Print
Email
Abscess
Abscesses may occur in the epidural or subdural spaces or within the substance of the brain, in which case they are examples of suppurative bacterial encephalitis.
Intracranial epidural abscess is usually associated with a local skull fracture, osteomyelitis, or inflammation of the transverse or sagittal sinuses. The abscess is frequently situated over the convexity of the brain, and the clinical features are those of a generalized infection, of a local destructive lesion compressing the brain, and of raised ICP. The usual organism found in spinal epidural abscesses is Staphylococcus aureus in the lumbar region or tuberculosis at thoracic levels. In tuberculosis, granulation tissue, pus, and the products of vertebral body and disk collapse to cause cord compression and local pain. Acute angulation (angular kyphosis) may result from the local infection and should be treated first by the usual antituberculous agents to render the contents of the abscess sterile; it can then be surgically drained, with later stabilization of the spine. Should the abscess cause neurologic signs, emergency surgical intervention will be required. Problems may arise in the differential diagnosis of acute lumbar spinal epidural abscess and acute transverse myelopathy that is usually of viral origin (and eight times as common). Both cause root pain in girdle distribution, stiff neck, marked muscle spasms, and local tenderness of the spine, with the usual neurologic deficit of paraparesis with a sensory level, fever, and increased cells and protein in the CSF. However, the erythrocyte sedimentation rate (ESR) is always high in epidural abscesses, but not necessarily with transverse myelitis. Evidence of block of CSF passage, radiographic findings of osteomyelitis of the appropriate vertebrae, recent bacterial infection elsewhere, and perhaps slower clinical development (so that the maximal deficit is not reached until the third or fourth day) are all factors in favor of epidural abscess. Transverse myelitis is also more common at thoracic levels and less so at lumbar levels. In children, transverse myelitis sometimes presents without any pain in the back. The underlying cause in at least 80% of cases of subdural abscess is disease of the nasal sinuses or of the middle ear, whether by direct extension or as a result of thrombophlebitis leading to focal intracranial infection. Paranasal infection commonly results in frontal abscesses, and otitis causes posterior cerebral and cerebellar abscesses. Subdural abscesses also occur when a subdural hematoma or effusion (particularly if secondary to meningitis in infants) becomes infected, when a cerebral abscess ruptures into the subdural space, or after a penetrating wound. The bacteria responsible for subdural abscesses are usually mixed aerobic and anaerobic streptococci, less commonly staphylococci, gram-negative cocci, or Clostridia. The disease occurs particularly between the ages of 10 and 20 years with paranasal infection and after the age of 40 with an otitic origin. The usual features of subdural abscess include evidence of skull osteomyelitis (local tenderness, swelling, and cellulitis), systemic signs of infection, altered consciousness, headache, fever, meningism, and focal signs appropriate to the area of cerebral involvement. These patients are severely ill, and seizures of any type are common. The diagnosis is suggested by the findings of nasal sinus or middle ear infection in the presence of the above signs. An EEG will show local slow wave activity, and plain skull radiographs may show sinus opacity or osteomyelitis (and sometimes a shift of the pineal gland). An enhanced CT scan localizes the abscess precisely. The abscess should be surgically drained. Cloxacillin and metronidazole are recommended in the same regimen as for intracerebral abscess (see below), and the treatment should be continued for 1 month. The mortality rate in subdural abscess is about 10%; residual seizures and focal neurologic deficits are common, so anticonvulsants are routinely prescribed. Consultation and referral are mandatory to ensure timely and optimal treatment for all intracranial abscesses. Over half of all cases of intracerebral abscess complicate an ear or paranasal sinus infection. Skull fractures, facial or dental infections, and congenital heart disease also predispose, and hematogenous spread of Neonates, diabetics, immunocompromised patients, heroin and alcohol addicts, patients with prosthetic or congenitally damaged heart valves, and those with lymphomas are especially at risk. Immunocompromised patients may develop candidal abscesses with intracerebral vasculitis; they present with fever but few focal signs. In many patients the infection can be traced to endocarditis or other septic foci. An abscess may spread directly or as a result of septic thrombophlebitis, in which the infected clot may extend backwards along a large vein to infect other areas of the brain. The organisms most frequently cultured include streptococci, staphylococci, klebsiella, proteus, bacteroides, pneumococcus, and anaerobic organisms. The symptoms of intracerebral abscess may for a time be vague and nonspecific; they include fever, mild drowsiness, and headache, followed by evidence of focal brain destruction, meningism, and raised ICP. Seizures are particularly common with cerebral abscesses in the frontal, temporal, and parietal regions. Often there is little systemic evidence of sepsis, and the patient presents in lethargic delirium. However, cerebellar abscesses produce rapidly rising ICP and brainstem signs. Diagnosis of an intracerebral abscess should be suggested by the clinical pictures of lung, ear, or sinus disease with signs of intracranial infection and seizures; meningitis with a focal deficit; stroke with fever; or raised ICP with no obvious cause. The EEG is invariably abnormal, with prominent focal slow waves. A CT or MRI scan will localize the abscess and will determine the degree of capsule formation. LP is potentially lethal. Initial treatment consists of surgical aspiration of pus from the abscess cavity; this will allow identification of the organisms and use of appropriate intravenous antibiotics in high doses. If the origin of the abscess is sinusitis, anaerobic streptococci will grow in culture and penicillin and chloramphenicol or metronidazole should be given to the patient. Otitic abscesses imply mixed organisms and will respond to gentamicin, as well as the above drugs. Traumatic abscesses usually yield staphylococci, for which cloxacillin is recommended. Multiple broad-spectrum antibiotic therapy is required for abscesses of metastatic origin; cloxacillin 12 g/day, with metronidazole, 500 mg every 8 hours, and a third-generation cephalosporin might be employed. ICP is likely to be raised as a result of vasogenic edema around the abscess; steroids may be expected to help relieve it, but antibiotic treatment should be started before steroids are given. Patients who have recovered from an acute cerebral abscess frequently go on to have seizures. If it is likely that the abscess developed by hematogenous spread, congenital heart disease with a right-to-left shunt, pulmonary disease such as bronchiectasis, and sepsis elsewhere in the body must be excluded. The physician should look for needle marks and other signs of intravenous drug use; many younger patients use dirty syringes to mainline drugs. Cerebral abscesses are serious emergencies and require rapid diagnosis so that antibiotic therapy can begin and surgical intervention is expedited. Even in these days of new antibiotics, steroids, and CT scanning, these abscesses still carry a 10% mortality rate.
 |
Textbook of Primary Care Medicine, 3rd ed
By: T. Jock Murray, William Pryse-Phillips © 2005 ELSEVIER Inc. All Rights Reserved |
Related Learning Centers |
 |
 |
 |
Advertise | Terms of Use | Privacy Policy