Professional Documents
Culture Documents
CASE REPORT
TUBERCULOUS MENINGITIS
PRESENTED BY
MUKHAMAD FARIED
110100351
110100362
SUPERVISED BY:
dr. Wisman Dalimunthe, Sp.A (K)
ACKNOWLEDGMENTS
We are greatly indebted to the Almighty One for giving us blessing to finish this
case report about Tuberculous Meningitis. This case report is a requirement to
complete the clinical assistance program in Department of Child Health in H.
Adam Malik General Hospital, Medical Faculty of North Sumatra University.
We are also indebted to our supervisor and adviser, dr. Wisman
Dalimunthe, Sp.A (K) for much spent time to give us guidances, comments, and
suggestions. We are grateful because without him this case report wouldnt have
taken its present shape.
This case report has gone through series of developments and corrections.
There were critical but constructive comments and relevants suggestions from the
reviewers. Hopefully the content will be useful for everyone in the future.
Presentators
TABLE OF CONTENTS
ACKNOWLEDMENTS....................................................................................................
ii
TABLE OF CONTENTS...................................................................................................
1
CHAPTER 1 INTRODUCTION......................................................................................
2
CHAPTER 2 LITERATURE REVIEW..........................................................................
4
CHAPTER 3 CASE REPORT..........................................................................................
17
CHAPTER 4 DISCUSSION.............................................................................................
56
CHAPTER 5 SUMMARY.................................................................................................
58
REFERENCES..................................................................................................................
59
CHAPTER 1
BACKGROUND
1.1 Background
Tuberculosis (TB) is a significant bacterial disease which principally affects the
lungs. Its causal agent is Mycobacterium tuberculosis (Mtb) an intracellular
facultative organism which can produce progressive disease or latent
asymptomatic infection. Although TB is essentially a pulmonary disease, other
organs and tissues can be infected, being cerebral TB is the most severe form.1
There is high prevalence of tuberculous meningitis (TBM) in developing
countries, including indonesia, and the disease has a high mortality rate among
infants and children. Neurological complication are common, and early diagnoseis
and specific treatment for tuberculosis (TB) are essential for prevention of squelae
or fatal outcomes.2
TBM is the most severe complication of TB and frequently occurs in
childhood. Lympho-hematogenous spread from primary pulmonary focus leads to
the development of Rich focus in the brain. Rupturing of this cseous granuloma
into the subarachnoid space causes 3 features responsible for the clinical
manifestations
of
TBM:
development
of
further
tuberculomata;
basal
inflammatory exudates that cause cranial nerve palsies and obstruct cerebrospinal
fluid (CSF) passages, resulting in hydrocephalus; and obliterative vasculitis
leading to infarctions. Once the Rich focus has ruptured, a prodormal period of
CHAPTER 2
LITERATURE REVIEW
2.1
Tuberculous Meningitis
2.1.1
Definition
Epidemiology
Mortality rates for instance have been described to range from 7 40% in
developed countries, while the percentages from TB endemic countries as well as
countries with high HIV prevalence have been found to be significantly higher,
reaching a 69% in South Africa. The key point in understanding the
epidemiological pattern of the disease is the fact that TBM and tuberculosis
infection are closely related in this aspect, so that it is generally accepted that
occurrence of the former in a community is correlated with incidence of the latter
and vice versa. It is therefore considered safe to assume that at a global level these
two entities share a common trend. According to the latest available data, in 2009
the global incidence of TB was 9.4 million cases which is equivalent to 137 cases
per 100.000 population with most of them occurring in Asia and Africa and a
smaller proportion occurring in Europe and the Region of the Americas.
Developing countries in particular account for more than 80% of the active cases
in the world. The global incidence rate after an initial fall during the 20th century
rose due to the HIV epidemic with a peak in 2004 and a subsequent slow but
steady decline that also involves the absolute number of TB related deaths. This
impact of HIV on TB has accordingly influenced the pattern of TBMs incidence
rates. In fact, HIV infection constitutes the most important determinant for the
development of TBM followed by age. As far as the latter is concerned it is in turn
determined by the socioeconomic status of a certain population. Therefore in
populations with a low TB prevalence adults seem to be more affected than
children. This is reversed in populations with a higher TB prevalence. Concerning
childhood disease, TBM appears to affect mainly children under the age of 5 years
with the mean age ranging from 23 to 49 months and according to literature close
contact with a confirmed case of pulmonary tuberculosis is usually the culprit.6
2.1.3
Etiology
alcohols and dilute solutions of strong mineral acids such as hydrochloric acid.
This ability is attributed to a waxlike layer composed of mycolic acids in their
cell wall. As a result, they are termed acid-fast bacilli (AFB) after Ziehl-Neelsen
(ZN) staining. The causative agents of TBM are mainly the members of M.
tuberculosis complex and less commonly NTM. The incidence of CNS infection
due to the latter has increased substantially since the onset of the HIV epidemic.6
2.1.4
Pathogenesis
The initial point of tuberculosis infection is entry of the bacilli into the lungs via
inhalation of infectious droplets, whereupon the bacteria colonize macrophages
within the alveoli. During the progression of active pulmonary disease, bacteria
may disseminate to local lymph nodes and bloodstream, whereupon spread
throughout the systemic circulatory system may occur. It is also likely that
extensive bacteremia following dissemination from the lungs increases the
probability that a sub-cortical focus will be established in the CNS. Therefore,
higher numbers of bacilli in the circulatory system may be associated with
increased likelihood of CNS invasion and subsequent CNS TB.7
The CNS is protected from the systemic circulatory system by the
physiological blood brain barrier (BBB). This barrier is principally composed of
tightly apposed human brain microvascular endothelial cells (Fig. 1). The basal
portion of these endothelial cells is supported by astrocyte processes interspersed
with the extracellular matrix. Paracellular transport is limited by the presence of
endothelial cell tight junctions, while transcellular movement is restricted by the
relative paucity of endocytic vesicles. Such properties render the barrier
impermeable to many large, hydrophilic molecules and circulating pathogens.
Also protective of the CNS is the blood-cerebrospinal fluid (CSF) barrier,
providing spatial separation of the circulatory system from the CSF at the choroid
plexus. Cells lining the blood-CSF barrier share similar properties to those lining
the BBB, with enhanced tight junctions and more stringent regulation of
transcytosis. Despite the integrity of this barrier, however, there are a number of
bacterial and viral pathogens capable of crossing the BBB and causing subsequent
meningitis / encephalitis.7
CSF cytokine levels in patients with TB meningitis have found elevated levels of
TNF- and IFN-. The clinical manifestation of CNS tuberculosis is primarily a
consequence of the inflammation which develops in response to M. tuberculosis in
the CNS. Obstruction of the CSF by inflammatory infiltrate leads to
hydrocephalus, and vasculitis contributes to infarction, causing potentially
irreparable neurological damage. Inhibition of this inflammation may therefore
help in preventing the sequelae of CNS TB. Though thalidomide, which inhibits
TNF-, has not be shown to be beneficial for the treatment of TB meningitis in
children, corticosteroids such as dexamethasone which suppress the production of
inflammatory cytokines and chemokines lead to better outcomes and are
recommended as adjunctive treatment for patients with TB meningitis.7
2.1.5
Clinical manifestation
10
Cranial nerve that most commonly affected are N. VI that was followed by
N. III, N. IV, and N. VII which can cause strabismus, diplopia, ptosis, and
decreased pupil reaction to light. Older children will complain of severe
headache and vomiting, while the baby would seem irritable and vomiting.
The child may have symptoms of encephalitis in the form of a real focal
neurological deficits accompanied by involuntary movements and speech
disorders. Hydrocephalus that occure before symptoms of encephalitis is
one characteristic of tuberculous meningitis.8
3. Stage III: Terminal.
This stage takes place quickly, as long as 2-3 weeks. brainstem
infarction due to vascular lesions or strangulation by exudates which
experienced organization. Consciousness decreased to stupor or coma,
more severe form of focal neurological deficits (hemiplegia to paraplegia).
hyperpyrexia, papilaedema, hyperglycemia, opistotonus, decerebrate
posture, pulse and irregular breathing, dilated pupils, and not react to light,
or even death.8
2.1.6
Diagnosis
11
12
concentrations
should
be
assessed.
Mild-to-moderate
Intensive phase
This phase is given on 2 months, using 4 or 5 anti-tuberculosis drugs, that
is isoniazid (INH) rifampin (RIF), pyrazinamide (PZA), ethambutol (E)
13
Advanced phase
This phase is given on next 10 months, using 2 anti-tuberculosis drugs that
is INH and RIF.8
to
evaluate
patients
commitment,
diseases
progressivity
and
manifestation, and adverse effect of the drugs. Liver function test is evaluated
when anti-tuberculosis therapy is started, then evaluate on weeks 2, 4, 6, 8 and
every month.8
On the first weeks therapy, PMN count increasing and hypersensitivity
reaction can be found caused by releasing of bacterial cell wall protein when the
bacteria is lysis. So corticosteroid can be given to suppress inflammation process
and reducing oedem, that is prednisone with dosage 11-2 mg/kgBW/day on 4-6
14
weeks and tapered off until 2-4 weeks. Steroid therapy can reduce mortality rate,
long-term complications, and permanent sequelae.8 The use of corticosteroids may
be indicated in the presence of increased intracranial pressure (ICP), altered
consciousness focal neurological findings, spinal block, and tuberculous
encephalopathy. Treatment of tuberculoma consist of high dose steroids and
continuation of anti-tuberculosis therapy, often for a prolonged course. 8
Symptomatic therapy can be given if there is seizure, correction of dehydration
caused by low nutritional intake or vomiting, and phisiotherapy.3
If there is a sign of obstructive hydrocephalus and neurologic worsening
surgical action such as ventriculo-peritoneal shunt (VPS) may be needed.8 Studies
suggest that prompt ventriculo-atrial or ventriculo-peritoneal shunting improves
outcome, particularly in patients presenting with minimal neurological deficit. 9
Surgical therapy for tuberculoma isnt important because it will be a resolution
with pharmacologic therapy. Unfortunately, tuberculoma can resist for a long
time, for months or for years.8
BCG vaccination offers a protective effect (approximately 64%) againts
tuberculous meningitis. Improvement in weight for age was associated with a
decreased risk of the disease, however, further studies are needed to evaluate the
association, if any, between nutritional status and vaccine effeicacy.9
2.1.8 Differential Diagnoses
The differential diagnoses of this cases is every condition that induced fever and
sensory changes, in which CNS infection by bacteria, fungi (such as
histoplasmosis, cryptococcus) virus (aseptic meningoencephalitis), spiroseta or
parasite. It must be considered of malignancy metastasis possibility, lymphoma,
epidural abscess, subdural hematoma or subdural empyema. 8 Diagnostic confuion
often exists between tuberculous meningitis and other meningoencephalitides, in
particular partially treated meningitis.9 The characteristic of CSF have a specific
presentation between bacterial, tuberculous, or viral meningitis.
15
Bacterial
Tuberculous
Viral Meningitis
Normal
Stain
Meningitis
Purulent, cloudy
Meningitis
Xanthochrome,
Clear
Pressure
200-750+
fibrin clots
150-750+
count >300/L)
Normal or slightly
<160
(mmH2O)
Cell
Thousands
(>1000
200-500,
increased
50-300,
0-5 lymphocyte,
count /L
cell/L),
mainly
lymphocyte
mainly
mainly
lymhocyte
PMN
lymphocyte
on neonatus, 20cell
20-125 (normal or
50 erytrocyte
15-35 (lumbal),
thousands
Very
decreased,
count increased
Very decreased,
slightly increased)
Normal or slightly
5-15 (ventricle)
50-80 (2/3 of
CSF/blood
CSF/blood
decreased
blood glucose)
Protein
Hundreds
(mg/dL)
Glucose
(mg/dL)
to
ratio
0,6 on neonatus,
45-1000,
ratio
0,4
Complication
16
CHAPTER III
CASE REPORT
17
3.1 Objective
The objective of this paper is to report a case of a 11 month old boy with a
diagnosis of bronkopneumonia.
3.2 Case
AS, a 11 month old boy, with 6,5 kg of BW and 66 cm of BH, came to Haji Adam
Malik General Hospital Medan on 12th November at 22.30. His chief complaint
was dyspnea.
History of disease:
AS, a 11 month old boy, with 6,5 kg of BW and 66 cm of BH, came to Haji Adam
Malik General Hospital Medan on 12th November at 22.30 with dyspnea as chief
complaint. The patients have been experienced this about 1 week before admitted
to hospital. Dyspnea was not directed with weather and activity. Cyanosis (-),
patient also experienced cough since 2 weeks ago followed by sputum. History of
contact with adult cough (-). Fever has been experienced by patient since 2 weeks
and the body temperature rises and drop. Shivering was not found. Vomiting (-)
and nausea (-). Defecation and urination is normal. History of weight loose is not
found.
History of medication:
O2, IVFD ringer lactate, nebule ventolin, inj meropenem, triamsinolon,
bromhexine an salbutamol
History of family:
There is no famiy history of similar disease found.
18
Patients mother was 31 years old during pregnancy. She regularly goes for
control. No history of complication neonate and maternal problem. Consumtion of
herbal medication (-)
History of birth:
Patient was first child. Gestational age was preterm (28 weeks). Body weight was
1200 gram, body length was not measured. Birth was assisted by traditional
midwife. Baby was born normally and cried spontaneously. Blusih was not found.
History of immunization:
Not complete
History of growth and development:
Patients mother explained that he grew normally. He was able to crawl and sit
appropriately based on his age.
Physical Examination:
Present status:
Sensorium : CM, body temperature: 37,6C, HR: 138 bpm, RR: 54 x/i, BW: 6,5
kg, BH: 66 cm, BW/A: Z score < -3 , BL/A: Z score < -3, BW/BL: Z score < -3,
anemic (-), icteric (-), dyspnea (+), cyanosis (-), edema (-).
Localized status:
Head : Face: within normal range
Eyes: light reflex +/+, isochoric pupil, pale inferior
palpebral conjunctiva -/-, superior and inferior palpebra
edema-/Ears: within normal range
Nose: nasal flaring
Mouth : within normal range
19
normal
Extremities : pulse 138 bpm regular, adequate p/v, felt warm, CRT
< 3
Working diagnosis
: DD
bronkopneumonia
bronchiolitis
Laboratory finding
Complete blood analysis (12th November 2015 / 23.03)
Test
Result
Unit
References
Hemoglobin
9.20
g%
11.3-14.1
Erythrocyte
3.51
106/mm3
4.40-4.48
Leucocyte
19.74
103/mm3
6.0-17.5
Thrombocyte
263
103/mm3
217-497
Hematocrite
28.70
37-41
Eosinophil
0.50
1-6
Basophil
0.500
0-1
Neutrophil
51.00
37-80
Lymphocyte
39.90
20-40
Monocyte
8.10
2-8
Neutrophil absolute
10.08
103/L
1.9-5.4
Lymphocyte
7.88
103/L
3.7-10.7
1.59
103/L
0.3-0.8
absolute
Monocyte absolute
20
Eosinophil absolute
0.09
103/L
0.20-0.50
Basophil absolute
0.10
103/L
0-0.1
MCV
81.80
Fl
81-95
MCH
26.20
Pg
25-29
MCHC
32.10
g%
29-31
Result
Unit
References
Blood Glucose
71.70
mg/dL
40-60
Ureum
14.70
mg/dL
< 50
Creatinine
0.23
mg/dL
0.17-0.41
Natrium
136
mEq/L
135-155
Potassium
5.3
mEq/L
3.6-5.5
Chloride
100
mEq/L
96106
Procalcitonin
0.42
ng/mL
<0.05
7.155
7.35-7.45
pCO2
38.7
mmHg
38-42
pO2
177.5
mmHg
85-100
mmol/L
2-26
Total CO2
14.5
mmol/L
19-25
-14.5
mmol/L
(-2) (+2)
O2 Saturation
98.8
95-100
21
Therapy:
Follow Up
13th Novemember 2015
S
Dyspnea(+)
O
Sensorium: CM, Temp: 37,2C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Major was closed
-
CRT < 3
DD/Broncopneumonia
Bronchiolitis
O2 1 L/min nasal canule
IVFD D5% NaCl 0,225 % 25gtt/i (micro)
22
Paracetamol 3x 75 mg
Inj Ampicilin 160 mg/6h
Inj Gentamycin 40 mg/24h
Nebule Ventolin 1 respul+ NaCl ,9 % /6h
Meylon 28 mEq, dosis I: 14 mEq meylon dalam 100cc D5% in 4 hours
Diet Su 650 kkal and 13 gr protein
At 22.30
S
dyspnea , fever (+)
O
Sensorium: GCS 13 (E4, V3, M6) , T= 38,8 C
Ear: yellow discharge (+)
Thorax: Simetris Fusiformis, retraksi (+) epigastrial
HR: 165x/i, reg, murmur (-)
RR: 65x/i, reg, stridor (+), ronchi (+)
P
Nebule Ventolin 1 respul+ NaCl 0,9% / 8 h
R
Check blood gas analysis, Check electrolite post correction
Advise from dr. Wisman Dalimunthe, SpA
-
7.427
7.35-7.45
pCO2
27.9
mmHg
38-42
pO2
165.0
mmHg
85-100
mmol/L
2-26
Total CO2
18.9
mmol/L
19-25
-5.5
mmol/L
(-2) (+2)
O2 Saturation
99.4
95-100
mg/dL
40-60
Carbohydrate Metabolism
Blood Glucose ad 108.3
23
random
Electrolyte
Calsium
8.0
mg/dL
8.4-10.4
Natrium
135
mEq/L
135-155
Potassium
4.8
mEq/L
3.6-5.5
Chloride
102
mEq/L
96106
Clinical Chemistry
Liver Function Test
Fosfatase Alkalase (ALP)
148
U/L
<4,62
AST/SGOT
46
U/L
<38
ALT/SGPT
22
U/L
<41
11,6
0,22
mg/dL
mg/dL
<50
0.17-0,42
Immunoserology
Autoimmune (CRP Kuantitatif)
Other Test (Procalcitonin)
5,6
0.17
mg/dL
ng/mL
<0,05
24
CRT < 3
DD/Broncopneumonia
Bronchiolitis
O2 1 L/min nasal canule
25
16thNovemember 2015
S
O
26
Bronchiolitis
O2 1 L/min nasal canule
Aff NGT
Consul for Cardiology Division (echocardiography)
Tappering off Inj dexamethasone
27
CRT < 3
DD/Broncopneumonia
Bronchiolitis
O2 1 L/min nasal canule (intermitten)
Dyspnea (-)
Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Mayor was closed
-
CRT < 3
DD/Broncopneumonia
28
Bronchiolitis
IVFD D5% NaCl 0,225 % 25gtt/i (micro)
dyspnea (-)
Sensorium: CM, Temp: 37C, BW: 6,5 kg, BH: 66 cm
Head : Fontanella Mayor was closed
-
CRT < 3
Broncopneumonia
IVFD D5% NaCl 0,225 % 25gtt/i (micro)
Inj Ampicilin 160 mg/6h/iv
Inj Gentamycin 40 mg/24h/iv
Paracetamol 75 mg (if needed)
Nebule Ventolin 1 respul+ NaCl ,9 % /8h
CHAPTER IV
29
DISCUSSION
Case
Theory
Experienced
symptoms
of
bronchopneumonia include fever,
shortness of breath
30
CHAPTER V
SUMMARY
31
DM, a girl, 3 years and 1 months old, weighted 7 kg and heighted 78 cm,
from General Hospital Medan on September 11th 2015 at 20.25 PM develops loss
of consciousness. Patient was diagnosed as tuberculous meningitis. Patient was
treated with Phenytoin, Ceftriaxsone, Paracetamol, Furosemide, spironolactone,
diamox, rifampicin, INH, pyrazinamide, ethambutol, prednisone, vit. B complex,
and Vit. C.
REFERENCES
32