Case Presentation: Acquired thrombotic thrombocytopenic purpura (TTP) is a rare antibody-mediated thrombotic microangiopathy that requires prompt identification and treatment. We present the case of a 32-year-old female with a history of systemic lupus erythematosus, asthma, augmentation mastopexy (11 years prior), and an antecedent episode of TTP following silicone breast implant placement who presented with back pain, generalized fatigue, confusion, and anemia for a week. She experienced increased bruising but denied any overt bleeding. The patient was 5 months post-partum at presentation and her pregnancy was complicated by right breast swelling requiring recurrent fluid aspiration in the outpatient setting, of which cytology was negative for anaplastic large cell lymphoma (ALCL). After giving birth, she experienced intermittent right breast tenderness and pruritus and on examination, the right breast was larger than the left. She reports having similar symptoms with her TTP episode, in which the suspected trigger was immune response to silicone breast implants. To date, one case of silicone breast implant-associated TTP has been reported (1). Physical exam was notable for a significantly enlarged right breast with palpable fluid collection, petechiae and ecchymoses on extremities. Notable labs were hemoglobin 7.1 g/dL, MCV 81.5 fl, platelet count 17 K/uL (baseline 188 K/uL), haptoglobin < 20 mg/dL, LDH 495 U/L, reticulocyte percent 3.7%, and dsDNA level 4 IU/mL. Peripheral smear showed normocytic normochromic RBCs with anisocytosis, marked schistocytes, macrocytes, increased nucleated red blood cells and polychromasia, consistent with intravascular hemolysis. CT head was negative for any acute intracranial process and CTA chest demonstrated bilateral breast implants with irregular contour and adjacent subcapsular fluid, with a large collection surrounding the right breast suggestive of bilateral implant rupture. Differential diagnosis included TTP vs other acute hemolytic syndromes such as acute hemolytic uremic syndrome. PLASMIC score for risk stratification of TTP was 7 points, indicating high risk for ADAMTS13 deficiency. Emergent treatment was performed with 2 units of fresh frozen plasma, therapeutic plasmic exchange, and prednisone 1 mg/kg with gradual rise in platelet count to >200 K/uL on hospital day four. ADAMTS13 level resulted as < 1% confirming the diagnosis of TTP. On day seven, 700mg rituximab was given and surgical removal of bilaterally ruptured breast implants occurred on day eleven. There were no further clinical or laboratory signs of relapse during this inpatient treatment.
Discussion: Cosmetic procedures, including silicone breast implants, have been increasing in popularity and reported immune-mediated adverse events associated with breast implants include breast implant illness, fibrosis and capsular contraction, connective tissue disorders, and ALCL. It has become increasingly critical to obtain a detailed medical and surgical history, including cosmetic procedural history which may contribute to immune mediated presentations such as TTP relapse.
Conclusions: We describe a case of acquired TTP associated with silicone breast implants. To our knowledge, this is the second reported case of breast implant-associated TTP, highlighting the necessity of a comprehensive medical and surgical history to identify a potential trigger of this condition and initiate prompt treatment.