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Blood transfusion. พญ.เพชรรัตน์ วิสุทธิเมธีกร พ.บ., ป. ชั้นสูงสาขาวิสัญญีวิทยา, วว. ( วิสัญญี ) ภาควิชาวิสัญญีวิทยา วิทยาลัยแพทยศาสตร์กรุงเทพมหานคร และวชิรพยาบาล. Topic modules. Blood blank practices Indication to blood transfusion Complication
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Blood transfusion พญ.เพชรรัตน์ วิสุทธิเมธีกร พ.บ., ป. ชั้นสูงสาขาวิสัญญีวิทยา, วว.(วิสัญญี) ภาควิชาวิสัญญีวิทยา วิทยาลัยแพทยศาสตร์กรุงเทพมหานคร และวชิรพยาบาล
Topic modules Blood blank practices Indication to blood transfusion Complication Alternative strategies for management of blood loss during surgery
Blood blank practices Human red cell membrane : least 300 different antigen fortunately, only the ABO and the Rh systems are important in the majority of blood transfusion History Hct. Infection : Hepatitis B,C syphillis HIV-1,2 HTLV-I,II
Blood blank practices #Crossmatching (50 min) Confirms ABO and Rh typing Detects antibodies to the other blood group systems 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 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
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. 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 transfusionwith 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 * prophylacticpreoperative : plt.counts below 50,000 *Microvascular bleeding in surgical patient with platelets < 50,000 *Neuro/ ocular surgery > 75,000
Intraoperative transfusion practices • *Massive transfusion with microvascular bleeding with platelets < 100,000 • 2 BVs = 50,000 • *Qualitative dysfunction with microvascular bleeding (may be > 100,000) 3.PLATELETS
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)
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) Intraoperative transfusion practices
Alternative strategies for management of blood loss during surgery Autologous transfusion Blood salvage & refusion 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 แล้วคุณหมอเป็นไงบ้าง หัวบวมหรือยังคะ
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
Chills , fever Facial flushing Hypotension Renal failure DIC Chest pain Dyspnea Generalized bleeding Hemoglobinemia Hemoglobinuria Shock Nausea Vomitting Back pain Pain along infusion vein Signs and Symptoms of AHTR
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! • 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-HostDisease ( 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-HostDisease ( 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 • 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) 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