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Thrombotic Thrombocytopenic Purpura Relapse During Induction of Labor
Abstract Number: F-70
Abstract Type: Case Report/Case Series
Thrombotic thrombocytopenic purpura (TTP) is a rare etiology of thrombocytopenia during pregnancy. Most cases of TTP are due to hereditary or acquired inhibition of the enzyme ADAMTS-13 (A Disintegrin And Metalloprotease with ThromboSpondin type 1 domain 13), a metalloprotease that cleaves von Willebrand factor (vWF) so that it does not thrombose the microvasculature. In TTP, vWF multimers bind platelets causing thrombocytopenia, microangiopathic hemolytic anemia, and arterial ischemia.1 We report a patient with TTP who had an acute crisis during induction of labor (IOL) and was treated with tranexamic acid (TXA).
A 26-year-old primigravida with an 8-year history of hereditary TTP, and undetectable ADAMTS-13 levels, was admitted for IOL at 41 weeks gestation. She was previously treated with therapeutic plasma exchange (TPE), immunoglobulin, steroids, and rituximab. Due to multiple TPEs, she was alloimmunized to HLA antigens with one TPE complicated by anaphylaxis. The patient was in remission for two years prior to pregnancy, and remained well until IOL.
The patient’s initial platelets were 33 x 10^9/L. A hematology consultant felt the TTP was active and recommended prednisone treatment and aborting the IOL. Despite this, the TTP worsened over three days, with platelets decreasing to 17 x 10^9/L, but without other symptoms. The decision was made for Cesarean delivery. Platelet transfusions are contraindicated in TTP; TPE with FFP was contraindicated in this particular case due to hypersensitivity. We decided to administer two doses of TXA (10 mg/kg) intraoperatively at incision and closing. The patient underwent general anesthesia with an estimated blood loss of 1 liter. On day four, her platelets were 6 x 10^9/L, with hemolytic anemia requiring blood transfusions. The patient was transferred to the ICU and improved with TPE and high dose steroids. She was discharged home three weeks later without complications.
It is important, but difficult, to distinguish TTP from other pregnancy-related thrombocytopenic disease states since it carries a poor prognosis and high fetal mortality.2 Pregnancy itself may precipitate TTP because ADAMTS-13 activity is decreased while vWF increases. All thrombocytopenias may deteriorate rapidly, and misdiagnosis can be fatal, especially when TTP is overlooked. TXA prevents the conversion of plasminogen to plasmin, thereby limiting fibrinolysis. Although generally contraindicated in prothrombotic states such as TTP, TXA has minimal complications with typical doses.3,4 We believed the risk of significant blood loss in this patient outweighed the risk of thrombosis. Further research into the use of TXA in pregnancy is needed.
1. NEJM 2002; 347:589-600
2. Br J Haematol 2009; 144:742–54
3. Eur J Obstet Gynecol Reprod Biol 2004; 112:154–157
4. The Lancet 2010; 376:23–32