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A Spinal Anesthetic with a Platelet Count of 7,000 x 109/L in a Patient with Undiagnosed Acquired Thrombotic Thrombocytopenic Purpura
Abstract Number: RF7B10-115
Abstract Type: Case Report Case Series
A 24-year-old G2P1 at 35w4d underwent urgent cesarean delivery (CD) for suspected placental abruption and non-reassuring fetal status. Obstetric history included one uncomplicated vaginal delivery. The platelet count was pending at the time of CD but was recently 285,000 x 109/L. A spinal was inserted on first attempt. Despite confirming abruption, estimated blood loss was only 500 mLs. After delivery and placental separation, the platelet count returned at 7,000 x 109/L. Due to good hemostasis, labs were redrawn and she went to recovery. One unit of platelets was transfused after a repeat set of labs revealed a platelet count of 11,000 x 109/L. Hourly neurologic exams were performed. She never developed signs of a spinal hematoma and had a normal recovery of neurologic function after receiving neuraxial anesthesia while severely thrombocytopenic.
Hematology was immediately consulted. A hemolytic screen (undetectable haptoglobin, LDH 4085 U/L, reticulocyte count 92 109/L, hemoglobin 9.3 g/dl, and blood smear with schistocytes) confirmed the diagnosis of a microangiopathic hemolytic anemia (MAHA). ADAMTS13 was low at 16%, and the ADAMTS13 inhibitor was present, leading to a diagnosis of acquired thrombotic thrombocytopenic purpura (TTP). She developed acute kidney injury and transient altered mental status. Steroids and plasmapheresis were initiated. Sequential compression devices were used for DVT prophylaxis until pharmacologic anticoagulation was initiated at a platelet count of 50,000 x 109/L. The patient was discharged on post-CD day 11 with a platelet count of 190,000 x 109/L but was readmitted twice for relapse requiring plasmapheresis and Rituximab.
Thrombotic microangiopathies (TMAs) are MAHAs with thrombocytopenia and end-organ damage and can be inherent to pregnancy (preeclampsia, HELLP, placental abruption) or precipitated by pregnancy (lupus, hemorrhage, TTP, hemolytic uremic syndrome). TTP is often misdiagnosed as preeclampsia or HELLP because of the overlapping symptoms of hypertension, proteinuria, renal impairment, and liver dysfunction. A high index of suspicion is necessary to distinguish TTP from the TMAs more commonly seen in pregnancy. TTP differs by persistent profound thrombocytopenia (platelets often less than 30,000 x 109/L), anemia, markedly elevated LDH, absent coagulopathy, and lack of resolution with delivery. ADAMTS13, a substance that cleaves Von Willebrand multimers, is deficient in TTP, and an inhibitor is present in the non-congenital form. Its absence leads to platelet aggregation and microemboli formation, which is most likely why intraoperative blood loss was less than expected with severe thrombocytopenia. Treatment of acquired TTP consists of plasmapheresis to remove the ADAMTS13 inhibitor from circulation, steroids and Rituximab for immunosuppression, avoidance of platelet transfusion to prevent exacerbation, and DVT prophylaxis because of the hypercoagulable state.
Blombery P, Scully M. J Blood Med. 2014