A 55-year-old man with a history of sickle cell disease (sickle cell hemoglobin C) but no history of sickle cell crises was seen with an episode of acute abdominal pain and fever. He had no significant medical history, including no antecedent neurologic problems. He became unresponsive during 24 hours, necessitating intubation and ventilation. On examination before intubation, he was febrile, anarthric, and quadraparetic. In addition, he was unable to track objects in his visual fields or follow simple commands. His blood test results were consistent with disseminated intravascular coagulation (9.9 g/dL hemoglobin level, 35 ×103/µL platelet count, 1.7 international normalized ratio, 5928 U/L lactate dehydrogenase level, 42 000 µg/mL D-dimer level, and 100 mg/L C-reactive protein level), which was thought to have occurred secondary to sepsis (to convert hemoglobin level to grams per liter, multiply by 10.0; platelet count to ×109/L, multiply by 1.0; lactate dehydrogenase level to microkatals per liter, multiply by 0.0167; D-dimer level to nanomoles per liter, multiply by 5.476; and C-reactive protein level to nanomoles per liter, multiply by 9.524). Results of initial brain computed tomography before and after intubation were normal, but subsequent brain magnetic resonance imaging (MRI) (T2-weighted * susceptibility-weighted imaging [SWI]) revealed extensive microhemorrhages supratentorially and infratentorially (Figure). He was managed supportively in the intensive care unit for a few weeks. Although initially following discharge from the intensive care unit he was anarthric and intermittently responsive to external stimuli, he had a significant cognitive and physical recovery during 2 months, following which he was discharged to a specialist center for further cognitive rehabilitation.
Neligan A, Rajakulendran S, Nortley R, Manji H. Extensive Cerebral Microhemorrhages Caused by Acute Disseminated Intravascular Coagulation Secondary to Sepsis. JAMA Neurol. 2014;71(4):510–511. doi:10.1001/jamaneurol.2013.223
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