This document discusses neonatal thrombocytopenia, defined as a platelet count below 150,000/cu.mm in newborns. It can be mild, moderate, or severe. Incidence is 1-5% in healthy newborns and higher in preterm/sick infants. Causes include placental insufficiency, infection, maternal conditions, and genetic disorders. Thrombocytopenia is classified as early onset (<72 hours) or late onset (>72 hours) based on time of presentation. Evaluation involves blood tests and smears to identify the cause and guide management, which may include platelet transfusions for severe cases.

1. Neonatal Thrombocytopenia
Dr. Jyoti Shrivastava
Associate Professor
Deptt.of Pathology
G.R.Medical College,Gwalior

2. Introduction
Normal Platelet count is above 150000 /
cu.mm
Fetus(second trimester)
Newborn
Child
Adult
(150000 – 450000 / cu.mm

3. Definition
Neonatal thrombocytopenia is defined as
Platelet count less than 150000 / cu.mm

4. Thrombocytopenia:
MILD - 1.0-1.5 lakh /mcL
MODERATE - 50000 -1.0 lakh /mcL
SEVERE - less than 50000 /mcL

6. Incidence
Newborn : 1-5%
1% -healthy term neonates
Rest – preterm / sick /IUGR
NICU : 22-35%
(50% severe)
6%- total neonates
8% - preterm

7. Thrombocytopenia
Thrombocytopenia
Increased platelet
consumption
Impaired
Megakaryopoiesis

8. Table 1: Classification of fetal and neonatal
thrombocytopenias(Roberts and Murray 2003)
FOETAL
1.Neonatal Alloimmune Thrombopenia (NAIT)
2.Maternal Autoimmune Disease (e.g. ITP, SLE)
3. Aneuploidy (e.g. trisomies 18, 13, 21, or triploidy)
4. Congenital infection (e.g. CMV, toxoplasma, rubella, HIV)
5.Severe Rh- HDN
6.Rare inherited disorders WAS ,TAR

10. Table 1: Classification of fetal and
neonatal
thrombocytopenias
Early onset (<72 hours)
Placental insufficiency (e.g. PET, IUGR, diabetes)
Perinatal asphyxia
Perinatal infection (e.g. E coli, Haemophilus influenzae)
DIC
NAIT (FMAITP)

11. Table 1: Classification of fetal and neonatal
thrombocytopenias
 Congenital infection (e.g. CMV, toxoplasma, rubella, HIV)
 Thrombosis (e.g. aortic, renal vein)
 Bone marrow replacement (e.g. congenital leukaemia)
 Kasabach-Merritt syndrome
 Congenital/inherited (e.g. TAR, Cong.Amegakaryocytic TP)

12. Table 1 Classification of fetal and neonatal
thrombocytopenias
Late onset (>72 hours)
Late onset sepsis
NEC
Congenital infection (e.g. CMV, toxoplasma, rubella, HIV)
Autoimmune
 Kasabach-Merritt syndrome
Congenital / inherited (e.g. TAR, CAMT)

13. Table 3: Comparison of natural history of early
and late onset thrombocytopenia in neonates
EARLY LATE
.
Mild to moderate . Severe
(platelet nadir rarely <50 × 109/l) . (platelet nadir frequently <50 × 109/l)
Evolves slowly over several Rapid onset and progression over 24–48
hours. hours
.
Associated with: Associated with: Sepsis and NEC
pregnancies (PET, IUGR, maternal Dm)
Mechanism: Mechanism:
Impaired platelet production Combined platelet consumption and
impaired production
 Rarely requires specific treatment Multiple platelet transfusions often
required.

14. Thrombocytopenia: assesment
Term or preterm?
Other medical conditions
Are there features suggestive of
congenital infection?
Congenital anomalies/dysmorphism

15. Pathogenesis
 Pre-eclampsia (Early onset)
 Thrombopenia with neutropenia
 Nadir at 3-4 days of life, recovering to normal levels by
day 7-10
 Disruption of hematopoietic progenitor cell
commitment to megakaryopoiesis
 Prematurity may exacerbates.

16. Pathogenesis
Bacterial Sepsis(late onset)
endothelial damage,
 immune mediated destruction,
platelet aggregation
decreased platelet production.
DIC

17. Pathogenesis
1.Viral infections
Viral neuraminidase causes sialic acid loss
from platelet membranes
Intravascular platelet aggregation
2. Congenital infections
Hypersplenism

18. Healthy /Term Neonate
Neonatal alloimmune thrombocytopenia
Maternal autoimmune thrombocytopenia
Occult infection

19. Neonatal alloimmune
thrombocytopenia (NAIT)
 Feto-maternal Alloimmune thrombocytopenia (FMAIT)
 A mother lacks a platelet antigen that her fetus
inherited from father.
 Maternal IgG vs “foreign” antigen on fetal platelets
cross the placenta and destroy them
 Most common platelet antigen HPA-1a and HPA-5b

20. Maternal autoimmune
Thrombocytopenia
Ex. ITP, SLE
Maternal antibodies vs. platelet antigens
a) Glycoprotein IIb/IIIa and Ib/IX
b) Antibodies cross placenta and bind to
these antigens on fetal platelets.

22. Laboratory Investigations
CBC
Platelet count
BT
Blood smear
PT,aPTT
Fibrinogen
FDP
D-dimer

23. Peripheral Smear Examination
Most important
Anticoagulant induced
Pseudothrombocytopenia-EDTA,Citrate
and Heparin
Cold Agglutinins

25. EDTA Smear

26. Heparin Smear

27. Management
1.Severe thrombopenia:50,000/ cu.mm or less
Platelet transfusion
1.pl.count
2.Term/preterm
3.Clinical condition
4.Presence /absence of bleeding

28. Platelet Bags

29. Platelet Indices
Mean Platelet Volume (MPV)
PDW
Guide to Platelet Transfusion

30. MPV: 7.5-11.5 fL
MPV (high)- Increased destruction
MPV (low) – Reduced production
Low MPV-7.5 fL

31. Conclusions
1.Neonatal Thrombocytopenia
newborns/sick/preterm.
2.Initial assessment
gestational age,
co-morbid conditions,
congenital-physical anomalies.
3.mild/moderate
Resolves spontaneously.
4.Severe thrombopenia
Treatment

32. References
 NeoReviews.org: Approach to the Newborn who
has thrombocytopenia. Vol.5 No.10 October 2004
 Curr opinion Obst Gynecol: Platelet disorders in
pregnancy. 2001;13:115-119
 CurrOpinPediatr.2001 Feb;13(1):16-21
 CurrHematol Rep. 2006 Mar;5(1):55-63
 Early Hum Dev.2005 Jan;81(1):35-41
 Avery’s Diseases of the Newborn. Taesch et
Ballard.