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Diabetic Ketoacidosis

Neurologic Collapse During Treatment Follo wed by Se vere De velopmental Morbidity

Divisions of Developmental Pediatrics and Developmental Disabilities and of General Pediatrics, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York, Departments of Neurology and Radiology, Robert Warner Rehabilitation Center, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York

Irene Sills, MD

Divisions of Developmental Pediatrics and Developmental Disabilities and of General Pediatrics, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York, Departments of Neurology and Radiology, Robert Warner Rehabilitation Center, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York

Michael Cohen, MD

Divisions of Developmental Pediatrics and Developmental Disabilities and of General Pediatrics, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York, Departments of Neurology and Radiology, Robert Warner Rehabilitation Center, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York

F. Glen Seidel, MD

Divisions of Developmental Pediatrics and Developmental Disabilities and of General Pediatrics, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York, Departments of Neurology and Radiology, Robert Warner Rehabilitation Center, Children's Hospital of Buffalo, State University of New York at Buffalo, School of Medicine and Biomedical Science, Buffalo, New York

Diabetic Ketoacidosis (DKA) remains the leading cause of death in children with type I diabetes mellitus. Complications occurring during DKA treatment include cerebral edema and neurologic collapse. Developmental outcomes following neurologic deterioration during DKA have varied from no sequelae to severe developmental disabilities.

A total of three children developed neurologic deterioration during treatment of DKA at Buffalo Children's Hospital between 1984 and 1987. The authors treated aggressively for cerebral edema. Characteristic findings on the computed tomography (CT) scans and magnetic resonance imaging (MRI) of the brain included hemorrhagic infarctions of the thalami, basal ganglia and lentiform nuclei.

The authors conducted developmental follow-up examinations between 1-1/2 - 3 years following recovery from DKA coma. Although they noted significant recoveries over time, developmental disabilities persisted.

The clinical courses and neuroradiographic findings of these patients are compatible with sequelae of central brain stem herniation and cytotoxic brain injury. Continued efforts are needed in the prevention and early detection of clinically significant cerebral edema during treatment of DKA.

Clinical Pediatrics, Vol. 29, No. 8, 451-456 (1990)
DOI: 10.1177/000992289002900807


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