Intracranial sepsis

Dr Juliet Sekabunga Nalwanga

Brain Abscess
Introduction
• Brain abscess is a focal area of necrosis with a surrounding membrane
within the brain parenchyma, may result from an infectious process or
a traumatic process
• The incidence: 8% of intra-cranial masses, developing countries and 1–
2% developed countries.
• Despite the breakthrough advances in management, they can be fatal.
• A multidisciplinary approach and eradication of the primary foci of
infection is important
• The causative pathogens vary according to geographic location, age,
underlying medical and/or surgical condition, and mode of infection.
Epidemiology
• The incidence in the western population is approximately 1500–
2500 cases/year
• The prevalence is higher in ISS and Tetralogy of Fallot patients
• The male to female ratio: 1.3:1 to 3.0:1
• Fungal brain abscesses are a/w use of broad-spectrum antibiotics and
ISS agents like steroids.
• Prevalence is highest in adult men < 30 years, children 4 to 7 years
and neonates
• They can occur due to paranasal sinuses and otogenic
infections
History
• The first successsful surgery: French surgeon S.F. Morand in 1752 on a
temperoethmoidal abscess.
• In 1893, William Macewen- draining the abscess and treating the
underlying causative sinus infections.
• In 1918, Warrington-etiological factors
• 1924: King introduced marsupialization
• 1926: Dandy introduced aspiration
• 1928: Sargent - enucleation of an encapsulated brain abscess
• 1936: Vincent - complete excision and proved its value
• 1971: Heineman and colleagues - successful medical management of a
brain abscess.
Etiology
• The age of the patient
• Underlying disease or immune status
• The causes are contiguous, hematogenous or metastatic
• The paranasal sinus and mastoid sinus infection
• Cyanotic heart disease and right-to-left shunts.
• Post neurosurgical procedures or head trauma and other facial
procedures
• The hematogenous spread of bacteria is associated with underlying
cardiac disease, pulmonary disease, or distant foci of infection
Organisms
Bacterial: Staphylococcus and Streptococcus. Especially
Staphylococcus aureus and Viridian streptococci are the commonest.
Fungal:Toxoplasma
Atypical: TB
Direct Local Spread
• Head and neck sites:
• Otitis media (5%)and mastoiditis (inferior temporal lobe and
cerebellar brain abscesses)
• Paranasal sinus infection: approximately 30% to 50%
• Frontal or ethmoid sinus infection: frontal lobes
• Dental infection: frontal lobar abscesses.
• Facial trauma, and neurosurgical procedures, can result in necrotic
tissue, and brain abscesses.
• Metal fragments or other foreign bodies left in the brain parenchyma
Generalized Septicemia and
Hematogenous Spread
• pulmonary infections, such as
lung abscess and empyema,
• pneumonia, pulmonary
arteriovenous malformation, and
bronchopleural fistula.
• Cyanotic congenital heart
diseases in children: more than
60%.
• Bacterial endocarditis
• ventricular aneurysms
• thrombosis
• Skin
• Pelvic
• Intraabdominal infections
Pathogenesis
1) early cerebritis (1–4 days)
2) late cerebritis (4–10 days)
3) early capsule formation (11–14 days)
4) late capsule formation (>14 days).
The glial cell activation is through parenchymal microglia and astrocytes.
Activated microglia has the potential to influence the type and extent of
antibacterial adaptive immune response
The continued release of proinflammatory mediators could damage the surrounding
brain parenchyma.
Cytokines IL-1 and TNF-alpha dictate essential functions for establishment of an
effective antibacterial response in the CNS parenchyma.
CFs
• Basic syndromes: focal mass expansion, intra-cranial
hypertension, diffuse destruction, focal neurological deficit.
• A headache (69% to 70%)
• Mental status changes (65%) lethargy progressing to coma is
indicative of severe cerebral edema and a poor prognostic sign.
• Focal neurologic deficits (50% to 65%)
• Pain is usually localized to the side of the abscess (sudden or gradual)
• The pain is most severe in intensity and not relieved by over-the-
counter pain medications.
• Fever (45% to 53%)
• Seizures (25% to 35%) can be the first manifestation of brain abscess.
• Nausea and vomiting (40%)
• Nuchal rigidity (15%) is most commonly associated with occipital lobe
abscess or an abscess that has leaked into a lateral ventricle.
• Third and sixth cranial nerve deficits.
• Rupture of abscess usually presented with suddenly worsening
headache and followed by emerging signs of meningismus.
Diagnosis
• Blood work
• CT: early detection, exact localization, and accurate characterization,
determination of number, size and staging of the abscess.
• It also detects hydrocephalus, raised ICP, edema and associated
infections like subdural empyema, ventriculitis
• hematogenous abscesses are usually multiple, identified at the
grey–white junction, and located in the middle cerebral artery
territory.
MRI
• A central area of liquefaction gives high signals while the surrounding
edematous brain tissue gives low signals onT1 weighted images.
• On T2 weighted images, the necrosis shows higher signals similar to
the grey matter.
• The abscess cavity shows a hyperintense rim on non-contrast T1-
weighted images and a hypointense rim on T2WI.
• Abscesses tend to grow toward the white matter, away from the
better-vascularized grey matter, with thinning of the medial wall.
Differential diagnosis
• Radiological features alone are • toxoplasmosis
inadequate to differentiate pyogenic
brain abscess from • metastasis
• fungal, • glioma
• nocardial • resolving haematoma
• tuberculous abscess • infarct
• Inflammatory • hydatid cyst
granuloma(tuberculoma)
• lymphoma
• neurocysticercosis
• radionecrosis
Management
• Antibiotics
• Initial therapy should be commenced with broad spectrum antibiotics which
cross blood–brain and blood–CSF barriers
• After the pus is drained and the antibiotic sensitivity reports become available,
specific bactericidal agents for the organism cultured should be administered.
• Negative cultures: CT broad spectrum antibiotics.
• Impiric antibiotic regiment: Cefotaxime/Ceftriaxone/Ceftazidime, Vancomycin and
metronidazole.
• Antibiotics are given for 3–12 months.
• Steroid administration: use only if signs of meningitis or
disproportionate cytotoxic edema posing a life threatening problem.
• Anticonvulsant therapy: for 5 years to all patients with cerebral
abscess.
• Discontinuation of antiepileptic drugs can be considered when patient
is seizure free for at least 2 years after surgery and EEG shows no
epileptic activity.
Surgery
• Pyogenic abscesses require surgical intervention while most of the
tuberculous abscesses were managed conservatively.
• The initial approach is to drain the abscess through a twist drill
craniotomy.
• If the pus is thick or there is inadequate drainage of abscess, burr-hole
drainage should be done.
• Deep seated abscess like a thalamic abscess should be drained by a CT
guided stereotactic procedure.
• The indications for craniotomy are multiloculated abscess and thick
pus.
• In case of otogenic abscesses, mastoidectomy should be performed at
the earliest.
• Small brain abscesses have been treated empirically with antibiotics.
• Rapidly progressive neurological deficits due to the mass effect of the
neuroradiologically then urgent decompression
• Excision: multiloculated abscesses, posttraumatic abscesses
containing foreign bodies or contaminated retained bone fragments,
and abscesses due to fistulous communication.
• Stereotactic aspiration
Intraventricular rupture of abscess
• Intraventricular rupture of abscess can herald significant morbidity
and potential mortality.
• A combination of intrathecal and intravenous antimicrobial treatment
has been recommended.
• Urgent craniotomy for rapid evacuation of the abscess lavage of the
ventricles and ventriculostomy placement
Outcome
• In the pre CT era, the mortality was ranged 40–60% and has been
reduced to between 17% and 32%.
• Poor prognosis is reported in patients who are immunocompromised,
having diabetes mellitus or cirrhosis and a low GCS score.
• Poorer prognosis reported from patients presenting with lower
Glasgow coma scale.
• Intraventricular rupture is a devastating and often fatal complication
of brain abscess, associated with high mortality.
Cerebellar abscess
• These comprise of 6–35% of all brain abscesses.
• Middle ear suppurative disease may extend to temporal lobe or
cerebellum via various routes.
• Antibiotics are very effective in early and late cerebritis stages.
• Surgical intervention is essential once the capsule is well formed and CSF
diversion in presence of overt or incipient hydrocephalus
• Persistent hydrocephalus is treated with a shunting procedure.
• Surgical intervention can be either by repeated aspiration or excision.
• Steroids reduce brain edema but diminish the effectiveness of the host
defense mechanisms that assist in containment of infection.
Treatment
• Bur hole and drainage
• Radical or cortical mastoidectomy with preservation of hearing is performed
concurrently with abscess drainage
• Stereotactic aspiration and endoscopic drainage
• Drainage via a twist drill (2–3 mm) craniostomy is as effective as a burrhole in
draining the pus.
• Cerebellar abscess should be completely excised through a suboccipital
craniectomy or a craniotomy.
• The prognosis following evacuation of cerebellar abscess is excellent.
• The long-term outcome of patients with cerebellar abscess is directly
proportional to their preoperative consciousness level.
Delayed “Glue” abscess complicating an embolized
cerebral arteriovenous malformation (AVM)
• Complications of AVM embolization include development of a delayed
multiloculated abscess.
• The duration of the procedure and repeated handling of the catheters
and use of large amount foreign material or Hysto-acryl “glue” can
precipitate infection.
• Cure of the lesion can only be obtained by surgical excision of the
infected and partially embolized AVM.
Cyanotic heart disease and brain abscess
• 5–18% population with cyanotic heart disease (CHD).
• Individuals with CHD are 10 times more prone to develop brain
abscess than those with no CHD.
• Fallot’s tetralogy is the most common cause.
• Intracardiac right to left shunt by-pass allows direct entry of blood
containing bacteria to the cerebral circulation without pulmonary
filtration.
• Hypoxaemia, metabolic acidosis and increased blood viscosity from
compensatory polycythemia results in low perfusion areas
(microinfarcts) in the brain.
• Microinfarcts provide a milieu where seeded microorganism can
sustain growth and multiply to form abscess.
• Anaerobic streptococci are most common agents.
• These patients have cardiopulmonary risk, coagulation defects and
variable degree of ISS states increasing the risk of anesthesia and
surgery.
• A deeply located parieto-occipital abscess larger than 2 cm diameter
which causes mass effect, should be aspirated.
• Intravenous Beta-lactam antibiotics are started immediately.
Multiple abscesses
• These account for 5–50% of all brain abscesses.
• They are a result of hematogenous spread from systemic infections
• Streptococcus and Staphylococcus are common organisms.
• Multiple abscesses are found more often in immunocompromised patients
• The frequency of intraventricular rupture is also more in these cases.
• Risk factors include AIDS, organ transplant recipients, IV drug abuse,
chemotherapy for lymphoma, cardiac anomaly or prosthetic cardiac valves,
diabetes, and regional enteritis.
• Broad spectrum antibiotics should be instituted and follow-up CT scans to
assess response to treatment.
• If the antibiotic sensitivity of organisms is unknown, aspiration of most
superficial or larger lesions and treat the remaining lesions with antibiotics
• If abscess recollects or fails to decrease or previously small abscess
enlarges, serial or staged stereotactic aspiration can be performed.
• All abscesses, >3 cm diameter and those causing mass effect particularly
deeply located in brain stem or close to ventricular wall should be aspirated
with stereotactic technique.
• If all the abscesses are of <2.5 cm size, still most accessible abscess should
be aspirated.
• In multiple abscesses antibiotics are continued for 3 months.
• Differential Diagnosis • Prognosis
• Bacterial meningitis • With the advent of antimicrobials
• Brain tumors and imaging studies the mortality
• Demyelination rate has reduced from 5% to 10%.
• Epidural/subdural abscess • Rupture of a brain abscess,
• Encephalitis however, is more fatal.
• Fungal or parasitic • The long-term neurological
infestations: Cryptococcosis/Cysticercos sequelae after the infection
is
depend on early diagnosis and
• Mycotic aneurysm administration of antibiotics.
• Septic dural sinus thrombosis
Complications
• Meningitis
• Ventriculitis
• Increased intracranial pressure
• Brain herniation
• Seizures
• Septicemia
• Neurological deficits
• Thrombosis of intracranial blood vessels
• Death
Subdural empyema
• Intracranial subdural empyema (ISE) is an infection of the brain with
the purulent collection located in the subdural space.
• Prior to the advent of antibiotics, morbidity, and mortality affected
near 100% of patients within 24-48 hours of presentation.
• The combination of improvement of investigations and management
strategies have decreased mortality to 4-9%.
• This is largely credited to decreased time to diagnosis and a
subsequent reduction in the time to treatment.
Epidemiology
• ISE can occur in any age group, gender or population
• In children and young adults (<20 years of age) males have the highest risk
• This was a/w sinusitis and otogenic infections (41-78% of cases)
• Other causes included meningitis, neurosurgical procedures, and head
trauma.
• The younger male population have a higher risk to develop sinusitis,
meningitis, otitis media and undergo trauma compared to their older and
female counterparts.
• There is greater vascularity of the diploic veins in the younger male which
may increase the risk of septic embolism
• In the older group there is a slight male predisposition
• In this group patients tend to be older (age 40-50) and associated
more with neurosurgical procedures
• Head trauma/surgery associated ISE in older population is more
evident.
• Other risk factors for developing ISE include smoking, diabetes, low
socioeconomic status, and low health literacy
Pathogenesis
• One of the pathways is haematogenic from emboli via intracranial vessels
such as diploe veins or endolymphatic channels
• The younger male patient is at higher risk developing ISE from this pathway.
• The second pathway is from the suppurative process within the sinus and ear.
• The progressive infection causes osteomyelitis and direct invasion into the
intracranial compartment
• This pathway leads to temporal lobe and cerebellum ISE with identifiable
areas of bone and dural defects adjacent to the ISE.
• The third is direct inoculation, as seen with trauma and neurosurgical
procedures.
• In infants, and young SE is associated with meningitis
• A subdural effusion forms secondary to meningitis (12%); this effusion
subsequently becomes infected forming a subdural empyema.
• The direct mechanism of infection of the subdural space is by erosion
through the posterior wall of the frontal sinus and dura
• Retrograde spread of septic trombophlebitis occurs from the
superficial mucosal veins into the dural venous sinuses, cortical
bridging veins and cortical veins because these veins are valveless,
and eventually the invasion of the subdural space.
CFs
• The infection poses a significant risk of venous stasis, venous thrombosis,
cerebritis, and stroke over a large area of brain
• This can lead to rapid deterioration with symptoms presenting as early as 1
day or late as 6 weeks, with mean time of 15 days
• headaches (77-83%), fevers (72-96%), altered sensorium (56-67%), vomiting
(50%) and seizures (29-56%)
• Mass effect: papilledema, cranial nerve palsy and hemiparesis
• The risk of developing ISE from sinusitis and otogenic infections remains
significantly low < 0.1%
• In cases of sinus and otogenic complications cranial imaging and thorough
examination of ear, nose and throat should be done
Investigations
• Laboratory analysis of blood tests are non-specific and can show
raised white cell count, C-reactive protein and erythrocyte
sedimentation rate
• Blood cultures can have poor yield as low as 5%.
• Intra-operative sampling and cultures are performed in all surgeries.
• Invasive procedures such as lumbar puncture (LP) are not
recommended as there is risk of neurological deterioration and
herniation
• CT: subdural collection including associated brain injury, bony
destruction and adjacent sinus and otogenic pathology.
• The empyema appears as a thin, hypodense subdural lesion with linear
enhancement of the medial surface.
• The mass effect due to cerebritis and cerebral ischemia contribute to
oedema
• MRI: gold standard in all patients with suspicion of ISE.
• MRI: The empyema is represented as a T2 hyperintense collection in the
subdural compartment with associated T1 hypointensity.
• MRV can be done to assess for venous sinus thrombosis.
Management
• Broad spectrum antibiotics
• Prophylactic anticonvulsants and medical therapy for raised intracranial
pressure
• Elevation of head of bed, normocapnia and normotensive
• The drainage of the collection provides source control and accelerates
recovery: burr-holes or craniotomy
• Craniotomy has the benefit of providing the option of assessment of
loculations, removal of membranes, repair of dural breach as well as an
adequate washout in the subdural compartment.
• If there is contamination of bone with evident osteomyelitis, or raised
intracranial pressure craniectomy is the procedure of choice.
Epidural abscess
• An epidural abscess is an infection within the epidural space anywhere in the
brain or spinal cord.
• Intracranial pressure (ICP) elevation related to infections, inflammation, or tumors
opens up the epidural space and separates bone from the tissue.
• This newly formed epidural space may contain blood, pus, or an abscess.
• Below the foramen magnum, the epidural space extends the length of the spine.
• It has 2 compartments:
a true space posterior and lateral to the spinal cord containing a cushioning layer
of fat embedded with penetrating arteries and an extensive venous plexus, and
a potential anterior space where the dura adheres to the posterior surface of the
vertebral body.
• Epidural abscesses occur as a result of infections involving the spinal
or cranial epidural space.
• Intracranial epidural abscesses (IEA) are complications of cranial
surgery or trauma; they may also complicate otorhinolaryngological
infections or other neck and thoracic procedures.
• Spinal epidural abscess (SEA) can have an acute and chronic
presentation.
• Acute SEA is usually less than 2 weeks in duration with fever and signs
of systemic inflammation from a hematogenous source.
• This is in contrast with subtle, afebrile, and long-standing chronic SEA
that has resulted from a direct extension of vertebral osteomyelitis.
• Both present with back and radicular pain, but leukocytosis (in serum
and CSF) is more likely in the acute form
• Acute forms are posterior to the spinal cord, but chronic forms are
commonly anterior to the cord.
• Gross pathology is purulent and exudative in acute, but with
granulation tissue in chronic.
Etiology

• IEA usually starts with an exogenous port of entry, either the paranasal
sinuses or ears.
• IEA can be a complication of neurosurgery
• Infection can also spread inward from osteomyelitis of the skull or fetal
monitoring probes applied to the skull during birth.
• Bacterial SEA make-up the major cause of this entity.
• Tuberculous, fungal, and parasitic abscesses of the spinal epidural space
typically evolve more insidiously than pyogenic bacterial ones.
• Other than candida infections, these etiologies are more frequently
encountered in tropical and subtropical regions
Epidemiology
• The incidence of the SEA is 0.2 to 1.2 cases per 10,000 hospital
admissions.
• Risk factors include diabetes, intravenous drug use, chronic renal
failure, alcoholism, or immunosuppression.
• SEA is nine-time more common than IEA and also more likely to be
acute.
• IEA is still the third most common focal pyogenic intracranial
infection, after brain abscess and subdural empyema.
• It is a result of head and neck infections such as sinusitis, mastoiditis,
and otitis and neurosurgery procedures
Pathophysiology

• The infection enters the epidural space by direct extension from a

contiguous site or by hematogenous/lymphatic seeding from a remote
site.
• IEA is mostly a localized lesion with a central collection of pus
surrounded by a wall of inflammatory reaction.
• Dura is rigid and tight around the base of the skull and therefore
prevents the downward transmission of the infection into spinal epidural
space.
• SEA spreads quickly since spinal epidural space is a connected space and
the infection is more of a granulation tissue rather than a purulent
nature.
History and Physical
• SEA: vague and subtle symptoms, it causes neurologic deficits.
• Localized vertebral tenderness to palpation or percussion is almost
always present.
• This pain will inevitably become more severe and harder to treat.
• During the illness, usually, a few days after the onset of spine
tenderness, 90% of patients will develop radicular pain.
• Most patients will also develop fevers above 38 C. Other nonspecific
findings may also be present such as generalized malaise, fatigue,
headaches, irritability, or vomiting.
• Progression of symptoms:
spinal ache (or back pain): 3-4 days
root (or radicular) pain: 4-5 days
weakness
paralysis.
• Early symptoms of backache may be indolent and persist for weeks,
• Severe back pain progresses to root pain within 3 to 4 days.
• This is followed by advanced signs of spinal cord dysfunction within
the next 4 to 5 days.
• The neurologic deficits at this stage are often still reversible; yet, rapid
surgical intervention may be needed
• Neurologic signs depend upon the level of spinal cord involvement.
• These signs are another factor that influences the differential
diagnosis at the time of presentation.
• In IEA, signs and symptoms can happen because of infection or
because of slowly increasing intracranial pressure (ICP).
• More common symptoms are fever, headache, lethargy, nausea,
vomiting, and photophobia.
• More common signs are papilledema, sinus drainage, cranial nerve
palsies, and focal neurologic deficits.
Evaluation
• Lab findings for these patients are nonspecific.
• Patients may have mild leukocytosis and elevated C-reactive protein.
• Blood cultures are positive in SEA but not so in IEA.
• Bone and gallium scans and even computed tomography are
equivocal and can delay definitive diagnostic testing.
• The gold standard for diagnosis of SEA is myelography which has
mostly replaced by magnetic resonance imaging (MRI).
• CT-guided needle aspiration is more frequently
Treatment / Management
• SEA: decompressive surgery and drainage of the abscess, and
parenteral antibiotic therapy
• Posterior epidural abscesses by posterior laminectomy, drainage of
infected and granulation tissue, and normal saline irrigation.
• Third-generation cephalosporin (ceftriaxone) with another
antimicrobial showing antistaphylococcal activity (rifampicin, nafcillin,
or fosfomycin) is recommended.
• Antibiotic therapy for 4 to 6 weeks osteomyelitis, 6 to 8 weeks.
• CT-guided needle aspiration instead of surgery in select cases with no
major spinal cord compression signs or neurologic deficit.
• IEA treatment usually requires a combination of a drainage procedure and
antibiotic therapy
• Craniotomy or simple burr holes for drainage.
• After clinicians get samples and cultures, they should start antibiotics as soon
as possible.
• Antibiotics for Streptococcus, Hemophilus, and anaerobes to cover infections
that have spread from the ear, sinuses, or other areas of the head and neck.
• Third-generation cephalosporins plus vancomycin plus metronidazole is one
regimen. Change treatment based on cultures and sensitivities.
• Antibiotic therapy is usually 6 to 8 weeks of intravenous agents
Prognosis
• With prompt and accurate diagnosis and time-sensitive management,
the prognosis for both IEA and SEA is very good.
Complications
• neurological complications of the SEA could arise from either pressure
causing compression of the spinal cord or septic thrombophlebitis
causing ischemic necrosis.
• Complications can ensue abruptly and unpredictably, without
warning. The resultant paresis or paralysis may not be reversible even
if surgery is performed urgently.