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1. NEONATAL
THROMBOCYTOPENIA
By:
Adrian B. Jayawon
Ma. Joselle L. Balasa
Katrina Kaye C. Bañas
Nikki Marie O. Blanco
Karleen T. Buenasflores
2. Thrombocytopenia
• Defined as a reduction of platelet in the
peripheral blood count of < 150, 000µL.
• Reconfirmation of the platelet count should be
done.
• Confirmation by Blood Film
3. Pathophysiology
• Decreased platelet production (usually in sick or
premature infants)
• Increased platelet destruction (immune or
consumptive)
• Platelet pulling to splenomegaly (rare)
4. Decreased Production
• Thrombocytopenia in sick neonates is low to the
secondary to decreased megakaryopoiesis as
a result of neonatal asphyxia or infection.
• In very sick neonates with disseminated
intravascular coagulopathy (DIC), there may
be platelet destruction
• Bacterial or viral sepsis with or without
disseminated intravascular coaguopathy.
5. Increased Platelet
Destruction
• Infants with immune-mediate
thrombocytopenia have increased platelet
destruction, usually without decreased
production.
• Compensatory increase in megakaryopoiesis is
often observed in the bone marrow.
• Thrombocytopenia occurs in about 10% of
infants whose mothers have ITP.
6. • Infants with Kasabach-Merrit Syndrome (KMS)
usually have severe thrombocytopenia, and
often have evidence of DIC.
• Thrombocytopenia and coagulopathy is
presumed to be due to platelet trapping on the
endothelium of the Kaposiform
Hemagioendothelioma (KHE), but can also be
a result of DIC.
7. • May also occur secondary to thrombosis of a
major vessel.
• Result from platelet consumption at the site of
thrombosis.
9. Neonatal Alloimmune
Thrombocytopenia
• Most frequent cause of thrombocytopenia in
the first few days of life of a healthy infants.
• Severe and can cause serious bleeding; such as
intracranial hemorrhage (ICH)
10. Etiology
• Antibodies to the HPA-1a is responsible for more
than 75% of NAIT cases, while antibodies to the
HPA-5b and other platelet antigens being
implicated in a minority cases.
11. • The risk of HPA-1a alloimmunization is highest in
women who are HLA class II DRB3*0101
12. Pathophysiology
• Maternal IgG alloantibodies formed in the
maternal circulation and cross the placenta
that leads to the destruction of fetal platelets.
• The mother has a normal platelet count, while
the fetus can be severely thrombocytopenic.
13.
14. Clinical Manifestation
• Occur as early as 20 weeks gestation, often
severe (platelet count <20, 000/ µL)
• Major bleeding, particularly intracranial
hemorrhage (ICH), occurs in 10-20% of
untreated NAIT cases.
• Affected infants may present asymptomatic
severe thrombocytopenia, or with mild
bleeding symptoms such as petechiae or
purpura
15.
16. Diagnosis and Treatment
• Diagnosed when platelet antigen
incompatibility is found between the parents,
maternal serum of antibody reacts with
platelets from the infant and father not with
platelets from the mother
• Peripheral smear for the abnormalities and
confirmation of thrombocytopenia is important
17. Autoimmune Neonatal
Thrombocytopenia
Etiology:
Neonatal autoimmune thrombocytopenia can
occur in infants born to women with ITP. Maternal IgG
autoantibodies cross the placenta and bind to neonatal
(and fetal) platelets, and cause platelet destruction by
macrophages in the reticuloendothelial system.
18.
19. Pathophysiology
There was a concomitant drop in the level of
maternal antiplatelet antibody on the child’s platelets.
21. Diagnosis and Treatment
• Blood Test
• CBC
• Platelet antibody tests
• All neonates of mothers with autoimmune disease
should have a cord blood platelet count
determined at birth and again at 24 hours.
• IVIG regardless of whether or not there is evidence
of bleeding
Notas do Editor
These mechanisms are not mutually exclusive, and some infants (particularly sick or premature infants) present with a combination of these mechanisms.
Alloimmunization to inherited paternal platelet antigens and destruction of fetal platelet can occur during the first pregnancy with an antigen incompatible fetus thus presenting a severe thrombocytopenia in an otherwise healthy neonate.
The mom produces antibodies that attack the baby's platelets causing thrombocytopenia. The baby has one platelet antigen from the mom, which the mom recognizes as &quot;self&quot; and one from the father that is of the opposite type, which triggers the immune response.
The Ab is directed against antigens common to maternal and neonatal platelets.
the platelet count should be repeated daily for the next three to four days, as platelet counts are commonly at their lowest during this time before rising spontaneously by day 7 in most cases. As most babies found to have an ICH secondary to maternal autoimmune disorders have had platelet counts of < 30 ´ 109/l.
