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Cerebral Sinovenous Thrombosis in Children: Another Reason to Treat Iron Deficiency Anemia

Division of Pediatric Neurology, Departments of Pediatrics and Neurology, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT, susan.benedict{at}hsc.utah.edu

Joshua L. Bonkowsky, MD, PhD

Division of Pediatric Neurology, Departments of Pediatrics and Neurology, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT

Joel A. Thompson, MD

Division of Pediatric Neurology, Departments of Pediatrics and Neurology, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT

Colin B. Van Orman, MD

Division of Pediatric Neurology, Departments of Pediatrics and Neurology, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT

Richard S. Boyer, MD

Department of Medical Imaging The University of Utah and Primary Children's Medical Center, Salt Lake City, UT

James F. Bale, JR, MD

Division of Pediatric Neurology, Departments of Pediatrics and Neurology, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT

Francis M. Filloux, MD

Division of Pediatric Neurology, Departments of Pediatrics and Neurology, The University of Utah and Primary Children's Medical Center, Salt Lake City, UT

Iron deficiency anemia is a rare cause of cerebral sinovenous thrombosis in children. We report three cases of cerebral sinovenous thrombosis and iron deficiency anemia treated at Primary Children's Medical Center in Salt Lake City, Utah, between 1998 and 2001. The children were 9, 19, and 27 months old at the time of admission. Hemoglobin levels ranged from 6.6 to 7.0 g/dL, mean corpuscular volume levels from 45 to 56 fL, and platelet counts from 248,000 to 586,000/µL. Magnetic resonance imaging and magnetic resonance venography revealed thrombosis of the straight sinus and internal cerebral veins in all three children, with the addition of the vein of Galen, left transverse and sigmoid sinuses, and upper left internal jugular vein in one child. Recovery ranged from excellent to poor in 3 months to 3 years of follow-up. Four additional cases, ages 6 to 22 months, were found in the English-language literature. Evaluation for prothrombotic disorders was negative in all children, including the current cases. Treatments have included thrombectomy, corticosteroids, mannitol, heparin, low-molecular-weight heparin, warfarin, aspirin, blood transfusion, and iron supplementation, but there is no consensus regarding therapy, other than to correct the anemia and treat iron deficiency. Iron deficiency anemia, a preventable cause of cerebral sinovenous thrombosis, deserves consideration when cerebral sinovenous thrombosis is detected in young children. (J Child Neurol 2004;19:526—531).

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