Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

25
DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
25
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

30
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...
30
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

19
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...
19
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

20
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...
20
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

53
DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
53
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

52
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
52

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The Queensland Bloodstream Infections (QBSI) study: rationale, protocol development and future directions.

Infectious diseases (London, England)·2026
Same author

Hypophosphatemia in Diabetic Ketoacidosis During Intensive Care Admission.

Medical sciences (Basel, Switzerland)·2026
Same author

Integrating Microscopy Methods to Study Gene and Protein Expression alongside Metal Ion Distribution and Speciation: A Case Study of Iron within Pyramidal Neurons from Distinct Hippocampal CA1 Subregions.

Chemical & biomedical imaging·2026
Same author

Validation of PaO2:FiO2 for predicting hospital mortality in critically ill patients with acute hypoxaemic respiratory failure: a retrospective binational registry-based study.

Critical care science·2026
Same author

Cryo-Correlative Light and X-ray Microscopies: Expanding the Intracellular Chemical Map.

ACS nano·2026
Same author

Safety and Efficacy of Stored Wet-Preprimed Extracorporeal Membrane Oxygenation Circuits: A Scoping Review.

ASAIO journal (American Society for Artificial Internal Organs : 1992)·2026

Related Experiment Video

Updated: May 6, 2026

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
10:59

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury

Published on: November 19, 2012

15.9K

Association Between Hyperchloremia and Neurological Outcomes in Traumatic Brain Injury: A Narrative Review.

Philippa McIlroy1,2, Mahesh Ramanan3,4,5, Kyle C White6,7

  • 1Cairns Hospital, Cairns, QLD 4870, Australia.

Healthcare (Basel, Switzerland)
|March 14, 2026
PubMed
Summary

High serum chloride levels in traumatic brain injury (TBI) patients are linked to increased mortality. This review explores the complex relationship between chloride, TBI outcomes, and fluid management strategies, highlighting an evidence gap in intracranial pressure correlation.

Keywords:
chlorideintracranial pressuremortalityneurological outcometraumatic brain injury

More Related Videos

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
07:21

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury

Published on: May 27, 2022

3.7K
Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging
08:27

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging

Published on: April 11, 2025

1.1K

Related Experiment Videos

Last Updated: May 6, 2026

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
10:59

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury

Published on: November 19, 2012

15.9K
Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
07:21

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury

Published on: May 27, 2022

3.7K
Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging
08:27

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging

Published on: April 11, 2025

1.1K

Area of Science:

  • Neurology
  • Critical Care Medicine
  • Nephrology

Background:

  • Traumatic brain injury (TBI) is a significant global health concern.
  • Electrolyte imbalances, particularly elevated serum chloride, are common in TBI patients.
  • Chloride dysregulation may negatively impact neurological outcomes via mechanisms like ferroptosis and cytotoxic edema.

Purpose of the Study:

  • To review the association between serum chloride levels and patient outcomes following TBI.
  • To explore the role of chloride in TBI pathophysiology and its implications for fluid management.

Main Methods:

  • Comprehensive literature review of studies reporting serum chloride levels and TBI outcomes.
  • Inclusion of all study types and patient groups measuring serum chloride.
  • Analysis of outcomes including mortality, surgical intervention, intracranial pressure, and neurological scores.

Main Results:

  • Small studies indicate a correlation between high serum chloride and increased TBI mortality, independent of hypernatremia.
  • Balanced crystalloid solutions, despite lower chloride, may be linked to worse TBI outcomes than saline.
  • Chloride levels, not total load, are more associated with adverse outcomes; non-hypertonic saline contributes significantly.

Conclusions:

  • Hyperchloremia appears independently associated with increased TBI mortality, though causality is unproven.
  • Findings challenge fluid management norms and underscore chloride's complex role in TBI.
  • A critical gap exists in studies correlating chloride levels with intracranial pressure, necessitating future research.