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Topic modules
1. Blood blank practices
2. Indication to blood transfusion
3. Complication
4. 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
#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
Blood blank practices
# Antibody screen : Indirect Coombs test
(45 mins)
the subject serum + red cells
( antigenic composition) ----- red cell agglutination
# Type&screen
# Emergency transfusion
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
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 practices1.1. PRCPRC 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*( Hctตั้��งตั้�น –Hctที่�ยอมรั�บได้�)/ Hctเฉลี่�
ย 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
Intraoperative transfusion practices
2. FFPFFP ( 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
3.3. PLATELETSPLATELETS
**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
3.3. PLATELETSPLATELETS
*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
3.3. PLATELETSPLATELETS
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
4.4. CRYOPRECIPITATE 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
TRANSFUSION REACTIONSTRANSFUSION REACTIONS
• is any unfavorable transfusion-related event occurring in a patient during or after transfusion of blood components
TRANSFUSION REACTIONSTRANSFUSION 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
Ab (in recipient serum) + Ag (on RBC donor)
-Neuroendocrine responses
-Complement Activation
-Coagulation Activation
- Cytokines Effects
Acute hemolytic transfusion reaction
Pathophysiology
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
• Chills , fever• Facial flushing• Hypotension• Renal failure• DIC• Chest pain• Dyspnea• Generalized bleeding
• 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!@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) – 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!@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
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 COMPLICATIONSINFECTIOUS 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, 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• Trypanosoma cruzi (Chaga’s disease) • Malaria• Toxoplasmosis• Leishmaniasis
Serological Testingfor Infectious markers
• 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