Cerebral Edema In Diabetic Ketoacidosis Research Articles

Cerebral hyperemia and impaired cerebral autoregulation associated with diabetic ketoacidosis in critically ill children*

Cerebral edema associated with diabetic ketoacidosis is an uncommon but severe complication of insulin-dependent diabetes mellitus with unclear pathophysiology. We sought to determine whether cerebral edema in patients with diabetic ketoacidosis was related to changes in cerebral blood flow, autoregulation, regional cerebral saturation, or S100B. Prospective case series. Pediatric intensive care unit of a tertiary children's hospital. Six patients with diabetic ketoacidosis and altered mental status, requiring computed tomographic scan of the head. Study evaluations included: 1) transcranial Doppler evaluations to determine middle cerebral artery flow velocities and cerebral autoregulation, defined by the autoregulatory index, at 6 and 36 hrs; 2) continuous monitoring of regional cerebral oxygenation on the left lateral forehead using near-infrared spectroscopy for the first 24 hrs of admission; 3) serial measurement of S100B as a marker of central nervous system injury; and 4) follow-up head computed tomographic scan. Serial computed tomographic scans showed that four of six patients had changes in brain volume without overt cerebral edema. Initial scans showed narrowing of the third and lateral ventricles when compared with follow-up. There was no difference in middle cerebral artery flow velocities between admission and recovery at 36 hrs, despite Paco2 increasing during treatment. Cerebral flow was normal to increased, despite hypocapnia. Cerebral autoregulation was impaired in five of six patients at 6 hrs and normalized by 36 hrs. Mean regional cerebral oxygenation was measured in five of six patients and decreased linearly with time. Two patients showed maximal regional cerebral oxygenation before returning to baseline. There were no periods of low regional cerebral oxygenation in any patient at any time. No elevation in S100B was found. We found normal to increased cerebral blood flow, elevated regional cerebral oxygenation, impaired autoregulation, and changes in brain volume in clinically ill pediatric patients with diabetic ketoacidosis. We found no evidence of cerebral ischemia. These findings suggest that the pathophysiology of cerebral edema in diabetic ketoacidosis may involve a transient loss of cerebral autoregulation, allowing a paradoxic increase in cerebral blood flow and the development of vasogenic cerebral edema.

Cerebral edema in diabetic ketoacidosis: an underestimated complication?

Cerebral edema in diabetic ketoacidosis: an underestimated complication?

Hyperventilation in severe diabetic ketoacidosis*

To explore whether the carbon dioxide-bicarbonate (P(CO(2))-HCO(3)) buffering system in blood and cerebrospinal fluid (CSF) in diabetic ketoacidosis should influence the approach to ventilation in patients at risk of cerebral edema. Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967. A clinical vignette is used--a child with severe diabetic ketoacidosis who presented with profound hypocapnia and then deteriorated--as a basis for discussion of integrative metabolic and vascular physiology. Studies included reports in diabetic ketoacidosis where arterial and CSF acid-base data have been presented. Studies where simultaneous acid-base, ventilation, respiratory quotient, and cerebral blood flow data are available. We revisit a hypothesis and, by reassessing data, put forward an argument based on the significance of low [HCO(3)](CSF) and rising Pa(CO(2))- hyperventilation in diabetic ketoacidosis and the limit in biology of survival; repair of severe diabetic ketoacidosis and Pa(CO(2))-and mechanical ventilation. The review highlights a potential problem with mechanical ventilation in severe diabetic ketoacidosis and suggests that the P(CO(2))--HCO(3) hypothesis is consistent with data on cerebral edema in diabetic ketoacidosis. It also indicates that the recommendation to avoid induced hyperventilation early in the course of intensive care may be counter to the logic of adaptive physiology.

Cerebral edema in diabetic ketoacidosis and other acute devastating complications: recent observations

Pediatric DiabetesVolume 6, Issue 1 p. 41-49 Cerebral edema in diabetic ketoacidosis and other acute devastating complications: recent observations Arlan L. Rosenbloom, Corresponding Author Arlan L. Rosenbloom Department of Pediatrics, University of Florida College of Medicine, Gainesville, FL, USA *Arlan L. Rosenbloom, MD Children's Medical Services Center 1701, SW 16th Avenue Gainesville, FL 32608, USA Tel: +1 352 334 1393; fax: +1 352 334 1476; e-mail: rosenal@peds.ufl.eduSearch for more papers by this author Arlan L. Rosenbloom, Corresponding Author Arlan L. Rosenbloom Department of Pediatrics, University of Florida College of Medicine, Gainesville, FL, USA *Arlan L. Rosenbloom, MD Children's Medical Services Center 1701, SW 16th Avenue Gainesville, FL 32608, USA Tel: +1 352 334 1393; fax: +1 352 334 1476; e-mail: rosenal@peds.ufl.eduSearch for more papers by this author First published: 23 March 2005 https://doi.org/10.1111/j.1399-543X.2005.00092.xCitations: 5Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume6, Issue1March 2005Pages 41-49 RelatedInformation

Bumetanide Reduces Cerebral Edema Formation in Rats With Diabetic Ketoacidosis

The mechanisms responsible for cerebral edema formation in diabetic ketoacidosis (DKA) are not well understood, although evidence suggests ischemia as a contributing factor. Previous studies have shown that the Na-K-Cl cotransporter of cerebral microvascular endothelial cells and astrocytes is a major participant in ischemia-induced cerebral edema in stroke. The present study was conducted to test the hypothesis that the Na-K-Cl cotransporter also contributes to cerebral edema in DKA. Sprague-Dawley rats were administered streptozotocin to induce DKA, and then cerebral edema was assessed by determination of apparent diffusion coefficients (ADC) with magnetic resonance diffusion-weighted imaging. Cerebral ADC values in DKA rats were significantly reduced in both cortex and striatum compared with non-DKA control rats, indicating the presence of cerebral edema. Intravenous administration of bumetanide to DKA rats abolished the drop in cortical ADC values, while having no significant effect in the striatum. Insulin and saline treatment had no effect when given after bumetanide but increased both cortical and striatal ADC values when given before bumetanide. Evidence is also presented here that acetoacetate and beta-hydroxybutyrate stimulate brain microvascular Na-K-Cl cotransporter activity. These findings suggest that the Na-K-Cl cotransporter contributes to brain edema in DKA.

Study of Subclinical Cerebral Edema in Diabetic Ketoacidosis by Magnetic Resonance Imaging T2 Relaxometry and Apparent Diffusion Coefficient Maps

Cerebral edema is the most significant complication in children with diabetic ketoacidosis (DKA). Our goal was to study whether subclinical cerebral edema was preferentially vasogenic or cytotoxic. Magnetic resonance imaging (MRI)—diffusion-weighted imaging (DWI) and T2 relaxometry (T2R)—were obtained in pediatric patients presenting with severe diabetic ketoacidosis (DKA) 6–12 hours after initial DKA treatment and stabilization and 96 hours after correction of DKA. T2 relaxometry was significantly increased during treatment in both white and gray matter, in comparison to the absolute T2R values 96 hours after correction of DKA (p = .034). Classic intracellular cytotoxic edema could not be detected, based on the lack of a statistically significant decrease in ADC values. ADC values were instead elevated, implying a large component of cell membrane water diffusion, correlating with the elevated white and gray matter T2R. We discuss the findings in relation to cerebral blood volume, cerebral vasoregulatory dysfunction, and cerebral hyperemia.

Use of hypertonic saline in the treatment of cerebral edema in diabetic ketoacidosis (DKA).

Cerebral edema is the primary cause of morbidity and mortality in children and adolescents with diabetic ketoacidosis (DKA). We report a case of an adolescent female with life-threatening DKA-related cerebral edema who responded to a combination of mannitol and hypertonic saline. This is the first report of the use of hypertonic saline in the treatment of cerebral edema due to DKA.

Fluid Therapy in Diabetic Ketoacidosis: Comparative Study

Fluid Therapy in Diabetic Ketoacidosis: Comparative Study