Gestational hemorhagic thrombocytopenia (GTP) is the most common type of thrombocytopenia. It accounts for between 70 and 80% of cases. This benign condition is usually cured within the first few weeks of pregnancy. Though the exact cause of this condition is unknown, it is thought to be caused by increased platelet consumption and pregnancy-related hemodilution. The remaining 20-30% of cases are due to life-threatening conditions such as thrombocytopenia during pregnancy. Although there are cases of GT recurring in women, not many cases report more than three episodes. A young woman suffered from gestational hemorhage during the third trimester in each of her four pregnancies. After that, she was completely healed. We excluded other potentially life-threatening causes for thrombocytopenia during pregnancy. Her platelet count decreased from normal to below-normal during each of her pregnancies. The lowest point was at the end. During her four pregnancies, all other hematological indexes were within the normal pregnancy-specific reference range. This case supports the idea that pregnancy-related hemodilution is not a significant factor in gestational bloody syndrome. When separating the different causes of thrombocytopenia, it is crucial to use a systematic approach.
Thrombocytopenia is a blood platelet count below 150 x 109/L. It is classified by the platelet count as mild (100 – 150 x 10).9/L), moderate (50–100 x 10).9/L), or severe (< 50 x 109/L). Thrombocytopenia can complicate 7-10% all pregnancies . Gestational hemorhagic thrombocytopenia (GT), which accounts for 70-80% of all cases, is the most common cause. GT is a benign condition and usually recovers fully after birth. . While the exact cause of GT remains unknown, hemodilution, which can be caused by increased plasma volume, elevated peripheral platelet consumption and hypersplenism, increased platelet intake, hypersplenism or reduced platelet production, has all been suggested. .
The remaining 20-30% are caused by other more serious causes of thrombocytopenia during pregnancy. These include pre-eclampsia/eclampsia, hemolytic-elevated-liver-enzymes-low-platelet (HELLP) syndrome, acute fatty liver of pregnancy, immune thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, autoimmune diseases (lupus, antiphospholipid syndrome), infections (hepatitis, human immunodeficiency virus, sepsis), disseminated intravascular coagulation, drugs (heparin), vitamin B12/folate deficiency, bone marrow dysfunction and hypersplenism .
GT is a diagnosis for exclusion. A systematic approach is essential when distinguishing between the many causes of thrombocytopenia. This will avoid unnecessary investigation and anxiety for women suffering from GT. GT patients typically have mild thrombocytopenia (100 to 150 x 10).9/L) in the third trimester that recurs in subsequent pregnancies, spontaneous recovery soon after delivery, normal platelet counts when not pregnant, and no associated conditions that could otherwise account for the thrombocytopenia [2,3]. The fetal platelet count is also normal.
Although there are some reports of GT recurrences in women, not many cases report more than three episodes. A young woman suffered GT during the third trimester in four consecutive pregnancies. After each pregnancy, she was fully recovered.
Prezentation of a Case
Demographics and medical history
A 29-year-old woman had a coincidental finding of mild thrombocytopenia during a routine joint obstetric/endocrinology clinic visit. She was 28 weeks into her fourth baby (gravida 4, para 3) On systemic review, she had no symptoms. She did not have any history of menorrhagia. Her medical history included Graves’ hyperthyroidism and sickle cell trait. Her three previous pregnancies had all seen low platelet counts. Before her first pregnancy, there was no history or low platelet count. Prenatal vitamins, ferrous Sulfate, and omeprazole were some of her medications. She did not take any medication that could cause thrombocytopenia or had any drug allergies. She was an ex-smoker and had never drank alcohol. Her family history included no bleeding or bruising disorders. Her examination revealed no signs of bleeding, bruising or gravid uterus. Normal blood pressure. She had no ankle swelling (she hadn’t had any in previous pregnancies).
A hematological examination revealed a low platelet count at 116 x 10.9/L at 28 week gestation. Her platelet count was within the normal range during the first trimester and the second. Red blood cell count (white blood cell count), hemoglobin (packed cell volume), and hemoglobin were all within the pregnancies-specific reference range (Table 1).
Normal reticulocyte counts (percentage of reticulocytes) and coagulation profiles (fibrinogen and prothrombin times, activated partial thromboplastin time, and activated partial hemoplastin clotting speed) were both found in her. Hemoglobinopathy screening revealed no evidence of thalassemia and sickle cell trait. Group B-negative was determined by blood grouping. The blood film examination showed no abnormalities, such as red cell fragmentation, platelet accumulation, or clumping. Biochemical investigations showed normal thyroid, renal, and liver function. Normal levels of serum albumin, vitamin D, and calcium were found. Serum ferritin was slightly low at 29 µg/L (normal range: 30-400), and her serum vitamin B12 and folate levels were normal. The serum electrophoresis was normal. An immunological examination revealed that serum immunoglobulins fell within the third-trimester limit. Anti-cardiolipin, anti-nuclear, anti-beta-2-glycoprotein-1, and antiphospholipid antibodies were all negative. Her anti-thyroid peroxidase antibody levels were slightly raised at 92 IU/ml (normal range: < 34). At the initial diagnosis, her thyroid receptor antibodies were positive but negative. The screen for the human immunodeficiency and hepatitis viruses was negative. An abdominal ultrasound examination previously showed that the liver and spleen were normal in size.
Historical records show that her pregnancies had been marked by thrombocytopenia. The onset occurred at 28 weeks. A nadir occurred between 37 and 40 weeks. During the previous three pregnancies, liver enzymes were not abnormal. A normal coagulation profile was available for her third pregnancy. Although she had normal platelet count after each pregnancies except for the second, her platelet counts were still high (Table 2).
The patient was diagnosed with gestational thrombocytopenia. The patient was not given any specific treatment, other than regular platelet count monitoring throughout her pregnancy. The patient was informed that gestational hemorhocytopenia is usually harmless and will likely recur in the third trimester.
Follow-up and outcome
The pregnancy was monitored closely for any changes in her platelet counts. Her platelet count fell to 100 x 10.9/L at 38 weeks of gestation (hemoglobin, liver enzymes normal), then rose to 111×109/L at 39 weeks gestation. The delivery of her baby girl was uneventful at 40 weeks gestation. A blood test for mild postpartum hemorhage (700ml) revealed a normal hemoglobin and platelet count of 121×10 in the baby girl.9/L. A follow-up test showed a normal platelet count (197 x 10).9/L) in the second week (nine day) after delivery.
Even though the patient’s platelet counts were consistently low during the third trimester of each of her four consecutive pregnancies, the other hematological indices always remained within the pregnancy-specific reference range (Figure 1).
Gestational thrombocytopenia is generally benign and characterized by complete platelet healing in the postpartum period. However, patients who are affected may be subject to excessive investigation, over-treatment, delay or misdiagnosis for a more serious cause of thrombocytopenia during pregnancy. Because of the current lack in knowledge about platelet function and expected kinetics of GT, patients with affected conditions are at greater risk of not receiving regional anesthesia during labor. . GT can therefore be used to diagnose and manage problems until full recovery is confirmed.
The average platelet count is over 100 x 10.9GT patients have a /L, but there have been cases of severe/moderate thrombocytopenia. A case of severe thrombocytopenia was reported in a case where a woman suffering from severe thrombocytopenia was treated with ITP and blood transfusions. The diagnosis was changed to GT only after complete recovery was made soon after the delivery. . There is no reliable laboratory method to distinguish between ITP and gestational thrombocytopenia during pregnancy. Both conditions can result in elevated platelet antibody levels. . If you have a history or low platelet count before pregnancy, and a lower platelet count than 70×10, ITP should be suspected.9/L in the first and second trimesters of pregnancy. The presence of immature plates on blood film examination . Our case report describes a woman who had GT in four consecutive pregnancies. She also experienced moderate thrombocytopenia in her second pregnancy. She was not able to have any complications at delivery and didn’t require any treatment.
A meta-analysis based on longitudinal studies found that plasma volume rose by 3-9% in the first trimester, 12-36% in second trimester, 38-51% in third trimester. This hemodilution leads to a decline in hemoglobin, red cell count and hematocrit (packed cells volume) throughout pregnancy. Other nutritional biomarkers may also be affected but hemoglobin, red cell count, hematocrit and hemoglobin are the main indicators of hemodilution. [8,9]. During her four pregnancies, our patient experienced similar drops in her platelet count. Although there were small but not significant drops in hemoglobin, hemoglobin, and hematocrit during her pregnancies, they remained within the normal range for pregnancy. This suggests that the hemodilution in this case did not contribute significantly to GT.
Hemodilution theory has been challenged by the results of a large, case-control study that included over 3500 pregnancies. . All pregnancies experience plasma volume expansion and hemodilution. However, GT was found in only 12%. This condition seems to be more patient-specific than pregnancy-specific. Also, the small drop in hemoglobin levels did not match the large decrease in platelet counts . The same study found that patients with GT had a higher mean platelet size than patients without GT. This suggests that there is increased platelet turnover in GT patients. The platelet counts also increased rapidly within one week of delivery, which makes an autoimmune mechanism unlikely. The authors concluded that GT was not explained by hemodilution resulting from increased plasma volume and that an autoimmune process is highly unlikely. GT could be explained by increased platelet turnover due to the increased uteroplacental bloodflow during the third trimester for women with genetically sensitive genes . To understand platelet kinetics, and genetic susceptibility of patients with GT, more research is necessary.
We show that hemodilution does not contribute to GT in our case report. Although each episode of thrombocytopenic activity was mild at the start of the third trimester and the nadir at the end was each pregnancy with documented recovery, the magnitude of the decrease in platelet count was far greater than any drop in the usual hemomatological markers of bleeding. Through the four pregnancies, the hemoglobin, hemoglobin and red cell count markers of hemodilution remained within the appropriate pregnancy-specific range.
Patients who have used proton pump inhibitors (which are specific to pantoprazole) have had thrombocytopenia reported in very rare cases. . Our patient had taken omeprazole during her fourth pregnancy. She also did not have any history of having used proton pump inhibitors in her past pregnancies. Her platelet count did not change while she was taking omeprazole. It was similar to her previous pregnancies.
Many cases of GT recurrences in women have been reported. However, there are no reports that more than three episodes per year. An earlier case report reported severe GT in two consecutive pregnancies. Both episodes were discovered later (after 35 weeks gestation). . The platelet count was almost back to normal shortly after the delivery. Even though the woman had no history of GT, she still needed to be thoroughly examined and monitored feto-maternally in case there was another cause. . Another case report describes moderate thrombocytopenia in two consecutive pregnancies. This was discovered after 35 weeks of gestation. The first pregnancies of the patient were characterized by a one unit platelet transfusion. The second pregnancy was a normal one. There were no bleeding complications in both pregnancies. . These case reports, along with similar reports of recurrence, suggest that GT can be a problem for women who have a history of GT.
While there is consensus that GT does not require any specific therapy, there is still concern among anesthetists and obstetricians about regional anesthesia for delivery and lower platelet counts. . If you have a history or thrombocytopenia, it is best to monitor your platelet count at least once every four weeks. During the third trimester, more frequent monitoring may be necessary . It is important to consider the importance of awareness as well as local and national recommendations.
The case presented here is one of recurrent GT. Each episode lasted through the third trimester in four consecutive pregnancies. While the platelet counts fell below the pregnancies-specific reference ranges, the hemodynamic markers of hemodilution were not affected. This case supports that GT is not just pregnancy-related hemodilution.
GT women may have lower platelet counts which can lead to suspicions of other serious causes of thrombocytopenia during pregnancy. Some patients will still need to be subjected to extensive investigation and antenatal monitoring. It is important to use a systematic approach in separating the different causes of thrombocytopenia. This will avoid over-investigating pregnant women and causing unnecessary anxiety.
Leave a Reply