INTRACRANIAL SEPSIS

NEUROSURGERY
GROUP D AND E
OBJECTIVES
INTRODUCTION
EPIDEMIOLOGY
ETIOLOGY
PATHOGENESIS
CLINICAL PRESENTATION
DIAGNOSIS
MANAGEMENT
OUTCOME
INTRODUCTION
Sepsis is a life-threatening organ dysfunction caused by a dysregulated host
response to infection. Sepsis causes cerebral dysfunction in the short and
long term and induces disruption of the blood–brain barrier (BBB),
neuroinflammation and hypoperfusion.
Changes in brain matter and brain atrophy can be detected using brain
imaging,
EPIDEMIOLOGY
The male-to-female ratio was 3.6:1 and 70 to 80% of patients were under the age of
20 years. Spread from the paranasal sinus or ear was the most common mechanism
of infection. Hematogenous processes accounted for 22% of cases and the origin was
undetermined in 11% to 26% of cases.
Staphylococcus aureus and enteric gram-negative bacilli were the most common
bacteria identified but cultures were reported as sterile in 30% to 50% of cases.
While ultrasonography can be useful in newborns with an open fontanelle,
arteriography is often the only feasible procedure for diagnosis in Africa.
CONT.
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
• 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.
 ETIOLOGY
1. The age of the patient
2. Underlying disease or immune status
3. Cyanotic heart disease and right-to-left shunts.
4. Post neurosurgical procedures or head trauma and other facial procedures.

To establish intracranial infection, bacteria reach the brain via three main routes:
5.Extension from a contiguous
6.Haematogenous (metastatic) spread from a distant extracranial source
7.Direct inoculation following neurosurgery or penetrating trauma
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 Otogenic and paranasal sinus

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HEMATOGENOUS SPREAD

Typically, multiple or multi-loculated abscesses are seen, occurring predominantly

within the territory of the middle cerebral artery, often at the grey white matter
interface where blood flow is most marginal

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HEMATOGENOUS: OTHER
SOURCES

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PENETRATING TRAUMA

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BRAIN ABSCESS
• Brain abscess is a focal area of necrosis with a surrounding membrane
within the brain parenchyma that may result from an infectious
process or a traumatic process
OR
A focal, suppurative infection with in brain parenchyma typically surrounded by
vascularized capsule.
OR
A localized collection of pus surrounded by pyogenic membrane inside the brain
Cerebritis is employed to describe nonencapsulated brain abscess.
PATHOGENESIS AND HISTOPATHOLOGY
OF BRAIN ABSCESS
Brain abscesses occur at focal points of bacterial multiplication within
the brain parenchyma; they begin as a localised area of cerebritis and
later progress into a collection of pus surrounded by a vascularised
capsule.

By virtue of the impermeability of the blood-brain barrier, the brain

parenchyma is relatively resistant to the establishment of focal
bacterial infection.
An area of necrosis caused by for example micro-infarction or
hypoxaemia is necessary to act as a nidus for bacterial multiplication.

Several stages of development en route to the formation of a mature

encapsulated brain abscess following bacterial ingress have been
defined by neuroimaging studies
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 Stages of Development and Pathogenesis of
Brain Abscesses
1.Early Cerebritis
Days 1-3: Perivascular inflammation, characterised by neutrophil infiltration, occurs
around the site of focal infection with a surrounding area of oedema.

2. Late Cerebritis
Days 4-9: A central area of necrosis develops as the surrounding oedema progresses.
Peripheral accumulation of fibroblasts preludes the development of a capsule.
3. Early Capsule
Days 10-14: Establishment of a ring-enhancing capsule of well-vascularised tissue with
further fibroblast migration and adjacent reactive astrocytosis.

4. Late Capsule
Day 14 and beyond: Collagen fibre and granulation tissue deposition leads to a
thickening of the capsule effectively walling off the area of focal suppurative infection.

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 Clinical presentation :
Occur in majorities in the first 2 decades of life
Males more affected ( cause is unknown )
adults depend on immune status
Infants : increase in head circumference , bulging fontanel ,
separation of cranial sutures , vomiting , irritability , seizures

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 Symptoms :
1. Head ache ( 90 %)
2. Change in conscious level ( 60 %)
3. FND ( 60 %)
 Parietal lobe : hemiparesis
 Temporal lobe : dysphasia
 Cerebellar : ataxia and nystagmus

4.Fever (more than 50 %)

5. Nausea and vomiting ( 50 %)
6. Seizure ( 50 %)
7.Papilledema and meningismus

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LABORATORY FINDINGS
1. WBC : normal or mild increase
2. ESR : increase in 90%
3. CSF : not specific
1. Opening pressure
2. Protein
3. Glucose
4. Culture

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4. radiological characteristic of brain abscess
1. Brain CTS with contrast
 ring enhancement
 Multi loculation
 Multiplicity
 Finding of gas

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MRI :
T1 :
 necrotic center ( hypointense)
 Capsule ( hyperintence)
 Edema ( hypointence)

T2 :
 necrotic center ( hyperintence)
 Capsule ( hypointence)
 Edema ( hyperintence

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MANAGEMENT
The main treatment strategies are:

Antimicrobial agents

Needle aspiration - often using stereotactic guidance

Complete surgical excision

In addition, adjunctive therapies such as corticosteroids and anticonvulsant agents are variably used.

A combination of antimicrobial therapy and aspiration is now used for the majority of cases, with medical therapy alone
and complete surgical excision reserved for particular circumstances

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 MANAGEMENT
1. Antibiotic therapy :
Antibiotic is mandatory and should given
Imperial treatment depend on the etiology
 Sinusitis : ( penicillin + metronidazole )
 Otitis : ( penicillin + metronidazole + 3rd generation cephalosporin)
 Metastatic abscess :(metronidazole + 3rd generation cephalosporin)
 Post traumatic abscess ( vancomycin)

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 antibiotic therapy
It may also be considered for…
• Multiple small abscesses
• Abscesses located in surgically unaccessible or eloquent areas

It is most likely to be successful if…

• Abscesses are small (i.e. <1.5cm)
• In cerebritis stage
• Located in a well vascularised cortical area
Frequent interval scans should be performed to assess therapeutic response and to
identify complications requiring definitive surgical management.

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Corticosteroids
 Adjuvant corticosteroids are often used to reduce vasogenic oedema associated with
brain abscesses.
There are important concerns regarding steroid use…

• Effectiveness in reducing oedema and mass effect not established in human clinical
trials
• May retard abscess capsule development
• May reduce antimicrobial penetration
• Give false impression of a therapeutic response by reducing ring-enhancement on
follow-up scans
corticosteroids are reserved for situations of raised intracranial pressure resulting in a
clear risk of brainstem herniation or other significant neurological deficit.

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Anticonvulsants

 Seizures are a frequent complication of brain abscess both in the acute setting and for a prolonged
period after the resolution of the acute infection.

 Some advocate the use of seizure prophylaxis for extended periods in every case of brain abscess

 If commenced, anticonvulsants should probably be continued for 6-12 months and then only withdrawn
if the patient is seizure-free, the EEG normal and no signs of on going inflammation on neuroimaging.

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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/Cysticercosis sequelae after the infection
Mycotic aneurysm depend on early diagnosis and
Septic dural sinus thrombosis
administration of antibiotics.
ASPIRATION

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FOLLOW UP
CT weekly during antibiotic therapy
And then monthly CT
2-3 week decrease size of abscess
3-4 months complete resolution of abscess
6-9 months no residual contrast enhancement

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OUTCOME OF ABSCESS :

Mortality influenced by ( herniation , rupture of abscess to the ventricle , clinical

course of the patient, type of abscess, neurological state of patient at time of
diagnosis)

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1. Long term morbidity : ( seizure , FND, Cognitive dysfunction)

2. Recurrence: ( 5-10%) causes ( inadequate antibiotic therapy, incorrect choice of

AB, presence of foreign body , failure to eradicate source of the abscess)

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COMPLICATIONS
Meningitis
Ventriculitis
Increased intracranial pressure
Brain herniation
Seizures
Septicemia
Neurological deficits
Thrombosis of intracranial blood vessels
Death
SUBDURAL EMPYEMA
Suppurative infection within the subdural space. There is pus collection within the subdural space.

Etiology
paranasal sinusitis (especially frontal)
otitis (usually chronic otitis media)
post surgical (neuro or ENT)
trauma
meningitis
congenital heart disease
Others- osteomyelitis, pneumonia, unrelated infection (e.g. foot cellulitis) in diabetics.
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.
CLINICAL FEATURES
The infection poses a significant risk of altered mental status
venous stasis, venous thrombosis,
cerebritis, and stroke over a large area of seizures
brain. sinus tenderness, swelling or
This can lead to rapid deterioration with inflammation
symptoms presenting as early as 1 day or
late as 6 weeks, with mean time of 15 days nausea and/or vomiting
fever homonymous hemianopsia
headache speech difficulty
meningismus (nuchal rigidity) papilledema
hemiparesis
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.
Empyema appears as hypodense (but denser than CSF) crescentic or lenticular
extracerebral lesion with dense enhancement of medial membrane, inward
displacement of gray-white interface, ventricular distortion and effacement of basal
cisterns are common findings.
The mass effect due to cerebritis and cerebral ischemia contribute to oedema
MRI: gold standard in all patients with suspicion of ISE. 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.
CT SCAN MRI
MANAGEMENT
Antibiotics- similar to treatment for cerebral abscess.
Anticonvulsants- prophylactically or if seizures occur.
Medical therapy for raised intracranial pressure.
Surgical drainage: burr hole or craniotomy can be done. Early in the course, the pus
tends to be more fluid and may be more amenable to burr hole drainage. Later,
loculations develop which may necessitate 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 EMPYEMA
An epidural abscess is an infection within the epidural space anywhere in the brain
(Intracranial) or spinal cord(spinal).
There is formation of an epidural space that separates tissue from bone and it 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.
ETIOLOGY
As a complication of cranial surgery or trauma.
Hematogenous spread- skin infections, parenteral drug use, bacterial endocarditis, UTI, pharyngeal or
dental abscess, respiratory tract infection eg sinusitis, otitis media
Direct extension- penetrating trauma, psoas abscess, pharyngeal infections, mediatinitis
Other neck and thoracic procedures.
Infection can also spread inward from osteomyelitis of the skull or fetal monitoring probes applied to
the skull during birth.

Risk factors- diabetes, intravenous drug use, chronic renal failure, alcoholism, or
immunosuppression. Other rare ones include- cancer, recurrent UTI, Pott’s disease, chronic steroid
use, trauma
CAUSATIVE AGENTS
Bacterial- Staph. aureus, Streptococci, Pseudomonas aeruginosa, E.coli, Enterobacter,
etc
Chronic infections- TB usually associated with Potts’s disease, fungal-
cryptococcosis, aspergillosis, brucellosis, parasitic- echinococcus
Tuberculous, fungal, and parasitic abscesses of the spinal epidural space typically
evolve slower than pyogenic bacterial ones.
Other than candida infections, these etiologies are more frequently encountered in
tropical and subtropical regions
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. Symptoms
may be due to mechanical compression of the spinal cord or vascular pathology such
as thrombophlebitis of epidural veins.
CLINICAL FEATURES
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.
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.
Fevers above 38 C are common.
Other nonspecific symptoms that can be present include: generalized malaise,
sweats, fatigue, headaches, irritability, or vomiting.
Progression of symptoms:
Back pain to root symptoms- 3 days
Root pain to weakness- 4 to 5 days
Weakness to paraplegia- 24 hours
Early symptoms of backache may be mild 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.
Symptoms include: bowel/bladder disturbances, weakness, para or quadriplegia.
The neurologic deficits at this stage are often still reversible but rapid surgical
intervention may be needed
Neurologic signs depend upon the level of spinal cord involvement.
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.
INVESTIGATIONS
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 frequent.
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 with osteomyelitis, 6 to 8 weeks.
CT-guided needle aspiration instead of surgery is done in selected 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.
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