GRAMNEGATIVE CONTAMINANTS, ARE THE RESULT
OF INFUSED ENDOTOXINS FORMED WITHIN THE
CONTAMINATED STORED COMPONENT.

80.  WHEN THESE REACTIONS ARE SUSPECTED, THE
TRANSFUSION MUST BE STOPPED IMMEDIATELY.
 THERAPY IS DIRECTED AT REVERSING ANY SIGNS
OF SHOCK, AND BROAD-SPECTRUM ANTIBIOTICS
SHOULD BE GIVEN.
 THE BLOOD BANK SHOULD BE NOTIFIED TO
IDENTIFY ANY CLERICAL OR SEROLOGIC ERROR.
 THE BLOOD COMPONENT BAG SHOULD BE SENT
FOR CULTURE AND GRAM STAIN.

95.  Most patients do
 not have repeated allergic reactions, but those with a history of
 atopy are at higher risk for additional reactions. For patients with
 repeated allergic reactions, premedication with an H1-blocking
 antihistamine is usually sufficient for prevention. If maximal
 premedication fails to control the allergic response, reducing
 the plasma content of the transfused blood product is another
 option. This can be accomplished by centrifuging the product and
 removing
 almost all the plasma or by red cell washing.

96.  In patients with severe anaphylactoid or anaphylactic reactions,
 antibodies reacting with IgA in donor plasma should
 be considered. The incidence of genetically determined IgA
 deficiency in the otherwise normal population is high, ranging
 from 1 in 400 to 1 in 500.467 Without necessarily having prior
 transfusion exposure, approximately 20% to 25% of such patients
 produce antibodies to IgA, generally class-specific (i.e., reacting
 with all IgA molecules). Such patients should be transfused, when
 necessary, with washed red cells468 or with IgA-deficient blood
 products. In addition, many patients with normal IgA levels have
 antibodies that react with some, but not all, IgA molecules; the
 incidence of such limited-specificity antibodies has been reported
 at 2% of normal adults,469 but the incidence may be as high as
 21% in multiply transfused patients.440 The concentration of such
 limited-specificity antibodies generally is low, and the resulting
 reactions are usually milder, but the possibility of a major reaction
 exists.417