Brain abscess in Children - Pathogenesis, diagnosis and management

Table of contents

  • Definition
  • Pathology
  • Source of Infection
  • Pathogenesis
  • Clinical menifestation
  • Diagnosis
  • Treatment - Empirical/Medical/Surgical
  • Prognosis

DNB Question asked

  1. Enumerate risk factors for brain abscess.Outline a scheme for investigating and treatment of a 10 year old child with brain abscess.(June 2008) Marks - 10
  2. Enumerate risk factors for brain abscess. Outline investigations and treatment of brain abscess in children. (Dec 2009) Marks 4+2+4


A brain abscess is a focal, suppurative infection within the brain parenchyma, typically surrounded by a vascularized capsule. The term cerebritis is often employed to describe a nonencapsulated brain abscess. 

The most common age of presentation: 4 and 8 yr and neonates.


  •  • Cerebral abscesses are evenly distributed between the two hemispheres
  •  • ≈80% of cases are divided equally between the frontal, parietal, and temporal lobes. 
  •  • 20% of the cases Brain abscesses in the occipital lobe, cerebellum, and brainstem.
  •  • Most brain abscesses are single, but 30% are multiple and may involve more than one lobe. 
  •  • An abscess in the frontal lobe is often caused by extension from sinusitis or orbital cellulitis.
  •  • Abscesses located in the temporal lobe or the cerebellum is frequently associated with chronic otitis media and mastoiditis. 
  •  • Abscesses from penetrating injuries tend to be singular and caused by Staphylococcus aureus.
  •  • Abscess resulting from septic emboli, congenital heart disease, or meningitis often have several causal organisms. PATHOLOGY

common organism causing brain abscess

Source of Infection / Routes of Entry : 

  1. As a direct spread from a contiguous cranial site of infection, such as paranasal sinusitis, otitis media, mastoiditis, or dental infection, soft tissue infection of the face or scalp, orbital cellulitis, Meningitis. Following head trauma or a neurosurgical procedure. 
  2. As a result of hematogenous spread from a remote site of infection ( CHD like TOF, immunodeficiency, infected VP shunt). 
  3. In up to 25% of cases, no obvious primary source of infection is apparent (cryptogenic brain abscess).

The responsible bacteria include:

  1. Streptococci: S. milleri, S. pyogenes group A or B,  S. pneumoniae, S. faecalis 
  2. Anaerobic organisms : gram-positive cocci, Bacteroides spp., Fusobacterium spp., Prevotella spp., Actinomyces spp. 
  3. Gram-negative aerobic bacilli: Haemophilus aphrophilus, H. parainfluenzae, H. influenzae, Enterobacter, E. coli, Proteus spp.

Few Important points

  1. Citrobacter is most common in neonates. 
  2. One organism is cultured in the majority of abscesses (70%), two in 20%, and three or more in 10% of cases.
  3. Abscesses associated with mucosal infections (sinusitis) frequently have anaerobic bacteria. Fungal abscesses (Aspergillus, Candida) are more common in immunosuppressed patients.   


The intact brain parenchyma is relatively resistant to infection. 

4 stages of brain abscess development.
various stages of brain abscess
 The gliotic process may contribute to the development of seizures as sequelae of brain abscess.   


The early stages of cerebritis and abscess formation are associated with nonspecific symptoms, including low-grade fever, headache, and lethargy. As the inflammatory process proceeds, vomiting, severe headache, seizures, papilledema, focal neurologic signs (hemiparesis), and coma may develop. 

 A cerebellar abscess is characterized by nystagmus, ipsilateral ataxia and dysmetria, vomiting, and headache. 

If the abscess ruptures into the ventricular cavity, overwhelming shock and death usually ensue.


  1. CBC: cell count can be normal or elevated, and the blood culture is positive in ≈10% of cases.
  2. CSF examination: variable results; the white blood cells and protein may be minimally elevated or normal, and the glucose level may be low. 
  3.  CSF cultures: are rarely positive; aspiration of the abscess is much more likely to establish a bacteriologic diagnosis. 
  4.  Remember "CSF is contraindicated in raised ICP"
  5. The electroencephalogram (EEG): shows corresponding focal slowing, and the radionuclide brain scan indicates an area of enhancement due to disruption of the blood-brain barrier in >80% of cases. 
  6.  CT with contrast and MRI: are the most reliable methods of demonstrating cerebritis and abscess formation. MRI is the diagnostic test of choice. 
  7. CT findings: Cerebritis are characterized by a parenchymal low-density lesion, and MRI T2 weighted images indicate increased signal intensity. 
  8.  An abscess cavity shows a ring-enhancing lesion by contrast CT, and the MRI also demonstrates an abscess capsule after gadolinium administration.


Initial Empirical Therapy:

  1. A combination of vancomycin, + a 3rd-generation cephalosporin + metronidazole is commonly used. The same regimen is initiated when otitis media, sinusitis, or mastoiditis is the likely cause. 
  2.  Penetrating head injury, head trauma, or neurosurgery:  vancomycin plus a 3rd-generation cephalosporin is appropriate. 
  3. Cyanotic congenital heart disease: if CCHD is the predisposing factor, ampicillin-sulbactam alone or a 3rd-generation cephalosporin plus metronidazole may be used. 
  4.  Meropenem has good activity against gram-negative bacilli, anaerobes, staphylococci, and streptococci, including most antibiotic-resistant pneumococci, and may be used alone to replace the combination of metronidazole and a β-lactam in the previous regimens. 
  5.   Meropenem does not provide activity against methicillin-resistant S. aureus and may have decreased activity against penicillin-resistant strains of S. pneumonia, indicating that vancomycin should remain a part of the initial regimen when these organisms are suspected.
  6. Abscesses due to an infected ventriculoperitoneal shunt: may be initially treated with vancomycin and ceftazidime. 
  7.  Citrobacter meningitis (often in neonates):  related abscess formation, a 3rd-generation cephalosporin is used, typically in combination with an aminoglycoside. 
  8.  Listeria monocytogenes may cause a brain abscess in the neonate and if suspected, ampicillin should be added to the cephalosporin. In immunocompromised patients, broad-spectrum antibiotic coverage is used, and amphotericin B therapy should be considered

Medical treatment: If

  1. The abscess is less than 2 cm in diameter
  2. The illness is of short duration (less than 2 wk)
  3. There are no signs of increased intracranial pressure, the child is neurologically intact.

If the decision is made to treat with antibiotics alone, the child should have weekly neuroimaging studies to ensure the abscess is decreasing in size. An encapsulated abscess, particularly if the lesion is causing a mass effect or increased intracranial pressure, should be treated with a combination of antibiotics and aspiration. Surgical excision of an abscess is rarely required, because the procedure may be associated with greater morbidity compared with the aspiration of a cavity.

Surgery is indicated: If

  1. The abscess is >2.5 cm in diameter
  2. Gas is present in the abscess
  3. The lesion is multiloculated, 
  4.  The lesion is located in the posterior fossa
  5. A fungus is identified in cultures. 
  6.  Associated infectious processes, such as mastoiditis, sinusitis, or a periorbital abscess, may require surgical drainage.

The duration of antibiotic therapy:

It depends on the organism and response to treatment but is usually 4–6 wk.


The mortality rate associated with brain abscess has decreased significantly to ≈15–20 % with the use of CT or MRI and prompt antibiotic and surgical management.

Factors associated with a high mortality rate at the time of admission :

  1. Age less than 1 yr 
  2. Multiple abscesses.
  3. Coma.
  4. Lack of CT facilities.

Long-term sequelae :

  1. Occur in at least 50% of survivors 
  2.  Include hemiparesis, seizures, hydrocephalus, cranial nerve abnormalities, 
  3. Behavior and learning problems.

About Author:

Ranjith C S. DNB (Pediatrics), DM (Medical Oncology)

Ranjith has completed Pediatric Residency from Kanchi Kamakoti Childs Trust Hospital and further trained in Medical Oncology from JIPMER.