This document discusses thrombocytopenia in neonates. It begins by defining thrombocytopenia as a platelet count below 150,000/mcL and notes its incidence is 0.7-0.9% generally but higher (22-35%) in NICUs. It then classifies thrombocytopenia by severity and lists various potential causes including alloimmune conditions, infections, genetic disorders, and others. Guidelines are provided for evaluation and management of early-onset versus late-onset thrombocytopenia as well as criteria for platelet transfusion in neonates. Specific conditions like NAIT are also explained in more detail.

1. Dr. Shantanu
2nd Yr DNB,
DEPT OF PEDIATRICS
J.L.N.Hospital & Research centre,
Bhilai Steel Plant

2. WHAT ARE THE TOPICS?
Definition and classification
Causes
APPROACH TO NEONATAL THROMBOCYTOPENIAS
NAIT
GUIDELINE FOR PLATELET TRANSFUSION IN NICU

3. Thrombocytopenia in neonates is traditionally
difined as a platelet count <150000/mcL
OveralI ncidence of neonatal
thrombocytopenia is (0.7%–0.9%)
In Neonatal Intensive Care Unit (NICU) it is
very high (22%–35%)

4. Mild- (PC = 100000 – 150000/mcl)
Moderate (PC = 50000 – 99000/mcl)
Severe (PC < 50000/mcl)

5. CONDITION
Fetal Alloimmune condition
Congenital infection (e.g., CMV,
toxoplasma, rubella, HIV)
Aneuploidy (e.g., trisomy 18,13, or 21,
or triploidy)
Autoimmune condition (e.g., ITP,
SLE)
Severe Rh hemolytic disease
Congenital/inherited (e.g., Wiskott-
Aldrich syndrome)

6. CONDITION
Early-onset
neonatal (<72
hr)
Placental insufficiency (e.g., PET, IUGR, diabetes)
Perinatal asphyxia
Perinatal infection (e.g., Escherichia coli, GBS, Haemophilus
influenzae), DIC
Alloimmune condition
Autoimmune condition (e.g., ITP, SLE)
Congenital infection (e.g., CMV, toxoplasma, rubella, HIV)
Thrombosis (e.g., aortic, renal vein)
Bone marrow replacement (e.g., congenital leukemia)
Kasabach-Merritt syndrome
Metabolic disease (e.g., proprionic and methylmalonic acidemia)
Congenital/inherited (e.g., TAR, CAMT)

7. Late-onset
neonatal (>72 hr)
Late-onset sepsis
NEC
Congenital infection (e.g., CMV, toxoplasma,
rubella, HIV)
Autoimmune
Kasabach-Merritt syndrome
Metabolic disease (e.g., proprionic and
methylmalonic acidemia)
Congenital/inherited (e.g., TAR, CAMT

9. Early-onset thrombocytopenia (<72 hr)
MILD TO
MODERATE
(PC 50000 -
149000)
-BABY WELL
-EVIDENCE OF PLACENTAL
INSUFFICIENCY
Pc not raising
pc not n by 10
days
Motherwith <pc
pe s/oTAR PRUS
trisomy13,18, 2
1
noonan, Turnar
syn
Pc raising pc
n by 10 days
No further
evaluation
-BABY ILL
- NO EVIDENCE OF
PLACENTAL
INSUFFICIENCY
Evaluate sepsis
, dic
Evidence of
sepsis.DIC pc
>with Tt
No further
evaluation
No evidence of
sepsis,DIC persistent
thrombocytopenias
Mother with <pc
pe s/o TAR PRUS
trisomy 18, 21,13
turnar, Noonan syndrome
SEVERE
PC <50000
Next slde

10. Severe (PC <50000)
Evaluate for sepsis , DIC , NAIT
No sepsis,DIC, NAIT Persistent
thombocytopenias
Mother <PC
Pe s/oTAR PRUS
trisomy 18, 21,13
Noonan, Turnar
syn
Evidence of sepsis,DIC,NAIT
PC improved with Tt
No further evaluation

11. Mother <PC
Pe s/oTAR PRUS
trisomy 18, 21,13
Noonan, Turnar syn
If no to all questions, consider:
TORCH infections Viral
infections (HIV, enterovirus)
Chromosomal abnormalities
Inborn errors of metabolism
Thrombosis (i.e., RVT)
Congenital thrombocytopenias
Yes to any q:
confirmatory
test

13. Late-onset
Thrombocytopenia
Evaluate for sepsis , NEC
Evidence of
sepsis,NEC
PC normal with Tt
No further
evaluation
No Evidence of
sepsis,NEC
• DIC
Viral infection (i.e., HSV, acquired CMV)
Thrombosis (especially if central line
present)
drug-induced thrombocytopenia
inborn errors of metabolism
Fanconi anemia

14. Immune thrombocytopenia occurs due to the passive
transfer of antibodies from the maternal to the fetal
circulation.
Types:
1) Neonatal alloimmune thrombocytopenia (NAIT)
2) Autoimmune thrombocytopenia

15. The antibody is produced in the mother against a specific
human platelet antigen (HPA) present in the fetus but
absent in the mother.
The antigen is inherited from the father of the fetus.
Early onset severe thrombocytopenia.
The combination of severe neonatal thrombocytopenia with
a parenchymal (rather than intraventricular) intracranial
hemorrhage is highly suggestive of NAIT.

16. Investigation:
1)Antigen screening (HPA 1,3,5,9,15,4)
2)Brain imaging studies
Management:
1) Suspected NAIT in an unknown pregnancy
2) Known case of NAIT
3)Antenatal management of pregnant woman with previous
history of NAIT

17. Management of the neonate with suspected NAIT in
an unknown pregnancy.
1) Random-donor platelet transfusion
2)IVIG (1g/kg/day for 2 days)
3) Antigen-negative platelet transfusion
4) Methylprednisolone (1 mg/kg bid for 3–5 days)
Management of the neonate with known NAIT
Antigen-negative platelet transfusion
Antenatal management of pregnant women with
previous history of NAIT
IVIG to mother

19. Platelet Count (*10000mcl)
<30 Transfuse all
30-49 Transfuse if:
• BW <1,500g and & 7 days old
• Clinically unstable
• Concurrent coagulopathy
• Previous significant hemorrhage
(i.e., grade 3 or 4 IVH)
• Prior to surgical procedure
• Postoperative period (72 hours)
50–100 Transfuse if:
• Active bleeding
• NAIT with intracranial bleed
•Before or after neurosurgical
procedures

20. Dose: 10 -15ml/kg
Complications:
Transfusion-transmitted CMV infections
Graft-versus-host disease (GVHD)
TRALI

21. THANK YOU