Case Report

TUBERCULOUS SPONDYLITIS

SUPERVISOR

: dr. Nelly Rosdiana, Sp. A (K)

PRESENTATOR

: Glancius Nironsta H (110100066)

Jos Bryan R.H.S

(110100302)

DEPARTMENT OF CHILD HEALTH

MEDICAL FACULTY NORTH SUMATRA UNIVERSITY
H. ADAM MALIK GENERAL HOSPITAL
MEDAN
2015

2
ACKNOWLEDGMENTS

We are greatly indebted to the Almighty One for giving us blessing to finish this case
report,Tubeculous Spondylitis.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. Nelly Rosdiana, Sp.A (K) for
much spent time to give us guidances, comments, and suggestions. We are grateful because
without Her 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.

Medan, 7th Desember 2015

Presentator

1.1

Introduction
Spinal tuberculosis infection, or commonly referred as spondylitis

tuberculosis (TB) or vertebral osteomyelitis tuberculosis or Potts disease [1], is

one of the oldest demonstrated diseases of humankind, having been documented
in spinal remains from the Iron Age in Europe and in ancient mummies from
Egypt and the Pacific coast of South America.[1, 2] In 1779, Percivall Pott, for
whom the disease is named, presented the classic description of spinal
tuberculosis. Tuberculous spondylitis caused by the Mycobacterium tuberculosis
bacteria that attacks the corpus vertebrae, potentially causing serious morbidity,
including neurological deficits and permanent spine deformity. The most common
deformity is kyphotic deformity, known as the gibbus. Tuberculous spondylitis
(TS) or spinal tuberculosis is usually secondary to pulmonary or intestinal
tuberculosis and may also be the first manifestation of tuberculosis (TB).(iran)
The diagnosis is usually established at advanced stage, where severe spinal
deformity and neurological deficits such as paraplegia are evident [2,3].
(bandung)
Spinal TB, an advanced disease, requiring meticulous assessment and
aggressive systemic therapy [1]. Despite its common occurrence and the high
frequency of long-term morbidity, there are no straightforward guidelines for the
diagnosis and treatment of spinal tuberculosis. Early diagnosis and prompt
treatment is necessary to prevent permanent neurological disability and to
minimize spinal deformity.1,2(india) In addition to systemic therapy of TS,
surgical intervention may be indicated. Surgery is indicated for diagnostic
dilemma, neurological complication and prevention of kyphosis progression [2].
(iran)
Physicians should keep the diagnosis in mind, especially in a patient from
a group with a high rate of tuberculosis infection. In endemic countries TS usually
occurs in young adults, but in developed countries it has become a disease of
older persons (iran).
Tuberculosis is common in the developing world and its incidence is
increasing. Spinal tuberculosis is associated with great potential morbidity and
mortality hence the importance of proper and quick diagnosis.(Uganda). Indonesia

is ranked after India and China as country with most population infected by TB
[4]. Approximately 20% of pulmonary TB infection will spread outside the lung
(extrapulmonary TB) [5]. Eleven percent of extrapulmonary TB is osteoarticular
TB, and approximately half of the patients have spinal TB infection [6]. The
management of spondylitis TB in general includes anti- TB drugs, immobilization
with or without surgical intervention. (Bandung)
1.2.

Objective
The objective of this paper is to report a case of a 15 years and 7 months

girl diagnosed with Suspect of Tuberculousis Spondylitis.

LITERATURE REVIEW
2.1.

Tuberculous spondylitis

2.1.1. Definition and Etiology

Tuberculous spondylitis is defined as an infection by a specific organism caused

by the Mycobacterium tuberculosis bacteria that attacks of one or more components

of the spine, namely the vertebra, intervertebral discs, paraspinal soft tissues, and epidural
space [1](ajr).
M.tuberculosis (MTB) belongs to the genus Mycobacterium that includes more
than 80 other species. Tuberculosis (TB) is defined as a disease caused by members of the
M. tuberculosis complex, which includes the tubercle bacillus (M. tuberculosis), M.
bovis, M. africanum, M. microti, M. canetti, M. caprae and M. Pinniped.

The mycobacterial cell envelope is composed of a core of three macromolecules

covalently

linked

to

each

other

(peptidoglycan,

arabinogalactan,

and

mycolicacids)andalipopolysaccharide,lipoarabinomannan (LAM), which is thought to be

anchored to the plasma membrane [7].
MTB are aerobes. Their reproduction is enhanced by the presence of 5-10% CO2
in the atmosphere. They are grown on culture media with high lipid content, e.g.
Lowenstein-Jensen (LJ) medium. The generation time of TB is approximately 12-18
hours, so that cultures must be incubated for three to six weeks at 370C until proliferation
becomes microscopically visible. [9] Broth-based culture systems to improve the speed
and sensitivity of detection have been developed [10]. In AFB smear-positive specimens,
the BACTEC system can detect M. tuberculosis in approximately eight days (compared
to approximately 14 days for smear-negative specimens

The cell wall components give mycobacteria their characteristic staining

properties. The organism stains positive with Grams stain. The mycolic acid structure
confersthe ability to resist destaining by acid alcohol after being stained by certain aniline
dyes, leading to the term acid fast bacillus (AFB). Microscopy to detect AFB (using
Ziehl-Neelsen or Kinyoun stain) is the most commonly used procedure to diagnose TB; a
specimen must contain at least 10 [5] colony forming units (CFU)/mL to yield a positive
smear [8]. Microscopy of specimens stained with a fluorochrome dye (such as auramine
O) provides an easier, more efficient and more sensitive alternative. However,
microscopic detection of mycobacteria does not distinguish M. tuberculosis from nontuberculous mycobacteria.

2.1.2. Epidemiology
Bone and soft tissue tuberculosis accounts for approximately 10-15% of
extrapulmonary tuberculosis cases and between 1% and 2% of total cases. Tuberculous
spondylitis is the most common manifestation of musculoskeletal tuberculosis,
accounting for approximately 40-50% of cases. (Medscape).

2.1.3. Pathogenesis
Infective spondylitis may result from hematogenous spread, lymphatic
spread from paraaortic lymph nodes possible but rare, direct external inoculation
or from contiguous tissues. The hematogenous arterial route is predominant,
allowing seeding of infection from distant sites onto the vertebral column. Wiley
and Trueta [25] demonstrated that metaphyses and cartilaginous end plates are
starting areas for blood-borne infections, showing how bacteria could easily
spread hematogenously to the metaphyseal region of adjacent vertebrae [26]. In
pyogenic spondylitis, once microorganisms enter in vascular arcades in the metaphysis, the infection spreads. The disc is destroyed by bacterial enzymes in a
manner similar to the destruction of cartilage in septic arthritis. Pyogenic infection
commonly involves the thoracic and lumbar spines. In contrast to pyogenic
infections, tuberculous infection commonly results from venous spread, Batsons
paravertebral venous plexus. Tuberculous spondylitis typically involves initial
destruction of the anteroinferior part of vertebral bodies and may then spread
beneath the anterior spinal ligament, involving the anterosuperior aspect of
adjacent inferior vertebra. Further spread may result in adjacent abscesses [27].

Anterior type involvement of the vertebral bodies seems to be due to the extension
of an abscess beneath the anterior longitudinal ligaments and the periosteum.
However, tuberculous spondylitis does not destroy the disc until very late in the
disease (Asian spine jurnal)
2.1.4. Classification
New classification system in which spinal TB is classified in to three main
types, with type I lesions being subdivided in to two subtypes. In this
classification system, lesions are classified as follows (ASJ):
1) Type I, one-level disc involvement and soft tissue infiltration without abscess,
collapse and neurologic deficit.
2) Type I-A, lesions only limited to vertebra and therefore, manageable with fine
needle biopsy and medical therapy.
3) Type I-B, abscess formation exceeds the vertebra and the treatment is
debridement using an anterior, posterior or endoscopic approach.
4) Type II, one- or two-level disc degeneration, abscess formation and mild
kyphosis correctable with anterior surgery. Although instability is not seen in this
type, neurological deficit may be present. The treatment includes debridement
with an anterior approach and fusion with strut tri-cortical graft.
5) Type III, one- or two-level disc degeneration, abscess formation, instability and
deformity that cannot be corrected without instrumentation. Decompression and
stabilization of the deformity via an anterolateral, posterior, or combined approach
is necessary.

2.1.5. Clinical Manifestations

The characteristic clinical features of spinal tuberculosis include local
pain, local tenderness, stiffness and spasm of the muscles, a cold abscess, gibbus,
and a prominent spinal deformity. The cold abscess slowly develops when
tuberculous infection extends to adjacent ligaments and soft tissues. Cold abscess
is characterized by lack of pain and other signs of inflammation.
The progression of spinal tuberculosis is slow and insidious. The total
duration of the illness varies from few months to few years, with average disease

duration ranging from 4 to 11 months. Usually, patients seek advice only when
there is severe pain, marked deformity, or neurological symptoms.2931. The
classical constitutional features of tuberculosis indicating presence of an active
disease are malaise, loss of weight and appetite, night sweats, evening rise in
temperature, generalized body aches, and fatigue.
Back pain is the most frequent symptom of spinal tuberculosis. Pain is
typically localized to the site of involvement and is most common in the thoracic
region. The pain may be aggravated by spinal motion, coughing, and weight
bearing, because of advanced disk disruption and spinal instability, nerve root
compression, or pathological fracture. Neurologic deficits are common with
involvement of thoracic and cervical regions. Paraplegia may occur at any time
and during any stage of the vertebral disease. In cervical spinal tuberculosis,
patients manifest with symptoms of cord or root compression. The earliest signs
are pain, weakness, and numbness of the upper and lower extremities, eventually
progressing to tetraplegia. If the thoracic or lumbar spine is involved, upper

extremity function remains normal while lower-extremity symptoms progress

over
time eventually leading to paraplegia.20 Patients with cauda equina compression
due to lumbar and sacral vertebral damage have weakness, numbness, and pain,
but have decreased or absent reflexes among the affected muscle groups. This is in
contrast to the hyperreflexia seen with spinal cord compression along with bladder
involvement (cauda-equina syndrome). (SCM)
Frequency of clinical, laboratory and imaging findings among studied
patients with spinal tuberculosis.(194323)
Variables
Clinical
Fever
Night sweating
Weight loss
Back pain
Local tenderness
Paraparesis
Laboratory
Leukocytosis
ESR >20
Positive CRP

Percentage
26.1
17.4
14.5
98.5
84.1
26.1
14.5
92.8
86.9

2.1.6. Diagnosis
Differentiating spinal TB from pyogenic and fungal vertebral osteomyelitis
as well as primary and metastatic spinal tumors may be difficult when only
clinical and radiographic findings are considered [8]. A history of tuberculosis, a
positive skin test (its value declines in endemic areas), and an elevated erythrocyte
sedimentation rate (ESR) may be useful in the diagnosis of spinal TB [8,9].
Biopsy plays a valuable role in the diagnosis of spinal TB infection. The use of
DNA amplification techniques (polymerase chain reaction or PCR) may facilitate
rapid and accurate diagnosis of the disease [10]. Culturing the organisms is slow
and may be inaccurate.
Computed tomography (CT) provides bony detail, while MRI evaluates
the involvement of soft tissue and abscess formation. The relative preservation of
the disc, rarefaction of the vertebral endplates, anterior wedging, the presence of
separate pre- and paravertebral or intra-osseous abscesses with a subligamentous
extension and breaching of the epidural space, concentric collapse of vertebral

body, ivory vertebra which is seen at conventional radiographs and refers to an

increase in opacity of a vertebral body while preserving its size and contours (with
no change in the opacity and size of adjacent intervertebral discs), neural arch
tuberculosis,

circumferential

or

pan

vertebral

involvement,

extradural

tuberculoma, subdural granuloma, intramedullary tuberculoma, and multilevel

spinal TB are considered as the diagnostic clues for this disease in various
imaging modalities [8,9,11-14]. Significant bone destruction can be detected on
plain radiographs or CT scan [15]. However, epidural granulomatous tissue or
tuberculoma of the spinal cord may not be detected by these tools [8]. (ASJ)
2.1.7. Treatment
2.1.7.1. Medical Therapy (ASJ)
Spinal TB is a medical disease and antituberculosis drugs have a main role
in the recovery and response of patients [9,38-43]. Adequate early pharmacological treatment can prevent severe complications [44]. Combination of
rifampicin, isoniazid, ethambutol, and pyrazinamide for two months followed by
combination of rifampicin and isoniazid for a total period of 6, 9, 12 or 18 months
is the most frequent protocol used for treatment of spinal TB [9].
The proposed regimen of World Health Organization (WHO) with total
duration of 6 months consists of primary treatment with isoniazid, rifampicin,
pyrazinamide, and ethambutol for two months followed by four months of therapy
with isoniazid and rifampicin (Table 1) [50]. WHO does not give much attention
to spinal TB but the American Thoracic Society recommends 9 months of
treatment with the same first drugs consumed for the first two months following
by seven months of therapy with isoniazid and rifampicin in the continuation
phase, while the Canadian Thoracic Society recommends a total time of treatment
as long as 9 to 12 months.
2.1.7.2. Surgical considerations
Indications for surgery in acute spondylitis TB :
1. Progressive neurologic deficit.
2. Progressive increase of spinal deformity (more than 40 of segmental
kyphosis, anteroposterior or lateral translation).
3. Conservative treatments futile including point 1 and 2 above.

4. Severe pain due to abscess or spinal instability.

5. Uncertain diagnosis: this could be an inability to obtain microbiological
diagnosis from microscopy, culture or even via detection of mycobacterium DNA
using PCR. (bandung)
2.1.8. Differential Diagnosis
There are a few differential diagnosis of Tuberculous Spondylitis, such as:

10

CASE REPORT
3.1.

Case
AW, 16 years and 7 month girl, BW 25 kg, BH 122 cm admitted to

Pediatric Department of Infection Unit in H. Adam Malik General Hospital

Medan on November 12th 2015 at 18.00 PM with a complain lump at the back.
3.3 History of Disease
AW was admitted to Haji Adam Malik General Hospital Medan
complaining lump at the back since 15 years ago without any pain. The posture
of the body became hunch. Traumatic history was found when patient was 11
months. Patient had experienced fever since the last 3 months. Temperature is
unstable, sometimes high grade fever and it is was reduced with antipyretics.
Shiverring and convulsions were not found. Cough without sputum was found in
this 3 months. Patient reported vomiting since 1 week ago 3-4 times a day with
the volume of a cup. It was food and drink that she ate. Sometimes, patient
also reported headache and pain around the neck since last 1 week. Her parents
realized that patient was pallor since 1 week. Loss of body weight was found
since 1 months around 12 kg. History of contact with the long cough patient was
not found. Riwayat benjolan di daerah lipatan paha kiri dan di atas tulang pinggul
belakang serta bernanah dijumpai. History of TB medication was denied.
Previous illness: Referred from RS Pertamina Pangkalan Brandan and diagnosed
with Spondilitis TB + Suspect Lung TB.
History of medication: Ambroxol, ranitidine, cefoperazine and aminofluid
injection
History of family: None
History of parents medication: None
History of Pregnancy: The age of mother was 27 years old during pregnancy.
The gestation was normal, 36 weeks.

11

History of Birth: Birth was assisted by midwife. The patient was born pervaginal
and cried immediately after birth. Body weight at birth was 2800 gram, body
length at birth was 50 cm.
History of feeding: Unclear
History of immunization: BCG scar (+), incomplete immunization
History of growth and development: The patients mother reported that AW
grew normally. AW had developed talking, crawling, and walking skills on time.
Physical Examination :
Present Status: Level of consciousness: Alert, Compos mentis. Blood pressure :
100/50 mmHg, Respiratory rate: 24 x/i, regular. Pulse : 108 x/i reguler, Body
temperature: 36,7C, Body weight : 25 kg, Body height : 122 cm. BW/A: 46%,
BH/A: 74%, BW/BH: 108%, anemic (-), ikteric (-), dyspnea (-), cyanotic (-),
edema (-).
Localized Status
Head: Eye: Eye light reflect +/+, isochoric pupil, pale conjunctiva palpebral
inferior -/-, Ear/nose/mouth : Within normal range.
Neck: Jugular Vein Pressure : R-2 cmH2O; Lymph node enlargement(-)
Thorax: Symetrical fusiformis, Retractions (-), Respiratory Rate : 24 x/i, regular,
ronchi -/-. Heart rate : 108 x/i, regular, murmur (-)
Thoracolubal : Gibbus (+), Kyphosis (+), tenderness (-), ROM limited
Abdomen: Soepel, Peristaltic (+) normal, Hepar/Lien: not palpable
Extremities: Pulse: 108x/i, regular, adequate pressure and volume, warm, CRT <
3, Pale (-), Pretibial edema (-), Blood pressure: 100/50 mmHg, thinning of
subcutaneous fat, hypotrophy of muscle (+)
Laboratory Findings :
13th November 2015
Complete blood count:
Test
Hemoglobin

Result

Unit

Referal

11.60

g%

12.0-14.4

12

Erythrocyte

4.7

106/mm3

4.75-4.85

Leucocyte

5.18

103/mm3

4.5-11.0

Thrombocyte

238

103/mm3

150-450

Hematocryte

34.50

36-42

Eosinophil

0.80

1-6

Basophil

2.30

0-1

Neutrophil

65.60

37-80

Lymphocyte

19.70

20-40

Monocyte

11.60

2-8

Absolute neutrophil

3.40

103/L

2.7-6.5

Absolute lymphocyte

1.02

103/L

1.5-3.7

Absolute monocyte

0.60

103/L

0.2-0.4

Absolute basophil

0.12

103/L

0-0.1

MCV

73.40

fL

75-87

MCH

24.70

Pg

25-31

MCHC

33.60

g%

33-35

RDW

15.60

11.6-14.8

MPV

8.40

fL

7.0-10.2

PCT

0.15

PDW

8.7

fL

13

Electrolyte
Test
Natrium
Kalium
Chloride

Result
139
3.4
105

Carbohydrate Metabolism
Blood Glucose
Renal Function
Ureum
Creatinin

Unit
mEq/L
mEq/L
mEq/L

Referal
135-155
3.6-5.5
96-106

98.9

mg/dL

< 200

19.30
0.42

mg/dL
mg/dL

< 50
0.50-0.90

Differential Diagnosis:

Spondylitis ec M. tuberculous
Pyogenic
traumatic
Brucellar
metastatic

Diagnosis : Suspect Tuberculousis Spondylitis + Pulmonary TB + Malnutrition

Therapy :
-

Diet F75 210 cc/3jam + Min Mix 4,2 cc

Vit B comp 1x1
Vit C 1x 100
Folic acid 1x5mg 1x1 mg
Further Investigation Plan:
- Blood culture and lumbal punctie
-

Head CT scan

Thoracolumbal MRI

Follow Up
S
O

13-15 November 2015

Cough (+), dyspnoe (-), decrease appetite (+), fever (-)
Sensorium: Compos Mentis, Temp: 37oC.
Head:

14

-Eye: Eye light reflect +/+, isochoric pupil, pale conjunctiva palpebral
inferior -/-Ear/nose/mouth : Within normal limit.
-Neck: Jugular Vein Pressure : R-2 cmH2O; Lymph node enlargement(-)
-Thorax: Symetrical fusiformis, Retractions (-), Respiratory Rate : 24 x/i,
regular, ronchi -/-. Heart rate : 108 x/i, regular, murmur (-)
-Thoracolumbal : Gibbus (+), Kyphosis (+), tenderness (-), ROM limited
-Abdomen: Soepel, Peristaltic (+) normal, Hepar/Lien: not palpable
-Extremities: Pulse: 108x/i, regular, adequate pressure and volume, warm,
CRT < 3, Pale (-), Pretibial edema (-), Blood pressure: 100/50 mmHg,
A
P -

thinning of subcutaneous fat, hypotrophy of muscle (+)

Suspect Tuberculousis Spondylitis + Pulmonary TB + Malnutrition
Diet F75 210 cc/3jam + Min Mix 4,2 cc
Vit B comp 1x1
Vit C 1x 100
Folic acid 1x5mg 1x1 mg
R/ Consuled to metabolic disease and nutrition divison, mantoux test,
expertise foto, BTA sputum 3x atau bilas lambung, cek LFT, CRP,

Procalcitonin, urinalysis, Blood culture, urine culture

Laboratorium result :
Complete blood count: Hb/Ht/Leuko/Tromb : 11,6/ 34,5/ 5.180/ 238.000
MCV/MCH/MCHC : 73,4/ 24,7/ 33,6
Diftel : 2,3/ 0,8/ 65,6/ 19,7/ 11,6
HST : PT: 15,6(14,0) INR: 1,14 APTT: 29,0 (33,0) TT: 14,5 (17,0)
Albumine : 3,7 g/dl ; KGD adr :139,2
RFT : Ur/Cr/As. Urat : 14,7/0,43/2,0
LFT : ALP/SGOT/SGPT : 68/18/11
CRP :5,6 Procalcitonin: 0,15
Urinalysis: colour : Yellowish; Glucose : +1; Bilirubin: - ;Keton: - ; BG: 1,015 ;
pH: 8,0 ; protein: - ; Uro:- ; Nit:- ; Leuko:- ; Blo:Sedimen : Eri/Leu/Epi/Casts/Crys : 0-1/0-1/0-1/-/-

16-18 November 2015 Modul Nutrisi dan Penyakit Metabolik

Cough (+), dyspnoe (-), decrease appetite (+), fever (-), vomiting (-), loose

stools (-)
Sensorium: Compos Mentis, Temp: 37oC.
BBM: 25kg

PB:122cm

BB/U: 46%

15

BBS: 25kg

HA: 7 tahun

PB/U: 74%

BBI: 23kg

LLA: 16,5 (<p5th)

BB/PB: 108%

RDA: 80kkal Total Kalori: 1840 kkal

- Wajah: old man face (-)
- Thoracolumbal : Gibbus (+), Kyphosis (+), tenderness (-), ROM limited
- Abdomen: soepel, peristaltic: (+) N, Hepar/Lien: not palpable
- Extremities : thinning of subcutaneous fat, hypotrophy of muscle (+)
A Suspect Tuberculousis Spondylitis + Pulmonary TB + Malnutrition
P - Diet F75 210 cc/3jam + Min Mix 4,2 cc
- Vit B comp 1x1
- Vit C 1x 100
- Folic acid 1x5mg 1x1 mg
R/ Bilas lambung (H1)
Susul hasil expertise foto pelvic, thoracolumbal
Susul hasil bilasan Lambung H1 dan H2 (18/11/2015)
Thorax photo result: Miliary Pulmonal TB
Lumbal photo result in 2 position: Kifosis vertebra thoracolumbal +
spondylitis (Advice Thoracolumbal MRI)
Pelvic photo result : suspect right ingunal lymph node

9- November 2015
Cough (+), dyspnoe (-), decrease appetite (+), fever (-), vomiting (-), loose

stools (-)
Sensorium: Compos Mentis, Temp: 37oC.
BBM: 25kg

PB:122cm

BB/U: 46%

BBS: 25kg

HA: 7 tahun

PB/U: 74%

BBI: 23kg

LLA: 16,5 (<p5th)

BB/PB: 108%

RDA: 80kkal Total Kalori: 1840 kkal

- Wajah: old man face (-)
- Thoracolumbal : Gibbus (+), Kyphosis (+), tenderness (-), ROM limited
- Abdomen: soepel, peristaltic: (+) N, Hepar/Lien: not palpable
- Extremities : thinning of subcutaneous fat, hypotrophy of muscle (+)
A Suspect Tuberculousis Spondylitis + Pulmonary TB + Malnutrition
P - Diet F75 210 cc/3jam + Min Mix 4,2 cc
- Vit B comp 1x1
- Vit C 1x 100
- Folic acid 1x5mg 1x1 mg

16

R/ Bilas lambung (H1)

Susul hasil expertise foto pelvic, thoracolumbal
Susul hasil bilasan Lambung H1 dan H2 (18/11/2015)
Thorax photo result: Miliary Pulmonal TB
Lumbal photo result in 2 position: Kifosis vertebra thoracolumbal +
spondylitis (Advice Thoracolumbal MRI)
Pelvic photo result : suspect right ingunal lymph node

17

S
Fever (-)

O
A
Sens: Alert, T: 36,8 oC, BW: Malaria+

P
IVFD D5% NaCl 0,45% 30

14 kg, BH: 104 cm

gtt/i,

anaemia

Head: eye reflect +/+, isocor,

DHP tablet 1x1 for 3 days

pale conj. palpebral inferior

(Day 1)

+/+, ear/nose/mouth: normal

Diet MB 1200 kcal with 28

Neck: JVP R-2 cmH2O

gram protein

Thorax: Symetris fusiformis,

Planned to check RDT, thin

retraction (-), HR: 140x/i,

blood smears, G6PD, LFT,

regular, murmur (-), RR: 24

RFT,

x/i, Ronchi -/-

culture,

Urinalysis,
and

Urine
PRC

Transfusion (11-5,6) x 4 x

Abdomen: Soepel, Normal

14 = 300

peristaltic, Hepar : palpable

Kemampuan : 5 x 14 = 75

2 cm BAC, Lien : palpable S

cc/12 hours

II
Extremities: Pulse: 140 x/i,

Result ( 07.00 pm)

regular, adequate pressure

Clinical Pathology

and volume, warm, CRT <

Hematologi

3, pale (+), pretibial edema

Malaria (+)

(-)
Others: Normal

Morfology
Erythrocytes: Ring form (+),
Trophozoite (+)

th

15 September 2015
S
O
A
o
Fever (-),
Sens: Alert, T: 36,8 C, BW: Malaria+
14 kg, BH: 104cm

anaemia

P
IVFD D5% NaCl 0,45% 50
gtt/i

Head: eye reflect +/+, isocor,

DHP tablet 1x1 for 3 days

pale conj. palpebral inferior

(Day 2)

+/+, ear/nose/mouth: normal

Diet MB 1200 kcal with 28

Neck: JVP R-2 cmH2O

gram protein

Thorax: Symetris fusiformis,

PRC Tranfusion 75 cc (Bag

18

retraction (-), HR: 120 x/i,

1)

regular, murmur (-), RR: 24

x/i, regular, Ronchi -/Abdomen: Soepel, Normal
peristaltic, Hepar: palpable 2
cm BAC, Lien : palpable S
II
Extremities: Pulse: 120 x/i,
regular, adequate pressure
and volume, warm, CRT <
3, pale (+), pretibial edema
(-)
Others: Normal
16 September 2015
S
O
A
o
Fever (-)
Sens: Alert, T: 36,8 C, BW: Malaria+anaemi
th

14 kg, BH: 104 cm

P
IVFD D5% NaCl 0,45% 50
gtt/i

Head: eye reflect +/+, isocor,

DHP tablet 1x1 for 3 days

pale conj. palpebral inferior

(Day 3)

Diet MB 1200 kcal with 28

Neck: JVP R-2 cmH2O

gram protein

Thorax: Symetris fusiformis,

PRC Tranfusion 75 cc (Bag

retraction (-), HR: 110 x/i,

2)

/+, ear/nose/mouth: normal

murmur (-), RR: 24 x/i,

Ronchi -/Abdomen: Soepel, Normal
peristaltic, Hepar: palpable 2
cm BAC, Lien : palpable S
II
Extremities: Pulse: 110 x/i,
regular, warm, CRT < 3,
pretibial edema (-)

Clinical Pathology
(11.42 AM)
Urinalysis
Complete Urine Morphology
Color : Yellow

19

Glocose : (-)
Bilirubin : (-)
Keton : (-)
Berat Jenis : 1.015
pH : 6
Urobilinogen : (-)
Nitrit : (-)
Leucocyte : (+)
Blood : (-)
Urine Sediment
Erythrocyte : 0-1
Leucocyte : 1-2
Epytel : 0-1
Casts : (-)
Crystal : (-)
th

17 September 21015
S
O
A
o
Fever (-)
Sens: Alert, T: 36,8 C, BW: Malaria+
14 kg, BH: 104 cm

anaemia

P
IVFD D5% NaCl 0,45% 50
gtt/i

Head: eye reflect +/+, isocor,

Diet MB 1200 kcal with 28

pale conj. palpebral inferior

gram protein

/-, ear/nose/mouth: normal

PRC Tranfusion 75 cc (Bag

Neck: JVP R-2 cmH2O

3)

Thorax: Symetris fusiformis,

Primakuin tablet 1 x 1/4 for

retraction (-), HR: 94 x/i,

14 days (Day 1)

murmur (-), RR: 20 x/i,

Ronchi -/Abdomen: Soepel, Normal
peristaltic, Hepar: palpable 2
cm BAC, Lien : palpable S
II
Extremities: Pulse: 94 x/i,

G6PD Deficiency : (-)

20

regular, warm, CRT < 3,

pretibial edema (-)
18th September 2015
S
O
Fever (-)

Sens: Alert, T: 36,6 oC, BW: Malaria

IVFD D5% NaCl 0,45% 50

14 kg, BH: 104 cm

gtt/i

Head: eye reflect +/+, isocor,

Diet MB 1200 kcal with 28

pale conj. palpebral inferior

gram protein

/-, ear/nose/mouth: normal

Primakuin tablet 1 x 1/4 for

Neck: JVP R-2 cmH2O

14 days (Day 2)

Thorax: Symetris fusiformis,

PRC Tranfusion 75 cc (Bag

retraction (-), HR: 100 x/i,

4)

regular, murmur (-), RR: 22

x/i, regular, ronchi -/Abdomen: Soepel, Normal
peristaltic, Hepar: palpable 2
cm BAC, Lien : palpable S
II
Extremities: Pulse: 110 x/i,
regular, warm, CRT < 3,
pretibial edema (-)

Check

Complete

Blood

Count after transfusion

Complete

Blood

Count

(09.11)
Test

Result

Hemoglobin

10.40

Erythrocyte

2.70x103

Leucocyte

5.40x103

Thrombocyte

275x103

Hematocryte

23.20

Eosinophil

7.40

Basophil

0.600

Neutrophil

35.90

Lymphocyte

49.40

Monocyte

6.70

Absolute

3.67

neutrophil

21

19th September 2015

S
O
A
o
Fever (-)
Sens: Alert, T: 36,8 C, BW: Malaria

Absolute

1.65

lymphocyte
Absolute

2.67

monocyte
Absolute

0.03

basophyl
MCV

85.90

MCH

38.50

MCHC

44.80

RDW

22.40

MPV

10.20

PCT

0.28

PDW

12.4

P
IVFD D5% NaCl 0,45% 50

14 kg, BH: 104 cm

gtt/i

Head: eye reflect +/+, isocor,

Diet MB 1200 kcal with 28

pale conj. palpebral inferior

gram protein

/-, ear/nose/mouth: normal

Primakuin tablet 1 x 1/4 for

Neck: JVP R-2 cmH2O

14 days (Day 3)

Thorax: Symetris fusiformis,

retraction (-), HR: 100 x/i,
murmur (-), RR: 24 x/i,
Ronchi -/Abdomen: Soepel, Normal
peristaltic, Hepar: palpable 2
cm BAC, Lien : palpable S
II
Extremities: Pulse: 100 x/i,
regular, warm, CRT < 3,
pretibial edema (-)
20th September 2015

22

S
Fever (-)

O
A
Sens: Alert, T: 36,6 oC, BW: Malaria

P
IVFD D5% NaCl 0,45% 50

14 kg, BH: 104 cm

gtt/i

Head: eye reflect +/+, isocor,

Diet MB 1200 kcal with 28

pale conj. palpebral inferior

gram protein

/-, ear/nose/mouth: normal

Primakuin tablet 1 x 1/4 for

Neck: JVP R-2 cmH2O

14 days (Day 4)

Thorax: Symetris fusiformis,

retraction (-), HR: 84 x/i,
murmur (-), RR: 20 x/i,
Ronchi -/Abdomen: Soepel, Normal
peristaltic, Hepar: palpable 2
cm BAC, Lien : palpable S
II
Extremities: Pulse: 84 x/i,
regular, warm, CRT < 3,
pretibial edema (-)

DISCUSSION AND SUMMARY

4.1.

Discussion
Malaria is one of endemic disease in tropical country or subtropic country.

Malaria is a health problem in Mexico, Caribia, Central America, Africa, India,

South East, and Indo Cina. It is estimated the prevalence of malaria up to 160-400
million cases. In Indonesia, malaria is still found in some provinces. Plasmodium

23

falciparum and Plasmodium vivax are the most species in Indonesia. Children are
one of most vulnerable groups affected by malaria.3,6 In this case, the patient is
children, 5 years, 11 month and has Plasmodium vivax malaria.
According to Pemprov (2010), in North Sumatera there are some endemic
regions of malaria, such as: Kabupaten Langkat, Deli Serdang, Labuhan Batu,
Serdang Bedagai, Asahan, Samosir, Tapanuli Tengah, Tapanuli Utara, Tapanuli
Selatan, Mandailing Natal, Nias, Batu Bara, Padang Lawas, Padang Lawas Utara
dan Kabupaten Labuhan Batu Utara.8 In this case, the patient is from Langkat.
In this case, the patient has a history of fever with unstable temperature.
Sometimes high grade fever and reduced with antipyretics. Patient also complain
shiverring while high fever. Patient also reported headache, myalgia if she had
fever . Cough and coryza was found in this 1 week. Her parents realized that
patient was pallor since 1 week. From physical examination, found that patient
has hepatosplenomegaly. Patient didnt have a travel to endemic area, but she lives
in endemic area, that is Langkat. The history, clinical manifestation and physical
examination are suitable with the theory. Based on Behrman, R.E (2004), children
with malaria often have special clinical features that differ from those of adults. In
children older than 2 months of age, symptoms of malaria vary widely from lowgrade fever and headache to a temperature greater than 104F with headache,
drowsiness, anorexia, nausea, vomiting, diarrhea, pallor, cyanosis, splenomegaly,
hepatomegaly, or any combination of these manifestations.2
Anemia is one of important pathologic processes have been identified in
patients with malaria. Anemia is caused by hemolysis, sequestration of
erythrocytes in the spleen and other organs, and inhibition of erythropoiesis by
TNFa. 5,6 In this case, patient has an anemia with Hemoglobin count is 5.60 gr/dl.
All episodes of malaria should be treated with at least two effective
antimalarial medicines with different mechanism of action that is by using
Artemisinin base Combination treatment (ACT) combined with Primaquine.1 ACT
which available in Indonesia are:
Artemether

Lumefantrine

Artesunate + Amodiaquine ( AS+AQ) ,

(AL),

and

Dihydroartemisinin-+Piperaquine

(DHP ).11 Based on a randomized study by Pasaribu et al (2013), Artesunate +

Amodiaquine and Dihydroartemisinin-+Piperaquine combined with primaquine

24

were effective for blood stage parasite clearance of uncomplicated P. vivax. Both
treatment were safe, but Dihydroartemisinin-+Piperaquine was better tolerated. 13
Patient treated with Dihydroartemisinin-+Piperaquine combined with Piperaquine.
Primaquine has oxidative side effect causing intravascular hemolysis in
populations in whom glucose-6-phosphate dehydrogenase (G6PD) deficiency. So,
before receive Primaquine, patient should be tested glucose-6-phosphate
dehydrogenase (G6PD) deficiency.12,13 In this case, patient was screened for
(G6PD) deficiency and the result was negative. So, the patient receive Primaquine
teraphy for 14 days.
4.2.

Summary
So the summary is, SS, 15 years and 7 months girl, that weighted 25 kg

and heighted 122 cm, admitted to Pediatric Department Unit in H. Adam Malik
General Hospital Medan on November 12th 2015 at 18.00 PM complaining lump
at the back since 15 years ago without any pain. The posture of the body became
hunch. She is diagnosed with Suspect Tubeculous Spondylitis + Pulmonary
Tuberculosis + malnutrition. Patients was treated with Antituberculousis Drug for

25

REFERRENCES
1. World Health Organization. Guidelines for The Treatment of Malaria. 3 rd
Edition.

2015.

Available

from:

http://www.who.int/about/licensing/copyright_form/en/index.html.

Accesed

on 11 September 2015.
2. Behrman, R.E; Kliegman, R.M; Jenson, H; Saunders, W.B. Nelson Textbook
of Pediatrics. 17th Edition. Elsevier; 2004.
3. World Health Organization. World Malaria Report 2014. Available from:
http://www.who.int/malaria/publications/world_malaria_report_2014/en.
Accesed on 12 September 2015.
4. World Health Organization. Malaria in Children. 2015. Available from:
http://www.who.int/malaria//areas/high_risk_groups/children/en/ . Accesed on
12 September 2015.
5. Kayser, F.H; Bienz, K.A; Eckert, J; Zinkernagel, R.M. Medical Microbiology.
2005.
6. Ikatan Dokter Anak Indonesia. Buku Ajar Infeksi dan Pediatri Tropis. Jakarta:
Badan Penerbit IDAI; 2008.
7. Mehta,

P.N.

Pediatric

Malaria.

2015.

Available

from:

http://emedicine.medscape.com/article/99842. Accesed on 11 September 2015.

8. Rizky, A. Peran Serta Masyarakat dalam Pencegahan Penyakit Malaria di
Desa Gunung Manaon Kecamatan Penyabungan Kabupaten Mandailing Natal.
2013. Available from: http://repository.usu.ac.id. Accesed on 17 September
2015
9. Centers for Disease Control and Prevention. Malaria. 2012. Available from:
http://www.cdc.gov/malaria. Accesed on 12 September 2015.
10. Departemen Kesehatan Republik Indonesia. Pedoman Penatalaksanaan Kasus
Malaria di Indonesia. 2008
11. Buletin Jendela Data dan Informasi Kesehatan Kementrian Kesehatan
Republik Indonesia. Epidemiologi Malaria di Indonesia. Triwulan I. 2011.
12. Peraturan Menteri Kesehatan Republik Indonesia. Pedoman Tata Laksana
Malaria. 2013.

26

13. Pasaribu, A.P; Chokejindachai,W; Sirivichayakul,C; Tanomising,N; Chavez, I;

et al. A Randomized Comparison Dihydroartemisinin-Piperaquine and
Artesunate-Amodiaquine Combined with Primaquine for Radical Treatment
of Vivax Malaria in Sumatera,Indonesia. The Journal of Infectious Diseases.
2013.

27