Extensive stroke associated with tranexamic Acid therapy.

نویسندگان

  • Fernando Cabrera-Naranjo
  • Ayoze González-Hernández
  • Oscar Fabre-Pi
  • Ana Carolina
  • López Veloso
  • Santiago Díaz-Nicolás
  • Alberto Cubero-González
چکیده

CASE REPORT A 38-year-old woman was admitted to the hospital because of sudden, right-sided weakness and impaired language expression and comprehension. The patient had a history of tuberculosis ten years prior and of thrombophlebitis in the lower-left limb five months prior. She was taking oral contraceptives. Three weeks before admission she started treatment with daily tranexamic acid (500 mg tid) under gynecological supervision due to onset of active metrorrhagia, but no other risk factors for vascular disease were present. The patient had been well until the day of admission. The morning of hospital admission the patient had sudden rightsided hemiparesis and impaired language expression and comprehension. On examination, the mucous membranes were pale. The blood pressure was 110/65 mm Hg, and the pulse 100 beats per minute. The respiratory rate was 14 breaths per minute and oxygen saturation 93%, while she was breathing ambient air. She was not able to follow simple commands, nor to repeat words, name objects or speak at all. The pupils were round and reactive to light and the eyes were conjugately deviated to the left. There was a lack of menace reflex on the right side, a right-side facial droop, a right hemiplegia and a Babinski reflex of the right big toe (National Institute of Health Stroke Scale = 17). The computerized tomography and the cranial magnetic resonance imaging revealed an extensive middle cerebral artery (MCA) infarct (Figure). The administration of intravenous tPA thrombolysis was ruled out because of active metrorrhagia. The serum levels of electrolytes and the results of renal and liver function tests were normal. Hemoglobin concentration was 7.7 g/dL. Coagulation parameters were normal. Antinuclear, anti-neutrophil cytoplasmic and anticardiolipin antibodies all were negative. The lupus-anticoagulant was also negative. The proteinogram was normal. The plasmatic homocisteine level was 16.4 umol/L [4-15 umol/L]. Tumor markers (carcinoembryonic antigen, carbohydrate antigen 19.9, cancer-antigen 125, alpha phetoprotein and β-2 microglobulin) were normal. The hereditary thrombophilia test, including Factor V Leiden, protein C, protein S and antithrombin 3, was negative. The eco-Doppler Extensive Stroke Associated with Tranexamic Acid Therapy

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عنوان ژورنال:
  • The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques

دوره 37 5  شماره 

صفحات  -

تاریخ انتشار 2010