Download Blood transfusion

Blood transfusion
Topic modules
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2.
3.
4.
Blood blank practices
Indication to blood transfusion
Complication
Alternative strategies for management of
blood loss during surgery
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
Blood blank practices
#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
# Antibody screen : Indirect Coombs test
(45 mins)
the subject serum + red cells
( antigenic composition) ----- red cell agglutination
# Type&screen
# Emergency transfusion
Type and screen vs Type and crossmatch
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
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
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
Intraoperative transfusion practices
1. PRC
Ideal for patients requiring red cells but not volume replacement
Only one – Increase O2 carrying capacity
AGE
Neonates
Premature
Full-term
Infants
Adults
Men
Women
BLOOD VOLUME
95 ml/kg
85 ml/kg
80 ml/kg
75 ml/kg
65 ml/kg
Allowable blood loss = EBV*( Hctตั้งต้น –Hctที่ยอมรับได้)/ Hctเฉลี่ย
Hct. 30% not magic number
Jehovah” s witness
Practice guideline
$$ case series : reports of Jehovah witness;
some may tolerate very low Hb< 6-8 g/dl in
the perioperative period without an incresae
in mortality
Practice guideline
$$ 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
คุณหมอขาหนูหน้าซี ดแล้วต้องให้เลือดหนูหรื อเปล่าคะ
Intraoperative transfusion practices
2. FFP ( initial therapeutic dose : 10-15 ml/kg )
isolated factor deficiencies
reverse warfarin therapy
correction of coagulopathy associated with liver disease
used in patients who are received massive blood transfusion
with microvascular bleeding
Complications (PATCH) Platelets – dec,Potassium – inc., ARDS,
Acidosis,Temp dec., Citrate intoxication, Hepatiti
>1 BV/ 24 HR> 50 % BV within 3 hrs > 150 ml/min
antithrombin III deficiency
TTP ( Thrombotic thrombocytopenic purpura )
Do not use for volume
Intraoperative transfusion practices
3. PLATELETS
**thrombocytopenia or dysfunction platelets in
the presence bleeding
* prophylactic : plt.counts below 10,000-20,000
* prophylactic preoperative : plt.counts below
50,000
*Microvascular bleeding in surgical patient with
platelets < 50,000
*Neuro/ ocular surgery > 75,000
Intraoperative transfusion practices
3. PLATELETS
*Massive transfusion with microvascular
bleeding with platelets < 100,000
2 BVs = 50,000
*Qualitative dysfunction with microvascular
bleeding (may be > 100,000)
Intraoperative transfusion practices
3. PLATELETS
50 ml: 0.5- 0.6 x 10 9 platelets (some
RBC’s and WBC’s)
Single donor apheresis OR
Random donor (x 6)
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)
Alternative strategies for management of blood loss
during surgery
1) Autologous transfusion
2) Blood salvage & refusion
3) Normovolemic hemodilution
“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
คุณหมอขาตัวหนูแดงทั้งตัวแล้ว แล้วคุณหมอเป็ นไงบ้าง หัวบวมหรื อยังคะ
TRANSFUSION REACTIONS
• is any unfavorable transfusion-related event
occurring in a patient during or after transfusion of
blood components
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)
Acute Hemolytic Transfusion Reaction
Pathophysiology
Ab (in recipient serum) + Ag (on RBC donor)
-Neuroendocrine responses
-Complement Activation
-Coagulation Activation
- Cytokines Effects
Acute hemolytic transfusion reaction
Acute Hemolytic Transfusion Reactions
 Acute onset within minutes or 1-2 hours
after transfuse incompatible blood
 Most common cause is ABO-incompatible
transfusion
Signs and Symptoms of AHTR
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Chills , fever
Facial flushing
Hypotension
Renal failure
DIC
Chest pain
Dyspnea
Generalized bleeding
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Hemoglobinemia
Hemoglobinuria
Shock
Nausea
Vomitting
Back pain
Pain along infusion
vein
– 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
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
– 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!
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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)
– noncardiogenic pulmonary edema
– Supportive therapy
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
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
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
• 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
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
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
@Platelets!
Alloimmunization
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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
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
INFECTIOUS COMPLICATIONS
I. Viral (Hepatitis 88% of per unit viral risk)
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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
• 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
CJD (and variant CJD)
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
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
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Trypanosoma cruzi (Chaga’s disease)
Malaria
Toxoplasmosis
Leishmaniasis
Serological Testing
for Infectious markers
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HIV – Ag
Anti – HIV
HBsAg
Anti – HCV
Test for syphilis
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.