Thrombocytopenia is defined as a platelet count below 150×10⁹/l, caused by accelerated platelet destruction or decreased production. It is classified as mild with a platelet count of 100-150×10⁹/l, moderate at 50-100×10⁹/l and severe with less than 50×10⁹/l [1].

Thrombocytopenia is secondly to anaemia as the most common hematologic abnormality during pregnancy [2].

Indeed, a platelet count <150×10⁹/l can be observed in 6 to 15% of pregnant women at the end of pregnancy. Thrombocytopenia is usually moderate (<100×10⁹/l in only 1% of women) and often incidentally detected on routine blood count [3].

Gestational Thrombocytopenia (GT) is considered the most prevalent cause of thrombocytopenia during pregnancy accounting for about 75% of cases [1].

The etiology is unknown, but it is considered to be due to the relative hemodilution of pregnancy, amplified by the capture or destruction of platelets in the placenta [4,5].

GT is considered a minor form of thrombocytopenia, with no substantial risk of hemorrhage for both the mother and the infant.

Gestational thrombocytopenia is characterized by:

− Asymptomatic, mild thrombocytopenia (platelet count >70×10⁹/l).

− No past history of thrombocytopenia (except during a previous pregnancy).

− Occurrence during the 3^rd trimester.

− No fetal / neonatal thrombocytopenia.

− Spontaneous postpartum resolution.

Thrombocytopenia can also be associated with several diseases, either pregnancy-related or not, such as preeclampsia and HELLP syndrome (haemolysis, elevated liver enzymes, low platelet count), which represents about 18% of cases, and Idiopathic Thrombocytopenic Purpura (ITP), which is found in about 5% of cases [6]. Some rare conditions, such as thrombotic thrombocytopenic purpura, haemolytic uremic syndrome, disseminated intravascular coagulation and others account for about 2% of the total [7,8] (Table 1).

Table 1: Causes of thrombocytopenia in decreasing order of frequency during pregnancy.

The Authors present here the results of a retrospective study concerning maternal platelet count fluctuation during pregnancy and puerperium and its correlation with the newborn’s platelet levels in a group of 36 patients referred to the haematology-clinic for gestational thrombocytopenia and who delivered in the same hospital during a period of four years.

Between January 2006 and December 2009, 36 patients with GT (mean gestational age at diagnosis 5 months ± 3 months) who delivered at the Santo Bambino Hospital, c/o Azienda Ospedaliero- Universitaria Policlinico-Vittorio Emanuele, Catania, Italy were enrolled in this study, after carefully excluding other possible causes of this condition, and evaluated retrospectively. GT was defined as an asymptomatic thrombocytopenia occurring during gestation, in patients with a normal platelet count at the beginning and or immediately before pregnancy and without antiplatelet- antibodies. The presence of EDTA-dependent pseudothrombocytopenia was ruled out by performing platelet count also in samples anticoagulated with sodium heparin and trisodium citrate and by examination of a May- Grunwald stained peripheral smear.

A maternal platelet count was determined at the minimum three times during pregnancy and once after delivery in each enrolled patient and at least once in every relative newborn at birth (first time on cord blood). All patients underwent specific tests for the presence of antiplatelet- autoantibodies.

Maternal thrombocytopenia was pharmacologically treated only for platelet count ≤ 90,000/ml with the following drugs: vitamin C (1-2.5 g/die) and tranexanic acid (tranex) 2-2.5 g/die, until 3-4 hours before delivery and for two days after birth.

When maternal platelet count was between 50,000 and 60,000/ ml, prednisone (deltacortene) 0.5-1 mg/kg/die was administered antenatally for about 30 days.

Mothers and their related foetuses-newborns were evaluated retrospectively for symptoms and/or signs of external and internal haemorrhage throughout pregnancy and early puerperium, even in relationship with mode of delivery (caesarean section versus spontaneous vaginal delivery).

A total of 36 patients were retrospectively followed, (22 primigravida). The mean age was 30 ± 2 years. Only 6 women had developed thrombocytopenia in a previous pregnancy (Table 2).

Table 2: Characteristics of patients.

About 45% of the enrolled patients had a caesarean delivery (however only in 1 case, patient 14, table 4, the clinical indication was merely the significant maternal thrombocytopenia and the suspect of a concomitant severe fetal thrombocytopenia by the attending obstetrician , although no maternal antiplatelet-autoantibodies had been identified in this case.

The mean gestational age at the time of diagnosis was 12 ± 3 weeks for the 6 women with a previous history of gestational thrombocytopenia and 28 ± 3 weeks in all the other patients (Table 3).

Table 3: Gestational age at diagnosis.

Initially, when GT was diagnosed in the 36 studied patients, the average platelet count was at the lowest level, 101 ( ± 26.3) × 10⁹/l, it increased to108 ( ± 18.8) × 10⁹/l subsequently during pregnancy and it went further up, 129 (± 27.3) × 10⁹/l, at the time of delivery, reaching the highest level in puerperium: 154 (± 27.9) × 109⁹/l (Figure 1 and Table 4).

Figure 1: Average maternal platelet count fluctuation.

Table 4: Maternal and neonatal platelet count: absolute values.

The search for antiplatelet antibodies was negative in all women; Women during pregnancy didn’t show any sign of hemorrhage and were given a vitamin supplementation (vitamin C), and tranexamic acid only in the presence of platelet count ≤ 90×10⁹/l, and deltacortene (0.5-1 mg/kg/die) for platelet count between 50,000 and 60,000/ml (Table 5).

Table 5: Treatment of thrombocytopenia and type of delivery.

Fetal-neonatal bleeding symptoms were not observed, and only two cases of mild transitory thrombocytopenia were recorded, as reported in Table 6.

Table 6: Maternal thrombocytopenia and neonatal complications.

Thrombocytopenia has been more commonly diagnosed in pregnant women in the last 20 years. It may result in bleeding into mucous membranes presenting as petechiae, ecchymosed, epistaxis, gingival bleeding etc. Moreover, bruising, hematuria, gastrointestinal bleeding and rarely intracranial hemorrhage can occur [9].

The diagnosis of ITP is very difficult during pregnancy because its presentation may closely resemble gestational thrombocytopenia [10,11].

The diagnosis of ITP should be suspected in case of:

− Thrombocytopenia discovered before the 3rd trimester or present before pregnancy.

− Platelet count <75×10⁹/l during pregnancy (in our series 7 cases).

− Presence of autoantibodies (in our series no cases).

− Persistence of thrombocytopenia postpartum (sometimes even thrombocytopenia due to ITP may promptly normalize after delivery).b

The Authors found that, despite the defining criteria, GT may include cases with moderate (n=6) and severe (n=1) maternal thrombocytopenia and, although the absence of antiplatelet-autoantibodies, it may be incidentally associated with mild neonatal thrombocytopenia: 2 cases in this series.

The present study confirm that all observed cases of GT have an uncomplicated course with no related perinatal and maternal morbidity even in patient with initial platelet count <75,000/ml independently from the mode of delivery.

In case of gestational thrombocytopenia, a complete normalization of maternal platelet count should be expected during the postpartum period, even if a diagnosis of a concomitant incidental neonatal thrombocytopenia cannot be excluded.

No intervention, such as a foetal platelet count or caesarean section, is necessary. Periodic platelet counts, either once a trimester or every month, are recommended depending on the level of thrombocytopenia

In cases of thrombocytopenia ≤ 90,000/ml, patients should be given drugs such as: vitamin C (1-1.5 g/die) and tranexanic acid (tranex) 2-2.5 g/die to improve platelet count.

In the past, it has been common practice to perform caesarean section on mothers with severe thrombocytopenia and presence of circulating antiplatelet autoantibodies to lessen the risk of neonatal intracranial haemorrhage due to the trauma of vaginal delivery, especially with foetal platelet counts <50×10⁹/l.

In the above clinical scenario, however, caesarean delivery has not been proved to decrease the incidence of either maternal and or neonatal haemorrhage and of course this is particularly true in case of GT as the present study demonstrates.

Valentina Pafumi has carried out English language editing for this article.