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ANESTHESIA PRACTICE 2 > BLOOD PRODUCTS AND ADMINISTRATION > Flashcards

BLOOD PRODUCTS AND ADMINISTRATION Flashcards

1
Q

what is the normal Hg of men vs. women?

what is the normal Hct of men vs. women?

A

Hg: men ≥ 14gm/dL women ≥ 12gm/dL
(Hct = 3X Hg)
Hct: men ≥ 42% women ≥ 38%

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2
Q

define hematocrit

A

the volume percentage of RBCs in blood; also known as PCV (packed cell volume)

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3
Q

when was whole blood first given in US?

A

1960s

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4
Q

when was component therapy given?

A

1970s-1980s

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5
Q

during what period were infectious concerns/transfusion triggers debated?

A

1970s-1990s

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6
Q

during what period did (reconstituted) whole blood return as component transfusion ratios?

A

1990-2005

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7
Q

how long have we seen reduced infectious risks, revision of transfusion triggers and computerization of blood banks?

A

since 2005

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8
Q

name two types of blood products

A

packed RBCs, fresh whole blood

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9
Q

in what instances should PRBCs be administered?

A

severe anemia

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10
Q

define anemia

A

reduced oxygen carrying capacity

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11
Q

define severe anemia

A

Hg

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12
Q

define splanchnic

A

term used to describe organs in the abdominal cavity (visceral organs)

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13
Q

what risks are associated with severe anemia and perioperative anemia (hence the need for PRBC administration)?

A

inadequate splanchnic and preportal oxygen delivery – acute kidney injury (AKI) and mortality

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14
Q

how does the 1988 NIH consensus conference define perioperative determinants for PRBC necessity?

A

Hg > 10gm/dL – rarely requires PRBCs

Hg

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15
Q

how are the liberal vs. conservative/restrictive threshold camps defined?

A

liberal transfusion threshold ≤ 9-10gm/dL

conservative/restrictive transfusion threshold ≤ 7-8gm/dL

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16
Q

according to 2006 ASA recommendations, define transfusion indications

A

Hg > 10gm/dL – transfusion rarely indicated

Hg

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17
Q

according to 2006 ASA recommendations, the determination of whether intermediate Hg concentrations (6-10gm/dL) justify or require RBC transfusion should be based on what?

A

should be based on pt’s risk for complications of inadequate oxygenation

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18
Q

define allogeneic

A

tissues or cells that are genetically dissimilar and hence immunologically incompatible, although from individuals of the same species

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19
Q

what is in PRBCs?

A

(contains as much Hg as) whole blood with most of plasma removed, CPDA/CPDA-1

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20
Q

what are the components/functions of CPDA

A

citrate – anticoagulant
phosphate – pH buffer
dextrose – nutrition
adenine – for ATP synthesis (extends storage time from 21-35 days)

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21
Q

what are the nutritional components of CPDA-1 that increase shelf life?

A

CPDA-1/AS-1 – adsol (adenine, glucose, mannitol and NaCl)
CPDA-1/AS-3 – nutricel (adenine, glucose, citrate and phoshpate)
CPDA-1/AS-5 – optisol (adenine, dextrose, mannitol and NaCl)

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22
Q

what percentage of transfused RBCs must remain in circulation for 24hr after infusion?

A

70%. RBCs that survive 24hr after transfusion disappear from the circulation at a normal rate

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23
Q

what is the Hct of whole blood?

A

40%

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24
Q

what is the Hct/total volume/plasma volume of CPDA?

A

Hct 65%, total volume 250ml, plasma volume, 70ml

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25
Q

what is the Hct/total volume/storage sln volume of CPDA-1

A

Hct 40%, total volume 310ml, storage sln volume 100ml

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26
Q

which crystalloid are PRBCs normally reconstituted with and why?

A

NS; Ca2+ in LR activates clotting factors

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27
Q

how does the pH of PRBCs change with time?

A

become more acidic: pH from 7.55 to 6.71 over 35d

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28
Q

how does the plasma Hg (mg/dl) of PRBCs change with time?

A

increases from 0.5mg/dl to 246mg/dl over 35d

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29
Q

how does the plasma potassium (mEq/L) of PRBCs change with time?

A

increases from 4.2mEq/L to 76mEq/L over 35d

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30
Q

how does the plasma sodium (mEq/L) of PRBCs change with time?

A

decreases from 169mEq/L to 122mEq/L over 35d

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31
Q

how does the blood dextrose (mg/dl) of PRBCs change with time?

A

decreases from 440mg/dl to 84mg/dl over 35d

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32
Q

how does the 2,3-diphosphoglycerate (µM/ml) of PRBCs change with time?

A

decreases from 13.2µM/ml to 1.0µM/ml over 35d

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33
Q

how does the survival percentage of PRBCs change with time?

A

decreases from 100% to 71% over 35d

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34
Q

how do ‘blood type’ and surface antigens/plasma antibodies relate?

A

blood type = surface antigen expressed; has opposite plasma antibody
type A blood: A surface antigen, B plasma antibody
type B blood: B surface antigen, A plasma antibody
type AB blood: A&B surface antigens, no plasma antibodies
type O blood: no surface antigens, A&B plasma antibodies

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35
Q

describe the negative effect of giving ABO incompatible blood

A

if plasma antibodies target the surface antigen expressed on transfused RBCs, the antibodies activate complement agglutination (clumping), leading to hemolysis

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36
Q

what percentage of the population is Rh(D)-positive (express surface antigen D)?

A

85%

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37
Q

if blood typing produces clumping, what does it mean?

A

administration of the antigen specific antibody has produced a positive result, meaning that the RBCs express the targeted antigen

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38
Q

what is the purpose of the type and screen?

A

determines ABO-Rh blood type and presence of most commonly found unexpected antibodies in the pt’s serum

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39
Q

how are serum antibodies screened?

A

donor serum is added to commercially supplied RBCs (with optimal number of antigens to react to most common antibodies to cause a hemolytic reaction)

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40
Q

how is a type and crossmatch performed?

A

a “test transfusion” in a test tube – donor RBCs mixed with recipient plasma to detect a potential for serious transfusion reaction

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41
Q

how long (total) do the three phases of type and crossmatch take?

A

45min

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42
Q

what are the three phases of the type and crossmatch?

A
  1. immediate – (room temp) major ABO rxns
  2. incubation – (37ºC) Rh and other major antibody rxns in albumin or low-ionic strength salt solution; no agglutination
  3. antiglobulin – addition of anti globulin sera to incubated test tubes; tests lesser antibody rxns; agglutination
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43
Q

why are the incubation and antiglobulin phases of T&C especially important?

A

the antibodies appearing in these phases are capable of causing serious hemolytic rxns

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44
Q

why not T&C every patient for surgery?

A

need 1-2d minimum for PRBCs to be removed from circulation and reserved for pt – leading to higher incidence of PRBC expiration

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45
Q

Is a T&C necessary for all pts?

A

*yes for ABO/Rh compatibility

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46
Q

what are the reaction prevention percentages of the three typing procedures?

A 
blood typing (alone) prevents reactions in 99.8% of cases
type and screen prevents serious reactions in 99.94% of cases
type and cross prevents serious reactions in 99.95% of cases
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47
Q

what are the best, next best, and most often scenarios of blood transfusion in trauma and emergency cases?

A

Best: typed and partially crossed (ABO-Rh & immediate-phase (major ABO rxns)
Next best: typed and uncrossed (caution for those who have previously had transfusion or previously pregnant)
Most often: type O, Rh-negative uncrossed (PRBCs)

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48
Q

why is type O, Rh-negative most often given in trauma, emergency scenarios?

A

type O blood lacks A and B antigens; cannot be hemolyzed by anti-A or -B antibodies in the recipients blood

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49
Q

why are type O, Rh-negative PRBCs (vs. whole blood) given in trauma, emergency scenarios?

A

some type O donors produce high titers of hemolytic ommunoglobulin (IgG), IgM, anti-A and anti-B antibodies; use of PRBCs reduces risks associated with these

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50
Q

describe what is meant by the point of no return when administering O-negative blood in trauma, emergency situations

A

switching to correct T&C blood after administration of > 2-4 units O-negative PRBCs can cause major intravascular hemolysis of donor RBCs by increasing titers of anti-A and anti-B, thus increasing risk of immune system response

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51
Q

what are the positive effects of giving PRBCs?

A

1 unit PRBCs increases Hg by 1-2gm/dl, Hct by 3-5%

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52
Q

what are the four major negative effects of PRBCs?

A
  1. decreased 2,3-DPG levels (decreased O2 offloading)
  2. thrombocytopenia (low platelets decreased clotting/free bleeding)
  3. decreased factor V, fibrinogen, factor VII levels (decreased clot formation/coagulation)
  4. citrate intoxication (can lead to hypocalcemia => hypotension, decreased pulse pressure, arrhythmias)
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53
Q

how does blood loss change as the classification for acute hemorrhage increases?

A

blood loss increases from 750 to ≥ 2000ml from class I to class IV (from 15 to ≥ 40% of volume)

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54
Q

how does pulse, blood pressure, and pulse pressure change from class I to class IV acute hemorrhage?

A 
pulse increases from 100 to ≥ 140 from class II to IV
blood pressure decreases from class II to IV
puls pressure remains normal (or increased) for class I, but decreases as the class of hemorrhage increases
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55
Q

how does the respiratory rate change from class I to class IV acute hemorrhage?

A

respiratory rates increase from 14-20 bpm to 35 bpm

56
Q

how does urine output change from class I to class IV acute hemorrhage?

A

urine output decreases to almost negligible as acute hemorrhage class increases

57
Q

how does mental status change as acute hemorrhage class increases?

A

pt goes from slightly anxious to anxious, confused, and lethargic

58
Q

what is the storage time/conditions for fresh whole blood?

A

1hr to 5 days before administration

stored at RT for a few hours; cooled for remainder

59
Q

how does whole blood compare to PRBCs after 35d?

pH? plasma hemoglobin? plasma potassium? plasma sodium? blood dextrose? DPG? percent survival?

A

pH: roughly the same (6.73 vs. 6.71)
plasma hemoglobin: lower (46 vs. 246mg/dl)
plasma potassium: lower (17.2 vs. 76mEq/L)
plasma sodium: higher (153 vs. 122mEq/L)
blood dextrose: higher (282 vs. 84mg/dl)
DPG: same (1.0M/ml)
percent survival: slightly higher (79% vs. 71%)

60
Q

what are the three types of autologous blood transfusions?

A

preoperative autologous donation (PAD)
acute normovolemic hemodilution (ANH)
intraoperative blood recovery (cell saver)

61
Q

what are the criteria for preoperative autologous donation (PAD)?

A
  • only for elective surgeries with high risk of blood transfusion
  • baseline Hg ≥ 11.5g/dl, Hct ≥ 34.5% before donation (max donation 10.5ml/kg blood)
  • donations 1-2x/week * erythropoietin supplementation
  • last donation ≥ 72hr before surgery
62
Q

what are the benefits of PAD?

A
  • avoidance of adverse PRBC reactions
  • avoid using valuable red cross supplies
  • lower risk of infection
  • provides patients with rare blood phenotypes and antibodies with safer blood
63
Q

what are the drawbacks of PAD?

A
  • perioperative anemia (if RBCs don’t replenish in time)
  • preoperative MI risk
  • administration to wrong patient
  • higher cost to system
  • less stringent donor criteria
64
Q

describe acute normovolemic hemodilution

A

the removal of whole blood from pt while restoring the circulating blood volume with an acellular fluid shortly before an anticipated significant surgical blood loss – reducing RBC loss intraoperatively/ iatrogenic lowering of Hct. blood is returned to circulation after blood loss

65
Q

what is the target Hct of ANH?

A

~28%

66
Q

how are crystalloids/colloids administered to compensate for the blood loss after ANH?

A

3: 1 – crystalloid:blood
1: 1 – colloid:blood

67
Q

what order are ANH blood units reinfused after surgical loss?

A

blood units are reinfused in the reverse order of collection; the first unit collected is the last to be infused bc it has highest Hct and concentration of coagulation factors and platelets

68
Q

calculate estimated blood volume (formula)

A

EBV = weight (kg) X average blood volume

69
Q

what is the average blood volume for a premature neonate? a full term neonate? an infant? an adult man? an adult woman?

A

premature neonates: 95ml/kg
full term neonates: 85ml/kg infants: 80ml/kg
adult men: 75ml/kg
adult women: 65ml/kg

70
Q

calculate allowable blood loss (formula)

A

(EBV x (Hi - Hf)) / Hi = ABL

  • Hi = initial Hct
  • Hf = final lowest acceptable Hct
71
Q

what are the patient selection criteria for ANH?

A
  • likelihood of transfusion exceeding 10% blood volume (ANH ≤ 15% blood volume = 0.5 unit PRBCs saved; ANH to 28% Hct = 3 units ANH = 1 unit PRBCs saved)
  • preoperative Hg ≥ 12g/dl
  • absence of clinically significant coronary, pulmonary, renal, or liver disease
  • absence of sever hypertension
  • absence of infection and risk of bacteremia
72
Q

what are the benefits of ANH?

A
  • less risk of adverse reactions to PRBCs
  • avoid using valuable red cross supplies
  • oxygenation of tissues with ANH usually unchanged
  • preservation of hemostasis: coagulation factors and platelet levels/function still high after 8hrs of storage
  • minimal time and cost
  • no preoperative testing needed
  • minimal clerical or administrative errors
  • minimal bacterial contamination
73
Q

what are the drawbacks of ANH?

A
  • may result in signs and symptoms of hypovolemia if volume replacement not done
  • theoretical risk of bacterial growth past 6hr of storage => bacteremia
74
Q

describe the technique used for cell saver technology

A

blood suctioned/collected from wound/pools under surgical site, washed, and concentrated into 225ml units with Hct 50-60%; reinfused in patient during surgery
* provides the equivalent of (max) 12u/hr of banked blood (to a massively bleeding pt)

75
Q

how long can cell-saver blood be stored at room temp?

A

≤ 4hr

76
Q

what are the indications for use of cell saver?

A

only for surgeries with higher blood loss

  • orthopedic and cardiac surgeries
  • cost effectiveness with 1- 2 units
  • slow bleeding has higher levels of hemolyzed blood and thus suboptimal cell saver blood
77
Q

what are the benefits of cell saver?

A

basically the same as that of ANH

  • same efficacy and survival as PRBCs
  • avoidance of adverse reactions to PRBCs
  • avoid using valuable red cross supplies
  • no preoperative testing needed
  • minimal clerical or administrative errors
  • minimal bacterial contamination
78
Q

what are the drawbacks of cell saver?

A
  • some surgical substances (topical collagen; i.e., methylmethacrylate) cause systemic inflammation and prevent cell saver use
  • suctioning can cause hemolysis (max vacuum setting of 150mmHg recommended => free Hg
  • potential nephrotoxicity with large amounts of cell saver blood due to higher serum free Hg levels (free Hg is toxic to kidneys)
79
Q

which coagulation pathways do partial thromboplastin time (PTT) and PT/INR measure?

A

PTT measures the intrinsic coagulation pathway PT/INR measures the extrinsic coagulation pathway

80
Q

describe plasma mediated hemostasis

A

plasma proteins, activated by exposure to tissue factor or foreign surfaces, initiate a cascading series of reactions culminating in conversion of soluble fibrinogen to insoluble fibrin clot
* an amplification system to accelerate thrombin generation from an inactive precursor (i.e., prothrombin)

81
Q

which pathway of the coagulation cascade is the initiating step in plasma-mediated hemostasis?

A

the extrinsic pathway; begins with exposure of blood plasma to tissue factor

82
Q

which pathway of the coagulation cascade is the amplification system of plasma-mediated hemostasis?

A

the intrinsic pathway: amplifies thrombin generation initiated by the extrinsic pathway

83
Q

what are normal values for PT, INR, and PTT

A

PT: 11.5-13sec
INR: 0.8-1.1 (no unit of measure)
PTT: 25-35sec (~2x PT)

84
Q

what do PT, INR, and PTT measure?

A

PT (prothrombin time): measures how long it takes blood to clot
INR (international normalized ratio): standardization of PT tests, regardless of the testing method
PTT (partial thromboplastin time): measures how long it takes for blood to coagulate

85
Q

what is the most frequently used plasma product?

A

FFP (fresh frozen plasma); 200-250ml volumes; stored at 4ºC

86
Q

what does FFP contain?

A

all plasma proteins and fibrinogen – particularly factors V and VIII; does not contain RBCs

87
Q

how is FFP tested?

A

FFP is ABO tested; Rh compatibility not necessary

88
Q

according to 2006 ASA recommendations, when do we give FFP? (5)

A
  1. replacement of inherited single coagulation factor deficiencies for which no virus-safe products exist
  2. replacement of multiple coagulation factor deficiencies with associated bleeding, DIC, or both
  3. as a component of plasma exchange in pts with thrombotic thrombocytopenic purpura
  4. reversal of warfarin anticoagulation when severe bleeding is present and prothrombin complex concentrations are not available
  5. prevention of dilutional coagulopathy in pts with major trauma and/or massive hemorrhage
89
Q

according to AABB transfusion practices committee, when should you give FFP? (3)

A
  1. trauma patients with substantial hemorrhage
  2. complex CTS patients
  3. ICH (intracerebral hemorrhage) patients needing emergent reversal of warfarin induced coagulopathy
90
Q

according to Miller’s anesthesia, when should FFP be administered? (3 sequential)

A
  1. generalized bleeding that cannot be controlled with surgical sutures or cautery, AND
  2. PTT ≥ 1.5x normal (nl 25-35sec), AND
  3. platelet count > 70,000/mm3 (to rule out thrombocytopenia)
91
Q

name two disease processes that do not need FFP

A

liver disease and elevated INR (nl: 0.8-1.1)

92
Q

how much does 1 unit FFP increase clotting factor?

A

1 unit FFP increases clotting factor level by 2-3%

93
Q

what is the dosing of FFP necessary to restore clotting factors to 30-50% of nl with warfarin toxicity?

A

15-30ml/kg

* not realistic because you don’t start out at zero, and you don’t need to get to 100%…ever

94
Q

what is a normal value for platelets?

A

150,000-400,000 plts/µL

95
Q

what are platelets (for transfusion)?

A

platelets with minimal plasma or RBCs

  • about 180-360ml/bag
  • either pooled concentrations from 4-6 donors or apheresis from one donor
96
Q

how long can platelets be stored?

A

stored at RT on agitator – expire 7d after collection

97
Q

what tests are platelets subjected to?

A

ABO testing (difficult but done)
* if possible use ABO compatible plts, but use of ABO incompatible plts produce good hemostasis
(possible hemolytic reaction with large volumes of plts)

98
Q

in what instances does the ASA suggest that platelet transfusion is not indicated?

A
  • when thrombocytopenia is due to increased platelet destruction (idiopathic throbocytic purpura)
  • in surgical patients with thrombocytopenia because of decreased platelet production when platelet count is greater than 100k/µL
99
Q

in what instances does the ASA suggest that platelet transfusion is indicated?

A

platelet counts ≤ 50k/µL – surgical and obstetric patients
* with intermediate platelet counts (50k to 100k/µL), the determination should be based on the patient’s risk for more significant bleeding

100
Q

by how much does 1 unit of plts increase platelet counts?

A

1 unit of plt concentrate increases plt count by 7k-10k plts/µl at 1hr post transfusion

  • pooled and apheresis platelet bags are usually 4-6u, thus 1 bag = 28k-60k plts/µL
  • about 10u needed (~2 bags) for 100k increase
101
Q

what are the most aggressive transfusion ratios?

A

1.5 PRBCs:1 FFP; 6 PRBCs: 1 bag of plts

102
Q

what are the risks for aggressive FFP transfusions?

A

higher incidence of TRALI, acute respiratory distress syndrome (ARDS), and organ dysfunction

103
Q

what is the normal fibrinogen level?

A

200-400mg/dl

104
Q

what is cryoprecipitate?

A

concentrated factor VIII, fibrinogen, factor XIII, and vWF

105
Q

how much fibrinogen is in each bag of cryoprecipitate?

A

each bag has 5u cryoprecipitate; each unit has 200-600mg fibrinogen, thus each bag has 1000-3000mg fibrinogen

106
Q

how is cryoprecipitate stored?

A

stored frozen at -40ºC and thawed for use

* once thawed, must be used within 6hr; cannot be refrozen

107
Q

what method of testing is most important for cryoprecipitate?

A

although ABO testing is done, and cryoprecipitate often give as ABO compatible, Rh testing is more important!
* RBC fragments may cause Rh sensitization in an Rh negative patient (same Rh precautions apply as with PRBCs)

108
Q

when do we give cryoprecipitate? (3)

A
  1. factor VIII deficiency
  2. hemophilia A (genetic factor VIII deficiency)
  3. low fibrinogen states – surgically:
    * major aortic surgery using CPB
    * open heart surgery involving > 1 valve
    * “redo” open heart surgery with combined valve/CABG
109
Q

according to 2006 ASA recommendations, when should fibrinogen supplementation begin? what is the target level?

A

when fibrinogen

110
Q

in an actively bleeding patient where fibrinogen is being consumed, what is the target fibrinogen level increased to?

A

≥ 250mg/dl

111
Q

how much fibrinogen is in 2 bags of cryoprecipitate, and how much does it raise body levels of fibrinogen?

A

10u (2 bags) have 3g of fibrinogen; 3g fibrinogen raises body levels 80-100mg/dl in a non-obese patient

112
Q

what is the emory protocol for post CPB based on CPB-60 fibrinogen levels?

A

> 250mg/dl = no cryoprecipitate
201-250mg/dl = 5u (1bag)
151-200mg/dl = 10u
101-150mg/dl = 15u

113
Q

when giving platelets and cryoprecipitate, which is given first and why?

A

give cryoprecipitate first; factor VIII and vWF in cryoprecipitate help platelets adhere to endothelium

114
Q

what is prothrombin complex concentrate (PCC)?

A

concentrated factors II, VII, IX and X

* while from humans, they do not cause blood transfusion reactions

115
Q

when do we give PCC? (4)

A
  1. factor IX deficiency
  2. hemophilia B (genetic factor IX deficiency)
  3. severe acute bleeding
  4. warfarin reversal/overdose (preparations with factor VII)
116
Q

what are the risks associated with PCC?

A
  • risk of hepatitis
  • increased thrombogenecity
  • donor pools of 3,000-20,000 ppl; potential for pathogen transmission
117
Q

what is fibrinogen concentrate?

A

fibrinogen from human plasma, but just fibrinogen (no blood transfusion reactions documented)
* not usually on formula for hospital-based fibrinogen replacement

118
Q

when do we give factor VII?

A
  • hemophilia A (factor VIII deficiency)
  • factor VII deficiency
  • inherited qualitative platelet disorders
  • an adjunct with thrombocytopenia
  • off label for profuse bleeding
  • off label for warfarin reversal when vitamin K is not working
119
Q

what are the study dosage ranges for factor VII?

A

15-180µg/kg

120
Q

what is the recommended dosage of factor VII?

A

one 4.8mg vial per does to 50-100kg patient (50-100µg/kg dose)

121
Q

what is the most common transfusion related cause of fatality?

A

TRALI

122
Q

what is the biggest cause of hemolytic transfusion reactions?

A

PRBCs – ABO incompatibility (occurs with ≥ 10ml wrong PRBCs)

123
Q

what are the effects of hemolytic transfusion reactions?

A

patient’s antibodies lyse donor RBCs leading to:

  • anemia
  • hypotension
  • Hg nephrotoxicity (hemoglobinuria, renal failure)
  • DIC (disseminated intravascular coagulopathy)
  • flu-like symptoms
124
Q

what is the treatment for hemolytic transfusion reactions?

A
  1. STOP THE TRANSFUSION!!!!
  2. maintain urine output at a minimum of 75-100ml/hr (generous administration of fluids/mannitol 12.5-50g given over 5-15min OR furosemide 20-40mg IV)
  3. alkalinize the urine (40-70mEq sodium bicarbonate/70kg body weight will raise urine pH to 8)
  4. labs: urine and plasma haptoglobin and hemoglobin, bilirubin, PT, PTT, platelet count, direct antiglobulin
  5. inform blood bank; return unused blood to blood bank for repeat crossmatch
  6. send patient’s blood and urine sample to blood bank for examination
  7. prevent hypotension to ensure adequate renal blood flow
125
Q

what are delayed hemolytic transfusion reactions (immune extravascular reactions)?

A
  • a PRBC problem
  • usually patients who have “lesser” antibodies to antigens (kell, kidd, duffy, and Rh – patients formerly pregnant or previously given PRBCs)
  • slow immune system response (2-21 days s/p PRBC transfusion; extravascular hemolysis)
126
Q

what are the effects of delayed hemolytic transfusion reactions?

A
  • usually just reduced Hg levels

* less common: jaundice, hemoglobinuria, renal dysfunction

127
Q

what are non-hemolytic transfusion reactions?

A
  • involves PRBCs, FFP, platelets, cryo, but most often PRBCs
  • fever and flu-like symptoms (from donor WBCs)
  • allergic reactions – usually minor; caused by the presence of foreign protein in the transfused blood
128
Q

what are the treatments and preventative methods for non-hemolytic transfusion reactions?

A
  • fever and flu-like symptoms: prevent with leukoreduced vs. irradiated blood
  • minor allergic reactions: treat with antihistamines
  • full anaphylaxis: treat by stopping transfusion and treat anaphylaxis as normal; prevent with IgA washed blood
129
Q

what is TRALI?

A
  • involves PRBCs, FFP, platelets and cryo, but most often FFP
  • most common cause of transfusion related deaths
  • occurs in the absence of excessive intravascular volume and cardiac failure
  • donor antibodies interact with recipient WBCs, causing WBCs to aggregate in the lungs
130
Q

what are the effects of TRALI?

A

noncardiogenic pulmonary edema, hypoxia, fever and respiratory failure
* symptoms 1-2hr after transfusion; near peak severity 6hrs after transfusion

131
Q

what is the treatment for TRALI?

A
  1. stop the transfusion (if still going)
  2. supportive measures
  3. inform blood bank
  4. await resolution of symptoms (most patients do recover within 96hr)
132
Q

what is TACO, what are the blood products involved, and what is the treatment?

A

TACO – transfusion-associated circulatory overload – excessive administration of blood associated with all products
* Tx: decrease rate of infusion, administration of diuretics

133
Q

what is TRIM, what are blood products involved?

A

TRIM – transfusion-related immunomodulation – PRBCs – suppression of the immune system bc of circulating lymphocytes

134
Q

what is microchimerism and what blood products are involved?

A

all products – donor lymphocytes persistent in a pt.

135
Q

what is post transfusion purpura, what blood products are involved and what is the treatment?

A

recipient aloo-antibodies attacking donor platelet antigens associated with PRBCs and platelets especially
* Tx: intravenous immunoglobin

136
Q

what is the highest infection risk associated with transfusion?

A

HBV – 1:280,000

ANESTHESIA PRACTICE 2 (5 decks)

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