Thrombocytopenia, defined as a platelet count below 150 × 10⁹/L, is the second most frequent hematologic disorder seen during pregnancy. The International Working Group (IWG) specifies immune thrombocytopenia using a lower diagnostic cutoff of 100 × 10⁹/L, a condition affecting fewer than 1% of pregnancies. Low platelet counts in pregnancy may arise from obstetric causes, such as gestational thrombocytopenia or preeclampsia/eclampsia, or from systemic diseases including thrombotic thrombocytopenic purpura and immune thrombocytopenia.
For clinical evaluation, the timing of onset whether in the first, second, or third trimester along with the underlying etiology, provides a practical framework for assessment and management. Although thrombocytopenia is relatively common in pregnancy, it rarely results in life-threatening complications on its own. Treatment strategies are directed toward addressing the primary cause rather than targeting platelet levels. Platelet transfusions are generally reserved for patients with active bleeding rather than for prophylactic use.
Institutional protocols often determine platelet thresholds for intervention, and these may vary considerably. Nonetheless, referral to a hematologist is recommended when platelet counts fall below 70 × 10⁹/L or if a concomitant bleeding disorder is suspected or confirmed.
Epidemiology
Thrombocytopenia affects 7–11% of pregnancies, but fewer than 1% experience platelet counts below 100 × 10⁹/L. It is the second most common hematologic disorder in pregnancy after anemia. Gestational thrombocytopenia accounts for nearly 75% of cases and is especially common in the third trimester. Pre-eclampsia, which complicates 2–8% of pregnancies, is responsible for about 20% of thrombocytopenia cases, while immune thrombocytopenia (ITP) is the leading cause in the first trimester, affecting 1–4% of pregnancies. HELLP syndrome, acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura (TTP), atypical hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC) are rare but clinically significant causes associated with high maternal morbidity and mortality. Other uncommon etiologies include hereditary thrombocytopenia, bone marrow failure syndromes, autoimmune conditions, paroxysmal nocturnal hemoglobinuria, antiphospholipid antibody syndrome, type II von Willebrand disease, and drug-induced thrombocytopenia. Although these rare causes occur in less than 1% of pregnancies, they often signal severe disease requiring urgent management.
Anatomy
Pathophysiology
Gestational thrombocytopenia is believed to arise from physiological changes of pregnancy rather than from a pathological process. Suggested mechanisms include dilution due to plasma volume expansion, increased platelet pooling or consumption within the placenta, altered activity of von Willebrand factor and ADAMTS-13, elevated placental production of macrophage colony-stimulating factors, and a relatively inadequate response to thrombopoietin. It usually develops in the later stages of pregnancy, often recurs in subsequent pregnancies, and resolves quickly after delivery, which supports the idea that it is a pregnancy-specific physiological phenomenon rather than an autoimmune condition.
Immune thrombocytopenia is a heterogeneous autoimmune disease that can either be present before pregnancy or become apparent during it. In the majority of cases, it is driven by antibodies against platelets, while in others it is related to abnormalities in T-cell or antigen-presenting cell function. Immune thrombocytopenia may also occur in association with systemic autoimmune conditions such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, or antiphospholipid antibody syndrome.
Thrombotic microangiopathies represent a group of disorders defined by the presence of microangiopathic hemolytic anemia, thrombocytopenia, and organ injury. Pathologically, they are characterized by small vessel thrombosis and endothelial injury. In pregnancy, they are most often seen in association with pre-eclampsia, HELLP syndrome, or acute fatty liver of pregnancy, conditions thought to be linked to placental hypoxia and the release of antiangiogenic factors that cause endothelial dysfunction. Non-pregnancy-related forms include thrombotic thrombocytopenic purpura, which results from deficiency or inhibition of ADAMTS-13, and atypical hemolytic uremic syndrome, which arises from genetic or functional defects in complement regulation.
Disseminated intravascular coagulation is another important cause of thrombocytopenia. It reflects an imbalance between activation of procoagulant pathways and impaired anticoagulant and fibrinolytic activity, leading to platelet consumption and fibrin deposition. In pregnancy, it can develop as a complication of delivery events such as postpartum hemorrhage, uterine atony, abruptio placentae, or retained products of conception. It can also arise in association with pregnancy-related conditions including HELLP syndrome, acute fatty liver of pregnancy, and other thrombotic microangiopathies.
Etiology
Thrombocytopenia in pregnancy arises from diverse causes with varying mechanisms and presentations. Common etiologies include gestational thrombocytopenia, immune thrombocytopenia (ITP), and thrombotic microangiopathies (TMA). TMAs may be pregnancy-specific, such as pre-eclampsia, HELLP syndrome, and acute fatty liver of pregnancy, or unrelated to pregnancy, including thrombotic thrombocytopenic purpura (TTP), atypical hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC). Other contributors are hereditary thrombocytopenias linked to genetic mutations, bone marrow failure syndromes, hematologic malignancies, marrow infiltrative disorders, paroxysmal nocturnal hemoglobinuria (PNH), and drug-induced thrombocytopenia, as well as conditions like type IIB von Willebrand disease and heparin-induced thrombocytopenia (HIT).
The differential diagnosis also depends on gestational age and platelet count. In the first trimester, ITP is most frequent, though hereditary and thrombotic causes should be considered. In the second trimester, platelet counts above 100 × 10⁹/L are usually due to gestational thrombocytopenia, ITP, or pre-eclampsia/HELLP, while counts below 100 × 10⁹/L point more toward ITP, hereditary causes, or TMAs. In the third trimester, gestational thrombocytopenia predominates when counts exceed 100 × 10⁹/L, with pre-eclampsia/HELLP as the next most likely cause. However, when counts fall below 50 × 10⁹/L, pre-eclampsia/HELLP is the leading diagnosis, followed by ITP, TMAs, and hereditary thrombocytopenia.
Genetics
Prognostic Factors
The prognosis of thrombocytopenia in pregnancy depends largely on its underlying cause. Gestational thrombocytopenia is benign, self-limiting, and typically resolves within 4 to 8 weeks postpartum, though it often recurs in later pregnancies without major maternal or neonatal complications. Immune thrombocytopenia carries a higher risk, as it may cause maternal bleeding and transient neonatal thrombocytopenia, but serious neonatal events such as intracranial hemorrhage are very rare, occurring in less than 1% of cases. Thrombotic microangiopathies, whether pregnancy-related such as pre-eclampsia, HELLP, and acute fatty liver of pregnancy, or non-pregnancy-related such as thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome, are associated with significant maternal and neonatal morbidity and mortality, though thrombocytopenia itself is not the main driver of complications. Other rare causes, including bone marrow failure syndromes and paroxysmal nocturnal hemoglobinuria, should be managed according to their primary etiology. Neonatal outcomes are excellent in gestational thrombocytopenia, while in ITP, platelet counts may fall transiently but usually recover, with severe bleeding being exceptionally uncommon.
Clinical History
A detailed history and physical examination are essential for identifying the cause of thrombocytopenia. Symptoms usually appear only when platelet counts are very low or when the underlying disorder manifests. While the temporal pattern of thrombocytopenia or bleeding (acute, chronic, or relapsing-remitting) does not establish the cause, it helps characterize the clinical phenotype. Past medical history, including autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis, infections, malignancies, or prior transplants, is important for diagnosis. Medication history, recent vaccinations, travel, dietary practices, and high-risk behaviors including smoking, alcohol use, sexual practices, and illicit drug use provide additional clues. Family history is particularly valuable for identifying congenital thrombocytopenia, which can first present in adulthood.
Physical examination offers further guidance. Women with gestational thrombocytopenia are generally healthy and asymptomatic, with low platelet counts discovered incidentally. In contrast, patients with thrombotic microangiopathies are often acutely ill and may require high-risk obstetric care. Mucocutaneous bleeding is a common finding, whereas joint or severe bleeding should prompt evaluation for serious coagulopathies such as disseminated intravascular coagulation. Examination should also assess for hepatomegaly or splenomegaly, skeletal abnormalities such as absent radius or humeral deformities seen in syndromes like thrombocytopenia absent radii, and characteristic skin findings including petechiae or purpura in immune thrombocytopenia or eczema in Wiskott-Aldrich syndrome.
Physical Examination
Age group
Associated comorbidity
Associated Comorbidity or Activity:
Gestational thrombocytopenia – Occurs in otherwise healthy women, usually without comorbidities; often discovered incidentally during routine pregnancy labs.
Immune thrombocytopenia (ITP) – May coexist with autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, or antiphospholipid antibody syndrome.
Pregnancy-related TMA (PEC/HELLP/AFLP) – Strongly associated with hypertensive disorders of pregnancy, abnormal liver function, and metabolic disturbances.
Non-pregnancy-related TMA (TTP, atypical HUS) – May be linked to inherited enzyme deficiencies (ADAMTS-13), complement pathway mutations, or prior personal/family history of TMA.
Disseminated intravascular coagulation (DIC) – Associated with obstetric complications such as postpartum hemorrhage, abruptio placentae, amniotic fluid embolism, or retained products of conception.
Other rare causes – Bone marrow failure syndromes, hematologic malignancies, paroxysmal nocturnal hemoglobinuria, and drug-induced thrombocytopenia.
Associated activity
Acuity of presentation
Gestational thrombocytopenia is almost always asymptomatic, discovered incidentally, and progresses gradually, making it a mild and non-acute condition. Immune thrombocytopenia may present either acutely with a flare during pregnancy or more chronically if pre-existing, though most women remain stable with only mild bleeding risk. Pregnancy-related thrombotic microangiopathies such as pre-eclampsia, HELLP syndrome, and acute fatty liver of pregnancy usually present acutely in the second or third trimester, often with systemic symptoms like hypertension, hemolysis, and liver dysfunction, requiring urgent intervention. Non-pregnancy-related TMAs such as thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome typically present with abrupt and severe symptoms, including hemolysis, thrombocytopenia, and organ failure, and are medical emergencies. Disseminated intravascular coagulation also presents acutely, often triggered by obstetric catastrophes such as postpartum hemorrhage or placental abruption, and carries high maternal and fetal risk. Other causes such as hereditary thrombocytopenia or bone marrow failure syndromes tend to present chronically and are usually identified before or early in pregnancy.
Differential Diagnoses
Gestational thrombocytopenia
Immune thrombocytopenia (ITP)
Pre-eclampsia (PEC)
HELLP syndrome
Acute fatty liver of pregnancy (AFLP)
Thrombotic thrombocytopenic purpura (TTP)
Atypical hemolytic-uremic syndrome (aHUS)
Disseminated intravascular coagulation (DIC)
Hereditary thrombocytopenia
Bone marrow failure syndromes
Paroxysmal nocturnal hemoglobinuria (PNH)
Type II von Willebrand disease (VWD)
Hematologic malignancies
Drug-induced thrombocytopenia
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Gestational thrombocytopenia: Usually requires no treatment, as it is self-limiting and resolves postpartum. Monitoring of platelet counts is sufficient.
Immune thrombocytopenia (ITP): Treatment is indicated for maternal bleeding, very low platelet counts, or prior to delivery. First-line therapy includes corticosteroids or intravenous immunoglobulin. Platelet transfusions are reserved for severe bleeding or peripartum management.
Pregnancy-related thrombotic microangiopathies (PEC, HELLP, AFLP): Definitive treatment is delivery of the fetus. Supportive care includes blood pressure control, seizure prophylaxis, and monitoring for maternal organ dysfunction. Platelet transfusions may be used if significant bleeding occurs or for invasive procedures.
Non-pregnancy-related TMAs (TTP, aHUS): Require specialized therapy such as plasma exchange for TTP or complement inhibitors for atypical HUS, along with supportive care.
Disseminated intravascular coagulation (DIC): Treat the underlying cause (obstetric complications or systemic illness) with supportive care, including blood products, coagulation factor replacement, and careful hemodynamic management.
Hereditary thrombocytopenia and other rare causes: Management is tailored to the specific disorder, including genetic counseling, disease-specific therapy, and supportive care as needed.
Delivery planning: Mode of delivery is based on obstetric indications and maternal platelet counts. A hematologist should be involved when counts are critically low or complex disorders are present.
Rituximab: Monoclonal antibody targeting CD20 on B-cells, reducing autoantibody production against platelets.
Caplacizumab: vWF-directed antibody fragment that blocks the A1 domain of von Willebrand factor, preventing platelet adhesion and microvascular thrombosis.
Eculizumab: Humanized monoclonal antibody against complement protein C5, preventing formation of the membrane attack complex and reducing complement-mediated hemolysis.
Confirm thrombocytopenia with repeat platelet counts.
Obtain a detailed history including prior thrombocytopenia, autoimmune disorders, medications, infections, family history, and obstetric complications.
Perform a thorough physical examination to look for bleeding, organomegaly, or congenital syndromes.
Identify the underlying etiology through laboratory tests and, if needed, specialized investigations (e.g., ADAMTS-13, complement studies, bone marrow evaluation).
Risk Stratification and Monitoring
Assess maternal bleeding risk based on platelet count and clinical symptoms.
Monitor platelet trends throughout pregnancy.
Evaluate fetal risk, particularly in immune-mediated thrombocytopenia.
Determine timing and mode of delivery based on obstetric indications and platelet counts.
Targeted Treatment
Gestational thrombocytopenia: Usually observation only.
Immune thrombocytopenia: Corticosteroids, IVIG, or other immunosuppressants if indicated; platelet transfusion for bleeding or peri-delivery.
Pregnancy-related TMA (PEC, HELLP, AFLP): Delivery of the fetus with supportive care.
Thrombocytopenia, defined as a platelet count below 150 × 10⁹/L, is the second most frequent hematologic disorder seen during pregnancy. The International Working Group (IWG) specifies immune thrombocytopenia using a lower diagnostic cutoff of 100 × 10⁹/L, a condition affecting fewer than 1% of pregnancies. Low platelet counts in pregnancy may arise from obstetric causes, such as gestational thrombocytopenia or preeclampsia/eclampsia, or from systemic diseases including thrombotic thrombocytopenic purpura and immune thrombocytopenia.
For clinical evaluation, the timing of onset whether in the first, second, or third trimester along with the underlying etiology, provides a practical framework for assessment and management. Although thrombocytopenia is relatively common in pregnancy, it rarely results in life-threatening complications on its own. Treatment strategies are directed toward addressing the primary cause rather than targeting platelet levels. Platelet transfusions are generally reserved for patients with active bleeding rather than for prophylactic use.
Institutional protocols often determine platelet thresholds for intervention, and these may vary considerably. Nonetheless, referral to a hematologist is recommended when platelet counts fall below 70 × 10⁹/L or if a concomitant bleeding disorder is suspected or confirmed.
Thrombocytopenia affects 7–11% of pregnancies, but fewer than 1% experience platelet counts below 100 × 10⁹/L. It is the second most common hematologic disorder in pregnancy after anemia. Gestational thrombocytopenia accounts for nearly 75% of cases and is especially common in the third trimester. Pre-eclampsia, which complicates 2–8% of pregnancies, is responsible for about 20% of thrombocytopenia cases, while immune thrombocytopenia (ITP) is the leading cause in the first trimester, affecting 1–4% of pregnancies. HELLP syndrome, acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura (TTP), atypical hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC) are rare but clinically significant causes associated with high maternal morbidity and mortality. Other uncommon etiologies include hereditary thrombocytopenia, bone marrow failure syndromes, autoimmune conditions, paroxysmal nocturnal hemoglobinuria, antiphospholipid antibody syndrome, type II von Willebrand disease, and drug-induced thrombocytopenia. Although these rare causes occur in less than 1% of pregnancies, they often signal severe disease requiring urgent management.
Gestational thrombocytopenia is believed to arise from physiological changes of pregnancy rather than from a pathological process. Suggested mechanisms include dilution due to plasma volume expansion, increased platelet pooling or consumption within the placenta, altered activity of von Willebrand factor and ADAMTS-13, elevated placental production of macrophage colony-stimulating factors, and a relatively inadequate response to thrombopoietin. It usually develops in the later stages of pregnancy, often recurs in subsequent pregnancies, and resolves quickly after delivery, which supports the idea that it is a pregnancy-specific physiological phenomenon rather than an autoimmune condition.
Immune thrombocytopenia is a heterogeneous autoimmune disease that can either be present before pregnancy or become apparent during it. In the majority of cases, it is driven by antibodies against platelets, while in others it is related to abnormalities in T-cell or antigen-presenting cell function. Immune thrombocytopenia may also occur in association with systemic autoimmune conditions such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, or antiphospholipid antibody syndrome.
Thrombotic microangiopathies represent a group of disorders defined by the presence of microangiopathic hemolytic anemia, thrombocytopenia, and organ injury. Pathologically, they are characterized by small vessel thrombosis and endothelial injury. In pregnancy, they are most often seen in association with pre-eclampsia, HELLP syndrome, or acute fatty liver of pregnancy, conditions thought to be linked to placental hypoxia and the release of antiangiogenic factors that cause endothelial dysfunction. Non-pregnancy-related forms include thrombotic thrombocytopenic purpura, which results from deficiency or inhibition of ADAMTS-13, and atypical hemolytic uremic syndrome, which arises from genetic or functional defects in complement regulation.
Disseminated intravascular coagulation is another important cause of thrombocytopenia. It reflects an imbalance between activation of procoagulant pathways and impaired anticoagulant and fibrinolytic activity, leading to platelet consumption and fibrin deposition. In pregnancy, it can develop as a complication of delivery events such as postpartum hemorrhage, uterine atony, abruptio placentae, or retained products of conception. It can also arise in association with pregnancy-related conditions including HELLP syndrome, acute fatty liver of pregnancy, and other thrombotic microangiopathies.
Thrombocytopenia in pregnancy arises from diverse causes with varying mechanisms and presentations. Common etiologies include gestational thrombocytopenia, immune thrombocytopenia (ITP), and thrombotic microangiopathies (TMA). TMAs may be pregnancy-specific, such as pre-eclampsia, HELLP syndrome, and acute fatty liver of pregnancy, or unrelated to pregnancy, including thrombotic thrombocytopenic purpura (TTP), atypical hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC). Other contributors are hereditary thrombocytopenias linked to genetic mutations, bone marrow failure syndromes, hematologic malignancies, marrow infiltrative disorders, paroxysmal nocturnal hemoglobinuria (PNH), and drug-induced thrombocytopenia, as well as conditions like type IIB von Willebrand disease and heparin-induced thrombocytopenia (HIT).
The differential diagnosis also depends on gestational age and platelet count. In the first trimester, ITP is most frequent, though hereditary and thrombotic causes should be considered. In the second trimester, platelet counts above 100 × 10⁹/L are usually due to gestational thrombocytopenia, ITP, or pre-eclampsia/HELLP, while counts below 100 × 10⁹/L point more toward ITP, hereditary causes, or TMAs. In the third trimester, gestational thrombocytopenia predominates when counts exceed 100 × 10⁹/L, with pre-eclampsia/HELLP as the next most likely cause. However, when counts fall below 50 × 10⁹/L, pre-eclampsia/HELLP is the leading diagnosis, followed by ITP, TMAs, and hereditary thrombocytopenia.
The prognosis of thrombocytopenia in pregnancy depends largely on its underlying cause. Gestational thrombocytopenia is benign, self-limiting, and typically resolves within 4 to 8 weeks postpartum, though it often recurs in later pregnancies without major maternal or neonatal complications. Immune thrombocytopenia carries a higher risk, as it may cause maternal bleeding and transient neonatal thrombocytopenia, but serious neonatal events such as intracranial hemorrhage are very rare, occurring in less than 1% of cases. Thrombotic microangiopathies, whether pregnancy-related such as pre-eclampsia, HELLP, and acute fatty liver of pregnancy, or non-pregnancy-related such as thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome, are associated with significant maternal and neonatal morbidity and mortality, though thrombocytopenia itself is not the main driver of complications. Other rare causes, including bone marrow failure syndromes and paroxysmal nocturnal hemoglobinuria, should be managed according to their primary etiology. Neonatal outcomes are excellent in gestational thrombocytopenia, while in ITP, platelet counts may fall transiently but usually recover, with severe bleeding being exceptionally uncommon.
A detailed history and physical examination are essential for identifying the cause of thrombocytopenia. Symptoms usually appear only when platelet counts are very low or when the underlying disorder manifests. While the temporal pattern of thrombocytopenia or bleeding (acute, chronic, or relapsing-remitting) does not establish the cause, it helps characterize the clinical phenotype. Past medical history, including autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis, infections, malignancies, or prior transplants, is important for diagnosis. Medication history, recent vaccinations, travel, dietary practices, and high-risk behaviors including smoking, alcohol use, sexual practices, and illicit drug use provide additional clues. Family history is particularly valuable for identifying congenital thrombocytopenia, which can first present in adulthood.
Physical examination offers further guidance. Women with gestational thrombocytopenia are generally healthy and asymptomatic, with low platelet counts discovered incidentally. In contrast, patients with thrombotic microangiopathies are often acutely ill and may require high-risk obstetric care. Mucocutaneous bleeding is a common finding, whereas joint or severe bleeding should prompt evaluation for serious coagulopathies such as disseminated intravascular coagulation. Examination should also assess for hepatomegaly or splenomegaly, skeletal abnormalities such as absent radius or humeral deformities seen in syndromes like thrombocytopenia absent radii, and characteristic skin findings including petechiae or purpura in immune thrombocytopenia or eczema in Wiskott-Aldrich syndrome.
Associated Comorbidity or Activity:
Gestational thrombocytopenia – Occurs in otherwise healthy women, usually without comorbidities; often discovered incidentally during routine pregnancy labs.
Immune thrombocytopenia (ITP) – May coexist with autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, or antiphospholipid antibody syndrome.
Pregnancy-related TMA (PEC/HELLP/AFLP) – Strongly associated with hypertensive disorders of pregnancy, abnormal liver function, and metabolic disturbances.
Non-pregnancy-related TMA (TTP, atypical HUS) – May be linked to inherited enzyme deficiencies (ADAMTS-13), complement pathway mutations, or prior personal/family history of TMA.
Disseminated intravascular coagulation (DIC) – Associated with obstetric complications such as postpartum hemorrhage, abruptio placentae, amniotic fluid embolism, or retained products of conception.
Other rare causes – Bone marrow failure syndromes, hematologic malignancies, paroxysmal nocturnal hemoglobinuria, and drug-induced thrombocytopenia.
Gestational thrombocytopenia is almost always asymptomatic, discovered incidentally, and progresses gradually, making it a mild and non-acute condition. Immune thrombocytopenia may present either acutely with a flare during pregnancy or more chronically if pre-existing, though most women remain stable with only mild bleeding risk. Pregnancy-related thrombotic microangiopathies such as pre-eclampsia, HELLP syndrome, and acute fatty liver of pregnancy usually present acutely in the second or third trimester, often with systemic symptoms like hypertension, hemolysis, and liver dysfunction, requiring urgent intervention. Non-pregnancy-related TMAs such as thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome typically present with abrupt and severe symptoms, including hemolysis, thrombocytopenia, and organ failure, and are medical emergencies. Disseminated intravascular coagulation also presents acutely, often triggered by obstetric catastrophes such as postpartum hemorrhage or placental abruption, and carries high maternal and fetal risk. Other causes such as hereditary thrombocytopenia or bone marrow failure syndromes tend to present chronically and are usually identified before or early in pregnancy.
Gestational thrombocytopenia
Immune thrombocytopenia (ITP)
Pre-eclampsia (PEC)
HELLP syndrome
Acute fatty liver of pregnancy (AFLP)
Thrombotic thrombocytopenic purpura (TTP)
Atypical hemolytic-uremic syndrome (aHUS)
Disseminated intravascular coagulation (DIC)
Hereditary thrombocytopenia
Bone marrow failure syndromes
Paroxysmal nocturnal hemoglobinuria (PNH)
Type II von Willebrand disease (VWD)
Hematologic malignancies
Drug-induced thrombocytopenia
Gestational thrombocytopenia: Usually requires no treatment, as it is self-limiting and resolves postpartum. Monitoring of platelet counts is sufficient.
Immune thrombocytopenia (ITP): Treatment is indicated for maternal bleeding, very low platelet counts, or prior to delivery. First-line therapy includes corticosteroids or intravenous immunoglobulin. Platelet transfusions are reserved for severe bleeding or peripartum management.
Pregnancy-related thrombotic microangiopathies (PEC, HELLP, AFLP): Definitive treatment is delivery of the fetus. Supportive care includes blood pressure control, seizure prophylaxis, and monitoring for maternal organ dysfunction. Platelet transfusions may be used if significant bleeding occurs or for invasive procedures.
Non-pregnancy-related TMAs (TTP, aHUS): Require specialized therapy such as plasma exchange for TTP or complement inhibitors for atypical HUS, along with supportive care.
Disseminated intravascular coagulation (DIC): Treat the underlying cause (obstetric complications or systemic illness) with supportive care, including blood products, coagulation factor replacement, and careful hemodynamic management.
Hereditary thrombocytopenia and other rare causes: Management is tailored to the specific disorder, including genetic counseling, disease-specific therapy, and supportive care as needed.
Delivery planning: Mode of delivery is based on obstetric indications and maternal platelet counts. A hematologist should be involved when counts are critically low or complex disorders are present.
Rituximab: Monoclonal antibody targeting CD20 on B-cells, reducing autoantibody production against platelets.
Caplacizumab: vWF-directed antibody fragment that blocks the A1 domain of von Willebrand factor, preventing platelet adhesion and microvascular thrombosis.
Eculizumab: Humanized monoclonal antibody against complement protein C5, preventing formation of the membrane attack complex and reducing complement-mediated hemolysis.
Azathioprine: Immunosuppressant that interferes with DNA synthesis in rapidly dividing immune cells, reducing autoantibody formation.
Cyclosporine: Inhibits calcineurin, suppressing T-cell activation and modulating the immune response against platelets.
Argatroban, Bivalirudin: Bind and inhibit thrombin, preventing clot formation in heparin-induced thrombocytopenia.
Fondaparinux: Synthetic pentasaccharide that inhibits factor Xa, providing anticoagulation without cross-reacting with heparin-dependent antibodies.
Initial Assessment and Diagnosis
Confirm thrombocytopenia with repeat platelet counts.
Obtain a detailed history including prior thrombocytopenia, autoimmune disorders, medications, infections, family history, and obstetric complications.
Perform a thorough physical examination to look for bleeding, organomegaly, or congenital syndromes.
Identify the underlying etiology through laboratory tests and, if needed, specialized investigations (e.g., ADAMTS-13, complement studies, bone marrow evaluation).
Risk Stratification and Monitoring
Assess maternal bleeding risk based on platelet count and clinical symptoms.
Monitor platelet trends throughout pregnancy.
Evaluate fetal risk, particularly in immune-mediated thrombocytopenia.
Determine timing and mode of delivery based on obstetric indications and platelet counts.
Targeted Treatment
Gestational thrombocytopenia: Usually observation only.
Immune thrombocytopenia: Corticosteroids, IVIG, or other immunosuppressants if indicated; platelet transfusion for bleeding or peri-delivery.
Pregnancy-related TMA (PEC, HELLP, AFLP): Delivery of the fetus with supportive care.
Thrombocytopenia, defined as a platelet count below 150 × 10⁹/L, is the second most frequent hematologic disorder seen during pregnancy. The International Working Group (IWG) specifies immune thrombocytopenia using a lower diagnostic cutoff of 100 × 10⁹/L, a condition affecting fewer than 1% of pregnancies. Low platelet counts in pregnancy may arise from obstetric causes, such as gestational thrombocytopenia or preeclampsia/eclampsia, or from systemic diseases including thrombotic thrombocytopenic purpura and immune thrombocytopenia.
For clinical evaluation, the timing of onset whether in the first, second, or third trimester along with the underlying etiology, provides a practical framework for assessment and management. Although thrombocytopenia is relatively common in pregnancy, it rarely results in life-threatening complications on its own. Treatment strategies are directed toward addressing the primary cause rather than targeting platelet levels. Platelet transfusions are generally reserved for patients with active bleeding rather than for prophylactic use.
Institutional protocols often determine platelet thresholds for intervention, and these may vary considerably. Nonetheless, referral to a hematologist is recommended when platelet counts fall below 70 × 10⁹/L or if a concomitant bleeding disorder is suspected or confirmed.
Thrombocytopenia affects 7–11% of pregnancies, but fewer than 1% experience platelet counts below 100 × 10⁹/L. It is the second most common hematologic disorder in pregnancy after anemia. Gestational thrombocytopenia accounts for nearly 75% of cases and is especially common in the third trimester. Pre-eclampsia, which complicates 2–8% of pregnancies, is responsible for about 20% of thrombocytopenia cases, while immune thrombocytopenia (ITP) is the leading cause in the first trimester, affecting 1–4% of pregnancies. HELLP syndrome, acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura (TTP), atypical hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC) are rare but clinically significant causes associated with high maternal morbidity and mortality. Other uncommon etiologies include hereditary thrombocytopenia, bone marrow failure syndromes, autoimmune conditions, paroxysmal nocturnal hemoglobinuria, antiphospholipid antibody syndrome, type II von Willebrand disease, and drug-induced thrombocytopenia. Although these rare causes occur in less than 1% of pregnancies, they often signal severe disease requiring urgent management.
Gestational thrombocytopenia is believed to arise from physiological changes of pregnancy rather than from a pathological process. Suggested mechanisms include dilution due to plasma volume expansion, increased platelet pooling or consumption within the placenta, altered activity of von Willebrand factor and ADAMTS-13, elevated placental production of macrophage colony-stimulating factors, and a relatively inadequate response to thrombopoietin. It usually develops in the later stages of pregnancy, often recurs in subsequent pregnancies, and resolves quickly after delivery, which supports the idea that it is a pregnancy-specific physiological phenomenon rather than an autoimmune condition.
Immune thrombocytopenia is a heterogeneous autoimmune disease that can either be present before pregnancy or become apparent during it. In the majority of cases, it is driven by antibodies against platelets, while in others it is related to abnormalities in T-cell or antigen-presenting cell function. Immune thrombocytopenia may also occur in association with systemic autoimmune conditions such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, or antiphospholipid antibody syndrome.
Thrombotic microangiopathies represent a group of disorders defined by the presence of microangiopathic hemolytic anemia, thrombocytopenia, and organ injury. Pathologically, they are characterized by small vessel thrombosis and endothelial injury. In pregnancy, they are most often seen in association with pre-eclampsia, HELLP syndrome, or acute fatty liver of pregnancy, conditions thought to be linked to placental hypoxia and the release of antiangiogenic factors that cause endothelial dysfunction. Non-pregnancy-related forms include thrombotic thrombocytopenic purpura, which results from deficiency or inhibition of ADAMTS-13, and atypical hemolytic uremic syndrome, which arises from genetic or functional defects in complement regulation.
Disseminated intravascular coagulation is another important cause of thrombocytopenia. It reflects an imbalance between activation of procoagulant pathways and impaired anticoagulant and fibrinolytic activity, leading to platelet consumption and fibrin deposition. In pregnancy, it can develop as a complication of delivery events such as postpartum hemorrhage, uterine atony, abruptio placentae, or retained products of conception. It can also arise in association with pregnancy-related conditions including HELLP syndrome, acute fatty liver of pregnancy, and other thrombotic microangiopathies.
Thrombocytopenia in pregnancy arises from diverse causes with varying mechanisms and presentations. Common etiologies include gestational thrombocytopenia, immune thrombocytopenia (ITP), and thrombotic microangiopathies (TMA). TMAs may be pregnancy-specific, such as pre-eclampsia, HELLP syndrome, and acute fatty liver of pregnancy, or unrelated to pregnancy, including thrombotic thrombocytopenic purpura (TTP), atypical hemolytic-uremic syndrome (HUS), and disseminated intravascular coagulation (DIC). Other contributors are hereditary thrombocytopenias linked to genetic mutations, bone marrow failure syndromes, hematologic malignancies, marrow infiltrative disorders, paroxysmal nocturnal hemoglobinuria (PNH), and drug-induced thrombocytopenia, as well as conditions like type IIB von Willebrand disease and heparin-induced thrombocytopenia (HIT).
The differential diagnosis also depends on gestational age and platelet count. In the first trimester, ITP is most frequent, though hereditary and thrombotic causes should be considered. In the second trimester, platelet counts above 100 × 10⁹/L are usually due to gestational thrombocytopenia, ITP, or pre-eclampsia/HELLP, while counts below 100 × 10⁹/L point more toward ITP, hereditary causes, or TMAs. In the third trimester, gestational thrombocytopenia predominates when counts exceed 100 × 10⁹/L, with pre-eclampsia/HELLP as the next most likely cause. However, when counts fall below 50 × 10⁹/L, pre-eclampsia/HELLP is the leading diagnosis, followed by ITP, TMAs, and hereditary thrombocytopenia.
The prognosis of thrombocytopenia in pregnancy depends largely on its underlying cause. Gestational thrombocytopenia is benign, self-limiting, and typically resolves within 4 to 8 weeks postpartum, though it often recurs in later pregnancies without major maternal or neonatal complications. Immune thrombocytopenia carries a higher risk, as it may cause maternal bleeding and transient neonatal thrombocytopenia, but serious neonatal events such as intracranial hemorrhage are very rare, occurring in less than 1% of cases. Thrombotic microangiopathies, whether pregnancy-related such as pre-eclampsia, HELLP, and acute fatty liver of pregnancy, or non-pregnancy-related such as thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome, are associated with significant maternal and neonatal morbidity and mortality, though thrombocytopenia itself is not the main driver of complications. Other rare causes, including bone marrow failure syndromes and paroxysmal nocturnal hemoglobinuria, should be managed according to their primary etiology. Neonatal outcomes are excellent in gestational thrombocytopenia, while in ITP, platelet counts may fall transiently but usually recover, with severe bleeding being exceptionally uncommon.
A detailed history and physical examination are essential for identifying the cause of thrombocytopenia. Symptoms usually appear only when platelet counts are very low or when the underlying disorder manifests. While the temporal pattern of thrombocytopenia or bleeding (acute, chronic, or relapsing-remitting) does not establish the cause, it helps characterize the clinical phenotype. Past medical history, including autoimmune diseases such as systemic lupus erythematosus or rheumatoid arthritis, infections, malignancies, or prior transplants, is important for diagnosis. Medication history, recent vaccinations, travel, dietary practices, and high-risk behaviors including smoking, alcohol use, sexual practices, and illicit drug use provide additional clues. Family history is particularly valuable for identifying congenital thrombocytopenia, which can first present in adulthood.
Physical examination offers further guidance. Women with gestational thrombocytopenia are generally healthy and asymptomatic, with low platelet counts discovered incidentally. In contrast, patients with thrombotic microangiopathies are often acutely ill and may require high-risk obstetric care. Mucocutaneous bleeding is a common finding, whereas joint or severe bleeding should prompt evaluation for serious coagulopathies such as disseminated intravascular coagulation. Examination should also assess for hepatomegaly or splenomegaly, skeletal abnormalities such as absent radius or humeral deformities seen in syndromes like thrombocytopenia absent radii, and characteristic skin findings including petechiae or purpura in immune thrombocytopenia or eczema in Wiskott-Aldrich syndrome.
Associated Comorbidity or Activity:
Gestational thrombocytopenia – Occurs in otherwise healthy women, usually without comorbidities; often discovered incidentally during routine pregnancy labs.
Immune thrombocytopenia (ITP) – May coexist with autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, or antiphospholipid antibody syndrome.
Pregnancy-related TMA (PEC/HELLP/AFLP) – Strongly associated with hypertensive disorders of pregnancy, abnormal liver function, and metabolic disturbances.
Non-pregnancy-related TMA (TTP, atypical HUS) – May be linked to inherited enzyme deficiencies (ADAMTS-13), complement pathway mutations, or prior personal/family history of TMA.
Disseminated intravascular coagulation (DIC) – Associated with obstetric complications such as postpartum hemorrhage, abruptio placentae, amniotic fluid embolism, or retained products of conception.
Other rare causes – Bone marrow failure syndromes, hematologic malignancies, paroxysmal nocturnal hemoglobinuria, and drug-induced thrombocytopenia.
Gestational thrombocytopenia is almost always asymptomatic, discovered incidentally, and progresses gradually, making it a mild and non-acute condition. Immune thrombocytopenia may present either acutely with a flare during pregnancy or more chronically if pre-existing, though most women remain stable with only mild bleeding risk. Pregnancy-related thrombotic microangiopathies such as pre-eclampsia, HELLP syndrome, and acute fatty liver of pregnancy usually present acutely in the second or third trimester, often with systemic symptoms like hypertension, hemolysis, and liver dysfunction, requiring urgent intervention. Non-pregnancy-related TMAs such as thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome typically present with abrupt and severe symptoms, including hemolysis, thrombocytopenia, and organ failure, and are medical emergencies. Disseminated intravascular coagulation also presents acutely, often triggered by obstetric catastrophes such as postpartum hemorrhage or placental abruption, and carries high maternal and fetal risk. Other causes such as hereditary thrombocytopenia or bone marrow failure syndromes tend to present chronically and are usually identified before or early in pregnancy.
Gestational thrombocytopenia
Immune thrombocytopenia (ITP)
Pre-eclampsia (PEC)
HELLP syndrome
Acute fatty liver of pregnancy (AFLP)
Thrombotic thrombocytopenic purpura (TTP)
Atypical hemolytic-uremic syndrome (aHUS)
Disseminated intravascular coagulation (DIC)
Hereditary thrombocytopenia
Bone marrow failure syndromes
Paroxysmal nocturnal hemoglobinuria (PNH)
Type II von Willebrand disease (VWD)
Hematologic malignancies
Drug-induced thrombocytopenia
Gestational thrombocytopenia: Usually requires no treatment, as it is self-limiting and resolves postpartum. Monitoring of platelet counts is sufficient.
Immune thrombocytopenia (ITP): Treatment is indicated for maternal bleeding, very low platelet counts, or prior to delivery. First-line therapy includes corticosteroids or intravenous immunoglobulin. Platelet transfusions are reserved for severe bleeding or peripartum management.
Pregnancy-related thrombotic microangiopathies (PEC, HELLP, AFLP): Definitive treatment is delivery of the fetus. Supportive care includes blood pressure control, seizure prophylaxis, and monitoring for maternal organ dysfunction. Platelet transfusions may be used if significant bleeding occurs or for invasive procedures.
Non-pregnancy-related TMAs (TTP, aHUS): Require specialized therapy such as plasma exchange for TTP or complement inhibitors for atypical HUS, along with supportive care.
Disseminated intravascular coagulation (DIC): Treat the underlying cause (obstetric complications or systemic illness) with supportive care, including blood products, coagulation factor replacement, and careful hemodynamic management.
Hereditary thrombocytopenia and other rare causes: Management is tailored to the specific disorder, including genetic counseling, disease-specific therapy, and supportive care as needed.
Delivery planning: Mode of delivery is based on obstetric indications and maternal platelet counts. A hematologist should be involved when counts are critically low or complex disorders are present.
Rituximab: Monoclonal antibody targeting CD20 on B-cells, reducing autoantibody production against platelets.
Caplacizumab: vWF-directed antibody fragment that blocks the A1 domain of von Willebrand factor, preventing platelet adhesion and microvascular thrombosis.
Eculizumab: Humanized monoclonal antibody against complement protein C5, preventing formation of the membrane attack complex and reducing complement-mediated hemolysis.
Azathioprine: Immunosuppressant that interferes with DNA synthesis in rapidly dividing immune cells, reducing autoantibody formation.
Cyclosporine: Inhibits calcineurin, suppressing T-cell activation and modulating the immune response against platelets.
Argatroban, Bivalirudin: Bind and inhibit thrombin, preventing clot formation in heparin-induced thrombocytopenia.
Fondaparinux: Synthetic pentasaccharide that inhibits factor Xa, providing anticoagulation without cross-reacting with heparin-dependent antibodies.
Initial Assessment and Diagnosis
Confirm thrombocytopenia with repeat platelet counts.
Obtain a detailed history including prior thrombocytopenia, autoimmune disorders, medications, infections, family history, and obstetric complications.
Perform a thorough physical examination to look for bleeding, organomegaly, or congenital syndromes.
Identify the underlying etiology through laboratory tests and, if needed, specialized investigations (e.g., ADAMTS-13, complement studies, bone marrow evaluation).
Risk Stratification and Monitoring
Assess maternal bleeding risk based on platelet count and clinical symptoms.
Monitor platelet trends throughout pregnancy.
Evaluate fetal risk, particularly in immune-mediated thrombocytopenia.
Determine timing and mode of delivery based on obstetric indications and platelet counts.
Targeted Treatment
Gestational thrombocytopenia: Usually observation only.
Immune thrombocytopenia: Corticosteroids, IVIG, or other immunosuppressants if indicated; platelet transfusion for bleeding or peri-delivery.
Pregnancy-related TMA (PEC, HELLP, AFLP): Delivery of the fetus with supportive care.
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