CASE PRESENTATION

RHEUMATIC FEVER IN CHILDREN

Supervisor:
dr. Ulynar Marpaung, Sp.A

Created by:
Nevy Ulfah Hanawati
1102014192

DEPARTMENT OF PEDIATRIC
BHAYANGKARA TK.I RADEN SAID SUKANTO HOSPITAL
FACULTY OF MEDICINE YARSI UNIVERSITY
ROTATION PERIOD 10th SEPTEMBER – 17th NOVEMBER
2018
 CONTENTS

CONTENTS ............................................................................................................ 1
PREFACE ............................................................................................................... 2
CHAPTER I – CASE ILLUSTRATION ................................................................ 3
CHAPTER II – FOLLOW UP .............................................................................. 21
CHAPTER III – LITERATURE REVIEW .......................................................... 40
CHAPTER IV – CASE ANALYSIS .................................................................... 52
REFERENCE ........................................................................................................ 54

1
 PREFACE

Rheumatic fever (RF) is a leading cause of acquired heart disease in children

and young adults in many parts of the world. Previous series have reported that RF
both is uncommon and may present differently in children who are younger than 5
years.
Acute rheumatic fever results from an autoimmune response to infection
with the group A streptococcus (GAS)—Streptococcus pyogenes. The illness is
characterised by varying degrees of inflammation of the joints and the heart,
typically manifesting as polyarthritis and valvular regurgitation. Less commonly,
involvement of the basal ganglia during the autoimmune process results in chorea.
Except for the valve lesions, all other manifestations of acute rheumatic fever
resolve without sequelae. As the acute illness resolves, valvular lesions usually
reduce in severity, but can persist or progress, leading to chronic rheumatic heart
disease. Although acute rheumatic fever itself is rarely life-threatening, rheumatic
heart disease can cause heart failure, stroke, or death. Acute rheumatic fever and
rheumatic heart disease are diseases of poverty, and have largely disappeared from
affluent parts of the world.
Acute rheumatic fever is an inflammatory response to group A streptococcal
infection which typically occurs two to three weeks after a throat infection. Acute
rheumatic fever is characterised by a clinical syndrome, and the most common
manifestations are painful joints and carditis. Carditis occurs in about 80% of
people with rheumatic fever and commonly affects the mitral and aortic valves,
resulting in regurgitation. Other less common clinical features include abnormal
involuntary movements (chorea), rash (erythema marginatum), and subcutaneous
nodules.
The inflammatory process slowly resolves over weeks to months, but about
half of individuals are left with chronic rheumatic heart disease. Although death
from acute rheumatic carditis is not common, chronic rheumatic heart disease
causes considerable morbidity including arrhythmias, stroke, infective endocarditis,
pregnancy complications, and premature death.

2
 CHAPTER I
CASE ILLUSTRATION

A. IDENTITY
1. Patient
a. Name : Child BD
b. Date of birth : 09th May 2002
c. Sex : Male
d. Address : Jl. Swadaya I No. 49, South Jakarta
e. Tribe : Javanese
f. Religion : Islam
g. Education : High school
2. Parents
Table 1. Identity of Parent’s Ch. BD
Father Mother
Name Mr. D Mrs. AY
Date of birth 6rd January 1966 14th May 1970
Sex Male Female
Address Jl. Swadaya I No. 49, South Jakarta Jl. Swadaya I No. 49, South Jakarta
Tribe Javanese Javanese
Religion Islam Islam
Education High school High School
Occupation Laborer Housewife

Relationship with patient: Biological parents

B. HISTORY
History was taken from the patient (autoanamnesis) at Parkit I Bhayangkara
Hospital R. Said Sukanto, East-Jakarta on September 11th 2018.
1. Chief Complaint
Fever since 5 days before admission to hospital.
2. Additional Complaint
Cough, nausea, vomiting and headache

3
3. History of Present Illness
16 years old boy came to the hospital emergency room with main
complaint fever since 5 days before admission to hospital. Additional
complaint are cough, nausea, vomiting, and headache.
Since 7 days before patient entered the hospital, patient complained
about cough. Cough with sputum, color of sputum is white, there is no
blood. He feels coughing all day. He had taken the medicine but did not
recover.
Since 5 days before patient entered the hospital, the patient
complained about fever and It feels up and down. The temperature rises at
night but the highest temperature is not measured at home. Patient has taken
paracetamol. After that, the fever was felt down but 4 hours later the fever
returned.
Since 2 days before patient entered the hospital, patient also
complained of nausea, vomiting and headache. Patient vomiting only
1x/day, vomit contains liquid and food, volume of vomiting as much as 1/2
cup of glass. But, patient vomiting doesn’t contains blood, the colour of
vomit not blackish or green, and vomiting doesn't spray.
4. History of Past Illness
Table 2. History of Past Illness
Disease Age
Upper Respiratory Infection (e.g.
Pharyngitis/Tonsilitis)
Diarrhea -
Otitis -
Pneumonia -
Tuberculosis + (10 years old)
Seizure -
Heart -
Blood -

4
 Diphtheria -
Measles -
Mumps -
Dengue fever -
Typhoid fever -
Worms infection -
Allergy -
Accident -

5. Allergy history
a. Food allergy: denied
b. Drugs allergy: denied
c. Asthma bronchial: denied
6. Dietary History
Table 3. Dietary history
Age Breast/formula Fruit/ Milk Steam Rice & Side
(years) milk biscuit porridge Rice dishes
0-6 ASI ad libitum - - - -
months
6 months- ASI ad libitum - Porridge - -
1 year 3x/day
1-2 years ASI ad libitum - Porridge - -
and formula 3x/day
milk (SGM)
2-5 years Formula milk Fruit/ - Steam
(SGM) biscuit rice
5-9 years Formula milk Fruit/ - - Rice & Side
(SGM) biscuit dishes 2-
3x/day

7. Growth and Development History

a. First dentition : 6 months old

5
 b. Gross motor
a) Head up : 1 month old
b) Prone : 4 months old
c) Sit : 6 months old
d) Crawl : 8 months old
e) Stand : 9 months old
f) Walk : 11 months old
g) Run : 13 months old
c. Fine motor
a) Reaches for objects : 3 months old
b) Puts objects in mouth : 6 months old
c) Throw objects : 8 months old
d) Scribbling paper : 14 months old
d. Social skills
a) Smile : 1 month old
b) Hugs and kisses : 11 months old
c) Initiates play : 13 months old
d) Imitates adult activities : 15 months old
e. Language skills
a) Vocalized : 1 months old
b) Laughs : 2 months old
c) Squeals : 2 months old
d) Jabbers : 6 months old
e) Speaks : 1 year old
f) Development disorder : None
g) Mental/emotion : Stable
8. Marital History
a. Mother’s Pregnancy History
The mother routinely checked her pregnancy to midwife. She
denied any problem noted during her pregnancy. She took vitamins
routinely given.

6
 b. Child’s Birth History
a) Maternity care : Midwife
b) Mode of delivery : Normal, spontaneous, no complication
c) Gestational age : 39 weeks
c. Child status
a) Weight of birth : 3200 gr
b) Length of birth : 51 cm
c) Head circumference : 34 cm
d) Congenital anomaly : -
According to the mother, the baby started to cry and the baby's skin is red.
9. Immunization History
Table 4. Immunization History
Immunization Frequency Time
BCG 1 time 1 month old
Hepatitis B 3 times 0, 1, 6 months old
DPT 3 times 2, 4, 6 months old
Polio 4 times 0, 2, 4, 6 months old
Hib 3 times 2, 4, 6 months old
Measles 2 times 9 months old, 6 years old
Varicella 1 times 7 years old

10. Family history

a. Reproduction Pattern
Table 5. Reproduction pattern
No Age Sex Alive Stillbirth Abor Death Health
tion (cause) status
1. 25 yo Male V - - - Healthy
2. 16 yo Male V - - - Patient

 Patient’s both parents were married when they were 26 years old and 22
years old, and this is their first marriage.

7
  There are not any significant illnesses or chronic illnesses in the family
declared.
b. History of Disease in Other Family Members / Around the House
There is no one living around their home known for having the
same condition as the patient.
C. PHYSICAL EXAMINATION
Physical examination was held on September 11th 2018 at Parkit I ward
Bhayangkara Hospital, R. Said Sukanto Jakarta.
1. General Examination
a. General condition : Mild ill
b. Awareness : Composmentis
c. Vital sign :
a) Blood Pressure : 110/80 mmHg
b) Heart rate : 92 bpm
c) Respiratory rate : 22 times/min
d) Temperature : 39,8 C
d. Anthropometry :
a) Body weight : 67 kg
b) Body height : 173 cm
2. Nutritional Status
Nutritional status measured based on National Center for Health
Statistics (2000):
a. WFA : 67/62 x100 = 108% (Good)
b. HFA : 173/174 x 100 = 99,4% (Good)
c. WFH : 67/60 x 100 = 111% (Good)
Conclusion: Nutrition status of the patient is good

8
Figure 1. Nutrition Status of the Patient

9
3. Head to Toe Examination
a. Head :
a) Measurement : Normocephalic
b) Hair and scalp : Black, normal distribution, strong
c) Eyes : Pale conjunctiva -/-, icteric sclera -/-, pupil
isokor 3/3 mm, direct and indirect light response +/+ and +/+
d) Ears : Normotia, secret/cerumen -/-, hyperemia -/-
e) Nose : Septum deviation (-), nostril breathing (-),
edema conca -/-, secret (-)
f) Mouth
 Lips : Dry
 Teeth : Caries dentist (-)
 Tongue : Dirty, tremor (-)
 Tonsil : T1/T1, detritus (-), wide crypt (-)
 Pharynx : Hyperemia (-)
b. Neck : No enlargement of lymph node
c. Thorax :
a) Chest wall : Retraction (-)
b) Pulmo :
 Inspection : Symmetric when static and dynamic
 Palpation : Vocal fremitus +/+
 Percussion : Sonor +/+
 Auscultation : Vesicular +/+, rhonchi -/-, wheezing -/-
c) Cor :
 Inspection : Ictus cordis can’t be seen
 Palpation : Ictus cordis felt in ICS V Linea MCS
without thrill
 Percussion :
- Margin of right heart : ICS IV Linea PSD
- Margin of left heart : ICS V Linea MCS

10
 - Margin of waist heart : ICS III Linea PSS
 Auscultation : S1S2 regular, murmur (-), gallop (-)
d. Abdomen:
a) Inspection : Even, there is no a widening of the veins, no spider
nevi
b) Auscultation : Bowel sound (+) normal
c) Palpation : Hepar and lien not palpable, epigastric tenderness
d) Percussion : Tympani
e) Other : Ballotement (-)
e. Anal and rectum : anal exist, no abnormalities
f. Genital : Normal
g. Extremities : Warm +/+/+/+, edema -/-/-/-, CRT < 2s, normal
ROM
h. Skin : Cyanosis (-), icteric
i. Vertebrae : Deformity (-), gibbus (-), kyphosis (-), scoliosis (-),
lordosis (-)
4. Neurologic examination
a. Physiologic reflex:
a) Brachioradialis : +2/+2
b) Biceps : +2/+2
c) Triceps : +2/+2
d) Patella : +2/+2
e) Achilles : +2/+2
b. Pathologic reflex :-
c. Motoric :5555 5555
5555 5555
d. Meningeal sign :-

11
D. DOCUMENTATION

12
 Figure 2. Documentation of Patient
E. LABORATORIUM EXAMINATION
a. Laboratory on September 11th 2018
Table 6. Routine Blood Count
Results Normal range
Haemoglobin 15,2 g/dl 12-14 g/dl
Leucocyte 4.300 u/l 5.000-10.000 u/l
Haematocrit 42 % 37-43 %
Thrombocyte 149.000 /ul 150.000-400.000 /ul

13
 b. Laboratory on September 12th 2018
Table 7. Routine Blood Count
Results Normal range
Haemoglobin 14,5 g/dl 12-14 g/dl
Leucocyte 3.600 u/l 5.000-10.000 u/l
Haematocrit 41 % 37-43 %
Thrombocyte 136.000 /ul 150.000-400.000 /ul

Table 8. Clinical Chemistry Examination

Results Normal range
Natrium 131 mmol/l 135-145 mmol/l
Potassium 3,5 mmol/l 3,5-5,0 mmol/l
Chloride 96 mmol/l 98-108 mmol/l

Table 9. Serology/Immunology of Widal

Results Normal range
Thypi O +1/80 Negative
Parathypi AO Negative Negative
Parathypi BO Negative Negative
Parathypi CO Negative Negative
Thypi H +1/80 Negative
Parathypi AH Negative Negative
Parathypi BH Negative Negative
Parathypi CH Negative Negative

c. Laboratory on September 13th 2018

Table 10. Routine Blood Count
Results Normal range
Haemoglobin 13,7 g/dl 12-14 g/dl
Leucocyte 5.200 u/l 5.000-10.000 u/l
Haematocrit 40 % 37-43 %
Thrombocyte 101.000 /ul 150.000-400.000 /ul

14
 d. Laboratory on September 14th 2018
Table 11. Routine Blood Count
Results Normal range
Haemoglobin 13,2 g/dl 12-14 g/dl
Leucocyte 5.800 u/l 5.000-10.000 u/l
Haematocrit 38 % 37-43 %
Thrombocyte 105.000 /ul 150.000-400.000 /ul

e. Laboratory on September 15th 2018

Table 12. Routine Blood Count
Results Normal range
Haemoglobin 14,0 g/dl 12-14 g/dl
Leucocyte 11.800 u/l 5.000-10.000 u/l
Haematocrit 40 % 37-43 %
Thrombocyte 114.000 /ul 150.000-400.000 /ul

f. Laboratory on September 16th 2018

Table 13. Routine Blood Count
Results Normal range
Haemoglobin 12,7 g/dl 12-14 g/dl
Leucocyte 7.400 u/l 5.000-10.000 u/l
Haematocrit 36 % 37-43 %
Thrombocyte 148.000 /ul 150.000-400.000 /ul

Table 14. Serology/Immunology

Results Normal range
Widal
Thypi O Negative Negative
Parathypi AO Negative Negative
Parathypi BO Negative Negative
Parathypi CO Negative Negative
Thypi H +1/80 Negative

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Parathypi AH Negative Negative
Parathypi BH Negative Negative
Parathypi CH Negative Negative
Anti Dengue Ig G – Ig M
Ig G Negative Negative
Ig M Negative Negative

Table 15. Complete Urine Examination

Results Normal range
Color Light Yellow
Appearance Clear
Specific Gravity 7,0 5-8,5
pH 1,010 1,000-1,030
Protein - Negative
Bilirubin - Negative
Glucose - Negative
Ketones - Negative
Blood/Hb - Negative
Nitrite - Negative
Urobilinogen 0,1 0,1-1,0 IU
Leucocyte - Negative
Sediment
WBC 0-1/LPB 0-5/LPB
RBC 0-1/LPB 1-3/LPB
Epithelial cells +
Cylinder -
Crystal -
Others -

16
 g. Laboratory on September 17th 2018
Table 16. Mycrobiology
Results Normal range
BTA 3x
BTA Sewaktu Negative Negative
BTA Pagi Negative Negative
BTA Sewaktu Negative Negative
Gram Coloring
Leucocyte cells 2-3 /LPI
Epithelial cells Little (3-5 /LPI)
Basil Bacterial
Positive Gram Not Found
Negative Gram 10-15 /LPI
Coccus Bacterial
Positive Gram Not Found
Negative Gram Not Found
Tetracoccus Bacterial Not Found
Coccobacil Bacterial
Negative Gram Not Found
Xpert MTB-RIF
Assay G4 (In Vitro Negative Not Detected
Diagnostic)

17
 h. Laboratory on September 18th 2018
Table 17. Routine Blood Count
Results Normal range
Haemoglobin 13,6 g/dl 12-14 g/dl
Leucocyte 8.600 u/l 5.000-10.000 u/l
Haematocrit 40 % 37-43 %
Thrombocyte 259.000 /ul 150.000-400.000 /ul
Blood 65 mm/jam <15 mm/jam
Sedimentation Rate
Table 18. Serology/Immunology of Widal
Results Normal range
Thypi O Negative Negative
Parathypi AO Negative Negative
Parathypi BO Negative Negative
Parathypi CO Negative Negative
Thypi H +1/80 Negative
Parathypi AH Negative Negative
Parathypi BH Negative Negative
Parathypi CH Negative Negative

i. Laboratory on September 19th 2018

Table 17. Serology/Immunology
Results Normal range
Rheumatoid Factor Reactive Not Reactive

j. Laboratory on September 20th 2018

Table 17. Routine Blood Count
Results Normal range
Haemoglobin 13,4 g/dl 12-14 g/dl
Leucocyte 6.700 u/l 5.000-10.000 u/l
Haematocrit 40 % 37-43 %
Thrombocyte 239.000 /ul 150.000-400.000 /ul

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F. THORAX RONTGEN

Figure 3. Thorax Rontgen

a. Sine / diaphragm well
b. Mediastinum does not widen
c. Cor good impression
d. Pulmo: rough complexion, right paracardial patches
e. Pleural space does not widen
f. Hilus calcification (+)
g. Bone does not appear to be abnormal
h. Impression: Bronchopneumonia dextra

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G. SUMMARY
A 16 years old boy came to emergency room, Bhayangkari R. Said
Sukanto’s hospital with her parents because of fever since 5 days before
admission to hospital. Complaints are associated with nausea, vomiting and
headache. On physical examination patient looked mild ill, temperature: 39,8
C, and dry lips. Additional examination theres: Hemoglobin 15,2 g/dl,
leucocyte 4.300 u/l, haematocrit 42%, and thrombocyte 149.000 /ul.
H. WORKING DIAGNOSIS
1. Prolonged Fever ec suspec Rheumatic Fever
2. Bronchopneumonia dextra
3. Normal Growth Status
4. Good Nutritional Status
5. Complete Immunization Status
I. PROGNOSIS
Quo ad vitam: ad bonam
Quo ad functionam: ad bonam
Quo ad sanationam: dubia ad bonam
J. TREATMENT
a. IVFD RL 1750 cc/24 hr (20 TPM macro)
b. Rantin 2 x 50 mg IV
c. Paracetamol 3 x 500 mg PO

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 CHAPTER II
FOLLOW UP
Table 18. Follow Up of Patient
September 12th 2018
A 16 years old boy, 1 day treatment with a major complaint: fever since
5 days before admission to hospital. Additional complaint: nausea,
S vomiting and headache.
- Fever (+)
- Rash (+)
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 120/80 mmHg
Temperature : 38,2 °C
Pulse : 101 x/min
Respiratory rate : 20 x/min
Head
 Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
O appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck

21
  Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Dengue Hemorraghic Fever
 IVFD RL 2500 cc/24 jam (21 TPM)
P  Rantin 2 x 50 mg IV
 Paracetamol 3 x 500 mg PO
September 13th 2018
A 16 years old boy, 2 days treatment with Dengue Hemorraghic Fever
- Fever (+)
S
- Vomitus (+)
- Rash (+)
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 100/60 mmHg
O Temperature : 38,5 °C
Pulse : 94 x/min
Respiratory rate : 22 x/min
Head

22
  Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Dengue Hemorraghic Fever
P  IVFD RL 2500 cc/24 jam (21 TPM)

23
  Cefotaxime 2 x 1 gr IV
 Rantin 2 x 50 mg IV
 Paracetamol 3 x 500 mg PO
 Ondancentron 3 x 4 mg IV
September 14th 2018
A 16 years old boy, 3 days treatment with Dengue Hemorraghic Fever
- Fever (+)
S
- Nausea (+)
- Cough (+)
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 100/70 mmHg
Temperature : 37,5 °C
Pulse : 100 x/min
Respiratory rate : 22 x/min
Head
 Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
O appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck

24
  Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Dengue Hemorraghic Fever
 IVFD RL 2500 cc/24 jam (21 TPM)
 Cefotaxime 2 x 1 gr IV
P  Rantin 2 x 50 mg IV
 Paracetamol 3 x 500 mg PO
 Ondancentron 3 x 4 mg IV
September 15th 2018
A 16 years old boy, 4 days treatment with Dengue Hemorraghic Fever
and Suspect Thypoid Fever
- Fever (+)
S
- Nausea (+)
- Cough (+)
- Limp (+)
Consciousness : Compos Mentis
O General condition : Mild ill
Blood pressure : 110/80 mmHg

25
Temperature : 36,2 °C
Pulse : 80 x/min
Respiratory rate : 28 x/min
Head
 Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.

26
 Extremities
 Warm, no cyanosis, no oedema or gross deformities.
 Dengue Hemorraghic Fever
A
 Susp thypoid fever
 IVFD RL 2500 cc/24 jam (21 TPM)
 Ceftriaxone 1 x 2 gr IV
P  Rantin 2 x 50 mg IV
 Paracetamol 3 x 500 mg PO
 Ondancentron 3 x 4 mg IV
September 16th 2018
A 16 years old boy, 5 days treatment with Prolonged Fever ec Drug
Fever
- Fever (+)
S - Nausea (+)
- Cough (+)
- Limp (+)
- Sometimes hard to breath
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 100/60 mmHg
Temperature : 38 °C
Pulse : 100 x/min
Respiratory rate : 24 x/min
O Head
 Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.

27
 Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Prolonged Fever ec Drug Fever
 IVFD RL 2500 cc/24 jam (21 TPM)
 Ceftriaxone 1 x 2 gr IV
P  Rantin 2 x 50 mg IV
 Paracetamol 3 x 500 mg PO
 Ondancentron 3 x 4 mg IV
September 17th 2018
S A 16 years old boy, 6 days treatment with Drug fever

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 - Fever (+)
- Nausea (+)
- Cough (+)
- Limp (+)
- Joint pain
- Sometimes hard to breath
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 110/70 mmHg
Temperature : 37,8 °C
Pulse : 80 x/min
Respiratory rate : 28 x/min
Head
 Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
O
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest

29
  No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Prolonged Fever ec Drug fever
P All procedures are terminated
September 18th 2018
A 16 years old boy, 7 days treatment with Prolonged Fever ec Drug
fever
- Fever (+)
- Nausea (+)
S
- Vomiting (+)
- Cough (+)
- Limp (+)
- Joint pain
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 110/70 mmHg
Temperature : 38 °C
O
Pulse : 98 x/min
Respiratory rate : 22 x/min
Head
 Normocephal

30
 Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Prolonged Fever ec Drug Fever
 Ambroxol 3 x 1 tab PO
P
 Neurobion 3 x 1000 mg PO

31
September 19th 2018
A 16 years old boy, 8 days treatment with Prolonged Fever ec Drug
fever
- Fever (+)
S - Nausea (+)
- Vomiting (+)
- Cough (+)
- Joint pain
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 110/70 mmHg
Temperature : 38 °C
Pulse : 98 x/min
Respiratory rate : 22 x/min
Head
 Normocephal
Eyes
 Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
O
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No

32
 lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Prolonged Fever ec Drug Fever
 Ambroxol 3 x 1 tab PO
P  Aspilet 3 x 2 tab PO
 Azitromicyn 1 x 1 tab PO
September 20th 2018
A 16 years old boy, 9 days treatment with Prolonged Fever ec Drug
S fever
- No complaint
Consciousness : Compos Mentis
General condition : Mild ill
Blood pressure : 100/60 mmHg
Temperature : 37 °C
O Pulse : 90 x/min
Respiratory rate : 20 x/min
Head
 Normocephal
Eyes

33
  Pupils equal, round and reactive to light. Extraocular muscle
appeared intact. Pale conjungtiva -/-, icteric -/-
Ears
 Clear external auditory canals. No erythema or bulging.
Nose
 Normal pink mucosa, no discharge or blood visible. Normal
midline septum.
Mouth
 Dry lips, dirty tongue
Pharynx
 Hyperaemic pharynx (-), T1-T1
Neck
 Grossly non-swollen. No tracheal deviation. No
lymphadenopathy.
Chest
 No increase of accessory muscles.
Lungs
 Lungs are clear to auscultation bilaterally. No stridor, wheezes,
and rhonci.
Cor
 Normal S1-S2 rate and rhythm. No murmurs, gallops or rubs.
Abdomen
 Soft, non-tender, non-distended. Bowel signs present. No
Hepatomegaly and Splenomegaly.
Extremities
 Warm, no cyanosis, no oedema or gross deformities.
A Prolonged Fever ec Drug Fever
 Ambroxol 3 x 1 tab PO
P  Aspilet 3 x 2 tab PO
 Azitromicyn 1 x 1 tab PO

34
 CHAPTER III
LITERATURE REVIEW
A. Definition
Acute rheumatic fever results from an autoimmune response to infection
with the group A streptococcus (GAS)—Streptococcus pyogenes. The illness is
characterised by varying degrees of inflammation of the joints and the heart,
typically manifesting as polyarthritis and valvular regurgitation.4
B. Epidemiology
The incidence of acute rheumatic fever varies widely, mainly by
socioeconomic development. Although the disease is no longer a public health
problem in highincome countries, occasional outbreaks do occur, and the
disease continues to persist in some of these countries. Data from prospective
studies suggest that acute rheumatic fever annual incidence ranges between
eight and 51 per 100 000 among children and young people. More recent reports
from two endemic regions indicate annual rates that are lower than 20 per 100
000,7,8 but incidence remains high in the South Pacific, and among indigenous
people in Australia and New Zealand. However, the true incidence of acute
rheumatic fever in large parts of Africa and Asia is unknown, because of the
absence of regional data (table 1).4

Table 19. Epidemiology of Rheumatic Fever

35
 There is little data regarding disease burden in low income countries
most affected by the disease. However, in recent years epidemiological studies,
including surveys using portable echocardiographic screening, have described
rheumatic heart disease burden in Africa, Asia, and Oceania, with prevalence
varying between 2% and 6% and around 90% of cases detected by
echocardiography being asymptomatic and subclinical.6
Although high rates of acute rheumatic fever and rheumatic heart
disease have been observed within particular families and ethnic groups,
susceptibility is incompletely understood. Even in populations where there is
ongoing exposure to group A streptococcus, only a small proportion, estimated
to be up to 6%, will develop acute rheumatic fever or rheumatic heart disease.
Risk is strongly associated with household crowding and socioeconomic
deprivation. Currently a large African genome-wide association study aims to
determine whether there is a genetic susceptibility to rheumatic heart disease.6
C. Etiology
Poverty and social disadvantage are among the strongest predisposing
factors for developing acute rheumatic fever, acting possibly through household
overcrowding, which facilitates easy transmission of GAS. Ethnicity could be
another predisposing factor, but the increased susceptibility in some ethnic
groups might be explained by the higher prevalence of poverty and
overcrowding in these groups, rather than genetic susceptibility.4
The incidence of acute rheumatic fever is highest among children aged
10–14 years, followed by those aged 5–9 years. Children younger than 5 years
rarely develop acute rheumatic fever, and a first episode is rare beyond age 30
years. Recurrences can occur at older ages but are rare beyond 40 years. Males
and females are equally likely to have acute rheumatic fever, although
rheumatic heart disease is more common in females.4
Streptococcal pharyngitis is a common infection in childhood.
Pharyngitis caused by rheumatogenic strains of group A streptococcus in a
susceptible host triggers an abnormal immune inflammatory response. The
exact nature of this response is incompletely understood. It is thought to involve

36
 cross reactivity of streptococcal antibodies against myocardium, synovial
tissue, and, in chorea, the basal ganglia. Molecular mimicry directs the immune
response, and the cross reacting antibodies activate the inflammatory process in
body tissues. In carditis, activated monoclonal autoantibodies produce T cell
infiltration in the valve endothelium.
D. Pathophysiology
The pathogenesis of acute rheumatic fever remains incompletely
understood. Evidence supports the view that acute rheumatic fever is the result
of an autoimmune response to pharyngeal infection with GAS in genetically
predisposed individuals, which is mediated through molecular mimicry. About
0,3–3% of people with GAS pharyngitis develop acute rheumatic fever,
depending on genetic predisposition and the virulence of the infecting strain.
Although some genetic and epidemiological evidence exists for skin infection
as the event that leads to acute rheumatic fever, pharyngeal infection is
considered to be the trigger in most cases. Streptococcal antigens activate
humoral and cell-mediated immune pathways leading to the production of
antibodies against streptococcal components, which cross-react with human
proteins. This results in immune-mediated inflammation and injury (figure 2).
Evidence from numerous small candidate-gene studies, and more
recently, two genome-wide association studies, suggests that genetic
susceptibility could be conferred by polymorphisms of genes involved both in
the innate and adaptive immune pathways (panel 2). The genetic susceptibility
to acute rheumatic fever is heritable, as shown by the higher risk of concordance
among monozygotic twins than dizygotic twins (44% vs 12%). Inheritance is
non-Mendelian and polygenic, with variable and incomplete penetrance.
Ongoing large genome-wide association studies will provide further insights.
There are several reasons why molecular mimicry is believed to be the
most likely mechanism underlying the development of autoimmunity in acute
rheumatic fever. First, the GAS M protein and the carbohydrate antigen (N-
acetyl-beta-D-glucosamine) share antigenic epitopes with human cardiac
myosin and laminin on heart valves. Second, monoclonal antibodies against

37
these antigens, derived from tonsillar and peripheral blood lymphocytes of
patients with acute rheumatic fever, cross-react in vitro with human myosin and
valvular endothelium. Finally, immunisation with recombinant streptococcal M
protein induces autoantibody formation and valvulitis in Lewis rats. Structural
similarity between the myosin epitopes and heart valve proteins, such as laminin
and vimentin, could be the basis of antibody-mediated damage to valve
structures. Although a wide variety of GAS emm types can induce carditis, a
mechanism common to all of them could be the targeting of epitopes in the S2
subregion of human cardiac myosin by autoantibodies. Molecular mimicry also
underlies the cell-mediated immune inflammation that occurs in acute
rheumatic fever. T-cell clones derived from rheumatic lesions react with myosin
and valvederived proteins, and release inflammatory cytokines upon exposure
to these antigens in vitro.

Figure 4. Mediators of genetic susceptibility to acute rheumatic fever

Valve damage in acute rheumatic fever occurs as a result of both
humoral and cellular immune responses against valve proteins. Binding of
cross-reactive antibodies at the valve surface induces the upregulation of
vascular cell adhesion molecule 1, which facilitates the adherence and

38
infiltration of activated CD4 T cells and B lymphocytes. Local tissue damage is
mediated predominantly through a T helper cell 1 response, leading to
production of inflammatory cytokines such as interferon γ and tumour necrosis
factor α, with decreased concentrations of interleukins 4 and 10 (figure 2). Local
epitope spreading results in the identification of other self-antigens (vimentin
and collagen), which causes amplification of immune damage. Inflammation
leads to neovascularisation and healing by fibrosis, causing the characteristic
valve lesions of rheumatic heart disease. Likewise, antibodies against GAS N-
acetyl-beta-D-glucosamine cross-react with neuronal cells in the basal ganglia,
causing the release of excess dopamine, which leads to chorea. Accumulation
of immune complexes can cause the transient, migratory joint manifestations
associated with acute rheumatic fever.

Figure 5. Pathophysiology of Rheumatic Fever

39
 Mechanisms other than molecular mimicry have also been proposed to
explain the pathogenesis of acute rheumatic fever. Streptococcal M protein
binding to basement membrane collagen type 4 epitopes can induce
autoimmunity to collagen, resulting in inflammation and scarring of valve
leaflets. However, antibodies against collagen do not induce valvulitis in animal
models. Therefore, molecular mimicry is probably essential for induction of
autoimmunity and initiation of valve damage during acute rheumatic fever, and
antibodies against collagen could contribute to disease progression.
E. Diagnosis Investigation
In endemic regions in low-income countries, less emphasis should be
placed on obtaining evidence of preceding streptococcal infection, because
bacteriological diagnosis is seldom sought, and anti-streptolysin O titres alone
might not be sufficiently sensitive or specific. Similarly, temperature records
during fever might not be available, and fever could be masked by the use of
overthe-counter antipyretics. Despite these barriers to the strict application of
the Jones criteria, correctly identifying patients who will develop chronic
rheumatic heart disease is imperative. Cardiac involvement at baseline, detected
by echocardiography, is the best predictor of developing rheumatic heart disease
in the future. Because 70–90% of patients with acute rheumatic fever have
echocardiographic carditis, all patients with a high probability of acute
rheumatic fever based on clinical symptoms should under go echocardiography.
Although in developed countries acute rheumatic fever as a cause of joint
symptoms is rare both in the community and in hospital settings, the small
amount of data available from developing countries indicate a high likelihood
of acute rheumatic fever among patients presenting with joint symptoms. In
hospital-based studies, the proportion of patients with arthritis who had acute
rheumatic fever was 15% in the West Indies and 41% in India. Therefore, we
suggest that all children and adolescents in endemic regions who have joint
manifestations (polyarthritis, polyarthralgia, or monoarthritis), with evidence of
elevated erythrocyte sedimentation rate (ESR) or C-reactive protein, with or
without fever, should have echocardiography for the detection of carditis.

40
 Figure 6. Common Clinical Features of Acute Rheumatic Fever
Carditis should be diagnosed using the modified World Heart Federation
criteria suggested by Gewitz and colleagues. The presence of carditis should be
sufficient to make a diagnosis of acute rheumatic fever (figure 3). A normal
echocardiogram documented during the index illness rules out carditis. If
facilities for echocardiography are not available locally (as can often be the
case), patients should be referred to an equipped centre for evaluation within 12
weeks of the onset of symptoms. This flexibility in the timing to obtain an
echocardiogram can ensure feasibility in most situations. Patients who have a
normal echocardiogram can be further assessed for acute rheumatic fever
(without carditis) based on the 2015 Jones criteria. The implications of incorrect
diagnosis in the absence of carditis are small, because cardiac involvement is

41
 unlikely during recurrences because of its mimetic nature. The suggested
approach is very similar to that used for the diagnosis of acute rheumatic fever
in patients presenting with chorea, and will improve sensitivity in moderate and
high-risk populations.
F. Differential Diagnosis

Figure 7. Differential Diagnosis of Acute Rheumatic Fever

42
G. Complications
For many people with mild to moderate carditis the degree of valvular
regurgitation stabilises or improves within 12 months after diagnosis.
Individuals who experience severe carditis during the initial episode, or
recurrences of rheumatic fever, are at greatest risk of severe chronic rheumatic
heart disease, which is associated with an increased risk of heart failure,
infective endocarditis, pregnancy complications, stroke, arrhythmias, and
premature death. Careful attention to ensure good adherence to benzathine
penicillin prophylaxis is required.
Antibiotic prophylaxis for endocarditis before dental procedures is
recommended for all individuals with rheumatic heart disease in Australasia, in
contrast with the American Heart Association guidelines, which restrict
antibiotics to a small group at highest risk of adverse outcomes from
endocarditis, and the UK, where the National Institute for Health and Care
Excellence (NICE) advocates that prophylactic antibiotics are not given in any
circumstances.
H. Treatment
Not all treatments for RF are based on randomised controlled trials.
Some are based on anecdotal evidence, common sense and proven safety.
1. Antibiotics
Penicillin (or erythromycin) in adequate doses given for 10 days is
considered mandatory to eradicate persistent group A streptococci from the
pharynx though this treatment has not been shown in controlled studies to
alter the cardiac outcome after one year.
2. Rest in bed
All patients with RF should be hospitalized and kept in bed for the
first three weeks of illness because carditis, if not already present, may
appear during this period.
a. Patients with polyarthritis only, are usually asymptomatic by the 2nd
or 3rd week of salicylate therapy and may then be gradually ambulated
while continuing on salicylates.

43
 b. Patients with significant murmurs (or echocardiographic evidence of
carditis), but no definite cardiomegaly or heart failure (with or without
polyarthritis), should be kept in bed for four weeks. This bed rest need
not be strict and in the last week may be broken by periods of
supervised ambulation of a few hours per day.
c. Patients with carditis and cardiomegaly, but no heart failure (with or
without polyarthritis), should be kept on bed rest for six weeks, the first
two weeks of which should be strict.
d. Patients with carditis and heart failure (with or without polyarthritis),
should be kept on strict bed rest until failure is controlled. It is wise to
maintain a modified bed rest until four weeks after anti-inflammatory
treatment is stopped (if no rebound occurs) or two weeks after the
spontaneous subsidence of a rebound.
e. No randomized studies have been done on the value of bed rest in RF.
3. Salicylates and/or steroids
a. In patients with arthralgia or mild arthritis only, salicylates should be
given in analgesic dosage. This is particularly wise when the diagnosis
is not definite.
b. Patients with moderate or severe arthritis but no carditis or with carditis
but no cardiomegaly or failure, should be treated with salicylates 90-
120 mg/kg/day for the first two weeks and then two-thirds of the dose
for the next 4-6 weeks.
c. Patients with carditis and cardiomegaly but no heart failure (±
polyarthritis), should be treated with salicylates as above. However, in
patients with marked cardiomegaly, salicylates are often insufficient to
control fever, discomfort and tachycardia or do so only at toxic or near
toxic doses. These patients may then be switched to steroids.
d. Patients with carditis and heart failure (± polyarthritis), should receive
prednisolone in a dose of 2mg/kg/day to be increased if control of heart
failure is not achieved. In severe cases, therapy may be initiated with
intravenous methylprednisolone. After 2 or 3 weeks, prednisolone may

44
 be slowly withdrawn, decreasing the daily dose at the rate of every 2
or 3 days and adding salicylates at standard doses. Salicylates should
be continued for 3 or 4 weeks after prednisolone is stopped. This
“overlap” therapy reduces the incidence of posttherapeutic clinical
rebounds.
e. Findings of meta-analyses indicate no benefit of salicylates over
corticosteroids or vice-versa in reducing the subsequent development
of RHD.
4. Other therapies
a. Naproxen has been used successfully as an alternative to salicylates in
one small randomized trial.
b. The heart failure of rheumatic carditis is often controlled with bed rest
and steroids only. If it is not, diuretics may be added first followed by
digitalis, if needed. Diuretics and vasodilators may be used in patients
with more severe haemodynamic decompensation. Digoxin should be
used with caution because of the risk of toxicity in the presence of
active myocarditis. Surgical treatment in the acute stage should be
considered when clinical therapy is ineffective to control cardic failure.
Valve repair, although technically more difficult, is the first choice for
younger patients.
c. Most cases of mild Sydenham chorea need no treatment. The condition
is usually benign and self-limited and many of the drugs are potentially
toxic. Treatment should be reserved for individuals with moderate to
severe chorea refractory to conservative management (reassurance and
moving of patient to a quiet and calm environment) or if movements
are distressing to patient or family. Findings of a small study concluded
that valproic acid was more effective than carbamazepine or
haloperidol.
d. Intravenous immunoglobulin does not seem to alter the extent and
severity of carditis or decrease chronic morbitidy.

45
 5. Treatment of rebounds
a. The termination of anti-inflammatory treatment may be followed in all
RF patients by the re-appearance within 2 or 3 weeks of lab
abnormalities (lab rebounds) or clinical abnormalities as well (clinical
rebounds).
b. All the lab rebounds and most of the clinical rebounds are best left
untreated or should be treated symptomatically with analgesic doses of
salicylates lest the full treatment be followed by another rebound and
the duration of the attack be lengthened. Only the most severe clinical
rebounds necessitate re-institution of the full original treatment.
c. Once rheumatic fever has subsided and more than 2 months have
elapsed after stopping treatment with anti-inflammatory drugs, RF
does not re-appear unless a new streptococcal infection occurs.
I. Prognosis
Rheumatic fever will go resolved spontaneously within 12 weeks even
if is not treated. With treatment, it can resolved within 2 weeks.
The ultimate prognosis, how ever, is determined by the level ogf heart
involvement with rheumatic fever. If the heart is severely affected, the patien
may go on to developed rheumatic heart disease. If it not treated, rheumatic
heart disease can cause scarring of the heart valves such as mitral stenosis, or
aortic stenosis. If not treated, destruction and scarring of the valves can lead to
heart failure.
Unfortunatelly, if a person has had one bout of rheumatic fever, he or
she is at higher risk for future bouts of rheumatic fever. There is seems to be
highes in the first ten years after the first bout of rheumatic fever. Because of
this risk, most pasien who have had one bout episode of rheumatic fever will be
placed on long term antibiotics to prevent another strep infection. This is usually
done with either panicillin by injection every three to four weeks or by taking
daily panicillin by oral. If the patient is allergic to penicillin, other antibiotics
such as eritromisin or clindamicin can be used.

46
 CHAPTER IV
CASE ANALYSIS
Table 20. Case Analysis

Case Theory

Unknown, patient there is no has Streptococcal pharyngitis is a

systematic disease, infections, common infection in childhood.
haematological disease, or consumed Pharyngitis caused by
Etiology
drugs before sick. rheumatogenic strains of group A
(Cause)
streptococcus in a susceptible host
triggers an abnormal immune
inflammatory response.

Patient complained fever, nausea, Fever, arthralgia, Polyarthritis,

Clinical
vomiting, headache, cough, and joint Erythema marginatum
Manifestation
pain. Subcutaneous nodules

Anamnesis
 Two major or one major and
Chief Complaint: fever since 5 days
two minor manifestations must
before admission to hospital.
be present, plus evidence of
Additional Complaint: nausea,
antecedent group A
vomiting, headache, cough, joint pain
streptococcus infection.
Physical Examination
 Major manifestations: carditis,
Vital Sign :
polyarthritis, chorea, erythema
Diagnosis
BP: 110/80 mmHg
marginatum, and subcutaneous
HR: 92 bpm
nodules
RR: 22 times/min
 Minor manifestations:
T: 39,8 C
arthralgia, fever, raised
Lips: dry
erythrocyte sedimentation rate
Ext: pain and heat in the joint
or Creactive protein
Laboratory
concentrations, and prolonged
ESR: 65 mm/hour

47
 Rheumatoid factor: reactive PR interval on
electrocardiogram
 Evidence of antecedent group
A streptococcus infection:
positive throat culture or rapid
antigen test for group A
streptococcus, raised or rising
streptococcal antibody titre

Treatment  Aspilet 3 x 2 tab PO  Antibiotics

 Azitromicyn 1 x 1 tab PO Penicillin (or erythromycin) in
 Neurobion 3 x 1000 mg PO adequate doses given for 10 days is
considered mandatory to eradicate
persistent group A streptococci from
the pharynx though this treatment
has not been shown in controlled
studies to alter the cardiac outcome
after one year.
 Salicylates and/or steroids
In patients with arthralgia or mild
arthritis only, salicylates should be
given in analgesic dosage.

48
 REFERENCE
1. Mistry, Raakhi M. 2015. Septic Arthritis and Acute Rheumatic Fever in
Children: The Diagnostic Value of Serological Inflammatory Markers. Journal
Pediatric Orthopedhy; 35(3): 318 – 322.
2. Tani, Lloyd Y. 2003. Rheumatic Fever in Children Younger Than 5 Years: Is
the Presentation Different?. Pediatric; 112(5): 1065 – 1068.
3. Young N S, Kaufman D W. 2008. The Epidemiology of Rheumatic Fever.
Pediatrica.
4. Karthikeyan, Ganesan. 2018. Acute rheumatic fever. Department of
Cardiology, Cardiothoracic Sciences Centre, All India Institute of Medical
Sciences, New Delhi, India.
5. Helena, Rachel. 2015. Acute rheumatic fever. BMJ; 351: 3443 – 3451.
6. G N Lucas. 2007. Diagnosis and treatment of rheumatic fever. Sri Lanka
Journal of Child Health; 36: 60-64.
7. Gipson, et al. 2009. Management of Childhood Rheumatic Fever. Journal of the
American Academy of Pediatrics; 124( 2): 747-757.
8. Mallory L. Downie, et al. 2017. Rheumatic Fever in infants and children:
pathophysiology and management. Paediatrics and International Child Health;
37(4): 248-258.

49