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Brain abscess
Brain abscess

Brain abscess

Brain abscess are a form of intracranial abscess (along with subdural abscess and extradural empyema). They are are with around 1 in 100,000 affected annually but are more common in the developing world. They are life-threatening and need to be managed appropriately and swiftly.

Pathophysiology

The central nervous system has many barriers and mechanisms in place to safeguard it from infections. Some of these include the meninges, the blood-brain-barrier (made up of tight junctions between endothelial cells and astrocyte foot processes), CSF circulation, microglial immune function.

However, despite these numerous techniques, breaches do occur in certain instances which can lead to the development of brain abscesses.

Let’s look at the potential causes that allow infection to spread in the brain:

  • Contiguous spread - spread from other adjacent sites of infection.

      • Common sites that allow for contiguous spread:

    1. Otitis media - most commonly affects the temporal lobe and cerebellum.
    2. Sinusitis - more commonly affects the frontal lobe.
    3. Mastoiditis
    4. Oral infections
    5. Meningitis
  • Direct access - for example after trauma or neurosurgery.
  • Haematogenous spread - this is the least common route and is more prevalent in individuals who are immunocompromised (such as patients on chemotherapy, patients with HIV & AIDS, and transplant patients).

      • Certain conditions and infections can predispose haematogenous spread, too:

    1. Cyanotic heart disease (such as arteriovenous right-to-left shunts) - as they bypass the pulmonary circulation’s filtration and can carry septic thrombi into the brain which can lead to multiple abscess formation along the vascular supply of the cerebral cortex.
    2. Pulmonary arteriovenous fistula
    3. Dental abscess
    4. Endocarditis
    5. Cystitis
    6. Peritonitis
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💡 Contiguous spread leads to a single abscess while haematogenous spread is more likely to lead to multiple abscesses.

Once the infection reaches the brain parenchyma, the infection passes through the following stages:

  1. Early cerebritis - in the first 3-5 days of infection. Neutrophil infiltration leads to cerebral oedema. Necrosis occurs and microglia and astrocytes are also activated but there is no fibrous capsule formation yet.
  2. Late cerebritis - this happens after 4-9 days of infection. Further tissue necrosis along with macrophage activation leads to a fibrotic capsule forming around the lesion.
  3. Early abscess - happens after day 10. Encapsulation of the infection allows for a suppurative collection.

🦠 Causative agents

Cerebral (and cerebellar) abscesses are increasingly polymicrobial:

  • Common pathogens:
    • ⭐️ Streptococci
      • Strep pneumoniae
      • Viridans streptococci - usually from sinusitis. Sinusitis may also be from Streptococcus milleri.
    • Staphylococci
      • Staphylococcus aureus
      • Coagulase-negative staphylococci such as Staphylococcus epidermidis.
  • Less common pathogens:
  • Obligate anaerobes - such as the bacteroides spp. (common in dental infections).
  • Gram negative aerobic bacteria, such as pseudomonas spp. and enterobacteria
  • In immunocompromised states it becomes commoner to be infected with parasites or fungi:
  • Parasitic infections- such as Toxoplasma gondii.
  • Fungal infections - such as Aspergillus, Candida spp., Mucormycosis, Cryptococcus.
  • Listeria - a bacterial infection more common in pregnant women and older people.

⚠️ Risk factors

Risk factors for haematogenous spread:

  • Congenital heart disease
  • Pulmonary arteriovenous malformations and fistulae
  • Infective endocarditis
  • Intravenous drug use
  • Lung infections

Risk factors for contiguous spread:

  • Systemic sepsis
  • Dental abscesses
  • Sinonasal infections

😷 Presentation

The presentation is variable depending on location and size of the abscess. The onset may be acute or may develop over several weeks (subacute).

Symptoms may include:

  • Dull, persistent headache - if the abscess ruptures the headache may suddenly worsen.
  • Meningismus - if coupled with radiological findings it is suggestive of brain abscess. Meningismus is the clinical syndrome of headache, neck stiffness, photophobia, nausea and vomiting.
    • Focal neurological deficits - commonly secondary to raised intracranial pressure.
      • Oculomotor nerve palsy - leads to a fixed and dilated pupil.
      • Abducens nerve palsy - leads to convergent strabismus due to paralysis of the lateral rectus muscle (inability to abduct the eye).
  • Raised intracranial pressure
    • Vomiting
    • Papilloedema
    • Cushing’s triad - raised blood pressure, bradycardia, irregular respiration.
  • Fever
  • Kernig and Brudzinki signs
  • Bulging fontanelle (in children)
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🔍 Investigations

🧪
Laboratory tests:
  • Bloods
    • CRP and ESR - raised.
    • FBC - leukocystosis.
    • Blood cultures - not helpful in diagnosis. they are only positive in about 15% of cases.

⚠️ Lumbar puncture is not done due to the risk of raised ICP (which is a contraindication), and because it may precipitate transtentorial (uncal) herniation and because CSF findings are nonspecific.

📷
Imaging:
  • 🥇 CT or MRI - this is the best initial investigative test. It is also used to confirm the diagnosis and to localise the lesion (as well as size and number of lesions). It can be used to monitor response to treatment as well.

      • MRI provides more detail, thus allowing us to differentiate a brain abscess from other ring-enhancing lesions, like brain tumours that have a nectrotic centre that makes them look similar to an abscess.

      Findings on MRI and CT include:

    1. CT - intraparenchymal lesions with a central hypodense (dark) necrotic area  and peripheral ring enhancement (a bright ring surrounding it).
    2. T1-weighted MRI with contrast - central hypointense (dark) lesions with ring-formed contrast enhancement, potentially in the perifocal hypointense regions due to surrounding oedema.
    3. T2-weighted MRI - central hyperintense region (bright) with an isointense rim and perifocal hyperintense regions (perifocal oedema).
    4. Diffusion weighted imaging (DWI) - hyperintense (bright) lesion.
      5. T1-weighted with contrast with a hypointense lesion, hyperintense ring, hypointense perifocal oedema.
      T1-weighted with contrast with a hypointense lesion, hyperintense ring, hypointense perifocal oedema.
      T2-weighted with a a hyperintense lesion, isointense ring, hyperintense perifocal oedema.
      T2-weighted with a a hyperintense lesion, isointense ring, hyperintense perifocal oedema.
      DWI with a hyperintense lesion.
      DWI with a hyperintense lesion.

🏆 Aspiration and drainage - this is the best test to confirm diagnosis and also to culture. It is done via craniotomy or image-guided aspiration. A biopsy can also be done to distinguish an abscess from a tumour.

🧰 Management

🧰
Management of a brain abscess:
  • Early surgical drainage and biopsy
  • IV antibiotics - usually for 6-8 weeks, following drainage. Therapy should be given intravenously for at least the first week.
    • Initial empirical therapy: 
      • Ceftriaxone or cefotaxime (3rd gen cephalosporins) + metronidazole
      • ± Vancomycin (if staphylococcal infection is suspected)
      • ± Ampicillin or chloramphenicol (if listeria is possible or the patient is immunocompromised)
    • If a fungal cause is suspected - amphotericin, flucytosine, fluconazole or voriconazole are indicated.
    • For toxoplasmosis: pyrimethamine + sulfadiazine.
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  • Seizure prophylaxis
  • Raised ICP management - [link to CCC on raised ICP once completed]