Q&A

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Question Anwser
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-History Taking :
We found altered consciousness, low grade fever 2 weeks, decrease appetite
-physical and neurogical examination
Buldging large fontanel
Right N VI palsy, increase physiologic reflex increase, clonus is positive
-support examination
We found from Head CT Scan : meningeal enhancement, infraction in basal ganglia, hydrocephalus
CSF analysis :
Color, appearance is colorness, clear, Nonne pandy is positive, count cell is 154, with dominan
mononuclear cell, glucose CSF and plasma ratio is less than 0.5%

Base on history taking, physical neurogival examination and support examination, we combine with
1. Dasar diagnosis marais score (or TBM score) is 14 so we diagnosed patient with meningitis tuberculous grade 2

Marais Score/TBM score patient :

Clinical criteria :
-symptom duration > 5 days (score 4), cranial nerve Vi right palsy (score 1), altered consciousness (score
1) ~ total score 6
Cerebrospinal fluid criteria :
Clear appearance (score 1), cell count 154/uL (score 1), Mononuclear predominance (score 1), CSF
glucose and plasma ratio < 50% (score 1) ~ totral score 4
Cerebral imaging criteria :
Hydrocephalus (score 1), basal meningeal enhancement (score 2), infract (score 1) ~ total score 4
Evidence of tuberculous elsewhere :
Radiograph suggestive TB (score 2)
1. Tuberculin skin test (Mantoux test): It may be nonreactive in 50% cases of CNS TB. Hence, it is
helpful in supporting the diagnosis of TBM when positive, but an isolated positive Mantoux cannot
be used to label a case of TBM as false positive/false negative reactions are commonly known.[11,12]
2. Chest X-ray: It helps to localize the signs of active TB but it may be normal in 20%–50% of the cases
of TBM.
3. Measurement of IFN-γ released by lymphocytes: It is a specific (70%–90%) test but with a low
sensitivity (50%–70%). It is available as enzyme-linked immunospot (ELISpot) and QuantiFERON
Gold for the diagnosis of latent TB. But currently, the use of these tests is restricted in the developing
What are another
countries because of the high cost.
2. diagnostic test in
4. Xpert MTB/RIF assay[13]: With a sensitivity of 67%–85% and a specificity of 94%–98%, it is a
TMB?
definitive diagnostic test that uses real-time polymerase chain reaction to amplify and detect M.
tuberculosis and identifies drug resistance. A meta-analysis of studies reported up to October 2011
estimated that Xpert MTB/RIF was 80.4% sensitive compared with culture. A study of Xpert
MTB/RIF in India for the diagnosis of extrapulmonary TB included 142 CSF samples and reported
that the assay was nearly 12 times more sensitive than microscopy. The cost of processing one Xpert
MTB/RIF test, however, was 82 times higher than the cost of microscopy. Larger studies to assess
Xpert MTB/RIF for the diagnosis of TBM are urgently needed. It may be used as an adjunctive test
for TBM.
3. Patient result X-pert With a sensitivity of 67%–85% and a specificity of 94%–98%, it is a definitive diagnostic test that uses
Mtb/Rif CSF negative, real-time polymerase chain reaction to amplify and detect M. tuberculosis and identifies drug resistance.
why u diagnosed A meta-analysis of studies reported up to October 2011 estimated that Xpert MTB/RIF was 80.4%
patient with Mtb? sensitive compared with culture.

but a negative Xpert result does not rule out tuberculosis disease, therefore clinicians should still consider
initiation of tuberculosis treatment in children with history and clinical features suggestive of tuberculosis
disease despite a negative Xpert result.
 sensitivity and specificity Xpert and microscopy in CSF of TBM patient?
Based on literature, in children with TBM, positive result of MTB microbiology from CSF was low, only
….%
Because of that literature, and less sensitive and specific from CSF microbiology, so for diagnostic
approach we used clinical sign and symptom, CSF analysis and also neuroimaging approach, and we have
some diagnostic criteria to establish TBM diagnosis in children such as Marais score.
  Basal meningeal enhancement75%
 Infarcts8%–44%
 Communicating hydrocephalus80%
Neuroimaging finding
4.  Tuberculomas8%–31%
in TBM
MRI has a higher sensitivity than a CT scan. A CT scan may itself be normal initially in almost 30% of
the cases. Hence, a normal neuroimaging initially does not rule out the possibility of TBM
The recommended daily doses of ATT include H 10 (7-15) mg/kg, R 15 (10-20) mg/kg, Z 35 (30-40)
mg/kg and E 20 (15-25) mg/kg  therapy TBM 2months RHZE with 10 months of RH regimen
5. Treatment TBM
H has good CSF penetration and can achieve CSF levels over 30 times the minimum inhibitory
concentration (MIC) of Mtb rapidly and use prednisone 2mg/kgbb for 4weeks,

Side effect
6. AntiTuberculousTerap
i

Risk Factor in the

7.
patient
8. Eficasy vaccine BCG 30-40%

Masa inkubasi TBC

9.
Walgreen TBC

From Walgreen TBC and incubation period for TBC infection. Hematogenous can occur in 3months after
primary infection of TBC, so we can conclude this patients has hematogenous phase of TB infections
around in 3months since first of symptom occur.
 A thick gelatinous exudate containing erythrocytes, neutrophils, macrophages and lymphocytes is formed
around the brain stem, sylvian fissures and basal cisterns, causing obstruction to the flow of CSF from the
cerebral aqueduct or fourth ventricle. Absorption of CSF is also interfered leading to raised intracranial
pressure (ICP) and hydrocephalus. The basal exudates may lead to periarteritis of the cerebral arteries
Mekanisme TTIK,
10. leading to infarction of the caudate nucleus and internal capsule. There may be oedema of the brain,
hydrocephalus
perivascular infiltration and inflammation of the blood vessel walls leading to narrowing or occlusion by
thrombi resulting in infarcts in the distribution of the medial striate and thalamic perforating arteries

 dipersingkat lagi aja mas jadi 1-2kalimat yg jelas

Immediate
 Electrolyte disturbances: Hyponatremia is the most common (35%–65% cases). This can be due to
cerebral salt wasting/syndrome of inappropriate secretion of anti-diuretic hormone (ADH)/increased
renal sensitivity to ADH.
 Seizures: Almost 50% of children present with seizures. They may be focal or generalized tonic–
clonic depending on the underlying CNS involvement. Phenytoin remains the most common
antiepileptic drug of choice. Others including valproate should be avoided due to increased risk of
hepatotoxicity. Other antiepileptic drugs may affect the metabolism of ATT drugs as well.
 Raised intracranial tension: Should be closely monitored for the same, with anti-raised intracranial
pressure measures.
 Vasculitis: May develop due to cerebral vasospasm or inflammation of meninges or obliterative
vasculopathy. The distal internal carotid artery, proximal middle cerebral artery, and its perforating
branches remain the most common sites involved. Corticosteroids because of their anti-inflammatory
role have been used widely. But recent studies suggested that corticosteroids do not significantly affect
the number of new infarcts or the extent of residual hemiplegia in children or adults. Only aspirin
might reduce the incidence of stroke, but this effect still needs to be confirmed in larger studies.[19,20]
Short term
 Hydrocephalus: Almost 80% of cases of TBM present with hydrocephalus, communicating being
more common than the noncommunicating type. Most cases can be managed medically using
acetazolamide and furosemide. But a failed medical treatment warrants surgery and
ventriculoperitoneal (VP) shunting. As hydrocephalus can be present in a case of pyogenic meningitis
Komplikasi selama as well, the possibility of that must also be considered
11.  Cranial nerve palsy
perawatan
 Diabetes insipidus
 Raised intracranial tension
Long term
 Cognitive disability
 Epilepsy
 Stroke
 Hydrocephalus
 Myeloradiculopathy
 Hypothalamic involvement: obesity, precocious puberty, diabetes insipidus, Frohlich syndrome, and
growth retardation
Sequelae
 Cognitive defects/intellectual disability
 Emotional effects: unhappy and moody, short-tempered, obstinate, and aggressive
 Physical limitations
 Headache
 Epilepsy
 Neurological deficit
 Behavior problems
 Drooling
 Blindness
 Deafness
 10 criteria for a healthy home according to the Ministry of Health:
1. Building materials are not made from materials that release dangerous substances such as asbestos,
dust, lead. And it is not made from materials that harbor pathogenic microorganisms
2. Components and layout of the house: the floor is waterproof and easy to clean. The room walls have
good air ventilation. The bathroom walls are watertight, the roof of the house is at least 10 meters high,
the division of rooms is appropriate to function and capacity. The kitchen has a smoke exhaust pipe
3. Room occupancy density: min 8m2, max capacity 2 people, except children <5 years old
12. Criteria Healthy Home
4. Lighting: either natural or man-made, intensity 60 lux
5. Air quality: temperature 18-30C pay attention to air exchange, air humidity
6. Ventilation: min 10% of floor area
7. Water quality: min capacity 60 L/day/person, suitable for drinking
8. There is a food storage area so that it is hygienic
9. Have regulation and management of household waste (solid and liquid)
10. No disease-transmitting animals (cockroaches, rats, maggots)
Indicator :
 95% reduction by 2035 in number of TB deaths compared with 2015.
 90% reduction by 2035 in TB incidence rate compared with 2015.
 Zero TB-affected families facing catastrophic costs due to TB by 2035.

Pillar and Components :

 Integrated, patient-centred care and prevention
o Early diagnosis of tuberculosis including universal drug-susceptibility testing, and systematic
screening of contacts and high-risk groups.
o Treatment of all people with tuberculosis including drug-resistant tuberculosis, and patient support.
Global End Pilar o Collaborative tuberculosis/HIV activities, and management of co-morbidities.
13.
Strategy TB o Preventive treatment of persons at high risk, and vaccination against tuberculosis.
 Bold policies and supportive systems
o Political commitment with adequate resources for tuberculosis care and prevention.
o Engagement of communities, civil society organizations, and public and private care providers.
o Universal health coverage policy, and regulatory frameworks for case notification, vital registration,
quality and rational use of medicines, and infection control.
o Social protection, poverty alleviation and actions on other determinants of tuberculosis.
 Intensified research and innovation
o Discovery, development and rapid uptake of new tools, interventions and strategies.
o Research to optimize implementation and impact, and promote innovations.
Tuberculosis prevention in Indonesia 2020-2024 will be implemented in six ways strategy, namely:
• Strategy 1. Strengthening central government commitment and leadership, provinces, and districts/cities
to support accelerated elimination tuberculosis 2030.
• Strategy 2. Increase access to quality and supportive tuberculosis services patient.
• Strategy 3. Optimizing promotional and prevention efforts, giving tuberculosis prevention treatment and
infection control.
• Strategy 4. Utilization of research results and screening, diagnosis and technology Tuberculosis
Strategy National End management.
14.
TB • Strategy 5. Increase the participation of communities, partners and other multi-sectors in the elimination
of tuberculosis.
• Strategy 6. Strengthening program management through system strengthening health.
The six strategies above consist of three functional strategies and three enabling strategies. Functional
strategies (Strategies 2,3,5) are technical strategies that focus on intervention areas: case finding,
treatment, and prevention. Enabling strategy (Strategy 1,4,6) is a strategy that focuses on contextual

factors that can become a leverage for achieving functional strategies .

15. TPT

Different Diagnosis
16
Anemia

16 Criteria Anemia WHO

7 for child

18. Criteria General GENERAL CONDITION CRITERIA (Keadaan Umum) OF THE PATIENT.
Condition of patient A.Fully alert, consist of :
-Conscious/ compos Mentis
-Vital signs/ stable
-Fulfill independent needs
B.Moderatelly ill. Have at least 3 (three) points below:Consists of:
-Conscious to Apathy
-Vital signs stable
-Requires medical procedure & injury/wounds at least 3x/day
-Requires observation
-Fulfillment of needs assisted
C. Severely ill. Have at least 2 (two) points below Consists of:
-Full awareness to somnolence
-Vital signs are unstable
-Using vital organ aids (such as ventilator)
 -Requires intensive care
-Requires close observation
-Fulfillment of needs assisted entirely

Vasogenic cerebral edema, the most common form, results from the disruption of the blood-brain-
19. Edema Cerebrii barrier. With the disrupted blood-brain-barrier ions and proteins flow more freely into the extravascular
space which causes osmotic draw of fluid into the brain interstitium. For example, vascular endothelial
growth factor (VEGF), glutamate, and leukotrienes produced locally increase the permeability of vessels
around tumors.[4] These factors and a lack of tight endothelial cell junctions in the vessels around the
tumors cause this increased permeability, which allows for an influx of proteinaceous solute and fluid into
the brain parenchyma, particularly in the white matter.[5] Peritumor edema, for example, leads to 65% of
patients developing cognitive impairment resulting from displacement and damage to white matter tracts.
[6]
Cellular or cytotoxic edema often results within minutes of the insult/injury and affects glial, neuronal,
and endothelial cells within the brain. In cytotoxic edema, the cells lack hemostatic mechanisms, and
primarily sodium enters the cell freely, with the failure of the export mechanism. Anions then follow,
attempting to return neutrality to the cell, resulting in intracellular edema as the cells swell with increased
water following the ions into the intracellular compartment.[7] Traumatic brain injury and stroke cause
this form of edema.
Interstitial cerebral edema results from the outflow of cerebrospinal fluid from the intraventricular space
to the interstitial areas of the brain. Patients with hydrocephalus or meningitis are examples of
those affected by this etiology. The increased pressure, against the cerebrospinal fluid (CSF) and brain,
drives fluid into the brain parenchyma. The fluid accumulates in the extracellular space of mostly the
white matter causing the cerebral edema.
Symptoms appear as the intracranial pressure (ICP) rises above 20 cm H2O in most patients. Treatment
for cerebral edema targets the underlying cause and any life-threatening complications. Treatments
include hyperventilation, osmotherapy, diuretics, corticosteroids, and surgical decompression .

Why choice mannitol Because mannitol can improve and increase cerebral perfusion pressure in patients with cerebral edema,
20. in the patient, didn’t patients also tend to have high sodium levels and Hyperosmolar saline is chosen in patients with
choice HS hypovolume and hyponatremia.
 Head up or Head up 15-30 : cerebral perfusin pressure increase, and promote cerebral venous drainage
21. Oxygen Oxygen suplementation : for ensure saturation oxygen of more than 90% and prevent hypoxia in patient
suplementation with cerebral edama
1. Hernia Subfalcine
2. Hernia Tentorial Lateral or uncal
22. Herniasi Otak
3. Hernia Tentorial Central or axial
4.Tonsiller

Cerebral Salt Wasting

23.
(CSW) dan SIADH