The relationship between basal cisterns on CT and time-linked intracranial pressure in paediatric head injury

Alison J Kouvarellis1, Ursula K Rohlwink, Vishesh Sood

  • 1Division of Neurosurgery, School of Child and Adolescent Health, Red Cross War Memorial Children's Hospital, University of Cape Town, Cape Town, South Africa.

Insights

Open basal cisterns in pediatric severe traumatic brain injury (TBI) do not rule out elevated intracranial pressure (ICP). This finding suggests that open cisterns on CT scans should not deter ICP monitoring in these patients.

Area of Science:

  • Pediatric neurosurgery
  • Neurocritical care
  • Neuroradiology

Background:

  • Intracranial pressure (ICP) monitoring is crucial for managing severe traumatic brain injury (TBI) in children.
  • Decisions regarding ICP monitoring often rely on head CT scan findings, particularly basal cistern patency.
  • The significance of open basal cisterns in relation to ICP levels in pediatric TBI remains unclear.

Observation:

  • This study analyzed ICP data from 104 pediatric severe TBI patients.
  • Basal cisterns were classified as open, effaced, or obliterated on head CT scans.
  • ICP values were assessed in relation to CT scan timing.

Findings:

  • Over 40% of scans with open basal cisterns showed episodes of ICP ≥ 20 mmHg.
  • 14% of scans with open cisterns had a mean ICP ≥ 20 mmHg.
  • The specificity of open cisterns for predicting ICP < 20 mmHg was poor (57.9%), with worse outcomes in younger children.

Implications:

  • Open basal cisterns on CT scans in children with severe TBI do not exclude the possibility of elevated ICP.
  • ICP monitoring should not be withheld solely based on the presence of open basal cisterns.
  • These findings may refine clinical decision-making for ICP monitoring in pediatric TBI management.
Abstract

Related Concept Videos

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 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...
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...
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...