Emergency Neurological Life Support: Intracranial Hypertension and Herniation

Robert D Stevens1, Michael Shoykhet2, Rhonda Cadena3

  • 1Departments of Anesthesiology and Critical Care Medicine, Neurology, Neurosurgery, and Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. rstevens@jhmi.edu.

Neurocritical Care
|October 7, 2015
PubMed

Insights

Recognizing "brain codes" like intracranial hypertension and herniation is critical for immediate neurological emergency treatment. This protocol outlines a stepwise algorithm for managing these life-threatening brain events to prevent irreversible damage.

Area of Science:

  • Neurology
  • Emergency Medicine
  • Critical Care

Background:

  • Sustained intracranial hypertension and acute brain herniation represent critical neurological emergencies.
  • These conditions, termed "brain codes," necessitate urgent intervention to avert irreversible brain injury and mortality.

Purpose of the Study:

  • To establish an evidence-based, standardized protocol for the evaluation and management of intracranial hypertension and brain herniation.
  • To guide the organized, stepwise implementation of emergency neurological life support.

Main Methods:

  • Development of a management algorithm based on current evidence.
  • Standardization of diagnostic and therapeutic approaches for patients presenting with signs of increased intracranial pressure or herniation.

Main Results:

  • The protocol provides a structured approach to managing complex neurological emergencies.
  • Implementation aims to improve patient outcomes by ensuring timely and appropriate interventions.

Conclusions:

  • A standardized emergency neurological life support protocol is essential for managing "brain codes."
  • This evidence-based approach is crucial for optimizing the care of patients with intracranial hypertension and brain herniation.

Related Concept Videos

Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
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...