Intracranial
infection
Meningitis
Bacterial meningitis, although potentially a
life-threatening infection, seldom requires neurosurgical intervention. Treat-
ment involves confirming the diagnosis and identifying the organism by obtaining a CSF sample, usually via lumbar puncture (LP). Broad-spectrum intravenous (i.v.) antibiotics with good CSF penetration should then be commenced without delay (ceftriaxone 2 g 12 hourly and metronidazole 400 mg 8 hourly) and adjusted as cultures and sensitivities become available. In situations where lumbar puncture is deemed impossible or unsafe, unless CSF can be obtained by other means, treatment might have to be empirical. Studies have demonstrated that steroids, commenced early and in combination with antibiotics, can improve outcome by reducing oxygen free radical attack on the brain. Complications are more likely to occur if treatment is not commenced early and may require neurosurgical intervention. The major complications are: cerebral oedema, seizures, hydrocephalus (communicating), subdural effusion, subdural empyema, brain
abscess and ventriculitis.
Brain abscess
The treatment of brain abscess has been
revolutionised by the availability of CT scanning, metronidazole and stereotaxis.
Prior to these modalities, the mortality for brain abscesses ranged between 15
and 40 per cent. Pyogenic inflammation of the brain leading to cerebral abscess
may result from:
haematogenous spread from a known septic site
or occult focus (particularly in patients with right to left cardiac shunts) (Fig. 35.24);
contiguous spread from
an adjacent infected sinus presumably via retrograde thrombophlebitis; and
direct inoculation from trauma. In 20 per cent of patients no cause can be
identified (Fig
35.25
,FIG.
35.26—Fig 35.27).
The
organisms most commonly responsible vary depending on the aetiology. With
otitis media anaerobic streptococci, Haemophilus
and Gram-negative anaerobes are involved; with sinusitis Streptococcus milleri and Staphylococcus.
Clinical features
Patients can present with either features of
raised pressure, seizures, meningeal irritation or focal signs, each of which
occurs in 50 per cent of patients. Systemic features of infection including
pyrexia are frequently absent but the history is usually short with rapid
clinical progression. Diagnosis is confirmed by demonstrating a single or
multiple low attenuation and smooth, symmetric, ring-enhancing mass lesions
with variable oedema on CT. MRI with enhancement will demonstrate similar
findings including high signal on 12-weighted images from the surrounding oedema.
These lesions arise in an area of cerebritis and can often be multiloculated.
Opacification of the sinuses or mastoids can be recognised on both CT and skull
X-ray (SxR). Infection markers will demonstrate a leucocytosis and a raised erythrocyte
sedimentation rate (ESR) and C-reactive protein (CRP), but may
initially be normal.
Treatment
Unless
very small, intracranial abscesses require surgical management. This is
performed by either aspiration through a burr hole, with or without stereotaxis
(repeated as necessary) or formal excision. The latter is undertaken if there
is persistent reaccumulation of pus despite serial aspirations. Excision may
also be considered if the abscess is superficial and easily accessible, and if
there is a well-formed capsule which fails to collapse despite repeated
aspirations. Patients should have regular follow-up CT scans with contrast until
the abscess stops reaccumulating. Anticonvulsant therapy is routinely
instituted.
Subdural
empyemas
Subdural empyemas, although uncommon, may
develop from sinusitis or mastoiditis. The infective agent is frequently S.
milleri, although other anaerobic or aerobic streptococci, other anaerobes
and Staphylococcus aureus may also be
responsible. These patients are systemically unwell with rapidly progressive
neurological signs, a depressed level of consciousness and hemi paresis. Epilepsy
occurs in most patients and can often progress to status epilepticus.
Despite
this being a surgical emergency, diagnosis is often delayed as the collection on
CT scanning is usually subtle to the untrained eye and frequently missed.
Treatment is as for an intracranial abscess but the collection requires a formal
craniotomy for drainage with exploration of the interhemispheric fissure. The
combination of fever and seizures with a background of sinusitus is usually
diagnostic of this lesion. Complications include refractory status epilepticus
and cortical vein/venous sinus thrombosis.
Surgical management
has now become routine to treat the patient first with a full course of antitoxoplasma treatment. Should this fail or the patient’s clinical condition deteriorate, or both, then a stereotactic biopsy should be considered. The differential diagnosis is then between infection with an organism thus far not covered with the therapy given, or tumour, principally lymphomas, or the condition of progressive multifocal leucoencephalopathy (CML). The current clinical course is one of rapid and relentless deterioration and, indeed, when a stereotactic biopsy is required for diagnostic purposes in AIDS, then the overall prognosis is poor. However, biopsy and histological diagnosis allow patients, their partners and families to be counselled as regards prognosis. Furthermore, a histological diagnosis also allows a prospective study of new therapies for AIDS which, it is hoped, will lead to improved long-term prognosis.