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Chapter: Paediatrics: Neonatology

Paediatrics: Neonatal haematology

Antenatal: Alloimmune haemolytic disease, e.g. Rhesus disease.

Neonatal haematology







   Alloimmune haemolytic disease, e.g. Rhesus disease.


   Twin to twin transfusion syndrome.


   Parvovirus B19 infection.


   Antepartum haemorrhage.


   Red cell defects or aplasia.




   Nutritional deficiency.


   Chronic illness.


   Anaemia of prematurity occurs 6–12wks after preterm delivery and is caused by:

   repeated and frequent blood sampling;

   shorter hbf red cell half-life;

   ‘fall’ erythropoietin;

   fast growth rate.




   Pallor and tachycardia.


   ‘rise’ O2 requirement or apnoea.


   Poor feeding.


   Growth failure.




   Start iron supplement at 4wks old for 12mths if <35wks gestation.


   Further research is required to establish appropriate blood transfusion thresholds for preterm infants. Transfuse if clinically indicated. Volume to transfuse (mL) = desired rise in Hb (g/dL) x weight (kg) x [4 (packed cells) or 6 (whole blood)]. Alternatively, give 20mL/kg over 4hrs. Blood should be CMV –ve and irradiated.


   Erythropoietin is useful, but not cost-effective for routine use and may increase the risk of retinopathy of prematurity. Use is limited to infants from Jehovah’s witness families.




Defined as arterial or venous packed cell volume (PCV) >65%. More common if placental insuffi ciency, maternal diabetes mellitus, Down’s syndrome, or after twin to twin transfusion. Risk of complications due to thrombosis and or microvascular sludging.




   If symptomatic: (lethargy, seizures, respiratory distress, poor feeding, thrombocytopenia, stroke, renal failure, NEC) perform dilutional exchange transfusion with 20–30mL/kg of normal saline over 30–60min.


   If asymptomatic: it is probably wise to perform dilutional exchange transfusion if PCV >70% to prevent complications.



Common neonatal causes include:

Sepsis, including congenital infection.






Maternal idiopathic thrombocytopenic purpura (ITP) (due to passive transfer of autoimmune IgG antiplatelet antibodies).


Neonatal alloimmune thrombocytopenia (NAIT) resulting from transplacental passage of maternal specific IgG antiplatelet antibodies sensitized to differing foetal human platelet antigen (HPA). In 85% antibody is to HPA1 antigen.


Placental dysfunction.












Intracranial haemorrhage (10–20%) particularly with NAIT.





Platelet transfusion 10–15mL/kg if platelet count is <50 and active bleed-ing or <30 plus additional haemorrhagic risk factor or <20 in a well baby.


NAIT-specific treatment


Antenatal: foetal platelet transfusion. Maternal IV immunoglobulin.


Postnatal: observe if platelets >40 x 109/L. If platelets less or infant symptomatic, give platelet transfusion (HPA1-negative if relevant) and consider corticosteroids, IV immunoglobulin, or even exchange transfusion (liaise with blood transfusion/haematology).


Coagulation disorders


The most common neonatal cause is DIC. Rarely, there is a specific coagulation defect, e.g. haemophilia, or haemorrhagic disease of newborn.


Haemorrhagic disease of newborn


Bleeding is due to deficiency of vitamin K dependent factors resulting from:

Poor transplacental supply.


Lack of enteric bacteria.


Maternal anticonvulsants.


Low vitamin K levels in breast milk.


Typical presentation: is at age 2–7 days with bruising and spontaneous bleeding, e.g. from umbilicus, GI tract, or intracranial.


Investigation: shows ‘rise’prothrombin time (PT) and partial thromboplastin time (PTT), whilst platelet count is normal.


Prevention: vitamin K1 at birth.


Treatment: immediate IV vitamin K1 1mg and fresh frozen plasma 10mL/kg.



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