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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.
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.[4, 5]
- 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 and references
Beckham JD, Tyler KL; Neuro-intensive care of patients with acute CNS infections. Neurotherapeutics. 2012 Jan9(1):124-38.
Udoh D; Uncommon intracranial abscesses. J West Afr Coll Surg. 2012 Jan2(1):75-83.
Ozsurekci Y, Kara A, Cengiz AB, et al; Brain abscess in childhood: a 28-year experience. Turk J Pediatr. 2012 Mar-Apr54(2):144-9.
Sowerby LJ, Wright ED; Intracranial abscess as a complication of nasal septal abscess. CMAJ. 2013 Apr 2185(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 Dec30(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-Dec158(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-Jun75(5-6):716-26
Muzumdar D, Jhawar S, Goel A; Brain abscess: an overview. Int J Surg. 20119(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 Jun71 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-Apr27(2):525-51.
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