Subclinical cerebral edema in children with diabetic ketoacidosis randomized to 2 different rehydration protocols

Nicole S Glaser1, Sandra L Wootton-Gorges, Michael H Buonocore

  • 1Department of Pediatrics, School of Medicine, University of California Davis, Davis, California, USA. nsglaser@ucdavis.edu

Pediatrics
|December 12, 2012
PubMed

Insights

Intravenous fluid rates do not significantly impact vasogenic cerebral edema (CE) during diabetic ketoacidosis (DKA) treatment in children. This study quantified subclinical CE using MRI, finding no substantial difference between rapid and slow fluid administration rates.

Area of Science:

  • Pediatric Endocrinology
  • Neuroimaging
  • Critical Care Medicine

Background:

  • Diabetic ketoacidosis (DKA) in children can lead to vasogenic cerebral edema (CE).
  • The influence of intravenous fluid administration rates on CE during DKA treatment remains unclear.
  • Quantifying subclinical CE is crucial for understanding DKA treatment complications.

Purpose of the Study:

  • To investigate the role of intravenous fluid rates in the development of subclinical vasogenic cerebral edema (CE) during diabetic ketoacidosis (DKA) treatment in children.
  • To utilize magnetic resonance diffusion-weighted imaging to measure CE non-invasively.
  • To compare CE severity in children receiving DKA treatment with different intravenous fluid infusion rates.

Main Methods:

  • Children with DKA were randomized into two groups receiving intravenous fluids at either a rapid or slower rate.
  • Diffusion-weighted imaging (DWI) was performed during DKA treatment (3-6 and 9-12 hours) and after recovery (≥72 hours).
  • Apparent diffusion coefficient (ADC) values were calculated to quantify brain water content and assess CE severity.

Main Results:

  • Mean brain ADC values were significantly higher during DKA treatment compared to post-recovery, confirming vasogenic CE.
  • No significant differences in ADC elevation were observed between children receiving rapid versus slower intravenous fluid rates.
  • The rate of fluid administration did not substantially influence the degree of subclinical CE.

Conclusions:

  • The rate of intravenous fluid administration does not appear to be a major factor in the development of vasogenic cerebral edema during DKA treatment in children.
  • Subclinical CE, indicated by ADC changes, occurs during DKA treatment.
  • Further research may explore other contributing factors to CE in DKA.
Abstract

Related Concept Videos

Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...