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Post-traumatic thrombotic microangiopathy following pelvic fracture treated with transcatheter arterial embolization: a case report.
Journal of Medical Case Reports 2018 August 10
BACKGROUND: Thrombotic microangiopathy is caused by various conditions, but few cases secondary to trauma have been reported. We present the rare case of a patient with thrombotic microangiopathy-induced high-impact trauma with hemorrhagic shock.
CASE PRESENTATION: An 86-year-old Japanese woman was transferred to our hospital after a traffic accident. A whole-body computed tomography scan revealed pelvic fractures with massive extravasation. She received a blood transfusion and emergency angiographic embolization. On post-traumatic day 1, she showed unexplained severe hemolysis, thrombocytopenia, and renal failure despite her stable condition. Disseminated intravascular coagulation was excluded because her activated partial thromboplastin time and prothrombin time-international normalized ratio were normal. Her fragmented red blood cell concentration was 28.8%. We suspected clinical thrombotic thrombocytopenic purpura and started plasma exchange. She recovered fully after the plasma exchange and was discharged on day 31. We eventually diagnosed thrombotic microangiopathy because her ADAMTS13 activity was not reduced.
CONCLUSIONS: It is important to recognize the possibility that thrombotic microangiopathy may occur after severe trauma. In the critical care setting, unexplained thrombocytopenia and hemolytic anemia should be investigated to eliminate the possibility of thrombotic microangiopathy. Early plasma exchange may help to prevent unfortunate outcomes in patients with thrombotic microangiopathy following trauma.
CASE PRESENTATION: An 86-year-old Japanese woman was transferred to our hospital after a traffic accident. A whole-body computed tomography scan revealed pelvic fractures with massive extravasation. She received a blood transfusion and emergency angiographic embolization. On post-traumatic day 1, she showed unexplained severe hemolysis, thrombocytopenia, and renal failure despite her stable condition. Disseminated intravascular coagulation was excluded because her activated partial thromboplastin time and prothrombin time-international normalized ratio were normal. Her fragmented red blood cell concentration was 28.8%. We suspected clinical thrombotic thrombocytopenic purpura and started plasma exchange. She recovered fully after the plasma exchange and was discharged on day 31. We eventually diagnosed thrombotic microangiopathy because her ADAMTS13 activity was not reduced.
CONCLUSIONS: It is important to recognize the possibility that thrombotic microangiopathy may occur after severe trauma. In the critical care setting, unexplained thrombocytopenia and hemolytic anemia should be investigated to eliminate the possibility of thrombotic microangiopathy. Early plasma exchange may help to prevent unfortunate outcomes in patients with thrombotic microangiopathy following trauma.
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