BLOOD COMPONENT THERAPY 2002 EVAN G. PIVALIZZA, FFA Department of Anesthesiology University of Texas...
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Transcript of BLOOD COMPONENT THERAPY 2002 EVAN G. PIVALIZZA, FFA Department of Anesthesiology University of Texas...
BLOOD COMPONENT BLOOD COMPONENT THERAPYTHERAPY
2002
EVAN G. PIVALIZZA, FFA
Department of Anesthesiology
University of Texas at Houston
A. BLOOD PRODUCTSA. BLOOD PRODUCTS
22 x 106 components p.a.
50-70 % peri-operatively
18-57% inappropriate (NIH reviews in 80’s)
Blood preservation and Blood preservation and storagestorage
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)
DODO22 / VO / VO22
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 Indications for PRBC transfusiontransfusion
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 transfusionIndications 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 Indications for cryoprecipitate transfusiontransfusion
10 ml: fibrinogen (150-250 mg), VIII (80-145 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 Indications for platelet transfusiontransfusion
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 B. TRANSFUSION REACTIONSREACTIONS
RBC’s Nonhemolytic
– 1-5 % transfusions: fever, chills, urticaria– Slow transfusion, diphenhydramine
Hemolytic– Immediate: ABO incompatibility (1/ 12-
33,000) 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 C. INFECTIOUS COMPLICATIONSCOMPLICATIONS
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, 10-20
% 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 UKTF 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 D. METABOLIC COMPLICATIONSCOMPLICATIONS
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. REFERENCESE. 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