Lec 17 - Transfusion Reactions Flashcards
clinical use of Rh immune globulin
-prevents problems in future pregnancies
historical significance of autologous donation
- youre more likely to get a transfusion if you donate your own blood for yourself
- usually donated before the surgery or whatever so the pt is slightly anemic = inc chances of ischemia
- usually blood isnt tested for viruses as much so then dont know if pt wants his virus laden blood or another donors blood
historical significance of directed donation
-donating blood to some one you know
hydrops fetalis basic mechanism and causes
imbalance of interstitial fluid production nd lymphatic return (caused by congestive heart failure, obstructed lymphatic flow, decreased plasma oncotic pressure)
body tries to compensate but ultimately increased venous pressure = edema and effusion
consequences of accelerated RBC destruction:
hyperbillirubinemia (unconjugated) == kernicterus - yellow staining of the basal ganglia
HDN caused by Rh antigens other than D
- Less immunogenic than D, so less severe
- Anti-E & C are most likely to cause severe HDFN
Which non-Rh antibodies are most likely to cause significant HDFN?
Anti-Kell
-Kell antigen present on RBCs & erythroid precursors in marrow
*Consequences of accelerated RBC destruction in HDFN
- Hydrops fetalis
- Accumulation of fluid in fetus (edema, effusion etc)
- Many causes: Rh immunization, congenital heart disease, arrhythmia etc. - Kernicterus: Yellow staining of basal ganglia
- Hyperbilirubinemia (unconjugated) from RBC destruction; immature liver can’t conjugate all
Hydrops fetalis pathophysiology
Imbalanced interstitial fluid production & lymph return-> Body compensation-> ↑Venous P.-> ↑edema & effusion (cycle)
Maternofetal hemorrhage occurs when/how?
- Mostly in last trimester & delivery
- Many other causes (abortion, trauma etc)
*RhoGAM/ Rh immune globulin use & mechanism
- Prevent HDFN
- Unknown mechanism:
1. The Anti-D masks antigen sites on fetal Rh+ cells in maternal circulation, preventing recognition
2. The Anti-D Helps clear antibody-coated Rh+ cells before they can be recognized by maternal immune system
When to administer RhoGAM
- 28 weeks gestation
(Rarely Rh alloimmunization before 28wk) - W/i 72hr. of delivery
- Possible extra dose if beyond 40wk gestation
Chance of developing Anti-D when D- pt. is transfused w/ D+ blood?
20%
*Most common cause of HTR?
Clerical error
wrong label, wrong blood hung etc
*Signs/symptoms of Acute intravascular HTR?
- Fever/chills (80%)
- Back/flank/infusion site pain
- HypOtension/shock
- Hemoglobinuria
- “Impending sense of doom”
Tx of acute intravascular HTR
- Hydration/diuresis (protect kidneys)
- Consider RBC exchange for high volume incompatible transfusions
- Most frequently reported transfusion reaction (FNHTR)
- Sign/symptoms
- Tx
Febrile Non-hemolytic transfusion reaction
- Unexplained ↑temp. of 1C+, Chills, rigors
- Premedicated FNHTR (acetaminophen) can still have chills but not fever
- Tx= Acetaminophen
*Schistocytes are present in ______ hemolysis
Intravascular
-Antibodies->complement->lysis
helmet cells
most important factor when patient is having a hemolytic reaction to trasnfusion?
HOW MUCH BLOOD DID THEY GET?
STOP THE TRANSFUSION!
What kind of RBC are present in extra vascular hemolysis?
SPHEROCYTES
-In extravascular, IgG coats-> Spleen/liver phagocytosis
TACO is
a circulatory overload - gets better with diuretics
TRALI is associated with
fever
does not get better with diuretics
septic transfusion reaction most commonly involves…?
endotoxin making gram neg rods (yersinia or E Coli) from the donors blood
platelets stored at room temp most commonly have what organsims?
gram pos cocci (staph epi and staph aureus)
another type of septic transfusion reaction
symptoms of septic transfusion reaction?
fever
RIGORS (NOT CHILLS - MUSCLE TENSE UP A LOT!)
shock
