2. Topic modules
1. Blood blank practices
2. Indication to blood transfusion
3. Complication
4. Alternative strategies for management of
blood loss during surgery
3. Blood blank practices
1. Human red cell membrane : least 300
different antigen
2. fortunately, only the ABO and the Rh
systems are important in the majority of
blood transfusion
3. History
Hct.
Infection : Hepatitis B,C syphillis HIV-1,2
HTLV-I,II
4. #Crossmatching (50 min)
1) Confirms ABO and Rh typing
2) Detects antibodies to the other
blood group systems
3) Detects antibodies in low titers or
those that do not agglutinate easily
Blood blank practices
5. Blood blank practices
# Antibody screen : Indirect Coombs test
(45 mins)
the subject serum + red cells
( antigenic composition) ----- red cell agglutination
# Type&screen
# Emergency transfusion
6. T&S -determines ABO and Rh status and the
presence of most commonly encountered
antibodies – risk of adverse rxn is 1:1000
-takes about 5 mins
T&C -determines ABO and Rh status as well
as adverse rxn to even low incidence
antigens – risk of rxn is 1:10,000
-takes about 45 mins
Type and screen vs Type and crossmatch
7. Type and screen vs Type and crossmatch
T&S:
Type O red cells are mixed with pt serum Antibody screen
T&C
Type O red cells are mixed with pt serum Antibody screen
Donor red cells are then mixed with the pt’s serum
to determine possible incompatibility
:
8. Blood blank practices
All units – RBC @ PRC 1unit (250 ml
Hct.70%)
--platelet@ 1 unit (50-70 ml, stored at
20-24c for 5 days)
--plasma @ FFP
--cryoprecipitate @ high conc. Of
factor VII, fibrinogen
9. Intraoperative transfusion practices
1. PRC
Ideal for patients requiring red cells but not volume replacement
Only one – Increase O2 carrying capacity
AGE BLOOD VOLUME
Neonates
Premature 95 ml/kg
Full-term 85 ml/kg
Infants 80 ml/kg
Adults
Men 75 ml/kg
Women 65 ml/kg
Allowable blood loss = EBV*( Hctตั้งต้น –Hctที่ยอมรับได้)/ Hctเฉลี่ย
Hct. 30% not magic number
Jehovah” s witness
10. Practice guideline
$$ case series : reports of Jehovah witness;
some may tolerate very low Hb< 6-8 g/dl in
the perioperative period without an incresae
in mortality
11. Practice guideline
$$ In healthy, normovolemic individual, tissue
oxygenation is maintained and anemia tolerated
at Hct as low as 18-25%(Hb 6-8gm%)
$$ RBC transfusion is rarely indicated when Hb> 10
g/dl and is almost always indicated when Hb< 6
g/dl
American Society Anesthesiologist : 1996
17. Intraoperative transfusion practices
4. CRYOPRECIPITATE
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)
18. Alternative strategies for management of blood loss
during surgery
1) Autologous transfusion
2) Blood salvage & refusion
3) Normovolemic hemodilution
19.
20. “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
22. TRANSFUSION REACTIONS
• is any unfavorable transfusion-related event
occurring in a patient during or after transfusion of
blood components
23. TRANSFUSION REACTIONS
@RBC’s !
• Nonhemolytic 1-5 % transfusions
Causes -Physical or chemical destruction of
blood: freezing, heating, hemolytic drug
-solution added to blood
-Bacterial contamination
: fever, chills, urticaria
– Slow transfusion, diphenhydramine , antipyretic for fever
• 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
Complement activation, RBC lysis, free Hb (+ direct Coombs Ab
test)
24. Acute Hemolytic Transfusion Reaction
Ab (in recipient serum) + Ag (on RBC donor)
-Neuroendocrine responses
-Complement Activation
-Coagulation Activation
- Cytokines Effects
Acute hemolytic transfusion reaction
Pathophysiology
25. Acute Hemolytic Transfusion Reactions
Acute onset within minutes or 1-2 hours
after transfuse incompatible blood
Most common cause is ABO-incompatible
transfusion
27. – 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)
– Correct bleeding, Rx. DIC
28. Laboratory investigation for AHTR
• sample from blood bag Repeat ABO, Rh, Ab screening
• Patient sample
Pre Tx sample Repeat ABO, Rh, Ab screening
Post Tx sample Repeat ABO, Rh, Ab screening, DAT,
CBC, UA, Bilirubin, BUN, Cr,
Coagulation screening
• Repeat compatibility test
- Pre Tx sample & Donor unit
- Post Tx sample & Donor unit
29. – 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
30. @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
31. • TRALI (Transfusion related acute lung injury)
– Donor Ab reacts with recipient Ag (1/ 10,000)
– noncardiogenic pulmonary edema
– Supportive therapy
32. Transfusion-related Acute Lung Injury
(TRALI)
Pathophysiology
Leukocyte Ab in donor react with pt. leukocytes
Activate complements
Adherence of granulocytes to pulmonary
endothelium with release of proteolytic enz.&
toxic O2
metabolites
Endothelial damage
Interstitial edema and fluid in alveoli
33. Transfusion-related Acute Lung Injury
(TRALI)
Acute and severe type of transfusion reaction
Symptoms and signs
• Fever
• Hypotension
• Tachypnea
• Dyspnea
• Diffuse pulmonary infiltration on X-rays
• Clinical of noncardiogenic pumonary edema
34. Transfusion-related Acute Lung Injury
(TRALI)
Therapy and Prevention
• Adequate respiratory and hemodynamic
supportive treatment
• If TRALI is caused by pt. Ab use LPB
• If TRALI is caused by donor Ab no special
blood components
35. • Transfusion-associated Graft-versus-Host
Disease ( TA-GVHD)
– Rare: immunocompromised patients
– Suggestion that more common with
designated donors
– BMT, LBW neonates, Hodgkin's disease,
exchange Tx in neonates
36. Transfusion-associated Graft-versus-Host
Disease ( TA-GVHD)
Pathophysiology
Infusion of Immunocompetent Cells
(Lymphocyte)
Patient at risk
proliferation of donor T lymphocytes
attack against patient tissue
37. Graft-versus-Host Reaction
Signs & Symptoms
Onset ~ 3 to 30 days after transfusion
Clinical significant – pancytopenia
Other effects include fever, liver enzyme,
copious watery diarrhea,
erythematous skin erythroderma
and desquamation
38. @Platelets!
Alloimmunization
– 50 % of repeated platelet transfusions
– Ab-dependent elimination of platelets with lack of response
– Use single donor apheresis
– Signs & Symptoms
• mild slight fever and Hb
• severe platelet refractoriness with bleeding
Post-transfusion purpura
– Recipient Ab leads to sudden destruction of platelets
1-2 weeks after transfusion (sudden onset)
– Rare complication
39. 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
40. • 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
41. 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
42. 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
43. HIV
• 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
44. 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
CJD (and variant CJD)
45. 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
46. II. Bacterial
• Contamination unlikely in products stored for > 72
hours at 1-6 0 C
• gram –ve, gram +ve bacteria
most frequent – Yersinia enterocolitica
Produced endotoxin
Platelets stored at room temperature for 5 days, with
infection rate of 0.25%
III. Protozoal
• Trypanosoma cruzi (Chaga’s disease)
• Malaria
• Toxoplasmosis
• Leishmaniasis
48. 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
49. 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
50. 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
51. 2, 3 DPG
• Depleted within 96 hours of storage
• O2 Hb DC to left
• Restored within 8- 24 hours of
transfusion
52. 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.