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Central Brain Herniation Secondary to JuvenileDiabetic Ketoacidosis

David A. ShrierGo,a, Dean K. Shibataa, Henry Z. Wanga, Yuji Numaguchia and James M. Powersa

a From the Departments of Radiology (D.A.S., D.K.S., H.Z.W., Y.N.) and Pathology and Lab Medicine (J.M.P.) University of Rochester School of Medicine and Dentistry, Strong Memorial Hospital, Rochester, NY.



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  		FIG 1. Nine-year-old boy with diffuse cerebral edema and central herniation secondary to treatment of DKA.

A, Axial noncontrast CT scan shows diffuse cerebral edema with effacement of sulci and basal cisterns.

B, Axial noncontrast CT scan obtained 2 days after A shows marked low-density infarcts in the gyrus recti and medial orbital gyri (arrows), globus pallidi, hippocampi/parahippocampal gyri, hypothalamus, midbrain, and posterior right temporal lobe.

C–D, Axial noncontrast T2-weighted (4000/105/1) (C) and coronal postcontrast T1-weighted SPGR (14.4/3.7/1) (D) MR images obtained 24 days after A show cavitary infarcts in the gyrus recti and medial orbital gyri (arrows), medial temporal lobes, midbrain and thalami. Enhancement is present within the thalamic and midbrain lesions. There is diffuse cerebral atrophy.

E, Coronal gross pathologic sections through cerebrum and axial section through midbrain show remote infarctions involving the basilar cerebral structures, basal ganglia, thalami, hippocampi and midbrain (arrows).





Copyright © 2008 by the American Society of Neuroradiology. Print ISSN: 0195-6108 Online ISSN: 1936-959X