PSEUDOMONAS AEROGINOSA CAUSE

ABCESS CEREBRI WITH CHRONIC OTITIS

MEDIA SUPPRATIVE IN A CHILD

Oleh:
Kadek Ayu Atrie S, dr.

Pembimbing:
Prof. Dr. Darto Suharsono, dr., SpA(K)
Prastya Indra Gunawan, dr., SpA

LAB/SMF ILMU KESEHATAN ANAK

 FAKULTAS KEDOKTERAN UNIVERSITAS
AIRLANGGA
RSU Dr. SOETOMO SURABAYA
2016

INTRODUCTION

Brain abscess is a serious, life threatening health problem in the

world due to its high morbidity rate, high mortality rate, and high costs rate.
Brain abscess can occur in all age groups but tends to occur in young age.
From all cases of brain abscess, children account for up to 25% of cases
and mostly in age 4-7 years old. In 1961-1977 Levine and De Souza
reported 50 patients with chronic suppurative otitis media (CSOM) who
suffered with intracranial complications. More than 50% of intracranial
complication were brain abscess with temporal lobe abscess 5 times more
frequent than cerebellum abscess. According to Austine, the highest
frequency of intracranial complications following chronic suppurative otitis
media are meningitis 34%, brain abscess 25% (15% temporal lobe and
1% cerebellum), labyrinthitis 12%, otitis hydrocephalus 12%, dural sinus
thrombosis 10%, extradural abscess 10%, and subdural abscess 1%. 1
Brain abscess caused by invasion of infectious microorganism to
the brain parenchyma. The spread of infectious microorganism from
contiguous focus of infection to the brain can happen through several
mechanism: direct spread of infection from a site contiguous to the brain,
via a hematogenous route, post skull trauma or surgery, and meningitis.
The location of primary infection can be predicted by knowing the location
of abscess in the brain. Chronic suppurative otitis media with
cholesteatoma or granulation tissue is the most common predisposing
condition of brain abscess. (E8/103171) Otogenic brain abscess is
intracerebral collection of pus due to complication of chronic suppurative
otitis media rather than acute otitis media. Otogenic brain abscess usually
occur following a malignant type of chronic suppurative otitis media.
Complication of otitis media can occur in acute phase of infection such as
acute otitis media or by destructive mechanism due to chronic activity of
bioenzym such as cholesteatoma. (the encyclope horton)
Computerized Tomography (CT) scan dan Magnetic
Resonance Imaging (MRI) are sensitive tools to diagnose brain abscess
accurately. With the availability of neuroimaging, morbidity and mortality
rate of brain abscess have been decreased drastically. Advances
technology in neuroimaging, blood culture, medical treatment, and surgical
treatment have improved outcome and decreased mortality rate. However,
brain abscess still a life threatening infection and leave a significant
permanent sequela such as epilepsy, sensorimotor deficits, cognitive
deficits, visual field loss, and hydrocephalus. (moscote, muzumdar)
The optimal treatment of brain abscess is complex and requires a
multidisciplinary approach from neurosurgeon, neurologist, an infectious
disease specialist, and neuroradiologist. This approach include use of
antibiotics, surgical intervention, neuroradiological evaluation, and
eradication of primary infected loci. (Brain abcess current management).
Broadspectrum antibiotics which can cross blood brain barier in adequate
concentration are recomended for initial therapy. Delay administration of
antibiotics is associated with proorer outcome in patient with brain
abscess. (shachor, brouwer)
The purpose of this paper is to present a case with abses cerebri
and chronic otitis media suppuratif maligna type focusing on diagnostic
and therapy approach.
CASE REPORT

A 12-year-old girl was referred to dr. Soetomo hospital from

sumenep hospital due to progressively worsening headache, right-sided
facial drop, slurred speech and altered mental status. Since June 28th
2016 she was suffered with headache, nausea, vomiting, and fever. She
was admitted at Sumenep hospital and treated with antibiotic,
dexamethasone, and ranitidine. After nine days of hospitalization without
any improvement, she was discharge against medical advice. She was
admitted again at Sumenep hospital on July 7th 2016 and then reffered to
dr. Soetomo hospital on July 21st 2016. From her past medical history we
found that she suffered with clear and foul smelling of discharge from both
of her ears since age of 7 years. Her left ear was responded well with
therapy from a public health service but her right ear continued to produce
purulent discharge with blood stained, foul smelling, and thick in
consistency. She visited another public health service and finally her right
ear responded to the treatment but since then the discharge from her right
ear was repeatedly returns.
She was born at 38 weeks of gestation via vaginal delivery by
midwife with a birth weight of 3100 gramm. Her mother was in healthy
condition, with no significant antenatal history. There was no history of
jaundice, cyanosis, or anemia. She was exclusively breast-fed until 1 year
of age and start to consume family food since 1 year of age. According to
the mother, her immunization was complete.
Physical examination on admission showed a girl with height 150
cm, weight 35 kg (body mass index 15.5 kg/m2), and head circumference
51 cm. She has a good nutritional status (weight for age at P10-25, height
for age at P25-50, BMI for age at P5-10, and head circumference at 0SD-
(-2SD). Her blood pressure was 100/70 mmHg, pulse was 78 bpm,
respiratory rate was 20 times per minute, and temperature was 37.40 C.
There was no anemic, icteric, and cyanosis noted. The thyroid gland was
not palpated.

Figure 1. Head Circumference Chart9

Source: Nellhaus G. Head circumference from birth to eighteen years. Practical
composite international
and interracial graphs. Pediatrics. 1968;41:106-14.

BMI P10

Body
Height
P 25-50

Body
Weight
at P25-50

Figure 2. Growth Chart10

 Source: CDC Growth Chart, 2000

From thorax examination we found symmetric chest, no accessory

muscles were being used, lungs are clear to percussion, the breath sound
was vesicular, no wheezing or rhonchi were present bilaterally, and no
murmur was found. The abdomen was flat and tender, liver and spleen
were not palpable, bowel sound was normal. The extremity was warm,
normal dorsalis pedis and posterior tibial pulses, and normal reflexes,
proprioception, vibration, and monofilament sensation.
Neurological examination revealed, an alert girl with normoreactive
isochoric pupils (3mm/3mm), no ptosis, no decreased of visual acuity, and
with peripheral facial nerve palsy. Meningeal signs were negative, bilateral
deep tendon reflexes were normal, pathological reflexes (babynski and
chaddock) were negative.
The initial complete blood count revealed leucocyte 11.630/cmm,
hemoglobin 13.3mg/dl, hematocrit 38.5%, and platelets 407.000/cm.
Erythrocyte sedimentation rate was increased (20mm/h) and CRP was
normal (2.56mg/dl). Creatinine serum and BUN were within normal limit
(0.53mg/dl and 10mg/dl respectively). Liver function test was normal
(SGOT 30U/l, SGPT 35U/l, albumin 3.73g/dl), blood sugar level was
106mg/dl, serum electrolyte within normal limit (calcium 9.6mg/dl, sodium
142mmol/l, potassium 5.2mmol/l, chloride 107mmol/l), APTT 28 seconds
(26.5), and PPT 10.3 seconds (10.9). Contrast enhance CT Scan revealed
a 4.1 x 2.6 x 2.5 cm lesion on the right hemispheres of cerebellum which
compressed the IV ventricle to the left causing constriction of the IV
ventricles suggestive to an abscess with non-communicating
hydrocephalus.
The patient was started with ceftriaxone 1500 mg twice daily,
metronidazole 225 mg twice daily, novalgin 300 mg three times daily, and
dexamethasone 5 mg three times daily. Formula feeding were given by
enteral feeding. Consultation were planned to Ophthalmology department,
ENT department, and neurosurgical department.
 From the ophthalmology department by direct ophthalmoscopy
revealed no papilledema which is one of the signs of increased intracranial
pressure. It can be concluded that the non-communicating hydrocephalus
was not associated with increasing in intracranial pressure.
The ENT department revealed granulation tissue and
mucopurulent secretions on the right ear. Tympanic membrane was
difficult to evaluate. She was diagnosed with chronic suppurative otitis
media type malignant. They suggest to do a CT scan focussing on
mastoid, treat the patient with tarivid ear drop, and planned for canal wall
down (CWD) mastoidectomy.
Consultation to neurosurgical department, based on CT scan
results, revealed ventricular dilatation indicating a non-communicating
hydrocephalus and cystic mass on infratemporal wall indicating a
cerebellar abscess. She was diagnosed with Non-communicating
hydrocephalus et causa suspected meningitis and cerebral abscess. No
medical treatment from neurosurgical department, but they planned to do
an abscess evacuation.
 Figure 3 : Head CT Scan

Consultation to neurosurgical department, based on CT scan

results, revealed ventricular dilatation indicating a non-communicating
hydrocephalus and cystic mass on infratemporal wall indicating a
cerebellar abscess. She was diagnosed with Non-communicating
hydrocephalus et causa suspected meningitis and cerebral abscess. No
medical treatment from neurosurgical department, but they planned to do
an abscess evacuation.
On the 3rd day of admission, patient still had headache and otorrhea
from her right ear. The treatment were added with mannitol loading dose
22.5 gram and maintenance dose 15 mg three times daily. The surgery
from both ENT and Neurosurgery department were planned in couple of
days.
On the 5th day of admission CWD mastoidectomy on the right ear
and cerebral abscess evacuation were done. Post-operation treatment
were oxygen mask 8 lpm, 30 0 head up, intravenous fluid D5 1/2 NS 1500
cc for 24 hours, ceftriaxone 1500 mg twice daily, metronidazole 225 mg
twice daily, novalgin 300 mg three times daily, dexamethasone 5 mg three
times daily, and mannitol 50 ml four times daily. Patients were admitted at
ROI GBPT for 3 days and then transferred to pediatric neurology ward.
She was alert and still had headache with stable vital signs.
On the 1st day post operation, patient not complaining about
headache anymore. Physical examination revealed a stable vital signs
(blood pressure 110/60, regular heart rate of 80 beats per minute,
respiratory rate 20 times per minute, and no fever). Peripheral facial nerve
palsy still present, normal thorax and abdominal examination. Laboratory
evaluation revealed hemoglobin 13 g/dL, hematocrit 36.7%, white blood
cell count 35030 /μL, platelet 68.900/µL, albumin 3.73 g/dl, potassium
5.2mmol/L, natrium 142 mmol/L, chloride 107 mmol/L, calcium 9.6 mg/dl.
We continue ceftriaxone 1500 mg twice daily, and injection metronidazole
225 mg twice daily for 42 days.
On the 5th day of post-operation, patient still has peripheral facial
nerve palsy with stable vital signs. We consult Physical medicine and
rehabilitation department and they suggested proper positioning,
mobilization, warm compress followed by circular massage on the right
face, facial muscle exercise with mirror, using an eye patch on the right
eye during sleep. After 5 days continue the treatment with with short wave
diathermy (SWD) at stylomastoid area and electrical stimulation on weak
facial muscles.
On 8th day post operation, blood culture resulted no growth on the
right side and positive for Staphylococcus hominis (gram-positive cocci
bacteria) on the left side. It was susceptible to gentamicin, tetracycline,
fosfomycin, daptomycin. Cholesteatoma culture resulted no growth for
anaerobic bacteria but positive for Pseudomonas aeruginosa (aerobic
gram-negative rod-shaped bacteria) and Enterococcus raffinosus (gram-
positive cocci), sensitive to astreonam, ceftazidine, cefoperazone
sulbactam, meropenem, ampicillin, penicillin G, tetracycline, daptomycin.
Bacterial culture from aspiration of brain abscess were negative.
On 15th day post operation, due to allergic reaction from ceftriaxon,
we replaced it with meropenem and she was given cetirizine 1x10 mg. On
33th day post operation, after she finished her 42 days antibiotic treatment
and stable vital signs, she was discharge.
Discussion

A 12-year-old girl was referred to dr. Soetomo hospital from

sumenep hospital due to progressively worsening headache, right-sided
facial drop, slurred speech and altered mental status. Since June 28th
2016 she was suffered with headache, nausea, vomiting, and fever. Her
left ear was responded well with therapy from a public health service but
her right ear continued to produce purulent discharge with blood stained,
foul smelling, and thick in consistency.
The presenting signs of brain abscess are variable and
nonspecific. Patients most commonly present with headache (49%-93%),
fever (14%-88%), altered mental status (33%-70%), focal neurologic
symptoms (29%-71%), and nausea and vomiting (26%-71%).2-7,9-16,24
Seizures are less common (2%-49%) and may have either focal or
generalized presentation. Rarely, brain abscess will present with status
epilepticus (0.3%).7 Neck stiffness and meningismus have been reported
(4%-23%).2,3,6,7,11,13-16 These symptoms may suggest a temporal or
cerebellar location6 but often occur in the context of a concomitant
meningitis or prior intraventricu- lar rupture. Papilledema should be sought
on physical exami- nation but is an insensitive sign (1%-19%).3,7,14,16
The classic clinical triad of fever, headache, and focal neurologic deficit is
suggestive of abscess, but recent reports indicate that this constellation
occurs in a minority of cases (2%-34%).6,10,11,13,14,16 (Bacterial Brain
Abscess Kevin Patel, MD1, and David B. Clifford, MD2)
Brain abscesses may be unicentric or multifocal. Majority, about
90% result from pericranial infection (sinusitis, mastoiditis, otitis media)
and many who are hematogenous borne (those from bacterial
endocarditis) are multifocal, especially from cyanotic congenital heart
disease. The clinical syndrome will be caused by the forces involved in the
host organism interaction, number and size and distribution of abscess,
specific brain structures involved and the neighbourhood anatomy
disturbances involving cisterns, ventricles, and the dural venous sinuses. A
pontine abscess may bulge posteriorly compressing the aqueduct of
sylvius causing obstructive hydrocephalus or an occipital abscess may
rupture into ventricle causing ventriculitis or ependymitis or it may cause
septic thrombophlebitis of the transverse sinus causing venous
hypertension, edema, seizures and raised intracranial pressure. Majority
of the abscesses were in the frontal, temporal and posterior fossa region.
(Brain abscess: An overview Dattatraya Muzumdar*, Sukhdeep Jhawar, A.
Goel Department of Neurosurgery, Seth Gordhandas Sunderdas Medical
College and King Edward VII Memorial Hospital, Mumbai, India)
From laboratory finding she had increasing white blood cell and
erythrocyte sedimentation rate. From Head CT Scan results seem
impressive ventricular dilatation hydrocephalus non communicans and
looked at the wall infratemporal cystic mass suggests a cerebral abscess.

Figure 4
Brain imaging is critical to diagnosis and management and is
critical to improving outlook for brain abscess. The early stages of
cerebritis are characterized on noncontrast computed tomography (CT) by
localized hypoattenuation. Contrast enhancement is variable in this stage

and when present may demonstrate a nodular or ring-like pattern. 27

(Bacterial Brain Abscess Kevin Patel, MD1, and David B. Clifford, MD2)
 Four stages of maturation of brain abscess have been recognized:
1) “early cerebritis” stage within the first 1 to 3 days with direct inoculation
of organisms into the brain, with focal areas of suppurative inflammation
appearing as a patchy or nonenhancing hypodensity/ intensity on CT or
MRI; 2) “late cerebritis” stage during days 4 to 9 with the early
development of a necrotic center, seen as edema and ring enhancement
on CT or MRI; 3) “early capsule” stage, with clear ring enhancing capsule
on neuroimaging; and finally 4) “late capsule” stage, with maturation of the
capsule that occurs about 2 weeks after development of the abscess.
(Diagnosis and Management of Brain Abscess and Subdural Empyema
Gary L. Bernardini, MD, PhD)

Figure 5. The characteristic ring-enhancement with marked

surround- ing edema suggests a mature abscess.
 Figure 6. Multiple ring-enhancing abscess lesions seen on
computed tomography scan of the head following intravenous contrast.

From laboratory reveal she had increasing white blood cell and
erythrocyte sedimentation rate. There is indicator he prevalence of serious
infections ranged from 4.5% to 29.3%. Tests were carried out for C
reactive protein (five studies), procalcitonin (three), erythrocyte
sedimentation rate (one), interleukins (two), white blood cell count (seven),
absolute neutrophil count (two), band count (three), and left shift (one).
(Diagnostic value of laboratory tests in identifying serious infections in
febrile children: systematic review)
Tabel 1. Differential diagnose abscess cerebral
Epidural empyema dan subdural empyema
Metastatic or primary brain tumors
Pyogenic meningitis
Subdural empyema represents loculated infection between the
outermost layer of meninges, and may occur either intracranially or in the
spinal canal. (Subdural Empyema John E. Greenlee, MD). Frontal sinusitis
was the most common cause, followed by postoperative infection,
meningitis, and trauma. Intracranial empyema resulting from
hematogenous spread developed in one patient with a long history of drug
abuse and a lung abscess. (Subdural Empyema: CT Findings1).
Manifestation clinic epidural empyema are headache, fever, photophobia,
neck pain (Sinogenic Intracranial Empyema in Children Noemi Adame,
MD*; Gary Hedlund, DO‡; and Carrie L. Byington, MD*)

Figure 7. Epidural Empyema CT Scan

Figure 8. Sudrural Empyema CT Scan

 Pyogenic meningitis, the signs and symptoms of raised intracranial
pressure are known to be unreliable, variable, unusual, and even absent,
fever, headache/ irritability, neck stiffness. A tense anterior fontanelle does
not show the extent to which the pressure is raised, 8 whereas direct
measurement is unequivocal, therefore if coma was present (to the extent
of failure to localise pain) a computed tomogram was performed to
determine if the basal cisterns were open and there was no space
occupation. (Cerebrospinal fluid pressure in pyogenicmeningitis R A
MINNS, H M ENGLEMAN, AND H STIRLING).
Brain tumors can cause either focal or generalized neurologic
symptoms. Generalized symptoms reflect increased intracranial pressure
and consist of head- ache and, when the illness is severe, nausea,
vomiting, and a sixth-nerve palsy. Focal symptoms and signs, such as
hemiparesis and aphasia, reflect the intracranial location of the tumor.
Other symptoms that reflect the location of the tumor, such as hemiparesis
or aphasia not associated with seizures, typically have a subacute onset
and are progressive. The exception is a visual-field deficit that may
develop progressively but that often goes unnoticed by the patient until it
contributes to an accident (frequently an automobile accident). The only
test needed to diagnose a brain tumor is cranial magnetic resonance
imaging (MRI). Computed tomography (CT) can miss structural lesions,
particularly in the posterior fossa, or nonenhancing tumors such as low-
grade gliomas. Therefore, if a brain tumor is a diagnostic consideration,
MRI with gadolinium enhancement is the test of choice; a normal contrast-
enhanced MRI scan essentially rules out the possibility of a brain tumor.
(BRAIN TUMORS LISA M. DEANGELIS, M.D.)
In our case had been evacuated abscess and CWD
mastoidectomy for cholesteatoma and granulation tissue in the mastoid.
And then we do examination culture from cholesteatoma and abscess.
Cholesteatoma culture resulted no growth for anaerobic bacteria but
positive for pseudomonas aeruginosa (aerobic gram-negative rod-shaped
bacteria) and enterococcus raffinosus (gram-positive cocci), sensitive to
astreonam, ceftazidine, cefoperazone sulbactam, meropenem, ampicillin,
penicillin G, tetracycline, daptomycin. Bacterial culture from aspiration of
brain abscess were negative.
Etiology can be identified in many cases, but the source of
infection remains unclear in a significant proportion of those with abscess
even after a thorough investigation.2,3,6-8,11,13,14,16,17 Brain
abscesses are often attributed to hematogenous spread, contiguous
spread, recent neurosurgical procedure, or penetrating head trauma.
Rarely, authors report bacterial meningitis as a source of hematogenous
spread.3,7 Hematogenous spread accounts for 9% to 43% of brain
abscesses.2,6,7,9-12,14 Contiguous infection may result from primary
dental, sinus, ear infections, or mastoiditis 2,3,6-16 and represents 14% to
58% proportion of brain abscess. Invasive neurosurgical procedures are a
known risk factor for development of brain abscess. They account for 3%
to 18% of brain abscess.2,3,7,8,11-15 (Bacterial Brain Abscess Kevin
Patel, MD1, and David B. Clifford, MD2)
Table2. Predisposing Conditions and Microbial Isolates in Patients with Brain
Abscess
Predisposing Condition Common Microbial Isolates

Immunocompromise

HIV infection Toxoplasma gondii, HIV infection Toxoplasma gondii,

nocardia and Mycobacterium
species, Listeria monocytogenes,
Cryptococcus neoformans
Neutropenia
Nocardia and Mycobacterium
species, Listeria monocytogenes,
Cryptococcus neoformans
Aerobic gram-negative bacilli,
Aspergillus species, Mucorales,
candida and Scedosporium species

Transplantation Aspergillus and Candida species,

Mucorales, Scedosporium species,
Enterobacteriaceae, Nocardia
species, T. gondii, Mycobacterium
tuberculosis

Contiguous spread of bacteria

Penetrating trauma or neurosurgery Staphylococcus aureus, S.

epidermidis, Streptococcus species
(anaerobic and aerobic),
 Enterobacteriaceae, Clostridium
species

Otitis media or mastoiditis Pseudomonas, Streptococcus

species (anaerobic and aerobic),
Bacteroides and Prevotella species,
Enterobacteriaceae

Paranasal sinusitis Streptococcus species (anaerobic

and aerobic), Bacteroides species,
Enterobacteriaceae, S. aureus,
Haemophilus species

Hematogenous spread of bacteria

Lung abscess, empyema, Fusobacterium, Actinomyces,

bronchiectasis Bacteroides, Prevotella, Nocardia,
Streptococcus species

Bacterial endocarditis S. aureus, Streptococcus species

Congenital heart disease Streptococcus and Haemophilus

species

Dental infection Mixed infection with Fusobacterium,

Prevotella, Actinomyces,
Bacteroides, and Streptococcus
species (anaerobic and aerobic)

(Brain Abscess Matthijs C. Brouwer, M.D., Ph.D., Allan R. Tunkel, M.D.,

Ph.D., Guy M. McKhann II, M.D., and Diederik van de Beek, M.D., Ph.D.)
Otogenic abscess is most often associated with Proteus,
Streptococcus milleri group organisms, and Streptococcus
pneumoniae.6,7,20 Mixed and negative cultures are more common in
otogenic abscess.12,20 Anaerobic organisms are isolated more frequently
in this population.16 Paranasal sinusitis is most often associated with
intracranial complications from Streptococcus sp, Staphylococcus sp, and
less commonly by the Enterobacteriaceae.7,26 Staphylococcus aureus,
Staphylococcus epidermidis, and Enterobacteriaceae (with Pseudomonas
aeruginosa being the most common pathogen in this group) are the most
common organisms found in abscess related to traumatic brain injury.
Similarly, S aureus, S epidermidis, P aeruginosa, and Propionibacterium
acnes are associated with abscess related to neurosurgical
procedure.8,12,13
The aerobic microorganisms most frequently isolated in chronic
suppurative otitis media are Pseudomonas aeruginosa (in 18-67% of
ears), Staphylococcus aureus (14-33%), Gram-negative organisms, such
as Proteus spp., Klebsiella spp., and Escherichia spp. (4-43%), and
Haemophilus influenzae (1-11%). The most frequently isolated anaerobic
organisms are Bacteroides spp. (1-91%) and Fusobacterium spp. (4-15%).
(Chronic suppurative otitis media: A review Monique Verhoeffa, Erwin L.
van der Veena, Maroeska M. Roversa,b,c, Elisabeth A.M. Sanders c, Anne
G.M. Schilder a,)
In our case from her past medical history we found that she
suffered with clear and foul smelling of discharge from both of her ears
since age of 7 years. Her left ear was responded well with therapy from a
public health service but her right ear continued to produce purulent
discharge with blood stained, foul smelling, and thick in consistency.
Chronic suppurative otitis media remains one of the most common
childhood chronic infectious diseases worldwide, affecting diverse racial
and cultural groups both in developing and industrialized countries. The
prevalence of chronic suppurative otitis media in Indonesia in general was
3.9%. It involves considerable morbidity and can cause extra and
intracranial complications. (Chronic suppurative otitis media: A review
Monique).
Chronic suppurative otitis media is persistent inflammation of the
middle ear or mastoid cavity. Synonyms include “chronic otitis media
(without effusion)”, chronic mastoiditis, and chronic tympa- nomastoiditis.
Chronic suppurative otitis media is characterised by recurrent or persistent
ear dis- charge (otorrhoea) over 2–6 weeks through a perforation of the
tympanic membrane. Typical findings may also include thickened granular
middle ear mucosa, mucosal polyps, and cholesteatoma within the middle
ear. Chronic suppurative otitis media is differentiated from chronic otitis
media with effusion, in which there is an intact tympanic membrane with
fluid in the middle ear but no active infection. Chronic suppurative otitis
media does not include chronic perforations of the eardrum that are dry, or
only occasionally discharge, and have no signs of active infection. Chronic
suppurative otitis media with cholesteatoma is not dealt with in this review.
Chronic suppurative otitis media is assumed to be a complication
of acute otitis media, but the risk factors for chronic suppurative otitis
media are not clear. Frequent upper respiratory tract infections and poor
socioeconomic conditions (overcrowded housing, [2] and poor hygiene
and nutrition) may be related to the development of chronic suppurative
otitis media. [3] [4] Improvement in housing, hygiene, and nutrition in Maori
children was associated with a halving of the prevalence of chronic
suppurative otitis media between 1978 and 1987. [5] See also acute otitis
media. The most com- monly isolated microorganisms are Pseudomonas
aeruginosa and Staphylococcus aureus; [6] P aeruginosa has been
particularly implicated in the causation of bony necrosis and mucosal
disease. However, a systematic review found no clear evidence that
antibiotics are effective in preventing the progression of acute to chronic
suppurative otitis media even among children who are at high risk for the
disease. [7] (Chronic suppurative otitis media)
Chronic suppurative otitis media is chronic inflammation of the
middle ear and mastoid mucosa in which the tympanic membrane is not
intact (perforation or tympanostomy tube) and discharge (otorrhea) is
present. There is, however, no consensus about the duration of the
symptoms. The World Health Organisation (WHO) defines chronic
suppurative otitis media as ‘‘otorrhea through a perforated tympanic
membrane present for at least 2 weeks’’, while others define ‘‘chronic’’ as
symptoms persisting for more than 6 weeks. (Chronic suppurative otitis
media: A review)
In our case, patient treated with ceftriaxone 1500 mg twice daily,
metronidazole 225 mg twice daily until 42 days, novalgin 300 mg three
times daily, dexamethasone 5 mg three times daily, and mannitol 50 ml
four times daily.
Medical management. Classically, penicillin G and chloram-
phenicol were the antimicrobials of choice in the treatment of abscess. The
emergence of antibiotic resistance and the development of agents with
improved tolerability have led to a shift in preferred agents over the past
several decades. A recent retrospective analysis based on a prospectively
designed antibiotic treatment protocol concluded that the com- bination of
cefotaxmine and metronidazole may be a safe and effective regimen for
empiric coverage. Parenteral antibiotics should be continued for a
minimum of 6 to 8 weeks. A shorter course of parenteral therapy, poten-
tially as short as 2 weeks, has been suggested; the data for this approach
are limited.5 (Bacterial Brain Abscess Kevin Patel, MD1, and David B.
Clifford, MD2)
Corticosteroid use in the management of brain abscesses is
controversial because steroids are known to inhibit the immune responses
that play a role in limiting brain abscesses. The use of steroids is generally
considered indicated when there is considerable mass effect secondary to
significant cerebral edema leading to neurological deficits and or
impending herniation. (Management of brain abscesses in children
JAMES L. FRAZIER, M.D., EDWARD S. AHN, M.D., AND GEORGE I.
JALLO, M.D. Department of Neurosurgery, Johns Hopkins University,
Baltimore, Maryland ) (Brain abscess: Current managementHernando
Alvis Miranda, Sandra Milena Castellar Leones, Mohammed Awad
Elzain1, Luis Rafael Moscote-Salazar2)
 SUMMARY
A case of chronic otitis suppurative media with abscess cerebral
has been reported. patient with chief complain of ear discharge since age
7 years. Right and left ear discharge is clear and odor. Left ear already
improve was taken for treatment but differences with right ear still have
viscous discharge, bloody and odor. She is go to public health service
already improved but still relapse. And then June 28, 2016 patients have
headache, nausea, vomiting and fever. On July 7, 2016 Increasingly
headache, asymmetric face, loss of speech and altered mental status.
From laboratory reveal LED 20mm/jam, leucocytosis 35.030/cmm. Results
from head CT Scan with contrast enhancement of lesion size of 4.1 x 2.6 x
2.5 cm on the right side of the hemispheres cerebelli urgent IV ventricle to
the left side, causing constriction of the ventricles IV leads to an overview
of infection (abscesses) and the non-communicating hydrocephalus.
Based on history taking, physical examination, and laboratory
examination, the baby assessed with chronic otitis suppurative media with
abscess cerebral. The patient was hospitalized in primarily of diagnostic
and therapy.
Chronic otitis media suppurtive chronic with type malignancy and
brain abscess treatment give antibiotic for 6 weeks. In this patient there
was neurological deficit in peripheral nerve 7.
1. Management of brain abscesses in children. Neurosurg Focus.
2008;24:1–10.