Brain abscess

Can arise from direct implantation of organisms, local extension from the mastoid or sinuses, and hematogenous spread from heart, lungs, bones or following tooth extraction.

Multiple lesions can come from acute bacterial endocarditis.

Can be associated with cyanotic congenital heart disease and chronic pulmonary infections.

In most patients results from predisposing factors such as an underlying disease process like HIV, history immunosuppressive drug use, abnormal protective barriers surrounding the brain related to surgery, trauma, mastoiditis, sinusitis, dental infections, or systemic source infection such as endocarditis or bacteremia.

In up to 35% of cases is unclear.

Severe immunocompromised conditions are often associated tuberculosis or nonbacterial causes of infection, such as fungi or parasite related brain abscess.

HIV infections are associated with bring abscesses caused by Toxoplasma gondii and also Mycobacterium tuberculosis.

Patients who have received solid organ transplants have an increased risk of norcardia brain abscesses and also fungal abscesses to include Aspergillus or Candida species.

Fungi are responsible for 90% of brain abscesses among patients with solid organ transplantation.

Bacteria enter the brain parenchyma by direct spread in about half of the cases and through hematogenous dissemination in one third of cases, with unknown source accounting for the remaining cases.

The hematogenous spread of bacteria to brain is associated with underlying cardiac disease processes including congenital heart defects, , endocarditis, and to pulmonary diseases, or to distant foci of infection primarily in the skin, sinuses, and teeth.

Brain abscesses that occur after neurosurgical procedures or head trauma are often caused by skin colonizing bacteria such as staphylococcal aureus and staph epidermidis or gram-negative bacilli.

Staphylococci and Streptococci most commonly associated organisms.

Gram negative bacteria are also common pathogens.

Up to 68% of patients with brain abscess have polymicrobial infections.

Brain abscesses due to the contiguous spread from para meningeal foci which includes the middle ear, mastoids, and sinuses are frequent caused by streptococcal species, but staph and polymicrobial abscesses including those by anaerobic gram-negative bacilli also occur.

Patients with Vascular Diseases have an increase in pro inflammatory mediators that may damage the surrounding brain  parenchyma, this increasing host susceptibility to the development of a marine abscess.

Paranasal sinus or dental infections with brain abscesses are often polymicrobial.

Brrain abscess is uncommonly caused by infectious endocarditis despite the presence of continuous bacteremia, of less than 8% in most series.

Disruption of the mechanical barriers, such as an open cranial fracture and neurosurgery, aew risk factors associated with brain access Prairie

Discrete lesions with central liquefaction necrosis, surrounded by edema and a fibrous capsule.

Most frequent areas of the brain are the frontal lobe, parietal lobe and the cerebellum.

Diagnostic brain MRI is the preferred radiologic method for diagnosis and differentiation.

Disruption of mechanical barriers, such as open cranial fracture and neurosurgeon surgery are risk factors for brain abscess.

Most patients with brain abscesses are older and have multiple underlying comorbidities.

Up  to 80% of patients have no definitive source of infection, and almost 20% of patients have no comorbid condition that would predispose them to abscess.

Most bacteremia does not cause brain abscess and hematogenous spread has been reported in 25% of cases.

Causes progressive focal deficits as a result of brain destruction and clinically can have signs of increased CNS pressure.

Bacteremia is associated with brain abscess in about 11% of patients.

Lumbar tap shows increased CSF pressure, increased white blood cells and protein levels with normal CSF sugar level.

Initial stage of brain abscess formation is cerebritis, which may lead to perivascular inflammatory response surrounding a necrotic center, with increased edema in the surrounding white matter.

When the brain abscess necrosis reaches maximum size a capsule is formed with accumulation of fibroblasts, neovascularization and collagen.

Clinically manifests with headache, and fever, altered mental status may be absent.

Neurologic findings depend on the site of the abscess.

The front lobe is the largest lobe and is the most common location for an abscess, and usually correlates with a sinus infection.

Early in the process neurological findings may be absent or subtle for days to weeks.

Involvement of the brainstem or cerebellum may be associated with cranial nerve palsies, gait disorders, or either headache or altered mental status due to the development of hydrocephalus.

Patients may present with seizures in about 25% of cases.

Larger abscesses are associated with more clinical manifestations as surrounding edema increases.

Patients may present with symptoms of their underlying infection.

Can lead to progressive intracranial pressure and brain herniation.

Rupture of the abscess can cause meningitis, ventriculitis and sinus venous thrombosis.

Differential diagnosis includes: brain tumors, stroke, bacterial meningitis, epidural abscess, and subdural empyema.

On suspected brain abscess imaging studies should be done.

CT scan of the brain with contrast is a rapid test to detect size, number, and localization of the brain abscesses.

MRI with diffusion-weighted imaging is a valuable diagnostic tool differentiating brain abscess from primary, cystic, or necrotic tumors.

MRI is the preferred radiologic method of diagnosis and differentiation.

Brain imaging is not sufficient to determine accurately the underlying etiology of a ringed enhancing mass and still requires the need for a biopsy.

Blood and CSF cultures can identify the cause of the involved organism in approximately one quarter of patients.

In the presence of an underlying dental, sinus, otic, or skin infection the site should be cultured, or removed surgically if necessary.

Combining Medical and surgical Approaches is crucial in managing brain abscess.

Medical management alone is considered when deep-seated infection is not amenable to surgery, when there are smaller multiple abscesses, or coexisting meningitis exists.

Selecting appropriate anti-microbial therapy is critical and should be targeted against suspected microorganisms, or those identified in tissue cultures.

Because of the risk of brain herniation lumbar puncture should be performed when there is clinical suspicion of meningitis or abscess that has ruptured into the ventricle and when there are no contraindications to LP, such as brain shift on cranial imaging or coagulation disorders.

Mortality rate with surgery and antibiotics is less than 10%.

Surgical aspiration is recommended for abscesses larger than 2.5 cm in diameter.

Open excision rather than aspiration may be preferred for more thorough irrigation, removal of purulent material and results in an abbreviated length of hospitalization in need for rehabilitation.

Cure rates  with combined medical and surgical management exceed 90%, and most patients with bacterial brain abscess undergo  surgical treatment to achieve cure rather than medical therapy alone.

Bacterial brain abscesses or treated with anti-microbial therapy for 4 to 8 weeks based on clinical and radiographic infection resolution.

Many  patients, about 43%, recover without neurologic sequelae.