Brain abscess is a life threatening illness,demanding rapid diagnosis and treatment. A brain abscess is an intraparenchymal collection of pus. Its development requires seeding of an organism into the brain parenchyma, often in an area of damaged brain tissue or in a region with poor microcirculation. The lesion evolves from cerebritis stage to capsule formation. Brain abscesses can be caused by contiguous or haematogenous spread of an infection, or by head trauma/ neurosurgical procedure. The most common presentation is that of headache and vomiting due to raised intracranial pressure. Seizures have been reported in up to 50% of cases. Focal neurological deficits may be present, depending on the location of the lesion. Treatment of a brain abscess involves aspiration or excision, along with parenteral antibiotic therapy. The outcome has improved dramatically in the last decades due to  improvement in diagnostic techniques, neurosurgery, and broad-spectrum antibiotics. The authors provide an overview of the pathogenesis, diagnosis and management of brain abscesses.

Sveinsson OA, Asgeirsson H, Olafsson IH

1. Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. 2. Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden. 3. Department of Neurosurgery, Landspitali, The National University Hospital of Iceland Reykjavik

Table I. Certain bacterial pathogens can indicate the possible origin of a haematogenous brain abscess. 14

Endocarditis – Viridans streptococcus, Staphylococcus aureus.

Pulmonary infections – Streptococcus species.

Congenital heart disease with right to left shunt– Streptococcus species.

Gatrointestinal infections – Enterobacteriaceae, anaerobic bacteria.

Urinary tract infections – Enterobacteriaceae.

Wound infections – S. aureus, Streptococcus species.

 

Table II. Situations where antibiotic treatment is sometimes used alone without a surgical intervention. 14,22

Multiple abscesses

Abscess located in an area where it is difficult to apply surgery

Abscess located in an eloquent area

Concomitant meningitis

Abscess less than 2-3 cm in diameter

Abscess which shrinks quickly with antibiotic treatment

Cerebritis

Patients state of health does not allow operation

 

Table III. Factors associated with worse prognosis of brain abscess. 14,22

Symptoms and signs indicating hearniation at diagnosis

Low Glasgow coma scale score at diagnosis

Large lesion with pressure effect (increasing oedema, midline shift)

Short period of symptoms before diagnosis

Delay in surgery

Gram negative infection

Other underlying diseases or immunosuppression

Nocardial abscess

Intraventicular rupture

 

Figure 1. An older gentleman complained of a worsening headache and left sided weakness over three days. On the fourth day, at the hospital, he was almost hemiplegic on the left side and had reduced consciousness (12 points on the Glasgow Coma Scale). Body temperature was 37°C. CRP was 63 mg/L. An acute CT scan of the brain with contrast (1a) showed a 35x35x40 mm lesion with ring enhancement in the right frontal lobe with surrounding edema and a slight midline shift to the left. This raised the suspicion of a brain abscess. MRI (T1) after gadolinium (1b) showed an expanding process with ring like contrast enhancement. On another slice (1c) one could see how the abscess became thinner towards the right ventricle and was close to rupture, in to the ventricle. To exclude a malignancy, a diffusion weighted imaging image (DWI) (1d) was performed which showed an increased signal (white) which indicated that it was an abscess. This was confirmed with an apparent diffusion coefficient (ADC) map (1e) which showed reduced signal (black) in the lesion. Treatment was initiated with intravenous corticosteroids (betamethasone 8mg bid), cefotaxime 3g tid and metronidazole 1g sid. The patient underwent under an open craniotomy and out came pus. After this the clinical situation improved. He returned to normal consciousness and regained strength on the left side to a large degree. Blood cultures were negative but from the abscess grew Streptococcus milleri, cefotaxime sensitive. Extensive investigations did not reveal the origin of the infection. The patient was treated for four weeks with cefotaxime and the corticosteroids were tapered over three weeks. After a rehabilitation period there was a mild weakness on the left side.

 

Figure 2. An older female sought her general practitioner because of right ear pain and leaking of pus. A clinical diagnosis of external otitis was made, treated with ear drops. The day after she had a seizure and was transported to the emergency department. Her temperature was 39.5°C and she was in a delirious state. CRP was 365 mg/L. A CT scan of the head showed signs of mastoiditis and raised a suspicion of cerebritis in the right temporal lobe. MRI (T1) with gadolinium showed signs of inflammation in the temporal lobe without contrast enhancement.  On T2 the inflammation was more visible (figure 2). She seized two more times and was treated with fosphenytoin and levetiracetam. Treatment was initiated with cefotaxime 3g tid. Streptococcus pyogenes grew from blood and nasopharynx cultures. Surgery was performed on the mastoid bone, and from there grew S. pyogenes og Staphylococcus aureus. After 11 days the patient got a skin rash, and the antibiotic treatment was changed to meropenem 2g tid for additional two weeks. She was discharged with ertapenem 2g sid for nine more days. The patient recovered fully and the anti epileptic treatment was stopped after one year.