Thrombocytopenia, defined as a platelet count below 150,000 per microliter of blood, is the second most common blood disorder encountered during pregnancy, affecting between 7% and 12% of all pregnancies. Platelets are cell fragments that circulate in the blood and play a fundamental role in clotting. A low platelet count is a significant concern during pregnancy because it increases the risk of hemorrhage during delivery and can influence the safety of procedures like neuraxial anesthesia, such as an epidural. While a platelet count of 70,000 to 80,000 per microliter is often considered a minimum threshold for regional anesthesia, a count below 50,000 per microliter can carry a notable risk of spontaneous bleeding.
Gestational Thrombocytopenia
Gestational thrombocytopenia is the most frequent cause of a low platelet count during pregnancy, accounting for 70% to 80% of all cases. This condition is considered a physiological change of normal pregnancy and is typically mild. The reduction in platelet count is thought to be caused by a combination of factors, including the normal expansion of blood volume, known as hemodilution, which effectively dilutes the concentration of platelets.
Increased platelet consumption and clearance also contribute, as platelets are used or removed more quickly in the circulation around the placenta. This condition typically appears late in the second or during the third trimester of pregnancy, and the platelet count rarely drops below 70,000 per microliter.
Gestational thrombocytopenia is a diagnosis of exclusion, meaning other pathological causes must be ruled out first. It causes no complications for the mother or the fetus and resolves spontaneously after delivery, with the platelet count returning to normal within two months postpartum.
Hypertensive Disorders of Pregnancy
Thrombocytopenia is a common feature of hypertensive disorders of pregnancy, particularly Preeclampsia and its more severe variant, HELLP syndrome. Preeclampsia is characterized by new-onset hypertension and organ dysfunction, and it is the second most common cause of a low platelet count, accounting for up to 20% of cases. The mechanism linking these conditions involves widespread damage to the endothelial cells lining the blood vessels.
The damaged endothelium triggers the activation of the coagulation cascade, leading to the formation of small clots and the consumption of circulating platelets. This process, known as microangiopathy, is the direct cause of the low platelet count. Thrombocytopenia is often a sign that the underlying hypertensive disorder is worsening, with the severity of the low count directly correlating with the disease’s progression.
HELLP syndrome, which stands for Hemolysis, Elevated Liver enzymes, and Low Platelets, represents the most severe manifestation of this process. The low platelet count in HELLP can be profound. Delivery is the only definitive treatment for severe Preeclampsia and HELLP syndrome, as it removes the source of the underlying placental dysfunction.
Autoimmune and Immune-Mediated Causes
Immune Thrombocytopenia (ITP) is a less common but significant cause of thrombocytopenia in pregnancy, arising from an autoimmune process. In ITP, the mother’s immune system mistakenly produces antibodies that bind to and destroy her own platelets, primarily in the spleen. This condition may pre-date the pregnancy or be newly discovered during routine prenatal screening.
ITP differs from gestational thrombocytopenia in that it can occur earlier in pregnancy and often results in a more profoundly low platelet count, frequently falling below 50,000 per microliter. The antibodies responsible for destroying the maternal platelets can cross the placenta, potentially causing a low platelet count in the fetus and newborn.
Other systemic autoimmune conditions, such as Systemic Lupus Erythematosus (SLE), can also cause immune-mediated thrombocytopenia during pregnancy. In these cases, the low platelet count is a feature of the broader autoimmune disease activity. Management of immune-mediated thrombocytopenia often requires treatment with steroids or intravenous immunoglobulin to suppress the immune attack on the platelets, especially before delivery.
Rare Thrombotic Microangiopathies
Rare conditions known as thrombotic microangiopathies (TMAs) can also cause severe thrombocytopenia. The most notable of these are Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS), which are characterized by widespread micro-clotting within the small blood vessels. It is important to differentiate these conditions from HELLP syndrome, as the treatment is fundamentally different.
TTP is typically caused by a severe deficiency of the ADAMTS13 enzyme, which is responsible for cleaving large von Willebrand factor molecules. Without this enzyme, the uncleaved molecules spontaneously bind to platelets, causing uncontrolled formation of micro-clots throughout the circulation. This severe platelet consumption results in a very low platelet count, often below 30,000 per microliter.
Atypical HUS (aHUS) is another severe TMA, often triggered by pregnancy in women with an underlying genetic dysregulation of the complement system. This uncontrolled activation of the complement pathway directly damages the vascular endothelium, leading to the formation of platelet-rich thrombi and severe kidney injury. While HELLP is treated by delivery, TTP requires urgent plasma exchange to replace the deficient enzyme, and aHUS is managed with complement-inhibiting drugs, underscoring the need for rapid and accurate diagnosis.