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Neonatal Thrombocytopenia
Dr. Jyoti Shrivastava
Associate Professor
Deptt.of Pathology
G.R.Medical College,Gwalior
Introduction
Normal Platelet count is above 150000 /
cu.mm
Fetus(second trimester)
Newborn
Child
Adult
(150000 – 450000 / cu.mm
Definition
Neonatal thrombocytopenia is defined as
Platelet count less than 150000 / cu.mm
Thrombocytopenia:
MILD - 1.0-1.5 lakh /mcL
MODERATE - 50000 -1.0 lakh /mcL
SEVERE - less than 50000 /mcL
Incidence
Newborn : 1-5%
1% -healthy term neonates
Rest – preterm / sick /IUGR
NICU : 22-35%
(50% severe)
6%- total neonates
8% - preterm
Thrombocytopenia
Thrombocytopenia
Increased platelet
consumption
Impaired
Megakaryopoiesis
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
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)
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)
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)
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.
Thrombocytopenia: assesment
Term or preterm?
Other medical conditions
Are there features suggestive of
congenital infection?
Congenital anomalies/dysmorphism
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.
Pathogenesis
Bacterial Sepsis(late onset)
endothelial damage,
 immune mediated destruction,
platelet aggregation
decreased platelet production.
DIC
Pathogenesis
1.Viral infections
Viral neuraminidase causes sialic acid loss
from platelet membranes
Intravascular platelet aggregation
2. Congenital infections
Hypersplenism
Healthy /Term Neonate
Neonatal alloimmune thrombocytopenia
Maternal autoimmune thrombocytopenia
Occult infection
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
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.
Laboratory Investigations
CBC
Platelet count
BT
Blood smear
PT,aPTT
Fibrinogen
FDP
D-dimer
Peripheral Smear Examination
Most important
Anticoagulant induced
Pseudothrombocytopenia-EDTA,Citrate
and Heparin
Cold Agglutinins
EDTA Smear
Heparin Smear
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
Platelet Bags
Platelet Indices
Mean Platelet Volume (MPV)
PDW
Guide to Platelet Transfusion
MPV: 7.5-11.5 fL
MPV (high)- Increased destruction
MPV (low) – Reduced production
Low MPV-7.5 fL
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
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.
Neonatal thrombocytopenia

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Neonatal thrombocytopenia

Editor's Notes

  1. Cm’nest hematolo.abnormay.pediatricians n in labs
  2. Severe –concern,treatment,Intracranial bleed mostly in NICU neonates
  3. Severe thrombopenia in term infants rare3/1000 term infants.1.deg.of thro.penia inversly prop.to gestational age. 2.Severe thrombopenia,risk of bleed
  4. Plat.synthesis/production sick/ill newborn-both mechanisms-low platelets
  5. Classifin based on time of presentation
  6. Majority episodes present within 72 hrs . PET Pre-eclampsia , maternal diabetes with vasculopathy
  7. direct cytotoxicity of on hematopoietic cells, immune-mediated destruction of infected cells, or impaired bone marrow stromal function by . nonspecific autoantibodies that cause antibody-mediated platelet destruction…coagulopathy,hemangiomas n thrombocytopenia
  8. CAMT-ong.amegakaryocytic
  9. Megakaryocytes less,thrombopoietin more
  10. Aggregn.du 2 bact.products,infected b.marrow. Dic complicates sepsis
  11. Any healthy infant,
  12. Determine the mother’s platelet count. cord bld.plt. count, scalp veinsampling, counts repeated 3-4 days.
  13. Screening lab tests in bleedg newborns
  14. Otherwise healthy neonates,no history. Otherwise healthy neonates,no history of disease or abnormality
  15. Altered conformation of plat.memb.Gp and anionic phospholipids-binds Ig-plat.aggregation
  16. Heparin with plat.factor 4,a/b binds.activates plateletes-clumping…………excluded before T/t
  17. No accepte safe level…..Potential triggers. Risks,limited supply,judicious
  18. MCV and RDW
  19. . Plat. Causes MPV less than 7.5-transfusion indicated
  20. Regular follow up,wait n watch