043 brain abscess

Brain Abscess

YOUMANS Chapter 43

Outline

• Epidemiology• Etiology• Initiation of infection• Stage of infection• Clinical finding• Diagnosis• Management

Epidemiology

• 0.3 -1.3 cases per 100,000 person• Male : Female 2:1• Median age 30-40 years– Otitic focus : < 20 Yrs , >40 Yrs– Paranasal sinus : 30 – 40 Yrs

• After cranial operation : 0.2 % of 1587 , 10 of 16540• Commonly in Immunocompromised : infected with HIV,

receiving chemotherapy for cancer, receiving immunosuppressive therapy after organ transplantation, or after prolonged use of corticosteroids.

Risk factor

• Pulmonary abnormality– Infection– AV fistula

• Congenital cyanotic heart disease• Bacterial endocarditis• Penetrating trauma• Chronic sinusitis or otitis media• AIDS

Pathogenesis

• Organism transmit– contiguous source of infection, 25-30 % of case– hematogenous dissemination 20-35% of cases– trauma

Pathogenesis• Contiguous source : middle ear, mastoid cells, paranasal sinuses• From purulent sinusitis : spread by osteomyelitis or by phlebitis

of emissary vein• Rare in infant because they lack aerated paranasal and mastoid

air cells• Localize of Contiguous source – Otitis media : temporal lobe or cerebellum– Paranasal sinusitis : frontal lobe– Sphenoid sinusitis(less common for sinusitis ) : temporal lobe, sella

turcica– Dental infection(most common molar) : frontal lobe

Pathogenesis

• Hematogenous dissemination : multiple, multiloculated abscesses, higher mortality rate

• Most common source in adult– Most common : pyogenic lung diseases (especially lung

abscess)– bronchiectasis – Empyema– cystic fibrosis– Skin infection, osteomyelitis, pelvic infections, and intra-

abdominal infections

Pathogenesis

• In children • Cyanotic congenital heart disease (tetralogy of Fallot)

because increase Hct and low PO2 provide and hypoxic environment suitable for abscess proliferation

• Right to left shunt• Streptococcal oral flora from oral dental procedure

Pathogenesis

• Trauma : open cranial fracture with dural breach or foreign body injury or as a sequela of neurosurgery

• Nosocomial brain abscess : halo pin insertion,after electrode insertion to localize seizure foci,and in malignant glioma patients treated by placement of Gliadel wafers in the tumor bed to release carmustine

Etiology• Bacterial : most common, streptococci (aerobic, anaerobic,

and microaerophilic), 70%• Streptococcus anginosus (milleri) : oral cavity, appendix,

and female genital tract• Staphylococcus aureus : cranial trauma or infective

endocarditis• Enteric gram-negative bacilli ,25-30% (e.g., Proteus spp.,

Escherichia coli, Klebsiellaspp., Pseudomonas aeruginosa, and Enterobacterspp.) : otitis media, bacteremia, neurosurgical procedures, and the immunocompromised state

• Negative culture : 0-43% (previous use ATB)• Listeria monocytogenesis uncommon (<1% of cases),

considered in patient who are immunocompromised (e.g., leukemia, lymphoma, HIV infection, and conditions requiring corticosteroids or other agents that cause immunosuppression)

• Salmonella, Nocardia, Streptococcus pneumoniae, Haemophilus influenzae, Burkholderia pseudomallei, and Actinomyces species

Etiology

Etiology

• the incidence of fungal brain abscess has been rising as a result of the increased use of corticosteroid therapy, broad-spectrum antimicrobial therapy, and immunosuppressive agents

• Candida : microabscesses, macroabscesses, noncaseating granulomas, and diffuse glial nodule

Etiology

• Risk factors for candidal brain abscess include the use of broad-spectrum antimicrobial agents, corticosteroids, and hyperalimentation; premature birth; malignancy; neutropenia; chronic granulomatous disease; diabetes mellitus; thermal injury; and the presence of a central venous catheter

• Aspergillosis : neutropenia, hepatic disease, diabetes mellitus, chronic granulomatous disease, Cushing’s syndrome, HIV infection, injection drug use, organ transplantation, and bone marrow transplantation

Etiology

• Mucorales group : Diabetes mellitus, patients with acidemia from profound systemic illness (e.g., sepsis, severe dehydration, severe diarrhea, chronic kidney disease)

• Scedosporium : immunocompetent and immunocompromised hosts

• Cryptococcus neoformans, the endemic mycoses (Coccidioides spp., Histoplasma spp., and Blastomyces dermatitidis)

Etiology

Initiation of infection

• The brain appears to be significantly more sensitive to infection than many other tissues.

• The brain may also be more susceptible to infection by different organisms

Stages of infection

Host defence mechanism

• Although the brain is generally protected from infection by an intact blood-brain barrier, once infection is established, immune defenses are usually inadequate to control the infection

• Encapsulate bacteria : E.coli, B.fragilis

Clinical finding

Clinical finding

• Newborn– Patent suture– Seizure– Meningitis– Irritabilitiy– Increasing OFC(occipital-frontal circumference)– Failure to thrive – May afebrile

Clinical finding

Clinical finding

• Intraventricular rupture of brain abscess : severe headaches and signs of meningeal irritation were prominent findings before rupture

• Intraventricular rupture appears to be more likely if the abscess is deep-seated, multiloculated, and in close proximity to the ventricular wall

Clinical finding

• Related to pathogen– Nocardia : concomitant pulmonary, skin, or muscle

lesions– Aspergillus brain abscess : commonly manifest signs of a

stroke syndrome as a result of ischemia or intracerebral hemorrhage, or both

– rhinocerebral mucormycosis : symptoms referable to the eyes or sinuses and complaints of headache, facial pain, diplopia, lacrimation, and nasal stuffiness or epistaxis cranial nerve involvement blindness

Clinical finding

• Related to pathogen– Scedosporium apiospermum brain abscess : • occur in immunocompromised patients or in

individuals 15 to 30 days after an episode of near-drowning• cerebrum, cerebellum, or brainstem• Clinical finding : seizures, altered consciousness,

headache, meningeal irritation, focal neurological deficits, abnormal behavior, and aphasi

Diagnosis

• WBC : mildly elevate (>10,000)• Blood C/S : should be obtain (usually negative)• ESR : may be normal• CRP : may arise• LP : dubious, OP increase, WBC count, Protein

elevate, risk for tantentorial herniation

Diagnosis• MRI is more sensitivity than CT, early detection of cerebritis,

more conspicuous spread of inflammation into the ventricles and subarachnoid space, and earlier detection of satellite lesions

• T1 : the abscess capsule often appears as a discrete rim that is isointense to mildly hyperintense

• T1 c Gad : rim enhancement, cerebral edema• T2 : zone of edema : hyperintensity, capsule : ill-defined

hypointensity• DWI : restricted diffusion (bright signal) may be seen• ADC : Dark

Diagnosis

Diagnosis

• Aspergillosis : finding of a cerebral infarct, which typically develops into either single or multiple abscesses, in immunocompromised patients, there may be little or no contrast enhancement on MRI

• Rhinocerebral mucormycosis : sinus opacification, erosion of bone, and obliteration of deep fascial planes; cavernous sinus thrombosis

Diagnosis

• stereotactic MRI- or CT-guided aspiration• Specimens sent for : Gram stain, routine aerobic

and anaerobic culture, modified acid-fast smears, acidfast smears and culture, and fungal smears and culture

• Aspergillus brain abscess : septate hyphae with acute-angle, dichotomous branching

• Mucormycosis : irregular hyphae with right-angle branching.

Diagnosis

Diagnosis

• Scedosporiumspecies are indistinguishable from those caused by Aspergillus species. The hyphae of dematiaceous fungi may be brownish on hematoxylin-eosin staining but are not distinguishable from those of other molds.

Management

• Multidisciplinary, neuroradiologist, neurosurgeon, and infectious disease specialist

• Larger than 2.5 cm : excision• Smaller than 2.5 cm : aspiration for definite diagnosis• Empirical ATB : metronidazole + third-generation

cephalosporin • S.aureus consider : add vancomycin• gram-negative bacilli such as P. aeruginosa :

ceftazidime, cefepime, or meropenem

Management

• no clear predisposing factors : combination of vancomycin, metronidazole, and a third- or fourth-generation cephalosporin

• Once the infecting pathogen is isolated, antimicrobial therapy can be modified for optimal treatment

Medical management alone

• Treatment began in cerebritis• Small lesion 0.8-2.5 cm• Duration of symptom < 2 Wk• Patient show clinical improvement in 1 wk

Surgical treatment

• Significant mass effect exerted by lesion• Difficult in diagnosis• Proximity to ventricle• Evedence of significane increase intracranial

pressure• Poor neurological condition• Traumatic abscees associated with foreign material• Fungal abscess

Management

Bacterial brain abscess• The principles of antimicrobial therapy for bacterial brain

abscess– penetrate the abscess cavity– in vitro activity against the isolated pathogen

• Metronidazole– excellent in vitro activity against strict anaerobes– an excellent pharmacokinetic profile– good oral absorption – penetration into brain abscess cavities– must always be used in combination with an agent effective

against streptococci

Bacterial brain abscess

• Vancomycin, The third generation cephalosporins are common used

• Imipenem : pyogenic and nocardial brain abscess, beware seizure

• Meropenem : Enterobacter cloacae

Bacterial brain abscess• Surgical therapy : aspiration after bur-hole placement or

complete excision after craniotomy• Stereotactic aspiration : eloquent or inaccessible regions• Complete excision by craniotomy

– patients with multiloculated abscesses in whom aspiration techniques have failed

– for abscesses containing gas– for abscesses that fail to resolve– posttraumatic abscesses that contain foreign bodies or

retained bone fragments to prevent recurrence


• In patients with intraventricular rupture of a purulent brain abscess : – rapid evacuation and débridement of the abscess cavity

via urgent craniotomy and ventricular drainage– intravenous or intrathecal ATB

• groups of patients may be treated with medical therapy alone– medical conditions that increase the risk associated with

surgery– multiple abscesses


• groups of patients may be treated with medical therapy alone– abscesses in a deep or dominant location– the presence of coexisting meningitis or ependymitis– early reduction of the abscess with clinical improvement

after antimicrobial therapy– abscess size less than 3 cm


• ATB optimal duration : 6-8 Wk IV then follow by oral ATB for 2-3 Mo

• Repeat neuroimaging studies performed biweekly for up to 3 months after completion of therapy has been suggested to monitor for reexpansion of the abscess or failure of resolution

Nocardial brain abscess

• Sulfonamide with or without trimethoprim is recommend

• Alternative agent : minocycline, imipenem, amikacin, third-generation cephalosporins, and linezolid

• In immunocompromised patients or those in whom therapy fails : combination treatment with regimens + a third-generation cephalosporin or imipenem + a sulfonamide or amikacin

Nocardial brain abscess

• Craniotomy with total excision is difficult in patients with Nocardia brain abscess because these abscesses are often multiloculated

• ATB duration : 3-12 Mo but in immunocompromised should be up to 1 Yr

Fungal brain abscess

• Candidal brain abscess : amphotericin B preparation plus 5-flucytosine

• Aspergillusbrain abscess : voricazole• CNS mucormycosis : amphotericin B deoxycholate

or a lipid formulation of amphotericin B with aggressive surgical debridment

• Scedosporiumspecies : surgery

Management

Adjunctive Therapy• Steroid effect

– Reduced edema– Decrese likehood of fibrous encapsulation– May be reduced penetration of antibiotic into abscess

• Corticosteroid use– edema and mass effect– progressive neurological deterioration– impending cerebral herniation

• High dose : dexamethasone 10 mg q 6 hr and then tapered

Cranial Subdural empyema and Epidural abscess

YOUMANS Chapter 43

Epidemiology and Etiology

• Cranial subdural empyema : collection of pus between the space of the dura and arachnoid, 15-20 % intracranial lesion

• Less common than brain abscess• SDE may be complicated by cerebral brain abcess,

cortical vein thrombosis, localized cerebritis• Location : 70-80 % convexity, 10-20% parafalcine


• most common predisposing conditions : otorhinologic infections, especially of the paranasal sinuses

• Other predisposing conditions : skull trauma, neurosurgical procedures, and infection of a preexisting subdural hematoma


• Organisms– aerobic streptococci (25% to 45%)– staphylococci (10% to 15%)– aerobic gram-negative bacilli (3% to 10%)– anaerobic streptococci– other anaerobes

• If the predisposing condition is postoperative or posttraumatics : staphylococci and aerobic gram-negative bacilli

Clinical finding

• Clinical manisfestation of subdural empyema– rapidly progressive, with symptoms and signs related to

increased intracranial pressure (headache, vomiting)– meningeal irritation– focal cortical inflammation (hemiparesis and hemiplegia,

ocular palsies, dysphasia, homonymous hemianopia, dilated pupils, and cerebellar signs

– Altered mental status– Seizure – Fever

Clinical finding

• Clinical manisfestation of cranial epidural abscess– Insidious onset– Abscess enlarge too slowly to produce a sudden onset of

major neurological deficits, as is seen in patients with cranial subdural empyema

– Most common : fever, headache– If the location of the epidural abscess is near the petrous

bone, Gradenigo’s syndrome may develop (involvement of cranial nerves V and VI and manifested clinically as unilateral facial pain and weakness of the lateral

rectus muscle)

Diagnosis

• Cranial subdural empyema should be suspected in any patient with meningeal signs and a focal neurological deficit

• CT brain : iv contrast : hypodense crescentric• LP : potential hazardous for herniation

Diagnosis

• MRI in Cranial subdural empyema : crescentic or elliptical area of hypointensity (on T1 images) below the cranial vault or adjacent to the falx cerebri, high signal on T2

• MRI in cranial epidural abscess : superficial, circumscribed area of diminished intensity with pachymeningeal enhancement.

Management ofCranial subdural empyema

• Cranial subdural empyema is a surgical emergency because antimicrobial therapy alone does not reliably sterilize the empyema

• The goals of surgical therapy are to achieve adequate decompression of the brain and to evacuate the empyema completely.

• The optimal surgical approach is controversial.


• Patients who underwent drainage via bur holes or craniectomy required more frequent operations to drain recurrent or remaining pus and exhibited higher mortality rates and worse outcomes

• Drainage via bur holes or craniectomy is therefore recommended only for– patients in septic shock, those with localized parafalcine

collections– children with subdural empyema secondary to meningitis

because there is usually no brain swelling and the pus is thin


• S. aureusis suspected : vancomycin• suspected anaerobes : metronidazole • aerobic gram-negative bacilli are suspected,

empirical : ceftazidime, cefepime, or meropenem• ATB continued for 3-4 wk after drainage


• ATB alone in – patients with cranial subdural empyema who have

minimal or no impairment of consciousness– no major neurological deficit– limited extension of the empyema with no

midline shift– early improvement with antimicrobial therapy

Management ofCranial epidural abscess

• combined medical and surgical approach• Empirical antimicrobial therapy is similar to that for

cranial subdural empyema• For surgical drainage, craniotomy or craniectomy

is generally preferred over bur-hole placement or aspiration of purulent material through the scalp

• ATN length 3-6 wk or longer in osteomyelitis

Thank you

043 brain abscess

Health & Medicine