Brain Abscess Flashcards

1
Q

A focal suppurations infection within the brain parenchyma typically surrounded by a vascularised capsule

A

Brain abscess

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2
Q

Nonencapsulated abscess

A

Celebrities

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3
Q

In immunocompetent individuals the most important pathogens

A

Streptococcus species 40%

Enterobacteriaceae( proteus, e.coli,kleibseilla)

Anaerobic bacteria Bacteriodes, fusobacterium

Staphylococcus

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4
Q

Brain abscess ethology

A
  1. Direct spread
  2. Trauma
  3. hematogenous spread

25% no obvious source: cryptogenic brain abscess.

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5
Q

Ethology of brain abscess

A
  1. Ontogenic: temporal lobe (55-75%) and cerebellum (20-30%)
  2. direct spread: frontal, ethmoidal, sphenoid sinuses and those that occur due to dental infections.
  3. 10% brain abscess are associated with paranasal sinuses: common in young males.
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6
Q

Paranasal sinusitis common pathogen

A

Streptoccoci, haemophilia Sapporo. Bacteriodes sap. Pseudomonas app. And staphylococcus aureus.

Dental infection:
1. Step staph Bacteriodes app, fusobacterium app.

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7
Q

Hematogenous spread: 25% of brain abscess

A

Predilection for the territory of the middle cerebral artery 9 posterior lobes

  • in the junction of gray and white matter and are poorly encapsulated.
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8
Q

Abscess due to complications of infective endocarditis: viridans streptococci or s. Aureus

A

Pyogenic lung infections such as lung abscess

  1. Streptococci
  2. staphylococci
  3. bacteriodes species
  4. fusobacterium
  5. enterobacteriaceae.

Head trauma: MRSA, s. Epidermidis, enerobacteriaceae, ppseudomonas app. Clostridium app.

Clostridium, and enterobacteriacea common with urinary sepsis.

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9
Q

Stages of brain abscess

A
  1. Early celebrities 9day 1-3)
  2. Late celebrities (4-9)
  3. early capsule formation (day 10-13)
  4. late capsule formation (day 14 and beyond)
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10
Q

Characterised by perivascular infiltration of inflammatory cells, surround a central core and coagulation necrosis. Marked edema surrounds the lesion at this stage.

A

Early celebrities

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11
Q

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.

A

Late stage celebrities.

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12
Q

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

A

Early capsule formation 9day (10-13)

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13
Q

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

A

Late capsule formation

Day 14-beyond)

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14
Q

Clinical prenration of abscess

A
  1. Headache
    2.fever
    3.focal neurological directives
    50% 0f cases.

Most common symptom: headache
-constant dull,aching, either hemicranial, or generalised

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15
Q

Clinical presentation of abscess

A
  1. Frontal lobe: hemiparesis
  2. Temporal lobe: disturbance of language (dysphasia) or upper homonymous quadratanopia
  3. Cerebellum abscess: nystagmus and ataxia
  4. Cerebellum; increase ICP
    Papilledema, nausea, vomiting, confusion and drowsiness
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16
Q

Treatment for brain abscess

A

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……..

17
Q

Medical therapy alone is reserved to patients with

A

Surgically inaccessible, small (<2-3cm) or nonencapsulated abscesses (cerebritis) and or patients whose condition is too tenuous to allow performance of the neurosurgical procedure.

18
Q

Duration for antibiotic therapy for brain abscess

A

6-8 weeks of parent earl antibiotic therapy…

19
Q

Prophylactic anticonvulsant therapy

A

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

20
Q

The most common parasitic disease of the CNS worldwide

A

Neurocystecercosisingestion of food contaminated with T. Sodium

21
Q

Acquired from ingestion of undercooked meat and from handling ca feces

A

Toxoplasmosis

22
Q

Clinical price notation of neurocysticercosis

A

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

23
Q

Manifestation of primary toxoplasmosis

A

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

24
Q

Treatment for focal CNS lesions

A

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

25
Q

Stages of cyst

A

Vesicular stage: cyst contains living larva

Colloidal stage: larva degenerates edema surrounds the lesion are treated with anticysticidal therapy

Granulomatous-modular stage: sorrounded by a contrast-enhancing ring
Calcified lesions

26
Q

Treatment for toxoplasmosis

A

Combination of sulfadiazine 1.5-2.0g orally aid plus pyrimethammine 100mg orally to load, ten 75-100mg orallyqd plus folk if acid 10-15mg orally qD

Folinic acid is added to prevent megaloblastic anemia.

Treatment ranges up to 6 weeks

And ten sulfadiazine is reduced to 2-4 grams/day and pyrimethamine tip 50mg/d

Alternative; Clin dams in plus pyrimethamine

27
Q

Pus between the ura and the arachnoid membrane

A

Subdural empyema

28
Q

A rare disorder that account for 15-25% focal suppurative CNS infections

  • sinusitis is the most common predisposing condition
  • affecting the frontal sinuses
  • re-election to young males
A

Subdural eempyma

29
Q

SDE most common complaint at time of presentation

A

Headache

Contralateral or hemiplegia: is the most common focal neurological deficit and can occur from the direct effects of the SDE on the cortex or as a consequence. Of venous infarction

Diagnosis: MRI is superior
CT scan: crescent-shaped hypodense lesion over one or both hemispheres or in the interhemispheric fissure.

LP not needed

30
Q

Treatment for Subdural empyema

A

Medical emergency
Emergent neurosurgical evacuation

empirical antimicrobial therapy: community acquired SDE combination of their generation cephalosporin 9cefotaxime or ceftriaxone) c=vancomycin and metronidazole

Hospital-acquired: MRSA or pseudomonas (meropenem) and vancomycin

Minimum 3-4 weeks after SDE drainage

31
Q

Less common than either brain abscess or SDE and accounts for <2% of focal suppurative CNS infections

A

Epidural abscess
Contagious to the area of osteomyelitis, frontal sinus, middle ear, mastoid or orbit can reach the epidural space through retrograde sprea of infection from septic thrombophlebitis in the emissary veins that drain areas or by direct spread through osteomyelitis

Epidural space: potential rather tan compartment

Dura: tightly adherent to inner skull table
-smaller than SDE

Staphylococci or gram negative organisms are the usual causes f an epidural abscess that develops as complications of craniotomy or compound skull fracture

32
Q

Bacterial meningitis is a common predisposing condition for the septic thrombosis of the superior Sagitta sinus

A

Cerebral veins and venous sinuses have no valves

Superior Sagitta sinus is the largest of the venous sinuses
: receive blood, from frontal, parietal,and occipital superior cerebral veins and the diploid veins and communicate with the meningieal veins.

33
Q

Superior Sagitta sinus: rains to the transverse sinuses

Middle and mastoid cells to the Sagitta sinus

Transverse sinus becomes sigmoid sinus before draining into the internal jugular vein

Septic transverse/sigmoid sinus thrombosis can be complications to acute and chronic otitis media or mastoiditis

From the emissary veins

A

Drains to the superior Sagitta sinus, provide a route for the spread of infection from meninges, especially in cases where there is purple to exudate near areas of the superior Sagitta sinus.

Cavernous sinus are inferior to the superior Sagittal sinus at the base of the skull.

  • receive blood from facial veins (sphenoid and ethmoid)
  • most common site for primary infection in septic cavernous sinus thrombosis.
34
Q

Clinical manifestation of septic thrombosis of the superior sagittal sinus

A

Headache, fever,nausea and vomiting, confusion and focal or generalised seizure

  • rapid development of stupor and coma
  • weakness of the lower extremities with bilateral Babinski
  • oculomotor, torchbearer,abducens , ophthalmic and maxillary branches of the trigeminal nerve and the internal carotid artery passs through the cavernous sinus
35
Q

Septic cavernous sinus

A

Fever, headache, rental, and retroorbital pain, and Diplopoda

Classic signs; ptosis,proptosis,chemists and extra ocular dysmotility, and Diplopoda
Due to cranial III, IV,VI hyper Esther’s is of the ophthalmic and maxillary division of the fifth cranial nerve and decrease corneal reflex may be detected

Dilated,tortuous retinal veins and papilleema

36
Q

Transverse sinus:

A

Headache and earache are the most frequent

Otitis media, sixth nerve palsy and reetroorbital or facial pain

Gradenigo’s syndrome

Sigmoid sinus and internal jugular vein thrombois: present wit neck pain

37
Q

Diagnosis of septic venous thrombosis

A

Suggested by an absent flow void within the affected venous sinus on RI and confirmed by MRI, CT angiogram or the venous phase of cerebral angiography

Cerebral angiography for definitive diagnosis.

38
Q

Treatment: suppurative thrombophlebitis

A

Septic venous sinus thrombosis is treated with antibiotic, hydration and removal of infected tissue and thrombus in septic lateral or cavernous sinus thrombosis

Duration of therapy is 6 months

Anticoagulation : is for aseptic venous sinus thrombosis and in the treatment of septic venous thrombosis complicating bacterial meningitis in patients who have progressive neurological deterioration despite antimicrobial therapy and intravenous fluids.