Gestational thrombocytopenia affects between 5% - 11% of normal pregnancies and is usually an incidental finding [2]. It is responsible for 75% - 80% of all cases of thrombocytopenia in pregnancy [3]. As risk factors there is a history of a previous episode, which increases the risk 14.2 times and twin pregnancy [2] [3] [4] [17]. As the cause has been proposed and increase in consumption of platelets by the presidential circulation, inhibition of megakaryocytes induced by hormonal influx and hemodilution [5].

The main characteristics are [2] [3] [7]:

• Asymptomatic

• Occurs more frequently in the second trimester

• Platelet count between 100 - 149 × 10⁹/L (only 1% is less than 100 × 10⁹/L)

• No history of pregestational thrombocytopenia

• Return to normal platelets levels in the first two months post-partum

• Diagnosis of exclusion

Thrombocytopenia is found in about 23.5% of patients with pre-eclampsia [5]. And it is responsible for 15% - 22% of the causes of thrombocytopenia in pregnancy [2] [17]. Thrombocytopenia (100 × 10⁹/L) is included as a diagnostic and severity criterion for preeclampsia, in the presence of arterial hypertension associated with non-proteinuria [18].

It is also well described that microangiopathic hemolytic anemia can occur in the clinical context of preeclampsia, this can precipitate a marked decrease in platelets levels associated with liver dysfunction (HELLP syndrome: Hemolysis, Elevated Liver enzymes, Low Platelet count). It can also be associated with disseminated intravascular coagulation. These two manifestations of the same entity are the main causes that must be ruled out in a patient with thrombocytopenia [3] [7] [8].

Defined as a platelet count below 100 × 10⁹/L without evidence of concomitant disease or etiology [17] [19]. It is responsible for 1% - 4% of all thrombocytopenia cases in pregnancy [17] [20]. The pathophysiologic mechanism has been described as an increase in platelet destruction mediated by antibody production directed against glycoproteins Ia/IIIa arranged in the platelet surface, once the antibodies bind the platelets, they are phagocyted by macrophages and destroyed by cytotoxic T cells. Additionally, insufficient production caused by low levels of thrombopoietin, and a dysfunction of platelet precursor megakaryocytes plays a fundamental role [19] [21] and is classified as:

• Primary or idiopathic ITP (80% of cases)

○ Autoimmune disorder with isolated thrombocytopenia < 100 × 10⁹/L

○ Diagnosis of exclusion

○ Risk of bleeding

• Secondary ITP: Any other immune thrombocytopenia

○ Triggered by viral infections, medications, or vaccines

Or according to the duration:

• De Novo: up to 3 months

• Persistent 3 - 12 months

• Chronic > 12 months

For the differentiation between ITP and gestational thrombocytopenia, it is more likely that it is an ITP if the platelet count is less than 50 × 10⁹/L, if there is a history of pre-pregnancy thrombocytopenia, if it presents from the first trimester, or if it persists postpartum [18]. Another manifestation that can help differentiate them is that in ITP a decrease in platelets is common in the newborn, particularly in the first 2 weeks, and that it is associated with an increased risk of neonatal bleeding [2] [17].

This is a group of diseases with primary involvement of the endothelium that are characterized by microangiopathic hemolytic anemia (schistocytes in the peripheral blood smear, elevated LDH and elevated reticulocytes), associated with thrombocytopenia and organ involvement [20]. They include 4 clinical syndromes that are life-threatening (Table 1): HELLP syndrome, typical or infection-associated hemolytic uremic syndrome, atypical hemolytic uremic syndrome (aHUS) and thrombotic thrombocytopenic purpura (TTP).

When TTP is suspected, ADAMTS13 activity levels should be requested, low levels are confirmatory. However, the result may take several days and if the diagnostic suspicion is high, plasma exchange therapy should be started, since without treatment the mortality rate is 90% [22]. The coexistence of HELLP syndrome must also be considered [23].

Immune complication secondary to the use of heparin, due to the formation of antibodies against the complex formed by the association of heparin with platelet factor 4, this creates a state of hypercoagulability due to monocyte and platelet activation. Occurs in 0.2% - 3% of patients exposed to heparin [25] [26]. The main clinical finding is thrombocytopenia seen in more than 95% of patients with temporary exposure to heparins. The usual drop is 30% - 50% in relation to the baseline count, it is usually a moderate thrombocytopenia between 50 - 70 × 10⁹/L.

Thrombotic events affect veins subjected to punctures or trauma, but can also cause arterial thrombosis of extremities, skin, coronary arteries, among others. In pregnancy, the incidence of thrombotic events in HIT has been reported around 50% [19], usually occurs between 5 - 14 days after the start of heparins. In patients with recent exposure (last 100 days) can occur in the first 24 hours by

preformed antibodies [25] [26]. This diagnosis is therefore highly probable in a patient with thrombotic manifestations and thrombocytopenia.

Although DIC may originate from insults other than sepsis, it is particularly common in sepsis and trauma. Generalized inflammation causes tissue factor dependent coagulation activation associated with uncontrolled plasminogen activation that simultaneously causes prothrombotic and hemorrhagic phenomena with subsequent platelet consumption [27]. There are some triggering causes in pregnancy such as: premature detachment of the placenta, amniotic fluid embolism, sepsis, retained dead fetus, posthemorrhagic shock, hydatidiform mole and gynecological neoplasms [30].

Other causes of thrombocytopenia in pregnancy include fatty liver of pregnancy a rare condition with 1 case between 5000 - 10,000 deliveries, that presents as nausea, vomiting, hypoglycemia, leukocytosis coagulopathy and encephalopathy [17]; folic acid deficiency; leukemia; aplastic anemia; hypersplenism; lupus erythematosus. Those mentioned above have their own characteristics and can be excluded by history or by their specific clinical picture [7] [14] situations that are beyond the scope of this review.