Brain Abscess
Dr. Shatdal Chaudhary, M.D.
Associate Professor
Universal College of Medical Sciences,
Bhairahawa, Nepal
Ema...
Definition


Brain abscess is a focal suppurative infection within
the brain parenchyma, typically surrounded by a
vascul...
Epidemiology



Relatively uncommon
Incidence~.3-1.3:100000 person per year
Etiology


Brain abscess may develop by
1. Direct spread from a contiguous cranial site of infection
 2. Head trauma, ne...
Predisposing conditions








Otitis media
Mastoiditis
Paranasal sinusitis
Pyogenic infection of chest or any oth...
In Immunocompetent persons:
 Streptococcus spp. (aerobic, Anaerobic and
viridans) 40%
 Enterobacteriaceae (Proteus, E.co...
In immuno-compromised host
 Nocardia
 T gondii
 Aspergillus
 Candida
 C. neoformans
Stages


1. Early Cerebritis: 1-3days




2. Late Cerebritis: 4-9 days




Pus formationin necrotic center which is s...
Clinical Presentation






Typically presents as an expanding intracranial
mass rather than as a infectious process
S...
Symptoms


Classical triad: seen in <50% patients
Headache 75%
 Fever 50%
 Focal neurologic deficit 15-35%



Focal neurologic deficit
Aphasia
 Hemiparesis
 Visual field defect
 Ataxia
 Nystagmus
 Seizures
 Raised ICP-Papil...
Investigations





TLC, DLC
ESR, CRP
Blood cultures
Neuroimaging studies:
MRI: better esp can detect early stages of ...
MRI
CT Scan
Microbiological Evaluation
CT-guided stereotactic needle aspiration
Gram’s Stain
 Culture : Aerobic, Anaerobic, Mycobacte...
D/D








Bacterial Meningitis
Meningoencephalitis
Acute disseminated encephalomyelitis
Empyema
Saggital Sinus Th...
Treatment




Combination of high dose parentral antibiotics
and neurosurgical drainage
Third/fourth grneration
cephalo...


Prophylactic anticonvulsant




Should continue atleast 3 months after resolution of
abscess

Role of steroids
Not gi...




Aspiration and Drainage of the abscess under
stereotactic guidance
Craniotomy and Complete excision of a
bacterial a...
Prognosis



Mortality rate <15%
Neurological sequelae ≥20% of survivors
Acute Viral Meningitis








Enterovirus(coxaschie viruses, echovirus,human
enterovirus68-71
HSV 2
HIV
Arbovirus
V...
Introduction


Encephalitis is an acute inflammatory process affecting the brain
parenchyma




Meningoencephalitis
En...
Causes of Viral Encephalitis












Herpes viruses – HSV-1, HSV-2, varicella zoster virus, cytomegalovirus,...
What Is An Arbovirus?





Arboviruses = arthropod-borne viruses
Arboviruses are maintained in nature through
biologica...
Major Arboviruses That Cause
Encephalitis


Flaviviridae
Japanese encephalitis
 St. Louis encephalitis
 West Nile



...
Japanese Encephalitis
Japanese Encephalitis





Flavivirus related to St. Louis
encephalitis
Most important cause of arboviral
encephalitis ...
History of Japanese Encephalitis


1800s – recognized in Japan



1924 – Japan epidemic. 6125 cases, 3797 deaths



193...
Distribution of Japanese
Encephalitis in Asia, 1970-1998
West Nile Virus
West Nile Virus





Flavivirus
Primary host – wild birds
Principal arthropod
vector – mosquitoes
Geographic distribut...
St. Louis Encephalitis
St. Louis Encephalitis





Flavivirus
Most common
mosquito-transmitted
human pathogen in the
US
Leading cause of
epide...
Eastern Equine Encephalitis






Togavirus
Caused by a virus transmitted to
humans and horses by the bite of
an infec...
Western Equine Encephalitis





Togavirus
Mosquito-borne
639 confirmed cases in
the US since 1964
Important cause of
...
La Crosse Encephalitis







Bunyavirus
On average 75 cases per year reported
to the CDC
Most cases occur in childre...
Summary – Confirmed and Probable
Human Cases in the US
Virus

Years

Total cases

Eastern Equine

1964-2000

182

Western ...
Clinical Manifestations
Symptoms


Fever



Headache,
Malaise, Anorexia, Nausea and Vomiting
Abdominal pain
Altered level of consciousness



...


Focal neurologic deficits:


Virtually every possible focal neurological disturbance has
been reported.



Aphasia
At...
Patient History






Detailed history critical to determine the likely cause of encephalitis.
Prodromal illness, rec...
Lab Investigation


CSF examination: Should be performed in all the
patients until contraindicated



Diagnosis is usual...
Laboratory Diagnosis


CSF PCR techniques
Detect specific viral DNA in CSF
 Usually available for HSVCMV, EBV, HHV6,
ENT...
MRI/ CT Scan



Can exclude subdural bleeds, tumor, and sinus thrombosis
Help by



Focal or diffuse ence4phalitis pro...
MRI
MRI
EEG


In HSV: Periodic focal temporal lobe spikes on
a background of slow or low amplitude activity.
Brain Biopsy


Is generally reserved for patients in whom CSF
PCR fail to lead a specific diagnosis



Reserved for pati...
D/D













Tuberculosis, Fungal, Rickettsia, Mycoplasma, Bacterial
Anoxic/Ischemic conditions
Metabolic ...
Treatment


Suppportive
Vital monitoring
 ABC
 IVF
 Treatment of raised ICP
 Bed Care
 Nutrition
 DVT prophylaxis

Supportive Therapy





Fever, dehydration, electrolyte imbalances, and
convulsions require treatment.
For cerebral ede...
Acyclovir


Acyclovir is a synthetic purine nucleoside
analogue with inhibitory activity against HSV-1
and HSV-2, varicel...
Acyclovir Action









Thymidine Kinase (TK) of uninfected cells does not use acyclovir as a
substrate.
TK enco...


Ganicyclovir/Foscarnet: For CMV related CNS
infection
Ganicyclovir 5mg/kg (over 1 hr) 12 hrly during
induction therapy ...
Dexamethasone






Synthetic adrenocortical steroid
Potent anti-inflammatory effects
Dexamethasone injection is gener...
Prognosis


The mortality rate varies with etiology, and epidemics due to the
same virus vary in severity in different ye...
Prognosis w/ Treatment


Considerable variation in the incidence and severity of sequelae.




NIAID-CASG trials:


...
Vaccination



None for most Encephalitides
JE




Appears to be 91% effective
There is no JE-specific therapy other ...
Brain abscess dr shatdal
Brain abscess dr shatdal
Brain abscess dr shatdal
Brain abscess dr shatdal
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Diagnosis And Treatment of Brain Abscess

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Brain abscess dr shatdal

  1. 1. Brain Abscess Dr. Shatdal Chaudhary, M.D. Associate Professor Universal College of Medical Sciences, Bhairahawa, Nepal Email: shatdalchaudhary@yahoo.com
  2. 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.
  3. 3. Epidemiology   Relatively uncommon Incidence~.3-1.3:100000 person per year
  4. 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
  5. 5. Predisposing conditions        Otitis media Mastoiditis Paranasal sinusitis Pyogenic infection of chest or any other part of body Penetrating head injury Neurosurgical procedure Dental infection
  6. 6. In Immunocompetent persons:  Streptococcus spp. (aerobic, Anaerobic and viridans) 40%  Enterobacteriaceae (Proteus, E.coli, Klebsella) 25%  Anaerobes (Bacteroides, Fusobacterium) 30%  Staphylococci 10%  Taenia solium(NCC)  Mycobacterial infection (tuberculoma)
  7. 7. In immuno-compromised host  Nocardia  T gondii  Aspergillus  Candida  C. neoformans
  8. 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. 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.
  10. 10. Symptoms  Classical triad: seen in <50% patients Headache 75%  Fever 50%  Focal neurologic deficit 15-35% 
  11. 11.  Focal neurologic deficit Aphasia  Hemiparesis  Visual field defect  Ataxia  Nystagmus  Seizures  Raised ICP-Papilledema  Meningismus Uncommon unless abscess rupture in ventricle 
  12. 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) 
  13. 13. MRI
  14. 14. CT Scan
  15. 15. Microbiological Evaluation CT-guided stereotactic needle aspiration Gram’s Stain  Culture : Aerobic, Anaerobic, Mycobacterial and fungal cultures  Blood Culture LP: do not perform
  16. 16. D/D        Bacterial Meningitis Meningoencephalitis Acute disseminated encephalomyelitis Empyema Saggital Sinus Thrombosis Primary or Secondary brain tumor CVA
  17. 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. 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. 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.
  20. 20. Prognosis   Mortality rate <15% Neurological sequelae ≥20% of survivors
  21. 21. Acute Viral Meningitis       Enterovirus(coxaschie viruses, echovirus,human enterovirus68-71 HSV 2 HIV Arbovirus VZV EBV
  22. 22. 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 
  23. 23. 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
  24. 24. 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
  25. 25. Major Arboviruses That Cause Encephalitis  Flaviviridae Japanese encephalitis  St. Louis encephalitis  West Nile   Togaviridae Eastern equine encephalitis  Western equine encephalitis   Bunyaviridae  La Crosse encephalitis
  26. 26. Japanese Encephalitis
  27. 27. 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.
  28. 28. 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.
  29. 29. Distribution of Japanese Encephalitis in Asia, 1970-1998
  30. 30. West Nile Virus
  31. 31. 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
  32. 32. St. Louis Encephalitis
  33. 33. St. Louis Encephalitis    Flavivirus Most common mosquito-transmitted human pathogen in the US Leading cause of epidemic flaviviral encephalitis
  34. 34. 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.
  35. 35. Western Equine Encephalitis     Togavirus Mosquito-borne 639 confirmed cases in the US since 1964 Important cause of encephalitis in horses and humans in North America, mainly in the Western parts of the US and Canada
  36. 36. 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
  37. 37. 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
  38. 38. Clinical Manifestations
  39. 39. 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
  40. 40.  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
  41. 41. 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.
  42. 42. 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
  43. 43. Laboratory Diagnosis  CSF PCR techniques Detect specific viral DNA in CSF  Usually available for HSVCMV, EBV, HHV6, ENTEROVIRUS, VZV   CSF CULTURE
  44. 44. 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
  45. 45. MRI
  46. 46. MRI
  47. 47. EEG  In HSV: Periodic focal temporal lobe spikes on a background of slow or low amplitude activity.
  48. 48. 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.
  49. 49. D/D             Tuberculosis, Fungal, Rickettsia, Mycoplasma, Bacterial Anoxic/Ischemic conditions Metabolic disorders Nutritional deficiency Toxic (Accidental & Intentional) Systemic infections Critical illness Malignant hypertension Hashimoto’s encephalopathy Traumatic brain injury Epileptic (non-convulsive status) CJD (Mad Cow)
  50. 50. Treatment  Suppportive Vital monitoring  ABC  IVF  Treatment of raised ICP  Bed Care  Nutrition  DVT prophylaxis 
  51. 51. 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.
  52. 52. 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 
  53. 53. 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.
  54. 54.  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 
  55. 55. 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
  56. 56. 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.
  57. 57. 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.
  58. 58. 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
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