WRITE UPS - MISCELLANEOUS: (OB) - Thrombo Cytopenia During Pregnancy

Platelets or thrombocytes are one of the finest friends of obstetricians and their pregnant subjects. The protective responses to pregnancy that are abundantly found in nearly all systems of the mother’s body also include important changes in the platelets. If a subject enters pregnancy with a disorder that keeps her platelet count autoimmunologicaly low like I.T.P. there can be a risk to her as well as her child.

Infact, the commonest platelet anomaly encountered in clinical practice is thrombocytopenia. A thrombocytopenia could be due to four types of conditions.

A) Gestational Thrombocytopenia

B) Thrombocytopenia associated with maternal disease

C) Auto-Immune Thrombocytopenic Purpura

D) Allo-Immune Thrombocytopenia.

Before going into details of these conditions it will be appropriate to consider the physiology of hemostasis in pregnancy.


Never is a woman as greatly exposed to the risks of bleeding as in pregnancy and labor. It is therefore understandable that profound changes take place in the physiology of a pregnant mother so as to generate a tendency of hemostasis. The changes affect the procoagulants and anticoagulants. They affect the pro-fibrinolytic and anti-fibrinolytic, in such a way that ultimate effect is that of hypercoagulability. In a recent study, it has been found that there is an increase in all coagulation factors with the sole exception of factor XI C (1) In this study it was found that the greatest changes were noted in factor VIII C having increased 65% above the baseline at term. This rise was sustained upto 3rd day post partum. The only clotting factor that fell during pregnancy was factor XI –C. Mean anti-thrombin activity was slightly higher in women at term. Though Protein-C remained same in its activity before delivery, it was found to be maximally active in 3 days post partum.

There are major changes in the balance of fibrinolytic system during pregnancy. The concentration of plasminogen and plasminogen activators increase significantly during pregnancy (2). It is now well known that following placental separation maternal plasma fibrinolytic activity increases rapidly.

  We now come to the conditions associated with low platelets in pregnancy.


In an interesting study by Kaplan et-al (3) showed that platelet count decreases with gestation by about 12% between 20 to 40 weeks. In most of these cases thrombocytopenia is mild with platelet counts between 70,000 to 1,50,000/cu. mL (4). These states, in absence of any autoimmune cause are described as gestational thrombocytopenia. This condition could occur due to hormonal depression of megakaryopoesis or placental destruction of platelets. This condition is not associated with any untoward feto-maternal complication (4) and therefore warrants no treatment (5).


Acquired hemolytic anemia, SLE, Septicemia, HIV infection, etc. are associated with thrombocytopenia. One of the recent entries to this list is Antiphospholipid Antibody syndrome (6). Pregnancy complications like P.I.H., placental abruption, etc. and drugs like heparin and aspirin can also produce thrombocytopenia. Kelton et al (7) have shown that all obstetric causes of D.I.C. together can add upto 21% of causes producing thrombocytopenia in pregnancy. Treatment of the parent conditions and that of the obstetric complications thereof manages the conditions of such thrombocytopenia.


Autoimmune thrombocytopenic Purpura (AITP) is 1 to 2 per 1000 pregnancies (4).  Antibodies directed against platelets tend to produce this autoimmune condition. These antibodies are of Ig G types They can cross the placenta and cause thrombocytopenia in the fetus. The platelets that are so coated by the antibodies tend to sludge in the R.E. system where they are conveniently phogocytosed.

The course of pre-existing thrombocytopenia is not affected by pregnancy, but may influence the pregnancy outcome including a grave risk of PPH (8). Severe fetal thrombocytopenia can occur in 12% of such pregnancies and in about 1% there is fetal intra cranial hemorrhage (9). The differentiation of this condition from maternal gestation thrombocytopenia is difficult but more or less academic rather than of significant practical bearing.


Maternal management of AITP in pregnancy rests on three pillars:

A)    Corticosteroids: Prednisolone in a dose of 0.25 – 1 mg/kg/day given upto delivery gives a satisfactory response in upto 90% of cases. This drug inhibits the antibody production and the response is seen within 3 week of starting of steroids (10)(11).

B)    Intravenous Gamma Globulin (Ig G) is effective in 80% of subjects. Its effect is seen within 5-10 days and lasts upto 3 weeks. This treatment acts by interfering with Fc receptor mediated clearance of IgG – coated platelets.(12)

C) Splenectomy: This is usually reserved for those subjects who do not respond to the above two modalities of treatment.

Other therapeutic modalities like Danazol have been tried but with modest success.


Risk of severe fetal thrombocytopenia at term is negligible in the absence of a history of AITP before pregnancy. Currently percutaneous fetal cord blood sampling is the procedure of choice for estimating fetal thrombocytopenia. It is recommended if: there is history of AITP with identifiable PA Ig G antibodies in current pregnancy. Fetuses with severe thrombocytopenia (Count 50,000/ml.) are preferably delivered by cesarean section.

In neonatal period an immediate cord blood platelet count must be performed. In cases with platelet counts < 50000/ml. and petechiae, steroids or preferably IgG should be administered. Platelet concentrate transfusions are indicated in cases of mucous membrane bleeding. Neonatal platelet counts falls further in the first few days of life, hence complications are likely to occur then evaluation of platelet count for the first week is indicated in those neonates with thrombocytopenia at delivery.


It is quite paradoxical to note that this is a serious fetal disorder that has no maternal significance (13). Maternal IgG antibodies directed against fetal platelets causes it. Its mechanism is similar to red cell isoimmunization (8). However, the problem lies in the fact that in nearly half of these cases, the diagnosis is made in retrospect i.e. after the birth of the child. This is also because, it occur predominately in primiparous women (14)(15). In subsequent pregnancies it is estimated to recur in 75% to 90% of cases. The seventy is either similar or worse but never ameliorates.

The first affected child is unsuspected as PLª typing is not done routinely. Also, in Rh isoimmunization, one uses antibody titers to monitor the severity of the disease, similar monitoring has not been found to be useful in this condition. Reznikoff (16) interestingly should that high mild from of the disease and low titters were associated with hemorrhages.

Fetal blood sampling and fetal transfusion by PLª negative platelets is the best way to treat the problem. In high-risk cases when past history of such a condition exists, it is wise to perform cord blood sampling as early as 20 weeks of pregnancy. Goldman (17) and Sagol (18) suggested an alternative approach. They suggested a cordocentesis in all cases at 20 weeks to determine the PLª genotype of the father. If the genotype is heterozygous than only 50% risk of the fetus getting affected. If the father is found to be homozygous for PLª2 than cordocentesis and maternal treatment are necessary. If on cordocentesis the fetal platelet count is >1,00,000/ml., it may be repeated after 10 weeks. If the same is between 50-1,00,000/ml than maternal steroids and Ig G are administered. If the count is 50,000/ml, platelet transfusions – preferably PLª negative is done.


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