Abscessos intracranianos

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.

Epidemiologia

• Incidence is estimated at 0.3-1.3 per 100,000 people per year (non-HIV infected).¹

• 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.²

• Brain abscesses are rare in developed countries but remain a significant problem in the developing world.

• A decrease in meningite due to the Haemophilus influenzae vaccine has reduced the prevalence in young children.

• The prevalence of brain abscess is higher in patients with infecção por HIV. They are usually caused by opportunistic fungal or protozoal infection.

• Cyanotic congenital heart disease was the most common predisposing factor in children.³

Causative organisms include:

• Bactérias: common bacterial causes include Staphylococcus aureus, e Streptococcus, Bacteroides e Listeria species. Approximately 40% of abscesses originate from infection of adjacent structures - eg, otitis media, dental infection, mastoiditis, sinusitis.⁴⁵

• Fungos: 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).⁶

• Protozoa: Toxoplasma gondii, Entamoeba histolytica, Trypanosoma cruzi e 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%.⁷

Sintomas

A low index of suspicion is essential.²Onset 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.

Sinais

• Febre.

• Focal motor or sensory deficits.

• Raised blood pressure and bradycardia associated with raised intracranial pressure.

• Papilloedema.

• Ataxia.

• Confusion, drowsiness.

• Bulging fontanelle in infants.

• Meningite.

• Encefalite.

• Tumor cerebral or other intracranial lesão ocupando espaço.

• 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.¹⁰

  • 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

• 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.

Cirúrgico

• 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.

• Epilepsia 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.