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80 Cards in this Set

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acute hemolytic blood transfusion reaction is caused by
ABO incompatibility, (misidentification of patient, blood specimen, blood unit)
how common is acute hemolytic blood transfusion reaction
symptoms of acute hemolytic blood transfusion reaction if awake
chills, nausea, fever, dyspnea, chest pain, flank pain, headache
symptoms of acute hemolytic blood transfusion reaction if asleep under anesthesia
increased temperature, unexplained tachycardia, hypotension, hemoglobinuria, oozing, DIC, shock, renal failure
what symptom of acute hemolytic blood transfusion reaction if under general anesthesia is not likely to be explained by other causes
if suspect an acute hemolytic blood transfusion reaction
recheck blood, stop transfusion, notify blood bank, send unused blood and tubing back, draw CBC, coags, type and cross, check urine for hemoglobinuria, osmotic diuresis with mannitol and fluids (to flush out kidneys), low dose dopamine, replace blood loss, platelets, FFP, steroids possibly
characteristics of a delayed hemolytic reaction after blood transfusion
mild, less common antigen-antibody reaction, 1:1,500 transfusions, 2 - 21 days after transfusion
symptoms of delayed hemolytic reaction
malaise, jaundice, fever
treatment for delayed hemolytic reaction
nonhemolytic immune reactions occur because
recipient is sensitized to donors WBC, platelets, or plasma proteins
most common symptom of nonhemolytic immune reaction to a blood transfusion
fever (3-5% of all transfusions)
treatment for nonhemolytic immune febrile reaction
stop infusion, antipyretices
in future transfusions patient should only receive leukocyte poor transfusions
types of nonhemolytic immune reactions
febrile, uticarial reaction, anaphylactic reaction, TRALI
symptoms of uticarial reaction
erythema, hives, itching, no fever
treatment for uticarial reaction to a blood transfusion
Antihistamine blockers H1 and H2
how common are uticarial reactions to blood transfusions
1% of all transfusions
possible cause of uticarial reactions
sensitization to transfused plasma proteins
how common are anaphylactic reactions to blood transfusions
anaphylactic reactions to blood transfusions caused by
IgA antibodies
treatment for anaphylactic reaction to blood transfusion
epinephrine, corticosteroids, H1 and H2 blockers, cardiovascular support (in the future patient should only receive washed cells and IgA free blood)
symptoms of anaphylactic reaction under anesthesia
hives, elevation in airway pressures, wheezing, decreased pulse ox, tachycardia
TRALI stands for
transfusion related acute lung injury
TRALI is how common
TRALI caused by
white cells aggregating in pulmonary circulation causing alveolar capillary damage
treatment and symptoms of TRALI
same as ARDS
TRALI resolves within
12 - 48 hours
what to check when checking blood
right patient (all must have ID band)
right MRN
right unit
right blood type
expiration date
(read out loud, repeat out loud)
graft-host disease occurs in what patient population
immunocompromised patients
graft-host disease in blood transfusions is caused by
the lymphocytes of the donor blood attacking the host
for immunocompromised people needing blood, you should give
only irradiated blood products that have hopefully killed the lymphocytes since filters do not effectively remove all the lymphocytes
how is the immune system is affected by blood transfusion
the transfusion of leukocytes causes immunosuppression which is good in organ transplants but bad if it helps tumors grow
infection risk of hepatitis A
infection risk of hepatitis B
1:30,000 to 250,000
infection risk of hepatitis C
1:30,000 to 150,000 (most common infection from blood transfusion)
infection risk of HIV
1:200,000 to 2,000,000
infection risk of human T-lymphocyte virus I/II (HTLV)
1:250,000 to 2,000,000
what % of the population has been exposed to CMV (cytomegalovirus)
50% - 80% of the population - 50% of donors have an antibody presence
symptoms of CMV are
mono-like in healthy people
CMV can cause severe infections in immunocompromised patients such as
retinitis, pneumonitis, gastroenteritis, hepatosplenomegally, risk of death
reduce incidence of CMV with blood transfusions by
leukocyte filters
risk of Parvovirus B-19 with blood transfusion is
parvovirus b-19 is a problem for
pregnant patients - may cause hydrops fetalis, stillbirth
other diseases possibly transmitted by blood transfusions (very rare)
Epstein-Barr, Human herpes 4 and 6, Syphilis, West Nile (no proven cases), Creutzfeld Jakob (not sure either - but seems possible)
what about syphilis and blood transfusions
syphilis doesn't survive cold storage, but platelets are kept at room temperature so could be a risk
Creutzfel Jakob disease is
a fatal neurodegenerative disease transmitted by prion infected meat and dura mater grafts, corneal transplants, reuse of EKG electrodes, pituitary growth hormone injections, and potentially blood transfusions
examples of prion caused diseases
Scrapie (sheep), bovine spongiform encephalopathy (mad cow disease), chronic wasting disease (deer and elk), Kuru (New Guinea tribe that ate the brains)
prions infect and propagate by
folding themselves into protein structures in the cells
why did the Red Cross have to pay 4.5 million $$$$
did not ask blood donors if they had been to Europe and eaten beef
What is the chance of receiving contaminated PRBCs
death rate if receive contaminated PRBCs
chance of receiving contaminated platelets
1:12,000 - high death rate
contamination in PRBC or platelets is due to
bacteria on the skin during the donation process
changes in stored blood
increased plasma potassium, ammonia, lactate levels, red cell lysis
decreased pH, 2,3 DPG, RBC ATP levels
what is citrate intoxication
the CPDA anticoagulant preservative solution in a unit of PRBCs contains citrate that binds ionized calcium - so large transfusions (more than 1 unit) can cause a reduction in serum ionized calcium
signs and symptoms of citrate intoxication
hypotension, narrow pulse pressure, prolonged Q-T, wide QRS, coagulopathy
what to remember about Citrate
it is metabolized by the liver to bicarb over a few days - so watch for alkalosis later on
treatment for citrate intoxication
0.2 - 0.25 ml/kg calcium chloride (10%) over 10 minutes and recheck ionized calcium
CPDA binds calcium causing
decreased heart contractility, decreased clotting, vasodilation because decreased smooth muscle contractility
why don't we give LR with PRBCs
LR contains calcium and citrate will bind to the calcium to cause microaggregate clot formation (may lead to TRALI). Also, LR is slightly hypoosmotic
successive[frequent] occurrence, a succession[series] (of events) [continue + appear]
what is the cause of metabolic acidosis during blood transfusions
usually due to an effect of hypoperfusion not the blood transfusion, the body is very effective at buffering several units of blood
why and when do you see metabolic alkalosis related to blood transfusions
citrate metabolism to bicarb in the liver so will see metabolic alkalosis several days after blood transfusions sometimes
does the oxyhemoglobin dissociation curve shift left or right with blood transfusions
overall left shift with banked blood because of reduced temperature and reduced 2,3 DPG even though the acidosis would want to shift it right
why risk of hyperkalemia with blood transfusions (Gayles never seen this as a real problem)
as H+ increase, K+ moves out of cells to maintain neutrality
red cell lysis if PRBCs transfused through small bore catheter
hypotonic infusion solution
problems from hypothermia in RBC transfusion
decreased CO, vasonconstriction, shift left on oxyhemoglobin dissociation curve, coagulopathy, shivering
shivering increases O2 consumption by
when transfusing cold blood
WARM it (will help anesthesia work better as well as prevent other side effects of hypothermia)
what lab values will you see with dilutional coagulopathy from RBC transfusions
thrombocytopenia will develop before loss of coag factors so give platelets
how to differentiate between dilutional coagulopathy and DIC
platelets will be the issue with dilutional coagulopathy whereas DIC will see big increase in FSP (D-dimer)
what is D-dimer
one of the FSP
risks associated with blood transfusions
disease transmission, graft-host disease, immune suppression, citrate intoxication, left shift of dissociation curve, hyperkalemia, hypothermia, dilutional coagulopathy, acute hemolytic reactions, non-hemolytic reactions, TRALI
What to know about Jehovah's witnesses and blood transfusions
will not accept donated blood or blood that has left the circulation, closed systems are sometimes OK (CABG), sign blood refusal form, eliminate religious pressure by talking to patient alone, remember some other products are partial blood products, may give procrit, epogen for 2-6 weeks before seeing result
conservation strategies for preventing too much blood loss
autologous blood, discourage family donation of blood, cell saver, CT autotransfusions, tourniquets, acute normovolemic hemodilution
What about cell saver?
anticoagulate blood - spins out RBC's, washes the cells with saline, all platelets coags removed, Hct 45 - 50%,
Secured Party versus Purchaser
1. General rule = secured party prevails
2. Debtor has permission to sell = purchaser prevails
3. Secured party unperfected at time of purchase - purchaser wins if (1) buyer gives value, (2) receives delivery of item, and (3) has no knowledge of security interest at time of delivery; but if PMSI creditor perfects within 20 days after debtor receives collateral but after debtor sells collateral to purchaser, creditor will prevail over the "gap" purchaser
4. Buyers in the ordinary course of business can prevail even over a perfected creditor if (a) good faith, (b) without knowledge of security interest violation, (c) purchase of goods that are not farm goods, (d) ordinary purchase from person in the business of selling goods of the kind, (e) security interest created by seller, and (f) creditor not perfected by possession
why not family donated blood
sets up family for deception
describe acute normovolemic hemodilution
remove blood prior to surgery, replace with crystalloid so fewer RBCs are loss during surgery, return with own blood after surgery with none of the risks associated with storage of blood
contraindications for acute normovolemic hemodilution
anemia, decreased renal function, CAD, carotid disease, pulmonary disease, liver disease, inadequate vascular access
2 complications of acute normovolemic hemodilution
MI and cerebral hypoxia