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Case Febris convulsion+KP
Case Febris convulsion+KP
Presented by:
Agus Heriyanto
0110028
Counselor:
H. Tisna Sukarna, dr, SpA, MBA.
DEPARTMENT OF PEDIATRIC
MEDICAL FACULTY
MARANATHA CHRISTIAN UNIVERSITY
BANDUNG
2006
0
I. Patient Identification
1
II. Anamnesis
2.1. Heteroanamnesis was given by her mother on May, 19th 2006
2
2.2. Birth History
The patient is the 3rd child from 4 children. No stillbirth and no abortus.
Birth: aterm, spontaneous, directly cry and helped by a traditional (paraji).
Birth weight: 4200 grams. Birth length: 50 cm.
Turn over : 6 months
Sitting down with aid : 8 months
Sitting down without aid : 9 months
Standing up : 11 months
Walking : 14 months
Read : 4 years
Writing : 5 years
2.5. Immunizations
Booster Recommended
Vaccine Basic Vaccination
Vaccination Vaccination
BCG + (scar + ) - - - HiB : none
Polio + + + - - - MMR : none
DPT + + + - - - Hep A : none
Hep B + + + - - - Varicella : none
Measles + - - - Typhim/typha : none
Influenzae : none
2.6. Nutrition and Feeding
0 –6 months : breast feeding on demand
6 months-2 years : breast feeding and Vitalac
2 years- now : family menu
3
2.7. Past Illnesses
Typhoid when she was 5 years old.
Chronic cough with fever since 3 months ago
3.3. Measuring
Age : 8 years old
Weight : 30 kg
Height : 131 cm
( 111% standard Weight/Age )
( 95,3 % standard Height/Age )
( 108% standard Weight/Height )
Nutrition status : good (standard Weight/Height )
Circumference of the head : 52,5 cm
Circumference of the chest : 63,5 cm
Circumference of the abdomen : 61 cm
Circumference of the upper arms : 20 cm
4
IV. Systematic examinations
4.1. Skin : icteric - , pale -, cyanosis -, skin’s turgor was immediately returns to its
normal position
4.2. Head
Small Fontanel: closed
Hair : black, disseminated, not easy to yanked out
Eyes : conjunctiva anemic -/-, sclera icteric -/-,light reflek +/+
Nose : nasal flare -/-, secrets -/-
Ears : symmetric, left was equal to right, no discharge
Lips : wet, anemic -, cyanosis -
Mouth : wet mucosa
Gums : no bleeding, no hyperemic, no hypertrophy
Palate : no disparity
Tongue : coated tongue -, wet
Pharynx : hyperemic -
Tonsil : hyperemic -, T0 = T0
4.3. Neck
Nuchal rigidity : +
JVP : 5+0 cmH2O
Lymph node : not palpable
4.4. Thorax
Lungs
Inspection : shape and movement was symmetric, right was equal to left,
retractions (intercostal, suprasternal, epigastrium) -
Palpation : vocal fremitus right was equal to left
Auscultation : vesicular breath sound +/+, rales -/-, wheezing -/-
Heart
Inspections : ictus cordis was not seen
Palpations : ictus cordis was palpable at ICS 4 linea midclavicularis
5
sinistra
Percussions : normal
Auscultations : heart sounds regular, shuffle -
4.5. Abdomen:
Inspections : flat
Auscultations : bowel sound (+) normal
Percussions : tympanic, Traube’s space: tympanic
Palpations : Soepel, tenderness (-),
Liver impalpable
Spleen impalpable,
Kidney impalpable
V. Laboratory finding
16/05/2006 03.15
Hb : 12,9 gr/dl
6
Ht : 39 %
Leukocyte : 15.500 / mm3
Thrombocyte : 310.000 / mm3
Thorax photo: specific process still active
16/05/2006 12.27
Hb : 12,4 gr/dl
Ht : 39 %
Leukocyte : 13.400 / mm3
Thrombocyte : 305.000 / mm3
IgM and IgG anti dengue negative
PPD tes ++
17/05/206
Rapid ICT TBC POSITIVE
Widal
Titer O Titer H
Typhoid 1/20 -
Paratyphoid A - -
Paratyphoid B - -
Paratyphoid C - -
VI. Resume
7
She also had fever for 1 weeks, that was raising slowly, gradually. Fever
was gone after patient went to doctor. The fever came along with cough, however it
was cough without mucous.
She also had headache, during seizure, patient was temporarily half-
parallyzed (right of the body) and patient’s lip also temporarily turned blue. Patient
gradually got well afterwards
Mictie: the color is yellow; there is no blood, normal in frequency and volume,
with no pain.
Past medical history: chronic cough with fever for 3 months, felt down and the right
hand(wrist) movement is relatively limited, seizure -
Record of family health: his family denied got sick like this.
Medical effort : The patient was went to Bina Sehat before come to Immanuel
hospital because of the convultion, and had been given Stesolid,
Oxygen, and NaCl, and delivered to Immanuel hospital for next
treatment.
Vital signs
Pulse : 100 times a minute, fast, equal, weak
Respiration : 40 times a minute, abdominothoracal type
Temperature : 37,8 ºC, axiler
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Lips : wet, anemic -, cyanosis -
Mouth : wet mucous
Thorax
Heart : In normal limits
Lungs : Retraction (-) suprasternal, subcostal,epigastrium, VBS +/+, Rales
-/-, Wheezing -/-
Abdomen
Flat, bowel sound (+) normal, soepel, tympanic, tenderness (-), liver and spleen
impalpable, Traube’s space : tympanic.
Extremities : No disparity
Neurological Examination : Nervi craniales : normal
Meningeal stimulation : Nuchal Rigidity ±
Brudzinky +
Physiological reflex +/+
Pathological reflex : -/-
VII. Diagnosis
Differential Diagnosis
Meningitis e.c DD/:
Tuberculosis
Bacterial
Viral
9
Mixed infection
Working diagnosis Nutritional status :
Meningitis e.c Good (standard Weight/Height)
Tuberculosis
Additional Diagnosis : -
10
VIII. Suggested Further Studies
- Lumbal Punctie
- Culture and resistance test from blood and Spinal fluid
- Thorax photo for evaluation on treatment
- Acid Basil Strain (BTA)
- BSE and Diff Count
- Viral isolation
- CT-scan
2. Medicamentous
- Luminal 3x10mg(16/5)
- Valium 5mg 3x5mg (17/5-22/5)
- Broadced 1gr 2x1gr (16/5-22/5)
- Novalgin 150mg 3x150mg ( 16/5-22/5)
- Netromycin 50mg 2x50mg (16/5-22/5)
- Rifampicin 450mg 1x1 tab (18/5-22/5)
- PZA 500mg 1x1 tab (18/5-22/5)
- Pehadoxin +TB vit 1x1 tab (18/5-22/5)
- Corticosteroid
- Streptomycin
X. Prognosis
11
XII. Discussion
Physical Verification :
Condition : severe sickness
Temperature 37,8 C
12
FOLLOW UP
13
Abdomen Flat, soepel, BS + ↑ Flat, soepel, BS + ↑ Flat, soepel, BS + ↑
Doctor advice (03:00) dr. Tisna SpA (10:00) dr. Tisna, (09.30) dr. Tisna,SpA
Adv: SpA - Continue the
- inf RL15 gtt/mn - Continue the therapy
- Novalgin therapy PPD
3x150mg OAT :
- Broadced -Rifampicin 450mg
2x1gr PZA 500 mg
- Netromycin INH 300mg
2x50mg 1.
- Check: Hb, 3
Ht, Leu,Tc, x ray
thorax
(18.30)
Dr Tisna SpA Adv:
- luminal 2.
stop
- PPD tommorow
- Anti TB
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19/05/2006 20/05/2006 21/05/2006
15
Liver :1 cm BAC
Doctor advice (10:00) dr. Tisna SpA (10:00) dr. Tisna, (09.30) dr. Tisna,SpA
Adv: SpA - Continue the OAT
- Continue - Continue the therapy
the therapy therapy - Maxpro 2x1/2cth
- Force leave - Bufect 3x1cth
- Imunos 2x1cth
- Luminal 3x30mg
3.
3
4.
22/05/2006 23/05/2006
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Appearance moderate illness moderate illness
Pulse 108x/minute 120x/minute
Respiration 30x/minute 28x/minute
MENINGITIS TUBERCULOSIS
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Pathophysiology:
In those who develop TBM, bacilli seed to the meninges or brain parenchyma,
resulting in the formation of small subpial or subependymal foci of metastatic caseous
lesions. These are termed Rich foci, after the original pathologic studies of Rich and
McCordick. Tuberculous pneumonia develops with heavier and more prolonged
tuberculous bacteremia. Dissemination to the CNS is more likely, particularly if
miliary TB develops.
The second step in the development of TBM is increase in size of a Rich focus
until it ruptures into the subarachnoid space. The location of the expanding tubercle
(ie, Rich focus) determines the type of CNS involvement. Tubercles rupturing into the
subarachnoid space cause meningitis. Those deeper in the brain or spinal cord
parenchyma cause tuberculomas or abscesses. While an abscess or hematoma can
rupture into the ventricle, a Rich focus does not.
Tuberculomas are conglomerate caseous foci within the substance of the brain.
Centrally located, active lesions may reach considerable size without producing
meningitis (Rich and McCordock, 1933). Under conditions of poor host resistance,
this process may result in focal areas of cerebritis or frank abscess formation, but the
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usual course is coalescence of caseous foci and fibrous encapsulation (ie,
tuberculoma).
19
o Negative history for bacille Calmette-Guérin (BCG)
vaccination
20
Less frequent presentations include atypical febrile seizures in
children, isolated cranial nerve palsies, bilateral papilledema, and acute
confusional state.
21
o Spondylitis also can result in various symptoms,
including local and radicular pain, limb motor and sensory loss, and
sphincter disturbances.
STAGING :
22
In 1948, British Medical Research Council developed a method
for staging the severity of the disease.
Visual findings
Neurologic findings
23
o Cranial neuropathies, most often involving CN VI, may
be noted. CN III, IV, VII and, less commonly, II, VIII, X, XI, and XII
also may be affected.
Causes:
Mycobacterium tuberculosis
24
and dilute solutions of strong mineral acids such as
hydrochloric acid. This ability is attributed to a waxlike layer
composed of long-chain fatty acids, the mycolic acids, in their
cell wall. As a result, mycobacteria are termed "acid fast" and
are called acid-fast bacilli (AFB).
Risk factors
25
o Homeless persons, people in correctional facilities, and
residents of long-term care facilities also have a higher risk of
developing active TB than the general population.
Lab Studies:
Urinalysis
o Protein
26
false-negative results potentially occur in samples containing very few
organisms (<2 colony forming units (CFU)/mL).
o Syphilis serology
Tuberculin test: Negative result on PPD does not rule out TB; if
the 5-tuberculin test (TU) skin test is negative, repeat the test with 250-TU.
Note that this test is often nonreactive in TBM.
Imaging Studies:
o Hilar lymphadenopathy
o Simple pneumonia
o Infiltrate
o Fibronodular infiltrate/cavitation
27
CT scan and MRI of the brain reveal hydrocephalus, basilar
meningeal thickening, infarcts, edema, and tuberculomas (see Image 2).
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o Tuberculous spondylitis
29
are particularly involved, owing to associated arachnoiditis. Meningeal
enhancement is more common in HIV-infected patients.
Other Tests:
30
slowing in 22 patients, intermittent rhythmic delta activity in the frontal region
in 15 patients, right-to-left asymmetry in 5 patients, and epileptiform
discharges in 4 patients. At the end of 3 months, 5 patients had died, while
recovery was poor in 13 patients, partial in 3, and complete in 11. EEG
findings correlated with severity of meningitis and degree of coma; outcome at
3 months was assessed by Barthel index score.
Dot-immunobinding assay
31
o CSF levels of amino acids, nitrite (a metabolite of nitric
oxide), vitamin B-12, and homocysteine were quantitated in both
groups of patients.
Procedures:
Spinal tap
32
o Inspect the CSF visually and note its gross appearance.
It typically is clear or slightly turbid. If the CSF is left to stand, a fine
clot resembling a pellicle or cobweb may form. This faintly visible
"spider's web clot" is due to the very high level of protein in the CSF
(ie, 1-8 g/L, or 1000-8000 mg/dL) typical of this condition.
33
(35-85) of adults and children, respectively. Failure to respond to
treatment should prompt a search for fungal infections or malignancy.
34
Histologic Findings: The Ziehl-Neelsen stain uses the properties of the cell
wall to form a complex that prevents decolorization by acid or alcohol. Fluorochrome
tissue stains also can be helpful in diagnosis of TBM (see Image 3).
Medical Care: The duration of chemotherapy for TBM is unclear, and the
benefits of adjuvant corticosteroids remain in doubt. Death may occur as a result of
missed diagnoses and delayed treatment.
35
Studies have shown that young children with TBM can be
treated safely for 6 months with high doses of anti-TB agents without overt
hepatotoxicity and with a low risk of relapse. Children must be treated for 12
months with combination antibiotic therapy and adjunctive corticosteroids.
Twelve months is probably a conservative estimate of the time required for
bacterial cure. The rationale behind the use of adjuvant corticosteroids lies in
reducing the harmful effects of inflammation as the antibiotics kill the
organisms. The use of corticosteroids in adults is controversial; they may be
indicated in the presence of increased intracranial pressure, altered
consciousness, focal neurological findings, spinal block, and tuberculous
encephalopathy.
Surgical Care:
36
Potential new agents include oxazolidinone and iseponicin. Fluoroquinolones
useful in the treatment of TBM include ciprofloxacin, ofloxacin, and levofloxacin. A
new rifamycin called rifapentine has been developed.
Trials for novel agents for the treatment of tuberculosis are under way. Long-
acting rifamycin derivatives and potent fluoroquinolone antibiotics have been studied,
and they lead the way for improved regimens against active and latent tuberculosis.
The recent rapid increase in knowledge of mycobacterial pathogenesis is likely to lead
to the advent of potent new drugs in latent disease as well as against the phenomenon
of persistence. Without a doubt, sustained and increased funding for basic research
plays a key role in eradicating this global epidemic altogether.
37