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The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ from the mimics. Brain Abscess. - PowerPoint PPT Presentation
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The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with
immune deficiency and how they differ from the mimics
Brain Abscess
• A brain abscess is a collection of immune cells, pus, and other material in the brain, usually from a bacterial or fungal infection.
• Majority is always secondary to purulent focus elsewhere in the body (only 10% introduced from the outside)
• 40% related to d/s in the paranasal sinuses, middle ear and mastoid cells
• Purulent pulmonary infection
Brain Abscess
• Mortality/Morbidity– With the introduction of antimicrobics and imaging 5-15%
decrease in Mortality Rate.– Rupture of a brain abscess, however, is associated with a high
mortality rate (up to 80%).– The frequency of neurological sequelae in persons who survive
the infection varies from 20-79%.• Sex
– More common in males.• Age
– Brain abscesses occur more frequently in the first 4 decades of life.
Pathophysiology
• Caused by intracranial inflammation with subsequent abscess formation.
• In at least 15% of cases, the source of the infection is unknown (cryptogenic).
• Infection may enter the intracranial compartment directly or indirectly via 3 routes.
• Three Routes:1. Contiguous suppurative focus2. Hematogenous spread from a distant focus3. Trauma
Contiguous suppurative focus
Bone of the middle earor nasal sinuses becomes the
seat of osteomyelitis
Spread along the veins
Abcess at a considerable distance from primary site of focus
Hematogenous spread from a distant focus
• 1/3 of all brain abcess• Majority -ABE and septic focus on
the lungs or pleura• Others - congenital heart defect,
pulmonary AV malformation
• Middle cerebral artery• multiple
Trauma
• 10% of cases• Open skull fracture allows organisms to seed
directly in the brain. • Brain abscess can also occur as a complication
of intracranial surgery, foreign body, bullets, and shrapnel.
Clinical Diagnosis
• The symptoms and signs include the following: – Low- or high-grade fever – Persistent headache (often localized) – Drowsiness – Confusion – Stupor – General or focal seizures – Nausea and vomiting – Focal motor or sensory impairments – Papilledema – Ataxia – Hemiparesis
Clinical Diagnosis
• The symptoms and signs include the following: – Localized neurologic signs
a. Cerebellar abscess - Nystagmus, ataxia, vomiting, and dysmetria
b. Brainstem abscess - Facial weakness, headache, fever, vomiting, dysphagia, and hemiparesis
c. Frontal abscess - Headache, inattention, drowsiness, mental status deterioration, motor speech disorder, hemiparesis with unilateral motor signs, and grand mal seizures.
d. Temporal lobe abscess - Headache, ipsilateral aphasia (if in the dominant hemisphere), and visual defect.
Causes
• Anaerobic and microaerophilic cocci and gram-negative and gram-positive anaerobic bacilli are the most important isolates.
• The predominant organisms include the following: – Staphylococcus Aureus– Aerobic, anaerobic, and microaerophilic streptococci, including
alpha-hemolytic streptococci and Streptococcus milleri – Bacteriodes, Prevotella, and Fusobacterium species – Enterobacteriaceae organisms, including Klebsiella pneumonia,
Escherichia coli, and Proteus species (Rare isolates include Enterobacter species, Actinobacillus actinomycetemcomitans, and Salmonella species)
– Pseudomonas species – Other anaerobes
Differential Diagnosis
• Cryptococcosis• Cysticercosis• Epidural Abscess• Meningitis
Laboratory Studies
• Routine tests – CBC count with differential and platelet count – Erythrocyte sedimentation rate (ESR; elevated in up to two thirds
of patients) – Serum C-reactive protein (CRP) or Westergren sedimentation
rate – Serological tests for some pathogens (eg, serum immunoglobulin
G antibodies, CSF polymerase chain reaction for Toxoplasma) – Blood cultures (at least 2; preferably before antibiotic usage) – Results:
• Moderate leukocytosis is present, • ESR and CRP level are generally elevated. • Serum sodium levels may be low because of inappropriate antidiuretic
hormone production. • Platelet counts may be high or low.
Laboratory Studies• Cerebrospinal fluid
– Elevated protein level, pleocytosis with variable neutrophil count, a normal glucose level, and sterile cultures.
– A lumbar puncture is mostly of value to rule out other disease processes, especially bacterial meningitis.
– The white blood cell reaches 100,000/µL or higher when the abscess ruptures into the CSF.
– Many red blood cells are generally observed at that time, and the CSF lactic acid level is then elevated to more than 500 mg.
• Abscess aspirate (obtained via stereotactic CT or surgery)– Culture aspirates of abscesses for aerobic, anaerobic, and acid-fast
organisms and fungi – Gram stain, acid-fast stain (for Mycobacterium), modified acid-fast stain
(for Nocardia), and special fungal stains (eg, methenamine silver, mucicarmine)
– Histopathological examination of the brain tissue.
Imaging Studies
• CT imaging of the brain (with and without contrast) is the most readily available study for establishing diagnosis of brain abscess – Early in the course: abscess appears as a low-
density, irregular zone – As the disease progresses: distinctive "ring
enhancement“
Other Causes of Pus• subdural empyema (from sinusitis, mastoiditis -
rare, 20% mortality)• meningitis, encephalitis, AIDS, toxoplasmosis
(see Neurology Chapter)• osteomyelitis of skull (Pott’s puffy tumour),
usually seen with sinusitis • granuloma (TB, sarcoid)
Surgical Measures• mandatory when neurologic deficits are severe or
progressive• used when the abscess is in the posterior fossa• Abscess drainage - (via needle) under stereotactic CT
guidance through a burr hole under local anesthesia, is most rapid and effective method. May be repeated if needed.
• Craniotomy - if abscess is large or multilocular
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Treatment• Antibiotics according to organism if known• Pen G and metronidazole, or chloramphenicol if
unknown• Add oxacillin or nafcillin if trauma or IV drug user ;
use vancomycin in penicillin-sensitive patients• If gram(-)organism suspected (otic, GI, GU organ)
add third-generation cephalosporin • Abscess associated with HIV infection assumed to be
due to Toxoplasma gondii - daily doses of sulfadiazine and pyrimethamine.
Treatment• Anticonvulsants - phenytoin until abscess resolved or
perhaps longer. Obtain anticonvulsant levels.• Following surgical procedure - corticosteroids to
reduce edema. Dexamethasone. Taper rapidly. Use usually limited to 1 week. Continue antibiotics for 6-8 weeks.