1. Neonatal Transfusion

2. Transfusion in the newborn requires selection of appropriate donor, measures to minimize donor exposure and prevent graft versus host disease and transmission of Cytomegalovirus.
Component therapy rather than whole blood transfusion, is appropriate in most situations.
A clear cut policy of cut-offs for transfusions in different situations helps reduce unnecessary exposure to blood products.
Transfusion triggers should be based on underlying disease, age and general condition of the neonate.

3. Neonatal Blood Transfusion
Ahmad Sh. Silmi Msc, FIBMS
Medical laboratory sciences
IUG

4. Introduction Neonatal period – birth to 4 months.
Indications for transfusion DIFFERENT
Weight
Gestational age
Circumstances of delivery
Maturation

5. Introduction Ill Infants most transfused patients in hospital.
Iatrogenic blood loss carefully monitored.
Once significant, transfuse
Transfusion service must provide specialized service
Minimize donor exposure if possible.
Use one unit with satellite bags
Use sterile docking device

6. Introduction
Double volume exchange transfusion is mainly used for the management of hyperbilirubinaemia and haemolytic disease of the newborn, when other methods of treatment such as early and intensive use of phototherapy have been ineffective

7. The aim of an exchange transfusion is:
To lower the serum bilirubin level and reduce the risk of brain damage (kernicterus);
To remove the infants' affected red blood cells and circulating maternal antibodies to reduce red cell destruction;
To correct anaemia and treat any potential for heart failure whilst maintaining euvolaemia.

8. Fetal and Neonatal Erythropoiesis
Appropriate transfusion practice requires knowledge of neonatal physiology and careful clinical observation.
As embryo develops predominant sites of hematopoiesis change:
at about the 9th week of gestation shifts from wall of yolk sac to liver.
at about the 24th week from liver to bone marrow.
Hematopoiesis regulated by gradually increasing erythropoietin levels stimulated by low oxygen tensions during intrauterine life.
At 40 weeks (full term), normal infants have cord blood hemoglobin of 19 +/- 2.2 g/dL.
Neonates of lower birth weight have lower normal hemoglobin levels.

9. Fetal and Neonatal Erythropoiesis
Fetal red cells have life span of days, 53-95% hemoglobin F
Physiologically adapted to low intrauterine oxygen tensions
High oxygen affinity allow red cells to acquire oxygen from maternal RBC throughout pregnancy and release tissues.
High oxygen affinity results in poor tissue oxygenation after birth.
Hemoglobin A replaces hemoglobin F after birth
Oxygen delivery to tissues remains satisfactory despite a physiologic fall in hemoglobin concentration.
Oxygen dissociation curve shifts to the right, reflecting improving oxygen delivery to the tissues.
Premature infants have lower hematocrits and greater percentage of hemoglobin F in their RBC than term newborns.

10. Fetal and Neonatal Erythropoiesis
As tissue oxygenation improves, erythropoietin decline and erythropoiesis diminishes.
Decline in RBC produces a "physiologic anemia of infancy“.
Normally developing infant maintains adequate tissue oxygenation despite lower hemoglobin levels.

11. Haemolytic disease: Indications for exchange transfusion
Cord Hb < 12 mg/dl and/or cord SBR > 5mg/dl : immediate exchange transfusion
Exchange transfusion if rate of rise in SBR is such that SBR is likely to reach 17mg/dl.
( aim to keep SBR below 20 mg/dl).

12. Unique Aspects of Neonatal Physiology
Differences between newborns and adults dictate differences in transfusion practice.
Newborns are small and physiologically immature.
Those requiring transfusion are often premature, sick and unable to tolerate minimal stresses.

13. Unique Aspects of Neonatal Physiology
Infant size
Full-term newborns blood volume approximately 85 ml/kg
Premature infants average blood volume of 100 ml/kg.
Survival rates continue to improve for infants weighing 1000 g (2.2 lbs) or less at birth
Transfusion service must provide blood components for patients whose total blood volume is less than 100 mLs.
Small blood volumes and need for frequent laboratory test makes replacement of iatrogenic blood loss most common indication for transfusion.

14. Unique Aspects of Neonatal Physiology
Infants do not compensate for hypovolemia well.
Results in diminished cardiac output, resulting in
poor tissue perfusion,
low tissue oxygenation and
metabolic acidosis.
Bone marrow responds more slowly to anemia.
If hemolysis occurring due to maternal antibody may be no increased erythropoiesis for 2-3 weeks.

15. Unique Aspects of Neonatal Physiology
Cold stress (hypothermia) causes exaggerated effects:
increased metabolic rate
hypoglycemia
metabolic acidosis
tendency to apneic episodes that may lead to hypoxia, hypotension and cardiac arrest.
Blood for transfusion should be warmed if given in large amounts, small amounts reach RT in about 20 minutes and does not need to be warmed.

16. Unique Aspects of Neonatal Physiology
Immunologically immature, antibodies present in plasma originate almost entirely from maternal circulation.
IgG only immunoglobulin class that crosses the placenta.
Passively acquired antibody conserved during the neonatal period due to slow catabolism by the fetus.
Infants exposed to an infectious process in utero or shortly after birth may produce small amounts of IgM detectable by sensitive techniques, but rarely form RBC antibodies of either class during the neonatal period.

17. Unique Aspects of Neonatal Physiology – Metabolic Problems
Immature kidneys have reduced glomerular filtration rate and concentrating ability, the newborn may have difficulty excreting potassium, acid and/or calcium loads.
Acidosis or hypocalcemia may also occur postransfusion because immature liver metabolizes citrate in banked blood inefficiently.
Studies have shown older units do not affect the infant for routine transfusion purposes.

18. Unique Aspects of Neonatal Physiology – 2,3-DPG
Tissue oxygenation poor due to high percentage of hemoglobin F.
Hemoglobin F does not release oxygen to the tissues like adult hemoglobin.
Respiratory distress syndrome (RDS) or septic shock have decreased levels of 2,3-DPG, alkalosis and hypothermia can further increase the oxygen affinity of hemoglobin.
2,3-DPG levels decrease in stored blood, newborns should be given freshest blood available, less than 5 days old if possible.
Controversy in the field about the practice of using fresh blood.
Greater importance to decrease donor exposures rather than give fresh blood.
Allow CPD donor units to be put on hold for infant for 21 days.
Exception is for massive transfusion

19. Informed Consent
Before the commencement of any blood or blood product infusion the medical officer or registered nurse administering the blood product must ensure that parents have given an informed consent for the procedure.
Benefit versus risk - In otherwise well babies the risk of exchange transfusion are usually small but in preterm babies who are unwell the risks of exchange transfusion are increased and the procedure must be balanced the high morbidity associated with bilirubin encephalopathy.

20. Collection of blood samples and ordering of Red Blood Cells and FFP:
Liaise with the obstetric team and notify blood bank of a possible exchange transfusion before the delivery of an Rh- affected fetus.
Stored red blood cells (RBCs) have a predictable packed cell volume of 60% (+/- 2%) so measurement of haematocrit levels is no longer necessary. In order to dilute the RBCs by 10% you will also need to order Fresh Frozen Plasma (FFP) of suitable type.
A request for RBCs for exchange transfusions is normally considered an urgent request. The RBCs should be ready within 2 hours of request provided antibody testing has been completed.

21. Types of Red Blood Cells
Rh haemolytic disease of the newborn: RBCs less than 5 days old are used.
O Rh negative RBCs do not have major blood group antigens so they are not haemolysed by maternal antibodies that may still be present in the infant's circulation.
If the RBCs are made available before delivery of the sensitised infant the RBCs must be O Rh negative and cross matched against the mother. If the RBCs are sourced after delivery the RBCs must be cross matched against the infant.

22. ABO incompatibility:
Use group O, Rh specific RBCs. These RBCs contain low levels of antibodies and lack antigen that could trigger any circulating maternal antibodies in the newborn. Subsequent transfusions should be done with RBCs that are compatible with that of the mother and infant.

23. Volume of RBCs and FFP to be ordered
The volume required is dependent on the reason for exchange and is determined by the formula next page.

24. SINGLE VOLUME EXCHANGE (anaemia with normovolaemia)
Estimated blood volume depends gestational age and timing of cord clamping ranging from ml/kg/min. Mean blood volume was 70 ml/kg (early cord clamping) versus 90ml/kg (delayed cord clamping for infants weighing g.

25. DOUBLE VOLUME EXCHANGE (for established hyperbilirubinaemia or to prevent hyperbilirubinaemia)
Double volume exchange removes about 85% of the infant's red blood cells. At the end of the exchange blood transfusion the bilirubin should be about 50% of pre exchange level. It will rebound at about 4 hours to 2/3rds the pre-exchange level.

26. Ordering blood
A cross match request form must be hand written and collection witnessed and signed by a second MO / RN. Specimen must be labelled by hand
When ordering red cells for an exchange transfusion, remember the priming volume of the exchange circuit is approx 50ml so additional RBCs should be ordered.
Always communicate with blood bank.

27. Collection of blood and plasma from Blood Bank
Blood Bank will notify the nursery when the RBCs and FFP are ready to be collected.
The Ward Assistant will need both the Intravenous Infusion Order Form and the RPA Blood Product Issue Form to collect the blood products form Blood Bank.

28. Possible Complications
These are unusual if the exchange is performed slowly and often the best
management is to slow down or pause the exchange. Any of the following can happen
Complications
Prevention & Management
Hypothermia - if babys skin temperature falls below 36oC.
Confirm placement of temperature probe and take axilla reading. Confirm blood warmer is at 37oC
Turn up the servo control or isolette and slow the exchange.
Hyperglycaemia donor blood is preserved in dextrose.
Blood glucose levels can be elevated during the exchange and generally resolve without intervention.

29. Complications
Prevention & Management
Hypoglycaemia: may occur during and shortly after the exchange.
If baby's reagent strip blood glucose is less than 2.5 mmol/L give slow push of 2 ml/kg of 10% dextrose (via peripheral line or flush catheter dead space before & after dextrose injection). Repeat screening blood glucose level on next cycle. Continue to monitor glucose levels.
Hyperkalaemia: unlikely to happen with red blood Cells less than 5 days old but is more likely to happen with a sick preterm infant refer to hyperkalaemia protocol
If K+ > 6.0mmol/L give calcium gluconate if Ca <2.0 mmol/L and recheck K+ frequently. Stop exchange if K+ >7.0 mmol/L and treat until K+ < 6.0 and then restart exchange. Peaked T waves / widened QRS / VEBs can be seen with hyperkalaemia.
Hypocalcaemia: This is rare with the preservative anticoagulants used now and will rarely need
treating.
If Ca++ drops to < 1.5 mmol/l then flush catheter dead space with normal saline and give Urgent IV Correction: mmol/kg (1-2ml/kg of calcium gluconate 10%) by slow IV injection of diluted solution over 10 minutes. Do not give into a peripheral vein. Prolonged QT interval can be seen with hypocalcaemia.

30. Complications
Prevention & Management
Metabolic acidosis: Mild metabolic acidosis is common and usually doesnt need treating. Correct hyperkalaemia / hypocalcaemia before giving H2CO3.
If baby's base excess falls below minus 10mmol/l then flush catheter dead space with normal saline, and Half correct with 4.2% sodium bicarbonate (mmol of bicarbonate = [body weight x base excess x 0.3]/2). If acidosis worsens or persists, then consider stopping exchange
Thrombocytopaenia: Stored red cells are platelet depleted, so the platelet count will tend to fall during the exchange transfusion. This rarely needs intervention.
If the platelet count falls to < 50,000 consider stopping exchange and arrange a platelet transfusion through a peripheral vein.
Air Embolus:
Ensure lines are set up and primed correctly.
Observe lines for presence of air during exchange & ensure 3-way taps are closed to the infant when filling or expelling contents of syringe.

31. Complications
Prevention & Management
Anaemia/ Polycythaemia:
Ensure HCT of RBCs / FFP infusion is kept
consistent throughout procedure. Gently agitate
burette at frequent intervals to prevent separation
of red cells and FFP.
Necrotising Enterocolitis: Ensure the UVC is in correct position.
Perform isovolumetric exchange transfusion or use small aliquots if single lumen technique used

32. Transfusion Associated Graft versus Host Disease (TA-GVHD)
TA-GVHD reported in newborns receiving intrauterine transfusion followed by postnatal exchange transfusion.
Lymphocytes given during intrauterine transfusion may have induced host tolerance, so that lymphocytes given in subsequent exchange transfusion were not rejected in the normal way.
GVHD not felt to be significant clinical problem for immunologically normal newborns who receive multiple exchange transfusions.

33. Transfusion Associated Graft versus Host Disease (TA-GVHD)
Irradiation of blood kills immunologically competent lymphocytes.
Irradiated blood given to low birth weight, low gestational age or septic premature neonates such infants are immunologically more vulnerable to TA-GVHD.
Blood for intrauterine transfusion should be irradiated.
Any directed donor blood from a relative should be irradiated.

34. Cause of Hemolytic Disease
Maternal IgG antibodies directed against an antigen of paternal origin present on the fetal red blood cells.
IgG antibodies cross the placenta to coat fetal antigens, cause decreased red blood cell survival which can result in anemia.
Produced in response to previous pregnancy with antigen positive fetus OR exposure to red blood cells, ie transfusion.

35. Cytomegalovirus (CMV) Infection
Infection by CMV may occur in the perinatal period, either in-utero or during birth, by breast feeding or by close contact with mothers or nursery personnel.
CMV mays also be transmitted by transfusion, virus seems to be associated with leukocytes in blood and components.
Infection in newborns is extremely variable in its manifestations, ranging from asymptomatic seroconversion to death.
Symptomatic infection may produce pulmonary, hepatic, renal, hematologic and/or neurologic dysfunction.

36. Cytomegalovirus (CMV) Infection
This neonate was found to have respiratory distress, an extensive rash and hepatomegaly.
Results of CMV IgM and IgG tests and both serum and plasma DNA polymerase-chain-reaction assays were positive.

37. Cytomegalovirus (CMV) Infection
Epidemiology and prevention of post transfusion CMV in neonatal patients have been under intense investigation.
The following observations have been noted:
Where CMV rate is high, symptomatic infection is low.
Babies of seropositive moms unlikely to develop CMV.
Premature infants born of seronegative mothers, weigh less than 1200 grams and require multiple transfusions at risk for symptomatic postransfusion infections.
The risk of CMV increases with number of donor exposures.
Risk of transmission decreases by using seronegative donors or components depleted of leukocytes.

38. Cytomegalovirus (CMV) Infection
Standards states that in geographic areas where postransfusion CMV transmission is a problem, blood with minimal risk of transmitting CMV be used for:
newborns weighing less than 1200 g,
born to mothers who lack CMV antibodies or
whose antibody status is unknown.
Most blood banks make it standard practice to transfuse all infants with CMV negative blood.

39. Hemolytic Disease of the Fetus and Newborn - HDFN
HDFN, red cells of fetus coated with IgG alloantibody of maternal origin, directed against antigen of paternal origin present on fetal cells.
IgG coated cells undergo accelerated destruction, both before and after birth.
Clinical severity of the disease is extremely variable, ranging from intrauterine death to a condition that can be detected only by serologic tests on blood from an apparently healthy baby.

40. HDFN - Pathophysiology
Shortened RBC survival causes fetal hematopoietic tissue increase production of RBCs, causes increase in nucleated red cells (NRBCs).
Organs containing hematopoietic tissue increase in size, particularly liver and spleen (hepatosplenomegaly).
If increased hematopoiesis cannot compensate for the immune destruction, anemia becomes progressively more severe.

41. HDFN - Pathophysiology
Severely affected fetus may develop high output cardiac failure with generalized edema, a condition called hydrops fetalis, death may occur in utero.
If live-born, severely affected infants exhibit heart failure and profound anemia.
Less severely affected infants continue to experience accelerated red cell destruction, which generates large quantities of bilirubin.

42. HDFN - Pathophysiology
In-utero fetal bilirubin processed by maternal liver.
After birth neonatal immature liver takes over.
Deficient in uridine diphosphoglucoronyl transferase, bilirubin rises.
Bilirubin 20mg/dL> results in mental retardation or death, condition known as kernicterus.

43. Kernicterus
Kernicterus (bilirubin encephalopathy) results from high levels of indirect bilirubin (>20 mg/dL in a term infant with HDN).
Kernicterus occurs at lower levels of bilirubin in the presence of acidosis, prematurity, hypoalbuminemia and certain drugs (e.g., sulfonamides).

44. Kernicturus Affected structures have bright yellow color.
Unbound unconjugated bilirubin crosses blood-brain barrier and, because it is lipid soluble, penetrates neuronal and glial membranes.
Bilirubin is thought to be toxic to nerve cells
Mechanism of neurotoxicity and reason for topography of lesions are not known.
Patients surviving kernicterus have severe permanent neurologic symptoms (choreoathetosis, spasticity, muscular rigidity, ataxia, deafness, mental retardation).

45. Three Classifications of HDN
ABO
“Other” – unexpected immune antibodies other than anti-D – Jk, K, Fy, S, etc. Rh
Immune anti-D alone
Immune anti-D along with other Rh antibodies – anti-C, -c, -E or –e.

46. Maternal Immunization
Fetal cells possessing paternal antigen mother does not possess enter her circulation and stimulate antibody production.
D antigen most immunogenic but other blood group antigens may also immunize.
Fetal cells enter maternal circulation during pregnancy.
Biggest exposure during birth.

47. Maternal Immunization
Can occur with exposure to <0.1mL
Immunization to D correlates with  volume of RBCs entering D neg mom’s circulation.

48. Maternal Immunizing Events
Other than birth can be due to:
Amniocentesis
Miscarriage
Abortion
Chorionic villus sampling
Cordocentesis
Blunt trauma to the abdomen
Rupture of an ectopic pregnancy

49. Maternal Immunization - Transfusion
Severe HDFN in D neg women transfused with D pos RBCs and develop anti-D
Must give D neg RBC and platelet products to females.
If D pos platelets or granulocytes given must give Rh prophylaxis, i.e., RhIg
Avoid directed donation from husband to wife

50. ABO Hemolytic Disease Mother group O, baby A or B
Group O individuals have anti-A, -B and –A,B in their plasma, fetal RBCs attacked by 2 antibodies
Can occur in any ABO incompatible pregnancy
Occurs in only 3%, is severe in only 1%, and <1:1,000 require exchange transfusion.
The disease is more common and more severe in African-American infants.

51. HDFN Other Than ABO
If this pregnancy is the immunizing event first baby is not affected or only mildly affected.
Primary immune response – IgM
During pregnancy IgG may not be produced in sufficient quantity to cause problems.
Severity of HDFN in future pregnancies due to “other” immune antibodies variable.
If anti-D future pregnancies severely affected.

52. Prenatal Serologic Tests
ABO/D type and antibody screen.
If antibody screen positive
Identify antibody
Determine clinical significance
If clinically significant patient history important, previously affected infant.
IgM antibodies are not of concern

53. Prenatal Serologic Tests
In primary immune response IgM antibodies may demonstrate high thermal amplitude.
Treat serum with 2-mercaptoethanol (2ME) or Dithiothreitol (DTT) to determine if IgG is present.
Antibody may be present but fetus may be antigen negative.
If anti-D test father to determine zygosity of D antigen.

54. Amniotic Fluid Analysis
Assess probable severity of HDFN.
Based on history of antibody AND maternal history with previous pregnancies.
Monitor antibody titer, perform if rising.
Measure bile pigments at 450 nm
Level correlates with severity of hemolysis.
Result will determine action plan.

55. Amniotic Fluid Analysis
Maternal titer greater than 32 for anti-D and 8 for anti-K OR four fold increase in titer indicates need for analysis of amniotic fluid.
Amniocentesis
Perform at 28 wks if HDN in previous child
Perform at 22 wks if previous child severely affected
Perform if maternal antibody increases before 34th wk.
High values of bilirubin in amniotic fluid analyses by the Liley method or a hemoglobin concentration of cord blood below 10.0 g/mL.
Type fetus -recent development in fetal RhD typing involves the isolation of free fetal DNA in maternal serum. In the United Kingdom, this technique has virtually replaced amniocentesis for fetal RhD determination in the case of a heterozygous paternal phenotype
Maternal plasma exchange may be instituted if the fetus is too young for intrauterine transfusion.

56. Amniocentesis

57. Amniotic Fluid Analysis
Zone 1- unaffected or mildly affected
Zone 2 – Deliver at weeks based on fetal lung maturity.
Zone 3 – Seriously affected, intrauterine transfusion and preterm delivery indicated.

58. Amniotic Fluid Analysis

59. Amniotic Fluid Analysis
Weigh risks in severely affected pregnancy
Respiratory Distress Syndrome (RDS)
Due to inadequate surfactant and lecithin
Determine fetal lung by L/S ratio and phosphotidylcglycerol (PG) in amniotic fluid.
If lungs not mature, intrauterine transfusion.

60. Amniotic Fluid Analysis and Fetal Blood Sampling
Amnio can cause fetomaternal hemorrhage (FMH)
If amnio done for other reasons and woman unsensitized D neg, give RhIg
D type of fetus is unknown, prevent immunization
Cordocentesis – draw blood from umbilical cord for laboratory analysis
Use non-invasive procedures when possible.

61. Intrauterine Transfusion (IUT)
Performed after careful evaluation due to high risk to fetus.
Given to prevent hydrops fetalis and fetal death.
Rarely feasible before 20th week gestation.
Once started administer every 2 weeks.

62. Intrauterine Transfusion (IUT)
Blood must be:
Less than 5 days old
Low risk of CMV (CMV neg or safe)
Hematocrit 80% or higher
O negative and COMPATIBLE WITH MOM
Lack antigens which antibody(ies) are directed.
Irradiated
75-175mLs determined by fetal size and age

63. Intrauterine Transfusion (IUT)
After multiple IUTs RBC testing will not be accurate:
Will type as O neg as 90% of circulating RBCs will be donor cells.
Direct Antiglobulin test will be negative
Indirect Antiglobulin Test will be positive.
Cord bilirubin not an accurate indicator of rate of hemolysis or of likelihood of need for exchange transfusion after birth.

64. Intrauterine Transfusion (IUT)
Done in the hospital
Ultrasound to determine the position of the fetus and placenta.
Local anesthetic to numb site.
Medicate fetus to stop or slow movement.
Ultrasound used to guide needle through abdomen into fetus's abdomen or umbilical cord vein.
Peritoneal cavity versus cord vein.

65. Intrauterine Transfusion (IUT)

66. Intrauterine Exchange Transfusion
Replace fetal blood with donor blood.
Use ultrasound to cannulate umbilical vein.
Take blood sample H&H and verification of catheter location in the fetal circulation.
Small volume donor blood transfused, wait, small volume removed.
EXCHANGE fetal blood with donor blood.

67. Intrauterine Transfusion - Risks
Fetal Loss - risk variable depending on condition of fetus, overall 1-2%, range <1% - 50%.
Bradycardia - common but usually transient
Bleeding - usually transient and mild
Preterm Labor

68. Fresh Frozen Plasma

69. Fresh frozen plasma and Cryoprecipitate Recommendations for use of Fresh frozen plasma:
Indications
Severe clotting deficiency (including DIC) with bleeding
Severe clotting deficiency in a neonate undergoing an invasive procedure
Vitamin K deficiency with bleeding
Dilutional coagulopathy with bleeding
Severe anticoagulant protein deficiency
Reconstitution of packed RBC for exchange transfusion

70. Incorrect indications for which FFP is often prescribed but should not be used
Prevention of intraventricular hemorrhage in premature neonates
Volume replacement in the management of sepsis
As an adjunct in the management of thrombocytopenia
To “correct” prolonged indices of coagulation

71. Fresh Frozen Plasma
The volume to be transfused is usually ml/kg.
FFP for neonates will be pathogen inactivated by methylene blue treatment (MB-FFP) from non-UK sources

72. Treatment of hypovolaemic shock/plasma volume expanders
Albumin is not superior to crystalloids in the management of hypovolaemic hypotension Fresh frozen plasma should not be used unless there are co-existing coagulation abnormalities.

73. Recommendations for Factor VIII/ cryoprecipitate:
Congenital factor deficiencies are rare in the neonatal period. While treating bleeding neonates, cryoprecipitate is often considered an alternative to FFP because of its small volume. However, cryoprecipitate contains only factors VIII, XIII and fibrinogen and is not effective in treating the more extensive clotting factor deficiencies.

74. Fresh frozen plasma
Preparation & characteristics: FFP is made by freezing plasma obtained by centrifugation of fresh whole blood. It contains albumin and factors II, VII, X and XI. Antibodies and Factors V, VIII and XIII are also present, but in insignificant quantities, thus precluding the use of FFP as replacement for these substances.
Storage and viability: FFP is stored at -20°C. After thawing it should be used immediately as there is a rapid fall in the concentration of clotting factors.

75. Platelets

76. Platelet Transfusions
Thrombocytopenia is more hazardous in neonates than adults and therapy is probably justified prophylactically at a platelet count of, 20-30x10⁹/l, and if very sick and premature with signs when counts fall below 50x10⁹/l. Platelets should be transfused if the patient is clinically bleeding and the platelet count is <50x10⁹/l.
Platelets should be
HPA compatible in neonates with alloimmune thrombocytopenia (see separate neonatal guideline*).
Irradiated if the child has been transfused in utero.
The volume to be transfused is ordinarily 10-20ml/kg.

77. Platelet Transfusions
Evidence: Asymptomatic thrombocytopenia occurs in about 1% of term and 25% of preterm neonates.
Platelet transfusions are common in the NICU, being administered to 2% - 9.4% of neonates admitted to NICUs.
Majority of platelet transfusions were used prophylactically in non-bleeding neonates with platelet counts in the range of 30 to 50 x 109/L.
Repeated platelet transfusions were common with more than 50% infants receiving more than one platelet transfusion during their NICU stay.

78. Thrombocytopenic neonates who receive platelets are up to 10 times more likely to die than neonates who do not receive platelet transfusion (usually to causes unrelated to severe hemorrhage).
Andrew et al found no benefit in terms of hemorrhage when maintaining a normal platelet count by platelet transfusion in a study of preterm neonates compared with controls with moderate thrombocytopenia (platelets (50 to 150 x 109/L).

80. Platelet concentrate
Preparation and characteristics: Platelets separated by centrifugation are pooled to make random donor platelet packs which have a volume of ml and contain about 5 to 7 x 1010 platelets. Platelets obtained by aphaeresis from a single individual (single donor platelets) provides about 3 to 4 x 1011 platelets. Platelet packs contain leucocytes, plasma and some red cells.
Storage: platelet packs are stored at 22°C with continuous agitation of the bag.

81. Typing: Platelet specific antigen and antibody testing has bearing on the management of alloimmune thrombocytopenia but it is not readily available. All platelet packs are contaminated with some RBCs, plasma and leucocytes, theoretically leading to ABO and Rh group incompatibility if similar group is not used. Ideally, therefore, group specific platelets should be used. However, unless repeated transfusions are required, different group platelets may be used in an emergency.

82. Dosage: One unit of random donor platelets per 10 kg body weight increases the platelet count by x 109/L. This can be achieved by infusion of 5-10 ml/kg of standard donor platelets.
The goal of platelet transfusion is to raise the platelet count to 100 x 109/L.
Frequency of transfusion: Normal half life of stored platelets is 3-5 days. In vivo life span is shorter, especially if there is platelet consumption. A repeat platelet count should be performed after 12 hours of transfusion.

83. Thank you