Central Nervous System Infections: Cerebral Abscess



Remember: Haematogenous spread is the commonest cause of brain abscess.





Pathology/Pathogenesis

Streptococcus is the commonest organism. Multiple organisms are cultured in up to 30% of cases and usually include anaerobic, predominantly Bacteroides, species. The commonest posttraumatic and postneurosurgical organism is Staphylococcus aureus. Toxoplasma and Nocardia are likely organisms in immunocompromised patients.


There are four stages to the formation of a cerebral abscess, progressing from the early cerebritis phase, characterised by early focal parenchymal infection and infiltration, through late cerebritis (up to day 9, characterised by development of central necrosis) to capsule formation (early up to day 13 and late after day 14) with development of a collagen capsule, peri-capsular gliosis and a definite necrotic centre. The administration of corticosteroids tends to slow the progression.


History


  • Symptoms suggestive of raised intracranial pressure, including headache, nausea and vomiting; irritability in children and seizures (may be focal or generalised and develop in up to 50% of cases).
  • Development of a neurological deficit related to the abscess location; acute neurological deterioration may suggest intraventricular rupture of a brain abscess.
  • Symptoms of primary infectious cause may be evident.

Examination


  • Signs of elevated intracranial pressure, including impairment of consciousness, neck stiffness and focal neurological deficit.
  • Evidence of primary infection, for example lung or sinuses.
  • May not necessarily be associated with pyrexia.

Investigations


  • Peripheral white cell count, erythrocyte sedimentation rate and blood cultures—often within normal limits or negative.
  • C-reactive protein may be elevated in relation to the primary or systemic infection.
  • Imaging is the investigative modality of choice. CT with contrast can be used to demonstrate ring enhancement (Figure 22.1). A mature encapsulated abscess shows ring enhancement of the capsule on postcontrast MRI. Extensive pericapsular oedema is evident. The necrotic centre demonstrates restricted diffusion on diffusion-weighted imaging. In the early cerebritis phase, the lesion is hypointense and hyperintense on T1- and T2-weighted images, respectively. Magnetic resonance spectroscopy shows high lactate, alanine and glycine in the necrotic centre of a mature abscess, while N-acetyl aspartate, creatine and choline peaks are reduced (compare with choline peaks in malignant glioma) (Table 22.1).
  • Other investigations directed at finding the source of abscess: Echocardiogram, CT of chest and abdomen, orthopantomogram (dental X-ray), CT of sinuses and so on.




< div class='tao-gold-member'>

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jul 16, 2016 | Posted by in NEUROSURGERY | Comments Off on Central Nervous System Infections: Cerebral Abscess

Full access? Get Clinical Tree

Get Clinical Tree app for offline access