CASE OF INFECTION JUNE 2020

BRAIN ABSCESS
Presented by
KASMAWATI AMIN
C155182001

Supervisor
Dr.dr.JUMRAINI TAMMASSE, Sp.S(K)

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 REGISTRATION

 Name : Mrs.S
 Date of birth : 9 t h august 1965
 Age : 54 years old
 Address : North Konawe
 Phone number : 085342426082
 Medical record : 904196
 Date of addmision : 10 t h December 2019
 Date of discharged : 30 t h December 2019
 Hospital : Wahidin sudirohusodo

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 HISTORY OF DISEASE

Nausea -Experienced
and since ± 2
Weakness vomiting months before
in all four being
limbs hospitalized
A history of
TB Chief -slowly
treatment complaint: -like depressed
exists,
treatment
headache
is not A history of Often
complete diabetes forgetful
mellitus, no
regular
treatment

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 PHYSICAL EXAMINATION

Generalist Status
Blood pressure : 110/70 mmHg
Heart rate : 93 beats/minute, regularly
Respiratory rate : 20 times/minute
Temperature : 37 º celcius
NPRS :8

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NEUROLOGICAL STATUS

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 LABORATORY (2019/12/10)

SUPPORTING EXAMINATION
WBC 14.900 4.000-10.000/uL

RBC 3.490.000 4.000.000-6.000.000/uL

HGB 10,4 12,0-16,0 g/dl

PLT 459.000 150.000-400.000/uL

HCT 31,7 37,0-47,0%

GDS 109 140 mg/dl

Ureum 42 10-50 mg/dl

Kreatinin 0,32 L(<1,3);P(<1,1) mg/dl

SGOT 32 <38 U/L

SGPT 32 <41 U/L

Natrium 135 136-145 mmol/l

Kalium 3,7 3,5-5,1 mmol/l

Clorida 104 97-111 mmol/l

Anti HIV Non reactive Non reactive 6

 SUPPORTING EXAMINATION

LABORATORY (2019/12/12)

HbA1c 6,9 4-6%

GDP 137 110 mg/dl

GD2PP 151 <200 mg/dl

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 MICROBIOLOGY EXAMINATION (2019/12/11)
GRAM COLORING
SPECIMEN SPUTUM
Gram affinity Gram positive & gram negative Not found

Shape and configuration Paired coccus and single bacil Not found

Quantity Positive (2+) and positive (3+) Not found

Localization - Not found

Other cells Leukocytes(2+) and epithelial cells (3+) Not found

Fungus Spores and hypha Not found

FUNGUS
Specimen type Sputum -
Fungus Spores and hypha Not found
(17/12/2019)
SPUTUM BTA 3X (COLORING)
Specimen type Sputum -
BTA 1 coloring Negative Negative
BTA 2 coloring Negative Negative
BTA 3 coloring Negative Negative
     
Detection of micobacterium TB Not detected Not detected

Inspection method Automatic

2019/12/17) -

Specimen type Blood -

Culture and sensitivity No aerob bacterial growth - 8

 ELECTROCARDIOGRAPHY

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Conclusion : normoaxis, sinus rhytm HR 83 bpm
THORAX X-RAY

2019/12/04, BAHTERAMAS HOSPITAL

 Cor : the right border of the heart is

closed cloaking
 Lung : looks infiltrate in the right
parahilar
 right phrenicocostalis sinus closed
cloaking, left sharp
conclusion :
-bronchopneumonia suspicious of a
specific process DD/dextra lung
abscess
-right pleural effusion

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CT SCANS BRAIN WITHOUT CONTRAST
2019/12/05, BAHTERAMAS HOSPITAL

Conclusion :
-multiple thick wall cavities
suspected of multiple cerebral
abscesses,
DD/neurocysticercosis
-hyperdense lesions (57 HU)
tubular shape with a size of
about 2x0.7 cm in the left lateral
periventricular area posterior
cornu
-cerebri edema
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MRI BRAIN WITH CONTRAST
(2019/12/17)
-multiple isointense lesions in the stinging T1WI
post contrast with ring enhancing images, firm
boundaries, irregular surfaces and hyperintense
in T2WI and FLAIR in both cerebral
hemispheres
-sulci and gyri are normal
-the interhemispheric fissure position appears
normal in the midline
-subarachnoid space and ventricular system are
within normal limits
-pons and cerebellum are within normal limits
-the oculi bulb and the retrobulbar structure that
are detected are within normal limits
-the bones are intact
Conclusion :
multiple nodules in the bilateral cerebral
hemisphere support a cerebral abscess
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14
MSCT THORAX WITHOUT CONTRAST
(2019/12/17)

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 MSCT THORAX WITHOUT CONTRAST

 visible cavity bounded firmly, thick-walled, irregular edges, non-

calcified with air fluid level inside - / + 3,8x4,2x3,9 cm in contrast
to the wall in the posterolaterobasal segment of the right lung
inferior lobe
 trachea in midline
 brochus within normal limits
 there was no bilateral enlargement of the paratrachea, subcarina
and peribronchial lymph nodes
 cor : not enlarged, aortic calcification. Other large blood vessels
within normal limits
 visible fluid density in the right pleural cavity
 liver, gastric and splenic lesions are within normal limits
 the bones are intact
Conclusion :
-right pulmo abscess
-dekstra pleural effusion 16
 DIAGNOSIS

Clinical diagnosis : Acute cephalgia +

Tetraparese flaccid + Multiple cranial nerve
palsy

Topis diagnosis : Hemisfer Cerebri Bilateral

Etiological diagnosis : Multiple Cerebral

Abscesses

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 MANAGEMENT

Infus natrium chlorida 0,9% 20 drops per minute

 1.Citicoline 500mg/12hours/IV
 2.Dexametasone 10 mg loading dose continue it to 5 mg/6
hours/IV (tapp off/3 day)
 3.Omeprazole 40mg/24 hours/IV
 4.Mecobalamin 500 mcq/24 hours/IV
 5.Ceftriaxone 2 gr/12 hours/IV
 6.Metronidazole 500 mg/8 hours/IV
 7. Ketorolac 30 mg/ekstra/IV

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FOLLOW UP

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FOLLOW UP

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FOLLOW UP

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FOLLOW UP

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DISCUSSION

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 DEFINITION

-Cerebral abscess is a focal intracerebral infection

that starts as localized cerebritis and develops into a
collection of pus surrounded by capsules .
- Cerebral abscess is a life-threatening infectious
disease.
- Epidemiology :Male > female 3 : 1, aged around 38-
78 years with a death rate of 55%

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 CLINICAL MANIFESTATION

 Systemic : subfebril fever or no fever, <50% of cases

 General cerebral : often associated with intracranial pressure,
that is:
-Progressive chronic headache (>50%)
-Nausea, vomit
-Loss of conciousness
-Papillary edema
 Focal cerebral :
-Seizure, often general (40%)
-Change in mental status (50%)
-Motor focal neurological deficit, sensory, cranial nerve (50%)

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 PATHOGENESIS

Direct extension of infection contact (25-

50%):derived from sinuses, teeth, middle ear or
mastoid.
Hematogenous (30%): derived from the focus of
distant infections such as bacterial endocarditis,
primary pulmonary and pleural infections. Often
produces multiple cerebral abscesses.
Head trauma and neurosurgical procedures involving
dura and leptomeningeal(10%).
Criptogenic (30%) there was no clear source of
infection.

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 PATHOLOGY
Early cerebritis
(day 1-day 3)
-formation of a center of necrosis
-inflammation cells
-the limit of edema is difficult to
determine
The early capsule stage
(day 10-day 13)
-resolution of cerebritis areas
-necrotic area shrinkage
-begin to form capsules that
surround the lesion
Late cerebritis
(day 4-day 9)
-characterized by fibroblasts and
neovascular enhancement at the
edge of the necrotic region
The late capsule stage
(≥ day 14)
-Necrotic central areas are
increasingly clearly formed
surrounded by inflammatory
regions, collagen tissue and
neovascular layers
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The possible location and location of microbial flora of cerebral abscesses based on the
source of infection
No. Source of infection Location of abscess Main pathogen
1. Paranasal sinuses Frontal lobe Streptococci, Staphylococcus
aureus, Haemophillus sp,
Bacteroides sp
2. Autogenic infection Temporal lobe, Streptococci, Bacteroides sp,
cerebellum Enterobacterial (Proteus sp),
Pseudomonas sp,
Haemophilus sp
3. Odontogenic infection Frontal lobe Streptococci, Staphilococci,
Bacteroides, Actinobacillus
sp
4. Bacterial endocarditis usually multiple Staphylococcus aureus,
abscesses, which can be Streptococcus viridans
in any lobe
5. Pulmonary infection usually multiple Streptococci, Staphilococci,
(abscess, emphyema, abscesses, which can be Bacteroides, Actinobacilus sp
bronchiectasis) in any lobe
6. Right to the left shunt usually multiple Streptococcus,
(cyanotic heart disease, abscesses, which can be Staphylococcus,
pulmonary AVM) in any lobe Peptostreptococcus sp.
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No. Source of infection Location of abscess Main pathogen
7. Penetrating or Depends on location Staphyilococcus aureus,
postoperative trauma Staphylococcus epidermidis,
Streptococus, Enterobacter,
Clostridium sp.
8. Patients with Often multiple Aspergilus sp,
immunosuppression abscesses, which can be Peptostreptococcus sp,
in any lobe Bacteroides sp, Haemophilus
sp, Staphylococcus.
9. Patients with AIDS Often multiple Toxoplasma gondii,
abscesses, which can be Criptococcus neoforman,
in any lobe Listeria, Mycobacterium sp,
Candida, Aspergilus.

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 SUPPORTING EXAMINATION

Laboratory
 Leukocytosis PMN or usually within normal, ↑ LED
 Positive blood cultures → only 30% of cases, cultures from
other tissues that are thought to be the focus.
 Lumbar puncture is not recommended, results are less
specific, danger of herniation
Radiological examination
- CT scan (without and with contrast) : is the quickest and
cheapest investigation to confirm diagnosis and plan treatment
→ “ring enhancement
- MRI is more sensitive because it is seen in early phase of
infection and lesion in fossa posterior.

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 A. CT scan without contrast showing a mass lesion in the frontal
region at the white-Gray Matter border surrounded by vasogenic
edema.
B. MRI T2
C. MRI T1 post contrast showing picture enhancement ring
 
 
MODUL NEUROINFEKSI 2019 32
 TREATMENT

 Must overcome cerebral edema and treatment of local primary

infections :
 antibiotics are given immediately, both with and without surgery
and blood samples have been taken.
 Empirical antibiotic therapy must have a broad spectrum, 6-8
weeks or depending on clinical conditions.
 cerebral abscesses that are likely community-based are suggested
by generation III cephalosporin antibiotics
 Surgical excision of the abscess (craniotomy and excision)
Medical therapy alone without operative action is considered in
conditions such as:
 single abscess, size less than 2 cm
 multiple abscesses or sites that are difficult to reach
 critical state, in the final stages

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 MODUL
NEUROINFEKSI 35
2019
Brain abscess handling
algorithm

MODUL NEUROINFEKSI
2019

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 PROGNOSIS

-The prognosis of cerebral abscess is influenced by the

virulence of the organism, the patient's age, comorbid
conditions, neurologic and precisely therapeutic.
-As management improves, survival rates for cerebral
abscesses improve. Good prognosis is determined by:
young age
no neurological deficit or loss of consciousness at
the onset of the disease
comorbid diseases are not found

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THANK
YOU
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