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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

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Page 1: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 2: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 3: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.

Page 4: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 5: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 6: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 7: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.

Page 8: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 9: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.

Page 10: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 11: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

Differential Diagnosis

• Cryptococcosis• Cysticercosis• Epidural Abscess• Meningitis

Page 12: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.

Page 13: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.

Page 14: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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“

Page 15: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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)

Page 16: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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

Page 17: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

Available online at http://www.catalog.nucleusinc.com

Page 18: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.

Page 19: The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ

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.