4th Pediatric Infectious Diseases Conference
 
 
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Pedi Poll
Today's Poll
Should teicoplannin, colistin be used in case of neonatal sepsis where culture does not reveal any organism_?
No, it should be used only after drug sensitivity report
Yes, under guidance of an infectious disease expert
NEONATAL THROMBOCYTOPENIA - A CHALLENGE
NEONATAL THROMBOCYTOPENIA - A CHALLENGE
Dr.M.R.Lokeshwar, Dr.Manisha Bavdekar, Dr.
Shilpa Kulkarni, Dr. Nitin Shah
 

Classification of Thrombocytopenia :

Thrombocytopenia in neonates, as in adult can be caused by decreased production, increased platelet destruction and platelet pooling in enlarged spleen or by combination of these mechanisms. Characterization of mechanism responsible for the thrombocytopenia has practical implication in the management of these patients. For example, transfusion of platelets into an infant with consumptive coagulopathy or peripheral destruction may be of limited or no benefit, since the platelets transfused will be destroyed in a very short time. Most infants in whom thrombocytopenia develops are ill, are premature or associated with other disorders that will contribute to thrombocytopenia including bacteremia, sepsis, DIC, etc. Usually the thrombocytopenia is caused by maternal factors such as anti-platelet-allo or autoantibodies that have crossed the placenta. However, commonest cause of low platelet count is improper collection of blood or inadequate anticoagulants and hence it is wise to confirm the laboratory reports of low platelet count with peripheral blood smear examination which will show clumps of platelet when platelet count and functions are normal.

On the basis of pathophysiological factors, neonatal thrombocytopenia can be classified as: -

  • Immune-mediated

  • Associated with infection - Bacterial or Non-bacterial

  • Drug-Related

  • Increased peripheral consumption of platelets - Disseminated Intravascular Coagulation, Narcotizing enterocolitis, hypersplenism

  • Genetic and Congenital Anomalies

  • Miscellaneous.

Immune-mediated Thrombocytopenia

Immune mediated neonatal thrombocytopenia could be due to:

  • Neonatal allo-immune thrombocytopenia (NAIT)

  • Incidental thrombocytopenia of pregnancy or Gestational thrombocytopenia

  • Autoimmune thrombocytopenic purpura

Neonatal allo-immune thrombocytopenia (NAIT)

When there is incompatibility within parental platelet antigen, mother can become sensitized to an antigen expressed on fetal platelet. This mechanism resembles to that of erythroblastosis fetalis associated with Rh-incompatibility. Maternal antibody is formed in response to fetal platelet antigen inherited from father which is not present on mother's platelet, crosses the placenta and bindsto fetal platelet which are then removed from circulation by fetal reticuloendothelial system. Platelet antigen appears in fetus early in gestation and maternal antibodies can cross placenta early in 2nd trimester thereby inducing severe thrombocytopenia. In the study of 110 fetus with history of sibling allo-thrombocytopenia, Bussel et al (29) reported thrombocytopenia in 50% of fetus with initial platelet < or = 50,000/ul at gestational age of 25 ± 4 weeks. Exact incidence of Feto-Maternal Allo-Immune Thrombocytopenia (FMAIT) is not known but is reported in range of 1 in 1000 to 1 in 5000 births. This is due to incompatibility for human platelet antigen (HPA), most frequently HPA-IA. Immune thrombocytopenia can occur during first pregnancy in more than 50% cases of NAIT and there are no routine screening tests being done (27-35).

Multiple antigens are expressed on the platelets, which include Class I Antigen (HLA), ABO antigen and several bi-allelic platelet alloantigen. Recently the platelet antigens nomenclature have been changed to Human Platelet Antigen (HPA) and different allelic forms are distinguished "a" or "b". "a" indicated more common and "b" indicated more rare allele. Following table give various types of antigen along with previous old names (16).

Antigen systems Other names Antigens Other names
HPA-1 Zw, P1A HPA-1a Zwa,P1A1
    HPA-1b Zwb,P1A2
HPA-2 Ko, Sib HPA-2a Kob
    HPA-2b Koa, Siba
HPA-3 Bak, Lek HPA-3a Bakb
    HPA-3b Baka,Leka
HPA-4 Pen, Yuk HPA-4a Pena,Yukb
    HPA-4b Pena,Yu0a
HPA-5 Br,Zav,Hc HPA-5a Brb,Zavb
    HPA-5b Bra,Zava,Hca
HPA-6 Ca, Tu HPA-6b Ca, Tu
HPA-7 Mo HPA-7b Moa
HPA-8 Sr HPA-8b Sra
HPA-9W Max HPA-9Wb Maxa
HPA = Human Platelet Antigens, W = Workshops (refers to systems that are still under evaluation). Adapted from American Medical Association Manual of Style, ed 9. Baltimore, Williams and Wilkins, 1998, p. 343.

 
 
 
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