PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.
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).
- Intracranial abscess, although uncommon, have relatively higher occurrence in low socio-economic settings where previous antibiotic abuse and lack of modern culture techniques makes isolation of organisms difficult.
- Brain abscesses are rare in developed countries but remain a significant problem in the developing world.
- 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.
- Cyanotic congenital heart disease was the most common predisposing factor in children.
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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.
- 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, corticosteroids or illness (eg, HIV or tuberculosis).
- 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. 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%) and pulmonary infection (7%). The cause was unknown in 4%.
A low index of suspicion is essential. 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.
- Focal motor or sensory deficits.
- Raised blood pressure and bradycardia associated with raised intracranial pressure.
- Confusion, drowsiness.
- Bulging fontanelle in infants.
- 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 - 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. 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.
- 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:
- 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.
- 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 long-term in 30-50%, 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.
Mortality ranges between 17% and 32%. Poor prognosis is reported in patients who are immunocompromised, have diabetes mellitus or cirrhosis and presentation with a low Glasgow Coma Score. Intraventricular rupture as a complication of brain abscess is associated with high mortality. Pre-treatment neurological state of the patient is the most influential independent factor related with the outcome. Patients with deep-seated infection (basal ganglion or thalamus) have worse outcome caused by the higher incidence of intraventricular rupture in these patients.
Further reading & references
- Beckham JD, Tyler KL; Neuro-intensive care of patients with acute CNS infections. Neurotherapeutics. 2012 Jan;9(1):124-38.
- Udoh D; Uncommon intracranial abscesses. J West Afr Coll Surg. 2012 Jan;2(1):75-83.
- Ozsurekci Y, Kara A, Cengiz AB, et al; Brain abscess in childhood: a 28-year experience. Turk J Pediatr. 2012 Mar-Apr;54(2):144-9.
- Sowerby LJ, Wright ED; Intracranial abscess as a complication of nasal septal abscess. CMAJ. 2013 Apr 2;185(6):E270. doi: 10.1503/cmaj.120431. Epub 2012 Sep 4.
- Leskinen K, Jero J; Acute complications of otitis media in adults. Clin Otolaryngol. 2005 Dec;30(6):511-6.
- 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.
- 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.
- Muzumdar D, Jhawar S, Goel A; Brain abscess: an overview. Int J Surg. 2011;9(2):136-44. doi: 10.1016/j.ijsu.2010.11.005. Epub 2010 Nov 16.
- Bonfield CM, Sharma J, Dobson S; Pediatric intracranial abscesses. J Infect. 2015 Jun;71 Suppl 1:S42-6. doi: 10.1016/j.jinf.2015.04.012. Epub 2015 Apr 24.
- 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.
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.
Dr Hayley Willacy
Dr Colin Tidy
Dr Adrian Bonsall