Optic Nerve Sheath Diameter Ultrasonography in Pediatric Patients with Diabetic Ketoacidosis

Abstract Objectives Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of...

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Published inCanadian journal of diabetes Vol. 40; no. 2; pp. 126 - 130
Main Authors Hansen, Gregory, MD, FRCP(C), MSc, MPH, Sellers, Elizabeth A.C., MD, FRCP(C), MSc, Beer, Darcy L., MD, FRCP(C), Vallance, Jeff K., PhD, Clark, Ian, MA, MB, BChir, FRCSEd (Ophth)
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LanguageEnglish
Published Canada Elsevier Inc 01.04.2016
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Abstract Abstract Objectives Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of this study was to examine the utility of ONSD ultrasonography to evaluate intracranial pressures in children with DKA. Methods This prospective cohort evaluated pediatric patients who presented to the emergency department of the Children's Hospital at the University of Manitoba with DKA within 3 hours of initial treatment. A pediatric bedside neurologic evaluation tool for cerebral edema was utilized 1) within the first hour of the intravenous fluid initiation (t=0 hr); 2) 8 hours after initiation of treatment (t=8 hr); and 3) at hours after presentation (t=24 hr). At each time interval, 3 images of the patients' ONSDs were scanned by an 11 MHz linear array transducer. Increased intracranial pressure was considered in all patients whose mean ONSDs were >4.5 mm. Results We evaluated 7 patients, aged 4 to 17 years. No patients were clinically assessed as having cerebral edema. Overall, no significant differences emerged among the 3 time points (t=0 vs. t=8 hr; t=0 vs. t=24 hr; t=8 vs. t=24 hr) (all p>.216). Effect sizes were small at 0.14 (t=0 vs. t=8 hr); 0.27 (t=8 vs. t=24 hr); and 0.07 (t=0 vs. t=24). Conclusions Although not statistically significant, subtle changes in intracranial pressure may have been detected with ONSD ultrasonography in pediatric patients with DKA.
AbstractList Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of this study was to examine the utility of ONSD ultrasonography to evaluate intracranial pressures in children with DKA. This prospective cohort evaluated pediatric patients who presented to the emergency department of the Children's Hospital at the University of Manitoba with DKA within 3 hours of initial treatment. A pediatric bedside neurologic evaluation tool for cerebral edema was utilized 1) within the first hour of the intravenous fluid initiation (t=0 hr); 2) 8 hours after initiation of treatment (t=8 hr); and 3) at hours after presentation (t=24 hr). At each time interval, 3 images of the patients' ONSDs were scanned by an 11 MHz linear array transducer. Increased intracranial pressure was considered in all patients whose mean ONSDs were >4.5 mm. We evaluated 7 patients, aged 4 to 17 years. No patients were clinically assessed as having cerebral edema. Overall, no significant differences emerged among the 3 time points (t=0 vs. t=8 hr; t=0 vs. t=24 hr; t=8 vs. t=24 hr) (all p>.216). Effect sizes were small at 0.14 (t=0 vs. t=8 hr); 0.27 (t=8 vs. t=24 hr); and 0.07 (t=0 vs. t=24). Although not statistically significant, subtle changes in intracranial pressure may have been detected with ONSD ultrasonography in pediatric patients with DKA.
Abstract Objectives Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of this study was to examine the utility of ONSD ultrasonography to evaluate intracranial pressures in children with DKA. Methods This prospective cohort evaluated pediatric patients who presented to the emergency department of the Children's Hospital at the University of Manitoba with DKA within 3 hours of initial treatment. A pediatric bedside neurologic evaluation tool for cerebral edema was utilized 1) within the first hour of the intravenous fluid initiation (t=0 hr); 2) 8 hours after initiation of treatment (t=8 hr); and 3) at hours after presentation (t=24 hr). At each time interval, 3 images of the patients' ONSDs were scanned by an 11 MHz linear array transducer. Increased intracranial pressure was considered in all patients whose mean ONSDs were >4.5 mm. Results We evaluated 7 patients, aged 4 to 17 years. No patients were clinically assessed as having cerebral edema. Overall, no significant differences emerged among the 3 time points (t=0 vs. t=8 hr; t=0 vs. t=24 hr; t=8 vs. t=24 hr) (all p>.216). Effect sizes were small at 0.14 (t=0 vs. t=8 hr); 0.27 (t=8 vs. t=24 hr); and 0.07 (t=0 vs. t=24). Conclusions Although not statistically significant, subtle changes in intracranial pressure may have been detected with ONSD ultrasonography in pediatric patients with DKA.
Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of this study was to examine the utility of ONSD ultrasonography to evaluate intracranial pressures in children with DKA. This prospective cohort evaluated pediatric patients who presented to the emergency department of the Children's Hospital at the University of Manitoba with DKA within 3 hours of initial treatment. A pediatric bedside neurologic evaluation tool for cerebral edema was utilized 1) within the first hour of the intravenous fluid initiation (t=0 hr); 2) 8 hours after initiation of treatment (t=8 hr); and 3) at hours after presentation (t=24 hr). At each time interval, 3 images of the patients' ONSDs were scanned by an 11 MHz linear array transducer. Increased intracranial pressure was considered in all patients whose mean ONSDs were >4.5 mm. We evaluated 7 patients, aged 4 to 17 years. No patients were clinically assessed as having cerebral edema. Overall, no significant differences emerged among the 3 time points (t=0 vs. t=8 hr; t=0 vs. t=24 hr; t=8 vs. t=24 hr) (all p>.216). Effect sizes were small at 0.14 (t=0 vs. t=8 hr); 0.27 (t=8 vs. t=24 hr); and 0.07 (t=0 vs. t=24). Although not statistically significant, subtle changes in intracranial pressure may have been detected with ONSD ultrasonography in pediatric patients with DKA. L'œdème cérébral subclinique a été rapporté chez les patients de pédiatrie souffrant du diabète de type 1 et d'acidocétose diabétique (ACD) par l'imagerie par résonance magnétique. L'ultrasonographie du diamètre de la gaine du nerf optique (DGNO) a été utilisée pour évaluer la pression intracrânienne. L'objectif de cette étude était d'examiner l'utilité de l'ultrasonographie du DGNO pour évaluer les pressions intracrâniennes chez les enfants souffrant d'ACD. Cette cohorte prospective évaluait les patients de pédiatrie qui se présentaient au service des urgences de l'Hôpital pour enfants de l'Université du Manitoba en raison d'une ACD au cours des 3 heures suivant le traitement initial. Un outil d'évaluation neuropédiatrique de l'œdème cérébral au chevet du patient était utilisé 1) au cours de la première heure après l'administration d'un liquide par voie intraveineuse (t=0 h); 2) 8 heures après le début du traitement (t=8 h); 3) dans les heures après l'arrivée (t=24 h). À chaque intervalle de temps, 3 images des DGNO des patients étaient balayées par une sonde linéaire de 11 MHz. L'augmentation de la pression intracrânienne était considérée chez tous les patients dont la moyenne du DGNO était>4.5 mm. Nous avons évalué 7 patients âgés de 4 à 17 ans. Aucun patient n'était cliniquement évalué comme souffrant d'un œdème cérébral. Dans l'ensemble, aucune différence significative n'est apparue entre les 3 moments temporels (t=0 vs t=8 h; t=0 vs t=24 h; t=8 vs t=24 h) (tous p>0.216). Les petites tailles de l'effet se situaient à 0.14 (t=0 vs t=8 h); 0,27 (t=8 vs t=24 h); 0,07 (t=0 vs t=24). Bien que non significatifs sur le plan statistique, les changements subtils de la pression intracrânienne pouvaient être détectés à l'ultrasonographie du DGNO chez les patients de pédiatrie souffrant d'ACD.
OBJECTIVESSubclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of this study was to examine the utility of ONSD ultrasonography to evaluate intracranial pressures in children with DKA.METHODSThis prospective cohort evaluated pediatric patients who presented to the emergency department of the Children's Hospital at the University of Manitoba with DKA within 3 hours of initial treatment. A pediatric bedside neurologic evaluation tool for cerebral edema was utilized 1) within the first hour of the intravenous fluid initiation (t=0 hr); 2) 8 hours after initiation of treatment (t=8 hr); and 3) at hours after presentation (t=24 hr). At each time interval, 3 images of the patients' ONSDs were scanned by an 11 MHz linear array transducer. Increased intracranial pressure was considered in all patients whose mean ONSDs were >4.5 mm.RESULTSWe evaluated 7 patients, aged 4 to 17 years. No patients were clinically assessed as having cerebral edema. Overall, no significant differences emerged among the 3 time points (t=0 vs. t=8 hr; t=0 vs. t=24 hr; t=8 vs. t=24 hr) (all p>.216). Effect sizes were small at 0.14 (t=0 vs. t=8 hr); 0.27 (t=8 vs. t=24 hr); and 0.07 (t=0 vs. t=24).CONCLUSIONSAlthough not statistically significant, subtle changes in intracranial pressure may have been detected with ONSD ultrasonography in pediatric patients with DKA.
Author Clark, Ian, MA, MB, BChir, FRCSEd (Ophth)
Hansen, Gregory, MD, FRCP(C), MSc, MPH
Sellers, Elizabeth A.C., MD, FRCP(C), MSc
Vallance, Jeff K., PhD
Beer, Darcy L., MD, FRCP(C)
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2016 Canadian Diabetes Association
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Keywords Pédiatrique
Acidocétose diabétique
Diabetic ketoacidosis
Ultrasonography
Diamètre de la gaine du nerf optique
Œdème cérébral
Ultrasonographie
Cerebral edema
Pediatric
Optic nerve sheath diameter
Language English
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Snippet Abstract Objectives Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic...
Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging....
OBJECTIVESSubclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance...
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SubjectTerms Acidocétose diabétique
Adolescent
Cerebral edema
Child
Child, Preschool
Diabetes Mellitus, Type 1 - complications
Diabetes Mellitus, Type 1 - diagnostic imaging
Diabetes Mellitus, Type 1 - pathology
Diabetic ketoacidosis
Diabetic Ketoacidosis - diagnostic imaging
Diabetic Ketoacidosis - etiology
Diabetic Ketoacidosis - pathology
Diamètre de la gaine du nerf optique
Emergency Service, Hospital
Endocrinology & Metabolism
Female
Follow-Up Studies
Humans
Intracranial Hypertension - diagnostic imaging
Male
Optic Nerve - diagnostic imaging
Optic Nerve - pathology
Optic nerve sheath diameter
Other
Pediatric
Pilot Projects
Prognosis
Prospective Studies
Pédiatrique
Ultrasonographie
Ultrasonography
Ultrasonography - methods
Œdème cérébral
Title Optic Nerve Sheath Diameter Ultrasonography in Pediatric Patients with Diabetic Ketoacidosis
URI https://www.clinicalkey.es/playcontent/1-s2.0-S1499267115005559
https://dx.doi.org/10.1016/j.jcjd.2015.07.007
https://www.ncbi.nlm.nih.gov/pubmed/26704639
https://search.proquest.com/docview/1778399428
Volume 40
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