BLOOD COMPONENT THERAPY
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Transcript BLOOD COMPONENT THERAPY
BLOOD COMPONENT
THERAPY
2002
EVAN G. PIVALIZZA, FFA
Department of Anesthesiology
University of Texas at Houston
A. BLOOD PRODUCTS
22 x 106 components p.a.
50-70 % peri-operatively
18-57% inappropriate (NIH reviews in 80’s)
Blood preservation and
storage
75 % RBC’s in circulation @ 24 hrs
Within 4 hrs, WB separated
WB: 63 ml preservative (HCT 36-40%)
– CPD- A (citrate, phosphate, dextrose, adenine)
shelf-life 35 days @ 1-60 C
PRBC: (HCT 60%)
– CPD-A
– ADSOL (adenine, dextrose, saline, mannitol)
shelf-life 42 days
Deglycerolized blood
– Frozen with glycerol for storage, washed before
transfusion (years)
Leucocyte depleted blood (see later)
Washed (IgA deficiency)
DO2 / VO2
DO2 = CO x [(Hb x SaO2 x 1.34) + PaO2 x
0.003]
Flow pressure, 1/R4, viscosity
Balance hematocrit/ viscosity + 30%
Compensations chronic anemia
– viscosity = flow, venous return, SV
– O2 extraction except cardiac and cerebral
circulation
– O2 DC shifted to right
– DO2 adequate to Hct 18-25%
Indications for PRBC
transfusion
ONLY: Increase O2 carrying capacity
Use of single ‘trigger’ transfusion inappropriate
TRICC: ? more conservative trigger in ICU (7-9
vs 10-12)
– NOT apply to > 55, bleeding, cardiac surgery
Determination transfusion based patient risks for
complication of inadequate DO2
10 ml/kg Hct 10 %
Indications for FFP transfusion
2 million units p.a.
200-260 ml: procoagulants (1U/ml) and fibrinogen
(3-4 mg/ml)
Urgent reversal of coumadin therapy (5-8 ml/ kg)
Correction of known coagulation factor
deficiencies (no concentrates available) to + 30%
(10-15 ml/ kg)
Microvascular bleeding with PT/ PTT > 1.5
normal
Massive BT with microvascular bleeding
– >1 BV/ 24 hours
– > 50 % BV within 3 hrs
– > 150 ml/min
Plasmapheresis for TTP
AT-III deficiency
Succinylcholine apnea
– S.D plasma
– Pooled plasma, Rx solvent and detergent
– Virus inactivated, bacteria, WBCs
– Consistent coagulation factors (1 U 2-3%)
BUT:
– Cost
– ? Transmission unknown particles
Indications for cryoprecipitate
transfusion
10 ml: fibrinogen (150-250 mg), VIII (80145 U), fibronectin, XIII
1U/ 10kg fibrinogen 50 mg/dL (usually a
6- pack)
Hypofibrinogenemia (congenital or
acquired)
Microvascular bleeding with massive BT
(fibrinogen < 80-100mg/dL)
– 2 BVs = < 100 mg/dL
Bleeding patients with vWD (or
unresponsive to DDAVP)
Indications for platelet
transfusion
7 million units p.a.
50 ml: 0.5- 0.6 x 10 9 platelets (some RBC’s
and WBC’s)
Single donor apheresis OR
Random donor (x 6)
Decreased production
Prophylactic for surgical patient with
platelets < 50,000
Microvascular bleeding in surgical patient
with platelets < 50,000
Neuro/ ocular surgery > 75,000
Massive transfusion with microvascular
bleeding with platelets < 100,000
– 2 BVs = 50,000
Qualitative dysfunction with microvascular
bleeding (may be > 100,000)
Assessment of platelet function (TEG,
Sonoclot) in O.R.
B. TRANSFUSION
REACTIONS
RBC’s
Nonhemolytic
– 1-5 % transfusions: fever, chills, urticaria
– Slow transfusion, diphenhydramine
Hemolytic
– Immediate: ABO incompatibility (1/ 1233,000) with fatality (1/ 500-800,000)
– Majority are group O patients receiving
type A, B or AB blood
Anesthesiologist major trauma hospital:
Transmit HIV once / 1,000 years
Hep C 200
Hep B 100
Administer incorrect blood 30
– UK: 1996-99 – 97 life-threatening
ABO incompatible transfusions
Complement
activation, RBC lysis, free
Hb (+ direct Coombs Ab test)
– Anesthesia: hypotension, urticaria,
abnormal bleeding
– Stop infusion, blood and urine to blood
bank, coagulation screen (urine/plasma Hb,
haptoglobin)
– Fluid therapy and osmotic diuresis
– Alkalinization of urine (increase solubility
of Hb degradation products)
– Delayed: (extravascular immune)
– 1/ 5-10,000
– Hemolysis 1-2 weeks after transfusion
(reappearance of Ab against donor Ag from
previous exposure)
– Fever, anemia, jaundice
– Alloimmunization
– Recipient produces Ab’s against RBC
membrane Ag
– Related to future delayed hemolytic reactions
and difficulty crossmatching
WBC’s
Europe: All products leukodepleted
USA: Initial FDA recommendation now reversed
pending objective data (NOT length of stay for
expense)
Febrile reactions
– Recipient Ab reacts with donor Ag, stimulates pyrogens
(1-2 % transfusions)
– 20 - 30% of platelet transfusions
– Slow transfusion, antipyretic, meperidine for shivering
TRALI (Transfusion related acute lung
injury)
– Donor Ab reacts with recipient Ag (1/ 10,000
but causes 15 % of mortality due to BT)
– Noncardiogenic pulmonary edema
– Supportive therapy
– ? relation to multiparous donors (> 4
pregnancies)
GVHD
– Rare: immunocompromised patients
– Suggestion that more common with designated
donors
– BMT, LBW neonates, Hodgkin's disease,
exchange Tx in neonates
Platelets
Alloimmunization
– 50 % of repeated platelet transfusions
– Ab-dependent elimination of platelets with lack
of response
– Use single donor apheresis
Post-transfusion purpura
– Recipient Ab leads to sudden destruction of
platelets 1-2 weeks after transfusion (sudden
onset)
Immunomodulatory effects of transfusion
Wound infection: circumstantial evidence (?
leukocyte filters for immunocompromised)
Beneficial effects on renal graft survival
(now < NB with CyA)
– 97: 9% graft survival advantage after 5 years
Nonspecific overload of RES
– lymphocytes, APCs
– Modification T helper/suppressor ratio
– Allogeneic lymphocytes may circulate for years
after transfusion
Cancer recurrence (mostly retrospective)
– Colon: 90 % studies suggest increased
recurrence
– Breast: 70 % studies
– Head and neck: 75 % studies
“Allogeneic blood products increase cancer
recurrence after potentially curative surgical
resection” - Landers
Evidence circumstantial NOT causal
However, 2 recent prospective, randomized
studies: no effect on tumor related
morbidity/mortality, but poorer outcomes
Conservative trigger (< 3 units)
Clinical judgment to weigh risk-benefit
ratio
C. INFECTIOUS
COMPLICATIONS
I. Viral (Hepatitis 88% of per unit viral risk)
Hepatitis B
Risk 1/ 200,000 due to HBsAg, antiHBc
screening (7-17 % of PTH)
Per unit risk 1/63-66,000
0.002% residual HBV remains in ‘negative’
donors (window 2-16 weeks)
Anti-HBc testing retained as surrogate
marker for HIV
NANB and Hepatitis C
Risk now 1/ 103,000 (NEJM 96) with 2nd/
1/ 125,000 with 3rd generation HCV Ab/
HVC RNA tests
Window 4 weeks
70 % patients become chronic carriers, 1020 % develop cirrhosis
HIV
29 cases -transfusion recipients 93
7,800 by 12/ 95
Current risk 1/ 450- 660,000 (95)
With current screening (Abs to HIV I, II and
p24 Ag), window 6-8 weeks (third
generation ELISA tests in Europe)
sero -ve window to < 16 days
HTLV I, II
Only in cellular components (not FFP, cryo)
Risk 1/ 641,000 (window period unknown)
Screening for antibody I may not pick up II
CMV
Cellular components only
Problem in immunocompromised, although
80 % adults have serum Ab
WBC filtration decreases risk of
transmission
CMV -ve blood:
– CMV -ve pregnant patients, LBW
neonates, CMV -ve transplant recipient,
– CMV-ve/ HIV +ve
CJD (and variant CJD)
BB implementing donor deferrals
– 1980-96:
> 3 months UK
TF in UK
> 5 years in France
II. Bacterial
Contamination unlikely in products stored
for > 72 hours at 1-6 0 C (10 cases Yersinia)
Platelets stored at room temperature for 5
days, with infection rate of 0.25%
III. Protozoal
Trypanosoma cruzi (Chaga’s disease)
D. METABOLIC
COMPLICATIONS
Citrate toxicity
Citrate (3G/ unit WB) binds Ca2+ / Mg+
Metabolized liver, mobilization bone stores
Hypocalcemia ONLY if > 1 unit/ 5 min or
hepatic dysfunction
Hypotension more likely due to cardiac
output/ perfusion than calcium (except
neonates)
Worse with hypothermia/ hepatic
dysfunction
Hyperkalemia
After 3 weeks, K+ is 25- 30 mmol/l
Only 8- 15 mmol per unit PRBC/ WB
Concern with > 1 unit/5 min @ infants
Acidosis
Acid load after after 3 weeks 30-40 mmol/l
(pH 6.6 - 6.9)
Metabolic acidosis more likely due to
decreased perfusion, hepatic impairment,
hypothermia
NaHCO3 or THAM if base deficit > 7-10
mEq/l
2, 3 DPG
Depleted within 96 hours of storage
O2 Hb DC to left
Restored within 8- 24 hours of transfusion
E. REFERENCES
Practice Guidelines for Blood Component
Therapy (ASA Task Force). Anesthesiology
1996; 84: 732-47.
Safety of the Blood Supply. JAMA 1995;
274:1368--73.
Infectious Disease Testing for Blood
Transfusions (NIH Consensus Conference).
JAMA 1995; 274: 1374-9.
Blood Transfusion- Induced
Immunomodulation. Anesth Analg 1996;
82: 187-204
ASA Questions and Answers about
Transfusion Practices (3rd ed., 1997)
Immunomodulatory aspects of transfusion.
Anesthesiology 1999; 91: 861-5.
“Blood is still the best possible thing to
have in our veins” - Woody Allen
“Blood transfusion is a lot like marriage. It
should not be entered upon lightly,
unadvisedly or wantonly, or more often than
is absolutely necessary” - Beal