Related Experiment Videos

Intracranial suppuration

Nicole Leotta1, Ray Chaseling, Glen Duncan

  • 1Department of Allergy, Immunology and Infectious Diseases, Children's Hospital at Westmead, New South Wales, Australia.

Insights

This study evaluated children with subdural empyema (SDE) and brain abscess (BA), finding that while mortality is low, neurological complications remain high. Early diagnosis and treatment of these pediatric intracranial infections are crucial.

Area of Science:

  • Pediatric Neurology
  • Infectious Diseases
  • Neurosurgery

Background:

  • Intracranial suppuration, including subdural empyema (SDE) and brain abscess (BA), is a serious condition in children.
  • Understanding the specific characteristics and outcomes of SDE and BA is vital for effective management.

Purpose of the Study:

  • To determine the prevalence, age distribution, predisposing factors, bacteriology, clinical features, and outcomes of pediatric SDE and BA.
  • To identify differences in presentation and outcomes between SDE and BA in children.

Main Methods:

  • A retrospective hospital-based study was conducted.
  • Clinical data of children diagnosed with SDE or BA over 10.75 years at a tertiary children's hospital were reviewed.

Main Results:

  • Forty-six children with intracranial suppuration were identified (26 BA, 16 SDE, 4 both).
  • Sinusitis was a predisposing factor for SDE; Streptococcus milleri was common in SDE. Periorbital edema and photophobia were associated with SDE.
  • Mortality was low (3/46), but neurological complications were high (54.3%), more frequent in BA. Outcomes varied by age, with peaks for SDE at <2 and >7 years, and for BA at 9-11 years.

Conclusions:

  • Intracranial suppuration in children has a low mortality rate but high morbidity.
  • Prompt diagnosis and treatment are essential to improve outcomes and reduce neurological deficits.
Abstract

Related Concept Videos

Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
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...
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...
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...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...