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Wednesday, 21 March 2012


The incidence of cerebral abscess case /100.000 population is estimated at 1 per year. This incidence decreased after 1950 in line with the increasingly widespread use of antibiotics. Comparison of prevalence between men and women are 3:1.
75-90% is a solitary abscess, of which 35-45% are located in the frontal lobe, temporal lobe at 30-40%, 15-20% in the parietal lobe, and 15% in the occipital, cerebellum and brain stem.


Brain abscess is an infection process by which localized pus between brain tissue caused by a wide variety of bacteria, fungus and protozoa. Brain abscess were present in all ages. Most at the age of the second decade of life, between 20-50 years.Comparison between male patients with female is 3:1.

Etiology and predisposing

Much of the spread of brain abscess arising directly from middle ear infections, sinusitis, or mastoiditis. Can also be caused by systemic pulmonary infection, acute and subacute bacterial endocarditis, and sepsis mikroemboli to the brain. Other causes but rarely is osteomyelitis of the skull, sellulitis, erysipelas of the face, tooth infections, puncture wounds to the skull by the trauma. Infection of the paranasal sinuses, can be spread by retrograde thrombophlebitis through the veins diploika valve toward the frontal or temporal lobes. Usually form a single absesnya, suferfisial located in the brain, close to the source of the infection. Frontal sinusitis can cause abscesses in the anterior or inferior frontal lobes. Sfenoidalis sinusitis, abscesses usually found in the frontal lobe or temporal. Maxillary sinusitis absesnya found in the temporal lobes. Sinusitis etmoidalis absesnya found in the frontal lobes. Middle ear infection can spread to the temporal lobes. Infection of the mastoid may spread into the cerebellum. Localization of brain abscess is hematogenous spread is consistent with the circulation of blood, most often on areas that are distributed by the middle cerebral artery, especially in the parietal lobe.
For other precipitating factors is the occurrence of penetrating trauma to the head, especially when found foreign bodies left in the brain tissue, eg bone. Skull base fractures are accompanied by leakage of cerebrospinal fluid can cause meningitis resulting in brain abscess. At craniotomy, if there is infection osteomyelitis of "bone flap", the possibility can lead to brain abscess.

According bacterial cause, the etiology of brain abscess can be divided into:
A. Aerobic organisms:
• Gram positive: Streptococcus, Staphylococcal, Pneumococcal
• Gram negative: E. coli, Hemophilus influenza, Proteus, Pseudomonas
2. Anaerobic organisms: B. fragilis, Bacteroides sp, Fusobacterium sp, Prevotella sp, Actinomyces sp, and Clostridium sp.
3. Fungi: Candida, Aspergillus, Nokardia
4. Parasites: E. histolytica, Schistosomiasis, Amoeba


Mechanisms of infection in cerebral abscess:
Direct spread from a primary focus (> 50% of cases), such as sinusitis, dental infections, middle ear, mastoid, which can directly or indirectly through the dura mater following the veins.
Dissemination via the blood (25% of cases), derived from primary lung infection, heart and skin. Half of all cases of hematogenous abscesses associated with chronic infection of the lungs (bronchiectasis, lung abscess). Direct exposure to the organism as a result of penetrating head trauma or neurological complications of surgery (35-40% of cases).
AS occur at an early stage of diffuse inflammatory reaction in brain tissue edema accompanied by leukocyte infiltration, and congestion perlunakan brain tissue, sometimes accompanied by bleeding spots. After a few days to several weeks and liquefaction necrosis in the center of the lesion so as to form an abscess cavity. Astroglia, fibroblasts and macrophages surrounding the necrotic tissue. At first the abscess is not demarcated but over time with progressive fibrosis formed a capsule with a concentric walls. Capsule thickness between a few millimeters to several centimeters.

Some experts divide the pathological changes in four stages, namely the United States:

1) Stage serebritis early (Early Cerebritis) (days 1-3)
Local inflammatory reaction with infiltration polymofonuklear leukocytes, lymphocytes and plasma cells in peripheral blood flow shift, which begins on the first day and increased on day 3. Inflammatory cells present in the tunica adventisia of blood vessels and surrounding necrotic areas of infection. Perivascular inflammation is called cerebritis. When this occurs around the brain edema and mass effect of the increase due to enlargement of the abscess.

2) further serebritis Stadium (Late Cerebritis) (days 4-9)
Currently there are very significant histological changes. The central area of ​​necrosis enlarged because of increased acellular debris and pus formation due to the release of enzymes from inflammatory cells. On the edge of the central area of ​​necrosis was found inflammatory cells, macrophages and a large picture of scattered fibroblasts. Fibroblasts from a reticulum which will form the collagen capsule. In this phase so that the maximum spread of brain edema lesions become very large

3) Stadium early capsule formation (Early Capsule Formation) (days 10-13)
Central necrosis began to shrink, acellular debris ingestion macrophages and fibroblasts increased the formation of the capsule. Forming a layer of fibroblast reticulum webbing around the center of necrosis. In daerahventrikel, wall formation is very slow because of lack of vascularization in the white substance than the substance of the ash. Capsule formation is delayed in the middle of the surface allows the abscess enlarges into a white substance. If the abscess is large enough, can be torn into the lateral ventricle. On
capsule formation, seen the woven reticulum scattered collagen capsule form, the reaction of astrocytes in the brain began to increase.
4) Advanced Stage capsule formation (Late Capsule Formation) (day> 14)
At this stage, there is a complete development of an abscess with a histological picture as follows:
• The center is filled by the acellular necrotic debris and inflammatory cells.
• The area consists of the edge of central necrosis of inflammatory cells, macrophages, and fibroblasts.
• a thick collagen capsule.
• Neurovascular layer with respect to ongoing serebritis.
• The reaction of astrocytes, gliosis, and edema of the brain outside the capsule.

Abscess in the capsule white matter can be further enlarged and extended to the ventricle so that in the event of rupture, can cause meningitis. Facial tissue infection, orbital cellulitis, sinusitis etmoidalis, meningoensefalokel nasal amputation and apical dental abscess can cause the U.S. is located in the frontal lobes. Otitis media, mastoiditis, especially the U.S. led to the temporal lobes and cerebellum, parietal lobe abscesses are usually hematogenous.

            Cerebral abscess usually appears as a subacute process and the onset of symptoms within 2 weeks. But if the temporal location is large enough, then the symptoms can occur acutely (days) or chronic (months). This depends on the suppression of mass effects in the brain.
            In early-stage U.S. clinical picture is typical, there are symptoms of infection such as fever, malaise, anorexia and symptoms of intracranial pressure elevation of vomiting, headaches and seizures. With symptoms of cerebral abscess the size of a typical form of brain abscess triad consisting of symptoms of infection, elevation of intracranial pressure and focal neurologic symptoms.

Manifestations of brain abscess is actually based in the presence of:

1. Manifestations of increased intracranial pressure, headache, vomiting, and papilledema.

2. Manifestations of intracranial suppuration iritabel, drowsiness, or stupor, and signs of meningeal stimulation.

3. Signs of infection include fever, chills, leukocytosis.

4. Local signs of brain tissue affected by the form of seizures, cranial nerve disorders, aphasia, ataxia, paresis.

Abscess in the frontal lobe is usually quiet and when there are neurological symptoms such as hemikonvulsi, hemiparesis, hemianopsia homonym with a decreased awareness showed unfavorable prognosis due to disc herniation and perforation usually occurs into the ventricular cavity.
Temporal lobe abscess in addition to causing hearing loss and found disfasi taste, vision defects and contralateral quadrants hemianopsi complete pedestal. Motor disorders, especially the face and upper limbs may occur if an abscess extension into the frontal lobe is relatively asymptomatic, located primarily in the anterior region so that the focal symptoms are symptoms sensorimotorik. Cerebellar abscess is usually located on one hemisphere and lead to coordination problems such as ataxia, tremor, and nystagmus dismetri. Brain stem abscesses are rare, usually from haematogenous and fatal.

In the laboratory tests obtained leukocytes> 10,000 (50%) or an increase of> 20,000 (<5%), LED increases> 40 mm / h (25-30%), and increased C reactive protein (85-90%).


CT-scan picture of the abscess:
I. Early cerebritis (days 1-3): areas of inflammation, focal, and edema
II. Late cerebritis (days 4-9): there are areas of inflammation and necrosis extends from the central zone of inflammation.
III. Early capsule stage (days 10-14): gliosis post infection, fibrosis, hipervaskularisasi on the perimeter of the infected area. At this stage the picture can be seen ring enhancement.
IV. Late capsule stage (days> 14): there is a hypodense central area (central abscess) are surrounded by contrast - ring enhancement (abscess capsule).

CT scan may be considered as a choice of diagnostic procedures, because the sensitivity can reach 90% for the diagnosis of cerebral abscess. To consider is that although the CT picture typical for an abscess, but did not rule out the possibility of appeal was diagnosed with a tumor (glioblastoma), infarct, metastasis, hematoma is absorbed and granuloma.
Although difficult to distinguish between abscesses and tumors (glioblastoma, metastasis) of the CT scan, there are several parameters that can be used to differentiate the two include: patient age, the thickness of the ring (a ring of thin only 3-6 mm) and usually uniform, ring diameter, the ratio lesion and ring. In 50% of cases, the medial capsule is thinner than the capsule subcortical. This suyggests at least vascularity of the mass of the white / white matter.
          Hematogenous cerebral abscess is characterized by a focus of infection (the commonest of the lung), the location of the area supplies by middle cerebral artery in the border area a mass of white and gray with a high mortality rate.
          While the CT scan picture of glioblastoma is a tumor of mixed density, ring enhancement of squiggly perifokal with extensive edema.


Definitive treatment for an abscess involving:
A. The management of mass effect (abscess and edema) which can be life threatening
2. Antibiotic therapy and test the sensitivity of the material culture of the abscess
3. Neurosurgical therapy (aspiration or excision)
4. Treatment of primary infection
5. Prevention of seizures
6. Neurorehabilitasi

Therapy recently recommended replacing the third-generation cefalosporin penicillin plus metronidazole for anaerobic bacteria combined with vancomycin or nafsilin to antistafilokokal.
Studies show that cefotaxime and ceftazidime is an antibiotic that can penetrate the abscess capsule well, and the results of clinical trials also support the effectiveness of cefotaxime and metronidazole combination therapy in the treatment of cerebral abscess.
 Nafcillin used in patients with suspected abscess is hematogenous spread. Vancomycin is used in patients with postoperative cerebral abscess or abscesses obtained from the hospital (hospital acquired). Antibiotics are used for 4-6 weeks.

            Most clinical studies indicate that steroid use can affect the penetration of certain antibiotics and may block the formation of an abscess capsule. But its use may be considered in cases where there are potential risks in an increase in intracranial pressure. The dose you take 10 mg of intravenous dexamethasone every 6 hours, and tappering off in 3-7 days.
 In patients, the corticosteroid is given in consideration of increased intracranial pressure, optic disc edema and extensive edema picture and midline shift on CT scan. Corticosteroids given in 2 weeks after that in the tap-off, and seen that the headache gradually reduced and the XV day of the examination is not available NO papil edema.

Surgical therapy

            Optimal therapy in dealing with cerebral abscess is a combination of antimicrobials and surgery. In the latter study, excision and drainage of abscess therapy through a craniotomy is a procedure of choice. But at certain centers preferred the use of stereotactic aspiration or MR-guided aspiration and biopsy. Common aspirations of the action performed on multiple abscesses, abscesses and brain stem lesions are more widely used excision.
In some circumstances the operative therapy is not much benefit, such as: small deep abscess, abscess and multiple cerebritic early stage. Most studies show that there was no significant difference between patients who received conservative treatment with therapy or excision in reducing the risk of seizures.


The use of anticonvulsants is also influenced by the location of the abscess and its position on the cortex. Therefore, when an anticonvulsant is stopped depends from case to case (determined by the duration of seizure-free, no abnormalities neurological examination, EEG and neuroimaging).


            With advances such as the use of neuroimaging and diagnostic neurosurgikal techniques and the use of effective antimicrobial can reduce the risk of death from 40% to 10%. Focal deficits can be improved, but seizures can be settled on 50% of patients.


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Scheld WM, Whitley RJ, Durack. Brain Abscess. In Infection of the Central Nervous System. New York, USA: Raven Press, 1991:457-586

Tyler KL. Bacterial Brain Abscess. AAN 2000 : 2FC.004-20-35

Lindsay KW, Bone I, Callander R. Intracranial Abscess. In Neurology and Neurosurgery Illustrated. 2nd ed. Hongkong: Churchill Livingstone, 1991: 343-346

Wood M, Anderson M. Brain Abscess. In Neurological Infections. London:WB Saunders Company, 1998:250-265

Wilkinson IMS. Infections of the Nervous System. In Neurology. 3rd ed. London:Blackwell Science Ltd, 1999: 226-232

Grumme T, Kluge W, Kretzschmar K, Roesler A. Cerebral Inflammations. In Cerebral and Spinal Computed Tomography. 3rd ed. Berlin:Blackwell Science, 1998:127-131

Grumme T, Kluge W, Kretzschmar K, Roesler A. Neoplasms. In Cerebral and Spinal Computed Tomography. 3rd ed. Berlin:Blackwell Science, 1998:138-148

Weisberg LA. Focal Intracranial Bacterial Disease. In Decision Making in Adult Neurology. Philadelphia:Manlygraphic Publishers PteLtd, 1988:214-217


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