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Introduction
Epidemiology:
Approximately 1500-2500 cases per year in U.S. Higher incidence in developing countries. Male: female ratio is 1.5: 3.1
Risk factors:
Pulmonary abnormalities (infection, A-V fistula,..) Cong. Cyanotic heart disease (CCHD). Bacterial endocarditis. Penetrating head trauma. AIDS (Immunocompromized patients).
Vectors of spread
1. Hematogenous dissimination. 2. Contiguous (local) spread. 3. Following penetrating cranial trauma or
neurosurgical procedure
1. Hematogenous dissimination:
The most common vector nowadays. Multiple in 10-50%. No source in up to 25%. Chest is the most common source. In adults: lung abscess, bronchiectasis and empyema. In children: CCHD (risk of 4-7%) especially Fallots tetralogy due to increased Hct and low PO2. Patients with left to right shunts lose the filtering effect of the lungs. Pulmonary A-V fistulas (5% will eventually develop B.A.). Bacterial endocarditis, especially with acute form. Dental abscess. GI infections
patients with injury traversing an air sinus associated with CSF leak not repaired surgically. An abscess following penetrating trauma can not be treated by simple aspiration, open surgical debridement is required. Abscess formation has been reported following use of intracranial pressure monitors and halo traction devices.
Pathogens
Cultures are sterile in up to 25% of cases. Streptococcus is the most frequent, 33-50% anaerobic or
microaerophilic. Multiple organisms may be cultured to varying degrees. In fronto-ethmoidal sinusitis:Strept.Melleri & Strep. Angiosus. In otitis media, mastoiditis or lung abscess: multiple organisms including anaerobic strept., Bacteroides, Proteus. Post traumatic abscess is usually due to Staph aureus or Enterobactericeae. In Transplant patients, fungal infections are common. In immunocompromized patients, organisms that may produce abscesses include toxoplasmosis and nocardia.
Clinical Presentation
No specific symptoms for brain abscess. Symptoms of increased ICP ( headache, nausea and
vomiting, lethargy) due to surrounding edema. Hemiparesis and seizures develop in 30-50% of cases. Papilledema is rare before 2 yrs of age. In newborns: there may be seizures, meningitis, irritability, increasing head circumference, and failure to thrive. Most newborns with brain abscess are afebrile.
Investigations
Bloodwork:
Peripheral WBC may be normal or mildly elevated. Bl. Culture: usually negative. ESR may be normal. C-reactive protein: non specific for cerebral abscess and may be elevated in other inflammatory conditions. No characteristic findings diagnostic of abscess. There is a high risk of transtentorial herniation. It is better to be avoided.
Lumbar puncture:
inflammation, poorly demarcated from surrounding brain, toxic changes in neurons, perivascular infiltrates. Late cerebritis: (days 4-9) developing reticular matrix and developing necrotic center. Early capsule: (days 10-13) neovascularity, necrotic center, reticular network surrounds. Late capsule: (>day 14) well-formed collagen capsule, necrotic center, gliosis around capsule.
Treatment
There is no single best method for treating a brain abscess. Treatment usually involves surgical drainage or excision,
correction of the primary source, and long term use of antibiotics (often IV x 6-8 weeks followed by oral route x 4-8 weeks). Poor surgical candidates. Multiple abscesses especially if small. Abscess in eloquent areas like motor cortex or brain stem. Concomitant meningitis or ventriculitis.
External drainage: controversial. Instillation of antibiotics directly into the abscess: has not been extremely effective, although it may be used as a last resort in Aspergillus abscesses.
Cultures
Aspirated material should be sent for the following: 1. Stains:
Gram stain Fungal stain AFB stain Routine cultures: aerobic and anaerobic Fungal culture TB culture
2. Cultures:
outcome
In the pre CT era, mortality ranged from 40-60%. With improvement in antibiotics, surgery and diagnostic
tools, mortality rate has been reduced to 10%. Morbidity remains high with permanent neurological deficit or seizures in up to 50% of cases. A worse prognosis is associated with poor neurological function, intraventricular rupture of abscess, and almost 100% mortality with fungal abscesses in transplant recipients.
Case presentation
10 year-old girl, a known case of Downs syndrome with CCHD, Fallots tetralogy and PDA. She has underwent cardiac surgery 3 years ago and has been following up with pedia cadiology. 20 days prior to admission, she developed fever, diagnosed as ? Infective endocarditis and received IV antibiotics. However, she did not improve and, instead, started to develop attacks of cyanosis and irritability and was admitted to pediatric ward to continue antibiotic therapy. During her stay in the hospital, she developed drowsiness, Rt-sided weakness and focal fits. Neurosurgery consultation was done and CT brain was requested.
Hospital course
The patient started immediately to receive imperically:
IV vancomycin 350 mg q 8 hours IV ceftriaxone 105 mg q12 hours IV metronidazol 200 mg q 6 hours Tab phenobarbiton 75 mg BID
Needle aspiration of the largest two daughter abscesses was done under GA and 70 ml of pus were drained. Patients conscious level and irritability significantly improved. Cultures were negative for aerobic, anaerobic and TB organisms
Re-tapping of the residual (or re-accumulating) cavity was done and further 20 CCs of pus were drained . Patient completed 6 weeks on IV antibiotics and further 6 weeks on oral antibiotics in the form of cloxacillin, clindamycin, and suprax.