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Background Cerebral edema is a fatal complication that can occur in children with diabetic ketoacidosis (DKA). Its clinical signs are generally not explicit, and subclinical cerebral edema can occur. This study is one of the few longitudinal studies conducted to identify cerebral edema in patients with DKA by measuring the optic nerve sheath diameter (ONSD). The aim of this study was to investigate cerebral edema in children with DKA with serial measurement of ONSD, which is an early and reliable indicator of cerebral edema, and to monitor changes in ONSD during therapy. Methods The study was conducted by measuring ONSD ultrasonographically at baseline and during the course of therapy in patients with DKA. All participants were diagnosed and received therapy at our unit between May 2016 and June 2017. The study was registered with the Clinical Trials database, with a study number of NCT02937441. Measurements were obtained while the patients were in the supine position with their eyes closed, and axial transbulbar images of both eyes were obtained with a 6-15-MHz linear probe. Results The ONSD values of children with DKA changed during the treatment, reaching the highest values at 12-16 h of therapy, and the greatest ONSD was observed in children who had moderate and severe DKA. Conclusions During treatment of children with DKA, it is possible to predict cerebral edema by measuring ONSD, and this may contribute to clinical management, especially fluid treatment.
This article was published in the following journal.
Name: Journal of pediatric endocrinology & metabolism : JPEM
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The purpose of this study is to determine cerebral edema with evaluation of measurement of diameter of optic nerve sheath.
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Atrophy of the optic disk which may be congenital or acquired. This condition indicates a deficiency in the number of nerve fibers which arise in the RETINA and converge to form the OPTIC DISK; OPTIC NERVE; OPTIC CHIASM; and optic tracts. GLAUCOMA; ISCHEMIA; inflammation, a chronic elevation of intracranial pressure, toxins, optic nerve compression, and inherited conditions (see OPTIC ATROPHIES, HEREDITARY) are relatively common causes of this condition.
Ischemic injury to the OPTIC NERVE which usually affects the OPTIC DISK (optic neuropathy, anterior ischemic) and less frequently the retrobulbar portion of the nerve (optic neuropathy, posterior ischemic). The injury results from occlusion of arterial blood supply which may result from TEMPORAL ARTERITIS; ATHEROSCLEROSIS; COLLAGEN DISEASES; EMBOLISM; DIABETES MELLITUS; and other conditions. The disease primarily occurs in the sixth decade or later and presents with the sudden onset of painless and usually severe monocular visual loss. Anterior ischemic optic neuropathy also features optic disk edema with microhemorrhages. The optic disk appears normal in posterior ischemic optic neuropathy. (Glaser, Neuro-Ophthalmology, 2nd ed, p135)
Conditions which produce injury or dysfunction of the second cranial or optic nerve, which is generally considered a component of the central nervous system. Damage to optic nerve fibers may occur at or near their origin in the retina, at the optic disk, or in the nerve, optic chiasm, optic tract, or lateral geniculate nuclei. Clinical manifestations may include decreased visual acuity and contrast sensitivity, impaired color vision, and an afferent pupillary defect.
Set of cell bodies and nerve fibers conducting impulses from the eyes to the cerebral cortex. It includes the RETINA; OPTIC NERVE; optic tract; and geniculocalcarine tract.
Benign and malignant neoplasms that arise from the optic nerve or its sheath. OPTIC NERVE GLIOMA is the most common histologic type. Optic nerve neoplasms tend to cause unilateral visual loss and an afferent pupillary defect and may spread via neural pathways to the brain.
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