Spinal Care, Neurology, Spinal Medical Advice and Information.
A brain abscess consists of localized free or encapsulated pus within the brain substance. Brain abscess is uncommon in children. It is hardly ever secondary to meningitis however, brain abscess may give rise to meningitis as a consequence of rupture into the ventricle or rarely into the subarachnoid space. In infants, especially neonates, it is often uncertain which came first and the abscess may become very large before it is recognized clinically.
It is estimated that brain abscess accounts for approximately 1 in 10,000 general hospital admissions. Male predominance of 2.5:1 is noted. Approximately 25% of all brain abscesses occur in children less than 15 years of age, with a peak incidence between ages 4 and 7 years. However, they are extremely rare before the age of 2 years. A brain abscess may occur as a solitary nodule or a multilobular process. The most common sites are the frontal and temporal lobes. These are followed by abscesses in the frontoparietal, parietal, cerebellar, and occipital lobes, in descending frequency. Thalamic abscesses are rare.
Formation of the abscess begins with entry of a microorganism into the brain, which produces an initial area of focal cerebritis leading to softening, edema, hyperemia and petechial hemorrhage. Fibroblasts from the capillaries adjacent to the focal cerebritis deposit collagen fibers to contain and encapsulate the purulent focus. Encapsulation usually takes two weeks. A mature brain abscess consists of three layers: a center of PMN leukocytes and necrosis, a collagenous capsule surrounding the central area and peripheral gliosis.
Brain abscesses develop in four clinical settings: associated with a contiguous infection, after hematogenous spread from a distant focus, after trauma finally 20% of the cases will be identified as cryptogenic where no focus is recognized. Whenever symptoms and signs of intracranial disease develop in a patient with infection of the middle ear, mastoid, sinuses, soft tissue of the face, orbit and scalp, brain abscess should be considered. The infection is most often subacute or chronic and spreads by infected veins or less commonly by osteomyelitis.
Congenital lesions including dermal sinuses and various forms of ruptured encephalocele may provide direct microorganisms to brain tissue. Hematogenous brain abscess may be replacing contiguous foci as the primary cause of brain abscess. These lesions occur most often with infections of the chest or as a result of cyanotic congenital heart disease. One study reported 17% association with congenital heart disease, 16% with pulmonary infection and 12% were noted to occur in compromised host. Evidence of associated endocarditis in the patient with congenital heart disease is rare but acute bacterial endocarditis may be complicated by septic infarction of the brain and therefore abscess formation.
Peripheral arteriovenous shunts, pulmonary A-V fistula like in patients with Osler Weber Rendu, lung abscess, pulmonary thrombophlebitis and collections of purulent material elsewhere in the body may provide an infective source. Recently, esophageal dilatation has been associated with brain abscess.
The incidence of brain abscess following open head trauma such as depressed skull fracture ranges between 5-11%. Abscess also may follow intracranial surgery. In addition, in infants and young children, a sharp object may penetrate the skull, leaving minimal external evidence of trauma mainly with orbital trauma because of the thin posterior wall of the orbit and therefore introduce the infective agent.
The most common organisms cultured include various strains of streptococci that account for around 60-70% of all brain abscess formation. Strep milleri is a common inhabitant of the oral cavity and the gastrointestinal tract. Strep milleri has a predilection for causing focal suppurative disease and is probably the most common strep group implicated in brain abscess formation. It is also part of the normal vaginal flora. Staph aureus is the cause of 10-15% of all abscesses and is most common in trauma related and post surgical infection. Enterobacteriaceae, proteus and escherichia and pseudomonas collectively account for 24% of all cases. Proteus and citrobacter are commonly recovered from abscesses in neonates.
Other bacteria found in abscesses include clostridium, nocardia and monocytogenes. These are usually associated with distant sites of primary infection. Yeast and fungi such as candida and cryptococcus neoformans have assumed an increasing role in the etiology of brain abscess and have been implicated as the cause of 9-17% of cases.
Compromised hosts are at risk of fungal infections. In most of these cases, the mortality is high. Toxoplasma gondii and amebic abscesses are the cause in less than 1%. However, Toxoplasma is becoming an important infection in patients with AIDS and it has been documented in as many as 30% of all AIDS patients with CNS involvement. Toxoplasma-contaminated meats account for more cases than contact with cat feces.
The course for brain abscess patients may range from indolent to fulminant; in approximately 75% of patients the duration of symptoms is 2 weeks or less. Only a minority <50% of patients display the classic triad of fever, headache, and focal neurologic deficit. The prominent clinical manifestations are due to the space occupying mass rather than to infection and physicians should maintain a high index of suspicion for brain abscesses in patients with presumptive diagnosis of brain tumor when the usual predisposing factors are not readily apparent. A moderate to severe headache, often hemicranial but also generalized, is the most common symptom (approximately 70% of cases). Fever occurs in only 45-50% of patients. A change in mental status ranging from lethargy to frank coma occurs in most patients.
Focal neurologic findings are present in approximately 50% of cases and are dependent on the location and size of the lesion and concurrent surrounding edema; hemiparesis is the most common manifestation. Nausea and vomiting occur in half of the patients secondary to raised intracranial pressure. Seizures occur in 25-35% of patients; they are often generalized and are common with frontal lobe lesions. Nuchal rigidity and papilledema are present in about 25% of cases. Aphasia may occur with temporal lobe lesions when they occur in the dominant hemisphere, and a contralateral upper quadrant visual field defect or complete hemianopsia may be demonstrated. Cerebellar abscesses are associated with ataxia, dizziness, deviation of the eye and abducens nerve palsy.
Sudden death occurs from apnea associated with herniation of cerebellar tissue through the foramen magnum. Rupture of an abscess into the ventricle with consequent ventricular empyema is a dreaded complication because the mortality exceeds 50%, and residual neurologic deficits including hydrocephalus, are the rule in those who survive. Frequently, rupture occurs before the diagnosis of abscess is established. A sudden worsening in the patient's clinical state heralds this event. High fever, shock, meningismus, and altered consciousness are prominent in this condition.
CT with IV contrast is needed otherwise an abscess may be missed. The contrast media demonstrates capsular enhancement commonly referred to as "ring enhancement". MRI is also an excellent diagnostic procedure. The findings on EEG may be localized and help excluding a more generalized, bilateral, intracranial disease, such as encephalitis. Unilateral slow waves (delta 1 to 3 sec) characterize the usual finding in cerebral abscess. Because the CSF pressure is elevated with brain abscess, herniation of cerebral tissue at either the tentorium or foramen magnum can occur even in the absence of lumbar puncture. Therefore, if brain abscess is suspected, CSF examination should be deferred until the appropriate imaging is done to rule out the abscess.
Surgery remains the definitive treatment for cerebral abscess, but controversy continues as to whether excision is preferable to single or multiple aspirations of the cavity. Recent experience suggests that precise needle aspiration of abscess contents can be achieved using CT to facilitate accurate placement of the needle, the size of the abscess being monitored by serial CT or in young infants by ultrasound. Spread of infection is minimized by administering antibiotics, usually IV penicillin and chloramphenicol, in doses appropriate for meningitis before, during and following surgery depending on the clinical status. If the gram stain suggests staph infection, an antibiotic such as nafcillin should be added. When the organism or organisms and their sensitivities are known, the most appropriate antibiotic should be used.
Regardless of the therapeutic modalities employed, neurologic deficits remain high, up to 50% of cases in recent series, although widespread availability of CT scanning has allowed for a reduction in mortality of from 30-40 to about 10%.