Chronic Encephalitis develop a fever by benbenzhou

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									Chronic Encephalitis                                           Subacute Sclerosing Panencephalitis
                                                                 Rare progressive demyelinating disease of the CNS
Progressive Multifocal Leukoencephalopathy                         assoc with a chronic infection of brain tissue with
A. Clinical Features & Pathology                                   measles virus
  Progressive disorder characterized pathologically by:         Hx of primary measles infection at an early age (2
       multifocal areas of demyelination of varying size          y/o)
         distributed throughout the CNS                          followed after a latent interval of 6 to 8 years by the
       cytologic alterations in both astrocytes &                 development of insidious intellectual decline and
         oligodendrocytes                                          mood and personality changes
  Astrocytes:                                                   Typical signs of a CNS viral infection, including fever
       Enlarged                                                   & headache, do not occur
       Hyperchromatic, deformed
       Bizarre nuclei                                         As the disease progresses, there is the occurrence of:
       Frequent mitotic figures                                  Focal and/or generalized seizures
  Oligodendrocytes:                                              Myoclonus
       Enlarged                                                  Ataxia
       Densely staining nuclei that contain viral                Visual disturbances
         inclusions formed the crystalline arrays of JC
         virus particles                                         EEG: characteristic periodic pattern with bursts every
  Clinical features:                                             3-8s of high-voltage, sharp slow waves, followed by
       Visual defects (45%)                                      periods of attenuated ("flat") background
       Homonymous hemianopia                                    CSF: acellular with a normal or mildly elevated
       Mental impairment—dementia, confusion,                    protein level & a markedly elevated ?-globulin level
         personality changes (38%)                                (>20% of total CSF protein)
       Motor weakness—not present early in the disease          CSF anti-measles antibody levels: invariably
         but eventually occurs in 75% of cases                    elevated; oligoclonal anti-measles antibodies are
  Almost all pxs have an underlying immunosuppressive            often present
    disorder                                                     CT and MRI show evidence of multifocal white matter
                                                                  lesions & generalized atrophy.
B. Diagnostic Studies                                            Measles virus can be cultured from brain tissue
  MRI reveals multifocal asymmetric, coalescing white           Viral genome can be detected by in situ hybridization
     matter lesions located:                                      or PCR amplification
        Periventricularly
        In the centrum semiovale                              Treatment
        In the parietal-occipital region                        Isoprinosine (Inosiplex) (100 mg/kg per day): alone
        In the cerebellum                                         or in combination with intrathecal or intraventricular
  These lesions have:                                             interferon
        ↑ T2 & ↓ T1 signal
        generally nonenhancing or show only minimal           Progressive Rubella Panencephalitis
          peripheral enhancement                                 Extremely rare disorder
        not assoc with edema or mass effect                     Primarily affects males with congenital rubella
  MRI for the diagnosis of PML: show hypodense                    syndrome
     nonenhancing white matter lesions                           After a latent period of 8-19 years, pxs develop
  CSF findings:                                                   progressive neurologic deterioration
        Typically normal                                        Manifestations: similar to SSPE
        Although, mild elevation in CHON &/or IgG               CSF shows:
        Pleocytosis (25%)—predominantly mononuclear &                  a. mild lymphocytic pleocytosis
          rarely >25cells/uL                                            b. slightly elevated protein level
  PCR amplification of JC virus from CSF: an impt                      c. markedly increased ?-globulin
     diagnostic tool                                                    d. rubella virus-specific oligoclonal bands.
        high specificity, but sensitivity has varied among      No therapy is available
          studies
  Diagnostic of PML: (+) CSF PCR for JC virus DNA in
     association with typical MRI lesions in the appropriate
     clinical setting
  Pxs with (-) CSF PCR studies may require brain biopsy
     for definitive diagnosis; JC virus antigen and nucleic
     acid can be detected by immunocytochemistry, in
     situ hybridization, or PCR amplification

C. Treatment
  No effective therapy is available.
Brain Abscess                                                        Most common pathogens in brain abscesses
  Focal, suppurative infection within the brain                       associated with paranasal sinusitis:
    parenchyma                                                            streptococci (especially S. milleri)
  Surrounded by a vascularized capsule                                   Haemophilus spp.
                                                                          Bacteroides spp.
Cerebritis                                                                Pseudomonas spp., and
  Often employed to describe a nonencapsulated brain                     S. aureus.
    abscess                                                          
                                                                - Dental infections are associated with ~2% of brain
A. Epidemiology                                                 abscesses, although it is often suggested that many
    A bacterial brain abscess is a relatively uncommon         "cryptogenic" abscesses are in fact due to dental
       intracranial infection                                   infections.
    Incidence: ~1 in 100,000 persons/yr                        The most common pathogens in this setting are
    Predisposing conditions:                                            a. streptococci
          otitis media & mastoiditis                                    b. staphylococci
          paranasal sinusitis                                           c. Bacteroides and
          pyogenic infections in the chest or other body                d. Fusobacterium spp.
          sites
          penetrating head trauma or neurosurgical             - Hematogenous abscesses account for ~25% of brain
          procedures                                           abscesses.
          dental infections                                    - show a predilection for the territory of the middle
    Modern causes:                                             cerebral artery (i.e., posterior frontal or parietal lobes).
          Toxoplasma gondii                                    - often located at the junction of the gray and white
          Aspergillus spp.                                     matter
          Nocardia spp.                                        - often poorly encapsulated.
          Mycobacteria spp.                                    - often multiple
          C. neoformans                                        - microbiology of these hematogenous abscesses is
    The said organisms are almost exclusively                  dependent on the primary source of infection
       restricted to immunocompromised hosts:                             Examples:
         a. HIV infection                                                 1. brain abscesses that develop as a complication
         b. organ transplantation                               of infective endocarditis are often due to viridans
         c. cancer                                              streptococci or S. aureus.
         d. immunosuppressive therapy                                     2. Abscesses associated with pyogenic lung
                                                                infections such as lung abscess or bronchiectasis are often
B. Etiology                                                     due to Streptococci, staphylococci, or Bacteroides or
     A brain abscess may develop:                              Fusobacterium spp.
                                                                          3. Enterobacteriaceae and P. aeruginosa are
           by direct spread from a contiguous cranial site
                                                                important causes of abscesses associated with urinary
            of infection, such as paranasal sinusitis, otitis
                                                                sepsis.
            media, mastoiditis, or dental infection;
                                                                          4. Abscesses that follow penetrating head trauma
           following head trauma or a neurosurgical
                                                                or neurosurgical procedures are frequently due to
            procedure; or
                                                                staphylococci, Enterobacteriaceae, and Pseudomonas
           as a result of hematogenous spread from a           species.
            remote site of infection
     25% of cases: no obvious primary source of
                                                                - Congenital cardiac malformations that produce a right-
       infection
                                                                to-left shunt (congenital cyanotic heart disease), such as
     1/3 of brain abscesses: assoc with otitis media &         tetralogy of Fallot, patent ductus arteriosus, and atrial
       mastoiditis, often with an cholesteatoma                 and ventricular septal defects, allow bloodborne bacteria
     Otogenic abscesses occur predominantly in the:            to bypass the pulmonary capillary bed and reach the
           temporal lobe (55 to 75%)                           brain.
           cerebellum (20 to 30%)                              - Similar phenomena can occur with pulmonary
     Common organisms:                                         arteriovenous malformations. The decreased arterial
           Streptococci                                        oxygenation and saturation from the right-to-left shunt
           Bacteroides spp.                                    and polycythemia may cause focal areas of cerebral
           P. aeruginosa                                       ischemia, thus providing a nidus for microorganisms that
           Enterobacteriaceae                                  bypassed the pulmonary circulation to multiply and form
     Abscesses that develop as a result of direct spread       an abscess.
       of infection from:                                       - Streptococci are the most common pathogens in this
           Frontal                                             setting.
           Ethmoidal
           Sphenoidal sinuses                                  PATHOGENESIS AND HISTOPATHOLOGY
     Those that occur due to dental infections: usually
       located in the frontal lobes                             -intact brain parenchyma is relatively resistant to
     ~10% of brain abscesses: assoc with paranasal             infection
       sinusitis
Prerequisite   for effective bacterial invasion                          - and its absence should not exclude the
        a.      preexisting brain ischemia                      diagnosis.
        b.      necrosis, or
        c.      hypoxia                                         Focal neurologic deficits
                                                                          -new onset of focal or generalized seizure
- Once infection is established, brain abscess frequently       activity is a presenting sign in 15 to 35% of patients.
evolves through a series of stages, influenced by:                        - includes hemiparesis, aphasia, or visual field
         a. the nature of the infecting organism and            defects
         b. by the immunocompetence of the host                           - part of the initial presentation in >60% of
                                                                patients.
Early cerebritis stage (days 1 to 3)
         - characterized by a perivascular infiltration of      The clinical presentation of a brain abscess depends on:
inflammatory cells, which surround a central core of                     a. location
coagulative necrosis.                                                    b. the nature of the primary infection if
         - Marked edema surrounds the lesion                                  present, and
                                                                         c. the level of the ICP
Late cerebritis stage (days 4 to 9)
         - pus formation leads to enlargement of the            Hemiparesis
necrotic center, which is surrounded at its border by an                 - most common localizing sign of a frontal lobe
inflammatory infiltrate of macrophages and fibroblasts.         abscess.
         - A thin capsule of fibroblasts and reticular fibers
gradually develops, and the surrounding area of cerebral        A temporal lobe abscess may present with:
edema becomes more distinct than in the previous stage.                 a. disturbance of language (dysphasia) or
                                                                        b. upper homonymous quadrantanopia.
Early capsule formation (days 10 to 13)
          - characterized by the formation of a capsule         - Nystagmus and ataxia are signs of a cerebellar abscess.
that is better developed on the cortical than on the
ventricular side of the lesion.                                 - Signs of raised ICP — papilledema, nausea and vomiting,
          -This stage correlates with the appearance of a       and drowsiness or confusion — can be the dominant
ring-enhancing capsule on neuroimaging studies.                 presentation of some abscesses, particularly those in the
                                                                cerebellum
Late capsule formation (day 14 and beyond)
         - defined by a well-formed necrotic center             Meningismus
surrounded by a dense collagenous capsule.                               -not present unless the abscess has ruptured into
         - surrounding area of cerebral edema has               the ventricle or the infection has spread to the
regressed, but marked gliosis with large numbers of             subarachnoid space.
reactive astrocytes has developed outside the capsule.
         - gliotic process may contribute to the                DIAGNOSIS
development of seizures as a sequelae of brain abscess.
                                                                - made by neuroimaging studies
CLINICAL PRESENTATION
                                                                MRI
- typically presents as an expanding intracranial mass                   - better than CT for demonstrating abscesses in
lesion, rather than as an infectious process.                   the early (cerebritis) stages
- evolution of signs and symptoms is extremely variable,                 - superior to CT for identifying abscesses in the
ranging from hours to weeks or even months                      posterior fossa
- most patients present to the hospital 11 to 12 days                    - A mature brain abscess appears on CT as a focal
following onset of symptoms.                                    area of hypodensity surrounded by ring enhancement.
                                                                         - CT and MRI appearance, particularly of the
The classic clinical triad (present in <50% of cases)           capsule, may be altered by treatment with glucocorticoids
         a. headache
         b. fever, and                                          Microbiologic diagnosis of the etiologic agent
         c. a focal neurologic deficit                                   - is most accurately determined by Gram's stain
                                                                and culture of abscess material obtained by stereotactic
Headache                                                        needle aspiration
         -most common symptom in patients with a brain                   - Up to 10% of patients will also have positive
abscess (>75% of patients)                                      blood cultures.
         -often characterized as a constant, dull, aching
sensation, either hemicranial or generalized                    - LP168 should not be performed in patients with known
         -becomes progressively more severe and                 or suspected focal intracranial infections such as abscess
refractory to therapy.                                          or empyema
                                                                - CSF analysis contributes nothing to diagnosis or therapy
Fever
         - is present in only 50% of patients at the time of    Laboratory studies
diagnosis                                                                - may provide clues to the diagnosis of brain
                                                                abscess in patients with a CNS mass lesion.
        a. 50% of patients have a peripheral leukocytosis    - Anticonvulsant therapy is continued for at least 3
        b. 60% an elevated ESR                               months after resolution of the abscess
        c. 80% an elevated C-reactive protein.               - decisions regarding withdrawal are then based on the
                                                             EEG.
DIFFERENTIAL DIAGNOSIS
                                                             EEG is abnormal - continue anticonvulsant therapy
Conditions that can cause headache, fever, focal             EEG is normal - anticonvulsant therapy can be slowly
neurologic signs, and seizure activity include:              withdrawn, with close follow-up and repeat EEG after the
        a. brain abscess                                     medication has been discontinued.
        b. subdural empyema
        c. bacterial meningitis                              Glucocorticoids
        d. viral meningoencephalitis                                  - should not be given routinely to patients with
        e. superior sagittal sinus thrombosis                brain abscesses.
        f. acute disseminated encephalomyelitis.                      - IV dexamethasone therapy (10 mg every 6 h) is
                                                             usually reserved for patients with substantial periabscess
- When fever is absent, primary and metastatic brain         edema and associated mass effect and increased ICP.
tumors become the major differential diagnosis                        - Dexamethasone should be tapered as rapidly as
                                                             possible to avoid delaying the natural process of
TREATMENT                                                    encapsulation of the abscess.

Combination of high-dose parenteral antibiotics and          Serial MRI or CT scans
neurosurgical drainage                                                - should be obtained on a monthly or twice-
        - optimal therapy of brain abscesses                 monthly basis to document resolution of the abscess
                                                                      - A small amount of enhancement may remain for
Empirical therapy of community-acquired brain abscess in     months after the abscess has been successfully treated.
an immunocompetent patient typically includes:
        a.          a third-generation cephalosporin
                    (e.g., cefotaxime or ceftriaxone) and
        b.          metronidazole                            PROGNOSIS

- In patients with penetrating head trauma or                - In modern series the mortality is typically <15%
recent neurosurgical procedures treatment should
include:                                                     Significant sequelae includes (occur in 20% of survivors)
          a.         ceftazidime as the third-generation              a. seizures
                     cephalosporin to enhance coverage of             b. persisting weakness
                     Pseudomonas spp.                                 c. aphasia, or
          b.          vancomycin for coverage of                      d. mental impairment.
                     staphylococci.

- Meropenem plus vancomycin also provides good               NONBACTERIAL CAUSES OF INFECTIOUS FOCAL CNS
coverage in this setting.                                    LESIONS

- Aspiration and drainage of the abscess under stereotaxic   ETIOLOGY
guidance are beneficial for both diagnosis and therapy.
- Empirical antibiotic coverage should be modified based     Neurocysticercosis
on the results of Gram's stain and culture of the abscess             -is the most common parasitic disease of the CNS
contents                                                     worldwide.
                                                                      - Humans acquire cysticercosis by the ingestion
Complete excision of a bacterial abscess via craniotomy or   of food contaminated with the eggs of the parasite T.
craniectomy                                                  solium.
         - generally reserved for multiloculated abscesses            - Eggs are contained in undercooked pork or in
or those in which stereotactic aspiration is unsuccessful.   drinking water or other foods contaminated with human
                                                             feces.
- Medical therapy alone is not optimal for treatment of               T. gondii is a parasite that is acquired from the
brain abscess and should be reserved for patients whose      ingestion of undercooked meat and from handling cat
abscesses are:                                               feces.
         a. neurosurgically inaccessible
         b. for patients with small nonencapsulated          CLINICAL PRESENTATION
abscesses (cerebritis), and
         c. patients whose condition is too tenuous to       New-onset partial seizures with or without secondary
allow performance of a neurosurgical procedure               generalization
                                                                     - most common manifestation of
- All patients should receive a minimum of 6 to 8 weeks of   neurocysticercosis
parenteral antibiotic therapy.
- Patients should also receive prophylactic anticonvulsant   Cysticerci may develop in:
therapy because of the high risk of seizures.                         a. brain parenchyma
                  - cause seizures or focal neurologic        - Approximately 85% of parenchymal cysts are destroyed
         deficits                                             by a single course of albendazole (15 mg/kg per day in
         b. subarachnoid or ventricular spaces,               two doses for 8 days)
                  - produce increased ICP by interference     - ~75% are destroyed by a single course of praziquantel(50
         with CSF flow.                                       mg/kg per day for 15 days)
         c. Spine
                  - mimic the presentation of intraspinal     Long-term antiepileptic therapy
         tumors.                                                       - recommended when seizures occur after
                                                              resolution of edema and resorption or calcification of the
- When the cysticerci first lodge in the brain, they          degenerating cyst.
frequently cause little in the way of an inflammatory
response.                                                     CNS toxoplasmosis is treated with a combination of:
                                                                      a. sulfadiazine, 1.5 to 2.0 g orally qid, plus
Cysticercal cyst degeneration                                         b. pyrimethamine, 100 mg orally to load then
         - elicits an inflammatory response that may                      75 to 100 mg orally qd, plus
present clinically as a seizure.                                      c. folinic acid, 10 to 15 mg orally qd.
         - Eventually the cyst dies, a process that may
take several years, and is typically associated with          - Folinic acid is added to the regimen to prevent
resolution of the inflammatory response and often             megaloblastic anemia.
abatement of seizures.                                        - Therapy is continued until there is no evidence of active
                                                              disease on neuroimaging studies, which typically takes at
Primary toxoplasma infection                                  least 6 weeks, and then the dose of sulfadiazine is
         - often asymptomatic                                 reduced to 2 to 4 g/d and pyrimethamine to 50 mg/d.
         - however, during this phase parasites may
spread to the CNS, where they become latent.                  Clindamycin plus Pyrimethamine
         - Reactivation of CNS infection is almost                     - an alternative therapy for patients who cannot
exclusively associated with immunocompromised hosts,          tolerate sulfadiazine, but the combination of
particularly those with HIV176 infection                      pyrimethamine and sulfadiazine is more effective.
         - patients present with headache, fever,
seizures, and focal neurologic deficits.

DIAGNOSIS                                                     SUBDURAL EMPYEMA

- The lesions of neurocysticercosis are readily visualized    - collection of pus between the dura and arachnoid
by MRI or CT scans                                            membranes

Parenchymal brain calcifications                              EPIDEMIOLOGY
        - most common finding.
                                                              - rare disorder that accounts for 15 to 25% of focal
- The scolex can often be visualized on MRI                   suppurative CNS infections
- A very early sign of cyst death is hypointensity of the
vesicular fluid on T2-weighted images when compared           Sinusitis
with CSF.                                                              -most common predisposing condition
- MRI findings: of multiple lesions in the deep white                  -typically involves the frontal sinuses, either
matter, the thalamus, and basal ganglia and at the gray-      alone or in combination with the ethmoid and maxillary
white junction in the cerebral hemispheres                    sinuses.
- With contrast administration, the majority of the lesions
enhance in a ringed, nodular, or homogeneous pattern          - Sinusitis-related Subdural empyema has a striking
and are surrounded by edema.                                  predilection for young males
- In the presence of the characteristic neuroimaging          -~3:1 male:female predominance
abnormalities of this parasitic infection, serum anti-T.      - 70% of cases occurring in the second and third decades
gondii antibodies should be obtained; if positive, the        of life.
patient should be treated.
                                                              -SDE may also develop as a complication of head trauma
                                                              or neurosurgery.
TREATMENT                                                     -Secondary infection of a subdural effusion may also result
                                                              in empyema, although secondary infection of hematomas,
Anticonvulsant therapy                                        in the absence of a prior neurosurgical procedure, is rare.
        - initiated when the patient with
neurocysticercosis presents with a seizure.                   ETIOLOGY

Albendazole and praziquantel                                  Most common causative organisms of sinusitis-associated
        -used in the treatment of neurocysticercosis.         SDE:
                                                                      a. Aerobic and anaerobic streptococci
                                                                      b. Staphylococci
                                                                      c. Enterobacteriaceae, and
         d.     anaerobic bacteria
                                                                DIAGNOSIS
Staphylococci and gram-negative bacilli
        -often the etiologic organisms when SDE follows         -MRI is superior to CT186 in identifying SDE1 and any
neurosurgical procedures or head trauma.                        associated intracranial infections
                                                                -Administration of gadolinium
                                                                          greatly improves diagnosis by enhancing the rim
PATHOPHYSIOLOGY                                                 of the empyema and allowing the empyema to be clearly
                                                                delineated from the underlying brain parenchyma
-Sinusitis-associated SDE182 develops as a result of either:
          (1) retrograde spread of infection from septic        Cranial MRI   also extremely valuable in:
thrombophlebitis of the mucosal veins draining the sinuses               a.    identifying sinusitis
          (2) contiguous spread of infection to the brain                b.    other focal CNS infections
from osteomyelitis in the posterior wall of the frontal or               c.    cortical venous infarction
other sinuses.                                                           d.    cerebral edema, and
                                                                         e.    cerebritis.
-may also develop from direct introduction of bacteria
into the subdural space as a complication of a                  - CT may show a crescent-shaped hypodense lesion over
neurosurgical procedure.                                        one or both hemispheres or in the interhemispheric
-evolution of SDE can be extremely rapid because the            fissure.
subdural space is a large compartment that offers few           - Frequently the degree of mass effect, exemplified by
mechanical barriers to the spread of infection                  midline shift, ventricular compression, and sulcal
- suppuration typically begins in the upper and anterior        effacement, is far out of proportion to the mass of the
portions of one cerebral hemisphere and then extends            SDE.
posteriorly.
                                                                CSF examination
 SDE is often   associated with other intracranial infections            -avoided in patients with known or suspected
including                                                       SDE188 as it adds no useful information and is associated
          a.    epidural empyema (40%)                          with the risk of cerebral herniation.
          b.    cortical thrombophlebitis (35%), and
          c.    intracranial abscess or cerebritis (>25%).      DIFFERENTIAL DIAGNOSIS

- Cortical venous infarction produces necrosis of               The differential diagnosis of the combination of
underlying cerebral cortex and subcortical white matter,        headache, fever, focal neurologic signs, and seizure
with focal neurologic deficits and seizures (see below).        activity that progresses rapidly to an altered level of
                                                                consciousness includes:
CLINICAL PRESENTATION                                                     a. subdural hematoma
                                                                          b. bacterial meningitis
-SDE typically presents with fever and a progressively                    c. viral encephalitis
worsening headache.                                                       d. brain abscess
-diagnosis of SDE should always be suspected in a patient                 e. superior sagittal sinus thrombosis, and
with known sinusitis who presents with new CNS1 signs or                  f. acute disseminated encephalomyelitis.
symptoms
                                                                presence of nuchal rigidity
Headache                                                                 - unusual with brain abscess or epidural
         - is the most common complaint at the time of          empyema
presentation                                                             -should suggest the possibility of SDE when
         - initially it is localized to the side of the         associated with significant focal neurologic signs and
subdural infection                                              fever.
         - then becomes more severe and generalized.

Contralateral hemiparesis or hemiplegia                         TREATMENT
         - most common focal neurologic deficit
         - can occur from the direct effects of the SDE on      -SDE is a medical emergency.
the cortex or as a consequence of venous infarction
- Seizures begin as partial motor seizures that then            Burr-hole drainage or craniotomy
become secondarily generalized                                           - definitive step in the management of this
                                                                infection.
Seizures may be due:
        a.        direct irritative effect of the SDE on        Empirical antimicrobial therapy should include a
                  the underlying cortex or                      combination of:
        b.        result from cortical venous infarction                a.          a third-generation cephalosporin
                                                                                    (e.g., cefotaxime or ceftriaxone)
- In untreated SDE, the increasing mass effect and                      b.          vancomycin, and
increase in ICP cause progressive deterioration in                      c.          metronidazole
consciousness, leading ultimately to coma.
- Parenteral antibiotic therapy should be continued for a                f.   Periorbital edema and Potts puffy
minimum of 4 weeks.                                                           tumor(~40%) reflecting underlying associated
-Specific diagnosis of the etiologic organisms is made                        frontal bone osteomyelitis.
based on Gram's stain and culture of fluid obtained via
either burr holes or craniotomy                                 - In patients with a recent neurosurgical procedure,
                                                                wound infection is invariably present, but other symptoms
                                                                may be subtle and can include:
PROGNOSIS                                                                 a. altered mental status (45%)
                                                                          b. fever (35%), and
Prognosis is influenced by:                                               c. headache (20%)
         a.          level of consciousness of the patient
                     at the time of hospital presentation       - the diagnosis should also be considered when fever and
         b.          size of the empyema, and                   headache follow recent head trauma or occur in the
         c.          speed with which therapy is                setting of frontal sinusitis, mastoiditis, or otitis media.
                     instituted.
                                                                DIAGNOSIS
- Long-term neurologic sequelae, which include seizures
and hemiparesis, occur in up to 50% of cases.                   - Cranial MRI is the procedure of choice to demonstrate a
                                                                cranial epidural abscess
                                                                          T2-weighted images - appears as a lentiform or
                                                                crescent-shaped fluid collection that is hyperintense
EPIDURAL ABSCESS                                                compared to CSF
                                                                          T1-weighted images - the fluid collection has a
- suppurative infection occurring in the potential space        signal intensity that is intermediate between that of brain
between the inner skull table and dura                          tissue and CSF.
                                                                          Gadolinium - a significant enhancement of the
                                                                dura is seen on T1-weighted images. In distinction to
ETIOLOGY AND PATHOPHYSIOLOGY                                    subdural empyema, signs of mass effect or other
                                                                parenchymal abnormalities are uncommon.
- less common than either brain abscess or SDE
-accounts for <2% of focal suppurative CNS infections           - CT appearance of an epidural empyema is that of a lens
                                                                or crescent-shaped hypodense extraaxial lesion
Develops as:
        a. a complication of a craniotomy
        b. compound skull fracture or                           TREATMENT
        c. as a result of spread of infection from the
             frontal sinuses, middle ear, mastoid, or           - Immediate neurosurgical drainage is indicated.
             orbit.
                                                                - Empirical antimicrobial therapy, pending the results of
- Infection in the frontal sinus, middle ear, mastoid, or       Gram's stain and culture of the purulent material obtained
orbit can reach the epidural space through retrograde           at surgery, should include a combination of:
spread of infection from septic thrombophlebitis in the                  a. a third-generation cephalosporin
emissary veins that drain these areas or by way of direct                b. nafcillin or vancomycin
spread of infection through areas of osteomyelitis.                      c. metronidazole

- rarely result from hematogenous spread of infection           - Ceftazidime should be substituted for ceftriaxone or
from extracranial primary sites.                                cefotaxime in neurosurgical patients.

The bacteriology of a cranial epidural abscess is similar to    - Meropenem and vancomycin also provide effective
that of SDE                                                     empirical therapy in postneurosurgical cases.

- etiologic organisms of an epidural abscess that arises        -Antibiotics should be continued for at least 3 weeks after
from frontal sinusitis, middle ear infections, or mastoiditis   surgical drainage.
are usually streptococci or anaerobic organisms.
- Staphylococci or gram-negative organisms are the usual
cause of an epidural abscess that develops as a
complication of craniotomy or compound skull fracture.          PROGNOSIS

CLINICAL PRESENTATION                                           -Mortality is <5% in modern series
                                                                -full recovery is the rule in most survivors.
Patients present with:
         a. fever (60%)
         b. headache (40%)
         c. nuchal rigidity (35%)                               Suppurative Thrombophlebitis
         d. seizures (10%), and                                   Septic venous thrombosis of cortical veins and
         e. focal deficits (5%)                                     sinuses.
  May occur as a complication of:                                     - Bacteria in the sphenoid and ethmoid sinuses
     a. bacterial meningitis                                   can spread to the cavernous sinuses via the small emissary
     b. SDE                                                    veins.
     c. epidural abscess; or
     d. infection in the skin of the face, paranasal           Sphenoid and ethmoid sinuses
        sinuses, middle ear, or mastoid.                                -most common sites of primary infection
                                                               resulting in septic cavernous sinus thrombosis.
A. Anatomy & Pathophysiology
    Cerebral veins and venous sinuses have no valves;         CLINICAL MANIFESTATIONS
      therefore, blood within them can flow in either
      direction.                                               Septic thrombosis of the superior sagittal sinus presents
                                                               with:
Superior sagittal sinus                                                 a. headache
         - largest of the venous sinuses                                b. fever
         - receives blood from the frontal, parietal, and               c. nausea and vomiting
occipital superior cerebral veins and the diploic veins,                d. confusion, and
which communicate with the meningeal veins.                             e. focal or generalized seizures.

Bacterial meningitis                                           - There may be a rapid development of stupor and coma.
         - a common predisposing condition for septic
thrombosis of the superior sagittal sinus                      - Weakness of the lower extremities with bilateral
                                                               Babinski signs or hemiparesis is often present.
Diploic veins
         - drain into the superior sagittal sinus              - When superior sagittal sinus thrombosis occurs as a
         - provide a route for the spread of infection from    complication of bacterial meningitis, nuchal rigidity and
the meninges, especially in cases where there is purulent      Kernig's and Brudzinski's signs may be present.
exudate near areas of the superior sagittal sinus.
                                                               Structures that pass throuth the cavernous sinus:
- Infection can also spread to the superior sagittal sinus              a. oculomotor nerve
from nearby SDE195 or epidural abscess.                                 b. trochlear nerve
                                                                        c. abducens nerve
Contributory   to cerebral venous sinus thrombosis                      d. ophthalmic and maxillary branches of the
        a.     Dehydration from vomiting                                    trigeminal nerve, and
        b.     hypercoagulable states, and                              e. internal carotid artery
        c.     immunologic abnormalities, including the
               presence of circulating antiphospholipid        The symptoms of septic cavernous sinus thrombosis are:
               antibodies                                             a. fever
                                                                      b. headache
- Thrombosis may extend from one sinus to another, and                c. frontal and retroorbital pain, and
often at autopsy thrombi of different histologic ages can             d. diplopia. T
be detected in several sinuses.
                                                               The classic signs (due to deficits of CN III, IV, and VI)
-Thrombosis of the superior sagittal sinus is often                     a. ptosis
associated with thrombosis of superior cortical veins and               b. proptosis
small parenchymal hemorrhages.                                          c. chemosis, and
                                                                        d. extraocular dysmotility
Transverse sinuses
          - drainage of the Superior Sagittal Sinus            - hyperesthesia of the ophthalmic and maxillary divisions
          - also receive venous drainage from small veins      of the fifth cranial nerve and a decreased corneal reflex
from both the middle ear and mastoid cells.                    may be detected.
          - becomes the sigmoid sinus before draining into     - There may be evidence of dilated, tortuous retinal veins
the internal jugular vein.                                     and papilledema.
Septic transverse/sigmoid sinus thrombosis
          - can be a complication of acute and chronic         Headache and earache
otitis media or mastoiditis                                             -most frequent symptoms of transverse sinus
          - Infection spreads from the mastoid air cells to    thrombosis.
the transverse sinus via the emissary veins or by direct                - may also present with otitis media, sixth nerve
invasion.                                                      palsy, and retroorbital or facial pain (Gradinego's
                                                               syndrome).
Cavernous sinuses
          - inferior to the superior sagittal sinus at the     - Sigmoid sinus and internal jugular vein thrombosis may
base of the skull                                              present with neck pain.
          - receive blood from the facial veins via the
superior and inferior ophthalmic veins.                        DIAGNOSIS
          - Bacteria in the facial veins enter the cavernous
sinus via these veins.
- suggested by an absent flow void within the affected
venous sinus on MRI

Magnetic resonance venography or Venous phase of
cerebral angiography
         - for diagnostic confirmatioin

Intracerebral hemorrhage
         -suggests the diagnosis of thrombophlebitis of
intracerebral and meningeal veins
         -requires cerebral angiography for definitive
diagnosis.


TREATMENT

- usually treated with antibiotics and hydration.

- choice of antimicrobial therapy is based on the bacteria
responsible for the predisposing or associated condition.

- Optimal duration of therapy is unknown, but antibiotics
are usually continued for 6 weeks or until there is
radiographic evidence of resolution of thrombosis.

Anticoagulation with dose-adjusted heparin
         - reported to be beneficial in patients with
aseptic venous sinus thrombosis
         - also used in the treatment of septic venous
sinus thrombosis complicating bacterial meningitis in
patients who are worsening despite antimicrobial therapy
and intravenous fluids.

- presence of a small intracerebral hemorrhage from
septic thrombophlebitis is not an absolute
contraindication to heparin therapy.

-Successful management of aseptic venous sinus
thrombosis has been reported with urokinase therapy and
with a combination of intrathrombus recombinant tissue
plasminogen activator (rtPA) and intravenous heparin, but
the efficacy of these therapies in septic venous sinus
thrombosis is unknown.

								
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