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![Pediatric age group
From birth to 18 years of age [IAP]
up to the age of 21 [U.S. FDA]](https://image.slidesharecdn.com/totransfuse-170824005741/75/To-transfuse-2-2048.jpg)
![Human Blood Group Systems
The term human blood group systems is defined by International
Society of Blood Transfusion as systems in the human species
where cell-surface antigens—in particular, those on blood cells—are
"controlled at a single gene locus or by two or more very closely
linked homologous genes with little or no observable recombination
between them",[1]
It includes the common ABO and Rh- (Rhesus) antigen systems, as
well as many others; thirty-five major human systems are identified
as of November 2014.[2]
ABO blood groups were discovered by Landsteiner in 1901 Later on
Rhesus blood groups were discovered by Landsteiner and Wiener in
1940. [3]
1. ISBT (2016). "International Society for Blood Transfusion (ISBT) Committee on Terminology for
Red Cell Surface Antigens, Terminology Home Page". Retrieved 20 February 2016
2. ISBT (2014). "Table of Blood Group Systems v4.0 (November)" (PDF). International Society
of Blood Transfusion. Retrieved 19 February 2016
3. Landsteiner K, Wiener AS (1940). An agglutinable factor in human blood recognized by immune sera for
Rhesus blood. Proc. Soc Exp. Biol. Med. 43:223-224.](https://image.slidesharecdn.com/totransfuse-170824005741/75/To-transfuse-5-2048.jpg)
![Blood grouping and crossmatching
Blood grouping
The most fatal of all transfusion-related reaction is ABO
incompatibility causing complement-mediated intravascular
hemolysis. Hence, correct blood grouping and typing, and cross-
checking with the blood requisition form is of utmost importance.
ABO typing is carried out by testing RBCs for the A and B antigens
and the serum for the A and B antibodies before transfusion. The
next step involves Rh typing with only 15% of the population being
Rh-negative.
Cross-matching
Cross-matching involves mixing of donor RBCs with the recipient
serum to detect fatal reactions. [19] . Among the three phases, the first
two phases are more important as they detect those involved in fatal
HTR. The total time taken for all the three phases is in between 45
and 60 min.
Mitra R, Mishra N, Rath GP. Blood groups systems. Indian J Anaesth 2014 [cited 2017 Feb
10];58:524-8.
Miller RD. Transfusion therapy. In: Miller RD, ErikssonLI, Fleischer LA, Wiener-
Kronish JP, Young LA, editors. Miller's Anesthesia. 7 th ed. Philadelphia: Churchill
Livingstone Elsevier; 2010. p. 1739-66.](https://image.slidesharecdn.com/totransfuse-170824005741/75/To-transfuse-28-2048.jpg)
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Similar to To transfuse !!!!
To transfuse !!!!
- 1. BLOOD TRANSFUSION To transfuse!!!! or not to transfuse??? Dr Charul Jakhwal
- 2. Pediatric age group From birth to 18 years of age [IAP] up to the age of 21 [U.S. FDA]
- 3. A Little AboutThe History! 1628 English physician William Harvey discovers the circulation of blood. He was the first known to describe completely and in detail the systemic circulation and properties of blood being pumped to the brain and body by the heart. 1665 The first recorded successful blood transfusion occurs in England: Physician Richard Lower.( dogs) 1667 successful transfusions from lambs to humans 1795 the first human blood transfusion 1818 first successful transfusion of human blood to a patient for the treatment of postpartum hemorrhage 1900 Karl Landsteiner, an Austrian physician, discovers the first three human blood groups, A, B, and C. Blood type C was later changed to O.
- 4. The majorchanges in blood transfusion practice over the last 100 years have largely occurred based on the experience of military physicians during the major conflicts of the 20th century. The first use of preserved blood for transfusion was carried in 1917 in United States Transfusion methods altered dramatically around the time of the Vietnam War in the 1970s, when practice changed from using whole blood to component therapy.
- 5. Human Blood GroupSystems The term human blood group systems is defined by International Society of Blood Transfusion as systems in the human species where cell-surface antigens—in particular, those on blood cells—are "controlled at a single gene locus or by two or more very closely linked homologous genes with little or no observable recombination between them",[1] It includes the common ABO and Rh- (Rhesus) antigen systems, as well as many others; thirty-five major human systems are identified as of November 2014.[2] ABO blood groups were discovered by Landsteiner in 1901 Later on Rhesus blood groups were discovered by Landsteiner and Wiener in 1940. [3] 1. ISBT (2016). "International Society for Blood Transfusion (ISBT) Committee on Terminology for Red Cell Surface Antigens, Terminology Home Page". Retrieved 20 February 2016 2. ISBT (2014). "Table of Blood Group Systems v4.0 (November)" (PDF). International Society of Blood Transfusion. Retrieved 19 February 2016 3. Landsteiner K, Wiener AS (1940). An agglutinable factor in human blood recognized by immune sera for Rhesus blood. Proc. Soc Exp. Biol. Med. 43:223-224.
- 6. ABO blood groupsystem divided into four blood types on the basis of presence or absence of A and B surface antigens. The blood groups are A, B, O and AB. The frequency of four main ABO blood groups varies in the population throughout the world. ABO blood group system derives its importance from the fact that A and B are strongly antigenic and anti A and anti B naturally occurring antibodies present in the serum of persons lacking the corresponding antigen, and these antibodies are capable of producing intravascular hemolysis in case of incompatible transfusion Zaman et al. Study of ABO and Rh-D blood group among the common people of Chittagong city corporation area of Bangladesh. Journal of Public Health and Epidemiology Vol. 7(9), pp. 305-310, September 2015
- 7. Rh blood groupsystem It is the second most important blood group system, after ABO, and it consists of 50 defined blood- group antigens, among which the five antigens D, C, c, E, and e are the most important. The commonly used terms Rh factor, Rh positive and Rh negative refer to the D antigen only. Rh antibodies are immunoglobulin G (IgG) may cross freely from the placenta into fetal circulation Rh incompatibility can occur by 2 main mechanisms 1. secondary to fetomaternal hemorrhage 2. when an Rh-negative female receives an Rh-positive blood transfusion
- 8. Davis PJ, CladisFP, Motoyama EK (eds). Smith’s Anesthesia for Infants and Children, 8th ed. Philadelphia, PA: Elsevier Mosby; 2011: Ch. 3
- 9. Blood components!!!1 unitwhole blood =350/450ml plasma Platelets poor plasma 200ml Platelets 50-70ml RBC 250ml CPDA1-35 days SAGM-42days 1-6’C storage Frozen in hypertonic saline – 10years Rapid Freezing with in 1hour- FFP Preserves factor 5 & 8 After thawing to be used within 24 hours Used with in 5 days Stored at 20-24’C Produced by apharesis or BCT The total blood requirement for a child may be as low as 25-100 ml and the child may also require multiple transfusions. This can be achieved by aliquoting one PRBC unit (About 200 ml) into Pedi-packs. This will avoid multiple donor
- 10. Pediatric Blood transfusion Childrenof <4 months 1. Physiological anemia 2. Predominance of HbF 3. the lower oxygen delivering capacity. 4. inefficient humoral system with attenuated formation of antibodies to allogeneic RBCs 5. the premature infant's have limited EPO response to decreased oxygen delivery 6. Relatively Greater blood volume Children of >4 months 1. No Physiological anemia 2. Predominance of HbA 3. Better oxygen delivering capacity 4. Strong immune system 5. Normal EPO response to decreased oxygen delivery 6. Relatively lower blood volume Smith’s Anesthesia for Infants and Children, 9th Edition, by Drs. Peter Davis and Franklyn Cladis
- 11. RED BLOOD CELLS Childrenof <4 months Indications: 1. Massive blood loss or acute blood loss due to trauma, surgery or other cause associated with hypovolemic shock 2. Hgb < 8 g(dL (Hct < 24%) in stable neonates with clinical manifestations of anemia (tachycardia, tachypnea, poor feeding, poor weight gain, apnea) 3. Hgb < 10 g/dL (Hct < 30%) in neonates with: a. 02 requirement < 35% by hood or nasal cannula b. On continuous positive airway pressure (CPAP) or stable ventilator setting (mean airway pressure < 6 cm of water) c. Significant apnea or bradycardia, significant tachycardia or tachypnea d. Low weight gain (poor feeding) Children of >4 months Indications: 1. Massive blood loss or acute blood loss due to trauma, surgery, or other cause associated with hypovolemic shock (>15% total blood volume) 2. Hgb < 8 g/dL emergent/urgent surgery; symptomatic anemia (tachypnea, tachycardia, hypotension), chemo/radiotherapy; hernodynamically stable pediatric ICU patients 3. Significant preoperative anemia when other corrective therapy not available 4. Hgb < 10 g/dL and severe brain injury *Blood center of Wisconsin 2015
- 12. RED BLOOD CELLS Childrenof <4 months 4. Hgb < 12 g/dL (Hct < 35%) in neonates with: a. Fi02 requirement > 35% b. On CPAP or IMV (Intermittent Mandatory Ventilation) with mean airway pressure 6-8 cm of water c. Deteriorating respiratory status d. With hypotension or shock requiring vasopressors e. Recovering from major surgery f. Severe traumatic brain injury 5. Hgb < 15 g/dL (Hct < 45%) in neonates a. With cyanotic congenital heart disease Children of >4 months 4. Hgb < 13 g/dL cyanotic heart disease, ECMO, severe pulmonary disease 5. Patients with hemoglobinopathies and/or chronic hemolytic anemias (e.g. Sickle cell disease, thalassemia) and undergo chronic or episodic transfusions for specific clinical indications *Blood center of Wisconsin 2015
- 13. Dosing Recommendations: •10-15 ml/kg of body weight should raise the Hgb by 2-3 g/dL or the Hct by 6%. • Transfusion rate is dependent on the clinical condition and age of the infant/pediatric patient; rate of transfusion should be prescribed by the ordering physician. *Blood center of Wisconsin 2015
- 14. Platelets Indications: Childrenof < 4 and >4 months: 1. Active bleeding or prior to invasive procedures a. Platelet count < 50,000/uL in neonates b. Platelet count < 100,000/uL in sick preterm neonates or those who need CNS surgery c. Platelet dysfunction (acquired, including post- cardiopulmonary bypass, or inherent), regardless of platelet count 2. As a part of a massive transfusion protocol 3. Prophylactic use may be indicated in patients with a platelet count < 30,000/uL (depending on age) *Blood center of Wisconsin 2015
- 15. Platelets -Dosing Recommendations: Childrenof < 4 months: • 10-15 ml/kg of body weight gives an expected platelet count rise of 30,000/uL to 50,000/uL Children of < 4 months: The following dose usually raises the platelet count by 30,000/uL to 50,000/uL: 1. If child less than 10 kg of body weight, 1/4 apheresis platelet 2. If child 10-30 kg of body weight, 1/2 apheresis platelet 3. If child greater than 30 kg of body weight, 1 adult apheresis platelet *Blood center of Wisconsin 2015
- 16. Plasma Children of <4 months: Indications 1. Documented coagulopathy and bleeding or thrombosis 2. Support during Disseminated Intravascular Coagulation (DIC), Massive Transfusion, and during or within 24 hours after ECMO/CPB 3. Replacement therapy for clinically significant deficiency, including: a. Multiple coagulation factor deficiency (i.e. liver disease) b. When specific factor concentrates are not available (i.e. Factor II, Factor V, Factor X, Factor XI) c. Clinically significant plasma protein deficiency (i.e. ADAMTS13, protein S) 4. Emergent correction of vitamin K deficiency (i.e. active bleeding, emergent surgery); but this does not preclude Vitamin K replacement 5. Neonates with unexplained bleeding unresponsive to other measures may be given plasma without PT, PTT. Children of > 4 months: Indications: 1. Support during Disseminated Intravascular Coagulation (DIC), Massive Transfusion, and during or within 24 hours after ECMO/CPB 2. Replacement therapy for clinically significant deficiency, including: a) Multiple coagulation factor deficiency (i.e. liver disease) b) When specific factor concentrates are not available (i.e. Factor II, Factor V, Factor X, Factor XI) c) Clinically significant plasma protein deficiency (i.e. ADAMTS13, protein S) 3. Emergent reversal of vitamin K antagonist or correction of vitamin K deficiency (i.e. active bleeding, emergent surgery)
- 17. Dosing Recommendations: •A dose of 10-20 mL/kg of body weight typically raises procoagulant factors into hemostatic levels; monitor for desired outcome.
- 18. Cryoprecipitate (all ages) Rich in– Fibrinogen, von Willebrand factor, Factor XIII and factor VIII Supplied as single unit for smaller patients(neonates) or as 5- pool for larger patients Indications: 1. Hypofibrinogenemia (Fibrinogen < 125 mg/dL) or dysfibrinogenemia, with active bleeding or undergoing an invasive procedure' 2. Hemophilia A (deficiency in factor VIII) or von Willebrand disease, only when virally-inactivated or recombinant concentrate is unavailable or DDAVP is not appropriate. 3. Replacement therapy in Factor XIII deficiency with active bleeding or undergoing an invasive procedure' Dosing Recommendations:One single unit of cryoprecipitate (20-25mL) per 7 kg of body weight will typically raise the fibrinogen by 100 mg/dL. Monitor for desired outcome. *Blood center of Wisconsin 2015
- 19. Why it isimportant to give blood? Anaemia is the commonest encountered abnormal laboratory finding in critical care (Vincent et al CCM 2006) Inadequate O2 delivery with severe anemia RBC transfusion improves O2 delivery Critically ill patients more susceptible to adverse effects of oxygen depletion • impairs oxygen delivery to critical organs • cardiovascular system must compensate RBC transfusion should improve outcomes Sepsis in European Intensive Care Units: Results of the SOAP Study Vincent et al CCM 2006
- 20. Anemia from acuteinflammatory response in critical care Reduction in red cell production Increased red cell destruction Blood loss (acute or chronic) Diminished erythropoietin response Impaired proliferation and differentiation of erythroid progenitors in the bone marrow Phlebotomy ACCP Critical Care Medicine Board Review: 21st Edition > < Previous Chapter Next Chapter > Chapter 22. Anemia and RBC Transfusion in the ICU 2015
- 21. Trauma resuscitation! Pediatric massiveblood transfusions Massive transfusion in the pediatric population is defined as the transfusion of blood components equaling one or more blood volumes within a 24-hour time frame or half of a blood volume in 12 hours. Whole blood- obsolete deficient in clotting factors and has high levels of potassium, ammonia, and hydrogen ions. Volume overload Blood component therapy Packed red blood cells Fresh frozen plasma (FFP) Platelets Plasma, red blood cell and platelet ratios of 1:1:1 appear to be the best substitution for fresh whole blood Sara J. Chidester et al. A pediatric massive transfusion protocol J Trauma Acute Care Surg. 2012 Nov; 73(5): 10
- 22. Sara J. Chidesteret al. A pediatric massive transfusion protocol J Trauma Acute Care Surg. 2012 Nov; 73(5): 10
- 23. Smith’s Anesthesia forInfants and Children, 9th Edition, by Drs. Peter Davis and Franklyn Cladis
- 24. Whole blood transfusion! Smith’sAnesthesia for Infants and Children, 9th Edition, by Drs. Peter Davis and Franklyn Cladis
- 26. Sloan SR, BenjaminRJ, Friedman DF, Webb IJ, Silberstein L. Transfusion medicine. In: Nathan & Oski’s Textbook of Hematology of Infancy and Childhood, 6th ed. Philadelphia: Saunders, 2003:1709−56. Children are quite different from adults during growth and development, and that should be taken into different consideration.
- 27. Transfusion complications Transfusion complicationsthat are generally common between adult and pediatric patients include Acute hemolytic transfusion reactions, Febrile non-haemolytic transfusion reactions (FNHTR) Allergic transfusion reactions, Delayed hemolytic transfusion reactions, Transfusion-related acute lung injury, Transfusion-associated graft-versus-host disease, and Infectious complications.
- 28. Blood grouping andcrossmatching Blood grouping The most fatal of all transfusion-related reaction is ABO incompatibility causing complement-mediated intravascular hemolysis. Hence, correct blood grouping and typing, and cross- checking with the blood requisition form is of utmost importance. ABO typing is carried out by testing RBCs for the A and B antigens and the serum for the A and B antibodies before transfusion. The next step involves Rh typing with only 15% of the population being Rh-negative. Cross-matching Cross-matching involves mixing of donor RBCs with the recipient serum to detect fatal reactions. [19] . Among the three phases, the first two phases are more important as they detect those involved in fatal HTR. The total time taken for all the three phases is in between 45 and 60 min. Mitra R, Mishra N, Rath GP. Blood groups systems. Indian J Anaesth 2014 [cited 2017 Feb 10];58:524-8. Miller RD. Transfusion therapy. In: Miller RD, ErikssonLI, Fleischer LA, Wiener- Kronish JP, Young LA, editors. Miller's Anesthesia. 7 th ed. Philadelphia: Churchill Livingstone Elsevier; 2010. p. 1739-66.
- 30. In emergencylifesaving resuscitation, the risk of hemolytic transfusion reactions from transfusion of group O blood to nongroup O recipients constitutes risk that is outweighed by the benefits.
- 34. Autologous/placental RBC transfusion In small pilot studies, there has been no benefit in autologous transfusion in neonates as compared with standard allogeneic transfusion.42,43 Additionally, there is limited benefit due to low volume of collection in extremely low birth weight infants.42,44–46 The shelf-life of umbilical cord blood autologous product is also shorter at 14–21 days.47 In addition to these concerns, bacterial contamination and high cost continue to hamper clinical usage.42,44 42. Strauss RG, Widness JA. Is there a role for autologous/placental RBC transfusions in the anemia of prematurity. Transfus Med Rev. 2010;24(2):125–129. 43. Brune T, Garritsen H, Hentschel R, Louwen F, Harms E, Jorch G. Efficacy, recovery, and safety of RBCs from autologous placental blood: clinical experience in 52 newborns. Transfusion. 2003;43(9):1210–1216. 44. Eichler H, Schaible T, Richter E, et al. Cord blood as a source of autologous RBCs for transfusion of preterm infants. Transfusion. 2000;40(9):1111–1117. 47. Khodabux CM, van Beckhoven JM, Scharenberg JG, El Barjiji F, Slot MC, Brand A. Processing cord blood from premature infants into autologous red blood cell products for transfusion. Vox Sang. 2011;100(4):367–373.
- 35. 82. Cervia JS,Wenz B, Ortolano GA. Leukocyte reduction’s role in the attenuation of infection risks among transfusion recipients. Clin Infect Dis. 2007;45(8):1008–1013. 83. Fergusson D, Hébert PC, Lee SK, et al. Clinical outcomes following institution of universal leukoreduction of blood transfusions for premature infants. JAMA. 2003;289(15):1950–1956. Blumberg N, Fine L, Gettings KF, Heal JM. Decreased sepsis related to indwelling venous access devices coincident with implementation of universal leukoreduction of blood transfusions. Transfusion. 2005;45(10):1632–1639.
- 36. Leukoreduction Removal ofleucocytes from various blood products
- 37. ADVANTAGES OF LEUKOREDUCTION Thereduction in the number of leukocytes, in allogenic blood products has been proven to be clinically relevant in the following: 1. Reducing the frequency and severity of Febrile Non-Hemolytic Transfusion Reactions (FNHTRs). 2. Reducing the risk of cytomegalovirus (CMV) transmission. 3. Reducing the risk of HLA-alloimmunization and platelet-refractoriness. Cervia JS, Wenz B, Ortolano GA. Leukocyte reduction’s role in the attenuation of infection risks among transfusion recipients. Clin Infect Dis. 2007;45(8):1008–1013.
- 38. Transfusion Triggers Restrictive Hb<7g/dl Low Hb Transfusion Trigger liberal HB <10g/dl High Hb Transfusion Trigger “a particular hemoglobin level of discomfort for the prescribing physician, not defined by clear physiologic parameters” at which blood transfusion is required
- 39. Restrictive versus LiberalTransfusion Strategy. Definitions for a restrictive versus liberal strategy for blood transfusion vary in the literature, although hemoglobin criteria for transfusion less than 8 g/dl and hematocrit values less than 25% are typically reported as restrictive. The report suggests Meta-analysis of RCTs comparing restrictive with liberal transfusion criteria report fewer red blood cell transfusions when restrictive transfusion strategies are employed Anesthesiology 2015; 122:241-75
- 40. P H BBolton-Maggs, M F Murphy Blood transfusion Arch Dis Child 2004;89:4–7
- 41. The availabilityof blood and platelet transfusion support has permitted increasingly more intensive chemotherapy regimes to be used in malignant disease at all ages,19 Children with haemoglobinopathies such as beta thalassaemia major, or with red cell aplasia are dependent on regular transfusions. These children should have a more extended blood group undertaken prior to the first transfusion in order to minimise the development of red cell alloantibodies,
- 42. George K. IstaphanousPediatrRed blood cell transfusion in critically ill children: A narrative review Crit Care Med 2011 Vol. 12, No. 2
- 43. Multi-centre, prospective,randomized study > 24 h ICU stay expected Hb < 9.0 g/dL within 72 h Volume resuscitated or normovolaemic Restrictive: Maintain 7-9 g/dL (APACHE II: 20.8) Liberal: Maintain 10-12 g/dL (APACHE II: 21.3)
- 44. Avnish Bharadwaj, MamtaKhandelwal1, Suresh Kumar Bhargava2, Perioperative neonatal and paediatric blood Transfusion. Indian Journal of Anaesthesia | Vol. 58 | Issue 5 | Sep-Oct 2014
- 45. METABOLIC CONSEQUENCES AND COMPLICATIONS OFMASSIVE BLOOD TRANSFUSION The metabolic consequences of large blood transfusions also occur in adults but are more frequent in children due to the relationship between blood component administered and their circulating blood volume Hypocalcaemia may be treated by administration of calcium fluoride 5-10 mg/kg IV or calcium gluconate 15-30 mg/kg. If the blood loss is continuous and prolonged infusion of calcium chloride at the rate of10 mg/kg/h may be used. Hyperkalaemia Use of blood collected within 7 days and administration slowly with total volume < 1.0 ml/kg/min is recommended. Intravenous sodium bicarbonate 1 m mol/kg and calcium chloride 20 mg/kg or calcium gluconate 60 mg/kg may be used to treat hyperkalaemia causing arrhythmias. Use of intravenous dextrose insulin, hyperventilation and sympathomimetics can be useful HypomagnesaemiaIV magnesium sulphate administered at 25-50 mg/kg Acid-base disorders Hypothermia Use of blood warmers, maintaining OT temperature, use of warming blankets and warm fluids for irrigation and intravenous infusion with monitoring of electrocardiogram, SpO2, skin and core temperature can be helpful in preventing hypothermia and consequent complications.
- 50. Conclusions Theadministration of blood per se did not lead to increased postoperative infection. Clinicians should reconsider withholding blood transfusion in patients solely owing to concerns of predisposition to infection.
- 52. In thepresent study, we found that shorter storage RBCs transfusion significantly improved ChE recovery and reduced the amount and duration of atropine usage Нese results suggest that RBCs transfusion could improve clinical therapeutic effects on OPs intoxication patients. Red blood transfusion may deliver additional erythrocyte cholinesterase, which could be the potential target substrate for OP packed RBCs transfusion has advantages over whole blood transfusion, since the total volume administrated into patients is less that could avoid risks of overloading and fever or allergy by substances in serum Concludes early blood transfusion can e ٴوectLvel reduce the extent of toxic symptoms and prevent further progression, especially when oximes are not available.
- 53.