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Brain abscess dr shatdal
1. Brain Abscess
Dr. Shatdal Chaudhary, M.D.
Associate Professor
Universal College of Medical Sciences,
Bhairahawa, Nepal
Email: shatdalchaudhary@yahoo.com
2. Definition
Brain abscess is a focal suppurative infection within
the brain parenchyma, typically surrounded by a
vascularized capsule.
Cerebritis: is often employed to describe a
nonnencapsulated brain abscess.
4. Etiology
Brain abscess may develop by
1. Direct spread from a contiguous cranial site of infection
2. Head trauma, neurosurgical procedures
3. Hematogenous spread
25% cases : There isno primary source of infection
8. Stages
1. Early Cerebritis: 1-3days
2. Late Cerebritis: 4-9 days
Pus formationin necrotic center which is surrounded by
inflammatory cells and fibroblast
3. Early Capsule Formation: 10-13 days
A perivascular infiltration of inflammatory cells around a
central core of coagulation necrosis
A capsule that is better develop on corticalthen on ventricle
side of lesion
4. Late Capsule Formation: beyond 14 days
A well defined necrotic center surrounded by a dense
collageous capsule
9. Clinical Presentation
Typically presents as an expanding intracranial
mass rather than as a infectious process
Symptoms are gradual in onset
Patients present weeks to month
Usually presents 11-12 days following onset of
symptoms.
12. Investigations
TLC, DLC
ESR, CRP
Blood cultures
Neuroimaging studies:
MRI: better esp can detect early stages of cerebritis
CT Scan: a focal area of hypodensity surrounded by
ring enhancementwith surrounding edema
(hypodensity)
17. Treatment
Combination of high dose parentral antibiotics
and neurosurgical drainage
Third/fourth grneration
cephalosporin+Metronidazole
Patients with neurodurgery/Head trauma
Vancomycin+Ceftazidine
Meropenem+Vancomycin
Modify antibiotics as per culture results
Duration: Min 6-8 weeks
18.
Prophylactic anticonvulsant
Should continue atleast 3 months after resolution of
abscess
Role of steroids
Not given routinely
Usually reserved forof significant periabscess edema
with mass effect and raise ICP
Dexamethasone 10 mg 6 hrly
19.
Aspiration and Drainage of the abscess under
stereotactic guidance
Craniotomy and Complete excision of a
bacterial abscess: reserved for multiloculated
abscess or in those where aspiration is
unsucessful.
25. Introduction
Encephalitis is an acute inflammatory process affecting the brain
parenchyma
Meningoencephalitis
Encephalomyelitis
Encephalomyeloradiculitis
Viral infection is the most common and important cause, with over
100 viruses implicated worldwide
Incidence of 3.5-7.4 per 100,000 persons per year
~20,000 cases reported anually in USA
26. Causes of Viral Encephalitis
Herpes viruses – HSV-1, HSV-2, varicella zoster virus, cytomegalovirus, EpsteinBarr virus, human herpes virus 6
Adenoviruses
Influenza A
Enteroviruses, poliovirus
Measles, mumps, and rubella viruses
Rabies
Arboviruses – examples: Japanese encephalitis; St. Louis encephalitis virus; West
Nile encephalitis virus; Eastern, Western and Venzuelan equine encephalitis virus;
tick borne encephalitis virus
Bunyaviruses – examples: La Crosse strain of California virus
Reoviruses – example: Colorado tick fever virus
Arenaviruses – example: lymphocytic choriomeningitis virus
27. What Is An Arbovirus?
Arboviruses = arthropod-borne viruses
Arboviruses are maintained in nature through
biological transmission between susceptible
vertebrate hosts by blood-feeding arthropods
Vertebrate infection occurs when the infected
arthropod takes a blood meal
28. Major Arboviruses That Cause
Encephalitis
Flaviviridae
Japanese encephalitis
St. Louis encephalitis
West Nile
Togaviridae
Eastern equine encephalitis
Western equine encephalitis
Bunyaviridae
La Crosse encephalitis
31. Japanese Encephalitis
Flavivirus related to St. Louis
encephalitis
Most important cause of arboviral
encephalitis worldwide, with over
45,000 cases reported annually
Transmitted by culex mosquito,
which breeds in rice fields
Mosquitoes become infected by
feeding on domestic pigs and wild
birds infected with Japanese
encephalitis virus. Infected
mosquitoes transmit virus to
humans and animals during the
feeding process.
32. History of Japanese Encephalitis
1800s – recognized in Japan
1924 – Japan epidemic. 6125 cases, 3797 deaths
1935 – virus isolated in brain of Japanese patient who
died of encephalitis
1938 – virus isolated from Culex mosquitoes in Japan
Today – extremely prevalent in South East Asia.
30,000-50,000 cases reported each year.
35. West Nile Virus
Flavivirus
Primary host – wild birds
Principal arthropod
vector – mosquitoes
Geographic distribution Africa, Middle East,
Western Asia, Europe,
Australia, North
America, Central
America
http://www.walgreens.com/images/library/healthtips/july02/westnilea.jpg
38. Eastern Equine Encephalitis
Togavirus
Caused by a virus transmitted to
humans and horses by the bite of
an infected mosquito.
200 confirmed cases in the US
1964-present
Human cases occur relatively
infrequently, largely because the
primary transmission cycle takes
place in swamp areas where
populations tend to be limited.
40. La Crosse Encephalitis
Bunyavirus
On average 75 cases per year reported
to the CDC
Most cases occur in children under 16
years old
Zoonotic pathogen that cycles between
the daytime biting treehole mosquito,
and vertebrate amplifier hosts
(chipmunk, tree squirrel) in deciduous
forest habitats
1963 – isolated in La Crosse, WI from
the brain of a child who died from
encephalitis
41. Summary – Confirmed and Probable
Human Cases in the US
Virus
Years
Total cases
Eastern Equine
1964-2000
182
Western Equine 1964-2000
649
La Crosse
1964-2000
2,776
St. Louis
1964-2000
4,482
West Nile
1999-present
> 9,800
43. Symptoms
Fever
Headache,
Malaise, Anorexia, Nausea and Vomiting
Abdominal pain
Altered level of consciousness
Mild lethargy to Coma
Behavioral changes, hallucinations, agitations,
personality changes, frank psychosis
44.
Focal neurologic deficits:
Virtually every possible focal neurological disturbance has
been reported.
Aphasia
Ataxia
Weakness: Hemiparesis with hyperactive tendon reflexes
Cranial nerve deficits
Involantary movements- tremors, myoclonic jerks
Seizures >50% patients
SIADH
45. Patient History
Detailed history critical to determine the likely cause of encephalitis.
Prodromal illness, recent vaccination, development of few days → Acute
Disseminated Encephalomyelitis (ADEM) .
Biphasic onset: systemic illness then CNS disease → Enterovirus encephalitis.
Abrupt onset, rapid progression over few days → HSE.
Recent travel and the geographical context:
Africa → Cerebral malaria
Asia → Japanese encephalitis
High risk regions of Europe and USA → Lyme disease
Recent animal bites → Tick borne encephalitis or Rabies.
Occupation
Forest worker, exposed to tick bites
Medical personnel, possible exposure to infectious diseases.
46. Lab Investigation
CSF examination: Should be performed in all the
patients until contraindicated
Diagnosis is usually based on CSF
Mild increase in protein
Inrease cells with predominantly lymphocytes
Normal glucose
Absence of bacteria on culture.
Viruses occasionally isolated directly from CSF
Less than half are identified
47. Laboratory Diagnosis
CSF PCR techniques
Detect specific viral DNA in CSF
Usually available for HSVCMV, EBV, HHV6,
ENTEROVIRUS, VZV
CSF CULTURE
48. MRI/ CT Scan
Can exclude subdural bleeds, tumor, and sinus thrombosis
Help by
Focal or diffuse ence4phalitis process
In HSV encephalitis- 80% abnormalities in temporal lobe
51. EEG
In HSV: Periodic focal temporal lobe spikes on
a background of slow or low amplitude activity.
52. Brain Biopsy
Is generally reserved for patients in whom CSF
PCR fail to lead a specific diagnosis
Reserved for patients who are worsening, have an
undiagnosed lesion after scan, or a poor response to
acyclovir.
55. Supportive Therapy
Fever, dehydration, electrolyte imbalances, and
convulsions require treatment.
For cerebral edema severe enough to produce
herniation, controlled hyperventilation, mannitol, and
dexamethasone.
Patients with cerebral edema must not be
overhydrated.
If these measures are used, monitoring ICP should
be considered.
If there is evidence of ventricular enlargement,
intracranial pressure may be monitored in conjunction
with CSF drainage.
56. Acyclovir
Acyclovir is a synthetic purine nucleoside
analogue with inhibitory activity against HSV-1
and HSV-2, varicella-zoster virus (VZV),
Epstein-Barr virus (EBV) and cytomegalovirus
(CMV)
In order of decreasing effectiveness
Acyclovir 10 mg/kg 8 hrly 14-21day
57. Acyclovir Action
Thymidine Kinase (TK) of uninfected cells does not use acyclovir as a
substrate.
TK encoded by HSV, VZV and EBV2 converts acyclovir into acyclovir
monophosphate.
The monophosphate is further converted into diphosphate by cellular
guanylate kinase and into triphosphate by a number of cellular enzymes.
Acyclovir triphosphate interferes with Herpes simplex virus DNA polymerase
and inhibits viral DNA replication.
Acyclovir triphosphate incorporated into growing chains of DNA by viral
DNA polymerase.
When incorporation occurs, the DNA chain is terminated.
Acyclovir is preferentially taken up and selectively converted to the active
triphosphate form by HSV-infected cells.
Thus, acyclovir is much less toxic in vitro for normal uninfected cells because:
1) less is taken up; 2) less is converted to the active form.
58.
Ganicyclovir/Foscarnet: For CMV related CNS
infection
Ganicyclovir 5mg/kg (over 1 hr) 12 hrly during
induction therapy the od in maintenance therapy
Foscarnet: 60mg/kg 8hrly during induction then
maintenance 60-120 mg/kg
59. Dexamethasone
Synthetic adrenocortical steroid
Potent anti-inflammatory effects
Dexamethasone injection is generally
administered initially via IV then IM
Side effects: convulsions; increased ICP after
treatment; vertigo; headache; psychic
disturbances
60. Prognosis
The mortality rate varies with etiology, and epidemics due to the
same virus vary in severity in different years.
Bad: Eastern equine encephalitis virus infection, nearly 80% of survivors
have severe neurological sequelae.
Not so Bad: EBV, California encephalitis virus, and Venezuelan equine
encephalitis virus, severe sequelae are unusual.
Approximately 5 to 15% of children infected with LaCrosse virus have a
residual seizure disorder, and 1% have persistent hemiparesis.
Permanent cerebral sequelae are more likely to occur in infants,
but young children improve for a longer time than adults with
similar infections.
Intellectual impairment, learning disabilities, hearing loss, and other
lasting sequelae have been reported in some studies.
61. Prognosis w/ Treatment
Considerable variation in the incidence and severity of sequelae.
NIAID-CASG trials:
Hard to assess effects of treatment.
The incidence and severity of sequelae were directly related to the age of the
patient and the level of consciousness at the time of initiation of therapy.
Patients with severe neurological impairment (Glasgow coma score 6) at initiation
of therapy either died or survived with severe sequelae.
Young patients (<30 years) with good neurological function at initiation of
therapy did substantially better (100% survival, 62% with no or mild sequelae)
compared with their older counterparts (>30 years); (64% survival, 57% no or
mild sequelae).
Recent studies using quantitative CSF PCR tests for HSV indicate that clinical
outcome following treatment also correlates with the amount of HSV DNA
present in CSF at the time of presentation.
62. Vaccination
None for most Encephalitides
JE
Appears to be 91% effective
There is no JE-specific therapy other than supportive care
Live-attenuated vaccine developed and tested in China
Vero cell-derived inactivated vaccines have been developed in
China
Appears to be safe and effective
Chinese immunization programs involving millions of children
2 millions doses are produced annually in China and Japan
Several other JE vaccines under development