This document discusses neonatal thrombocytopenia. It defines thrombocytopenia in neonates as a platelet count below 150,000/mcL. The incidence is 0.7-0.9% overall but higher in NICUs at 22-35%. Causes include fetal alloimmune conditions, infections, genetic disorders, placental insufficiency, and perinatal complications. Evaluation and management depends on timing of onset (early vs late) and severity (mild, moderate, severe). Testing may include antigen screening for conditions like NAIT. Treatment involves treating any underlying conditions, IVIG, and platelet transfusions following guidelines based on platelet count and clinical status.

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

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

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

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

13. Late-onset
Thrombocytopenia
Evaluate for sepsis , NEC
Evidence of No Evidence of
sepsis,NEC sepsis,NEC
PC normal with Tt
• DIC
Viral infection (i.e., HSV, acquired CMV)
Thrombosis (especially if central line
present)
No further drug-induced thrombocytopenia
evaluation 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 -15 ml/kg
 Complications:
Transfusion-transmitted CMV infections
Graft-versus-host disease (GVHD)
TRALI

21. THANK YOU