1/13 Blood Products - Corbett Flashcards
ABO groups
basics
H antigen is precursor onto which terminal sugars are added to yield
- A antigen (GalNac)
- B antigen (Gal)
when individuals LACK a carbohydrate antigen, they form an IgM antibody against it
- important bc IgM can fix complement → intravascular hemolysis
front typing vs back typing
front typing: pt blood + known antibody
back typing: pt serum + known cells
what happens if A, B, and O clot during a typing test?
rare phenotype: BOMBAY - lacks H antigen
- lack fucosyl transferase which adds fucose, which has to be added before A or B sugars can be added
Rh system
- protien antigens expressed by RBCs
- D antigens are VERY IMMUNOGENIC → considered most imp Rh antigen in transfusion practice
- Rh+ : D antigen present, no anti-D
- Rh- : D antigen absent, no anti-D UNLESS EXPOSED (ex. childbirth)
***both types lack anti-D antibodies at default state
antiD antibodies
IgG : too small to engage antigen AND fix complement at the same time
- instead, just bind to antigen surface and opsonize them → cause extravascular hemolysis (RES system in liver and spleen, where Fc portion of ab is recognized)
CAN CROSS PLACENTA
hemolytic disease of newborn
1st pregnancy
mom Rh-
baby Rh+
fetal-maternal blood transfer during labor → mom is sensitized to RhD antigen
- can try to prevent with Ig therapy
- can check for sensitization with Coombs test
NOW, mom has antiD antibodies in her circulation just waiting to pour through the placenta during her next pregnancy!
- issue: next Rb+ baby will have problems
hemolytic disease of newborn
second pregnancy
sensitized mother and Rh+ baby
- next contact with fetal RhD antigen
FETAL OR NEWBORN HEMOLYTIC ANEMIA
- mild: mild anemia, jaundice
- severe: incr bilirubin, CNS damage, death → erythroblastosis fetalis
hydrops fetalis
fluid in two or more fetal compartments
immune and non-immune causes, but root cause is fetal RBC destruction, leading to:
- extramedullary hematopoiesis → liver failure → low plasma oncotic pressure
- low O2 delivery triggering higher CO → heart failure → contributes to liver failure and also high central venous pressure
overall: high interstitial fluid
tx to prevent hemolytic disease of newborn
RHOGAM is IgG antiD
- antibody given close to birth to prevent mom from being sensitized
- mom wont react to Rh+ kid, no B cell activation and memory cell formation takes place
ABO hemolytic disease
mom O
baby A or B
- in very small group, some antiA, antiB, and antiAB antibodies of IgG class can develop
more common and more severe in African American infants
HDN can occur in first pregnancy bc prior sensitization not necessary
less severe than Rh HDN bc…
- amount of cross passing antibody is less than Rh
- ABO antigens are in low number
- retal RBCs less developed at birth
- presence of ABO antigens in tissues and secretions
ABO vs Rh incompatibility
blood component therapy
four main derivatives
why collected in citrate?
a unit of whole blood is processed through a series of centrifugations into four main derivatives for transfusion into recipient:
-
packed red cells
- 3-6 week shelf life: lose 2,3BPG, pH drop, K rise
- platelet concentrate
- fresh frozen plasma (FFP): coag factors II, VII, IX, X, XII, protein C, protein S
- cryoprecipitate: fibrinogen, vWF
why collected in citrate?
citrate binds Ca in blood → prevents Ca from triggering coag
treatment for packed RBCs
- refrigerate
- leukodepletion: filter granulocytes and lymphocytes
- irradiation: kill all leukocytes (esp T cells) to prevent graft vs host disease
fresh frozen plasma
contains all coagulation factors and other proteins present in original unit of blood (including antiA, antiB, antiD antibodies)
i.e MUST BE ABO COMPATIBLE
- frozen: good for 1yr
- thawed: use in 24hr
- after 24hr, F VIII level drops
cryoprecipitate
all ABO acceptable
contains proteins:
- F VIII (12h halflife)
- fibrinogen (4-7d halflife)
- vWF (24h halflife)
- F XIII (1-2wk halflife)
platelets
major risk
all ABO acceptable BUT donor match recommended
- do have antigens on their surface but don’t cause a reaction
- however, could trigger sensitization that makes subsequent transfusions more difficult
stored at room temp bc if you store in cold, you’ll activate vWF in plasma and cause clumping of vWF-platelets
major risk: bacterial contamination/infection during platelet transfusion
- storing at room temp → bacteria can proliferate rapidly
- 1/2000 chance for platelets (vs 30k for RBC)
summary guide to products
issues with transfusing lots of blood
(3 or more units of pRBCs/hr)
- coagulopathy: coagulopathy
- (have to make sure you’re putting back volume proportionally 1:1:1, RBC: plasma: platelets)
- hypothermia
- (need to warm the blood)
- citrate issues → chelates Ca out of blood
- hypocalcemia
- metabolic alkalosis (if renal insufficiency)
- hyperkalemia (longer storage time → more K in blood)
complications of transfution
common
uncommon
rare
suspect problem if adverse signs/sx during/within 24h of transfusion
- fever/chills
- pruritis, urticaria
- resp distress, hypotn
- hemoglobinuria, flank/back pain, oliguria
- disseminated bleeding or oozing from IV sites
common:
- febrile non-hemolytic transfusion rxn
- leukocytes generate cytokines (IL1, 6, 8, TNFalpha) which accumulate during storage of blood components
- urticaria
uncommon
- TACO
- TRALI
rare
- anaphylaxis
- acute hemolytic transfusion reaction
- fever, flank pain, red/brown urine, pink plasma, anxiety, pain at infusion site, diffuse bleeding (DIC)
AHTR
pathogenesis
cause
dx
consequences
treatment
MEDICAL EMERGENCY
cause: ABO incompatibility
- donor RBCs dont match → rapid destruction of transfused blood by preformed antibodies in recipient
- naturally occuring IgM antibodies fix complement and lyse donor cells
dx:
- plasma free Hb 25-40mg/dL
- direct coombs test will be positive
if allowed to continue: DIC, shock, acute renal failure
- treatment: STOP transfusion, save bag
- supportive care
- saline infusion IV to save kidneys: maintain urine output at 100-200cc/hr
- send blood sample for direct Coomb’s test and figure out cause of error
delayed hemolytic transfusion rxn
definition
cause
hemolysis occuring 3-30 days post-transfusion
cause: “anamnestic” antibody response
- reexposure to previously encountered foreign red cell antigen (i.e. in prior transfusion, transplantation, pregnancy)
- pt had preformed IgG antibody - commonly ab to Kidd or Rh that was undetectable on screening
since IgG → extravascular hemolysis
- decr hematocrit
- slight fever
- mild jaundice
- spherocytosis
- test again? positive direct Coombs
tx: supportive care
urticarial transfusion rxn
mech: allergenic substance in plasma of donated pdt reacts with preexisting IgE in recipient
- mast cell and basophil degranulation occur to cause hives
tx:
- STOP transfusion
- provide diphenhydramine
- once stable, continue
anaphylactic transfusion rxn
MEDICAL EMERGENCY
very rapid onset (seconds to minutes) following transfusion containing plasma/RBC/platelets/granulocytes/cryoprecipitate/gamma glob
rapid onset of anaphylaxis
- shock
- hypotension
- angioedema
- respiratory distress
typical occurs in setting of IgA deficiency and who have class-specific IgG anti-IgA antibodies
tx: stop transfusion
- epinephrine
- fluid resuscitation of hypotensive pt
- airway maintenance
- oxygenation
- vasopressors (DA) if necessary
transfusion associated lung injury
sudden onset of hypoxemic respiratory insufficiency during or shortly after transfusion of blood product
- hypoxemia
- pulmo infiltrates on chext radiography
- pink frothy airway secretions
- fever
- hypotension
- cyanosis
pathogenesis: neutrophil sequestration and priming in lung microvasc + activation of neutrophils by factor in blood
TRALI
transfusion related acute lung injury
(analogous to ARDS)
transfusion associated circulatory overload
TACO
(volume overload)
- most common in elderly
- risk factors
- compromised cardiac fx
- positive fluid balance
- rapid blood product admin
TRALI vs TACO
