3. Intracranial Abscesses

Intracranial Abscesses

This PatientPlus article is written for healthcare professionals so the language may be more technical than the condition leaflets. You may find the abbreviations list helpful.

Intracranial abscesses are uncommon, serious, life-threatening infections. They include brain abscess and subdural or extradural empyema. A high number of brain abscesses are polymicrobial.

  • Incidence is estimated at 0.3-1.3 per 100,000 people per year (non-HIV infected).[1] 
  • Brain abscesses are rare in developed countries, but are a significant problem in the developing world; they are twice as common in males and have a peak incidence at around 40 years of age.[2]
  • A decrease in meningitis due to the Haemophilus influenzae vaccine has reduced the prevalence in young children.
  • The prevalence of brain abscess is higher in patients with HIV infection. They are usually caused by opportunistic fungal or protozoal infection.

Causative organisms include:

Bacteria: common bacterial causes include Staphylococcus aureus, and Streptococcus, Bacteroides and Listeria species. Approximately 40% of abscesses originate from infection of adjacent structures - eg, otitis media, dental infection, mastoiditis, sinusitis.[3]

Fungi: Aspergillus, Candida, Cryptococcus, Coccidioides, Histoplasma, and Blastomyces species. The frequency of fungal brain abscess has increased because of the frequent administration of broad-spectrum antimicrobials, immunosuppressive agents or illness (HIV or tuberculosis[4]) and corticosteroids.

Protozoa: Toxoplasma gondii, Entamoeba histolytica, Trypanosoma cruzi, and Schistosoma spp.

Helminths: Taenia solium.

Abscess formation can also develop following blood-borne spread from a remote site - eg, in patients with cyanotic congenital heart disease, endocarditis, and dental caries.[5] In at least 20% of cases no source can be identified. In one South African study precipitating events were as follows: oto-rhino infection (38%), trauma (37%), pulmonary infection (7%) and cryptogenic (4%).[6] 

Symptoms

Onset may be sudden or subacute over several weeks.

  • Common presenting symptoms include fever, headache, changes in mental state (drowsiness, confusion), focal neurological deficits, grand mal seizures, nausea and vomiting, neck stiffness.
  • A suddenly worsening headache, followed by emerging signs of meningism, are often associated with rupture of the abscess.

Signs

  • Fever.
  • Focal motor or sensory deficits.
  • Raised blood pressure and bradycardia associated with raised intracranial pressure.
  • Papilloedema.
  • Ataxia.
  • Confusion, drowsiness.
  • Bulging fontanelle in infants.
  • Meningitis.
  • Encephalitis.
  • Brain tumour or other intracranial space-occupying lesion.
  • FBC: marked leukocytosis.
  • Raised ESR and CRP.
  • Renal function and electrolytes: serum sodium levels may be lowered as a result of inappropriate antidiuretic hormone production.
  • Blood cultures: at least two, and preferably before antibiotics are started.
  • Serological tests: available for some pathogens.
  • Cerebrospinal fluid: lumbar puncture is rarely helpful (unless required to rule out meningitis) and is contra-indicated if increased intracranial pressure is present. Lumbar puncture in the presence of raised intracranial pressure can precipitate a tentorial or tonsillar herniation.
  • CT scanning is the investigation of choice.[7] Cerebral abscesses appear as a radiolucent space-occupying lesion:
    • As the disease progresses, a distinctive 'ring enhancement' appears on contrast-enhanced CT, as the abscess wall thickens.[8]
    • They are often surrounded by oedema.
    • The position, size and number of abscesses may suggest underlying pathology.
    • MRI scans provide greater contrast between cerebral oedema and the brain and early detection of satellite lesions.
  • Aspiration of abscess for culture.
  • Biopsy of cerebral lesion.

The principles of treatment are:[1][7]

  • Drain intracranial collection; supratentorial abscesses can be drained via a burr hole. Pus should be sent for culture.
  • Administer effective antibiotic therapy; early treatment is essential.
  • Eliminate the primary source of infection.

Initial antimicrobial therapy should be started immediately and then modified according to the results of cultures.

  • Initial therapy should be guided by local guidelines and the advice of a microbiologist:
    • Initial empirical therapy usually consists of a third-generation cephalosporin (eg,  ceftriaxone), metronidazole and vancomycin (if staphylococcal infection is suspected), and ampicillin or chloramphenicol (if listeria is possible or the patient is immunocompromised).
    • If a fungal cause is suspected then amphotericin, flucytosine, fluconazole or voriconazole are indicated.
    • The treatment of choice for toxoplasmosis is a combination of pyrimethamine and sulfadiazine.
    • Therapy should be given intravenously for at least the first week.
  • Patients presenting with seizures require intubation and hyperventilation. Seizures should be treated aggressively to decrease the risk of increases in intracranial pressure.
  • Corticosteroids: intravenous dexamethasone is used if massive cerebral oedema is seen on the CT scan.

Surgical

  • Once an abscess has formed, surgical excision or drainage through a burr hole, combined with prolonged antibiotics (usually 4-8 weeks), remains the treatment of choice.
  • Aspiration is the most common procedure and is often performed using a stereotactic procedure with the guidance of CT scanning or MRI. Craniotomy is generally performed in patients with larger, multiloculated abscesses and for those whose conditions failed to resolve.
  • Management of subdural or epidural empyema requires prompt surgical evacuation of the infected site and antimicrobial therapy.
  • Intracerebral abscesses may rupture into the ventricular system and produce ventriculitis.
  • Epilepsy occurs in around 30%, particularly with temporal lobe abscess and subdural empyema. Anticonvulsants may be required.
  • Mainly depending on the speed of diagnosis and treatment, 20-80% of survivors have neurological sequelae - eg, hemiparesis, visual field loss.
  • Prompt treatment results in mortality of less than 10%, but a delay in diagnosis increases mortality to above 50%.
  • Rupture of a brain abscess is associated with mortality of up to 80%.
  • 50% of survivors have neurological sequelae which may include hemiparesis, visual field losses and epilepsy.[7]
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Further reading & references

  1. Beckham JD, Tyler KL; Neuro-intensive care of patients with acute CNS infections. Neurotherapeutics. 2012 Jan;9(1):124-38.
  2. Thomas LE et al; Brain Abscess in Emergency Medicine, Medscape, Sep 2012
  3. Leskinen K, Jero J; Acute complications of otitis media in adults. Clin Otolaryngol. 2005 Dec;30(6):511-6.
  4. Gump WC, Summers LE, Walsh JW; Tuberculosis infection presenting as brain abscess in an immunocompromised host. J La State Med Soc. 2006 Nov-Dec;158(6):292-5.
  5. Oxford Textbook of Medicine 4th edition; Section 24.138; Teddy PJ; Intracranial Abscess.
  6. Nathoo N, Nadvi SS, Narotam PK, et al; Brain abscess: management and outcome analysis of a computed tomography era experience with 973 patients. World Neurosurg. 2011 May-Jun;75(5-6):716-26; discussion 612-7.
  7. Central nervous system infections: Intracranial abscess; Surgical Tutor
  8. Smirniotopoulos JG, Murphy FM, Rushing EJ, et al; Patterns of contrast enhancement in the brain and meninges. Radiographics. 2007 Mar-Apr;27(2):525-51.
Original Author: Dr Colin Tidy Current Version: Peer Reviewer: Dr Adrian Bonsall
Last Checked: 10/12/2012 Document ID: 2334  Version: 23 © EMIS

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

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