Brain Abscess Flashcards
A focal suppurations infection within the brain parenchyma typically surrounded by a vascularised capsule
Brain abscess
Nonencapsulated abscess
Celebrities
In immunocompetent individuals the most important pathogens
Streptococcus species 40%
Enterobacteriaceae( proteus, e.coli,kleibseilla)
Anaerobic bacteria Bacteriodes, fusobacterium
Staphylococcus
Brain abscess ethology
- Direct spread
- Trauma
- hematogenous spread
25% no obvious source: cryptogenic brain abscess.
Ethology of brain abscess
- Ontogenic: temporal lobe (55-75%) and cerebellum (20-30%)
- direct spread: frontal, ethmoidal, sphenoid sinuses and those that occur due to dental infections.
- 10% brain abscess are associated with paranasal sinuses: common in young males.
Paranasal sinusitis common pathogen
Streptoccoci, haemophilia Sapporo. Bacteriodes sap. Pseudomonas app. And staphylococcus aureus.
Dental infection:
1. Step staph Bacteriodes app, fusobacterium app.
Hematogenous spread: 25% of brain abscess
Predilection for the territory of the middle cerebral artery 9 posterior lobes
- in the junction of gray and white matter and are poorly encapsulated.
Abscess due to complications of infective endocarditis: viridans streptococci or s. Aureus
Pyogenic lung infections such as lung abscess
- Streptococci
- staphylococci
- bacteriodes species
- fusobacterium
- enterobacteriaceae.
Head trauma: MRSA, s. Epidermidis, enerobacteriaceae, ppseudomonas app. Clostridium app.
Clostridium, and enterobacteriacea common with urinary sepsis.
Stages of brain abscess
- Early celebrities 9day 1-3)
- Late celebrities (4-9)
- early capsule formation (day 10-13)
- late capsule formation (day 14 and beyond)
Characterised by perivascular infiltration of inflammatory cells, surround a central core and coagulation necrosis. Marked edema surrounds the lesion at this stage.
Early celebrities
Pus formation leads to enlargement of the necrotic center, which is sorrounded at its border by an inflammatory infiltrate of macrophages and fibroblast.n capsul of firoblast and reticular fibres gradually develops, and the surrounding edema becomes more distinct.
Late stage celebrities.
Formation of capsule, that is better developed on the cortical than in the ventricular side of the lesion.
Appearance of ring enhancing capsule on neuro imaging
Early capsule formation 9day (10-13)
Defined as well formed necrotic center surrounded by a dense colllagenous capsul. The sorroundeing edema has regressed but marked by glossing with large numbers of reactive astrocytes has developed outside the capsul.
The gliotic process: contribute to development of seizures
Late capsule formation
Day 14-beyond)
Clinical prenration of abscess
- Headache
2.fever
3.focal neurological directives
50% 0f cases.
Most common symptom: headache
-constant dull,aching, either hemicranial, or generalised
Clinical presentation of abscess
- Frontal lobe: hemiparesis
- Temporal lobe: disturbance of language (dysphasia) or upper homonymous quadratanopia
- Cerebellum abscess: nystagmus and ataxia
- Cerebellum; increase ICP
Papilledema, nausea, vomiting, confusion and drowsiness
Treatment for brain abscess
Immunocopetent brain abscesss Platient
3rd-4th generationcephalosphorin
(Cefotaxime,ceftraixone, cefipime) and metronidazole
Penetrating head trauma: Ceftazidime 3rd gen cephalosporin with enhance coverage to pseudomonas spp.
Staphylococci: vancomycin
Meropenem should be added……..
Medical therapy alone is reserved to patients with
Surgically inaccessible, small (<2-3cm) or nonencapsulated abscesses (cerebritis) and or patients whose condition is too tenuous to allow performance of the neurosurgical procedure.
Duration for antibiotic therapy for brain abscess
6-8 weeks of parent earl antibiotic therapy…
Prophylactic anticonvulsant therapy
All patient should receive prophylactic anticonvulsant therapy
35% risk for focal generalised seizure
Continued for at least 3 months after resolution of the abscess. And the withdrawal should be based on EEG
The most common parasitic disease of the CNS worldwide
Neurocystecercosisingestion of food contaminated with T. Sodium
Acquired from ingestion of undercooked meat and from handling ca feces
Toxoplasmosis
Clinical price notation of neurocysticercosis
New onset partial seizure with or without secondary generalisation
Cysticerrci may develop in the brain parenchyma and cause seizures or focal neurological deficits.
When present in the subarachnoid or the ventricular spaces: increase ICP
Spinal cystecerci can mimic the presentation of intraspinal Tumors
Manifestation of primary toxoplasmosis
Often asymptomatic
May spread to the CNS where the become latent
Reactivation occurs with immunocompromised hosts, particularly with those HIV infection
Fever headache, seizure, focal neurological deficits
Treatment for focal CNS lesions
Anticonvulsant therapy when they present with seizure
Albendazole 15mg/kg/day in two dose for 8 days
Praziquantel 50mg/kg per day for 15 days
Prednisone and defame that’s one should be added to reduce host anti inflammatory response
Colloidal stage: treated with anticysticidal therapy