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BRAIN ABSCESS.pptx
- 1. BRAIN ABSCESS OLUWATAYO SAMUEL OLUWAKEYE VICTOR TAYO
- 2. INTRODUCTION • A brain abscess (or cerebral abscess) is a focal collection within the brain parenchyma which can arise as a complication of a variety of infections, trauma, or surgery. • It results from inflammation and collection of infected material, coming from local (ear infection, dental abscess, infection of paranasal sinuses, infection of the mastoid air cells of the temporal bone, epidural abscess) or remote (lung, heart, kidney etc.) infectious sources, within the brain tissue.
- 4. EPIDEMIOLOGY • Brain abscesses are rare in developed countries but are a significant problem in developing countries. • Brain abscesses are more common in males than in females. • Brain abscesses occur more frequently in the first 4 decades of life.
- 5. ETIOLOGY The microbial etiology of brain abscess depends on the • patient's age, • site of primary infection, and • the patient's immune status.
- 6. ETIOLOGY cont’d • A significant number of brain abscesses are polymicrobic but the most common agents are bacterial. • The predominant organisms include the following: • Staphylococcus aureus, including methicillin-resistant • Streptococcus viridans • Anerobic bacteria • Etc
- 7. ETIOLOGY cont’d • The incidence of fungal brain abscess has been rising as a result of increased use of corticosteroid therapy, broad-spectrum antimicrobial therapy, and immunosuppressive agents. Common agents include • Aspergillus, Candida, Cryptococcus • Other agents are • Protozoa e.g. Toxoplasma gondii • Helminths e.g. Taenia solium • Co-infection with bacterial, viral, and fungal organisms can occur.
- 8. PATHOPHYSIOLOGY • Brain abscess is caused by intracranial inflammation secondary to infection with subsequent abscess formation. • Infection may enter the intracranial compartment directly or indirectly via 3 routes • Contiguous suppurative focus • Hematogenous spread from a distant focus • Trauma
- 9. PATHOPHYSIOLOGY cont’d The process of abscess formation occurs in four stages- • Early cerebritis (days 1–3) • Late cerebritis (days 4–9) • Early capsule formation (days 10–13) • Late capsule formation (>14 days)
- 10. CLINICAL FEATURES- History • Most symptoms are a result of the size and location of the space- occupying lesion or lesions. • The frequency of common symptoms and signs is as follows: • Headache - 70% • Mental status changes (may indicate cerebral edema) - 65% • Focal neurologic deficits - 65% • Fever - 50% • Seizures - 25-35% • Nausea and vomiting - 40% • Nuchal rigidity - 25% • Papilledema - 25%
- 11. CLINICAL FEATURES- Examination • On examination, the following signs might be present- • Low-grade or high-grade fever • Confusion • Stupor • Focal motor or sensory impairments • General or focal seizures • Papilledema • Ataxia • Hemiparesis • Neck stiffness
- 12. INVESTIGATIONS • FBC count with differential • Erythrocyte sedimentation rate (ESR) • Serum C-reactive protein (CRP) • Serological tests for some pathogens • Blood cultures for aerobic and anerobic bacteria (at least 2; preferably before antibiotic usage) • Abscess aspirate • Culture • Histopathological examination • Lumbar puncture is rarely warranted
- 13. INVESTIGATIONS cont’d • CT Scan • MRI • Biopsy of cerebral lesion • Immunochemical tests
- 14. Brain CT Brain MRI
- 15. TREATMENTS • Medical • Abscesses in a deep or dominant location • The presence of coexisting meningitis or ependymitis • Early reduction of abscess with clinical improvement after antimicrobial therapy • Abscess size less than 2.5 cm • Surgical • Significant mass effect exerted by lesion • Proximity to ventricles • Evidence of significant increased intracranial pressure • Traumatic abscess associated with foreign material
- 16. TREATMENTS • Larger than 2.5 cm – excision • Smaller than 2.5 cm – aspiration for definitive diagnosis • Empirical ATB – metronidazole + third-generation cephalosporin • Once the infecting pathogen is isolated, antimicrobial therapy can be modified for optimal treatment • Antibiotics optimal duration is about 6 to 8 wks IV followed by oral antibiotics for 2 to 3 months.
- 17. TREATMENTS Surgical therapy – • Aspiration after bur-hole placement • Stereotactic aspiration • Complete excision by craniotomy
- 18. COMPLICATIONS • Rupture of abscess into ventricles or subarachnoid space. • Recurrence of abscess • Uncal or tonsillar herniation due to increased intracranial pressure • Long-term neurologic sequelae in 50 percent of patients e.g. hemiparesis, seizures, etc.
- 19. PROGNOSIS • The mortality rate from brain abscess is currently approximately 10% • However, if the abscess ruptures into the ventricular system, the mortality rate may be 80%. • Morbidity in survivors is generally due to residual neurologic defects, increased incidence of seizures due to scar tissue foci, or neuropsychiatric changes.
- 20. THANK YOU
Editor's Notes
- Contiguous suppurative focus Direct extension may occur from necrotic areas of osteomyelitis in the posterior wall of the frontal sinus, the sphenoid and ethmoid sinuses, mandibular dental infections, as well as from subacute and chronic otitis media and mastoiditis. Usually causes a single brain abscess. Hematogenous spread from a distant focus Frequently found in the distribution of the middle cerebral artery. The most common effected lobes (in descending frequency) are the fontal, temporal, parietal, cerebellar, and occipital. These abscesses are more commonly multiple and multiloculated. Hematogenous spread is associated with cyanotic heart disease (mostly in children), pulmonary arteriovenous malformations, endocarditis, chronic lung infections (eg, abscess, empyema, bronchiectasis), skin infections, abdominal and pelvic infections, neutropenia, transplantation, esophageal dilatation, injection drug use, and HIV infection. Trauma Trauma that causes an open skull fracture allows organisms to seed directly in the brain. Brain abscess can also occur as a complication of intracranial surgery, and foreign body, such as pencil tip, lawn dart, bullets, and shrapnel.
- The early stage of brain abscess (first 7-14 days) is called cerebritis and is associated with edema. Necrosis and liquefaction occur after 2-3 weeks, and the lesion becomes gradually surrounded by a fibrotic capsule Early cerebritis- days 1–3 Acute inflammatory cells, bacteria present on Gram stain Rapid perivascular infiltration of neutrophils, plasma cells and mononuclear cells Reticulin formation begins Marked cerebral edema Late cerebritis- days 4–9 Enlarging necrotic center reaching maximum size Inflammatory cells Maximal extent of cerebritis, rapid increase in new vessel formation Appearance of fibroblast with rapid formation of reticulin Prominent cerebral edema Appearance of reactive astrocyte Early capsule formation- days 10–13 Decrease in necrotic center Increased numbers of fibroblasts and macrophages Maximal degree of neovascularity Evolution of mature collagen Regression of cerebral edema Increase in reactive astrocyte Late capsule formation Further decrease in necrotic center Further increase in fibroblasts Cerebritis restricted to outside of collagen capsule Reduced neovascularity Capsule completed by end of second week Regression of cerebral edema Marked gliosis/ outside capsule by end of third week
- Moderate leukocytosis is present, and the ESR and CRP level are generally elevated. Serum sodium levels may be low because of inappropriate antidiuretic hormone production. Platelet counts may be high or low. Serological tests for some pathogens (eg, serum immunoglobulin G antibodies, CSF polymerase chain reaction [PCR] for Toxoplasma) Blood cultures for aerobic and anerobic bacteria (at least 2; preferably before antibiotic usage) Lumbar puncture is rarely warranted and is contraindicated if increased intracranial pressure is present because of the potential for CNS herniation and death.