Bronko Pneumonia

i

CASE REPORT

TUBERCULOUS MENINGITIS

PRESENTED BY

MUKHAMAD FARIED 110100351

TESAR AKBAR NUGRAHA 110100362

SUPERVISED BY:

dr. Wisman Dalimunthe, Sp.A (K)

PEDIATRIC HEALTH DEPARTMENT

HAJI ADAM MALIK GENERAL HOSPITAL

UNIVERSITY OF NORTH SUMATERA

2015

ACKNOWLEDGMENTS

ii

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 wouldn’t 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.

Medan, 15th October 2015

Presentators

1

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

2

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

3

nonspecific symptoms, such s fever, vomiting, and behavioral changes, develops.

As the disease progresses, neck stiffness, loss of consciousness, motor deficits,

and convulsions will follow. TBM diagnosis is often only considered once

irreversible neurologic damage has already occured.2

The outcome of TBM is known to be affected by age, stage of the disease

at admission, and whether riased intracranial pressure (ICP) caused by obstructive

hydrocephalus is actively treated.2

1.2 Objective

This paper is one of the requirements to fullfil in the senior clinical assistance

programs in Pediatric Department of Haji Adam Malik General Hospital,

University of North Sumatra. In addition, this paper can be used as reference to

know and understanding a litle about meningitis TB.

4

CHAPTER 2

LITERATURE REVIEW

2.1 Tuberculous Meningitis

2.1.1 Definition

Tuberculous meningitis is an inflammation of the meningen that cause by primary

tuberculosis.3 Tuberculous meningitis (TBM) is caused by Mycobacterium

tuberculosis (M. tuberculosis) and is the most common form of central nervous

system (CNS) tuberculosis (TB).4 Central nervous system (CNS) tuberculosis

occurs in approximately 1% of all patients with active tuberculosis. It results from

the haematogenous dissemination of Mycobacterium tuberculosis from primary

pulmonary infection and the formation of small subpial and subependymal foci

(Rich foci) in the brain and spinal cord. In some individuals foci rupture and

release bacteria into the subarachnoid space causing meningitis. In others, foci

enlarge to form tuberculomas without meningitis. Tuberculous meningitis (TBM)

is the most dangerous form of infection with Mycobacterium tuberculosis.5

2.1.2 Epidemiology

Tuberculosis of the central nervous system is the most severe manifestation of

extrapulmonary TB and constitutes approximately 1% of all new cases annually,

with Tuberculous Meningitis (TBM) being the commonest form of the disease.

Several studies have attempted to assess its epidemiology with variable

conclusions as the disease’s incidence and mortality rates differ from country to

country according to their individual socioeconomic and public health statuses.

5

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 TBM’s 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

Mycobacteria are aerobic, nonmotile, gram-positive rods ranging in appearance

from spherical to short filaments, which may be branched. Their cell wall contains

lipids, peptidoglycans, and arabinomannans. One distinct characteristic is their

ability to retain dyes that are usually removed from other microorganisms by

6

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

7

bacterial and viral pathogens capable of crossing the BBB and causing subsequent

meningitis / encephalitis.7

Fig. (1). Blood Brain Barrier.7

Much of the current understanding of the pathogenesis of CNS TB and

subsequent meningitis comes from the meticulous work of Arnold Rich and

Howard McCordock, who demonstrated upon autopsy that the majority of TB

meningitis patients displayed a caseating focus in the brain parenchyma or the

meninges. Rich postulated that these foci, also termed as “Rich foci,” develop

around bacteria deposited in the meninges and brain parenchyma during the initial

bacteremic phase. Much later, the rupture of these foci allowed dissemination of

the bacilli into the subarachnoid space, causing diffuse, inflammatory meningitis

(Fig. 2). Since the meninges and the brain parenchyma are anatomically and

physiologically protected from the systemic circulation by the BBB, the

mechanism by which the bacilli initially invade this barrier need to be elucidated.

8

Theoretically, M. tuberculosis can cross the BBB as a free (extra-cellular)

organism or via infected monocytes/neutrophils. While the latter hypothesis seems

attractive, such cellular traffic is severely restricted into the CNS prior to invasion

by the offending pathogen. Intravenous inoculation of free M. tuberculosis or M.

bovis in guinea pigs and rabbits has been shown to produce CNS invasion as

evidenced by the formation of tuberculomas in their brain parenchyma. Further,

one report utilizing CD18 leukocyte adhesion deficient mice, suggests that free

mycobacteria may transverse the BBB independent of leukocytes or macrophages.

Finally, it is unclear whether, after invading the CNS, M. tuberculosis reside

primarily within the parenchyma of the brain, the vessel wall, or the endothelial

cells lining the microvasculature. Significant vasculitis associated with CNS

tuberculosis and robust human endothelial cell invasion observed in vitro may

suggest that M. tuberculosis reside, at least initially, in the endothelial cells lining

the microvasculature.7

Fig. (2). Pathogenesis of Central Nervous System tuberculosis and

subsequent tuberculous meningitis.7

The spread of M. tuberculosis into the subarachnoid space following

rupture of a Rich focus triggers a robust inflammatory T cell response. Studies of

9

CSF cytokine levels in patients with TB meningitis have found elevated levels of

TNF-α and IFN-γ. 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-α, 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

Generally, the progression of tuberculous meningitis has 3 stage:8

1. Stage I: Prodormal

This stadium will progress in 1 – 3 week without any special

clinical symptoms and without any neurological disorder. Experienced

symptoms include fever, malaise, anorexia, abdominal pain and

headaches, sleep cycles change, nausea, vomiting, constipation, irritable to

apathy, but without loss of consciousness. Physical examination showed

the large fontanelle bulging in infants. older children will experience a

change of mood and decreased school performance. intermittent seizures

may arise.8

Prodromal stage may last a very short when tubercles broke into

the subarachnoid space arrived - arrived so the trip can last clinical jump

to the next stage quickly.8

2. Stage II: Transitional

At this stage exudate was collected in cerebral gyrus which make

the meningeal refleks positive, ie a stiff neck, Kernig, and brudzinsky

(except in infants frequently meningeal refleks is negative). Decreased of

10

consciousness (but not coma or delirium), hydrocephalus, papilaedema

light, and the presence of tubercles in the choroid, and cranial nerve palsy.

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

The diagnosis of tuberculous meningitis is not a simple work up especially on

mild stage. It cannot be made or excluded on the basis of clinical findings2.

Suspecting a tuberculous meningitis is a must if there is prolonged fever (>14

days, or >7 days if there is contact history with TB-confirmed family), patient still

unconscious after antimicrobial treatment, positive meningeal sign, hydrocephalus

and stroke with unclear etiology.8

Evaluate contact history to TB-confirmed family, immunodeficiency

possibility or drug-induced immunodepression. Evaluate BCG vaccination

history, because BCG vaccination can decrease tuberculous meningitis risk until

50-80%.8

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Positive tuberculin test and chest radiography can confirm the suspicion,

but the negative result doesn’t eliminate the suspicion because non-reactive

tuberculin and normal chest radiography is found at almost 50% patient. A

complete blood count testing should be performed, and the erythrocyte

sedimentation rate should be determined.8 Positive tuberculin test, chest

radiography abnormal finding and the finding of infection source in family only

can support the diagnoses. Tuberculin test often negative because of anergy,

especially on terminal stage.3

The gold standard of diagnosis is to find M. tuberculosis bacilli on

cerebrospinal fluid (CSF) culture, but to growing the bacteria up needs long time

at least 3-6 weeks and the positive result is found only on 50-75% cases if the

CSF is enough (5-10 ml). So the therapy can be given based on CSF analysis

result or the finding of acid-resistant bacteria on the microscopic test.8 Spinal tap

carries some risk of herniation of the medulla in any instance when intracranial

pressure (ICP) is increased, but if meningitis is suspected, the procedure must be

performed regardless of the risk, using suitable precautions and obtaining

informed consent before the procedure. Use manometrics to check CSF pressure.

Typically, the pressure is higher than normal.9

CSF analysis result show xhantochromic color, with fibrin sediment,

leucocyte count increases to 10-500 cell/mm3 (almost of them is lymphocyte, but

on early stage PMN is dominantly found), protein is very increased (0,4-1,3 g/dL)

low glucose (<40 mg/dL, infrequently to <20 mg/dL, or glucose-serum/CSF ratio

≤0.4).8 So the serum glucose level should be measured as comparison with the

glucose level measured in the CSF. Hemorrhagic CSF also has been recorded in

proven cases of TBM, this is attributed to fibrinoid degeneration of vessels

resulting in hemorrage.9

CSF acid-resistant staining can detect acid-resistant bacteria only on 30%

cases and needs high CSF amount as on culture. Low CSF amount can lowering

detection rate.8 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 the diagnosis of tuberculous meningitis.9

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Ziehl-Neelsen staining lacks sensitivity, and culture results are often too

late to aid clinical judgment. Semi-automated radiometric culture systems, such as

Bactec 460, and automated continuously monitored system have reduced culture

times. Newer methods involving amplification of bacterial DNA by polymerase

chain reaction (PCR) and comparable system have not been assessed completely

and may not be suitable for laboratories in developing countries with limited

resources.9

Computed tomography (CT) scanning and magnetic resonance imaging

(MRI) lack specificity but help in monitoring complications that require

neurosurgery.9 CT-scan or MRI testing is the most useful diagnosis on terminal

stage because it can detect complications, like communicans hydrocephalus,

cerebral oedem, ischemia, lesion on basal and tuberculoma. Tuberculoma can be

single or multiple, on CT scan or MRI is seen as lesion with clear border

surrounded by oedematous tissue. Strengthening with contrast will show ring-like

lesion.8

In one study, findings from electroencephalography (EEG) were abnormal

in some cases. EEG findings correlated with severity of meningitis and degree of

coma. Brainstem auditory evoked potential abnormalities were observed in some

cases. Motor and somatosensory evoked potentials may be helpful in objective

documentation of respective motor and sensory functions in patients with TBM

and altered sensorium.9

Electrolyte concentrations should be assessed. Mild-to-moderate

hyponatremia is present roughly 45% of patients, in some cases constituting a true

syndrome of inappropriate diuretic hormone secretion (SIADH). Blood urea

nitrogen (BUN) and creatinine levels should be measured as well. Urinalysis

should be performed.9

2.1.7 Treatment

Tuberculous meningitis therapy based on Indonesia guideline is given on 12

months and also follow general tuberculosis therapy concept.8

Intensive phase

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This phase is given on 2 months, using 4 or 5 anti-tuberculosis drugs, that

is isoniazid (INH) rifampin (RIF), pyrazinamide (PZA), ethambutol (E)

and streptomycin (SM). Streptomycin is given if there is anti-tuberculosis

drugs resistance.8

Advanced phase

This phase is given on next 10 months, using 2 anti-tuberculosis drugs that

is INH and RIF.8

The dosage of anti-tuberculosis drugs given is:

Isoniazid 5-15 mg/kgBW/day, max 30 mg/day

Rifampin 10-20 mg/kgBW/day, max 600 mg/day

Pyrazinamide 20-40 mg/kgBW/day, max 2 g/day

Ethambutol 15-25 mg/kgBW/day, max 1,25 g/day

Streptomycin 15-40 mg/kgBW/day, max 1 g/day

The second-line therapy is ethionamide, cycloserine, ofloxacin, and para-

aminosalicylate acid (PAS).8 The best anti-tuberculosis treatment of tuberculous

meningitis include isoniazid, rifampin, pyrazinamide, and streptomycin, all of

which enter CSF readily in presence of meningeal inflammation. Ethambutol is

less effective in meningeal disease unless used in high doses. INH, RIF, and PZA

are bactericidal. RIF and SM achieve optimal CSF levels when the meninges are

inflamed.9

Although anti-tuberculosis drug therapy have been started, culture and

sensitivity test are still performed to get a suitable therapy for the bacteria

sensitivity.8

During anti-tuberculosis therapy, monitoring must be performed every

month to evaluate patient’s commitment, disease’s 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

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and reducing oedem, that is prednisone with dosage 11-2 mg/kgBW/day on 4-6

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 isn’t 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.

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Table.1. CSF Characteristic on Bacterial, Tuberculous, and Viral Meningitis.8 Condition Bacterial

Meningitis

Tuberculous

Meningitis

Viral Meningitis Normal

Stain Purulent, cloudy Xanthochrome,

fibrin clots

Clear (except cell

count >300/µL)

Clear

Pressure

(mmH2O)

200-750+ 150-750+ Normal or slightly

increased

<160

Cell

count /µL

Thousands (>1000

cell/µL), mainly

PMN

200-500, mainly

lymphocyte

50-300, mainly

lymhocyte

0-5 lymphocyte,

1-3 PMN on 3-

first month,

30 lymphocyte

on neonatus, 20-

50 erytrocyte

Protein

(mg/dL)

Hundreds to

thousands

45-1000, cell

count increased

20-125 (normal or

slightly increased)

15-35 (lumbal),

5-15 (ventricle)

Glucose

(mg/dL)

Very decreased,

CSF/blood ratio

≤0,6 on neonatus,

≤0,4 on older child

Very decreased,

CSF/blood ratio

≤0,4

Normal or slightly

decreased

50-80 (2/3 of

blood glucose)

Tuberculous meningitis must be differentiated not only from other forms

of acute and subacute meningitis but also from conditions such as viral infection

and cerebral abscess. The radiological differential diagnoses includes cryptococcal

meningitis, cytomgalovirus encephalitis, sarcoidosis, meningeal metastases, and

lymphoma.9

2.1.9 Complication

Complication can occurred because of inadequate or late treatment.9 Tuberculous

meningitis got high complication rate, major or minor, even after treated and has

been confirmed healed. Permanent major neurologic symptom such as cerebral

palsy, mental retardation, epileptic, paraplegia, and sensory changes on extremity.

Minor neurologic symptom such as cranial nerve palsy, nystagmus, ataxia, and

mild changes of coordination and spastiity.8

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Mental retardation rate is almost 70%, intracranial calcification about

30%, and endocrine changes such as precocious puberty, hyperprolactinemia,

growth hormone deficiency, diabetes insipidus, corticotrophin, and gonadotropin

caused by hypofisis and hypothalamic disturbances is about 20% of cases. The

complication can affect eye that caused optical atrophy and blindness, and affect

ear that caused hearing loss.8

Tuberculous radiculomyelitis (TBRM) is a rare complication of

tuberculous meningitis. It develops at various intervals after tuberculous

meningitis, even in adequately treated patients after sterilization of the CSF. The

most common symptoms are subacute paraparesis, radicular pain, bladder

disturbance, and subsequent paralysis.9

2.1.10 Prognosis

The prognosis depends on patient’s stage when diagnosed and treated. On early

stage the prognosis is great, but most of patients on late stages experienced

permanent neurologic symptoms. Patient’s age under 3 years got worse prognosis.

Untreated patient can caused patient’s death.8 Before anti-tuberculosis drugs had

been found, tuberculous meningitis mortality is almost 100%. With anti-

tuberculous treatment, mortality can be reduced even still high that is about 10-

50%.3

17

CHAPTER III

CASE REPORT

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

History of parent’s medication:

Not found

History of pregnancy:

Patient’s 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:

Patient’s 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: 37,6°C, 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-/-

19

Ears: within normal range

Nose: nasal flaring

Mouth : within normal range

Neck : lymph node enlargement (-)

Thorax : Symmetrical fusiform, retraction intercostal and epigastric

(+)

HR: 138 bpm, regular, murmur (-)

RR: 54x/i, regular, ronchi (+/+), wheezing (-/-)

Abdomen: Symmetric, supple, normal peristaltic, liver and spleen:

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

20

Lymphocyte 39.90 % 20-40

Monocyte 8.10 % 2-8

Neutrophil absolute 10.08 103/µL 1.9-5.4

Lymphocyte

absolute

7.88 103/µL 3.7-10.7

Monocyte absolute 1.59 103/µL 0.3-0.8

Eosinophil absolute 0.09 103/µL 0.20-0.50

Basophil absolute 0.10 103/µL 0-0.1

MCV 81.80 Fl 81-95

MCH 26.20 Pg 25-29

MCHC 32.10 g% 29-31

Clinical chemistry (12 November 2015 / 23.03)

Test 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 96–106

Procalcitonin 0.42 ng/mL <0.05

21

Gas blood analysis (12 November 2015 / 23.03)

pH 7.155 7.35-7.45

pCO2 38.7 mmHg 38-42

pO2 177.5 mmHg 85-100

Bicarbonate (HCO3) 13.4 mmol/L 2-26

Total CO2 14.5 mmol/L 19-25

Base Excess (BE) -14.5 mmol/L (-2) – (+2)

O2 Saturation 98.8 % 95-100

Therapy: - O2 1-2 L/ min via nasal cannula

- IVFD D5% NaCl 0,225% 25 gtt/menit (micro)

- Inj Ceftriaxone 300 mg/ 12 hours /iv

- Paracetamol 3x cth 1/2

- Fluid challenge 10 cc/kgBB (65 cc)

Follow Up

13th Novemember 2015

22

S Dyspnea(+)

O Sensorium: CM, Temp: 37,2°C, BW: 6,5 kg, BH: 66 cm

Head : Fontanella Major was closed

- Eye : Light reflex (+/+), isochoric pupil, pale inferior conjunctiva

palpebra (-/-), sclera icteric (-/-)

- Ear : within normal range

- Nose : nasal flaring

- Mouth : within normal range

Neck : lymph node enlargement

Thorax : symmetrical fusiform, retraction (+) intercostal, epigastric

- HR: 140 bpm, regular, murmur (-)

- RR : 52x/i, regular, ronchi (+/+), wheezing(-/-)

- Abdomen : supple, peristaltic (+)N, Liver and Spleen: no palpable

- Extremities : pulse 140 bpm, regular, adequate p/v , felt warm,

CRT < 3”

A DD/Broncopneumonia

Bronchiolitis

P O2 1 L/min nasal canule

IVFD D5% NaCl 0,225 % 25gtt/i (micro)

Paracetamol 3x 75 mg

Inj Ampicilin 160 mg/6h

Inj Gentamycin 40 mg/24h

Nebule Ventolin 1 respul+ NaCl ,9 % /6h

Meylon 28 mEq, ½ 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 (-)

23

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

- Mucolitic :GE 3 x ½ tab (pulv)

- Analgetic Paracetamol: 4 x 10 mg (pulv)

- Consult to THT

- Cultur the ear discharge

Gas blood analysis (13 November 2015 / 20.59)

pH 7.427 7.35-7.45

pCO2 27.9 mmHg 38-42

pO2 165.0 mmHg 85-100

Bicarbonate (HCO3) 18.0 mmol/L 2-26

Total CO2 18.9 mmol/L 19-25

Base Excess (BE) -5.5 mmol/L (-2) – (+2)

O2 Saturation 99.4 % 95-100

Carbohydrate Metabolism

Blood Glucose ad

random

108.3 mg/dL 40-60

Electrolyte

Calsium 8.0 mg/dL 8.4-10.4

24

Natrium 135 mEq/L 135-155

Potassium 4.8 mEq/L 3.6-5.5

Chloride 102 mEq/L 96–106

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

Renal Function Test

Ureum 11,6 mg/dL <50

Creatinin 0,22 mg/dL 0.17-0,42

Immunoserology

Autoimmune (CRP Kuantitatif) 5,6 mg/dL

Other Test (Procalcitonin) 0.17 ng/mL <0,05


S dyspnea (+)

25

O Sensorium: CM, Temp: 37°C, BW: 6,5 kg, BH: 66 cm

Head : Fontanella Major was closed












CRT < 3”


Bronchiolitis




Inj Ampicilin 160 mg/6 jam/iv

Inj Gentamycin 40 mg/24 jam/iv

Inj Dexametason 2,5 mg/8 jam/iv

Nebule Ventolin 1 respul+ NaCl ,9 % /8 jam

Diet Su 650 kkal dengan 13 gr protein

Answer from ENT division

S Fluid in left ear (-), pain (+), cough and flu (about 1 week)

O left ear: secret (+), thick, yellowish, central perforation

A Acute Otitis Media

P -

Result of Radiology examination

26

- Both of sinus costophrenicus are sharp. Diafragma is smooth

- Infiltrate on suprahilar, perihiler, dan parakardial paru bilateral

- No cardiomegaly (CTR 45%)

- Trachea in middle

- Bones and soft tissue normal

- Conclusion : Bronkopneumonia bilateral


S Shortness of breath (+)

O Sensorium: CM, Temp: 37,1°C, BW: 6,5 kg, BH: 66 cm

Head : Fontanella Mayor was closed




- Nose : pernafasn cuping hidung








CRT < 3” , blood pressure: mmHg.


Bronchiolitis




Inj Ampicilin 160 mg/6 jam

Inj Gentamycin 40 mg/24 jam

27


Inj Aminophylline MD 1 cc/12 jam/iv diencerkan in 5 cc NaCl 0,9 %

bolus pelan

Nebule Ventolin 1 respul+ NaCl ,9 % /6 jam

16thNovemember 2015

S Shortness of breath (+) ↓↓O Sensorium: CM, Temp: 37°C, BW: 6,5 kg, BH: 66 cm

Head : Fontanella mayor was closed












CRT < 3” , blood pressure: mmHg.


Bronchiolitis



Inj Ampicilin 160 mg/6 jam

Inj Gentamycin 40 mg/24 jam


Inj Aminophylline MD 1 cc/12 jam/iv diencerkan in 5 cc NaCl 0,9 %

bolus pelan

28

Paracetamol 75 mg (k/p)

GE 3x ½ tab

Advise from dr. Wisman Dalimunthe, SpA

- Aff NGT- Consul for Cardiology Division (echocardiography) - Tappering off Inj dexamethasone


S Shortness of breath (+) ↓↓O Sensorium: CM, Temp: 37°C, BW: 6,5 kg, BH: 66 cm





- Nose : within normal range








CRT < 3”


Bronchiolitis

P O2 1 L/min nasal canule (intermitten)




Inj Dexametason 2mg/12 jam/iv (tapering off)

Inj Aminophylline (MD) 1 cc/12 jam/iv diencerkan in 5 cc NaCl 0,9 %

29

bolus pelan

Paracetamol 75 mg (k/p)

Nebule Ventolin 1 respul+ NaCl ,9 % /8jam


S Dyspnea (-)









Thorax : symmetrical fusiform, retraction (-)





CRT < 3”


Bronchiolitis

P IVFD D5% NaCl 0,225 % 25gtt/i (micro)



Inj Dexametason 2mg/12 jam/iv (tapering off)

Inj Aminophylline (MD) 1 cc/12h /iv diluted in 5 cc NaCl 0,9 % bolus

slowly

Paracetamol 75 mg (if needed)

Nebule Ventolin 1 respul+ NaCl ,9 % /8jam

30


S dyspnea (-)









Thorax : symmetrical fusiform, retraction (-)





CRT < 3”

A Broncopneumonia

P 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

DISCUSSION

Case Theory The chief complaint of this patient

was loss of consciousness. Seizure has Experienced symptoms of

bronchopneumonia include fever,

31

been experienced three times, the duration of seizure at least 5 minutes. Fever is experienced by patient with high temperature. Cough experienced, History of loose of weight is found.

shortness of breath

Patient has history of fever, since 1 week before admitted to hospital with high temperature

Patient’s mother is diagnosed as lung tuberculosis

Patient has no history of immunization

Suspecting a tuberculous meningitis is a must if there is prolonged fever (>14 days, or >7 days if there is contact history with TB-confirmed family

Evaluate contact history to TB-confirmed family, immunodeficiency possibility or drug-induced immunodepression.

Evaluate BCG vaccination history, because BCG vaccination can decrease tuberculous meningitis risk until 50-80%

Based on Chest X-Ray The Patient has abnormal inhomogeneous infiltrate tuberculosis impression

Positive tuberculin test, chest radiography abnormal finding and the finding of infection source in family only can support the diagnoses

CSF acid resistant staining test on this patient shows negative result

CSF acid-resistant staining can detect acid-resistant bacteria only on 30% cases and needs high CSF amount as on culture. Low CSF amount can lowering detection rate

The patient is treated with rifampicin, INH, pyrazinamide and ethambutol

Patient is treated with corticosteroid prednisone

Symptomatic therapy of this patient is head elevation, IVFD NaCl + KCl, phenytoin, O2, paracetamol,

Anti-tuberculosis drug given is isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), ethambutol (E) and streptomycin (SM). Streptomycin is given if there is anti-tuberculosis drugs resistance

Corticosteroid can be given to suppress inflammation process and reducing oedem, that is prednisone

Symptomatic therapy can be given if there is seizure, correction of dehydration caused by low

32

furosemide, spironolactone, and additional therapy is vit. B complex, vit. C, folic acid and diet F75

nutritional intake or vomiting, and phisiotherapy

CHAPTER V

SUMMARY

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.

33

REFERENCES

1. Isabel BE, Pathogenenesis and Immune Response in Tuberculous Meningitis,

Malays J Med Sci. Jan-Feb 2014; 21(1): 4-10.

2. Dimyati Y, Outcomes of tuberculous meningitis in children: a case review

study, Pediatricia Indonesiana, Vol. 51, No. 5, 2011.

3. Hassan R, Buku Kuliah Ilmu Kesehatan Anak edisi 11, Bagian Ilmu Kesehatan

Anak Fakultas Kedokteran Universitas Indonesia, 2007.

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4. Marx GE, Tuberculous Meningitis: Diagnosis and Treatment Overview,

Tuberculosis Research and Treatment, Volume 2011.

5. Thwaites G, British Infection Society guidelines for the diagnosis and treatment

of tuberculosis of the central nervous system in adults and children, Journal of

Infection. 2009; 167-187.

6. Kechagia M, Tuberculous Meningitis, InTech, 2012.

7. Be NA, Pathogenesis of Central Nervous System Tuberculosis, Curr Mol Med.

2009; 9(2): 94-99.

8. Tanto C, Kapita Selekta Kedokteran, Media Aesculapius, 2014.

9. Ramachandran TS, Tuberculous Meningitis, Emedicine Medscape, 2014.

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