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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.

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Presentation on theme: "The clinical manifestations of abcess and focal infections due to local spread, hematogenous d/s associated with immune deficiency and how they differ."— Presentation transcript:

1 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

2 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

3 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.

4 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 focus 2.Hematogenous spread from a distant focus 3.Trauma

5 Contiguous suppurative focus Bone of the middle ear or nasal sinuses becomes the seat of osteomyelitis Spread along the veins Abcess at a considerable distance from primary site of focus

6 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

7 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.

8 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

9 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.

10 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

11 Differential Diagnosis Cryptococcosis Cysticercosis Epidural Abscess Meningitis

12 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.

13 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.

14 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“

15 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)

16 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

17 Available online at http://www.catalog.nucleusinc.c om

18 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.

19 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.


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